1

CARDIOVASCULAR SYSTEM
!0 marks
1. Name the different properties of cardiac muscle. Describe the properties and their physiological
significance
2. Define cardiac cycle. Name the events occurring in one cardiac cycle & give their normal duration.
Describe the mechanical events of cardiac cycle
Describe briefly the changes in following during cardiac cycle:
(With the help of a schematic diagram (WIGGER’S))
 Right ventricular pressure
 Left ventricular pressure
 Right atrial pressure/Jugular venous pulse
 Aortic pressure
 Pulmonary arterial pressure
 Ventricular volume
 ECG
 Heart sounds
3. Define & give the normal values of
a. Cardiac output
b. Stroke volume
c. Cardiac index
d. Peripheral resistance
e. End Diastolic Volume
f. End Systolic Volume
g. Ejection fraction
Name the determinants of cardiac output
Which methods are commonly used to measure cardiac output? What are the advantages &
disadvantages of each method
Describe the process of regulation of cardiac output
4. Define heart rate. Give its average value & range. Describe the factors influencing it
Describe the regulation of heart rate
5. What are heart sounds? Give the factors contributing to heart sounds. Describe the heart sounds
Draw a normal phonocardiogram and explain the various events in it
6. Define and give the normal range of:
 Blood pressure
 Systolic BP
 Diastolic BP
 Mean pressure
 Pulse pressure
Explain in detail the short term & long term regulation of BP
7. Circulatory shock
 Definition
 Types of shock
 Name the stages of circulatory shock
 Describe the immediate & long term compensatory mechanisms of hemorrhagic
shock
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5 marks
1. Depict diagrammatically the pacemaker potential & the influence of hormones. Explain the ionic basis.
What are the effects of sympathetic & parasympathetic stimulation of pacemaker potential?
2. Differentiate between pacemaker potential & ventricular potential
3. Briefly describe the origin & spread of cardiac impulse / Trace the electrical activity in the heart during
the process of depolarization with proper diagram & labeling
5. Describe the conducting system with a schematic diagram.
6. Draw a labeled diagram of JVP & give the physiological basis of genesis of each wave of JVP
7. Describe sino-aortic or Marey’s reflex or baroreceptor reflex /.What are buffer nerves? Explain their
role in regulation of Bp.
8. The physiology of coronary circulation – Diagrammatic representation of phasic flow, the special
features of coronary circulation & the factors influencing it
9. Draw ECG from lead II. Explain the physiological basis of genesis of the waves, and how to calculate
heart rate using an ECG
10. Discuss autoregulation. Describe its role in physiology briefly
11. Outline the changes in duration of systole & diastole that occur with changes in HR & discuss their
physiological consequences.
12. Explain the physiological basis of ECG abnormalities in heart blocks
13. What is laminar blood flow in blood vessels? What are the causes for turbulent blood flow?
14. Define Frank-Starling’s law. How is it related to cardiac output?
15. What are the effects of increased temperature on blood pressure?
3 marks
1. What is A – V nodal delay and its physiological significance?
2. Cardiac muscle can not be tetanized. Justify the statement with proper diagram & labeling
3. Define refractory period. What is the significance of this period in heart
4. Extrasystole is followed by compensatory pause- Explain the statement
5. Explain vagal tone and its maintenance. How it can be proved?
6. What is ejection fraction and its significance?
7. What is Starling’s law of muscle contraction? How is it applicable to cardiac muscle?
8. Describe the mechanism of autoregulation of cardiac output
9. Describe the factors affecting venous return
10. What is preload & after load in the heart & how it affects the functioning of heart?
11. Explain vagal tone & its maintenance. How it can be proved?
12. Write the physiological basis of splitting of second heart sound.
13. Draw ECG from aVR lead. Mention the significance of bifid QRS complex.
14. What is the significance of P-R interval in ECG?
15. State the reason for negative deflection in aVR lead
17. What is Bainbridge reflex? Briefly explain the mechanism of Bainbridge reflex
18. Explain the effect of increased intracranial pressure on systemic blood pressure
19. Explain the components of triple response giving their physiological basis.
20. What is Windkessel effect? Mention the physiological significance of it.
21. What is CNS ischaemic response? What is its significance?
22. Give the reason for increase in cardiac output during anxiety & excitement.
23. Mention the cardiovascular compensatory adjustments on assuming upright posture
24. Explain the effect of posture on cardiovascular system or explain the changes in blood pressure &
pulse rate during the change of posture.
25. Draw a diagram of radial pulse tracing and mention its clinical significance
26. Draw a labelled diagram of normal sphygmogram & Phlebogram
27. Significance of low arterial blood pressure in pulmonary circulation
28. Outline the unique features of cerebral circulation
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29. Write briefly on Cushing’s reflex

30. Discuss in brief – sympathetic and parasympathetic innervation of the heart.
31. What are the causes for hypovolemic shock? Brief out the physiological basis of treatment of
hypovolemic shock.
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1. CARDIAC CYCLE

Definition: The cyclical changes that take place in the heart during each beat (one systole and
one diastole)
Duration for one cycle = 0.8 sec
Phases:
 Atrial systole - 0.1 sec
 Atrial diastole- 0.7 sec
 Ventricular systole – 0.3 sec
 Ventricular diastole – 0.5 sec
ATRIAL SYSTOLE
 Contraction of atria & expulsion of blood into ventricles
 Contributes 25% of the ventricular filling
 Last phase of ventricular diastole
 Produces fourth heart sound
ATRIAL DIASTOLE
 Gradual filling of atria by blood brought by veins
VENTRICULAR SYSTOLE
 Contraction of ventricles & expulsion of blood into respective blood vessels
 Includes three phases
Isovolumetric contraction-0.05sec
Maximal ejection – 0.1 sec
Reduced ejection – 0.15 sec
Isovolumetric contraction
 Period between closure of AV valves & opening of semilunar valves
 Ventricles contract as closed chambers
 No change in the volume of blood in the ventricles
 Intraventricular pressure increases
Maximal Ejection phase
 Increase in intraventricular pressure
 Semilunar valves are forced to open
 Due to High Pressure gradient, blood is rapidly ejected out of ventricles
 About 2/3rd of stroke volume is ejected
Reduced ejection
 Due to decreased pressure gradient, the rate of ejection of blood is reduced
 About 1/3rd of stroke volume is ejected
VENTRICULAR DIASTOLE
 Filling of ventricles by the blood flowing from atria
 Includes five phases
Protodiastolic period – 0.04 Sec
Isovolumetric relaxation – 0.08 Sec
Rapid inflow – 0.11
Diastasis – 0.19
Atrial systole – 0.11
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Protodiastolic phase
 Ventricle relaxes
 Intraventricular pressure in less than the pressure in the aorta/Pulmonary Arteries
 Semilunar valves close to prevent the back flow of blood from arteries into ventricles
 Closure of SLV produces second heart sound
Isovolumetric relaxation
 Period between closure of semilunar valves & opening of AV valves
 SLV and AV valves are closed
 Ventricle relaxes as closed chamber
 No change in the volume of blood in the ventricles
 Intraventricular pressure decreases
Rapid inflow phase
 Intraventricular pressure less than intra atrial pressure
 Hence AV valves open
 Blood flows from atria to ventricle at a faster rate
 Turbulence due to rapid flow produces third heart sound
Diastasis
 Increase in intraventricular pressure
 Blood flow from atria to ventricle at low rate or static
Atrial systole
 Last phase of ventricular diastole
 Contributes additional 25% of ventricular filling
HEART SOUNDS
4 recordable heart sounds (Phonocardiogram)
 First heart sound-S1 – Caused by closure of AV valves. Occurs at the beginning of
ventricular systole
 Second heart sound S2- Caused by closure of Semi Lunar Valves. Occurs at the end
of ventricular systole
 Third heart sound- Due to rapid ventricular filling
 Fourth heart sound- Caused by atrial systole
HEMODYNAMIC CHANGES
Pressure and volume changes in the atria & ventricle during cardiac cycle
 Intra atrial pressure curve
 Intraventricular pressure curve
 Aortic pressure curve
 Ventricular volume curve
Intra-atrial pressure curve
3 Positive waves – a, c & v (caused by increase in intraatrial pressure)
2 Negative waves - x & y (caused by decrease in intraatrial pressure)
 ‘a’ wave - due to atrial systole
 ‘c’ wave – due to bulging of AV valve into the ventricles during isovolumetric
contraction
 ‘v’ wave – due to filling of atria after the closure of AV valves
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Intraventricular pressure curve: (Left ventricular pressure)

 During isovolumetric contraction phase – Pressure rises steeply due to a rise in
tension
 Maximum ejection phase – Maximum pressure (120 mmHg) develops as the ventricle
is contracting with a maximum force
 Reduced ejection phase – Pressure is less during this phase
Aortic pressure Curve:
 During diastole of heart, the aortic pressure is maintained at 80 mmHg
 During systole of the heart, it rises to 120 mmHg
Ventricular volume curve:
 End diastolic volume – During diastole, ventricular volume increases. The maximum
volume of blood in the ventricle at the end of diastole is called End Diastolic
volume. It is normally 130 ml.
 Stroke Volume: Volume of blood ejected out from ventricle during systole. It is 80 ml
 End Systolic Volume: The minimal volume of blood remaining in the heart at the end
of systole
ECG:
“P” wave = is due to atrial depolarization which occurs before atrial systole
“QRS” complex = is due to ventricular depolarization which occurs before ventricular
Systole
“T” wave is due to ventricular repolarization which occurs before ventricular diastole

Wiggers Chart
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2. CARDIAC OUTPUT
A) Definition:
Cardiac output (CO) – Volume of blood ejected by each ventricle / minute
Stroke volume (SV) – Volume of blood ejected by each ventricle / beat
Cardiac Index (CI) – Cardiac output / square meter of the body surface Area
End Diastolic Volume (EDV) – Volume of the blood in the ventricle at the end of diastole
Ejection Fraction (EF) – Fraction of the end diastolic volume that is ejected
Peripheral Resistance (PR) – The resistance offered to the blood flow in the peripheral
blood vessels
B) Normal values:
Cardiac output – 5 lts / min
Stroke volume – 70 ml/ beat
Cardiac index – 3 lts/ min/square metre of body surface area
End diastolic volume – 120 ml
Ejection Fraction -- 65%
METHODS TO DETERMINE CARDIAC OUTPUT
Direct method
Indirect method
 Fick principle
 Dilution principle (Dye. Isotope & Thermo dilution)
 Ballistocardiography
 Pulse pressure contour
 X – ray cardiometry
FICK PRINCIPLE
The cardiac output is calculated by the following formula
X
Q = ----------
A – V difference
Q – Blood flow
X – Amount of substance taken up by an organ
A -- V difference = Arterio venous difference in the concentration of a substance
As pulmonary blood flow is equal to cardiac output, pulmonary blood flow determined
by Fick principle is taken as cardiac output.
Pulmonary blood flow = amount of O2 taken by the lungs/minute
--------------------------------------------------
Arterio venous difference of O2
For example
Amount of oxygen taken by lungs / minute = 250 ml
(Determined by spirometer)
Arterial oxygen content = 20 ml / 100 ml of blood
(Estimated from any peripheral artery)
Venous oxygen content = 15 ml / 100 ml of blood
(Estimated from right atrium)
Pulmonary blood flow = 250
--------- X 100 = 5000 ml 0r 5 lts
20 - 15
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As pulmonary blood flow = cardiac output, CO = 5 lts

DYE DILUTION PRINCIPLE
A known amount of dye is injected into the peripheral vein and blood samples are
collected from the peripheral artery and the concentration of the dye in each sample is
estimated.
Cardiac output can be calculated by using the following formula:
Amount of the dye injected
-----------------------------------------
Mean concentration of the dye over a period of 1 minute
The commonly used dye is EVAN”S BLUE (T—1824)
C) Regulation of Cardiac output:
Cardiac output = Stroke volume x Heart rate
-------------------------------------
Peripheral resistance

Stroke volume = Myocardial contractility X End Diastolic Volume (EDV)

Heart rate End Diastolic Volume

(chronotropic) Cardiac Output (Pre load)

Myocardial Peripheral resistance

Contractility (After load)
(Ionotropic)

Cardiac Output Regulation

Heterometric regulation Homometric regulation

(Factors which cause an increase in the initial (Factors which do not cause any change
length of cardiac muscle before contraction) in the initial length of cardiac muscle
before contraction)
Heterometric regulation of cardiac output
I. Intrinsic factors regulating myocardial contractility
Frank – Starling Phenomenon:
The force of contraction is directly proportional to the initial length of the
cardiac muscle. The initial length of the muscle depends on the end diastolic
volume. Any increase in the EDV stretches the ventricular myocardium,
increasing the length of the muscle fiber
Importance:
– helps to match the stroke volume of the ventricles
– helps to maintain the minute output
– prevents venous engorgement
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Force Frequency relation:

Any increase in the frequency of heart beat increases myocardial contractility
within physiological limits. The increase in contractility is due to accumulation of
intracellular calcium ions
II. End Diastolic volume:
End Diastolic Volume (EDV) is the volume of blood in the ventricles
at the end of diastole. Any increase in the EDV increases the cardiac output by
increasing the stroke volume.
Mechanism: Increase in EDV  stretching of ventricular muscle fibres 
Increase in the length of fibres  stronger muscle contraction
Increase in cardiac output (Frank Starling’s law)
Factors influencing EDV:
i) Venous return
ii) Ventricular compliance
iii) Diastolic pause
iv) Atrial systole
Venous return: The volume of blood that returns to the atria through the veins in
one minute. This increases EDV & there by increases cardiac
output.
Factors influencing venous return:
1. Cardiac pump: The pumping action of ventricles increases
venous return by 2 forces:
 Vis – a – tergo (propelling force from behind):
- Left ventricular contraction during systole and
elastic recoiling of arteries during diastole push
the blood from aorta towards the right atrium
 Vis – a –fronte (suction force from front) – Right
atrial pressure:
- Less pressure in right atrium during diastole helps
in suction of blood from the great veins into the
right atrium
2. Capacity of venous reservoir: This factor is inversely
proportional to venous return .
Venoconstriction  decrease in venous capacity  increase
in venous return
3. Blood Volume: Directly proportional to venous return.
e.g., hemorrhage  decrease in blood volume  decrease in
venous return
4. Respiratory pump: Venous return increases during inspiration
Inspiration  negative intrathoracic pressure  suction of
blood into thoracic big veins  increased venous return
5. Muscle pump: Intermittent contractions of skeletal muscle
particularly leg muscle  squeeze the veins  increases the
flow of venous blood towards the heart  increase in venous
return
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6. Abdominal pump: Contractions of abdominal muscles 

compresses the great veins, pushing venous blood towards the
heart

Right atrial pressure

Blood volume Respiratory pump

Cardiac pump Venous return Vascular capacity

Abdominal pump Muscle pump

Ventricular compliance:
- refers to the stretchability of ventricular myocardium
- any increase in the compliance reduces EDV and thereby stroke volume
e.g constrictive pericarditis & pericardial effusion
Diastolic pause:
- refers to the duration of diastole of ventricles
- this influences the ventricular filling
- this factor is directly related to EDV within physiological limits
Atrial systole:
- contributes 20% of ventricular filling at rest
- influences EDV directly
e.g
- increase in atrial systole during exercise  increase in EDV
- in atrial flutter & fibrillation, the contribution of atrial systole in ventricular
filling is reduced
Homometric Regulation of Cardiac Output
I . Extrinsic Factors Regulating Myocardial Contractility
a) Neural factors:
Sympathetic stimulation: Releases nor-epinephrine  binds to β1 receptors  increases
cAMP  increase in intracellular calcium  increase in myocardial contractility
Parasympathetic stimulation: Releases acetylcholine  binds to muscarinic receptors
(M2)  hyperpolarization of SA nodal and myocardial cells  decrease in myocardial
contractility
b) Hormones:
Epinephrine & Nor-epinephrine: Bind to β1 receptors increase in cAMP  increase in
intracellular calcium  increase in myocardial contractility
Glucagon: Increases myocardial contractility by increasing intracellular calcium without
binding to β1 receptors
Thyroxine: Increases the myocardial contractility by increasing the metabolic rate.
c) Ions:
Sodium & Potassium – decreases the myocardial contractility
Calcium – increases the myocardial contractility
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d) Drugs:
β – blockers: e.g Propanaolol – block the β – receptors and decreases the myocardial
contractility
Calcium-channel blocker: e.g Verapramill – block the calcium channel  decrease in
intracellular calcium  decrease in myocardial contractility
Digitalis: Blocks Na+ - K+ ATPase  decrease in Na+ gradient across the membrane 
calcium accumulation inside the cell  increase in myocardial contractility
e) Coronary blood flow:
Decrease in coronary blood flow
↓
Hypoxia, hypercapnia & acidosis
↓
Decrease in myocardial contractility

Intrinsic Factors Extrinsic Factors

M
Sympathetic
Y
Frank-Starling phenomenon O Neural
C Parasympathetic
A
R Catecholamines
D Hormonal Glucagon
I Thyroxine
Force – Frequency relation A
L Ions (Na+, K+ & Ca2+)
C β-blockers
O
Drugs Calcium channel blockers
N
T Digitalis
R
A Coronary blood flow
C
T
I
L
I
T
Y

Influence of heart rate on cardiac output

- Direct relationship between heart rate and cardiac output
Increase in HR
↓
Increase in intracellular calcium
↓
Increase in force of contraction
 9

- This happens by two ways:

1. As a multiplying factor
2. Staircase phenomenon
(This relation is linear upto 180 BPM. Beyond this level, venous return falls 
decrease in cardiac output)
Influence of peripheral resistance on cardiac output:
- Initially, the variation in peripheral resistance tends to influence cardiac output
- But the indirect effects maintain the cardiac output
---------------------------------------------------------------------------------------------------------------------
3. BLOOD PRESSURE
Definition:
Blood Pressure : The lateral pressure exerted by the moving column of blood on the walls
of the arteries
Systolic BP : The maximum BP in the arteries during systole of the heart.
Diastolic BP : The minimum BP in the arteries during diastole of the heart.
Pulse pressure : The difference between systolic and diastolic pressure
Mean Arterial BP : The average BP in the arteries. This is calculated as Diastolic BP + 1/3 of
pulse pressure
Normal Values:
Blood Pressure : 120/80 mm Hg
Systolic BP : 90 – 140 mm Hg
Diastolic BP : 60 – 90 mm Hg
Pulse pressure : 40 mm Hg
Mean Arterial BP : 95 mm Hg

Regulation Of Arterial Blood Presssure:

Short – Term or Rapid Acting Mechanisms

1. Baroreceptor reflex
2. Chemoreceptor reflex
3. Cushing reflex
4. Stress relaxation & inverse stress relaxation
5. Capillary fluid shift
6. Hormones
Baroreceptor reflex:
- Also called as “Marey’s reflex” or “Sino-Aortic reflex”
- Initiated by increase in blood pressure
- Receptors are mechanoreceptors which respond to stretch in blood vessel wall
- Receptors are called “Baroreceptors”. They are present in the carotid sinus and
aortic arch
- This mechanism can correct 2/3rd of fall in BP
- The working range of BP is 60-200 mm Hg
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Increase in BP
↓
Stimulation of baroreceptors
(Carotid sinus and aortic arch)
↓
Stimulation of NTS (Nucleus of Tractus Solitarius) in medulla
↓

Inhibition of VMC Stimulation of CVC

(Vasomotor center) (Cardiovascular center-
Nucleus Ambiguus)

Inhibition of SNS
(Sympathetic Nervous Stimulation of vagus
System)

Decreased Increased vagal tone

sympathetic tone

Blood vessel Adrenal medulla Heart

Vasodilatation Decreased catecholamine Bradycardia

Venodilatation secretion

Net effect:
Decreased Peripheral resistance
&  Decrease in BP
Decrease in cardiac output

Decrease in BP
↓
Inhibition of baroreceptors
(Carotid sinus and aortic arch)
↓
NTS is not stimulated
↓

stimulation of VMC Inhibition of CVC

(Vasomotor center) (Cardiovascular center-
Nucleus Ambiguus)
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Stimulation of SNS
(Sympathetic Nervous Inhibition of vagus
System)

Increased sympathetic Decreased vagal tone

tone

Blood vessel Adrenal medulla Heart

Vasoconstriction Increased catecholamine Tachycardia

Venoconstriction secretion

Net effect:
Increased Peripheral resistance
&  Increase in BP
Increase in cardiac output

CNS ischemic response:

- This mechanism occurs due to ischaemia of brain
- This may result due to severe fall in BP below 40 mmHg
- If this response is specifically due to increase in intracranial pressure, it is called
as “Cushing reflex”
- The response is called “last ditch effort” as it tries to prevent the death of a
person
- The working range for this mechanism is 15-50 mm Hg
- It can correct 90% of the fall in BP
Decrease in BP (below 40 mm hg)
↓
Decreased blood flow to the brain
↓
Ischemia of brain
↓
Stimulation of VMC
(Vasomotor center)
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Stimulation of SNS
(Sympathetic Nervous
System)

Increased sympathetic
tone

Blood vessel

Vasoconstriction

Increase in BP

Chemoreceptor Reflex:
- Receptors respond to chemicals. So called as chemoreceptors
- Two types of receptors – peripheral & central chemoreceptors
- Peripheral chemoreceptors - Carotid bodies & Aortic bodies
- Stimuli for receptors : Hypoxia, Hypercapnia & Acidosis

Decrease in BP (<40 mm Hg)

Cerebral hypoxia, hypercapnia & acidosis

Stimulation of VMC
(Vasomotor center)

Stimulation of SNS
(Sympathetic Nervous
System)

Increased sympathetic
tone
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Blood vessel

Vasoconstriction

Stress relaxation and reverse stress relaxation mechanism:

Increase in BP  Stretching of blood vessels  Stress relaxation  Loss of
vasomotor tone  increased capacity of vascular bed  Pooling of blood 
Decrease in circulating blood volume  Decrease in BP

Decrease in BP Blood vessels are not stretchedIncrease in vasomotor tone 

decreased capacity of vascular bed Increase in circulating blood volume Increase
in BP
Capillary Fluid Shift Mechanism:

Increase in BP Decrease in BP

Increase in capillary Decrease in capillary

Hydrostatic pressure Hydrostatic pressure

Fluid Decrease in BP Fluid Increase in BP

Interstitial space Interstitial space

Hormones:
1. Catecholamines: Fall in BP  release of catecholamines (epinephrine &
norepinephrine) from adrenal medulla  Vasoconstriction & increase in cardiac output
 increase in BP
2. ADH: In large amounts ADH causes vasoconstriction  increase in BP
3. Glucocorticoids: Cortisol and corticosterone sensitize the vascular smooth muscle to the
action of catecholamines (permissive role)
4. Nitric oxide (Endothelium Derived Relaxing factor) :released by endothelium and acts
locally causing vasodilatation
Long Term Regulation of Blood Pressure
1. Renal body fluid mechanism
2. Renin-Angiotensin mechanism
3. Hormones – Aldosterone & ADH
 14

Renal body fluid mechanism:

Increase in BP Decrease in BP

Increase in renal blood flow Decrease in renal blood flow

Increase in GFR Decrease in GFR

Increase in urine formation Decrease in urine formation

Decrease in ECF volume Increase in ECF volume

Decrease in BP
Increase in BP
(Restoration of BP)
(Restoration of BP)

Renin – Angiotensin Mechanism:

Decrease in BP

Decrease in renal blood flow

Decrease in GFR

Renal ischemia or decreased

Na+ & Cl- at macula densa

Release of renin from

juxtaglomerular cells of
kidney
 15

Angiotensinogen Angiotensin I

Angiotensin II
&
Angiotensin III

Angiotensin II & Angiotensin III

Vasoconstriction reabsorption of Aldosterone ADH secretion

Na+ & Cl- secretion
(direct effect on kidney)

reabsorption of reabsorption of
Na+ & Cl- water

Increase in ECF volume

Increase in blood volume

Increase in blood pressure

Hormones Regulating Blood Pressure:

Aldosterone: Secreted from adrenal cortex in response to decrease in ECF volume.
Increases the reabsorption of Na+ & Cl- in kidney tubules. This causes
increase in ECF volume and blood pressure
ADH: Secreted from posterior pituitary. Increases water reabsorption from kidney 
increase in ECF volume and blood pressure
ANP: Secreted from atrial myocardium in response to increase in ECF volume facilitates
Na+, Cl-& H2O excretion into urine  decrease in ECF volume & blood pressure
 1

CVS -- 5 MARKS
1. . PACE MAKER POTENTIAL
• Potential that is produced in pacemaker cells of heart (mainly by SA node)
• R.M.P is low(–60mV )
• Unstable RMP - ie there is a slow depolarization between Action potentials,&
when it reaches threshold value action potential is triggered
• After repolarization again there is a slow depolarization & an action potential &
this process is repeated
• The slow depolarization between action potentials is the Pacemaker potential or
prepotential
Ionic basis of pacemaker potential
• Is due to decrease in Potassium efflux-forming the 1st part of the prepotential
• In the later part Transient (T) Ca ++ channels open up completing the
prepotential
• Slow depolarization occurs till threshold (firing level) is reached
• At the threshold level long lasting Ca ++ channels (L channel) open up causing
Action potential
• Action potential is largely due to Ca++ entry with very little contribution by Na+
• When AP reaches the peak the K+ channel open up K + efflux occurs &
repolarization follows

Action potential
Ca++(L)

Prepotential

1
 2

Effect of Stimulation of Sympathetic

• Stimulation increases the slope of prepotential (steep)
• Facilitates opening of Ca++ channel & Ca ++ entry 
• Reaches the firing level sooner
• So heart rate is rapid

Sympathetic
stimulation

Vagal stimulation

Effect of Stimulation of Vagus

• When the vagal fibre are stimulated the membrane becomes hyperpolarized &
the slope of the prepotential is  (slope is flat) because of  K permeability
• So there is a delay in reaching the firing level & the rate is slow
------------------------------------------------------------------------------------------------------------
2. CONDUCTING SYSTEM OF HEART

2
 3

Origin & Conduction of cardiac impulse

Internodal pathways
• Connects S-A node to A-V node
• Comprise of three bundles
• Anterior - Bachman
• Middle – Wenkebach
• Posterior - Thorel
Conduction Rate (meter/second)
• SA Node ---- -- 0.05 m/s
• AV Node ----- -- 0.05 m/s
• Atrial Pathway ----- 1 m/s
• Ventricular Muscle— 1 m/s
• Bundle of his ---------- 1 m/s
• Purkinje Fibres -------- 4 m/s
AV Nodal Delay
• AV Nodal Delay- O.1sec
• Allows Atria to complete its contraction
• Helps in proper filling of ventricles
• Decreases in stimulation of sympathetic nerves
• Increases in stimulation of vagus
Septal activation
 Depolarization of the ventricular muscle starts on the left side of the
interventricular septum and moves to the right across the mid portion of the
septum
 Wave of depolarization spreads down the septum to the apex of the heart &
activates the apex on either side
• From the apex the impulse passes along the ventricular walls towards the base of
the heart at the AV groove
• Endocardial surface of the ventricle is activated by the Purkinje fibres
• Impulse passes from the endocardial to epicardial surface of the ventricle
• The last part of the heart to be depolarized posteriobasal portion of the left
ventricle (Pulmonary conus & uppermost portion of the septum)

3
 4

3. THE PHYSIOLOGY OF CORONARY CIRCULATION

Arterial supply
• 2 coronary arteries.
• 20% humans - left coronary artery predominates.
• 50% - right coronary artery predominates
• 30% - equal supply by both.
• Main arteries lie on the surface, while small arteries penetrates the muscle mass.
Venous drainage
• 2 systems (superficial & deep)
• Superficial – Ends in coronary sinus & anterior cardiac vein.
• Deep system – opens directly in to the cardiac chambers.
Via 3 sets of vessels (arteriosinusoidal, arterioluminal, thebesian)
SPECIAL FEATURES OF CORONARY CIRCULATION
1. 1st branch to arise from aorta.
2. Blood flow is more during diastole.
3. Only organ to generate its own perfusion pressure.
4. Coronary arteries are functional end arteries, however, when occlusion occurs
slowly collaterals do develop.
5. Shortest circulation - Mean transit time. 6 – 8 seconds.
6. The veins drain directly in to the chambers adding deoxygenated blood to the
oxygenated blood.(Physiological shunt).
7. The diameter of the cardiac muscle fiber is smaller than the skeletal muscle fiber
& the capillary density is more than the skeletal muscle.
8. Autoregulation in coronary blood flow is present between 60 – 150 mmHg of
mean arterial pressure.
9. Hypoxia – Powerful vasodilator (Acts via adenosine)
ATP becomes ADP,  adenosine, acts on vessel wall  vasodilatation.
10. Oxygen extraction is nearly maximal even at resting heart rate,
Arterial PO2 = 19 ml %.
Venous PO2 = 7 – 8 ml %.

19 – 07 X 100 = 63 %
19
ie oxygen utilization by the cardiac muscle at rest is more ( 63%) than other organs
in the body (25%)
11. During systole the pressure in the subendocardial muscle is more than the outer
layers ( Epicardial).
Applied – subendocardium is maximally prone for ischemia.
12. Compensatory protective mechanism for the left ventricular subendocardium is
(1)  Capillary density.
(2)  Myoglobin content

4
 5

PHASIC FLOW OF CORONARY CIRCULATION

PHASIC CORONARY FLOW

During isovolumetric contraction
• Ventricles contract without any change in the length of the muscle fiber.
• Blood is not leaving the chamber.
• Blood flow to LV muscle reduces to zero
During ejection
Aortic pressure increases but the contracting ventricles are compressing the vessels,
thus the flow is present but less.
During isovolumetric relaxation
• Ventricles are relaxing.
• Sharp increase in the coronary blood flow
• Maximum coronary blood flow
During diastasis & late filling
• Aortic pressure decreases, so the coronary blood flow is less

Regulation of Coronary Blood Flow

Mechanisms involved:
1. Autoregulation
2. Neural regulation
3. Hormonal regulation
Autoregulation:
- Heart regulates its own blood flow. This is called as autoregulation
- Autoregulation is by two mechanisms – Myogenic & chemical

5
 6

Myogenic: The contraction and relaxation of the vascular smooth muscle

adjust the coronary blood flow when the blood flow is altered
Chemical regulation:
1. Hypoxia
2. Other metabolites ( CO2, H+, K+ & lactate)
3. Local vasodilators
Hypoxia: Increases coronary blood flow by causing vasodilatation
This is done by two mechanisms:
a. Direct effect:
Decreased myocardial oxygen
↓
Intracellular acidosis
↓
Less calcium binding
↓
Relaxation of vascular smooth muscle
↓
vasodilatation
↓
Increase in coronary blood flow

b. Trough adenosine: (Berne’s hypothesis)

 in myocardial metabolism
↓
Hypoxia & adenosine (from ATP)
↓
Vasodilatation
↓
Increase in coronary blood flow
Other metabolites : ( CO2, H+, K+ & lactate)
Decrease in coronary blood flow
↓
Accumulation of metabolites
↓
Vasodilatation
↓
Increase in coronary blood flow
Local vasodilators: (NO (EDRF), Prostacyclin & bradykinin)

Decrease in coronary blood flow

↓
Release of vasodilators by vascular endothelium
↓
Vasodilatation
↓
Increase in coronary blood flow

6
 7

Neural regulation:
Sympathetic nervous system (nor-adrenergic fibers)
• Stimulation of the  receptors  vasoconstriction decrease in coronary blood
flow (direct effect)
• Stimulation of  receptors  increase in heart rate & myocardial contractility 
accumulation of metabolites  vasodilatation  increase in coronary blood flow
(Indirect effect)
• Coronary vascular dilatation  Preservation of the supply to the heart.
parasympathetic nervous system
• Stimulation
-- directly  vasodilatation.
-- indirectly  vasoconstriction
Hormonal regulation:
1. Catecholamines: Same as that of sympathetic stimulation
2. Acetylcholine: Same as that of parasympathetic stimulation
3. Vasopressin: Vasoconsrtiction
4. Angiotensin: Vasoconstriction
5. Thyroxine: Increases metabolism  Hypoxia  vasodilatation  increase in
coronary blood flow
---------------------------------------------------------------------------------------------------------------------
4. Describe the factors affecting venous return
Venous return: The volume of blood that returns to the atria through the veins in
one minute. This increases EDV & there by increases cardiac output
Factors influencing venous return:
1. Cardiac pump: The pumping action of ventricles increases venous return by 2
forces:
 Vis – a – tergo (propelling force from behind):
- Left ventricular contraction during systole and elastic recoiling of
arteries during diastole push the blood from aorta towards the right
atrium
 Vis – a –fronte (suction force from front) – Right atrial pressure:
- Less pressure in right atrium during diastole helps in suction of
blood from the great veins into the right atrium
2. Capacity of venous reservoir: This factor is inversely proportional to venous
return .
Venoconstriction  decrease in venous capacity  increase in venous return
3. Blood Volume: Directly proportional to venous return.
e.g., hemorrhage  decrease in blood volume  decrease in venous return
4. Respiratory pump: Venous return increases during inspiration
Inspiration  negative intrathoracic pressure  suction of blood into thoracic
big veins  increased venous return
5. Muscle pump: Intermittent contractions of skeletal muscle particularly leg
muscle  squeeze the veins  increases the flow of venous blood towards
the hear t  increase in venous return
6. Abdominal pump: Contractions of abdominal muscles  compresses the great
veins, pushing venous blood towards the heart

7
 8

Right atrial pressure

Blood volume Respiratory pump

Cardiac pump Venous return Vascular capacity

Abdominal pump Muscle pump

3 marks:
1. Draw a labeled diagram of JVP & give the physiological basis of genesis of each wave of
JVP

Jugular Venous Pulse / Phlebogram

As the jugular vein is directly connected to right atrium, the right atrial pressure changes
are reflected in the venous pulse
3 Positive waves – a, c & v (caused by increase in intraatrial pressure)
2 Negative waves - x & y (caused by decrease in intraatrial pressure)
 ‘a’ wave - due to atrial systole
 ‘c’ wave – due to bulging of AV valve into the ventricles during isovolumetric
contraction
 ‘v’ wave – due to filling of atria after the closure of AV valves
 ‘x’ wave – due to downward movement of AV ring during ejection phase
 ‘y’ wave – due to the rushing of blood from atria to ventricles immediately after
the opening of AV valves

2. What is A – V nodal delay and its physiological significance?

 The delay in the conduction of cardiac impulse through AV node is called
AV nodal delay
 It is for about 0.1 second
Causes:
- Small & primitive fibers
- Presence of few gap junctions
- RMP is more negative
Significance:
- Gives sufficient time for completion of atrial contraction
- Prevents overlapping of atrial and ventricular systole
- Allows sufficient time for ventricular filling

8
 9

3. Cardiac muscle can not be tetanized. Justify the statement with proper diagram &
labeling / Define refractory period. What is the significance of this period in heart?

Refractory period: It is the period of excitation during which the muscle will not respond
to a second stimulus. It includes two phases – absolute & relative
Absolute refractory period: During this phase, even a stronger second stimulus will not
produce any response. It is for about 200 ms
Relative refractory period: During this phase, a second stronger stimulus may produce a
response. It is for about 50 ms
Significance:
- The whole contraction period of cardiac muscle is refractory period
- Cardiac muscle cannot be tetanized because of this long refractory period

4. What is ejection fraction and its significance?

The fraction of the end diastolic volume that is ejected out of ventricle is called ejection
fraction

It is calculated by: EDV – ESV EDV-End Diastolic Volume

----------------- ESV- End Systolic Volume
EDV
Normally it is about 65%

5. What is Starling’s law of muscle contraction? How is it applicable to cardiac muscle?

Starling’s law of muscle contraction: The initial length of muscle is directly
proportional to the force of contraction within physiological conditions.
Application to cardiac muscle: Increase in venous return  Increase in End Diastolic
Volume  Stretching of ventricular myocardium  Increase in the initial length of
cardiac muscle  increase in strength of myocardial contractility

9
 10

6. Explain the components of triple response giving their physiological basis.

Triple Response of Lewis:

A three phased cutaneous response that occurs from firm stroking of the skin is
called as triple response.
Phases:
Red reaction: Reddening along the line of stroke
Flare: Spread of reddish colour around the redline
Wheal: Local diffuse swelling along the line of stroke
Red reaction:
- Occurs within 10 seconds of application of the stroke
- It is due to relaxation of precapillary sphincters which increases blood
flow through capillaries
- This is mediated through histamine and bradykinin
- Not dependent on nerves
Flare:
- Occurs within 15-20 seconds of application of the stroke
- It is due to dilatation of arterioles, venules & relaxation of precapillary
sphincters
- Dependent on nerves. Caused by axonal reflex
Mechanism of axonal reflex:
Chemicals released from injured tissue
↓
Stimulate sensory nerve endings
↓
Sensory impulses to spinal cord
↓
Antidromic conduction of impulses through
Collateral fibers to blood vessels
↓
vasodilatation
Wheal:
- Occurs within 1-3 minutes of application of the stroke
- It is due to increase in permeability of capillaries and venules 
exudation of protein rich fluid from the capillaries and venules

10
 11

- Caused by chemicals such as histamine, bradykinin, P substance, K+ and

prostaglandins from the injured tissue
- Not dependent on nerves
7. What is Windkessel effect? Mention the physiological significance of it.
- Large arteries (Aorta & their branches) have more elastic & collagen
fibers in their walls. So these vessels are stretchable
- During systole, when excess blood is pumped into these vessels. They
expand to accommodate excess blood temporarily
- During diastole, when heart is not pumping, their elastic walls recoil, and
blood in them is propelled forward
- This property of large arteries is called Windkessel effect.
Functions:
- Pulsatile ejection of blood is converted to steady outflow
- Maximum exchange between blood & tissues is achieved
Significance:
- Helps to prevent too much rise of pressure in the arteries during systole
- Helps to maintain pressure & blood flow when heart is not pumping in
diastole
Applied:
In old age, loss of windkessel effect due to hardening of arterial walls leads
to hypertension
8. Draw a labelled diagram of normal sphygmogram

11
 1

CVS applied K.Senthamil selvi

1. ECG - normal diagrammatic representation & the changes in heart block,
myocardial infarction & ischemia

ECG changes in the following conditions:

Heart block –
I degree - PR interval prolonged
II degree –
a) Mobitz type 1 (Wenkebach phenomenon) – Gradual prolongation of PR interval
followed by dropping of one ventricular beat & followed by a normal beat
b) Mobitz type II – PR interval remains constant but A-V ratio is 6:5 or 8:7
Myocardial infarction –
Initially absence of Q wave & ST segment elevation
Later – Prominent Q wave , ST segment elevation & T wave inversion
Myocardial ischemia – ST segment depression
2. A person was brought to the hospital from the site of an accident. On examination he
was restless, extremely weak, skin was pale, cold and clammy with low BP, RAPID &
thready pulse.
What is your diagnosis?
What is the immediate treatment?
Diagnosis - hypovolemic shock.
Immediate treatment - to transfuse compatible whole blood
3. A patient complaints of dysponea at rest which is aggravated in supine posture.
O/E, he was found to have increased JVP & pedal edema.
What is your provincial diagnosis?
What is the clinical name of this dysponea?
Why there is edema formation?
Diagnosis – Left ventricular failure
Clinical name of the dysponea – Orthopnea
Pedal edema is due to damming up of blood in peripheral blood vessels which leads
to increase in peripheral capillary pressure & increased filtration
 2

4. Effect of ionic changes on ECG

Hyperkalemia –
Moderate – Tall T wave & ST segment elevation
Severe – Absence of P wave, Widened QRS complex, Tall T
Wave & Absence of ST segment
Hypokalemia – Prominent U wave, ST depression
Hypercalcemia – Shortened QT & QTc interval, widening of T wave & presence of J
waves
Hypocalcemia – Prolonged QT & QTc interval, & flattening of T wave
5. Mention the significance of bifid QRS complex.
Significance of bifid QRS complex – indicates bundle branch block
6. What is the significance of P-R interval in ECG?
- PR interval denotes the time taken by the impulse to travel from atria to ventricles.
- Prolongation of this interval indicates heart block
7. What is hypertension? Classify
Sustained elevation of Bp is called Hypertension (Systolic Bp > 140mmHg &
Diastolic BP > 90 mmHg)
Classification – Primary or essential hypertension & secondary hypertension
8. What is the cause of dysponea in Left ventricular failure?
Left ventricular failure (decrease in the ejection of blood from left ventricle) 
Pulmonary congestion (accumulation of blood in the pulmonary circulation) 
Increase in pulmonary capillary pressure  increased filtration of fluid into the
alveolar tissue (pulmonary edema)  dysponea
9. Physiological basis of development of orthopnea in heart failure
Orthopnea is dysponea in supine position. This occurs in left ventricular failure which
leads to pulmonary congestion. This congestion is aggravated in lying position &
dysponea occurs
10. Murmur- physiological basis
Murmur is abnormal heart sound that arises due to turbulence in the blood flow.
11. Why patients with severe aortic stenosis are more prone for MI?
In aortic stenosis, intraventricular pressure is increased to force blood through stenosed
valve. This causes compression of coronary vessels during systole. More over
myocardium requires more oxygen as the work load is increased. Both the factors lead
to deficiency of oxygen supply to myocardial cells. This myocardial ischemia makes
the myocardium to be prone for MI
12. The message of a close relative’s death causes fainting in a woman. What is the
condition and what is the cause?
It is called neurogenic shock. Also called as vasovagal attack.
Cause: Sudden autonomic activity causes vasodilation & pooling of blood in the lower
Extremities. So the blood flow to brain decreases causing fainting
13. Which phase of cardiac cycle murmur is produced by mitral stenosis?
Diastolic murmur
14. Physiological basis for hypertension in patients with chronic kidney diseases.
Hypertension occurs in chronic kidney diseases by two ways:
1) Reduction in the ability of kidney to excrete sodium and water
2) Release of renin from ischemic renal tissues which convert Angiotensin I to
 3

Angiotensin II (vasoconstrictor)
15. Reason for negative deflection in aVR lead
aVR lead looks at the cavities of the ventricles. Atrial depolarization, ventricular
depolarization & repolarization move away from the exploring electrode which is placed
in the right arm. .So P wave, QRS complex and T wave are all negative (downward)
deflections 4
16. MI- signs & symptoms, management
Signs & symptoms:
- severe pain behind the sternum which is radiating the lunar side of left upper arm
- profuse sweating
- cold extremities
- dysponea.
- anxiety & restlessness
- Variation in HR & BP
Management:
- Streptokinase, urokinase or tPA (tissue plasminogen activator) to dissolve the clots
- β-blockers to reduce the oxygen demand
- Anticoagulants like heparin or warfarin to prevent further spread of thrombus
- ACE inhibitors
- Calcium channel blockers
17. ECG changes in 1st degree heart block- diagrammatic representation

18. A 55 year old man with past history of angina pectoris complaint of loss of
consciousness for few minutes and recovery. Mention the probable diagnosis and
the physiological basis for the same.
Diagnosis – Stokes – Adams syndrome
Physiological basis – In patients with complete heart block, the heart rate becomes so
low that sometimes there may be periods of asystole lasting a minute or more. The
resultant cerebral ischemia causes dizziness and fainting
19. A man aged 60 years, suffering from chronic ventricular failure has engorged
neck veins and edema on the feet. Explain the underlying mechanisms for these
two signs
1. Ventricular failure  stasis of blood in the peripheral veins Engorged neck veins
2. Ventricular failure  stasis of blood in peripheral blood vessels increased
capillary pressure  increased filtration of fluid in to the interstitial spaces 
peripheral edema
20. Following Lumbar sympathectomy, a patient experiences orthostatic hypotension.
Give the reason
Orthostatic hypotension – Developing low blood pressure when changing posture
from lying to standing position
 4

Lumbar sympathectomy  loss of sympathetic tone over the blood vessels of lower
extremities  failure of vasoconstrictor compensatory mechanism during change of
posture  decrease in venous return  decreased cardiac output  hypotension
21. A 40 year old person complaints to the doctor that he is having severe pain
behind the sternum which is radiating the lunar side of left upper arm and with
profuse sweating .
ECG showed the ST segment elevation with T wave inversion.
a) Diagnose the above condition
b) What is the principle of management?
a) Diagnosis : M I – Myocardial infarction
b) Management :
- streptokinase, urokinase or tPA(tissue plasminogen activator) to dissolve
the clots
- β-blockers to reduce the oxygen demand
- Anticoagulants like heparin or warfarin to prevent further spread of
thrombus
- ACE inhibitors
- Calcium channel blockers
22. A 45 year old male had an attack of acute myocardial infarction
a) What will be the ECG findings?
b) What are the reasons for the ECG changes?
a) ECG findings : ST segment elevation & T wave inversion
b) Reason:
Delayed depolarization during early part of depolarization & rapid
repolarisation during latter part of repolarisation (due to loss of K+ ions from
ICF as a result of accelerated opening of K+ channels) makes the infarcted
area positive to the surrounding area.This causes elevation of ST segment.
23. Cardiac function tests in a patient showed the following findings:
Cardiac output = 3.5 lt/min; ejection fraction of 45% and stroke volume = 50 ml
a) Interpret these values comparing with the normal standard values
b) Briefly outline one method for estimation of cardiac output
a) Normal cardiac output- 5lt/min, Normal ejection fraction – 65% and normal
Stroke volume – 70ml.
As all the values are less than the normal values, the values indicate less
efficiency of heart.
b) DYE DILUTION PRINCIPLE
A known amount of dye is injected into the peripheral vein and blood
samples are collected from the peripheral artery and the concentration of the
dye in each sample is estimated.
Cardiac output can be calculated by using the following formula:
Amount of the dye injected
-----------------------------------------
Mean concentration of the dye over a period of 1 minute
The commonly used dye is EVAN”S BLUE (T—1824)
 5

24. Give the physiological basis of use of Beta blockers & calcium channel
blockers for the treatment of Hypertension.
Beta blockers block the beta receptors and prevent the binding of Norepinephrine
with the beta receptors and there by decrease the strength of contraction of heart. The
cardiac output decreases and there by BP also.
Calcium channel blockers block the calcium channels & prevent the entry of
calcium into the cardiac muscle and there by reduce the force of contraction
25. A patient has been brought to emergency with the history of severe blood loss
having intense thirst, O/E Hypotension, rapid thready pulse, cold pale skin with
tachypnoea
a) What is the diagnosis?
b) What might be the cause?
a) Diagnosis : Hypovolemic shock
b) Cause : due to activation of sympathetic nervous system
26. During a clinical examination, a medical intern comes across a murmur
heard at the mitral area of auscultation and suspects narrowing (stenosis) of the
mitral valve
a) What is the physiological basis of a murmur?
b) During which phase of cardiac cycle is the above murmur likely
to be produced?
a) Turbulence in the normal laminar flow of blood is heard as murmur.
b) During ventricular diastole, the flow of blood through the stenosed mitral
valve produces murmur
27. During recording of ECG in a male aged 35 years it was found that there is an
increase in the heart rate during inspiration & decrease during expiration.
a) What is this condition called?
b) Explain the basis
a) Condition : Sinus arrhythmia
b) Basis : During inspiration – impulses in the vagi from the stretch receptors of
the lungs inhibit the vagal tone and the heart rate increases.
28. In some individuals quiet standing causes fainting
a) What is the cause for fainting?
b) How will you treat?
a) Cause : Venous pooling of blood – pulling of blood into the capacitance vessels
increased filtration pressure in the capillaries  Decreased venous
return  decreased cardiac output decreased cerebral blood flow 
fainting
b) Treatment: The patients can be asked to make some little movements during
standing for a long time or they can be asked to wear stockings which
will prevent venous pooling.
29. A patient complaint of dysponea at rest, which is aggravated in supine posture. On
examination, he was found to have increased JVP & pedal edema. What is your
provincial diagnosis and what is the clinical name of this dysponea? Give the
physiological mechanisms of edema formation in this condition.
Diagnosis – Left ventricular failure
Clinical name of the dysponea – orthopnea
 6

Cause for edema :

Ventricular failure  stasis of blood in peripheral blood vessels increased
capillary pressure  increased filtration of fluid in to the interstitial spaces 
pedal edema
30. In aortic regurgitation diastolic pressure may fall all the way to zero. Explain
Normally the diastolic pressure in aorta is maintained at 80 mmHg by the complete
closure of aortic valve. In aortic regurgitation, due to incomplete closure of aortic valve
the diastolic pressure falls & in severe cases may fall to zero.
31. Explain why is the subendocardial muscle more susceptible to infarction?
The coronary blood vessels are compressed during systole. As the pressure in the left
ventricle is slightly higher in left ventricle, blood flows through the arteries supplying the
subendocardium only during the diastole. Because there is no blood flow during systole in
the subendocardial portion of the left ventricle, this region is prone to ischemic damage
and is the most common site of myocardial infarction
32.What is Stokes Adam syndrome? Such syndrome is an indication for pace maker
implantation for the safety of the patients. Give your reasons
Stokes Adam syndrome is characterized by dizziness & fainting due to cerebral ischemia.
This occurs in III degree heart block. The ventricular rate may be very low
(15beats/minute) and there may also be periods of asystole lasting for a minute or more.
33.What is Sick-sinus syndrome?
The disease affecting the SA node leads to marked bradycardia, accompanied by
dizziness & syncope. These subjects are treated by implanting artificial pacemakers
34. Why do some people faint when they shift from supine to standing position?
Shifting of posture from supine to standing  venous pooling of blood – pulling of
blood into the capacitance vessels  increased filtration pressure in the capillaries 
Decreased venous return  decreased cardiac output decreased cerebral blood flow
This is corrected by barereceptor reflex which cause reflex sympathetic
stimulation & vasoconstriction. But in people with autonomic insufficiency the
correction is not possible & the person faints
35. A patient came with a cardiac problem. On investigation, the ECG showed repeated
sequence of heart beat in which the P-R interval lengthened progressively until the
ventricular beat dropped. The P-R interval that followed each beat was normal.
What is the condition?
What is its type?
The condition is called II degree heart block.
It is Mobitz type I (Wenkebach phenomenon)
36. A 20 year young man c/o palpitation after climbing up 3 storied building
a) What is palpitation?
b) What is the cause for it?
Awareness of one’s own heart beat is called palpitation.
The cause is cardiac arrhythmia
37. What are the causes for hypovolemic shock? Brief out the physiological basis of
treatment of hypovolemic shock.
Causes – Haemorrhage, trauma, surgery, burns & fluid loss in vomiting, diarrhea,
excessive sweating, nephrotic kidney and adrenocortical insufficiency .
Treatment – Transfusion of whole blood or blood substitutes, keeping the subject in
 7

head-down leg-up position, hyperbaric oxygen therapy, keeping the subject in cool
ambience and administration of glucocorticoids
38. Explain the physiological basis of bradycardia in athelets.
Due to increased vagal tone caused by regular physical activity, athletes have
bradycardia
39. What is the ECG change in left bundle branch block?
Left axis deviation, prolonged & bifid QRS complex
40. What are murmurs? Systolic murmur is heard in mitral regurgitation – Explain
the statement
Murmurs are abnormal heart sounds. Mitral regurgitation occurs in mitral valve
incompetency – inability to close completely when ventricular systole begins. So during
ventricular systole the regurgitation of blood through the incompletely closed valve
produces murmur
41. Name the conditions causing systolic & diastolic murmur
Mitral stenosis – Diastolic murmur
Mitral regurgitation – Systolic murmur
Aortic stenosis – Systolic murmur
Aortic regurgitation – Diastolic murmur
42. A patient treated with intravenous injection of a drug developed hypotension,
rapid thready pulse, cold & clammy skin, rapid respiration & thirsty.
a) What is the type of shock he suffered?
b) What is your immediate treatment?
a) Anaphylactic shock
b) Administration of antihistaminase drugs & vasoconstrictors especially epinephrine
43. Briefly describe the mechanism of effect of following substances in controlling MI
a) Nitroglycerine
b) Streptokinase
c) Ca+ channel blocker
d) Aspirin
e) Follic acid & vitamin B12
a) Nitroglycerine - causes vasodilation of coronary vessels by activating Guanylyl
cyclase enzyme producing cGMP which inturn mediates the
relaxation of vascular smooth muscle
b) Streptokinase – causes lysis of clots inside the coronary vessels (thrombolytic
agent)
c) Ca+ channel blockers – reduces the strength of contraction of heart there by
reducing the O2 demand of cardiac muscle
d) Aspirin – Aspirin reduces clot formation by the following mechanism.
Arachidonic acid
↓ Cyclooxygenase (inhibited by low doses of aspirin)
Prostaglandins
↓
Platelet aggregation & consequent clot formation
 8

e) Follic acid & vitamin B12 – Homocysteine is a substance which damages

endothelial cells & induces atherosclerotic plaque in coronary & other
arteries. Vitamin B12 & Follic acid convert this into nontoxic
methionine thereby reduce its effect in producing atherosclerosis.
44. In a person of hemorrhagic shock with cold clammy skin, tachycardia & thready
pulse, which of the following may help in improving the condition – explain the
reason also
i) covering him with blanket / keeping him in a cool ambience
ii) keeping him in sit down posture / lying posture with head down & legs up
iii) as a drug of choice dopamine is preferred / nor adrenaline is preferred
i) Keeping the subject in cool ambience – to reduce body temperature
(Covering with blanket will elevate body temperatures which may cause
cutaneous vasodilation. This will worsen the condition)
ii) In lying posture with head down & legs up – increases venous return &
cardiac output
iii) Dopamine is preferred over noradrenaline – Dopamine causes vasodilation in
renal & mesenteric circulation where as vasoconstriction in other
areas. This causes increase in systolic pressure and no change in
diastolic pressure
45. What is the effect of
a. Increased PCO2
b. Kinins
c. Histamine
d. Angiotensin II — on blood flow to tissues
a) Increased PCO2 – vasodilation
b) Kinins – vasodilation
c) Histamine – vasodilation
d) Angiotensin - vasoconstriction
46. What is the effect of the following substances on blood vessels:
1. Angiotensin 2. Bradykinin 3. NO 4. Histamine
Angiotensin – vasoconstriction
Bradykinin –
NO - vasodilation
Histamine - vasodilation
47. What is the effect of histamine, Ach & adrenaline on coronary blood vessels
Histamine -- vasodilation
Ach – vasodilation
Adrenalin -- vasoconstriction
48. Give one example each for a substance which crosses BBB rapidly & slowly.
Substance that crosses BBB rapidly – drug like L- dopa
Substance that crosses BBB slowly – glucose
49. A patient C/O pain over the medial side of left upper arm. What may be the
probable cause? Explain briefly
Probable cause: Myocardial infarction
Cause for pain in the medial side of left upper arm:
- Referred pain
 9

Explanation:
Heart & inner side of left upper arm develop from the same embryonic
Segment or dermatome and supplied by same spinal nerve root. So the pain
arising from heart due to myocardial infarction is referred to inner/medial
side of left upper arm
50. A patient who has got admitted in a hospital for infection with gram negative
bacteria has developed the following features. High fever, marked vasodilation,
development of micro blood clots.
i) What type of shock he has developed?
ii) Why there is disseminated intravascular coagulation?
i) Type of shock – Septic shock
ii) Cause for development of micro blood clots – Endotoxins, the cell wall
lipopolysacharides produced by the bacteria initiate a complex series
of coagulant reactions.
51. A person who stands most of the time has developed large, bulbous protrusions of
the veins beneath the skin of the entire leg.
i) What is the abnormality called?
ii) What treatment can be given?
i) Abnormality: Varicose vein
ii) Treatment: Surgery
52. What is orthostatic hypotension? What are the causes for it?
Orthostatic hypotension: Fall in blood pressure on sudden standing
Causes:
- Damage of sympathetic nerve fibers ( e.g Diabetes mellitus & syphilis)
- Administration of sympatholytic drugs
- Primary autonomic failure
53. A 35 year old man comes to you with his ECG recording. As a first year student,
what are the informations you can collect regarding his cardiac functioning?
Heart rate from R-R interval, Heart block (P-R interval),Myocardial infarction
& myocardial ischemia (S-T segment) bundle branch block (QRS complex) & Axis
deviation
54. What is the clinical importance of inversion of “T’ wave in ECG?
Indicates myocardial ischemia
55. A 45 year old patient complaints of chest pain and difficulty in breathing at rest.
He develops pedal edema.
i) What is the condition?
ii) What is the cause for pedal edema?
i) Condition: Congestive heart failure
ii) Cause for pedal edema: Failure of heart to pump blood  stasis of blood in
the peripheral blood vessels  increased capillary pressure  increased
filtration of fluid in to the interstitial spaces  Accumulation of fluid in the
interstitial spaces (edema)
56. Explain bradycardia and pulse deficit. What are the causes for the above two?
Bradycardia – Decreased heart rate.
Causes: Athletes (increased vagal tone), increased intracranial pressure (Activation of
Cushing reflex),Myxoedema (decreased receptor number & activity to
 10

Epinephrine), Obstructive jaundice (inhibition of SA node by bile salts), Heart

blocks, Propanolol(β blocker) & Digitalis (vagal nuclei stimulation).
Pulse deficit – Decrease in the pulse rate when compared to heart rate.
Causes: Occurs in atrial fibrillation and in some ectopic rhythm. Some ventricular beats
are so weak that they fail to produce an adequate stroke volume to cause pulse.
Hence there is difference between pulse rate & heart rate
57. What circulatory changes occur after burns and discuss the pathophysiology of
them?
- Circulatory shock – due to fluid loss as plasma is lost as exudate from the
capillaries in the damaged areas
Hypotension – due to loss of fluid and electrolytes
Increased hematocrit – due to hemoconcentration
58. What is the normal cerebral blood flow? Discuss briefly the factors regulating
cerebral blood flow.
Normal cerebral blood flow – 750 ml/minute
Factors regulating –
1. Cerebral vascular resistance:
Refers to resistance offered to the blood flow by the cerebral
blood vessels. This depends upon diameter of blood vessels and
viscosity of blood.
Diameter is influenced by :
Chemical factors:
PCO2 – Hypercapnia  vasodiation
PO2 - Hypoxia  vasodilation
H+ - acidosis of CSF or interstitial fluid of brain  vasodilation
Neural factors:
Sympathetic stimulation  vasoconstriction.
Parasympathetic stimulation  vasodilation.
2. Effective perfusion pressure:
Effective perfusion pressure = Mean arterial BP – internal jugular venous
pressure
As internal jugular venous pressure is very less, mean arterial BP is taken
as the effective perfusion pressure
3. Role of intracranial pressure:
i) Monroe Kellie Doctrine – The total volume of the contents of skull
(brain,CSF & blood vessels) at any time
Remains constant
E.g
a) increase in blood flow reduction in CSF
b) increase in CSF ( increased intracranial pressure)  compression
of blood vessels  decreased blood flow
ii) Cushing reflex :
Increased intracranial pressure  compression of cerebral blood
vessels  decrease in cerebral blood flow  activation of sympathetic
nerves  vasoconstriction  increase in systemic blood pressure 
restoration of blood flow
 Respiratory system

10 marks
1. Describe the mechanism of respiration
2. Describe the process of transport of O2 & CO2 in the lungs.
3. Draw a labeled diagram of respiratory centers. Discuss the neural & chemical regulation of
Respiration

5 marks
1. List out respiratory & non respiratory functions of lungs
2. Illustrate graphically changes occurring in IPP, Intra alveolar pressure & TV during normal breathing
Explain the significance of negative IPP.
3. Describe about surfactant & its functions
4. Draw spirogram. Define & give the normal values of lung volumes & capacities
5. What are the salient features of pulmonary circulation?
6. Draw the normal ODC curve. What is the significance of sigmoid shape of the curve? Describe the
factors influencing the curve
7. What is Bohr effect & Haldane effect?
8. Explain chloride shift and its significance
9. Draw the respiratory centers, its interconnections among themselves & their afferent
connections from the lungs with their proper labeling ( showing + or – to show the influences)
Describe the genesis of normal rhythm.
10. Define & give the normal value of vital capacity. Describe the factors influencing vital capacity
11. Explain the compensatory mechanisms when a individual is exposed to hypoxia at an high altitude

3 marks
1. Define compliance. What is its significance? What are the factors that influence compliance?
2. What is dead space? What are the two types? Give the normal values. Describe a method to measure
3. FRC- normal value & functional importance.
4. What is timed vital capacity? What is its significance?
5. Draw the respiratory membrane & label its component
6. What are the factors affecting diffusion of gases across the respiratory membrane?
7. Give the comparison of diffusing capacity of O2 & CO2 in the lungs.
8. What is the significance of low arterial pressure in pulmonary circulation?
9. Describe the law of Laplace as it relates to pulmonary function
10. What is the reason for shifting of O2 dissociation curve to right during muscular exercise?
11. Give a short account on peripheral chemoreceptors.
12. What is the role of BBB in regulation of respiration?
13. What is acclimatization? What are cardiorespiratory changes that occur at high altitude?
 RESPIRATORY SYSTEM
10 marks

1. Draw the respiratory centers. Explain in detail the mechanism of neural regulation
of respiration.
Respiratory Centers

Medullary centers Pontine centers

Dorsal Group Ventral Group Apneustic center Pneumotaxic center

Of neurons of neurons

NERVOUS CENTERS FOR RESPIRATION

PONS
inhibits

MEDULLA

Respiratory Centres:
Medullary respiratory Centers
a) Dorsal respiratory group (DRG) of neurons
b) Ventral respiratory group (VRG) of neurons
Pontine respiratory centers:
a) Pneumotaxic center (Upper pons)
b) Apneustic Center (lower pons)
PNEUMOTAXIC CENTRE:
Location: Located bilaterally in the upper pons (Nucleus Parabrachialis)
Functions: Shortens inspiration through ‘Apneustic center’ & switching
off the ‘DRG’  Increases respiratory rate & decreases the depth of
respiration.
APNEUSTIC CENTRE:
Location: Located bilaterally in the lower part of the pons
Function: Prevents the switch off of the ‘DRG’

’ Increases the tidal volume & duration of inspiration

Deeper and more prolonged inspiratory effort (Apneusis)

DRG:
Location: Located in the nucleus of Tractus solitarius (NTS) of medulla.
Function: Spontaneous rhythmic discharge of impulses
 2

Causes inspiration
(impulses are called ‘inspiratory ramp signals’ )
VRG:
Location: Located lateral & ventral to DRG in the nucleus ambiguus.
Function: Discharge impulses during forced breathing
Inactive during quiet breathing.
Pre-Bert Zinger Complex:
Location: On either of medulla between nucleus ambiguus & lateral reticular
nucleus.
Functions: Initiate the respiratory rhythm.
Experimental evidences:
Complete transection of brain stem above the pons breathing continues
Complete transection of the brain stem below medulla breathing stops
Section at mid pontine level Apneusis (arrest of respiration in inspiration)
Section between pons & medulla rhythmic, but irregular respiration
Mechanism of respiratory rhythm:
DRG Neurons (Dorsal Respiratory Groups of Neurons at Medulla)

Discharge of impulses steadily & spontaneously (Called as inspiratory ramp signal)

Steady & Sustained contraction of inspiratory muscles.

Expansion of chest wall & lungs.

Entry of air into the lungs (Inspiration)

Impulses through vagal afferent fibers & impulses from pneumotaxic center.

Arrest of inspiratory ramp from DRG.

Relaxation of inspiratory musles.

Recoiling of lung & chest wall.

Air is expelled out of lungs (Expiration)

Interconnections Between Respiratory Centres

Upper Pons: Pneumotaxic

Center

-
Lower Pons: Apneustic
Center
-
+
Medulla: Ventral Respiratory Dorsal Respiratory
Neurons Neurons
+ -
Inspiratory Muscles Vagal Afferents

Inspiration From Lung

Factors That Influence Respiratory Centers:

REFLEXES HIGHER CENTERS

 3

Herring-Breuer Reflex Cerebral Cortex

Sneezing Reflex Limbic System
Coughing Reflex Hypothalamus
Swallowing Reflex
Speech
RESPIRATORY CENTERS

DRUGS PERIPHERAL RECEPTORS

Catecholamine Baroreceptors
Caffeine, Nicotine Chemoreceptors
Anesthetics J - receptor
Proprioceptor
Pain receptor
Thermoreceptors
Higher centers:
Cerebral cortex – voluntary control over respiration
Limbic system – control ventilatory changes during emotions
Hypothalamus - Influences ventilatory changes to temperature
Peripheral receptors:
Baroreceptors: Stimulation of Baroreceptors  inhibits respiratory centers
Chemoreceptors: Stimulation of chemoreceptors  stimulation of respiratory
Centers
J – receptors: Stimulation of J receptors  apnoea followed by tachypnoea
Proprioceptor: Stimulation of propioceptors  stimulates breathing
Reflexes:
Herring – Breuer reflex: When tidal volume increases above 1000 ml 
stimulation of pulmonary stretch receptors arrest of inspiration 
initiates expiration  increase in respiratory rate
Sneezing reflex: Irritation of nasal mucosa  deep inspiration followed by
explosive expiration through nose
Coughing reflex: Irritation of the tracheobronchial mucosa  deep inspiration
followed by explosive expiration through mouth
Swallowing reflex: Swallowing  stops respiration (deglutition apnoea)
Drugs : Catecholamines, caffeine, nicotine & nikethamide  stimulates respiration
Anaesthetic agents & sedatives  inhibits respiratory centers ↓ventilation
-------------------------------------------------------------------------------------------------------
2. Where is chemosensitive area situated? Describe the chemical control of
respiration.
The activity of the respiratory center is altered by the variation in the chemical
composition of plasma, CSF and interstitial fluid of the brain.
Chemicals that alter the activity of the respiratory center
1) Carbon dioxide (CO2)
2) Oxygen (O2)
3) Hydrogen (H+)
Mechanism of action of the chemicals on respiratory centers.
The chemicals act through chemoreceptors
Types of Chemoreceptors:
Peripheral chemoreceptors
Central chemoreceptors

Peripheral Chemoreceptors
Includes aortic bodies & carotid bodies
Location: -
 4

- Carotid bodies are located on either side near the bifurcation

of common carotid artery.
- Arotic bodies are located near the arch of aorta.
Afferent nerve:
- Sinus nerve (Branch of IX cranial nerve from carotid bodies)
- Aortic nerve (Branch of X cranial nerve from aortic bodies)

Central chemorceptors:
Location: Located in the ventral surface of the medulla.
Function: Monitor the H+ ion concentration of CSF & interstitial fluid of the
brain.
Ventilatory Responses to oxygen, Co2 & H+ ions.
Ventilatory response to O2 content:
(Effect of Hypoxia on Respiration)

PO2 in inspired air

Alveolar PO2

Arterial PO2 (below 60mm Hg)

Stimulation of peripheral Chemoreceptors

Activity of respiratory center

Contractility of inspiratory muscles

Ventilation

Ventilatory response to CO2

(Effect of Hypercapnia on respiration)
 5

Hypercapnia ( PCO2 in the inspired air)

Aleveolar PCO2

Arterial PCO2

Arterial H+ PCO2 of brain CSF

Activity of peripheral H+ ions of brain CSF

Chemoreceptors
Activity of central
Chemoreceptors

Activity of respiratory center

Ventilation

Ventilatory response to H+ ions

(Effect of acidosis on respiration)

Diabetic ketoacidosis, starvation ketoacidosis, Loss of alkali in diarrhoea, renal

failure to excrete H+ ions.
Accumulation of lactic acid

In arterial pH (Metabolic acidosis)

Stimulation of peripheral chemoreceptors

Stimulation of respiratory center

Increase of pulmonary ventilation

Overall chemical regulation of respiration

1. H+ ions in ECF of brain 1. Arterial PCO2 (Hypercapnia)

2. Arterial PCO2 2. Arterial H+ (acidosis)

3. Arterial PO2 (Hypoxia)

Central chemoreceptors Peripheral chemoreceptors

at medulla (Carotid body, aortic body)

Stimulation of respiratory Centers

Ventilation

-----------------------------------------------------------------------------------------------------
3. Describe the process of transport of Gases
Transport of Oxygen
Oxygen is transported by the blood from the lungs to tissues
 6

This transport can be dealt under the following events

- Uptake of oxygen in the lungs by pulmonary blood
- Transport in the blood
- O2 dissociation curve and the factors influencing it
- O2 delivery to the tissues
Uptake of O2 in the lungs
Due to the pressure gradient between alveolar oxygen & pulmonary capillary blood
oxygen, oxygen diffuses from alveolus into the pulmonary capillary blood

Transport in the blood

Oxygen is transported in the arterial blood in two forms
- In dissolved form (3%)
- In combination with hemoglobin (oxyhemoglobin) (97%)
In dissolved form
O.3 ml of O2 is dissolved in the plasma of 100 ml of blood
The dissolved oxygen is proportional to PO2
In combination with Hemoglobin
Oxygen from alveolus

Enters into the blood

Combines with Hb by the process of Oxygenation

Steps involved

Hb4+O2 Hb4O2
Hb4O2+O2 Hb4O4
Hb4O4+O2 Hb4O6
Hb4O6+O2 Hb4O8

i.e., four oxygen molecules combine with one molecule of hemoglobin

O2 carrying capacity of Hb
1 molecule of Hb - 4 molecules of O2
1 gm of Hb - 1.34 ml of O2
15 gms/100 ml of blood - 1.34 X 15 = 20 ml of O2
Oxygen – dissociation curve
- Curve obtained by plotting the relationship between PO2 (partial
pressure of oxygen) and the percentage of Hb saturation
- the percentage saturation of Hb increases with the increase in PO2 of
arterial blood
- the curve is sigmoid shaped due to variation in the affinity of Hb to O2 at
varied atmospheric PO2
 7

- the pleateau (upper flat part) of the curve is the loading zone which is
related to the process of O2 uptake in the lungs
- the steep portion the curve is the dissociation (unloading) zone which is
concerned with the O2 delivery in the tissue
O2– Dissociation Cuve

97

90
%
s 75
a
t
u
r 50
a
t
i
o
n

PO2 (mm Hg)

-At PO2 of 26 mm Hg – 50% saturation (p-50)
-At PO2 of 40 mm Hg – 75% saturation (Venous blood)
100

-At Po2 of 95 mm Hg – 97% saturation (Arterial blood)

Curve shifting to Right
- signifies the decreased affinity of Hb for O2
Factors causing right shift
- Decrease in PO2 (hypoxia)
- An increase in Pco2 (Bohr’s effect)
(loading of Co2 by the blood causes unloading of oxygen from blood to
tissues)
- A decrease in the pH of blood
- An increase in the temperature
- An increase in the concentration of 2,3 – BPG
Factors causing left shift
- Decreased PCO2 of blood
- Increased pH of blood
- Decreased temperature
- Fetal Hb
 8

Delivery of O2 to body cells per minute

Arterial O2 content = 20 ml / 100 ml of blood
Venous O2 content = 19 ml / 100 ml of blood
Cardiac out put = 5 lt / minute
O2 delivery to the entire body /minute = 20-15/100 X5000 = 1000 ml or 1lt/mt
Transport of CO2
CO2 is transported by blood from tissues to lungs
The transport of Co2 can be described under the following events
- Uptake of CO2 by the blood in the tissues
- Transport in the blood
- CO2 dissociation curve
- CO2 delivery in the lungs
Uptake of CO2 by the blood in the tissue
- The pressure gradient is the motive force for the diffusion of CO2 from
tissue cell to the capillary blood

Transport of CO2 in the blood

CO2 is transported in the blood in three forms
- In dissolved state (7%)
- In bicarbonate form (70%)
- In carbamino compound form (23%)
In dissolved form
0.3 ml of CO2 is transported from tissues to lungs in dissolved form
 9

In bicarbonate form
CO2 is converted into bicarbonate inside the RBC and then diffuses into plasma
-the steps involved are
CO2 in the tissues

Enters into the blood

Enters into the RBC

Combines with H2O to form carbonic acid in the presence of enzyme “carbonic
Anhydrase”

Carbonic acid dissociates into bicarbonate ions (HCO3-) and Hydrogen ions (H+)

Diffusion of bicarbonate into the plasma and H+ are buffered by hemoglobin

Chloride Shift:

- Diffusion of HCO3- out of RBC into plasma  less negative inside to

neutralize this effect negatively charged chloride ions diffuse from
plasma into the RBC
- this movement of chloride ions into the RBCs is called chloride shift

In carbamino form
CO2 + Aminogroup of plasma proteins – Carbamino proteins
CO2+ Aminogroup of Hb - Carbaminoglobin
CO2 dissociation curve
- Curve obtained by plotting the relationship between PCO2 and total
CO2 content of the blood
- the total CO2 content of the blood is directly proportional to PCO2 of
the blood
Factors affecting the curve
1) Oxygen
- Increase in PO2 causes increase in CO2 dissociation (Haldane’s effect)
(loading of O2 in lungs causes unloading of CO2)
- Shifts the curve to right
2) 2, 3 – DPG
- Competes with CO2 to combine with Hb
- Shifts the curve to right
 10

Delivery of CO2 in the lungs:

Involves the following steps
1. Release of CO2 from carbaminohaemoglobin into plasma
Entry of O2 into RBC – Oxygenation of Hb

Oxyhaemoglobin has low affinity for CO2

Release of CO2
2. bicarbonate is converted into CO2 by reverse chloride shift
Oxyhemoglobin releases H+ ions

Entry of HCO3- from plasma into RBC in exchange for Cl- ions
(Reverse chloride shift)
H+ combines with HCO3- to form carbonic acid

Carbonic acid dissociates into H20 & CO2

CO2 diffuses out of RBC into plasma

Diffusion of CO2 from plasma to alveoli

- Difference in the partial pressure of CO2 between alveoli and

pulmonary capillary blood makes the CO2 to diffuse out of blood
into the alveoli
Amount of CO2 delivered in the lungs
CO2 content of venous blood – 52 ml/100 ml
CO2 content of Arterial blood – 48 ml/100 ml
So CO2 delivered into the lungs – 4 ml / 100 ml
Total amount of CO2 transported = 4 /100 X 5000 (cardiac output) = 200 ml/minute

4. Describe the mechanism of respiration

Respiration is the process by which the body acquires oxygen and expels carbon di
oxide. It includes two phases:
1. Inspiration
2. Expiration
Inspiration:
- It is the process of air entering into the lungs
- It is an active process
Mechanism:
The contraction of the inspiratory muscles  expansion of thoracic cavity 
intrapleural pressure becomes more negativeincrease in transpulmonary pressure
 lungs expand  decrease in intrapulmonary pressure  air flows in to the lungs
Inspiratory muscles
Diaphragm – 75% of the increase in intrathoracic volume (increases the vertical
diameter of chest)
External intercostal muscles – increases the anteroposterior diameter of the chest
Accessory muscles during deep inspiration
Scalene and sternocieido mastoid muscles
Movement of ribs:-
a. Bucket handle movement
(upward and outward) - Increase in transverse diameter of thoracic cage
 11

b. Pump handle movement

(upward and forward) - Increase in anteroposterior diameter of thoracic cage

Volume changes during inspiration:

Tidal volume – Volume of air in the lungs increases by 500 ml
Pressure changes during inspiration
a) Intrapulmonary pressure
At the end of inspiration and expiration – 0mm Hg (same as that of
atmospheric pressure i.e., 760 mm Hg)
During inspiration ----- - 1 mm Hg (759 mm Hg)
During expiration ----- +1 mm Hg (760 mm Hg)
b) Intrathoracic pressure
At the end of inspiration and expiration -- - 2.5 mm Hg (757.5 mm Hg)
During inspiration ---- - 6 mm Hg (754 mm Hg)
During forced inspiration ---- - 30 mm Hg
 12

b) Work of breathing during inspiration

1. Elastic resistance work (65%)
2. Non elastic resistance
a) Viscous resistance work (7%)
b) Airway resistance work (28%)
Expiration:
- It is the process of air expulsion from the lungs
- It is a passive process
Mechanism:
The relaxation of the inspiratory muscles  recoiling of thoracic cavity 
intrapleural pressure is restored to normal  decrease in transpulmonary pressure 
lungs recoil  increase in intrapulmonary pressure  air flows out of lungs
Accessory muscles during forced expiration
Internal intercostal muscles & abdominal muscles
-----------------------------------------------------------------------------------------------------
 1

Respiratory system – Part 2

5 marks
Illustrate graphically changes occurring in IPP, Intra alveolar pressure & TV during normal
breathing. Explain the significance of negative IPP.
Pressure Changes:
a. Intrapulmonary pressure: (Pressure inside the alveoli)
At the end of inspiration & expiration ---- O mm Hg
(same as that of atmospheric pressure - 760 mm Hg)
During inspiration -- -1 mm Hg
(1 mm Hg less than the atmospheric pressure -759 mm Hg)
During expiration -- +1 mm Hg
(1 mm Hg more than the atmospheric pressure - 761 mm Hg)
b. Intrapleural pressure: (pressure inside the pleural cavity)
At the end of inspiration & expiration -- -2.5 mm Hg (757.5 mmHg)
During inspiration -- - 6 mm Hg (754 mm Hg)
During expiration -- returns back to -2.5 mm Hg
Cause for negative intrapleural pressure
Due to balance of two opposite forces
- recoil tendency of the lungs to collapse
- recoil tendency of the thoracic cage to expand
Significance of negative intrapleural pressure
- keeps the lungs in a stretched condition which prevents the collapse of lungs
- facilitates venous return
Transpulmonary pressure:
The pressure difference across the lung is called transpulmonary pressure
Transpulmonary pressure = Intrapulmonary pressure – intrapleural pressure
Volume changes
Tidal volume
During inspiration – The volume of air in the lungs increases by 500 ml.
During expiration – The volume of air in the lungs decreases by 500 ml.
 2

2. Describe about surfactant & its functions

 Surfactant is a mixture of phospholipids, proteins & ions
 The major phospholipid is dipalmitoyl – phosphotidylcholine (DPPC)
 The proteins are SPA, SPB, SPC and SPD
 Secreted by type II alveolar epithelial cells
Primary function:-
Reduces the surface tension of intra alveolar fluid by reducing the attraction between water
molecules
Secondary functions
 Stabilizes alveolar size during inspiration and expiration.
During inspiration, surfactant layer becomes thin. This can not reduce the surface tension.
The surface tension opposes further expansion of alveoli during inspiration. During
expiration, surfactant layer becomes thick. This reduces surface tension. This prevents
alveolar collapse during expiration. Thereby the alveolar size is stabilized

 Prevents pulmonary edema

Since surface tension of intra alveolar fluid is one of the causes for pulmonary edema, by
reducing surface tension the surfactant prevents pulmonary edema
 Increase in compliance
Increases compliance by decreasing the elastic recoiling of the lungs which tend to
collapse the lung
 Reduces the work of breathing by causing easy expansion of alveoli
 Facilitates the reopening of collapsed airway & alveoli
 Facilitates phagocytosis of micro-organisms by alveolar macrophages
Factors affecting the secretion of pulmonary surfactant
decrease in secretion increase in secretion
- Hyperbaric O2 therapy for a - Thyroid hormones
Long time
- Hypoxia - Glucocorticoids
- Cigarette smoking
- bilateral vagotomy - Vagal stimulation
 3

Applied (clinical significance)

RDS (respiratory distress syndrome of newborn)
Decreased surfactant secretion in new born babies (especially premature) causes difficulty in
breathing due to pulmonary edema & lung collapse (atelectasis) The infant may die if not
treated
---------------------------------------------------------------------------------------------------------------------
3. Draw spirogram. Define & give the normal values of lung volumes & capacities
Pulmonary Volumes
• Tidal Volume (TV)
• Inspiratory Reserve Volume (IRV)
• Expiratory Reserve Volume (ERV)
• Residual volume (RV)
Pulmonary Capacities
• Total Lung Capacity (TLC)
• Vital Capacity (VC)
• Inspiratory Capacity (IC)
• Functional Residual Capacity (FRC)

• Tidal Volume (TV)

Volume of air breathed in or out during quiet respiration.
Normal value – 500 ml
• Inspiratory Reserve Volume (IRV)
Maximum volume of air breathed in after a normal tidal inspiration.
Normal value – 3000 ml
• Expiratory Reserve Volume (IRV)
Maximum volume of air breathed out after a normal tidal expiration.
Normal value – 1100 ml
• Residual Volume (RV)
Volume of air remaining in the Lungs after a maximal expiration.
Normal value – 1200 ml
Pulmonary Capacities
TLC = IRV + TV + ERV + RV
VC = IRV + TV + ERV
IC = IRV + TV
FRC = ERV + RV
• Total Lung Capacity (TLC)
Volume of air in the lungs after a maximal inspiration
Normal value – 5800 ml
• Vital Capacity (VC)
Maximal volume of air expelled Out from the lungs by forceful expiration after a
maximum inspiration
Normal value – 4600 ml
• Inspiratory Capacity (IC)
Maximum volume of air which is inspired from the resting expiratory level
Normal value – 3500 ml
 Functional Residual Capacity (FRC)
Volume of air remaining in the lungs after normal expiration
Normal value – 2300 ml
 4

-----------------------------------------------------------------------------------------------------------------
4. What are the salient features of pulmonary circulation?
Pulmonary circulation
Right ventricle  Pulmonary artery Pulmonary capillariesPulmonary veins
Functions of pulmonary circulation
 Respiratory gas exchange (diffusion of O2 into the blood & CO2 out of the blood)
 Reservoir for left ventricle
 Removal of emboli & other particles from blood
 Removal of third from alveoli
 Absorption of drugs
 Synthesis of ACE (Angiotensin Converting Enzyme)
Special features of pulmonary circulation
1. Entire blood volume passes through the two lungs in one minute
2. Differences compared to systemic circulation
Pulmonary circulation Systemic circulation
1. Artery carries deoxygenated blood 1. Artery carries oxygenated blood
2. Vein carries oxygenated blood 2. Vein carries deoxygenated blood
3. Capillary gives up CO2& takes in O2 3. Capillary gives up O2 & takes in CO2
3. High capillary density. Blood flow is referred to as “sheet flow”. Helps in quick exchange of gases
4. It is a low pressure system.
Pulmonary artery – 15 mmHg
Pulmonary capillary – 6-8 mmHg
Cause for low arterial pressure
Pulmonary vessels are thin walled and distensible (high-compliance circulation)
Significance of low arterial pressure
Keeps the alveoli dry. This prevents the formation of pulmonary edema
5. Blood flow during respiration
Inspiration - blood flow is increased
Expiration - blood flow is decreased
6. Hypoxia  Vasoconstriction
 5

Significance:
Diversion of blood flow from a poorly ventilated area to a well ventilated region
7. Pulmonary blood flow is always equal to cardiac output in all physiological conditions
8. Effect of gravity on pulmonary circulation
Base of the lungs – more blood flow
Apex of the lungs – less blood flow
Significance of low pressure in pulmonary circulation:
Pulmonary circulation is a low pressure low resistance & high capacitance system
Pulmonary arterial pressure – Systolic pressure - 25 mm Hg
Diastolic pressure - 9 mm Hg
Pulmonary capillary pressure – 6-8 mm Hg
Significance of low pressure:
- Capillary pressure is less than colloidal osmotic pressure (25 mm Hg)

- Draws fluid from alveolar interstitial space into pulmonary capillaries

Keeps the alveoli dry

(a safety factor against pulmonary edema)
------------------------------------------------------------------------------------------------------------
5. Draw the normal ODC curve. What is the significance of sigmoid shape of the curve?
Describe the factors influencing the curve
Definition: Curve obtained by plotting the relationship between PO2 (partial pressure of
oxygen) and % of Hb saturation.
Characteristic features of curve:
 sigmoid or S-shaped
 Consists of two zones:
1. Loading zone refers to plateau (upper flat part)
- This is related to the process of O2 uptake in the lungs
- At PO2 of 100 mm Hg, the Hb is 97% saturated (Arterial blood)
2. Unloading (dissociation) zone refers to the steep portion of the curve at PO2
below 60 mm Hg
-concerned with O2 delivery in the tissues
-At PO2 of 40 mm Hg, the Hb is 75% saturated (venous blood)
Advantages of sigmoid shape of ODC
 Allows greater uptake of O2 at lungs inspite variation in alveolar PO2
 Tissues are supplied with O2 according to the needs of tissues
 Hb acts as a buffer for O2 & maintains tissue PO2 at 40 mm Hg.
Factors influencing ODC
Several factors affect the affinity of Hb for O2 & shift the ODC either to right or left
Shifting of curve to right
- Hypoxia
- Increase in PCO2
- Decrease in pH of blood (Accumulation of acidic products like lactic acid, CO2 etc.,)
- Increase in temperature
- 2, 3, DPG (diphosphoglycerate)
-
 6

Shifting of curve to left

- decreased PCO2 of blood
- increased pH of blood
- decreased temperature
- Fetal Hb
Effect of exercise on ODC
As exercise leads to increase in PCO2 (due to increase in metabolism), decrease in pH
(accumulation of acids) & increase in temperature (due to increase in metabolism), the
ODC is shifted to right

---------------------------------------------------------------------------------------------------------------------
6. What is Bohr effect & Haldane effect?
Bohr effect:
The effect of increased PCO2 on oxygen dissociation curve is called Bohr effect
In tissues, increase in PCO2 causes unloading of oxygen from Hb and loading of CO2
This shifts the curve to right
Significance of Bohr effect
This helps to supply oxygen to the tissues and remove CO2 from tissues
 7

Haldane effect:
The effect of increased PO2 on CO2 dissociation curve is called Haldane effect
In lungs, increase in PO2 causes unloading of CO2 from Hb and loading of oxygen
This shifts the curve to right
Significance of Haldane effect
This helps to deliver CO2 in the lungs so that it can be expelled out of lungs

----------------------------------------------------------------------------------------------------------------
7. Explain chloride shift and its significance
CO2 is converted into bicarbonate inside the RBC and then diffuses into plasma
-the steps involved are
CO2 in the tissues

Enters into the blood

Enters into the RBC

Combines with H2O to form carbonic acid in the presence of enzyme “carbonic Anhydrase”

Carbonic acid dissociates into bicarbonate ions (HCO3-) and Hydrogen ions (H+)

Diffusion of bicarbonate into the plasma and H+ are buffered by hemoglobin

Chloride Shift:

- Diffusion of HCO3- out of RBC into plasma  less negative inside  to

neutralize this effect negatively charged chloride ions diffuse from plasma into
the RBC
- this movement of chloride ions into the RBCs is called chloride shift
 8

RBC

Plasma

-
Significance of chloride shift:
- maintains the membrane potential of RBC
- causes movement of other ions into RBC which is followed by osmosis of water
into RBC. This increases the volume of RBC in venous blood. This increases the
hematocrit value of venous blood
---------------------------------------------------------------------------------------------------------------------
8. Define & give the normal value of vital capacity. Describe the factors influencing vital
capacity
Definition
Maximal volume of air expelled out from the lungs by forceful expiration after a maximum
inspiration (IRV + TV + ERV)
Normal values : Males – 4.8 lts & Females – 3.2 lts
Factors influencing :
1. Respiratory muscle power
2. Airway patency (resistance)
3. Compliance of the lungs
4. Elasticity and viscosity of lung
Physiological variations
• Increased in: Athletes, Europeans, Divers, Swimmers, Standing Posture, High altitude
• Decreased in: Old age, sedentary life & Obesity, Lying Posture
Pathological variations
Decreased in
Pulmonary congestion Myasthenia gravis
Emphysema Chronic asthma
Bronchitis Poliomyelitis
Pleural effusion Pulmonary fibrosis
Respiratory obstruction Pneumothorax
Asthma
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 9

3 marks
1. Define compliance. What is its significance? What are the factors that influence compliance?
Definition: The change in lung volume per unit change in transpulmonary pressure.
Normal value: 0.22 l/cm H2O
Factors that influence compliance:
- Surface tension
- Lung volume
- Phase of respiratory cycle
- Effect of gravity
Significance:
Compliance is increased in emphysema & old age, decreased in pulmonary congestion,
pulmonary fibrosis & pulmonary edema
--------------------------------------------------------------------------------------------------------------------
2. What is dead space? What are the two types? Give the normal values. Describe a method to
measure
Definition
The air in the respiratory tract that does not take part in the gas exchange process.
Types
Anatomical dead space
Physiological dead space
Anatomical dead space
The volume of air present in the conducting zone of respiratory passage, i.e. from nose to
terminal bronchiole
Physiological dead space
Total dead space which includes anatomical dead space + alveolar dead space.
Alveolar dead space
Air in the alveoli that does not take part in the gas exchange
Alveolar dead space caused by
1. Obstruction to pulmonary capillary blood flow (no perfusion)
e.g. pulmonary embolism
2. over ventilation of alveoli
e.g. emphysema and Bronchiectasis
Normal values
Healthy adult:
Anatomical dead space = Physiological dead space
Young males – 150 ml
Young females – 100 ml
Older subjects – 200 ml
Measurement of dead space
Anatomical dead space: Fowler’s method
Physiological dead space: Bohr’s equation
Fowler’s method
Quiet expiration

Deep breathing of pure O2

Breathing out slowly and evenly into a nitrometer

 10

No N2 in the earlier part (Area with Dots)

&
N2 concentration gradually rises in the latter part (Area of diagonal lines) and reaches 60%

Area of dots
Dead space = --------------- X Volume of expired air (TV )
Area of dots and diagonals
Measurement of Physiological dead space
Bohr’s equation:
TV (PACO2 – PECO2)
Dead space (VD) = -------------------------
PACO2
TV – Tidal volume
PACO2 – Partial pressure of CO2 in alveolar air
PECO2 – Partial pressure of CO2 in expired air
Increased physiological dead space
Pulmonary embolism
Bronchiectasis
Emphysema
Effect : Hypoxia
------------------------------------------------------------------------------------------------------------------------------
3. FRC (Functional Residual Capacity) - normal value & functional importance.
Definition
Volume of air remaining in the lungs after normal expiration
Normal value – 2300 ml (ERV + RV)
Measurement
• Spirometry cannot measure
• Thus Functional Residual Capacity (FRC) cannot be determined using spirometry alone.
• FRC can be determined by
1) Helium dilution technique
2) Nitrogen washout technique
Physiological significance
1. Helps in continuous exchange of gases between the lungs and blood between two breaths.
(Prevents the marked rise or fall of blood O2 and CO2 level between respirations)
2. Required for breath holding
3. Dilution of toxic inhaled gases
4. Reduces the work of breathing by preventing the collapse
 11

Conditions Affecting FRC

Increased in - Emphysema, COPD & Old age
Decreased in - Pulmonary fibrosis (scarring of lung tissue) & Atelectasis (collapse of lung)
---------------------------------------------------------------------------------------------------------------------
4. What is timed vital capacity? What is its significance?
TIMED VITAL CAPACITY (FORCED VITAL CAPACITY)
Definition:
It is the volume of air that can be expired with maximum effort after a maximal inspiration in a given
unit time
Components
FEV1 (forced expiratory volume in 1st sec)

FEV2 (forced expiratory volume in 2nd sec)

FEV3 (forced expiratory volume in 3rd sec)

TVC in normal individuals

FEV1% = FEV1
----------*100 = 80%
FVC
FEV2% = 90%
FEV3% = 100%
Significance
Helps in differentiating the obstructive lung diseases from the restrictive lung diseases
Obstructive lung diseases Restrictive lung diseases

FEV1 < 80 % FEV1 = normal

 12

5. Draw the respiratory membrane & label its components

---------------------------------------------------------------------------------------------------------------------
6. Give a short account on peripheral chemoreceptors.
Peripheral chemoreceptors are the sensory nerve endings which are present in the peripheral
blood vessels and stimulated by changes in O2 & CO2 content of blood
Location :
- Carotid sinus (carotid bodies)
- Aortic arch (aortic bodies)
Structure:
- 2 types of cells (type I & type II cells)
- Unmyelinated nerve endings are found at intervals between type I & type II cells
- Type I cells consists of dopamine which is released in hypoxia and stimulates the
nerve endings via D2 receptors
 13

Nerve supply:
- Carotid body -- By sinus nerve, a branch of glossopharyngeal (IX nerve)
- Aortic body --- by aortic nerve, a branch of vagus (X nerve)

Blood supply:
- 2000 ml/ 100 gm/ mt (highest blood flow in the body)
- O2 needs of the receptor cells are met by dissolved oxygen content
Mechanism of stimulation: Hypoxia  inhibition of K+ channels  decrease in K+ efflux
increase in Ca++ influx  depolarization of type I cells  release of neurotransmitter 
stimulation of afferent nerve endings
Effect of stimulation:
- Stimulation of peripheral chemoreceptors  increase in both rate & depth of
respiration
- Carotid bodies are seven times more effective in stimulating respiration than the
aortic bodies
- Not stimulated in anemia or carbon monoxide poisoining as dissolved O2 content
is normal
-------------------------------------------------------------------------------------------------------------------
7. What is acclimatization? What are the cardiorespiratory changes that occur at high altitude?
Definition:
Changes in body mechanisms to bring an adaptation of the person to the high altitude
Changes in Respiratory System
Hyperventilation
Hypoxemia (decreased O2 tension of blood) – stimulation of peripheral
chemoreceptors – hyperventilation – increased PO2 & decreased PCO2 (Starts within
the 1st few hours of exposure)
Increase in lung volumes & capacities
Hypertrophy of respiratory muscle power  ↑ chest size and somewhat ↓body size
high ventilatory capacity to body mass  Increase in lung volumes & capacities
 14

↑ Diffusion capacity
– ↑ pulmonary capillary blood volume
– ↑ lung volume
– ↑ pulmonary arterial pressure
Respiratory alkalosis
Hypoxia  Hyperventilation  Washout of CO2  Respiratory alkalosis (↑pH)
Shift of ODC curve to right
• ↑ in 2,3 DPG
• Hypoxia
Changes in Cardiovascular System
Hypoxia

Activation of sympathoadrenal system

↑in HR, CO & BP ↑ Muscle blood flow ↑ Coronary blood ↓in cutaneous &
(vasodilatation) flow Splanchnic
blood flow (vasodilatation)
(vasoconstriction) (Indirect effect)
 1

Respiratory system – Part 3

Hypoxia

1. What is hypoxia? Explain the different types of hypoxia with examples. Describe the
effectiveness of O2 therapy in various types of hypoxia
Definition: Decreased PO2 in the tissue is called hypoxia
- due to inadequate supply of O2 to tissue
- due to failure of tissue to utilize the available O2
Types:
a) Hypoxic hypoxia
b) Anemic hypoxia
c) Stagnant hypoxia
d) Histotoxic hypoxia
a) Hypoxic hypoxia
– decreased O2 tension of the arterial blood
– also called as arterial hypoxia
Causes:
– low PO2 in the inspired air (High altitude)
– hypoventilation (Asthma – Air way obstruction)
– diffusion of oxygen across respiratory membrane (Lung collapse)
b) Anemic hypoxia
– decreased O2 transport or O2 dissociation from Hb
Causes:
- decreased Hb content (anemia)
- decreased saturation of Hb (carbon monoxide poisioning)
c) Stagnant hypoxia
– Inadequate blood flow to the tissues
Causes :
– slow flow of blood (congestive heart failure)
– obstruction in blood flow (vasoconstriction)
d) Histotoxic hypoxia
– tissue can not utilize O2
Causes :
– paralysis of cytochrome oxidase enzyme (Cyanide poisoning)
Oxygen therapy
a) Hypoxic hypoxia - highly beneficial – O2 therapy increases the alveolar PO2 and also the
entry of O2 into the blood – increases the arterial blood content of O2 both in
dissolved and combined forms
b) Anemic hypoxia – moderately beneficial - helpful in increasing the dissolved oxygen
c) Stagnant hypoxia – less useful
d) Histotoxic hypoxia – not useful - as tissue is not able to utilize the oxygen that is
delivered.
---------------------------------------------------------------------------------------------------------------------
 2

2. What is cyanosis? Differentiate peripheral and central cyanosis

Cyanosis is a diffused bluish colouration of the skin and mucous membranes
Cause: caused by increased amount of reduced hemoglobin (deoxyhemoglobin)
To produce cyanosis the reduced Hb should be more than 5 gms / 100 ml of blood
Types
1) Peripheral cyanosis
2) Central cyanosis
Peripheral cyanosis
- Due to stagnant hypoxia
- Venous unsaturation is more
- only skin becomes bluish
Conditions which cause peripheral cyanosis
- cardiac failure
- shock
- exposure cold environment (Peripheral vasoconstriction --- stagnant hypoxia)
Central cyanosis

- Due to hypoxic hypoxia

- Arterial unsaturation is more
- Skin & mucous membranes become bluish
Conditions which cause central cyanosis
- congenital heart diseas
- AV admixture
- Lung diseases
- Presence of methaemoglobins and sulphaemoglobin
Reason for absence of cyanosis in the following condition
Anemic hypoxia: As the anemic patients have less hemoglobin, they can not produce
more than 5 gms of reduced hemoglobin / 100 ml of blood so cyanosis does not
occur
Histotoxic hypoxia: As tissues do not utilize oxygen, oxygen is not dissociated from Hb.
So reduced Hb is not formed in greater amounts (more than 5 gms/100 ml of
blood) to produce cyanosis.
Carbonmonoxide (CO) poisoning: Causes cherry red colour which hides the bluish
Colouration
---------------------------------------------------------------------------------------------------------------------
3. Decompression Sickness /Caisson’s disease /Dysbarism /sickness/Diver’s
palsy/bends
Definition: The symptoms produced when an individual ascends rapidly to sea level after
sufficient exposure to high atmospheric pressure in deep sea
Mechanism or physiological basis:
At high atmospheric pressure, nitrogen dissolves in the body fluids. As nitrogen is lipid
soluble, it get dissolved in the cell membranes & sphingomyelin of myelim sneath.
During rapid ascent, the gas (nitrogen) escapes from the tissue at a faster rate. This
forms bubbles which block the blood vessels producing tissue ischaemia & tissue death.
 3

Symptoms or features:
a) Pain in joints and muscles of legs (called as bends)
(Presence of bubbles in the myelin sheath of sensory nerve fibers in joints and muscles)
Paraesthesia – pricking & itching may follow
b) Temporary paralysis due to bubbles in motor nerve fibers
c) Chokes – shortness of breath due to bubbles in pulmonary veins
d) Myocardial ischaemia – due to bubbles in coronary blood vessels.
e) Brain damage due to bubbles in cerebral blood vessels.
Prevention:
Slow decompression (the ascend to the surface should not be faster than 3 km/ hour)
Treatment:
Recompression followed by slow decompression along with hyperbaric O2 therapy.
---------------------------------------------------------------------------------------------------------------------
4. Asphyxia
Definition:- Condition in which hypoxia (PO2) is associated with hypercapnia (PCO2) due to
obstruction in the air way.
Causes: Strangulation, drowning, tracheal obstruction (due to entry of food or choking) and
paralysis of diaphragm.
Stages:
I stage - Stage of hyperopnea
II stage - Stage of central excitation
III stage - Stage of central depression

I-Stage of hyperopnea:- (lasts for 1 minute)

Features
 increase in rate & depth of respiration
 Expiratory effort
 Dysponea, cyanosis
 Prominence of eyeballs
(due to stimulation of respiratory centers by PCO2)
II – stage of convulsions (lasts for a minute)
Features
 Violent expiration
 increased HR & systolic BP
 constriction of pupil
 exaggeration of all reflexes
 convulsions & loss of consciousness
(due to stimulation of respiratory centers by PCO2 & O2)
III- Stage of exhaustion & collapse (lasts for 2-3 minutes)
 Convulsions disappear
 HR & systolic BP
 Dilatation of pupil
 Gasping (shallow & low frequency respiration)
 Death
 4

5. Pneumothorax
- refers to presence of air in the pleural space
Cause: Either through a rupture in the lung or a hole in the chest wall (stab injury, gun shot
wound etc.,)
Types:
a) Open or sucking pneumothorax
b) Closed pneumothorax
c) Tension pneumothorax
Open or sucking pneumothorax:
The communication between the pleural space and the exterior remains open
Closed pneumothorax:
Hole through which the air enters the pleural space is sealed off.
Tension pneumothorax:
A flap of tissue lies over the hole in the lung or chest wall acts as a valve. This will allow
air to enter the pleural space during inspiration but does not allow air to exit during
expiration.
Features:
- Collapse of lung on affected side (As the pleural pressure becomes positive, the
elastic recoil of lungs leads to collapse)
- Mediastinum shifted towards normal side
- Respiratory distress (due to stimulation of respiratory centers by hypoxia and
hypercapnia)
--------------------------------------------------------------------------------------------------------------------
6. Periodic breathing
- Periodic breathing is characterized by alternate periods of apnoea and hyperopnea
Types:
1. Cheyne – stokes respiration
2. Biot’s breathing
Cheyne – stokes respiration – characterized by gradual waxing and waning, followed by a
period of apnoea
Condtions: Premature infants, High altitude, voluntary hyperventilation, heart failure
Physiological basis:
Hyperventilation  Wash out of CO2 (respiratory alkalosis) Inhibition of respiratory
Center Apnoea (cessation of breathing) Build up of PCO2 & in PO2 (Hypoxia and
hypercapnia) Stimulation of respiratory center Hyperopnea
(The cycle continues till normal breathing is restored)
Biot’s breathing: Abrupt apnoea & hyperopnea - No waxing and waning
Conditions: increase in intracranial pressure, morphine poisioning & damage to brain stem
-------------------------------------------------------------------------------------------------------------------
7. Mountain sickness
Symptoms that occur due to rapid ascend to high attitude are together called as mountain
sickness
Types:
a) Acute mountain sickness
b) Chronic mountain sickness
 5

Acute mountain sickness:

(Symptoms appear within a day after reaching the high attitude and last for 4-8 days)
Features:
fatigue, headache, insomnia, irritablity and palpitation
loss of co-ordination and memory, Euphoria and emotional changes
(Above features are due to mild cerebral hypoxia & also due to mild cerebral edema)
-Nausea, vomiting & diarrohoea
(due to distension of GIT by expansion of gases in hypoxia)
-Hyperopnea & dysponea
(due to stimulation of respiratory center by hypoxia)
Physiological basis
All the effects are due to hypoxia in high attitude
Treatment:
- Shifting the person to a lower attitude
- Hyperbaric O2 therapy to relieve hypoxia
- Glucocorticoids to reduce cerebral edema
- Carbonic anhydrase inhibitor ( reduce cerebral edema)
- Nifedipine (Ca+ channel blocker) to reduce pulmonary hypertension
Chronic mountain sickness (Monge’s disease)
Seen in long term residents of high attitude
Features:
Polycythemia, fatigue, pulmonary hypertension, right ventricular failure and heart
failure (due to chronic hypoxia)
---------------------------------------------------------------------------------------------------------------------
8.Oxygen toxicity
Increase in the amount of dissolved O2 -- increases the PO2 proportionally. This is called as
oxygen toxicity
Causes: Breathing O2 at a higher pressure
Conditions: Hyperbaric O2 therapy (100% O2 therapy for more than 8 hours)
Deep sea diving
Features:
On CNS:
Nausea, irritability, dizziness, disorient at facial twitching and convulsions.
On respiration:
- Congestion and irritation of the airway
- in surfactant
- Pulmonary edema
- Atelectasis (collapse of lung)
On special senses:
- Tinnitus (spontaneous ringing in the ear)
- Loss of equilibrium
- Blurring of vision
- Retrolental hyperplasia ((formation of an opaque membrane behind the lens)
Physiological basis:
Accumulation of oxidizing free radicals like super oxide (O3), hydrogen peroxide (H2O2) 
Oxidise the PUFA (Poly unsaturated fatty acids) & destroy the cellular enzymes
 6

9.Artificial Respiration
- Refers to ventilation of lung artificially when there is respiratory failure
Indications:
In subjects with respiratory deficiency but with a functional heart
Conditions: Drowning, gas poisoning, electric shock, overdose of sedatives, head injury
surgery etc.,
Methods:
Positive pressure
1. Instrumental
Negative pressure
2. Manual methods
Instrumental:
Positive pressure method – Lung is inflated with air +O2 mixture at positive pressures (used in
operation theater)
Negative pressure method – Alternate compression and relaxation of chest wall
Drinker’s mehod
Bragpaul method
Boyle”s apparatus
Manual methods
Holger – Neilson Method
Eve’s rocking method
Mouth to mouth breathing:
Mouth to mouth breathing:-
Mechanism - Subject in supine position
- Clean the mouth and nose of food, vomitus etc.,
- Head is extended backward
- Kneel on one side, open the mouth of subject and close the nose
- Exhale air smoothly into the mouth of victim
- This inflates the subject’s lungs
- remove the mouth to allow for passive expiration
- repeat this procedure three times to saturate the victim’s blood with O2
- continue the procedure regularly at the rate of about 12 times per minute

Advantages of this method:

- can be applied immediately and quickly
- simple and most effective (most effective because CO2 present in the expired air
directly stimulate the respiratory center and facilitate the onset of respiration)
- large tidal volume of about 1000 ml (1 liter can be obtained)
- Can be applied in all age groups.
 1
RESPIRATORY SYSTEM Applied K.Senthamil selvi
1. Mountain sickness- features, possible causes and treatment
Features - causes
-nausea, vomiting - Due to distension of GIT by expansion of
Gases in GIT
-fatigue, headache, insomnia,
Irritability, palpitations, loss of - may be due to cerebral hypoxia or mild
Coordination & memory cerebral edema

- Hyperventilation - stimulation of respiratory centre by hypoxia

Treatment:
1. Transferring the person immediately to a lower altitude
2. Providing hyperbaric oxygen therapy
3. Treating with drugs like carbonic anhydrase inhibitors, glucocorticoids &
nifidepine (calcium channel blocker)
2. Tidal volume-475 cc, VC- 2.65lt, FEV1- 45% & FEV2 - 70%
Explain this case & identify the disorder
The vital capacity is lower than normal (normal – 4.6 lts)
FEV1 percentage is also lower (normal – 80 %)
- the above values indicate the obstructive lung disease
3. Asphyxia – definition & stages
Definition – Hypoxia associated with hypercapnia mainly develops by physical or
mechanical obstruction in the airway.
Stages :
1. Stage of exaggerated breathing
2. Stage of convulsions
3. Stage of exhaustion & collapse
4. Physiological basis of oxygen treatment in different types of hypoxia
Hypoxic hypoxia – Oxygen therapy is highly beneficial. Alveolar PO2 is increased
which increases the pressure gradient between alveoli & blood. The diffusion of O2 is
facilitated
Anemic hypoxia – moderately useful. 100% O2 therapy will increase the oxygen
content in the dissolved form. This will supply extra O2 to the tissues
Stagnant hypoxia – less useful. Increase the dissolved form
Histotoxic hypoxia – As tissues are not in a state to utilize O2, O2 is not beneficial
5. What is periodic breathing? Mention two types of periodic breathing.
It is a type of breathing in which breathing is interrupted by alternate apnoea i.e.,
hyperopnea & apnoea alternate periodically.
2 types:
1. Cheyne – Stokes respiration
2. Biot’s respiration
6. Reason for less vital capacity in lying position.
1. As diaphragm is pushed up by abdominal organs the vertical diameter of the
thoracic cavity is reduced. This decreases the thoracic volume and vital capacity is
reduced.
2. The pulmonary circulation is congested by increase in the venous return. This also
reduces the vital capacity.
7. Reason for absence of cyanosis in histotoxic hypoxia
In histotoxic hypoxia, the tissues are not in a condition to utilize oxygen. The oxygen
does not dissociate from Hb and the amount of reduced Hb formed is less. So cyanosis
1
 2
will not occur in this type of hypoxia
8. Physiological basis of hyaline membrane disease or IRDS
 Surfactant, a chemical produced in the alveoli helps to prevent the collapse of alveoli,
increase the compliance & keeps the alveoli dry. Deficiency of surfactant at birth leads to
a disease of the new born called Neonatal respiratory distress syndrome (NRDS) or
Hyaline membrane disease.
Features:
 Several areas of collapse
 Reduced compliance
 Poor expansion of lungs
 Presence of fluid in the alveoli
9. Describe two important complications of O2 toxicity
1. On CNS – nausea, irritability, dizziness, disorientation, facial twitching &
Convulsions
2. On respiration – congestion and irritation of the airway, decrease in the surfactant
level, pulmonary edema and atelectasis
10. Briefly describe Pneumothorax
It is a clinical condition in which air enters into the pleural space through either a
rupture in the lung or a hole in the chest wall.
Features:
- the lung on the affected side collapses because of the elastic recoil
- shifting of mediastinum towards normal side as the intrapleural pressure on the
affected side become atmospheric
Types:
1. Open pneumothorax – communication between pleural space & exterior remains
open
2. Tension pneumothorax – a flap of tissue in the communication acts as a valve
3. Closed pneumothorax – the communication is sealed off
11. Reason for development of carpopedal spasm after voluntary hyperventilation
Voluntary hyperventilation  washout of CO2  alkalosis (high pH )  ionization
of plasma proteins  protein anions bind Ca+ ions  Plasma ionic calcium level
decreases  Tetany
12. In patients with respiratory failure with hypercapnia & hypoxia, administration of
oxygen may stop respiration and even cause death if artificial respiration is not initiated.
Why?
In these patients hypoxia is the only stimulant for respiration. Hypercapnia depress the
respiratory centre. Administration of O2 may remove the hypoxic drive & stop respiration.
Artificial respiration will keep the respiratory centres stimulated
13. Significance of timed vital capacity in distinguishing obstructive lung diseases from
restrictive lung diseases.
The FEV1 value is normal (80% of vital capacity) in restrictive lung disease. But it is
decreased in obstructive lung disease
14. Mention the types of hypoxia not accompanied by cyanosis. Give the reasons.
Anemic hypoxia – The Hb amount itself is less. So reduced Hb can not be formed to a
level of producing cyanosis
Histotoxic hypoxia – already discussed

2
 3
15. Why sudden ascend from deep sea is dangerous? / What is decompression sickness?
Explain the features, causes & treatment
Sudden ascend from deep sea leads to decompression sickness.
Decompression sickness: Refers to symptoms that develop in an individual who ascends to
the surface rapidly after sufficient exposure to high atmospheric pressure in deep sea
Cause:
The nitrogen which gets dissolved in the body fluids under high pressure in deep sea form
bubbles when trying to come out of body when the person is suddenly exposed to low
pressure. Presence of bubbles blocks the blood vessels producing tissue ischemia & tissue
death
Symptoms/Features:
 Pain in joints and muscles of leg
 Paraesthsia (Altered sensation)
 Temporary paralysis
 Chokes
 Myocardial ischemia
 Brain damage
Prevention:
Slow decompression
Treatment:
Recompression followed by slow decompression along with oxygen therapy
16. Explain the effects of the following on Timed Vital Capacity
a) Bronchial asthma
b) Fibrosis of the lung
a) Bronchial asthma – FEV1 value is decreased  Obstructive lung disease
b) Fibrosis of lungs – FEV1 value is normal  restrictive lung disease
17. Explain why expiration is more difficult than inspiration in an asthmatic patient
During expiratory effort, there is a compression on the bronchioles by the external
pressure. This will further occlude the already occluded bronchioles (due to constriction) in
the asthmatic patients. So expiration becomes difficult. But during inspiration , air is sucked
into the slightly inflated bronchioles because of negative pressure
18. Explain why a deep sea diver ascend fast to the surface complaints of pain in joints
The nitrogen which gets dissolved in the body fluids under high pressure in deep sea form
bubbles when trying to come out of body when the person is suddenly exposed to low
pressure. Presence of bubbles in the myelin sheath of sensory nerve fibres produces severe
pain in the tissues especially joints.
19. Explain the effect of the following conditions on lung compliance
a) Emphysema
b) Pulmonary Fibrosis
a) Emphysema – Alveolar wall destruction causes permanent dilatation of alveoli. So
the compliance is more
b) Pulmonary fibrosis – the spongy elastic tissue is replaced by fibrotic connective
tissue. The expansion is restricted. So the compliance is reduced
20.Name the condition when air enters the pleural space through a hole in the chest
wall. Explain why lung collapses on this condition
The condition is called Pneumothorax. As the air enters into the pleural space through
the hole, the negativity of intrapleural pressure which keeps the lungs in a slight
inflated position is lost. Because of the elastic recoil of the lungs, the lung collapses
on the affected side.

3
 4
21. A person acclimatized to high altitude passes alkaline urine. Give the reason.
Hyperventilation wash out of CO2  alkalosis (high pH) of body fluid  kidney
starts excreting bicarbonate without reabsorbing it  alkaline urine
22. A member of the mountaineering expedition suddenly developed nausea, Vomiting ,
Headache, Breathlessness, Disorientation &Tachycardia
a) What is the possible cause for this condition?
b) How the condition can be treated?
The condition is called mountain sickness.
Reason or cause, features and the treatment for the condition are already
discussed
23. Briefly give the reasons for the decompression sickness
Decompression sickness occurs when a person exposed to high pressure air is
suddenly exposed to a low pressure. This is because at high pressure nitrogen get
dissolved in the body fluids as well as lipid structures of the body. At low
atmospheric pressure nitrogen tries to escape from the body. On sudden exposure
to low pressure escape of nitrogen forms bubbles. These bubbles are responsible
for decompression sickness
24.Explain cyanosis and its clinical significance
Cyanosis is bluish coloration of the skin and mucous membrane. It occurs when
the amount of reduced haemoglobin in the blood exceeds 5gm/ 100 ml of blood.
Clinical significance:
Cyanosis occur in clinical conditions like congenital heart diseases, AV
admixture, peripheral vascular disease, shock & lung diseases.
25. Name the types of hypoxia. Give one example for each type
1. Hypoxic hypoxia - high altitude
2. Anemic hypoxia – Carbon mono oxide poisoning
3. Stagnant hypoxia – circulatory shock
4. Histotoxic hypoxia – Cyanide poisoning
26. What are the indications for artificial respiration?
• Artificial respiration is given
– In respiratory deficiency or arrest till normal respiration is restored
• Rapid Respiratory failure:
Anesthetic accident
Barbiturate poisoning
CO poisoning
Drowning
Electric shock
Fatal Head injury
• Gradual Respiratory failure:
Poliomyelitis
Motor neuron disease
Myopathies
27. A premature newborn baby develops difficulty in breathing immediately after
birth. X ray chest showed areas of atelectasis
a) What is the probable diagnosis?
b) What is the cause?
a) Hyaline membrane disease or Respiratory Distress Syndrome of newborn
b) Deficiency of surfactant

4
 5
28. What role does the BBB play in the regulation of respiration?
H+ ions can not pass through the blood brain barrier. CO2 can pass through easily.
. After entering into the CSF, CO2 combines with a water molecule to form carbonic
acid which dissociates into H+ ions & HCO3 – ions . Increase in H+ ion content
stimulates the respiratory centre
29. Why is the PO2 of blood in Aorta slightly less than the PO2 of blood in pulmonary vein?
Reasons:
1. Physiological shunt – Venous blood of lungs is drained in to pulmonary veins
2. Venous blood of heart is drained by thebesian vessels into all the four cardiac
chambers
30. What is the physiological basis of RDS?
Deficiency of surfactant  collapse of the lungs as surface tension of intra alveolar fluid is
not reduced  Distress in the respiration
31. Name the test used to differentiate obstructive airway disease from restrictive airway
disease. How is it interpreted?
Timed Vital Capacity : FEV1 which is expressed as percentage of vital capacity that is
expelled in 1st second is normally 80%.. This value will be normal in restrictive lung disease
but less in obstructive lung disease.
32. Explain the cause of respiratory depression seen after hyperventilation.
Hyperventilation  Wash out of CO2  Hypocapnia  Inhibition of respiratory centre 
respiratory depression
33. a) Pulmonary tuberculosis affects mostly the apex of the lung.
b) Anemic hypoxia without increase in the respiratory rate
Explain the physiological basis of these two conditions
a) High ventilation /perfusion ratio at the apex accounts for the increased effect of
tuberculosis in the apex. The reason for this is the presence of high alveolar PO2 which
provides a favorable environment for the growth of the tuberculosis bacteria
b) In anemic hypoxia, the dissolved O2 content is normal. Only the O2 carried by Hb will be
less. The PO2 which is determined by dissolved O2 is normal. So the respiratory centre
which is sensitive to changes in PO2 is not stimulated
34. What is the normal compliance of the lungs? Mention two respiratory diseases in
which it is reduced.
Normal compliance – 0.2 lt/ cm H2O
Disaeases (Decrease in compliance) – Pulmonary congestion & interstitial
Pulmonary Edema
35. A child of two years old is brought to emergency with severe respiratory
distress. X ray revealed a foreign body obstruction in the throat. The child died
in operation table before he could be given any relief. What is the cause of death?
Explain briefly.
What is the name of the condition?
What is the cause of death?
The condition is asphyxia
The cause for death – In this condition there is hypoxia associated with hypercapnia.
Hypoxia leads to death at last.
36. What are the consequences when a person consumes cyanide?
Cyanide inhibits the function of cytochrome oxidase enzyme thereby inhibits the tissue
oxidation processes. So tissue does not utilize oxygen & this condition is called histotoxic
hypoxia. The oxygen content of the arterial blood is normal

5
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37. Hypoxic stimulation of respiratory center is absent in carbonmonoxide poisioning &
anemic hypoxia. Explain the physiological basis
In both the conditions, the dissolved oxygen content is normal. So PO2 is normal
Only the O2 carried by Hb will be less. The PO2 which is determined by dissolved O2
is normal. So the respiratory centre which is sensitive to changes in PO2 is not stimulated
38. A person was exposed to environment rich in CO. What type of hypoxia he is likely to
suffer? Briefly explain the physiological basis of management of this type of hypoxia?
Hypoxia that occur in CO poisioning is anemic hypoxia.
Treating by hyperbaric O2 therapy (100% oxygen) facilitates not only dissociation of
CO from Hb but also increases the transport of O2 in dissolved state.
39. A man was found unconscious in a closed garage with the engine of a car kept on. His
skin & mucous membrane were cherry red in colour. He had no sign of dysponea &
hyperventilation.
What could be the cause & what type of hypoxia he develops?
Why didn’t he develop hyperventilation?
How he could be treated?
Rich carbon monoxide in the car fuel causes anemic hypoxia. In anemic hypoxia, the
dissolved O2 content is normal. Only the O2 carried by Hb will be less. The PO2 which is
determined by dissolved O2 is normal. So the respiratory centre which is sensitive to changes
in PO2 is not stimulated.
Treatment - Treating by hyperbaric O2 therapy (100% oxygen) facilitates not only
dissociation of CO from Hb but also increases the transport of O2 in dissolved state.
40. Severe hypoxia produces pulmonary hypertension, pulmonary edema & righ
ventricular failure(Cor pulmonale). How?
Hypoxia causes pulmonary vasoconstriction which produces pulmonary hypertension. This
leads to increase in pulmonary capillary pressure & filtration of fluid into alveoli causing
pulmonary edema. Due to high pressure in pulmonary artery, right ventricular work load
increases which leads to right ventricular failure
41. Mention four diseases in which compliance is abnormal
Increased compliance is seen in Emphysema & decreased compliance is seen in
pulmonary fibrosis, pulmonary edema & structural abnormalities like kyphosis & scoliosis
42. What is ARDS. Explain the physiolological mechanism involved in it. ARDS is Acute
or Adult Respiratory Distress syndrome.
It is caused by circulatory shock, sepsis, lung contusion, trauma & other serious
conditions. This condition is characterized by acute respiratory failure. The common feature
seems to be damage to capillary endothelial cells & alveolar epithelial cells, with release of
cytokines.
43. A person who was drowned in river water was brought to you without any
respiratory movement. His HR is 60/mt. What type of first aid would you like to
give? Why?
The first aid should be artificial ventilation since there is respiratory failure but HR is normal.
The best method is mouth to mouth respiration as it is a simple technique.
44. Prompt resuscitation with normal O2 was resorted to combat birth asphyxia in a new
born. What is the physiological basis of administration of O2?
What would be the toxic effects if it is given in excess?
Asphyxia is a condition which is characterized by hypoxia associated with hypercapnia. So
restoring the O2 level help to relieve the newborn from complications due to hypoxia.
Toxicity due to excess of O2 – Bronchopulmonary dysplasia (lung cysts & densities)
& retrolental hyperplasia (formation of opaque vascular tissue in the eyes)

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45. Explain the cause of cyanosis on exposure to extreme cold weather.
Cold weather causes cutaneous vasoconstriction which leads to stagnant hypoxia. In
this the flow of blood is very slow which allows more time for removal of oxygen by
the tissues. So more of reduced Hb is formed which produces cyanosis
46. Explain the effects of rebreathing of expired air for a short period of time & the
mechanism involved
Rebreathing of air increases CO2 level in the blood which stimulates respiratory center &
causes hyperventilation
47. Patients who breathe through the tracheostomy opening tend to get crusting lung
infection.Explain why
Lack of defence provided by upper respiratory tract against microbes leads to crusting
lung infections
48. A permaature newborn baby develops difficulty in breathing immediately after
birth. X ray chest showed areas of atelectasis.
What is the probable diagnosis?
What is the cause?
Diagnosis – Hyaline membrane disease
Cause – lack of surfactant
49. What is pulmonary edema? What are its causes, features & treatment?
Pulmonary edema: Accumulation of fluid in the interstitial spaces and alveoli of
lungs.
Causes:
 Increase in pulmonary capillary hydrostatic pressure
 Increased alveolar surface tension
 Decreased oncotic pressure
 Increased capillary permeability
Features:
 Hypoxemia and hypercapnia due to decreased gas exchange
 Increased air way resistance
 Decreased lung compliance
 Dysponea
Treatment:
- Diuretics ( decrease blood volume  decrease in pulmonary capillary
pressure)
- Digitalis ( increases the left ventricular function)
- Vasodilators (relax the systemic blood vessels)
50. Mention four conditions where hyperbaric oxygen therapy is used.
Hopoxia in high altitude, Asphyxia, Pulmonary edema & pulmonary fibrosis
51. Why the gas exchange system in lungs is affected in chronic smokers?
Effect of chronic smoking – Increase in pulmonary alveolar macrophages  release
A chemical substance  attraction of more leucocytes  release elastase which destroy the
elastic tissue in the lungs & the oxygen radicals produced by leucocytes inhibit α antitrypsin
inhibitor which inactivates elastase. The walls between the alveoli break down so that the
alveoli are replaced by large air sacs.
The inadequate & uneven alveolar ventilation & perfusion of underventilated
alveoli leads to hypoxia & hypercapnia. This condition is called emphysema which is
characterized by barrel shaped chest, dysponea, increased airway resistance,
decreased diffusing capacity of the lungs & extremely abnormal V-P ratio

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52. A 45 year old chronic smoker with barrel shaped chest complaints of dusponea.
Investigations revealed increased airway resistance, decreased diffusing capacity
of the lungs & extremely abnormal V-P ratio
-From what disease he is suffering
-Why dysponea in this condition?
- What treatment is advised?
The disease is emphysema
The inadequate & uneven ventilation of alveoli & perfusion of underventilated
alveoli leads to hypoxia & hypercapnia. So the inspiration & expiration become labored
Treatment – Quit smoking, administration of bronchodilators
53. A neurotic patient who chronically hyperventilates
a) What type of acid base disorder he will have?
b) What are the other causes for the above disorder?
a) Respiratory alkalosis due to washout of CO2
b) Voluntary hyperventilation & high altitude
54. Draw a schematic diagram showing periodic breathing in case of left ventricular
failure & give its explanation
Left ventricular failure
↓
Pulmonary edema
↓
Hypoxia & hypercapnia
↓
Periodic breathing (a cycle in which apnoea is followed
by hyperpnoea)
Explanation:
Hypercapnia & hypoxia  stimulates respiratory center  Hyperopnea
 washout of CO2  inhibition of respiratory center  apnoea
55. A male patient admitted in the hospital with severe dysponea. Various
examinations & investigations revealed the following – RR 22/m, expiration
prolonged & labored, breath sound diminished, Ronchi – plentiful, V.C – 4.2 lts,
FEV1 – 1.2lts.Other system examination showed nothing abnormal. Write your
diagnosis with justification
Diagnosis – Asthma. Asthma is a obstructive lung disease in which expiration is
prolonged & labored , presence of rhonchi (abnormal breath sound ) & FEV1 is less than
80%
56. Why prolonged hyperventilation produces blackout & giddiness?
Prolonged hyperventilation leads to washout of CO2. Since CO2 is a vasodilator, hypocapnia
leads to vasoconstriction. Constriction of cerebral blood vessels leads to blackout &
giddiness
57. Which hypoxia causes central cyanosis & which hypoxia causes peripheral
Cyanosis?
Central cyanosis -- Hypoxic hypoxia
Peripheral cyanosis -- Stagnant hypoxia
58. What will happen to the respiration after vagotomy and if the vagi are cut after
damage to the pneumotaxic center?
Vagotomy – The depth of respiration is increased
Vagotomy after damage to pneumotaxic center – Apneusis (Prolonged inspiratory
spasm that resembles breath holding)

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 9
60. A patient with barrel shaped chest has the following changes in the lungs.
- Alveoli are replaced by large air sacs
- Work of breathing is greatly increased
i) What is that respiratory disease?
ii) What is the most common cause for this disease?
Disease – Emphysema
Most common cause: Smoking
61. What is hypoxia? Mention the types of hypoxia. Explain the pathophysiology of
each type
Hypoxia is oxygen deficiency at tissue level.
Type Pathophysiology
Hypoxic hypoxia - Decreased PO2 of arterial blood
Anemic hypoxia - Amount of hemoglobin available to carry O2 is less
Stagnant hypoxia - Blood flow to a tissue is very low
Histotoxic hypoxia - Inability of tissue to utilize oxygen due to the action of a
toxic agent
62. What respiratory disorder will be developed in patients who have already had
chronic heart failure for a long time?
Pulmonary edema
63. Why a small percentage of people who ascend rapidly to high altitude become
acutely weak and can die if not treated? What is the cause for this weakness?
Due to hypoxia at high altitude
64. What is atelectasis? What are the causes for atelectasis?
Atelectasis – Collapse of alveoli
Causes:
- Bronchiolar obstruction
- Deficiency of surfactant
- Pneumothorax
- hydrothorax
- Hemothorax
65. Describe briefly the resuscitation mechanism followed to save a drowned person
The best method is mouth to mouth respiration as it is a simple technique which can
be applied immediately.
Mouth –Mouth Respiration: Steps:
 Place the subject in supine position
 Clean the mouth & nose
 Extend the neck backward
 Kneel on one side
 With the left hand hold the lower jaw & open the mouth of the subject
 With the right hand close the nose
 Place the mouth over the mouth of subject & enclose the subject’s mouth
between the lips
 Exhale smoothly in to the subject’s airway (This inflates the lungs)
 Remove the mouth for passive expiration
 Continue this procedure regularly at a rate of 12 times/ minute

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66. Some people who go to high altitude develop cerebral edema and pulmonary
edema. Explain its physiological basis
- Hypoxia in high altitude leads to pulmonary vasoconstriction  increase
in pulmonary hydrostatic pressure  increase in capillary filtration 
pulmonary edema
- Hypoxia in high altitude leads to cerebral vasodilation  increased
filtration  cerebral edema

67. The chloride ion concentration inside red blood cells in venous blood is greater
than that in red blood cells in arterial blood. Explain the cause
CO2 entering into the blood from tissues first moves into the RBC and gets converted into
HCO3-. HCO3- comes out of RBC into plasma. For each bicarbonate ion coming out of RBC,
one chloride ion enters into RBC. This Chloride-bicarbonate shift during CO2 transport in
venous blood increases the chloride ion concentration inside RBCs
68. Explain why oxygen therapy is not very useful in anemic hypoxia.
Anemic hypoxia is caused by decreased hemoglobin content of blood. Oxygen therapy
can only increase the dissolved oxygen content but can not increase the total oxygen
content of blood

10
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CENTRAL NERVOUS SYSTEM

10 marks
1. Name the different ascending tracts carrying conscious & unconscious sensations. Write in short about
dorsal column tract with proper diagram & labeling. What are the sensations carried by dorsal column
2. With the help of a labeled schematic diagram, trace the pathway for fine touch
3. Trace the pain pathway
4. Describe the origin, course, termination of corticospinal tract with a diagram. Explain its functions
5.List out the functions of thalamus
6. Draw a schematic diagram the cerebellum & label its various parts. Mention the functional divisions of
cerebellum. Describe the connections and functions of cerebellum
7. Name the nuclei of basal ganglia. Briefly discuss the connections & functions of basal ganglia with a
note on basal ganglia disorders
8. Name the hypothalamic nuclei. Describe the functions of hypothalamus
9. Describe briefly about CSF formation, circulation & functions.

5marks
1. With the help of suitable diagram, explain the mechanism of synaptic transmission.
2. Explain synaptic inhibition & facilitation
3. Explain the properties of synapse.
4. List out the properties of receptors
5. Describe the following:
- Stretch reflex
- Inverse stretch reflex (Clasp knife)
6. List out the properties of reflexes. Explain irradiation of reflexes
7. Briefly explain the mechanism of ‘endogenous painelief system / Describe about the modulation of
pain
8. Draw a schematic diagram of cross section of spinal cord showing the location of tracts.
9. Briefly describe the role of thalamus in the perception of somatic sensations
.10. Name the cortical areas & their functions
.11. Write in brief about the Parkinson’s disease. How is it treated? Write the physiological basis of
treatment?
12. Describe the role of hypothalamus in the regulation of water balance of the body
13. Briefly describe the role of hypothalamus in the regulation of food intake & body temperature.
14. Draw a labeled diagram of muscle spindle with its innervations
15. Describe the structure & functions of muscle spindle
16. Briefly describe the role of muscle spindle & strength reflex in the maintenance of muscle tone.
17. What is muscle tone? How is it regulated? Explain the rigidity of Sherrington’s animal preparation
18. What is decerebrate rigidity? Explain the mechanism of decerebrate rigidity.
19. Enumerate & explain the functions of reticular formation
20. Briefly describe the role of limbic system in the control of emotion & behaviour
21. Define memory and discuss briefly about the types of memory
22. What is memory? Describe the different types of memory. Explain the different mechanisms
involved in it
23. Describe the neural mechanism involved in written & spoken speech
24. What is sleep? Write about mechanism of sleep and different types of sleep
25. Enumerate the functions of BBB
26. Explain conditioned reflex
27. What are the structures of limbic system? And list out the functions of limbic system.
 2

3 marks
1. Mention the causes of synaptic delay
2. Mention some of the excitatory & inhibitory neurotransmitters
3. What is Weber Fechner’s law? Mention its significance
4. Explain reciprocal innervations with example
5. Explain crossed extensor reflex with example
6. Explain withdrawl reflex with example
7. What is synthetic sense?
8. Name the extrapyramidal pathways
9. What is Broca’s area? What happens when there is lesion in it?
10. Describe the Papez circuit & its importance
11. Describe the role of presynaptic facilitation i& its role in memory
12. Describe the role of limbic system in memory
13. Explain the EEG waves. What is alpha block?
14. Name the circumventricular organs & explain their significance
15. Explain habituation and sensitization

.
10 marks
1. Pyramidal tract
Origin :
 Primary motor Cortex (Area 4 – from large cells of Betz in the v layer of precentral
gyrus) - 30 %
 Premotor Cortex (area 6) & Supplementary motor cortex (Area 6) - 30%
 Somatosensory cortex (Areas 3,1, 2, 5 & 7) - 40%
Course:
 Corona radiata: Fibers forming a radiating pattern in the subcortical areas
 Internal Capsule: Converge through the genu and anterior 2/3rd of posterior limb of
internal capsule
 Mid brain: Fibers occupy middle 1/5th of cerebral peduncles
 Pons: The tract is split into a number of bundles by the presence of pontine nuclei
 Medulla:
Upper part:
Fibers join to form a single bundle. This forms a distinct bulge anteriorly close to the
midline called pyramid
Lower part:
80% of the fibers cross to the opposite side & 20% of the fibers descend on the same side
(The crossing of fibers from each side to opposite side is called motor decussaation)
 Spinal cord:
The crossed fibers form the lateral corticospinal tract and descend in the lateral white
column of spinal cord.
The uncrossed fibers form the anterior corticospinal tract and descend in the anterior
white column of spinal cord
Termination:
Fibers of lateral corticospinal tract – synapse with anterior horn cells directly and supply to
the distal limb muscles
Fibers of anterior corticospinal tract – cross at the segmental level and synapse with the anterior horn
cells through internuncial neurons. The fibers of this tract supply the axial and proximal limb
muscles
 55 % of the fibers end in the cervical region
 20% of the fibers end in the thoracic region
 25 % of the fibers end in the lumbosacral region
Functions:
 Control of voluntary fine and skilled movements (lateral corticospinal tract)
 Control of gross voluntary movements (anterior corticospinal tract)
 Facilitates muscle tone
 Facilitates superficial reflexes
 Mediates the actions of basal ganglia and cerebellum
 Concerned with direct sensory – motor coordination

( Refer book for diagram)

 2. CEREBELLUM

Functional divisions, their connections & functions

Functional divisions:
 Vestibulocerebellum (Flocculonodular lobe)
 Spinocerebellum (Vermis & intermediate zone)
 Neocerebellum (cerebrocerebellum)

Vestibulocerebellum:
 Connected to vestibular apparatus
 Role in control of body posture, equilibrium & visual fixation
Spinocerebellum:
 Mainly connected to spinal cord
Vermis: Controls muscle movements of axial body, neck, shoulder, hips  Maintains
posture via vestibulospinal & reticulospinal pathways
Intermediate zone: Control of muscular contraction of upper & lower limbs via
corticospinal tract
Cerebrocerebellum:
 Connected with pons and cerebral cortex
 Concerned with overall planning and programming of sequential motor movements
 Coordinates the timing and duration of contraction of different groups of muscles
Connections:

Peduncles Afferent fibers Efferent fibers

Superior Cerebellar Ventral spinocerebellar tract Dentato thalamocortical fibers
Peduncle Tectocerebellar Dentatorubral fibers
Trigemino cerebellar fibers

Middle Cerebellar Cerebro ponto cerebellar ----------------------

Peduncle

Inferior Cerebellar Dorsal spinocerebellar Cerebello reticular

Peduncle Cuneo cerebellar Cerebello vestibular
Reticulo cerebellar
Vestibulo cerebellar
Olivo cerebellar

Functions:
1. Control of body posture & equilibrium (Vestibulocerebellum & Spinocerebellum)
 Influences antigravity muscles through medial motor system and maintains
posture
 Influences muscles through vestibulospinal tract and maintains equilibrium during
standing, walking etc.,
(Vestibular apparatus  Vestibular nucleus of brain stem Vestibulo cerebellar
fibers  Vestibulocerebellum  Cerebello vestibular fibers  Vestibular
nucleus  Vestibulospinal tract)
2. Control of Gaze (Movements of eyeballs) – Vestibulocerebellum
 Controls eye movements and coordinates with head through medial longitudinal
fasciculus
3. Control of muscle tone & Stretch reflex (Spinocerebellum)
 Facilitates γ motor neurons in the spinal cord
 Forms an important site of α – γ linkage
4. Control of voluntary movements (Neocerebellum)
 Regulates time, rate, range(extent), force and direction of muscular activity
 Controls coordination of movements, but does not initiate movements
 Influences the activity of agonists, antagonists & synergistic muscles
 Planning and programming of voluntary movements
 Correction of purposeful movements (comparator of a servo-mecanism)
 Smooth transition of movements
 Cognition
 Learning of motor skills
 Mental rehearsal of complex action
5. Other functions: Influences autonomic functions
 3. BASAL GANGLIA / BASAL NUCLEI-
 Subcortical nuclear masses of grey matter, present at the base of the cerebral hemispheres
Components:
1. Caudate nucleus
2. Putamen
3. Globus pallidus
- Externa
- Interna
4. Substantia nigra
- Pars compacta
- Pars reticulata
5. Subthalamic Body of Luys
Connections:

Direct pathway:
+ Cortex

+ Glutamine

Striatum Dopamine Substantia nigra

D1

- GABA
Globus pallidus Interna

+
Thalamus
- Excitatory pathway
- Facilitates the intended movement

Indirect pathway:
-
Cortex

+ Glutamine

Globus pallidus Externa Striatum Dopamine Substantia nigra

D2
- GABA
Subthalamic nucleus + Globus pallidus Interna

PPN -
Brain stem & Spinal cord Thalamus

- Inhibitory pathway
- Inhibits the unwanted movement
Basal Ganglia functions
 Lower animals – center for motor activity
 Initiation of voluntary movements
 Suppression of unwanted movements
 Planning and Programming of a voluntary movement
 Execution of automatic associated movement
- Swinging of arms during walking
- Gestures during speech
 Cognitive control of motor activity ie., timing and scaling of movements through caudate circuit
 Inhibits muscle tone – inhibits γ motor neuron discharge by stimulating inhibitory medullary
reticular formation
 Regulation of posture
 Role in mood & behavior
-------------------------------------------------------------------------------------------------------------------------------

4. PAIN PATHWAY
Pain is carried by two pathways:
i) Neospinothalamic pathway
ii) Paleospinothalamic pathway
Neospinothalamic tract: (carries fast pain)

1st order neuron: Aδ fibers from receptors to lamina I and V of spinal cord

2nd order neuron: From dorsal horn of spinal cord  cross to opposite side  ascend in the lateral
white column  end in the ventral postero lateral (VPL) & ventral postero
medial (VPM) nuclei of thalamus.
(Gives few collaterals to reticular formation)

3rd order neuron: From VPL & VPM nuclei of thalamus to somatosensory cortex (areas 3, 2 &1)
of post central gyrus.

Paleospinothalamic tract: (carries slow pain)

1st order neuron: ‘C’fibers from receptors to lamina IV and V of spinal cord

2nd order neuron: From dorsal horn of spinal cord  cross to opposite side  ascend in the lateral
white column  end in intralaminar & midline nuclei of thalamus
(Gives collaterals to reticular formation, PAG and tectum of midbrain)

3rd order neuron: Arise from intralaminar & midline nuclei of thalamus & reach the entire cerebral
Cortex
Special features:
Neospinothalamic tract: concerned with localization and interpretation of quality of pain
Paleospinothalamic tract: concerned with perception of pain, arousal and alertness
 (Refer book for diagram)

Please learn dorsal column tracts from the book

 1

CNS Notes 2nd Part

1.Synaptic inhibitions & facilitation

1. Direct postsynaptic inhibition:
Stimulation of an afferent neuron inhibits an efferent neuron. The inhibition is direct and is
usually through an internuncial neuron. The neurotransmitter released is inhibitory in nature
Example: Golgi bottle neuron inhibition in reciprocal innervation and crossed extensor reflex
Mechanism : Stimulation of an afferent neuron from muscle spindle activates a golgi bottle
neuron that releases glycine which causes hyperpolarisation of the motor neuron
that supply to the antagonistic muscles.
2. Indirect postsynaptic inhibition:
Inhibition that occurs due to the effects of previous discharge from the postsynaptic neuron.
Mechanism: 2 ways:
i) Postsynaptic neuron remains refractory to the incoming stimuli because it has just fired and is
in the refractory period
ii) Neurons which initiate an excitatory impulse may inhibit themselves in a negative feedback
fashion.
Example: Renshaw cell inhibition:
The spinal motor neuron regularly gives recurrent collateral which synapses with an inhibitory
interneuron that terminates on the cell body of the same neuron. This inhibitory interneuron is
called Renshaw cell . This prevents excess discharge from the anterior horn cell
3. Presynaptic inhibition:
Inhibition occurs usually at the presynaptic terminals before the signal reaches the synapse.
Mostly modulatory in nature and usually axo-axonic type.
Example: Pain modulation in the spinal cord
Mechanism: A reflex response to stimulation of an afferent nerve is either abolished or
decreased by stimulating another afferent nerve .The second afferent nerve ending
synapses with presynaptic nerve terminal through an inhibitory interneuron. The
inhibitory neurotransmitter (Eg . GABA) released by this interneuron decreases
the depolarization of the presynaptic nerve terminals. Calcium entry into the
nerve terminals is decreased causing a decreased release of excitatory
neurotransmitter. This leads to a reduced response
4. Feedforward inhibition:
The afferent fibers first stimulate the efferent fibers and then inhibit the same fibers through
interneurons
Example: In cerebellum , the afferent fibers first stimulate the deep nuclei and then inhibit
them through purkinjee cells.
PRESYNAPTIC FACILITATION
A reflex response to stimulation of an afferent nerve is increased by stimulating another afferent
nerve.The second afferent nerve ending synapses with presynaptic nerve terminal through an
interneuron. The excitatory neurotransmitter (mostly serotonin) released by this interneuron
decreases the K+ current at presynaptic nerve terminals and increases the duration of
depolarization of the presynaptic nerve terminals. Calcium entry into the nerve terminals is
increased causing a increased release of excitatory neurotransmitter. This leads to an increased
response
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 2

2. Properties of Receptors
a. Specificity:
Each type of receptor is highly specific for a particular stimulus for which it is designed and is
non responsive to normal intensities of other type of stimuli (e.g) Rods and cones respond to
normal intensities of light, but respond to only high intensity of touch.
b. Adequate stimulus:
The stimulus which can easily stimulate a receptor is the adequate stimulus for that receptor.
(e.g) Light is the adequate stimulus for rods & cones.
c. Labelled Line Principle:
The specificity of nerve fibers for transmitting only one modality of sensation is called labeled
line principle.
d. Doctrine of specific nerve energies:
Also called as Muller’s law. The sensation evoked by impulses generated in a receptor depends
in part upon the specific part of the brain they ultimately activate.
e. Law of projection:
When a stimulus is applied anywhere in the pathway of a sensation, the sensation is projected to
the receptors. (e.g) Phantom limb & Phantom pain
Phantom Limb: The non existing limb in an amputated person gives the sensation of pain &
proprioception as if it is existing.
Phantom pain: The pain sensation from the non existing limb of an amputated person can be
explained by law of projection ie., the stimulus applied anywhere in the pathway causes
projection of sensation to receptors)
Mechanism
Amputation  formation of neuromas  discharge of impulses by pressure or
Spontaneously sensation produced is projected to the place where the receptors were
presented.
f. Adaptation:
Reduction in sensitivity of receptors in the presence of a constant stimulus
 Phasic receptors: Fast adapting receptors (e.g) receptors for smell & pacinian corpuscles.
 Tonic receptors: Slow – adapting receptors (e.g) proprioceptors
 Receptors that do not adapt at all - Pain receptors (Nociceptors)
g. Intensity discrimination:
Weber Fechner Law: The magnitude of sensation felt is proportionate to the log of intensity of
stimulus
R=KSA
(R = Magnitude of sensation felt, S=intensity of stimulus, K & A = constants)
Intensity discrimination depends upon
 Number of receptors stimulated (spatial summation)
 Frequency of action potential reaching the cortex (Temporal summation)
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 3

3. Sensory Tracts
1.Dorsal column pathway
Origin: From the dorsal column of spinal cord
Course:
I order neuron
 In the posterior nerve root
 After entering into spinal cord, ascend in the dorsal column of spinal cord
 Terminate in the nucleus gracilis & nucleus cuneatus of medulla
II order neuron
 From nucleus gracilis & nucleus cuneatus
 Cross to the opposite side (sensory decussation)
 Crossed fibers (called as inter nal arcuate fibers) upward in the medial lemniscus through pons &
mid brain.
 Terminate in the ventral postero lateral nucleus of thalamus (VPLN)
III order Neuron
 From VPLN of thalamus
 Pass through posterior limb of internal capsule
 Terminates in the SI & SII areas of cortex
 Sensations carried:
Fine touch, tactile localization, tactile discrimination, vibration, pressure, pain, conscious
proprioception & stereognosis.

2. Antero – lateral pathway

Origin: From the dorsal horn of spinal cord
Course:
I order neuron
 In the posterior nerve root
 After entering into spinal cord ascend up 1-3 segments or immediately end in nuclei of dorsal
horn.
II. Order neuron
 Starts from dorsal horn spinal cord
 Cross to opposite side in the anterior commissure
 Form 2 pathways
- Anterior spinothalamic tract
- Lateral spinothalamic tract
 Anterior spinothalamic tract runs in the anterior white column
 Lateral spinothalamic tract runs in the lateral white column of spinal cord
 Pass through medulla, pons, & mid brain
 Terminate in the VPLN of thalamus
III. Order neuron:
 from VPLN of thalamus
 pass through internal capsule
 terminate in the somatosensory cortex
Sensations carried:
Anterior spinothalamic tract – crude touch & pressure
Lateral spinothalamic tract – pain & temperature
 4

4. Regulation of Muscle Tone

Resistance of the muscle to stretch due to continuous state of tension in the muscle is called
muscle tone
Control of muscle tone:
 Muscle tone is purely a spinal segmental reflex.
 Produced by continuous, asynchronous, low frequency discharge from anterior horn motor
neurons
 This depends up on the activation of muscle spindle & stretch reflex.
Role of muscle Spindle
 Receptor organ present in the muscle
 Consists of infrafusal fibers (nuclear bag and nuclear chain fibers)
Sensory supply
 Group-Ia (annulospiral ending) – supply both fibers
 Group-II (Flower spray endings) – supply only nuclear chain fibers
Motor nerve supply
Gamma motor neuron
Muscle spindle participate in stretch reflex which play an important role in regulation of muscle tone
and posture
Role of stretch reflex
Reflex arc:
 Receptor - Muscle spindle
 Stimulus – Stretch
 Afferent – Group Ia & II fibers
 Center – Spinal Cord
 Efferent limb – motor nerve fiber ( α motor neuron)
 Response: Contraction of extra fusal fibers
Two types of reflexes
Dynamic stretch reflex: (phasic stretch reflex)
Activation of Group Ia fibers - contraction of agonist muscle and relaxation of antagonistic
muscle (helps is movement)
Tonic stretch reflex:
Activation of Group Ia & II fibers - continuous steady contraction of the antigravity muscles due
to asynchoronous discharge of motor units supplying the muscle
(necessary for maintaining muscle tone and posture)
Role of γ motor neurons on muscle tone
 γ motor neuron increases the sensitivity of muscle spindle to stretch
 increase inγ motor (gamma motor) neuron discharge increases muscle tone
 γ motor neuron discharge is increased in following conditions
noxious (painful) stimulation of skin
anxiety
Jendrassik phenomenon
Role of higher centers in regulation of muscle tone
Brainstem:
Brain stem reticular formation
Facilitatory reticulospinal tract(Pons) Inhibitory reticulospinal tract(Medulla)

Facilitates motor neuron discharge Inhibits motor neuron discharge

↑muscle tone ↓muscle tone

 5

Cerebellum: Increases muscle tone by

Facilitating motor cortex
Facilitating descending pathways
Cerebral cortex

Cerebral cortex Indirect pathway

Pyramidal tract Brain stem nuclei

Facilitates muscle tone Inhibits muscle tone

Applied
Hypotonia: ↓in muscle tone (lower motor neuron lesion & cerebellar lesion)
Hypertonia: ↑ in muscle tone (UMN lesion)
Spasticity – hypertonia only in antagonistic muscles (clasp knife rigidity)
(e.g) Hemiplegia due to pyramidal lesion
Rigidity: Hypertonia in both agonistic & antagonistic muscle
e.g Basal ganglia lesion – Parkinsonism
-------------------------------------------------------------------------------------------------------------------------------
5. VESTIBULAR APPARATUS
Components:
Vestibule (Utricle & Saccule)
Semicircular canals
Receptors:
Vestibule (otolithic organ) – Macula
Semicircular canals – Crista ampullaris
Stimulus
Vestibule - Linear acceleration
Semicircular canals – angular rotation
Activation of semi circular canals
Angular rotation

Movement of fluid in the semi circular canals

Bending of stereocilia towards the kinocilium

Entry of K+ into the hair cell

Depolarization

Calcium influx

Release of excitatory neurotransmitter (Glutamate)

On the opposite side:
Stereocilia move away from kinociliun

Hyperpolarization

Inhibition of Semicircular canals on opposite side

-Both of these cause relaxation of muscles on same side & contraction of muscles on opposite side
 6

Functions of Semicircular canals:

-helps to maintain equilibrium during rotational movements
-helps in visual fixation during angular rotation of head (vestibule-ocular reflex)

Otolith organ (vestibule) activation

Utricle responds to horizontal acceleration & Saccule responds to vertical acceleration
Functions of otolithic organ:
-gives information about static position of head
-respond to linear acceleration in different directions
Vestibular pathway

Vestibular apparatus

Vestibular division of VIII cranial nerve

Vestibular nucleus (Brain stem)

Vestibulo – cerebellar tract

Vermis of cerebellum

Cerebellar cortex Vestibular nucleus Vestibulospinal tract Spinal cord

6. Nuclei & Functions of Hypothalamus (important - regulation of water
balance, regulation of food intake & body temperature)
Nuclei of hypothalamus
1. Supra optic area: Includes supra optic, Suprachiasmatic, paraventricular & anterior nuclei
2. Preoptic area: Medial & lateral preoptic nuclei
3. Tuberal area: Ventromedial, dorsomedial, arcuate, lateral & posterior nucleus
4. Mammillary area: Medial & lateral mamillary, pre & supramamillary nuclei.
Functions of Hypothalamus
a) Regulation of food intake

Ventromedial Nucleus Lateral Nucleus

(Satiety center) (Feeding Center)

Inhibits feeding center Hunger

↑Food intake ↓food intake

b) Regulation of water intake

Tonicity of body fluid ECF volume

Osmoreceptors Baroreceptors

Thirst center Thirst center Angiotensin II

↑Water intake ↑Water intake Subfornical organ

Thirst center
 7

c) Regulation of body Temperature

Pre optic nucleus of anterior hypothalamus (heat loss center)  Sweating and vasodilatation
Posterior hypothalamus (heat gain center)  Shivering & vasoconstriction
d) Control of ANS
(Acts as a head ganglion of ANS)

Stimulation of anterior Stimulation of posterior

Hypothalamus Hypothalamus

↑HR, BP & HCL secretion ↓HR & BP, Pupillary dilatation,

Micturition, erection of penis sweating & piloerection
(Parasympathetic effects) (sympathetic effects)
e) Control of Pituitary
Hypothalamus Supra optic & paraventricular nuclei of hypothalamus

Releasing &
inhibitory
Hormones

Anterior pituitary Posterior pituitary

Trophic hormones ADH Oxytocin

Target endocrine gland Water re-absorption Milk secretion

In kidney in mammary glands
&
contraction of uterus
f) Role in circadian rhythm
-Hypothalamus play a role in influencing the changes in body functions tuned to the day and night
cycle (circadian rhythm)

Retina

Optic tract

Suprachiasmatic nucleus of hypothalamus

Pineal gland

Melatonin

Day & night variations

g) Role in emotions:
Hypothalamus is a part of papez circuit which is responsible for emotional behavior.
 8

h) Role in stress
Hypothalamus helps to protect the body from damaging effects of stress
Stress

Cerebral cortex & Limbic system

Sympathetic
Nervous system Hypothalamus Adrenal cortex Adrenal medulla

Glucocorticoids Catecholamines
i) Role in sleep wakeful cycle
Hypothalmus has 2 sleep centers
- diencephalic sleep zone
- basal fore brain sleep zone
j) Role in sexual behavior
Hypothalamic areas (Preoptic & anterior hypothalamus) are responsible for sexual behavior like
mating, attracting the opposite sex etc.
k) Reward & punishment
Ventromedial nucleus – Reward center
Posterior & lateral nucleus - Punishment center
Important Functions:
a) Role of Hypothalamus in food intake
Food intake is controlled by 2 nuclei. They are
i) Ventromedial nucleus (VMN) – Satiety center
Inhibits the feedings center
Produces satiety (satisfaction) after taking food
Destruction of VMN - Hyperphagia & obesity
Stimulation of VMN - Hypophagia (↓food intake)
ii) Lateral nucleus (LN) – Feeding center
Stimulaters appetite
Produces hunger
Destruction of LN – aphagia & starvation
Stimulation of LN – Hyperphagia (↑ food intake)
Hypothesis about food intake
1. Glucostatic Hypothesis
Hyperglycemia in blood  ↓VMN activity  ↓ food intake
Hypoglycemia in blood ↑VMN activity ↑ food intake
2. Lipostatic Hypothesis:
Adipose tissue secretes “leptin”  inhibits hypothalaminus ↓ food intake
3. Gut peptide Hypothesis
Presence of food in GI tract  release of intestinal peptides (GRP, glucagon, somatostatin &
CCK)  acts on brain  satiety
4. Thermostatic Hypothesis
↓Body temperature ↑ food intake
↑Body temperature ↓ food intake
b) Role of Hypothalamus in regulation of water intake
 Mainly involves ‘thirst center
 Dorsal or lateral hypothalamus acts as thirst center
 Water intake mainly depends upon the stimulation of thirst center
 Thirst center is stimulated in 2 conditions
 9

a) in the increased tonicity of the body fluid

b) in the decreased ECF volume
a) Increase in the tonicity of body fluid

Stimulation of osmoreceptors

Stimulation of thirst center

Water intake
b) Decrease in ECF volume

Baroreceptors

Stimulation of Thirst center Angiotensi II

↑Water intake Subfornical organ

Thirst center
C. Regulation of Body Temperature
 Hypothalamus is called as ‘biological thermostat as it controls the body temperature constant
 Involves preoptic region of the anterior hypothalamus & posterior hypothalamus
Preoptic nucleus of anterior hypothalamus -- heat loss center
Posterior hypothalamus -- heat gain center
Stimulation of the centers occurs through 2 mechanisms
a) Cutaneous thermoreceptors
b) Blood flowing through hypothalamus
(-mediated through serotonergic pathway)
Stimulation of anterior hypothalamus Stimulation of posterior hypothalamus

Vasodilatation, sweating Vasoconstriction

& panting Shivering & Piloerection
-------------------------------------------------------------------------------------------------------------------------------
7. THALAMUS
Specific sensory nuclei
 ventrobasal group (VPLN & VPMN)
 medial & lateral geniculate bodies
Non specific sensory nuclei
 midline & intralaminar nuclei
Nuclei concerned with efferent control
 ventrolateral & ventro Anterior Nuclei
Nuclei concerned with higher functions
 dorsomedial, dorsolateral, pulvinar, posterolateral & Anterior nucleus
Functions
a) Sensory Relay Center:
sensory relay center for the following sensations:
 Tactile sensation
 vibration
 pressure
 conscious proprioception
 10

 stereognosis
 sexual sensation
 visual sensation (LGB)
b) Centre for crude sensations:
 Perceives the crude touch, pain & Temperature Sensation
c) Integrator of motor signals
 controls the smooth, slow and coordinated movements by its connections with cerebellum basal
ganglia & cerebral cortex.
d) Role in memory & emotions
 Being a part of Papez circuit, it influences recent memory & emotions.
Papez circuit
Mammillary body of Hypothalamus

Anterior Nucleus Hippocampus

Of thalamus

Cingulate gyrus
e) Role in sleep wakefulness cycle
 influences sleep wakefulness cycle.
 stimulation causes alertness of animal which facilitates learning process
 produces the B-rhythm of EEG
 Non-specific Nuclei are responsible for them
 Connections involved. (Reticulo thalamo cortical & Cortico thalamo reticular)
--------------------------------------------------------------------------------------------------------------------
8. Withdrawl reflex
Refers to the withdrawal of body parts by flexion of limbs when a painful (noxious)
stimulus is applied.
 -It is a polysynaptic reflex
Receptors: Nociceptors
Afferent Limb: Type III & IV somatic afferents
Center: Spinal Cord
Efferent fibers: Somatomotor neuron supplying the flexor muscles of same side and
extensor muscles of opposite side.
Response:
Mild stimulus- flexion of limb of same side and extension of limb of opposite side.
Stronger stimulus - response in all four limbs.
(Reason: a) Irradiation of impulse, b) Recruitment of more motor units)
Special features:
 Withdrawl reflex is a protective reflex (protects the tissue from damage)
 Pre potent (stops all other spinal reflexes temporarily)
 Shows local sign ie., response depends upon the location of the stimulus
 Stronger stimulus causes wide spread and prolonged response
(Causes: After discharge due to involvement of many interneuronal pathways
& reverberatory circuits in the spinal cord)
 11

----------------------------------------------------------------------------------------------------
9. Modulation of Pain/ Endogenous Pain Relief System
Analgesia [inhibition of pain]:
1. Gate control theory
2. Endogenous pain relief from PAG(Peri Aqueductal Grey matter) & NRM / Central Pain
suppressing Mechanisms
3. By release of Endogenous opioid peptides (Enkephalins & Endorphins)
Gate control theory of pain
- the posterior or dorsal horn acts as a Gate for pain
- pain impulses in the spinal cord can be modified or gated by other afferent impulses [touch
,pressure vibration] that enter the spinal cord
- Large myelinated A fibers interact with small unmyelinated C fibers via
inhibitory cells of the Substatia gelatinosa of the spinal cord
- Stimulation of C fibers inhibits SG cells & favours passage of impulses along
the pathway of pain in the spinal cord.
- Stimulation of large ‘A’ fibers increases SG activity & block impulse
transmission to nerve cells concerned with pain-
(inhibit transmission of pain from the ‘C’ fibers to Spinothalamic tract.-
presynaptic inhibition)
- pain inhibiting opioids also act at the level of gate
Endogenous pain relief from PAG/central pain suppressing mechanism
- Descending pathways arise from Periaqueductal gray matter [surrounding aqueduct of Sylvius]
[release Encephalin]  Descend & connect with Nucleus raphe magnus of medulla release
of Serotonin  posterior horn cells of spinal cord  inhibits the release of substance “P” from
the pain fibers
 12

Opioid peptides:
oEnkephalins—
 Met enkephalins ,Leu enkephalins
o Endorphins-
 Beta endorphins, & Dynorphins
o Similar in action to Morphine
o Present in PAG (peri aqueductal gray matter),NRM( nucleus raphae
magnus),periventricular
o areas, posterior horn cells, GITract & Hypothalamus
o Endogenous morphine - ENDORPHINE
 Two sites of action:
-Terminals of pain fibers (receptors) & decrease the response of the receptors
to nociceptive stimuli
-At spinal level – binds to opioid receptors & decreases the release of
substance - P
---------------------------------------------------------------------------------------------------- --

10. REFERRED PAIN

Visceral pain instead of being felt at the site of the viscera is frequently felt at some
distance,on somatic structures. This is called referred pain
Eg: Appendicitis pain at the umbilicus
Cardiac pain at the inner aspect of left arm
Cholecystitis at the tip of the shoulder.
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain- both from the viscus & the
corresponding dermatome (somatic structures) converge on the same pathway to
the cortex
2. Facilitation theory: The visceral pain produces a subliminal fringe effect on the
Substantia Gelatinosa Rolando [SGR] cells which receive somatic pain nerves

CONVERGENCE THEORY
 13

11. Inverse Stretch Reflex

Refers to relaxation of muscle in response to a strong stretch.
Also called as lengthening reaction or clasp knife reflex.
Receptors: Golgi tendon organ
Afferent fibers: Group Ib fibers
Center: Corresponding spinal segment
Efferent fibers: α motor neuron to the corresponding muscle
Response: Inhibition of α motor neuron by the inhibitory interneuron and relaxation of the
corresponding muscle.
Functions:
-Monitors the force generated in the muscle
-reflex is called autogenic inhibition
-monitors muscle tension and prevents rupture of muscle
-along with stretch reflex maintains optimal motor responses for postural adjustments
-----------------------------------------------------------------------------------------------------------------------------------
12. Reciprocal innervations
-refers to the contraction of agonist muscles and relaxations of the antagonistic muscles in response to
the stimulation of an afferent nerve
Circuit:
Afferent fibers: Group Ia & II fibers
Center: spinal card
Efferent fibers: motor neurons supplying agonist and antagonistic muscle
Response: contraction of agonist muscle and relaxation of antagonistic muscle
(relaxation is due to stimulation of an inhibitory interneuron)
Importance:
-essential for normal physiological movements like walking
-useful in eliciting crossed extensor reflex between two upper limbs

13. Crossed extensor reflex

- stimulation of a limb causes flexion of limb on same side and extension of opposite limb.
- Mediated through interneurons
-Take part in withdrawal reflex
 1

CONDITIONED REFLEXES
Learning refers to a neural mechanism by which the individual changes his or her behavior on the
basis of past experience or acquisition of new information by the individual

Learning

Reflex Learning Incidental Learning

Non Associative Associative

Associate learning can be studied by conditioned reflexes
Conditioned Reflexes

Classical conditioning Operant conditioning

Classical conditioning
-refers to a reflex response to a stimulus that is acquired by repeatedly pairing the stimulus with
another stimulus that does not normally produce the response.

The stimulus which normally produce the response-- unconditioned stimulus

The stimulus that normally does not produce the response – conditioned stimulus

Pavlov’s experiment
Meat placed in the mouth of a dog --- salivation
(unconditioned stimulus)

Bell ringing alone --- no salivation

(conditioned stimulus)

UCS + CS --- salivation

After repetition of UCS + CS for many times

Conditioned stimulus alone ---salivation

(bell ringing)

Operant conditioning

The animal has to operate first to learn the process

(e.g) the animal presses a bar to get a food pellet.

Features of conditioned reflexes

If the CS is presented repeatedly without UCS, the conditioned reflex eventually disappears. This
is called extinction or internal inhibition.

It the CS is presented repeatedly with UCS, the conditioned reflex is reinforced. This is a must
for maintaining a conditioned reflex.

Physiological basis of conditioned reflex

The development of a conditioned reflex is due to formation of a new functional connection
between the neurons of CNS

HABITUATION & SENSITIZATION

Habituation
Refers to decrease in response to a benign stimulus when the stimulus is presented repeatedly.
When the stimulus is applied for the first time. It is novel & evokes reaction. This response is
called “orientation reflex” or “what is it” response.
Eventually the subject totally ignores the stimulus and gets habituated to it.
 2

Physiological basis of Habituation

Gradual inactivation of Calcium channels and consequent reduction in the release of a
neurotransmitter.
Example for Habituation
Riding a bicycle for the first time may be exciting. After repeating it, it becomes a habit.
Sensitization
When a habituated stimulus is coupled with a distinctly pleasant or unpleasant stimulus, a greater
response is produced.
Physiological basis of Sensitization
-due to increased levels of cAMP via an increase in Ca2+ levels in the post synaptic neuron
-the response in transient but can be prolonged
Example for sensitization
-the mother who sleeps through many kinds of noise but wakes promptly when her baby cries.
Importance of / significance of Habituation and sensitization
-Habituation & sensitization take part in learning & memory
-Habituation takes part in negative memory which prevents over burdening of memory storage.
-Sensitization takes part in positive memory
---------------------------------------------------------------------------------------------------------------------
Papez Circuit
Mammillary body of Hypothalamus
Mammillo thalamic
tract

Anterior Nucleus of thalamus Hippocampus

Cingulate gyrus
Significance of this circuit
-Hippocampus connections to diencephalon (thalamus & hypothalamus) takes part in recent
memory
-Hippocampal connections to amygdala is involved in emotions related to memory
-Hippocampus is a part of limbic system which is concerned with emotional behavior like anger,
fear, etc.,
-Anterior Nucleus of thalamus forms a part of diencephalic sleep zone – stimulation of which
produces slow waves in EEG –
---------------------------------------------------------------------------------------------------------------------
Memory
-Refers to the ability to recall past events at a conscious or a subconscious level.
Types of memory
On the basis of recall of stored information
a) Non declarative (implicit) memory
-Subconscious recall of skills, habits & classical conditioned reflexes
-Also called as reflexive memory
(e.g) cycling, driving etc.,)
b) Declarative (Explicity) memory
-conscious recollection of stored information
2 types
i) short term memory
-recalling within a few minutes or few days
(e.g) recalling a phone number to dial immediately after memorizing it.
ii) Long term memory: (remote memory)
-recalling the stored information even after few days or few years
(e.g) remembering about the picnic enjoyed
Mechanism of short term memory
1. Post titanic potentiation or facilitation
When an excitatory presynaptic neuron is stimulated for a brief period by a tetanizing current,
the synapse becomes more excitable after stoppage of stimulus.This is due to accumulation of
Calcium in presynaptic nerve endings.
 3

2. Reverberatory circuit theory

Reverberation of impulses between cerebral cortex brainstem and subcortical nuclei
through reverberating circuits.
3. Presynaptic facilitation
The presynaptic neuron is facilitated for a long time by neurons that lie on presynaptic
Terminals. Neurotransmitter involved is serotonin
Mechanism of long term memory
Long term potentiation
Physiological changes
-changes in the gene expression in postsynaption neuron
- in the synthesis and release of excitatory neurotransmitter
-changes in the response of receptors in the post synaptic membrance
Anatomical changes
-changes in the member & shapes of dendritic spines
-changes in number & size of synapses
-thickening of cortex
-formation of new synaptic connections
Chemical changes
-increase in RNA, protein & neurotransmitter synthesis
Consolidation of recent memory into permanent (long term memory)
-refers to the transfer of information from short term memory to long term memory
-recent memory initiates chemical, physical and structural changes in the synapses that
are responsible for permanent memory
-Hippocampus is the area mainly responsible for recent memory and its consolidation in
permanent memory
-consolidation will be lost in case of
-brain injury
-electric shock
Neural connections involved in memory (Learn from book)
Applied
Amnesia – loss of memory
Korsakoff’s syndrome – loss of memory in alcoholics
Reterograde amnesia – inability to remember the events that occurs before the
impairment of brain function
Anterograde amnesia – failure to learn new things, but long term memory is intact
CEREBROSPINAL FLUID
Cerebrospinal fluid is the fluid present in te ventricular system of the brain, subarachnoid space &
central spinal canal
Formation of CSF

CSF is mainly formed by choroidal plexus, which are covered by specialized ependymal cells.
The choroidal plexus are located in the cerebral ventricles (lateral, third and fourth). About 500
ml of CSF is secreted per day.

Normal CSF pressure – 60 – 100mm Hg of water

Amount of CSF - 160 Mgml

Circulation:
Lateral ventricles
Foramen of Manroe
III Ventricle
Aqueduct of sylvius
IV ventricle

Foramina of magendie Foramina of luschka

Subarachnoid space Subarachanoid space

80% dural sinus 20% spinal veins

 4

Absorption
Arachnoid villi play an important role in absorption of CSF
The CSF is removed through arachnoid villi into dural venous sinuses in the cranium

Functions:
1) Protective function:
-forms a liquid cushion surrounding brain and spinal cord. The brain simply floats in the fluid.
This prevents any mechanical injury
-gives buoyancy to brain. This reduces brain weight by 97% and thus prevents the brain from
crushing under its own weight

2) Medium of exchange
-nutritive substances are provided to the cells of CNS by CSF only. CSF is in direct contact with
neurons.
-CSFacts as a lymph and removes proteins and waste products of metabolism from the cells.

3. Reservoir function / regulation of cranial content volume

Monro Kellie Doctrine – The volume of blood, CSF & brain in the cranium at any time must be
relatively constant.
CSF regulates the contents of cranium
-increase in blood volume of brain  drainage of CSF
-decrease in blood volume of brain  retention of CSF
Thus the total volume of cranial content is kept constant.
4.Other functions
- Provides a proper chemical environment for the optimal activity of the neurons
-Useful for the diagnosis of brain disorder as it reflects the brain function
Applied
1. Lumbar puncture:- CSF is drawn from subarachnoid space by inserting needle between the L3
& L4
CSF can also be drained by cisternal and ventricular puncture
2. Hydrocephalus: Accumulation of CSF
Causes: increase in production of CSF, obstruction to CSF circulation
If CSF accumulates in ventricles --- internal hydrocephalus
If CSF accumulates in subarachnoid space --- external hydrocephalus
3.Counter – coup injury: When the head receives a severe blow, the brain gets injured on the
opposite side of blow
-----------------------------------------------------------------------------------------------------------------
APHASIA
Definition
Speech disorders in the comprehension or production of spoken or written language. The
disorders are not due to defects of vision or hearing or due to motor paralysis, but caused by
lesions in the association areas which are responsible for integrating activity.
Types
Sensory or wernicke’s or Fluent aphasia
Motor or Broca’s or Non-fluent aphasia
Global Aphasia
Anomic Aphasia
Causes:
1. Cerebral thrombosis
2. Cerebral infarction
3. Injury to the brain during accidents
4. Inadequate blood flow to the parts of the brain due to vascular changes
5. Tumours of the brain
 5

Type of Site of lesion Characteristic features Characteristic

Name errors (e.g)
aphasia Chair
Fluent Wernicke’s area Excessive talk with full of Stool or choss
a) Wernicke’s (Area 22) Jargon & Neologisms (Neologisms)
aphasia
(sensory
aphasia)
b) Conduction
Aphasia

1) Pure word Angular gyrus/ Trouble in understanding the I know.. I have

blindness Visuopsychic area written language or pictures. lots of them
Can not name the colors or
objects
(Pure word blindness)
2) Pure word Areas 40, 41 & 42 Trouble in comprehending the Flair……. no
deafness (in and around spoken word. Unable to repeat swair……..fair
auditory cortex) or write on dictation
Non fluent Broca’s area (Area Slow speech, words are hard to “Tssair”
c) motor/ Broca’s 44) come by, limited to two or three
aphasia words to express the whole
range of meaning & emotion
d) Global Both wernicke’s & Scanty non fluent speech.
Aphasia Broca’s area All aspects of speech and
language are impaired

-----------------------------------------------------------------------------------------------------------------
Reticular Formation
Reticular formation – Functions
1. Role in muscle tone regulation:
- Descending extrapyramidal tracts from reticular formation (Reticulo spinal tract) -
regulate muscle tone, posture & equilibrium
- mainly modulates the tone of antigravity muscles.
Two tracts:
Lateral Facititatory reticulo spinal tract from pons
Medial Inhibitory reticulo spinal tract from medulla
2. Role in sleep & wakefulness cycle
The ascending reticular activating system of reticular formation has a role in this process
ARAS:
RF of midbrain

Intralaminar Nuclei of Thalamus (Non specific nucles)

Cerebral cortex (all parts)

Activation of ARAS Wakefulness, alertness & consciousness

Inactivation of ARAS  Sleep
Other functions of ARAS
- Influences learning and memory
- Keeps the person in alert state
- Responsible for the genesis of EEG waves
3) Modulation of pain:
Raphae magnus nucleus of retircular formation

Descending serotonergic fibers

Excites SGR (substantia gelatinosa of Rolando) cells of spinal cord

Modulation of pain
 6

4) Control of visceral / vegetative functions:-

VM (Vaso Motor Center), Cardia Center, Respiratory center
Vomiting Center, Salivary Centers, etc., in descending Reticular formation of brain stem

Through Autonomic Nervous system

Control visceral functions (Gastric Secretion, GI mofility, BP, heart rate, respiratory rate,
salivation, vomiting etc.,

5) Control of neuroendocrine systems in the hypothalamus

6) Influences biological clocks (circadian rhythm) by its connections with hypothalamus
--------------------------------------------------------------------------------------------------------------
ELECTROENCEPHALOGRAM(EEG)
Definition:
Electroencephalogram is a record of summated potentials of the cerebral cortex recorded from the
surface of the scalp
Hans Berger is called the father of modern electroencephalography

Normal EEG pattern: (the waves of normal EEG)

Alpha rhythm
Beta rhythm
Theta rhythm
Delta rhythm

α Rhythm : (alpha rhythm)

-prominent component of EEG
-obtained from adult humans who are awake but with closed eyes.
-recorded from parieto – occipital area
-also called as Berger rhythm
Frenquency: 8-13 Hz
Voltage: 50uv

β(beta) rhythm:
-obtained when the eyes are opened
-indicates an alert state
-recorded from parietal and frontal regions
Frequency: 18-30 Hz (Faster rhythm)
Voltage: 5-10 uv
Theta rhythm:
-recorded from the parietal and temporal regions of children.
-do not occur in normal waking adult
But obtained from adults in emotional stress and many brain disorders
Frequency: 4-7 hz
Amplitude: (10uv)
Delta waves:
-present during sleep
-absent in wakeful adults, but present in wakeful infants
-presence of these waves in wakeful adults indicates some lesion of the brain
-recorded from occipital and other regions.
Frequency: 1-4 Hz
Amplitude: 200 uv
Applied – alpha block
-refers to a phenomenon in which alpha waves are replaced by B-rhythm (fast, irregular
waves of low amplitude)
Occurs in
-when the eyes are opened
-in conscious mental activity
-application of a stimulus
 7

USES OF EEG

Useful in:

Diagnosis of epilepsy
Localization of lesions in brain
Neurophysiological investigation
Studying of sleep pattern
Finding out the prognosis of head injuries and vascular lesions
Differentiating organic and functional disorders of brain

--------------------------------------------------------------------------------------------------------------------
SLEEP
What are the types of sleep? Differetniate them
Types of sleep:
Rapid eye movement sleep (REM)
Slow wave sleep or NREM
Differences

NREM Sleep REM Sleep(Parodoxical sleep)

1. Rapid Eye movement Absent Present
2. Brain activity Less More
3. Muscle tone Hypotonia More hypotonia
4. EEG δ( Delta) waves) β (beta) rhythm
5. Dreams Can not be recalled can be recalled
6. PGO (ponto
Geniculo occipital
Spikes No PGO spikes Present

7. Pulse, BP &
Respiratory rate Low & regular increased & irregular

8. Hormonal level Decrease in serotonin Decrease in nor adrenaline

content of raphae content in locus cerulus
Nucleus Increase in Acetylcholine
Of cortex
9. Threshold for arousal Elevated Further elevated

10. % of total sleep

Duration 75% 25%

11. O2 consumption Less More

-------------------------------------------------------------------------------------------------------------------

LIMBIC SYSTEM
Components
Amygdala
Hippocampus
Cingulate gyrus
Septal Nuclei
Medial Forebrain Bundle
Pre pyriform cortex
Entorhinal cortex
Diagonal brand of Broca
 8

Functions
a) Emotional behavior
Seat of emotions
mainly due to papez circuit involvement
Physical changes during emotions.
a) Somatic changes – Grinding of teeth, shouting, crying etc.,
b) Visceral changes -↑HR,↑RR,↑BP, Sweating etc.,
Mental changes
Awareness of sensation (cognition)
Feeling (Affect)
Urge to take action (conation)
- Amygdala stimulates emotions
- Lesion of amygdala  placidity
b) Feeding behavior
- Limbic system is responsible for discriminative feeding
- Amygdala is mainly involved
- Lesion in amygdala  hyperphagia with indiscriminative ingestion of all kinds
of food.
c) Maternal behavior
- refers to the nursing (breastfeeding) and protection of the off spring by the mother.
- Cingulate gyrus & retrosplenial portion of the limbic cortex are involved in this
- Lesion in these areas depress mater nal behavior
d) Sexual behavior
- refers to the basic sex drive (urge to copulate)
- Limbic system suppress the sexual behaviour
- Piriform cortex of limbic lobe is involved
- Bilateral lesion in this area ↑ in sexual activity
- (attempt to copulate even the animals of other species & inanimate things)
e) Motivational behavior
- refers to the motivation of learning and behavior
- reward & punishment centers in the limbic system are responsible for motivation
- septal nuclei (Reward center) & entorhinal cortex (punishment center) are parts of
limbic system
f) Autonomic functions
- Stimulation of many parts of the limbic system specially that of amygdala produces
autonomic responses such as
- changes in cardiovascular system
- changes in respiratory system
- changes in GI system
- changes are mediated through hypothalamus
 1

NERVOUS SYSTEM - applied K.Senthamil selvi

1. Following haemorrhage in to the internal capsule paralysis of limbs of
opposite side was observed.
a) On which side would be facial paralysis?
b) Mention why facial muscles of upper half are spared.
a) Opposite side
b) There is bilateral supply of upper motor neuron for the muscles of upper half.
2. A 65 year old person suddenly fainted and became unconscious. On
regaining consciousness he was unable to move his left side arm and leg.
After six weeks there was spastic paralysis with exaggerated tendon reflex
and left side facialparalysis.
a) What is your diagnosis?
b) Where is the probable site of lesion?
a) The condition is called Hemiplegia
b) Above pons. Most probable site is internal capsule
3. A 65 year old patient complains to the doctor that his muscles are stiff and
can initiate movements with difficulty. On examination it is found that
there is rigidity, resting tremor, absence of automatic associated movements
a) What is your diagnosis?
b) How will you treat?
a) Parkinsonism
b) With L-Dopa
4. Sensory & motor changes in Hemisection of spinal cord
BROWN SEQUARD SYNDROME
- a group of complications that arise due to lesion of one lateral half of spinal
segment
Causes;
Cord hemisection
Trauma or tumor

SAME SIDE OPPOSITE SIDE

BELOW Loss of sense of position, movement, Loss of pain &

THE Sensory vibration, tactile discrimination and temperature sensation
LEVEL OF localisation
LESION
Motor UMN type paralysis
- Hypertonia
- Exaggerated deep No motor changes
Reflexes
-Babinski sign +ve

vasomotor paralysis – dilatation of blood

vessels
No changes
 2

AT THE Sensory complete loss of sensation No change

LEVEL (anesthesia)
OF LESION
Motor LMN type paralysis No change
- Flaccidity
- Loss of both superficial &
deep reflexes
- Babinski sign – ve

vasomotor Paralysis – vasodilation No change

Above the Level of lesion – Hyperaesthesia (due to irritation by cut fibers) on the same
side & referred hyperaesthesia on opposite side
5. A patient presents with the history of unilateral facial paralysis of abrupt onset, in-
ability to close the eye, loss of taste sensation O/E Hyperacusis present
a) What is the name of this condition?
b) What is the cause?
a) Bell’s palsy
b) Lesion of facial nerve in Facial canal (may be due to repeated middle ear
infections
6. Give the physiological basis of Saturday night palsy where there is muscle weakness &
diminished sense of touch & pressure. Pain is not affected
Saturday night palsy is due to the effect of mechanical pressure or compression on radial
nerve. Type A fibres are more susceptible to pressure followed by type B fibres. That is why
there is muscle weakness (motor neuron – Type A) & diminished sense of touch &
pressure ( type B) . The least affected fibres are type C fibres which carry pain sensation. So
pain is not affected
7. A patient was admitted to the hospital with the following complaints:
inability to perform alternate movements rapidly and oscillatory movements of
hand during a voluntary movement but not at rest.
a) What is medical terminology used for the above symptoms?
b) Where is the probable site of lesion?
a) Inability to perform alternate movements – Adiadocokinesia
Oscillatory movements of hands during movements – intention tremors
b) Cerebellar lesion
8. A patient was admitted to hospital with involuntary rhythmic movements of his hands
which disappear on voluntary movements. On examination he showed rigidity through
out passive movement
a) What is the lesion? Where is it located?
b) What is the possible cause of this disease?
a) Lesion of nigrostriatal fibres in the basal ganglia
b) Defeciency of dopamine
 3

9. Effects of lesions at different levels of corticospinal tract

Effect of lesion of pyramidal tract during its course
• Motor areas of cortex – monoplegia
• Corona radiata – monoplegia
• Internal capsule – contralateral hemiplegia
• Brain stem – above decussation – contralateral hemiplegia
• Upper part of mid brain – cont. hemiplegia & ipsilateral III N palsy
(Weber’s syndrome)
• Pons – cont. hemiplegia & ipsilateral VI N palsy (Raymond’s syndrome)
--cont. hemiplegia & ipsilateral VII N palsy (Millard Gubler syndrome)
• Medulla – cont.hemiplegia & ipsilat. XII N palsy.
• Lateral corticospinal tract – ipsilateral UMN type of palsy
• Above C5 – both upper & lower limbs (Quadriplegia)
• Below T1 – only lower limbs(Paraplegia)
10. A 60 year old male shows the following personality changes
-distractability, difficulty in fixing attention
-inability to solve complex problems
-flight of ideas
-impairment of moral and social sense
a) What is the condition he is suffering from?
b) Comment on his memory impairment
a) Prefrontal lobe syndrome
b) Loss of short term memory
11. Physiological basis of hypertonia in Parkinson”s disease
Parkinson’s disease is due to lesion of basal ganglia.
Basal ganglia have a inhibitory control over the muscle tone. Basal ganglia lesion leads
to the removal of this inhibition and excessive excitation leads to hypertonia
12. Physiological basis of hypotonia on the same side in cerebellar lesions
Cerebellum has got a excitatory influence over excitatory reticulospinal&
vestibulospinal tract of same side. So lesion of cerebellum leads to loss of this
excitation and there by hypotonia occurs
13. Physiological basis of using L-Dopa in treating parkinsons disease
Parkinson’s disease is due to the deficiency of Dopamine. But dopamine can not pass
through Blood Brain Barrier. So it is given in the form of L-Dopa which will cross the
BBB easily
14. A patient was admitted to the hospital with complete loss of voluntary movements of
left lower limb. O/E, he had hypotonia, loss of reflexes and muscle atrophy.
a) What is the type of neurological disorder?
b) Where is the probable site of lesion?
a) Lower motor neuron lesion
b) The probable site of lesion is anterior nerve root of Lumbo – sacral nerves
15. A 20 year old male was brought to intensive medical care unit following a head on
collision with a truck. MRI revealed complete transection of the spinal cord at T1
level. What are the effects of transection.
- complete loss of all sensations below the level of section
- Paraplegia ( paralysis of the lower limbs only)
- respiration is not affected
- Maximum fall of BP due to loss of sympathetic tone
 4

16. Following chronic infection in middle ear, there is deviation of the angle of mouth
and incomplete closure of the eyelid on the same side.
Name this condition. What could be the cause and where is the site of lesion?
The condition is called Bells palsy. Caused by infranuclear lesion of facial nerve
. Site of lesion may be at stylomastoid foramen
17. Describe the mechanism of referred pain
--Visceral pain instead of being felt at the site of the viscera is frequently felt at some
distance,on somatic structures.
Eg: Appendicitis pain at the umbilicus
Cardiac pain at the inner aspect of left arm
Cholecystitis at the tip of the shoulder.
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain- both from the viscus & the
corresponding dermatome (somatic structures) converge on the same pathway to
the cortex
2. Facilitation theory: The visceral pain produces a subliminal fringe effect on the
Substantia Gelatinosa Rolando [SGR] cells which receive somatic pain nerves

CONVERGENCE THEORY

18. A sixty year old man has expressionless face and tremor of hands even at
rest. Name the condition and the physiological basis for the use of L-
Dopa in his treatment
The condition is called Parkinsonism.
Physiological basis of using L-Dopa – already discussed
19. Tabulate the differences between REM & NREM sleep
NREM sleep REM sleep
1. No rapid movements of eyeballs 1. Rapid movements of eyeballs
2.75% of total sleep 2. 25% of total sleep
3. Show б (delta) waves in ECG 3. Show β (beta) waves in ECG
4. No pontogeniculo occipital spikes 4. PGO spikes are present
5. Hypotonia 5. More hypotonia
6. Pulse, BP & respiration are slow 6. Pulse, BP & respiration are high & irregular
& regular
7. Brain activity is less 7. Brain activity is high
8. O2 consumption is less 8. O2 consumption is more
9. Decline in serotonin level 9. Decline in Noradrenalin & increase in Ach
10. Dreams can not be recalled 10. Dreams can be recalled
11. Threshold for arousal by 11. Threshold for arousal by sensory
sensory stimulus is elevated stimulus is further elevated
 5

20. How the receptors in semicircular canals get stimulated & explain the
functional significance of this
Same side: The receptors (Crista ampullaris ) are stimulated during angular rotation
of head in the same plane. The endolymph in the canal moves in the opposite
direction. Bending of stereocilium towards Kinocilium  movement of K+ ions
inside  depolarization
Opposite side: opposite movement of hair cells  hyperpolarisation
Function – maintains equilibrium during rotational movements
21. Mention any four neuro-transmitters within the brain and their physiological
role
1. Acetylcholine – excitatory neurotransmitter in various parts of brain
2. Dopamine – inhibitory neurotransmitter in basal ganglia
3. Serotonin – affects the mood of a person
4. Opiod peptides – takes part in modulation of pain
22. Explain why an infant with high levels of Bilirubin develops KERNICTERUS –
and not an adult
The Blood Brain Barrier which does not allow the passage of bilurubin is not
developed in the infants. So the bilirubin pass into the cerebral blood & accumulates
in the basal ganglia cells to produce Kernicterus. But in adults BBB is well
developed & bilirubin can not enter in to brain
23. What are opiod peptides? How do they alter pain sensation?
Opiod peptides are endogenous (produced inside the body) neurotransmitters which
bind to opiod receptors. They are enkephalins & endorphins. They inhibit the release
of Substance ‘P’ the neurotransmitter in the pain fibres. Thus they inhibit pain
transmission
24. What is Babinski’s sign? What is its physiological & pathological significance?
Babinski’s sign is abnormal plantar reflex in which the response is dorsiflexion of big
toe & fanning out of all other toes.
Physiological significance – This response is normal in infants before one year of age
Pathological significance – Presence of this sign indicates Upper motor neuron lesion
25. Explain why, irritation of viscus produces pain which is not felt not in
the viscus but in somatic structure that is distance away
This is referred pain.
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain- both from the viscus & the
corresponding dermatome (somatic structures) converge on the same pathway to
the cortex
2. Facilitation theory: The visceral pain produces a subliminal fringe effect on the
Substantia Gelatinosa Rolando [SGR] cells which receive somatic pain nerves
26. What is saltatory conduction? Give the advantages of saltatory conduction.
Jumping of impulse from one node of Ranvier to another node in myelinated nerve
fibres is called saltatory conduction .
Advantage: Helps in rapid conduction of impulse
 6

27. A 65 years old man came to the doctor with the complaint that his movements
were slow with no appreciated swinging of arms while walking, difficulty in
standing up, tremors in the hand at rest. O/E, there was muscular rigidity, mask-
like face, “ pill- rolling” movements in the fingers and the speech was slurred and
monotonous. No sensory loss was seen and the stretch reflexes were normal.
a) What is your diagnosis?
b) Which part of the CNS is affected?
c) What is the treatment?
a) Parkinsonism
b) Basal ganglia
c) L- Dopa ( a derivative of dopamine)
28. Name the normal EEG rhythms. Explain alpha block
Alpha rhythm ( α)
Beta rhythm (β)
Delta rhythm
Theta rhythm
Alpha block – The synchronized (regular slow waves) alpha rhythm is replaced by
desynchronized (irregular waves) when the mental activity is increased i.e., when
the eyes are opened & the mind is focused on some activity
29. Differentiate the features of UMN lesion from LMN lesion
UMN Lesion LMN Lesion
1. Damage to the motor tracts 1. Damage to the anterior horn cell & below
above the anterior horn cell
2. Spastic paralysis 2. Flaccid paralysis
3. Exaggeration of deep reflexes 3. Loss of both superficial & deep reflexes
& loss of superficial reflexes
4. Babinski sign positive 4. Babinski sign negative
5. No muscular atrophy 5. Atrophy of paralysed muscle
6. Muscle groups are affected 6. Individual muscle is affected
7. EMG normal 7. EMG shows fibrillation & fasciculation
e.g Hemiplegia e.g Poliomyelitis
30. Explain the mechanisms of differences between upper and lower motor neuron paralysis
Physiological basis of UMN lesion:
Spasticity – Interruption of corticoreticular fibers causes inhibition of medullary
reticulospinal tract which reduces muscle tone. Also facilitates the excitatory
reticulospinal pathway from pons. Hence hypertonia & spasticity
Exaggeration of deep tendon reflexes – Loss of inhibitory influence causes increased
gamma motor neuron discharge. This increases the sensitivity of muscle spindle to stretch
Loss of superficial reflexes – As efferent pathway is disrupted, superficial reflexes are
lost.
Babinski’s sign (Extensor plantar reflex) – Positive - Loss of inhibitory influence on
lower motor neurons supplying extensor muscles causes dorsiflexion of big toe
Physiological basis of LMN lesion:
Flaccidity – Denervation of muscle abolishes influence of gamma motor neurons there by
reduces tone
Reflexes – loss of lower motor neurons disrupts the reflex arc of the stretch reflexes as well
as the superficial reflexes. So both the reflexes are lost
 7

Babinski’s sign – Negative-due to loss of lower motor neuron activity

Muscle atrophy – Loss of innervation stops the secretion of nerve growth factors
31. Following brain injury, a patient developed hypersexuality, hyperphagia, and visual
agnosia and started exploring objects orally. What is your provisional diagnosis? Name
the parts of the brain affected in this dysfunction
Diagnosis – Cluver Bucy syndrome
Parts affected – Temporal lobe particularly involving amygdala
32. A patient complaints of incordination of movement and instability in maintaining
posture. O/E, he was found to have intention tremor and inability to perform rapid
alternate movement. Which structure of the CNS is most likely involved in this
dysfunction? What will be the state of muscle tone in this disease and what is the
physiological basis of change of the muscle tone?
Structure involved – Cerebellum
Muscle tone status – Hypotonia
Physiological basis – Cerebellum has got a excitatory influence over excitatory
reticulospinal & vestibulospinal tract of same side. So lesion of cerebellum leads to loss
of this excitation and there by hypotonia occurs
33. What happens when there is a lesion in Broca’s area?
Broca’s area ( area 44 ) is motor area for speech. It is located in the frontal lobe of
dominant hemisphere. Lesion causes motor aphasia.
34. Name the disease that results after destruction of the dopamine secreting fibers of the
substantia nigra. Mention two important clinical features of the condition
Parkinsonism. Clinical features – Rigidity & tremor at rest
35. A 50 year old person is admitted with paralysis of the right arm & leg for the past 6
weeks. He has spasticity of muscles on the affected side and deep reflexes are
exaggerated.
i) What is your diagnosis and where is the site of lesion?
ii) What is the response in plantar reflex?
i) Hemiplegia & the probable site of lesion is below the pyramidal decussation.
ii)The response in plantar reflex is dorsiflexion of big toe & fanning out of other toes.
36. If a person’s speech is slow and words are hard to come by, limited to 2 or 3 words with
which to express the whole range of meaning and emotion
i) What type of abnormality of language function he has?
ii) Which cortical area is affected?
iii) What is the most common cause for this disorder?
i) The dysfunction is motor aphasia.
ii) Area affected is Broca’s area (area 44)
iii) Most common cause – Injury or vascular accident
37.Mention the name of the diseases which have the following movements
1. Rapid, involuntary dancing movements
2. Continuous, slow writhing movements
3. Flailing movements of an entire limb
1. Chorea 2. Athetosis 3. Hemi Ballism
 8

38. A 5 year old boy complains of pain in the back & neck. He had a body temperature of
102®F. The following morning, there was complete paralysis of the right leg. On
examination, the muscle tone was greatly reduced, tendon reflexes were abolished in
affected limb. After a month, the muscles of the affected limb showed marked atrophy.
There was no sensory loss.
1. What is your diagnosis?
2. What is the type of lesion?
1. Poliomyelitis
2. LMN lesion
39. A man walking with barefoot had a thorn prick on his right sole
i) What is the posture he will adopt immediately?
ii) What are the reflexes that act quickly to maintain his posture?
- Flexion of right limb & extension of left limb
- Withdrawl reflex & crossed extensor reflex
40. Name the features of cerebellar lesion
Posture – Head rotated to normal side. The trunk is bent with the concavity towards the
affected side.
Equilibrium – Loss of equilibrium
Gait – Drunken gait
Tone – Hypotonia on the same side
Movements
a) Ataxia – incordination of movements
b) Asynergia:
Dysmetria – overshooting & undershooting the targets
Intention tremor – tremor that develops during movement
Decomposition of movement – movement occurring in stages
Rebound phenomenon – failure of termination of movement
Dysdiadochokinesia or Adiadochokinesia – inability to carry rapid supination &
Pronation
c) Nystagmus – Jerky movements of eyes
d) Scanning speech
41. Explain the mechanism of polyphagia in diabetic patients
Polyphagia in diabetes is due to decreased activity of VMN (Satiety center) which
requires insulin for glucose uptake.
42. List out the features of hemiplegia.
1. Impairment of voluntary movement
2. Impairment of fine skilled movements
3. Hypertonia – spasticity (clasp knife rigidity)
4. Loss of superficial reflexes
5. Exaggerated tendon reflexes
6. Extensor plantar reflex (Babinski sign positive)
 9

43. Explain the types of aphasia.

Speech disorders in the comprehension or production of spoken or written language are
called aphasias.
Types:
- Wernicke’s aphasia ( Sensory or fluent )
- Conduction aphasia ( Pure word deafness & blindness)
- Broca’s aphasia (motor or non fluent)
- Global aphasia
- Anomic aphasia
Type of aphasia Site of lesion Characteristic features
Fluent Excessive talk with full of
1. Sensory or Wernicke’s area (Area Jargons & Neologisms
Wernicke’s 22)

2. Conduction aphasia Speak well, good auditory

Areas 40,41& 42 ( in and comprehension but can not
around auditory cortex) Put parts of words together
Non fluent Broca’s area (Area 44) Slow speech, words are hard to
Motor/Broca’s aphasia come by, limited to two or three
words to express the whole range of
meaning and emotion
Anomic aphasia Angular gyrus -No difficulty in speech
-No difficulty in understanding
the auditory information
-Trouble in understanding the
written language or pictures
Global aphasia Both Wernicke’s and Scanty, non fluent speech
Broca’s area
44. A suspected case of meningitis was admitted in hospital for treatment. Doctors after
thorough investigation confirmed the case as the same. CSF examination report shows
rise in CSF pressure and some alterations in its chemical composition.
– Give your comments on the consequence
– of high CSF pressure with special reference to Monro Kellie doctrine
Monro Kellie doctrine – The cranial cavity consists of brain, CSF & cerebral blood
Vessels. The total volume of the contents at any time remain constant.
Consequence of high CSF pressure : Increases the intracranial pressure which
compresses the cerebral blood vessels & reduces the blood flow. This maintains the
volume constant.
45. Touch sensation is not totally abolished following hemisection of spinal cord – explain
The fibers carrying fine touch impulses ascend in the same side of spinal cord where as
the crude touch fibers are crossing to the opposite side and ascend. So the touch
sensation is not totally abolished in Hemisection of spinal cord
46. List out the features of thalamic syndrome
Thalamic syndrome :
Changes occurring in the contralateral half of the body when there is a lesion in
Thalamus
Features:
- Loss of sensations on the contralateral half of the body
- Astereognosis (failure to recognize the shape, size and texture of the object with
closed eyes)
 10

- Sensory ataxia
- Thalamic pain (development of spontaneous excruciating pain)
- Thalamic phantom limb
- Ameliognosis (failure to feel the limb)
- Hypotonia
47. A 12 year boy fell from a tree and was admitted to the hospital. O/E, he had loss of all
sensations, muscle tone, voluntary movements and reflexes from both lower limbs and
BP was 70/50
i) What is the cause for the above clinical condition?
ii) Why there is decrease in BP?
The condition is called paraplegia.
As the sympathetic fibers are affected, the blood vessels dilate due to loss of
sympathetic tone. This decreases BP.
48. Pain sensation is least affected following ablation of primary sensory cortex
Crude(protopathic) part of pain sensation terminates at thalamus. The epicritic part of
pain sensation is projected to somatosensory cortex. So after ablation(removal) of
primary sensory cortex, the person gets the perception of pain sensation. But the ability
to locate the pain sensation is lost.
49. Explain clasp knife type of paralysis in hemiplegia.
When a limb is passively flexed in a hemiplegic person, one finds a lot of resistance. This
is due to activation of muscle spindle in the antagonistic muscle which gets stretched.
The antagonistic muscle contracts & resistance in felt. When flexed with force it finally
gives way and a flexion can be achieved. This is due to relaxation of antagonistic muscle
which is caused by activation of Golgi tendon organ. This resembles the folding of a
clasp knife. So called as clasp knife rigidity
50. A patient with gun shot injury at thoracic region of spinal cord shows signs of motor
nerve lesion
i) Write the type of motor lesion happened below the level in this case.
ii) How can you confirm it clinically?
i) Upper motor neuron lesion
ii) Byeliciting Babinski’s sign. It will be positive in this condition
51. EEG of a young adult subject in lying down position who is fully awake with eyes closed,
physically and mentally in resting state showing predominantly synchronized waves.
These waves are suddenly replaced by desynchronized waves following opening of eyes
i) What is the synchronized and desynchronized waves?
ii) What is the cause for this change over?
i) Regular rhythmic ECG waves (alpha rhythm) recorded with closed eyes from the
parieto – occipital area in a resting man are synchronized waves.
Waves of faster rhythm with low voltage (beta rhythm) are called desynchronized
waves.
ii) The replacement of alpha rhythm by beta rhythm is due to the activity of ARAS
following sensory stimulation. The sensory impulses enter the ARAS through
collaterals from specific sensory pathway. From ARAS the impulses are relayed
through nonspecific thalamic projection system to the cortex, causing
desynchronization.
52. In cerebrovascular accident there is a spastic paralysis while selective lesion of
pyramidal tract causes hypotonia - justify
Pyramidal tract always facilitates the muscle tone. So selective lesion of pyramidal tract
alone causes hypotonia. But in most of the CVAs, extrapyramidal fibers also get
damaged. So spasticity develops instead of hypotonia
 11

53. What type of motor dysfunction you will expect when complete transaction of spinal
cord is done at T1 level?
Paraplegia – loss of muscle tone, voluntary movements and reflexes from both lower
limbs
Maximum fall in BP
54. What is mass reflex? What is its clinical significance?
It is obtained when a scratch is applied at any point on the lower limb or on the
anterior abdominal wall below the lesion. The responses in the reflex are :
- Flexion of lower limbs and contraction of anterior abdominal wall
- Evacuation of the bladder and the rectum
- Profused sweating below the level of lesion
This reflex is seen several months after the spinal cord lesion due to irradiation of
afferent stimuli from one reflex center to another center.
Clinical significance: Elicited to evacuate rectum & urinary bladder in patients with
spinal cord lesion
55. What are the effects of degeneration of cerebellar cortex with loss of Purkinjee fibers?
Posture – Head rotated to normal side. The trunk is bent with the concavity towards
the affected side.
Equilibrium – Loss of equilibrium
Gait – Drunken gait
Tone – Hypotonia on the same side
Movements
a) Ataxia – incordination of movements
b) Asynergia:
Dysmetria – overshooting & undershooting the targets
Intention tremor – tremor that develops during movement
Decomposition of movement – movement occurring in stages
Rebound phenomenon – failure of termination of movement
Dysdiadochokinesia or Adiadochokinesia – inability to carry rapid supination &
Pronation
c) Nystagmus – Jerky movements of eyes
d) Scanning speech
Motor skills; Inability to learn new motor skills as Purkinjee fibers are responsible for
learning new motor skills
56. Explain the phenomenon of hyperrigidity in Parkinsonism.
Parkinsonism is due to basal ganglia lesion. Basal ganglia control reflex muscular
contraction (muscle tone) through suppressor motor areas and inhibitory medullary
reticular formation. In lesions of basal ganglia there is exaggeration of the muscle tone
57. What is an intention tremor? Why does it occur in cerebellar lesion?
Tremor that develops during movement is called intension tremor. This is due to
dysmetria ( failure to judge the distance, direction, range & force of movement) that is
caused by cerebellar lesion. In a healthy person, error during a movement is corrected
in a single attempt. In lesion of neocerebellum or intermediate zone of cerebellum, there
is a defective planning or failure to correct the errors during movement. It takes several
attempts to correct the error. Hence tremor occurs during movement
58. Why does a strong noxious stimulus produce a prolonged withdrawal response?
A stronger noxious stimulus produces a prolonged withdrawal response due to
prolonged & repeated firing of the target motor neurons. This process is called after
discharge. After discharge is due to two mechanisms:
- Involvement of many interneuronal pathways
- Presence of reverberating circuits in the interneuronal pathways in the spinal cord
 12

59. What is the physiological role of ‘P’ factor in muscle pain?

When there is a occlusion of blood flow to the muscle, contraction of that muscle causes
pain. This may be due to the release of a chemical agent(Lewis ‘P’ factor) which causes
pain when its local concentration is high enough. This pain disappears when the blood
flow is restored as the material is washed out or metabolized. The identitity of the P
factor may be K+. Angina pectoris & intermittent claudication are examples for the
accumulation of ‘P” factor.
60. Describe about the Vannilloid receptors.
Vannilloid receptors are the receptors that respond to noxious heat. There are two
types: VRL-1 & VR1). Vanillin is a group of compounds, including capsaicin, which
produces pain.VR1 receptors respond to capsaicin , Protons & temperatures above
43° C. VRL-1 respond to temperatures above 50° C, but not to capsaicin
61. What is syncope? Briefly explain any one type of syncope
Transient loss of consciousness accompanied by loss of postural tone is called syncope.
Types:
Postural syncope
Micturition syncope
Cardiogenic syncope
Deglutition syncope
Effort syncope
Carotid sinus syncope
Postural syncope:
Definition: Syncope caused by sudden standing
Cause: Pooling of blood in the dependant parts of the body
62. What are astrocytes? Give two important functions of astrocytes
Astrocytes are neuroglial cells (cells of supporting tissue of nervous system)
Functions:
1. Produce substances which help in the growth of neurons
2. Processes of astrocytes take part in forming Blood Brain Barrier
63. What is stereognosis? Mention the sensory modalities carried by the posterior column
of the spinal cord.
Stereognosis: Ability to identify familiar objects with closed eyes by recognizing size, shape
and texture of the objects.
Sensory modalities carried by the posterior column of the spinal cord.
- Fine touch
- Tactile localization
- Two point discrimination
- Pressure
- Vibration
- Stereognosis
- Conscious proprioception
64. Give an account of lumbar puncture and its clinical applications
Lumbar puncture is tapping of CSF from lumbar cistern. It is performed by inserting
a needle in between the L2and L3 vertebrae.
Clinical applications: CSF examination is required in many disorders of CNS. Mainly done
for
a) Diagnostic purposes
b) For relieving the intracranial pressure temporarily
 13

65. What is Papez circuit? What is the significance of this circuit?

The limbic structures are interconnected by circuitous tracts which were initially
described by Papez, hence called ‘’Papez circuit”.

Cingulate gyrus

Hippocampus Anterior nucleus

Mammillary body

Significance: Responsible for emotions and resting EEG

66. What is alpha block in ECG? What does it represent?
Replacement of the regular alpha rhythm by irregular low voltage activity in the EEG
recording is called alpha block.
It represents the aroused, alert state of the mind
67. What are receptor functions of Muscle spindle and golgi tendon organ? What is the
major difference in the excitation of golgi tendon organ versus muscle spindle?
Muscle spindle – Receptor organ of muscle. Muscle spindle & its reflex connections
constitute a feedback device that operates to maintain muscle length.
Excitation leads to stretch reflex- stretching of muscle causes shortening
of muscle
Golgi tendon organ – Receptor organ of tendon. Functions as a transducer in a
feedback circuit that regulates muscle force. Excitation leads to
inverse stretch reflex- strong stretch & great tension in the muscle
cause relaxation of the muscle
Difference in the excitation:
 Muscle spindle is excited only by passive stretching of the muscle & stops
firing in active contraction of muscle
 Golgi tendon organ is excited by both passive stretch and active
contraction of muscle
68. Why rubbing the skin near painful areas is often effective in relieving pain?
This can be explained with the help of gate control hypothesis. According to this
Hypothesis, Aβ (large myelinated fibers) afferents carrying tactile sensation interact
with small unmyelinated C and A delta fibers carrying pain sensation. The
interaction is through inhibitory cells of SG (Substantia Gelatinosa) in the dorsal
horn of spinal cord. Stimulation of touch fibers enhances the SG activity and blocks
the transmission of pain
69.If a person is having ataxia, past-pointing, intention tremor
i) Where is the lesion?
ii) Reason out the above abnormalities
iii) What are the other abnormal features of the lesion?
i) Lesion is at cerebellum
ii) Ataxia – incoordination of movements
Past pointing (Dysmetria) – attempting to touch an object with a finger results in
overshooting to one side or other
Intention tremor – Dysmetria in the movement initiates a gross corrective action,
 14

but the correction overshoots to the other side. Hence, the finger
oscillates back and forth causing intention tremor
(The above features are due to errors in the rate, range, force and
direction of movements)
iii) The other abnormal features of cerebellar lesion are already discussed)
70. Explain vertigo and motion sickness. Give physiological basis for the above two.
Vertigo is a type of dizziness, where there is a feeling of motion when one is
Stationary. It is commonly associated with vomiting or nausea,
unsteadiness, and excessive perspiration. Blurred vision, difficulty
speaking, a lowered level of consciousness, and hearing loss may also
occur. Central nervous system disorders may lead to permanent symptoms.
Motion sickness – a type of dizziness caused by any kind of movement. People tend to get
motion sickness on a moving boat, train, airplane, car, or amusement park rides.
The most common signs and symptoms of motion sickness include:

 Nausea
 Pale skin
 Cold sweats
 Vomiting
 Dizziness
 Headache
 Increased salivation
 Fatigue

Physiological basis:
Vertigo – the most common cause is Benign paroxysmal positional vertigo (BPPV) which is a
disorder caused by problems in the inner ear. Its symptoms are repeated episodes of
positional vertigo, that is, of a spinning sensation caused by changes in the position of
the head.
Motion sickness occurs when the body, the inner ear, and the eyes send conflicting signals to the
Brain
71. A person scratches with a sharp pin over the skin. Discuss the responses you get
The response will be a three phased reaction called “Triple Response”. It is produced due to
the release of histamine from the mast cells.
Components of the Triple Response:
1.Red reaction: red line (transient local vasodilation due to histamine), appears in few seconds.
2.Flare: redness in the surrounding area due to arteriolar dilatation mediated by axon
reflex appears slowly.
3.Wheal: localized edema in the region of the redline (increased capillary permeability and
exudation of fluid from capillaries and venules due to histamine release), appears in 1
minute
 15

72. Correlate ECG waves with sleep and wakefulness with diagram

73. What is phantom limb? What is the cause for it?

Some of the amputated patients complaint of pain and proprioceptive sensations in
the absent limb. This is called phantom limb.
Cause: The ends of the nerves cut at the time of amputation form nerve tangles called
neuromas. These neuromas may discharge spontaneously or when pressure is
put on them. The impulses produced are in nerve fibers that previously came from
the sense organs in the amputated limb and the sensations evoked are projected to
where the receptors used to be present.
 16

74. After a brain injury, a man developed an aphasia when he talked rapidly, but made little
sense of wat he talked. What type of aphasia he developed and what is the probable site of
lesion?Mention the functions of the area involved in the abnormality.
 CNS NOTES - APPLIED
1. Differentiate UMN & LMN lesion
UMN Lesion LMN lesion
1. Damage to the motor tracts above the anterior 1. Damage to the anterior horn cell and
horn cell below
2. Spastic paralysis 2. Flaccid paralysis
3. Exaggeration of deep reflexes & loss of 3. Loss of both superficial and deep
superficial reflexes reflexes
4. Babinski Sign positive 4. Babinski sign negative
5. No muscular atrophy 5. Atrophy of paralysis
6. Muscle group are affected 6. Individual muscle is affected
7. EMG normal 7. EMG shows fibrillations and
fasciculations
(E.g) Hemiplegia and Parkinsonism (E.g) Poliomyelitis

------------------------------------------------------------------------------------------------------------------------------------------
2. Hemiplegia
- refers to paralysis of one half of the body
Cause: Pyramidal lesion
Main site of lesion: Internal capsule
Main cause of lesion: rupture of tenticulostriated artery, a branch of middle cerebral artery
3 stages of clinical features
A .stage of shock:
Loss of muscle tone
Loss of voluntary movements
Loss of all the reflexes
B. stage of recovery:
-hypertonia (spasticity)
-hemiplegic posture
-Exaggerated deep reflexes
-Babinski’s sign positive
-Loss of superficial reflex
-spastic gait
C. Stage of reflex failure
-Loss of muscle tone and wasting of muscles
-Loss of all reflexes
-Development of bed sores
-Patient may die
------------------------------------------------------------------------------------------------------------------------------------------
 3. Complete transection of spinal cord
-Spinal cord is completely separated from the higher centers
Cause: Gunshot wounds, occlusion of blood vessel due to thrombosis
Features:
A. Stage of spinal shock:
-Complete functional loss below the transection
-Flaccid paralysis due to loss of muscle tone
-Loss of all reflexes
-Loss of vasomotor tone if transection occurs above the lower thoracic level of spinal cord
-Loss of all sensations.
Different levels:

Above C8 - Quadriplegia (Paralysis of both upper and lower limb)

Below C8 - Paraplegia (Paralysis of only lower limbs)
Above C3 - No respiratory paralysis

At T1 -
-Complete anesthesia below the section
- Paraplegia (Paralysis of only lower limbs)
-Maximum fall in blood pressure (due to loss of vasomotor tone)
-Horner’s syndrome (due to sympathetic failure)

Below lower thoracic - Fall in BP is less

---------------------------------------------------------------------------------------------------------------------------------------

4. Hemisection of spinal cord (Brown – sequard syndrome)

Refers to lesion in one lateral half of the spinal cord

Level of spinal cord Same side Opposite side

Below the level of section Sensory: Sensory:
Damage of dorsal column -Loss of pain
tracts Temperature and crude touch
-Loss of fine touch, tactile
discrimination, pressure, Motor : Normal
vibration, kinaesthetics and
stereognosis Vasomotor: Normal
Motor: UMN paralysis
Vasomotor: Temporary loss of
vasomotor tone
(vasodilatation)
At the level of lesion Sensory Sensory: Not affected
-Anaesthesia (complete loss of
sensation) Motor: Not affected
Motor: LMN paralysis
Vasomotor: Loss of Vasomotor: Not affected
vasomotor tone
4. Differentiate between Sherrington’s Classical and Ischaemic Decerebrate
Rigidity

Sherrington’s classical decerebrate rigidity Ischaemic decerebrate rigidily

1. Produced by section at mid collicular level Produced by ligation of 2 carotid

(in between superior colliculus and inferior arteries and the basilar artery
colliculus)
2. Fatal and traumatic procedure 2. Safe procedure

3. Rigidity is due to increased gamma motor neuron 3. Rigidity is due to alpha motor neuron
discharge caused by simultaneous activation of discharge caused by activation of
facilitatory reticulospinal tract and removal of vestibulospinal tact
inhibition by inhibitory tracts

4. Features 4. Features are same

-Hyper extension of head, neck, back and tail
(opisthotonus)
-Extension of all four limbs
-No righting reflexes
-Presence of tonic reflexes

5. Rigidity can be abolished by deafferentiation 5. Rigidity cannot be abolished by

deafferentiation

------------------------------------------------------------------------------------------------------------------------------------------
5. PARKINSONISM
-a disease caused by lesion in basal ganglia also called as “Paralysis Agitans’ or “Shaking Palsy”
-first described by James Parkinson in 1817
Pathogenesis
Imbalance between excitation and inhibition in the basal ganglia mainly caused by the loss of
dopaminergic inhibition of the putamen.
Causes
Degeneration of dopaminergic fibers from substantia migra (pars compacta) to striatum
(Nigrostriatal fibers)
Old age
Drugs chloropromethazine
MPTP (Methyl phenyl tetrahydro pyridine) poisioning
Clinical Features
Involves a triad of akinesia, tremor & rigidity
Akinesia – hypokinetic feature
Rigidity Tremor - hyperkinetic features
Akinesia / Bradykinesia
-Lack of initiation of movements
-retardation of movements
 - loss of automatic, associated movements (statue like appearance, mask like face)
-Defect in speech
-loss of timing & scaling of movements (micrographia)
Rigidity
 Hypertonia in the agonistic and antagonistic (mostly proximal) muscle
 Caused by increased discharge of gamma motor neuron due to loss of inhibitory control
 2 types of rigidity
Cog wheel - resistance to passive movement disappears intermittently
Lead pipe – continuous resistance to passive movement

Posture – stupor (flexion attitude)

Tremor
 Occurs at rest
 Pill rolling tremor
 Alternate contraction & relaxation of agonists and antagonist of hands and fingers at a
frequency of 6-8
o hertz/second
 Absent in sleep

Festinant gait
 body is bent forward
 moves forward with short quick shuffling steps as if to catch center of gravity
 when pushed forward or backward, the subject is unable to stop quickly. This is called
retropulsion.

TREATMENT
Levo Dopa --- can cross the blodd brain barrier, but dopamine cannot cross
Carbidopa – inhibits decarboxylation of L-dopa in peripheral tissues
Anticholinergics – Atropine
Dopamine agonists – Bromocriptin

Surgical
Pallidotomy
VL N of thalamus destroyed

Chorea – Rapid involuntary dancing movement (Lesion in caudate nucleus)

Athetosis – continuous, slow writing movement (Lesion in putamen)
Ballism – wild, flinging involuntary movements of extremities
Features seen in one side of the body is called “Hemiballism”
(caused by lesion in subthalamic nucleus)
 6. CEREBELLAR LESION
Features: (4 A, 4 D & SIN)

Ataxia Dysmetria Scanning speech

Atonia Decomposition Intention tremor
Asynergia Dysdiadochokinesia Nystagmus
Asthenia Drunken gait

Physiological Basis:
Ataxia - In co-ordination of movements
Atonia/ Hypotonia - Cerebellum has got a excitatory influence over excitatory reticulospinal &
vestibulospinal tract of same side. So lesion of cerebellum leads to loss of this
excitation and there by hypotonia occurs
Asynergia – Lack of coordination between protogonistics, antagonists & synergists muscles
Asthenia – Slow movements (muscles get tired easily)

Dysmetria - errors in the rate, range, force and direction of movements (This leads to
decomposition of movement, overshooting & undershooting the targets (intention
tremor), Dysdiadochokinesia, Rebound phenomenon etc.,)
Dysdiadochokinesia - Inability to perform rapid, alternate movements(supination & pronation of
hands)
Decomposition of movement – movement occurring in stages
Drunken gait – Walking in a clumsy manner with a wide base (walks in a zig zag line)

Scanning speech – Slow and lalling (Like a baby) – due to imperfect use of the movements of the
laryngeal muscles and tongue
Intention tremors - Oscillatory movements of hands during movements/ tremor that develops during
movement
This is due to dysmetria ( failure to judge the distance, direction, range & force of
movement) that is caused by cerebellar lesion. In a healthy person, error during
a movement is corrected in a single attempt. In lesion of neocerebellum or
intermediate zone of cerebellum, there is a defective planning or failure to
correct the errors during movement. It takes several attempts to correct the
error. Hence tremor occurs during movement
Nystagmus - Jerky movements of eyes when trying to fix the eyes on a subject (due to slow to – and-
frow movements of eyes on looking to affected side due to hypotonia and a rapid to-and
–fro movement on looking to opposite side)

Other Features:
Posture – Head rotated to normal side. The trunk is bent with the concavity towards the
affected side.
Equilibrium – Loss of equilibrium
Rebound phenomenon – failure of termination of movement
 7. Effect of lesion of pyramidal tract At Various Levels
Motor areas of cortex – monoplegia
Corona radiata – monoplegia
Internal capsule – contralateral hemiplegia
Brain stem – above decussation – contralateral hemiplegia
Upper part of mid brain – contralateral hemiplegia & ipsilateral III N palsy
(Weber’s syndrome)
Pons – contralateral hemiplegia & ipsilateral VI N palsy (Raymond’s syndrome)
--contralateral hemiplegia & ipsilateral VII N palsy (Millard Gubler syndrome)
Medulla – contralateral hemiplegia & ipsilateral XII N palsy.
Lateral corticospinal tract – ipsilateral UMN type of palsy
Above C5 – both upper & lower limbs (Quadriplegia)
Below T1 – only lower limbs (Paraplegia)
 1

Special senses

10 marks
Describe the visual pathway & the effect of lesions at various levels with the suitable
diagram
The visual pathway consists of
1. Retina
2. Optic nerve
3. Optic chiasma
4. Optic tract
5. Lateral geniculate nucleus
6. Optic radiation(geniculo-calcarine tract)
7. Visual cortex
 2

1. Retina:
- rods & cones in the retina convert light in to electrical impulses.
2. Optic nerve:
- formed by the fibers of ganglion cells.
- the fibers in the lateral (temporal ) half of the nerve carry the impulses from the nasal field of the
same eye.
- the fibers in the medial half of the nerve carry impulses from the temporal field of the same eye.
3. Optic chiasma:
- formed by the crossing of medial fibres of both the optic nerves.
4. Optic tract:
- consists of nasal fibres from the opposite optic nerve and temporal fibers from the optic nerve of the
same side.
- fibres run backwards and relay in lateral geniculate nucleus of thalamus.
5. Lateral geniculate nucleus(LGN):
- The LGN is divided into six layers of cells.
- The crossed fibers of the optic tract terminate in layers 1, 4 and 6 while the uncrossed fibers terminate
in layers 2, 3 and 5.
6. Optic radiation:
- arise from the LGN
- is also referred as geniculo-calcarine tract
- the fibers are arranged supero medially & infero laterally
- terminates in primary visual area(17)
- also projected to visual association areas 18 and 19.
7. Visual cortex:
- The primary visual cortex is Brodmann area 17
- also known as V1
- located on the medial surface of the occipital lobe along the walls and lips of calcarine fissure.
Other connections
1. to suprachiasmatic nucleus of hypothalamus - concerned with circadian rhythm.
2. to pretectal nucleus which inturn sends fibres to 3rd cranial nerve nucleus = mediates the light
reflex.
3. From the occipital cortex to the frontal eye field (area 8) - concerned with the movement of
eyeball (convergence) & accommodation reflex
4. From occipital cortex to superior colliculi and from there to III, IV, VI cranial nuclei and to the
spinal cord - mediate tone, posture, equilibrium and visuospinal reflexes.

Effect of lesion of visual pathway at different levels

• The loss of vision in one entire visual field is referred as anopia.

• Loss of vision in one half of the visual field is called hemianopia. It is of two types:
– Homonymous hemianopia
– Heteronymous hemianopia
 3

Site of lesion Condition Diagram

1 Right optic Right eye anopia
nerve
2 Optic Bitemporal
chiasma hemianopia
3 Lateral Binasal
Fibers hemianopia
4 Right optic Left homonymous
Tract Hemianopia

5 Rjght optic Left homonymous

radiation Hemianopia
1 6 Inferolateral Left homonymous
2
3 fibers of Superior
optic Quadranopia
radiation
4
7 Superomedial Left homonymous
Fibers of Inferior
5 Optic Quadranopia
radiation
6
8 Inferolateral Left homonymous
fibers of Superior
7 optic Quadranopia
radiation in With macular
calcarine Sparing
fissure
8 9 Superomedial Left homonymous
9 fibers of Inferior
optic Quadranopia
radiation in With macular
10 calcarine Sparing
fissure
10 Visual cortex Left homonymous
Hemianopia
With macular
Sparing
 4

5 marks
1. Describe the circulation & functions of aqueous humour.
Aqueous humour
 Homogenous fluid that fills the anterior & Posterior chambers
 pH 7.1-7.3
 Refractive index 1.33
 Composition – Less glucose & more Lactic Acid than plasma with high ascorbic acid
Formation of Aqueous Humour:
 Formed by the ciliary processes-
 Mechanism:
1. Active secretion
2. Ultra-filtration
 Rate of formation: 2-3 cu.mm per minute
Circulation of Aqueous Humour:
 Aqueous humor circulates within the eye
 Formed by the ciliary processes
 Secreted into posterior chamber
 Passes between ligaments of lens
 Passes through pupil into Anterior chamber
 Flows into angle between cornea & iris
 Flows through trabeculae
 Flows into canal of Schelmn & extra ocular veins
 Re-enters blood circulation

Functions Of Aqueous humour:

 Provides nutrition to cornea & lens (avascular structures)
 Maintains IOP (Intra ocular pressure)
 Maintains shape of eyeball
 Acts as refractive medium
------------------------------------------------------------------------------------------------------------------------------
2. Describe the mechanism of accommodation for near vision
• It is the ability of the eye to see distant and near objects clearly. This involves the process of
adjusting the shape of the lens so that the external image falls exactly on the retina.
Accommodation of the Lens for near vision
• Ciliary muscles contract
• Ciliary body pulls forward and inward
• Tension on suspensory ligaments of lens is decreased
• Lens becomes thicker (rounder) due to its elasticity
• Pupils constricts
Near point:
• It is the nearest point to the eyes at which an object can be brought into clear focus by
accommodation.
– At age 10: Near point – 9 cm
– At age 60: Near point – 83 cm
• The near point recedes with age.
Near response
1. Convergence of eye ball
2. Constriction of pupil
3. Curvature (anterior) change in lens
 5

Accommodation of the Lens for far vision

• Ciliary muscle is relaxed
• Ciliary body is pulled backward and outward
• Tension on suspensory ligaments of lens is increased
• Lens becomes thinner (flatter) due to its elasticity
• Pupils dilate
Accommodation Reflex
Changes in the eye in response to changing the gaze from long distant to short distant
Responses:
Constriction of pupil
Convergence of eyes (medial )
Curvature of lens (increase in anterior)
Pathway of the Accommodation reflex

Near vision
.
Retina

Optic nerve

LGN

Visual cortex

Frontal eye field

Superior colliculus

III cranial nerve nucleus

Ciliary ganglion

Short ciliary nerve

Sphincter papillae Ciliary muscle Medial rectus

Constriction of pupil Curvature of lens Convergence of eye balls

(increase in anterior)
 6

-------------------------------------------------------------------------------------------------------------------------------
3. Briefly describe the mechanism of dark adaptation
Adaptation to dark (Scotopic vision)
On entering dark room from bright area, initially the vision is poor, later it improves.This decline
in visual threshold is called dark adaptation.
Time duration for dark adaptation depends
1. Intensity of light
2. Duration of exposure
3. Vit A Content
Two phases
1. Adaptation of the cones (5min)
2. Adaptation of rods (20min)

Changes in the eye during dark adaptation

1. Pupils dilate
2. Sensitivity of the photoreceptors to light increases
3. Resynthesis of photo pigments
4. Decrease in visual acuity
5. Vision changes from cone to rods (photopic to scotopic). This is called PURKINJE SHIFT.
Visual Purple//Rhodopsin Cycle

Rhodopsin (11 cis retinal+ opsin ) Pre-lumi rhodopsin

Light
Dark Lumi rhodopsin

Meta rhodopsin I
Opsin
Meta rhodopsin II
+
Retinal isomerase
11 cis retinal All transretinal
Isomerase
11 cis retinol All transretinol (Vitamin A)
 7

---------------------------------------------------------------------------------------------------------------------------
4. Write short notes on colour vision
• A sensation evoked by different wavelengths of light.
• Function of cones.
Physiological Basis of colour vision
• Three different types of cones
• Three types of pigments (the opsin protein part differs from rhodopsin),
• Each pigment has maximum absorption at different wavelengths
• blue-absorbing cones – cyanopsin pigment (max absorption at 445nm)
• green-absorbing cones – Iodopsin pigment (max absorption at 535 nm)
• red-absorbing cones – porphyropsin pigment (max absorption at 570 nm)
Primary colours
• Red
• Green
• Blue
Theories of colour vision
• Young – Helmholtz theory
• Granit modulator & dominator theory
• Hering opponent colour theory
• Land’s retinex theory
Young – Helmholtz theory
• Trichromatic theory
• Red , green , blue – 3 primary colours
• The 3 types of cones have 3 different pigments
• Each pigment is maximally sensitive to one primary colour
- But also responds to other 2 primary colours
• Sensations of various colours are due to stimulation of different receptors at
different intensities.
Processing of colour perception
• Analysis of colour occurs in the retina
• Information is then passed on to the brain for interpretation.
• Centre of fovea is blue blind.
• Blue cones are absent here.
• Retina , lateral geniculate nucleus , visual cortex all have a combined role in
perception of colour.
Colored light strikes the retina
↓
Depending on the color mixture cone will respond
↓
Response is in the form of local potentials
↓
LP transmitted in bipolar cells
↓
Ganglion cells activated
↓
Signals from the 3 cones are processed in the ganglion cell
↓
Reach the layers of LGN
↓
Processed in LGN
 8

↓
Transmitted to cortex V1
↓
Impulses reach V4

COLOUR BLOBS

• Primary visual area 17 contains color blobs – clusters of colour sensitive peg shaped neurons.
------------------------------------------------------------------------------------------------------------------------------

5. What are the errors of refraction? How will you correct it?
• In a normal human eye light rays are focused on retina.
• If not focused on retina-called Refractive errors.
• Due to abnormality in cornea or lens.
• Normal eye is called Emmetropic Eye
• Abnormal focus is called Ametropic Eye
Refractive Errors
1. Myopia (short sight)
2. Hypermetropia (Long sight)
3. Presbyopia
4. Astigmatism
5. Anisometropia
6. Aphakia
7. Cataract
Error Defect Cause Feature Correction

Myopia Long distant objects Longer eye ball / high Light rays are Biconcave
not clear refractive power of lens focused in front of lens
retina

Hypermetropia Short distant objects Shorter eye ball / Low Light rays are Biconvex
not clear refractive power of lens focused behind the lens
retina

Presbyopia Short distant objects Loss of elasticity & Decrease in the Biconvex
not clear plasticity of lens and power of lens
also decrease in power accommodation of
of ciliary muscle due to eye
aging

Astigmatism Blurring of vision Ununiform curvature of Light is focussed Cylindrical

the cornea at multiple points lens
on retina

Aniso Difference in the Congenital Eye with high Correction

metria refractive power refractive power – of each eye
between the two eyes Dominant eye separately
Eye with less with
refractive power – appropriate
 9

Suppressed eye lenses

Aphakia Diplopia & Removal of lens Complete loss of Wearing

Astigmatism due to following cataract accommodation spectacles
absence of lens surgery / dislocation of (hypermetropic) with power
lens of + 11
diopters/IOL
implantation

-----------
--------------------------------------------------------------------------------------------------------------------6.
Describe the functions of middle ear.
Components of middle ear:
1. Three small bones (ossicles):
1)Malleus
2)Incus
3)Stapes
2. Two small muscles:
1)Tensor tympani
2)Stapedius muscle
Functions of middle ear
1. Tympanic Reflex:
• When loud sounds are transmitted through the ossicular system (Malleus, Incus, stapes) into
the CNS, a reflex occurs to cause contraction of both Stapedius and tensor tympani muscles.
This is called tympanic reflex or attenuation reflex
• The contraction of tensor tympani muscles pulls the handle of the malleus inward, while the
stapedius muscle contraction pulls the stapes outward
• These two forces oppose each other and this causes rigidity of the entire ossicular system
which greatly reduces the transmission of low frequency sounds.
Significance of tympanic reflex
to protect the cochlea from damaging vibrations caused by excessive loud sound i.e. low
frequency sounds.
2. Impedance Matching:-
• Whenever sound wave travels from a thinner medium to denser medium, some
amount of sound energy is lost at the interphase of two medium.
• This happens in ear also. When sound travels from air filled middle ear into
denser fluid medium of inner ear, there is a loss of sound energy at oval window
• Middle ear compensates this by increasing the sound energy level by several times at oval
window.
• Middle ear achieves this by three mechanism which are combinely referred as impedance
matching.
The mechanism are:-
1. Area difference
• As the area of the tympanic membrane is large than the area of the oval window,
the forces collected over the tympanic membrane are concentrated on a smaller
area of oval window.
• This increases the pressure at the oval window by 17 times.
2. Lever action of the middle ear bones.
• The arm of incus is shorter than that of malleus and this produces a lever action.
• This increases the force by 1.32 times and decreases the velocity at the stapes.
 10

3. Buckling factor:-
• The tympanic membrance is conical in shape. As the membrane moves in and out
it buckles so that the arm of the malleus moves less than the surface of the
membrane.
• This also increase the force and decreases the velocity
3. Function of Eustachian tube:
Equalizes the pressure on both sides of tympanic membrane
-------------------------------------------------------------------------------------------------------------------------------
7. Describe organ of corti
Organ of Corti
• Receptor organ of hearing
• Situated on the basilar membrane
• Extends from the base to apex of cochlea
Main components of Organ of Corti

1. Inner hair cells

2. Outer hair cells
3. Rods of corti
4. Tunnel of Corti
5. Lamina reticularis
6. Basilar membrane
7. Tectorial membrane
8. Deiters' cells
9. Hensen's cells

2 7

1 5

3 9

8
6
4

• INNER HAIR CELLS

- one row ( 3500 in number)
- flask shaped
- connected to lamina reticularis
- Stereocilia of hair cells float freely
• OUTER HAIR CELLS
- three or four rows ( 20000 in number)
- test tube shaped
- stereocilia –embedded in the tectorial membrane
 11

8. Trace the pathway for hearing

I order neuron :
From the bases of the hair cells  cell bodies form the spiral ganglion around the modiolus
 axons form the cochlear nerve joins with the vestibular nerve to form the
vestibulocochlear nerve  end in cochlear nuclei
II order neuron :
From cochlear nuclei  ascend to the nearby superior olivary nucleus (of both sides)  then
ascend in the lateral lemniscus  end in inferior colliculi of midbrain
III order neuron:
From inferior colliculi to medial geniculate bodies of thalamus
IV order neurons: complete the pathway from thalamus to primary auditory complex
 12

9. Trace the olfactory pathway

receptor cell axon

↓
pierce the cribriform plate of ethmoid
↓
enters olfactory bulb
↓
synapse with dendrites of mitral cells to form olfactory glomeruli
↓
axons of mitral cells pass posteriorly through olfactory stria
↓
olfactory cortex
(anterior olfactory nucleus, olfactory tubercle, prepyriform cortex, amygdala, entorhinal cortex
↓
From the olfactory cortex signals reach
↓
– Orbito frontal cortex
– Hypothalamus
– Hippocampus
Thus olfactory impulses are projected both to
– Neocortex
Perception & discrimination of odours
– Limbic system
Emotional, motivational, behavioral & physiological effects of odours

Olfactory
Cribriform plate of ethmoid bone Glomerulus
straie
bone

Olfactory bulb

Olfactory
neuron

Olfactory receptors
 13

10. High light the special features of olfactory pathway

Pathway involves only two sets of neurons

Receptor is a modified neuron
Neurons are in direct contact with external environment
Neurons degenerate & regenerate periodically
No relay in thalamus
Olfactory signals do not reach somatosensory cortex but reach orbitofrontal cortex
Impulses reach limbic system & so related to food and sex related beaviour
-------------------------------------------------------------------------------------------------------------------
11. Trace the taste pathway
Taste buds

Taste fibres in vii, ix & x nerves (I order neuron)

Tractus solitarius (in medulla)

Nucleus tractus solitarius (II order neuron)
 Cross over
Joins medial leminiscus

VPM (Ventral Postero Medial Nucleus of thalamus (III order neuron)

Brodman’s area 43

Gustatory Pathway from Taste

Buds

Figure 16.2
 14

12. Name the primary taste sensation. How are they distributed on the tongue?
Outline the basic taste modalities & explain the mechanism of taste sensation

Primary taste sensations

1. Sweet
2. Salt
3. Sour
4. Bitter
5. Umami

BASIC TASTE PRODUCED BY MECHANISM OF PART OF TONGUE MOST

SENSATIONS STIMULATION SENSITIVE

Sweet Sugars, glycols & ↑ cAMP→↓K+ Tip

aldehydes. conductance

Bitter Alkaloids ↑ IP3→ ↑Ca++ release Back

Sour H+ ions Blocking K+ channels Posterior ½ of lateral

Salt Anions of ionised salts Na+ ion permeability Anterior ½ of lateral

Umami Monosodium -------- ---------

Glutamate
 1

SPECIAL SENSES - Applied

1. Mention the visual field defects that occur when optic tract is cut.
Right optic tract – Left homonymous hemianopia
Left optic tract – Right homonymous hemianopia
2. Why unilateral cerebral/brain stem lesion can not produce unilateral deafness?
1.The auditory signals from both the ears are transmitted through the pathways of
both sides of the brain.
2. In three places in the brain stem , crossing – over occurs between the two pathways
3. How is hearing affected in middle ear diseases?
Block the conduction & magnification of sound energy in the middle ear. So no
stimulation of receptors & no generation & transmission of impulses. This type of loss
of hearing is called conduction deafness.
4. Describe the formation of image in hypermetropic eye. How is it corrected?
The image is formed behind the retina. This is corrected by using convex lens which
refract the light rays & converge them on retina
5. Diagrammatically represent image formation & its correction in myopic eye

Light rays focused in front of retina

- can be corrected by using concave lens (diagrammatic representation – refer

book)
6. What type of deafness is expected in the middle ear infection.
Conduction deafness
7. Name the type of defect due to loss of accommodation of the eye
Presbyopia
8. Explain how color blindness can be inherited
Colour blindness is inherited as X-linked recessive trait. Mostly the males are
affected and the females act as carriers
9. Mention any two tests to distinguish between nerve & conduction deafness
Rinnie’s test & Weber’s test
10. What is the effect of lesion of nasal fibres at optic chiasma?
Bitemporal Hemianopia
11. Name the types of deafness. Mention the tests used to determine the type of
deafness
Types of deafness: Conduction deafness & nerve deafness
Tests to determine : Rinnie’s test , Weber’s test & Audiometry
12. What will happen in diseases affecting stapedius muscle?
Attenuation reflex will be lost & that leads to a condition called hyperacusis
13. A 70 year old man complaints of defective hearing over the last few years
 2

a. What is the reason for his loss of hearing?

b. What are the tests that can be employed to diagnose the condition?
a. Degeneration of auditory fibres due to aging
b.Tests – already discussed
14. Explain terms anosmia and Parosmia
Anosmia – absence of smell sensation
Paraosmia – altered sensation of smell
15. A patient suffering from otosclerosis developed poor hearing ability leading to
deafness
a) How would you distinguish between nerve deafness and conduction
deafness
b) Explain the effect of masking
a) The tests are Rinnie’s ,Weber’s & Audiometry
b) Masking effect- The low frequency sounds in a loud environment cover the high
frequency sounds. Because of this masking effect, the auditory mechanism is
unable to separate the total stimulation in to separate components
16. When a Myope and Hypermetrope (of same age) are compared, who will
develop Prespyobia at an earliest age- Give reasons
In myopic subjects, the near point in his youth is so close to the corneal surface that
even in his old age his near point may be at a distance which is normal for a young
person. So he does not need any correction & the development of presbyopia in old
age is delayed.
But in hypermetropic subjects, his near point of vision is far away from
corneal surface. It moves farther away in old age. More over far vision also is
possible only with some accommodation which makes the eye tired. So if
hypermetropic individual suffers from presbyopia, he requires correction at an early
age.
17. A patient came with complaints of inability to hear on the right ear. O/E, his
right side ear showed a positive response for Weber’s test and negative response
for Rinne’s test.
Identify the problem and explain the differences in the responses to both these
tests
The problem with hearing is conduction deafness of right ear.
Air conduction is affected in this. So in Rinie’s test, bone conduction is longer than
air conduction. This response is Rinnie’s negative
In the right ear, as the environmental sound is not conducted, there is no
masking effect on bone conduction of tuning fork sound. This loss of masking
effect makes the sound to be heard louder in affected ear (right ear). This is what
meant by Weber’s test positive
18. With the suitable diagram, explain the effect of transection at various levels of
visual pathway
Refer the book
19. A man aged 45 years had difficulty in reading books comfortably. His
visual vicinity was 6/6. He had no other complaints in his eyes
a) Mention the type of visual defect and give reasons for this & how
can this be corrected
 3

b) Mention whether this is a physiological or pathological condition

a) This condition is presbyopia at early stage or hypermetropia of old age. This is
corrected by using biconvex lens.
b) It is a physiological condition that arises due to the effect of aging
20. What is glaucoma? How is it produced?
Increase in intraocular pressure above 80 mm Hg is called as glaucoma.
It is caused by accumulation of intraocular fluid in the eyes.
This condition is produced either by increased secretion of intraocular fluid or
by blockage of the canal of Schlemm which drains the fluid from the eye
21. A 50 year old woman complains that she could not read the news paper
while keeping the paper at a normal distance
a) Identify the above condition
b) How do you manage the above condition?
a) Presbyopia
b) By using convex lens
22. How do you test the middle ear functions?.
Tests:
Rinnie’s , Weber’s & Audiometry
23. The young man is unable to pick up his red color hat from a bundle of
different colours
Name the defect. What is the physiological basis for this?
The condition is called protonopia. This due to the absence of porphyropsin.
24. Explain why audiogram is superior to tuning fork tests to assess hearing
Impairment?
1. can asses the degree of deafness
2. can assess the frequency range in which deafness is most affected
- these advantages of this test help in designing hearing aids to overcome some of the
hearing problems of the individual patient
25. What is the effect of a large pituitary tumor on the visual field?
Large pituitary tumor damage the crossed fibres & leads to bitemporal hemianopia
26 Following repeated middle ear infection on left side, a little girl
complained of some hearing impairment. O/E, the rinnie’s test was
negative
a) What is the type of deafness?
b) How is it caused?
a) conduction deafness
b) May be due to damage of tympanic membrane or ear ossicles
27. Why does pain occur in the ear after common cold & sore throat?
Common cold & sore throat  blockage of Eustachian tube  retraction of
tympanic Membrane  stimulation of pain receptors in the tympanic membrane
28. Mention the visual field defects that occur when right optic tract is cut.
Left homonymous hemianopia
29. What is colour blindness?
Inability to distinguish certain colours is called colour blindness. Classified as
follows:
1) Trichromats – Presence of all three cone systems but one of them is defective
 4

Protonamaly – Defective red cone system

Deuteronomaly – Defective green cone system
Tritanomaly – Defective blue cone system
2) Dichromats – Presence of two cone systems & absence of one cone system
Protanopia – absence of red cones
Deuteranopia – absence of green cones
Tritanopia – absence of blue cones
3) Monochromats – Presence of only one system. They see only black & white
& shades of gray
30. Briefly explain the role of Vit.A in scotopic vision? How the process of dark
adaptation is affected in Vit.A deficiency?
Dim light vision is called scotopic vision. In dim light vision, rods play an important
role. Retinal, a chromatophore in rods is an aldehyde of vitamin A. This helps in the
resynthesis of rhodopsin during dark adaptation. In deficiency of Vit.A, resynthesis
of rhodopsin is affected and dark adaptation does not take place. This is called as
night blindness.
31. While performing Weber’s test, it was found that the patient was able to hear
better on the left ear than on the right ear.
a) What type of deafness he is suffering from?
b) Explain the basis.
a) Conduction deafness in left ear.
b) Basis: In Weber’s test, bone conduction is tested. Due to loss of masking effect
of environmental sound over the sound transmitted through bone, the sound is
heard louder in affected ear than normal ear
32. Radiologists wearing red goggles in bright light has some advantage when he
resumes his work in dim light. What is this advantage?
During dark adapation in dim light, rods take a long time ( 20 – 25 minutes ) for
adaptation compared to cones ( 4 – 5 minutes). By wearing red goggles in bright
light will reduce the time taken for rod adaptation. Because the light wavelengths in
in the red end of the spectrum stimulate the rods only to a slight degree while
permitting the cones to function reasonably well in bright light.
33.Draw a diagram of light reflex pathway with proper labeling. Locate the site of
lesion in the diagram in case of a neurosyphilitic patient showing Argyll
Robertson Pupil with a cross mark.
Draw the pathway from book. Put X mark on pretectal nucleus
34.A child of 6 years old had difficulty in seeing pictures in TV screen. After a
thorough check up he was given a glass for correction. Explain what the problem
was & how it was rectified?
TV is normally seen from long distance(more than 20 feet). Inability of the eye to see
long distance objects is called myopia or short sight. It can be rectified by wearing
biconcave lens

35. A middle aged man was found to have unsteadiness of gait with eyes closed and
the bladder incontinence. On examination, his eyes showed papillary
constriction (miosis) to near vision, but no miosis when light was thrown in his
eyes.
 5

a) Name the condition of the pupil.

b) Draw the reflex pathway which is impaired
c) What may be the overall diagnosis? What may be the cause?
a) Argyll Robertson pupil
b) Impairment of light reflex pathway
c) Neurosyphilis.
- Destruction of pretectal nucleus causes loss of light reflex.
- Damage of dorsal nerve roos leads to sensory ataxia(unsteadiness of
gait with eyes closed) & bladder incontinence
36. A 36 year old male with eyes deviated inwards fail to move downwards. In this
case, it would be because of either nerve or muscle involved.
Which nerve & muscle could have been involved?
Muscle impaired – Superior oblique
Nerve impaired – Trochlear nerve
37. A motorist while driving observed something catching his attention (out of
corner of his eye). He immediately turn to the object of his attention & found his
friend waving his hand.
- What is the visual mechanism responsible for detecting the object of attention?
- What is the visual mechanism responsible for identifying the object finally?
- List the differences between two mechanisms at retinal level.
- Peripheral visual mechanism
- Macular vision
- Peripheral visual mechanism involves rods which are situated at the periphery of
retina. Macular vision involves cones.
38. In dim light colours are not appreciated properly and the coloured objects
appear as shades of grey. Explain
Cones are responsible for colour vision. In dim light, rods play an important role in
vision. So colours are not appreciated properly in dim light
39. Write in short about various errors in refraction in image forming mechanism.
Learn about myopia, hypermetropia, astigmatism & presbyopia
40. Discuss the relation between olfaction & sexual behaviour.
The sense of olfaction plays an important role in food & sex-motivated behaviour.
This is mainly because of projection of olfactory fibers to limbic system which is
concerned with control of sexual behaviour
Moreover the sexual behaviour is associated with odoriferous hormone like
substance called pheromones secreted by the opposite sex.
41. Give physiological basis of blurred vision following installation of homatropine
into the eye.
Homatropine is a parasympatholytic drug which causes pupillary dilatation when
installed in to the eye. This is the reason for blurred vision. This is done to carry out
fundus examination through opthalmoscope.

42. Give physiological basis of decrease in olfaction if a person suffers from common
cold.
Nasal congestion prevents the contact of odoriferous substances with the
olfactory epithelium. This decreases the perception of smell.
 6

43. Watching TV for long periods may produce severe headache. Why?
Watching TV for long periods causes strain on ocular muscles which leads to
headache
44. A 60 year old man complaints of sudden loss of vision. O/E, his intraocular
vision was 70 mm Hg.
a) What is the clinical condition?
b) What is the cause for loss of vision?
a) The clinical condition is glaucoma.
b) Severe glaucoma may lead to gradual atrophy of retina that causes loss of
vision
45. A school girl was found to have difficulty in reading words written on black
board, but no difficulty in reading her text books.
a) What common refractive error could cause this?
b) How is the error corrected?
- Myopia
- corrected by biconcave lens
46. Explain why, colour blindness skips generation and appears in males of every
second generation.
It is a X-chomosome linked inherited disorder. As males have only one X chrosome
they exhibit this disorder when affected. But in females, as they have two X
chromosomes, they will not exhibit this disorder & they will carry the affected gene
to the next generation males
47. What is the normal intraocular tension? What is the condition called glaucoma?
Normal intraocular pressure is 15 mmHg.
A rise in intraocular pressure above the normal range is called glaucoma
48. Why, a person who entered a cinema theater, little late, was not able to locate
his seat immediately.
When a person entered into a dark room from a bright area, it takes time for the eye
to get adapted to the dark environment. This is called dark adaptation. Adaptation of
cones take 4 – 5 minutes. Adaptation of rods take 20--25 minutes
49. When a person aged 80 shows progressive loss of hearing without any middle
ear dysfunction. What may be the probable diagnosis & name of the condition?
How will you establish your diagnosis with the help of tuning fork tests?
Diagnosis – nerve deafness due to aging. The condition is called presbycusis.
Rinnie’s test – Negative in affected ear
Weber’s test – sound is lateralized to normal ear
50. List out differences between presbyopia & cataract. How are they rectified?
Presbyopia Cataract
Loss of accommodation due to loss Opacity of lens due to aging or
of elasticity of lens diseases like diabetes
Corrected by wearing bifocal lens Corrected by surgical replacement of
lens
51. What results from poor drainage of aqueous humour & how
parasympathomimetic drugs can help in such conditions?
Accumulation of aqueous humour leads to increase in intraocular pressure. This
condition is called glaucoma. Parasympathomimmetic drugs like pilocarpine
 7

facilitates the outflow by causing meiosis.

52. How pupillary dialatation facilitates dim light vision?
Pupillary dialatation allows more light to enter into the eye. This facilitates dim
light vision
53. What is night blindness? How is it corrected?
Night blindness is failure of dark adaptation and the person will not be able to see the
objects in dim light. This is due to deficiency of Vit.A as vitamin A is required for
synthesis of rhodopsin. Rhodopsin helps in dim light vision.
Can be corrected by administering therapeutic doses of vit.A
54. When the person was looking at the stars in the sky he could see a cluster of dim
stars at the corner of his eye. When he looked at them directly he could not see
them. Explain this visual magic
When the image falls on the peripheral part of retina, he was able to see the stars.
Because peripheral part consists of rods which help to see the stars at night (dim light
vision). When he looked directly at stars the image falls on central part of retina
where only cones are present. As cones help in bright light vision, the stars are not
seen in dark
55. Explain how the sudden pressure changes act against the ear drum.
Sudden pressure changes produced by sound waves

tympanic membrane moves in and out

Tympanic membrane acts as a resonator and reproduces the vibrations of the sound
Source

Auditory ossicles (Malleus, Incus & Stapes act as lever system and convert the
resonant vibrations of ear drum into movements of Stapes against perilymph filled
scala vestibuli of the cochlea

This increases the sound pressure at oval window

60% of the sound energy impinged on the tympanic membrane (ear drum) is
transmitted to the fluid in the cochlea
56. Name the primary colours. What is colour blindness?
Red, Green & Blue are primary colours.
Colour blindness – inability to detect one or two colours
57. What substance is frequently used by psychologists for demonstrating taste
blindness?
Phenyl thiocarbamide
58. What is the fifth taste sensation which is triggered by glutamate and particularly
monosodium glutamate?
Umami is added as fifth taste sensation triggered by glutamate and particularly
monosodium glutamate
 8

59.
 1

Environmental physiology (High altitude, Deep sea, Space, Cold & Hot environment)

1. Explain the cause of cyanosis on exposure to extreme cold weather

Exposure to extreme cold weather  Vasoconstriction  stagnant hypoxia
 peripheral cyanosis
2. What is the effect of Hypothermia on
a) Pulse pressure
b) Heart rate
c) Peripheral resistance
d) Ejection fraction
a) Pulse pressure decreases as the systolic pressure decreases and diastolic
pressure increases ( vasoconstriction)
b) Heart rate is decreased as S.A.Node is depressed
c) Peripheral resistance increases as vasoconstriction occurs
d) Ejection fraction decreases as the heart contractility is decreased
3. What are the changes seen in the Total body Water and electrolyte level during Heat stroke.
How can it be treated?
Decrease in TBW & electrolyte level due to excessive loss of fluid & electrolytes
in the sweat.
Treatment:
- Placing the person in a cold water bath
- Sponge or spray cooling of the body
4. Explain why perspiration aggravates the effect of sun stroke.
During perspiration (excessive sweating) the sweat spreads over a greater area of skin before it
evaporates. It delays the cooling of body & aggravates the effect of sunstroke
5. Explain how humidity aggravates effects of sunstroke
Humidity causes excessive sweating (perspiration). During perspiration the sweat spreads over a
greater area of skin before it evaporates. It delays the cooling of body & aggravates the effect of
sunstroke
6. Explain the mechanism of alteration of cutaneous circulation in response to altered
environmental Temperature
- High environmental temperature  stimulation of anterior hypothalamus  vasodilation
- Low environmental temperature  stimulation of posterior hypothalamus  vasoconstriction
7. Describe the features of hypothermia
Effects of hypothermia on CVS
- Stimulation of posterior hypothalamus  vasoconstriction
- Vasoconstriction  stagnant hypoxia  peripheral cyanosis
- Pulse pressure decreases as the systolic pressure decreases and diastolic pressure increases
( vasoconstriction)
- Heart rate is decreased as S.A.Node is depressed
- Peripheral resistance increases as vasoconstriction occurs
- Ejection fraction decreases as the heart contractility is decreased
Signs & Symptoms:

Mild hypothermia:
-intense shivering
2