Scribd
Upload
192 views3 pages

Pa Tho Physiology of Diabetes Mellitus

This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

Uploaded by

Pong's Teodoro Salvador
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
192 views3 pages

Pa Tho Physiology of Diabetes Mellitus

This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

Uploaded by

Pong's Teodoro Salvador
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 3

PREDISPOSING FACTOR AGE: 80 yrs.

Old Family History of DIABETES Hereditary

PRECIPITATING FACTORS DIET: eating foods rich in sugar, carbs, and fats LIFESTYLE: smoking, drinking alcohol Compliance: no maintenance of meds. for DM

Exhaustion of beta cells occurs

Altered pancreatic insulin production Decreased insulin production Decreased absorption of glucose by the cells Glucose is unable to enter the cells Glucose remains in the blood stream Increased serum glucose level
HYPERGLYCEMIA (304 mg/dl, 13.2 mg/dl)

Sluggish flow of blood Impaired delivery of blood components Inadequate inflammatory response Microorganism would enter the body at any route

Serum osmolarity
Blood viscosity

Tissue perfusion of kidney


Impaired removal of waste Failure to initiate erythropoietin

Osmotic pressure in blood H20 from cell towards the blood

Glucose concentration in urine Reabsorption of glucose in renal tubule

Glucose intake of cells ATP production Energy for normal cells functions Cells starvation occurs Stimulation of the hunger mechanism Hunger occurs
POLYPHAGIA

Blood flow to the organs and extremities Tissue perfusion in nerves Nerve hypoxia Segmental demyelization Nerve damaged Excessive glucose is converted into SORBITOL w/c accumulate in nerves Sorbitol impairs motor nerve conduction

Impaired removal of waste from blood Glucose level exceeds renal threshold Impaired renal Fnx Permeability of the renal cell wall Filtration of macro cells & particles

Stimulation of the bone marrow fails RBC production decreased

Dehydration Stimulation of osmoreceptors thirst

Osmotic pressure H20 reabsorption Urine output

Infection occurs
WBC (14.4), eusinophils (7%)

POLYDIPSIA RBC (4.5) POLYURIA

Fatigue

Inadequate nutritional support

Poor wound healing

Paresthesia, numbness

Decreased PR (60 bpm)

Sugar+2, protein+2, blood+5, RBC >100/hpf

DIABETES MELLITUS
Pathophysiology of BPH

Thickening of the cardiac blood vessels wall Plaque formation begins

Occlusion of the blood vessels occurs

Blockage of blood flow

Myocardial ischemia occurs Decreased myocardial O2 supply

+ TROPONIN T ST-T abnormality

Half of the bundle of his loss its function Left fascicular block occurs

Increased cellular hypoxia


Mild left axis deviation

Increased lactic acid production release of metabolites Altered cell membrane functions

CHEST PAIN

MYOCARDIAL INFARCTION (ACS)

Ineffective right ventricular contractility

Reduced right ventricular pumping ability

Decreased cardiac output

Backflow of blood into the right atrium and peripheral circulation

Shifting of fluids into interstitial spaces

Grade 2 edema @ lower extremities

SINUS BRADYCARDIA

DOB, fatigue, with rales upon auscultation

Ineffective left ventricular contractility

Reduced left ventricular pumping ability

Decreased cardiac output

Backflow of blood into the left atrium and lungs

Pulmonary congestion

Pulmonary edema

HEART FAILURE

PREDISPOSING FACTORS AGE: 80 yrs. Old FAMILY HISTORY OF BPH NORMAL BODY CHANGES

PRECIPITATING FACTORS SMOKING WITH DM, HF, AND MI

As mans age increased prostate gland increased Androgen Testosterone Dihydrosterone Binds to nuclear androgen receptors

Deterioration of the blood vessel in the prostate Blood flow becomes abnormal and 02 supply impaired

Signals growth factors

Stimulation of cell growth

HYPERPLASIA
Encroaches upon the bladder neck occurs

Increased size of prostate

Reduced ability to funnel in response to micturition

Overwhelms the detrusor muscles ability to ensure effective bladder evacuation by micturition

UTI (1-2 PUS CELLS), HEMATURIA

Obstruction occurs

Increase urethral resistance

LUTS

Dribbling of urine

Feeling of incomplete emptying of the bladder

Increased daytime voiding frequency


POLYURIA

URGENCY

NOCTURIA

BENIGN PROSTATIC HYPERPLASIA

You might also like