#6-8 Drug acting on Automatic nervous system

Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Adrenaline  α effect vasoconstriction -> Non-selective
(epinephrine) 1)Shock increase BP α + β2 effect -
2)Acute heart failure Little increase of  β1 effect -> increase HR, > little / no
3)For stabilize BP BP CO change in BP
but need increase Increase CO  β2 vasodilation ->
HR patient decrease BP
 ALL receptor are activated
 Noradrenaline  α effect vasoconstriction -> Non-selective
(norephinephrine) increase BP
For weak heart
Increase BP, CO  β1 effect -> increase HR,
patient
CO
 β2 little effect
 Phenylephrine Nasal congestion  α effect vasoconstriction -> α-selective
 Methoxamine (swelling due to increase BP
inflammation of
nose)
 Phenylpropanolamine  Less CNS stimulation Suppress appetite Usually use
(PPA) Weight loss with anti-
Risk of histamine for
Sympathetic Nasal congestion
hemorrhage oral treatment
nervous system
stroke of brain (banned in
(Direct acting)
HK)
 Isoproterenol Increase CO  β1 effect -> increase HR & β1,2 selective
(Isoprenaline) Increase systolic CO
Shock,
pressure  β2 vasodilation ->
Acute Heart failure
Decrease diastolic decrease BP
pressure
 Dobutamine  β1 effect -> increase HR, β1 selective
Shock
Mostly increase CO contractility -> increase
Acute Heat failure
and maintain/raise CO
For weak heart
BP  some α effect -> small
patient
increase BP
 Terbutaline  Activation  Activation β2 selective
Delay or Relax Relax of β2 of β2 by inhalation
prevent airway uterine receptor receptor in
Asthma
premature smooth smooth in airway uterine
labor muscle muscle smooth
muscle
 Salbutamol Relax airway  Activation of β2 receptor in
Asthma
(albuterol) smooth muscle airway
  Ephedrine  Orally active Non-selective
 Sympathomimetic Plants
Colds, fever flu,
Clinical use  Release of stored Prohibited as
headaches, asthma,
(replace with more transmitters (NE) supplements
wheezing, nasal
selective drugs)  Some direct effect on by FDA but
congestion
adrenergic receptors restricted in
HK/CN
 Amphetamine  Stimulate CNS strongly Suppress appetite Non-selective
ADHD (attention-
Indirect acting Produce mood  More CNS action then Anorexiant
deficient
elevation ephedrine (a drug
hyperreactivity
Increase awareness  Cross blood barrier easily causes loss
disorder)
of appetite)
 Cocaine  Inhibition of transmitter Non-selective
Local anesthetic
reuptake at noradrenergic Inhalation /
action
synapses injection
Strong central
 Short acting but intense **Popular
effect
drug of abuse
 Phentolamine  Competitive antagonist for α receptor
α blockers  Tolazoline Hypertension Reduce BP α receptor

 Propranolol  Competitive antagonist for β1, 2

Reduce cardiac β receptor receptors
Hypertension  Block receptor -> reduce
workload
HR, contractility

 Timolol 1)
β1, 2
receptors
Reduce aqueous
*Topical
Glaucoma humor production
application
*Glaucoma; increase (which stimulated
pressure in eyes -> by β effect)
β blockers damage retina -. 2)
Loss of eyesight Release pressure of
eye without
affecting heart
 Metoprolol  (low dose) block cardiac Chance for β1 receptor
 Atenolol β1 but not β2 receptor in asthmatic attack (β1 selective)
respiratory tract Give seldomly
 Have danger to block β2
receptor which cause Px
cannot dilate bronchiole
  Acetylcholine (Ach) Produce short term
 Activate both nicotinic (N)
and muscarinic (M)
effect
receptors
 Carbachol  Activate both N and M Nausea Non-selective
receptors Vomiting Can pass out
 Not degraded by Blur vision by urination
cholinesterase
Relax bladder (clinically won’t give px for
Urinary retention
retention urinary retention immediately,
since don’t want to activate
whole body receptor -> too
many side effects) -> insert
Parasympathetic Foley instead
Nervous System  Bethanechol  Not degraded by M receptor
(Direct acting) Increase urinary cholinesterase (directly selective
Urinary retention muscle contraction bind to the receptor)
to initiate urination  Little CNS effect (poor lipid
solubility)
 Pilocarpine 1)Contract ciliary  Not degraded by Constrict pupil M receptor
muscle in eye cholinesterase Blur vision selective
Glaucoma 2)Improve drainage  Good lipid solubility Night vision **local
3)Reduce pressure application
in eyes
 Nicotine  Activate central N receptor Addictive effect N receptor
Make nicotine gum
-> stimulate CNS Hypertension selective
and patch for
Cardiac Contains in
smoking cessation
arrhythmias cigarettes
 Edrophonium Myasthenia gravis  Cholinesterase inhibitor ->
For diagnostic test
(immune diseases allow more Ach to bind
(patient with weak
due to reduced with receptor
muscle can move
nicotinic receptors in  Competitive inhibition
little more)
muscle0  Poor lipid solubility
 Neostigmine  Cholinesterase inhibitor Salivation By oral
 Competitive inhibition Sweating Duration: 0.5-
Indirect acting Muscle weakness  Charged molecule -> poor Gastric secretion 2 hrs
 Pyridostigmine lipid solubility Diarrhea Duration: 3-6
hrs
 Physostigmine Contract ciliary  Cholinesterase inhibitor Constrict pupil Doesn’t direct
muscle in eyes ->  Lipid soluble (seldom use, Blur vision Affect M
Glaucoma improve drainage as lipid drug will go to receptor
and reduce eye brain)
pressure
  Parathion  Cholinesterase inhibitor 1)Toxic to human 4)Neuro-
 Malathion  Lipid soluble 2)Excessive muscular
 (Organophosphate  All muscle contract -> stiff salivation & blockage
cholinesterase Kill insects Insecticide muscle -> cannot move -> sweating
inhibitor) kill the insects 3)Bronchial
constriction ->
breathing difficulty
Indirect acting  Donepezil  Alzheimer’s disease Intestinal Require good
caused by decreased ACh cramping -> distribution to
production -> cognitive activation of brain
Alzheimer’s disease function impairment intestinal muscle
(CNS disease)  Cholinesterase inhibitor
can increase action of ACh
-> improvement of
neurological function
 Atropine 1) Reduce heart
 Less effective for Dry mouth Muscarinic
endogenous release of Dysphagia blocker
block due to vagal
Bradycardia ACh Constipation
activity
Eye refraction  More effective against
2) Relax bronchi
Non-ulcer dyspepsia exogenous muscarinic
smooth muscles
Irritable bowel agonists
3) Relax gut while
syndrome  Blocks M receptors in
glandular
Diverticular disease peripheral tissue such as
secretions are
the heart, intestines,
reduced
bronchial muscle
 Ipratropium  Synthetic analog of Muscarinic
COPD
atropine blocker
Cholinergic Asthma (most
Dilate bronchial  Block the receptor -> By inhalation
receptor asthma patient use β
muscle cannot constrict bronchiole (not whole
blockers blocker, not useful
 Charged molecule -> less body absorb)
then use ipratropium)
absorption & CNS effect
 Scopolamine  More central than *need to take 0.5- Muscarinic
(hyoscine) peripheral effects 1 hr before getting blocker
sick (not work) if
Motion sickness Like atropine
take the drug
when vomited or
got sick
 Tubocurarine Hypertension  Block autonomic N Block skeletal Nicotinic
 Pancuronium (at past) Use as anesthesia receptor -> block both muscle N receptor receptor
Relax muscle as muscle relaxants SNS, PNS -> muscle
(will be discussed) relaxation
#9-10 Drug acting on Gastrointestinal tract
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Cimetidine  Inhibit the activity of H2 Generally well tolerated Drug interaction:
 Ranitidine receptor -> cAMP -> GI disturbance Inhibit cytochrome
 Nizatidine protein kinase -> decrease Headache p450 metabolizing
 Famotidine H+ production Dizziness enzymes
H2 antagonists (Cimetidine) -> inhibits Decrease
binding of metabolism of other
dihydrotestosterone -> drugs -> increase
impotence, gynecomastia drug blood level ->
drug toxicity
Decrease  Omeprazole  Inhibit H+/K+ ATPase Generally well tolerated
gastric acid  Esomeprazole Peptic ulcer proton pump -> decrease GI disturbance
secretion  Lansoprazole Proton pump H+ secretion Headache
 Pantoprazole inhibitors Dizziness
 Rabeprazole

 Pirenzepine  Inhibit M1 and M2 Dry mouth Rarely used now

 Dicyclmine receptor -> inhibit Blurred vision
Muscarinic histamine release and Cardiac arrhythmias
antagonists Ca++ production -> Urinary retention
decrease protein kinase ->
decrease H+ production
 Sodium  React with H+ to become Belching (Ca and Na) (Heart failure,
bicarbonate H2O/ CO2 (ca) -> hypercalcemia, renal hypertension, renal
 Calcium calculi, constipation insufficiency Px)
carbonate (Mg, Al) -> commonly used Exacerbate fluid
Neutralize acid Peptic ulcer Neutralize acid
 Magnesium together retention -> edema
hydroxide
 Aluminum
hydroxide
 Sucralfate  Sucralfate -> (presence of No systemic adverse effect Drug interaction
H+) release Al -> bind to (Antacid) reduce
+ve charged glycoprotein efficiency -> require
Promote -> form viscous gel -> acidic environment
Promote mucosal
mucosal Peptic ulcer protect the stomach for activation
defense
defense luminal surface (drug binding) ->
reduce absorption
Need to took empty
stomach
  Bismuth  Combines with mucus Darkening of stool, teeth,
glycoproteins -> stimulate tongue
secreationof mucus, (Px with renal failure) ->
bicarbonate, prostaglandin Encephalopathy
 Antimicrobial activity
against H.Pylori
Promote  Prostaglandins  Bind to PGE1 receptor ->
Promote mucosal
mucosal Peptic ulcer decrease H+ secretion
defense
defense  Increase mucus,
bicarbonate secretion
 Increase blood flow
 Misoprostol  Prostaglandin analogue GI discomfort
Miscarriage (pregnant
female)
 Amoxicillin  Inhibits transpeptidase -> Hypersensitivity reaction
interfere synthesis of GI disturbance
bacterial cell wall
 Clarithromycin  Bind to 50S subunit -> Hypersensitivity reaction
inhibits translocation GI disturbance
during synthesis of protein
 Tetracycline  Bind to 30S subunit -> Nausea
Eradication of Eradication of H. block the attachment of Vomiting
Peptic ulcer
H. Pylori Pylori tRNA Tooth discoloration
Enamel dysplasia
Reduced bone growth
 Metronidazole  Reduction -> Redox GI disturbance
enzyme pyruvate- Metallic taste
ferredoxin oxidoreductase Sensory neuropathy
(PFOR) -> inhibiting DNA (occasionally)
helix structure -> DNA
fragmentation
 Triple therapy:
 Proton pump inhibitor +
Recommended
 Clarithromycin +
regimens for
 Amoxicillin / Metronidazole
treating H.
 Quadruple therapy:
Pylori-
 Proton pump inhibitor +
associated
 Bismuth +
peptic ulcer
 Metronidazole +
 Tetracycline
 Muscarinic  Hyoscine  Block vestibular Drowsiness, Dizziness For motion
Muscarinic receptor  Nuclei -> stop vomiting Dry mouth sickness and
receptor
antagonists Blurred vision stimuli from
antagonists
Urinary retention pharynx & stomach
 Dimenhydrinate  Block vestibular nuclei, Dizziness For motion
 Promethazine nucleus of the solitary Sedation sickness and
tract -> reduce vomiting Confusion stimuli from
(inhibit muscarinic receptor) pharynx & stomach
H1 receptor H1 receptor
-> Drowsiness
antagonists antagonists
Dry mouth
Dizziness
Vomiting
Blurred vision
Urinary retention
 Ondansetron  Block chemoreceptor Headache Motion sickness
5HT3 receptor 5HT3 receptor trigger zone, visceral Dizziness Endogenous toxins
antagonists antagonists afferents -> reduce Constipation & drugs
vomiting
 Metoclopramide  Block chemoreceptor Motion sickness
 Domperidone trigger zone -> reduce Endogenous
vomiting Toxins and drugs
Stimulus from
Dopamine Dopamine pharynx and
receptor receptors stomach
antagonists antagonists  Increase ACh in myenteric
plexus -> lower
esophageal peristatic
pressure -> increase
Esophageal
gastric emptying
reflux
 Cisapride Gastric
 Stimulates 5HT4 Diarrhea
receptors -> increase Ach Abd. Cramp
emptying
and calcitonin gene- Risk of arrhythmia
disorder
related peptide (CGRP)
5HT4 agonists 5HT4 agonists
 Increase lower sphincter
pressure -> increase
gastric emptying, gut
motility
Bulk laxatives  Methylcellulose Bulk laxatives
 Increase fecal mass -> Flatulence Drink adequate
peristalsis Abd. Distension water
Constipation
 Lactulose  Increase the amount of Flatulence
Osmotic
Osmotic laxatives water in faces -> drawing Abd. Distension
laxatives
fluid form body
  Docusate  Detergent -> soften the (chronic use)
sodium stool Paraffinomas
 Glycerol  (sodium, glycerol) weak Impair absorption of fat-
Fecal softener Fecal softener
 Liquid paraffin stimulant laxatives soluble vitamins A, D
 (paraffin) lubricate feces,
assist evacuation
Constipation
 Bisacodyl  Stimulating sensory nerve Diarrhea
 Senna ending Abd. Cramp
Stimulant  (senna) Anthraquinones
Stimulant laxatives
laxatives release from the precursor
glycosides -> stimulate
myenteric plexus
 Codeine  Activate opioid receptors - Drowsiness
 Loperamide > decrease gut motility Dizziness
Opioid  Increase colonic transit Constipation
Opioid agonists time -> increase facial Paralytic ileus
agonists
Anti- water absorption -> stop
diarrheal diarrhea
 Kaolin  Bind toxins and diarrhea No evidence to
Absorbents  Pectin Adsorbents show their
effectiveness
 Hyoscine  Inhibit muscarinic Constipation
Diarrhea receptors in myenteric Tachycardia
Muscarinic
Irritable Muscarinic receptor plexus & smooth muscle Urinary retention
receptor
bowel antagonists cells -> smooth muscle Blurred vision
antagonists
disease cell relaxation Dry mouth

 Sulfasalazine Chronic  Unknown: Headache

5-
inflammatory 5-aminosalicyclic  Scavenging free radicals Rash
aminosalicyclic
bowel acid  Inhibiting prostaglandin Diarrhea
acid
disease
#11-12 Endocrine pharmacology
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Somatropin  Stimulate liver for Hypothyroidism Somatropin = native
separate growth Peripheral edema growth hormone
Replace therapy hormones to Papilledema -> visual
Deficient of growth
with somatropin -> peripheral tissues changes
hormone
resume normal Intracranial
(Dwarfism)
growth funciton hypertension
Impaired glucose
tolerance
 Octreotide  Inhibiting secretion GI disturbance (abd.
Growth
of growth hormone Cramp, nausea,
hormone Inhibiting secretion
from anterior vomiting, flatulence,
of growth hormone
pituitary steatorrhea)
Hypersecretion of from anterior
Gallstones
growth hormone pituitary
Postprandial
(Acromegaly,
hyperglycemia
Gigantism)
 Pegvisomant  Block the function Elevate liver enzymes
Inhibit the function of growth hormone Infection
of growth hormone in liver and Flu
peripheral tissue Nausea, vomiting
 Hydrocortisone  Promote cortisol Iatrogenic Cushing’s **glucocorticoid effect +
content in body syndrome: some mineralocorticoid
Deficiency of ACTH
 Stimulate Redistribution of fat effect
aldosterone and muscle wasting
 Hydrocortisone Replacement  Replacement Hyperglycemia **glucocorticoid effect +
 Fludrocortisone Addison’s disease
therapy therapy -> achieve Hypertension some mineralocorticoid
normal function Growth suppression in effect
(adrenal gland
children ** mineralocorticoid effect
dysfunction)
Osteoporosis
Adrenal
Peptic ulcer
hormones
 Trilostat  (trilostat) inhibit 3β Hypotension
 Metyrapone dehydrogenase Nausea
 (metyrapone) Vomiting
Cushing’s Inhibit the synthesis inhibit 11β Headache
syndrome, of cortisol and hydroxylase Dizziness
Hyperaldosteronism aldosterone  Suppress Rash
synthesis of
cortisol and
aldosterone
  Bromocriptine Hypersecretion of  Inhibit secretion of Postural hypertension Cabergoline: longer half-
 Cabergoline prolactin
Dopamine receptor
prolactin from Constipation life and higher selectivity
Prolactin (galactorrhea, anterior pituitary Nausea
agonists
hypogonadism, Vomiting
amenorrhea) Dizziness
 Vasopressin  Activate V2 Fluid retention
 Desmopressin receptor -> water Headache
reabsorption from Nausea
collecting duct (Vasopressin)
Administration of
ADH Diabetes insipidus Spasm of coronary
ADH
artery -> angina
Abd. Cramps
Uterine cramps

**Glucocorticoid effect:

1. increase uptake and utilization of glucose, increase gluconeogenesis -> increase blood glucose level
2. increase metabolism of protein, increase lipolysis -> maintenance of cardiovascular function by potentiation of noradrenaline effects
**Mineralocorticoid effect:
1. Act on distal tubule to enhance Na+ reabsorption and increase K+/H+ secretion
#13-14 Drugs used in treatment of metabolic disease
Categories Drug Name Mechanism Side effects Onset time Limitation
 Regular Human  Self-aggregate -> form dimers -> stabilize Appears: 30-60 min (self-aggregate) -> Slow onset
Insulin zinc ions to create hexamers Peak time: 1-2 hrs of action:
 (hexametric nature) -> delayed onset, Last for: 5-8 hrs 1) inconvenient adm. (need to
prolong time to peak actions get injection before 30mins for
Short acting
meal)
insulin
2) risk of hypoglycemia
(long duration) -> potential for
late postprandial
hypoglycemia
 Insulin Lispro  Reversing two amino acids near the Onset time: 10-15 /
carboxyl terminal of the B-chain min
 monomers Peak effect: 30-60
 closely mimics endogenous 1) min
Rapid-onset and Hypoglycemia
postprandial insulin secretion Duration: 2-4 hrs
ultra-short acting 2)
 Insulin Aspart  Substation of B-chain proline 28 with –ve Onset time: 10-20 /
charged aspartic acid Insulin allergy min
 Breaks to monomer and resistance Peak effect: 1 hr
3) Duration: 2-4 hrs
Lipodystrophy
 NPH, Neutral  (NPH) mixture of insulin and protamine Peak effect: 4-10 /
at injection
Intermediate Protamine (+ve charged polypeptide) hrs
 (Lente) mixture of 30% semilente with sites Duration: 10-18 hrs
acting Hagedorn
4)
 Lente Insulin 70% ultralente insulin
Abuse
 Ultralente  Entirely crystalline zinc Onset: 6-10 hrs /
Duration: 18-24 hrs
 Glargine  Attachment of two arginine to the B chain Duration: 24 hrs or *Cannot mixed with other
carboxyl terminals longer insulins
 Substitution of a glycine for asparagine at Peakless activity
Long acting the A chain 21
 Levemir  Developed by Novo Nordisk / /
 Myristic acid is added into the lysine
amino acid at position B29
 Bind to albumin in circulation -> extending
circulating life, prevent peak events
 Sulphonylureas  (Action site) Pancreatic β cells Weight gain Duration: 12-48 hrs 1st generation (e.g.
 Used for type 2 DM Px Hypoglycaemia chlorpropamide, tolbutamide):
 Bind to 140kDa high-affinity receptors GI upsets long duration, adverse
Insulin
 Increase insulin secretion from β-cells Teratogenic reactions
secretagogues
 Closing K+ channel -> membrane 2nd generation (e.g. glipizide,
depolarization -> Ca++ entry -> exocytosis glibenclamide): fewer adverse
-> insulin released effects, drug reactions
 Non-  Meglitinide  (Action site) Pancreatic β cells Weight gain (meglitinides) ->
analogs  Bind to sulfonylurea receptor of ATP- Hypoglycemia rapid onset and
sulphonylureas
insulin  Repaglinide sensitive K+ channels -> rapid, transient (lower rate than short duration
secretagogues  Nateglinide insulin release secretagogues)
 Good control of postprandial glucose
 Metformin HCL  (Action site) Liver GI upsets Contradicted Px with renal
 Activate AMP-activated protein kinase Lactic acidosis disease, alcoholism, hepatic
(AMPK) -> Inhibit hepatic glucose Vit. B12 disease and severe infection
production deficiency
Biguanides  Recommended for obese Px / Px with
insulin resistance
 Reduce hyperlipidemia
 Reduce risk of cardiovascular
complications
 Rosiglitazone  (Action site) adipose tissue, muscle, Weight gain Should not used in patients of
 Pioglitazone liver Fluid retention type 2 diabetes
Thiazolidinedion  (molecular target) peroxisome proliferator-
es activated receptor γ (PPAR γ)
(TZDs)  Possess anti-inflammatory properties
 Improve lipid profile
 Prevent type 2 DM
 Acarbose  (Action site) gut Flatulence
 Miglitol  Inhibit α-glucosidase though competition Diarrhea
α-glucosidase  Block postprandial digestion and Abd. Pain
inhibitors absorption of starch
 No effect on body weight
 Not cause hypoglycemia
 Exenatides  Increase resistance  (Action site) GI disorders *Only for injection
to DPP-4 -> pancreatic Dizziness
extends half life cells Headache
 Cause weight loss -  Increase insulin
> slow down gastric secretion but
Incretin analogs
emptying time block glucagon
 Decrease fatty liver secretion
 Liraglutide  Long acting GLP
analog
 Cancer concerns
 Sitagliptin  (Action site) gut URTI
 Vidagliptin  Increase GLP-1 levels Sore throat
 Blocking the activity of DPP-4 Diarrhea
DPP-4 inhibitors
 Use as monotherapy or combine with
metformin / PPAR-γ agonist
 Long term blood glucose control
  Orlistat  Inhibits pancreatic and gastric lipases GI symptoms
 Reduce of absorption of fat (oily spotting,
 Significant obesity fecal urgency,
increased
defecation)
Obesity Malabsorption
of fat-soluble
vitamins
 Phentermine  Suppression of appetite through CNS
 Sibutramine
 Rimonabant
#15-16 Drug used in the treatment of infectious disease (Anti-viral & Anti-parastics)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Acyclovir  Competitive substrate for DNA GI distress Oral
 Valacyclovir polymerase -> chain termination Headache Iv
 Famciclovir Herpes virus Tropical
Inhibiting DNA/RNA
 Ganciclovir infection application
synthesis
Herpes virus  Valganciclovir (caused by
varicella-zoster
 Cidofovir
virus(VZV))
 Docosanol  Inhibitis fusion between HSV
Inhibiting viral entry
envelop and plasma membranes
 Amantadine  Block pore formation by M2 GI irritation Shd be given
 Rimantadine proteins Dizziness within 48 hrs after
Inhibiting the  Prevents H+ ions from entering Ataxia coating
Influenza A
uncoating of the virus Slurred speech
infection
influenza A virus  Prevent acidification of the virus
core -> acquired for activation of
Influenza viral RNA transcriptase
 Oseltamivir  Binds to influenza More effective if
 Zanamivir neuraminidase used with 24 hrs
Influenza A or B Neuraminidase  Prevents the cleavage of sialic
infection inhibitor acids residues
 Inability to release progeny
virions
 Maraviroc  Block CCR-5 (transmembrane
chemokine receptor)
 Reduce viral attachment
 Enfuvirtide Entry/Fusion  Synthetic 36-aminoacid peptide Subcutaneous inj
inhibitors  Binds to the gp41 subunit of the only
viral envelope glycoprotein
Human  Prevents conformational
Immunodeficiency HIV infection changes
Virus (HIV)  Zidovudine  Similar to specific nucleoside /
 Abacavir nucleotides
 Diadanosine Nucleoside reverse  Act as terminators
 Lamivudine transcriptase  Lacks a 3’ hydroxyl group
 Emtricitabine inhibitors
 Stavudine
 Zalcitabine
  Tenofovir Nucleotide reverse
transcriptase
inhibitor
 Efavirenz Non-Nucleoside  Not competitive inhibitors Preventing HIV
 Nevirapine reverse  Directly binds to reverse vertical
transcriptase transcriptase -> change its transmission
inhibitors structure -> disrupt active site
 Raltegravir  Genome of virus must be
incorporate before getting into
Integrase inhibitor host
 Integration accompanied by
Human integrase
Immunodeficiency HIV infection
 Lopinavir  Genome of virus are just 1 large 1)
Virus (HIV)
 Atazanavir polypeptide chain with multiple Disorders in
 Indinavir proteins connected together carbohydrate
 Saquinavir  Cut apart from each other by & lipid
 Ritonavir HIV protease metabolism
 Nelfinavir  Inhibitor blocks the active site of (insulin
 Amprenavir Protease inhibitor HIV protease resistance,
hyperglycemia,
 Fosamprenavir
hyperlipidemia)
 Darunavir
2)
 Saquinavir Buffalo bumps
 Tipranavir 3)
Gynecomastia
 Iodoquinol  Iodine compound
Intestinal amebicide  Combination with tissue
amebicide
 Chloroquine  Form heme-chloroquine complex Oral
Tissue or in the ingested RBC -> toxicity to IMI
extraintestinal cell -> disrupt membrane
amebicide functions -> cell lysis
Protozoal  Prevent synthesis of hemozoin
Amebiasis
infection
 Metrondazole  Metronidazole is reduced by Contradiction;
reacting with reduced ferredoxin Pregnancy
Both intestinal and -> produce toxic products to cells Patients with blood
extraintestinal  Taken up into amoeba DNA -> disorders
amebiasis form unstable molecules Avoid alcohol
 Damage protozoa’s DNA and
inhibits DNA synthesis
  Chloroquine  Against erythrocytic forms
 Not effect against the tissue from
 For prophylaxis
 Form heme-chloroquine complex
in the ingested RBC -> toxicity to
cell -> disrupt membrane
functions -> cell lysis
 Prevent synthesis of hemozoin
 Mefloquine Chloroquine-  Inhibits heme polymerase,
Antimalarial  Halofantrine resistance stains hemozoin formation
Malaria antimalarial agents
agents
 Pyrimathamine  Inhibit folic acid formation
 Selective inhibitor of
dihydrofolate reductase of the
plasmodium
 Primaquine  Effective against exo-
erythrocytic or tissue forms
 For prophylaxis
 Generating reactive oxygen
 Interfering with the electron
transport in the parasite
 Mebendazole  Inhibit the worm’s ability to Fetal
absorb glucose -> stop ATP malformations
production Not for children
< 2yo
 Pyrantel /  Neuro-muscular blocking agent Not for
praziquantel  Cause paralysis of the muscles pregnancy
 Paralyzed worms -> expelled Not for young
Helminthiasis
from feces by bowel normal children <1yo
Anthelmintic arise from
actions
Parasitic worms
 Ivermectin  Act in muscle and nerve cells of Nausea
the parasitic worm Vomiting
 Bind to glutamate-gated chloride
ion -> increase the permeability
of the cell membrane to chloride
ions -> hyperpolarization of the
cell -> paralysis and death
#17-18 Drug used in the treatment of infectious disease (Anti-bacterial & Antibiotics)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Penicillin  Interfere peptidoglycan
 Cephalosporin synthesis
 Inhibit transpeptidase -> x
Antibiotics Beta-lactam
cross-linking step ->
Cell wall (Gram +ve antibiotics
compromising cell wall
synthesis bacterial structure integrity -> cell lysis
infection)  Bactericidal
 Vancomycin Non-beta-lactam  Inhibit early steps of
antibiotics peptidoglycan synthesis
 Polymyxins  Cyclic peptide with long Restricted topical
Antibiotics
hydrophobic tail -> emulsify the use
Cell membrane (Gram -ve Disrupt membrane
lipids -> kill the cell Last resort of
permeability bacterial permeability
 Disrupt the membrane antibiotics
infection
permeability
 Tetracyclines  Inhibit function of 30S subunit
 Aminoglycosides
 Macrolides  Inhibit function of 50S subunit
Inhibit protein inhibit protein
synthesis  Clindamycin synthesis
 Linezolid
 Chloramphenicol
 Streptogramins
 Sulfonamides Antibiotics  Similar structures -> Compete
Inhibits folate  Trimethoprim Folate synthesis with folate intermediates
synthesis inhibitor  Inhibit DNA synthesis
 Bacteriostatic
 Metronidazole Inhibit DNA  Bacteriostatic
Inhibit nucleic  Quinolones synthesis
acid synthesis  Rifampin Inhibit RNA  Bactericidal
synthesis
 Metronidazole Tissue and
 Intracellularly reduce
metronidazole to active form ->
luminal
covalently binds to DNA ->
amebicide
inhibits DNA synthesis
Amoebiasis  Diloxanide  Kills amoeba in intestine lumen
 Clear the amoeba may present
Luminal Dichloroacetamide
in the lumen -> eradicate
amebicide derivative
intraluminal
 Inhibit protein synthesis
  Artemisinin  Low bioavailability
 Poor pharmacokinetic
properties
 Derivatives improve these
properties
 Mechanism of action largely
unknown
 Primaquine  Effective against erythrocytic
forms
Protozoa  For radical care (once prarsites
infections: cleaned from blood stream ->
Malaria amoeba / remove tissue forms for 14
flagellates / day)
sporozoa  Low cure rate if used alone
 Prophylaxis for pateitns has
returned from malarious area
 Chloroquine  Used for prophylaxis -> given
before, during, after level or
residence in endemic areas
 Dapsone  Inhibit folate synthesis
Inhibit folate  Inhibit dihydrophobic acid ->
synthesis tetradrofolic acid -> prines ->
DNA
 Amphotericin B  Binds with ergosterol Renal toxicity IVF -> systemic
 Interferes with membrane Hypokalaemia fungal infection
Fungal cell permeability, transport Hypomagnesamia
Polyenes
membrane inhibitor functions
 Form large pores on
membrane -> fungal death
Antifungal drugs  Azoles  Binds to ergosterol on the
Ergosterol
fungal cell wall
synthesis inhibitor
 Arrests of fungal growth
 Echinocandins Fungal cell wall  Inhibits ergosterol production
synthesis inhibitor on the fungal cell wall
 Flucytosine Fluorinated  Leads to RNA miscoding and
pyrimidine analog interfere with DNA synthesis
Rules of using antibiotics

Rule Description
1 Prophylaxis VS Treatment
Treatment: know the disease or illness caused by bacterial infection
Prophylaxis: prevent bacterial infection -> likelihood of infection
2 Bacteriostatic vs. bactericidal drugs
Bacteriostatic Bactericidal
 Inhibit growth of bacteria  Kills bacteria directly
 Needs out body immune system to help and get rid of the  Infection requires “cidal” action
bacteria  E.g. meningitis , bacteremia, endocarditis
 Infection may relapse when drug is discontinued  E.g. pencillins
 E.g. tetracycline
3 Board spectrum vs Narrow spectrum
Board spectrum Narrow spectrum
 Effective against a wide range of bacteria, including Gram  Effective again a selected group of bacterial type
-ve, Gram +ve bacteria  To effect disease with known type of causation bacteria
 For a patient which an infection may not cause by one  E.g. Penicillin G, Vancomysin
type of bacteria
 E.g. tetracyclines, amoxillin, augmentin
4 Toxicity vs. Efficacy
 Need to know about the side effects or toxicities of the antibiotics or other drugs
 Toxicity associated with overdose / resulted from patient’s special conditions
5 Antibiotic resistance
Possible mechanisms:
1. Rapid exclusion / inhibiting entry of antibiotics
2. Degradation of antibiotics
3. Altering the antibiotics biochemically or the antibiotic agents
6 Combination antibiotics
Use of more than 1 antibiotics
 Synergistic action in the eradication of bacterial infection
 Treat mixed bacterial infection
 Overcome resistance to antibiotics
 Reduce toxicity -> lower dosage used for both two antibiotics
#19-20 Drug used in the treatment of Cardiovascular disease (Angina & Hypertension)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Nitroglycerin  nitrate induces nitric oxide 1. Tolerance Phosphodiesterase
 Isosorbide dinitrate (NO) -> production of (Tachyphylaxis) -> (PDE) inhibitor->
cyclic guanosine decrease response to relax tachycardia -
Vasodilation of monophosphate (cGMP) -> nitrates > BIG drop of BP
1) veins, dephosphorization of 2. Dependence ->
(administration)
2) large arteries, myosin light chain -> withdrawal
Sublingual (fast
3) collateral relaxation
Nitrates relieve, prevention
coronary artery (adverse effect)
of anginal pain),
4) decrease 1. Headache
oral, cutaneous,
coronary artery 2. Postural
transmucosal or
spasm hypotension
Buccal, IV
3. Tachycardia

 Nifedipine  Decrease oxygen demand Dependence on

 Amlodipine -> decrease force of selectivity on cardiac /
contraction -> decrease vascular smooth
Angina force of contraction muscle
(Stable,  Decrease peripheral (vascular activity)
Unstable, vascular resistance Headache, flushing
1) Decrease force of
Calcium Variant) (decrease BP) -> decrease Hypotension
contraction
channel cardiac workload -> (increase angina
2) Vasodilation
blockers decrease myocardial symptoms)
3) Decrease
(vascular/cardi oxygen demand Decrease coronary
coronary artery
ac selective)  Effective against variant perfusion
spasm
angina Reflex tachycardia
Cause peripheral
edema
 Diltiazem (cardiac activity)
 Verapamil -> Atrioventricular
block -> heart failure
 Propranolol  Reduce cardiac workload - 1. Bronchospasm
 Esmolol 1) reduce > decrease myocardial 2. Decrease force and
force & rate of oxygen demand -> rate of contraction of
β-Adrenoceptor
contraction of heart decrease force and rate of heart
Antagonists
2) increase artery contraction of heart 3. Hypoglycemia
spasm  Increase coronary artery
spasm
  Trimetazidine  Inhibit long-chain Parkinson Syndrome
mitochondrial 3-ketoacyl (reduced kidney
coenzyme A thiolase (3- function)
Metabolic Improve myocardial KAT) enzyme GI discomfort
modulators energy metabolism  Inhibit myocardial fatty acid Muscle cramp
Angina oxidation Dizziness
(Stable,  Increase efficiency of
Unstable, cardiac O2 utilization
 Ranolazine Variant)  Decrease Na+ influx -> Nausea
decrease activation of Dizziness
Decrease heart Na+/Ca++ exchanger ->
Miscellaneous
contractility decrease intracellular
[Ca++]
 Decrease O2 demand
 Furosemide  (action site) thick 1. Hypokalemia Used
 Bumetanide ascending lime of loop of (K+ lost in collecting for
Henle tubule) severe
(Efficacy)
 Reabsorption of NaCl by 2. Metabolic alkalosis HT
inhibiting Na+/K+/2Cl- (H+ lost) ->
Loop
cotransporter compromise cardiac fx Shorter
diuretics
Loop diuretics -> (1,2) -> treated by - acting
->
K+ replacement
Thiazide
3. Hyponatremia
diuretics
(depletion of Na+) ->
->
extra cellular depletion
K+-
(hypotension, Reduced
sparing
GFR)
diuretics
 Hydrochlorothiazide  (action site) distal tubule (1-3) like loop diuretics Mild to
Diuretics  Indapamide HT  Inhibit Na+/Cl- 4. Hyperglycemia Modera
Thiazide diuretics cotransporter -> inhibit 5. Hyperlipidemia te HT
Na+ & Cl- reabsorption ->
reabsorption of Ca++
 Amiloride  (action site) collecting 1. Hyperkalemia -> (multiple
tubule -> inhibit Na+ exacerbate cardiac drug
channel arrhythmia (reversed regimen)
 Inhibit Na+/K+ exchange in by thiazide diuretics) Enhance
the collecting tube -> 2. metabolic acidosis blood
Potassium-sparing
inhibit reabsorption of Na+ -> decrease excretion pressure
diuretics
-> decrease execration of of H+ -> compromise lowering
K+ cardiac function effect
 Spironolactone  (action site) collecting
tubule -> antagonize
aldosterone receptor
  Captopril  Decrease vasoconstriction Dry cough
Angiotensin
 Enalapril -> decrease peripheral Angioedema
Converting Enzyme
 Lisinopril (ACE) inhibitor
vascular resistance -> (due to increase level
Inhibitors of  Quinapril decrease blood volume -> of bradykinin)
Renin-  Losartan Angiotensin decrease edema Severe hypotension
HT
angiotensin  Valsartan Receptor Blockers Acute renal failure
system (ARB) Hyperkalemia
 Aliskiren Risk for fetal
Renin inhibitors hypotension, renal
failure or malformation
 Propranolol  Inhibit β-adrenoreceptors 1. bronchospasm ->
 Metoprolol Inhibit β-adrenoreceptors (heart) in heart -> decrease (Inhibit β-
 Pindolol cardiac output adrenoreceptors in
 Inhibit β-adrenoreceptors respiratory tract)
in kidney -> decrease Na+ 2. increase risk of
and water retention hypoglycemia ->
 Inhibit peripheral (Inhibit β-
presynaptic β- adrenoreceptors in
adrenoreceptors -> liver)
decrease vasoconstrictor 3. decrease rate of
nerve activity -> decrease contraction of heart ->
peripheral vascular increase risk of
Adrenoceptor resistance arrhythmia -> (Inhibit β-
HT
antagonists
 Latetalol  Inhibit β- & α- adrenoreceptors in
Sympathoplegi  Carvedliol β-adrenoreceptors antagonists with adrenoreceptors heart)
c
 Nebivolol vasodilating effects  Inhibit β1-adrenoreceptors
(Sympatholytic)
 Release NO
agents
 Esmolol  Inhibit β1-adrenoreceptors
 Short half-life
 Constant IV fusion
 Prazosin  Inhibit α1-adrenoceptors in Selectivity at α1-
 Doxazosin Inhibit α-adrenoreceptors (blood vessel) arterioles and venules -> adrenoceptors -> mild
decrease peripheral unwanted effects
vascular resistance (dizziness, palpations,
 Retention of Na+ and headache)
water
 Reserpine  Inhibit the uptake and 1. GI disturbance
storage of biogenic amines 2. CNS disturbance
Adrenergic Neuron-
into aminergic transmitter (sedation, mental
Blocking Drugs
vesicles -> depletion of depression)
neurotransmitters
Sympathoplegi  Methyldopa  Stimulation of α2- 1. CNS disturbance
c  Clonidine adrenoreceptors in (sedation, mental
HT Centrally acting presynaptic neurons depression)
(Sympatholytic)
 (Clonidine) -> decrease
agents
HR -> decrease CO
 Nifedipine  Inhibit calcium channels in 1. reflex tachycardia ->
 Amlodipine blood vessels -> decrease vascular-selective
 Diltiazem vasoconstriction -> diuretics (nifedipine)
 Verapamil Calcium channel
decrease peripheral 2. heart failure ->
vascular resistance cardiac-selective
blockers
 Inhibit calcium channels in blockers (verapamil)
heart -> decrease rate &
force of contraction ->
decrease CO
 Minoxidil  Dilators of arterioles -> Reflex tachycardia
Potassium channel
 Last resort for decrease peripheral Reflex retention of Na+
openers
severe HT vascular resistance and water
vasodilator HT
 Nitroprusside  Decrease vascular
 Nitroglycerine resistance -> decrease
amount of blood returning
to the heart
Nitrates  (nitroprusside) -> rapid
decrease BP and
breakdown to thiocyanate
 (organic nitrates,
nitroglycerin) -> tolerance
 Hydralazine 
Last resort
 Diazoxide
(not being used)
 Fenoldopam
1. Non-pharmacological approaches 1. Life long treatment
a. Decrease weight, sodium intake a. Compliance of treatment; oral preparation,
2. Pharmacological therapy monotherapy vs multiple drugs
a. Angiotensin inhibitors [A] b. Monitor of adverse effects
b. β-adrenoreceptor antagonists [B] 2. Choice of drugs
c. calcium channel blockers [C] Consideration of a. Level of BP
Hypertension d. thiazides diuretics [D] anti- b. Concomitant disease
Management 3. Alternative choices of monotherapy hypertensive i. (HT+angina) -> β-adrenoreceptor antagonists /
a. Sympathoplegic agents (not α-adrenoreceptor treatment calcium channel blockers
blockers) ii. (HT+Heart failure) -> diuretics / ACE inhibitors
4. Combination therapy iii. (HT+asthma) avoid β-adrenoreceptor
a. Thiazide diuretics plus others antagonists
#21-22 Drug used in the treatment of Cardiovascular disease (Angina & Hypertension)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Digoxin  Inhibit Na+/K+-ATPase -> Pro-arthythmic Anti-arrhythmic
increase intracellular Na+ GI disturbance drug
-> decrease Ca++ CNS disturbance NOT 1st line
Cardiac glycosides
expulsion -> increase Narrow safety margin therapy
intracellular [Ca++] Effect opposed by
increase K+ / Mg++
 Dobutamine  Activate β1-adrenoreceptor Pro-arthythmic
 Dopamine β-adrenoreceptors -> increase intracellular Pro-angina
stimulants [cAMP] -> active PKA -> Tachyphylaxis
increase Ca++ entry
Used for Acute
 Amrinone  Inhibit enzyme Pro-arthythmic
heart failure
Positive  Milrinone Heart phosphodiesterase III -> GI disturbance
inotropic drugs failure Phosphodiesterase decrease cAMP ->
inhibitors increase PKA activation ->
increase intracellular
[Ca++]
 Levosimendan  Stabilize the binding Headache IV use
between Troponin C and Hypotension Used for coronary
Calcium -> increase affinity and systemic
of troponin C and Ca -> vasodilator
Calcium sensitizer
increase sensitive to Ca ->
increase contractility
without increase
intracellular [Ca++]
 Captopril  Decrease fluid retention -> Severe hypotension
 Enalapril ACE inhibitors decrease blood volume -> Hyperkalemia
Angiotensin  Quinapril Heart decrease oedema
inhibitors failure  Decrease vasodilation ->
 Losartan Angiotensin decrease peripheral
Receptor Blockers vascular resistance
 Furosemide  Increase fluid excretion -> Refer to HT
Loop diuretics
 Bumetanide decrease pulmonary
 Hydrochlorothiazide vascular congestion ->
 Indapamide increase oxygenation of
Heart Thiazide diuretics blood -> improve
Diuretics
failure myocardial function
 Amiloride
 Spironolactone Potassium-sparing
 Eplerenone diuretics
  Isosorbide dinitrate  Decrease volume of blood
Dilation of veins returning to heart ->
decrease cardiac workload
 Hydralazine  Decrease resistance to
blood flowing from the
Dilation of arterioles
heart -> decrease cardiac
Heart workload
Vasodilators
 Nesiritide failure  Activates particulate Renal damage IV adm.
guanylyl cyclase -> Hypotension Used for acute
increase cGMP level -> heart failure
Synthetic Brain
arteriolar and venous
Natriuretic Peptide
dilation
 Increase glomerular
filtration rate -> diuresis
 Bisoprolol  Reversal of potentially
β-  Carvedilol harmful increase
adrenoreceptor  Metoprolol Heart Decrease force of sympathetic activity in
failure contraction of heart chronic heart failure
antagonists
 Improve survival in chronic
heart failure
1. Non-pharmacological approaches
a. Decrease cardiac workload (decrease activity, weight)
b. Decrease Na+ intake
2. Pharmacological 1st line treatments
Management of a. Diuretics
chronic heart b. Angiotensin converting enzymes inhibitors / angiotensin receptor blockers
failure 3. Cardiac glycosides (for heart failure / atrial fibrillation)
4. β-adrenoreceptor antagonists (for chronic severe heart failure)
5. Adjuncts
a. Vasodilators
b. Positive inotropic drugs
 Quinidine  (oldest group) intermediate 1. Pro-arrhythmia
 Procainamide rate of dissociation from (inhibition of K+
 Disopyramide sodium channel -> block channel) -> prolong
premature beats -> duration of action
moderately decrease potassium -> ectopic
Cardiac Sodium channel conduction beats
Class Ia drugs
arrhythmia blockers  Block potassium channels 2. tachycardia
-> decrease rate of 3. GI disturbance
repolarization -> increase 4. Lupus-related
duration of action potential symptoms (arthritis)
-> increase effective 5. decrease force of
refractory period (ERP) contraction of heart
  Lidocaine  Rapid kinetics CNS disturbance
 Mexiletine  Dissociate rapidly from (nausea, tremor,
Na+ channel within the drowsiness,
same frame of NORMAL convulsions)
Class Ib drugs heartbeat -> block
premature beats
 Selective for refractory
Sodium channel channels -> preferentially
blockers suppress depolarized cells
 Flecainide  Slow kinetics 1. Pro-arrhythmia
 Encainide  Markedly decrease (increase of sudden
 Propafenone conduction even at normal death)
Class Ic drugs heart beats 2. Worsen heart failure
(Propafenone) -> weak
β-adrenergic blocker
activity
 Esmolol selective  Oppose β-adrenergic 1 bronchospasm
 Metoprolol β1-adrenoreceptors stimulation (decrease HR, 2. decrease force and
Cardiac increase AV node rate of heart
antagonist
Class II drugs arrhythmia conduction time, decrease contraction
 Propranolol Non-selective intracellular Ca++ 3. hypoglycemia
(Vaughan- β-adrenoreceptors overload)
Williams antagonist
Classificati
 Dofetilide  Effective in maintaining Developing ectopic Avoid patient with
on)
sinus rhythm in Atrial beats renal failure or
Fibrillation patients (increase action inhibition of renal
potential -> cation transport
hypokalemia)
 Dronedarone  Highly effective 1. Pulmonary fibrosis (Dronedarone)
 Amiodarone  Additional effects to K+ 2. Photosensitivity -> similar mechanism
Potassium channel channel blocker skin rash and skin but with lower
blockers o Block inactivated Na+ discoloration incidence of
Class III drugs (decrease rate of channels 3. Corneal deposits -> adverse drug
repolarization of o Weak adrenergic blocking visual problems reactions
cardiac cells) activity 4. Thyroid
o Weak calcium channel abnormalities -> hyper-
blocking activity /hypo-thyroidism by
 Low incidence of high iodine content
developing ectopic beats 5. Pro-arrhythmias
 6. Drug interaction (by
liver cytochrome P450
enzymes)
  Sotalol Potassium channel
 Class III dug with class II Pro-arrhythmia
action Risk of developing
blockers
 Mixture of d- and l- Sotalol ectopic beats
Class III drugs Cardiac (decrease rate of
(only l-isomer contains β-
arrhythmia repolarization of
adrenoreceptor blocking
cardiac cells)
activity)
(Vaughan-
 Verapamil Williams
 Decrease HR 1. Decrease force of
 Diltiazem  Decrease AN nodal contraction of heart
Classificati
Calcium channel conduction velocity 2. Atrioventricular block
Class IV drugs on)
blockers  Decrease Ca++ overload 3. Hypotension
 Use-dependent block 4. (1-3) cause heart
failure
 Adenosine  Activate presynaptic Activation of A2 Rapid uptake into
purinergic receptors on receptors in vascular cells for
sympathetic nerve terminal smooth muscle cells metabolism
-> reduce release of (increase cAMP level (shorter half-life,
noradrenaline -> decrease -> vasodilation -> shorter duration of
normal automaticity flushing, hypotension, action, adverse
 Activate A1 receptors on cheat pain and SOB) effects rapidly
SA and AV nodes -> resolved)
reduce cAMP production
-> decrease Ca++
overload
 Activate potassium
channels in SA and AV
nodes -> increase rate of
Cardiac repolarization of cardiac
Miscellaneous cells -> decrease
arrhythmia
conduction velocity
 Magnesium  Affect ion channel activity
Electrolyte
 Sodium supplement
 Normalize potassium pool
in the body
 Digoxin  Anti-arrhythmic effect -> 1.ectopic beats
parasympathomimetic Pro-arrhythmic effect
effects -> decrease HR, -> increase intracellular
conduction velocity [Na+] -> decrease
Ca++ expulsion ->
Cardiac glycoside
increase intracellular
[Ca++]
2. GI disturbance
3. CNS disturbance
(disorientation)
  Atropine  Reduce vagal influence -> 1. tachycardia
increase HR, conduction 2. dry mouth
Cardiac Muscarinic receptor velocity 3. dilation of pupils
Miscellaneous
arrhythmia antagonist 4. constipation
(with overdose or
repeated dosing)
1. Causes of arrhythmia
a. Elimination of “reversible” cause (e.g. ischemia, acute cardiac dilation, drug toxity)
b. Appropriate therapy
Consideration 2. Route of administration
with anti- a. IV preparation preferred for emergency
arrhythmic 3. Therapy regimen
drugs a. Combination therapy -> prevent adverse effects
4. Justification
a. Decrease symptoms (e.g. palpitations, syncope or cardiac arrest)
b. Decrease long-term mortality in asymptomatic patients
Non- 1. Electrical cardioversion
pharmacologic 2. Implantable cardioverter-defibrillator
al therapy of 3. Pacemaker
cardiac 4. Catheter ablation
arrhythmias 5. Heart surgery
#23-24 Drug used in the treatment of Cardiovascular disease (Thrombosis & Atherosclerosis)
Categories Drug Name Treatment Function / Mechanism Side effects Remarks
Outcome
 Aspirin  Inhibit cyclooxygenase activity -> GI disturbance
decrease synthesis of Gastric damage
Aspirin thromboxane A2 (TxA2) -> (chronic usage)
decrease platelet aggregation Prolonged bleeding
 Potent drug -> low dosage -> inhibition TxA2
 Clopidogrel  Block ADP receptors on platelets - 1. GI disturbance 3,4 -> rare with
 Ticlopidine > inhibit expression of fibrinogen - 2. Haemorrhage clopidogrel >>>>
Adenosine > prevent linkage of platelets by 3. Thrombotic ticlopidione
Diphosphate fibrinogen -> decrease thrombocytopenic
(ADP) Receptor aggregation purpura
inhibitors 4. Leukopenia ->
(WBC count)
 Abciximab  Block glycoprotein IIb/IIIa -> Bleeding IV -> short-term
Antiplatelet  Eqtifibatide Glycoprotein inhibit linkage of adjacent platelets Thrombocytopenia treatment
Thrombosis IIb/IIIa inhibitors
drugs by fibrinogen
 Dipyridamole  Inhibits adenosine uptake -> Ineffective on its
adenosine remain extracellularly to own
activate A2 receptor -> inhibits Use in combination
cyclic nucleotide with aspirin /
phosphodiesterase warfarin
 Increase cAMP level ->
Miscellaneous vasodilation; decrease platelet
aggregation

 Cilostazol  Inhibits phosphodiesterase -> Use primarily ->

increase cAMP level -> intermittent
vasodilation; decrease platelet claudication
aggregation

 Heparin  Bind to anti-thrombin -> increase Haemorrhage IV/SC adm. (large

activity -> increase rate of Allergic response molecule -> cannot
inactivation of clotting factors Loss of hair absorbed by abd.)
Indirect thrombin (IIa,IXa, Xa) -> decrease formation Osteoporosis Unpredictable
Anticoagulants Thrombosis of fibrin Mineralcortricoid pharmacokinetics
inhibitors
 High molecular weight fraction -> deficiency Suitable for
high affinity for anti-thrombin (long Thromnocytopenia pregnant women
chain) (decrease platelet)
  Enoxaparin  Low molecular weight fractions Contraindicated
 Dalteparin  Advantage over UFH with renal impaired
 Tinzaparin o Decrease binding to plasma patient
proteins -> increase
bioavailability; decrease drug
resistance
Heparin o Longer half-life -> decrease
derivatives dosage frequency
o Renal clearance -> predictable
pharmacokinetics
 Fondaparinux  Synthetic form
 Pentasaccharide
 High affinity for anti-thrombin
 Hirudin Bivalent inhibitor of
 Lepirudin thrombin -> close
monitor aPTT
Kidney excretion
Long-term infusion
 Bivalirudin Bivalent inhibitor
Anticoagulants Thrombosis Parenteral Direct that also inhibits
thrombin platelet activation
inhibitors
 Argatroban Smaller molecule
 Directly bid to the active site of -> binds only at
thrombin -> inhibit its effects thrombin active site
 Independent of anti-thrombin Clearance
dependent on liver
function
 Dabigatran Bleeding Rapid onset
No interaction with
Oral direct P450 drugs
thrombin Renal clearance
inhibitors

 Rivaroxaban  Directly bind to factor Xa -> inhibit Risk of bleeding Fixed dosage -> no
 Apixaban Oral direct Factor
conversion of prothrombin to monitoring
thrombin Rapid onset of
Xa inhibitors
 Prolong action in elderly patients action
or renal impairment patient
  Warfarin  Inhibit the action of vitamin K Haemorrhage ->
epoxide reductase -> inhibit monitor INR & PT
conversion of inactive vitamin K Birth defects (avoid
epoxide to active form ->. during pregnancy)
Vitamin K
Anticoagulants decrease formation of functional
antagonists
clotting factors -> decrease
formation of thrombin
 Oral anticoagulant
 Protein bound -> long half-life
 Streptokinase Thrombosis  Increase formation of plasmin from Bleeding IV/IA adm
 Urokinase plasminogen -> increase (GI haemorrhage, For acute
degradation of insoluble fibrin stroke) myocardial
(reversed by infraction, multiple
Fibrinolytic  Alteplase  Selectivity on fibrin-bounded antifibrinolytic agent pulmonary emboli,
Fibrinolytic drugs
agents  Tenecteplase plasminogen -> confine fibrinolysis administration; central deep
to the formed thrombus (clot aminocaproic acid, venous thrombosis
selective) fresh-frozen plasma Expensive
or coagulation
factors
 Phytonadione  Formation of clotting factors
(vitamin K)  Depression of prothrombin activity
-> excess warfarin / vit.K
deficiency
 Plasma  Concentrated with clotting factors Risk of other
fractions  w/ heat or extracted solvent or transmissible
detergents -> reduce risk of disease (prions)
Reduce Bleeding transmission of viral diseases
Reduce bleeding
bleeding disorders  Tx/ clotting factor deficiency
 Fibrinolytic  Inhibit activation of plasminogen Intravascular
inhibitors  Tx/ bleeding or risk of bleeding thrombosis
(antifibrinolytic Hypotension
drugs) Myopathy
Abdominal
discomfort
 Lovastatin  Decrease synthesis of cholesterol GI disturbance Prevention of
Short half-life
3-Hydroxy-3-  Pravastatin in liver -> inhibit HMG-CoA Risk for atherosclerosis in
statin
Methylglutrayl-  Fluvastatin reductase hepatotoxicity -> patients with
Coenzyme A  Simvastatin Athero- Intermediate half-  Increase clearance of plasma LDL measuring ALT elevated LDL
(HMG-CoA) sclerosis life statin -> promoting synthesis of LOL Risk for myopathy Not for pregnant
Reductase  Atorvastatin receptors in liver (muscle pain, women or children
Inhibitors Long half-life  Modest decrease of plasma weakness, fatigue)
 Rosuvastatin statin triglycerides
  Vitamin B3  Decrease level of VLDL -> 1. flushing Normalize LDL in
inhibiting hormone-sensitive lipase 2. skin rashes most patient
in adipose tissue -> increase 3. GI disturbance with(out) genetic
hepatic triglyceride synthesis 4. Risk of defects of LDL
 Decrease level of LDL hepatotoxicity receptors
Niacin
Niacin  Increase level of HDL -> decrease 5. decrease glucose Effective in
(Nicotinic acid)
clearance of HDL apolipoprotein tolerance increasing HDL
A1 in liver 6. Increase uric acid level
levels
7. risk of birth
defects
 Clofibrate  Decrease VLDL level -> increasing 1. GI disturbance Treatment for
 Gemfibrozil syntheses of lipoprotein lipase; 2. rashes hyper-
 Fenofibrate increasing fatty acid oxidation in 3. increase risk of triglyceridemia
liver myopathy
 Increase/decrease LDL level 4. increase plasma NOT for pregnant
(decrease level of VLDL/ increase level of liver and children
Fibrates Fibrates
triglyceride breakdown) enzymes
 Modest increase HDL level 5. increase risk of
Athero-
(increase production of HDL cholesterol
sclerosis
apolipoproteins A-I and A-II gallstones
6. increase action of
warfarin
 Cholestyramine  Decrease liver cholesterol level -> 1. no systemic Useful in condition
 Colestipol binding to bile acids -> decrease toxicity with increase LDL
 Colesevelam reabsorption of bile acids 2. GI disturbance only
 Decrease plasma LDL level -> (bloating,
Bile acid- Bile acid-binding
promoting the synthesis of LDL dyspepsia, Bind digoxin ->
binding resins resins
receptors in liver constipation) good for digoxin
3. decrease toxicity
absorption from GI
tract
 Ezetimibe  Decrease absorption of intestinal 1. headache
cholesterol -> binding to NPC1L1 2. diarrhea
& inhibiting intestinal ACAT ->
Ezetimibe Ezetimibe decrease level of LDL
 Decrease plasma LDL level ->
promoting synthesis of LDL
receptors in liver
#25-26 Anti-inflammatory Drugs
Categories Drug Name Treatment Function / Mechanism Side effects Remarks
Outcome
 Aspirin  Block cyclooxygenase activity -> 1. GI disturbance Should not be used
 Diflunisal decrease prostanoids production 2. prolonged for children with
 Decrease vasodilation; vascular bleeding fever due to viral
permeability 3. skin reactions illness
Salicylates  Decrease sensitization of pain 4. renal insufficiency
nerve endings 5. liver disorders (Aspirin)
 Decrease set-point of the 6. bronchospasm irreversible
hypothalamic thermoregulatory (5,6) less common inhibition of
center -> relieve fever cyclooxygenase
 Ibuprofen Individual
Propionic acids
 Naproxen difference -> trail
 Indomethacin (clinical applications) for 1-2 week;
Acetic acids 1. Rheumatoid arthritis initiated with low
 Sulindac
 Piroxicam Oxicams 2. Seronegative dose
Spondyloarthropathies Avoid combination
Non-Steroidal  Meclofenamic
3. Localized Musculoskeletal of NSAIDs
Anti- acid
Anti- Syndromes
inflammatory
inflammation Fenamates 4. Osteoarthritis
drugs
5. Gout
(NSAID)

 Acetaminophen  Weak cyclooxygenase 1 and 2 Acetaminophen

(paracetamol) inhibitor induced
 Analgesic effect -> mild to Hepatotoxicity ->
moderate pain GSH-conjugation
Paracetamol
fully occupied ->
produce chemical
that lead to cell
death
 Celecoxib  Anti-inflammatory Lack of effects on
 Etoricoxib Selective  Analgesic and antipyretic effects platelets
cyclooxygenase-2  Decrease GI adverse effects Renal insufficiency
inhibitors Cardiovascular
thrombotic events
  Hydrocortisone  Inhibit interactions of White cell 1. Infections and Short and medium
 Prednisolone adhesion molecules with those on peptic ulcer acting
endothelial cells 2. Impaired wound
 Inhibit function of macrophages healing
and other antigen-presenting cells 3. Insomnia,
 Cause vasodilation Euphoria and
 Cortisone  Reduce capillary permeability Depression
Inactive (pro-drug)
 prednisone 4. Osteoporosis
-> converted by
Anti- 11β-hydroxysteroid
Steroids Steroids 5. hyperglycemia
inflammation dehydrogenase
(withdrawal of glucocorticoids) 6. muscle wasting
type 1 (11β-HSD1)
=> Iatrogenic Addison’s disease: and weakness
 Betamethasone muscle weakness; weight loss; 7. redistribution of Long-acting
 Dexamethasom hypotension; hyperpigmentation = fat
e (patchy or dark skin)
=> Iatrogenic
Cushing’s syndrome
#27-28 Antihistamines and Allergic Emergencies
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Diphenhydramine  Relieve allergic rhinitis; itching and Fatigue
swelling associated with Dizziness
uncomplicated allergic skin reactions; Sedation
First generation coughs due to cold or allergy
antihistamines  Can cross the blood-brain barrier ->
cause CNS impairment

 Fexofenadine Anti-  Use

 Ioratadine histamines  Allergic and inflammatory conditions
 Cetirizine  Motion sickness and nausea
 Mizolastine  Somnifacients
Second  Cannot across the blood-brain barrier
generation  Sedation is less common
antihistamines  Rapid onset
 Less frequent dosing

 Epipen  Inhibits the release of inflammatory

mediators
Anto-injectable  Stimulated the β2-adrenergic
Anaphylaxis receptors -> bronchodilation
adrenaline
 Increases peripheral vascular
resistance

 Cyclosporine  Binds to cyclophilin (CpN) -> inhibits Nephrotoxicity

calcineurin phosphatase -> prevents Infections
activation of nuclear factor -> inhibits Viral infections
synthesis id IL-2 for T cell-mediated Lymphoma
immunity Hypertension
Microbial products
Immuno- Immune (inhibitors of  Combined with corticosteroids and Hyperkalemia
suppressant disorders cytokine production antimetabolites Tremor
 Prophylaxis and treatment of Hirsutism
and function)
transplant rehection Glucose intolerance
 Alternative for the treatment of severe Gum hyperplasia
autoimmune disease (e.g. rheumatoid
arthritis, recalcitrant)
  Tacrolimus  Binds to FKBP -> inhibits calcineurin MORE SEVERE
phosphate -> prevents activation of nephrotoxicity;
nuclear factors -> inhibits synthesis of neurotoxicity
IL-2 in T-cells (tremor, seizures,
 Prevention of rejection of solid organ hallucinations)
 Given with corticosteroids and/or and Posttransplant
antimetabolite insulin-dependent
diabetes mellitus
Cardiovascular
toxicities (HT,
Microbial products
(inhibitors of hyperlipidemia)
 Sirolimus cytokine production  Binds to cytoplasmic FK-binding Hyperlipidemia
(Rapamycin) and function) protein -> interfering with mTOR Leukopenia
signal Thrombocytopenia
 Block the T-cell ability for proliferation Infection
in response of IL-2 stimulus
 High fat diets affect absorption
 Combine with cyclosporine/tacrolimus
+ corticosteroids -> kidney/heart
transplantation
Immuno- Immune
suppressant disorders
 Azathioprine  Prodrug (-> 6-mercaptipurine -> 6- Myelosuppression
thioinosinic acid Defective thiopurine
 Block de novo purine synthesis in methyltransferase
lymphocytes (TMPT) -> fatal
 Combination of corticosteroids and myelosuppression
cyclosporine/tacrolimus -> kidney Increase risk of
transplantation and autoimmune cancer
disorders (hemolytic anemia) GI irritation

 Mycophenolate Antimetabolites and  Inhibit inosine monophosphate Diarrhea Largely

mofetil cytotoxic agents dehydrogenase Nausea replaced
 Blocking de novo formation of Vomiting azathi-
guanosine phosphate -> depriving T- Abdominal pain porine
and B-cell component of nucleic acids Leukopenia
 Combination of corticosteroids, Anemia
calcineurin inhibitors,
cyclosporine/tacrolimus
 Sole agent for heart, kidney, liver
transplants
  Cyclophosphamide  Anti-neoplastic drug
 Treatment of autoimmune diseases
Immuno- Immune (hemolytic anemia, systemic lupus
suppressant disorder erythematosus (SLE), rheumatoid
arthritis), organ transplantation

 Antilymphocyte  Mediate antibody-dependent Chills and fever

globulins cytotoxicity Leukopenia
 Anti-body bounded cells -> depleted in Thrombocytopenia
spleen and liver Infections
 Used together with Skin rashes
immunosuppressive agents ->
prevention of severe rejection
episodes

 Rho(D) Immune  Prevention of Rho hemolytic disease

Globulin to the new born
 Maternal antibodies to Rh-positive
cells are not produced in subsequent
pregnancies -> averted hemolytic
Polyclonal & disease
Monoclonal
 Muromonab-CD3 antibodies  Antibody binds to the CD3 on T-cells - Cytokine release T cells
(OKT3) > prevents binding to antigen and the syndrome functions
antigen recognition complex -> blocks Anaphylactic return to
all T-cell functions and depletes T- reactions normal 48
cells hours
 Against the glycoprotein CD3 antigen
 Acute rejection of renal allografts
 Deplete T cells from donor bone
marrow prior to transplantation
 Pre-medicate with
methylprednisolone,
diphenhydramine, acetaminophen ->
alleviate the cytokine release
syndrome

 Basiliximab  Bind to the IL-2 receptor expressed on

 Daclizumab activated T cells -> inhibit IL-2
Interleukin-2 mediated activated and proliferation
Receptor Antagonists  Inducting therapy in transplantation
 Decreasing the incidence of acute
rejection
 Prednisone  Non-specific ant-inflammatory agents Diabetogenic,
 Methylprednisolone  Disrupting T cell activation and hypercholesterolemi
macrophage-mediated tissue injury a
 Inhibition of nuclear factor kappa B Cataracts
Corticosteroids activation (binding to glucocorticoid Osteoporosis
response elements) Hypertension
 Suppressing both acute rejection and
chronic graft-versus-host diseases,
autoimmune diseases
#29-30 Drugs used in the treatment of malignant diseases I & II
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Methotrexate  Blocking the active site of dihydrofolate Renal damage
(MTX) reductase (DFHR) -> necessary for Cirrhosis
methylation u various metabolic process Neurological
 MTX becomes polyglutamated toxicities
 Immunosuppressive effects -> treat
Folate antagonist inflammatory disease
 High dose of MTX -> form 7-
hydromethotrexate
Antimetabolites  Keep patient well hydrated
 Leucovorin  Leucovorin -> rescue normal cells
 6-mercaptopurine  Similar to normal nucleotides but Myelosuppression -
 6-thioguiane interfere with DNA synthesis > life-threatening
 Converted to the nucleotide analog (allopurinal) -> XO
Purine antagonists
 Inhibits de novo purine-ring biosynthesis; inhibitor -> reduce
block formation of AMP and xanthinuric 75%
acid from inosinic acid
 Vincristine  GTP dependent binding to tubulin Drug resistance
(Oncovin, VX)  Prevent polymerization Mylosuppressant
 Vinblastine Cancer  Dysfunctional spindle in metaphase -> Peripheral
Vinca alkaloids prevent chromosomal segregation and neuropathy
(Velban, VBL)
 Vinorelbine cell proliferation Granulocytopenia
(Navelbine, VRB)
 Paclitaxel (Taxol)  Bind  Combination of Myelosuppression
reversely to cisplatin -> lung and Alopecia-
the tubulin ovarian cancer neuropathy
Mitotic subunit  Premedicated with Mouth sores
inhibitors  Promote dexamethasone, Allergic reaction
polymerizatio  Diphenhydramine,
n and H1+H2 blocker
 Docetaxel Taxanes stabilization  NSCLC, breast, Neutropenia
(Taxotere)  Accumulation prostate, gastric Hypersensitivity
of cancer Fluid retention
nonfunctional  Semi-synthetic Rash, palmar-
microtubules derivative palmar
 Chromosome  Contraindicated with erythrodyesesthesia
s cannot cardiac disease Drug resistant
segregate
  Irinotecan  Unwind and wind DNA -> facilitate DNA
 Topotecan replication
 Inhibiting topoisomerase -> inhibiting the
molecules from religating DNA
 Stabilize the topoisomerase I enzyme-
Topoisomerase-I DNA complex -> prevent the single-
inhibitors strand (S-phase specific)
 (Topotecan) -> metastatic ovarian
cancer, small-cell lung cancer
 (Irinotecan + 5-FU + leucovorin) -> colon
or rectal cancer
Topoisomerase
 Etoposide  Act in the premitotic, G2 and S phases
inhibitors  Interfere with topoisomerase-II enzyme
 Teniposide
reaction
 Bind drugs to the enzyme-DNA complex
 Stabilization of topoisomerase II-DNA
intermediate -> break double strand of
Topoisomerase-II
DNA -> inhibiting DNA synthesis
inhibitors
 (Etoposide) -> oat-cell lung carcinoma
 (Etoposide + bleomycin + cisplatin) ->
Cancer testicular carcinoma
 (Teniposide) -> 2nd line treatment of
acute lymphocytic leukemia

 Cyclophosphamide  Attached to the guanine base of DNA -> Bone marrow

 Ifosfamide abnormal base pairing, DNA breakage, depression
cross-linking Hemorrhagic cystitis
 Mutagenic and carcinogenic -> 2nd Bladder fibrosis
malignancies
 Hydroxylation by cytochrome P450
 Reacts with DNA by alkylation

Alkylating  Carmustine  Highly lipophobic

agents  Lomustine  Penetrate into CNS
Nitrosoureas
 Treatment of brain tumors

 Cisplatin  Heavy metal platinum complex Severe nausea;

 Producing intra- and inter-strand linkage vomiting
in DNA Nephrotoxicity
 Treat almost every solid tumor and
lymphoma]
  Doxorubicin  Intercalating between base pairs of Dose-dependent
DNA/RNA -> disrupt DNA function cardiotoxicity
 Cell-cycle nonspecific Generation of free
 Topoisomerase II enzymes; preventing radicals
the relaxation of supercoiled DNA; induce Lipid peroxidation
Antitumor
double-strand DNA breaks
antibiotics  Treatment of sarcomas, breast and lung
carcinoma, lymphocytic leukemia,
lymphomas

 Dexrazoxane  Against the cardiotoxicity of Doxorubicin

 Tamoxifen  Treat estrogen receptor-positive breast Induce endometrial
Hormones and cancer cancer
hormone Antiestrogens  Binding to estrogen receptors Thromboembolic
Cancer
antagonists  Selective estrogen receptor modulator events
(SERM) Cataract formation
 Trastuzumab  Stimulate cell kinging -> targeting Congestive heart
(Herceptin) proteins on the surface of cancer cells failure
 Blockage of receptors -> blockade of
receipt for growth signals
 Immunotoxins -> antibodies carrying
toxic molecules to target cancer cells
Antibodies
 Targets the extracellular domain of HER2
growth receptor -> Inhibits the
proliferation of cells that overexpress the
HER2 protein
 (+paclitaxel) -> regression of breast
cancer, metastases
#31 Drugs used in the Treatment of Respiratory Diseases
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Salbutamol  Decrease permeability and oedema Tremor Inhalation
Short acting (Albuterol)  Increase mucociliary clearance due to Tachycardia IV
β2 agonists
 Terbutaline increase ciliary beat frequency Hypokalaemia
β2 agonists  Against all non-specific Desensitization
Long acting  Salmeterol
bronchoconstrictor stimuli Down-regulation
β2 agonists  Formoterol
(LABA)
 Theophyline  Increase cAMP -> smooth muscle Nervousness Used as
 Aminophylline relaxation Increase second line
Phosphodiesterase  Block adenosine receptors -> decrease chronotropic & drug
/ contraction of airway smooth muscle & inotropic
(PDE) inhibitors
decrease histamine release Nausea vomiting
Asthma Diuresis
 Ipratropium  Inhibit ACh-mediared bronchospasm ->
Short-acting Muscarinic binding all muscarinic receptors
Receptor  Decrease cholinergic tone; decrease
mucus secretion
 Tiotropium bromide Antagonist
Long-acting

 Monelukast Cysteinyl  Inhibit LTC4 and LTD4-mediated

 Zafirlukast Leukotriene bronchospasm
Add-on Receptor
therapy Antagonists
 Zileuton 5-Lipoxugenase  Block leukotriene production Not commonly
inhibitor used
 Budesonide  Suppressing inflammation -> decrease Oral >> inhaled
 Fluticasone synthesis and infiltration; decrease steroids
 Prednisolone oedema Osteoporosis
 Prednisone  Decrease airway mucus production Cataracts
Glucocorticoid  Increase the number of bronchial β2- Glucose
Glucocorticoids
s receptors and responsiveness of β2 intolerance
Anti- agonists Depressed
inflammatory immunity
Cushingoid
changes
 Cromolyn sodium  Inhibit mast cell degranulation and Dry mouth inhalation
Anti-allergic (sodium activation Irritating cough
Mast cell stabilizers
drugs cromoglicate)  Depress exaggerated neuronal reflexes
 Prophylactic
  Omalizumab  Stop immunoglobin E from binding to Anaphylaxis SC injection
(Xolair) mast cell and basophils Systemic every 2-4 wks
Anti-IgE Anti-
 Prophylactic treatment for severe reaction to an
antibody inflammatory
uncontrolled asthma allergen

Rationale:
Glucocorticoids reverse; restore β2-AR function and number in lung in viro
Inhaled glucocorticoid in combination with inhaled long-acting inhaled β2-agonist
Combination e.g.
therapy  Symbicort (budnedonide / formoterol)
 Seretide (fluticasone / salmeterol)
 Flutiform (fluticasone / formoterol)

Drugs that NSAID, e.g ibuprofen -> block cyclooxygenase -> produce leukotrienes through lipoxygenase -> asthma
provoke β-adrenergic receptor antagonists (blockers) (e.g. propanolol)
asthma
 Salbutamol Short-acting β2  Relieve symptoms
agonists  Prevent disease progression
 Salmeterol or Long-acting β2  Prevent and treat exacerbations
formoterol agonists  Prevent and treat complication
 Indaceterol Ultra long-acting β2  Reduce mortality
(onbrez) agonists  Improve exercise tolerance
 Ipratropium Short-acting  Improve health status
Induce
Muscarinic receptor
bronchospas
antagonists
m
 Tiotropium COPD Long acting
Muscarinic receptor
antagonists
 Acidinium (Tudorza
Ultra long acting
Pressair)
Muscarinic receptor
 Glycopyrronium antagonists
(seebri breezhaler)
Decrease  Glucocorticoids /
inflammatory  Roflumilast (Daxas) Selective PDE4
responses
 Theophylline inhibitor
Anticholinergics/β2-agonists glucocorticoids/β2-agonists
e.g. e.g. budesonide/formoterol (Symbicot)
Combination
ipratropium/salbutamol (Combivent) fluticasone/salmeterol (Seretide)
therapy for
umeclidinium/vilanterol (Anoro Ellipta) fluticasone/vilanterol (Relvar/Breo Ellipta)
COPD
glycopyrrondium/indacterol (Ulibro Breezehaler) anticholergic/glucocorticoid (under development)
glucocorticoids/β2-agonist/anticholinergics
  Codeine  Strong Non-productive cough
depressant
 Decrease sensitivity of CNS
 Dry cough
 NOT for cough accompanied with
Antitussives
excessive secretions
 dexotromethorphan  most popular antitussive Dizziness
 selectively depress the cough center in Drowsiness
the medulla Nausea
 for dry cough
 guaifenesin  assist the removal of secretion /
Cough exudates from the traches, bronchi or
depressants lungs
 increase amount but decrease viscosity
Expectorants Expectorants
of bronchial secretions
 increase cough centre
 stimulating the mucin secreting cells ->
mucin
 N-acetylcysteine  Breaks the disulphide binds crossing
links mucus glycoprotein molecules
 Easily transported out of the lungs
Mucolytics
 Dornase Recombinant  rhDNase -> cleaves DNA left behind by
human neutrophils
deoxyribonuclease I
 chlorphenamine  inflammation of nasal mucosa caused Anti-nausea
 promethazine Sedative by a type 1 hypersensitivity reaction to Anti-emetic
Anti-  diphenhydramine antihistamines allergens Local
histamines anaethesia
 Cetirizine Non-sedative
 Loratadine antihistamines
 Phenylephrine Allergic  Constricts dilated arterioles in the nasal
Decongestant rhinitis α1-adrenergic mucosa & reduce airway resistance
s agonists  Aerosol -> rapid onset
 Oral -> increase systemic effects
Glucocorticoid  Beclomethasone 
Glucocorticoids
s
 Cromolyn sodium Anti-allergic mast- 
cell stabilizers
#32 Drugs used in the Anxiety and Insomnia
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Midazolam Short-acting  Anxiolytic -> reduce anxiety Drowsiness, * = rapid
 Triazolam* Benzodiazepines  Hypnotic -> induce sleep when anxiety lethargy, fatigue onset
(BDZs) causes insomnia (higher dosage)
 Alprazolam  Bind allosterically in a site between the α and Dizziness
Both  Lorazepam Intermediate-acting γ subunits in GABAA receptor-chloride ion Impaired motor
 Temazepam Anti- BDZs channel complex -> open Cl- channel more coordination
anxiolytic /
anxiety frequenly Mood swings
hypnotic
 Chlordiazepoxide drugs Reduce anxiety Respiratory
drugs
 Clonazepam*  (alprazolam) -> anxiolytic-antidepressant depression,
 Diazepam* Long-acting BDZs  (diazepam) acute panic-anxiety death
(Valium)  (chlordiazepoxide) -> chronic anxiety
 Flurazepam
 Flumazenil  Competitive antagonist of benzodiazepines at Dizziness IV use only
the GABAA receptor Nausea
/ / BDZs antagonist  Reversal of BDZ overdose Vomiting
Seizures
 Thiopental Ultra-short-acting  Potentiate GABA action on chloride entry into Drowsiness Less
Barbiturates the neuron -> prolong the duration of the Decreased motor common
 Pentobarbital Cl- channel opening control use in
 Block excitatory glutamate AMPA receptors Induction of clinical
 Amobarbital Anti- Short-acting
Anxiolytic  Anesthetic concentration -> decrease P450 drug
 Secobarbital anxiety barbiturates
drugs neuronal activity Tolerance,
drugs
dependence
 Phenobarbital Respiratory
Long-acting
barbiturates depression and
coma
 Buspirone  Treatment of general anxiety disorder (GAD)
 Mediated by serotonin (5HT1A) receptors
 NO anticonvulsant, muscle-relaxant
/ properties
Anti-  Minimal sedation
Anxiolytic
anxiety
drugs
drugs

 Hydroxyzine  Patients with anxiety and drug abuse history Drowsiness

Antihistamine  Sedation prior to dental procedures/surgery
  Selective  Chronic anxiety disorders
serotonin  Managing symptoms
reuptake
inhibitors (SSRIs)
 Tricyclic
Antidepressants
Anxiolytic antidepressants
drugs (TCAs)
 Monoamine
oxidase inhibitors
(MAOIs)
 Propanolol β-blockers
 Somatic manifestations of anxiety (e.g. social
phobias, performance anxiety)
 Zolpidem  Selectively to BZ1 subtype of benzodiazepine Effect on the
 Zaleplon  Facilitates GABA-mediated neuronal inhibition stages of sleep
 Antagonized by flumazenil Nightmares
Anti-  NO muscle-relaxing and anticonvulsant Daytime
anxiety effects drowsiness
/
drugs (Zaleplon) Confusion
 resembles zolpidem GI discomfort
 Rapid onset Headache
 Fewer residual effect on pseudo-motor and
cognitive function
Hypnotic  Ramelteon  Selective agonist at the MT1 and MT2 Dizziness
drugs subtypes of melatonin receptors Fatigue
 Insomnia treatment Drowsiness
/
Increased
production of
prolactin levels
 Chloral hydrate  Trichlorinated derivative of acetaldehyde GI disturbance
/  Induced sleep in 30 mins Unpleasant taste
 Duration of sleep is about 6 hrs
 Diphenhydramine  Sedating properties Dry mouth
 Doxylamine antihistamine  Over the counter drug Blurred vision
 Promethazine Drowsiness
#33 Drugs used in Neurological Disorders I (Parkinson’s disease, Huntington’s disease, Alzheimer’s Disease)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Levodopa  Metabolic precursor of dopamine (Conversion of L- NOT give with
(L-dopa)  Covert in dopamine in the brain by dopa to dopamine) L-dopa:
DOPA decarboxylase Nausea Non-selective
 High therapeutic index -> symptom Vomiting MAO inhibitors
control for elderly Arrhythmias Pyridoxine
Postural Antipsychotics
Dopamine precursors hypotension
(overstimulation of
central dopamine
receptors)
Dyskinesia
Hallucination
Brain
Confusion
dopaminergic
 Carbidopa  Dopamine decarboxylase inhibitor
system
 Doesn’t cross blood brain barrier
(Sinemet)
 Combination of L-dopa and carbidopa,
4:1 ratio
Parkinson’s
Peripheral DOPA  Reduce metabolism of dopamine
disease
decarboxylase (periphery) ; increase availability of
(PD)
inhibitors dopamine (CNS)
 Benserazide  Peripheral DOPA decarboxylase
inhibitor
(Madopar)
 Combination of L-dopa and
benserazide, 4:1
 Bromocriptine  Ergot derivative Hallucination
 Dopamine receptor agonists at D2 Nausea; vomiting
receptors Cardiac
 Conjunction of L-dopa -> relieve arrhythmia;
rigidity; tremor postural
Dopamine Dopaminergic
hypotension
receptor agonists (Ergot
Erythromelalgia
agonists derivatives)
 Pergolide  Ergot derivative Confusions
 Dopamine receptor agonists at both Hallucination
D1 and D2 receptors Postural
 Combination of L-dopa/carbidopa and hypotension
anticholinergic drugs UTI
  Ropinirole  First-line therapy for younger patients Dyskinesia
 Pramipexole  Adjunct of L-dopa/carbidopa -> for Insomnia
patient with advanced PD Dizziness
Postural
Dopaminergic hypotension
agonists (Non-ergot
 Rotigotine  Dopamine D2-like receptor agonist Application site
derivatives)  Transdermal patches reactions;
hypersensitivity
Dizzy; Headaches
Nausea
 Selegiline  Decrease metabolism of dopamine in Hypertensive crisis
Dopamine  Rasagiline Monoamine Oxidase the periphery and CNS at high dose
receptor B  Increase brain dopamine levels
agonists (MAO-B) inhibitors  Enhance effects of L-dopa/carbidopa
 Entacapone Parkinson’s  Blocking the peripheral conversion of Diarrhea
disease levodopa to 3-O-methyldopa Postural
(PD)  ONLY adjuncts to L-dopa/carbidopa hypotension
COMT inhibitors therapy Dyskinesia
Hallucinations
 Tolcapone Hepatic necrosis
 Amantadine  Antiviral agent for influenza Confusion
 Enhance the release of dopamine Skin rash
Dopamine facilitator  Inhibit reuptake of dopamine Peripheral edema
Postural
hypotension
 Benztropine  Reduce cholinergic output of the Sedation
 Benzhexol striatum Urinary retention
Brain  Less effective than L-dopa Dry mouth
(Trihexyphenidyl) Central
cholinergic  Reduce primary symptoms (tremor,
 Biperiden anticholinergics Constipation
system rigidity) and secondary symptoms Confusion
(drooling)
 Tetrabenazine  Dopamine-depleting -> suppress
/
Movement involuntary jerking and movement
disorders  Haloperidol  Suppressing
 Risperidone Huntington’s Antipsychotic drugs movements
disease
 Fluoxetine (SSRI) (HD) Antidepressants  Treat depression
Psychiatric
disorders  Carbamazepine Mood-stabilizing  Treat irritability
drugs
 Donepezil  Increase the amount of acetylcholine Nausea; diarrhea
 Rivastigmine Acetylcholinesterase
(Ach) available for CNS function Anorexia
 Galantamine Alzheimer’s Inhibitors (AChEI)
Agitation
Bradycardia
diseases
Urine incontinence
(AD)
 Memantine  Improve cognitive ability Headache
NMDA receptor
 Protecting CNS neurons from the Dizziness
antagonists
excitotoxic effects of glutamate Confusion
#34 Drugs used in Neurological Disorders II (Epilepsy)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Phenytoin  Protein bounded -> drug-drug Osteoporosis Induces
interaction Ataxia hepatic
 Prevent sodium influx (fetus) cytochrome
 Inhibit calcium influx cleft palate; lip P450 activity

Sodium  Carbamazepine Sodium channel

 Stabilize them in the inactive site -> Dizziness
channel prevent repetitive firing of the axons -> Diplopia
blockers
blockers induce epilepsy Nausea
 Block sodium channel Ataxia
Blurred vision
 Lamotrigine  Block voltage-dependent sodium
channel
 Inhibiting glutamate release
 Ethosuximide  Calcium channel blockers Increased suicidal
thoughts
Calcium
Calcium current Liver/kidney
current
inhibitors disease
inhibitors
Concentration
problems
Antiepileptic
 Clobazam  (seizure) -> Imbalance between
drugs
 Clonazepam GABAA agonist excitatory and inhibitory activity of
 Phenobarbitone brain
 Tiagabine Uptake inhibitor  Influx of Cl- -> increase the negativity
Gamma- (inhibit GABA- inside the cell -> greater difficulty to
aminobutyric transporter) reach action potential level
acid (GABA)  Vigabatrin GABA-transaminase
enhancers (inhibit the
breakdown of GABA)
 Gabapentin GAD modulation
 Valproate (increase synthesis
of GABA)
 Topiramate  (glutamate) -> main excitatory amino Ataxia
acid neurotransmitter Concentration
 Inhibit AMPA and kainite subtype impairment
Glutamate glutamate receptor Confusions
Glutamate blockers
blockers  Inhibit sodium conductance Weight loss ->
 Enhance GABA appetite
 Influx of sodium, calcium; Out flux of suppression
potassium => excitation
  Progesterone  Inhibitory hormone
 Increasing chloride conductance at
GABAA receptors
Hormones Hormones  Decrease glutamate excitatory
response
 Increase glutamic acid decarboxylase
(GAD) mRNA
Synaptic  Levetiracetam  Binds to synaptic vesicle protein 2A Asthenia
Antiepileptic
vesicle Synaptic vesicle  Inhibits presynaptic calcium channels Dizziness
drugs
protein 2A protein 2A binding  Reduce neurotransmitter release Upper respiratory
binding agents tract infection
agents
 Retigabine  Potassium channel opener
Potassium  Prolonging the opening of potassium
Potassium channel
channel channels -> stabilizes membrane
openers
openers potential
 Add on therapy
#35-36 Drugs used in Metal Health Disorders I and II (Anti-depressant and anti-psychotic)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Fluoxetine  Block reuptake of serotonin Nausea; Gi upset;
(Prosac)  Maintaining high level of 5-HT in diarrhea
 Paroxetine the synapse Diminished sexual
 Citalopram  Inhibition of the serotonin function and
Selective
serotonin  Escitalopram Selective serotonin transporter interest
 Sertraline reuptake inhibitor  Serotonin = 5-HT Reduced
reuptake inhibitor
 Fluvoxamine (SSRI) coagulation;
(SSRI)
increase risk of
bleeding
Favors
vasoconstriction
 Atomoxetine  Block reabsorption of NA from the High BP
synapse Increase HR
Norepinephrine Norepinephrine
CNS activation
reuptake inhibitor reuptake inhibitor
(insomnia, anxiety,
agitation)
 Venlafaxine  Binds to both serotonin and Serotonergic
Serotonin-  Desvenlafaxine Serotonin- norephedrine transporters adverse effects
Anti-  Block norepinephrine and
Norepinephrine  Duloxetine Norepinephrine Norepinephrine
depressant
reuptake inhibitor  Bupropion reuptake inhibitor serotonin uptake reuptake inhibitor
 Mirtazapine
Tricyclic  Tricyclic  Affects uptake of serotonin,
antidepressants antidepressants norepinephrine, dopamine
(TCA) (TCA) neurotransmitters
Serotonin  Trazodone  Blocking 5-HT2A receptor
antagonist- Serotonin antagonist-  Blocking serotonin reuptake
reuptake reuptake inhibition transporter
inhibition  Agonist at 5-HT1A receptor
α2  Mianserin α2 adrenoreceptor
 Blocks α2 presynaptic
adrenoreceptor autoreceptor
antagonist
antagonist  Enhance noradrenaline release
 Phenelzine Non-selective  Increase levels of all three
Monoamine  Tranylcypromine Monoamine oxidase neurotransmitters by inhibiting an
inhibitors (MAOI) enzyme responsible for
oxidase
inhibitors  Moclobemide Selective monoamine inactivating them
oxidase inhibitors
(MAOAI)
  Agomelatine  Synthetic version of melatonin
(Valdoxan)  Does not increase serotonin level
Melatonin Anti-
Melatonin inhibitor  Increase concertation of
inhibitor depressant
dopamine and norepinephrine in
the brain
 Chlorpromazine  Extrapyramidal symptoms Failure of
 Fluphenazine  Hyperprolactinemia symptoms temperature
 Haloperiodol  Effective against positive signs regulation
Typical  Periciazine hallucinations, delusions, Medial emergency
antipsychotic  Perphenazine disorganized thinking, agitation
drugs  Pimozide
 Sulpiride
 Trifluoperazine
 Zuclopenthixol Anti-
 Amisulpride psychotic  5HT2 recepotrs binding exceed Increased risk of
 Ariprazole their affinity for dopamine D2 blood sugar
 Clozapine receptors Increase risk of
 Risperidone  Lower extrapyramidal side effects diabetes
Atypical
  Treat both negative and positive Severe weight
antipsychotics
sign of psychosis gain
Extrapyridmal
effects
#37 Drugs used in the control of pain
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Morphine  Standard for comparing with
Opioids another opioid
 Phenanthrene derivative
 Codeine  Methylmorphine Constipation
 Dihydrocodeine  Prodrug of morphine Disorientation
 Oxycodone  Undergo O-demethylation -> Excitement
morphine
 Exhibits genetic polymorphism
 Antitussive, antidiarrhoeal
 Combined with paracetamol and
NSAID
 Pethidine  Labour analgesia Renal failure Contraindicated
 Synthetic phenylpiperidine Significant BP fall with monoamine
derivative Tachycardia oxidase inhibitors
 Antimuscarinic agent -> relaxed Dry mouth patient
smooth muscles
 Fentanyl  Relieve chronic pain Respiratory
 Synthetic phenylpiperidine depression
Pain derivative Sedation
Pain control
control  Transdermal patch -> chronic Unconsciousness
pain conditions Muscular rigidity of
chest
 Remifentanil  Maintenance of anesthesia with Bradycardia
controlled ventilation Hypotension
 Rapid onset and offset Apnoea
 Muscle rigidity
 Alfentanil  Synthetic phenylpiperidine
derivative
 Structure similar to fentanyl
 Methadone  Potent opioid analgesic
 Substitute for opioids -> reduce
incidences of withdrawal
symptoms
 Tramadol  Inhibits neuronal reuptake of
norepinephrine
 Potentiates release of serotonin
 Cause descending inhibition of
nociception
  Buprenorphine  Highly lipid soluble Prolonged nausea
 Similar effects with morphine and vomiting
Diminish effects at
Partial opioid  Extremely high affinity for MOR
opioid receptors
 Respiratory depression -> treated
with doxapram
 Pentazocine  Poor mu opioid receptor efficacy Increase HR and
 kappa agonistics properties -> BP
dysesthesias Nausea; vomiting
 used as analgesics Bizarre dreams
 decrease abuse potential Hallucination
 Meptazinol Opioid agonists-  precipitate withdrawal Nausea
Pain antagonists Voiting
control Less respiratory
depression
 Nalbuphine
 Butorphanol
 Naloxone  Centrally and peripherally acting Hypertension
Competitive opioid  Beware of re-narcotization Pulmonary edema
antagonist Cardiac
arrhythmias
 Naltrexone  Treat opioid addiction;
Compulsive eating with morbid
obesity
#38 Drugs used in Anesthesia (General and local anesthestics)
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Isoflurane  Anaesthesia but not analgesia
 Decreased BP and SVR
 Increase HR
 Moderate
 Sevoflurane  Anaesthesia but not analgesia
 Decrease BP, SVR and BP
 Dose-dependent depression of
respiratory rate
 Non-irritant to airways
 Desflurane  Anaethesia but not analgesia
 Dose-dependent cardiovascular
depression; respiratory
depression
 Respiratory irritant -> increased
secretions
 Requires vaporizer
 Nitrous oxide  Analgesia
 Sedation
 Prolong use interferes with
vitamin B12
 Sodium  Prevents CO2 in air from forming
thiopental Barbiturates free acid
 Ketamine  Lipophobic Hallucinations
 Rapid onset ->longer duration of Agitation
action
 Dissociative anaesthesia -> not
necessary involve loss of
Phencyclidine
consciousness
derivatives
 Increase HR, BP and
catecholamine levels
 Mildly depress respiration
 Bronchodilator
 Protective airway reflexes
 Etomidate  Carboxylated imidazole
 Excitatory muscle movements
Imidazoles
 Inhibition of corticosteroid and
mineralocorticoid synthesis
  Propofol  Dose-dependent cortical
depression
 Used in sedation
 Suitable for total intravenous
anaesthesia
Phenols
 Attenuation of airway reflexes
 Reduction in vascular resistance,
myocardial depression ->
hypotension
 Respiratory depressant
 Benzodiazepam  Anaesthesia as premedication;
(Midazolam) sedate patients
 Anxiolytic, hypnotic,
anticonvulsant properties
 Blockade of voltage-gated sodium channel conductance
 Prevents axonal action potential generation or propagation
 Lignocaine  Solutions for surface application
to pharynx, larynx and trachea
 Spray for anaesthesia of the oral
cavity and upper respiratory tract
 Bupivacaine  Propensity of cardiotoxicity
Local
anaesthetic  Ropivacine  Preparation -> S-ropivacaine
enantiomer solutions
 Separation of sensory and motor
blockade
 Tetracaine  Topical anaesthesia Severe skin
 Ophthalmic procedures reddening
 (Ametop) aqueous cream
preparation; penetrates skin
rapidly
#39 Skeletal Muscle Relaxants
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Succinylcholine  Phase I -> twitching and Bradycardia
fasciculation -> Na+ channel get Anaphylaxis
activated -> flaccid paralysis -> Malignant hyperthermia
absence of fade and post-tetanic Increase intra-ocular
facilitation on PNS pressure; intra-gastric
Depolarizing
 Phase II -> prolonged block -> pressure
block
(PNS) fade of the train-of-four twitch Muscle pain
height response and post tetanic Prolonged block ->
facilitation phase II block
 Resembles non-depolarize block
 Partial reverse by AchE
 Pancuronium  Competitive blocvk by muscle
relaxants
 N atom attached to Ach receptors ->
Non-polarizing antagonists to Ach receptors, no
Muscle Long acting muscle
skeletal muscle conformational change at receptor
relaxants relaxants
relaxants  Can overcome by excess Ach
 Large muscles more resistant to
blockade compared to small
muscles
 Atracurium/ (Atracurium)
Cisatracurium  Release histamine
 Rocuronium  Organ independent elimination
 Vencuronium (Cisatracurium)
 Longer onset and duration
 Does not release histamine
(Vecuronium)
Intermediate acting  Lyophilized powder
muscle relaxants  Significant hepatic uptake and biliary
excretion
(Rocuronium)
 Alternative to succinylcholine in
larger doses for rapid sequence
intubation
 Reversed by gamma cyclodextrin
Sugammadex
 Mivacurium Short acting muscle 
relaxants
  Neostigmine  Reversible, acid-transferring
cholinesterase
 Accumulation of Ach at the NMJ ->
competitive antagonism
 Increase in ACh
 Sugammadex  Selective relaxant binding agent
 Reversal from neuromuscular
blockade from Rocuronium and
Vecuronium
 Encapsulates then inactivate them
 Dantrolene  Direction action on muscle fiber
 Inhibits Ca++ release and reuptake
into sarcoplasmic reticulum
Peripherally acting
Muscle relaxant  Prevents depolarization
muscle relaxant
 Treatment of malignant
hyperthermia; conditions associated
with spasticity
 Botulinum toxin  Binds pre-synaptically to high-affinity
A (Botox) recognitions on the cholinergic nerve
terminals
 Decrease release of acetylcholine ->
neuromuscular blocking effect
 Recovery by formation of new
neuromuscular junction
 Baclofen  Racemic GABAB receptor agonist Muscle weakness
 Inhibit activity of motor neurons in Confusion, headache,
the anterior horn of the spinal chord insomnia
Central acting
Nausea, constipation
muscle relaxant
Urinary frequency
Asthenia, dizziness,
somnolence
 Tizanidine  Clonidine derivative
 Short-acting presynaptic α2-
adrenergic receptor agonist actions
 Affect spinal motor neurons via
presynaptic inhibition
 Diazepam  Acting on GABAA receptor ->
increase GABAA receptors affinity
for GABA in brain and spinal cord
 Influx of Cl- -> hyperpolarization of
the postsynaptic cell
#40 Drug of Abuse and Drug Dependence
Categories Drug Name Mechanism Side effects Remarks
 Amphetamines  Synthetic drugs -> stimulate nervous system Nervousness
 Trigger release and block uptake of noradrenaline and Agitation
dopamine Irritability
 Produce high levels of energy -> no sleep Confusion
 Reduce appetite, increase HR, constrict blood vessels in Paranoia
skin and mucous membrane Hostility
 Develop tolerance
 Cocaine  Local painkiller or anesthetic
Central  Powerfully addictive drug
stimulants  Replaced by lidocaine
 Snorted / dissolved in water and injected
 Prevent reuptake of dopamine -> buildup of dopamine in
synapse -> Stimulate reward system
 Produce happy feelings, increased energy and alertness
 Nicotine  Stimulated dopamine neurons Lung cancer
 Addicting agent in tobacco Obstructive lung disease
Coronary heart disease
Peripheral vascular disease
 Alcohol  Change in membrane fluidity with changes in membrane Anxiety Synergistic with
protein functions (causing inhibitory postsynaptic potential Depression heroin and
(IPSP)) Weakness barbiturates
 Direct effect on GABAA receptors -> inhibit action of GABA in Restlessness
CNS Insomnia
Central  Inhibitory effect on glutamate activation of NMDA-glutamate Muscle tremor
depressants receptors in CNS Elevated BP, pulse,
 Biphasic effect -> initially stimulates; later depresses temperature
 Benzodiazewpines  Induce muscle relaxation; reduce anxiety; produce mild Slurred speech
 Barbiturates euphoria; aid sleep Impaired judgement
 Stimulate GABA system Accidental suffocation
 Tolerance and withdrawal presence
 Lysergic acid  Derivate form ergot Distressing anxiety; Fear of
Hallucinogens diethyamide (LSD)  death; Nausea; Numbness;
Tremor
  MDMA (Ecstasy)  Amphetamine with CNS stimulation and hallucinogenic Restlessness; Dizziness
effects Tremor; Talkativeness
 Central stimulation -> liberation of norepinephrine form Tenseness
Hallucinogens peripheral adrenergic terminals -> sympathomimetic effects Depression after stimulation
 Serotonin-depletion effect GI disturbance
Fetal poisoning ->
convulsion, coma, CV
 Mescaline collapse
Weight loss
Psychotic reaction with vivid
hallucination and paranoid
delusions
Muscle rigidity

 Ketamine  Dissociative anesthetic Unpleasant dreams

 Blocking activation of non-competitive N-methyl-D-aspartate Confusion
(NMDA) receptors -> dissociative anesthesia -> sensory Hallucinations
loss, analgesia, amnesia without loss of consciousness Irrational behavior
‘flashback’
Respiratory suppression
Dissociative Impaired memory
anesthetics Leaning and attentional
mechanisms
 Phencyclidine  Blocking the NMDA glutamate receptors -> serious of Loss of balance
hallucinogenic effects Slurred speech
 Euphoria; suicidal impulse; aggressive behaviors Delusions
Convulsions
Paranoia
 Marijuana  Used for painkiller; mild sedative; weakness; malaria;
 Tetrahydrocannabinol constipation
(THC)  1964 -> isolated to THC
Cannabis
 Used for reduction of excessive eye pressure in glaucoma;
lessoning of nausea by anti-cancer drugs; muscle relaxant;
increase appetite
 Morphine  Pain reliever
 Heroin  (heroin) high solubility of water -> easy preparation
Narcotics  (codeine) cough suppressant
analgesics  Codeine
 Methadone  Treatment of heroin addicts
 Similar drugs with less side effect in withdrawal
#41 Drugs in the Treatment of Ear, Nose and Throat Disease
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Ethanla 
Alcohols
 Isopropyl alcohol
 Iodine tincture 
Iodine
 Povidone-iodine
 Blench Chlorine 
 Phenylphenol  Corrosive and membrane
 Benzyl- disruption
cholorophenol 
Phenolics

 Hexachlorphene  Skin disinfectant

 Chlorhexidine  Absorb to bacterial membrane

 Chlorhexidine Chlorhexidine -> membrane leakage -> cell
digluconate damage
Antiseptics
and  Benzalkonium  Quaternary ammonium
chloride compounds
disinfectants  Detergent-like property

 Formaldehyde  Aldehydes
 Glutaraldehyde  Alkylating agents
 Formalin  (formalin) solution of
formaldehyde in water

Miscellaneous agents
 Hydrogen peroxide  oxidizing agent

 Silver  Bactericidal but less commonly

 Mercury used
compounds
 Olive oil  Clear ear canal
 Sodium  Antiseptic
bicarbonate
External ear
 Boric acid
canal
 Aluminum acetate  Drying agent
inflammation
 Corticosteroid  Anti-inflammatory agent
drops
  Topical antibiotics
 Paracetamol  Viral infection
Middle ear  Control pain
 Amoxicillin infection –  Systemic antibiotics
 Trimethoprim- otitis media
sulfamethoxazole (acute and
 Decongestant chronic)  Better drainage and reduction
of pressure
 Cromolyn sodium  Presence of allergens ->
increase of chemical mediators
-> inflammatory process and
symptoms
 Prophylactic use
 Antihistamine Nasal allergy  Decrease effect of histamine
 Beclomethasone  Anti-inflammatory agent
 Budesonide  Topical corticosteroids and
nasal spray
 Decrease inflammatory and
edema
 Xylometazoline  Blood vessel swelling + fluid Rebound nasal
 Oxymetazoline accumulation congestion
Nasal  Active α receptor in blood Less systemic effect
Decongestants
congestion vessels -> constrict blood with local application
vessels -> decrease swelling ->
improve airflow
 Antibiotics 
Nasal
 infection

Cream or ointment
 Hexetidine  Keep oral hygiene with mouth
 Chlorhesidine wash
 Hydrogen peroxide Oral
ulceration and
 Salt solution
inflammatory
 Bonjela (choline  Find out the underlying problem
salicylate,
cetalkonium)
Pain relieve
 Lozenges
(dequadin/
strepsils)
  Salivary substitutes
Dry mouth  Spray
 Solutions
#42 Drugs used in eye disorders
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
Antibacterial  Ofloxacin 
Anti-viral  Acyclovir 
Anti-fungal   *Fungal infection risk in
contact lens user
Eye infection:
 Pheniramine  Relieve of allergy and itchy
H1 blocker
 Antazoline Conjunctivitis
eyes
Antihistamines
 Naphazoline 紅眼症 vasoconstrictor
Keratitis
Mast cell  Cromolyn sodium 角膜炎
 Relieve of allergy and itchy
stabilizer  Nedocromil eyes
Blepharitis
 and stye
 Management of ocular Risk of steroid- Immune-modulatory
Glucocorticoid inflammation induced therapy
眼針
glaucoma
external eye
 Flurbiprofen  For seasonal allergic Topical use
infection
 Ketorolac conjunctivitis
NSAIDS  Diclofenac  Relieve post-op inflammation
 Bromfenac and pain
 Nepafenac
 Latanoprost  PGF2α analogs Eye drop
 Bimatoprost  Affect ciliary muscle open up Once a day
Prostaglandins PGF2α analogs
 Travoprost trabecular meshwork  Require refrigeration
facilitate aqueous outflow
 Timolol  Reduce aqueous humor may affect Only Betaxolol is β2
 Betaxolol production (which stimulated airway selective
β2-blockers  Carteolol by β effect) *asthma
 Levobuolol  Block β receptor  ↓aqueous patients
Glaucoma solution ↓pressure in eye
 Acetazolamide (open-angle:  Inhibit carbonic anhydrase in Topical: 3 times daily
Carbonic (oral) chronic; epithelium of ciliary body 
anhydrase  Dorzolamide closed-angle: ↓formation of bicarbonate ion
inhibitors  Brinzolamide acute, need  ↓fluid transport 
(topical) surgery) ↓pressure
 Pilocarpine  Contract ciliary muscle in eye Constrict pupil M receptor selective
 improve drainage  Blur vision Good lipid solubility,
reduce pressure Night vision not degraded by
Cholino-  (老人家本身早訓所以夜盲都冇 cholinesterase
mimetics 影響，又本身都眼矇矇所以唔
介意，衡量影響覺得 ok 嘅就會
開比老人家)
  Physostigmine Glaucoma  Lipid soluble  eye
(open-angle: drop can be absorbed
Cholinesteras chronic;
e inhibitor closed-angle:
acute, need
surgery)
 Atropine  Dilate pupil Need sunglasses after
(7-10day)   (if not dilated, light during procedure
*eye
 Homatropine exam cause pupil constriction)
Muscarinic examination,  block M receptor in sphincter
(3-7day)
receptor diagnostic
blocker  Cyclopentolate purpose
of iris
(1 day)
 Tropicamide
(0.25day) 
#43 Drugs used in skin disorders
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Cimetidine  Topical for localized and less
Antihistamines  Ranitidine H2 blockers severe cases
 Famotidine
Steroid  
 (cream, ointment, 
Emollients Pruritus
lotion)
 Menthol (itching)  Menthol may
 Camphor cause hemolysis
Coolants  Calamine in G6PD
deficiency
patients (but low
risk)
  Immunosuppressive and anti-
Glucocorticoid Skin atrophy inflammatory
 Systemic for severe case
 Methotrexate 
 Azathioprine Antimetabolites
Cytotoxic and  fluorouracil
immuno-
 Cyclophosphamide Psoriasis Alkylating agents 
suppressive
drugs  Cyclosporine 
Calcineurin
 Tacrolimus
inhibitors
 Pimercolimus
 Tretinoin ,  Vitamin A-like Topical once
 Adapalene  Bind to nuclear retinoid nightly
receptors Tretinoin: If meet
 Correct abnormal follicle sunlightsunburn
Acne keratinization, reduce bacterial Photolabile,
暗瘡 count inactivated by
 ↑cell turn over  skin peeling benzoyl peroxide
Acne vulgaris 粉
 Adapalene: Similar to tretinoin
Retinoid 刺 Retinoic acid
 Stable in sunlight and to
(skin disorder of benzoyl peroxide
 Benzoyl peroxide sebaceous  Effective topical agent Use with
follicle)  Benzoyl peroxide => Penetrate
 Azelaic acid antibiotics
and converted to benzoic acid
 Antimicrobial against
Propionibacterium acnes
 Skin drying and peeling effect
  Eczema 濕疹  Avoid soaps and
Antihistamines detergents 
Dermatitis
Corticosteroid moisturizer to
皮膚炎
relief dryness
Antihistamines  Urticaria  Frequently by
Glucocorticoids allergy
麻疹
Cooling
medications (acute/ chronic)
Skin cream &   Immune-mediated
moisture Psoriasis chronic skin
Topical problem
牛皮癬
corticosteroid Skin cells grow too
Retinoid quick
 Methotrezate  Systematic use
 Cyclosporine
 Salicylic acid Hyperkeratotic  Solubilize intercellular cement Need scratch to
disorder:  Reduce cell adhesion remove layer after
 Soften stratum corneum soften
Warts 疣  Wart: caused by human
papilloma virus HPV
Corns 雞眼
 Corn: harden skin on toe &
finger
 α-Hydroxy acid  Similar to salicylic acid
 Urea  Softening and moisturizing Other treatment:
effect cryosurgery
 Increase solubilization and (freezing) & laser
removal of cells from stratum treatment
corneum
#44 Fertility agents, contraceptives and oxytocics
Categories Drug Name Treatment Function / Outcome Mechanism Side effects Remarks
 Progestin-only  Inhibit hypothalamus Headache, breast Taken
contraceptives ↓frequency of GnRH pulse tenderness, continuously for
(mini-pill) generator  reduce/ inhibit depression, 28 days without
release of LH  prevent nausea, break
ovulation hypertension,
 Thickening of cervical mucus thromboembolism
Oral
 ↓sperm penetration (blood clot)
contraceptives ↑risk of breast
 Endometrial alteration 
↓implantation cancer
 Morning after pill  Strong progesterone -> Within 72
(Plan B pill) temporarily stop release of hours,
 Levonorgestrel egg from ovary -> prevent preferably 12
0.75mg fertilization and implantation hours
 Spermicide  Surfactant lyse the sperm
 (Nonoxynol-9) membrane
 Tamoxifen  Partial agonist inhibitor of Hot flush, nausea,
estrogen receptor vomiting
 Reduce contralateral breast
Selective Breast cancer
cancer
estrogen
 Chemoprevention in high risk
receptor
group
modulators
(SERMs)  Raloxifene Prevention of  Partial estrogen agonist- More expensive
osteoporosis in antagonist than estrogen
postmenopausal  Similar effect as stradiol on
women lipid and bone
 Clomiphene  Partial agonist and FSH multiple egg Not effective in
competitive endogenous development / ovarian and
estrogen inhibitor enlargement, pituitary failure
 Inhibit –ve feedback of abdominal
estrogen  ↑secretion of LH discomfort
& FSH  ↑estrogen & Risk of ovarian
progesterone  stimulation of cancer
Fertility Agent
follicles  maturation
ovulation
 FSH + hCG  Injection of FSH for 5-12 days
 ↑estrogen and growth of
Hormonal therapy follicles in ovary  injection of
human chorionic gonadotropin
(hCG)  produce ovulation
  Bromocriptine  Reduce prolactin released by
 Cabergoline Hormonal therapy pituitary
 GnRH  Stimulate LH and FSH release
Fertility Agent  Medrol  A steroid to assist pre-embryo
implantation
 Doxycylin  For male partner to reduce
levels of bacteria in semen
 Oxytocin  Increase sensitivity of uterus Uterine-
 Assist laboring in patients with stimulating
uterine dysfunction
Uterus stimulation
 Contract uterus  prevent or
control bleeding
Oxytocic  Stimulate milk let-down reflex
 Prostagladins Abortifacients  Induce cervical ripening Uterine-
 (PGE, PGF) (terminate  Control persistent postpartum stimulating
pregnancy) hemorrhage
 β2-adrenergic Delay premature  Inhibit uterine contraction Uterine-relaxing
agonists labor