PHARMACOLOGY &

THERAPEUTICS SUPPLEMENTS
NISHTAR MEDICAL UNIVERSITY MULTAN

ALI RAZA CHAUDARY (N67)

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ALI RAZA CHAUDARY (N67)

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REFERENCES
PHARMACOLOGY AND THERAPEUTICS
1. Katzung & Trevor’s Pharmacology, Examination & Board Review, 12th Ed. (MINI
KAZUNG)
2. Lippincott Illustrated Reviews: Pharmacolog, 6th Ed.
3. Basic and Clinical Pharmacology by Katzung, 14th Ed., Mc Graw-Hill (BIG
KATZUNG)
4. Kaplan USMLE Step 1 Video & Lecture Notes 2020: Pharmacology

CONTENTS
DESCRIPTION PAGE NO
MODULE NO. 1: GENERAL PHARMACOLOGY 5
MODULE NO. 2: AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY 26
MODULE NO. 3: AUTOCOIDS & NSAIDS PHARMACOLOGY 34
MODULE NO. 4: RESPIRATORY & GASTROINTESTINAL PHARMACOLOGY 39
MODULE NO. 5: CARDIOVASCULAR, DIURETIC & BLOOD PHARMACOLOGY 42
MODULE NO. 6: ANTIFUNGAL, ANTIVIRAL & ANTICANCER PHARMACOLOGY 54
MODULE NO. 7: ANTI-MYCOBACTERIAL & PARASITIC PHARMACOLOGY 58
MODULE NO. 8: ANTIBACTERIAL PHARMACOLOGY 62
MODULE NO. 9: ENDOCRINE PHARMACOLOGY 72
MODULE NO. 10: CENTRAL NERVOUS SYSTEM PHARMACOLOGY 79
MODULE NO. 11: DRUGS OF CHOICE 93

ALI RAZA CHAUDARY (N67)

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ALI RAZA CHAUDARY (N67)

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🢔1
PHARMACOKINETICS
🢖
G E N E R A L PHARMACOLOGY
1 S E Q + 5 M CQ s = 12 Marks

DESCRIPTION PAGE NO
6
PHARMACODYNAMICS 18
DRUG DEVELOPMENT & REGULATION 23

ALI RAZA CHAUDARY (N67)

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PHARMACOKINETICS
(The actions of the body on the drug) OR (It is study of ADME)
Four pharmacokinetic properties determine the onset, intensity, and the duration of drug action:
1. Absorption: Absorption from the site of administration permits entry of the drug (either directly or indirectly) into plasma.
2. Distribution: Drug may then reversibly leave the bloodstream and distribute into the interstitial and intracellular fluids.
3. Metabolism/Biotransformation: Drug may be biotransformed by metabolism by the liver or other tissues.
4. Elimination: Drug and its metabolites are eliminated from the body in urine, bile, tears, breast milk, saliva, sweat, or feces

ABSORPTION
(Absorption is the transfer of a drug from the site of administration to the site of action/bloodstream.)
▶ MECHANISMS FOR PERMEATION OF DRUGS
FEATURE PASSIVE FACILITATED ACTIVE ENDOCYTOSIS EXOCYTOSIS
TRANSPORT TRANSPORT TRANSPORT
Movement of drug
from region of Energy requiring
Movement of Type of vesicle Type of vesicle
higher to lower movement of
drug from region transport that transport that
Definition concentration by substances across
of higher to lower moves substances moves substances
the help of carrier a plasma
concentration into a cell. out of a cell.
or channel protein membrane.

Incidence Very Common Less Common Least Common Least Common Least Common
Process Slow & Passive Fast & Passive Very Fast & Active Very Fast & Active Very Fast & Active
Relation with Along the Against the Against the
Along the gradient Against the gradient
gradient gradient gradient gradient
Fick’s Law Applicable Not applicable Not applicable Not applicable Not applicable
Carrier Not required Required Required Required Required
Energy Not required Not required Required Required Required
Selectivity No Yes Yes Yes Yes
Saturablity No Yes Yes Yes Yes
Direction Bidirectional Bidirectional Unidirectional Unidirectional Unidirectional
Metabolic Inhibition No Yes Yes Yes Yes
Ions,
Aqueous or lipid Neurotransmitters,
Examples diffusion in Metabolites and Na/K ATPase Vitamin B12, Iron,
Neurotransmitters
capillaries Xenobiotics’ pump Proteins
transporters

▶ FACTORS AFFECTING ABSORPTION OF DRUGS

LOCAL FACTORS (RELATED TO BODY)
Fick’s Law
Rate = C1 − C2 × Permeability coefficient
Thickness
× Area

1. Area of Absorptive Surface (directly proportional) e.g. intestine > stomach

2. Contact time at the Absorption Site
 ⭡GIT Motility ⭢🢙Absorption
 🢙GIT Motility ⭢ Delayed absorption
3. Food/Other drugs (Dilutes the drug and slows gastric emptying i.e delayed absorption)
4. Blood Flow to Absorption Site (directly proportional) (Intramuscular, Subcutaneous & GIT sites)
5. Expression of P-glycoprotein (inversely proportional) (“pumps” drugs out of the cells & provide multidrug resistance)
6. Route of administration (affects rate and efficacy of the absorption)
7. Local pH
PHARMACOLOGICAL FACTORS (RELATED TO DRUG)
8. Solubility
1 1
Absorption 𝖺 𝖺
Aqueous Solubility ElectrostaticCharge (ionization & 𝑝𝑜𝑙𝑎𝑟i𝑡𝑦)
Absorption 𝖺 Lipid Solubility 𝖺 1
Charge

2. Degree of Ionization (inversely proportional) By Henderson-

Hasselbalch Equation
Pronated form
log ( ) = pKa
− pH Unpronated form
3. Nature of drug & pH of the medium (WHEN MEDIUM IS SAME,
DRUGS CAN CROSS THE MEMBRANE)
 Acidic pH (e.g. Stomach):
Weak acidic drugs become more unionized ⭢ More lipid soluble
⭢ More absorbable e.g. aspirin
Weak basic drugs become more ionized ⭢ More aqueous
soluble ⭢ Less absorbable e.g. amphetamine
 Alkaline pH (e.g. Intestine):
Weak basic drugs become more unionized ⭢ More lipid soluble ⭢ More absorbable
Weak acidic drugs become more ionized ⭢ More aqueous soluble ⭢ Less absorbable
4. ALI RAZA CHAUDARY
Size (inversely proportional) e.g. powder form is more absorbable (N67)
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▶ ROUTES OF ADMINISTRATION OF DRUGS
It is determined by
1. Properties of drug (solubility, ionization)
2. Therapeutic objectives (desirability of a rapid onset, need for long-term treatment, or restriction of delivery to a local site).
Routes of Drug Administration

Local Systemic

Topical Enteral Parenteral Others (Skin &

Mucous
Sub- Intra-
Intra-
Membrane)
Sub- Trans- Oral In-
Oral
Nasal In- lingual venous muscular cutaneous
dermal Rectal halarional halational
Intra-
articular

Intrathe
cal
ROUTE PATTERN ADVANTAGES DISADVANTAGES
LOCAL EFFECTS
 Applied on skin or mucous
membranes of eye, throat,  Low systemic effects
Topical  Not well absorbed in deeper layers
ear, nose, airway or vagina  Steady level of drugs to the system of skin
 E.g. clotrimazole applied to
skin for fungal infections.
 Difficult to hit joint surfaces
 Introduce drugs in to  Low systemic effects  Difficult to calculate dose for joints
Intraarticular inflamed joint cavity directly  Rapid delivery to the local tissue  Irritate joints and cause infections
 E.g. hydrocortisone  Painful procedure, expert is needed
 Introduce drugs directly into
Intrathecal/ the cerebrospinal fluid. For  Low systemic effects
 Painful procedure, expert is needed
 E.g. amphotericin B is used  Bypasses BBB and BCB
ventricular in cryptococcal meningitis
SYSTEMIC EFFECTS
ENTERAL ROUTE (through the mouth)
 Variable; many factors
 Drugs may be metabolized before
PREPARATIONS: systemic absorption (first pass
 Safest, most common, convenient,
 Enteric-coated e.g. aspirin and economical route effect)
Oral for protecting the
 Self administered  Limited absorption due to low GIT
(by mouth) stomach
 Toxicities overcome by antitodes pH
 Extended-release e.g. activated charcoal  Food may affect absorption
(ER/XR)  Patient compliance is necessary
e.g. morphine to prolong
duration of action for drugs
with small half lives
 Bypasses first-pass effect ,
Sublingual Depends on the drug:
(under tongue)  Absorb directly to systemic venous  Limited to certain types of drugs
OR  Few drugs (for example, circulation
nitroglycerin) have rapid,  Limited to drugs that can be taken
Buccal  Bypasses destruction by GIT acid
direct systemic absorption in small doses
(between  Drug stability maintained because
 Most drugs erratically or  May lose part of the drug dose if
cheek and the pH of saliva relatively neutral
incompletely absorbed swallowed
gum)  May cause immediate
pharmacological effects
PARENTERAL ROUTE (other the mouth)
Usage:
 Drugs poorly absorbed from the GI tract (e.g. heparin)
 Drugs unstable in GIT (e.g. insulin)
 Unable to take oral medications (unconscious patients)
 Require a rapid onset of action
Advantage: highest bioavailability (not subject to first-pass metabolism or the harsh GI environment)
Disadvantage: Irreversible and may cause pain, fear, local tissue damage, and infections
 Can have immediate effects  Unsuitable for oily substances
 Ideal if dosed in large volumes  Bolus injection may result in
 Suitable for irritating substances adverse effects like hemolysis and
Intravenous  Absorption not required and complex mixtures thrmobosis
(25° angle)  100% Bioavailability  Valuable in emergency  Most substances must be slowly
situations injected
 Dosage titration permissible  No antitodes like activated
ALI RAZA CHAUDARY
 Ideal for high molecular weight
(N67)
charcoal
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Depends on drug diluents.
PREPARATIONS:
 Suitable for slow-release drugs
 Aqueous solution: prompt  Pain or necrosis if drug is irritating
Subcutaneous  Ideal for some poorly soluble
 Depot preparations: slow  Unsuitable for drugs administered
(45° angle) suspensions
and sustained in large volumes
EXAMPLES:  Less adverse effects like hemolysis
and thrombosis as in IV bolus.
 Insulin
 Heparin
Depends on drug diluents.
PREPARATIONS:
 Affects certain lab tests (creatine
 Aqueous solution: prompt  Suitable if drug volume is moderate
kinase)
Intramuscular  Depot preparations: slow  Suitable for oily vehicles and
and sustained (non-  Can be painful
(90° angle) certain irritating substances
aqueous vehicle like  Can cause intramuscular
 Preferable to intravenous if patient hemorrhage (precluded during
polyethylene glycol) e.g. must self-administer
haloperidol & depot anticoagulation therapy)
medroxyprogesterone
OTHERS
 Slow and sustained
depending upon thickness  Bypasses the first-pass effect  Some patients are allergic to
of skin and lipid solubility at  Convenient and painless patches, which can cause irritation
site of administration  Drug must be highly lipophilic
Transdermal  Ideal for drugs that are lipophilic
(patch) EXAMPLES: and have poor oral bioavailability  May cause delayed delivery of drug
 Nitroglycerin to pharmacological site of action
 Ideal for drugs that are quickly
 Scopolamine eliminated from the body  Limited to drugs that can be taken
 Nicotine in small daily doses
 Partially bypasses first-pass effect
 Bypasses destruction by GIT acid  Drugs may irritate the rectal
Rectal/  Erratic (unpredicatable)  Ideal if drug causes vomiting mucosa
Suppository and variable  Ideal in patients who are vomiting,  Not a well-accepted route
or comatose
 Systemic absorption may
occur; this is not always  Absorption is rapid; can have
desirable immediate effects
EXAMPLES:  Ideal for gases e.g.
 Most addictive route (drug can
Oral Inhalational anesthesia enter the brain quickly)
Inhalation  Anesthesia  Effective for patients with  Patient may have difficulty
(Oral or Nasal)  Albuterol respiratory problems regulating dose
 Fluticasone  Dose can be titrated
Nasal Inhalational  Some patients may have difficulty
 Localized effect to target lungs: using inhalers
 Oxymetazoline, lower doses used compared to that
 Mometasone with oral or parenteral e.g.
 Desmopressin for diabetes bronchodilators & corticosteroids
insipidus.  Fewer systemic side effects

▶ BIOAVAILABILITY (F)
( rate and extent to which an administered drug reaches the systemic circulation)
DETERMINATION
 Unity (100%) for IV administration.
 Important for calculating drug dosages for non-IV routes of administration.
 Determined by comparing;
AUC Route
Bioavailability (F) = × 100
AUC
IV

ALI RAZA CHAUDARY (N67)

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FACTORS AFFECTING
1. First-pass hepatic metabolism:
 When a drug is absorbed from GIT, it enters initially in portal circulation and rapidly metabolized in liver or gut wall and
amount of unchanged drug entering the systemic circulation is decreased. Eg. nitroglycerin is primarily administered
via sublingual or transdermal.
 Results in lower systemic bioavailability of parent compound, diminished therapeutic response.
 Drugs with high first-pass metabolism should be given in doses sufficient to ensure that enough active drug reaches
desired site of action.
ORAL DOSE

 > Sublingual / Parenteral

 Marked individual variation
 ⭡Oral F Liver disease or when
in competition with other drug
 Short plasma t1/2.

SITE
2. Solubility of the drug:  Liver (major site)
 Hydrophilic ⭢ poorly absorbed in lipid bilayer membranes  Gut wall & lumen
 Lipophilic ⭢ poorly absorbed in aqueous body fluids
 For a drug to be readily absorbed, it must be largely lipophilic, yet have some solubility in aqueous solutions.
3. Chemical instability:
 Penicillin G, unstable in pH of gastric contents.
 Insulin, destroyed in GIT by degradative enzymes.
4. Nature of the drug formulation:
 Particle size
 Salt form
 Crystal polymorphism
 Enteric coatings
 Presence of excipients (such as binders and dispersing agents)

▶ EQUIVALENCE
FEATURE BIOEQUIVALENCE THERAPEUTIC EQUIVALENCE
Two drug formulations are therapeutically
Two drug formulations are bioequivalent if equivalent if they are pharmaceutically
they show comparable bioavailability and equivalent (that is, they have same dosage
Definition form, contain same active ingredient, and use
similar times to achieve peak blood
concentrations. same route of administration) with similar
clinical and safety profiles.
Rate Same -
Bioavailability Same -
Clinical Effect - Same
Safety Profile - Same
Pharmaceutical Equal 🗸 🗸
Pharmaceutical Alternative 🗸 🗴

DISTRIBUTION
(Process by which a drug reversibly leaves bloodstream and enters interstitium and tissues.)
For drugs administered IV, absorption is not a factor, and initial phase (from immediately after administration through rapid fall in
concentration) represents distribution phase, during which drug rapidly leaves the circulation and enters the tissues.

ALI RAZA CHAUDARY (N67)

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▶ FACTORS AFFECTING DISTRIBUTION OF DRUGS
1. Blood flow to capillaries (Does not affect the amount of drug in the tissue at equilibrium)
 Well-Perfused Tissues: Brain, Heart, Kidney, Splanchnic organs >>> Skeletal Muscles
 Poorly-Perfused Tissues: Fat, Bone and other viscera
 Example: IV bolus of propofol ⭢ High blood flow & high lipophilicity ⭢ Rapid distribution into CNS ⭢ Anesthesia
⭢ Hypnosis ⭢Subsequent slower distribution to skeletal muscle & adipose tissue ⭢ Plasma conc. lowered ⭢
Diffuses out of CNS down gradient ⭢ Consciousness regained
2. Capillary permeability (determined by capillary structure i.e. fraction of basement membrane exposed by slit junctions
between endothelial cells, and by chemical nature of drug)
 Liver & Spleen: Discontinuous capillaries + Slit junctions
 Brain: Continuous capillaries + Tight junctions (Lipid-soluble drugs readily penetrate CNS but ionized or polar
drugs e.g. levodopa, fail to enter CNS as tight junction formed by endothelial cells of BBB and is actively transport
mostly)
3. Binding of drug (directly proportional to drug distribution)
 Binding to plasma proteins: Reversible binding and sequesters drugs in a non-diffusible form that slows their
transfer out of the vascular compartment. Example: Warfarin is bound to Albumin.
 Acts as a drug reservoir
 Maintains free drug concentration in plasma.
 Binding to tissue proteins: Accumulate drug in tissues by binding to lipids, proteins and nucleic acids, leading to
higher concentrations in tissues than in extracellular fluid and blood. Example: acrolein accumulates in bladder
cause hemorrhagic cystitis
 Acts as a drug reservoir
 Prolong its actions or cause local drug toxicity.
4. Lipophilicity
 Lipophilic ⭢ rapidly absorbed in lipid bilayer membranes
 Hydrophilic ⭢ poorly absorbed in lipid bilayer membranes and have to pass through slit junctions
5. Size of organ (influence concentration gradient between blood and organ)
 Skeletal muscle > Blood: Take large amount of drug and have high blood-tissue gradient
 Brain < Blood: Take small amount of drug and have low blood-tissue gradient smaller
6. Pattern of drug distribution (2 forms)
 Bound form: Inactive, Non-diffusible, Cannot be metabolized or excreted by kidneys
 Free form: Active, Diffusible, Can be metabolized or excreted by kidneys
7. Apparent volume of distribution (Vd)

▶ EFFECTIVE DRUG CONCENTRATION

(Concentration of drug at the receptor site)
 Readily measured in blood
 Except for topical agents, it follows;
Effective Drug Concentration 𝖺 Concentration at receptor site 𝖺 Concentration in Plasma/Blood at equilibrium

FACTORS AFFECTING Cp or Cb
 Rate of input of drug by absorption
 Rate of distribution by Vd
 Rate of elimination by CL

▶ APPARENT VOLUME OF DISTRIBUTION (Vd)

(Fluid volume that is required to contain entire drug in body at same conc. measured in plasma)
 Apparent Vd has no physical equivalence that’s why it is called apparent.
 It relates the amount of drug in the body to the plasma (Cp) or blood (Cb) concentration at time zero as follow;
Amount of drug in the body Amount of drug in the
Vd = body =
Plasma drug concentration C
p

UNITS OF Vd
 Volume
 Volume/kg of body weight (if vary with body size)

ASPECTS
1. Distribution into water compartments in body: Once a drug enters the body, it distributes into any one of these or
sequestered in a cellular site.
PLASMA COMPARTMENT EXTRACELLULAR FLUID TOTAL BODY WATER
Model One compartment Two compartment Multicompartment
Drug HMW drug LMW drug LMW drug
Features Extensively protein bound drug Hydrophilic
Lypophilic
Crossing Cross slit junctions but not lipid Cross slit junctions and lipid
Cannot cross slit junctions
bilayers bilayers
Vd Vd = Plasma Volume = 4 L (4% of Vd = Plasma Volume + Interstitial Vd = Total body water = 42 L
Calculation weight) fluid volume = ECF Volume = (60% of weight)
14 L (20% of weight)
Vd Low Moderate High
ALI
Example RAZA Heparin CHAUDARY Aminoglycoside (N67) Ethanol
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2. Determination:

3. Effect on Half Life:

Half life 𝖺 Vd 𝖺 Duration of Action of Drug

METABOLISM/BIOTRANSFORMATION
(Chemical alteration of drug in body that converts non-polar or lipid soluble compounds to polar or lipid
insoluble compounds)

Biotransformation
Biotransformation is required for protection of body from toxic metabolites.

SITES EFFECTS ADVANTAGES

Primary Site Prodrug to Active Drug Active Drug to Active Drug to Active
Terminate drug action Liver Inactive Drug Metabolite
(Toxic Metabolism) ↓ Toxicity
🢙 Lipophilicity
⭡ Renal
excretion Other Sites ⭡Stability Propranolol Phenacetin to Paracetamol ⭡ Biliary
excretion
Kidney
⭡Bioavailability Morphine Digitoxin to Digoxin 🢙 Renal
reabsorption
Intestine
🢙Toxicity Paracetamol
Plasma
Lungs
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ALI RAZA CHAUDARY (N67)

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▶ CYTOCHROME P450 SYSTEM/ MIXED FUNCTION OXIDASES
(Microsomal enzyme ranking first among Phase I enzymes with respect to catalytic versatility)
Heme-containing proteins [Complex formed between Fe2+ and CO absorbs
light maximally at 450 nm (447-452 nm)]
 Substrate: Drug that is metabolized by the enzyme system
 Inducer: Drug that increase synthesis and activity of enzyme system
 Inhibitor: Drug that decrease the metabolism of a substrate
 At least 15 P450 enzymes identified in human liver microsomes.
% of Drugs Metabolized by Enzyme System
 3A4 & 5 50%
 2D6 25%
 1A2 15%
 2C9 Small but significant interactions
 2C19 Small but significant interactions
 2E1 ?

▶ TYPES OF METABOLIC REACTIONS

FEATURE PHASE I REACTIONS PHASE II REACTIONS

Reactions that convert the parent drug to a more polar Reactions that increase water solubility by
(water-soluble) or more reactive product by unmasking conjugation of the drug molecule with a polar moiety
Definition
or inserting a polar functional group such as -OH, -SH, such as glucuronate, acetate, sulfate, glutathione,
or -NH2 glycine, or methyl.
Non synthetic / Functionalization Synthetic / Conjugation
Other names
(A functional group is inserted) (An endogenous radical is conjugated)
Metabolite Polar + Active, Inactive or Unchanged Polar + Usually Inactive
Half life Short Long
Consequence May result in metabolic activation Facilitate Excretion (urine/ bile/ faeces)
Selectivity Not much selective Not much selective
Enzymes Cytochrome P450 Enzymes mainly Transferases mainly
True
Detoxification No Yes
reactions
Energy Not required Required
1. Microsomal Oxidation (9 types) 1. Glucuronidation (UDP glucuronyl transferase)
 N-oxidation: Chlorpheniramine  Aspirin, Acetaminophen, Digoxin
 S-oxidation: Chloramphenicol 2. Acetylation (N-Acetyl transferase)
 O-Dealkylaton: Phenacetin to Paracetamol  Isoniazid, Sulfonamids
 N-Dealkylaton: Theophylline 3. Glutathionation (Glutathione S- Transferase)
 S-Dealkylaton (Sulphur): 6-Methyl thiopurine  Ethacrynic Acid
 Deamination: Amphetamine 4. Acylation (N-Acyl trasferase)
 Desulfuration: Parathion to Paraoxon  Niacin, Salicylic Acid
 Aliphatic Hydroxylation: Ibuprofen 5. Sulfation (Sulfotransferases)
 Aromatic Hydroxylation: Propranolol  Acetaminophen
2. Non-microsomal Oxidation 6. Methylation (Methyl transferase)
 Mitochondrial enzymes – (MAO  Dopamine, Histamine
Adrenaline, 5-HT, Tyramine 7. Ribonucleotide or Ribonucleoside Synthesis
Examples  Cytoplasmic enzymes – (Dehydrogenases)  6 Mercaptopurine
Alcohol to Acetaldehyde & Acetic Acid
 Plasma oxidative enzymes – (Histaminase)
(Xanthine oxidase)
Allopurinol
3. Microsomal Reduction
 N-reduction: Chloramphenicol
 Keto-reduction: Cortisone
4. Microsomal Hydrolysis: Pethidine
5. Non-Microsomal Hydrolysis
 Esters: Aspirin
 Amides: Indomethacin
6. Cyclization: Proguanil
7. Decyclization: Phenytoin, Barbiturates

ALI RAZA CHAUDARY (N67)

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▶ DETERMINANTS OF BIOTRANSFORMATION
1. Chemical Factors
 Enzyme Induction (increased synthesis and expression of SER containing CYP450 enzymes by drugs or other
xenobiotic factors)
Examples: Bull Shit SCRAP PG
Barbiturates
St. John’s Wort
Sulfonylureas
Carbamazepin
e (auto-
inducer)
Rifampin (with contraceptives ⭢ 🢙therapeutic effect of contraceptives⭢pregnancy)
Alcohol (chornic)
Phenobarbital
Phenytoin
Griseofulvin
 Enzyme Inhibition
Examples:
SICKFACES.COM +
AQ G
Sodium Valporoate
Isoniazid
Cimetidine (Dcreases the metabolism of propanolol leading to enhanced bradycardia)
Ketoconazole
Fluconazole
Alcohol
Chloramphenicol
Erythromycin
Sulfonamides (Decrease the metabolism of phenytoin so that its blood levels become toxic)
Ciprofloxacin
Omeprazole
Metronidazole
Amidadrone
Quinine
Grape fruit
juice
 Intestinal P-Glycoprotein (P-gp or MDR-1) Inhibitors [An ATP-dependent transport molecule found in many
epithelial (intestine, BBB) and cancer cells, that expels drug molecules from mucosa to lumen or from cytoplasm
into extracellular space and contributes of first pass effect. Drugs include: Digoxin, Cyclosporine, Saquinavir]
Examples: Verapamil (Calcium Channel Blocker) Furanocoumarin (Grape fruit juice component)
2. Biological Factors
 Age
Infants CYP450 system not fully developed ⭢ 🢙 Metabolism
 Chloramphenicol: Grey baby syndrome
 Diazepam: Floppy baby syndrome
Elder patients’ organs shrunken⭢🢙 Blood flow ⭢ 🢙 Metabolism
 Gender
Males BMR Type ⭢ ⭡ Metabolism
> Women BMR Functional Element(Salicylates,
Defects orEthanol,
SNPs Propanolol, Benzodiazepines)
Drugs Affected
Womens on oral contraceptive ⭢ 🢙 Metabolism
CYP-3A4, 3A5 Cyclosporine toxicity ⭡
 Race (Antimalarials & Isoniazid)CYP-2D6 Codeine function & toxicity⭡
 DietPhase
(Deficiency of proteins,
I Enzymes vitamins & Minerals ⭢ 🢙 Metabolism)
CYP-2C9 Warfarin toxicity ⭡
 Genetic Polymorphs (Study of genetic factors affecting drug responses
CYP-2C19 is called metabolite ⭡🢙
Clopidogrel
pharmacogenetics) Dihydropyrimidine Dehydrogenase 5-Flurouracil toxicity⭡
UDP GT Irinotecan toxicity ⭡
Phase II Enzymes Thiopurine MT Thiopurine toxicity ⭡
G6DP Hemolysis ⭡
Transporter Organic Anion Transporter (OATP) Simvastatin myopathy ⭡
Receptor 1 receptor Metoprolol efficacy ⭡
3. Altered Physiological Factors
 Pregnancy Metabolism (⭡Phenytoin, 🢙 Phenobarbitone, 🢙 Pethidine)
 Hormonal Imbalance (Hypothyroidism & Hyperthyroidism)
 Disease states (CVS, Respiratory and Liver diseases impair metabolism & Renal diseases impair conjugation)
4. Temporal Factors
 ⭡Cortisterone Levels in afternoon ⭢ 🢙 Metabolism & vice versa for early morning
5. Route of Drug Administration
 Lignocaine is given topically not orally to avoid first pass metabolism
6. Environmental Factors
 Smoking, Chronic alcoholism & Pesticides or Organophosphate insecticides ⭢ Enzyme inducers.
 Hot and humid climate ⭢🢙 Metabolism
 High altitude ⭢🢙 Oxygen ⭢🢙 Metabolism

ALI RAZA CHAUDARY (N67)

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▶ TOXIC METABOLISM
(Active drug is converted to active metabolite i.e. toxic molecule)
Examples: Methyl alcohol, Ethylene glycol & large doses of acetaminophen

Metabolism of acetaminophen (Ac) to harmless conjugates or to toxic metabolites.

Acetaminophen glucuronide, acetaminophen sulfate, and the mercapturate conjugate
of acetaminophen all are nontoxic phase II conjugates. Ac* is the toxic, reactive phase I
metabolite, N-acetyl-p-benzoquinoneimine. Transformation to the reactive metabolite
occurs when hepatic stores of sulfate, glucuronide, and glutathione (GSH, Gs) are
depleted or overwhelmed or when phase I enzymes have been induced.

▶ ADVERSE DRUG EFFECTS

ADVERSE DRUG EFFECTS

Unpredictable Effects Predictable Effects

Allergy Idiosyncrasy Cummulation Teratogeni- Mutagenicity Carcinogeni- Tolerance

Dependence
/ Toxicity city city

Trait that is
Drug taken peculiar to a

Decreased
group or
as antigen iDrug induced
l Drug
induced Drug induced
Drug induced drug
Habituation/
ndividua
and immune
inutero fetal
gene
response
response mainly poisoning defects mutations cancer
due to many Addiction occurs because of
reasons
genetic
problem

Aspirin
Penicillin causes Large one
or Aflatoxins, Coal tar,
Ethanol, Anticancer
Vinyl Morphine,
Tobacco,
aphylac people with doses Warfarin drugs Chloride Nitrates
Morphine Shock G6DP
deficiency

ELIMINATION
(It is drug inactivation or removal from the body by metabolism or excretion)
ELIMINATION = METABOLISM + EXCRETION
Different from excretion in terms, ( drug may be eliminated by metabolism long before modified molecules are excreted from body.)
ALI RAZA CHAUDARY (N67)
1. Most drugs and their metabolites: hepatic metabolism, biliary elimination, or urinary elimination
PHARMACOLOGY SUPPLEMENTS
⮜15⮞
▶ DIFFERENCE BETWEEN FIRST ORDER AND ZERO ORDER ELIMINATION
FEATURE ZERO ORDER ELIMINATION FIRST ORDER ELIMINATION
A process that is independent of drug concentration
Definition involved in the process and is constant with passage A process that is directly proportional to drug
of time concentration involved in process
Process Constant Rate Process Linear Kinetic Process
Type Capacity limited elimination Flow dependent elimination
Rate Independent of drug concentration Directly proportional to drug concentration
General dc dc
= − K 0 C 0 = − K0 = − KC1 = − KC
Expression dt dt
Rate Constant (K Ko K
Units of K mg/min min-1, hr-1
C = C0 e−Kt OR
General
Equation
C = C0 − K 0 t log C = log C0 − Kt
2.3030

Graph

Clearance (CL) Not constant Constant (Rapid at first & slows as conc. decreases)
Constant (In first order kinetics, A drug infused at a
Half life (like constant rate takes 4–5 half-lives to reach steady
Not constant state. It takes 3.3 half-lives to reach 90% of the
CL)
steady-state level.)
𝐶0 1
Half life 𝑡1 = 0.5 𝑡1 = 0.693
𝐾 𝐾
expression 2 2
0
Dependence
Dependent on initial drug concentration Independent on initial drug concentration
(t½)
End At some time, comes to end Never comes to an end
At high/toxic doses:
Examples: Ethanol
Mostly drugs follows this
Aspirin
Phenytoin

▶ CLEARANCE (CL)
(Volume of blood or plasma that can be freed of a drug in a specific time)
 It relates the rate of elimination of drug to the plasma concentration at specific time as follow;
(Rate of Elimination of Drug)Organ (Rate of Elimination of
Drug)Organ
CL Organ = =
Plasma drug concentration C
p

UNITS OF CL
 Volume/time i.e. mL/min or L/h
 CL/kg of body weight

FACTORS AFFECTING CL
 Drug
 Blood flow
 Conditions of the organs of elimination i.e. kidney, liver, intestines etc
Clearance by an individual organ = Extraction capability for that drug ×
Rate of delivery of drug to organ.
 Clearance of a drug that is very effectively extracted by an organ is often flow-
limited.

▶ PLASMA HALF LIFE (t½ )

(Time required for the amount of drug in the body or blood to fall by 50%)
 Determines the rate at which blood concentration rises during a constant infusion and falls after administration is stopped
 It relates as follow;
Vd
t 1 = 0.693
2 CL

UNITS OF t½
 Time

FACTORS AFFECTING t½
Vd
Half life 𝖺 𝖺 Duration of Action of Drug
CL
 Vd
 CL ALI RAZA CHAUDARY (N67)
PHARMACOLOGY SUPPLEMENTS
⮜16⮞
▶ EXTRACTION RATIO
(fraction or percentage of the drug removed from perfusing blood during its passage through the organ
 After steady-state concentration in plasma has been achieved,
extraction ratio is one measure of elimination of drug by that organ.
 Drugs that have a high hepatic extraction ratio have a large first-
pass effect and bioavailability of these drugs after oral administration
is low.
 It is determined as follow;
Extraction by organ = Blood flow × (Input − Output)
Extraction by organ = Q × (Ci − Co )

▶ THERAPEUTIC WINDOW
(Safe range between the minimum therapeutic concentration and the minimum toxic concentration of a drug)
 Determine the acceptable range of plasma levels when designing a
dosing regimen
1. Minimum effective concentration = trough levels of a
drug
given intermittently
2. Minimum toxic concentration = permissible peak plasma
concentration
 For some drugs, therapeutic and toxic concentrations vary so greatly
among patients that it is impossible to predict therapeutic window in a
given patient. Such drugs must be titrated individually in each
patient.

▶ DOSAGE REGIMENS
(Plan for drug administration over a period of time)
 An optimal dosage regimen results in the achievement of therapeutic levels of drug in blood without exceeding the
minimum toxic concentration and depends on;
1. Minimum Therapeutic & Toxic Concentration
2. Vd & CL
FEATURE MAINTENANCE DOSE LOADING DOSE
The dose required for regular administration to maintain a The dose required to achieve a specific
Definition target plasma level i.e. to maintain a desired steady state plasma drug concentration level (Cp) with a
(SS). single administration.
Factors CL and t½ Vd
At Steady state:
(Rate of Dosing)SS = (Rate of Elimination)SS
(Rate of Dosing)SS = CL × Desired Cp Vd × Desired Cp
Expression Loading Dose =
F
(Rate of Dosing)SS
Maintenance Dose = ×
F
Dosing Interval
(Rate of Dosing)SS = Dose per unit time if CL is in mL/min
But
As for chronic therapy we give these doses once or a few
Units times per day, we convert it as follow; Loading Dose = milligrams
(dose per minute × 60 min/h × 24 h/d)

Maintenance Dose = milligrams

Smaller and more frequent maintenance doses, if difference Loading dose is large (Vd >Blood volume) then
Dosing between therapeutic and toxic conc. is small. dose is given slowly
Larger and less frequent maintenance doses, if difference Loading dose is small (Vd <Blood volume) then
between therapeutic and toxic conc. is large. dose is given rapidly

Graph

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜17⮞
▶ DOSAGE ADJUSTMENTS WHEN ELIMINATION IS ALTERED BY DISEASE
RENAL IMPAIRMENT:
 GFR disturbed
 Creatinine Clearance (CLCr) disturbed

1. For drugs to be removed by renal route only

Patient′ s CLCr
Corrected Dosage = Avergae Dose ×
100mL/min
2. For drugs to be removed 50% by renal route and 50% by liver
1
1
Patient′s CLCr
Corrected Dosage = Average Dose(Liver) + Average
Dose × (Kidney) 2 2
100mL/min
3. Shortcut for measuring CLCr directly by Cockcroft Gault Equation

(140 − Age) × Body weight in kg

CLCr(mL/min) = (× 0.85 if female)
72 × Serum
Cr
4. Shortcut for measuring GFR directly by MDRD Equation
2 175 (× 0.742 if female)(× 1.212 if African American)
GFR ((ml/min)/1.73m body surface area) =
S1.154 × Age0.203
Cr

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜18⮞
PHARMACODYNAMICS
(The actions of the drug on the body)
▶ RECEPTORS (A molecule to which a drug binds to bring about a change in function of the biologic system)
 Selective in their ligand binding characteristics
 Modifiable
 Mostly Proteins, but also Enzymes or Nucleic Acids in nature
[Response] 𝖺 Drug − Receptor Combinations 𝖺 Concentration of R a State
FEATURE TYPE-I TYPE-II TYPE-III TYPE-IV
Name Ligand Gated Ion G-Protein Coupled
Receptor Kinases Nuclear Receptors
Channels Receptors
Location Membrane Membrane Membrane Intacellular
Ligand Nature Hydrophilic Hydrophilic Hydrophilic Hydrophobic
Effector Ion Channel Channel or Enzyme Protein Kinases Gene Transcription
Monomeric or oligomeric
assembly of subunits Single transmembrane
Oligomeric assembly of comprising 7 trans- helix linking extracellular Monomeric structure
Structure subunits surrounding membrane helices with receptor domain to with receptor- and DNA-
central pore intracellular G protein– intracellular kinase binding domains
coupling domain domain

Protein phosphorylation Protein and receptor

Changes in membrane  Gi: 🢙cAMP phosphorylation by
Protein phosphorylation
Mode of Action potential or ionic
concentration within cell
 Gs: ⭡cAMP formation of dimers or
and altered gene
expression
 Gq: ⭡IP3, ⭡DAG multisubunit complexes

Domains Receptor Binding + Receptor Binding + Receptor Binding + Receptor Binding +

Channel Lining G-protein Catalytic DNA Binding
Coupling
Duration of Action Milliseconds Seconds Minutes to Hours Hours to Days
 Insulin  Steroid
 Nicotinic Ach
 Muscuranic Ach  Growth Factors  Vitamin D
 Serotonin 5-HT3  Adrenoceptors  ANP  NO
 Cytokines  Cytokines
 GABAA

Examples

▶ DIFFERENCE BETWEEN INERT BINDING SITE RECEPTOR SITE

&
Feature INERT BINDING SITE RECEPTOR SITE
Definition A molecule to which a drug may bind without changing Specific region of the receptor molecule to which the
any function drug binds
Play an important role in buffering concentration of a
Function drug because bound drug does not contribute directly Drug- receptor interaction initiates the drug action
to the concentration gradient that drives diffusion.
Example Primary receptor affinity is a basis of drug classification
Albumin & orosomucoid (α1-acid glycoprotein)
e.g. H1 for histamine receptors

▶ RECEPTOR REGULATIONS
SIGNAL AMPLIFICATION PROTECTION AGAINST EXCESSIVE STIMULATION
G-protein and Kinase-Linked Tachyphylaxis/Down-regulation: When a receptor is exposed to repeated
Receptors amplify signal duration and administration of an agonist, it becomes desensitized resulting in diminished effect.
intensity that give rise to spare  Blockage of access to G-proteins (-arrestin)
receptors.  Internalization/Sequestration of receptors ( or morphine receptors) – during recovery
Eg. unresponsive receptors are called refractory.
 Insulin receptors:  Depletion of essential substrate (thiol cofactors for nitroglycerin)
99% are spare Up-regulation: Repeated exposure of a receptor to an antagonist may result in up-
 Heart -receptors: regulation of receptors, in which receptor reserves are inserted into the membrane,
5-10% are spare increasing the total number of receptors available.
 Make the cells more sensitive to agonists
 More resistant to the effect of the antagonist
ALI RAZA CHAUDARY (N67)
PHARMACOLOGY SUPPLEMENTS
⮜19⮞
▶ EFFECTORS
(Component of a system that accomplishes the biologic effect after receptor is activated by an agonist)
1. Channel: Na/K channel for NN receptor
2. Transporter: M receptors
3. Enzyme: Adenylyl cyclase
4. May be part of the receptor molecule: Tyrosine kinase effector enzyme part of insulin receptor

▶ DIFFERENCE BETWEEN EFFICACY & POTENCY

Feature EFFICACY (Emax) POTENCY
Definition The largest effect that can be achieved with a particular The amount or concentration of drug required to
drug, regardless of dose produce a specified effect
 Nature of Drug
Factors  Receptor Affinity
 Nature of Receptor
Affecting  Number of Receptors available
 Nature of Effector
Graded Dose Median Doses
EC50; ED50; TD50
Response Can be measured by it
Curve (Concentration or dose that causes 50% of maximal
effect or toxicity)
Quantal Dose Median Doses
ED50; TD50; LD50
Response Cannot be measured by it
Curve (Concentration or dose that causes a specified
response in 50% of the population under study)
Graph Y-value (Emax) X-value (Median Doses)
Represents • ⭡ Y-value = ⭡ Emax = ⭡ Efficacy. Left shifting = 🢙ED50 = ⭡Potency = 🢙Drug needed
1
Mathematical EC 
E max  Efficacy 50
Form
Potency

Graph

▶ DIFFERENCE BETWEEN DOSE CURVE GRAPHS

FEATUR GRADED-DOSE RESPONSE GRADED-DOSE BINDING QUANTAL-DOSE RESPONSE
E RESPONSE
Graph between increase of Graph between receptors bound Graph between fraction of population
Definition response with increase of dose by drug with increase of dose of showing that response with increase of
of drug drug dose of drug
B max  DR Binding
1 Potency Variables
Emax  Efficacy K 
Data
Derived
1
d

Affinity
 Median effective dose (ED50)
EC50 
Potency (Kd = concentration of drug that  Median toxic dose (TD50)
binds 50% of receptors in  Median lethal dose (LD50)
system)
Relation Dose to intensity of effect Dose to intensity of effect Dose to frequency of effect

Graph

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜20⮞
▶ SPARE RECEPTORS (Receptor that does not bind drug when drug concentration is sufficient to produce Emax)
 Reason

E max < B max

OR

 Mechanisms EC50 < K d

1. Duration of effector activation > DR interaction
2. Receptors > Effectors
 Increases sensitivity to the agonist because the likelihood of a drug-
receptor interaction increases in proportion to the number of receptors
available

▶ THERAPEUTIC INDEX (TI)

(Ratio of median toxic dose (or median lethal dose) to median effective dose,
determined from quantal dose-response curves.)
 Formula
TD50 LD50
TI = 50
or
ED ED
50

 It estimates the safety of the drug.

 Safer drugs have higher TI values.
 Drugs with lower TI values frequently require
monitoring (eg, Warfarin, Theophylline, Digoxin,
Lithium)

▶ PHARMACOLOGICAL DRUG INTERACTIONS

CHEMICAL INTERACTIONS

Mechanims Classification

Pharmacokinetic Pharmacodynamic Additive Synergestic Potentiation Tachyphylactic Antagonism

Absorption Receptor Pharma-

cological
Distribution Non-receptor Physiological

Metabolism
Chemical

Elimination
TYPE DEFINITION EXAMPLE
Effect of substance A and B together is equal to the sum of their
Additive individual effects Aspirin and acetaminophen
i.e. A = 1, B = 1, A + B = 2
Effect of substance A and B together is greater than the sum of their
Synergistic individual effects Clopidogrel with aspirin
i.e. A = 1, B = 1, A + B > 2
Potentiation Presence of substance A is required for full effects of substance B Cortisol on catecholamine
A = 0, B = 1, A + B > 1 responsiveness
Tachyphylactic Acute decrease in response to a drug after initial/repeated
Nitrates, niacin, phenylephrine
administration
Antagonism See below
▶ AGONIST (A drug that activates its receptor upon binding)
 Equilibrium is formed between Rinactive (Ri) and Ractive (Ra) state in absence of ligand.
 The activity in the absence of agonist ligand is called constitutive activity.
 Ri state is favoured in absence of ligand.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜21⮞
▶ TYPES OF AGONISTS
FEATURE FULL AGONIST PARTIAL AGONIST NEUTRAL INVERSE AGONIST
ANTAGONIST
A drug that binds to its A drug binds with equal A drug that binds to
A drug capable of fully
receptor but produces a affinity to Ri & Ra states, non-active state of
activating the effector
Definition smaller effect (Emax) at preventing binding by receptor molecules and
system when it binds to
agonist and preventing decreases constitutive
the receptor full dosage than a full
any deviation from level activity.
agonist
of constitutive activity.
Ra > Ri
Affinity for state (in presence of full agonist
Ra >>> Ri Ra = Ri Ri > Ra
it acts as inhibitor)
Intrinsic Activity (I) I=1 I >0 but <1 I=0 I<0
Apripirazole at
D-receptors with Naloxone is a
Phenylephrine at H1 and H2
Example activate underactive competitive antagonists
-receptors at all opioid receptors antihistaminic
paths and inactive the s
overactive paths

Graph

▶ TYPES OF ANTAGONISM
COMPETITIVE NON-COMPETITIVE
FEATURE PHYSIOLOGICAL CHEMICAL
REVERSIBLE IRREVERSIBLE ALLOSTERIC
A drug that binds to A drug that A drug that
A pharmacologic counters the counters the
A pharmacologic a receptor molecule
antagonist that can without interfering effects of another effects of
antagonist that
be overcome by with normal agonist by binding to a another by
Definition cannot be overcome
increasing the by increasing agonist binding but different receptor binding the
concentration of concentration and causing agonist drug
alters response to
agonist opposing effects (not receptor)
normal agonist
Location At receptor site At receptor site Other than receptor Different receptor With drug
Overcome Yes (By agonists) No No - -
Emax  Efficacy
Emax - 🢙 (Down Shift) 🢙 (Down Shift) - -
Efficacy 🢙 🢙
EC50  1/(Potency)
EC50 ⭡ (Right shift) - - - -
Potency 🢙
Norepinephrine
Diazepam (agonist) (agonist) + Epinephrine’s
+ flumazenil phenoxybenzamine Picroton + GABA antagonism of Dimercaprol
Examples (noncompetitive
(antagonist) on linked Cl- channel bronchoconstrictio
GABA antagonist) on α- n by histamine Pralidoxime
receptor receptors

Graph

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜22⮞
▶ DIFFERENCE BETWEEN TACHYPHYLAXIS & TOLERANCE
FEATURE TACHYPHYLAXIS TOLERANCE (METABOLIC/
(PHARMACODYNAMIC TOLERANCE) PHARMACOKINETIC TOLERANCE)
Definition Rapid loss of drug effects caused by Decrease in clinical effects of drug after prolonged
compensatory neurophysiological mechanisms exposure to it
Onset Rapid (few minutes) Slow (days - months)
High Dose
No Yes
dependent
Effects with ⭡
Not Seen Seen
dose
Routine Practice Not Seen Seen
Examples Ephedrine, Nitroglycerin (TD) Barbiturates, Ethanol, Opium
 Blockage of access to G-proteins (-arrestin)
 Internalization of receptors  Congenital (Negroes are resistant to mydriatic
Causes (morphine receptor) effect of ephedrine)
 Sequestration of receptors ( receptors)  Acquired (morphine, ethyl alcohol, nitrates,
 Depletion of essential substrate (thiol cofactors ephedrine, and amphetamine)
for nitroglycerin)
CROSS TOLERANCE:
Tolerance between related drugs e.g. between ethyl alcohol and general anaesthesia.
1. Alteration in drug concentration that reaches the receptors due to an effect on absorption, distribution or elimination.
2. Variation in concentration of endogenous transmitters e.g. - blockers will slow heart rate markedly in patients with excess
endogenous catecholamines.
3. Alteration in the number or function of receptors, e.g. thyrotoxicosis increases the number and sensitivity of -receptors.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜23⮞
DRUG DEVELOPMENT & REGULATION
Sale and use of drugs are regulated in almost all countries by governmental agencies.
In the United States, regulation is by the Food and Drug Administration (FDA).
▶ NATURE/SOURCES OF DRUGS

SOURCES OF DRUG

Natural Synthetic Semisynthetic

Animals Plants Microorganisms Aspirin Ampicillin

Minerals
Sulfonamide from penicillin
Pethidine
Insulin Digoxin Penicillin Procaine
MgSO4
(pancreatic -cells) (Digitalis purpura) (P chrysogenum) (Laxative)
Heparin Quinine Streptomycin Mg trisilicate
(Liver extract) (Cinchona bark) (S. griseus) (Antacid)
Vitamin B12 Atropine Chloramphenic
(Liver) (Atropa ol
ADH belladonna) (S. venezuelae)
(hypothalamus)

▶ FORMS OF DRUGS
FORMS OF DRUG

SOLID LIQUID GASES

1. Tablets—Paracetamol 1. Injections—Benzyl penicillin Nitric Oxide

2. Capsules—Ampicillin 2. Mixtures—Potassium chloride
3. Powders—Dusting antiseptic powder 3. Solution—Eyedrop
4. Pressary—Antifungals 4. Suspension—Antacid
5. Suppository—Analgesics. 5. Emulsion—Cod liver oil
6. Lotions—After shave lotions
7. Enema—Barium enema

▶ NOMENCLATURE OF DRUGS

NOMENCLATURE OF DRUG

Official name or
Chemical Name Proprietary name Generic Name
nonproprietary name

Name chosen by the official Forms or class or genus in

Describes the chemistry of a Name chosen by the firm
bodies & used by which the drug in
drug manufacturing or marketing
pharmacopias question falls

EXAMPLE:
 Chemical name: 7 chloro 1,3 dihydro—1 methyl 5 phenyl 2H, 1,4 benzodiazepine—2.
 Official name: Diazepam
 Proprietary name: Valium
 Generic name: Benzodiazepine
▶ DRUGS CLASSIFICATION
A drug class is group of medications having similar chemical structures, mechanism of action and mode of action.
1. Prototypic/First-in-Class/Novel Drug: An individual drug that represents a drug class
2. Me-too Drugs: Drugs similar to prototypic drugs having same mechanism of action with:
 Faster onset of action
 Improved selectivity
 Increased potency
 Longer duration of action
 Less toxicity

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜24⮞
▶ DRUGS DEVELOPMENT

ANIMAL TESTING (PRE-CLINICAL)

One basis of two things evaluated:
1. Function of proposed use: Topical usage drugs require less testing than one for chronic systemic administration.
2. Urgency: Anticancer or anti-HIV drugs require less testing than one for life threatening diseases.
TEST DETERMINATION PERFORMANCE EXAMPLES
 All pharmacologic effects Effects on CVS, GIT, Respiration, Hepatic,
Pharmacological profile
 Graded & quantal dose response data Renal, Endocrine and CNS intestinal
Acute dose that is lethal Usually two species (1
Acute toxicity in approximately 50% rodent, 1 non-rodent), Determine the no-effect dose and the
animals. two routes. maximum tolerated dose.
The longer the duration of expected clinical
Subacute toxicity Three doses, two use, the longer the subacute test.
 Biochemical effects species for 2-4 weeks. 2 weeks - 3 months of testing may be
 Physiologic effects required before clinical trials.
Rodent & at least one Required when drug is intended to be used in
Chronic toxicity nonrodent species for ≥ humans for prolonged periods.
6 months. Usually run concurrently with clinical trials.
Effects on: Two species, (one
Teratogenic/
 Mating behavior rodent & rabbits) during
Reproductive Toxicity
early pregnancy
Teratogenesis is induction  Reproduction Examples: thalidomide, isotretinoin, valproic
(organogenesis take
of development defects in  Parturition acid, ethanol, glucocorticoids, warfarin,
place) and by later
somatic tissues of fetus  Progeny lithium, and androgens.
(examining fetuses or
(exposure to chemical,  Birth defects neonates for
infection, or radiation).  Postnatal development abnormalities).
Mutagenic Toxicity Test effects on genetic stability and mutations in:
Mutagenesis is induction of 1. Sallmonella bacteria in culture (Ames test): Aflatoxin, cancer
changes in genetic  Genetic stability drugs, and agents binding to DNA give this test positive
material of animals of any  Mutations 2. Mammalian cells in culture
age and therefore 3. Mice (Dominant lethal test): Clastogenicity in mice & exposure
induction of heritable is before mating
abnormalities.
Required when drug is intended to be used in
Carcinogenic Toxicity humans for prolonged periods.
Carcinogenesis is the  Gross pathology Examples: coal tar, aflatoxin,
induction of malignant Two years, two species. dimethylnitrosamine and other nitrosamines,
 Histologic pathology.
characteristics in cells. urethane, vinyl chloride, and polycyclic
aromatic hydrocarbons in tobacco smoke (eg,
benzo[a]pyrene) and other tobacco products

REPRODUCTIVE SAFETY (FDA RATINGS)

D
CATEGORY A B C X
(teratogenic but
(very safe) (safe) (may be safe) (teratogenic)
used when serious)
+
Animals - +/- +/0 +
+
Humans - -/0 0 +

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜25⮞
CLINICAL TESTING & MARKETING
PRECLINICAL PHASE 1 PHASE 2 PHASE 3 PHASE 4
~ 20-100 healthy
volunteers ~ 100- 200 patients Post marketing
2 different animal (Exception: Cancer & (most drugs ~ 1000-6000 patients surveillance (after FDA
species toxic drugs to target failed here) approval)
patients)
Effectiveness (check in
 Safety  Safety monitored patients) Confirm effectiveness &
Common as wells as
 Efficacy  Dosage with placebo in single common side effects
(double blind check) rare side effects
 Biological Activity  Pharmacokinetics or double blind
check

ORPHAN DRUGS
 An orphan drug is a drug for a rare disease (one affecting < 200,000 people in the United States).
 Study of such agents has often been neglected because profits from the sales of an effective agent for an uncommon
ailment might not pay the costs of development.
 Some countries bestow certain commercial advantages on companies that develop drugs for uncommon diseases

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜26⮞

🢔 2🢖
AUTONOMIC N E RVO U S
S YS T E M PH AR M ACO LOGY
1 S E Q + 6 M CQ s = 13 Marks

DESCRIPTION PAGE NO
INTRODUCTION TO AUTONOMIC PHARMACOLOGY 27
PARASYMPATHOMIMETICS 28
ANTICHOLINERGIC DRUGS 29
SYMPATHOMIMETICS 31
ADRENERGIC BLOCKERS 33
DRUGS USED IN GLAUCOMA 33

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜27⮞
INTRODUCTION TO AUTONOMIC PHARMACOLOGY
CLASSIFICATION OF CHOLINERGIC RECEPTORS
Mnemonic Location G Protein Mechanism
M1 Nadia Nerve Endings Gq ⭡IP3, DAG cascade
🢙cAMP, K+ channels
M2 Have Heart Gi
activate
Effective Effector Cells: Smooth Muscle, Glands,
M3 Gq ⭡IP3, DAG cascade
Endothelium
🢙cAMP, K+ channels
M4 Gi
CNS CNS activate
M5 Gq ⭡IP3, DAG cascade
NN Nerve Ganglia
- Na+/K+ depolarizing current
NM NeuroMuscular Junction
Anything that comes under parasympathetic control and not from M1 (Increased gastric secretions) and M2 (Heart
depression effects) will come under M3. Most of the functions are reverse of sympathetic control!

CLASSIFICATION OF ADRENERGIC RECEPTORS

Mnemonic Location G Protein Mechanism
1 England Effector Cells: Smooth Muscle, Glands Gq ⭡IP3, DAG cascade
2 Never Nerve Endings Gi 🢙cAMP
1 Have Heart, JG apparatus
2 Some Smooth Muscle, Liver, Heart
Gs ⭡cAMP
3 Apology Adipocytes
D1 and D5 Brain, Smooth Muscles of Renal Vasculature
D2 D3 and D4 Brain, Smooth Muscles, CVS Gi 🢙cAMP
 1-receptors are further classified to 1A, 1B & 1D while 2-receptors are into 2A, 2B & 2C.
 1-receptors follow BIG FISH BIG EYE theory! Imagine a Fish made of rope with a big Eye. And you pulled
rope and the Fish became smaller i.e. 1 has big eye (mydriasis) and other things generally constricted or
contracted.

 2-receptors resemble a fish bigger than 1-receptors. She was playing but some batameez betas (
receptors) start fighting with her. At the end, she won by eating the batameez betas but left some poop. So
what happens is 2-receptors have functions of opposing Batmez Betas. Poop represents platelets
aggregation.

 1, 2 and 3 receptors resemble heart and kidney; relaxing wings of butterfly; triglyceride molecule
respectively.

INNERVATIONS OF ORGAN SYSTEMS (Most by both SANS and PANS except)

 Only SANS supply; Save Blood Save Human (Sweat Glands, Blood Vessels, Spleen, Hair Follicles)
 Only PANS supply; Punjab Group of Colleges (Pancreatic Glands, Gastric Glands, Ciliary Muscle)
DRUGS MNEMONICS
Cholinergic Transmission: Hepatitis Virus B = Hemicholinium, Vesamicol, Botulinum
Adrenergic Transmission: MRGA (‫)غامر‬ = Me-tyros-ine, Re-serp-ine, Gua-nethid-ine, Amphetam-
ine
CT (‫)کٹ‬ = Cocaine, TCA
ERECTION & EJACULATION: (Point & Shoot) i.e. PANS & SANS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜28⮞
PARASYMPATHOMIMETICS
Parasympatho-
mimetics

Indirect Acting
Direct Acting
(AChE Inhibitors)

Muscuranic Intermediate acting Short acting Long acting

Both Receptors Nicotinic
cabamates alcohols organophosphates

Bethanechol Neostigmine Parathion

Acetylcholine Nicotine Malathion
Methacholine Varinicline Physostigmine Edrophonium
Carbachol Pilocarpine Sarin, Tubin
Succinylcholine Metrifonate
Muscarine Pyridostigmine
Lobeline Ambonemium

▶ WHY NEOSTIGMINE IS PREFERRED OVER PHYSOSTIGMINE IN TREATMENT OF

MYASTHENIA GRAVIS?
Neostigmine has quaternary nitrogen; hence, it is more polar and cannot cross BBB to enter CNS, but cross the
placenta. Physostigmine is lipid soluble and can cross BBB to enter CNS.
▶ DIFFERENCE BETWEEN PARATHION AND MALATHION
FEATURE MALATHION
PARATHION
Clinical Use Insecticide Insecticide + Scabicide
Duration Days to Weeks Days
Metabolized to inactive
Pharmacokinetics Lipid Soluble
form in mammals & birds
Danger Less
High

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜29⮞
ANTICHOLINERGIC DRUGS
Antiparkinsonims
& Dystonia when
Antimotion L-dopa is
CNS Sickness unresponsive
(Scopolamine) (Benztropine,
Biperiden,
Trihexiphenidyl)
Atropine (72h),
Eye Homatropine (24h)
(Mydriasis, Cyclopentolate (12h),
Cycloplegia) Tropicamide (4h)

Bronchi Ipratropium,
(Asthma, Tiotropium,
COPD) Aclidiunum
Anti-
muscuranics
Non Selective M1 Selective
Gut (Dicycloamine,
Glycopyrrolate) (Pirenzepine,
Telenzepine)

M3 Selective
(Tolterodine,
Bladder Non Selective Festerodine,
(Urinary (Oxybutynin, Propiverine,
Anticholinergic Urgency) Trospium) Darifenancin,
Drugs Solifenancin)
Intoxication of
AChE Atropine
inhibitors

Hexamethonium
Ganglion
Mecamylamine
Parasympatho Blockers Trimethaphan
-lytics
Anti-
nicotinics Nondepolarizing
Pan-curonium
Tubo-curarine
NMJ Depolarizing Ve-curonium
Blockers Succinylcholine Cis-atra-curium
Ro-curonium
Atra-curium
AChE Miva-curium
Oximes Pralidoxime
Regenerators

▶ TREATMENT OF ORGANOPHOSPHATE POISONING

1. Stabilize the patient vitally ABC.

2. Contaminated clothes should be removed and exposed skin should be washed with Na2CO3 solution.
3. Atropine 2 mg is given IM or IV at once and repeated every 15 min till mydriasis, tachycardia and dry mouth occurs.
4. Specific cholinesterase reactivator, Pralidoxime 1 gm in 100 ml normal saline or 5% glucose is given by IV infusion
and repeated as indicated by patient’s condition. It should be given as early as possible in order to be effective.
5. Artificial respiration with positive pressure device may be needed.
6. Airway should be kept clear as there is bronchoconstriction and excessive bronchial secretion. Endotracheal
intubation or tracheostomy with suction may be required.
7. Diazepam may be needed for convulsions.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜30⮞
▶ ATROPINE EFFECTS IN ORDER OF INCREASING DOSE
1. Decreased secretions (salivary, bronchiolar, sweat)
2. Mydriasis and cycloplegia
3. Hyperthermia (with vasodilation)
4. Tachycardia
5. Sedation
6. Urinary retention & constipation
7. Behavioral: excitation & hallucinations

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜31⮞
SYMPATHOMIMETICS
Sympathomimetics

Direct Acting Indirect Acting

Both

Reuptake
 &  Agonists  Agonists  Agonists Releasers Ephedrine
Inhibitors

Epinephrine
Amphetamine Nonselective (,) Nonselective
Cocaine Nore hrine
Oxymetazoline
Isoproterenol Methamphetamine TCA
pinep Tyramine
(, except 2)
Dopamine (D1,,
 selective
except 2) 1 1 selective
Phenylephrine
Dobutamine
Tetrahydrozolin
e Midodrine
2 selective
SHORT ACTING
 selective
2 Albuterol
Clonidine Metaproterenol
Methyldopa Terbutaline
Apraclonidine Ritrodrine
Brimonidine LONG ACTING
Salmeterol
Formoterol
Indacaterol
Vilanterol
Olodaterol

▶ SYMPATHOMIMETIC EFFECTS ON CVS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜32⮞
▶ WHY NOR EPINEPHRINE IS NOT USED IN ANAPHYLACTIC SHOCK?
Epinephrine and norepinephrine are very similar neurotransmitters and hormones. While epinephrine has slightly more
of an effect on your heart, norepinephrine has more of an effect on your blood vessels.

▶ WHY DOPAMINE IS GIVEN IV ONLY?

Since the half-life of dopamine in plasma is short—approximately one minute in adults, two minutes in newborn babies
and up to five minutes in preterm babies—it is usually given as a continuous intravenous drip rather than a single
injection.
▶ USES OF CLONIDINE IN DIABETIC DIARRHEA
Activate uninnervated 2 receptors and cause water and salt absorption in GIT that relieves diarrhea

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜33⮞
ADRENERGIC ANTAGONISTS
Adrenergic Antagonists

&
 Blockers  Blockers
Blockers

Labetolol 1 selective 2 selective Nonselective 1 selective 2 selective

Nonselective Parazosin
Carvedilol Yohimbine Acebutolol Butoxamine
Doxazosin Rauwolscine Propranolol Nebivolol
Terazosin Betaxolol Esmolol
Reversible & Irreversible & Silodosin Nadolol Metoprolol
Short Long Acting Tamsulosin Pindolol Atenolol
Acting Timolol Bisoprolol
Sotalol
Phentolamine Phenoxybenzamine

DRUGS USED IN GLAUCOMA

Drugs for Glaucoma
(All are qiven in TOPICAL DROPS except the highlighted)

Decrease Secretion of Removal of Water from

Increased Aqeuous Outflow
Aqueous Humour Eye

 Agonists Carbonic
2 selective Cholinomimetic Anhydrase Osmotic
 Blockers (uveoscleral Prostaglandins
Agonists s (Contraction) Inhibitors Agents
veins)
(HCO3 lack)

Pilocarpine Latanoprost Mannitol

Timolol Apraclonidine Epinephrine Acetazolamide
Betaxolol Brimonidine Physostigmine (IV) for acute
Bimatoprost (ORAL)
(GEL) closed
Unoprost angle
Travoprost
Dorzolamide

Brinzolamide

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜34⮞

🢔 3🢖
AUTOCOIDS & NSAIDS PHARMACOLOGY
1 S E Q + 7 M CQ s = 14 Marks

DESCRIPTION PAGE NO
AUTOCOIDS 35
EICOSANOID AGONISTS & ANTAGONISTS 36
NSAIDS, DMARDS & ANTI-GOUT DRUGS 37

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜35⮞
AUTOCOIDS
Drugs for Unit 16

Histamine Antagonists Serotonin Ergot Alkaloids

H1 Antagonists H2 Antagonists Serotonin Agonists Serotonin Antagonists Vessels

Ergotamine

1st Generation 5-HT1 Agonist 5-HT2 Antagonist

Cimetidine Suma-triptan
Diphenhydramine Ketanserin Uterus
Famotidine
Dimenhydrinate Riza-triptan Cycloheptadine Ergonovine
Ranitidine
Doxylamine Nizatidine Frova-triptan Phenoxybenzamine
Promethazine Almo-triptan
Cyclizine Ele-triptan
Zolmi-triptan Brain
Chlorpheniramine Lysergic Acid
Nara-triptan 5-HT3 Antagonist
Ondan-steron Diethylamide (LSA)
Grani-steron Bromocriptine
2nd Generation Dola-steron Pergolide
5-HT2 Agonist Cabergoline
Cetirizine Locaserin Palono-steron
Fexofenadine Alo-steron Methylsergide
Fenfluramine
Loratadine Dex-fenfluramine
Des-loratadine

5-HT4 Agonist
Tegaserod

▶ HISTAMINE METABOLISM ▶ SEROTONIN METABOLISM

DAO

HCl secretion in stomach

Inflammation
Strong Vasodilation (due to NO release)
Thepeuratic Value (none)
Allergy
Mast Cells (production)
IgE
Neurotransmitter or Narrow Airways (Bronchoconstriction)
E (x)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜36⮞
EICOSANOID AGONISTS & ANTAGONISTS
Eicosanoids

Agonists Antagonists

COX Inhibitors Phospholipase

Straight Chain Cyclic LT Antagonists
(NSAIDS) A2 Inhibitors

Leukotrienes Thromboxane LOX Inhibitor Non-Selective

TXA4 Corticosteroids
LTB4 Zileuton Reversible
LTC4 Ibuprofen
LTD4 Indomethacin
Prostacyclin LT2 Receptor Naproxen
PGI2 Inhibitor Piroxicam
Epo-prostenol Monte-lukast
Tre-prostinil Zafir-lukast
Non-Selective
Irreversible
Prostaglandins Aspirin
PGE1
Miso-prostol
Al-prostadil
PGE2 Selective COX2
Dino-prostone Inhibitor
PGF2 Cele-coxib
Latano-prost Rafe-coxib
Bimato- Valde-coxib
prost Uno- Meloxicam
prost Travo-
prost

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜37⮞
NSAIDS, DMARDS & ANTI-GOUT
DRUGS Drugs

Anti-inflammtory Gout Drugs

Analgesic Drug
drugs

COX Inhibitors Acet-amino-phen Acute Chronic

DMARDS
(NSAIDS) Phenacetin

Cytotoxic NSAIDS
Non-Selective Microtuble
Methotrexate Indomethacin Assembly Inhibitor
Reversible Phenylbutazone
Ibuprofen Col-chi-cine
Indomethacin
Naproxen Interfere T-Cell
Piroxicam Cyclosporine Glucocorticoids
Chloroquine Uricosurics
Abatacept Probenecid
Leflunomide Sulfinpyrazole
Non-Selective Sulfasalazine
Irreversible Col-chi-cine in low
Aspirin doses
Xanthine Oxidase
Interfere B-Cell Inhibitors
Belimumab Allopurinol
Selective COX2 Rituximab Febuxostat
Inhibitor
Cele-coxib
Rafe-coxib
Valde-coxib Interfere
Meloxicam Macrophages
Gold Compounds
Gold Sodium
Thiomalate
Aurothioglucose
Auranofin

Anti-TNF Drugs
Etanercept
Infliximab
Golimumab
Adalimumab
***Biological DMARDS

▶ PHARMACOLOGICAL EFFECTS OF ASPIRIN

DOSE MAJOR URIC ACID ACID & ELECTROLYTE BALANCE
ELIMINATION
EFFECT
Low:
Antiplatelet
(300 mg/d) ↓ tubular secretion →
Moderate: Analgesic + hyperuricemia
(300-2400 mg/d) Antipyretic
Mild uncoupling of oxi. Phosphorylation → ↑ respiration →↓ pCO2→
High: Anti- ↓ tubular reabsorption respiratory alkalosis → renal compensation →↑ HCO 3 – elimination
(2400-4000 mg/d) inflammatory → uricosuria →compensated respiratory alkalosis (pH = normal, ↓ HCO3−,
↓ pCO2)

Inhibits respiratory center →↓ respiration→↑pCO2→ respiratory acidosis (↓

pH, ↓ HCO 3 –, normalization of pCO2) plus inhibition of Krebs cycle and
severe uncoupling of oxi. phosphorylation (↓ ATP)
→metabolic acidosis, hyperthermia, and hypokalemia

Toxic Dose TOXICITY MANAGEMENT

1. No specific antidote.
2. Gastric lavage (  activated charcoal)
3. Ventilatory support
4. Symptomatic management of acid-base/
electrolyte imbalance, & hyperthermia & dehydration.
5. ⭡Urine volume & its alkalinization facilitate salicylate renal
elimination. (zero-order elimination)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜38⮞
▶ SELECTIVE COX-2 INHIBITORS vs
▶ NSAIDS vs ASPIRIN
NSAIDS
1. Analgesia: ketorolac > ibuprofen/naproxen > ASA
2. Gastrointestinal irritation: < ASA 1. Less gastrointestinal toxicity
3. Minimal effects on acid-base balance 2. Less antiplatelet action
4. No effects on uric acid elimination 3. Not effective as an antiinflammatory agent.
5. Allergy: common, possible cross-hypersensitivity with ASA 4. Exert prothrombotic effects via inhibition of endothelial cell
6. Renal: chronic use may cause nephritis, nephritic syndrome, function (MI and strokes).
acute failure (via ↓ formation of PGE2 and PGI2, which 5. Increased risk of Arterial Thrombosis
normally maintain GFR and RBF)

▶ ACETAMINOPHEN IS PREFERRED OVER

▶ ACETAMINOPHEN vs ASPIRIN
ASPIRIN
1. Renal Disease
1. No antiplatelet effect
2. Duodenal Ulcer
2. No implication in Reye Syndrome
3. Viral Infections
3. No effects on uric acid
4. Aspirin Allergies
4. Low GUT distress
5. Bleeding Disorder
5. Not bronchospastic
6. Late Pregnancy

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜39⮞

🢔 4🢖
RESPIRATORY PH AR M ACO LOGY
0.5 S E Q + 2 M CQ s = 5.5 Marks

GASTROINTESTINAL PHARMACOLOGY
0.5 S E Q + 3 M CQ s = 6.5 Marks

DESCRIPTION PAGE NO
DRUGS FOR ASTHMA & COPD 40
DRUGS FOR GASTROINTESTINAL DISORDERS 41

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜40⮞
DRUGS FOR ASTHMA
Drugs for Asthma

ACUTE ASTHMA CHRONIC ASTHMA BOTH

[Bronchodilators (Relievers)] (Controllers) (Leukotriene Antagonists)

Sympathomimetics Anti-inflammtory LOX Inhibitors

SHORT ACTING 2 AGONISTS Bronchodilators
Drugs Zileuton
(SABA)
Albuterol
Metaproterenol Corticosteroids
Terbutaline Sympathomimetics Receptor Inhibitors
LONG ACTING  2 INHALED (ICS)
Ritrodrine Mo-methasone Montelukast
AGONISTS (LABA) Zafirlukast
NON Flutica-sone
Salmeterol
SELECTIV Dexa-methasone
E DIRECT Formoterol Beclo-methasone
Epinephrine Olodaterol Flun-solide
Isoproterenol Bude-sonide
DIRECT/ SYSTEMIC
INDIRECT Prednisone
Ephedrine Prednilosone
Antimuscuranics Hydrocotisone
Ipratropium (Short Acting)

Anti-IgE Antibodies
Methyl-xanthines Omalizumab
Theophylline
Aminophylline
Release Inhibitors
Cromolyn
Nedocromil
*
▶ MANAGEMENT OF ASTHMA *
*
Bronchoconstrictive Results of peak flow or Quick relief of
Classification P
Long-term control
episodes spirometry Symptoms
Intermittent < 2 days per week
o
No daily medication
> Near normal* r
Mild persistent 2 days per week, not Low-dose ICS
daily p
Moderate h OR
Low-dose ICS + LABA SABA
Daily 60% to 80% of normal
persistent Medium-doseyICS
Severe Medium-dose ICS + lLABA OR
Continual < 60% of normal
persistent High-dose ICS +aLABA
x
▶ DRUGS FOR COPD
i
Drugs for COPD s

o
Bronchodilators Anti-inflammtory
f Drugs

Sympathomimetics A
Antimuscuranics Methyl-xanthines
SHORT ACTING 2 Ipratropium Rof-lumi-last
sCorticosteroids
INHALED (ICS)
AGONISTS (SABA) Tiotropium t Mo-methasone
Albuterol Aclidinum h Flutica-sone
Metaproterenol Beclo-methasone
Terbutaline m
Ritrodrine a Bude-sonide
LONG ACTING 2 AGONISTS
(LABA)
Salmeterol
Formoterol
Indacaterol
Vilanterol
Olodaterol

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜41⮞
DRUGS FOR GASTROINTESTINAL DISORDERS
1. Antacids: Mg(OH)2 ; Al(OH)3
2. H2 Blockers: Cimetidine; Famotidine; Ranitidine; Nizatidine
ACID PEPTIC 3. Proton Pump Inhibitors: Ome-prazole; Panto-prazole; Rabe-prazole;
DISEASE Dex-lanso-parazole; Lanso-prazole; Es-ome-prazole
4. Mucosal Protective Agents: Sucralfate; Misoprostol; Colloid Bismuth
5. Antibiotics: Amoxicillin, Metronidazole, Clarithromycin

PROKINETIC 1. D2 Blockers: Metoclopramide; Domperidone

AGENTS 2. Macrolides: Erythromycin
(⭡MOTILITY) 3. Cholinomimetics: Neostigmine

1. Bulk Forming: Psyllium, Methylcellulose, Polycarbophil

2. Osmotic: MgO, Mg(OH)2, Sorbitol, Lactulose, Mg citrate, Na3PO4,
Polyethylene glycol
LAXATIVES/ 3. Stool Softening/Lubricating/Surfactants: Docusate, Glycerin,
PURGATIVES Mineral oil
4. Stimulant: Aloe, Bisacodyl, Cascara, Castor oil, Senna
5. Chloride Channel Activator: Lubiprostone, Linaclotide (cGMP)
6. Opioid Antagonists: Methylnaltrexone, Alvimopan
1. Opoid Agonists: Loperamide; Diphenoxylate
ANTI- 2. Colloid Bismuth Compounds: Subsalicylate; Citrate
DIARRHEALS
3. Adsorbents: Kaolin + Pectin

1. 5-HT3 Blockers: Alo-setron

IRRITABLE 2. Anticholinergics: Dicycloamines, Hyoscyamine
Drugs for GIT BOWEL
SYNDROME 3. Chloride Channel Activators: Lubiprostone
Disorders 4. 5-HT4 Agonist: Tegaserod

1. Antimuscuranics: Scopolamine, Phenothiazines

2. Corticosteroids: Dexamethasone
3. Cannabinoids: Dronabinol; Nabilone
ANTIEMETICS 4. D2 Blockers: Phenothiazines; Metoclopramide
5. 5-HT3 Blockers; Ondan-steron; Grani-steron; Dola-steron; Palono-steron
6. H1 Blockers: Diphenhydramine, Dimenhydrinate, Cyclizine
7. NK1 Blockers: Apre-pitant, Netu-pitant, Rowa-pitant

1. Aminosalicylates (5-ASA): Me-salamine, Pentasa, Asacol, Lialda, Rowasa,

Canasa
2. AZO Compounds: Bal-salazide, Ol-salazine, Sulfa-salazine
INFLAMMATORY 3. Glucocorticoids: Budesonide
BOWEL DISEASE 4. Immunosuppressive Antimetabolites: 6-Mercaptopurine, Azathioprine,
Methotrexate
5. Anti-TNF Drugs: Infliximab, Golimumab, Adalimumab
6. B-Cell Intregrin Blocker: Natalizumab

PANCREATIC Pancrelipase
SUPPLEMENTS Pancreatin

BILE ACID Ursodiol

THERAPY

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜42⮞

🢔 5🢖
CAR D IOVASCUL AR , DIURETIC & BLOOD
PH AR M ACO LOGY
1.5 S E Q + 10 M CQ s = 20.5 Marks

DESCRIPTION PAGE NO
ANTIHYPERTENSIVE DRUGS 43
ANTIANGINAL DRUGS 44
HEART FAILURE DRUGS 45
ANTIARRHYTHMIC DRUGS 48
DIURETICS 50
DRUGS USED IN CYTOPENIAS/ ANEMIAS 51
DRUGS USED IN COAGULATION 52
ANTIHYPERLIPIDEMICS 53

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜43⮞
ANTI-
HYPERTENSIVE
DRUGS
Anti-Hypertension
Drugs

Diuretics oplegics Vasodilators

Sympath Angiotension
(Blood Volume 🢙 ) Renin
Antagonist
Antagonists
Thiazide Diuretics ceptor Calcium
Barore Channel ACE
(mild-moderate
Sensitizin Inhibitors Aliskiren
g Agents

Blockers
Capto-
pril
hypertension) (🢙SANS, ⭡Heart Dihydropyridines
Hydro-choloro- Benaze-pril
Vagal thiazide tone) Felo-dipine
Veratrum Lisino-pril
Chlorothiazide Alkaloids Isra-dipine
ural)
Enala-pril
Nicar-dipine
(Nat
Metolazone Nisol-dipine
Chlorthalidone Nife-dipine
ARBs
CNS Ac ting (2 Amlo-dipine
Cande-sartan
ists) Verapa-mil
Loop Diuretics Lo-sartan
Agon
🢙 TPR) Dilti-azem
(severe
(🢙CO, Irbe-sartan
hypertension) Clon idine

Val-sartan
Furosemide Methy ldopa NO Releasers
Bumetanide Hydrala-zine
Torsemide Ganglion Blockers Nitroprusside
Ethacrynic Acid Hexame thonium
Mecam ylamine
Postassium
Trimeth
Channel
HYPERTENSION DRUG

Minoxidil Sulfate
Postga nglionic Diazoxide
1. 🢙TPR
Neuron Blockers
2. 🢙CO
Rese rpine D1 Agonist
Guane 3. 🢙 Body
Fluid
thidine
Volume
Fenoldopam
Guan adrel
MAO in
COMPENSATORY RESPONSE:
hibitors

1. Reflex Tachycardia (⭡SANS) -

Baroreceptors
2
.
E
d
e
m
a
(
⭡
R
e
n
i
n
)
Adreno ceptor
Bloc kers
1 k
Blo e

ALI RAZA CHAUDARY (N67)

c r
(🢙 T s
PHARMACOLOGY SUPPLEMENTS
⮜44⮞
ANTI-ANGINAL DRUGS
Anti-Anginal Drugs

Others
Vasodilators Cardiac Depressents

Nitrates pFOX Inhibitors

Calcium Channel Blockers -Blockers Ranolazine
Trimetazidine
Ultrashort Ac
(Inhalat ting Dihydropyridines (Oral) Non-Selective  Blockers
iona l) Felo-dipine Propranolol
Amyl Selective
Isra-dipine HR🢙
nitrite Nicar- Ivabradine
dipine
Nisol-dipine
Nife-
lingual)
Short Acting dipine  Blockers
1
(Sub n Amlo-
Nitroglyceri dipine Atenolol
Isosorbide din
itrate
Nebivolol
Esmolol
Intermediate Actini
Verapa-mil (Oral & Metoprolol DYSFUNCT
Nitroglyceri Acebutalol
Isosorbide din g (Oral)
Parenteral) ION
Isosorbide mono n
Pentaerythritol tetr trate
ERECTILE
anitrate
Long Acting nitrate Dilti-azem (Oral & Nitrates + “-afils”
(Tran
Nitroglyceri Parenteral) i. Silden-afil
ii. Tadal-afil
▶ COMPENSATO
iii. Varden-
TREATMEN sdermal)
RY
afil
TY n
PE OF
ANGINA T STRATEGIES FOR ANGINA
TREATMENT STRATEGY

Atherosclerotic/ 🢙 Oxygen Requirement by 🢙 TPR, 🢙 CO or Both

Stable/ Classic ⭡ Coronary Blood Flow From action of nitrates:
Angina/ Angina of Acute Attack: Nitrates + Rest (Repeat in recurrence); Nifedipine can also be given 1. Reflex Tachycardia
Effort Prophylaxis: CCBs, -blockers
(⭡SANS) –
Vasospastic/ Rest/ ⭡Oxygen Delivery by reversing vasospasm
Baroreceptors
Variant/ ⭡ Coronary Blood Flow
Nitrates 2. ⭡ Heart Force
Prinzmetal’s
Angina Prophylaxis:
CCBs
Unstable/
Crescendo I/V nitrates (nitroglycerin) given
Angina/ Acute Definite: Myocardial Revascularization (Coronary Artery Bypass Grafting CABG, -
Coronary Percutaneous Transluminal Coronary Angioplasty PTCA)
Syndrome
▶ T OF CYANIDE POISONING
TREATME TREATMENT 1
N MetHb, which binds CN−
lation of amyl nitrite & IV administration of sodium nitrite promotes
formation of anoMetHb which prevents inhibitory action of CN− (complex IV of the less toxic
(3 step procedure) ETC)
1. Immediate inha reconverted to MetHb by treatment with IV sodium thiosulfate, forming MetHB
ions, forming cy and thiocyanate
2. CyanoMetHb is ted by kidney.
ion (SCN−) ed to OxyHb with methylene blue.
excre TREATMENT 2
3. MetHb is convert (preferred now)

Hydroxocobalamin

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜45⮞
HEART FAILURE DRUGS (A: ACUTE; C: CHRONIC)
Heart Failure Drugs

Positive Inotropic Drugs Vasodilators Miscellanous drugs for CHF

Cardiac Glycosides (CHF) Loop Diuretics (AHF +

Digoxin NO Releasers (AHF)
Nitroprusside CHF)
Digitoxin (long duration) Furosemide
Nitroglycerin
Bumetanide
Torsemide
-Agonists (AHF) Ethacrynic Acid
Dobutamine NO Releasers (CHF)
Dopamine Nitrates
Hydralazine Thiazide Diuretics (CHF)
Hydrochloro-thiazide
Chlorothiazide
PDE Inhibitors/Bipyridines Metolazone
(AHF) Chlorthalidone
Milrinone ADH
Theophylline
Antagonists
Coni-vaptan ACE Inhibitors (CHF)
Capto-pril
Tol-vaptan Benaze-pril
Enala-pril
Lisino-pril

ARBs (CHF)
Irbe-sartan
Cande-sartan
Lo-sartan
Val-sartan

Natriuretic Peptide (AHF)

Ne-siri-tide

-Blockers (CHF)
Bisoprolol
Carvedilol
Metoprolol
Nebivolol

K+ Sparing Diuretics (CHF)

Spironolactone
Eplerenone

** Yellow Highlighted for AHF

** Blue Highlighted for both AHF & CHF

HEART FAILURE DRUGS STRATEGY

1. 🢙 Preload (Blood Volume x Venous Tone)
a. 🢙 Blood Volume by Diuretics, ACEIs, ARBs
b. 🢙 Venous Tone by Venodilators
2. 🢙 Afterload (TPR or BP) by ACEIs, ARBs, -
blockers , Arteriodilators
3. ⭡Contractility by Positive Inotropic Drugs
4. 🢙 Remodeling of Heart Muscles by ACEIs, ARBs, -
blockers,

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜46⮞
▶ DIGOXIN MECHANISM OF ACTION & EFFECTS

Digoxin

Direct Effect Indirect Effect

Cardiac Na/K ATPase Inhibit Neuronal Na/K ATPase Inhibit Intracellular

Na⭡ & K🢙 ⭡ PANS Activity

NCX Exchanger (stops)

Atria

AV
Node
⭡Intracellar Ca (not removed)
🢙 ERP ;
⭡Conduction
Velocity

⭡ERP ;
🢙 Conduction
Velocity
⭡ Heart Force/ Contractility
(Positive Inotropy)

Negligible Effects on ECG

⭡PR Interval
(🢙 Ventricle ERP)

🢙 🢙QTHeart Rate (Negative

Interval

Chronotropy)
T-wave inversion
ST-segment depression

⭡CO, ⭡EF

Remodelling 🢙 🢙 SANS Tone

🢙 ESS (Vasodilation)
🢙 EDS 🢙 Preload
🢙 Afterload
🢙 Heart Rate (Negative
Chronotropy)

▶ TYPES OF HEART FAILURE & TREATMENT

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜47⮞
▶ HEART FAILURE DIFFERENCES

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜48⮞
ANTI-ARRHYTHMIC DRUGS
Anti-Arrhythmic Drugs

Group 2 Group 3 Group 4 Group 5

Group 1
INa Blockers -Blockers IK Blockers L-type ICa Misc.
Propranolol Prolong AP Blockers Adenosine
Metoprolol Sota-lol Verapamil
Group 1B Timolol Ibu-tilide Diltiazem Potassium
Group 1A Group 1C Esmolol
Shorten AP Dofe-tilide Amio-darone Magnesium
Prolong AP No effect on AP Sota-lol Amio-
Moderate Kinetics Fast Kinetics
Lidoca-ine Slow Kinetics Amio-darone darone Ranolazine
Procain-amide Flecain- Drone-
Disopyr-amide Mexilet-ine Ivabradine
Phenytoin ide darone
Quini-dine
Amio-darone

***Sotalol Effect: IK blocker > -blocker

***Amiodarone Effect: IK blocker > INa blocker > -blocker > ICa blocker

▶ PROPERTIES OF PROTOTYPIC
INa Block ANTI-ARRHYTHMIC
ER Period DRUGS
- (PM: PACE
ICaMAKER) PR
Group Drug AP PM Normal
QRS QT Ischemic Normal
Procaineamide Ischemic Block Block Interval Duration
- Interval Activity

1A Disopyramide ⭡ + +++ ⭡ ⭡⭡⭡ + + ⭡/🢙 ⭡⭡ ⭡⭡ 🢙

Quinidine -
Lidocaine
1B
Mexiletine 🢙 - +++ 🢙 ⭡⭡ - - - - -/🢙 🢙🢙
1C Flecainide - + +++ - ⭡ - - ⭡ ⭡⭡ - 🢙🢙
Propranolol - - + +++ - - -
2
Esmolol 🢙 ⭡⭡ ⭡⭡ 🢙🢙
3, 1A, Amiodarone
2, 4 Dronedarone
⭡ + +++ ⭡⭡ ⭡⭡ + + ⭡ ⭡⭡ ⭡⭡⭡⭡ 🢙🢙
Ibutilide - - ? - - - - -
3
Dofetilide ⭡ ⭡ ⭡⭡⭡
3, 2 Sotalol ⭡ - - ⭡⭡ ⭡⭡⭡ +++ - ⭡⭡ - ⭡⭡⭡ 🢙🢙
Verapamil - - + - + +++ - -
4
Diltiazem ⭡ ⭡⭡ 🢙🢙
5 Adenosine - - - - - + + ⭡⭡⭡ - - -

▶ ANTI-ARRHYTHMIC DRUGS THERAPY

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜49⮞
▶ CLINICAL USES OF ANTI-ARRHYTHMIC DRUGS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜50⮞
DIURETICS

Diuretics

Drugs that modify salt Drugs that modify water

excretion excretion

PCT TAL CCT Osmotic ADH Agonists ADH

DCT Diuretics Desmo- Antagonists
Mannitol pressin Coni-vaptan
Carbonic Loop Thiazides K+ Sparing Glycerin Tol-vaptan
Anhydrase Diuretics Diuretics Vaso-pressin
Diuretics Isosorbide Demeclocylcine
Inhibitors Furosemide Hydrochloro- Spironolactone
Aceta- Torsemide Urea Lithium
thiazide Eplerenone
zolamide Bumetanide Chlorothiazide Amiloride
Dor-zolamide Ethacrynic Acid Metolazone Triamterene
Brin-zolamide Chlorthalidone
SGLT2 Inhibitors
Can-agliflozin
Dap-agliflozin
Emp-agliflozin
Ipr-agliflozin

▶ ACIDOSIS & ALKALOSIS

▶ HYPOKALEMIA & METABOLIC ALKALOSIS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜51⮞
DRUGS USED IN CYTOPENIAS/ ANEMIAS
Cytopenia Drugs

Erythrocyte factors Granulocyte Factors Platelet Factors

Erythropoiesis- Myeloid Growth

Iron Vitamins Stimulating Agents Factors Megakaryocyte
(ESAs) - (IV/SC) (Subcutaneous) Growth
Factors

Iron Preparations Vitamin B12 G-CSF Agonist IL-11 Agonist

1-3 x per week
Oral (Parenteral) Fil-grastim Oprelvekin (SC)
Epoetin alfa
Ferrous sulfate Cyano-cobalamin Peg-fil-grastim
Ferrous gluconate Hydro-cobalamin Leno-grastim
Ferrous fumarate
Parenteral Thrombopoietin
Iron dextran Weekly Agonists
Iron sucrose Vitamin B9 (Oral) Darb-epoetin alfa Romiplostim (SC)
GM-CSF Agonist
Ferumoxytol Folic Acid (Folacin) Sargramostim Eltrombopag (Oral)
Sodium Ferric
Gluconate Complex
1-2 x per month
Methoxy polyethylene CXCR4 Antagonist
glycol-epoetin beta Plerixafor
Iron Chelators
Defera-sirox (Oral)
Defer-xamine
(Parenteral)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜52⮞
DRUGS USED IN COAGULATION DISORDERS
Coagulation Drugs

Anticlotting Drugs Drugs that facilitate clotting

Reversal Agents
Anticoagulants Thrombolytics (IV) Antiplatelets
Vitamin K1
(Phytonadione)
Protamine
Heparins (Parenteral) t-PA derivatives COX Inhibitor (oral)
Unfractioned heparin (selective for fibrin- Aspirin
LMW heparins bound plasminogen) Other NSAIDs Clotting Factors
Dalte-parin Recombinants Factor VIII
Enoxa-parin Al-teplase Plasma and Human
Tinza-parin Modified Purified Clotting Factors
Fonda-parinux Re-teplase GP IIa/IIIb Inhibitor (P) Desmopressin
Tenec-teplase Abc-iximibab
Eptifibatide
Direct Factor X Inhibitors Tirofiban
(P/O) Antiplasmin Agents
IV Recombinant Streptokinase Aminocaproic
Lepi-rudin (non-selective) Acid
Tranexamic Acid
IV Modified ADP Receptor
Desi-rudin Antagonist (oral)
Bevali-rudin Clopidogrel
Arga- Prausugrel
troban Oral Ticlopidine
Dabi-gatran Ticagrelor

Direct Thrombin Adenosine Uptake &

Inhibitors (Oral) PDE3 Inhibitors (oral)
Api-xaban Dipyridamole
Edo-xaban Cilostazol
Rivaro-xaban

Coumadin Anticoagulant
(Oral)
Warfarin
▶ DIFFERENCE BETWEEN LMW HEPARINS & HMW HEPARINS
Feature HMWH LMWH
Molecular Weight 15000-20000 Daltons 2000-6000 Daltons
Bioavailability Low High (90%)
Half Life Short (Dose dependent) Long (Dose independent)
Mode of Action Inactivates both factor IIa & Xa Inactivates only Xa
Anticoagulant Effect More effective Less Effective
Monitoring By aPTT Not required (given
once/twice a day)
Protamine Reversal More Effective Partially Effective
Heparin Induced Thrombocytopenia More risk Less risk
Osteroporosis More risk Less risk
Excretion Less reliable More
reliable

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜53⮞
ANTIHYPERLIPIDEMICS
Antihyperlipidemics

HMG-CoA Fibrates Bile Acid Binding Sterol Niacin Homozygous

Absoprtion Resins Inhibitor Familial
Reductase Hypercholestr-
Inhibitors(Statins) emia
Gemfibrozil Colestipol Ezetimibe
Cholestyramine
Pra-vastatin Fenofibrate Colesevelam Lomitapide
Sim-vastatin Mipomersen
Lo-vastatin
Ceri-vastatin
Rosu-vastatin
Ator-vastatin
Flu-vastatin

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜54⮞

🢔 6🢖
ANTIFUNGAL, ANTIVIRAL &
ANTICANCER PH AR M ACO LOGY
0.5 S E Q + 5 M CQ s = 8.5 Marks

DESCRIPTION PAGE NO
ANTIFUNGAL DRUGS 55
ANTIVIRAL DRUGS 56
ANTICANCER DRUGS 57

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜55⮞
ANTI-FUNGAL DRUGS
Anti-Fungal Drugs

Disrupt microtubule
Alter cell membrane Block nucleic acid functions + Inhibit synthesis
permeability (ergosterol) Block -glucan synthesis
synthesis of nucleic acids

Azoles Echinocandins Antimetabolite

Imid-azole (2 Nitrogens) Caspo-fungin Griseofulvin
Flu-cytosine/
Ketocon-azole Mica-fungin 5-Fluorocytosine
Micon-azole Anidula-fungin (5FC)
Clotrim-azole
Tri-azoles (3 Nitrogens)
Flucon-azole
Itracon-azole
Voricon-azole
Posacon-azole

Amphipathic Polyenes
Amphotericin B
Nystatin

Terbinafine

▶ SPECTRUM OF AZOLES
Name Spectrum Cutaneous Subcutaneous Systemi Opportunistic
Mycoses Mycoses c Mycoses
Mycoses
Ketoconazole +
Miconazole > Ketokonzaole Dermatophytes Candida (CMC)
Clotrimazole > Ketokonzaole
Coccidioide Candida
Fluconazole ++ Dermatophytes
s Cryptococcu
Blastomyce s
s
Coccidioides
Sporothrix Histoplasma Cryptococcu
Itraconazole +++ Dermatophytes
Chromomycosis Blastomyces s
Paracoccidioide Aspergillus
s
Candida
Voriconazole +++
Aspergillus
Candida
Posaconazole ++++ Aspergillus
Rizopus

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜56⮞
ANTIVIRAL DRUGS

Anti-Viral Drugs

Anti-Herpes Drugs Anti-HIV Drugs Anti-Influenza Drugs Drugs for Hepatitis HSV, VZV

NRTIs Influenza A

HBV
Acy-clovir Zido-vudine* Oselta-mivir
IFN-
Val-acy-clovir Sta-vudine* Zana-mivir Lami-
vudine Penci-clovir Lami-vudine* A-mantadine Telbi-vudine Famci-clovir
Abaca-vir* Ri-mantadine
Ade-fovir Docosanol Tenofo-vir
Teno-fovir
Cidofovir Didanosine*
Entecavir
Foscarnet Emtri-citabine*
Idox-uridine Zal-citabine
Influenza B
Trifl-uridine Oselta-mivir
Vidarabine Zana-mivir
HCV
IFN-
CMV Sofosbu-vir
Ga vir NNRTIs
Riba-virin
nci-clo
Val- ovir Dela-vird-ine
Bocepre-vir
ganci-cl
Cidofovir
Nevirap-ine*
Foscarnet Etravir-ine
Efa-virenz
Vidarabine
Fomivirsen

Protease Inhibitors
Indi-navir*
Saqui-navir*
Ataza-navir
Daru-navir
Tipra-navir
Nelfi-navir*
Rito-navir*
Fosampre-navir

Entry Inhibitors
CCR5 Antagonist:
Maraviroc
Fusion Inhibitor:
Enfuvirtide
Integrase Inhibitors:
Raltegraver

*
A
n
t
i
-
r
e
t
r
ALI RAZA CHAUDARY o (N67)
PHARMACOLOGY SUPPLEMENTS
⮜57⮞
ANTICANCER DRUGS

Anti-Cancer
Drugs

Alkylating Agents Antimetabolites Natural Product

Antitumour
Hormonal Misc.
Anticancer Drugs Antiboid
es
Anticanc
er
Drugs
Nitrogen Mustards Folic Acid Vinca Alkaloids Anthracyclines TK Inhibitors Glucocorticoids
Chlorambucil Antagonist Vin-blastine Doxo-rubicin Ima-tinib Prednisone
Cyclophosphamide Methotrexate Vin-cristine Dauno-rubicin
Dasa-tinib Mechlorethamine Vin-orelbine
Ida-rubicin Nilo-tinib
Epi-rubicin Bosu-tinib GH Inhibitors
Nitrosoureas Purine Mito-xantrone Suni-tinib
Podophyllotoxins Car-mustine AntagonistsTamoxifen
Pazopa-nib Eto-
poside Toremifene
Lo-mustine Mercaptopurine Sorafe-nib Flutamide Thioguanine
Teni-poside Bleo-mycin
Mito-mycin
Platinum Analogs Growth Factor
Cis-platin Camptothecins GnRH
Pyrimidine Receptor
Analogs
Carbo-platin Antagonists Topo-tecan Inhibitors
Leuprolide
Oxai-platin Irino-tecan Gose-relin
Fluorouracil Trastuzu-mab Nafa-relin
Cytarabine
Cetuxi-mab
Gemcitabine Pantiumu-mab
Alkyl Sulfonates Taxanes Gefi-tinib
Bu-sulfan Pacli-taxil Erlo-tinib
Aromatase
Doce-taxil
Inhibitors
Anas-trozole
Others VEGF Inhibitors
Le-trozole
Pro-carbazine Bevaci-zumab
Da-carbazine Ziv-aflibercept
Others
Rituximab
Proteosome

Asparaginase
Inhibitors

Interferons
Borte-zomib
Carfil-
zomib

*Green Highlighted are CCS (Cell

Cycle Specific) Drugs

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜58⮞

🢔 7🢖
ANTI-MYCOBACTERIAL &
PARASITIC PH AR M ACO LOGY
1 S E Q + 6 M CQ s = 13 Marks

DESCRIPTION PAGE NO
ANTIPROTOZOAL DRUGS 59
ANTIHELMINTHIC DRUGS 60
ANTIMYCOBACTERIAL DRUGS 61

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜59⮞
ANTI-PROTOZOAL DRUGS
Anti-Protozoal Drugs
for Intestinal & Urogneital Protozoans

Amebiasis Giardiasis Cryptosporidiosis Trichomoniasis Tissue Amebicides (act

Luminal Amebicides Metronidazole Paromomycin Metronidazole

Nitazoxanide Tinidazole
Metronidazole Diloxanide furoate
Tinidazole Iodoquinol
Chloroquine Paromomycin
Emetines

Anti-Protozoal Drugs
for Blood & Tissue Protozoans

Malaria Toxoplasmosis Pneumocystis Pneumonia Trypanosomiasis Leishmaniasis Tissue

TMP-SMZ TMP-SMZ American

type Visceral type

Schizonticides (kill Antifolates Pentamidine (Chagas Disease) Pentamidine
schizonts in liver) (Pyrimethamine + Atovaquone Nifurtimox
Paromomycin
Prima-quine Clindamycin + Primaquine + Clindamycin Miltefosine Folinic Acid)
Trimetrextae + Leucovorin
Trimethoprim + Dapsone

African type
Blood Suramin Cutaneous type
Schizonticides (kill Pentamidine Metrodinazole
schizonts in RBCs) Melarsoprol Fluconazole
Chloro-quine Eflornithine
Meflo-quine Nifurtimox
Qui-nine
Artemisi-nins
Mucocutaneous type
(Artesunate,
Amphotericin B
Artemether,
Dihydro-artemisinin)
All types
Sodium
Sporonticides
stibogluconate
(prevent sporogony)
Antifolates
(Sulfonamide,
Proguanil,
Pyrimethamine)

Other Malarial Drugs

Doxycycline
Atovaquone
Halofantrine
Amodiaquine
Lumefantrine

▶ DRUG REGIMEN IN TREATMENT OF MALARIA

DESCRIPTION DRUG
All Plasmodium species Chloroquine
(except Chloroquine-resistant P. falciparum)
Mefloquine
Quinine + Doxycycline
Quinine + Clindamycin
Chloroquine-resistant P. falciparum
Artemisinins + Lumefantrine
Artemisinins +
ALI RAZA CHAUDARY (N67)Amodiaquine
PHARMACOLOGY SUPPLEMENTS
⮜60⮞
ANTI-HELMINTHIC DRUGS
Anti-Helminthic Drugs

Nematodes Trematodes Cestodes

(roundworms) (flukes) (tapeworms)

All Roundworms All Flukes Beef/Pork/Fish

Albendazole Praziquantel Tapeworm
Praziquantel
Niclosamide

Intestinal Roundworms Sheep Liver Fluke

(except Strongyloides) Bithional Pork Larval Tapeworm
Mebendazole Triclabendazole Praziquantel
Albendazole

Tissue Roundworms Large Intestinal Fluke

(Wuchereria, Loa) Praziquantel Dog Tapeworm
Diethylcarbamazine Niclosamide Albendazole

Strongyloides, Larva Migrans S.haematoblium

Thiabendazole Metrifonate
Ivermectin (+ Onchocerca)

Ascaris S. mansoni
Piperazine Oxamniquine
Pyrantel pamoate (+
Hookworm)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜61⮞
ANTI-MYCOBACTERIAL DRUGS
Anti-Mycobacterial Drugs

Atypical Mycobacterial
Tuberculosis Drugs Leprosy Drugs
Infection Drugs

First Line Drugs Alternative/ 2nd Line Drugs Sulfones M. Avium Intracellulare
Isonazid Amikacin (Dapsone, Acedapsone) Drugs
Rifamycins Ciprofloxacin Clofa-zimine Clarithromycin/
(Rifampin, Ofloxacin Rifampin Azithromycin
Rifabutin, Ethionamide Ethambutol
Rifapentine) p-Aminosalicyclic Acid (PAS) Rifabutin
Ethambutol Caspreomycin
Pyrazinamide Cycloserine
Streptomycin
Other Atypical
Mycobacterium Drugs
First Line Anti-TB Drugs
Amikacin
Cephlosporins
Fluoroquinolones
Macrolides
Tetracyclines

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜62⮞

🢔 8🢖
ANTI-BACTERIAL PHARMACOLOGY
1 S E Q + 10 M CQ s = 17 Marks

DESCRIPTION PAGE NO
GENERAL CONSIDERATIONS 63
CELL WALL SYNTHESIS INHIBITORS 65
PROTEIN SYNTHESIS INHIBITORS & AMINOGLYCOSIDES 68
ANTIFOLATE DRUGS & FLUOROQUINOLONES 71

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜63⮞
GENERAL CONSIDERATIONS
▶ BASIS OF CLASSIFICATION OF ANTIMICROBIAL AGENTS
A. NATURE
 Antimicrobials are of two types:
 -cidal drugs = kills
 Beta-Lactams (Cell wall synthesis Inhibitors)
 Vancomycin & relatives
 Fluoroquinolones
 Aminoglycosides
 Cotrimoxazole
 Streptogramins
 -static drugs = inhibit growth
 All other then –cidal drugs
 Usage
 Immunocompetent person = Both types
 Immunocompromised person = Only – cidal drugs
B.TYPE OF MICRORGANISMS
C. CHEMICAL STRUCTURE
D. SOURCE
 Antibiotics
 Non-antibiotic
E. MECHANISM OF ACTION

▶ DIFFERENT PATTERNS OF ANTIMICROBIAL ACTION

FEATURE TYPE – I = CDK TYPE – II = TDK TYPE – III = Both CDK & TDK
Pattern of Concentration dependent with Time dependent with prolonged
Time dependent with minimal PAE
Activity prolonged PAE PAE
PK/PD AUC/MIC
Cmax/MIC T > MIC AUC/MIC
Parameter
Goal of therapy Maximize concentration Maximize duration of exposure Maximize amount of drug
Dosing More frequent (Multiple Small
Less frequent (Single High Dose) Depends
Doses)
Examples Aminoglycoside Beta Lactams Macrolides
s Vancomycin Tetracycline
Flouroquinilones

 MIC: Minimal Inhibitory Concentration:

An estimate of the drug sensitivity of pathognes for comparison with anticipated levels in blood or tissue
 PAE: Post Antibiotic Effect:
Antibacterial effect that persists after drug concentration falls below the MIC
 AUC: Area Under Curve

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜64⮞
▶ GRAPHS FOR PATTERNS OF ANTIMICROBIAL ACTION

▶ GENERAL MECHANISMS OF RESISTANCE TO ANTIMICROBIAL ACTION

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜65⮞
CELL WALL SYNTHESIS INHIBITORS
Cell Wall Synthesis
Inhibitors

Beta Lactams

Others

Pencillins
Cephalospori
ns**
Others

Glycoproteins
Vanco-mycin
Teico-planin
Wider Spectrum  Narrow Spectrum Wider Spectrum Mono-bactam Tela-vancin
Narrow Spectrum Beta Lactamase Actreo-nam
Inhibitors**
1st Generation 2nd Generation Lipoproteins (Gm +ve)
(Gm -ve > +ve) Carba-penems Dapto-mycin
Pencillinase Extended Cefazolin (P) Cefaclor (O) Mero-penem
Susceptible Spectrum Cefalexin (O) Cefamandol (O) Erta-penem
Peptide
Penicillin G Ampi-cillin Cefadroxil (O) Cefotetan (P) Dori-penem

Penicillin V Amoxi-cillin Cefoxitin (P) Imi-penem

Cefuroxime (O/P)
Pencillinase Anti-pseudomonal Beta Lactamase
Antimetabolite Resistant
Pipera-cillin 3rd Generation Inhibitors
Inhibitors
Methi-cillin Ticar-cillin (Gm +ve & -ve) Clavu-lanic Acid
Fosfo-
mycin
Naf-cillin Cefoperazone (P) Sul-bactam
Cyclo-
serine
Oxa-cillin Cefotaxime (P) Tazo-bactam
Dicl-oxa-cillin Cefixime (O)
Ceftazidime (P)
Ceftizoxime
(P)
Ceftriaxone (P)

4th Generation
(Gm -ve)
Cefepime (P)
Cefpirome (P)

5th Generation
(MRSA)
Ceftaroline (P)
** Extended & Antipseudomonal spectrum of Pencillins + Carbapenems = Stable to Pencillinases
** All cephalosporins can cross BBB except 1st generation, 2nd generation, Cefoperazone & Cefixime.

▶ SPECTRUM OF PENICILLIN
DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS SPIROCHETES
NARROW SPECTRUM
 Bacillus anthracis
Pencillinase  Streptococcus pyogenes  Neisseria  Treponema
🗴
Susceptible  Streptococcus viridians gonorrhoeae
A  Clostridium
pallidum
Penicillin G  Streptococcus  Neisseria  Leptospira
Penicillin V perfringens
pneumoniae A interrogans
meningitidis  Corynebacterium
diphtheriae
Pencillinase

🗴 🗴 🗴 🗴
Resistant
Methi-cillin  StaphylococciB
Naf-cillin
Oxa-cillin
BROAD SPECTRUM
Extended  S. pyogenes  Escherichia coli
Spectrum   S. viridians
🗴
C  Haemophilus
Beta Lactamase  S. pneumonia  N. gonorrhoeae  Listeria
infuenzae
Inhibitors B monocytogenes
 Staphylococci  N. meningitidis C  Proteus
Ampi-cillin
Amoxi-cillin ALI  Enterococci RAZA CHAUDARY (N67)
mirabilis
PHARMACOLOGY SUPPLEMENTS
⮜66⮞
▶ SPECTRUM OF CEPHALOSPORINS
DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS OTHERS
NARROW SPECTRUM
 Streptococcu
st s pyogenes
1 Generation  Escherichia coli
 Streptococcu
🗴 🗴 🗴
(Gm +ve)  Proteus mirabilis
Cefazolin s (anerobes)
 PRSPA  Klebsiella
Cefalexin
Cefadroxil  MSSAB
 Staphylococcu
s epidermidis
BROAD SPECTRUM
2nd Generation  E. coli
(Gm -ve > +ve)  S. pyogenes
 Neisseria  Haemophilus  Bacteroides
🗴
Cefaclor  Streptococcu fragilis
gonorrhoeae infuenzae
Cefamandol
Cefotetan
s (anerobes)
 PRSPA
  P. mirabilis (anaerobe)- Cefo
drugs
Moraxella  Klebsiella
Cefoxitin  MSSAB  Enterobacter
catarrhalis
Cefuroxime
3rd Generation  E. coli
(Gm +ve & -ve)  H. infuenzae
 S. pyogenes
Cefoperazone  P. mirabilis  Bacteroides
🗴
Cefotaxime  Streptococcu  N. gonorrhoeae –  Klebsiella fragilis
Cefixime s (anerobes) Cefixime,  Enterobacter (anaerobe)-
Ceftazidime  PRSPA Ceftriaxone  Serratia Ceftizoxime
Ceftizoxime  MSSAB  Pseudomonas
Ceftriaxone aeruginosa
4th Generation/
Anti-
pseudomonal  Combines the gram (+) activity of 1 generation with gram (-) activity of 3 generation cephalosporins.
st rd

(Gm -ve)  Used in P. aeruginosa mainly

Cefepime
Cefpirome

🗴 🗴 🗴 🗴
5th Generation
(MRSA)  MRSAC
Ceftaroline (P)
A. PRSP: Pencillin resistant pneumococci
B. MSSA: Methicillin suspectible staphylococci
C. MRSA: Methicillin resistant staphylococci

▶ SPECTRUM OF OTHER BETA LACTAMS

DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS OTHERS

🗴 🗴 🗴 🗴
 Klebsiella
Monobactam
 Serratia
Aztreonam  Pseudomonas
Pathogens inside &
outside enteric
tract
 Salmonella
 Escherichia coli
Pathogens outside  Bacteroides
Carbapenems  Neisseria  Listeria enteric tract fragilis
Mero-penem  Streptococci B monocytogenes  Klebsiella (anaerobe)
Erta-penemC  MSSAA gonorrhoeae  Fusobacterium
 Clostridium sp.  Serratia
Dori-penem  Enterococci  Neisseria  Gardnerella  Enterobacter (anaerobe)
Imi-penem meningitidis
B
vaginalis  Proteus  Actinomyces
 Providencia  Nocardia
 Pseudomonas
Respiratory Tract
 H. influenzae
Others
 Acinetobacter sp.
 Citrobacter sp.
Beta Lactamase
Inhibitors  Good inhibitors of Plasmid encoded beta-lactamases i.e. Streptococci, Gonococci, E. coli, H. influenza
Clavu-lanic Acid  Bad inhibitors of Chromosome encoded beta-lactamases i.e. Serratia, Enterobacter , Pseudomonas
Sul-bactam
tazo-bactam
A. MSSA: Methicillin suspectible staphylococci
B. Penicillinase producing strains
C. Not effective against P. auruginosa and Acinetobacter spp.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜67⮞
▶ SPECTRUM OF OTHER AGENTS
DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS OTHERS
 Streptococci  Listeria
Glycoproteins monocytogenes
🗴 🗴
 PRSP
Vanco-mycin  Clostridium difficle
Teico-planin  MSSA/ MRSA  Actinomyces
 S. epidermidis (Orally)
Tela-vancin  Clostridium sp.
 Enterococci
 Coryneabacterium
 Streptococci
 PRSP
 MSSA/ MRSA
Lipoprotein
Dapto-mycin


S. epidermidis
Enterococci
🗴  Coryneabacterium 🗴 🗴
 VRE A
 VISA B/VRSA C
Beta Lactamase
Inhibitors  Good inhibitors of Plasmid encoded beta-lactamases i.e. Streptococci, Gonococci, E. coli, H. influenza
Clavu-lanic Acid  Bad inhibitors of Chromosome encoded beta-lactamases i.e. Serratia, Enterobacter , Pseudomonas
Sul-bactam
tazo-bactam
A. VRE: Vancomycin resistant enterococci
B. VISA: Vancomycin intermediate staphylococci aureus
C. VRSA: Vancomycin resistant staphylococci aureus

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜68⮞
PROTEIN SYNTHESIS INHIBITORS & AMINOGLYCOSIDES

Protein Synthesis
Inhibitors

Inhibitors of 30S Inhibitors of 50S

Subunit Subunit

Broad Spectrum Broad Spectrum Moderate Spectrum Narrow Spectrum Tetracyclins

Chloramphenicol Macrolides Lincosamides

Doxy-cycline Clari-thro-mycin
Mino-cycline Ery-thro-mycin
Demeclo-cycline
Streptogramins
Quinupristin-dalfopristin
Ketolides
Teli-thro-mycin
Glycylcycline Oxazolidinone Tige-cycline
Linezolid

Aminoglycosides
Genta-micin
Tobra-mycin
Amika-cin
Strepto-mycin
Neo-mycin
Netil-micin
Kana-mycin
Spectino-mycin

▶ MECHANISM OF ACTIONS
DRUG CLASS MECHANISM OF EFFECT
ACTION
Blocks functioning of
initiation complex
Aminoglycosides Bactericidal
and causes
misreading of mRNA
Tetracyclines Blocks tRNA binding
Bacteriostatic
to ribosome
Blocks
Chloramphenicol peptidyltransferas Both*
e
i.e. transpeptidation
blocked
Macrolides Bacteriostatic
Telithromycin Blocks translocation Both*
Clindamycin Bacteriostatic
Linezolid Blocks early step in
Both*
ribosome
formation
Causes premature
Streptogramins release of peptide Both*
chain

*Primarily bacteriostatic but can be bacteriocidal depending on dose.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜69⮞
▶ SPECTRUM OF AMINOGLYCOSIDES
DRUG CLASS ORGANISMS/USES Route
E. coli
Enterobacter
Aerobic Gram Negative Rods
Klebsiella IV
(causing UTI or Sepsis)
Genta-micin Serratia
Ref: Levinson Microbiology 15th Ed. Page
Tobra-mycin Proteus
145
Amika-cin Pseudomonas
H. influenzae
Aerobic Gram Negative Rods M. catarrhalis IV
Shigella
Aerobic Gram Negative Rods Pseudomonas (pneumonia)
Aminoglycosides + IV
(causing UTI or Sepsis)
Cell Wall
Gram Positive Cocci Enterococci (carditis) IV
Synthesis
Gram Positive Rods Listeria IV
Inhibitors
Strepto-mycin + Aerobic Gram Negative Rods F. tularensis (tularemia)
Cell Wall Synthesis IV
(associated with animal sources) Yersenia pestis (plague)
Inhibitors Acid Fast Rods Mycobacterium tuberculosis IM
Amika-cin + Multidrug Resistant Strain of
Cell Wall Synthesis Acid Fast Rods Mycobacterium tuberculosis IM
Inhibitors resistant to Streptomycin
Neo-mycin
- Eliminate bowel flora Topical/
Kana-mycin
Oral
Genta-
micin
Netil-micin - Infections resistant to other AGs IV
Spectino-mycin Gonorrhea in patients allergic to
- IM
beta-lactams

▶ SPECTRUM OF OTHER PROTEIN SYNTHESIS INHIBITORS

DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS OTHERS
 Chlamydiae

🗴
 Rrickettsiae
Chloramphenicol  Streptococcus  Neisseria  Salmonella
 Spirochetes
pneumoniae meningitidis  H. influenzae
 Anaerobes (Bacteroides
fragilis)
Doxycycline
 Bacillus  Mycoplasma
Tetracyclines  Brucella sp.
anthracis  Chlamydiae
Tetra-cycline (T)  Streptococcus  Neisseria  Vibrio cholerae
 Clostridium  Rickettsiae
Doxy-cycline pneumoniae meningitides  Yersinia pestis
Mino-cycline (M) (M)  Spirochetes
 MSSA  Helicobacter
 Borrelia burgdorferi
Demeclo- perfringens pylori (T)
cycline  Clostridium  Leptospira interrogans
tetani  Treponema pallidum

 MRSA Extended Extended

spectrum gram
🗴
 VRE spectrum gram
Glycylcycline negative beta negative beta
 Multidrug  Acinetobacter
Tige-cycline resistant lactamase lactamase
streptococci producing bacteria
producing
bacteria
 Spirochetes (A)
 Bordetella  Treponema pallidum
pertussis  Chlamydia (A)
 Campylobacter  C. pneumoniae
Macrolides  Neisseria  Clostridum jejuni
 Streptococcus gonorrhoeae  C. psittaci
Azi-thro-mycin (A) difficile  H. infuenzae
pneumonia (A)  C. trachomatis
Clari-thro-mycin (C)
Ery-thro-mycin (E)
 Streptococcus
pyogenes
 (F)
Moraxella  Coryne-
(A)
 Helicobacter
 Mycoplasma (A)
 M. pneumonia
Fidaxo-micin (F) catarrhalis (A) bacterium pylori (C)
diphtheria (E)  Ureaplasma urealyticum
 Legionella  Other
pneumophila
 Mycobacterium avium
(A) complex (C)
Ketolide  Same as macrolides
Teli-thro-mycin  Also effective against multidrug resistant organisms and macrolide resistant organisms
Lincosamides
Clindamycin


Streptococci
MRSA 🗴 🗴 🗴  Anaerobes (Bacteroides
fragilis)
 PRSP

🗴 🗴 🗴 🗴
Streptogramins  MRSA
Quinupristin-  VRSA
dalfopristin  VRE (only E.
faecium)
ALI RAZA CHAUDARY (N67)
PHARMACOLOGY SUPPLEMENTS
⮜70⮞
 PRSP  Coryne-
 MRSA bacterium sp.
Oxazolidinone
Linezolid


MRSE
VRSA 🗴  Listeria
monocytogenes
🗴  Mycobacterium tuberculosis
 VRE  Clostridium
 Streptococci
perfringens

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜71⮞
ANTIFOLATES & FLUOROQUINOLONES
Drugs Interfering Folic
Acid Synthesis

Antifolates Fluoroquinolones
(DNA Gyrase/
Toposisomerase IV
Inhibitors)
Dihydro-pteroate
Synthase Inhibitors
(Sulfonamides)
SHORT ACTING Narrow Spectrum Wider Spectrum
(Oral)
Sulfis-oxazole
Sulfa-acetamide
Sulfa-diazine 1st Generation 2nd Generation 3rd Generation
INTERMEDIATE Nor-floxacin Cipro-floxacin (Respiratory)
ACTING (Oral) O-floxacin
Sulfameth- Gemi-floxacin
oxazole Moxi-floxacin
LONG ACTING Levo-floxacin
(Oral)
Sulfa-doxine
Sulfa-salazine
TOPICAL
Mafenide
Silver Sulfa-diazine
Dihydro-folate
Reductase Inhibitor
Trimethoprim

Combination
Co-trim-oxazole
(TMP-SMZ)

▶ SPECTRUM OF
DRUGS
DRUG GRAM + COCCI GRAM - COCCI GRAM + RODS GRAM - RODS OTHER ORGANISM
 E. coli
 H. infuenzae PARASITES
🗴
 Listeria
 Legionella  P. jirovecii
Co-trim-oxazole  S. aureus monocytogenes
 P. mirabilis  Toxoplasmosis
 S. typhi gondii
 Shigella
 E. coli
 H. infuenzae
 Legionella
 P. mirabilis
Fluoroquinolones  S. pneumoniae 🗴  Bacillus anthracis 

Shigella
P. aeruginosa
 M. tuberculosis

 Serratia
 Klebsiella
 Enterobacter

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜72⮞

🢔 9🢖
E N D O C R I N E PH AR M ACO LOGY
1 S E Q + 6 M CQ s = 13 Marks

DESCRIPTION PAGE NO
HYPOTHALAMIC & PITUITARY HORMONES 73
THYROID HORMONES 74
CORTICOSTEROIDS HORMONES 75
GONADAL HORMONES 76
PANCREATIC HORMONES 77
DRUGS AFFECTING BONE MINERAL HOMEOSTASIS 78

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜73⮞
HYPOTHALAMIC & PITUITARY HORMONES
Hypothalamic & Pituitary
Hormones

Hypothalamus Anterior Pituitary Posterior Pituitary

GnRH Analogs GH Agonists Oxytocin Agonist

Leu-prolide Somatotropin Oxytocin
Gonado-relin Mecasermin
Gose-relin
Buse-relin
Hist-relin
Nafa-relin Oxytocin Antagonist
Tripto-relin GH Antagonists Atosiban
Peg-visomant
Somatostatin
Analogs Oct-reotide
Lan-reotide
GnRH Antagonist D2 receptor Agonist Vasopressin Agonist
Aba-relix Bromo-criptine Vasopressin (V1,
Gani-relix V2) Desmopressin
Cetro-relix (V2)
Dega-relix

GT: FSH Analogs

Follitropin alfa Vasopressin
Follitropin beta Antagonist Coni-
Uro-follitropin vaptan (V1a, V2) Tol-
Menotropin vaptan (V2)

GT: LH Analogs
hCG
CG alfa
Lutropin
Menotropin

Prolactin Antagonist/
Dopamine Agonist
Bromociptine
Cabergoline
Pergolide

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜74⮞
THYROID HORMONES
Thyroid Hormones

Hypo-thyroidism Hyper-thyroidism

Thyroid Preparations Thioamides Iodide

Levo-thyroxine (T4) Methi-mazole Lugol's Solution
Lio-thyronine (T3) Propyl-thiouracil Potassium
(PTU) Iodide (KI)
Radioactive
Iodine (I131)

Anion Inhibitors Radiocontrast Media

Thiocyanate (SCN) Oral Dia-trizoate
Perchlorate IV Iohexol
(CLO4)

Beta Blockers Antiayyhythmic

Propanolol Amiodarone

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜75⮞
CORTICOSTEROID HORMONES
Corticosteroid Hormones

Agonists Antagonists

Glucocorticoid Agonists Mineralocorticoid Agonists Receptor Antagonists Synthesis Inhibitors

Cortisol Aldo-sterone Mife-pristone (GC) Ketoconazole
Beta-methasone Deoxy-cortisterone Spironolactone (MC) Aminoglutethimide
Beclo-methasone Fludro-cortisone Eplerenone (MC) Metyrapone
Bude-sonide
Dexa-methasone
Predni-sone
Triamci-nolone

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜76⮞
GONADAL HORMONES
Ovarian Hormones

Estrogens Progestins

Agonists Antagonists Agonists Antagonists

Estradiol Progesterone Mifepristone (RU 486) in
Ethinyl estradiol combination with PGE
Estradiol analog Misoprostol
cypionate
Estrone SERMS
Diethyl-stil-bestrol Tamo-xifen
Mestran Tore-mifene Synthetic Progestins
ol Ralo-xifene Medroxy-progesterone acetate
Bazedo-xifene Megestrol acetate
Clo-miphene

Full Receptor Antagonist Older 19-Nortestosterone

Fulve-strant Compounds
L-Nor-gestrel
Nor-ethindrone

Synthesis (Aromatase)
Inhibitors
Anas-trozole Newer 19-Nortestosterone
Le-trozole Compounds
Exemestane Nor-gestimate
Nor-elgestromin
Deso-gestrel
Etono-gestrel
GnRH Agonists
Leu-prolide

Spironolactone Derivatives
Dor-spirenone
GnRH Antagonists
Gani-relix
Cetro-relix

An
d
r
Agonists Antagonists
o
Testosterone
g
e Receptor Antagonist
Oral Androgens n Fl-utamide
Fluoxy-me-sterone Bical-utamide
Methyl-testosterone
H Nil-utamide
o Spironolactone
r
Esters
m
Testosterone cypionate 5-reductase Inhibitors
o Fin-asteride
n Dut-asteride
e
Anabolic Steroids
Ox-androlones GnRH Agonists
N-androlone Leu-prolide

GnRH Antagonists
Aba-relix
Dega-relix

Synthesis
Inhibitors
Ketocona
zole

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜77⮞
PANCREATIC HORMONES
Pancreatic Hormones

Antidiabetics Hyperglycemics

Insulin Non-Insulin Glucagon

Rapid Acting Insulin Secretagogues

Lispro 1st Gen-Sulfonylureas
Aspart Tolaz-amide
Glulisine Tolbut-amide
Inhaled Regular Chlorprop-amide
Acetohex-amide
2nd Gen-
Sulfonylureas
Gli-piz-ide
Short Acting Gli-mepir-ide
Regular Insulin Gly-bur-ide
Meglitinide
Analogs Repa-
glinide Nate-
glinide

Intermediate Acting
NPH
Biguanides
Metformin

Long Acting
Detemir Thiazolidinediones
Glargine Rosi-glitazone
Pio-glitazone

-glucosidase Inhibitors
A-carbose
Miglitol

Incretin Based Drugs

GLP-1 Agonists
Exenatide
Lira-glutide
Albi-glutide
Dula-glutide
DPP-4 Antagonists
Sita-gliptin
Saxa-gliptin
Lina-gliptin
Alo-gliptin
Vilda-gliptin

Amylin Analogs
Pramlintide

SGLT2 Inhibitors
Cana-gliflozin
Dapa-gliflozin

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜78⮞
DRUGS AFFECTING BONE MINERAL HOMEOSTASIS
Bone Homeostasis Regulators

Hormonal Non-hormonal

PTH Biphosphonates
Teri-paratide Alen-dronate
Eti-dronate
Rise-dronate
Iban-dronate
Pami-dronate
Vitamin D Analogs Tilu-dronate
Chole-calciferol Zole-dronate
Ergo-calciferol
Calcitriol
Doxer-calciferol
Pari-calcitol
Calci-potriene RANKL Inhibitor
Deno-sumab

Calcitonin
Calcimimetics
Cina-calcet

SERM
Ralo-xifene Misc.
Gallium Nitrate
Thiazide
Diuretics
Glucocorticoids Plicamycin
Mithramycin
Furosemide
Fluoride
Strontium Ranelate
Sevelamer

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜79⮞

🢔 10 🢖
CENT R AL N E RVO U S S YS T E M
PH AR M ACO LOGY
1 S E Q + 5 M CQ s = 12 Marks

DESCRIPTION PAGE NO
SEDATIVE HYPNOTICS 80
ALCOHOLS 81
ANTISEIZURE/ANTIEPILEPTIC DRUGS 82
GENERAL ANESTHETICS 83
LOCAL ANESTHETICS 84
SKELETAL MUSCLE RELAXANTS 85
DRUGS FOR MOVEMENT DISORDER 86
ANTIPSYCHOTIC & BIPOLAR DRUGS 87
ANTIDEPRESSANTS 89
OPIODS ANALGESICS & ANTAGONISTS 90
DRUGS OF ABUSE 92

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜80⮞
SEDATIVE HYPNOTICS
Sedative Hypnotics

Benzo-dia-zepines
Benzo-dia-zepines Barbiturates Misc.
Antagonist

Short Acting (3-8 hours) Ultra Short Acting Newer Hypnotics (BZ1)
Fluma-zenil
Oxa-zepam (20 minutes) Zolpi-dem
Tria-zolam Thio-pental Zalep-lon
Eszopic-lone

Intermediate Acting Short Acting (3-8 hrs)

(8-20 hrs) Pento-barbital Melatonin Agonists
Alpra-zolam Seco-barbital Ra-melteon
Clona-zepam Amo-barbital Tasi-melteon
Esta-zolam Buta-barbital
Lora-zepam
Tema-zepam
5-HT1A Agonist
Long Acting Bu-spirone
(1-2 days)
Long Acting (1-3 days) Pheno-
Clorazepate barbital
Chlordiazepoxide Orexin Antagonist
Dia-zepam Suvo-rexant
Flura-zepam

▶ CLINICAL INDICATIONS OF BARBITURATES

NAME OF DRUG CLINICAL INDICATIONS
Alpra-zolam Anxiety (Panic, Phobias)
Clona-zepam Anxiety, Bipolar disorder, Seizures disorder
Dia-zepam Anxiety, Anesthesia IV, Muscle Relaxation, Status epilepticus, Withdrawal states Lora-zepam
Anxiety, Status epilepticus
Chlordiazepoxide Withdrawal states
Mida-zolam Anesthesia IV
Flura-zepam
Esta-zolam
Tria-zolam

Sleep
disorders
Tema-zepam
Oxa-zepam
▶
DIFFERENCE
BETWEEN
Receptors
Act through BZ receptors Do not act through BZ
BENZODIAZE receptors
Dependence
PINES &
Liability
Less
These receptors are part of GABAA complex Highon GABAA complex
Have their own binding sites
BARBITURAT
Half lives 2-4 hours 4-60 hours
ESAntagonism By Fluma-zenil No
FEATURE

BENZODIAZEP
INES

BARBITURATE
S
P
o
t
e
n
t
i
a
ALI RAZA t
CHAUDARY (N67)
PHARMACOLOGY SUPPLEMENTS
⮜81⮞
ALCOHOLS
Alcohols

Alcohol Withdrawal Alcohol Dependency Methanol & Ethylene

Agonists
Drugs Drugs Glycol Poisoning Drugs

Ethanol Benzodiazepines Opioid Antagonist Alcohol Dehydrogenase

Methanol (Wood Alcohol) Diazepam Nal-trexone Inhibitor
Ethylene Chlordiazepoxide Fome-pizole
Glycol

NMDA Antagonist
Vitamin Acamprosate Alcohol
Thiamine
Ethanol

Aldehyde
Dehydrogenase Inhibitor
Disulfiram

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜82⮞
ANTISEIZURE/ANTIEPILEPTIC DRUGS
Antiseizure Drugs
(Clinical Uses)

Tonic-Clonic (Grand Absence (Petit Mal)

Mal) Seizures Partial Seizures Seizures Myoclonic Seizures Status Epilepticus

Drug of Choice Drug of Choice Drug of Choice Drug of Choice Short Acting
Phenytoin Phenytoin Ethosuximide Valproate Diazepam (IV)
Fos-phenytoin Fos-phenytoin Valproate Lorazepam (IV)
Carbama-zepine Carbama-zepine Phenobarbital (child)
Ox-carba- Ox-carba-
zepine zepine Back up &
Valproate Lamotrigine Back up & Adjunctives
Adjunctives Felbamate Long Acting
Clona-zepam Clona-zepam Phenytoin
Drug of Choice Back up & Lamotrigine Lamotrigine Fos-phenytoin
(infants) Adjunctives Levetiracetam Levetiracetam
Phenobarbital Gabapentin Zonisamide Topiramate
Primidone Felbamate Zonisamide
Pregabalin
Phenobarbital OTHER USES:
Topiramate
Back up & 1. Manic Phase of Bipolar Disorder: Valproate
Valproate
Adjunctives
2. Migraine: Phenytoin, Topiramate
Gabapentin
Lamotrigine 3. Neuropathic pain: Gabapentin, Pregabalin
Levetiracetam 4. Neuralgia (trigeminal): Carbamazepine, Oxcarbazepine
Topiramate 5. Bipolar disorders: Carbamazepine, Lamotrigine
Zonisamide

Mechanism of Actions
of Anti-seizure Drugs

Sodium Channel Calcium Channel Glutamate Receptor

GABA Related Targets
Blockade Blockade (T Blockade
type)

Therapuetic Doses GABAA Receptor Agonist Etho-suximide Phenobarbital

Phenytoin Benzodiazepines Valproate Topiramate
Topiramate (increase frequency of Cl- Gabapentin Felbamate
Car bama-zepine channel opening) Topiramate
Lamo-trigine Dia-zepam Pregabalin
Zonis- Clona-zepam
amide Lora-zepam
Barbiturates
(increase
High Doses duration of
Cl-
Pheno-barbital channel
Valproate opening)
Phenobarbita
l
GABA Transaminase Inhibitor
Vigabatrin
Valproate

GABA Reuptake Inhibitor

Tiagabine

GABA Analog
Gabapentin

GABA Facilitators
Felbamate
Topiramate
Valproate

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜83⮞
GENERAL ANESTHETICS
General Anesthetics

Inhaled Anesthetics Intravenous Anesthetics

Gas Volatile Liquid GABAA Receptor Glutamate NMDA Opoid Receptor 2 Agonist Nitrous
Oxide Halogenated Inhibition Facilitators Blockers
Agonists Dex-mede-
(N2O) Hydrocarbons BENZODIAZEPINES Ketamine Fenta-nyl
tomidine Des-flurane Midazolam
Al-fenta-nil
Sevo-flurane BARBITURATES Remi-fenta-
nil
Iso-flurane Thio-pental Morphine En-flurane Thio-amylal
Halothane Metho-hexital
Methoxy-flurane
IMIDAZOLE
Ethomidate
PHENOLS
Propofol
Fos-propofol

▶ DIFFERENCE BETWEEN NITROUS OXIDE & HALOTHANE

FEATURE HALOTHANE NITROUS OXIDE
Potency High Low
Induction Slow Rapid
Recovery Slow Rapid
Blood Gas Coefficient 2.30 0.47
MAC 0.75% > 100%
Metabolism > 40% None
Arrhythmia Increased risk None
Hepatotoxic Increased risk (not in children) None
Therapeutic Actions DOC in children Rapid onset and recovery
Good for asthmatic bronchodilation Good analgesia

▶ MERITS & DEMERITS OF HALOTHANE

MERITS DEMERITS
Potent Hypotension and Bradycardia
Less irritant Arrhythmiogenic
Smooth and rapid induction Hepatotoxic
Smooth and rapid recovery Shivering during recovery
Non inflammable Not an analgesic
Bronchodilator Variable muscle relaxation

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜84⮞
LOCAL ANESTHETICS
Local Anesthetics

Amides (2 i's) Esters (1 i)

Medium Acting Long Acting Surface Acting Short Acting Long Acting
Arti-caine Bu-piva-caine Benzo-caine Pro-caine Tetra-
Lido-caine Levo-bu-piva-caine Co-caine caine
Prilo-caine Me-piva-caine
Ro-piva-caine

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜85⮞
SKELETAL MUSCLE RELAXANTS
Skeletal Muscle Relaxants

Neuromuscular Blockers Spasmolytic Drugs

Depolarizing Acute Use Others

Non-Depolarizing Chronic Use Botulinum Toxin
Succinylcholine Cyclo-benz-apine
Meta-xalone Gabapentin
Metho- Pregablin
CNS Action carbamol
Rapid Acting Orphenadrine
Atra-curium (Spinal Cord)
Cis-atra-curium Baclofen
Diazepam
Tizanidine
Intermediate
Acting
Miva-curium Muscle Action
Ro-curonium Dantrolene
Ve-
curonium
Long Acting
Doxa-curium
Pan-curonium
Tubo-
curarine

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜86⮞
DRUGS FOR MOVEMENT DISORDERS
Drugs for Movement
Disorders

Parkisonism Physiological Huntington's Touretter's Drug Induced Restless Legs

(Paralysis & Essential Disease Syndrome
Dyskinesias Wilson's Disease Syndrome
Agitans) Tremor

Drug of Choice -Blockers Amine D2 Antagonists

Benzotropine Pencillamine Dopamine
Levodopa  Propran-olol Depletors Haloperidol Diphenhydramine
Tri-entine Agonists
Carbidopa Metopr-olol Reserpine Pimozide
Tetrathiomolybdate Ropinirole
Tetrabenazine
Pramipexole
Dopamine Antiseizure 2 Agonist
Agonists Drugs D2 Clonidine
Opoid
D2 AGONIST Gabapentin Antagonists
Analgesics
Apo-morphine Topiramatee Haloperidol
Ropinirole Primidone Perphenazine Benzodiazepine Bromocriptine
Benzodiazepine
Clonazepam
D3 AGONIST Others Atypical
Pramipexole Botulinum Antipsychotic Antiseizure Antisezure Toxin Olanzapine
Drugs Drugs
MAOB Inhibitors Carbamazepine Gabapentin
Rasa-giline
Sele-giline Atypical

Antipsychotic
COMT
Molindone
Inhibitors
Tol-capone
Enta-capone

Antimuscurani
c Benzotropine
Biperiden
Orphenadrine

Others
Amantadine

Increase Dopamine Function

Increase Dopamine
Decrease ACh
Function

▶ FUNCTIONAL CIRCUITRY BETWEEN CORTEX, BASAL GANGLIA AND THALAMUS

In Parkinson’s disease, there is

degeneration of pars compacta
of substantia nigra, leading to
overactivity in indirect pathway
(red)

and

increased glutamatergic activity

by subthalamic nucleus.

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜87⮞
ANTIPSYCHOTIC & BIPOLAR DRUGS
Antipsychotic
& Bipolar
Drugs

Antipsychotics

Bipolar Drugs
(Neuroleptics)

Classic Drugs Newer Drugs Classic Drug Newer Drugs

(D2 receptor (5HT2 receptor
affinity) affinity)
Lithium Acute Mania
Phenothiazines Thioxanthenes Butyrophenonones Aripipr-azole Olanz-apine
PROPYLAMINE Thiothixene Haloperidol Cloz-apine Queti-apine
SIDE-CHAIN Lox-apine
Valproate
Chlorprom-azine Olanz-apine Acute Mania 
PIPERIDINE Queti-apine
Prophylaxis
SIDE-CHAIN Molin-done Carbama-
zepine
Thiorid-azine Risperi-done Clona-zepam
PIPERAZINE Ziprasi-done Lamo-
trigine
SIDE-CHAIN
Trifluoper-azine
Fluphen-azine
Prochlorper-azine
Perphen-azine

**Sedation & anti-cholinergic effects decreases from top to bottom subclasses.

** Extrapyramidal effects increases from top to bottom subclasses.
** Extrapyramidal effects are maximum in this class of drugs.
** Least sedating of newer antipsychotics.

▶ ANTIPSYCHOTICS ADVERSE EFFECTS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜88⮞
▶ DIFFERENCE BETWEEN TYPICAL & ATYPICAL ANTIPSYCHOTICS
FEATURE TYPICAL ANTIPSYCHOTICS ATYPICAL ANTIPSYCHOTICS
Receptor Affinity D2 > 5-HT2 5-HT2 > D2
Schizophrenia Symptoms 🢙 Positive Symptoms 🢙 Positive & Negative Symptoms
Extrapyramidal Side Effects ⭡ tendency (maximum in Haloperidol) 🢙 tendency
Tardive Dyskinesias High risk Low risk
Metabolic Disturbances None May produce
Agranulocytosis None May produce (Cloz-apine)
QT Interval Prolongation None May produce (Queti-apine & Ziprasi-done)
Withdrawal Symptoms Less High

▶ TYPES OF PSYCHIATRIC ILLNESS

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜89⮞
ANTIDEPRESSANTS
Antidepressants

TCAs SSRIs Heterocyclics MAO Inhibitors

Ami-triptyline Fluo-xetine SNRIs MAOA & MAOB Inhibitor

Clo-mipramine Paro-xetine Levo-milna-cipran
Phenel-zine
I-mipramine Fluvo-xamine Dulo-xetine
Tranyl-cy-promine
Ser-traline Venla-faxine
Citalo-pram Des-venla-faxine
Es-citalo-pram
MAOB Inhibitor
5-HT2A Antagonists Sele-giline
Nef-azodone
Tr-azodone

Others
Amoxa-pine
Mirtaze-pine
Bu-pro-pion
Ma-pro-
tiline

▶ ANTIDEPRESSANTS ADVERSE EFFECTS

▶ ADVANTAGES OF SSRIs OVER TCAs

1. 🢙 Sedation
2. Not interfere with cognitive and anticholinergic effects
3. No postural hypotension (Suitable for elders)
4. Wide safety margin
5. Better patient acceptability
6. Preferred for porphylaxis of recurrent depression.
7. Additional use in NEUROSIS psychiatric illnesses

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜90⮞
OPIOID ANALGESICS & ANTAGONISTS
Opioid Drugs

Agonists Mixed Agonist-Antagonists Antagonists Others

Full Agonists  Agonist &  Antagonist Older Agents Antitussives

Fentanyl Butor-phanol (Crosses BBB) Codeine
Morphine Nal-buphine Nalo-xone Dextro-
Oxy- Penta-zocine Nalme-fene meth-
morphone Naltre-xone orphan
Hydro-morphone
Methadone
Meperidine  Agonist &  Antagonist Newer Agents/
Heroin Bupre-norphine Antidiarrheals
Levor-phanol (Do not cross BBB)
Loper-amide (Antidiarrheal) Methyl-naltre-xone
Diphenoxylate (Antidiarrheal)  Agonist & 5-HT Reuptake Alvimopan
Inhibitor
Tramadol
Partial Agonists
Codeine
Oxy-codone  Agonist & NE Reuptake
Hydro-codone Inhibitor
Tapentadol
Weak Agonists
Prop-oxy-phene

Overdose reversed by Naxolone

Overdose cannot be reversed by
▶ OPIOID RECEPTORS Naxolone
RECEPTOR FUNCTIONS ENDOGENOUS OPIOID PEPTIDE AFFINITY
Supraspinal and spinal analgesia
Respiratory inhibition
μ (mu) Hormone modulation Endorphins > enkephalins > dynorphins
Neurotransmitter release
Sedation
Slowed GIT transit
Supraspinal and spinal analgesia
δ (delta) Hormone modulation Enkephalins > endorphins = dynorphins
Neurotransmitter release
Tolerance development
Supraspinal and spinal analgesia
κ (kappa) Sedation Dynorphins > > endorphins = enkephalins
Slowed GIT transit
Psychotomimetic effects
▶ PHARMACOLOGICAL & ADVERSE EFFECTS OF OPIOIDS
ACUTE EFFECTS (BAD AMERICANS Hormones Imbalanced)
1. Bradycardias & hypotension
2. Analgesia (treatment of moderate to severe pain)
3. Dependence
4. Anorexia (poor appetite)
5. Miosis (characteristic of all opioids except meperidine)
6. Euphoria (state of excitement)
7. Respiratory depression
8. Increase smooth muscles activity (characteristic of all opioids except meperidine)
 Biliary tract constriction ⭢ Biliary Colic
 ⭡ Ureteral & bladder sphincter tone
 🢙 Uretrine tone ⭢ Prolongation of labor
9. Constipation (atidiarrheal agents)
10.Antitussive (suppression of cough reflex by inhibiting respiratory centres with decrease response to CO2 challenge)
11. Nausea and vomiting (activate chemoreceptor trigger zone)
12. Sedation and mental clouding (at higher doses)
13. Hormones Imbalanced
 ⭡ Release of ADH & Prolactin
 🢙 Release of LH
 Exaggerate response in adrenal insufficiency & hypothyroidism

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜91⮞
CHRONIC EFFECTS (TD)
1. Tolerance
2. Dependance ⭢ Abstinence Syndrome ⭢ GLARY De CMH (Gooseflesh, Lacrimation, Anxiety, Rhinorrhea,
Yawning, Diarrhea, Chills, Muscle aches, Hostility)

▶ ADVERSE EFFECTS OF OPIOIDS

(MORPHINE)
1. Miosis
2. Out of it i.e Sedation
3. Respiratory depression
4. Pneumonia (aspiration)
5. Hypotension
6. Infrequent urination
7. Nausea
8. Emesis

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜92⮞
DRUGS OF ABUSE
Drugs of Abuse

Sedative- Opioid CNS

Hallucinogens Marijuana Inhalants Steroids
Analgesics Stimulants
Hypnotics
Benzodiazepine Fentanyl Caffeine Phencyclidine Tetrahydro- Anesthetics
Barbiturates Morphine Nicotine LSD cannabinol Industrial Solvents
Ethanol Meperidine Cocaine Mescaline Cannabidiol Organic Nitrates
Heroin Amphetamines Cannabinol
Codeine Psilocybin
Oxy-codone

▶ MECHANISMS OF ACTION OF DRUGS OF ABUSE

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜93⮞

🢔 11
🢖
DESCRIPTION
AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY
PAGE NO
94
AUTOCOIDS & NSAIDS PHARMACOLOGY 95

D RU G S O F C H O I C E
RESPIRATORY PHARMACOLOGY
GASTROINTESTINAL PHARMACOLOGY
96
97
CARDIOVASCULAR PHARMACOLOGY 98
RENAL PHARMACOLOGY 99
BLOOD PHARMACOLOGY 100
ANTIFUNGAL PHARMACOLOGY 101
ANTIVIRAL PHARMACOLOGY 102
ANTI-MYCOBACTERIAL PHARMACOLOGY 103
PARASITIC PHARMACOLOGY 104
ANTIBACTERIAL PHARMACOLOGY 105
ENDOCRINE PHARMACOLOGY 107
CENTRAL NERVOUS SYSTEM PHARMACOLOGY 108

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜94⮞
AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Mushroom poisoning
– Early (Inocybe sp.) Atropine
– Delayed (Amanita sp.) Thioctic acid
Glaucoma
– Open angle Latanoprost
– Angle closure Acetazolamide
Myasthenia gravis
– Diagnosis Edrophonium
– Treatment Neostigmine/pyridostigmine
Belladona poisoning Physostigmine
Atropine poisoning Physostigmine
Dhatura poisoning Physostigmine
Alzhiemer’s dementia Donepezil/Rivastigmine/Gallantamine
Cobra bite Anti-venom
Anticholinesterase poisoning
– Organophosphate Atropine
– Carbamate Atropine
Colicky pain Anticholinergics like hyoscine/dicyclomine
Bronchial asthma Salbutamol
Refraction testing
– In adults Tropicamide
– In children Atropine
Fundoscopy Phenylephrine
Uveitis
– Iridocyclitis Atropine + steroids
– Posterior uveitis Steroids
– Panuveitis Steroids
Bradycardia Atropine
Atrioventricular block Atropine
Drug induced Parkinsonism Anticholinergics like benzhexol
Shock
– Cardiogenic Nor-adrenaline or dopamine
– with oligourea Dopamine
– Anaphylactic Adrenaline
– Distributive Nor-adrenaline or phenylephrine
– Septic Broad spectrum antimicrobials
– Shock due to adrenal insufficiency Corticosteroids
– Hypovolumic Fluids (crystalloids)
– Secondary Prazosin (α-blockers)
Postural hypotension Fludrocortisone
Attention deficit hyperkinetic disorder Methylphenidate
Narcolepsy Modafinil or armodafinil
Pheochromocytoma
– Before surgery Phenoxybenzamine
– Long term CCBs like nifedipine or nicardipine extended release
Cheese reaction Phentolamine or tolazoline
Rebound hypertension due to clonidine withdrawl Phentolamine or tolazoline
Raynaud’s phenomenon CCBs like nifedipine ER or amlodipine
Essential tremors Propanolol
Akathisia Propanolol
Hypertrophic obstructive cardiomyopathy Propanolol
Beta blocker poisoning Glucagon
Benign hyperplasia of prostate
– Without hypertension Tamsulosin
– With hypertension Prazosin or doxazosin
Performance anxiety Propanolol

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜95⮞
AUTOCOIDS PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Migraine
– Acute-mild to modrate NSAIDs
– Acute-severe Sumatriptan
– Prophylaxis Propanolol
Abortion < 7 weeks Mifepristone + misoprostol
Induction of labour Oxytocin
Post-partum hemorrhage Oxytocin
Cervical priming Misoprostol
NSAID-induced peptic ulcer Proton pump inhibitors
Open angle glaucoma Latanoprost
To maintain patency of ductus arteriosus Alprostadil
Treatment of patent ductus arteriosus (PDA) Indomethacin
Bartter syndrome Indomethacin
Pulmonary hypertension Oral diltiazem or amlodipine or nifedipine
Erectile dysfunction Sildenafil
Rheumatoid arthritis
– Pain relief NSAIDs
– Bridge therapy Corticosteroids
– DMARD Methotrexate
Flushing due to nicotinic acid Aspirin
Prophylaxis of MI and stroke Aspirin
Acetaminophen (Paracetamol) poisoning N-Acetyl cysteine
Anaphylactic shock Adrenaline
Acute mediterranean fever Colchicine
Cancer chemotherapy induced vomiting 5HT3 antagonists like ondansetron
Cisplatin induced vomiting
– Early Ondansetron
– Delayed Aprepitant
Gout
– Acute NSAIDs except aspirin
– Refractory acute Colchicine
– Chronic Allopurinol
– Chronic (in patient allergic to allopurinol) Febuxostat
Hyperuricemia secondary to anticancer drugs Allopurinol

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜96⮞
RESPIRATORY PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Bronchial Asthma
– Acute attack Salbutamol
– Acute attack in pregnancy Salbutamol
– Acute attack during labour Ipratropium
– Acute attack in patients on beta blocker therapy Ipratropium
– Prophylaxis Corticosteroids
Exercise-induced asthma
– Acute attack Salbutamol
– Prophylaxis Corticosteroids
Aspirin-induced asthma
– Acute attack Salbutamol
– Prophylaxis Corticosteroids

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜97⮞
GASTROINTESTINAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Peptic ulcer
– Gastric ulcer Proton pump inhibitors (PPI)
– Duodenal ulcer PPI
– Stress ulcer PPI
– NSAID-induced PPI
– H. pylori associated Lansoprazole + Amoxycillin + Clarithromycin
– Zollinger Ellison syndrome PPI
– Gastro Esophageal Reflux Disease PPI
Vomiting
– Chemotherapy induced 5-HT3 antagonists like palonosetron
– Levo-dopa induced Domperidone
– Migraine associated Metoclopramide
– Drug or disease associated Metoclopramide
– Post-operative Ondansetron
– Radiation induced Ondansetron
– Cisplatin induced
* Early 5-HT3 antagonists
* Delayed Aprepitant
– Prophylaxis of motion sickness Hyoscine
– Pregnancy (Morning sickness) Doxylamine + Pyridoxine
Opioid induced constipation Methyl naltrexone
Diarrhea in carcinoid syndrome Octreotide
To prevent dehydration in diarrhea ORS
Crohn’s disease Corticosteroids
Ulcerative colitis 5-ASA derivatives
Hepatic encephalopathy Lactulose

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜98⮞
CARDIOVASCULAR PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Diabetic nephropathy ACE inhibitors or ARBs
Scleroderma hypertensive crisis Captopril
Congestive heart failure
– Decompensated Dobutamine
– Compensated ACEI/ARB
Hypertrophic obstructive cardiomyopathy Propanolol
Angina pectoris
– Acute attack Sublingual nitroglycerine
– Prophylaxis Oral/transdermal nitrates
Esophageal spasm Nitroglycerine
Cyanide poisoning Hydroxocobalamin/amyl nitrite
Raynaud's phenomenon Nifedipine ER or amlodipine
Myocardial infarction
– Pain relief Sublingual nitroglycerine ↓ Morphine
– Prophylaxis Aspirin
– Thrombolytic for STEMI Reteplase or alteplase
Hypertension Thiazides
– With BHP Prazosin
– With diabetes mellitus ACE inhibitors
– With ischemic heart disease (angina) Beta blockers
– With chronic kidney disease ACE inhibitors
– In pregnancy Labetalol
Acute severe digitalis toxicity Digibind
Hypertensive emergencies Nicardipine + Esmolol
– In cheese reaction Phentolamine
– in clonidine withdrawl Phentolamine
– In aortic dissection Nitroprusside + esmolol
– In Pregnancy Labetalol
Hyperlipidemia
– Type IIa and IIb Statins
– Type III (hypertriglyceridemia) Fibrates
– Type IV Statins
– Secondary to diabetes or nephrotic syndrome Statins
Supraventricular tachycardia
– Narrow QRS complex Verapamil or beta blockers
– Wide complex Flecainide
– WPW syndrome Flecainide
Paroxysmal supraventricular tachycardia (PSVT)
– Acute treatment Adenosine
– Prophylaxis Verapamil
Ventricular tachycardia Lignocaine
– Digitalis induced Lignocaine
Long QT syndrome (Torsades' de pointes) Magnesium

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜99⮞
RENAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Edema
– Due to CHF Furosemide
– Due to renal disease or nephrotic syndrome Furosemide
– Pulmonary edema Furosemide
– Cerebral edema Mannitol
– Edema due to cirrhosis Spironolactone
Diabetes insipidus
– Central Desmopressin
– Nephrogenic Thiazides
– Lithium-induced Amiloride
Recurrent calcium stones in kidney due to hypercalciurea Thiazides
Acute congestive glaucoma Acetazolamide
Acute mountain sickness Acetazolamide
Nocturnal enuresis Desmopressin
SIADH Fluid restriction + Hypertonic saline +
Furosemide

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜100⮞
BLOOD PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Anemia
– Iron deficiency anemia Ferrous sulphate
– Megaloblastic anemia
* Folate deficiency Folic acid
* B12 deficiency Vitamin B12
* Pernicious anemia Vitamin B12
* Chemotherapy induced anemia Erythropoietin
– Anemia due to chronic kidney disease Erythropoietin
Iron poisoning
– Acute Desferrioxamine
– Chronic Deferipirone
Cyanide poisoning Hydroxocobalamin/Amyl nitrite
Deep vein thrombosis
– Prophylaxis Warfarin
– Initiation of therapy LMW heparin + warfarin
– With severe chronic kidney disease Unfractionated heparin
Pulmonary embolism
– Stable patient LMW heparin
– Unstable patient Thrombolytics (Reteplase)
Chronic Atrial fibrillation
– Prophylaxis Dabigatran or Rivaroxaban or Apixaban
– In mechanical prosthetic valves Warfarin
– Advanced kidney disease Warfarin
– Mitral stenosis Warfarin
Myocardial Infarction
– Acute STEMI Thrombolytics (Reteplase)
– Prophylaxis Aspirin
Heparin overdose Protamine
Warfarin overdose Vitamin K
Bleeding due to overdose of anticoagulants Fresh frozen plasma
(heparins or warfarin)
Fibrinolytic overdose Tranexamic acid or Epsilon Amino Caproic Acid
Chemotherapy induced leukopenia Sargramostim
Chemotherapy induced thrombocytopenia Oprelvekin
Immune thrombocytopenic purpura Corticosteroids
Heparin induced thrombocytopenia Argatroban

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜101⮞
ANTIFUNGAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Candida albicans Fluconazole
Candida glabrata Caspofungin
Candida krusei Caspofungin
Candida endocarditis Amphotericin B (AMB)
Histoplasmosis
– Meningeal AMB
– Non-meningeal Itraconazole
Coccidioidomycosis AMB
Para-coccidioidomycosis Itraconazole (For severe cases: AMB)
Sporotrichosis Itraconazole
Blastomycosis
– Mild and Non-CNS Itraconazole
– Severe or CNS AMB
Penicillium marneffei Itraconazole (For severe cases: AMB)
Chromoblastomycosis Itraconazole
Mycetoma
– Eumycetoma Itraconazole
– Actinomycetoma Itraconazole
Cryptococcal meningitis
– Induction AMB (for 2 weeks)
– Maintenance Fluconazole (for further 8 weeks)
Aspergillosis
– Invasive Voriconazole
– Allergic broncho-pulmonary (AMBA) Prednisolone + Itraconazole/Voriconazole
Mucormycosis AMB (Posaconazole should be given after disease has stabilized)
Pseudoallescheria boydii Voriconazole
Fusarium Voriconazole
Exserohilum AMB
Febrile neutropenia
– Treatment Voriconazole
– Prophylaxis Fluconazole

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜102⮞
ANTIVIRAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Herpes simplex
– Keratitis Topical vidarabine/Trifluridine
– Neonatal Acyclovir
– Encephalitis Acyclovir
– Dissemnated Acyclovir
– Esophagitis Acyclovir
– Genital Acyclovir
– Bell’s Palsy Prednisolone
Varicella Acyclovir
Herpes zoster
– Acute Valacyclovir
– Post herpetic neuralgia Gabapentin
Epstein Barr virus Symptomatic (no antiviral)
Cytomegalo virus
– Retinitis Ganciclovir
– Post-transplant
* Mild Valganciclovir
* Severe Ganciclovir
Measels Ribavirin (Indication: Severe pneumonitis)
Prion disease Flupirtine (🢙cognitive decline but does not stop mortality)
Viral hemorrhagic fever
– Lassa virus Ribavirin
– Rift Valley fever Ribavirin
– Congo crimean hemorrhage fever Ribavirin
– Hantaan virus Ribavirin
Respiratory syncytial virus
– High risk patient, acute Ribavirin (aerosolized)
– Prophylaxis (infants) Palivizumab
Influenza virus
– Seasonal influenza Oseltamivir
– Avian influenza (including bird flu) Oseltamivir
– Oseltamivir-resistant influenza Zanamivir
Human immunodeficiency virus (HIV)
– Treatment Zidovudine + Lamivudine + Nevirapine
– Post-exposure prophylaxis Zidovudine + Lamivudine ± Atazanavir

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜103⮞
ANTIMYCOBACTERIAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Tuberculosis
– Latent TB Infection (Chemoprophylaxis) Daily INH for 9 months
– Category 1 (New or previously untreated cases) 2HRZE + 4HR
– Category 2 (Previously treated cases; relapses 2HRZES + HRZE + 5HRE
and treatment defaults)
– Treatment failure and special cases:
a. Resistance (or intolerance) to H 6 RZE + Q (for extensive disease)
b. Resistance (or intolerance) to R 12 HZEQ + S (for extensive disease)
c. Intolerance to Z 2 HRE + 7 HR
d. MDR TB (resistance to H + R) HRZE
e. Extensive drug resistance (XDR) HRZE
Leprosy
– Multibacillary (x 12 months) Rifampicin (600mg) once monthly supervised
Clofazimine 300mg once monthly supervised
Dapsone 100 mg OD
Clofazimine 50mg OD
– Paucibacillary (x 6 months) Rifampicin 600 mg once monthly supervised
Dapsone 100 mg OD
– Type 1 Lepra reaction Corticosteroids
– Type 2 Lepra reaction Corticosteroids
M. avium intracellulare Azithromycin + Ethambutol ± Rifabutin
M. kansasii Isoniazid + Rifampicin ± Ethambutol
M. fortuitum chelonei Cefoxitin + clarithromycin
(Q: Fluoroquinolone, H: Isoniazid, R: Rifampicin, Z: Pyrazinamide, E: Ethambutol, S: Streptomycin)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜104⮞
PARASITIC PHARMACOLOGY

CONDITION DRUG O F C H O I C E
ANTI-PROTOZOAN
Ameobiasis
– Asymptomatic intestinal Diloxanide furoate
– Mild, moderate and severe intestinal Metronidazole + diloxanide
– Extra-intestinal (hepatic abcess) Metronidazole + diloxanide
– Primary ameobic meningo-encephalitis (Naegleria fowleri) AMB
– Acanthameoba keratitis Topical propamidine isethionate
Coccidiosis Nitazoxanide/Paromomycin
– Cryptosporidiosis
– Isoporiasis Cotrimoxazole
– Cyclosporiasis Cotrimoxazole
– Microsporidiosis Albendazole
– Sacrocytosis No treatment
– Trypanosomiasis
– East African sleeping sickness
* Early haemo lymphatic stage Suramin
* Late CNS stage Melarsoprol
– South-American (Chagas disease) Benznidazole (alternative is nifurtimox)
ANTI-HEMINTHICS
Flukes
– Fasciola Triclabendazole
– Schistosoma Praziquantal
– Clonorchis Praziquantal
– Opisthorchis Praziquantal
– Paragonimus Praziquantal
– Fasciolopsis Praziquantal
Tapeworms
– Taenia solium Praziquantal
– T. saginata Praziquantal
– D. latum Praziquantal
– H. nana Praziquantal
– Echinococcus Albendazole
– Neurocysticercosis Albendazole
Nematodes
– Ascaris Albendazole
– Trichuris Albendazole
– Ancylostoma Albendazole
– Necator Albendazole
– Enterobius Albendazole
– Trichinella Albendazole
– Cutaneous larva migrans Albendazole
– Visceral lara migrans Albendazole
– Dracunculus (Guinea worm) Metronidazole
Filarial worm
– W. bancrofti Di Ethyl Carbamezine (DEC)
– B. malayi Di Ethyl Carbamezine (DEC)
– B. timori Di Ethyl Carbamezine (DEC)
– Loa loa Di Ethyl Carbamezine (DEC)
– Onchocerca volvolus Ivermectin
Strongyloides stercoralis Ivermectin

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜105⮞
ANTIBACTERIAL PHARMACOLOGY

CONDITION DRUG O F C H O I C E
GRAM-POSITIVE COCCI
Streptococcus
• S. pneumoniae Penicillin G1
• Hemolytic, groups A, B, C, G Penicillin G1
• S. viridans Penicillin G1, 2
Staphylococcus
• Non penicillinase producing Penicillin G1
• Penicillinase producing Penicillinase resistant penicillin (cloxa, oxa, naf or
dicloxacillin)
• Methicillin resistant (MRSA) Vancomycin
• Coagulase negative Vancomycin
ENTEROCOCCUS
• faecalis Ampiillin3
• faecium Vancomycin3
GRAM-POSITIVE BACILLI
• Actinomyces Penicillin G
• Bacillus
– Anthracis Ciprofloxacin or Doxycycline
– Cereus and others Penicillin G
• Clostridium Pencillin G
• Corynebacterium Erythromycin4
• Listeria Ampicillin5
GRAM-NEGATIVE COCCI
• Neisseria
– meningitides Penicillin G
– gonorrhea Ceftriaxone + Azithromycin/Doxycycline
• Moraxella Fluoroquinolones
GRAM-NEGATIVE BACILLI
• Campylobacter Macrolides
• Legionella Macrolides
• Bordetella Macrolides
• Brucella Doxycyline + Rifampicin
• Acinetobacter Carbapenems
• Hemophilus
– Serious infections like meningitis Ceftriaxone
– Respiratory infections, otitis Cotrimoxazole
– Ducreyi (chancroid) Azithromycin
• Prevotella Clindamycin
• Bacteroides Metronidazole
• Pseudomonas Anti-Pseudomonal β-lactam (piperacillin or ceftazidime
or cefepime or imipenem) + Gentamicin
• Burkholderia
– mallei (glanders) Streptomycin + Tetracycline
– pseudomallei (melioidosis) Ceftazidime
• Helicobacter pylori Clarithromycin + Amoxycillin + Proton pump inhibitor
• Enterobactericiae
– Salmonella Ceftriaxone
– E. coli sepsis Ceftriaxone6
– Klebsiella Ceftriaxone7
– Proteus vulgaris Ceftriaxone8
– Enterobacter Carbapenems
– Serratia Carbapenems
– Shigella Fluoroquinolones
– Yersinia Streptomycin + tetracycline
SPIROCHETES
• Treponema
– pallidum (syphilis) Penicillin G
– pertenue (yaws) Penicillin G

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜106⮞
• Leptospira Penicillin G
• Borrelia
– burgdorferi (Lyme’s) Doxycycline
– recurrentis (Relapsing fever) Doxycycline
CHLAMYDIAE
• C. psittaci Doxycycline
• C. trachomatis Doxycycline
• C. pneumoniae Doxycycline
RICKETTSIAE
• R. prowazekii (Epidemic typhus) Doxycycline
• R. typhi (Endemic typhus) Doxycycline
• Orientia tsutsugamushi (scrub typhus) Doxycycline
• R. rickettssi (Rocky mounted spotted fever) Doxycycline
• R. akari (Rickettsial pox) Doxycycline
• Rickettsia fever Doxycycline
• Ehrlichia Doxycycline
• Coxiella burnetii (Q fever) Doxycycline
MYCOPLASMA Azithromycin
NOCARDIA Cotrimoxazole
1. Oral penicillin V can be used for mild cases
2. Addition of gentamicin decreases the duration of treatment
3. Gentamicin is added for meningitis or endocarditis
4. For C. jeikium, vancomycin is drug of choice
5. Gentamicin is added for first few days
6. For UTI by E.coli, nitrofurantion or fosfomycin are used
7. For ESBL producing strains, carbapenems are drug of choice
8. For P. mirabilis, ampicillin is drug of choice

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜107⮞
ENDOCRINE PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Infantile spasms ACTH
Hypothyroidism Levo-thyroxine
Myxedema coma Levo-thyroxine
Hyperthyroidism Carbimazole or methimazole
– In lactation Propylthiouracil
– In 1st trimester of pregnancy Prophylthiouracil
– In 2nd and 3rd trimester of pregnancy Carbimazole or methimazole
– Graves' opthalmopathy Methylprednisolone
Thyroid storm Propanolol (life saving)+ Iodides
Diabetes mellitus
Type 1 (IDDM) Insulin
Type 2 (NIDDM) Metformin
– In obese Metformin
– Uncontrolled Insulin
– Pregnancy Insulin
– To tide over stress Insulin
Diabetic ketoacidosis Insulin (Regular)
Post prandial hyperglycemia Nateglinide
Acute hyperkalemia Calcium gluconate
Beta blocker poisoning Glucagon
Hypoglycemia Glucose (oral or i.v.)
Adrenal insufficiency
– Acute Hydrocortisone
– Chronic (Addison's disease) Hydrocortisone
Erectile dysfunction Sildenafil
Contraceptive
– Newly married Combined oral contraceptives
– In lactation Mini pills
– Emergency contraceptive Levonorgestrel
Anovulatory infertility Clomiphene
Osteoporosis
– Post menopausal Alendronate
– Steroid-induced Alendronate
– In women with risk factors for breast cancer Raloxifene
Hypercalcemia of malignancy Bisphosphonates
Paget's disease of bone Bisphosphonates
Tetany Calcium
Induction of labour Oxytocin
Post partum hemorrhage Oxytocin
Acromegaly Cabergoline
Esophageal varices Terlipressin (if not available, octreotide)
Hyperprolactinemia Cabergoline
Androgenital alopecia Finasteride
Dysfunctional uterine bleeding
– Light bleeding Medroxyprogesterone acetate
– Heavy bleeding Combined oral contraceptives
– Intractable bleeding Leuprolide
Endometriosis Combined oral contraceptives
Ectopic pregnancy Methotrexate

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜108⮞
CENTRAL NERVOUS SYSTEM PHARMACOLOGY

CONDITION DRUG O F C H O I C E
Alcohol dependence
– Withdrawl symptoms (including seizures) Benzodiazepines like chlordiazepoxide or diazepam
– Maintenance therapy Chlordiazepoxide
– To prevent craving Naltrexone
Methanol poisoning Fomepizole
Ethylene glycol poisoning Fomepizole
Anxiety disorders
– Performance anxiety Propanolol
– Generalized anxiety disorder (GAD)
* Acute attacks Benzodiazepines
* Sustained treatment Antidepressants (venlafaxine/duloxetine)
– Panic disorder
* Acute panic attacks Benzodiazepines
* Sustained treatment SSRI (Sertraline)
Insomnia Zolpidem
Benzodiazepine poisoning Flumazenil
Epilepsy/seizure disorders
– Grand mal (GTCS) Valproate
– Petit mal (Absence) Valproate
– Focal Carbamazepine/Oxcarbazepine
– Myoclonic Valproate
– Atonic Valproate
– Infantile spasms
* Without tuberous sclerosis (TS) ACTH
* With TS Vigabatrin
– Febrile seizures Diazepam
– Status epilepticus Lorazepam
– Eclamptic seizures Magnesium sulphate
– Epilepsy in pregnancy Lamotrigine/Topiramate/levetiracetam
– Lennox-Gastaut syndrome Valproate/Rufinamide/Clonazepam
Neuropathic pain
– Trigeminal neuralgia Carbamazepine
– Post-herpetic neuralgia Pregabalin or gabapentin
– Diabetic neuropathic pain Pregabalin or gabapentin
Parkinsonism
– Early Pramipexole/Ropinirole
– Late Pramipexole/Ropinirole
– Drug induced Anticholinergics (Benzhexol)
Levo-dopa induced
– Vomiting Domperidone
– Psychosis Atypical antipsychotics (olanzapine)
Schizophrenia Olanzapine
– In non-compliant patients Risperidone LAI (long acting injection)
– Refractory Clozapine
Manic disorder
– Acute mania Benzodiazepines/Antipsychotics (olanzapine) + lithium
– Prophylaxis of mania Lithium
– Bipolar disorder Lithium
– Rapid cyclers Valproate
Gille de la Tourette syndrome 1. Haloperidol (FDA-approved)
2. Clonidine/Guanafacine (off label)
Relapsing remitting multiple sclerosis Beta-interferon
Huntington’s disease Tetrabenazine
Wilson disease Zinc
Depression SSRI
– Mild to moderate SSRI (Fluoxetine)
– Severe SNRI (Venlafaxine)
Neurotic disorders
– Obsessive compulsive disorder SSRI (Fluoxetine)
– Post-traumatic stress disorder SSRI (Sertraline)

ALI RAZA CHAUDARY (N67)

PHARMACOLOGY SUPPLEMENTS
⮜109⮞
– Bulimia SSRI (Fluoxetine)
– Phobia SSRI (Sertraline)
– Impulse-control disorders SSRI (Fluoxetine)
Attention deficit hyperkinetic disorder Methylphenidate
Nocturnal enuresis Desmopressin
Severe (cancer) pain Opioids (morpine)
Opioid poisoning
– Acute Naloxone
– Maintenance Naltrexone
Opioid de-addiction
– Maintenance therapy Methadone
– To prevent relapse Naltrexone
– To treat withdrawl symptoms Beta blockers/clonidine
Alzhiemer’s dementia Donepezil
Amyotrophic lateral sclerosis Riluzole
Extrapyramidal symptoms
– Acute muscular dystonias Benzhexol
– Parkinsonism Benzhexol
– Akathisia Propanolol
– Neurolept malignant syndrome Dantrolene
– Tardive dyskinesia No treatment (benzodiazepines may help)
Restless leg syndrome Pramipexole
Neurolept analgesia Droperidol + Fentanyl
Neurolept anaesthesia Droperidol + Fentanyl + Nitrous Oxide
GA for internal version Halothane
GA for asthma
– Inducing agent Ketamine
– Inhalational Halothane
GA to produce controlled hypotension Isoflurane
GA for cardiac surgery
– Inducing agent Etomidate
– Inhalational Isoflurane
GA for neurosurgery Isoflurane
Day care surgery Propofol
Total Intravenous Anaesthesia Propofol
GA for malignant hyperthermia Propofol
GA in patients with shock Ketamine
LA in patients with malignant hyperthermia Procaine
Intravenous Regional Anaesthesia (IVRA; Bier’s Prilocaine
block)
Malignant hyperthermia Dantrolene
Malignant Neuroleptic Syndrome Danrolene
MR in patients with asthma Vecuronium
MR in liver and kidney disease Atracurium or Cis-atracurium
MR for endotracheal intubation Succinylcholine
 GA : General Anaesthetic
 LA : Local Anaesthetic
 MR : Muscle Relexant

ALI RAZA CHAUDARY (N67)