Pharmacology PYQs

Dr. Priyanka Sachdev

Pharmacodynamics deals with

a. Effect of drugs on body

b. Effect of body on drugs

c. Absorption of drugs

d. Metabolism of drugs
Pharmacodynamics deals with

a. Effect of drugs on body

b. Effect of body on drugs

c. Absorption of drugs

d. Metabolism of drugs
Pharmacodynamics  What the drug does to the body
• Physiological and biochemical effects of drugs

• Their mechanism of action at organ system

Pharmacokinetics  What the body does to the drug

• Absorption

• Distribution

• Biotransformation (metabolism)

• Excretion of the drug

Pharmacokinetics includes study of all except -

a) Absorption

b) Distribution

c) Adverse effects

d) Excretion
Pharmacokinetics includes study of all except -

a) Absorption

b) Distribution

c) Adverse effects

d) Excretion
Pharmacodynamics includes -

a) Drug elimination

b) Drug excretion

c) Drug absorption

d) Mechanism of action
Pharmacodynamics includes -

a) Drug elimination

b) Drug excretion

c) Drug absorption

d) Mechanism of action
Which is the best way to manage a patient present
with aspirin poisoning:

a. Make urine acidic with NH4Cl

b. Make urine alkaline with NaHCO3

c. Treat with N-acetyl cysteine

d. Do gastric lavage
Which is the best way to manage a patient present
with aspirin poisoning:

a. Make urine acidic with NH4Cl

b. Make urine alkaline with NaHCO3

c. Treat with N-acetyl cysteine

d. Do gastric lavage
• Aspirin is an acidic drug; it readily crosses any acidic medium. To
treat this toxicity, make the urine alkaline with NaHCO3.

• Now, this acidic drug can't be reabsorbed from the basic medium, and
it readily gets excreted from the body.
• HA  H+ + A-

• BOH  B + + OH-

• Unionized form  Absorbed

• Ionised form  Excreted
For absorption  Same pH is required

• Weakly acidic drugs  unionize/absorbed more at  acidic Ph (Stomach)

• Weakly basic drugs  unionize/absorbed more at  basic pH (intestine)

For excretion  Opposite pHis required

• Weakly acidic drugs  ionize/excreted more at  basic pH (Alkaline urine)

• Weakly basic drugs  ionize/excreted more at  acidic pH (Acidic urine)

Remember

• Alkalinization of urine  done by IV infusion of sodium bicarbonate

• Acidification of urine  done by IV infusion of arginine hydrochloride

followed by ammonium chloride (NH4Cl)
Acidic drug is more ionized at –

a) Alkaline

b) Acidic pH

c) Neutral pH

d) None
Acidic drug is more ionized at –

a) Alkaline

b) Acidic pH

c) Neutral pH

d) None
About acidic drug true is -

a) Best absorbed in acidic medium

b) Best absorbed in alkaline medium

c) Not absorbed in acidic medium

d) Binds to alpha glycoprotein

About acidic drug true is -
a) Best absorbed in acidic medium

b) Best absorbed in alkaline medium

c) Not absorbed in acidic medium

d) Binds to alpha glycoprotein

Acetyl salicylate & phenobarbitone are better
absorbed from stomach because they are-
a) Weak acids remain non-ionic in gastric pH

b) Weak acids remain ionic in gastric pH

c) Strong acids fully ionised in gastric pH

d) Weak bases which are ionised at gastric pH

Acetyl salicylate & phenobarbitone are better
absorbed from stomach because they are-
a) Weak acids remain non-ionic in gastric pH

b) Weak acids remain ionic in gastric pH

c) Strong acids fully ionised in gastric pH

d) Weak bases which are ionised at gastric pH

Alkalinization of urine is done for:

(a) Weak acid drugs

(b) Weak basics drugs

(c) Strong acidic drugs

(d) Strong basic drugs

Alkalinization of urine is done for:

(a) Weak acid drugs

(b) Weak basics drugs

(c) Strong acidic drugs

(d) Strong basic drugs

All are prodrug EXCEPT:

a. Aspirin

b. Levodopa

c. Dipivefrin

d. Captopril
All are prodrug EXCEPT:

a. Aspirin

b. Levodopa

c. Dipivefrin

d. Captopril
 PRODRUGS
All – ACE inhibitors (except captopril and lisinopril
Prefer – Prednisone
– Proton pump inhibitors
– Proguanil
Doing – Dipivefrine
M – Mercaptopurine
– Methyldopa
– Minoxidil
D – Levo-dopa
In – Irinotecan
Clinical – Cyclophosphamide
– Clopidogrel
– Carbimazole
Subjects – Sulfasalazine
All drugs are metabolized by acetylation EXCEPT:

a. Phenytoin

b. Isoniazid

c. Procainamide

d. Hydralazine
All drugs are metabolized by acetylation EXCEPT:

a. Phenytoin

b. Isoniazid

c. Procainamide

d. Hydralazine
Classification of Biotransformation
1. Nonsynthetic / Phase I / Functionalization reactions

2. Synthetic/ Phase II / Conjugation reactions

Phase I reaction (Non polar  polar)
• Convert parent drug to a more polar metabolite by introducing or
exposing a functional group (chemically reactive group), such as -OH, -
NH7, -SH2, (hydroxyl, amine and thiol respectively)

1. Oxidation

2. Reduction

3. Hydrolysis

4. Cyclization

5. Decyclization
Phase II reaction (Non polar  polar)
• It is coupling between drug and an endogenous hydrophilic substrate such
as glucuronic acid, sulfuric acid etc. to create more polar conjugates
• Thus conjugation enhances drug hydrophilicity.

1. Glucuronide conjugation

2. Glycin conjugation

3. Glutathion conjugation

4. Sulfate conjugation

5. Methylation

6. Acetylation
Acetylation

MNEMONIC- CHIPS – ABC

§ Clonazepam (sedative)
§ Hydralazine (anti HTN)
§ Isoniazid (anti TB)
§ Procainamide (anti-arrhythmic)
§ Sulfonamides (dapsone)
§ Acebutalol, Amrinone, ASA
§ Benzocaine
§ Caffeine
All are enzyme inhibitors EXCEPT:

a. Carbamazipine

b. Cimetidine

c. Valproate

d. Ketoconazole
All are enzyme inhibitors EXCEPT:

a. Carbamazipine

b. Cimetidine

c. Valproate

d. Ketoconazole
 Microsomal enzymes

Induction Inhibition
 Microsomal Enzyme Inhibition
• One drug can competitively inhibit the metabolism of another if it utilizes
same enzyme

• Occurs by direct effect on the enzyme  fast (within hours)

• Precipitate toxicity of object drug

Microsomal Enzyme Induction

• Increase the synthesis of microsomal enzyme protein (cytochrome P-

450 and glucuronyl transferase)

• Many drugs interact with DNA  Slow

• Decreased intensity and duration of action of object drugs

 Hofmann elimination

• Inactivation of the drug in body fluids by spontaneous molecular

rearrangement without the agency of any enzyme

• e.g. Atracurium
Which of the following drug is an enzyme
inducer:

a. Rifampicin

b. Isoniazid

c. Ketokonazole

d. Erythromycin
Which of the following drug is an enzyme
inducer:

a. Rifampicin

b. Isoniazid

c. Ketokonazole

d. Erythromycin
Which is Cyt. P450 inhibitor -

a) Ketoconazole

b) Rifampicin

c) Phenytoin

d) INH
Which is Cyt. P450 inhibitor -

a) Ketoconazole

b) Rifampicin

c) Phenytoin

d) INH
Hofmann elimination is -

a) Inactivation of drug by metabolizing enzyme

b) Unchanged excretion by kidney

c) Excretion in feces

d) Inactivation by molecular rearrangement

Hofmann elimination is -

a) Inactivation of drug by metabolizing enzyme

b) Unchanged excretion by kidney

c) Excretion in feces

d) Inactivation by molecular rearrangement

True about zero order kinetics:

a. Rate of elimination is independent of plasma concentration

b. Rate of elimination is dependent on plasma concentration

c. Clearance of drug is always constant

d. Half-life of drug is constant

True about zero order kinetics:

a. Rate of elimination is independent of plasma concentration

b. Rate of elimination is dependent on plasma concentration

c. Clearance of drug is always constant

d. Half-life of drug is constant

Order of Kinetics

Rate of Elimination α (Plasma Concentration) order

1. Zero order kinetics

2. First order kinetics

Zero order kinetics
Rate of Elimination α (Plasma Concentration)0
(Plasma Concentration) 0 = 1

• Rate of elimination is independent of plasma concentration

• Rate of elimination is constant.

• CL decreases with increase in concentration

• A constant amount of the drug is eliminated in unit time

First order kinetics
• Rate of Elimination α (Plasma Concentration) 1

• Rate of elimination is proportional to plasma concentration for drugs

• CL remains constant

• A constant fraction of the drug present in the body is eliminated in

unit time.
 Zero order kinetics First order kinetics

(Plasma Concentration) 0 = 1 (Plasma Concentration) 1

• Rate of elimination is constant. • Rate of elimination is proportional

to plasma concentration for the
drugs

• CL decreases with increase in

• CL remains constant
concentration

• A constant fraction of the drug

• A constant amount of the drug is
present in the body is eliminated
eliminated in unit time
in unit time.
MNEMONIC

Zero - Zero order kinetics shown by

W - Warfarin
A - Alcohol and Aspirin
T - Theophylline
T - Tolbutamide
Power - Phenytoin
Patients are first enrolled in this phase of clinical trial:

a. Phase 0

b. Phase I

c. Phase II

d. Phase III
Patients are first enrolled in this phase of clinical trial:

a. Phase 0

b. Phase I

c. Phase II

d. Phase III
Phase I first In human Phase II first In patient Phase III multisite trial Phase IV post marketing
surveillance
10-100 participants 50-500 participants A few hundred to a few Many thousands of
thousand participants participants
Healthy volunteers Patient-subjects receiving Patient-subjects receiving Patients in treatment with
experimental drug experimental drug approved drug

Open label Randomized and Randomized and Open label

controlled (can be placebo controlled
controlled); may be (can be placebo
Blinded controlled) or
uncontrolled; may be
blinded
Safety and tolerability Efficacy and dose ranging Confirm efficacy in larger Adverse events,
Population compliance, drug-drug
interactions

1-2 years 2-3 years 3-5 years No fixed duration

Success rate: 50% Success rate: 30% Success rate: 25%-50% -
The site of action of the furosemide is

a. Thick ascending limb of loop of Henle

b. Descending limb of loop of Henle

c. Proximal convoluted tubule

d. Distal convoluted tubule

The site of action of the furosemide is

a. Thick ascending limb of loop of Henle

b. Descending limb of loop of Henle

c. Proximal convoluted tubule

d. Distal convoluted tubule

 DIURETICS

High ceiling Medium efficacy Weak/adjunctive

(Inhibitors of Na+ -K+ -2CI- (Inhibitors of Na+ -CI- diuretics
cotransport) symport)
Carbonic Osmotic
Benzothiadiazines Thiazide-like anhydrase diuretic
inhibitor Mannitol
Hydrochlorothiazide Chlorthalidone
Hydroflumethiazide Metolazone Acetazolamide Isosorbide
Benzthiazide Xipamide Glycerol
Indapamido
Clopamide Potassium sparing diuretics
Furosemide
(Frusemide)
Bumetanide Aldosterone Renal epithelial Na+
Torasemide antagonists
Spironolactone channel inhibitors
Eplerenone Amiloride Triamterene
COLT Pee

Carbonic anhydrase inhibitors  at pct

Osmotic diuretics  at Loop of Henle

Loop diuretics  at ascending loop

Thiazides  at DCT

Potassium-sparing diuretics  at collecting tubules

 DIURETICS

High ceiling Medium efficacy Weak/adjunctive

(Inhibitors of Na+ -K+ -2CI- (Inhibitors of Na+ -CI- diuretics
cotransport) symport)
Carbonic Osmotic
Benzothiadiazines Thiazide-like anhydrase diuretic
inhibitor Mannitol
Hydrochlorothiazide Chlorthalidone
Hydroflumethiazide Metolazone Acetazolamide Isosorbide
Benzthiazide Xipamide Glycerol
Indapamido
Clopamide Potassium sparing diuretics
Furosemide
(Frusemide)
Bumetanide Aldosterone Renal epithelial Na+
Torasemide antagonists
Spironolactone channel inhibitors
Eplerenone Amiloride Triamterene
Arrange the following diuretics according to their
site of action starting from proximal to distal parts
of the nephron.

A. Triamterene B. Hydrochlorothiazide
C. Acetazolamide D. Bumetanide

a. ABCD
b. CDBA
c. DBCA
d. BCAD
Arrange the following diuretics according to their
site of action starting from proximal to distal parts
of the nephron.

A. Triamterene B. Hydrochlorothiazide
C. Acetazolamide D. Bumetanide

a. ABCD
b. CDBA
c. DBCA
d. BCAD Answer: C D B A
Tetracycline inhibits protein synthesis by:

a. Inhibiting initiation and causing misreading of mRNA

b. Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

c. Inhibiting peptidyl transferase activity

d. Inhibiting translocation
Tetracycline inhibits protein synthesis by:

a. Inhibiting initiation and causing misreading of mRNA

b. Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

c. Inhibiting peptidyl transferase activity

d. Inhibiting translocation
Mechanism of action

1. Inhibit cell wall synthesis

2. Cause leakage from cell membranes

3. Inhibit protein synthesis

4. Interference with nucleic acid synthesis

STEPS OF TRANSLATION
INITIATION
Attachment of new aminoacyl
tRNA on A site
Peptide bond formation between
the newly attached aminoacid and
the nascent peptide chain
Transfer of peptide chain from
P site
The ribosome move along the mRNA to expose
the next codon.

Translocation of the elongated peptide chain

back from ‘A’ site to ‘P’ site
Protein synthesis inhibitors

1. Tetracyclines

2. Chloramphenicol

3. Aminoglycoside

4. Macrolide Antibiotics (Erythromycin)

INITIATION
Attachment of new aminoacyl
tRNA on A site
Peptide bond formation between
the newly attached aminoacid and
the nascent peptide chain

Transfer of peptide chain from

P site
The ribosome move along the mRNA to expose
the next codon.

Translocation of the elongated peptide chain back

from ‘A’ site to ‘P’ site
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction

Classification

Spectrum

MOA

Resistance

Adverse
effects

Uses
Tetracyclines

• Have nucleus of four cyclic rings

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction

Classification

Spectrum

MOA

Resistance

Adverse
effects

Uses
Classification
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction

Classification

Spectrum

MOA

Resistance

Adverse
effects

Uses
 Spectrum
1. All gram positive and gram negative Cocci

2. All gram positive and gram negative Bacilli

3. Spirochetes, including T. pallidum and Borrelia

4. Rickettsiae (typhus, etc.) and chlamydiae

5. Mycoplasma and Actinomyces

6. Protozoa like Entamoeba histolytica and Plasmodia

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction
I
Classification II
III
+c
-c S |R | M| P
Spectrum +b
-b

MOA

Resistance

Adverse
effects

Uses
 Mechanism of action
• Inhibit protein synthesis
 Tetracyclins enters inside bacteria

Binds to 30S ribosomes

Interfered with attachment of new aminoacyl t-RNA to acceptor (A) site of

mRNA-ribosome complex

Peptide chain fails to grow

Bacteriostatic
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction
I
Classification II
III
+c
-c S |R | M| P
Spectrum +b
-b
-30s
MOA X new tRNA on A-site
-bS

Resistance

Adverse
effects

Uses
Adverse Effects
L.K. ADVanI is P.T. teacher
L- liver damage
K- kidney damage
A- Antianabolic effect
D- Diabetis insipidus
V- Vestibular toxicity
I- Intracranial pressure raised
P- Phototoxicity
T- Teeth and bones

T- Teratogenic
 Uses

Tetracyclines are the first choice drugs:

VACUuM The BedRoom

Vibrio cholera
Acne
Chlamydia, LGV, Granuloma inguinale
Ureaplasma urealyticum
Mycoplasma pneumonae

Tularemia/ Plague

Borrelia burgdorferi (Relapsing fever)

Rickettsia
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction
I
Classification II
III
+c
-c S |R | M| P
Spectrum +b
-b
-30s
MOA X new tRNA on A-site
-bS

Resistance

Adverse
LK ADVanI PT
effects

Uses VACUM BR Too

 Chloramphenicol

• Nitrobenzene moiety  responsible for antibacterial activity

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2

I
Classification II -
III
+c
-c S |R | M| P
Spectrum +b
-b
-30s
MOA X new tRNA on A-site
-bS

Resistance

Adverse
LK ADVanI PT
effects

Uses VACUM BR Too

 Spectrum
1. All gram positive and gram negative Cocci

2. All gram positive and gram negative Bacilli

3. Spirochetes, including T. pallidum and Borrelia

4. Rickettsiae (typhus, etc.) and chlamydiae

5. Mycoplasma and Actinomyces

6. Protozoa like Entamoeba histolytica and Plasmodia

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2

I
Classification II -
III
+c
-c S |R | M| P
Spectrum +b
Same
-b
-30s
MOA X new tRNA on A-site
-bS

Resistance

Adverse
LK ADVanI PT
effects

Uses VACUM BR Too

 Mechanism of action
• Inhibit protein synthesis
 Chloramphenecol enters inside bacteria

Attaches to 50S ribosome

Prevents peptide bond formation between newly attached aminoacid

and nascent peptide chain

Interferes with transfer of peptide chain from P site

Inhibits bacterial protein synthesis

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2

I
Classification II -
III
+c
-c S |R | M| P
Spectrum +b
Same
-b
-30s -50S
MOA X new tRNA on A-site X P-P bond formation
-bS -bs

Resistance

Adverse
LK ADVanI PT
effects

Uses VACUM BR Too

Adverse effects

BIG Super Hypersensitivity

 Uses
Highly restricted due to fear of fatal toxicity

BARE TB
B - Bacterial meningitis/Pyogenic meningitis
A - Anaerobic infections
R - Ricketsia infection
E - Ear & Eye infection(conjunctivitis, endophthalmitis)
T - Typhoid
B - Brucellosis
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2

I
Classification II -
III
+c
-c S |R | M| P
Spectrum +b
Same
-b
-30s -50S
MOA X new tRNA on A-site X P-P bond formation
-bS -bs

Resistance

Adverse
LK ADVanI PT BIG Super H
effects

Uses VACUM BR Too BARE TB

Aminoglycosides

• Have amino groups linked glycosidically to two or more aminosugar

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Classification II -
III
+c
-c S |R | M| P
Spectrum +b
Same
-b
-30s -50S
MOA X new tRNA on A-site X P-P bond formation
-bS -bs

Resistance

Adverse
LK ADVanI PT BIG Super H
effects

Uses VACUM BR Too BARE TB

Classification

Systemic aminoglycosides (TANGSS KP)

Streptomycin Amikacin
Gentamicin Sisomicin
Kanamycin Netilmicin
Tobramycin Paromomycin

Topical aminoglycosides
Neomycin Framycetin
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same
-b
-30s -50S
MOA X new tRNA on A-site X P-P bond formation
-bS -bs

Resistance

Adverse
LK ADVanI PT BIG Super H
effects

Uses VACUM BR Too BARE TB

Spectrum

Gram negative aerobic Bacilli

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S
MOA X new tRNA on A-site X P-P bond formation
-bS -bs

Resistance

Adverse
LK ADVanI PT BIG Super H
effects

Uses VACUM BR Too BARE TB

Mechanism of Action
• Inhibit protein synthesis
Transport of aminoglycoside through bacterial cell wall and cytoplasmic
membrane (transport mechanism)

Binds to ribosomes 30S subunit, 50 subunit, 30S-50S interface

freeze initiation of protein synthesis

Prevent polysome formation

Distortion of mRNA codon recognition resulting in misreading of code

Inhibit protein synthesis  Bacteriostatic action

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H
effects

Uses VACUM BR Too BARE TB

Adverse effects

ONN HT
1. Ototoxicity

2. Nephrotoxicity

3. Neuromuscular blockade

4. Hypersensitivity reactions

5. Teratogenic
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
Uses
• For gram negative infections  UTI, meningitis, pneumonia, peritonitis,
burn, osteomyelitis, sepsis — gentamicin, sisomicin, tobramycin,
amikacin and netilmicin.

• For tuberculosis  streptomycin, kanamycin, amikacin, netilmicin.

• For intestinal amoebiasis and tape worm  paramomycin.

• For topical application (for infected wound, ulcers, burn, external ear
infections, conjunctivitis )  neomycin, framycetin
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
 Macrolide Antibiotics

• Have a macrocyclic lactone ring with attached sugars

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar Sugars

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
Classification

1. Erythromycin

2. Roxithromycin

3. Clarithromycin

4. Azithromycin

5. Spiramycin

• Immunosuppressant drug tacrolimus is also a macrolides

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar Sugars

I
Systemic
Classification II -
Topical
III
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic)
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
Spectrum

All bacterias except Gram negative Bacilli

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar Sugars

I
Systemic
Classification II -
Topical
III
+c
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic) -c -b
+b
-b
-30s -50S - 30S, 50S, 30+50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread
-bS -bs - bs & bc

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
 Mechanism of action

• Inhibit protein synthesis

 Erythromycin bind to 50S ribosome

Hinder translocation of elongated peptide chain back from ‘A’ site to ‘P’ site

Ribosome does not move along mRNA to expose next codon

Peptide synthesis prematurely terminated

 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar Sugars

I
Systemic
Classification II -
Topical
III
+c
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic) -c -b
+b
-b
-30s -50S - 30S, 50S, 30+50S -50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread X Translocation
-bS -bs - bs & bc - bs

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT
effects
-
-
Uses VACUM BR Too BARE TB
Adverse effects
MACRO
M - Motilin receptor agonists
A - Allergy
C - Cholestasis
R Reversible
O Ototoxicity
USES

CLAW

C - Chancroid by Haemophilus ducreyi (Azithromycin single dose),

Corynebacterium (diptheria). Campylobacter
L - Legionella infections
A - Atypical pneumonia
W - Whooping cough by Bordetetla pertussis
 Tetracyclin Chloramphenicol Aminoglycosides Erythromycin

Introduction NO2 NH2 - Sugar Sugars

I
Systemic
Classification II -
Topical
III
+c
+c
-c S |R | M| P
Spectrum +b
Same -b (aerobic) -c -b
+b
-b
-30s -50S - 30S, 50S, 30+50S -50S
MOA X new tRNA on A-site X P-P bond formation X Initiation – misread X Translocation
-bS -bs - bs & bc - bs

Resistance

Adverse
LK ADVanI PT BIG Super H ONN HT MACRO
effects
-
-
Uses VACUM BR Too BARE TB CLAW
Which of the following is a side effect of streptomycin?

a. Phototoxicity
b. Hepatotoxicity
c. Ototoxicity
d. All of the above
Which of the following is a side effect of streptomycin?

a. Phototoxicity
b. Hepatotoxicity
c. Ototoxicity
d. All of the above
Tetracycline inhibits protein synthesis by-

a) Inhibiting initiation and causing misreading of mRNA

b) Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

c) Inhibiting peptidyl transferase activity

d) Inhibiting translocation
Tetracycline inhibits protein synthesis by-

a) Inhibiting initiation and causing misreading of mRNA

b) Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

c) Inhibiting peptidyl transferase activity

d) Inhibiting translocation
Tetracyclines inhibit protein synthesis by acting on-

a) 30-S ribosome

b) 50-S ribosome

c) Both 30-S & 50-S ribosome

d) 60-S ribosome
Tetracyclines inhibit protein synthesis by acting on-

a) 30-S ribosome

b) 50-S ribosome

c) Both 30-S & 50-S ribosome

d) 60-S ribosome
Gray baby syndrome is caused by

a) Penicillin

b) Chloramphenicol

c) Rifampicin

d) Erythromycin
Gray baby syndrome is caused by

a) Penicillin

b) Chloramphenicol

c) Rifampicin

d) Erythromycin
Which of the following aminoglycosides is not
available for parenteral use?

a) Sisomycin

b) Amikacin

c) Framycetin

d) Gentamycin
Which of the following aminoglycosides is not
available for parenteral use?

a) Sisomycin

b) Amikacin

c) Framycetin

d) Gentamycin
Which of the follwing is a side effect of streptomycin?

a) Phototoxicity

b) Hepatotoxicity

c) Ototoxicity

d) All of the above

Which of the follwing is a side effect of streptomycin?

a) Phototoxicity

b) Hepatotoxicity

c) Ototoxicity

d) All of the above

Which of the following drugs acts on “motilin receptors

a) Erythromycin

b) Tetracycline

c) Norfloxacin

d) Chloramphenicol
Which of the following drugs acts on “motilin receptors

a) Erythromycin

b) Tetracycline

c) Norfloxacin

d) Chloramphenicol
Which of the following is a side effect of sulfonamide-

a. Constipation

b. Joint pain

c. Crystalluria

d. Hyperkalemia
Which of the following is a side effect of sulfonamide-

a. Constipation

b. Joint pain

c. Crystalluria

d. Hyperkalemia
Mechanism of action

1. Inhibit cell wall synthesis

2. Cause leakage from cell membranes

3. Inhibit protein synthesis

4. Interference with nucleic acid synthesis

 Sulfonamides Trimethoprim Quinolones

Introduction

Classification

Spectrum

MOA

Resistance

Adverse
effects

Uses
 Classification

1. Short acting - Sulfadiazine ,Sulfisoxaxole, Sulfamethizole, Sulfacystine.

2. Intermediate acting-Sulfamethoxazole.

3. Long acting-Sulfadoxine, Sulfamethopyrazine.

4. Topical Sulfonamides-Sulfacetamide sodium ,Mafenide, silver

sulfadiazine

5. Sulfonamide for RA and ulcerative colitis - Sulfasalazine.

Mechanism of action:
 Cotrimoxazole

• Combination of sulfamethoxazole and trimethoprim in a ratio of 5:1 to

provide a blood level in ratio of 20:1.

• This occurs because trimethoprim has a larger volume of distribution

than Sulfamethoxazole and attains lower plasma concentration
Adverse Effects of Sulfonamides

ABC of RASH

A - Aplastic anemia
B - Bilirubin displacement (kernicterus)
C - Crystalluria
R - Rash/Hypersensitivity (MC side effect)
A - Acetylation
S - SLE
H - Hemolysis in G-6-PD deficiency
 Adverse Effects of Trimethoprim

• Nausea, vomiting, stomatitis, headache and Rashes

• Megaloblastic Anemia  Due to folate deficiency

• Bone marrow toxicity Pancytopenia

• Hyperkalemia ( due to amiloride like action , amiloride is a Potassium

sparing diuretic ).

• Teratogenic  Neonatal haemolysis and methaemoglobinaemia can

occur if it is given near term.
Uses

SEPTRAN

• S - STD’s (Chancroid, LGV)

• E - Enteritis (E.coli, Shigella)

• P-PC , PJ

• T – Typhoid (Bacterial diarrhoeas and dysentery)

• R-RTI

• A - Acute uncomplicated UTI

• N - Nocardia
 Sulfonamides Trimethoprim Quinolones
Introduction -SO2 NH2 - 5:1 Quinolones
- 20:1  Synergistic
Classification Short – - 1st
Int. – -2nd
Long – -3rd
Topical – -4th
Spectrum – – 1st → gm-
– – 2nd → ex. gm-
– – 3rd → ex gm- & gm+
– – 4th → ex gm-, gm+,
anaerobes
MOA – FS – DHFR – DNA gyrase
– Topoisomerase IV
Adverse ABC of RASH - N/v GIT Photo
effects - Meg. Anemia CNS QT ↑
- BM tox. Bone DST Treating
- Mk
-Teratogenical
Uses SEPTRAN SEPTRAN 4G SPECRUM CT
Which of the following fluoroquinolone has broadest spectrum
activity against bacteria -

a. Ciprofloxacin

b. Norfloxacin

c. Trovafloxacin

d. Nalidixic acid
Which of the following fluoroquinolone has broadest spectrum
activity against bacteria -

a. Ciprofloxacin

b. Norfloxacin

c. Trovafloxacin

d. Nalidixic acid
 First generation

Moderate gram negative antimicrobial activity

1. Nalidixic acid
2. Oxalinic acid
Second generation

• Expanded gram negative activity with limited or no activity on gram

positive.

• Class I  Norfloxacin, lomefloxacin

• Class II  Ciprofloxacin, ofloxacin
 Third generation

• Expanded gram negative activity, additionally gram positive activity.

• Levofloxacin
• Spatfloxacin
• Gatifloracin
• Pefloxacin
• Temafloxacin
• Tosufloxacin
• Moxifloxacin
Fourth generation

• Maximally improved gram positive activity with retained

expanded gram negative activity and also have anaerobic
antimicrobial activity.

• Broadest spectrum

1. Trovafloxacin
2. Fleroxacin
3. Gamifloxacin
4. Prulifloxacin
5. Sitafloxacin
6. Clinafloxacin
 FQ
FQs bind to A subunit of DNA gyrase

Interfere with its strand cutting and

resealing function

Blockage of unwiding of double stranded

DNA during replication or transcription

Prevents replication or transcription

Adverse effects
1. GIT  Most common  Nausea, vomiting,Diarrhea.

2. CNS  due to GABA antagonistic action  Headaches, dizziness, sleep

disorders, mood changes and seizures.

3. Bone, soft tissue  tendonitis with risk of tendon rupture

contraindicated in children.

4. Phototoxicity  lomefloxacin (maximum), sparfloxacin and pefloxacin

5. Torsades de pointes  can prolong QT interval Sparfloxacin,

gatifloxacin and moxifloxacin

6. Teratogenicity
Uses

4G SPECTRUM CT

4G: Gonorrhoea, Gastroenteritis , gynaecological infections, Gram -ve

Infections
S: Septicemia
P: Prophylaxis
E: Enterocolitis
C: Chancroid
T: Typhoid
R: RTI
U: UTI
M: Meningitis
C: Conjunctivitis
T: Tuberculosis
 Sulfonamides Trimethoprim Quinolones
Introduction -SO2 NH2 - 5:1 Quinolones
- 20:1  Synergistic
Classification Short – - 1st
Int. – -2nd
Long – -3rd
Topical – -4th
Spectrum – – 1st → gm-
– – 2nd → ex. gm-
– – 3rd → ex gm- & gm+
– – 4th → ex gm-, gm+,
anaerobes
MOA – FS – DHFR – DNA gyrase
– Topoisomerase IV
Adverse ABC of RASH - N/v GIT Photo
effects - Meg. Anemia CNS QT ↑
- BM tox. Bone DST Treating
- Mk
-Teratogenical
Uses SEPTRAN SEPTRAN 4G SPECRUM CT
Which one of the anti-tubercular drug may precipitate goat -

a. Pyrazinamide

b. Rifempicin

c. Streptomycin

d. Isoniazid
Which one of the anti-tubercular drug may precipitate goat -

a. Pyrazinamide

b. Rifempicin

c. Streptomycin

d. Isoniazid
 ANTITUBERCULAR DRUGS

First line drugs Second line drugs

Isoniazide
Rifamcin
Pyrazinamide Fluoroquinolones Other oral Injectable
Ethambutol drugs drugs
Ofloxacin
Streptomycin
Levofloxacin Ethionamide Kanamycin
Moxifloxacin Prothionamide Amikacin
Ciprofloxacin Cycloserine Capreomycin
Terizidone
Paraaminosalicy
lic acid (PAS)
Rifabutin
Thiacetazone
 H R Z E S

INTRO

MOA

RESISTANCE

PK

ADVERSE
EFFECTS
Drug Bactericidal/ Hepatotoxicity Bacteria Inhibited
Bacteristatic

Isoniazid Cidal + Both

Rifampicin Cidal + Both

Pyrazinamide Cidal ++++ Intra

Ethambutol STATIC - No Both

Streptomycin Cidal - No Extra

Galactose Arabinose Acetyl Co-A

FAS-1

Fatty acid chain

Arabinosyl transferase

Arabinogalactan FAS-2

Mycolic acid

Mycobacterial Cell Wall

 Isoniazid
• Bacteriostatic against resting and bactericidal against rapidly
multiplying organisms.

• It is effective against intra- as well as extra-cellular mycobacteria.

• Drug of choice for TB

• Drug of choice for prophylaxis of tuberculosis

• Anti-tubercular drug which make the patient non-infectious earliest is

INH
Galactose Arabinose Acetyl Co-A

FAS-1

Fatty acid chain

Arabinosyl transferase

Arabinogalactan FAS-2

Mycolic acid

Mycobacterial Cell Wall

Adverse effects

1. Hypersensitivity reactions

2.Peripheral neuritis  Due to interference with production of the

active coenzyme pyridoxal phosphate from pyridoxine

3. Hepatitis

4. Hemolysis in patients with deficiency of G6PD

 Rifampin

• Bactericidal

• Action is most marked against slow and intermittent multipliers

• Both extra- and intracellular organisms are affected

• Most potent sterilising antitubercular drug  fastest to kill all bacilli

in the lesion.
Drug Bactericidal/ Hepatotoxicity Bacteria Inhibited
Bacteristatic

Isoniazid Cidal + Both

Rifampicin Cidal + Both

Pyrazinamide Cidal ++++ Intra

Ethambutol STATIC - No Both

Streptomycin Cidal - No Extra

 Rifampin inhibits rpoB gene

rpoB gene codes DNA-dependent RNA polymerase

So it is inhibited

Interrupts RNA synthesis of mycobacterium

Adverse effects
1. Urine and secretions may become orange-red— but this is
harmless.

2. Hepatitis: chronic alcoholics and patient with old age or chronic

liver disease are more prone for it.

3. Flu like syndrome with fever, chills, and myalgia

4. Blood dyscrasias
 Pyrazinamide

• Weakly tuberculocidal and more active in acidic medium

• Effective only against intracellular bacteria

Drug Bactericidal/ Hepatotoxicity Bacteria Inhibited
Bacteristatic

Isoniazid Cidal + Both

Rifampicin Cidal + Both

Pyrazinamide Cidal ++++ Intra

Ethambutol STATIC - No Both

Streptomycin Cidal - No Extra

Galactose Arabinose Acetyl Co-A

FAS-1

Fatty acid chain

Arabinosyl transferase

Arabinogalactan FAS-2

Mycolic acid

Mycobacterial Cell Wall

 Adverse effects
1. Hepatic damage  Pyrazinamide is most hepatotoxic
antitubercular drug

2. Decrease urate excretion  Hyperuricaemia (Gout can occur)

3. Arthralgia, anorexia, nausea, vomiting dysuria.

 Ethambutol
• Bacteriostatic effect

• Least toxic antibutercular drug

Drug Bactericidal/ Hepatotoxicity Bacteria Inhibited
Bacteristatic

Isoniazid Cidal + Both

Rifampicin Cidal + Both

Pyrazinamide Cidal ++++ Intra

Ethambutol STATIC - No Both

Streptomycin Cidal - No Extra

Galactose Arabinose Acetyl Co-A

FAS-1

Fatty acid chain

Arabinosyl transferase

Arabinogalactan FAS-2

Mycolic acid

Mycobacterial Cell Wall

 Adverse effects

• 1. Optic neuritis/ Retrobulbar neuritis  Decrease visual acuity and loss

of ability to differentiate red from green, hence it may produce green
vision  Reversible.

• 2. Increases blood urate because of decrease renal excretion

• 3. Rashes, drug fever, GI upset and pruritus.

• 4. CNS: Headache, dizziness, confusion, disorientation, hallucination,

arthralgia.
 Streptomycin
• First antitubercular drug

• Now being advocated for a shift to second line drug in view of toxicity
and less effectiveness

• It is tuberculocidal

• Acts only on extracellular bacilli

Drug Bactericidal/ Hepatotoxicity Bacteria Inhibited
Bacteristatic

Isoniazid Cidal + Both

Rifampicin Cidal + Both

Pyrazinamide Cidal ++++ Intra

Ethambutol STATIC - No Both

Streptomycin Cidal - No Extra

 Transport of the aminoglycoside through bacterial cell wall and
cytoplasmic membrane (transport mechanism)

Binds to ribosomes 30S subunit, 50 subunit, 30S-50S interface

Freeze initiation of protein synthesis

Prevent polysome formation and promote their disaggregation to
monosomes
Causes distortion of mRNA codon recognition resulting in misreading of
the code (wrong amino acids are entered in the peptide chain)

Inhibit protein synthesis

Bacteriostatic
Adverse effects MNEMONIC

ONN HT
1. Ototoxicity
2. Nephrotoxicity
3. Neuromuscular blockade
4. Hypersensitivity reactions
5. Teratogenic
Mycobacteria Most effective drug

1. Rapidly growing (wall of cavitary lesion) H

2. Slow growing (intracellular) Z

3. Spurters (within caseous material) R

Enalapril is contraindicated in all of the following
conditions except:

a. Diabetic nephropathy with albuminuria

b. Single kidney

c. Bilateral renal artery stenosis

d. Hyperkalemia
Enalapril is contraindicated in all of the following
conditions except:
a. Diabetic nephropathy with albuminuria

b. Single kidney

c. Bilateral renal artery stenosis

d. Hyperkalemia
DRUGS

ACE inhibitors
- Captopril
- Enalapril
- Lisinopril
- Perindopril
- Ramipril
- Fosinopril
- Quinapril
- Trandolapril
 Decrease BP

Decrease renal perfusion pressure

Renin is produced by juxtaglomerular cells of kidney

Renin acts on – Angiotensinogen (α2 globulin synthesized by the liver) and breaks
it into a Angiotensin-I (decapeptide)

Angiotensin-I is converted to Angiotensin-II (octapeptide) by ACE (present in

luminal surface of vascular endothelium)
 Decrease BP

Angiotensinogen (α2 globulin synthesized by the liver)

Renin (kidney)

Angiotensin-I (decapeptide)

ACE (lung)

Angiotensin-II (octapeptide)

Angiotensin-III (heptapeptide)

Angiotensin-IV (hexapeptide)
ACE secreated from lung also convert Kinins (bradykinin) and
substance P into inactive products.

Bradykinin and substance P

ACE

Inactive products
 Angiotensinogen
Renin

Angiotensinogen I Bradykinin

Ace

Angiotensinogen II Inactive Products

AT2 AT1
Aldosterone
Receptor Receptor
 Home Care Makes Patients Definitely Strong

Home  Hypertension

Care  CHF

Makes  MI

Patients  Prophylaxis in high cardiovascular risk

Definitely  Diabetic nephropathy

Strong  Scleroderma crisis

 ACE inhibitor side effects
(CAPTOPRIL)
C - Cough
A - Angioneurotic oedema
P - Proteinuria
T - Taste disturbance/ Teratogenic in 1st trimester
O - Other (fatigue, headache)
P - Potassium increased
R - Renal impairment
I - Itch
L - Loui BP (1st dose)
Contraindications

PARK
1. Pregnancy
2. Allergy or hypersensitivity
3. Bilateral renal artery stenosis,
4. Hyperkalaemia