6 Pharmacology

AIIMS NOVEMBER 2017 8. A diabetic and hypertensive patient taking several drugs
comes to you with Sr. Creatinine value 5.7mg/dl. Which of
1. Drug of choice for Insomnia in blind people is? the following drug should be immediately stopped?
a. Latanoprostene b. Zerviate a. Metformin
c. Tasimelteon d. Ramelteon b. Metoprolol
2. A patient in labour ward was given opioid analgesic. Which c. Insulin
d. Linagliptin

/e
drug should be kept ready for emergency?
a. Atropine b. Naloxone 9. A morbidly obese diabetic woman was on failed metformin
c. Lignocaine d. Fentanyl

,2
therapy. She has a history of Pancreatitis and family history
3. The most important mechanism of antibiotic resistance in of bladder cancer. Patient does not want to take injections.
biofilms is? Which of the following would be suitable to reduce her


a. Increased adhesion
b. Increased efflux of antibiotic

sy glucose levels?
a. Sitagliptin
b. Pioglitazone
Ea
c. Low mitotic rate
d. Decreased diffusion of antibiotic c. Canagliflozin
d. Liraglutide
4. What instructions you would give to a lactating mother
ed

regarding drug usage? 10. A person on antitubercular treatment taking following

a. Breastfed child just before taking next dose, when plasma drugs develops tingling sensation. Which of the following is
concentration of drug is least added to the regimen?
M

b. Give longer half lives drug to her •• Rifampicin: 15 mg/kg/d (10 to 20 mg/kg/day)
c. No advice as most of drugs are excreted negligibly in breast milk •• Isoniazid: 10 mg/kg/d (10 to 15 mg/kg/day)
d. Tell the mother to breastfeed when the drug is least efficacious •• Pyrazinamide: 35 mg/kg/d (30 to 40 mg/kg/day)
S

•• Ethambutol 20 mg/kg/d (15 mg to 25 mg/kg/d)

5. Mechanism of action of Vancomycin is?
IM

a. Folic acid
a. Cell membrane inhibition
b. Cobalamine
b. Cell wall synthesis inhibition
c. Pyridoxine
c. Peptide synthesis inhibition
AI

d. Thiamine
d. 50s Ribosome inhibition
11. Ceftriaxone is available in vial of 5 ml in concentration of
6. Which of the following is a placebo?
500 mg. You have to give 180 mg of drug to patient with
a. Sham Surgery
a syringe of 2ml having 10 divisions per ml. How many
b. Herbal medication with no effect known
divisions need to be given?
c. Physiotherapy
a. 1.8 b. 18
d. Cognitive Behavioural therapy
c. 20 d. 2
7. A new drug and a placebo was given to compare their action.
12. Drug that decrease size of prostate is?
Following data was obtained. Action of new drug can be
a. Flutamide b. Tamsulosin
described best as?
c. Finasteride d. Sildenafil
Drug Heart rate Cardiac output SBP DBP
13. A friend of yours is going on a hill station trip next morning
Placebo 72 5 110 80 and he had history of motion sickness. He asked you for
New drug 86 6 150 68 prescribing some drug. What would you prescribe?
a. Dimenhydrinate 1 hour before journey
a. M2 agonist and M3 agonist b. Ranitidine one night before and 1 hour before trip
b. Alpha 1 antagonist and beta 1 agonist c. Omeprazole one hour before trip
c. Alpha 1 agonist and beta 1 agonist d. Scopolamine transdermal patch a night before
d. Beta 1 agonist and beta 2 agonist

14. A patient presented with pain in the right lower quadrant
of abdomen. He has history of renal stones in right kidney.
He was prescribed an opioid which is partial agonist at mu
receptors and antagonist at kappa receptors. The likely drug
given was?
a. Pentazocin
b. Tramadol
c. Buprenorphine
d. Fentanyl
15. A patient come with acute exacerbation of bronchial asthma.
Salbutamol inhalation was given and no improvement
was noticed. Hence, Intravenous corticosteroids and
Aminophylline was added and condition improved. What is
the mechanism of action of corticosteroids in this condition?
a. They increase bronchial responsiveness to salbutamol
b. They cause direct bronchodilation when used with
xanthenes
c. They increase mucociliary clearance
d. They indirectly increases effectivity of xanthines on
adenosine receptors
AIIMS MAY 2017
16. Drug of choice for prophylaxis of Pneumocystis jirovecii in
an immunocompromised patient is?
Ea
a. Cotrimoxazole
b. Amoxycillin
c. Dexamethasone
d. Cephalosporin
ed
17. Mechanism of action of protease inhibitors is?
a. It inhibits translation
M
b. It inhibits assembly of virus protein
c. It inhibits proviral RNA synthesis
d. Inhibits conversion of RNA to DNA
S
18. A 40-year-old patient came with complaints of spikes of
IM
fever and difficulty in breathing. Transesophageal echo
found out vegetations in the heart. The culture showed
positive for Burkholderia cepacia. Which of the following is
AI
the first line management? Drug of choice for Burkholderia
cepacia pneumonia is?
a. Aminoglycosides and colistin
b. Carbapenems and 3rd generation cephalosporins
c. Tigecycline and cefepime
d. Cotrimoxazole with 3rd generation cephalosporin
19. Storage of drug in the tissues is suggested by?
a. Small volume of distribution
b. Large volume of distribution
c. Excretion in urine
d. Excretion in saliva
20. A patient came with complaints of high grade fever and
altered sensorium. He was diagnosed to be suffering from
meningococcal meningitis. Which of the following is the
most appropriate empirical treatment option? Empirical
drug of choice for treatment of meningococcal meningitis
a. Ceftriaxone b. Gentamycin
c. Cefepime d. Cefoxitin
AIIMS Nov 2013–May 2011
Questions with Explanations Covered in Volume II (Available Separately)
PHARMACOLOGY  • Questions 307
21. An epileptic adult man is on levetiracetam therapy 1 g BD.
He is seizure free for 2 years. Now, he started developing
irritability and lability of mood that is affecting his daily
life. What should the doctor do?
a. Stop levetiracetam therapy suddenly
b. Taper the drug over 6 months
c. Continue the medication for another 3 years
d. Stop levetiracetam and start another antiepileptic
22. A 70-year-old patient has diabetes mellitus and hypertension.
He presents with renal failure and does not want to take
insulin. Which antidiabetic drug will you prefer in this
patient that does not require dose modification in renal
disease?
a. Linagliptin b. Vildagliptin
c. Exenatide d. Repaglinide
23. All are idiosyncratic reactions to Carbamazepine EXCEPT:
a. Rash
/e
b. Steven Johnson syndrome
c. Blurred vision
,2
d. Agranulocytosis
24. Components of lente insulin is?
a. 30% amorphous + 70% crystalline
sy
b.
c.
30% crystalline + 70% amorphous
Same as NPH insulin
d. Only 70% amorphous
25. Mechanism of action of Oseltamivir is?
a. Neuraminidase inhibitor
b. Blocks viral M2 protein
c. Fusion inhibitor
d. RNA dependent DNA polymerase inhibitor
26. Antidote for overdose of fibrinolytic therapy is?
 (AIIMS May 2017, Nov 2015)
a. Heparin b. Epsilon amino caproic acid
c. Protamine d. rTPA
27. A drug X was administered by continuous IV infusion at the
rate of 1.6 mg/min. Clearance of drug X is 640 ml/min. If
the t1/2 of the drug is 1.8 hours, what would be the plasma
concentration of drug after achieving steady state?
a. 2.5 mg/L b. 5 mg/L
c. 7.5 mg/L d. 10 mg/L
28. A patient was administered 200 mg of a drug. 75 mg of the
drug is eliminated from the body in 90 minutes. If the drug
follows first order kinetics, how much drug will remain after
6 hours?
a. 12.5 mg b. 25 mg
c. 30 mg d. 50 mg
29. A 60-year-old patient who had myocardial infarction 2 weeks
back with TG- 262 mg/dl, LDL- 124 mg/dl, HDL - 32 mg/dl.
Which of the following will you use?
a. Atorvastatin 80 mg
b. Rosuvastatin 10 mg
c. Rosuvastatin + Fenofibrate
d. Fenofibrate
PHARMACOLOGY
312 Section I  •  Subject-wise MCQs and Answers with Explanations
115. All are true about Methadone EXCEPT:
a. Used in chronic pain
b. Mu receptor agonist
c. Onset in IV route is 30-60 min and oral route is 90-120 min
d. Onset of action quicker in IV route
ANSWERS WITH EXPLANATIONS
AIIMS NOVEMBER 2017
1. Ans. (c)  Tasimelteon
Ref: Sleep Medicine by Nick Antic 1st Ed Ch 35; Manual of
Clinical Psychopharmacology
By Alan F. Schatzberg 8th Ed
•• Given the inability of light to treat insomia in the blind, an
alternative therapy is required that will entrain the circadian
clock, and therefore the sleep/wake cycle.
•• Both melatonin and a melatonin agonist have been shown
to reset the circadian clock in the totally blind.
•• Tasimelteon is a melatonin MT1/MT2 agonist and is safe
and effective.
•• Ramelteon (Rozerem) is a specific melatonin MT1/MT2
Ea
receptor agonist that was approved in 2005 as the first FDA-
approved hypnotic that is not a controlled substance.
•• In 2014, a second MT1/MT2 agonist, tasimelteon, was
ed
approved for the treatment of non-24-hour sleep-wake
disorder in totally blind individuals. While not approved
for other forms of insomnia, tasimelteon has a clinical
M
profile similar to that of ramelteon.
2. Ans. (b)  Naloxone
S
Ref: K.D Tripathi 7th Ed Pg 472, 483
IM
•• Apnoea of the newborn may occur when morphine is given
to the mother during labour.
•• The blood-brain barrier of the foetus is undeveloped,
AI
morphine attains higher concentration in foetal brain than
in that of mother.
•• Naloxone 10 μg/kg injected in the umbilical cord is the
treatment of choice.Naloxone is the drug of choice for
morphine poisoning (0.4–0.8 mg i.v. every 2– 3 min: max
10 mg) and for reversing neonatal asphyxia due to opioid
use during labour (10 μg/kg in the cord).
•• It is also used to treat overdose with other opioids and
agonist- antagonists (except buprenorphine).
•• Naloxone (high dose) can prevent buprenorphine effect,
but does not reverse it when given afterwards; does not
precipitate buprenorphine withdrawal; probably because of
more tight binding of buprenorphine to opioid receptors.
3. Ans. (d)  Decrease diffusion of antibiotic
Ref: Goodman and Gilman’s 12th ed, pg 1367; HPIM 19th ed pg
145 e4 and 161 e1
AIIMS (Nov 2017–May 2014)
116. Which of the following is a both alpha and beta agonist
action?  (AIIMS May 2014, Nov 2013)
a. Epinephrine b. Dobutamine
c. Fenoldopam d. Phenylephrine
Recall Bias..................................................
Some recallers think that the question was asked in all Except format
Biofilm mechanism of resistance of antibiotics includes all
EXCEPT:
A. Increased excretion of antibiotics (Answer)
/e
B. Mechanical barrier
C. Decreased diffusion of antibiotic
,2
D. Adherence
“Bacterial and fungal biofilms are colonies of slowly growing
cells that are enclosed within an exopolymer matrix. The
sy exopolysaccharide is negatively charged, which restricts
positively charged antibiotics from reaching their target. This
physical barrier restricts the diffusion of antimicrobial molecules
and sometimes binds them. To be effective against infections in
these compartments, antibiotics have to be able to penetrate the
biofilm and endothelial barriers.” Ref: Goodman and Gilman
From the above explanation it is clear that resistance is
because of restriction of antibiotics to reach target site and
sometimes biofilm adheres the antibiotics, for sure it is not the
increased efflux or excretion of antibiotics. Ref: Harrison’s 19th
ed 145 e 4 and 161 e1:
•• Biofilms are surface associated communities of bacteria,
often embedded in a matrix, that allow the microbes
to persist and to resist the effects of host immunity and
antimicrobial agents.
•• Growth in biofilms leads to altered microbial metabolism,
production of extracellular virulence factors, and decreased
susceptibility to biocides, antimicrobial agents, and host
defense molecules and cells.
•• Examples of microbial biofilm growth associated with
human disease are:
ƒƒ P. aeruginosa growing on the bronchial mucosa during
chronic infection
ƒƒ Staphylococci and other pathogens growing on implanted
medical devices
ƒƒ Dental pathogens growing on tooth surfaces to form
plaque
4. Ans. (a)  Breastfed child just before taking next dose, when
plasma concentration of drug is least
Ref: Katzung’s 13th ed pg 1020
This line from Katzung gives you the answer: “If the nursing
mother must take medications and the drug is a relatively safe

one, she should optimally take it 30–60 minutes after nursing
and 3–4 hours before the next feeding. In some cases this may
allow time for drugs to be partially cleared from the mother’s
blood, and the concentrations in breast milk will be relatively
low.”
Readers please be careful if ‘option a’ was not as given in
question then the answer would be ‘option c’, see the following
line, from Katzung:
“Despite the fact that most drugs are excreted into breast
milk in amounts too small to adversely affect neonatal health,
thousands of women taking medications do not breast-feed
because of misperception of risk. Unfortunately, physicians
contribute heavily to this bias. It is important to remember
that formula feeding is associated with higher morbidity and
mortality in all socioeconomic groups.”
Important points regarding drug use during lactation:
•• Most drugs are excreted into breast milk and are detectable
also, but the amount is too small to adversely affect neonatal
health
•• The concentration of drugs achieved in breast milk is usually
low. Therefore, the total amount the infant would receive in
a day is substantially less than what would be considered a
“therapeutic dose.”
•• Most antibiotics taken by nursing mothers can be detected
in breast milk.
Ea
ƒƒ Tetracycline concentrations in breast milk are
approximately 70% of maternal serum concentrations
and present a risk of permanent tooth staining in the
ed
infant.
ƒƒ Isoniazid rapidly reaches equilibrium between breast
milk and maternal blood. The concentrations achieved
M
in breast milk are high enough so that signs of pyridoxine
deficiency may occur in the infant if the mother is not
given pyridoxine supplements.
S
•• Most sedatives and hypnotics achieve concentrations in
breast milk sufficient to produce a pharmacologic effect in
IM
some infants.
ƒƒ Barbiturates taken in hypnotic doses by the mother can
AI
produce lethargy, sedation, and poor suck reflexes in the
infant.
ƒƒ Chloral hydrate can produce sedation if the infant is fed
at peak milk concentrations.
ƒƒ Diazepam can have a sedative effect on the nursing
infant, but, most importantly, its long half-life can result
in significant drug accumulation.
•• Opioids such as heroin, methadone, and morphine enter
breast milk in quantities potentially sufficient to prolong the
state of neonatal narcotic dependence if the drug was taken
chronically by the mother during pregnancy.
PHARMACOLOGY  •  Answers with Explanations 313
ƒƒ If conditions are well controlled and there is a good
relationship between the mother and the physician, an
infant could be breast-fed while the mother is taking
methadone. She should not, however, stop taking
the drug abruptly; the infant can be tapered off the
methadone as the mother’s dose is tapered. The infant
should be watched for signs of narcotic withdrawal.
ƒƒ Although codeine has been believed to be safe, a recent
case of neonatal death from opioid toxicity revealed that
the mother was an ultra rapid metabolizer of cytochrome
2D6 substrates, producing substantially higher amounts
of morphine. Hence, polymorphism in maternal drug
metabolism may affect neonatal exposure and safety.
A subsequent case control study has shown that this
situation is not rare. The FDA has published a warning
to lactating mothers to exert extra caution while using
painkillers containing codeine.
•• Minimal use of alcohol by the mother has not been reported
/e
to harm nursing infants. Excessive amounts of alcohol,
however, can produce alcohol effects in the infant. Nicotine
,2
concentrations in the breast milk of smoking mothers are
low and do not produce effects in the infant.
•• Lithium enters breast milk in concentrations equal to
sy those in maternal serum. Clearance of this drug is almost
completely dependent upon renal elimination, and women
who are receiving lithium may expose the infant to relatively
large amounts of the drug.
•• Radioactive substances such as iodinated 125I albumin
and radioiodine can cause thyroid suppression in infants
and may increase the risk of subsequent thyroid cancer
as much as tenfold. Breast feeding is contraindicated after
large doses and should be withheld for days to weeks after
small doses. Similarly, breast-feeding should be avoided in
mothers receiving cancer chemotherapy or being treated with
cytotoxic or immunomodulating agents for collagen diseases
such as lupus erythematosus or after organ transplantation.
5. Ans. (b)  Cell wall synthesis Inhibition
Ref: Katzung 13th ed 773
•• Vancomycin inhibits cell wall synthesis by binding firmly
to the D-Ala-D-Ala terminus of nascent peptidoglycan
pentapeptide. This inhibits the transglycosylase, preventing
further elongation of peptidoglycan and crosslinking.
•• Beta-lactam antibiotics, structural analogs of the natural
D-Ala-D-Ala substrate, covalently bind to the active site of
PBPs. This binding inhibits the transpeptidation reaction
and halts peptidoglycan synthesis, and the cell dies. Beta-
lactam antibiotics kill bacterial cells only when they are
actively growing and synthesizing cell wall.
PHARMACOLOGY
314 Section I  •  Subject-wise MCQs and Answers with Explanations

Classification of Antibiotics
Mechanism of Action Examples
Inhibit cell wall synthesis •• Fosfomycin
•• Cycloserine
•• Bacitracin
•• Vancomycin
•• β lactam antibiotics (includes penicillins, cephalosporins, monobactams, carbapenems, and
β lactamase inhibitors)
Cause leakage from cell Polypeptides- Polymyxins, Colistin, Bacitracin. Polyenes-Amphotericin B, Nystatin, Hamycin.
membranes
Inhibit protein synthesis Tetracyclines, Chloramphenicol, Erythromycin, Clindamycin, Linezolid.
Cause misreading of m-RNA Aminoglycosides-Streptomycin,Gentamicin,
code and affect permeability
Inhibit DNA gyrase Fluoroquinolones-Ciprofloxacin. and others.
Interfere with DNA function Rifampin,Metronidazole.

/e
Interfere with DNA synthesis Acyclovir,Zidovudine.
Interfere with intermediary Sulfonamides, Sulfones, PAS, Trimethoprim,

,2
metabolism Pyrimethamine, Ethambutol.

sy
6. Ans. (a)  Sham Surgery have strong and prominent smell and taste. (Ref: Drug
Discovery and Clinical Research By S K Gupta page 435)
Ref: With Text A single herb can contain hundreds of natural constituent and
Ea
The confusion is between (A) Sham surgery and (B) Herbal most of herbal medicines contains mixture of herbs. It becomes
medication with no effect known. Option (C) Physiotherapy almost impossible to ascertain the effect. Clinical effects of
and Option (D) CBT are known therapies with known effects Herbal medicines are often related to traditional knowledge,
ed

and hence can not be used as Placebo. experience of Individual practitioners, theory and concepts of
Placebo (Latin- I shall please) is a substance or treatment traditional medicine. (Ref: The Problem of Herbal Medicines
with no active therapeutic effect. A placebo may be given to a Legal Status By JL Valverde page 12). Hence Herbal medicines
M

person in order to deceive the recipient into thinking that it is are not ideal for Placebo effect
an active treatment.
To establish whether or not the benefit of a particular surgical Note
S

intervention is due to the ‘placebo effect’, the intervention must Nocebo is the opposite of placebo, and refers to
be investigated using a placebo-controlled RCT. In surgery, negative psychodynamic effect evoked by the
IM

these placebo-controls are referred to as ‘sham procedures/ pessimistic attitude of the patient, or by loss of faith
surgeries’. One placebo controlled, randomized blinded trial in the medication and/or the physician. Nocebo
AI

of arthroscopic lavage versus arthroscopic debridement versus
sham knee surgery in patients with osteoarthritis demonstrated
no benefit to either arthroscopic lavage or debridement when
compared to sham surgery (Moseley et al., 2002) (Ref: Principles
and Practice of Surgery By O James Garden 7th ed page 139)
If the herbal medicine cannot be administered in a
predetermined standardized formulation, it will be impossible
to keep the treatment blinded. Otherwise also use of herbal
medicines as Placebo may not be always possible because of
ethical and technical issues. Like for example Herbal medicines
effect can oppose the therapeutic effect of active
medication.
7. Ans. (d)  Beta 1 agonist and beta 2 agonist
Ref: KDT 7th ed 101, 127,130
The new drug increases heart rate, cardiac output, Systolic
Blood pressure but decreases Diastolic Blood Pressure.
Let us review actions at various receptors:

M1 M2 M3
•• Location Authonomic Depolarization (late SA node: Hyperpolarization, Visceral smooth muscle:
and functin ganglia: Gastric EPSP) Hist. release, ↓ rate of impulse generation contraction
subseved glands: CNS action secretion AV node: a velocity of Iris: Constriction of pupil
learning, memory conduction Ciliary muscle: Contraction
motor functions Atrium: shortening of APD, ↓ Exocrine glands: secretion
contractility
Contd…

AIIMS (Nov 2017–May 2014)

 PHARMACOLOGY  •  Answers with Explanations 315

Ventricle: ↓ contractility Vascular endothelium:

(slight) (receptors sparse) release of NO→
Cholinergic nerve endings: ↓ vasodilatation
ACh release
CNS: tremor, analgesia
Visceral smooth muscle:
contraction
a actions b actions
•• Constriciton of arterioles and veins → rise in BP (a1 + a2) Dilatation of arterioles and veins → fall in BP (a2)
•• Heart—little action, arrhythmia at high dose (a1) Cardiac stimulation (a1), ↑ rate, force and conduction
velocity

Now let us discuss the options: 9. Ans. (c)  Canagliflozin

Option (A) Ref: Harrison 19th ed page 2414, Lippincott’s 4th Ed page 295,
M2 agonist and M3 agonist KDT 7th Ed Pg 274, 277, 278

/e
M2 agonism will decrease heart rate, and hence cardiac output See table of Glucose-Lowering Therapies for type 2 Diabetes
will decrease (C.O = heart rate X Stroke Volume). AIIMS MAY 2015 Pharmacology
Clue:

,2
Option (B)
There are 4 prerequisites given in this question.
Alpha 1 antagonist and beta 1 agonist 1. There is history of pancreatitis so the replacement drug
Alpha 1 antagonism will decrease SBP and Beta 1 agonism will
increase heart rate.Cardiac output may increase.
Option (C)
sy should not have pancreatitis in its side effects.
2. Family history of Bladder cancer, hence the replacement
drug should not have side effect of Bladder cancer risk.
Ea
Alpha 1 agonist and beta 1 agonist 3. Patient does not want to take injections so the drug needs to
Alpha 1 agonism will increase SBP. However, DBP will increase be given orally.
due to vasoconstriction due to alpha 1 action. Beta 1 agonism 4. Patient is Obese hence preferred drug should have
ed

will increase heart rate. Cardiac output will increase. characteristic of weight loss

Option (D) Option (A)

M

Beta 1 agonist and beta 2 agonist Sitagliptin is given orally and does not causes bladder cancer
Beta 1 agonism will increase heart rate . Beta 2 agonism will but it is known to cause pancreatitis. Sitagliptin has no effect
cause vasodilatation thus causing fall in DBP. Cardiac output on body weight. There are postmarketing reports of acute
S

will increase. This drug seems to have isoprenaline-like action pancreatitis (fatal and nonfatal) and severe allergic and
hypersensitivity reactions. Sitagliptin should be immediately
IM

on the body. SBP may increase. Also, it matches the parameters

in the question and hence is the answer. discontinued if pancreatitis or allergic and hypersensitivity
Adr: a1 + a2 + b1 + b2 and weak b3 action reactions occur. Hence should be avoided in this case.
AI

NA: a1+ a2 + b1 + b2 but no b3 action Option (B)

Iso: b1 + b2 + b3 nut no a action Pioglitazone is given orally, does not cause pancreatitis but it
is known to increase the risk of Bladder cancer. Side effects
8. Ans. (a)  Metformin
include weight gain. Hence can not be given in this case
Ref: KDT 7th ed page 276, Harrison 19th ed page 2413
Option (C)
In addition to general restrictions for use of oral hypoglycaemics,
Canagliflozin is in a class of medications called sodium-
metformin is contraindicated in hypotensive states, heart
glucose co-transporter 2 (SGLT2) inhibitors. It is given orally.
failure, severe respiratory, hepatic and renal disease, as well as
Acute pancreatitis is a very rare side effect with an incidence
in alcoholics because of increased risk of lactic acidosis (KDT)
<1%. Harrison 19th ed says “As part of the FDA approval of
Metformin should not be used in patients with renal
canagliflozin in 2013 postmarketing studies for cardiovascular
insufficiency (glomerular fùtration rate [GFR] <60 mL/
outcomes and for monitoring bladder and urinary cancer risk
min any form of acidosis, unstable congestive heart failure
are underway. Apart from this it also causes weight loss hence
(CHF), liver disease, or severe hypoxemia. Some feel that these
is ideal in the given patient.
guidelines are too restrictive. The National Institute for Health
and Clinical Excellence in the United Kingdom suggests that Option (D)
metformin be used at a GFR >30 mL/min, with a reduced dose Liraglutide is recently developed long-acting GLP-1 agonist. It
when the GFR is <45 mL/min. (Harrison) does not cause Bladder cancer.It also causes weight loss. But

PHARMACOLOGY
316 Section I  •  Subject-wise MCQs and Answers with Explanations

It’s known to cause Pancreatitis and given as Subcutaneous
Injected once daily. liraglutide is contraindicated in individuals
with a history of pancreatitis and should be permanently
discontinued if pancreatitis develops.Hence can not be given
in this case.
•• Side effects: decreased libido, impotence and decreased
volume of ejaculate (each in 3–4% patients). Gynaecomastia,
skin rashes, swelling of lips are rare.

10. Ans. (c)  Pyridoxine

Ref: K.D Tripathi 7th Ed Pg 916, Harrison 19th ed page 1116
•• The symptoms of the patient are related to the deficiency of
pyridoxine caused by isoniazid.
•• Isoniazid reacts with pyridoxal to form a hydrazone, and
thus inhibits generation of pyridoxal phosphate. Isoniazid
also combines with pyridoxal phosphate to interfere with
its coenzyme function. Due to formation of hydrazones, the
renal excretion of pyridoxine compounds is increased. Thus,
isoniazid therapy produces a pyridoxine deficiency state.
•• Pyridoxine is used to prevent and treat (10–50 mg/day)

/e
isoniazid induced neurological disturbances.
•• Acute isoniazid poisoning has been successfully treated

,2
with massive doses (in grams) of pyridoxine.

11. Ans. (b)  18

Ref: Pharmaceutical Calculations By Howard C. Ansel 14th ed
page 428 sy
Ea
500 mg/5ml means every 100 mg is present in 1 ml, Absolute surgical indications include
So 180 mg will be present in 1.8 ml a. Refractory urinary retention (failing at least one attempt at
10 divisions per ml means 0.1 ml per division catheter removal),
ed

So, 1.8 ml will be present in 18 divisions b. Recurrent urinary tract infection from BPH
c. Recurrent gross hematuria from BPH,
12. Ans. (c)  Finasteride
d. Bladder stones from BPH
M

Ref: KDT 7th Ed Page 302 e. Renal insufficiency from BPH

Finasteride is a competitive 5 alpha reductase inhibitor and f. Large bladder diverticula
S

is used in benign hypertrophy of prostate along with alpha 1

blockers like tamsulosin. 13. Ans. (d)  Scopolamine transdermal patch a night before
IM

The α1 blockers afford faster (within 2 weeks) and greater Ref: KDT 7th Ed Pg 168, 664, Harrison 19th ed page 260
symptomatic relief than finasteride which primarily affects static
•• Antiemetics with anticholinergic- antihistaminic
component of obstruction and has a delayed onset (around six
property are the first choice drugs for motion sickness.
AI

months) for clinical improvement. The α1 blockers do not affect

prostate size, but are more commonly used. Concurrent treatment
with both produces greater symptomatic relief.
Some details about Finasteride:
•• Competitive inhibitor
•• Relatively selective for 5 α-reductase type 2 isoenzyme
(predominates in male urogenital tract.)
•• Patients with large prostate (volume > 40 ml) obtain greater
relief than those with smaller gland.
•• Upto 20% reduction in prostate size may be obtained.
•• Withdrawal of the drug results in regrowth of prostate, but
with continued therapy benefit is maintained for 3 years or
more.
•• Other uses: Finasteride has also been found effective in
male pattern baldness (promotes hair growth and prevents
further hair loss), although hair follicles have primarily type
1 enzyme. Onset- 3 months, effective till 1 year after cessation.
Antidopaminergic and anti-HT3 drugs are less effective.
•• All anti-motion sickness drugs act better when taken
1⁄2–1 hour before commencing journey. Once sickness
has started, it is more difficult to control; higher doses/
parenteral administration may be needed.
•• Dimenhydrinate (anti histaminic with anticholinergic
activity) should be taken 1 hour before the journey. It
affords protection from motion sickness for 4–6 hours, but
produces sedation and dryness of mouth
Scopolamine: A transdermal patch can be applied behind
the pinna containing 1.5 mg of hyoscine (scopolamine), to be
given at least 4 hours before journey and to be replaced after 72
hours (3 days) if needed. Oral dose 0.4–0.6 mg one hour before
travel and then TID may be recommended. Scopolamine is the
most effective drug for motion sickness. With the advantage of
it having mild side effects, scopolamine seems to be the drug
of choice.

AIIMS (Nov 2017–May 2014)

 PHARMACOLOGY  •  Answers with Explanations 317

14. Ans. (c)  Buprenorphine

Ref: K.D Tripathi 7th Ed page 479

Opioid Drugs and Their Actions on Opioid Receptors

Strong opioid agonist
Moderate opioid agonist
Mixed agonist/antagonist
Weak opioid agonist
Pure antagonist
Morphine, Methadone, Heroin, Fentanyl
Codeine, Dihydrocodeine, Dextropropoxyphene
Buprenorphine Partial/weak µ agonist + kappa antagonist
Pentazocine Partial μ agonist with agonist activity at κ receptors too
Levallorphan Antagonist on μ-opioid receptor and agonist on kappa receptors
Tramadol Weak μ opioid receptor agonist
(Atypical opioid) Very low affinity for κ and δ opioid receptor.
Inhibits reuptake of Noradrenaline and 5-HT, increases 5-HT release,activates
monoaminergic spinal inhibition of pain.
Naloxone, Naltrexone, Nalmefene

/e
15. Ans. (a)  They increase bronchial responsiveness to Drugs of Choice for Infectious Disease Prophylaxis

,2
salbutamol
Disease Drug of choice
Ref: K.D.Tripathi 7th Ed Pg 229
Anthrax Ciprofloxacin/Doxycycline
KDT 7th Ed says: “Corticosteroids afford more complete
and sustained symptomatic relief than bronchodilators or
cromoglycate; improve airflow, reduce asthma exacerbations sy Cholera
Diphtheria
Doxycycline
Penicillin/Erythromycin
Ea
and may influence airway remodeling, retarding disease Endocarditis Amoxycillin/Clindamycin
progression. They also increase airway smooth muscle
Gonorrhoea/Syphilis Procaine penicillin
responsiveness to β agonists and reverse refractoriness to these
ed

drugs. Inhaled corticosteroids have thus markedly changed the Group B Streptococcal Ampicillin
outlook on asthma therapy” infection
Asthma attack not responding to intensive bronchodilator Influenza A and B Oseltamivir
M

therapy: start with high dose of a rapidly acting i.v.

H. influenzae Type B Rifampicin
glucocorticoid which generally acts in 6–24 hours—shift to
oral therapy for 5–7 days and then discontinue abruptly or Herpes simplex Acyclovir
S

taper rapidly. Malaria Chloroquine (for

IM

susceptible)/Mefloquine/
AIIMS MAY 2017 Doxycycline (endemic area
or chloroquine resistant)
AI

16. Ans. (a)  Cotrimoxazole

Meningococcal meningitis Rifampicin
Ref: KDT 7th edition page 706 to 708
Mycobacterium Avium Azithromycin/Clarithromycin
•• Cotrimoxazole is drug of choice for both treatment and Complex (MAC)
prophylaxis of P. jirovecii (Previously known as P. carinii)
Otitis media Amoxycillin
infection.
•• Cotrimoxazole is a fixed dose combination of trimethoprim Pertussis (Whooping cough) Azithromycin/Erythromycin
and sulfamethoxazole. Plague Tetracycline
•• The required plasma concentration ratio of sulfamethoxazole: Pneumocystis jirovecii Cotrimoxazole/Atovaquone/
trimethoprim is 20:1, which shows synergistic activity Dapsone
against most organisms. This is achieved by dose ratio of
5:1, because trimethoprim has high tissue distribution. For Rheumatic fever Benzathine penicillin
example, 1 Double Strength (DS) tablet = sulfamethoxazole Rickettsial infections Tetracyclines
800 mg + trimethoprim 160 mg. Surgical prophylaxis Cefazolin
•• For curative treatment of PCP = High dose cotrimoxazole
TB INH with/without Rifampicin
(4-6 DS tablets per day) + prednisone or methyl-
prednisolone as adjunctive Toxoplasmosis Cotrimoxazole
•• For prophylaxis of PCP low dose is used (1 DS tablet daily). Urinary tract infections Cotrimoxazole

PHARMACOLOGY
318 Section I  •  Subject-wise MCQs and Answers with Explanations

17. Ans. (b)  Inhibits assembly of virus protein Option (D)

Ref: Goodman & Gilman’s 12th ed pg 1628 to 1659; KDT 7th ed
pg 805, Harrison’s 19th Ed Pg 1274
Let us go through individual options:
Option (A)
It inhibits translation and Option (C) It inhibits proviral RNA
synthesis.
Translation and transcription of HIV viral DNA is by using
host (human) enzymes so as of now no drugs target this system.
Inhibits conversion of RNA to DNA
NRTI & NNRTI inhibit reverse transcriptase thereby
inhibiting conversion of RNA to DNA.
Option (B)
It is correct mechanism of protease inhibitors. Function of
HIV protease is cleavage of gag and pol precursor polypeptides
and other precursor proteins to final structural proteins of
mature virion.

/e
,2
sy
Ea
ed
M
S
IM
AI

Pathogenesis and targets of antiretroviral drugs (trends in pharmacological sciences)

Targets and Mechanism of Antiretroviral Drugs

Target Normal function in virus Drug class Mechanism of action
gp41 HIV attaches through gp Enfuvirtide Binds to gp41 → does not allow conformational changes
160 (which includes gp120 (Entry inhibitor) that allow fusion of virusè blocks entry of virus into host
& gp41) → gp 41 fuses viral cell.
envelop to host membrane
CCR5 Maraviroc (Entry Binds specifically to host protein ccr5 → blocks entry
→ entry of virus
inhibitor)
RT (Reverse RT then converts viral RNA NRTI [Nucleoside/ These drugs are purine or pyrimidine analogues that enter
transriptase) to DNA Nucleotide cells get phosphorylated and then blocks replication by 2 ways:
(tenofovir)] (1) Competitively inhibits incorporation of native nucleotides.
e.g. zidovudine, (2) once incorporated terminates elongation of nascent DNA
lamivudine, etc. because NRTI lack 3’ hydroxyl group
Contd…

AIIMS (Nov 2017–May 2014)

 PHARMACOLOGY  •  Answers with Explanations 319

Targets and Mechanism of Antiretroviral Drugs

Target Normal function in virus
Integrase Incorporates viral DNA into
host DNA.
Protease Proteolytic cleavage of
gag and pol precursor
polypeptides and other
precursor proteins to final
structural proteins of mature
virion
Drug class Mechanism of action
NNRTI Bind to NNRTI binding pocket in enzyme RT which is
(Nonnucleoside) e.g. separate from catalytic site and cause change in 3D
nevirapine structure of the enzymeè reducing its activity.
Integrase inhibitor These drugs bind to integrase enzyme and prevent viral
e.g. Raltegravir DNA strand transfer to host DNA
Protease inhibitors HIV protease inhibitors are peptide-like chemicals that
e.g. ritonavir, competitively inhibit the action of the viral protease thereby
saquinavir, etc. blocking formation of mature virions.

/e
18. Ans. (d)  Cotrimoxazole with 3rd generation cephalosporin •• Ionization at physiological pH (a function of its pKa)
•• Extent of binding to plasma and tissue proteins: Drugs
Ref: Katzung 13th ed page 802, 904, Harrison’s 19th ed page 1048

,2
extensively bound to plasma proteins are largely restricted
Note to the vascular compartment and have low volume of
distribution, e.g. diclofenac and warfarin

sy
Trimethoprim-sulfamethoxazole (TMP-SMX), also •• Presence of tissue-specific transporters
known as co-trimoxazole •• Differences in regional blood flow
ƒƒ Volume of distribution is the apparent volume required
Ea
•• What Harrison’s 19th Ed page 1048 says: to contain the amount of drug homogeneously at the
ƒƒ B cepacia is intrinsically resistant to most antimicrobials. concentration found in the plasma
ƒƒ TMP-SMX, meropenem, and doxycycline are most effective ƒƒ Drugs having high volume of distribution get sequestrated
ed

drugs. in various tissues and are unequally distributed and tend

ƒƒ Empirical treatment of choice is TMP-SMX or meropenem to have longer duration of action.
ƒƒ Some strains are susceptible to third-generation cephalo- ƒƒ Due to sequestration may exert local toxicity, e.g.
M

sporins and fluoroquinolones tetracyclines on bone and teeth, chloroquine on retina,

ƒƒ When serious pulmonary infection is there, e.g. cystic streptomycin on vestibular apparatus, emetine on heart
and skeletal muscle.
S

fibrosis then combination therapy is suggested, but

combination of meropenem and TMP-SMX is antagonistic. ƒƒ Large volume of distribution indicates good drug storage.
IM

ƒƒ Resistance to all agents has been reported. Small volume of distribution means drug stays in vascular
•• What Katzung pg 904 says compartment either due to high plasma protein binding or
DOC for B. Cepacia is TMP-SMX and alternative agents are due to less lipid solubility, therefore less drug is distributed
AI

Ceftazidime, chloramphenicol. to tissues. Lesser the distribution lesser will be the storage.

19. Ans. (b)  Large volume of distribution
Ref: KDT 7th ed page 21, Katzung 8th ed page 38
Indirect repeat Pharmacology AIIMS Nov 2015 (was asked in
reverse form i.e. What happen in Low volume of distribution)
The extent and pattern of distribution of a drug depends on its:
•• Lipid solubility
20. Ans. (a)  Ceftriaxone
Ref: Harrison’s 19th ed table 147-1 page 780, 889.
Meningitis can be broadly classified into community acquired
(usual case) or hospital acquired. The empirical therapy for
both of these is discussed in the table below.

Type of MC Cause Empirical Treatment Addition to Rationale

Meningitis Empirical Rx
Community S. Pneumonia 3rd/4th gen cephalosporin + Ampicillin 3 months of age, those >55, or immunocompromised
acquired (50%) and N. (ceftriaxone, cefotaxime, (to cover Listeria monocytogens)
meningitis meningitidis (25%) cefepime)
+ Metronidazole In patients with otitis, sinusitis, or mastoiditis (to
+ vancomycin
cover gram-negative anaerobes)
+ acyclovir
+ dexamethasone + Doxycycline In tick season (tick-borne bacterial infections)
Contd…

PHARMACOLOGY
320 Section I  •  Subject-wise MCQs and Answers with Explanations

Type of MC Cause Empirical Treatment Addition to Rationale

Meningitis Empirical Rx
Hospital Staphylococci and Vancomycin + ceftazidime or Ceftriaxone and cefotaxime do not provide activity
acquired gram -ve organisms cefepime or meropenem against CNS infection with pseudomonas therefore
meningitis (P. aeruginosa) replaced by active agents

Meningococcal Meningitis
Empirical Rx DOC if DOC if resistance to Chemoprophylaxis for adults and Alternate chemoprophylaxis for
suceptible Pencillin G children >1 year adults
Ceftriaxone or Penicillin G Ceftriaxone or 2-day regimen of rifampin One dose of azithromycin
cefotaxime cefotaxime (not recommended in pregnancy) (500 mg) or one im dose of
ceftriaxone (250 mg)

21. Ans. (b)  Taper the drug over 6 months drug is then further optimized based on seizure response
and side effects. Monotherapy should be the goal whenever
Ref: Katzung 13th ed page 414, Harrison’s 19th ed page 2556 possible”.

/e
This question is about whether to stop levetiracetam or to Based on above explanation option A and option C are wrong.
switch to different antiepileptic due to adverse effects of leve-

,2
Option (B)
tiracetam. Levetiracetam is a well tolerated antiepileptic with
very few adverse effects. Tapering is usually 2 to 3 months but may vary with different
•• The usual adverse effects include: somnolence, asthenia, drugs and different scenarios. Therefore over 6 months can be
ataxia, and dizziness.
•• Less common but important: mood and behavioral changes. sy regarded as true.
Option (D)
Ea
•• Rare: Psychotic reaction The patient is seizure free for 2 years, but other criteria like
type of seizure, neurologic examination and EEG has not been
Stopping an antiepileptic mentioned in question. Remember that all the criteria need
ed

Stopping or switching an antiepileptic is mandated based on to be met to stop the drug. This could have been the answer
2 parameters if tapering of levetiracetam over a period and then gradually
•• Seizure free period and shifting to other antiepileptic would have been mentioned.
M

•• Compliance or adverse effect of the drug

ƒƒ The appropriate seizure free interval is unknown and 22. Ans. (a)  Linagliptin
undoubtedly varies for different forms of epilepsy. It is
S

Ref: KDT 7th ed page 275, Katzung 13th ed page 1090 & 1091
reasonable to attempt withdrawal of antiepileptic after 2 Indirect Repeat (Different case description and options)
IM

years seizure free period if the patient meets the following Pharmacology AIIMS NOV 2016
criteria:
a.  Complete medical control of seizures for 1–5 years; Dipeptidyl peptidase-4 (DPP-4) inhibitors
AI

b.  Single seizure type, either focal or generalized;
c. Normal neurologic examination, including intelli-
gence; and
d.  Normal EEG.
Withdrawal of therapy should be gradual over a period of 2
to 3 months.
Switching to different antiepileptic:
•• If seizure free period is not sufficient to withdraw or
seizures are not controlled by the drug or if there is
significant toxicity then switching to another antiepileptic
may be considered.
•• “This is usually done by maintaining the patient on the first
drug while a second drug is added. The dose of the second
drug should be adjusted to decrease seizure frequency
without causing toxicity. Once this is achieved, the first
drug can be gradually withdrawn (usually over weeks
unless there is significant toxicity). The dose of the second
•• Sitagliptin, Vildagliptin, Saxagliptin, Alogliptin, Linagliptin.
•• The dose of Sitagliptin, Vildagliptin and saxagliptin should
be reduced if GFR falls below 50-60 ml/min.
•• Linagliptin is safe in renal failure or hepatic impairment.
There is no dose adjustment required for linagliptin in
renal failure patients (which is the only oral drug currently
licensed for this use)
23. Ans. (c)  Blurred vision
Ref: Katzung 13th ed pg 410, Harrison’s 19th ed pg 383
Diplopia (not blurred vision) is a adverse effect of carba-
mazepine not an idiosyncratic reaction
•• MC drugs causing Steven Johnson syndrome are (Harrison’s
19th pg 383): Sulfonamides, nevirapine, allopurinol, lamo­
trigine, aromatic anticonvulsants (including phenytoin,
carbamazepine, and barbiturates), and NSAIDs, specifically
oxicam.

AIIMS (Nov 2017–May 2014)

 PHARMACOLOGY  •  Answers with Explanations 321
•• Unpredictable reactions or type B or Bizarre reactions varies
Insulins
from patient to patient and are not due to drug as such.
These include idiosyncratic reactions (IR) and allergy. Insulin Insulin lispro Ultra short acting
•• Unpredictable reactions are rare. Carbamazepine is known analogues Insulin aspart
for unpredictable reactions. Insulin glulisine
•• Adverse drug effects are due to drug’s off target actions and Insulin glargine Long acting
on contrary reason for IRs is unpredictable and is considered
to be related to patient. Activity Profiles of Different Types of Insulin

Idiosyncratic Reactions due Adverse Effects of Carba-

to Carbamazepine are
•• MC IR is: Erythematous
skin rash (SJS)
•• Dangerous IRs but rare
include: Aplastic anemia
and agranulocytosis.
mazepine are
•• MC dose-related adverse
effects of carbamazepine
are diplopia and ataxia.
•• Other dose-related
complaints include mild
gastrointestinal upsets,

/e
unsteadiness, and, at much
higher doses, drowsiness.

•• Other IRs leukopenia
(common idiosyncratic
blood dyscrasia) and
hepatic dysfunction (rare)
24. Ans. (a)  30% amorphous + 70% crystalline
Ref: KDT 7th ed page 264
,2
•• Hyponatremia and water
intoxication are rare and
may be dose related.
sy
Ea
25. Ans. (a)  Neuraminidase inhibitor
Ref: Harrison’s 19th Ed page 21 5e-l, Katzung 13th ed page 886
ed

Lente insulin is a combination of 30% semilente (amorphous)

and 70% ultralente (crystalline) insulin zinc suspension See Drug section of table of “Influenza a Virus Including
Subtype H1N1” in Microbiology COLOUR PLATE 11 KEY
M

•• Oseltamivir and zanamivir are anti influenza agents

•• Influenza A is divided into various subtypes based on H
S

(haemagglutinin) and N (Neuraminidase) into various

subtypes. Important being H5N1 (avian), H1N1 (swine),
IM

H1N2 and H3N2.

•• Neuraminidase inhibitors: Oseltamivir and Zanamivir
AI

ƒƒ Influenza virus requires neuraminidase to sialic acid

Insulins residues in host membrane to get released from the cell
Highly purified Porcine Actrapid- Short acting ƒƒ Neuraminidase inhibitors interfere with release of
mono- Regular progeny influenza virus from infected host cells, thus
component halting the spread of infection within the respiratory
Porcine Monotard- Intermediate tract.
insulin Lente acting ƒƒ Inhibition of viral neuraminidase results in clumping of
Porcine Insulatard- NPH newly released influenza virions to each other and to the
Porcine Mixtard 30% regular, 70% membrane of the infected cell.
Isophane ƒƒ Active against both influenza A and B
•• Amantadine and its α-methyl derivative rimantadine,
Human insulin Human Actrapid- Short acting block the M2 proton ion channel (Option B) of the virus
Regular particle and inhibit uncoating of the viral RNA within
Human Monotard- Intermediate infected host cells, thus preventing its replication
Lente acting ƒƒ Active against influenza A only
Human Insulatard- NPH
26. Ans. (b)  Epsilon amino caproic acid
Human Mixtard 30% regular, 70%
Isophane Ref: Goodman 12th ed page 867, Katzung 12th page 616
Contd… Repeat Pharmacology AIIMS NOV 2015 (See for explanation)

PHARMACOLOGY
322 Section I  •  Subject-wise MCQs and Answers with Explanations

27. Ans. (a)  2.5 mg/L Indications Treatment Recommen-

Ref: KDT 7th ed page 32 dation
•• Plasma steady state concentration (Cpss) is achieved after Presence of clinical atherosclerotic High intensity statin or
repeated administration of drug leading to a balance cardiovascular disease moderate intensity statin if
between drug input and elimination. over age 75
•• Cpss is directly proportional to the dose rate and inversely Primary elevation of LDL cholesterol High intensity statin
to the clearance of the drug and the relation is as follows: ≥190 mg/dL (4.91 mmol/L)
Cpss = Dose rate/Clearance Age 40–75 Moderate intensity statin
Dose rate = 1.6 mg/ml, Clearance = 640 ml/min Presence of diabetes Or high intensity statin if
Cpss = 1.6/640 = 0.0025 mg/ml = 2.5mg/L LDL ≥70 mg/dL (1.81 mmol/L) 10-year CVD risk 7.5% or
higher
28. Ans. (c)  30 mg
Aged 40–75 Treat with moderate-to-
Ref: KDT 7th ed page 30 No clinical atherosclerotic high intensity statin
cardiovascular disease or diabetes
Explanation LDL 70–189 mg/dL (1.81–4.91
This question can be solved easily by the fact that in first order mmol/L)
kinetic “constant fraction of drug is eliminated per unit time” Estimated 10-year CVD risk 7.5% or

/e
•• Step 1: higher
ƒƒ In the question 75 mg out of total 200 mg is eliminated in

90 minutes. Means 75/200 × 100 = 37.5%
ƒƒ 37.5% (fraction) of drug will be eliminated every
90 minutes
•• Step 2: We have to find out how much drug remains in the
body at the end of 6 hours (4 times 90 mins)
Ea
ƒƒ At the end of 1st 90 mins: 200-75 = 125 mg is the remaining
amount
ƒƒ 2nd 90 min: Now 37.5% of 125 will be eliminated =
ed
,2
As per the table above patient comes under 1st category
(presence of clinical cardiovascular disease). It is also important
to point out that even if the patient is not having deranged lipid
sy profile he may be started with statin therapy.
•• High intensity statin therapy: lowers LDL cholesterol by
approximately 50%.
ƒƒ Atorvastatin 40–80 mg (Option A) and rosuvastatin 20–
40 mg/day

37.5/100 × 125 = 47 •• Moderate intensity statins lower LDL cholesterol by

Drug remaining at the end of 2nd 90 min (3 hours) = 125 – 47 approximately 30–50%.
= 78 ƒƒ Atorvastatin 10–20 mg, rosuvastatin 5–10 mg (Option B),
M

ƒƒ 3rd 90 min: 37.5% of 78 = 29.25 simvastatin 20–40 mg, pravastatin 40–80 mg, and
Drug remaining at the end of 3rd 90 min (4½ hours) = 78– lovastatin 40 mg.
29.25 = 48.75
S

ƒƒ 4th 90 min: 37.5% of 48.75 = 18.3 30. Ans. (a)  Ofloxacin

Drug remaining at the end of 4th 90 min (6 hours) = 48.7–
IM

18.3 = 30.4 = 30 mg Ref: KDT 7th ed page 782, 783

Thus the answer •• Among the given options ofloxacin, ciprofloxacin and
amoxicillin have bactericidal activity, but only ofloxacin is
AI

29. Ans. (a)  Atorvastatin 80 mg
Ref: CMDT 2017 page 1263-64
•• When lipid lowering agents are indicated the treatment is
started with HMG Co-A reductase inhibitors (statins)
Option (C) Rosuvastatin + Fenofibrate
Combination therapy is rarely indicated. Only ezetimibe plus
simvastatin has shown benefit in trials even though very small.
Gemfibrozil and HMG-CoA reductase inhibitors increases the
risk muscle and liver disease more than either drug alone.
Option (D) Fenofibrate
Fibrates are used to reduce triglycerides and increase HDL
levels, which is not the case here and also first line therapy is
always statins.
This table shown below serves as a guide to type of therapy
to be used under specific conditions.
anti-leprosy drug. Erythromycin is a bacteriostatic drug and
not used in leprosy.
•• Commonly used anti-leprosy drugs include: Dapsone,
Clofazimine, Rifampin, Ethionamide.
•• Other antibiotics effective against M leprae are: Ofloxacin,
Moxifloxacin, Minocycline and Clarithromycin
•• Bactericidal activity of anti-leprosy drugs is as follows
ƒƒ Rifampicin: Up to 99.99% M.leprae are killed in 3–7 days
by 600 mg/day dose.
ƒƒ Ofloxacin: Over 99.9% bacilli were found to be killed by
22 daily doses of ofloxacin monotherapy.
ƒƒ Clarithromycin: Monotherapy with 500 mg daily caused
99.9% bacterial killing in 8 weeks.
31. Ans. (a)  Methotrexate
Ref: Harrison’s 19th ed page 2145

AIIMS (Nov 2017–May 2014)