< >

< >
 -------------------------- --------MTC

Duration of actJon
------"'------
r ,
C
� C Therapeutic
max I Range
ftl I
�
... I

<
C I

>
� I
u
I
I
C

------------
I
0 I
(J I ------------ -------- MEC
I
I
I I
t I
t
'
I
I
I
I
I I
I

On et
bme Time

C max- Maximum plasma concentraon obtained

T MAX- is the me to reach C max (rate of absorpon )

AUC- bioavailability(extend of absorpon)

 -------------------
tox� level

Oral Oral
Crocin 500mg MetacinSOOmg

,,... __ ----­ ' >

I �·-.............C
.. .• •• ............ . ..........,___

.••. . .-
.
•• • • • ••
•...
I•• ••-·· ' ' .,....•••
------- ' .... ..

TIME
Same drug, same dose, same dosage forms- <20%- Bioequivalent
 GRADED DOSE RESPONSE CURVES

MAXIMAL
ESPONS

...-
• •
I
-0 '
U)
4

C
::, 0
< >
...
0 a.
.0 cu
u
0 � 0.5
01
(.) -
(U
0
.
Cl)
a:, �
MAXIMAL
0 DOSE
Dose
 LOG DOSE RESPONSE CURVE

MR
100
�- Emax
Efficacy

< 0
ED 50- >
a: II Potency
ED50
/I /
1 0 1 3 1.6 1 .9 0.2
Log doses
0 1 0.2 0.4 0.8 1 .6
Doses (µg/mr) on arithmetic scale
lg. 7.16 Cale lation of ED 50 from LOR Curve
 DOSE RESPONSE CURVES OF DRUGS

Drug A is more Drug C shows

potent than Drug lower potency
B. but both show and lower
the same efficacy. efficacy than
Drugs A and B.

- 100

< ::::
�

-
Q)
u 50 Drug A Drug B
>
en
-
-
0
0
al

Log drug concentration

0
• T '
ECso EC50 EC50
for for for
Drug A Drug B Drug B

Figure 2.7
Typical dose-response curve for
drugs showing differences in potency
and efficacy. (EC50 = drug dose that
shows fifty percent of max ma
response.)
 EDso & LDso

100 100
·-
..,_ C
ou
-0
U
o C O Q)
0 ·-
0 0
Q)
> "'
a.
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Q) 'O
> er, - 50 -
< ·- Q)
- L.

-:J -"'
a,
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0 I
I >
I
I :J ·-
I
E oQ) I �
- .Q-'
u
I :, (/)
:J ·- I
() .0
I
I 1 LD
:J
"' jED50 so

Log doses Log doses

• 7.22 Calculation of L050 from Quantal LOR
7.21 Calculation of ED50 from Quantal LOR

Lesser the ED50 more potent Larger the LOSO more safe
 DRUG SAFETY

THERAPEUTIC INDEX LDso

EDso

Theophylline
< Lithium
>
Anti epileptics
Anti arrhythmics
lmmunomodulators
 RECEPTOR ANTAGONISM

Drug with non­ Drug with

competi1ive competitive

-
antagonist antagoniS1
Drug
(,)
alone )
-
�

<
OJ

>
(,)

-
0,
0
·-
m
0

Drug concentration

EC 50
t r
EC so
for drug for drug
alone or in the presence
in the presence of a competitive
of a noncompetitive antagonist
antagonist

Figure 2.9
Effects of drug antagonists.
 -
After 5 half life - reaches steady state plasma level

2
187
C 175
·-
0
5th T1/2

- ·m� - -_
I,
150
.C
� 1.5
,

m
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< 0
(.)
1
----1 st T1/2 >
co
E
en
ro o.s
CL

1 2 3 4 5 6
Time (multiples oft½)
 OCULOMOTOR NERVE

,.. · pbinrur mtKClr

Miosis
-
- CONSTRICTOR

< P tq)I
>
Mydriasis

'I
Adrenergic drugs Anti cholinergic drugs
Only Mydriasis Mydriasis + Cycloplegia
(loss of light reflex)
 Renal damage

< >

Bull's eye renopathy Crystalline maculopathy

Chloroquine Tamoxifen

vigabatrin Field of vision defect

 whorl-like pattern
cornea verticillata Or ''vortex keratopathy''. AMIODARONE

< >
 Corneal pigmentaon
Renal degenaraon

Cataract
< >
Posterior sub capsular
cataract
Cataract
< >
< >
< >
 Systolic BP

Diastolic BP
lsoprenaline :
�1, �2, �3 no a action ISO- jSBP/l DBP, Reftahcy

< I NA: a1,a2, �1 no�2 action I NA- j SBP/ j DBP, Ref brady >
Adr: alpha1,2, B-1. 2

Dale's vasomotor reversal

phenomenon

Alpha blocker Adr

 Anaesthesed dog blood pressure

< >

• • • •
Tyramine 0.3 mg/kg. iv
 -
Bronchospasm

C d

< >
'

Iris
pigmentation

Latanoprost

Bimatoprost
 Identify what is drug A? by its action on rabbit ileum

t t t >
< Atropine Drug A
t Wash
Ach t t
Wash Drug A Wash I

Barium chloride or calcium chloride or any prokinetic

< >
< >

TARGET CELL
 ,
< >
 NO independent direct
Guanyl Cyclase activators

Riociguat, Cinociguat

< >

0 · ase inhibitor-
Fasud i I SAH, PII'I� Angina
 lnfliximab

< ANAKINRA
Etanercept
Adalimumab >
Golimumab
g o n ist
a n t a Certolizumab
\\.6 u 111 ab
1'oc il i �
1 u 111 a b
s a n
 Vasopepde
Pepde ANP BNP Urodilann
Funcon NATRIRESIS
DIURESIS
VASODILATATION

Analogue Carperide Nesiride Ularide

< •
>

Neprilysin (neutral endopeptidase)

 Heart Failure
+ +
Na K pump ISTAROXIME

<
Omecamitiv mecarbil (oirect mvasin acvator)- >
(+)ve inotrophic

Calcium Sensitiser
Pimobendan,Levosimendan
 Class la

Class Ill
< >
 VR V1
v,.

L--vaVL-
j
··--v -v
JI 1f
'=
v� V5

Jll VF

MORPHINE- Ml, LVF

pFOX inhibitors
Acute ASMI Trimetazidine
< >
Ranolazine
��=I'-:=;_;;;;;_�'"°1----r.....;..r-�y--,-�� '--v"'---JI/
a.'R
1 '-----ii I t Na ch ann e I b Ioc ke r
IVABADINE
v,
1t/l

Acute IWMI
 v,

\
'
For acute SVT ......., To prevent recurrance
Iv. Adenosine Oral beta blockers
Iv- Verapamil Oral Verapamil
<
'

�""' \ "'( �,, \

v,
>
V3

Jll

11

10. 0 �rtN
:is •/HC

_ ..... --·- ,4;"1nrt� the

 • --
-- �
ir

. ------.J'
11
I
VL 2

< >

' .
lbutilide K channel blocker
Amiodarone
=AF- "· .NSR
Vernakalent Multi ion channel blocker
 Delta wave

H
PR interval < 120 ms
< >
Wolff Parkinson White Syndrome
Flecainide
Atrioventrlculir
Node

Left Bundle
Branch

Right Bundle
Branch
 - '
T
I
T
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T

t
r
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l ;--- - � �- - .1
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ttr=-=r111-::·�1Hr=-�·t-t+2.·--f·-i'+1--�r-RRP:+�h�::;:==t=:::t.n;=!=t-�='r-�t4"±
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I

HYPERKALEMIA EMERGENCY
Insulin + glucose
Calcium gluconate
Salbutamol

�AM�
 MOUTH ULCERS

< >
< >
 AVASIMIBE -ACAT-1 Diet
cholesterol
( acyl coenzyme A: cholesterol acyl
transferase-1) which forms cholesterol
ester from cholesterol.

< >

'

EZETIMIBE
Mipomersen
S/C -Intestine
 Thiazide
Site of action
Diuretic having antidiuretic action

Diuretic causing maximum

erectile dysfunction

Diuretic useful

<
in liver failure
Diuretic useful in - >
Mountain sickness Disease modifying
If--! diuretic for
heart failure
Acetazolamide
Rapid relief of symptoms of Spirinolatone
heart failure

Furosemide
I Most ototoxic I Ethacrynic acid
 ,en- Collecting tnterstitium­
tubule blood

ENaC +
Na
+ I'"'"'

<
K ATP
K
>
@ II( ADH
Water
channel
H20 molecules
For cranial D1- Intercalated cell
DESMOPRESSI N (V2)
�

For nephrogenic DI ATP

THL"?IDES
< >
< >
 METHADONE
< Buprenorphine >
Naloxone Inhibit reuptake
__
Nalmefene of SHT, NE
Naltrexone(oral)
Methadone
Tramadol

NMDA blocker Methadone

 1ne
< >

Urinary retension

Potassum channel opener- partial seizure

 MELATONIN

< >

MT1 MT2
< )
< )
< >
< >
 ...

VINCA ROSEA
< ST john's wort >
< >

--
� -

- -

Digitalis purpurea
Foxglov Cinchona plant
CCF
< >

Dhatura stromomium Papver somniferum

 .....

Alanine ligase/racemase
Cycloserine

Enolpyruvate transferase
I Fosfomycin

Dephosporylation of bactoprenol Bacitracin

< Transglycosylase Vaneomycin

>
LINEZOLID
Transpepdase Beta Lactam STREPTOGRAMINS
Daptomycin
Tigicycline
 Resistance
Bactena don ting plasm ,.

•
Pl $fflid

< >

Batwr1um
receiving ______
< >
< >

steven Johnson syndrome

? 2 nd line An TB C/1- HIV

< >
Stavudine
Zidovudine
Protease inhibitors
 Ultra short acting-
( onset 10-20min, dur 3--4Hrs)

INSULIN LISPRO,
ASPART
GLULISINE

< Long acting- >

INSULIN GLARGINE
DETEMIR

Longest acting­
INSULIN DEGLUDEC
 GLP-1 analouge

Liraglutide FDA- obesity

< >
ADR
s/c GIT- N,V,D
 .....

DPP4 INHIBITORS

Linagliptin- excretion bile ( safe in RF)

< >
 .....

PltAMLINTIDE
-
Islet Amyloid PolyPepde analog

SIC
< Type 1 & 2 DM >
 SODIUM-GLUCOSE CO-TRANSPORTER 2 (SGLT2) INHIBITORS j

Canagliflozin
Serligiliflozin
Dapagliflozin
Empagliflozin
SGLT-2

< >
SGLT-1
Reabsorption 9Do/o _ Collecting
duct
ADR
UTI
Risk of breast/bladder Ca
10010

Glycosuria
 >

Osteonecrosis of femur neck

...
 ((J,

:tiel o,-1�
�er,;,.'il e
to
'1
< Linaclotide­
(CFTR ativator)
Cystic fibrosis transmembrane
conductance regulator activator­
increases chloride rich secretion-
1 ncreases bowl movement • at\ot\-
d
�
o o s\ ' tl
d c. e c. 1' o o e
. . d \o u � \ te
09,0' et"�\ t\ a
c.f C --
� ' �\"et1'
tJ\ o 9 a t\
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ot a , -
< >
 Neuro Kinin 1 antagonist

< >

Canabinoids

PALONOSETRON
 AML Cerebellar ataxia

< >

I
< >
< >
< >
 EGFR HER-2- TRASTUZUMAB
HER-1
Lapatinib
HER 1 & 2

< >
Malignant melanoma

Aldesleukin - IL2
RCC
 I Sedative, anti emetic f

< >

Category X
 FETAL CHONDRODYSPLASIA PUNTATA
CONTRADI SYNDROME

< >

UN SAFE
Misoprostol- Moebius syndrome

Abnormal development of cranial

nerves- VI &VII

>
Facial paralysis
inability to move the eyes
from side to side
 � - 0 D

< >

....
 DES

Hypospadias

< >

Female 7 Vaginal ca
 WARFARIN Protein C ••••
•••
••
V & VIII
Hypercoagulation & dermal necrosis

< >

Purple toe syndrome

 ••••
•••
••
PHENYTOIN

< Purple Glove Syndrome

Pseudo Lymphoma,
 ••••
•••••
Pseudo jaundice

Rifabutine 1

< >

Pseudo alcoholic liver damage

Amiodarone

Pseudo porphyria
Naproxen
1. ldcntify th e pharmacodynamic curve de picted in the picture:

Ol
.s
"0
c
0
a.
1/)
~
1/)

~ 50
E
::J
1/)
Q)
Ol
ro
c Q)
~
Q)
a..

Logdose --+

Fig. l1
(a) Graded dose response curve
(b) Log dose response curve
(c) Quanta! dose response curve ""
(d) Percentage dose response curve
2. Point A in the Fig. I 1 corresponds to:
(a) Potency
(b) Efficacy
(c) EDSO
(d) LDSO
3. The image sh ows the Log DRC of four drugs A,B,C and D. Which of the following statements about these drugs is true?

Ol
.S
"0
c
0
a.
1/)
Q)
0:::

Log dose ---+

Flg. l2
 (..1) l rug i-. nw-.t dfi~.al'U
(b) Drug 8 and dn•g C ar~.• t.'quip~)hn
( ) Drug 11 , ... mo-.t ..... ft~.h t.'
(d) Drug B ~ ... 11......... ~x,tcn but nwn.• dfk<~l'U than dru~ \

4. G h en image "hO"•" the log DR of,, d rug .1lo nc ( ) <~ n u in the pt cscncc of a ntagon is ts (8 and C) . Iden tify the type of
antagoni m "hown in the 1.. un l' Band cun c :

r
0>
c
i5
c
0
0.
IJl
Q)
0::

Logdose - +

Fig. l3
a B 15 competiti\ e and Cis no n competiti ve antagonism
(b) B lS non-competith e a n Cis compe titive antagonism
c) Both an~ competitive a ntagonis ts
(d) Both arc non-competitive a ntagonists

5. Which of the followi ng drug is likely to act by signal transduction mechanism show n in the image above?
L Drug X

Extracellular
Space

Cytosol

" "''" "''""'"'"' Intracellular

signaling prote1ns
Phospho/ P bound to
rylated P phosphorylated
tyros1ne tyros1nes

Inactive RTK K1naseactivity

stimulated
S1gnal relayed by
act1vated s1gnahng proteins
~nto the cell's interior

Fig. l4
 ~lut,\m)1
(t- -"'..., llonl\Olll'
( ~· ~1 ... C' )Jll'
( " '-.\) W'

b. Till" hat date the drug salbu tam ol c.1n be used i n th e image of the astha lin strip hown in Fig. J 5 above?

Fig . IS
(a) HJulv 2017
(b) 31 jul\' 2017
(c) 17 June 201-l

.-. d 3{l •une 2017

a
helf life of salbutamol in this preparation (s hown in Fig. I 5) is:
3 Years
(b) 1~ ~ears
(c 5 \·ears
d Cannot be J..no" n from the information
E'piry date s h own in the s trip of the tablet (show n in Fig. I 5) m eans:
a U this preparation is used after Jul~ 2017, it will lose its potency
(b U this preparation is used after July 2017, it" ill become toxic
(c) Qualitv of this medicine is not assured after July 2017
~ &thiandb ·
9. What does IP in the above image (Fig. I 5) stand for:
(a) Drug is meant for Intra Pulmonary use
(b) Intellectual Property right of the CIPLA
(c) Die standards according to Indian Pharmacopeia
tA Itt'> an In tant release Preparation
10. A drug having half life of 12 hours is administered orally twice a day. A graph is plotted between plasma dru£
concentration and time which is shown in the graph. How much time will be taken for the plasma concentration to
reach at poi nt A?

l
u
c:
8
m
E
IJ)
m
a:

nme ~

Fig. l6
 (a) 12 hours
(b) 24 hours
(c) 36 hours
(d) 60 hours
11. The unknown drug is likely to be:

Fig.l 7

(a) Low dose adrenaline

(b) High dose adrenaline
(c) Nor-Adrenaline
(d) Isoprenaline
12. What is this effect known as:

Fig . IS

(a) Tachyphylaxis
(b) :\icotinic actions of Ach
(c) Biphasic response of Adr
(d) Vasomotor re\ crsal of Dale
13. What is this effect known as:

Fig. l9
(a) Tachyphylaxis
(b) icotinic actions of Ach
(c) Biphasic response of Adr
(d) Vasomotor reversal of Dale
14. What is this phenomenon known as:

Fig . l10
(a) Tachyphylaxis
(b) Nicotinic actions of Ach
(c) Biphasic response of Adr
(d) Vasomotor reversal of Dale
15. Apart from the effects shown in the image, the light and corneal reflex were present. Drug A is likely to be:

In•••"'..' Ton1loa
8
L 8 L
'
Fig. l11
 (a) Par.1svmpathomimctic
(b) Sympathomimetic
(c) r·Jrasympatholvtic
(d) Sympathol) tic
16. Apart from the effects s hown in the image, the light a nd cornea l reflex were present. Drug A is likely to be:

tatt.ocut.t "renrion - - -!----'

L u L N u

Fig. l12
(a) Parasympathomimetic
(b) Sympathomimetic
(c) Parasvmpatholytic
(d) Local anaesthetic
17. Identify the unknown drug by its action on rabbit ileum:

t t
Atropine Drug A
t Wash
Ach Wash t
Dru A Wash

Fig. l1 3
(a) Acetylcholine
(b) Adrenaline
(c) Barium ch loride
(d) Papavcrin('
18. Identify the unknown drug by its action on rabbit ile um:

t t t
Drug B Wflsh Atrop1ne Drug B

Fig . 114
 (a) Acetylcho line
(b) Adrenaline
(c) Ba r iu m chloride
(d ) Papa\ e rine

19. Identify the unknown drug by its action on rabbit ileum:

t
t Propanolol Drug C
t
Drug c Wash

Fig. l15
(a) Acetvlcholine
(b) Adrenaline
(c) Barium chl o ride
(d) Papaverine
20. Identify the unknown drug by its action on rabbit ileum:

Drug C
t
Drug D Wash

Flg . l1 6

(a) Acetylcholine
(b) Adrcn<11inc
(c) Barium chloride
(d) PtlpJwrinc
21. Identify the unknown dru g by its action on rabbit ileum:

t t t
Drug E Wash Drug E
Wash

Fig . l17
(.1) Acetylcholine
(b) Adrenaline
(c) Barium chloride
(d) Papaverine
22. A 50 year old male presented with suicidal overdose of a drug. Patient is flabby and comatose with shallow fail i ;
respiration. The BP of the person is 80/40 mm Hg and the lesion on the right is shown in the image. The likely poisoni
is:

Fig. l18
(a) Heroin
(b) Phenobarbitone
(c) Imipramine
(d) Phenytoin
23. Which antiepile ptic drug can lead to this adverse effect

Fig. 119
(a) Phenytoin
(b) Carbamazepinc
(c) Valproate
(d) Lamotrigine
24. Drug A is likely to b e:

,1----10

Fig. l20

(a) Phenytoin
(b) Ethosuximide
(c) Vigabatrin
(d) Benzodiazcpincs
25. Drug B is like ly to be:

• "' Voltage gated

Na •
I Na • channel
"'
Depolanzation
I

'
"'
Vesicular

0 00 0

0 0
0
0 0 0
0
0

~IODW I~! IDIIIDDIIIDIOIDIUIJI ~ Uil t ~ 10iltU

KCNQ
K' channel
Cl-

Fig . l21
(a) La mo trig ine
(b) Levetiracetam
(c) Pera mpcncl
(d) Retigabine
26. Otug C i:.likt:ly lu ut::

@)-! GAT-1 0
0
0 0 0
0 '
0 ~ GAB : 0
0
I 0 0 T-type
0
0
I
I
0 0 0 ca ·
0 : 0

lmtDIUr~ WDDDL.,Wf
l 1101111 ! UDUU UIIUIDUIIDIDUUJ
GABAA : AMPA
receptor i receptor K channel
Cl o Na'

Fig. l22
(a) Gabnpcnlin
(b) Tiagabi ne
(c) Vigab<llrin
(d) Retigabinr
27· Drug Dis likely to be:

K' .r=Volt?ge-gated
Na •
Na channel
KCNQ \
K' channel

0
0 0 0 0
o o- GABA 0
T-tyoe
~ 0:
0
0
0 0 Ca 2'

IDIJDJJDJDUUDIDlWJiDJDU UDJDJD
GABAA
f nmir.'m1ii
receptor receptor
cr Na'

Fig. l23
(a) Phenytoin
(b) Ethosuximide
(c) Vigabatrin
(d) tlenzod•a7cpmcs
28. Drug E is likely to be:

K'
Na
I( Voltage-gated
.
: Na channel
KCNQ ...
Depolarizatton
I

...
I

Vesicular
// release ',,,
,/

0
0 Glutamate (!]
0 0 0 0
0
o- GABA 0
0
0 0
0
0 0 0
0 0

mmnm
K channel
Na
ca ·
Fig. l24

(a) Rcligabinc
(b) Lamotrigine
(c) Levctirclu•tam
(d) 1opiramal('
29. Drug F is likely to be:

K•

KCNQ \
K' channel

GAT-1
0
0 o- GABA
0
0
0
0

DlJUI~ ~ ~ IUJ
cr
Fig. l 25
(a) Phenytoin
(b) Ethosuximide
(c) Vigabatrin
(d) Perampanel
30. A patient of Park in sonism d eveloped this condition after treatment. Which of the following drugs is likely to c,. •
this adverse effect?

Fig. l26
(a) Lcvo-dopa
(b) /\m,mtadinc
(c) Sclegilirw
(d) Prumipexolc
31. , A, ~n. patient
t h
with Schizo P h rerua
· was prescnbed
. .
halopcndol. Next day she returned with the features shown in the image.
·yua s ou1d be the treatment?

Fig. l27
(a) Increase the dose of haloperidol
{b) Give Propanolol
(c) Give Benzhexol
(d) Reassurance is enough
32. Mechanism of action of 3 antihypertensive drugs (X, Y and Z) is shown in the given figure. These are likely to be (in
sequence):

fNa'and H20 1
l_wention J
Fig. l28
(a) Enalapril, Enalkerin and Losartan
(b) Losa rlan, Enalapril and Enalkerin
(c) Enalkcrin, Enalapril, Losartan
(d) Enalkerin, Losa rtan, Enalapril
33. Which of the following drug is likely to produce the effect on action potential as shown in the diagram:

-- - .....
I ....
....
I
I ''
I
I
''
I ' \
I Drug A \
I
I \
I \
\
I
\
I \
I
I '

Fig.l29
(a) Quinidine
(b) Amiodarone
(c) Lignocaine
(d) Flecainide

34. Urug wh1ch can act at both sites 1 and 2 as shown in the diagram is:

Fig. l 30
(a) Sacu bi Lril
(b) Samplrilat
(c) Losarlan
(d) Nesirilide
35. Which of the following is likely to be drug A?

2
Ca • senditizers

Fig. l31
(a) Digoxin
(b) Levosimendan
(c) Amrinone
(d) None of these
36. Which of the following drugs are likely to cause the given change in ECG?

Normal ECG Long-QT

R R

QT interval QT tntervat

Fig. 132

(a) Quinidine
(b) Lignocaine
(c) Verapamil
(d) Propanolol
37. The drug obtained from this plant (shown in Fig. I 33) is used for the treatmen t of:

Fig . l33
(a) Malaria
(b) Congestive heart failure
(c) Myocardial infarction
(d) Irid ocycl itis
38. The drug obtain ed from the plant (shown in Fig. I 34) is used for the treatment of:

Fig. l 34
(a) Malaria
(b) Congestive heart failure
(c) Myocardial infarction
(d) Iridocyclitis
39. The drug obtained from the plant (shown in Fig. I 35) is used for the treatment of:

Fig. l35
(a) '\1alaria
(b) Congesh' e heart fai lure
(c) \h ocardial infarction
(d) Iridocyclitis
40. The plant s hown in the Fig. I 36 is a source of:

Fig. l36
(a) Atropine
(b) Morphine
(c) Quinine
(d) Digoxin
41. A 30 year old female was treated with an antihypertensive drug and presented with following features. The likely drug w

Fig. l37
(a) Minoxidil
(b) Fenoldopam
(c) Methyl Dopa
(d) Enalapril
42. A 60 year old maJe presents w ith acute severe chest pain associated with sweating 30 min before. The ECG th
person is s hown below. Which of the following drug should be given to this person:

25m1n/s 1Om1n/mV 150Hz 0058 12SL 250

Flg. l38
 (.l) /\tropine
(b) Sl n,'plokin<lSt'
(c) 1\rniod<~c
(d) Adenosine
43. A 30 year
. old athlete w en t cor routme
· cxammation.
. . H e h as no symptoms . The ECG is show n below What ad · ·11
you g 1ve to him? · v1se wt

Fig. l39
(a) No treatment is required
(b) Permanent pacemaker should be placed
(c) Atropine should be given
(d) Electrical defibrillation sh ould be done
44. A new ~ g X is given orally t~ a h ealthy volunteer in a dose of 100 mg. Plasma concentration of the drug is measured
at hourly rnterval and a graph IS plotted between plasma concentration and time as shown below in Fig. I 40.

27 ······ ·· · ·· ·· ---- --- ---

25

i
::=-
20 t - -- +-------T------\- - - - -- --Minimum
toxic cone.

--
"0
0>
2;
15
0
c:
0 10 +-.; -~ - - Minmu
0 effective cone.
ro
E
Vl
ro 5
0:
1 2 3 4 5 6 7 8 9 10 11
Time after drug administration (hr) -----+

Fig. l40

Which of the following statements about drug X is TRUE?

(a) Its Cmax. Is 20 1-1g/ dl.
(b) AUC from the above graph reflects rate of absorption
(c) Tmax for drug X is 7 hours.
(d) Instead of 100 mg drug X should be given in divided doses.
J!;. A 30 year old theatre actress developed few wrinkles on the face. The treating physician advised her to have local
inj ectio ns of a drug. This d rug is a lso indicated in cervical dysto nia and other spastic disorders like cerebral palsy. Very
recently, it h as also been approved for prophylaxis of migraine. The physician warned of the drug to cause dry mouth
and blurring of vision. T he actress searched the compound on internet and found the site of action of the drug as shown
in the Fig. I 41.
 ChAT

ACh

/ ACh\
ATP
+
ACh --
Choline+
Acetate

Fig. 141

lVhich of the following drug is being talked about?

(a) Hemicholinium
(b) Vesamicol
(c) Botulinum toxin
(d) Physostigmine
46. A new antiarrhythmic drug is found to be effective against both atria l and ventricular arrhythmias. Its effect on a ·c
potential is shown as below in Fig. I 42. The effect of this new drug is most similar to:
(a) Lignocaine
(b) Propanolol
(c) Encainide
(d) Quinidine

I
~ ~ .,_ ____ Action potential
after drug
I
I therapy
I
I
I
I
I
I
I
I

I
I Normal
I
I
Action potential
I
I
I
I

I
I
''
I
I
'
'
\
I

I
I
' I
I
I

."::::==== -
\
' ~ ~- c.:_ - :.; - .: - _ - _ - _ __
Flg. l42
47. Which of the following drug is not indicated in a pers on w ith the given ECG?

Fig. l43
(a) Amiodarone
(b) Propanol ol
(c) Vera parnil
(d) Adenosine
 s . Identify ctntg A lin Fig. 1 44) by its nll'chanism of action:

~ UOP • • UDP -~ ~ - •- + r UDP

lJ
1 UDP-MurN~/
MLtra MurB MurC MurB
UDP-GicNAc t UDP-MurNAc
pentapeptide r
P --

[orug c]
MraY

Lipid II
- - ~ Lipd I
Cytoplasm MurG, UDP - ~ pp

Periplasm PP Transglycosylase pp

o'(oyoy •3_ o']' ~

jorug A~ f
~
Transpeptidase
? MurNAc

CJ GlcNac

:l:l:l Fig. l44

( P P)~ Bactoprenol
(pyrophosphate

(a) Cloxacillin
n (b) Vancomycin
(c) Bacitracin
(d) Fosfomycin
49. Identify drug 8 by its mechanism of action (as shown in Fig. I 44):
{a) Cloxacillin
(b) Vancomycin
(c) Bacitracin
(d) Fosfomyci n
Identify drug C by its mechanism of action (as s hown in Fig. I 44):
(a) Cloxacillin
(b) Vancomycin
(c) Bacitracin
(d) Fosfomycin
I. Identify drug D by its m echanism of action (as s hown in Fig. I 44):
(a) Cloxacillin
(b) Vancomycin
(c) Bacitracin
(d) Fosfomycin
In the given Fig. I 45 at which site does penicillinase work?

Fig. l45
 (a) Site A
(b) Site B
(c) Site C
(d) SiteD
53. T he drug shown in the f ig. I 46 is treatment of ch oice for:
OH 0 OH

OH N
H3c/ "'- cH3
Flg. l46
(<1) rntcric ft'H'f
(h) Q Fe\er
(') \1RSA
(d) C.onorrhea
54. Identify drug A by its mechanis m of action as s hown in the Fig. I 47:
Amino acid

Growing
protein D'RNA [!] ~
''
' .
'
'
Ribosome ''
50s '

.
..~
Fig. l 47
(a) Doxycycline
(b) Chloramphenicol
(c) \7ithromycin
(d) Pemcillin C
55. Jdentify drug B by it!t mech anis m of action as s hown in the Fig. I 47:
(a) Doxycycline
(b) Chloramplwnicol
(c) A/ithrom ycin
(d) Pt>nicillin C
56. Identify drug C by its mechanism of action as s hown in the Fig . I 47:
(.l) Doxycydme
(h) Chloramplwnicol
(c) '\nthronwcin
(d) Penicl (~
57. Mechanism of transfer of drug resis tance s how n in th e g iven fig ure I 48 is:

Transposon Donor cell Recipient cell

Fig. l48
 (a) Conjugation
(b) Transformation
(c) Transduction
(d) Mutation
58. Mechanism of transfer of drug resis tance sh own in the given figure 1 49 is:

- - - - - - - - - .Release of

~ ~ -:NA
Donor cell Antibiotic- Recipient cell
resistance gene

Flg. l49
(a) Conjugation
(b) Transformation
(c) Transduction
(d) Mutation
59. Mech anism of transfer of drug resistance sh own in the given figure I 50 is:

Release
Phage-infected donor cell of phage Recipient cell

Fig. ISO
(a) Conjugation
(b) Transformation
(c) Transduction
(d) Mutation
60. Bioch emical m echan isms of dru g resistan ce are show n in the given figure I 51. Most important mode of resistance in
M RSAis:

Target site
modification
IAl • Decreased
permeability
[Bl

•
Enzymatic
degradation
[g
Efflux
•
Bypass ~
[D)
Fig. I 51
(a) A
(b) B
{c) C
{d) D
61. Vancomycin develops resistance to Enterococcus by which mechanis m (as s hown in Fig. I 51)?
(a) A
(b) B
(c) C
(d) D
62. Cis the major mechanism of res istance (according to Fig. I 51) against:
(a) Fluoroquinoloncs
(b) Aminoglvcosides
(c) Tetracyclines
(d) Sufonamides
63. Major mechanism of development of resistance agains t cotrimoxazole (in Fig. I 51) is:
(a) B
(b) c
(c) D
(d) E
64. E is the major mode of resistance against (as shown in Fig. I 51):
(a) Tetracyclines
(b) Chloramphenicol
(c) Ampicillin
(d) Ciprofloxacin
65. The only oral drug (among the given options) effective for the treatment of the condition shown in the figure I 52 is:

Brow
prominent

Soft tissues
ur IIU:it:: , t::C:tr:;
lips enlarged

Fig. I 52
(a) Octretide
(b) Cabcrgolinc
(c) Pegvisomant
(d) L- thyroxine
66. A 40 year old male presented to emergency (as shown in Fig. I 53) with fever, extreme restlessness, confusion and
marked weakness. On examination, severe tachycardia and BP of 170/110 mmHg was noted. ECG revealed the presence
of atrial fibrillation. Which among the following is the only life saving drug that should be given immediately to this person:

Fig. I 53
(<1) C1rbirnazole
(b) R,ldionctiw iodine
 (c) Prop<molol
(d) l ioth\ ronml'
67. A J?atient presented to O PD with swelling in the neck a'l shown in the Fig. 1 54. He complains of decreased appetite,
fahgue and cold intoerancc. lie h as gain ed 8 Kg of weig ht in laqt 4 munt hc;. rl hyroid fu nction tests revealed normal T4
b u t elevated T II. llw patient s h ould be treated w ith:

Fig. I 54
(a) Lioth\ ro1\inc
(b) L-thYTO\:inc
(c) Carbimazole
(d) Steroids . .
68. A 40 year old male suffering from a chronic disease presents to OPD w t'th th e features shown in the Fig. I 55. This ts
likely to be adverse effect of:

Bruisablllty
ecchymosis

Red stration

~ - Pendulous
abdomen

Poor wound
heanng

osteoporosis
compressed
(codfish)
vertebrae
Fig. I 55
 (.1) Corticosteroids
(b) NSAIDs
(c) Infli>.imab
(d) Androgens
69. The medicine shown in the Fig. I 56 is used for:

... ... ... ...

... ... ... ...
3 4 5 6 7
t

t ...
14 13 12 11 10 9 8
....
15 16 17 18 19 21

28

Fig. I 56
(a) Multibacillary leprosy
(b) Paucibacillary leprosy
(c) Tuberculosis
(d) Contraception
70. The oral contraceptives shown in the Fig. I 57 are:

Fig. I 57
(a) Monophasic combirwd OCPs
(b) Biphasic combirwd Q(p..,
(c) Jriphasic combined OCJ>s
(d) Fmergenc; Pill..,
71. The oral contraceptives shown in the Fig. I 58 are:

Fig. I 58
(a) Monophasic combined OCPs
(b) Biphasic combined OCPs
(c) Triphasic combined OCPs
(d) Emergency Pills
72. A 52-year-old male, Vivek was treated with enalapril for hypertension. It was able to control his blood pressure. Which
of the following is the most likely combination of changes in response to this patient's treatment?

(a) i i .!, .!, i

(b) i t ,j. .!, ,j.

(c) t ,j. ,j. ,j. ,j.

{d) -!. -!. -!. No change

73. The drug Z show n in the Fig. I 59 is likely to be:

segments of-+ ~
proximal tubule

Reabsorption
Collecting
duct
S3 segments of
proximal tubule

No glucose
Fig. I 59
(a) Pramlintide
(b) Exenatide
(c) Canagliflozin
(d) S1tagliptin
74. Based on the given m echanism of action as shown in Fig. I 60, Drug A is likely to be:
Meal ingested

A
~e

Small
mtestlne i lnsulin relase
J..Giucagon release
Large
intestine

Panaeas

a-cells
Fig. I SO
(a) Exenatidc
(b) Vildagliptin
(c) Canagliflozin
(d) Pramlintidc
75. The drug X used in osteoporosis has the mechanism shown in the Fig. I 61. X is likely to be:

T RANKL Osteoblast

I RANK @ (0 ~ " - ..

'
....
Bone
Osteoblasts
0
0
0 0

Fig. l61
 (a) Tcriparatide
(b) Alendronatc
(c) Denosumab
(d) Estrogen

76. Cell cycle is s how n in the figure 1 62 below. Which of the fo llowing drug act specifically at the stage marked with
arrow?

G1-Growth
S-DNA synthesis
G2-Growth and
preparation for
mitosis
M-mitosis
(Cell division

Fig.l62
(a) Mechlorethamine
(b) Methotrexate
(c) Vincristine
(d) Paclitaxel
77. Figure I 63 shows the mechanism of action of:

Metaphase
Metaphase

Tubulin molecules fail

Tubulin
to polymerize in the
molecules
presence of vinca

-.
stacked to
alkaloids
form miotic
spindle
"
Anaphase

Anaphase 1

Fig. l63

(a) Vinblastine
(b) Cisplatin
(c) Imatinib
(d) Trastuzumab
78. A patient present with the features shown in the figure I 64 after treatment w ith an anticancer drug. The likely drug i:

Flg. l64
(a) Ch.platin
(b) 5 lluorout\lcil
(c) 1cthotre\clte
(d) lmatinib

79. A patient was given radiotherapy for head and neck cancer. After 6 months chemotherapy was started. The patient
presented with the features s hown in Fig. I 65 after start of chemotherapy. It is likely due to which drug?

Fig. l 65
(a) Doxorubicin
(b) Cisplatin
(c) Imatinib
(d) Methotrexate
80. Figure 1 66 shows the mechanism of action of which of the following drug?
ATP
I / ATP
-+AOP ¥
I r ~O ~
BCR-
ABL l!.TYR.0Sub-
BCR-
ABL
strate

Intracellular Intracellular
signals signals

Fig. l 66
 {.1) ilotnb~
(~) \ h.'thotn.·'·'h.'
(d l\.•rtucu m,\b
(d) l~p,1hn

bOlby W.t ~ born with the congenital malformations s hown in the figure 1 67. T he like ly teratogenic drug received by
4

l,
the mother is:

Fig. l 67
(a) Thalidomide
(b) Alcohol
(c) Carbimazole
(d) Heparin
.
!.. Based on the m echarusm s h own 1·n the figure 1 68, Drug A is likely to be:

Intracellular
signaling
activation

Fig. l68
 (a) Aspirin
(b) Clopidogrel
(c) Abciximab
(d) All of these
83. Based on the mechanism shown in the figure I 68, Drug B is likely to be:
(a) Aspirin
(b) Clopidogrel
(c) Abciximab
(d) All of these
84. Based on the mechanism shown in the figure I 68, Drug C is likely to be:
(a) Aspirin
(b) Clopidogr<'l
(c) Abciximab
(d) All of these
85. A patient was started on an anticoagulant therapy for DVT. Next day he presented 'th th f .
Fig. I 69. The implicated drug is: WI e eatures shown m the

Fig. J69
(a) Warfarin
{b) Heparin
(c) Rivaroxaban
{d) Dabigatran
86. A patient was started on an anticoagulant therapy for DVT. Next day he presented with the features shown in the
Fig. I 70. The implicated drug is:

Fig. l70
 (~ 1 ) \\ arfarin
(b) Heparin
(c) Rivaro>-aban
(d) Dabigatra:n
S". A 20-yea.r-old male Chintu i b . . . .
drug fr h . ' s emg treated With zafirlukast for bronchial asthma. The most likely site of action of this
om t e Fig. I 71 can be deciphered as:
(a) A
(b) B
(c) C
(d) D

Membrane phospholipids

l PhosphoHpaseA2 • ---------- - (A)

Arachidonic acid

cox LOX +----------- (B)

Prostanoids

T
Cys-LT receptors + -- (C)

l
Bronchoconstriction + --· (D)

Fig. l71

88. A 50-year-old male, Rajesh presented to OPD with fever and sore throat with mouth ulcers. He has a history of
m yocardial infarction and is taking several drugs. One month back he had an episode of transient ischemic attack. His
complete blood count shows:
Hb 14.2g/dL
WBC 900/mm'
Platelet 220000/mm'
If a n antipJatelet drug is responsible for the above symptoms of the patients, Which of the following drugs is most
likely m echanism of the drug as shown in Fig. I 72?
(a) A
(b) B
(c ) (
(d) D
 Subendothelial vWF
Colla en

ADP .-.- -
f 1. Adhesion

_. Fibrin
~Agreation

( o Xo Xo Xo Xo Xo Xo Xo Xo Xo )
%%%'6 %~ c%f%%'9 <%>%%'i!i ·'6<'&'8%'

Fig. l72

89. A 15-year-old female, Rashmi presents to the emergency in comatose state. She is a known case of type 1 diabete
mellitus. Immediate blood sugar is measured by glucometer and found to be 658 mgldl. Urine is found to be positiH
for glucose as well as ketone bodies. Which of the following insulin types depicted in the Fig. I 73 below is mos
appropriate for the treatment of this patient's condition?
(a) A
(b) B
(c) C
(d) D

Q)

"'0
(.)
A
..=!
Ol
-o
0
0
::0
.s
(ij D
u.

2 4 6 8 10 12 14 16 18 20 22
Time (h)
Fig. l 73
· ·sa known case of type 2 dia betes and was well controlled on metformin. But
90. A marnath , a 58 year o ld b usJOessma n t. · . . h bl d t
s ince last 5 years the different combinations of ora l antidiabetic drugs were ~te d_ and ~t l t e .00 sugar was n~
controlled. So, the physicia n thought of giving him ins ulin. Which of the fo llowtng m su l~n ~Fro1 Ftg._I 74) can be used
to maintain the basal levels of insulin without producing significant risk of hypoglycenua tn thts pahent:
(a) A
(b) B
(c) C
(d) 0
 <I>
Vl
0
(J
A
::J
c;,
-o
0
.2
.0
s
ro
u.. D

4 6 8 10 12 14 16 18 20 22
Time (h)

Fig. l 74
9 A n~w inhale~ anesthetic has been developed and is tested in a series of experiments. Anesthetic tension in the
art~ n~l blood tS shown on the graph below (in Fig. I 75) as a function of time after beginning inhalation (Drug A).
A s1milar curve for nitrous oxide is also shown:
\'\ hich_ of the following best describes the properties of the new anesthetic compared to nitrous oxide'?
(a) High b lood: gas partition coefficient
(b) Low solubility in the blood
(c) Rapid onset of action
(d) Low potency

~ Nitrous oxide

Drug A

Fig. l 75

92. A 53 yea r old male Arjun presented to emergency with blunt injury to abdomen and crushing of his left leg under
the tyrcs of a bus in a road traffi c accident. His blood pressure was 80/40 mmHg. Emergency laparatomy was planned
to repair the ruptured viscera and to know the cause of internal bleeding. Succynlcholine was used for intubation
and vecuronium for maintenance of muscle relaxation. Anaesthesia was induced by thiopentone and maintained
'Y halothane. J Jowcver, during intraoperative period, the patient developed arrhythmias as shown in ECG below
(Fi g. 1 76). Which of the following is the likely cause of this ECG finding?
(,l) t>rl'St' n<<'of .1ty pic,1l p ~e ud oc h o lir ws t e r ase i n this patient
(b) '1ur ciny lt holirw inducl'd hy pl•rk,ll t>mia
(<) V<•c trnm ium ovt•rdosc
(d ) A ~.·ti <d • nl intr ,l •" h.•rial injt•ction o f thiopr ntorw
 Fig . l 76
93. You are studying ph armacokinetic properties of thiopentone. A dose-time relationship in various tissues after a single
bolus of thiopentone is shown in the graph b elow (in Fig. I 77). Curves A, B and C in the graph represent:

B
Q) '
(J) '
0 '
""0
'
' ' c
0>
' '\
::J
..... I'
0

Time
Fig. l 77
Curve A Curve B Curve C
(a) Brain Blood Adipose tissue
(b) Blood Brain Adipose tissue
(c) Brain Adipose tissue Blood
(d) Adipose tissue Brain Blood
94. A 72-year-old male, Hemraj was admitted to the hospital with severe dyspnoea and orthopnea. On investigations a11d
clinical examination, he was found to be suffering from congestive h eart failure. He was given some drug intravenously
and the patient experienced brisk diuresis and significant relief of symptoms. This drug acts predominantly on which
of the following segments of nephron (From Fig. I 78)?
(a) A
(b) B
(c) C
(d) D

Medulla

Fig . l 78
1. Ans. (c) Q uanta! dose response curve
When the dose
called · response cu rv~ P1o ts num ber o f people rcspondmg
· (or percentage of people responding) on y axis then it is
DRC i quanta! DRC ~her 1f t~1erc is rcspon_se (or percentage response) on Y-axis, then it is called graded DRC. Quanta!
s employed f01 cond1h<.ms where there 1s all or none response. It is used to calculate EDSO and LDSO.
2. Ans. (c) EDSO
~D 50 or median effective dose is the dose at which 50 percent of the recipient gets the desired (or undesired) action. It
IS calculated from the quanta! DRC as shown in the figure. The same point is graded DRC corresponds to potency of the
drug.
3. Ans. (d) B is less _potent but more efficacious than drug A
In DRC, potency IS assessed by looking at the location of cur ve on X axis ie curves on right side are less potent drugs and
those on le~t ar~ more potent. On the other hand, efficacy is assessed by looking at the curves on Y axis. Higher curves are
of more eff1cac1ous drugs and lower for less efficacious ones. However, read the statement carefully, we cannot assess ef-
fectiveness from the DRC.
Therefore in the given image:
• A is most potent, not most efficacious
• Band Care equally efficacious, not equipotent
• D is most efficacious, not most effective
• B is less potent than drug A but has more efficacy than it
4. Ans. (a) B is competitive and C is non competitive antagonist
In rnmpPtitive antagonism, the DRC shifts towards right ie potency decreases but efficacy remains same. On the other
hand, in case of non-competitive antagnosim, the curve becomes flat ie potency remains same but efficacy decreases

- Ans. (b) G rowth H ormone

The given figure shows that the signal transd uction mechanism of the receptor is tlu·ough tyrosine kinase. The enzymatic
receptors arc present for
• Cytokines
• Prolactin
• Insulin
• Growth Hormone
Ans. (d) 301h June 2017 . .
The given strip shows the information that MFD (means manufacturing date) is July 2014 whereas expuy date 1s]unc 2017.
The drug can be used till last date of month of expiry date. Therefore this product can be used upto 30th June 2014

7. Ans. (a) 3years . . f ~ ust.•d

The shelf life is time in which drug can be used ie from manufacturing date to expiry date. In th1s ftgure, c rug can
from July 2014 till June 2017, so shelf life is 3 years.
B. Ans. (c) Quality of this medicine isnot assured after June 2017 1
1
The expiry date means the time till that the product should remain within specified limits if proper Y store(·

9. Ans. (c) The standards according to Indian Pharmacopoeia

The abbn.•viations written on the drug label
• IP: Indian Pharmacopoeia
• BP: British Pharmacopoeia
• USI': United Nations Pharmacopoeia
• BNF: Bri tish National Formulary

10. Ans. (d) 60 h ours . .15. 1 5 half IIVl'S. ;\.:. h.11f lill'
J he point A n'fers to steady state. The time taken to reach steady slate plasma conccntratwn 4 tc
of the drug is 12 hours in the question, so it will take 48-60 hours to reach tht• steady stc1te.
 11. Ans. (b) High dose Adrenaline
GiH'n figure shows that after giving a drug, blood pressure first increases and then decreases. It is known ac; biphasic re-
sponse'' hich 1s characteristic of high dose adrenaline. At low doses, adrenulinc stimulates only beta 2 receptors and thus
cause only fall 111 BP. But at high doses, It s timulates both a lpha and beta receptors and initially cause rise in BP due to
alpha receptor stunulation, however as plasma concentration falls, it lead to decrease in BP due to stimulation of only beta
2 receptors. 1his is kno ...vn as biphasic response
12. Ans. (d) Vasomotor reversal of Dale
Adrenaline norM I~ y ~r·oduce. biph~sc re~po_ns at high ~ l ~se as cxpl~ined _in ~he question above. However, if alpha
blocker (Phcntol.munc m the g1ven ftgure) ts gtven before g 1v1ng ad rena lm e, th1s b1phasic response is not seen. Only fall in
BP is noted. This is called vasomotor reversal of Dale
13. Ans. (b) icotinic actions of acetylch oline
An•t) kholine normally produces fall in BP due to its effect on musca rinic receptors to cau se vasodilation. However when
given in ' e•) high doses, it ca n s timu late nicotinic rece ptors pres<.'nt on the ganglia that can result in increase in blood
pressure. H owever, to demons trate this effect, musca rinic receptors s hould be blocked by giving high dose atropine.
14. Ans. (a) Tachyphy laxis
\Vhen repl'tlted doses of a drug produce lesser response than original, it is called tachy phylaxis. It is shown by indirectly
acting~' mpathomimetic drugs like tyramine and ephedrine
15. Ans. (b) Sympathomim e tic
rhe drug is causing m yd riasis with decrease in lOP whereas both light reflex and corneal reflex are present. These are
change~ of sympathomimetic drugs like adrenaline.
\\ e can identif\ the nature of some drugs by their action on rabbit eye.

Parasympathomimetics like pilocarpine Present Decreases

Parasympatholytics like atropine Absent No effect or incrco::;c
Local Anaesthetic like lignocaine No change Present Absent No effect
Cocaine Mydriasis Present Absent Decreases
16. Ans. (a) Parasympa thomimetics
As explained in the question a bove, th e drug is causing mios is with decrease in lOP whereas both light reflex and corneal
reflex are present. These arc c ha nges of parasympathomimetic drugs li ke pi locarpine.
17. A ns. (c) Barium chloride
The given figure shows that the dru g is s tim ulant at rabbit ileum and its stimulatory effects are not blocked by <~tropine.
So, it seems to be a directly acting stimulant like Barium chloride or calcium chloride.
We can identifv the nature of some drugs by their effect on rabbit ileum

Banum chloride Stimulant

Adrenaline Depressant Alpha and Beta receptors
~- - -r·
Papavenne Depressant
To identif\· the drug,
First St>l' ,~ · lwtr the drug incn•ases tht• tone (stimul.1nt) or decn•aS('S (dcpr<.'S'ic111t). . .
I( it is stimulant, it i~ likely to be acetylcholine or bilriu m c hloride. 1 hen set' '' hP_
t h_cr_ the.effect can be ab~he by atrop~ne
or not. If stimulant effect is absent <Iflcr iltropine, the drug is ,\n•tvlchohnt' but rf 1t 1s s ttll present, then 1t 1s d1recll) actmg
drug like barium or calci um c hloride. . . . , , ,
If it is depressant, it is likely to be adrenal me or papavt>riiW. I hen see"' ht>ther the cf~et can be abolrshed b) blockt r o_r not:
If deprt•ssant effect is absent or reduced after giving beta blocker (com~?lety aboh~ed by alpha plus beta blocket), the
drug is ,1 drerMfinc but if it is s till present, then it ic; directly ,wting drug like papavenne or KCl.

18. Ans. (a) Acetylcholine . . .

The drug is stimulant whose effect i~ abolished after g1vmg atroprne
19. Ans. (b) Adrenaline
The given drug is depressant whose effect is .:tbolishcd .1ftcr beta blockct
20. Ans. (b) Adrenaline
The giYen drug is depressant ''hose effect is significanlly reduced by beta blocker. So the drug is working through beta
receptors but as some effect is s till present means the drug is acting on alpha receptors also. The likely drug is adrenaline
21. Ans. (d) Papaverine
The given drug is a depressant whose effects arc not abolished by beta blocker. So the drug is directly acting depressant
like papaverine or KCl.
Ans. (b) Phenobarbitone
The clinical features points towards poisoning ca used by CNS depressan t drug. The figure shows the characteristic barbi-
turate blisters. So it is p henobarbitone poisoning.
' An . (a) Phenytoin
The figure shows the gum hypertrophy which is caused by phenytoin
The mechanism of action of antiepileptic drugs

Na Channel blockers Phenytoin

Carbamazepine
Lamotrigine
Valproate
Stimulate GABA-BZD Cl channel comples Barbiturates
Benzodiazepines
lnhrbit GABA transaminase Vigabatrin
Inhibit GAT-1 TioyJr~

Act on SV2A Levetiracetam

Open K + Channels Retigabine
Block NMDA receptors Felbamate
Block AMPA receptors Perampanel
Block L type Ca Channels Ethosuximide

2· Ans. (a) Phenytoin

2 Ans. (b) Levetiracetam
2 Ans. (b) Tiagabine
2 . Ans. (d) Benzodiazepines
2A .• Ans. (a) Retigabine
29. Ans. (d) Perampanel
30. Ans. (b) Amantadine . . . . . . "huacteristic ad,
The figure shows the livedo reticularis, a type o f skm ptgmentahon m the fonn of mesh (reticular). It 1" t •
verse effect of amantadine

31. Ans. (c) Give Benzhexol . & h ,, 1 j..; drug of

The figu re shows the torticollis. Thi!> is an ex trap yra mid<~l adversl' df~ct CMtsed b\ ilntips\'chohcs. ~ o z ~ 0
choice for this adverse effect.
32. Ans. (c) Enalkerin, EnaJapril, Losartan
The figure shows the drugs m~ibtng_he.raos pathway
• Renin inhbtor ~: Enalkerrn, Renukenn, Altsktren
• ACE inhibitor<;: I'nalapril, Ramipril, Perindopril
• ARB. Losartan, Valsartan, Telmisartan
33. Ans. (c) Lig nocaine , ·tion p1,tt•nti.,l
I he figure shows that the drug decn:•tls<.>s slope of phase 0 ( a channel hlock.1de) ,lnd also it dl'<t• '"~
dur.1tion (K channel opener) fhcse are the actions of t1nti,lrrhythmtl drugs lwongm~ to c I,,..,.., lh ht...e ·~w., 1 1
"
'c.. • "'
34. Ans. (b) Sampatrilat
S,1mpatrilat and 001tlptltrilat are vasopeptidase inhibitors th<lt inhibit both neutral endopeptidase as well a'> ACE.
35. Ans. (a) Digoxin
I he figure sho\\'l the mechanism of action of digitalis ie NJ K pump inhibitor drug
36. Ans. (a) Quinidine
Drugs that block K channels in the heart can cause increase in QT interval and predispose to Torsades' de pointcs. Antiar-
rh\ thmic drugs ha\'ing K channel blocking property are:
Cl~1s la. Quinidnc and Procainamide
CIJss :1: Amiodarone, Sotalol, Bretylium etc
37. Ans. (b) Congestive heart fa ilure
The figu re shows the plant digitalis purpura.lt ca n identified from name itself. The flowers of the plant can be put in fin-
gers (digits). Digoxin is the drug obtained from this plant and is used in CT TF
38. Ans. (a) Malaria
The figu re shows the bark of c inchona plant. The drugs obtained from this plant are quinine and quinidine. Former is used
for malaria whereas latter can be used for arrhythmias
39. Ans. (c) Myocardia l infarction
I'hc plant shown in the figure is papaver somniferum. Crud extract of this plant is known as opium which is source of
opioids like morphine.
40. Ans. (a) Atropi ne
The plant shown in the figure is dhatura stramomium w hich is source of atropine
41. Ans. (a) Mi noxidil
The fi g ure shows ma le pattern hair growth in females known as hirsutism. It is adverse effect of minoxidil. Other tmpor
tant drugs causing hirsutism are cyclosporine and pheny toin apart from androgens.
42. Ans. (b) Streptokinase
The gtven ELL. shows the ST elevation in leads v:; to V6 whereas there is associated ST depression in contiguous lead.,
I, II and aVF. These ECC findings along with clinical features points towards acuteST elevation MI. Thrombolytic" likl•
streptokinase a re indica ted in these patients.
43. Ans. (a) No treatment is required
The given ECC shows the patient in normal s inus rhy thm. llowcvcr, the heart rate is very low (approximately 50 lx•.1ts per
minute). As the patient is asymptomatic and is athlete (hcnrt rate is usua lly low in these pati e n~ s), no treatment is rcqui~ cd.
However this person s hou ld not be prescribed any drug that can reduce heart rate fUI'thcr (like beta blockers or Cillcllllll
channel blockers)
Also sec the ECG findings in different types of heart block
First degree block

Second degree type 1

Second degree type 2

;_j~ ~
44. Ans.. (d) Ins tea~ of 100 m g, drug X s ho u ld be given in divided doses. (Ref Goodman Gilman 12/e p35)
C , .., ts the maxtmum plasma concentration obtained. In this questin, C is 27 llg/ dl.
T """ is the time to reach Cn...,· It tells about rate of absorption. From the given graph, T "'"'is 4 hours.
AUC reflects extent of absorption and not the rate of absorption.
Thi., drug, when given as 100 mg, produce a C""'' which is higher than the minimum toxic concentration (20 llg/ dl.). Thus
to avoid the toxic effects, C n,.,, must be lower and to produce a lower Cnw,.,-' the dose has to be reduced.
l5. Ans. (c) Botulinu m toxin (Ref KK Sharma 2/e p211)
As shown in the diagram, the drug is inhibiting the exocytosis of ACh. Botulinum toxin act by this mechanism. Other
features pointing towards botulinum toxin are:
• Anticholinergic adverse effects (dry mouth, blurring of vision)
• Usc in wrinkles, spastic disorders, prophylaxis of migraine.
4 Ans. (d) Quinidine (Ref: KK Sharma 2/e p301)
This drug is decreasing the slope of phase 0 (Na+ channel blocking property) as well as increasing the action potential dura-
tion (K• channel blocking property). Thus, it exhibits the properties of class Ia anti-arrhythmic agents like quinidine.
4i Ans. (d) Adenosine (Ref Harrisons 19th/e p2080)
fhc ECG shows the features of atrial fibrillation as
rregularly irregular rhythm
Absence of P waves
The drugs used for atrial fibrillation include:
a. Anticoagulants like warfarin, heparin etc
b. Drugs to control atrial rate:
1. Beta blockers: Propanolol, metoprolol etc.
ii. Calcium channel blockers: Diltiazem and Verapamil
m. Digoxin
c. Drugs to control rhythm: . . .
i Sodium channel blockers: Fleca inide, Propafenone, qutmdmc
.. Pottasiurn channel blockers: Amiodarone, ibutilide, dofetil ide
Ad: ~·osine has very very short half li fe (less than 10 sec.). It is ind icated for treatment of PSVT only.

48 Ans. (a) C loxacillin . .

Mechanism of action of antim icrobtals acttng on cell wa ll

Fosfomycin Phosphoenolpyruvate
Cyclosenne Alanine-Alanine ligase

Bacitracin Bactoprenol
Vancomycin - - - - - - - ' -
T_
ransglycosylase
Beta lactams .L T~ran ~ s~p:e! .: td:ase :._ _ _ _ _ _ _ __ --1

49. Ans. (b) Va ncomyci n

SO. A ns . (d) Fosfomyci n
51. Ans . (c) Bacitracin
52. Ans (a) . . ·at activity. Beta lactamasc break this
The ·four member ring is beta lactam ring and i~s int:grity is rcqutred for anttbacten, ·
· b e t ween Nand C=O group and can result m reststance.
nng
53. Ans . (b) Q fev er . . . h, roup 'tetracyclines'. This is tht' chcmi-
Th e slructu rr s hows that
G
the drug contains
• •
four cycles, therefore Jtts c1 drug tn l ( g
cal structure of doxycycline. Doxycyclme IS DOC for Q fever.
54. Ans. (a) Doxycycline . . . . .
M echanis m of action of pr otem synthesiS mhtbttors
 50S Pept1dyl transferase and transfer of peptide cha1n from A to p srte
50S Translocation (transfer of peptide cha1n from P to A site)
50S Translocation
50S
----------------
50S
30S and 50S lnitiat1on and cause m1sreading of mRNA code

55. An~. (b) Ch loramphenicol

56. Ans. (c) Azithromycin
57. Ans. (b) Conjugation
Methods of horizontal transfer of drug res is tance

By forming sex pili between to bacteria through phys1ca1contact

Through environment

Transduction ---------------------------.IL...T_h_r_o....:
ug=-h--
B_a_
ct_e_rio....:p_h_a..:::g:....
e________ _ _ __ _ _ __ ____-.J
58. Ans. (b) Transformation
59. Ans. (c) Transduction
60. Ans. (a) Target site modification
Resistance in MRSA occurs mainly because of altered penicillin binding proteins
Biochemical mode of transfer of drug resistan ce

Enzymatic breakdown A : Aminoglycosides

B : Beta lactams
C: Chloramphenicol
Decreased permeability Aminoglycosides

Effiuxpumps_______ _ -+ ~ Tetra=cy ~ c ~ line=s - - -

4
Altered me t a bo :. l :. i c :!p : a:.th w .: a :. y ~ - ~ S :. u l:.f o :. n .: a :. m :. i ~ de .: s :_ _ _ __ __ .,
Altered target MRSA
Vancomycin
Fluoroquinolones

61. Ans. (a) Target site modification l 'l , , • ,"" \l \l)in~ t,, \.min~-
Vancomycm · r~,> s1~ tan ce occurs due to altered bindmg
· s1· te w 110s~ ' stru
• c·tttl'l' che1ngcs
<
1rorn ~ ' " 1' 11 t '

Lactate
62. Ans. (b) Aminoglycosides
63. Ans. (c) 0 . .· p, · i~t,nce to sulfon,unidcs ,m,\ thu" cotn·
C..otrimoxazole contains s ulfamcthoxazolc (a sulfol'h1midc) ,md tnnwthop•.111.'· '\lS ·f' .,, ,~folk \cid
moxa/ole occur'><.1uc to alternative metabolic pi'lthwuy .ll' lJ,1t' I t'rt•'
. ' IH'I utihllllg pn' 011 oCI..
s• I

64. (a) Tetracyclines

65. A ns. (b) CabergoJine . . . • .. s \ikl' bromocriptine and c,,bcrgoline ,m' tlw onh ()r,\\
'I he figure shovvs the features of acromcga ly. Dopammc agonist. th)rroxine h 1s no role in ,Kmtn\.')J,·'"
r> ~ · 1e an d pegv1o;omant 1 1
drugs for c1cromcgaly. vdrcotit · o· for acronwga \'· --
· · t'' bl e t II'LII'S
are 111JCC ' '·

66. Ans. (c) PropanoloJ . . r . we the life ·we need to imnwdi,,ll'\v t\'\ \.'r"l' ~ · ,\1
fhe fe,1turcs gi' rn in the question, points towards thyroto'\ic cnsls. 0 s, b •. ' ,. ~ 'nncl blockl'r" likt' , l'r,11),11l\ll \)\
1 01 1
di<)\ ,1scular svmptom'>. It can be done by beta blockt>rs l1.kl' prop.:tnololor Vl'<lllll ~ '"
diltiaNm
67. Ans. (b) L-lhyroxinc

lht.~
conothon. !~tuns «nd the invcstig«tions (elevated l'SH) points towMds hypothyroidism. L-thyroxine is drug of choice for this

68. Ans. (a) Corticosteroids

The figurc s hows the characteristic "C ushing '~ llabitus". It is the adverse effect of prolonged use of corticosteroids.
69. Ans. (d) Contraception
Th~figure s~o'" s the 28 dnv pills with 21 of different colou r and 7 of different. These arc combined oral contraceptive pills
whtch arc gl\ en for 21 dt'I)'S and last 7 days are hormone free tablets (containing only iron) are given.
70. Ans. (a) Monoph asic pills
The strip sho\\'S 28 tablets with 21 on one colour and 7 of different colour. These are monophasic combined OCPs. Here the
hormone content of 21 tablets is same whereas ? tablets contains on ly iron without any hormone. As all the tablets contain-
ing hormone arc satTIC (the content is not changed), these arc ca lled monophasic pills. On the other hand in biphasic pills
the first ll tablets have lesser progesterone and next 10 have higher progesterone. Similiarly in triphasic pills hormone
content is changed thrice ie less hormone for first 6 days then slightly more progesterone for 7-11 days and sti ll higher
progesterone in 12-21 dny tablet.
71. Arts. {c) Triph asic pills
72. Ans. (a) (Ref 1-..k Sllnrmn 2nd/265)
ACE inhibitors decrease angiotenisn 11 by inhibiting the conversion of Ang I to Ang IT and thus aldosterone also decrease.
Due to compensatory increase in plasma renin activity, renin and angiotensin I levels increase. By inhibiting the metabo-
lism of bradykinin, the level of these vasoactive peptides also increase.
73. Arts. (c) Canagliflozin . . .. . .
The figure shows the mechanism of drug action to be sodium glucose cotransporter 2 (SGLT2) inhib1tion. This 1s done by
canagliflozin, dapagli flozin and empagliflozin.

74. Ans (b) Vildag liptin db · li · 'ld li t'

The ·figure sh ows the drug action to be inhibition of enzyme DPP4. This mechanism is possesse y sttag p 1m, VI ag P m
like drugs.

75. Ans. (c) Oen?s

Denosumab monoc lona1 an t'b
1s aurnab 1 o d y against RANK liga nd. lt inhi bit interaction of RANK with its ligand on the surface
of osteoclasts and thus prevents its activation.

76. Ans.' (b) Methotrexate . ibitin the metabolism (antimetabolites) specifically act on S pha~e .of. cell cycle. Ar~.ti-
Antlcancer ~rugs that act by mh ? . (lik 6-merca to urine, 6-thioguanine) and pymrudme analogs 0tke
metabolites mclude methotrexate, punne analogs e P P
5-fluorouracil, capeci tabinc etc.)

77. Ans. (a) Vinblastine . . f b I' s the drug inhibit the spindle formation. This
The mechanism shows the inhibition of poly mcnzation o t.u u 111 • mean
mechanism is shown by vinca al ka101'd s l'k · cr'stine
t e vm 1 and vmblastme·

Vincristine, Vinolastine
Inhibit polymerization of tub._:li~n - - -+:=~ :; ;-
Paclilaxel. Docetax~.l _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ ___,
Inhibit depofymerizalion of tubulin_ _ _ _ _ _ _ ____L_ _____ _

78. Ans. (b) 5-Fiuorouracil I. h . I lcristic adverse effect of 5-fl uorouracil and capecitabine.
.
The f1gure sI1ows 1 l and and Foot syndrome w l iC IS c larac <

79. Ans. (a) D ox rub hic~., ·hows the characteri stic ' Radiation reca ll syndrome'. It is caused by doxorubicin.
The history and t c tgure s

80. Ans . (a) NHotinib f . , ll . CM I This en1.yme can be inhibited by

. kinase activalcd by abl-bcr us!On resu I 11 -·
Tyros1ne . 'b
B· Bosut1111
[·· Jmatinib
N·Nilotinib
0 : Dasiltinib
I';otcins: Ponatinib
81. Ans. (a) Tha lidomide
The figure ..,hO\\.., the babv \'\ ith p hocomelia. fhic; is charactcri..,tic teratogenic effect of thalidomide.
82. An . (a) Aspirin
\1cch,ml..-,m of ac.tion of anti-platelet drugs

Decrease formation of TXA2 by Inhibiting COX

1-
C - Io - p - td ;. g - re -1~l
Ttcloptdtne
'rev e rs tbl e P2Y1 2 receptor antagonists of ADP
Prasugrel
Cangrelor Reverstble P2Y12 receptor antagonists of ADP
TIC~grelo

AbCIXtmab
--------------T----
Gpllblllla antagonists
Tirofiban
Epttfibattde
Dtpyndamole POE inhibitor
Vorapaxar Antagonists of protease activated receptors (PAR) of thrombin
Atopaxar
83. An . (c) Abciximab
84. An . (b) Clopidogrel
85. An . (a) Warfarin
~e figure .... ho\\.., ~he den~ I vascular necrosis which is an early adverse effect of warfarin. It is mainh seen in patient
\\ tlh genehc protem C defic1ency. '
6. An . (a) Warfarin
Thi... ,.., abo dermal vascular necrosis also known as 'purple toe syndrome'
87. Ans. (c) kf: K t:, 1~ 11/e p349)
The drug zafirlukast is a cys-LT receptor ru1tagonist.
88. Ans. (a) A (Ref Katzu11g 11/c p598)
~1e patient ,..., ha\ mg neu.tro~ia ~ th~ drug most likely being discussed about is ticlopidine. Clopidogrel and ticlopi-
dm~ act as ADP ant~goms. ftcloptdme IS rarely used due to the occurrence of serious side effects like neutropenia thilt
typ1cally presents w1th fever and mouth ulcers. Though this is rare, it is a serious complication and complete blood count
should be monitored biweekly for the first three months.
89. Ans. (b) B (Ref: KK Sharma 2/e p633)
I ht<. i:; a ca<><.> of diabetic coma due to diabetic ketoacidosis (DKA). The insulin of choice for DKA is regular insu-
lin by intrav<.>nous routt>. Curve A shows rapidly acting inslulins like aspart, glulisinc and lispro (onset in 15-20 min.).
I lowen'r, tlws<.> are given by subcutaneous route and not thl' first choice in diabetic ketoacido is. Cun e B repre-
sents regular insulin that can be given i.v. and ic; insulin of choic(' for DKA. Curve C represents ultralente and cur-.;e
0 rcpre ...tmts insulin glarginc.
90. Ans. (d) D ' rfKK Slmrma 2/t.• p635)
Cur\l' D repre<,L'nts the ultra-long acting insulin al..,u 1-..nm' n "" pt'c1!...lec;s in..,ulin as glargine and detemir.
91. Ans. (a) High blood: ga'> partition coefficient (Uti k at 1111:< 1 1/t ' J' ~ ) )
• rhc dl•pth of ane..,tlwsta depend'> on the parti,tl prl'..,surL' of .ltwsthl'tic inC S. l he transfer of anesthetic into the brain
'ilMI'> onh after the blood is fully saturall'd (or, in ollwr "ord ... parti<ll prl'ssure of the anesthetic in blood equals the
partial prL''isure in the inspired air). 1 he spl't>d of tr,msfL•r of ;uw..,thetic to the brain determines its onset of action
(r.lpid 's slO\\ induction of am'sthesia) and i'> dt.>pl•ndt•nl on tlw solubility of anesthetic in the blood. Solubit~r of an
anesthetic is directl) related to its blood/gas pMtition col'fficicnt: highly soluble anesthetics have high blood/gas
partition coefficient.
• Jf tlw agent is poorly soluble the amount of gas needed to saturate the blood is small and saturation occurs fairly
quickh•. Nitrouc; oxide is an example of poorly soluble ga~ with a blood/ gas partition coefficient of 47. On the graph
a bow the curve of partial pressure of 0 in blood rises rapidly. In the highest point on the curve the partial pressure
on NO in blood equals that in the inspired air, and the transfer to br<lin occurs.
 •
~h1.' second curve (drug/\) portrays the process of blood saturation for a highly soluble gas. The higher the sol bT .
1 'c mo~c gns can bt' taken up by blood before it b saturated. Note that the curve of the partial pressure of d u ~)
?lood rts~ slower than that for NO. When the blood i'> fully saturated with f\0 the partial pressure of drug A~
1
~ apro~tmcly 25°r. of that in inspired air. For drug A, it takes a longer time to fully saturate the blood and to start
h at.1sfer tn ttssucs. Drug A, therefore is charactcri/cd with hig h blood/ gas partition coefficient and slower onset 0 f
action.

Equilibtium with the brain rapid sow

-~+
Onset of action rapid slow
92. Ans. (b) Succiny lcholine induced h y perkalemia (Ref Katzung 11/e p460)
Succinylcholine has high risk of causing hyperka lemia if used in patients with injury to muscles and nerves. The ECG
shows changes characteristic of hyperkalemia and the patient also has crush injury, so this seems to be the most likely
hyperkalemia caused by succinylcholine.
93. Ans. (b) Blood, Brain, Adipose tissue (Ref:Katzung 11/e p434)
Thiopentone is a short-acting barbiturate used for induction of anesthesia. After equilibration with the brain it rapidl}
redistributes into keletal muscles and adipose tissue, which results in rapid recovery from.
94. Ans. (b ) B (Ref' KK Slrarma 2/e p227)
The drug administered to this patient is most likely a loop diuretic that act on ascending limb of the loop of Henle.