1. AIIMS NOVEMBER 2015 QUESTIONS & ANSWERS

AIIMS NOVEMBER – 2015
QUESTIONS & EXPLANATORY ANSWERS (INCLUDING IMAGE BASED
QUESTIONS)
BY:DR MANJUNATH,
MBBS MD (MAULANAAZAD MEDICAL COLLEGE),
ALL INDIAFACULTY
DIRECTOR, DOCTORSACADEMY, DAVANAGERE
ANDSHIVAMOGGA .
REGULAR COURSE/FOUNDATION COURSE,
CONTACT: 9686252725, 9632241911 .WWW.DOCTORSACADEMYDVG.COM
DR MANJUNATH, DOCTORS ACADEMY, DAVANAGERE 1

AIIMS NOV 2015-QUESTIONS & ANSWERS WITH EXPLANATIONS-SOLVED BY
DR: MANJUNATH, MBBS, MD (MAMC NEW DELHI) DIRECTOR
DOCTORS ACADEMY DAVANAGERE & SHIMOGA
(www.doctorsacademydvg.com)
ANATOMY
1. WHICH OF THE
FOLLOWING MUSLE
HELPS IN PROTRUSION
OF MANDIBLE?
A) TEMPORALIS
B)LATERAL PTERYGOID
C) MEDIAL PTERYGOID
D)BUCCINATOR
• ANSWER: B) LATERAL PTERIGOID

AIIMS MAY 2015-QUESTIONS & ANSWERS WITH EXPLANATIONS-SOLVED BY
(www.doctorsacademydvg.com)-
• THE LATERAL PTERYGOID MUSCLE IS ALSO KNOWN AS PTERYGOIDEUS
EXTERNUS OR EXTERNAL PTERYGOID MUSCLE.
•
• GROSS ANATOMY
• THE LATERAL PTERYGOID IS A SHORT, THICK MUSCLE, SOMEWHAT CONICAL
IN FORM, WHICH EXTENDS ALMOST HORIZONTALLY, POSTERIORLY AND
LATERALLY BETWEEN THE INFRATEMPORAL FOSSA AND THE CONDYLE OF
THE MANDIBLE . IT ARISES BY TWO HEADS: AN UPPER (SUPERIOR) AND A
LOWER (INFERIOR).
• THE SUPERIOR PART ARISES FROM THE LOWER PART OF THE LATERAL
SURFACE OF THE GREATER WING OF THE SPHENOID AND FROM THE
INFRATEMPORAL CREST. IT INSERTS IN THE TMJ CAPSULE AND TMJ DISC
.
• THE INFERIOR PART ARISES FROM THE LATERAL SURFACE OF THE LATERAL
PTERYGOID PLATE AND INSERTS INTO A DEPRESSION IN FRONT OF THE
NECK OF THE CONDYLE OF THE MANDIBLE; THE PTERYGOID FOVEA.

(www.doctorsacademydvg.com)-
• ACTIONS OF LATERAL PTERIGOID
• THE SUPERIOR PART IS ACTIVE DURING RETRUSION (OPPOSITE OF
PROTRUSION) AND IPSILATERAL JAW MOVEMENT. IT IS ALSO
ESSENTIAL IN PULLING THE CAPSULE AND DISC FORWARD DURING
MOUTH OPENING, THEREBY MAINTAINING NORMAL RELATIONSHIP
BETWEEN THE CONDYLE OF THE MANDIBLE AND THE TMJ DISC.
• THE INFERIOR PART IS RESPONSIBLE FOR OPENING OF THE MOUTH,
PROTRUSION AND CONTRALATERAL JAW MOVEMENT.
• HYPERACTIVITY OF THE LPM MUSCLE HAS BEEN DESCRIBED IN TMJ
INTERNAL DERANGEMENT , ESPECIALLY WITH LONGSTANDING
ANTERIOR DISPLACEMENT OF THE DISC WITHOUT RECAPTURE.
THICKENING OF THE TENDON (INFERIOR PART) CAN GIVE RISE TO THE
"DOUBLE DISC SIGN".
• NERVE SUPPLY: MANDIBULAR NERVE

DR MANJUNATH, DOCTORS ACADEMY, DAVANAGERE
MUSCLES NERVE SUPPLY ACTION SPECIAL REMARKS
MASSETER ANTERIOR DIVISION OF
MANDIBULAR NERVE
ELEVATES THE MANDIBLE
RETRACTS THE MANDIBLE
SIDE MOVEMENT
EFFECTOR OF JAW JERK
IT IS HYPERTROPHIED IN
BRUXISM
TEMPORALIS ANTERIOR DIVISION OF
MANDIBULAR NERVE
ELEVATES MANDIBLE
PROTRACTION & SIDE TO SIDE MOVEMENT.
IT IS A FAN SHAPED MUSCLE
LATERAL PTERYGOID ANTRIOR DIVISION OF
MANDIBULAR NERVE
MOST IMPORTANT MUSCLE FOR OPENING
OF MOUTH ALONG WITH SUPRAHYOID
MUSCLES
LEFT & RIGHT MUSCLES CONTRACT
TOGETHER TO CAUSE PROTRUSION OF JAW
IF ONLY ONE LATERAL PTERYGOID
CONTRACTS, JAW IS PULLED MEDIALLY
TOWARD THE OPPOSITE SIDE.
MEDIAL PTERYGOID BRANCH FROM TRUNK OF
MANDIBULAR NERVE
CONTRACTION OF LATERLA & MEDIAL
PTERIGOID TOGETHER PROVIDE HELP IN
GRINDING FOOD BETWEEN TEETH OF THE
SAME SIDE.
NERVE TO MEIDAL PTERIGOID
SUPPLIES TENSOR VELI
PALATINI & TENSOR TYMPANI
THROUGH OTIC GANGLION
5

2. AXILLARY NERVE IS NOT
INJURED IN WHICH OF THE
FOLLOWING CONDITIONS?
A. FRACTURE OF SURGICAL
NECK HUMERUS
B. INTRAMUSCULAR INJECTION
C. IMPROPER USE OF CRUTCHES
D. SHOULDER DISLOCATION
• ANS: C. IMPROPER USE OF CRUTCHES
• REF: SNELL’S 9ED/354

(www.doctorsacademydvg.com): AXILLARY NERVE
• THE AXILLARY NERVE IS ONE OF FIVE TERMINAL BRANCHES
OF THE BRACHIAL PLEXUS, SUPPLYING MOTOR AND
SENSORY BRANCHES TO THE SHOULDER.
•
• SUMMARY
• ORIGIN: POSTERIOR CORD OF THE BRACHIAL PLEXUS
• COURSE: PASSES OUT OF AXILLA THROUGH THE
QUADRANGULAR SPACE TO THE UPPER ARM
• MAJOR BRANCHES: SUPERIOR LATERAL CUTANEOUS NERVE
OF THE ARM
• MOTOR SUPPLY: DELTOID AND TERES MINOR MUSCLES
• SENSORY SUPPLY: SKIN OVERLYING DELTOID MUSCLE
DR MANJUNATH, DOCTORS ACADEMY,
DAVANAGERE
7

DAVANAGERE
8

HIGH YIELDING INFORMATION:
NERVE DAMAGED EFFECT OF LESION
UPPER TRUNK OF BRACHIAL PLEXUS (ERB’S PALSY) POLICEMAN’S TIP HAND OR PORTER’S TIP HAND
LOWER TRUNK OF BRACHIAL PEXUS (KLUMPKE’S
PALSY)
CLAW HAND, HORNER’S SYNDROME
LONG THORACIC NERVE WINGED SCAPULA
MEDIAN POINTING INDEX, APE THUMB
UNLAR CLAW HAND (ULNAR CLAW HAND)
MEIDAN + ULNAR CLAW HAND (COMPLETE CLAW HAND)
RADIAL WRIST DROP
9

3. BUCCINATOR IS PIERCED
BY ALL OF THE
FOLLOWING EXCEPT ?
A. BUCCAL BRANCH OF
MANDIBULAR
B. LABIAL BRANCH OF FACIAL
ARTERY
C. PAROTID DUCT
D. MUCUS GLAND OF MOLARS
ANS: B. LABIAL BRANCH OF FACIAL ARTERY
(Ref: BDC vol3, 6ed/p63)

STRUCTURES PIERCING BUCCINATOR ARE:
PAROTID DUCT:
PAROTID DUCT
BUCCAL BRANCH OF MANDIBULAR NERVE
4-5 MOLAR MUCUS GLANDS LYING ON BUCCOPHARYNGEAL FASCIA AROUND PAROTID
DUCT
EMERGES AT ANTERIOR BORDER OF GLAND
RUNS OVER MASSETER
PIERCES BUCCINATOR TO ENTER MOUTH OPPOSITE UPPER SECOND MOLAR
11

4. WHICH OF THE
FOLLOWING ARTERY
DOES NOT SUPPLY
RECTUM?
A. SUPERIOR RECTAL ARTERY
B. INFERIOR RECTAL ARTERY
C. MIDDLE RECTAL ARTERY
D. MIDDLE COLIC ARTERY
ANS: D. MIDDLE COLIC ARTERY
Ref: BDC vol2, 6th ed/267-269

BLOOD SUPPLY OF RECTUM:
NAME OF ARTERY ARISES FROM SUPPLIES
SUPERIOR-RECTAL A INFERIOR MESENTERIC ARTRY MAIN SUPPLY FOR UPPER 2/3 OF
THE RECTUM
MIDDLE RECTAL A ANT DIV OF INTERNAL ILIAC
ARTERY
MIDDLE THRID OF RECTUM
INFERIOR RECTAL A AORTA DISTAL THIRD OF RECTUM
MEDIAN SACRAL A TERMINAL MIDLINE BRANCH OF
THE AORTA
POSTERIOR WALL OF ANORECTAL
JUNCTION ON SACRORECTAL
FASCIA
13

5. IDENTIFY VAGUS NERVE IN THE GIVEN DIAGRAM OF
TRANSVERSE SECTION OF THORAX?
A. VAGUS NERVE
B. AORTA
C. THORACIC DUCT
D. IVC
Ans: A VAGUS NERVE
Ref: Netter’s Anatomy Atlas 5th/27
DAVANAGERE
14

(www.doctorsacademydvg.com): HIGH YIELDING POINTS
LONGEST INTRACRANIAL COURSE → TROCHLEAR NERVE (ALL INDIA REPEAT)
LONGEST COURSE OVERALL AND MOST WIDELY DISTRIBUTED → VAGUS NERVE
SMALLEST (THINNEST) CRANIAL NERVE → TROCHLEAR NERVE
LARGEST (THICKEST) CRANIAL NERVE → TRIGEMINAL NERVE
CRANIAL NERVES CARRYING PARASYMPATHETIC FIBERS → 3, 7, 9, 10
THE ONLY CRANIAL NERVE DECUSSATING COMPLETELY BEFORE EMERGING → TROCHLEAR
NERVE
COMMONEST CRANIAL NERVE AFFECTED IN SPINAL ANESTHESIA → ABDUCENT NERVE
CRANIAL NERVE MOST COMMONLY INVOLVED IN INTRACRANIAL IN INTRACRANIAL
ANEURYSM → OCULOMOTOR NERVE
CRANIAL NERVE MOST COMMONLY INVOLVED IN BASED SKULL FRACTURE → FACIAL
NERVE
CRANIAL NERVE MOST COMMONLY INVOLVED IN RAISED INTRACRANIAL TESNION →
ABDUCENT NERVE
15

6. WHICH OF THE FOLLOWING IS NOT INVOLVED IN
FORMATION OF THORACIC DIAPHRAGM?
A. CENTRAL TENDON
B. BODY WALL
C. PERICARDIOPERITONEAL FOLD
D. SOMATIC PLEURIPERITONEUM
ANS: C. PERICARDIOPERITONEAL FOLD
REF: BDC 6TH ED, VOL1/193-194
DAVANAGERE
16

(www.doctorsacademydvg.com): EXTRA EDGE
EMBRYONIC STRUCTURE PART OF DIAPHRAGM
SEPTUM TRANSVERSUM STERNAL PART & CENTRAL TENDINOUS
REGION
PLEUROPERITONEAL MEMBRANES DORSAL PAIRED PORTION
DORSAL MESENTARY OF ESOPHAGUS UNPAIRED CRURAL PART
LATERAL BODY WALLS PERIPHERAL COSTAL PORTION
17

MAJOR OPENINGS IN DIAPHRAGM: SIM: SAVING INTO MEMEORY
OPENING PART OF DIAPHRAGM SHAPE STRUCTURES
PASSING
VENAE CAVAL T8
CENTRAL TENDON QUADRILATE
RAL
1.INFERIOR VENA CAVA
2. BRANCHES OF RIGHT
PHRENIC NERVE
OESOPHAGEAL T8
MUSCULAR PORTION
DERIVED FROM RIGHT CRUS
ELLIPTICAL 1.OESOPHAGUS
2.OESOPHAGUS
BRANCH OF
LEFT GASTRIC VESSELS
3. VAGUS/GASTRIC
NERVES
AORTIC
(OSSEOAPANEUROTIC)
T12
BETWEEN RIGHT AND
LEFT CRUS (POSTERIOR
TO DIAPHRAGM)
ROUND 1. AORTA
2. THORACIC DUCT
3. AZYGOUS VEIN
18

7. 8 YEAR OLD BOY PRESENTED TO OPD
WITH HYPEREXTENSION OF METACARPO
PHALANGEAL JOINT AND FLEXION OF
DISTAL PHALAGEAL JOINT OF LITTLE AND
RING FINGER. WHICH NERVE IS
INVOLVED?
A. ULNAR NERVE
B. RADIAL NERVE
C. ANTERIOR INTEROSSEOUS
NERVE
D. POSTERIOR INTEROSSEOUS
NERVE
ANS- A. ULNAR NERVE (DIAGNOSIS-ULNAR CLAW HAND)
Ref: BDC 5th/e vol 1, p110-111
19

(www.doctorsacademydvg.com): ULNAR NERVE-EVERY THING YOU SHOULD KNOW
THE ULNAR NERVE IS ONE OF THE TERMINAL BRANCHES OF THE BRACHIAL
PLEXUS AND HAS MOTOR AND SENSORY SUPPLY TO THE FOREARM AND HAND.
• GROSS ANATOMY
• ORIGIN
• THE ULNAR NERVE ORIGINATES AS A TERMINAL BRANCH OF THE MEDIAL CORD
OF THE BRACHIAL PLEXUS WITH NERVE ROOT FIBRES FROM C8-T1.
• COURSE
• ARM
• IN THE ARM, THE ULNAR NERVE RUNS MEDIAL TO THE AXILLARY ARTERY AND
SUBSEQUENTLY THE BRACHIAL ARTERY ON THE CORACOBRACHIALIS MUSCLE IN
THE ANTERIOR COMPARTMENT. THE NERVE PASSES TO THE POSTERIOR
COMPARTMENT THROUGH THE MEDIAL INTERMUSCULAR SEPTUM DISTALLY
RUNNING WITH THE SUPERIOR ULNAR COLLATERAL ARTERY. FURTHER ON, IT
RUNS BETWEEN MEDIAL HEAD OF TRICEPS BRACHII MUSCLE AND THE MEDIAL
INTERMUSCULAR SEPTUM TO PASS POSTERIOR TO THE MEDIAL HUMERAL
EPICONDYLE IN THE SUPERFICIAL CONDYLAR GROOVE (CUBITAL TUNNEL).
20

(www.doctorsacademydvg.com): ULNAR NERVE
• FOREARM
• THE ULNAR NERVE ENTERS THE FOREARM FROM THE ARM
VIA THE TWO HEADS OF FLEXOR CARPI ULNARIS (FCU)
MUSCLE. IT SUBSEQUENTLY LIES SUPERFICIAL TO FLEXOR
DIGITORUM PROFUNDUS AND DEEP TO FCU AND MEDIAL
TO THE ULNAR ARTERY. AT THE WRIST, THE ULNAR NERVE
RUNS LATERAL TO THE TENDON OF FCU.
• HAND
• THE ULNAR NERVE ENTERS THE HAND SUPERFICIAL TO
THE FLEXOR RETINACULUM AND INSIDE GUYON'S CANAL.
THEN IT DIVIDES INTO ITS TERMINAL BRANCHES AT THE
LEVEL OF THE PISIFORM BONE.
• PRIOR TO PASSING THE FLEXOR RETINACULUM AT THE
WRIST, THE ULNAR NERVE GIVES OFF THE DORSAL
CUTANEOUS BRANCH.
21

CUBITAL TUNNEL SYNDROME IS A TYPE OF ULNAR NERVE COMPRESSION NEUROPATHY
WHICH CAN OCCUR FROM A PATHOLOGICAL COMPRESSION OF THE ULNAR NERVE AT
THE CUBITAL TUNNEL.
• EPIDEMIOLOGY
• IT IS THE SECOND MOST COMMON PERIPHERAL NEUROPATHY OF THE UPPER
EXTREMITY.
• CLINICAL PRESENTATION
• ULNAR NERVE COMPRESSION CAN RESULT IN ALTERED SENSATION IN THE LITTLE AND
RING FINGERS. IN MANY PATIENTS, SENSORY LOSS IS OFTEN THE FIRST SYMPTOM TO
BE REPORTED. AS THE CONDITION PROGRESSES, THEY MAY BE CLUMSINESS IN THE
HAND, AS THE ULNAR NERVE IS THE PRINCIPAL MOTOR SUPPLY TO THE INTRINSIC
MUSCLES OF THE HAND. IN WELL‐ESTABLISHED CASES, THERE MAY BE MARKED
WASTING OF THE SMALL MUSCLES OF THE HAND AND THE ULNAR‐SIDED MUSCLES OF
THE FOREARM.
22

8. INCORRECT REGARDING LOCATION OF OTIC
GANGLION IS?
A. ANTERIOR TO MIDDLE MENINGEAL ARTERY
B. LATERAL TO MANDIBULAR NERVE
C. INFERIOR TO FORAMEN OVALE
D. LATERAL TO TENSOR VELI PALATINE
• ANS: B. LATERAL TO MANDIBULAR NERVE ( OTIC GANGLION IS MEDIAL TO
MANDIBULAR NERVE)
• Ref: Gray’s 3rd/988-989
26

OTIC GANGLION :
IT IS A SMALL, OVAL, REDDISH-GREY GANGLION SITUATED JUST BELOW
FORAMEN OVALE.
IT IS A PERIPHERAL PARASYMPATHETIC GANGLION
RELATED TOPOGRAPHICALLY TO MANDIBULAR NERV, BUT FUNCTIONALLY
WITH GLSSOPHARYNGEAL NERVE.
NEAR ITS JUNCTION WITH TRIGEMINAL MOTOR ROOT, MANDIBULAR NERVE
LIES LATERAL TO IT.
TENSOR VELI PALATINI LIES MEDIALLY, SEPARATING THE GANGLION FROM
CARTILAGINOUS PART OF THE PHARYNGOTYMPANIC TUBE
MIDDLE MENINGEAL ARTERY IS POSTERIOR TO THE GANGLION.
OTIC GANGLION USUALLY SURROUNDS THE ORIGIN OF THE NERVE TO MEDIAL
PTERYGOID.
27

9. TRUE STATEMENT ABOUT OSTEOBLASTS ARE
ALL EXCEPT?
A. DERIVED FROM OSTEOPROGENITOR
B. EXPRESS NEUROPEPTIDE RECEPTORS
C. HAVE SMOOTH PLASMA MEMBRANE OUTLINE
D. REGULATED BY BONE MORPHOGENIC FACTOR
ANS: C. HAVE SMOOTH PLASMA MEMBRANE OUTLINE
Ref: I.B Singh Histology 7/ed/pg 89-90
29

10. ALL OF THE
FOLLOWING
ARTICULATED
ARTICULATE WITH
MAXILLA EXCEPT?
A. LACRIMAL
B. NASAL
C. ZYGOMATIC
D. SPHENOID
ANS: D. SPHENOID (SPHENOID HAS NO
ARTICULATION)
Ref: Gray’s Anantomy 3rd e/p780-786
DAVANAGERE
30

• BIOCHEMISTRY
12. FOR THE TRANSCRIPTION OF SELENO-CYSTEINE,
CODON IS ?
A. UGA
B. UAA
C. UAG
D. GUA
ANS: A. UGA (SELENOCYSTEINE IS 21 ST AMINOACID HELPS IN DELAYING AGEING AND CANCER AND
HEART DISEASE)
REF: HARPER 29/e p270
AIIMS NOVEMBER 2015-QUESTIONS & ANSWERS WITH EXPLANATIONS-SOLVED BY
31

WHAT IS IT? IT IS AN L-AMINO ACID FOUND IN SOME PEROXIDASES & REDUCTASES WHERE IT PARTICIPATES
IN CATALYSIS OF ELECTRON TRANSFER REACTIONS.
STRUCTURE AS ITS NAME IMPLIES, A SELENIUM ATOM REPLACES THE SULFUR OF ITS STRUCTUAL ANALOG,
CYSTEINE.
SINCE SELENOCYSTEINE IS INSERTED INTO POLYPEPTIDES DURING TRANSLATION, IT IS
COMMONLY REFERRED TO AS “21ST AMINO ACID.”
PK Pk3 OF SELENOCYSTEINE, 5.2, IS 3 UNITS LOWER THAN THAT OF CYSTEINE
UNIQUE
FEATURE
UNLIKE THE OTHER 20 GENETICALLY ENCODED AMINO ACIDS, SELENOCYSTEINE IS NOT
SPECIFIED BY A SIMPLE THREE-LETTER CODON
CLINICAL
SIGNIFICANCE:
SELENOCYSTEINE IS PRESENT AT THE ACTIVE SITE OF SEVERAL HUMAN ENZYMES THAT CATALYZE
REDOX REACTIONS.
EXAMPLES: THIOREDOXIN REDUCTASE, GLUTATHIONE PEROXIDASE & DEIODINASE THAT
CONVERTS THYROXINE TO THIIODOTHYRONINE.
SIGNIFICANTLY , REPLACEMENTOF SELENOCYSTEINE BY CYSTEINE CAN SIGNIFICANTLY DECREASE
CATALYTIC ACTIVITY.
IMPAIRMENTS IN HUMAN SELENOPROTEINS HAVE BEEN IMPLICATED IN TUMORIGENESIS,
ATHEROSCLEROSIS & SELENIUM DEFICIENCY CARDIOMYOPATHY (KESHAN DISEASE).
(www.doctorsacademydvg.com): SELENOCYSTEINE
33

13. WHICH ONE OF THE
REACTION DOES NOT REQUIRE
BIOTIN?
A. ACETYL-COA TO MALONY-COA
B. PYRUVATE TO OXALOACETATE
C. GLUTAMINE TO GAMMA
CARBOXY GLUTAMATE
D. PROPIONYL COA TO METHYL
MALONYL COA
ANS- C. GLUTAMINE TO GAMMA CARBOXY
GLUTAMATE
Ref: Harper’s 26/e p153-156
BIOTIN DEFICIENCY
34

REACTIONS REQUIRING BIOTIN AS CO-ENZYME:
BIOTIN ENZYME BIOCHEMICAL FUNCTION
ACETYL-COA CARBOXYLASE LIPID SYNTHESIS FROM ACETATE
METHYLMALONYL-COA
CARBOXYLTRANSFERASE
PROPINONIC ACID SYNTHESIS BY
RUMEN BACTERIA
3-METHYLCROTONYL-COA CARBOXYLASE LEUCINE CATABOLISM
PROPINYL-COA CARBOXYLASE CONVERSION OF AMINO ACIDS AND
PROPIONATE TO GLUCOSE IN THE LIVER
PYRUVATE CARBOXYLASE LIVER GLUCONEOGENESIS
35

(www.doctorsacademydvg.com): BIOTIN FOOD SOURCES

14. HEME IS NOT
SYNTHESIZED IN?
A. RBC
B. OSTEOCYTE
C. LIVER PARENCHYMA
D. ERYTHROPOETIC PRECURSOR
CELLS IN BONE MARROW
ANS: A. RBC
Ref: Lippincott’s Illustrated Reviews:
Biochemistry 4/e p21
40

15. GLYCOGEN PHOSPHORYLASE IS REGULATED BY ALL
EXCEPT?
A. PROTEIN KINASE
B. CALMODULIN
C. C-AMP
D. GLYCOGENIN
ANS- D. GLYCOGENIN
Ref: Harper’s 26/e p145-147

EXPLANATION:
CYCLIC AMP INTEGRATES THE REGULATION OF GLYCOGENOLYSIS & GLCOGENESIS
THE PRINCIPAL ENZYMES CONTROLLING GLYCOGEN METABOLISM-GLYCOGEN
PHOSPHORYLASE AND GLYCOGEN SYNTHASE-ARE REGULATED BY ALLOSTERIC MECHANISMS
AND COVALENT MODIFICATION BY REVERSIBLE PHOSPHORYLATION AND
DEPHOSPHOSPHORYLATION IS INCREASED IN RECPONSE TO:
 CYCLIC AMP (cAMP) FORMED FROM ATP BY ADENYLYL CYCLASE AT THE INNER SURFACE
OF CELL MEMBRANES IN RESPONSE TO HORMONES SUCH AS EPINEPHRINE,
NOREPINEPHRINE, AND GLUCAGEN.
 cAMP IS HYPDRLYZED BY PHOSPHODIESTERASE, SO TERMINATING HORMONE ACTION; IN
LIVER INSULINE INCREASES THE ACTIVITY OF PHOSPHODIESTERASE.

16. IN A PATIENT WITH LEAD TOXICITY, WHICH HEME
PATHWAY INTERMEDIATE WILL INCREASE IN URINE?
A. ALA
B. PORPHOBILINOGEN
C. UROPORPHOBILINOGEN
D. COPROPORPHYRIN
ANS: A. ALA
(Ref: Harper 29/e p309-311)
CHILD WITH LEAD POISONING
43

EXPLANATION:
HEME SYNTHESIS:
STARTS WITH SUCCINYL-CoA, DERIVED FROM THE CITRIC ACID CYCLE IN MITOCHONDRIA,
AND THE AMINO ACID GLYCINE.
PYRIDOXAL PHOSPHATE IS ALSO NECESSARY IN THIS REACTION TO “ACTIVE” GLYCIN.
THE PRODUCT OF THE CONDENSATION REACTIOB BETWEEN SUCCINYL-CoA AND GLYCINE IS
α-AMINO-β-KETOADIPIC ACID, WHICH IS RAPIDLY DECARBOXYLATED TO FORM α
AMINOLEVULINATE (ALA).
• THIS REACTION REQUENCE IS CATALYZED BY ALA SYNTHASE, THE RATE-CONTROLLING ENZYME IN
PORPHYRIN BIOSYNTHESIS IN MAMMALIN LIVER. SYNTHESIS OF ALA OCCURS IN MITOCHONDRIA.
•IN THE CYTOSOL, TWO MOLECULES OF ALA ARE CONDENSED BY THE ENZYME ALA DEHYDRATASE
TO FORM TWO MOLECULES OF WATER AND ONE OF PORPHOBILINOGEN (PBG).
•ALA DEHYDRATASE IS A ZINC-CONTAINING ENZYME AND IS SENSITIVE TO INHIBITION BY LEAD, AS
CAN OCCUR IN KEAD POISONING.
•IT IS FOR THIS REASON THAT ALA GETS INCREASED IN LEAD POISONING.
44

17. GLUCOSE 6 PHOSPHATE PRODUCED IN CYTOPLASM OF
HEPATOCYTE DOES NOT GET ACTED UPON BY GLUCOSE 6
PHOSPHATASE ENZYME BECAUSE?
A. IT IS THEROMODYNAMICALLY VIABLE ONLY WHEN GLUCONEOGENESIS
HAS STARTED
B. IT REQUIRES ACTIVATION BY PYRUVATE KINASE
C. GLUCOSE 6 PHOSPHATASE IS PRESENT IN ENDOPLASMIC RETICULUM
D. STERIC HINDERANCE BY ALBUMIN
ANS: C. GLUCOSE 6 PHOSPHATASE IS PRESENT IN ENDOPLASMIC RETICULUM
(Ref: Chatterjee 5/e p488; Harper 29/e p19-21; 26/e p147)
DAVANAGERE
45

EXPLANATION:
•THE CONVERSION GLUCOSE 6-PHOSPHATE TO GLUCOSE IS CATALYZED BY GLUCOSE-6-PHOSPHATASE.
•IT IS PRESENT IN LIVER AND KIDNEY BUT ABSENT FROM MUSCLE AND ADIPOSE TISSUE, WHICH,
THEREFORE, CANNOT EXPORT GLUCOSE INTO THE BLOODSTREAM.
•GLUCOSE-6-PHOSPHATASE CONSISTS OF 357 AMINO ACIDS, AND IS ANCHORED TO THE
ENENDOPLASMIC RETICULUM (ER) BY NINE TRANSMEMBRANE HELICIES.
•ITS N-TERMINAL AND ACTIVE SITE ARE FOUND ON THE LUMEN SIDE OF THE ER AND ITS C-TERMINUS
PROJECTS INTO THE CYTOPLASM.
•THE TRANSFER OF THE GLUCOSE 6-PHOSPHATE IS CARRIED OUT BY A TRANSPORTER PROTEIN (T1)
AND THE ENDOPLASMIC RETICULUM (ER) CONTAINS STRUCTURES ALLOWING THE EXIT OF THE
PHOSPHATE GROUP (T2) AND GLUCOSE (T3).
46

18. WHICH IS NOT
GLUCOGENIC?
A. ACETYL COA
B. PYRUCATE
C. LACTATE
D. OXALOACETETE
ANS- A. ACETYL COA (ACETYL COA ENTERS KREB
S CYCLE FOR ATP PRODUCTION)
(Ref: Chatterjee 5/e p448: Harper 29/e p19-20;
26/e p153-155) DR MANJUNATH, DOCTORS ACADEMY,
DAVANAGERE
47

EXPLANATION:
GLUCONEOGENESIS
WHAT IS IT? IT IS THE TERM USED TO INCLUDE ALL PATHWAYS RESPONSIBLE FOR
CONVERTING NON-CARBOHYDRATE PRECUSORS TO GLUCOSE OR
GLYCOGEN RESERVES.
MAJOR SUB-STRATES GLUCOGENIC AMINO ACIDS, LACTATE, GLYCEROL & PROPIONATE
SITE LIVER AND KIDNEY ARE THE MAJOR GLUCONEOGENIC TISSUES.
PURPOSE • IT MEETS THE NEEDS OF BODY FOR GLUCOSE WHEN CARBOHYDRATE IS NOT
AVAILABLE IN SUFFICIENT AMOUNT FROM DIET OR FROM GLYCOGEN.
A SUPPLY OF GLUCOSE IS NECESSARY ESPECIALLY FOR CNS & RBCs.
HYPOGLYCEMIA CAUSES BRAIN DYSFUNCTION,
GLUCOSE IS ALSO IMPORTANT IN MAINTAINING LEVEL OF INTERMEDIATES OF
CITRIC ACID CYCLE
GLUCONEOGENESIS ALSO CLEARS LACTATE PRODUCED BY MUSCLE & RBCs AND
GLYCEROL PRODUCED BY ADIPOSE TISSUE.
48

19. WHICH IS NOT A METHOS
OF PROTEIN PRECIPITATION?
A. SALTING OUT WITH METALS
B. ACETONE & ALCOHOL
C. CHANGING PH OTHER THAN
ISOELECTRIC PH
D. TRICHLORO ACETIC ACID
ANS: C. CHANGING PH OTHER THAN
ISOELECTRIC PH
(Ref: Chatterjee 5/e p448: Harper 29/e p19-21)

EXPLANATION:
METHODS OF PROTEIN PRECIPITATION:
•SALTING OUT:
•EXCESS SALT PRECIPITATES PROTEINS BECAUSE MOST OF WATER MOLECULES BECOME
TIED UP IN FORMING HYDRATION SHELLS AROUND SALT IONS.
•SO, LESS WATER IS AVAILABLE TO DISSOLVE PROTEINS
•AMMONIUM SULFATE IS MOST COMMONLY USED REAGENT FOR SALTING OUT PROTEIN
•THE SALT CONCETRATION AT WHICH PROTEIN PRECIPITATES DIFFERS FROM ONE
PROTEIN TO ANOTHER. EG GLOBULIN PRECIPITATE AT HALF SATURATION WHILE
ALBUMIN PRECIPITATES AT FULL SATURATION OF AMMONIUM SULPHATE.
•BY ORGANC SOLVENTS(PROTEIN IS LEAST SOLUBLE AT ISOELECTRIC PH)
•BY HEAVY METALS (LEAD, CADMIUM, MERCURY)
50

PHYSIOLOGY
21. Na-IODIDE TRANSPORTER
IS PRESENT IN ALL EXCEPT?
A. PITUITARY
B. SALIVARY
C. PLACENTA
D. THYROID
ANS- A. PITUITARY
(Ref: Ganong 23/e p303)

DOCTORS ACADEMY, DAVANAGERE & SHIMOGA.
EXPLANATION:
“THE SALIVARY GLAND, THE GASTRIC MUCOSA, THE PLACENTA, THE CILIARY BODY OF
THE EYE, THE CHOROID PLEXUS, THE MAMMARY GLANDS, AND CERTAIN CANCERS
DERIVED FROM THESE TISSUES ALSO EXPRESS NA IODIDE TRANSPOTER, WHICH CAN
TRANSPORT IODIDE AGAINST A CONCENTRATION GRADIENT.”
BUT THE TRANSPORTER IN THESE TISSUES IS NOT AFFECTED BY TSH.
THE PHYSIOLOGIC SIGNIFICANCE OF ALL THESE EXTRATHYROIDAL IODIDE-
CONCENTRATING MECHANISM IS OBSCURE.
THEY MAY PROVIDE PATHWAY FOR RADIOABLATION OF NA IODIDE TRANSPORTER-
EXPRESSING CANCER CELLS USING IODIDE RADIOIDOTOPES.
THIS APPROACH IS ALSO USEFUL FOR THE ABLATION OF THYROID CANCERS.
52

22. ATRIAL NATRIURETIC PEPTIDE EXERTS ITS ACTION ON
ALL EXCEPT?
A. INHIBITION OF Na+ REABSORPTION IN PCT
B. DILATE AFFERENT ARTERIOLE
C. MESANGIAL CELL CONTRACTION
D. INHIBITION OF Na+ REABSORPTION IN MEDULARRY COLLECTING DUCT
ANS: C. MESANGIAL CELL CONTRACTION
(ANP is a powerful vasodilator, and a protein (polypeptide) hormone secreted by heart
muscle cells. It is involved in the homeostatic control of body water, sodium, potassium
and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of
the heart (atrial myocytes) in response to high blood volume. ANP acts to reduce the
water, sodium and adipose loads on the circulatory system).
(Ref: Ganong 23/e p675)

EXPLANATION:
ACTIONS OF ATRIAL NATRIURETIC PEPTIDE (ANP) & BRAIN NATRIURETIC PEPTIDE (BNP)
• THEY ACT ON THE KIDNEY TO INCREASE NA+ EXCRETION
• THEY APPEAR TO PRODUCE THIS EFFECT BY DILATING AFFERENT ARTERIOLES AND
RELAXING MESANGIAL CELLS. BOTH OF THESE ACTIONS INCREASE GLOMERULAR
FILTRATION
•THEY ACT ON THE RENAL TUBULES TO NHIBIT NA+ REABSORPTION.
•OTHER ACTIONS INCLUDE AN INCREASE IN CAPILLARY PERMEABILITY, LEADING TO
EXTRAVASATION OF FLUID AND A DECLINE IN BLOOD PRESSURE.
•THEY RELAX VASCULAR SMOOTH MUSCLE IN ARTERIOLES AND VENULES
54

23. INTERSTITIAL FLUID VOLUME CAN BE
DETERMINED BY ?
A. RADIOACTIVE SODIUM AND RADIOIODINE LABELLED ALBUMIN
B. RADIOACTIVE WATER AND RADIOLABELLED ALBUMIN
C. RADIOACTIVE SODIUM AND RADIOACTIVE WATER
D. DIIODOTHALMIUM IODIONE
ANS- A. RADIOACTIVE SODIUM AND RADIOIODINE LABELLED ALBUMIN
(Ref: Ganong 24e p3-5, Guyton 12/534-536, 541)

EXPLANATION:
MEASUREMENT OF BODY FLUID VOLUME
VOLUME INDICATORS
TOTAL BODY WATER 3H2O, 2H2O, ANTIPYRINE
EXTRACELLULAR FLUID 22NA, 125I-OTHAMAMATE, THIOSULFATE, INULIN
EXTRACELLULAR FLUID (CALCULATED AS TOTAL BODY WATER-EXTRACELLULAR FLUID VOLUME)
PLASMA VOLUME 125I-ALBUMIN, EVANS BLUE DYE (T-1824)
BLOOD VOLUME 51CR-LABELED RED BLOOD CELLS, OR CALCULATED AS BLOOD VOLUME= PLASMA
VOLUME/(1-HEMATOCRIT)
INTERSTITIAL FLUID (CALCULATE AS EXTRACELLULAR FLUID VOLUME-PLASM VOLUME)
56

24. THE CLOT FORMED IN NOT STABLE UNLESS EXTENSIVE CROSS
LINKING OCCURS. THIS IS DONE BY?
A. PLASMIN
B. THROMBIN
C. FACTOR XIII
D. HMWK
ANSWER: C. FACTOR XIII
REF: GANONG 23/E P531
57DR MANJUNATH, DOCTORS ACADEMY, DAVANAGERE

25. PHYSIOLOGICAL CHANGES IN LAPAROSCOPY INCLUDE ALL
EXCEPT?
A. INCREASED PCWP
B. INCREASED ICP
C. DECREASED FRC
D. INCREASED PH
ANSWER: D. INCREASED PH (THERE IS DECREASE IN PH UE TO METABOLIC ACIDOSIS)
REF: WYLIE CBURCBILL-DAVIDSON’S A PRACTICE OF ANAESTHESIA 7/E P896

26. ALL OF THE STATEMENTS ARE TRUE ABOUT SMOOTH
MUSLE CONTRACTION EXCEPT ?
A. TENSION DEVELOPED IS PROPORTIONAL TO OR AFFECTED BY FREQUENCY OF
SPIKE POTENTIALS
B. MUSCLE CONTRACTION IS RELATED TO THE AMPLITUDE OF BASAL ELECTRICAL
RHYTHUM (BER)
C. FREQUENCY IS AROUND 6/MIN
D. THRESHOULD IS -50mV
ANS- B. MUSCLE CONTRACTION IS RELATED TO THE AMPLITUDE OF BER (BER ITSELF RARELY
CAUSES MUSLE CONTRACTION)
(Ref: Ganong 24/e p498-499, 23/e p471)

29. IN THE FORMULA,
CLEARANCE C=U x V/P,U
STANDS FOR?
A. URINARY CONCENTRATION IN
GM/24 HRS
B. URINARY CONCENTRATION IN
MG/100ML
C. MICROALBIMINURIA
D. URINE OSMOLARITY
ANS- D. URINE OSMOLARITY (REF: GUYTON’S
12/E .663)
Ref: Guyton’s 12/e p663

30. ANATOMICAL DEAD SPACE IS MEASURED WITH ?
A. SINGLE BREATH NITROGEN TEST OR NITROGEN WASH OUT
B. BOHLERSETHOD
C. SPIROMETER
D. XENON ISOTOPES
ANS: A. SINGLE BREATH NITROGEN TEST
REF: GUYTON’S 12/E P883-885
(Nitrogen washout (or Fowler's method) is a test for measuring anatomic dead space in
the lung during a respiratory cycle , as well as some parameters related to the closure
of airways.)

PATHOLOGY
31. HISTOPATHOLOGY OF
SCHWANNOMA,FOLLOWING IS
SEEN?
A. ANTOMY A WITH VEROCAY BODY
B. ROSETTES
C. ANTOMY B WITH VEROCAY BODY
D. PALLISADING
ANS: A. ANTOMY A WITH VEROCAY BODY
REF:ROBBIN’S 9/E P1314; COMPLETE REVIEW OF
PATHOLOGY 1/E P710

FEATURES SCHWANNOMAS NEUROFIBROMAS
GENERAL
CHARACTERISTICS
 BENIGN TUMOR
 ARISE DIRECTLY FROM
PERIPHERAL NERVES.
 BENIGN TUMORS,
HETEROGEOUS IN
COMPOSITION
 NEOPLASTIC SCHWANN
CELLS MIXED WITH
PERINURIAL LIKE CELLS,
FIBROBLASTS, MAST CELLS,
AND CD34+ SPINCLE CELLS
GROSS  WELL-CIRCUMSCRIBED
&ENCAPSULATED
 BUT ASSOCIATED NERVE
WITHOUT INVADING
 NON-ENCAPSULATED MASS
MORPHOLOGY CONSISTS OF:
 ANTONI A: CELLULAR AREAS
 ANTONI B: LOOSE
EDEMATOUS AREAS
3 TYPES:
 LOCALIZED CUTANEOUS
NEURROFIBROMA
 DIFFUSE NEUROFIBROMA
 PLEXIFORMNEUROFIBROMA
65

(www.doctorsacademydvg.com): PATHOLOGY OF SCHWANNOMAS
• Schwannomas are benign encapsulated neoplasms of schwann cells (WHO
grade I). They arise eccentrically from their parent nerve. They are composed
of two cell types: Antoni A and Antoni B.
• The Antoni A cells are densely packed and arranged in fascicles; acellular areas
lie between opposing rows of parallel nuclei (Verocay bodies).
• The Antoni B cells are less compact and are prone to cystic degeneration.
• PATHOLOGIC VARIANTS INCLUDE :
• conventional (most common type): fibrous capsule, hyaline vessels, Antoni A
and loose textured Antoni B areas (Verocay bodies)
• cellular schwannomas (predominantly Antoni A tissue without Verocay bodies)
• melanotic schwannomas (dense melanin pigment)
• plexiform schwannomas (do not undergo malignant change, unlike plexiform
neurofibromas)

(www.doctorsacademydvg.com): VESTIBULAR SCHWANNOMA

32. A 30 YEAR OLD SOFTWARE ENGINEER CAME
TO OPD WITH CHIEF COMPLAINS OF
HEARTBURN. ON ENDOSCOPIC BIOPSY, THE
LESION SHOWS THE FOLLOWING (FIGURE
BELOW). IDENTIFY THE LESION, STAIN HAS
DONE FOR THE WHAT AND WHAT
ADDITIONAL FEATURES SHOULD BE LOOKED
FOR?
A. ADENOCACINOMA; PAS; MALIGNANCY
B. BARRETTS OESOPHAGUS; MUCIN STAIN;
DYSPLASIA
C. SQUAMOUS CELL CARCINOMA;
CYTOKERATIN, SQUAMOUS PEARLE
D. INFECTION; FUNGAL STAIN; INCLUSIO BODY
ANS: B. BARRETTS OESOPHAGUS; MUCIN STAIN; DYSPLASIA
REF: ROBBIN’S 9/757; COMPLETE REVIEW OF PATHOLOGY
1/E P482
DR MANJUNATH, DOCTORS
ACADEMY, DAVANAGEREDR. MANJUNATH, DOCTORS ACADEMY 68

EXPLANATION:
Barrett esophagus represents progressive metaplasia of oesophageal stratified
squamous cell epithelium to columnar epithelium.
Although the exact number varies, 90-100% of oesophgeal adenocarcinoma is thought
to arise from this metaplasia.
Although patients with Barrett oesophagus have a 30x risk of developing oesophageal
adenocarcinoma, the annual risk of developing adenocarcinoma depends on the
degree of histological dysplasia, but may be ~1% (range 0.1-2%), and the absolute risk
is low.
69

33. THE GIVEN FIGURE SHOWS WHICH OF
THE FOLLOWING?
A. AMYLOIDOSIS-GREY; VIABLE WHITE NECROTIC
B. NUTMEG LIVER-RED AREAS ARE VIABLE
PERICENTRAL AREAS; WHITE AREAS ARE
PERIPORTAL NECROTIC AREAS
C. RED AREAS ARE NECROTIC AREAS NEAR CENTRAL
VEIN, WHITE AREAS ARE VIABLE, FIBROTIC
PERIPORTAL AREA
D. AMYLOIDOSIS-NECROTIC WHITE PERIPORTAL VIABLE
GREY PERICENTRAL AREAS
ANS: C. RED AREAS ARE NECROTIC AREAS NEAR
CENTRAL VEIN, WHITE AREAS ARE VIABLE,
FIBROTIC PERIPORTAL AREA (CHRONIC HEAPTIC
CONGESTION)
REF: ROBBIN’S 9/129; COMPLETE REVIEW OF
PATHOLOGY 1/E P86

EXPLANATION:
ACADEMY, DAVANAGEREDR. MANJUNATH, DOCTORS ACADEMY
ACUTE PULMONARY CONGESTION:
 ENGORGED ALVEOLAR CAPILLARIES
 ALVEOLAR SEPTALEDEMA
 FOCAL INTRA ALVEOLAR HEMORRHAGE
CHRONIC PULMONARY CONGESTION
 SEPTA ARE THICKENED AND FIBROTIC
 HEMOSIDERIN-LADEN MACROPHAGES(HEART FAILURE CELLS)
ACUTE HEPATIC CONGESTION
 CENTRILOBULAR HEPATOCYTES: ISCHEMIC NECROSIS
 PERIPORTAL HEPATOCYTES-FATTY CHANGE
CHRONIC PASSIVE HEPATIC CONGESTION
 NUTMEG LIVER: CENTRILOBULAR REGIONS ARERED-BROEN AGAINST SURROUNDING ZONES
OF UNCONGESTED TAN LIVER
 INITIALLY CENTRILOBULAR NECROSIS & HEMOSIDERIN LADEN MACROPHAGES.
 LATER: HEPATIC FIBROSIS CALLED CARDIAC CIRRHOSIS.
71

34. WHICH OF THE FOLLOWING IS A IMMUNE
PRIVILEGED REGION?
A. AREA POSTREMA
B. SEMINIFEROUS TUBULES
C. KIDNEY
D. OPTIC NERVE
ANS: B. SEMINIFEROUS TUBULES
[REF: ROBBIN’S 9/215-216]

EXPLANATION:
IMMUNE-PRIVILEGED SITES:
 TESTIS, EYE AND BRAIN
 TISSUES IN WHICH THESE ANTIGENS ARE LOCATED DO NOT COMMUNICATE
WITH THE BLOOD AND LYMPH
 DIFFICULT TO INDUCE IMMUNE RESPONSES TO ANTIGEN INTRODUCED INTO
THESE SITES
 PROLONGED TISSUE INFLAMMATION ON INJURY & RELEASE OF ANTIGEN FROM
THESE SITES; POST-TRAUMATIC ORCHITIS & UVEIRIS
73

35. PATHOLOGIST EXAMINES BIOPSY
FROM A PATIENT PRESENTING WITH
BLEEDING PER RECTUM WITH A PAST
HISTORY OF INTUSSUPTION FOR THE
PAST 6MONTHS. HIS OBTAINED
FINDING HAS BEEN SHOWN BELOW.
IDENTIFY THE PATHOLOGY?
A. TUBULE VILLOUS ADENOMA
B. ADENO CARCINOMA
Ç. HAMARTOMA
D. JUVENILE POLYPOSIS SYNDROME
ANS: A. TUBULE VILLOUS ADENOMA
REF: ROBBIN’S 9/808-809; COMPLETE REVIEW OF
PATHOLOGY 1/E P517

EXPLANATION:
ADENOMAS CAN BE CLASSIFIED AS: (BASED ON THEIR ARCHITECTURE)
TUBULAR SMALL, PEDUNCULATED POLYPS COMPOSED OF ROUNDED,
OR TUBULAR, GLANDS
TUBULO-VILLOUS
(PICTURE)
MIXTURE OF TUBULAR AND VILLOUS ELEMENTS
VILLOUS LARGER AND SESSILE, ARE COVERED BY SLENDER VILLI
75

36. WHICH ONE IS BEST PROGNOSTIC FACTOR FOR
ALL?
A. HYPERPLOIDY
B. ORGANOMEGALY
C. TLC MORE THAN 50,000/UL
D. ENVIROMENTAL FACTORS
ANS: A

EXPLANATION:
PROGNOSTIC FACTORS IN ACUTE LYMPHOBLASTIC LEUKEMIA
DETERMINANTS FAVORABLE UNFAVORABLE
WBC/UL <10,000 >2,00,000
AGE 2-9 YR <1 Y,>10 Y
GENDER FEMALE MALE
ETHNICITY WHITE BLACK
L.NODE, LIVER. SPLEEN
ENLARGEMENT
ABSENT MASSIVE
TESTICULAR
ENLARGEMENT
ABSENT PRESENT
CENTRAL NERVOUS
SYSTEM LEUKEMIA
ABSENT PRESENT
77

37. 10 YEAR CHILD PRESENTED WITH BILATERAL
CERVICAL LYMPHADENOPATHY. LYMPHNODE
BIOPSY WAS PERFORMED, WHICH SHOWED
CELLS AS GIVEN IN THE FIGURE. WHICH OF THE
FOLLOWING IS TRUE REGARDING THIS
CONDITION?
A. HODGKIN LYMPHOMA;EBV AND EMBRYO
CELL
B. NON HODGKIN LYMPHOMA; HIV AND GIANT
B CELL
C. TB, MYCOBACTERIA AND TINY GRANULOMA
D. HODGKIN LYMPHOMA; EBV AND REED
STERNBERG CELL
ANS: D. HODGKIN LYMPHOMA; EBV AND REED
STERNBERG CELL
REF: ROBBIN’S 9/608-611; COMPLETE REVIEW OF
PATHOLOGY 1/E P285, 761

EXPLANATION:
Hodgkin’s Lymphoma:
• USUALLY PRESENTS AS SOLITARY OR GENERALIZED LYMPHADENOPATHY AND
MOST COMMONLY OCCURS IN YOUNG ADULTS, ALTHOUGH ANY AGE GROUP MAY
BE AFFECT ED.
• THE DISEASE APPEARS TO SPREAD IN A CONTIGUOUS FASHION, AND MOST
PATIENT PRESENT WITH DISEASE LIMITED TO THE LYMPH NODES OR TO THE
LYMPH NODES AND SPLEEN
• THE FIGURE GIVEN IN THIS EQUESTION IS “CLASSIC”HODGKIN LYMPHOMA.
• THE BACKGROUND IS PRIMARY LYMPHOCYTES, AND THE REED-STERNBERG CELLS
79

(www.doctorsacademydvg.com)- HODKINS LYMPHOMA

38. IRON METABOLISM AND
REGULATION ARE IMPORTANT FOR
RBC PRECURSOR CELL. WHICH OF
THE FOLLOWING HELPS IN
REGULATION OF IRON
METABOLISM BUT IS NOT SPECIFIC
FOR IRON?
• A. HEPCIDIN
• B. DMT-1
• C. FERROPORTIN
• D. FERRITIN
•
ANS- B. DMT-1
[REF: WINTROBE 13ED/PG 811]

EXPLANATION:
 *HEPHAESTIN IS SIMILAR TO CERULOPLASMIN, THE COPPER-CARRYING PROTEIN.
 **DIVALENT METAL TRANSPORTER TYPE 1 (DMT-1): ALSO KNOEN AS NATURAL RE-
SISTANCE MACROPHAGE-ASOCIATED PROTEIN TYPE 2 (NRAMP 2) OR DCT-1
 HEPCIDIN: PRINCIPAL IRON REGULATORY HORMONE; AND IS NEGATIVELY
REGULATED BY FERROPORTIN
 DMT1 HAS A STRICT REQUIREMENT FOR DIVALENT CATIONS, AND IT WILL NOR
TRANSPORT THE FE3+ FROM OF IRON
82

39. THERE ARE DIFFERENT
CHECK POINTS IN CELL
GROWTH AND REGULATION.
WHICH ONE IS THE PRIMARY
POINT FOR REGULATION OF
CELL GROWTH?
A. END OF G1
B. START OF G2
C. END OF S1
D. END OF M
ANS: A. END OF G1
REF: ROBBIN’S 9/25; COMPLETE REVIEW
OF PATHOLOGY 1/E P197

EXPLANATION
CELL CYCLE
Definition: Cell cycle is the sequence of events that results in cell division
 PHASES: G0→G1→S→G2→M
 G1: PRE-SYNTHETIC GROWTH
 S: DNA SYNTHESIS (MOST RADIO-RESISTANT PHASE)
 G2: PRE-MITOTIC GROWTH
 M: MITOTIC PHASE (MOST RADIO-SENSITIVE PHASE)
 G0: QUIESCENT CELLS THAT ARE NOT ACTIVELY CYCLING ARE SAID TO BE IN GO STATE
84

40. IDENTIFY THE CRYSTALS IN THE URINE ANALYSIS?
A. OXALATE
B. URIC ACID
C. PHOSPHAHATES
D. CYSTEINE
ANS: A. OXALATE

EXPLANATION
Crystals you can get in Urine
TRIPLE PHOSPHATE  SEEN IN ALKALINE URINE
 RECTANGULAR SHAPE
URIC ACID  SEEN IN ACIDIC URINE
 BROWN LEMONSHAPED
OR STAR SHAPED
 BIREFRINGENT WITH
POLARIZED LIGHT
CALCIUM OXALATE  ENVELOPE SHAPED
 SEEN IN ACIDIC URINE
86

41. CAVITATORY LESION IN RIGHT
LOWER LUNG WITH DYSPONEA
WITH FOLLOWING
HISTOPATHOLOGICAL
APPEARANCE?
A. ECHINOCOCCUS WITH 2 LAYERS
B. STRONGYLOIDES WITH 2 LAYERS
C. PARAGONIMUS WITH 2 LAYERS
D. CYSTICERCOSIS WITH 3 LAYERS
ANS: C. PARAGONIMUS WITH 2 LAYERS
REF: HARRISON’S 19/E P1429; CDC WEBSITE

EXPLANATION: THE FIGURE SHOWS: EGG OF PARAGONIMUS SP. TAKEN FROM A LUNG
BIOPSY STAINED WITH HEMATOXYLIN AND EOSIN
GEOGRAPHIC
DISTRIBUTION
 PARAGONIUM WESTERMANI IS DISTRIBUTED IN SOUTHEAST ASIA AND JAPAN.
CLINICAL PRE-
SENTATION
 ACUTE PHASE: DIARRHEA, ABDOMINAL PAIN, FEVER, COUGH, URTICARIA,
HEPATOSPLENOMEGALY & EOSINOPHILIA.
 DURING THE CHRONIC PHASE, PULMONARY MANIFESTATIONS INCLUDE COUGH,
EXPECTORATION OF DISCOLORED SPUTUM & HEMOPTYSIS
MODE OF
TRANSMISSION
 HUMANS ACQUIRE LUNG FLUKE INFECTION BY INGESTING INFECTIVE METACERCERCARIAE
ENCYSTED IN THE MUSCLES AND VISCERA OF CRAYFISH AND FRESHWATER CRABS.
 IN ENDEMIC AREAS, THESE CRUSTACEANS ARE CONSUMED RAW, MATINATED, OR PICKLED.
 ONCE THE ORGANISM REACH THE DUODENUM, THEY EXCYST, PENETRATE THE GUT WALL,
AND TRAVEL THROUGH THE PERITONEAL CAVITY, DIAPHRAGM, AND PLEURAL SPACE TO
REACH LUNGS
 MATURE FLUKES ARE FOUND IN THE BRONCHIOLES SURROUNDED BY CYSTIC LESIONS
 PARASITE EGGS ARE EITHER EXPECTORATED WITH SPUTUM OR SWALLOWED AND PASSED
TO THE OUTSIDE ENVIRONMENT WITH FACES
 THE LIFE CYCLE IS COMPLETED IN SNAILS AND FRESHWATER CRUSTACEANS.
88

MORPHOLOGY  ADULT LUNG FLUKES, WHICH ARE 7-12 MM IN LENGTH, ARE
FOUND ENCAPSULATED IN THE LUNGS OF INFECTED PERSONS.
RARELY, FLUKES ARE FOUND ENCYSTED IN CNS (CEREBRAL
PARAGONIMIASIS) OR THE ABDOMINAL CAVITY.
 WHEN MATIRUG FLUKES LODGE IN LUNG TISSUES, THEY CAUSE
HAEMORRHAGE AND NECROSIS, RESULTING IN CYST
FORMATION
 THE ADJACENT LUNG PARENCHYMA SHOWS EVIDENCE OF
INFLAMMATORY INFILTRATION, PREDOMINANTLY BY
EOSINOPHILS.
 CYSTS USUALLY MEASURE 1-2 CM IN DIAMETER AND MAY
CONTAIN ONE OR TWO WORMS EACH
 OLDER CYSTS DEVELOP THICKENED WALLS, WHICH MAY
UNDER GO CALCIFICATION.
 DURING THE ACTIVE PHASE OF PARAGONIMIASIS, LUNG
TISSUES SURROUNDING PARASITE CYSTS MAY SHOW
EVIDENCE OF PNEUMONIA, BRONCHIECTASIS, AND FIBROSIS.
89

DIAGNOSIS  PRODUCTIVE COUGH WITH BROWNISH SPUTUM OR FRANK
HEMOPTYSIS ASSOCIATED WITH PERIPHERAL-BLOOD
EOSINOPHILIA IS USUALLY THE PRESENTING FEATURE.
 CHEST EXAMINATION MAY SIGNS OF PLEURISY, BRONCHITIS OR
BRONCHIECTASIS MAY PREDOMINATE, RARELY LUNG ABSCESS.
 IMAGING OF LUNGS SHOWS PATCHY DENSITIES, CAVITIES,
PLEURAL EFFUSION, AND RING SHADOWS.
 PULMONARY PARAGONIMIASIS IS DIAGNOSED BY DETECTION
PARASITE OVA IN SPUTUM, LUNG BIOPSY AND/OR STOOLS.
 SEROLOGY IS OF CONSIDERABLE HELP IN EGG-NEGATIVE CASES
AND IN CEREBRAL PARAGONIMIASIS.
 THE DIFFERENTIAL DIAGNOSIS INCLUDES ACTIVE TUBERCULOSIS.
BACTERIAL LUNG ABSCESS, AND LUNG CARCINOMA.
TREATMENT THE DRUG OF CHOICE FOR TREATMENT IS PRAZIQUANTEL
90

42.ABSENT UROBILINOGEN IN
URINE WITH ICTERUS
INDICATES?
A. PERIHEPATIC OBSTRUCTION
B. HEMOLYSIS
C. HEPATITIS
D. LIVER FAILURE
ANS: A. PERIHEPATIC
OBSTRUCTION

EXPLANATION: UROBILIONGEN APPEARS IN URINE ONLY AFTER ENTROHEPATIC CIRCULATION, SO
ITS ABSECENCE WITH ICTERUS INDICATES POST HEPATIC JAUNDICE (PERIHEPATIC
OBSTRUCTION)
CONDITION SERUM BILIRUBIN URINE
UROBILINOGEN
URINE BILIRUBIN FECAL
UROBILINOGEN
NORMAL DIRECT 0.1-0.4
MG/DL
INDIRECT 0.2-07
0-4 MG/24H ABSENT 40-280 MG/24H
HEMOLYTIC
ANEMIA
↑ INDIRECT INCREASED ABSENT INCREASED
HEPATITIS ↑ DIRECT AND
INDIRET
DECREASED IF
MICROOBSTRUCTIO
N IS PRESENT
PRESENT IF
MICROOBSTRUCTIO
N
DECREASE
OBSTRUCTION
JAUNDICE
↑ DIRECT ABSENT PRESENT TRACE TO ABSENT
92

43. FOR WHICH PROCEDURE IS THE FOLLOWING INSTRUMENT
USED?
A. BONE MARROW EXAMINATION
B. LIVER BIOPSY
C. PLEURAL BIOPSY
D. LUMBAR PUNCTURE
ANS: A. BONE MARROW EXAMINATION
[REF: DACIE PRACTICAL HEMATOLOGY]

44. IN A PATIENT SUFFERING WITH SICKLE CELL ANEMIA,
ELETROPHORETIC MOBILITY OF HBS IN RELATION TO HBA
WILL BE?
A. RETARDED
B. ACCELERATED
C. SAME
D. WILL DEPEND UPON CONCENTRETATION OF HBS
ANS: A. RETARDED
[REF: COMPLETE REVIEW OF PATHOLOGY 1/343]

45. WHICH OF THE FOLLOWING MECHANISM IS MAINLY INVOLVED IN
EPIGENETICS?
A. METHYLATION
B. ACETYLATION
C. DEAMINATION
D. PHOSPHORYLATION
ANS: A. METHYLATION
(The term epigenetics refers to heritable changes in gene expression
(active versus inactive genes) that does not involve changes to the
underlying DNA sequence; a change in phenotype without a change
in genotype.)
[REF: ROBBIN’S 9/ EP5]

EXPLANATION
EPIGENETICS
DEFINITION HERITABLE CHANGES IN GENE EXPRESSION, NOT CAUSED BY ALTERATIONS
IN DNA SEQUENCE.
EPIGENETIC FACTORS HISTONES AND HISTONE MODIFYING FACTORS
o HISTONE METHYLATION
o HISTONE ACETLATION
o HISTONE PHOSPHORYLATION
98

SIGNIFICANCE  EPIGENETIC DYSREGULATION→CENTRAL ROLE IN MALIGNANCY
 MANY OTHER DIEASES ARE ASSOCIATED WITH INHERITED OR ACQUIRED
EPIGENETIC ALTERATIONS. EG GENOMIC IMPRINTING IN QUIRED
EPIGENETIC ALTERATION. EG GENOMIC IMPRINTING IN PRADER WILLI
SYNDROME
 EPIGENETIC ALTERATIONS LIKE HISTONE ACETYLATION AND DNA
METHYLATION ARE REVERSIBLE AND ARE RESPONSIVE TO DRUGS; SO,
HDAC INHIBITORS AND DNA METHYLATION INHIBITORS ARE BEING
TESTED IN THE TREATMENT OF CANCER
DIAGNOSIS  SEQUENCING
 CHIP ON CHIP (MICROARRAY TECHNOLOGY)
 USING METHYLATION SPECIFIC PRIMERS IN POLYMERASE CHAIN
REACTION (PCR)
 BISULPHITE METHOD: BISULPHITE CONVERTS UNMETHYLATED CYTOSINE
TO URACIL, WHICH ACTS LIKE THYMINE IN DOWNSTREAM REACTIONS.
THE UNMETHYLATED (MODIFIED) DNA IS DETECTED BY SEQUENCE
ANALYSIS.
99

PHARMACOLOGY
47. NEW ORAL DRUG APPROVED FOR
THE TREATMENT OF HEPATITIS C IS?
A. RIBAVIRINE
B. LEDIPASVIR
C. LAMIVUDINE
D. PEG INTERFERON
ANS: B. LEDIPASVIR (Ledipasvir (formerly GS-5885) is a drug for
the treatment of hepatitis C that was developed by Gilead
Sciences)
REF: HARRISON’S 19/E P2041-2047

EXPLANATION:
DISCUSSING ANOUT THE PTIONS ONE BY ONE:
(A) RIBAVIRINE  IT IS A NUCLEOSIDE INHIBITOR
 USED FOR SEVERE RSV, CHRONIC HEPATITIS C INFECTION
 RIBAVIRIN SHOULD NERVE BE GIVEM AS MONOTHERAPY.
 SHOULD BE GIVEN IN COMBINATION WITH PEGINTERFERON ALFA-2A;
 DAILT DOSE IS 800-1200 MG ADMINISTERED ORALLY
 MOST IMPORTANT SIDE EFFECT IS HEMOLYSIS
 CONTRA-INDICATED IN PREGNANCY & HEMOGLOBINOPATHIES
(B) LEDIPASVIR  LEDIPASVIR (FORMERLY GS-5885) IS A RECENTLY DEVELOPED DRUG FOR THE
TREATMENT OF EPATITIS C
 IT IS A POTENT INHIBITOR OF HCV NS5A, A VIRAL PHOSPOHOPROTEIN THAT
PLAYS AN IMPORTANT ROLE IN VIRAL REPLICATION, ASSE,BLY, AND
SECRETION.
 SOFTOSBUVIR IS A NUCLEOTIDE ANALOG INHIBITOR OF HEPATITIS C VIRUS
NS5B POLYMERASE
 FIXED DOSE COMBINATION LADIPASVIR-SOFOSBUVIR IS FDA-APPROVED FOR
THE TREATMENT OF CHRONIC HEPATITIS GENOTYPE 1
 MOST COMMON ADVERSE EFFECTS ARE FATIGUE AND HEADACHE.
101

(www.doctorsacademydvg.com): EXTRA EDGE NEW MCQS
© LAMIVUDINE  LAMIVUDINE, IS A NUCLEOSIDE ANALOG THAT INHIBITS HIV
REVERSE TRANSCRIPTASE AND HBC DNA POLYMERASE.
 FOLLOWING ORALADMINISTRATION. LAMIVUDINE IS
ABSORBED RAPIDLY WITH A BIOAVAILABILITY OF 80%
 LAMIVUDINE IS A WELL TOLERATED DRUG
 AMINOTRANFERASE RISES AFTER THERAPY MAY BE SEEN
(D) PEG INTERFERON  INTERFERONS (IFNS) ARE POTENT CYROKINES THAT POSSESS
ANTIVIRAL, IMMUNIMODULATING, AND ANTIPROLIFERATIVE
ACTIVITIES
 ORAL ADMINISTRATION DOES NOT RESULT IN DETECTABLE IFN
LEVEL IN SERUM, HENCE GIVEN SUBCUTANEOUS OR
INTRAMUSCULAR
 ATTACHMENT OF IFN PROTEINS TO LARGE, POLYETHYLENE
GLYCOL (PEG) MOLECULES SLOWS ABSORPTION, DECREASES
CLEARANCE, AND PROVIDES HIGHER & MORE PROLONGED SERUM
CONCENTRATIONS THAT ENABLE NCE-WEEKLY DOSING
 SIDE EFFECTS:ACUTE INFLUENZA B, DISCOMFORT AT THE
INJECTION SITE, AND LEUCOPENIA
 ONCE-A-WEEK ADMINISTERED LONG-ACTING PEG IFN IS MORE
EFFECTIVE THAN THE STANDARD IFN
102

48. MECHANISM OF ACTION OF ASPIRIN FOR ANTIPLATELET
ACTION IS?
A. BLOCKS TXA2 SYNTHESIS
B. COX 2 INHIBITOR
C. LIPOXYGENASE INHIBITOR
D. PLATELET DYSFUNCTION
ANS: A. BLOCKS TXA2 SYNTHESIS
REF: H19 746-747

EXPLANATION:
ASPIRIN
IMPORTANT INFO IT IS THE MOST WIDELY USED ANTIPLATELET AGENT
WORLDWIDE
MECHANISM OF ACTION  ASPIRIN PRODUCES ITS ANTITHROMBOTIC EFFECT BY
IRREVERSIBLY ACETYLATING & INHIBITING PLARELET
CYCLOOXY-GENASE (COX)-1, A CRITICAL ENZYME IN
THROMBOXANE A2 SYNTHESIS
 AT HIGH DOSES, ASPIRIN ALSO INHIBITS COX-2, AN
INDUCIBLE COX ISOFORM FOUND IN ENDOTHELIAL
CELLS AND INFLAMMATORY CELLS.
INDICATIONS  SECONDARY PREVENTION OF CARDIOVASCULAR EVENTS
IN PATIENTS WITH CORONARY ARTERY,
CEREBROVASCULAR OR PERIPHERAL VASCULAR DISEASE
 ASPIRIN PRODUCES A 25% REDUCTION IN THE RISK OF
CARDIOVASCULAR DEATH, MI, R STROKE
 ASPIRIN IS ALSO USED FOR PRIMARY PREVENTION IN
HIGH RISK PATIENTS
104

DOSAGE 75-325 MG ONCE DAILY
ADVERSE EFFECTS SIDE EFFECTS OF ASPIRIN ARE DOSE-RELATED
MOST COMMON ARE GASTROINTESTINAL (DYSPEPSIA, EROSIVE GASTRITIS,
PEPIC ULCERS WITH BLLEDING AND PERFORATION)
105

49. WHICH OF THE FOLLOWING IS
THE LATEST APPROVED DRUG
FOR TUBERCULOSIS?
A. ETHIONAMIDE
B. LEVOFLOXACIN
C. BEDAQUILINE
D. TIPRANAVIR
• ANS: C. BEDAQUILINE
• (Bedaquiline (trade name Sirturo,
code names TMC207 and R207910)
is a medication used to
treat tuberculosis)

EXPLANATION: SECOND-LINE DRUGS (HAVE LOWER EFFICACY & HIGHER TOXICITY, USED IN MDR &
XDR TB):
FLUOROQUINOLONES
(LEVOFLOXACIN & MOXIFLAXACIN
MOST EFFECTIVE)
INHIBIT MYCOBACTERIAL DNA GYRASE & TOPOISOMERASE IV,
PREVENTING CELL REPLICATION AND PROTEIN SYNTHESIS, AND ARE
BACTERICIDAL.
INJECTABLE AMINOGLYCONSIDES
(KANAMYCIN, AMIKACIN &
STREPTOMYCIN)
EXERT MYCOBACTERICIDAL ACTIVITY BY BINDING TO THE 16S
RIBOSOMAL SUBUNIT.
ADVERSE EFFECTS OTOTXICITY, NEPHROTOXICITY,A AND
NEUROTOXICITY.
CAPREOMYCIN USEFUL WHEN ADDITIONAL RESISTANCE TO AMINOGLYCOSIDES IS
DOCUMENTED. CAPREOMYCIN IS ADMINISTERED BY THE IM ROUTE;
ADVERSE EFFECTS; HYPOKALEMIA, HYPOMAGNESEMIA, OTO-AND
RENAL TOXICITY.
ETHIONAMIDE AND
PROTHIONAMIDE
(BACTERIOSTATIC)
INHIBITS INHA GENE PRODUCT ENOYL-ACYL CARRIER PROTEIN (ACP)
REDUCTASE, INVOLVED IN MYCOLIC ACID SYNTHESIS.
ADVERSE EFFECTS: SEVERE GI REACTIONS (INCLUDING ABDOMINAL
PAIN, NAUSEA, VOMITING), NEUROLOGIC SIDE EFFECTS, REVERSIBLE
HEPATITIS, HYPERSENSITIVITY REACTIONS, AND HYPOTHYROIDISM.
107

CYCLOSERINE AND TERIZIDONE
(THERIZIDONE)
PREVENTS CELL WALL SYNTHESIS & INHIBITS THE ACTION OF
ALANINE RACEMASE, INVOLVED IN PRODUCTION OF
PEPTIDOGLYCANS
IT IS WELL ABSORBED AFTER ORAL ADMINISTRATION AND IS
WELL DISTRIBUTED AFTER ORAL ADMINISTRATION AND IS WELL
DISTRIBUTED THROUGHOUT BODY FLUID, INCL CSF
SIDE EFFECTS INCLUDE SEIZURES, PSYCHOSIS, PERIPHERAL
NEUROPATHY, HEADACHE, SOMNOLENCE & ALLERGIC
REACTIONS.
PAS (PARA-AMINOSALICYLIC ACID) IT IS AN ORAL AGENT USED IN TREATMENT OF MDR-& XDR-TB.
ITS BACTERIOSTATIC ACTIVITY IS DUE TO INHIBITION OF FOLATE
SYNTHESIS AND OF IRON UPTAKE.
ADVERSE EFFECTS INCLUDE NAUSEA, VOMITING,
DIARRHEA, HEMOLYSIS IN C6PD DEFICIENCY.
108

(WWW.DOCTORSACADEMYDVG.COM)
50. DRUG USED FOR DETOXIFICATION IN CHRONIC
ALCOHOLISM ARE ALL EXCEPT?
A. NALTREXONE
B. FLUMAZENIL
C. DISULFIRAM
D. ACAMPROSATE
ANS: B. FLUMAZENIL
REF:HARRISON 19/E P2727

EXPLANATION:
MEDICATIONS FOR REHABILITATION IN CHRONIC ALCOHOLISM
NALTREXONE  AN OPIOID ANTAGONIST
 MAY BE TAKEN DAILY ORALLY, OR AS MONTHLY INJECTION
 SHORTENS SUB-SEQUENT RELAPSES
 BY BLOCKING OPIOID RECEPTORS, NALTREXONE DECREASES ACTIVITY IN
THE DOPAMINE-RICH VENTRAL TEGMENTAL REWARD SYSTEM &
DECREASES THE FEELING OF PLEASURE IF ALCOHOL IS IMBIBED.
ACAMPROSATE  IT INHIBITS NMDA RECEPTORS, DECREASING MILD SYMPTOMS OF
PROTRACTED WITHDRAWAL.
 DOSE~2 G.D DIVIDED INTO THREE ORAL DOSES
DISULFIRAM  IT IS AN ALDH INHIBITOR, USED AT DOSES OF 250 MG/D
 IT PRODUCES VOMITING & AUTONOMIC INSTABILITY IN THE
PRESENCE OF ALCOHOL AS A RESULT OF RAPIDLY RISING BLOOD
LEVELS OF ACETALDEHYDE.
 THIS REACTION CAN BE DANGEROUS, ESPECIALLY FOR ATIENTS
WITH HEART DISEASE, STROKE, DIABETES MELLITUS, OR
HYPERTENSION
 IT ALSO CARRIES POTENTIAL RISK OF DEPRESSION, PSYCHOTIC
SYMPTOMS, PERIPHERAL NEUROPAHY, AND LIVER DAMAGE
110

OTHER DRUGS UNDER INVESTIGATION  NALMEFENE (OPIOID ANTAGONIST)
 VARENICLINE (NICOTINIC RECEPTOR
AGONIST)
 ONDANSETRON (SEROTONIN ANTAGONIST),
 PRAZOSIN (Α-ADRENERGIC AGONIST)
 BACLOFEN (GABA B RECEPTOR AGONIST),
 TOPIRAMATE (ANTICONVULSANT)
111

51. ETANERCEPT IS?
A. COX 2 INHIBITOR
B. TNF INHIBITOR
C. IL 6 INHIBITOR
D. IFN GAMMA INHIBITOR
ANS: B. TNF INHIBITOR
REF: HARRISON 19/E P272E30

EXPLANATION
INDICATIONS OF ETANERCEPT:-
• ANKYLOSING SPONDYLITIS
• ADULT RHEUMATOID ARTHRITIS
• PSORIATIC ARTHRITIS
• PLAQUE PSORIASIS
113

52. WHICH OF THE FOLLOWING
ADVICE WILL YOU GIVE TO A
PATIENT WHEN HE IS GIVEN
BISPHOSPHONATES?
A. TAKE TABLET BEFORE FOOD WITH FULL
GLASS OF WATER
B. DISCONTINUE IF GASTRITIS PERSISTS
C. TAKE TABLET AFTER FOOD WITH FULL
GLASS OF WATER
D. WITHDRAW THE DRUG WHEN BONE PAIN
OCCURS
ANS: A. TAKE TABLET BEFORE FOOD WITH FULL GLASS
OF WATER
REF: HARRISON 19/E P2499

EXPLANATION: BISPHOSPHONATES
NAME OF DRUGS ALENDRONATE, RISEDRONATE, IBANDRONATE,
AND ZOLEDRONIC ACID
INDICATIONS  PREVENTION AND TREATMENT OF POST-
MENOPAUSAL OSTEOPOROSIS.
 TREATMENT OF STEROID-INDUCED
OSTEOPOROSIS,
 PREVENTION OF STEROID-INDUCED
OSTEOPOROSIS
 PAGET’S DISEASE
 HYPERCALCEMIA OF MALIGNANCY
MECHANISM OF ACTION  INHIBIT OSTEOCLAST MEDIATED BONE
RESORPTION
 INCREASES APOPTOSIS OF OSTEOCLASTS
 INHIBIT IL6, THEREBY SUPPRESSES
DIFFERENTIATION OF OSTEOCLAST PRECURSOR
TO MATURE OSTEOCLAST
115

PROCESS OF ADMINISTRATION  ALENDRONATE SHOULD BE GIVEN WITH A FULL
GLASS OF WATER BEFORE BREAKFAST, BECAUSE
BISPHOSPHONATES ARE POORLY ABSORBED.
 IT IS RECOMMENDED THAT PATIENTS REMAIN
UPRIGHT FOR AT LEAST 30 MIN AFTER TAKING THE
MEDICATION TO AVOID ESOPHAGEAL IRRITATION.
CONTRAINDICATION  BECAUSE OF THE POTENTIAL FOR ESOPHAGEAL
IRRITATION, ALENDRONATE IS CONTRAINDICATED
IN PATIENTS WITH HAVE STRICTURE OR
INADEQUATE EMPTYING OF THE ESOPHAGUS.
116

53. DRUG OF CHOICE IN PREGNANCY
INDUCED HYPERTENSION?
A. ACE INHIBITOR
B. ATENOLOL
C. ALPHA METHYL DOPA
D. NITROPRUSSIDE
ANS: C. ALPHA METHYL DOPA
REF:HYPERTENSION IN PREGNANCY (REPORT OF THE ACOG TASK FORCE
ON HYPERTENSION IN PREGNANCY) OBSTETRICS & GYNECOLOGY
VOL. 122, NO. 5 NOVEMBER 2013

55. WHICH OF THE FOLLOWING IS UREIDOPENICILLIN?
A. PENICILLIN V
B. METHICILLIN
C. PIPERCILLIN
D. CLAVULANIC ACID
ANS: C. PIPERCILLIN

56. WHILE PILOCARPINE ACTS ON SPHINCTER PAPILLAE. WHICH
OF THE FOLLOWING HAS ANALOGOUS EFFECT ON DILATOR
PUPILLAE?
A. EPINEPHRINE
B. TIMOLOL
C. COCAINE
D. LATANOPROST
ANS: A. EPINEPHRINE
(REF: K.D. TRIPATHI)

EXPLANATION:
PUPILLARY MYDRIASIS
THIS IS CAUSED BY DRUGS THAT ACTIVELY DILATE THE PUPIL (ACTING ON THE
DILATOR PAPILLA) ON PRESENT THE ACTIVE CONSTRICTION OF THE PPIL
(PREVENTING ACTION ON THE SPHINCTER PAPILLA).
THUS, DRUGS WHICH DILATE THE PUIL BY ACTIVELY ACTING ON THE SYMPATHETIC
INNERVATIONS OF THE DILATOR PAPILLA ARE CALLED SYMPATHOMIMETIC DRUGS
AND DRUGS WHICH RESULT IN DILATATION OF THE PUPIL BY PREVENTING THE
PARASYMPATHETIC ACTION OF THE SPHINCTER ARE CALLED PARASYMPATHOLYRIC
DRUGS.
121

57. PHASE 1 TRIAL IS DONE FOR?
A. HUMAN PHARMACOLOGY & SAFETY
B. THERAPEUTIC EXPLORATORY
C. MICRODOSING
D. PHARMACOKINETICS
ANS: A
(REF: K. D TRIPATHI 7/E P63-64)

EXPLANATION
PHASE NAME CONDUCRED ON PURPOSE
I HUMAN PHARMACOLOGY AND
SAFETY
HEALTH VOLUNTEERS
(20-100)
 SAFETY AND TOLERABILITY
 TO KNOW MAIMUM TOLERABLE
DOSES (MTD)
II THERAPEUTIC EXPLORATORY 100-150
PATIENTS
 TO ESTABLISH THERAPEUTIC
EFFICACY
 DOSE RANGING AND CEILING
EFFECT
III THERAPEUTIC CINFIRMATORY UPTO 5000 PATIENTS FROM
SEVERAL CENTRE
 TO CONFIRM THERAPEUTIC
EFFICACY
IV POST MARKETING SURVEILI
LUNCH
TREATED BY PRACTICING
PHYSICIANS
 TO KNOW RARE AND LONG
TERM ADVERSE EFFECTS
 SPECIAL GROUPS LIKE
CHILDREN, PREGNANCY ETC
CAN BE TESTED
0
(ZERO)
MICRODOSING STUDIES HEALTHY VOLUNTEERS
(SMALL NUMBER)
 VERY LOW DOSE 1/100 OF
HUMAN DOES; MAX 100 µG
123

58. WHICH ANTIDOTE IS REQUIRED FOR FIBRINOLYTIC
THERAPY?
A. tPA
B. PROTAMINE SULFATE
C. STREPTOKINASE
D. E-AMINO CAPROIC ACID
ANS: D. E-AMINO CAPROIC ACID
REF: K. D TRIPATHI 6/E P608-610

EXPLANATION
DISCUSSING THE OPTIONS ONE BY ONE,
(A) EACA EPSILON AMINO CAPROIC ACID (EACA) &
TRANEXAMIC ACID ARE SPECIFIC ANTIDOTES OF
FIBRINOLYTIC THERAPY
(B) PROTAMINE SULFATE IT IS AN ANTIDOTE OF HEPARIN
(C ) STREPTOKINASE IT FORMS A COMPLEX WITH PLASMINOGEN &
EXPOSES ITS ACTIVE SITE. THIS ALTERED
PLASMINOGEN ACTS LIKE TPA & ACTIVATES OTHER
PLASMINOGEN MOLECULES TO PLASMIN THUS,
STREPTOKINASE ACTS AS A FIBRINOLYTIC
(D) TPA TISSUE PLASMINOGEN ACTIVATOR SELECTIVELY
ACTIVATES PLASMINOGEN THAT IS BOUND TO
FIBRIN (IN THE THROMBUS)
125

59. WHICH ANTICHOLINERGIC IS
EXCLUSIVELY USED IN PRE-
ANAESTHETIC MEDICATION?
A. ATROPINE
B. PROMETHAZINE
C. GLYCOPYRROLATE
D. SCOPOLAMINE
ANS: C. GLYCOPYRROLATE (TO DECREASE
SECRETIONS)
REF: K. D TRIPATHI 7/E P110-112

60. DRUGS SOLD ONLY ON
PRESCRIPTION OF
REGISTERED MEDICAL
PRACTITIONER BE LONGS
TO WHICH SCHEDULE?
A) H
B) X
C) J
D) P
ANS: A) H
(REF: TEXTBOOK OF FORENSIC
MEDICINE AND TOXICOLOGY BY
N.G.RAO P356)

EXPLANATION
THE DRUGS AND COSMETIC RULES 1945
SCHEDULE DESCRIPTION
C BIOLOGICAL AND SPECIAL PRODUCTS
E LIST OF POISONS
F VACCINES AND SERA
G HORMONE PREPARATION;
H DRUGS (POISON TO BE SOLD ONLY ON THE PRESCRIPTION OF A REGISTERED MEDICAL
PRACTITIONER);
J LIST OF DISEASES FOR THE CURE OF WHICH NO DRUG SHOULD BE ADVERTISED
L ANTIBIOTICS, ANTIHISTAMINICS AND OTHER RECENT CHEMOTHERAPEUTIC AGENTS
128

61. A PATIENT WITH EPILEPTIC DISORDER PRESENTED WITH
CONCENTRIC VISUAL FIELD DEFECTS. WHICH DRUG WAS HE
TAKING ?
A. VALPROATE
B. ETHOSUXIMIDE
C. PHENOBARBITOL
D. VIGABATRIN
ANS: D. VIGABATRIN
(REF: NELSON 20/E P2846)

EXPLANATION
ANTIEPILETIC DRUG SIDE EFFECTS
ACETAZOLAMIDE MINOR: DIZZINESS, POLYURIA, ELECTROLYTE IMBALANCE SERIOUS: STEVENTS-
JOHNSON SYNDRINE
BENZODIAZEPINES MINOR: DOES-RELATED NEUROTOXICITY (DROWSINESS, SEDATION, ATAXIA),
HYPERACTIVITY, DROOLING INCREASED SECRETIONS SERIOUS APNEA
CARBAMAZEPINE NUISANCE: TICS, TRANSIENT LEUCOPENIA, HYPONATREMIA, WEIGHT GAIN,
NAUSEA, DIZZINESS
SERIOUS: STEVENS-JOHNSON SYNDROME, AGRANULOCYTSIS, APLASTIC ANEMIA,
LIVER TOXICITY
GABAPENTIN IN CHILDREN: ACUTE ONSET OF AGGRESSION, HYPERACTIVITY IN ADULTS:
EUPHORIA AND BEHAVIOURAL DISINHIITION, WEIGHT GAIN
LAMOTRINGINE MINOR: HEADACHE, ATAXIA, DIZZINESS, TREMOR, SERIOUS, STEVENS-JOHNSON
SYNDROME, RARELY LIVE TOXICITY
LEVETIRACETAM CNS ADVERSE EVENTS: SOMNOLENCE ASTHENIA DIZZINESS, BUTUSUALLY LESS
THAN OTHER AEDS
IN ADULTS: BEHAVIOURAL SYMPTOMS ARE COMMON, DEPRESSION
130

PHENOBARBITONE MINOR: NEUROTOXICITY INSOMNIA, HYPERACTIVITY, SIGNS OF DISTRACTIBILITY,
FLUCTUATION OF MOOD, AGGRESSIVE OUTBURSTS
SERIOS:LIVER TOXICITY, STEVENS-JOHNSON SYNDROME
PHENYTOIN AND OTHER
HYDANTOINS
MINOR: GINGIVAL HYPERPLASIA, COARSENING OF FACIES, HIRSUTISM,
CEREBELLOVESTIBULAR SYMPTOMS (NYSTAGMUS AND ATAXIA)
SERIOUS: STEVENS-JOHNSON SYNDROME LIVE TOXICITY
PREGABALIN MINOR: DIZZINESS, PERIPHERAL EDEMA, BLURED VISION WEIGHT GAIN,
THROMBOCYTOPENIA
SERIOUS: HYPERSENSITIVITY REACTIONS, RHABDOMYOLYSIS
TOPIRAMATE MINOR: CONGNITIVE DYSFUNCTION, WEIGHT LOSS, RENAL CALCULI, HYPOHIDROSIS,
FEVER
SERIOUS: PRECIPITATION OF GLAUCOMA
VALPROCIC ACID MINOR: WEIGHT GAIN; HYPERAMMONEMIA TREMOR, ALOPECIA, MENSTRUAL
IRREGULARITIES
SERIOUS: HEPATIC AND PANCREATIC TOXICITY
VIGABATRIN MINOR: HYPERACTIVITY
SERIOUS: IRREVERSIBLE VISUAL FIELD DEFICTS, RETINOPATHY THAT REQUIRES
FREQUENT OPHTHALMOGIC EVALUATIONS AND FOLLOW UP
131

62. DRUG WHOSE CONCENTRATION INCREASES AFTER A FATTY
MEAL ARE ALL EXCEPT?
A. AMPHOTERICIN B
B. AMPICILLIN
C. PPI
D. NIMESULIDE
ANS: C. PPI
(REF: NUTRITION IN PEDIATRICS /E P196)

EXPLANATION
DRUG ABRORPTION
REDUCED/DELAYED BY FOOD
DRUG ABSORPTION INCREASED BY FOOD
AMPICILLIN
ASPIRIN
ATENOLOL
AZITHROMYCIN
CAPTOPRIL
CEFACLOR
CEFIXIME
CEPHALEXIN
CIPROFLOXACIN
DIDANOSINE
ATOVAQUONE
CARBAMAZEPINE
CHLOROTHIAZIDE
CEFUROXIME
CLOFAZIMINE
DIAZEPAM
ERYTHROMYCIN ESTOLATE
GANCICLOVIR
HYDROCHLOROTHIAZIDE
ITRACONAZOLE
133

INDINARIR
ISONIAZID
LORATIDINE
NAFICILLIN
PENICILLIN G OR V
PHENOBARBITAL
PHENYTOIN
RIFAMPIN
SUCRALFATE
TERACYCLINE
DOXYCYCLINE
KETOCONAZOLE
LITHIUM
LOVASTATIN
METHYLPHENIDATE
METOPROLOL
NELFINAVIR
NITROFURANTOIN
PROPRANOLOL
PROPOXYPHENE
RITONAVIR
SAQUINAVIR
SPIRONOLACTONE
HYDRALAZINE
134

63. ALL OF THE FOLLOWING INHIBITS
NUCLEIC ACID SYNTHESIS EXCEPT?
A. QUINOLONES
B. NALIDIXIC ACID
C. LINEZOLID
D. RIFAMPICIN
ANS: C. LINEZOLID (LINEZOLID INHIBTS THE PROTEIN
SYNTHESIS)
(REF: HARRIOSN 19/E P931)

EXPLANATION
ANTIBACTERIAL AGENT MAJOR CELLULAR TARGET MECHANISM OF ACTION
Β-LACTAMS (PENICILINS
CEPHALOSPORINS)
CELL WALL INHIBIT CELL-WALL CROSS-LINKING
VANCOMYCIN CELL WALL INTERTERES WITH ADDITION OF NEW
CELL WALL SUBUNITS
(MURAMY PENTAPEPTIDES)
BACITRACIN CELL WALL PREVENTS ADDITION OF CELL-WALL-
SUBUNITS BY INHIBITING RECYCLING OF
MEMBRANE LIPID CARRIER
MACROLIDES (ERYTHROMYCIN) PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
LINCOSAMIDES (CLINDAMYCIN) PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
BLOCK PEPTIDE CHAIN ELONGTATION
CHLORAMPHENICOL PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
BLANK AMINOACYL TRNA ATTAXHMENT
136

TETRACYCLINE PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
BLOCK AMINOACYL TRNA
AMINOGLYCOSIDES
(GENTAMYCIN)
PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
INHIBIT TRANSLOCATION OF PEPTIDYL-
TRNA
LINEZOLID PROTEIN SYNTHESIS BIND TO 50S RIBOSOMAL SUBUNIT
INHIBITS INITIATION OF PROTEIN
SYNTHESIS
SULFONAMIDES AND TRIMETHOPRIM CELL METABOLISM COMPETITIVELY INHIBIT ENZYMES
INVOLVED IN TWO STEPS OF FOLIC ACID
BIOSYNTHESIS
RIFAMPICIN NUCLEIC ACID SYNTHESIS INHIBITS DNA-DEPENDENT-RNA
POLYMERASE
METRONIDAZOLE NUCLEIC ACID SYNTHESIS INTRACELLULARLY GENERATES SHORT-
LIVED RE-ACTIVE INTERMEDIATES THAT
DAMAGE DNA BY ELECTRON TRANSFER
SYSTEM
QUINOLONESS
(CIPROFLOXACIN)
DNA SYNTHESIS INHIBIT ACTIVITY OF DNA GYRASE (A
SUBUNIT) AND TOPOISOMERASE IV
137

NOVOBIOCIN DNA SYNTHESIS INHIBIT ACTIVITY OF DNA GYRASE ( B
SUBUNIT)
POLYMYXINS CELL MEMBRANE DISRUPT MEMBRANE PERMEABILITY
BY CHARGE ALTERATION
GRAMICIDIN CELL MEMBRANE FORM PORES
CHLORAMPHENICOL PROTEIN SYNTHESIS BIND 50S RIBOSOMAL SUBUNIT
BLOCK AMINOACYL TRNA
POSITIONING
OXAZOLIDINOMES (LINEZOLID
TEDIZOLID)
PROTEIN SYNTHESIS BIND 50S RIBOSOMAL SUBUNIT
INHIBIT IN;TIATIO OF PEPTIDE
SYNTHESIS
MUPIROCIN PROTEIN SYNTHESIS BLOCK ISOLEUCYL TRNA SYNTHEASE
SULFONAMIODES (SULFADIAZINE
SULFLSOXAZOLE AND
SULFAMETHOXAZOLE)
FOLATE SYNTHESIS INHIBITS DIHYDROFOLATE SYNTHETASE
TRIMETHOPRIN FOLATE SYNTHESIS INHIBITS DIHYDROFOLATE REDUCTASE
QUINOLONERS (NORFLOXACIN,
CIPROFLOXACIN, OFLOXACIN
LEVOFLOXACIN MOXIFLOXACIN
GEMIFLOXACIN)
DNA SYNTHESIS INHIBIT DNA GYRASE AND DNA
TOPOISOMERASE IV ENZYME-DNA-
DRUG COMPLEX:BLOCK REPLICATION
APPARATUS
138

RIFAMYCINS (RIFAMPIN
FIFABUTIN, RIFAPENTNE)
RNA SYNTHESIS INHIBIT RNA POLYMERASE
NITROFURANTOIN NUCLEIC ACID SYNTHESIS REDUCE REACTIVE DRUG
DERIVATIVES THAT DAMAGE DNA
METRONIDAZOLE NUCLEIC ACID SYNTHESIS BIND LPS AND MEMBRANE
CHANNEL AND MEMBRANE
LEAKAGE
POLYMYXIN E (CLISTIN) CELL MEMBRANE BIND LPS AND DISRUPT: BOTH
OUTER AND SYTOPLASMIC
MEMBRANE
DAPTOMYCIN CELL MEMBRANE PRODUCES MEMBRANES
CHANNEL AND MEMBRANE
LEAKAGE
139

64. GENDER SPECIFIC SIDE EFFECT OF VALPROATE IS?
A. WEIGHT GAIN
B. TREMORS
C. PCOD
D. ALOPECIA
ANS: C. PCOD
(REF: K.D TRIPATHY 7/E P405-409)
DR. MANJUNATH, DOCTORS ACADEMY 141

65. GLUCOCORTICOID IS NOT USED IN WHICH OF THE
FOLLOWING CONDITIONS?
A. MULTIPLE MYELOMA
B. KAPOSI SARCOMA
C. HODGKIN LYMPHOMA
D. CLL
ANS: B. KAPOSI SARCOMA
(REF: HARRISON’S 19/E P716)

EXPLANATION
DISCUSSING THE DRUGS USED IN THE TREATMENT OF ABOVE MALIGNANCIES
ONE NY ONE
(A) MULTIPLE MYELOMA THALIDOMIDE, DEXAMETHASONE, LENALIDOMIDE (A DERIVATIVE OF
THALIDOMIDE), BORTEZOMIB (A PROTEASOME INHIBITOR),
CYCLOPHOSPHAMIDE
(B) KAPOSI SARCOMA LIPOSOMAL DAUNORUBICIN, LIPOSOMAL DOXORUNICIN,
VINBLASTINE, AND PACLITAXEL-HAVE BEEN APPROVED BY FDA FOR
THIS INDICATION
(C) HODGKIN LYMPHOMA COMBINATION OF DOXOTUBICIN (ADRIAMYCIN), BLEOMYCIN
VINBLASTINE, AND DACARBAZINE (ABVD)
(D) CLL THE MOST COMMON TREATMENTS FOR PATIENTS WITH TYPICAL B-
CELL CLL/SMALL LYMPHOCYTIC LYMPHOMA HAVE BEEN
CHLORAMBUCIL OR FLUDARABINE, ALONE OR IN COMBINATION.
OTHER DRUGS USED: BENDAMUSTINE, CVP (CYCLOPHOSPHAMIDE,
VINCRISTINE, AND PREFNISONE) OR CHOP PLUS RITUXIMAB.
ALEMTUZUMAB (ANTI-CD52)
143

66. WHICH OF THE FOLLOWING IS A CALCINEURIN INHIBITOR?
A. CYCLOSPORINE
B. METHOTREXATE
C. LEFLUNOMIDE
D. MYCOPHENOLATE MOFETIL
ANS: A. CYCLOSPORINE
REF: K.D TRIPATHY 7/E P838-839

EXPLANATION:
BIND TO IMMUNIPHILLIN
↓
INHIBITS ACTIVATION OF NUCLEAR FACTOR OF ACTIVATED T CELLS (NFAT)
↓
INHIBITION OF TRANSCRIPTION FACTOR OF IL-2
↓
IMMUNISUPPRESSIVE ACTION
145

67. DRUG OF CHOICE FOR BIRD FLU?
A. OSELTAMIVIR
B. RIBAVIRIN
C. ENTECAVIR
D. ACYCLOVIR
ANS: A. OSELTAMIVIR
REF: HARRISON’S 19/E P1209-1213

68. AT A DOSE OF 3-
5MCG/KG/MIN, DOPAMINE
CAUSES?
A. β1 RECEPTOR STIMULATION
B. INCREASE IN RENAL FLOW
C. INCREASE BLOOD PRESSURE
D. VASOCONTRICTION
ANS: B. INCREASE IN RENAL
FLOW
(REF:GOODMAN & GILMAN
PHARMACOLOGY/CH 10)

69. URIPRISTAL ACETATE IS A ?
A. SELECTIVE ESTROGEN
RECEPTOR MODULATOR
B. SELECTIVE PROGESTERONE
RECEPTOR MODULATOR
C. GNRH ANATAGONIST
D. GNRH AGONIST
ANS: B. SELETIVE PROGESTERONE
RECEPTOR MODULATOR (SPRM)
(REF: HARRISON 19/E P2391)

MICROBIOLOGY
70. MOST COST EFFECTIVE WAY TO PREVENT INFECTION?
A. HANDWASHING
B. ANTIBIOTIC
C. CHEMOPROPHYLAXIS
D. CULTURE SENSITIVITY
ANS: A. HANDWASHING
(REF: HARRISON’S 19/E P152E9)

71. IDENTIFY THE ORGANISM IN THE GIVEN FIGURE?
A. HISTOPLASMOSIS
B. CANDIDA
C. CRYPTOCOCCUS
D. COCCIDIODOMYCOSIS
ANS: C. CRYPTOCOCCUS
(REF: ANANTNARAYAN P611)

EXPLANATION:
DIAGNOSIS OF CRYPTOCOCCUS INFECTION
INDIA INK STAINING  A DIAGNOSIS OF CRYPTOCOCCOSIS REQUIRES THE DEMONSTRATION OF
YEAST CELLS IN NORMALLY STERILE TISSUES.
 VISUALIZATION OF THE CAPSULE OF FUNGAL CELLS IN CEREBROSPINAL
FLUID (CSF) MIXED WITH INDIA INK IS A USEFUL RAPID DIAGNOSTIC
TECHNIQUE.
 CRYPTOCOCCAL CELLS IN INDIA INK HAVE A DISTINCTIVE APPEARANCE
BECAUSE THEIR CAPSULES EXCLUDE INK PARTICLES.
 HOWEVER, THE CSF INDIA INK EXAMINATION MAY YIELD NEGATIVE
RESULTS IN PATIENTS WITH A LOW FUNGAL BURDEN.
 THIS EXAMINATION SHOULD BE PERFORMED BY A TRAINED INDIVIDUAL,
SINCE LEUKOCYTES & FAT GLOBULES CAN SOMETIMES BE MISTAKEN FOR
FUNGAL CELLS.
151

(www.doctorsacademydvg.com): CRYPTOCOCCUS

72. STOOL SAMPLE FROM A PATIENT
SHOWS THE FOLLOWING. HOW DO
HUMANS GET THIS INFECTION?
A. INGESTION WITH FOOD
B. WORK IN DIRTY WATER
C. IMPROPERLY COOKED BEEF
D. DIRECT CONTACT
ANS: A. INGESTION WITH FOOD
(ENTAMOEBA CYST)
(REF: K. D CHATTERJEE COLOUR PLATES)

EXPLANATION:
CHARACTERISTIC FEATURES DIAGNOSIS
 10-15 UM SIZED
 ROUND YELLOW COLORED STRUCTURE SEEN
 BROWN COLOURED 1-4 NUCLEI AND GLYCOGEN MASS
CYST OF ENTAMEOBA
 PEAR SHAPED YELLOW COLOURED SEEN WITH VISIBLE
AXOSTYLE
TROPHOZOITE OF GIARDIA
 6-10 UM SIZED DISTINCT CYST WALL SURROUND WITH
VISIBLE AXOSTYLE
CYST OF GIARDIA
154

 40X60UM SIZED OVAL SHAPED YELLOW COLORED
STRUCTURE SEEN WITH LIGHTLY STAINED
BLASTOMERE
 SHELL MEMBRANE AND SEGMENTED OVUM WITH
LIGHT YELLOW STAINED BLASTOMERE
 CKEAR SHELL MEMBRANE AND BLASTOMERE
HOOKWORM EGG
 60X40 SIZED ROUND OVAL SHAPED YELLOW
COLOURED STRUCTURE SEEN WITH YELLOW STAINED
OUTER CORTICAL THICK CELL WALL
 UNSEGMENTED OVUM AND ALSO THE SPACE
BETWEEN THE SHELL AND OVUM AT EACH POLE ARE
STAINED YELLOW.
FERTILIZED EGG OF ASCARIS LUMBRICOIDS
 25X50 UM SIZED YELLOW COLORED,
 BARREL SHAPED STRUCTURE SEEN WITH LIGHTLY
STAINED MUCUS PLUGS AT EACH POLE
 EGG SHELL IS STAINED BROWN AND ENCLOSES THE
LIGHT YELLOW STAINED UNSEGMENTED OVUM
EGGS OF TRICHURIS TRICHURA
155

1. AIIMS NOVEMBER 2015 QUESTIONS & ANSWERS

1. AIIMS NOVEMBER 2015 QUESTIONS & ANSWERS

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