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Mock Test-3 (Surgery)

Anatomy
1. Regarding medulla oblongata-
a) It contains the spinal nucleus of the trigeminal nerve
b) Vagus nerve emerge between it and the interior cerebral peduncle
c) Gracile nucleus lies medial to hypoglossal nucleus
d) The vagus nucleus lies medial to hypoglossal nucleus
e) The pyramids decussate in the lower part of the medulla
TTFFT
Explanation:
c) Lies lateral
d) Lies lateral
[Ref: Snell’s/7th/P-198]
2. The neurotransmitter at-
a) Sympathetic postganglionic is noradrenaline Explanation:
b) Parasympathetic ganglion is acetylcholine  Both preganglionic & postganglionic NTMs in
c) Sympathetic preganglionic is noradrenaline parasympathetic system is acetylcholine.
d) Neuromuscular junction is noradrenaline  In sympathetic system, preganglionic NTMs are
e) Sympathetic postganglionic to sweat gland is Ach but post ganglionic are noradrenaline
acetylcholine adrenaline except sweat gland which is choline
TTFFT sympathetic.
 In NMJ NTMs always ach.
[Ref: Snell’s/8th/P-397]
3. The internal capsule of the brain-
a) Lies lateral to the thalamus
b) Contain pyramidal tract fibers in its genu
c) Is supplied by the thalamus striate artery
d) Is wedge shaped in coronal section
e) Radiates toward the calcarine sulcus known as corona radiate
TTFTT
Explanation:
c) Supplied by striate branch of middle & posterior cerebral artery.
[Ref: BD/8th/P-156-157]
4. Pneumatization is seen in-
a) Pterygoid process
b) Greater wing of the sphenoid Explanation:
c) Body of the sphenoid  Pneumatic bones of skull- Frontal, Sphenoid,
d) Lesser wing of the sphenoid Ethmoid, Maxilla, Temporal
e) Posterior clinoid process
FTTTF
[Ref: BD/8th/V-3/P-5]
5. Low ulnar nerve palsy is characterized by-
a) Wasting of the thenar muscle
b) Diminished/ absence of sensation of little finger
c) Clawing of little & ring finger
d) Weakness of flexor carpi ulnaris muscle
e) Positive formants sigh
FTTFT
Explanation:
a) Hypothenar
d) In high ulnar nerve palsy, lesion at elbow
e) It is positive in cubital tunnel syndrome, Guyon’s canal syndrome
[Ref: BD/8th/V-I/P-137]
Neuron Medical Academy 1|Page
6. Puborectalis muscle-
a) Is a component of the anorectal ring
b) Can be felt digitally especially on its anterior aspect
c) Is an important component in the continence mechanism
d) Is functionally distinct from the external anal sphincter
e) Gives off fibers to the longitudinal muscle layer
TFTFT
Explanation:
a) Anorectal ring is formed by the fusion of the puborectalis uppermost fiber of external sphincter & internal anal
sphincter.
b) Felt digitally on its posterior aspect.
c) Surgical division results in rectal incontinence.
d) The external anal sphincter forms a single functional and anatomical entity which upper most fibers blend with
fibers of puborectalis.
e) Conjoint longitudinal muscle coat is formed by fusion of puborectalis with the longitudinal muscle coat of rectum
(at the anorectal junction).
[Ref: A.K. Datta’s/9th/V-I/P-183]
7. The inferior epigastric artery-
a) Lies lateral to the deep inguinal ring
b) Originates from the internal iliac artery
c) Anastomoses with a branch of the internal thoracic artery
d) Pierces the fascia transversalis
e) Passes in front of the arcuate line
FFTTT
Explanation:
a) Lies medial to deep inguinal ring.
b) Originates from external iliac artery.
c) Anastomosis with superior epigastric artery which is branch of internal thoracic artery.
[Ref: A.K. Datta’s/9th/V-I/P-133]
8. The thoracic sympathetic trunk-
a) Possesses eleven ganglia
b) Lies in front of the neck of the ribs
c) Has no direct communication with the lumbar sympathetic trunk
d) Provides all the splanchnic nerves
e) Is independent of the thoracic spinal nerves
FTFTF
Explanation:
a) Possesses 12 ganglia.
c) Thoracic sympathetic ganglia are continuing above with cervical & below lumber sympathetic ganglia.
e) White & gray rami communicans are part of each spinal nerve.
[Ref: Lumley/Q-63/P-40]
9. The distribution of the left coronary artery shows that-
a) It trunk lies in the coronary sinus
b) The left anterior descending artery supplies parts of both ventricles
c) Its branches are the main supply to the A-V node in most cases
d) The left circumflex artery does not usually anastomose with any right coronary arterial branch
e) A left circumflex blockage would commonly cause septal ischemia
FTFFF
Explanation:
a) Lies in coronary sulcus.
c) Its branches are the supply to the A-V node in 10% cases.
d) The left circumflex artery usually anastomoses with any right coronary arterial branch.
e) Septal ischaemia is caused by blockage of LAD and PDA.
Neuron Medical Academy 2|Page
Information desk:
Area supplied by right coronary artery-
 Right atrium
 Most part of right ventricle except a portion adjacent to anterior inter-ventricular groove.
 A little portion of left ventricle adjacent to posterior inter-ventricular groove.
 The whole of the conducting system of the heart except left branch of AV bundle.
Area supplied by left coronary artery-
 Left atrium
 Most part of left ventricle except a small portion adjacent to posterior inter-ventricular groove.
 A small portion of right ventricle adjacent to the anterior inter-ventricular groove.
 Left branch of AV bundle and
 The SA node in 40% cases, AV node in 10% cases.
[Ref: BD Chaurasia’s/8th/V-1/P-298]
10. Development of the inter-atrial septum receives contribution from the-
a) Right venous valve
b) Septum primum
c) Septum secundum
d) Spiral septum
e) Septum spurium
FTTFF
Information desk:
Inter-atrial septum develops from-
1. Septum primum
2. Septum secundum
3. Endocardial cushion

[Ref: Langman’s/14th/P-190]
11. Barr body is-
a) Found in interphase of the cell cycle
b) Diagnostic of a genetic female
c) Discovered by Mary. Lyon
d) Located just below the nuclear membrane
e) Absent in normal male
TFTTT
Explanation:
b) It is present if female but not diagnostic.
Information desk:
 During interphase, somatic cell of normal female presents a heterochromatin plano-convex body
beneath the nuclear membrane.
 Present in Klinefelter’s syndrome.
 Murray Llewellyn Bar.
 Beneath the nuclear membrane.
 Present in female but not male.
[Ref: Junqueira’s/16th/P-54-55 & A.K. Datta’s/8th/P-224]
12. Multipolar neurons are-
a) Amacrine cells of the retina
b) Brush cells of the cochlear nucleus
c) Purkinje cells of the cerebellum
d) Pyramidal cells of the cerebrum
e) Olfactory receptor cells of the nasal mucosa
FFTTF

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Explanation:
a) Anaxonic neuron
b+e) Bipolar neuron
Information desk:
Neurons can be classified according to the number of processes extending from the cell body-
 Multipolar neurons, each with one axon and two or more dendrites, are the most common. E.g. purkinje
cells of the cerebellum, pyramidal cells of the cerebrum.
 Bipolar neurons, with one dendrite and one axon, comprise the sensory neurons of the retina, the olfactory
epithelium, and the inner ear.
 Unipolar or pseudounipolar neurons, which include all other sensory neurons, each have a single process
that bifurcates close to the perikaryon, with the longer branch extending to a peripheral ending and the
other toward the CNS.
 Anaxonic neurons, with many dendrites but no true axon, do not produce action potentials, but regulate
electrical changes of adjacent CNS neurons.
[Ref: Junqueira’s/14th/P-163 & Snell’s/7th/P-38]

13. Growing end of long bones are-


a) Upper end ulna
b) Upper end of humerus
c) Lower end of radius
d) Upper end of femur
e) Lower end femur
FTTFT
Explanation:
a) Lower end of ulna
d) Lower end of femur

[Ref: BD/7th/V-I/P-24]
14. Anal canal below the pectinate line-
a) Devoid of anal columns
b) Lined by simple columnar epithelium
c) Sensitive to touch and pressure sensation
d) Supplied by branch of hypogastric plexus of nerve
e) Drained in to superficial inguinal lymph node
TFTFT
Explanation:
a) Anal canal column above pectinate line consists of anal column.
b) Lined by non-keratinized stratified squamous epithelium.
c+d) Above pectinate line supplied by autonomic nerve (insensitive to touch, pressure) below pectinate line of anal
canal supplied by somatic nerve (sensitive to touch, pressure).
e) Above pectinate line lymphatic drainage into para aortic lymph node, below pectinate line lymphatic drainage
into superficial inguinal lymph node.
Information desk:
Differences between the upper & lower anal canals-
Features Upper anal canal (15mm) Lower anal canal (15+8mm)
Development From endoderm of the hind gut From ectoderm of proctodeum
Innervation Autonomic nerves, hence insensitive to Somatic nerves, hence insensitive to pain,
pain, touch & temperature touch & temperature
Epithelial lining Simple columnar Stratified squamous
Arterial supply Superior rectal artery Inferior rectal artery

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Venous drainage Superior rectal vein draining into portal Inferior rectal vein draining into canal
system system
Lymphatic Internal iliac lymph nodes Superficial inguinal lymph nodes (horizontal
drainage set)
Hemorrhoids Internal hemorrhoids External hemorrhoids
[Ref: BD/8th/V-2/P-485]
15. The paramesonephric ducts-
a) Develop as diverticula from the coelomic -cavity Information desk:
b) Form the uterine tube 1. Arsis as a longitudinal invagination of the
c) Have epithelial elements derived from endoderm epithelium on the anterolateral surface of the
d) Begin function before birth urogenital ridge.
e) Develop during the 2nd month of gestation 2. The two ducts initially separate by septum but
FTTTF later fuse to form uterus.
[Ref: Langman’s/14th/P-273-274] 3. Endoderm derivatives epithelium of uterine tube
& urethra.
4. Function at 3rd month of intrauterine life.
16. The medial meniscus of the knee joint-
a) Give attachment to the popliteal
b) Embraces the ends of the lateral meniscus
c) Give attachment posteriorly to the tendon of popliteus
d) Is formed by hyaline cartilage
e) Is more liable to injury
FTFFT
[Ref: Lumley/Q-230/P-146]
17. The renal arteries-
a) Arise from the aorta at the level of the 4th lumbar vertebra
b) Are related posteriorly to the crus of the diaphragm of the same side
c) Supply branches to the corresponding suprarenal gland
d) Give testicular branches
e) Are unequal in size
FTTFT
Explanation:
a) At L2 level
b) Gonadal artery branch of abdominal aorta.
[Ref: BD/8th/Fig-27.1/P-396]
18. The adductor tubercle-
a) Is related to the junction of the femoral and popliteal arteries
b) Gives attachment to the meniscus of the knee
c) Is situated on the upper aspects of the tibia
d) Gives origin to the popliteus
e) Provides attachment to the tendon of adductor Magnus
TFFFT
Explanation:
a) At the lower end of the adductor canal femoral artery passes through an opening in the adductor Magnus to
become continuous with the popliteal artery.
b) It receives insertion of adductor Magnus.
c) Situated on the lower end of the medial supracondylar ridge above the medial condyle of femur.
d) The adductor has three unique-
 Receives insertion of adductor Magnus.
 Epiphyseal line of lower end pass through.
 Bony landmark
[Ref: A.K. Datta’s/4th/V-3/P-143]
Neuron Medical Academy 5|Page
19. Carotid sheath-
a) Is attached superiorly to the base of the skull Information desk:
b) Fuse with the perichondrium inferiorly Carotid Sheath contains the common and internal carotid
c) Lies deep to the prevertebral fascia arteries, internal jugular vein, and vagus nerve.
 Does not contain the sympathetic trunk, which lies
d) Encloses external carotid artery
posterior to the carotid sheath and is enclosed in the
e) Encloses jugular vein and vagus nerve prevertebral fascia.
TTFFT  Blends with the prevertebral, pretracheal, and
Explanation: investing layers and also attaches to the base of the
a) Superiorly it attached to base of skull. skull.
b) Blend with the pericardium inferiorly. Structures piercing the carotid sheath-
c) It lies anterior to the prevertebral fascia. 1. External carotid artery.
d) It preloves common and internal carotid artery 2. Most the tributaries of internal jugular vein.
e) Encloses jugular vein, vagus nerve, common 3. Glossopharyngeal nerve.
4. Accessory nerve
carotid & internal carotid artery.
5. Hypoglossal nerve
[Ref: Lumley/P-349] 6. Cervical branches of vagus nerve.

20. The rima glottides is closed by the action of the-


a) Arytenoid
b) Cricothyroid Information desk:
c) Lateral cricoarytenoid Rima glottidis closed by-
d) Posterior cricoarytenoid  Lateral cricoarytenoid
e) Thyroarytenoid  Oblique aryenoid
TFTFF  Arytenoidus transversus
[Ref: BD Chaurasia’s/8th/P-292]
21. In coarctation of aorta-
a) The post-ductal type presents in infancy
b) A lateral chest x-ray may show dilated descending thoracic aorta
c) The isthmus of the aorta is the usual site
d) Bicuspid aortic valve is a recognized association
e) Berry aneurysms are a recognized complication
FTTTF
Explanation:
a) Post ductal type present in adults.
e) Association
[Ref: Vishram Singh/3rd/P-288]
22. The azygos vein-
a) Passes through the oesophgeal hiatus of the diaphragm
b) Crosses over the right bronchus T6 vertebra
c) Drains into the left brachiocephalic vein
d) Drains the lower intercostal spaces
e) Can provide an alternative path when either vena cava is blocked
FFFTT
Explanation:
a) Passes through the aortic hiatus of the diaphragm.
b) Crosses over the right bronchus T4 vertebra.
c) Drains into the superior vena cava.
[Ref: BD/8th/V-1/P-286, 302]

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23. The adult female mammary gland-
a) Lies deep to the deep fascia of the chest wall
b) Extends from the side of the sternum to the midaxillary line
c) Has no subcutaneous and sub-mammary plexus of lymph vessels
d) Develops from modified skin glands
e) Has a lymphatic drainage which extends to the anterior mediastinum
FTFTT
Explanation:
a) Lies deep to superficial fascia, but superficial to deep (pectoral) fascia.
b) Vertically, it extends from the 2nd to 6th rib, and horizontally, from the lateral border of the sternum to the mid-
axillary line.
c) Has subcutaneous and sub-mammary plexus of lymph vessels.
d) Develops from modified sweat glands.
e) Has a lymphatic drainage which extends to the axillary, internal mammary, posterior intercostal, anterior
mediastinum and sub diaphragmatic area.
[Ref: Lumley/Q-39 & BD/7th/V-I/P-38-39]
Microbiology
24. Bacteria lacking cell walls are-
a) Mycoplasma spp.
Information desk:
b) Citrobacter
 A protoplast is a bacterial, fungal, or plant cell that has had its cell
c) L-forms
wall completely or partially removed using either enzymatic or
d) E. coli
mechanical means. Cell walls are made of a variety of
e) Protoplasts
polysaccharides (peptidoglycan, chitin, cellulose).
TFTFF
 L-forms are bacterial variants that lack a cell wall and divide by a
variety of processes involving membrane blebbing, tubulation,
vesiculation and fission. Their unusual mode of proliferation
provides a model for primitive cells and is reminiscent of recently
[Ref: Lange/17th/P-12]
developed in vitro vesicle reproduction processes.
25. Facultative intracellular bacteria are-
a) Rickettsia Information desk:
b) Listeria  Some- Salmonella  Live- Listeria
c) Salmonella  Nasty- Neisseria  Facultative LY- Francisella,
d) Chlamydia  Bugs- Brucella Legionella, Yersinia pestis
e) Brucella  May- Mycobacterium
FTTFT
[Ref: Lange/17th/P-24-25, 38]
26. The pathogens isolated from patients with ventilator associated pneumonia-
a) Pseudomonas aeruginosa
b) Herpes simplex virus
c) Staphylococcus aureus
d) Mycoplasma spp.
e) Klebsiella spp.
TFTFT
[Ref: Lange/17th/T-76.2/P-647]
Information desk:
Pathogenic organisms commonly associated with HAP and VAP
Gram-negative bacteria-
 Pseudomonas
 Acinetobacter baumannii
 Enterobacteriaceae, such as escherichia coli, Klebsiella, Enterobacter, Proteus and Serratia spp.
 Stenotrophomonas maltophilia
 Haemophilus influenzae
(These are the most common causative organisms)

Neuron Medical Academy 7|Page


Gram-positive bacteria-
 Staphylococcus aureus (MSSA and MRSA)
 Streptococcus spp. (including Streptococcus pneumoniae)
Other pathogens-
 Anaerobic bacteria, such as Prevotella, Fusobacterium and Veillone
 Candida and Aspergillus spp.
 Other

27. Bloody diarrhea may be caused by-


a) Bacillus cereus food poisoning
b) Clostridium difficile
c) Vibrio cholerae
d) Salmonella typhi
e) Shigella flexneri
FTFTT
Explanation:
a+c) Watery
[Ref: Lange/17th/T-73.2, 73.3/P-625 & Davidson’s/24th/B-13.9/P-272]
28. Atypical pneumonia is caused by-
a) Hemophilus influenzae
b) Streptococcus pneumoniae
c) Chlamydia trachomatis
d) Respiratory syncytial virus
e) Legionella pneumophila
FFFTT
[Ref: Lange/17th/P-165, 190, 302]
29. Exotoxin mediated diseases are-
a) Tetanus Information desk:
b) Scarlet fever Important bacterial exotoxins-
c) Typhoid fever Bacterium Disease
d) Rheumatic fever Gram-positive rods
e) Botulism Corynebacterium diphtheriae Diphtheria
TTFFT Clostridium tetani Tetanus
Clostridium botulinum Botulism
Clostridium difficile Pseudomembranous colitis
Clostridium perfringens Gas gangrene
Bacillus anthracis Anthrax
Gram-positive cocci-
Staphylococcus aureus 1. Toxic shock syndrome
2. Food poisoning
3. Scalded skin syndrome
Streptococcus pyogenes Scarlet fever
Gram-negative rods-
Escherichia coli 1. Watery diarrhea
2. Bloody diarrhea
Shigella dysenteriae Bloody diarrhea
Vibrio cholerae Cholera
Bordetella pertussis Whooping cough
[Ref: Lange/17th/T-7.10/P-39]

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30. Chemical agents that destroy spores-
a) Phenol
b) Alcohol Information desk:
c) Formaldehyde Chemical agents destroy spores-
d) Ethylene oxide  Ethylene oxide, formaldehyde
e) Peracetic acid  Glutaraldehyde, Peracetic acid
FFTTT
[Ref: Lange/17th/P-12]
31. Important characteristics of Neisseria meningitidis is/are-
a) Polysaccharide capsule
b) IgA1 Protease
c) M protein
d) Pili
e) Protein A
TTFFF
Explanation:
c) M protein is the most important virulence factor of S. pyogens
d) N. gonorrhoeae- Possess pili
e) Protein A is the important virulence factors of S. aureus
[Ref: Lange/17th/P-124]
32. Characteristic features of secondary syphilis include-
a) Itchy rash
b) Severe prostration
c) Painless lymphadenopathy
d) Mucosal erosions
e) Interstitial keratitis
FFTTF
Explanation:
a) Maculopapular rash
b) Congenital syphilis
[Ref: Lange/17th/P-193-194]
33. Virus (es) responsible for haemorrhagic fever is (are)-
a) Dengue virus
b) Hepatitis B virus
c) Ebola virus
d) Yellow fever virus
e) Zika virus
TFTTF
Information desk:
Viral haemorrhagic fevers-
Disease-
 Lassa fever  Dengue  Bolivian and Argentinian haemorrhagic
 Ebola fever  Crimean-Congo haemorrhagic fever fever (Junin and Machupo viruses)
 Marburg fever  Rift Valley fever  Haemorrhagic fever with renal syndrome
 Yellow fever  Kyasanur fever (Hantaan fever)
 Severe fever with thrombocytopenia
syndrome (SFTS)
[Ref: Davidson’s/24th/B-13.35/P-289]

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34. Virus/es transmitted through haematogenous route is/are-
a) Hepatitis B virus Information desk:
b) Polio Viruses that commonly cause fetal and neonatal infections-
c) Measles Type of transmission Virus
d) Cytomegalovirus Transplacental Cytomegalovirus
e) Rubella Parvovirus B19 virus
TFFTF Rubella virus
Explanation: Zika virus
a) Also saliva & within birth canal Perinatal (at time of Hepatitis B virus
b) Poliovirus is transmitted by the fecal oral birth) Hepatitis C virus
route Herpes simplex virus type-2
c) Respiratory tract Human immunodeficiency virus
d) Also sexual, respiratory droplet & Human papillomavirus
transplacental Breast feeding Cytomegalovirus
e) Transplacental & respiratory route Human T-cell lymphotropic virus

[Ref: Lange/17th/T-7.2, 32.2/P-33, 250]


35. Following viruses have segmented genome-
a) Orthomyxo virus Information desk:
b) Herpes virus Viruses having segmented genome (AROB)-
c) Paramyxo virus  Arena virus (Lymphocytic choriomeningitis virus)
d) Bunya virus  Reo virus (Rota)
e) Rota virus  Orthomyxo virus (Influenza)
TFFTT  Bunya virus (Hanta virus)
Explanation:
a) Influenza
e) Reo virus
[Ref: Lange/17th/T-31.2/P-242]
36. Presence of inclusion bodies may be associated with following viruses-
a) Measles virus Information desk:
b) Rota virus A) Intracytoplasmic inclusion bodies-
c) Corona virus 1. Negri body: Rabies
d) Rabies virus 2. Perinuclear cytoplasmic: Cytomegalovirus
e) Cytomegalovirus 3. Guarneri body: Small pox & vaccinia.
TFFTT B) Intranuclear inclusion bodies-
1. Cowdry type A: Herpes
2. Intranuclear Inclusions: Adenovirus
C) Both intracytoplasmic and intranuclear inclusion bodies-
[Ref: Khaleque/2021/P-394] 1. Measles
2. Cytomegalovirus
37. The live vaccines are-
a) Oral polio vaccine Information desk:
b) BCG Vaccines in current clinical use
c) Rabies Live attenuated vaccines-
d) Measles  Measles, mumps, rubella (MMR)
e) Hepatitis B  Oral poliomyelitis (OPV, not used in UK)
TTFTF  Rotavirus
 Tuberculosis (bacille Calmette–Guérin, BCG)
 Typhoid (oral typhoid vaccine)
 Varicella zoster virus
[Ref: Lange/17th/P-278 & Davidson’s/24th/B-6.14/P-112]
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38. HPV infection is-
a) Common in young sexually active women
b) Associated with menorrhagia
c) The causes of cervical intraepithelial neoplasia
d) The cause invasive cervical cancer if persists for 10-15 years
e) Of low grade disease by HPV 16 & 18
TFTTF
Explanation:
b) Not associated
e) High grade disease by HPV 16 & 18
Information desk:
Human Papillomavirus (HPV)-
Diseases → Papillomas (warts); condylomata acuminata (genital warts)
Characteristics → Nonenveloped virus with icosahedral nucleocapsid and circular double-stranded DNA. No
virion polymerase.
Transmission → Direct contact of skin or genital lesions.
Laboratory diagnosis → Diagnosis is made clinically by finding koilocytes in the lesions. PCR assays that detect
HPV DNA are available.
Treatment → Treatment varies according to the site of lesions: liquid nitrogen is used for skin lesions, podophyllin
for genital lesions, and salicylic acid for plantar lesions.
Prevention → Three vaccines are available: one contains the capsid proteins of nine HPV types (6, 11, 16, 18 &
five others) and another contains only the capsid proteins of the four most common HPV types (6, 11, 16, 18)
that cause cancer. The third vaccine contains the capsid proteins of two types (16 & 18) that are the most
common cause of cervical cancer.
[Ref: Lange/17th/P-301 & DC Dutta’s/Gynae/8th/P-265]
39. Parasite/s that has/have intermediate host as part of its life cycle is/are-
a) Ascaris lumbricoides
b) Ancylostoma duodenale Explanation:
c) Echinococcus granulosus  Parasites having indirect life cycle
d) Taenia saginata requiring one intermediate host & one
e) Trichomonas vaginalis definitive host.
FFTTF

Information desk:
Parasite Definitive host Intermediate host
Protozoa-
Plasmodium spp. Female Anopheles mosquito Man
Babesia Tick Man
Leishmama Man, dog Sand-fly
Trypanosoma brucei Man Tsetse fly
Trypanosoma cruzi Man Triatomine bugs
Toxoplasma gondii Cat Man
Cestodes-
Taenia solium Man Pig
Taenia saginata Man Cattle
Echinococcus granulosus Dog Man
Trematodes-
Fascioloa hepatica Man Snail
Fasciolopsis buski Man, Pig Snail
Schistosoma spp. Man Snail

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Nematodes-
Trichinella spiralis Man Pig
Wuchereria bancrofti Man Mosquito
Brugia malayi Man Mosquito
Dracunculus medinensis Man Cyclops
[Ref: KDC/13th/P-146 & Paniker’s/9th/P-4]
40. Regarding leishmania donovani-
a) Causative agent of visceral leishmaniasis Explanation:
b) Kinetoplast is situated anterior to the nucleus in promastigote form c) LD bodies are present within-
c) LD body is present within RBC  Monocyte, Macrophage
d) Multiplies by binary fission  Bone marrow
e) Produces amastigote form in the sandfly  Spleen
TTFTF  Liver
e) Promastigote form in the sandfly

Information desk:
Genus leishmania, causes leishmaniasis (Caused by unicellular, flagellate, intracellular protozoa)
Species-
1. Visceral leishmaniasis (Kala azar)
2. Cutaneous leishmaniasis
3. Mucosal leishmaniasis
Vector-Sandfly (Phlebotomus ar.)
 L. Donovani has 2 form  Amastigote form (LD Body) found in-
 Promastigote(10-20micro m which have flagellum 1. Monocyte, Macrophage
with characteristic anterior kinetoplast) 2. Bone marrow
 Amastigote(2-4 micro m, Non flagellated) 3. Spleen
 Promastigote is infective form. 4. Liver
Clinical feature-
 Fever, Weakness, Weight loss  Cardiac failure (severe anaemia)
 Spleenomegaly  Pedal edema, ascites,anasarca
 Hyperpigmentation (Black fever/ Black sickness) (Hypoalbuminaenia)
 Bleeding from retina, nose, GIT
(Thrombocytopenia)
Diagnosis
CBC-
 Pancytopenia  Monocytosis
 Leucopenia. Leucocyte count progressively  High ESR
decreases as the diseases progresses  Hypoalbuminiaemia
 Relative lymphocytosis.  Hypergamaglobulinaemia
[Ref: Lange/17th/P-451-452 & Davidson’s/24th/P-326-327]
41. Nematodes that infect humans through skin penetration are-
a) Ascaris lumbricoides
b) Necator americanus Information desk:
c) Strongyloides stercoralis Penetration of skin-
d) Trichuris trichiura  Doudenale (Filariform larva)  Cutaneous larva migrans
e) Diphyllobothrium latum (cestodes/  N. Ameracana (Filariform larva) (Ancylostoma. Brazilensis &
tapeworms)  S. Stercoralis (Filariform larva) A.caninum)
FTTFF  Brugia malayi  Cercariae of schistosoma spp
[Ref: Lange/17th/P-476-477 & KDC/13th/P-8]

Neuron Medical Academy 12 | P a g e


42. Agents of invasive fungal infections are-
a) Candida spp
b) Aspergillus spp Information desk:
c) Rhizopus spp  Mainly systemic and opportunistic fungi
d) Malassezia furfur cause deep/ invasive fungal infections of
e) Medurella mycetomatis infections of internal organs.
TTTFF
Explanation:
d) Cutaneous fungus
e) Subcutaneous fungus
[Ref: Lange/17th/P-411, 418]
43. Cryptococcus neoformans-
a) Reproduces by the process of budding
b) Causes diseases in immunocompromised host
c) Forms germ tube in human serum
d) Possesses a polysaccharide capsule
e) Causes human to human transmission
TTFTF
Explanation:
c) Germ tube is formed in candida species.
e) No human to human transmission.
Information desk:
Cryptococcus neoformans:
 Disease → Cryptococcosis, especially cryptococcal meningitis.
 Characteristics → Heavily encapsulated yeast. Not dimorphic.
 Transmission → Inhalation of airborne yeast cells.
 Pathogenesis → Organisms cause influenza-like syndrome or pneumonia. They spread via the bloodstream
to the meninges. Reduced cell-mediated immunity predisposes to severe disease, but some cases of
cryptococcal meningitis occur in immunocompetent people who inhale a large dose of organisms.
 Laboratory diagnosis → Visualization of the encapsulated yeast in India ink preparations of spinal fluid.
Culture of sputum or spinal fluid on Sabouraud’s agar produces colonies of yeasts.
Cryptococcal antigen test (CRAG) is a latex agglutination test that detects polysaccharide capsular antigen
in spinal fluid.
 Treatment → Amphotericin B plus flucytosine for meningitis.
 Prevention → Cryptococcal meningitis can be prevented in AIDS patients by using oral fluconazole.
[Ref: Lange/17th/P-421-422]
44. Cellular components of innate immunity includes-
a) Helper T cell
b) Follicular dendritic cell
c) Macrophage
d) Natural killer cell
e) B cell
FTTTF
[Ref: Lange/17th/P-542-543 & Akram/5th/P-78]
45. Professional antigen presenting cell are-
a) Dendritic cells
b) Mast cells
c) Cytotoxic T lymphocytes
d) Macrophages
e) B lymphocytes
TFFTF
Neuron Medical Academy 13 | P a g e
Information desk:
Activated B lymphocytes are antigen presenting cell but not professional-
Macrophage Large phagocytes, located Engulfs and kills many Possess surface IgG receptors that
in all tissues, class II MHC classes of microbes fascinate phagocytosis
expression removal of debris tissue (opsonization) activated by IFN-γ,
repair TNF-α, from T-cells Professional APC
expressing class II MHC
Dendritic cell Sentinel cells with long Antigen uptake and Professional APC expressing class II
branches reside in epithelial presentation including MHC responsible for priming of
barriers and secondary cross presentation naïve T cells
lymphoid organs class II
MHC expression
Neutrophil Most common leukocyte in Enguifis and kills bacteria Attracted into tissues by
blood, first responder in and fungi, digests cellular chemoidines which are increased by
inflamed or necrotic tissue debris T-cells derived Ill-17
Eosinophil Eosinophils granules contain Granuie proteins are toxic Surface IgE receptors maturation
major basic protein, to cells involved in asthma and survival supported by IL-5 from
recruited into inflamed and allergic diseases and T-cells
tissue by exotoxin protective again invasive
helminth infection
Basophil Present at low frequency in Release histamine, IgE receptors acid IgE modules that
the blood proteases, chemokines survey for antigen
and cytokines,
contributes to allergic
diseases and anaphylaxis
Mast cell Distributed throughout the
tissues around the
vasculature
[Ref: Lange/17th/Fig-58.3/P-506]
46. Helper T-cell-
a) Has receptor for EBV
b) Needs MHC molecule for antigen recognition
c) Produces IL-1
d) Produces memory cell
e) Provides help for both humoral and cell mediated immunity
FTFTT
Explanation:
a) β-lymphocyte has recepton for EBV
c) Produces IL- 2, 4, 5
[Ref: Lange/17th/P-527-528]
47. Hypo-complementaemia is a feature of-
a) Systemic lupus erythematosus (SLE)
b) Minimal change nephrotic syndrome Information desk:
c) Rheumatoid arthritis Hypo-complementaemia: SLE-
d) Acute pyelonephritic  Post streptococcal glomerulonephritis
e) Post streptococcal glomerulonephritis  Disease of type-3 hypersensitivity
TFFFT
[Ref: Lange/17th/P-557 & Davidson’s/24th/B-18.17/P-576]

Neuron Medical Academy 14 | P a g e


48. During post-transplant period, the prospect of graft acceptance can be improved by- [Residency March- 23]
a) Irradiated blood Information desk:
b) Leukocyte depleted red blood cells  Irradiated blood and leucocyte depleted red cells
c) Intramuscular GM-CSF infusion prevent GVHD and increase acceptance of post-
d) Random donor HLA identical blood transplant graft.
e) Previous blood transfusion  Use of a myeloid growth factor (G-CSF or GM-CSF) post-
TTTTF transplant can accelerate recovery by 3-5 days, so
acceptance is improved.

[Ref: Harrison's Haematology & Oncology/2nd/B-28.3/P-407 & Oxford Handbookb of Clinical


[Haematology/4th/P-420, 775]
Biochemistry
49. Metabolic pathway/s in mitochondria is/are-
a) Glycogenesis
b) TCA cycle
c) Transamination
d) Beta-oxidation
e) Glycolysis
FTFTF
Information desk:
Metabolic pathways in Metabolic pathways in mitochondria Metabolic pathways in both
cytoplasm- (King COOOBRAS)- mitochondria & cytoplasm [H U G]-
1. Glycolysis 1. Ketogenesis & ketone body 1. Urea cycle (mainly in
2. HMP shunt oxidation cytoplasm)
3. Glycogenesis and 2. Carboxylation of pyruvate to 2. Gluconeogenesis (mainly in
glycogenolysis oxaloacetic acid. cytoplasm)
4. Lipogenesis (fatty acid 3. Oxidation of pyruvate to acetyl-CoA. 3. Heme synthesis
synthesis) 4. Oxidative deamination
5. Synthesis of TAG (fat) 5. Oxidation of alcohol.
6. Lipolysis (hydrolysis of 6. β-oxidation of fatty acid
fat) 7. Respiratory chain.
7. Synthesis of cholesterol 8. TCA cycle
8. Lipoprotein metabolism 9. Steroid hormones synthesis
9. Transamination
Liver is the only site for → Ketogenesis, Urea cycle
[Ref: ABC of Medical Biochemistry/8th/P-276]
50. Compounds produced from acetyl CoA are-
a) Pentose sugar
b) Ketone bodies
c) Citric acid
d) Cholesterol
e) Fatty acid
FTFTT
Information desk:
Metabolic fates: (AT KFC)-
1. Donation of acetyl group for synthesis of Acetyl choline.
2. Oxidation in TCA cycle
3. Synthesis of Ketone bodies (in starvation)
4. Synthesis of Fatty acid (in well fed state)
5. Synthesis of Cholesterol
[Ref: ABC of Medical Biochemistry/8th/P-199]
Neuron Medical Academy 15 | P a g e
51. Vitamins required for TCA cycle are-
a) Thiamine
b) Ascorbate Explanation:
c) Vitamin D Vitamins essential for TCA cycle are-
d) Nicotinic acid  Riboflavin, Niacin, Thiamine, Pantothenic acid
e) Vitamin A
TFFTF
[Ref: ABC of Medical Biochemistry/8th/P-178-179]
52. Major sites for glycogen storage are-
a) Adipose tissue
b) Adrenal gland
c) Muscle
d) Bone
e) Liver
FFTFT
Explanation & Information desk:
Glycogen is stored in Liver and muscle.
 It possesses high energy value than glucose.
 It does not diffuse out of its storage site as it is colloid in nature.
 In the form of glycogen large amount of glucose can be stored within cell without disturbing the osmotic
equilibrium between ICF and ECF.

[Ref: ABC of Medical Biochemistry/8th/P-196-197]


53. Hexose monophosphate shunt generates-
a) NADPH
b) FADH
c) NADH
d) GTP
e) Pentose sugar
TFFFT
Explanation & Information Key
Synonym: Pentose phosphate pathway/ Phosphogluconate pathway/ Hexose monophosphate shunt
Salient features-
 Substrate: Glucose 6-P
 Product: Ribose sugar/Pentose sugar and NADP2H
 Site: Liver, Adipose tissue, RBC, Gonads (testis and ovary), adrenal cortex, macrophage, lactating breast
 Compartment: Cytoplasm
 Rate limiting enzyme: G6PD (glucose 6-P dehydrogenase)
 Coenzyme needed: NADP, TPP
 ATP involvement: No ATP is directly consumed or produced
[Ref: ABC of Medical Biochemistry/8th/P-191-192]
54. Ammonia-
a) Helps in acidification of urine
b) Enters in circulation from colon
c) Is a nontoxic substance
d) Is freely permeable to blood-brain-barrier
e) Is produced from muscle break down
TTFTF
Explanation:
c) Toxic NH3 is converted to urea in liver by urea cycle.
e) A lesser amount of ammonia is produced from breakdown of RBC and metabolisms in muscles.

Neuron Medical Academy 16 | P a g e


Information desk:
Ammonia metabolism & excretion-
 The liver is critical for ammonia handling in the body. Ammonia levels must be carefully controlled because
it is toxic to the central nervous system (CNS), and freely permeable across the blood-brain barrier. The
liver is the only organ in which the complete urea cycle (also known as the Krebs-Henseleit cycle) is
expressed. This converts circulating ammonia to urea, which can then be excreted in the urine. Ammonia
in the circulation comes primarily from the colon and kidneys with lesser amounts deriving from the
breakdown of red blood cells and from metabolism in the muscles.
Distal acidification of urine-
 Secreted H+ (70 mmol/day) is titrated in tubular fluid by urinary buffers with net loss of H+ from blood as
NH4+, H2PO4- and net gain of HCO3- to blood (70 mmol/day) to raise serum bicarbonate concentration back
to normal. In tubular lumen NH4+ is formed by H+ and NH3 both of which are secreted by tubular cells. So
ammonia helps in distal acidification of urine.
[Ref: ABC of Medical Biochemistry/8th/P-331-332 & Ganong’s/26th/P-500]
55. Adipose tissue lipolysis is stimulated by-
a) Lipoprotein lipase
b) Hormone sensitive lipase
c) Insulin
d) Apo lipoprotein
e) Catecholamine
FTFFT
Information desk:
 In fasting & starvation, insulin secretion decreases but glucagon, cortisol, growth hormone, thyroid
hormone & catecholamine secretion increases. This hormonal scenario causes lipolysis by stimulating HSL
(Hormone sensitive lipase) and inhibiting TAG (fat) synthesis by inhibition of PDH, acetyl CoA Carboxylase,
fatty acid synthase & Glycerol 3-p acyl-transferase.
 Hormone sensitive lipase activated by Glucagon, Cortisol, Catecholamine (epinephrine, norepinephrine),
Growth hormone, Thyroid hormone, TSH, ACTH, Vasopressin and Caffeine.
 Hormone sensitive lipase inhibited by Niacin/Nicotinic Acid, Prostaglandin E1 and Insulin.
[Ref: ABC Biochemistry/8th/P-225-226, Harper’s Biochemistry/31st/P-601 & Satyanarayana/5th/P-288]
56. A person's daily calorie requirement depends on-
a) Body temperature
b) Basal metabolic rate
c) Vitamin intake
d) Thermic effect of food
e) Physical activity
FTFTT
Information desk:
Components of energy requirement/expenditure-
 BMR (It is the largest component of energy expenditure)
 SDA (Specific Dynamic Action) of food
 Physical activity-
 For light activity (Sedentary): 25-50% of BMR is added.
 For moderate activity: 50-100% of BMR is added.
 For heavy activity: ≥100% of BMR is added.
[Ref: ABC Biochemistry/8th/P-488]
57. Micro-minerals are-
a) Sodium
b) Iron
c) Calcium
d) Potassium
e) Zinc
FTFFT
Neuron Medical Academy 17 | P a g e
Information desk:
Minerals inorganic elements required in small amount by the body.
Dietary source: 1. Whole grain cereals and pulses, fruits and vegetable. 2. Milk and milk products, Meat, Fish.
Types of minerals-
 Macro-minerals (bulk elements): The minerals having total body content more than 5g and daily
requirement more than 100mg. They represent about 60-70 % of all inorganic matter of body e.g. Sodium,
potassium, calcium, magnesium, chloride, sulfur and phosphorus.
 Micro-minerals (trace elements): The minerals having total body content less than 5g and daily
requirement less than 100 mg. e.g. Iodine, zinc, iron, copper, manganese, cobalt, chromium, selenium,
fluoride, molybdenum.
 Iodine, molybdenum & selenium are ultra-trace element because their RDA is less than 1.0mg.
[Ref: ABC Biochemistry/8th/P-494]
58. Zinc-
a) Is an essential component of carbonic anhydrase enzyme
b) Deficiency causes goiter
c) Helps in iron absorption from gut
d) Is necessary for wound healing
e) Is used following diarrhea
TFFTT
Explanation:
a) Zinc is cofactor of the enzyme carbonic anhydrase
b) Iodine deficiency causes goiter
c) Copper is necessary for iron absorption and utilization
d) Zinc supports gonadal activity, growth and wound healing
e) Zinc supplementation is given diarrhea patient
[Ref: ABC of Medical Biochemistry/8th/P-496-497, Medical Biochemistry by DM Vasudevan/7th/P-521-522]

59. Hormones that regulate plasma calcium level are-


a) ADH
b) ACTH
c) Calcitonin
d) PTH
e) TSH
FFTTF
Information desk:
 Calcium level is regulated by PTH, calcitriol and calcitonin. PTH and calcitriol (vitamin D) increase plasma
calcium level when there is hypocalcaemia & on the other hand calcitonin decreases plasma calcium when
the level is increased.
[Ref: ABC of Medical Biochemistry/8th/P-372]
60. Skin changes are seen in the deficiency of following nutrients-
a) Vitamin A
b) Zinc
c) Iodine
d) Vitamin K
e) Folic acid
TTTFF
Explanation:
 Vitamins causing skin change → Vitamin-A, Vitamin-B3, Vitamin-B2 (seborrheic dermatitis), Vitamin-B7 , Zn
 Deficiency of iodine causes hypothyroid followed by skin change - dry skin.
[Ref: ABC Biochemistry/8th/P-496, 509-521]

Neuron Medical Academy 18 | P a g e


61. Vitamin-D-
a) Is a steroid hormone
b) Undergoes 25 hydroxylation in the kidney
c) Is stored in the liver
d) Undergoes 1-alpha-hydroxylation in the liver
e) Its synthesis in influenced by cortisol
TFTFF
Explanation:
a) T. Vitamin D is a hormone: Active vitamin D (calcitriol) is produced in kidney. From kidney via blood calcitriol
goes to its distant sites of action (intestine, kidney, bone). Therefore, the action of calcitriol is identical to that of
hormone. So vitamin D is regarded as hormone. Also vitamin D contains steroid nucleus.
b) F. Undergoes 25 hydroxylation in the liver
c) T. Is stored in the liver
d) F. Undergoes 1-alpha-hydroxylation in the kidney
e) F. Its synthesis in influenced by parathyroid hormone (PTH)
Information:
Function of calcitriole:
Calcitriole is responsible for-
 Calcium and phosphate homeostasis
 Immunoregulation
 Cellular differentiation
In bone (both anabolic and catabolic effect)-
 Stimulates calcium phosphate mobilization in presence
of PTH, increases calcification, increases bone
resorption.
In intestine-
 Stimulates intestinal calcium and phosphate absorption.
In kidney-
 Minimizes calcium loss by the kidney, increases calcium
and phosphate reabsorption.
[Ref: ABC of Medical Biochemistry/8th/P-510 & Vision Physiology/9th/P-458, 460-461]
62. Vitamin-K dependent clotting factor/s is/are-
a) Factor I
b) Factor II
c) Factor VI
d) Factor VII
e) Factor IX
FTFTT
Explanation & Information:
Function of vitamin K:
 Post translational maturation of clotting factors (factor II, VII, IX, X) – It is done by vitamin K dependent
carboxylation of certain glutamic acid residues of clotting factors II, VII, IX & X after their synthesis. Here
carboxylase enzyme act as catalyst & vitamin K act as coenzyme of carboxylase.
 Helps in coagulation (clot formation). [Ref: ABC of Medical Biochemistry/8th/P-515]

63. 1, 25-dihydroxycholecalciferol increases intestinal absorption of calcium ion by activating the-


a) Calcium binding protein
b) Protein kinase C
c) Alkaline phosphatase
d) Adenylcyclase
e) Calcium stimulated ATPase
TFTFT
Neuron Medical Academy 19 | P a g e
Explanation & Information desk:
 “Hormonal” Effect of Vitamin D to Promote Intestinal Calcium Absorption. 1, 25-Dihydroxycholecal-ciferol
functions as a type of “hormone” to promote intestinal absorption of calcium mainly by increasing, over
a period of about 2 days, formation of calbindin, a calcium-binding protein, in intestinal epithelial cells.
This protein functions in the brush border of these cells to transport calcium into the cell cytoplasm. The
calcium then moves through the basolateral membrane of the cell by facilitated diffusion. 'The rate of
calcium absorption is directly proportional to the quantity of this calcium-binding protein. Furthermore,
this protein remains in the cells for several weeks after the 1, 25-dihydroxycholecalciferol has been
removed from the body, thus causing a prolonged effect on calcium absorption.
 Other effects of 1, 25-dihydroxycholecalciferol that might play a role in promoting calcium absorption
are the formation of (1) a calcium-stimulated adenosine triphosphatase in the brush border of the
epithelial cells and (2) an alkaline phosphatase in the epithelial cells. The precise details of all these
effects are unclear.
 Vitamin D Promotes Phosphate Absorption by the intestines. Although phosphate is usually absorbed
easily, phosphate flux through the gastrointestinal epithelium is enhanced by vitamin D. This
enhancement is thought to result from a direct effect of 1, 25-dihydroxycholecalciferol, but it is possible
that it occurs secondarily from this hormone's action on calcium absorption, with the calcium in turn acting
as a transport mediator for the phosphate.
[Ref: Guyton and Hall Medical Physiology/14th/P-999]
64. Peripheral neuropathy may result from deficiency of-
a) Riboflavin
b) Thiamine
c) Pyridoxine
d) Iodine
e) Cyanocobalamin
FTTFT
Information desk:
Causes of peripheral neuropathy- (vitamin deficiency)
 Thiamine
 Pyridoxine
 Vitamin B12
 Vitamin E
[Ref: Davidson’s/24th/Fig-28.83/P-1192]
65. Glucose transport into the cells requires insulin in-
a) Adipocytes
b) Cornea
c) Skeletal muscle
d) The brain
e) Erythrocytes
TFTFF
Information desk:
 In adipocyte, skeletal muscle and cardiac muscle GLUT-4 is expressed; insulin helps in glucose entry into
these cells by increasing the number of GLUT-4 on their cell surface. GLUT-4 is insulin dependent.
 Insulin insensitive cells: The cells where insulin is not needed for glucose uptake.
 RBC, Neuron, Renal tubular cell, Hepatocyte, Enterocyte, Pancreatic β-cell, Leukocytes, Placenta, Retinal
cell, Lens & Cornea.
[Ref: ABC of Medical Biochemistry/8th/P-100-101, 560]

Neuron Medical Academy 20 | P a g e


66. The primary structure of a protein refers to the-
a) α-helices and β-sheets bonded by peptide linkage
b) Arrangement of subunits to form a functional structure
c) Amino acid sequence of the protein
d) Twist, fold or twist & fold of the amino acid sequence into stabilized structures within protein
e) Arrangement of twisted chains and folds within a protein into a stable structure
FFTFF
Explanation:
a) Secondary structure
b) Quaternary structure
d+e) Tertiary structure
[Ref: ABC of Medical Biochemistry/8th/P-68]
67. Amino acid/s that is/are required to synthesize purine nucleotide is/are-
a) Glycine
b) Lysine
c) Alanine
d) Aspartate
e) Glutamate
TFFTT
Explanation & Information:
Synthesis of purine bases occur mainly in liver. Purine nucleus is an aromatic heterocyclic nine atom ring
compound with 4 nitrogen and 5 carbons. Raw materials for purine nucleus synthesis are:
 Aspartic acid (Amino acid)
 Carbon dioxide
 Glutamine (Amino acid)
 Glycine (Amino acid)
 Formyl tetrahydrofolate: F-FH4
 Methenyl tetrahydrofolate: M-FH4
[Ref: ABC of Medical Biochemistry/8th/P-123]
68. Following are the cardiac enzymes-
a) Aspartate transaminase (AST)
b) Creatinine kinase BB (CKBB)
c) Lactate dehydrogenase (LDH)
d) Creatinine kinase MM (CKMM)
e) Creatinine kinase MB (CKMB)
TFTFT
Information:
Cardiac enzymes-
 CK-MB
 LDH
 AST
Cardiac protein-
 Myoglobin
 Troponin
[Ref: ABC Biochemistry/8th/P-589-590 & Vision Physiology/8th/P-124]
69. Radioactive isotope-
a) Helps in bone scan
b) Cannot convert to stable isotope
c) Safe in pregnancy
d) Capable to emit radiation
e) Not suitable for sterilization of medical instruments
TFFTF

Neuron Medical Academy 21 | P a g e


Information desk:
Unstable isotope (radioactive isotope): capable to emit radiation-
 These are the isotopes having neutron to proton (neutron/ proton) ratio far away from its stability ratio.
 Naturally occurring isotopes of heavy elements are usually unstable. e.g. Radium, uranium.
 Rarely some naturally occurring isotopes of lighter elements can also be unstable, e.g. 14C
 Unstable isotopes tend to become stable by radio-active decay.
Clinical use (clinical importance) of radioactive isotope:
 Diagnostic use:
 Iodine uptake test for diagnosis of thyroid disorders.
 Radio immune assay of hormones for diagnosis of hormone disorders.
 Organ scanning, e.g. bone scan, brain scan, thyroid scan.
 Absorption test, e.g. for iron, vitamin B12 etc.
 Isotope renogram for measurement of GFR and renal clearance.
 RBC life span measurement.
 Therapeutic use: e.g. radiotherapy in treatment of malignancy.
 Use in tracer technique: Isotopes are used as tracer in metabolic studies to outline the metabolic pathways.
 Measurement of volumes and spaces: e.g. ECF volume, blood volume, plasma volume, etc.
 Measurement of regional blood flow: e.g. cerebral blood flow, coronary blood flow, renal blood flow etc.
 Sterilization of medical instruments
Radio sensitive tissues (these are mostly rapidly dividing tissues):
 Bone marrow, Gonads, Lymph node, Skin, Intestine
Radiation hazards: Hazards (disadvantage) of radioactive isotope
1. Immediate hazards:
 Bone marrow depression & immune suppression
 Damage to intestinal mucosa causing, diarrhea and malabsorption
 Baldness, rough and scaly skin.
 In pregnancy: Fetal growth retardation, congenital malformations of fetus, fetal death, neonatal
death.
2. Delayed hazards e.g. Carcinogenesis, sterility, cataract.
3. Genetic effects e.g. DNA damage, mutation
[Ref: ABC of Medical Biochemistry/8th/P-29-30]

Pharmacology
70. Factor/s that may shorten the duration of action of drug is/are-
a) Co-administration of vasoconstrictor agents
b) Extensive plasma protein binding Information desk:
c) Rapid elimination through kidney Factor shortening D/A-
d) Rapid biotransformation  Metabolism  Absorption rate
e) Redistribution of drug  Rapid distribution  Biotransformation
FFTTF  Renal excretion  ↓PPB drug into tissue
Explanation:
a) Any vasoconstrictor- agent slows circulation thereby duration of action
b) Extensive PP binding drug duration of action
e) Redistribution of cellular component prolong drug action
[Ref: Katzung/15th/P-50-52]
71. Drug/s which undergo enterohepatic circulation is/are-
a) Estrogen Information desk:
b) Cefuroxime Drug undergoing enterohepatic circulation-
c) Rifampicin 1. Various antibiotics e.g. rifampicin, 5. Digoxin
d) Gentamicin metronidazole 6. Warfarin
e) Ciprofloxacin 2. NSAIDs 7. Paracetamol
TFTFF 3. Hormones (steroid) 8. Thyroxin
4. Opioids
[Ref: Vision’s/7th/P-21]
Neuron Medical Academy 22 | P a g e
72. An enzyme inducer, when used with another drug may cause-
a) Therapeutic failure
b) Tolerance of Co-administered drug
c) Increased potency of itself
d) Therapeutic potentiation
e) Toxicity
TTFFT
Explanation:
b) Its called metabolic tolerance
c) Decreased potency
d) Therapeutic failure
[Ref: Katzung/15th/P-60& Lippincott/8th]
73. Contraindications of β-blocker(s) is/are-
a) Bronchial asthma
b) Heart block
c) Glaucoma
d) Peripheral vascular disease
e) Ventricular tachycardia
TTFTF
Explanation:
c) Used in glucoma
e) Used in tachycardia

Information desk:
Indication- Contained-
 Angina, MI  Asthma
 HTN  Heart block
 Arrhythmia  PVD
 Obstructive cardiomyopathy  DM
 Hyperthyroidism  Sexual dysfunction
 Chronic HF  Hypotension (SL 90mmHg)
 Glucoma  Bradycardia (<55/min)
 Anxiety, migraine, essential tremor
 Phaeochromocytoma
[Ref: Katzung/15th/P-250]
74. Indications of adrenaline are-
a) Anaphylactic shock Information desk:
b) Hypertension Indication of adrenaline-
c) Acute severe asthma  Anaphylactic shock
d) Ischemic heart disease  Status asthmaticus
e) Type III hypersensitivity reaction  With local anesthetics
TFTFF  Cardiac arrest
[Ref: Vision Pharmacology/7th/P-82]  Hypoglycemic shock

75. Muscarinic actions of acetylcholine include-


a) Slowing of the heart Information desk:
b) Constriction of the pupil Muscarinic action of acetylcholine-
c) Accommodation of the eye for distant vision  Respiratory: Bronchorrhea, Bronchoconstriction
d) Increased secretions in the GIT  Decrease heart rate, decrease BP
e) Decreased peristalsis  Fever
TTFTF  Diplopia, miosis, lacrimation
[Ref: Katzung/15th/T-6.3 & Davidson’s/23rd/B-  Vomiting, diarrhea
7.14/P-146]  Salivation & sweating
 All secretion is increased

Neuron Medical Academy 23 | P a g e


76. Drugs used in glaucoma are-
a) Atropine
b) Pilocarpine
c) Scopolamine
d) Physostigmine
e) Echothiophate
FTFTT
Information desk:
Anti-glaucoma drugs-
Cholinomimetics Pilocarpine, Physostigmine, Carbachol, Echothiophate, Demecarium
Alpha agonists Epinephrine (Non-selective), Dipivefrin (Non-selective)
Apraclonidine (α2-selective), Brimonidine (α2-selective)
Beta -blockers Timolol (Non-selective)
Betaxolol (β1-secective), Carteolol (Non-selective), Metipranolol (Non-selective),
Leveobunolol (Non-selective), Levobetaxolol (Non-selective)
Diuretics Acetazolamide, Dorzolamide, Brinzolamide, Dichlorphenamide, Methazolamide
Prostaglandins Latanoprost, Unoprostone
[Ref: Katzung/15th/T-10.3 & Vision Pharmacology/7th/P-102]
77. Food containing tyramine should be avoided when taken with-
a) Tricyclic antidepressants (TCAs)
Information desk:
b) Mono amino oxidase inhibitors (MAO-I)
MAO inhibitors are associated with 2 severe drug interactions-
c) Selective serotonin reuptake inhibitors
a) Life threatening serotonin syndrome-
(SSRI)
 Cognitive: Delirium, coma
d) Atypical antidepressants
 Somatic: Hyperreflxia, tremor myoclonus
e) Antihypertensive medicines
 Autonomic: increase HR, increase BP
FTFFF
b) Cheese reaction (MAOI + Tyranine containing food)
Explanation:
b) MAO-I if taken with tyramine containing food it will precipitate hypertensive crisis.
d) Same explanation as. [Ref: Kumar & Clark’s/7th/P-843]

78. Beneficial drug combinations are-


a) Losartan + thiazide
b) Amoxicillin + clavulanic acid
c) Amiloride + thiazide
d) Iron + tetracycline
e) Aspirin + prednisolone
TTTFF
Explanation:
a) Synergistic antihypertensive effect.
b) Clavulanic acid is a beta lactamase inhibitor. It inhibits the enzyme beta lactamase & thus prevent the inactivation
of amoxicillin.
c) Thiazide causes hypokalaemia so it is used along with amiloride which causes potassium retention in the body.
d) Inorganic iron may form chelates with tetracycline, cause it to be less readily absorbed.
e) Both aspirin & prednisolone causes GIT adverse effects like peptic ulceration.

79. Propofol- Information desk:


a) Is water soluble induction agent Propofol-
b) Contains soyabean oil and egg lecithin  Highly lipid soluble
c) Decreases systemic vascular resistance & blood pressure  Contains soyabean oil & purified egg
d) Causes post-operative nausea & vomiting phosphatide.
e) Is used to terminate status epilepticus  Antiemetic action
FTTFT  No analgesic effect
 Less hangover effect
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Explanation:
a) Highly lipid soluble
d) Reduces post-operative nausea vomitting.

Indication- C/I- A/E-


1. Induction of anaesthesia 1. Airway obstruction  Cardio-resp. depression
2. TIVA 2. Known hypersensitivity  Excitatory phenomenon- convulsion,
3. Sedation in ICU myoclonus.
 Pain on injection
[Ref: Katzung/15th/P-466]
80. Following antibiotics have β lactam ring-
a) Benzathine penicillin
b) Tobramycin Explanation:
c) Mecillinum  Mecillinam is an extended spectrum penicillin antibiotic (has β
d) Monobactam lactam ring) active against gram negative bacteria.
e) Vancomycin  Vancomycin- is a glycolpeptide antibiotic, has no β lactam ring.
TFTTF  Tobramycin- is an aminoglycoside antibiotic, has no β lactam ring.

Information desk:
β lactam ring containing drugs are-
 Penicillins-
 Natural penicillins: benzylpenicillin, phenoxymethylpenicillin
 Penicillinase-resistant penicillins: methicillin, flucloxacillin, nafcillin, oxacillin
 Aminopenicillins: ampicillin, amoxicillin
 Carboxy- and ureido-penicillins: ticarcillin, piperacillin, temocillin
 Cephalosporins-
 First generation- Cefalexin, cefradine (oral), Cefazolin (IV)
 Second generation- Cefuroxime (oral/IV), Cefaclor (oral), Cefoxitin (IV)
 Third generation- Cefixime (oral), Cefotaxime (IV), Ceftriaxone (IV), Ceftazidime (IV)
 Fourth generation- Cefepime (IV)
 Fifth generation (also referred to as ‘next generation’)- Ceftobiprole (IV), Ceftaroline (IV)
 Monobactams- Aztreonam
 Carbapenems- Imipenem, meropenem, ertapenem, doripenem
[Ref: Katzung/15th/P-823, Bennet Brown/11th/P-173-180 & Davidson’s/24th/B-6.22P-117]
81. The following adverse effects are correctly paired with anti-TB drug-
a) Peripheral neuropathy → Isoniazid
b) Oto-toxicity → Rifampicin
c) Hyperuricaemia → Pyrazinamide
d) Retrobulbar optic neuritis→ Ethambutol
e) Hepatotoxicity → Streptomycin
TFTTF
[Ref: Davidson’s/23rd/B-17.53/P-593]
82. Side effect/s of loop diuretics is/are-
a) Hyponatraemia
b) Hypercalciuria Information desk:
c) Hypocalcemia A/E-
d) Metabolic acidosis  ↓Na+, ↓K+  Cholesterol
e) Hyperparathyroidism  Hypovolemia, Hypotension  Hypercaleiuria
TTTFF  ↓Ca 2+
, ↓Mg 2+
 Met. alkalosis
Explanation:  Uric acid
a) ↓Na+, ↓K+
d) Met. alkalosis
e) Hypoparathyroidism
[Ref: [Ref: Katzung/15th/P-271 & Lippincott’s/8th/P-269]

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83. Drugs used for managing hypertension in pregnancy are-
a) Hydrochlorothiazide
b) Atenolol
c) Labetalol
d) Captopril
e) α methyldopa
FFTFT
Explanation:
Others-
 Her-Hydralazine
 New-Nifedipine
 Lab-Labetalol
 Method-alpha methyldopa
 Done- Doxazosin

Information desk:
Drug treatment of hypertension during pregnancy-
Medication Dosage
Labetalol 100 mg twice daily to 600 mg four times a day
Nifedipine 5 mg once daily to 10 mg once daily
Amlodipine 10mg B.D. to 40mg B.D
Methyldopa 250 mg twice daily to 1000 mg three times a day
Doxazosin 0.5 mg twice daily to 8 mg three times a day
[Ref: Davidson’s/24th/B-32.7/P-1270]
84. Drugs that increase survival of patients with heart failure are-
a) Frusemide Information desk:
b) Carvedilol Drugs that decrease mortality of HF-
c) Milrinone  ACEI/ARB
d) Digoxin  β-blocker
e) Angiotensin-converting enzyme inhibitors  Diuretics (Spironolactone)
FTFFT  Sacubitril
[Ref: Katzung/15th/P-219]
85. Anticoagulants are-
a) Heparin
b) Enoxaparin
c) Rivaroxaban
d) Aspirin
e) Clopidogrel
TTTFF

Information desk:
Oral anticoagulants-
 Vitamin K antagonism - Warfarin/ coumarins
 Direct thrombin inhibition - Dabigatran
 Direct Xa inhibition – Rivaroxaban, Apixaban, Edoxaban
Injectable anticoagulants-
 Antithrombin-dependent inhibition of thrombin and Xa – Heparin, LMWH
 Antithrombin-dependent inhibition of Xa – Fondaparinux, Danaparoid
 Direct thrombin inhibition - Argatroban, Bivalirudin
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Antiplatelet drugs-
 Cyclo-oxygenase (COX) inhibition- Aspirin
 Adenosine diphosphate (ADP) receptor inhibition- Clopidogrel, Prasugrel, Ticagrelor
 Glycoprotein IIb/IIIa inhibition - Abciximab, Tirofiban Eptifibatide
 Phosphodiesterase inhibition - Dipyridamole
[Ref: Davidson/24th/B-25.26/P-948]
86. Drugs used in acute attack of migraine are-
a) Diazepam Information desk:
b) Paracetamol  Drugs used to abort an acute attack of migraine are either non-
c) Pethidine specific (analgesics) or specific (triptans and ergots).
d) Propranolol  Simple analgesics such as acetylsalicylic acid or acetaminophen, with
e) Sumatryptan or without the addition of caffeine, can often be effective for mild to
FTFFT moderate headaches.
 The addition of domperidone, prochlorperazine or metoclopramide
may help reduce nausea, and may have an abortive effect, even in the
absence of nausea.
 NSAIDs, such as naproxen, ibuprofen, or tolfenamic acid can also be
very useful, when tolerated.
 All tend to be most effective when given early during the headache.
[Ref: Clinical Pharmacology by Bennet Brown/12th/P-305]

87. Corticosteroids possessing potent mineralocorticoid activity are-


a) Mineralocorticoid
b) Deoxycorticosterone
c) Prednisolone
d) Dexamethasone
e) Aldosterone
TTFFT

Information desk:
Chart-
 Minimal glucocorticoid activity very high mineralocorticoid activity- Fludrocortisone.
 Glucocorticoid activity, high mineralocorticoid activity- Hydrocortisone
 Predominant glucocorticoid activity low mineralocorticoid activity- Prednisolone.
 Very high glucocorticoid activity minimal mineralocorticoid activity- Dexamethasone, Betamethasone.
[Ref: Katzung/15th/P-734 & Vision Pharmacology/7th/P-554]
88. Linagliptin-
a) Is an incretin mimetic Information desk:
b) Releases insulin from β-cell of pancreas
 Linagliptin is a DPP-4 inh. It inhibits DPP-4 activity,
c) Can cause invariable hypoglycemia
increasing post-prandial active incretin
d) Activates the enzyme dipeptidyl-peptidase-4
concentration.
e) Is an antagonist of GLP-1
 S/E- Urticaria, immune mediated dermatological
TTFFF
effect, heart failure hospitalization.
Explanation:
a) Linagliptin increase incretin level which increase secretion from B-cell of pancreas.
c) Insulin, salphonylurea & meglitinides (repaglinide, nataglinide)- causes hypoglycaemia.
d) Inhibits the enzyme DPP-4
e) Agonist of GLP-I increases post-prandial active incretin (GLP-I, GIP) concentration.
[Ref: Katzung/15th/P-795]

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89. Ototoxic drugs are-
a) Cisplatin
b) Cefixime
c) Gentamicin
d) Streptomycin
e) Acetaminophen
TFTTF

Information desk:
 All aminoglycosides are ototoxic and nephrotoxic. Aminoglycosides include streptomycin, neomycin,
kanamycin, amikacin, gentamicin, tobramycin, netilmicin and others.
 Cisplatin is chemotherapeutic drug (alkalyting agent) - toxicity include nephrotoxicity, peripheral
sensory neuropathy, ototoxicity.
 Acetaminophen is paracetamol has no ototoxic effect.
 Cefixime has no ototoxic effect
Ototoxic drugs are- aminoglycosides, salicylates, quinine, quinidine, frusemide, cisplatin, vancomycin
[Ref: Katzung/15th/P-683, 860, 992 & Dhingra/7th/P-36]
90. Following drugs require monitoring when used in renal failure patients-
a) Doxycycline
b) Diazepam
c) Propranolol
d) Pethidine
e) Lithium
FFFTT
Information desk:
Some drugs that require extra caution in patients with renal or hepatic disease-
Kidney disease Liver disease
Pharmacodynamic effects enhanced
 ACE inhibitors & ARBs (Renal impairment,  Warfarin (Increased anticoagulation because of
hyperkalaemia) reduced clotting factor synthesis)
 Metformin (Lactic acidosis)  Metformin (Lactic acidosis)
 Spironolactone (Hyperkalaemia)  Chloramphenicol (Bone marrow suppression)
 NSAIDs (impaired Renal function)  NSAIDs (Gastrointestinal bleeding, Fluid retention)
 Sulphonylureas (Hypoglycaemia)  Sulphonylureas (Hypoglycaemia)
 Insulin (Hypoglycaemia)  Benzodiazepines (Coma)
Pharmacokinetic handling altered (Reduced clearance)-
 Aminoglycosides (e.g. gentamicin)  Phenytoin
 Vancomycin  Rifampicin
 Other antibiotics (e.g. ciprofloxacin)  Propranolol
 Digoxin  Warfarin
 Lithium  Diazepam
 Atenolol  Lidocaine
 Allopurinol  Opioids (e.g. morphine)
 Cephalosporins
 Methotrexate
 Opioids (e.g. morphine)
ACE = Angiotensin-converting enzyme; ARB = Angiotensin receptor blocker; NSAID = Non-steroidal anti-
inflammatory drug.
[Ref: Davidson’s/24th/B-2.22/P-32]

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91. Colchicine-
a) Inhibits prostaglandin synthesis Information desk:
b) Inhibits the action of xanthine oxidase enzyme Colchicine is used to treat acute gout-
c) Reduces the production of Leukotriene B4  Colchicine is used to treat acute gout.
d) Reduces leucocyte migration and phagocytosis  It inhibits activation of innate immunity, CASPASE-
e) Selectively inhibits the microtubule assembly I activation, release of chemotactic factor &
FFTTT neutrophil recruitment.
Explanation:  It is an anti-mitotic drug that prevents
a) NSAIDs inhibit PG synthesis. microtubule polymer.
b) Allopurinol, febuxostat are xanthine oxidase inhibitor.
[Ref: Vision/7th/P-206 & Lippincott/8th/P-713]
Physiology
92. Refractory period in the ventricle corresponds to the-
a) Period of ventricular contraction
b) Period of ventricular action potential
c) QRS complex of ECG
d) PR interval of ECG
e) ST segment of ECG
TTTFF

Information desk:
Interval Events in the heart
P-R interval Atrio-ventricular conduction/ Atrial depolarization & AV nodal conduction
QRS complex Ventricular depolarization/ ventricular contraction/refractory period
QT Ventricular action potential
ST interval Plateau portion of the ventricular action potential
R-T interval Ventricular activation time
[Ref: C.C. Chatterjee/11th/P-247]
93. Viscosity of blood is-
a) A function of friction between molecules of following blood
b) A contributing factor to peripheral resistant
c) Increased in anemia
d) A determining factor of blood flow
e) Increased in hypoproteinemia
TTFTF
Explanation:
c) Viscosity ↑ in polycythemia
e) Viscosity ↑ in hyperproteinemia
[Ref: Guyton’s/14th/P-245 & Vision’s/9th/P-160]
94. Cardiac output is increased-
a) In rapid arrhythmia
b) By shortening of myocardial fiber
c) When heart rate is increased
d) By decreased sympathetic stimulation
e) By increased diastolic pressure
FFTFF

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Information desk:
Factors of cardiac output-
Physiological-
1. Age: Increase with increasing age 5. Exercise: Increased up to 700%
2. Sex: 10-20% less in female 6. Temp: Directly proportional
3. Surface area: Directly proportional 7. Pregnancy: Increases
4. Posture: Greater in sitting and lying posture 8. Sleep: No change (but HR decrease)
than erect posture 9. Digestion: Food intake increases CO.

Pathological factor
Increase CO-
1. Hyperthyroidism 5. Fibrillation and flutter
2. Anemia 6. Paget’s disease
3. Fever 7. Arteriovenous fistula
4. Hypoxia
[Ref: Bailey & Love’s/27th/P-21]
95. Amplitude of the pulse pressure in the aorta is directly proportional to-
a) Total peripheral resistance
Information desk:
b) Aortic compliance
Pulse Pressure depends on-
c) Stroke volume
 Age  Atherosclerosis
d) Velocity of blood flow
 SV  AR
e) Elasticity of vessel wall
 Arterial elastic constant  AV fistula
FFTFF
↑PP = ↑ age  Hyperthyroidism
Explanation:
𝐒𝐕 ↑SV ↓compliance  PDA
 P𝐏∞ ↓PP = ↑ HR ↑TPR  Hyperdynamic circulation
𝐂𝐨𝐦𝐩𝐥𝐚𝐢𝐧𝐜𝐞
[Ref: Guyton’s/14th/P-180]
96. Rate of gas diffusion through the respiratory membrane is-
a) Directly proportional to diffusion coefficient of the gas
b) Inversely proportional to the thickness of respiratory membrane
c) Inversely proportional to the pressure gradient between two sides of membrane
d) Directly proportional to molecular weight of the gas
e) Directly proportional to solubility of the gas
TTFFT
Explanation:
c) Directly propoional to the pressure gradient.
d) Inversely proportional to molecular weight of the gas.

Information desk:
Gas diffusion is directly proportional to-
 Surface area of membrane
 Diffusion co-efficient ∞ solubility of gas molecular got.
 Partial pressure difference between two sides of membrane.
 Gas diffusion is inversely proportional to thickness of membrane.
[Ref: Guyton’s/14th/P-516]
97. During normal quiet breathing-
a) Most of the tidal air enters into the apex of the lungs
b) Intra alveolar pressure is lowest at the end of inspiration
c) Intra-alveolar pressure is lowest at mid inspiration
d) Intrapleural pressure is lowest at the apex of the lungs
e) Intrapleural pressure is lowest at the end of inspiration
FFTTT
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Explanation:
a) Most of the tidal air enters into the base of the lungs.
b) Intra alveolar pressure is lowest at the mid of inspiration.
Information desk:
During normal quiet breathing-
1. At the end of inspiration: Both Intrapleural & intra esophageal pressure lowest.
2. At the end of expiration: Both Intrapleural & intra esophageal pressure highest.
3. At mid inspiration intrapulmonary (Interalveolar) pressure lowest rate of airflow greatest
4. At mid expiration: intra alveolar pressure highest.
[Ref: Roddie/6th/Q-145 & Guyton’s/14th/P-497]
98. The compliance of the lungs will be greater-
a) In infants than adults Information desk:
b) In apex than base of lungs Compliance of lung is greater in-
c) In saline filled than air filled alveoli  In standing than recumbent position
d) Than the compliance of the lungs and thorax together  In adult than infant
e) In recumbent position  Than the compliance of the lungs & thorax
FFTTF together
Explanation:  In obstructive lung disease
a) In adults than infants  Maximum at normal tidal range
b) Base > apex  In saline field than air
e) In standing then recumbent Other factor  compliance-
[Ref: Roddie/Q-151/P-65 & Ganong’s/26th/P-617]  Ageing process, emphysema
 Surfactant
99. Bohr effect-  Chronic obstructive pulmonary disease
a) Promotes O2 transport
b) Promotes CO2 Transport
c) Occurs when pH of the blood falls
d) Is not advantageous for tissue
e) Indicates the decrease affinity' of O2 to Hb
TFTFT
Explanation:
b) Promotes O2 transport
d) Advantageous for tissue as tissue get oxygenation.
Information desk:
Traits Haldane effect Bohr effect
Definition Binding of O2 with hemoglobin tends to The shifting of the O2 Hb dissociation
displace CO2 from the blood. This effect is curbe by the change in the blood CO2 &
called Haldane effect. H+ conc is called Bohr effect.
Depends on PO2 in blood PCO2 in blood
Effects In the tissue, increases pickup of CO2 by Hb. In the lungs increases pickup of O2 by Hb.
In the lungs , increases release of CO2 from In the tissue, increases release of O2 from
carbamino Hb. Hb-O2.
Importance Increases CO2 transport from the tissue to Increases O2 transport from the lungs to
the lungs. the tissue.
[Ref: Ganong’s/26th/P-631 & Guyton’s/14th/P-529]
100. IDA is associated with-
a) Low MCV
b) High serum ferrilua
c) Low serum iron
d) Low TIBC
e) Low RDW-CV
TFTFF
[Ref: Davidson’s/24th/P-950-951]
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101. Bleeding time is prolonged in-
a) Haemophilia
b) Von Willebrand disease
c) Dengue hemorrhagic fever
d) ITP
e) Henoch schonlein purpura
FTTTF
Explanation:
a) BT, PT, platelet count normal
e) Platelet count increased [*All causes of thrombocytopenia increases bleeding time]
[Ref: Hoffbrand/7th/P-277; Khaleque’s/2021/P-211, 213; Sembulingam/8th/P-139 & Vision’s/9th/P-76]
102. Renal vasodilatation is caused by-
a) Dopamine
b) Atrial natriuretic peptide Information desk:
c) Cortisol Mesangial cell relaxation (CAPD)-
d) Endothelin  CAMP
e) Angiotensin II  ANP
TTFFF  PGE2
Explanation:  Dopamine
d+e) Causes vasoconstriction.
[Ref: Ganong’s/26th/T-37.3/P-668]
103. Hormone regulating plasma osmolarity include-
a) Aldosterone
b) Antidiuretic hormone (ADH) Explanation:
c) Procalcitonin  Aldosterone
d) Atrial natriuretic peptide (ANP)  Antidiuretic hormone (ADH)
e) Epinephrine  Atrial natriuretic peptide (ANP)
TTFTF
[Ref: Ganong’s/26th/P-7 & ABC Biochemistry/7th/P-324]
104. The urine colour becomes dark on standing in the following conditions-
a) Alkaptonuria
b) G6PD deficiency
c) Chyluria
d) Metronidazole intake
e) Porphyria
TFFTT
Explanation: More- Imipenem, Cilastin, Methyldopa.

105. Glomerular function test include-


a) Water deprivation test Information desk:
b) Acid load test Glomerular function test includes-
c) Creatinine clearance test  eGFR  Renal clearance
d) Calorie deprivation test  GFR  Albumin in urine
e) Specific gravity of urine  S. creatinine  Albumin creatinine ratio
FFTFF  Blood Urea (ACR)
[Ref: ABC Biochemistry/7th/P-566-567] Tubular function test-
 Water deprivation test
 Acid load test
 Urine osmolarity/ Sp. gravity
 α2, β2 microglobulin defect in Urine

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106. Osmolarity of plasma-
a) Depends on electrolytes Information desk:
b) Depends on lipids  Laboratory facility to measure plasma osmolarity is
c) Is about 300 mosmol/L costly and not readily available. So, alternatively it is
d) Is about 28mm Hg. calculated out from plasma concentration of some
e) Measured by osmometer substances which are routinely measured in almost
TFTFT every patient. Calculated plasma osmolarity is claimed
Explanation: to be the valid approximation of instrumentally
a) Sodium and chloride are the main contributor measured plasma osmolarity. So, it is widely used
of plasma osmolarity. Potassium, urea and clinically for management of patients. Calculated
glucose have some contribution in plasma plasma osmolarity in mosm/L: 2[Na+] + 2[K+] + Glucose
osmolarity. + Urea [All measured in mmol/L].
b) Lipid has no role in plasma osmolarity.
c) Plasma osmolarity is 280-300 mosm/L.
d) Osmolarity of plasma is about 5441 mm of Hg at 37○C.
e) Osmometer is an instrument, which can measure osmolarity of a solution.
[Ref: Guyton’s/14th/P-308 & ABC Biochemistry/8th/P-337, 341]
107. Features of SIADH include-
a) Low plasma sodium concentration
b) High plasma osmolality
c) Urine osmolality > 150 mmol/L
d) Urine sodium concentration < 30 mmol/L
e) Raised plasma uric acid
TFFFF
Information desk:
Diagnosis of SIADH-
 Low plasma sodium concentration (typically < 130  Clinical euvolemia
mmol/L)  Absence of adrenal, thyroid, pituitary or
 Low plasma osmolality (<275 m0smol/kg) renal insufficiency
 Urine osmolality not minimally low  No recent use of diuretics
(typically >100 m0smol/kg)  Exclusion of other causes of
 Urine sodium concentration not minimally hyponatremia
low (>30 mmol/L)  Appropriate clinical context (above)
 Low- normal plasma urea, creatinine, uric acid
[Ref: Davidson’s/24th/B-19.11/P-624]
108. ECG changes in hypocalcaemia-
a) ST segment depression
b) ST segment prolongation
c) Prolong QRS
d) Loss of P wave
e) Prolonged QT interval
FTFFT
[Ref: Davidson’s/24th/P-663]
109. Dorsal column damage in the spinal cord results in-
a) Able to stand steadily with closed eye
b) Impaired pain sensation
c) Impaired touch sensation
d) Impaired vibration sensation
e) Flexor plantar response
FFTTT

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Explanation:
a) Unable
b) Pain sensation- lateral spinothalamic tract.
e) Plantar extensor in pyramidal tract lesion.
[Ref: Snell’s/8th/P-163]
110. Corticospinal tract lesion leads to-
a) Exaggerated knee jerk Information desk:
b) Loss of all tendon reflexes Lesion of pyramidal tract-
c) Increases muscle tone 1. Voluntary movements- There is loss of performance
d) Positive Babinski sign of fine-skilled voluntary movements. This occurs
e) Weakness of distal group of muscles of hands especially at the distal end of the limbs.
and feet 2. Muscle tone- Increased due to release phenomenon.
TFTTT 3. Reflexes-
Explanation:  Superficial reflex- Absent
b) Exaggerated tendon reflex  Deep reflex- Exaggerated
[Ref: Snell’s/8th/P-168]  Babinski sign- Positive
 Clonus- Present
111. Muscle spindle-
a) Contain extrafusal muscle fiber
b) Is innervated by gamma motor neuron
c) Detects change in length of muscle fiber
d) Can be stretched
e) Has sensory supply of Ib fiber
FTTTF
Explanation:
a) Intrafusal
e) Ia, Il
[Ref: Guyton’s/14th//P-687]
112. Life-saving hormones are-
a) Cortisol
b) Thyroxine Information desk:
c) Testosterone Life-saving hormones are-
d) FSH  Aldosterone / cortisol
e) Growth hormone  PTH
TFFFF
[Ref: Guyton/14th/T-75.1/P-917]
113. Cauda equina syndrome is characterized by-
a) Faecal incontinence Information desk:
b) Bladder dysfunction Clinical features of radicular pain-
c) Leg weakness Nerve root pain-
d) Hyper-reflex  Unilateral leg pain worse than low back pain
e) Saddle anaesthesia  Pain radiates beyond knee
TTTFT  Paraesthesia in same distribution
Explanation:  Nerve irritation signs (reduced straight leg raising that reproduces leg
d) Areflexia pain)
[Ref: Davidson’s/24th/B-26.20/P-  Motor, sensory or reflex signs (limited to one or adjacent nerve roots)
1004]  Often self-limiting, with 50% recovery at 6 weeks
Cauda equina syndrome-
 Difficulty with micturition
 Loss of anal sphincter tone or faecal incontinence
 Saddle anaesthesia
 Gait disturbance
 Pain, numbness or weakness affecting one or both legs

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114. Laboratory finding/s of primary hyperparathyroidism is/are-
a) Hypercalcaemia
b) Hyperphosphataemia
c) Increased serum parathyroid hormone
d) Decreased urinary phosphate
e) Increased serum alkaline phosphatase if bone involvement is present
TFTFT
[Ref: Davidson’s/24th/P-687-688]
115. Clinical feature/s consistent with primary adrenal insufficiency is/are-
a) Diarrhoea
b) Hypopigmentation
c) Hypotension
d) Polyphagia
e) Salt craving
FFTFT
[Ref: Davidson’s/24th/B-20.41/P-685]
116. Functions of Insulin include-
a) Promotes glucose uptake
b) Inhibits lipogenesis
c) Decreases K+ uptake by cells
d) Increases cell growth
e) Decreases release of gluconeogenic amino acid
TFFTT
Explanation:
b) ↑ Lipogenesis
c) ↑ Potassium uptake by cells
[Ref: Ganong’s/26th/T- 24.1, 24.2/P-426, Guyton’s/14th/P-975-979 & Davidson’s/24th/B-21.1/P-708]
117. In the stomach-
a) Acetylcholine stimulates secretion of gastrin
b) Histamine stimulates secretion of HCI
c) Gastrin stimulates secretion of histamine
d) Prostaglandin stimulates secretion of HCL
e) Acetylcholine stimulates chief cells
TTTFT
Information desk:
Control of acid secretion-
 Gastrin released from antral G cells in response to food (protein) binds to cholecystokinin receptors
(CCK-2R) on the surface of enterochromaffin-like (ECL) cells, which in turn release histamine. The
histamine binds to H2 receptors on parietal cells and this leads to secretion of hydrogen ions in exchange
for potassium ions at the apical membrane. Parietal cells also express CCK-2R and it is thought that
activation of these receptors by gastrin is involved in regulatory proliferation of parietal cells.
Cholinergic (vagal) activity and gastric distension also stimulate acid secretion; somatostatin, vasoactive
intestinal polypeptide (VIP) and gastric inhibitory polypeptide (GIP) may inhibit it. (ACh-R = acetylcholine
receptor; ATPase = adenosine triphosphatase).
[Ref: Ganong’s/26th/P-448-449 & Davidson’s/24th/Fig-23.3/P-785]
118. Pancreatic secretion-
a) Contains bicarbonate
b) Is acidic Information desk:
c) Is regulated by fat content of diet Pancreatic secretion-
d) Contains digestive enzymes Hydrolytic type- Ecbolic type-
e) Is not influenced by vagal stimulation  Contain fluid and HCO 3  Pancreatic enzyme: CCK-
TFTTF secretin. PZ & Ach acts thick
 Acts thin secretion on secretion on aciner cells.
ductal cells.

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Explanation:
b) Highly alkaline, pH-8 (Approximately).
c) When fat content reaches the duodemum, then pancreatic secretions are regulated through ach, CCK, secretion.
e) Vagal stimulation plays a less effective role in pancreatic secretion.
[Ref: Ganong’s/26th/P-452 & Guyton’s/14th/P- 825]
119. Elements absorbed from terminal ileum are-
a) Iron
b) Vitamin B12
c) Bile acid
d) Folic acid
e) Vitamin D
FTTFF
Explanation:
a) From duodenum
[Ref: Ganong’s/26th/B-26.2/P-470]
120. The liver is the principal site for-
a) Synthesis of plasma albumin
b) Synthesis of plasma globulins
c) Synthesis of vitamin B12
d) Storage of vitamin C
e) Storage of iron
TFFFT
Explanations:
b) Plasma globulins are synthesized in the liver except gamma globulins which are produced by plasma cell. So, liver
is no the principal size for globulin synthesis.
c) Vitamin B12 is stored rather synthesized in liver.
d) Liver stores large amount Vit-A, D, B12, small amount- iron, copper, vit- K, folate.
e) Liver stores iron, copper

Information desk:
Principal functions of the liver
Formation and secretion of bile
Nutrient and vitamin metabolism-
 Glucose and other sugars
 Amino acids
 Lipids-
 Fatty acids
 Cholesterol
 Lipoproteins
 Fat-soluble vitamins
 Water-soluble vitamins
Inactivation of various substances-
 Toxins
 Steroids
 Other hormones
Synthesis of plasma proteins-
 Acute-phase proteins  Clotting factors
 Albumin  Steroid-binding and other hormone-binding proteins
Immunity-
 Kupffer cells
[Ref: Ganong’s/26th/P-499, Vision/9th/P-261 & Davidson’s/24th/P-865]
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Pathology
121. Cellular adaptive responses include-
a) Necrosis Information desk:
b) Fatty change Cellular adaptations-
c) Metaplasia  Cellular adaptation occur in severe physiologic stresses and certain
d) Dysplasia pathologic stimuli and altered steady states are achieved.
e) Hyperplasia Cellular adaptation includes-
FFTFT 1. Hypertrophy: Hypertrophy refers to an increase in the size of cells, that
results in an increase in the size of the affected organ. The hypertrophied
organ has no new cells, just larger cells. The increased size of the cells is
due to the synthesis and assembly of additional intracellular structural
components.
2. Hyperplasia: Hyperplasia is defined as an increase in the number of cells
in an organ or tissue in response to a stimulus.
3. Atrophy: Atrophy is defined as a reduction in the size of an organ or
tissue due to a decrease in cell size and number.
4. Metaplasia: Metaplasia is a reversible change in which one
[Ref: Robbin’s/10th/P-35] differentiated cell type (epithelial or mesenchyme) is replaced by
another cell type.
122. Liquefactive necrosis is seen in-
a) Center of a granuloma
b) Heart
c) Brain
d) Wet gangrene
e) Abscess cavity
FFTTT
Explanation:
a) Caseous necrosis

Information desk:
Liquefactive necrosis or colliquative necrosis-
1. It results from autolysis and heterolysis in the pyogenic bacterial or occasionally fungal infections these
agents constitute powerful stimuli to the accumulation or inflammatory cells. It is also evoked by hypoxic
cell death in CNS.
2. Enzymes digestion is dominant. This results from autolysis or heterolysis by the action of powerful
catalysing enzyme.
3. Example: Liquefactive necrosis occurs in-
a) Suppurative inflammation
b) Hypoxic death of cell within brain
c) Foral bacterial or fungal infection
d) Wet Gangrene (If superimposed infection)
Morphology-
 Liquefaction completely digests dead cells and transforms the tissue into liquid viscous mass
 If initiated by acute inflammation the matter is frequently creamy yellow because of presence of dead
white cells called pus
 These occur softening of necropsied area. It then breaks up and turn into fluid.
 There may be cyst formations.
[Ref: Robbin’s/10th/P-40]

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123. Apoptosis is triggered by-
a) P53 gene
b) Bcl-2 gene
c) Fas-Fas ligand
d) Superoxide dismutase
e) Nitric oxide
TFTFF
Explanation:
a) Apoptotic gene
b) Anti-apoptotic gene
c) Cell surface receptor that act in death receptor pathway
d) Enzyme that breakdown free radical
e) Vasodilator mediator
Information desk:
Morphology/ Features of apoptosis-
The following changes characterize cells undergoing apoptosis and are seen best with the electron microscope.
1. Cell Shrinkage-
 Cell is smaller in size, cytoplasm is dense, eosinophilic and organelles are tightly packed.
2. Chromatin condensation-
 Most characteristic feature of apoptosis.
 Chromatin aggregates into dense masses under the nuclear membrane.
 Nucleus may break into two or more fragments.
 Pyknosis may be seen in apoptotic cell death.
3. Formation of cytoplasmic blebs and apoptotic bodies-
 There occurs marked surface blabbing.
 The apoptotic cell fragments into a number of apoptotic bodies which are membrane-bound and
consist of cytoplasm, organelles with or without a nuclear fragment.
4. Phagocytosis- Usually by macrophages or adjacent healthy parenchymal cells phagocytose the apoptotic
cells or cell bodies.
5. Apoptosis does not elicit inflammation.
N.B: Apoptosis is caused by Cysteine Proteases during Initiation Phase.
[Ref: Robbin’s/10th/P-44]
124. Free radicals-
a) May arise by absorption of radiant energy
b) Antioxidants block free radical formation
c) Are not a byproduct of metabolism
d) May cause peroxidation of lipids within plasma membrane
e) Can only form in the presence of oxygen
TTFTF

Information desk:
Generation of free radicals-
1. Reduction oxidation reaction during normal metabolic process 6. Nitric oxide (NO)
2. Absorption of radiant energy e.g. ultraviolet light X-rays 7. Reperfusion injury
3. Rapid bursts of ROS during inflammation (ROS-Reactive oxygen 8. Phagocytosis
specin) 9. Hydrolysis
4. Enzymatic metabolism of exogenous chemical or drugs 10. Anticancer drugs
5. Transition metals such as iron & copper as in Fenton reaction 11. Cellular aging
12. Both necrosis & apoptosis

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Removal of free radicals-
 Spontaneous decay
 Enzymes: catalase, Superoxide dismutase, Glutathione peroxidase
Anti-oxidants-
 Vit E  Glutathione
 Vit A  Transferrin, Ferritin, Lactoferrin
 Ascorbic acid  Ceruloplasmin
 Cysteine
Pathological effects-
 Lipid peroxidation
 Protein modification
 DNA damage
[Ref: Robbin’s/10th/P-52]
125. Features of acute inflammation are increased-
a) ESR
b) Monocyte count
c) IgG
d) Leukocyte count
e) Creactive protein
TFFTT
Information desk:
Events of acute inflammation-
A) Vascular, events changes in vascular flow & caliber-
 Transient vasoconstriction of arteriole persists few second
 Persistent vasodilation
 Slowing of the circulation
 Stasis
Increased vascular permeability (vascular leakage)
 Formation of endothelial gaps
 Endothelial retraction
 Increased transcytosis
 Direct endothelial injury
 Delayed prolonged leakage
 Leukocyte, mediated endothelial injury
B) Cellular events-
Leukocyte extravasation
Extravasation can be divided into the following steps-
 In the lumen- margination, rolling, adhesion
 Transmigration across the endothelium (diapedesis)
 Migration in interstitial tissue towards a chemotactic stimulus
[Ref: Robbin’s/10th/P-75-85]
126. In chronic granulomatous reaction-
a) Macrophages collect cytoplasm to convert into epithelioid cells
b) Neutrophils are arranged at the peripheral region
c) Fibroblasts fuse to form multinucleated giant cells
d) Signs of destruction of attempts of repair are present simultaneously
e) Caseous material is pathognomonic of tuberculosis
TFFTT
[Ref: Robbin's/10th/P-41, 99, 100, 386]

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127. Granulation tissue is composed of-
a) Young fibroblast
b) Histiocytes
c) Epithelioid cells
d) Newly formed blood vessels
e) Loose extracellular matrix
TFFTT
[Ref: Khaleque’s/2021/P-38]
128. Factors causing delay in wound healing are-
a) Infection
b) Ultraviolet light Explanation:
c) Foreign bodies  Infection in the most important cause of delayed
d) High protein diet wound healing. Presence of foreign body & early
e) Movement movement delayed wound healing.
TFTFT
[Ref: Khaleque’s/2021/P-40]
129. Brown induration is seen in-
a) COPD
b) Pulmonary oedema
c) Heart failure
d) Septic shock
e) Pulmonary embolism
FFTFF
Explanation:
b) Acute pulmonary does not cause brown induration
c) Heart failure (chronic) causes brown induration
[Ref: Khaleque’s/2021/P-46]
130. Coagulation failure is an important complication of-
a) Placenta praevia
b) Abruptioplacenta
c) Amniotic fluid embolism
d) Gram-negative septicemia
e) Uterine rupture
FTTTT
Information desk:
Causes of Disseminated intravascular coagulation (DIC)
1. Infection sepsis by- 4. Severe liver failure
 E. Coli 5. Malignancy- Solid tumours and leukaemia
 Streptococcus pneumoniae 6. Tissue destruction- pancreatitis, burns
 Neisseria meningitidis 7. Vascular abnormalities- Vascular aneurysm, Liver
 Malaria haemangiomas.
2. Trauma 8. Toxic/ Immunological- ABO incompatibility, Snake
3. Obstetric- bites, Recreational drugs.
 Amniotic fluid embolism
 Placental abruption
 Pre-eclampsia
[Ref: Robbin’s/10th/P-669-670]

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131. Clinical features of compensated shock are-
a) Decreased blood pressure
b) Increased respiratory rate Information desk:
c) Decreased urine output Features of compensated shock-
d) Lactic acidosis  Lactic acidosis  Normal Respiratory rate
e) Increased pulse rate  Normal urine output  Mildly increased pulse rate
FFFTT  Normal conscious level  Normotension
[Ref: Bailey & Love’s/27th/T-2.2/P-14]
132. Sex chromosomal abnormalities found in-
a) Down syndrome
b) Edward syndrome
c) Turner syndrome
d) Klinefelter syndrome
e) Patau syndrome
FFTTF

133. An XY individual who inherits mutated non-functional androgen receptor will have-
a) Female phenotype Information desk:
b) Non-functional gonad  An XY individual who inherit mutated non-functional
c) Mullerian duct derivatives androgen receptor, the genetic alteration they inherit,
d) External appearance of male prevents their body responding to testosterone. This
e) The ability to secret testosterone means male sex development does not happen as normal.
TTFFF The genitalias appear as female or under developed.
Uterus and ovansies also don’t develop internally.
134. Following are the autosomal dominant disorders-
a) Neurofibromatosis
b) Marfan syndrome
c) Wilson disease
d) Duchene muscular dystrophy
e) Hemophilia
TTFFF
Explanation:
a+b) AD
c) AR
d+e) XR
[Ref: Khaleque’s/2021/P-87]
135. Autosomal recessive disorders are-
a) Familial hypercholesterolemia
b) Hypertension
c) Thalassemia
d) Glycogen storage disease
e) Mosaicism
FFTTF

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Information desk:
Example of autosomal recessive-
1. Metabolic-
 Hemochromatosis  Glycogen storage disease
 Cystic fibrosis  Lysosomal (Hurler syndrome) Liposomal storage disease
 Phenylketonuria  Galactosemia
 Wilson disease
2. Hematopoietic- 4. Neurologic-
 Sickle cell anemia  Spinal muscular atropy
 Thalassemia  Neurogenic muscular atropy
 Friedreich ataxia
3. Endocrine- CAH 5. Skeletal-
 Alkaptonuria
 Ehler-danlos syndrome
[Ref: Robbin’s/10th/T-5.2/P-146]
136. Anaplasia means-
a) To form backward
b) Lack of differentiation
c) The tumour is malignant
d) Disordered growth
e) Absence of organization
TTTFF
Explanation:
d) Dysplasia means disordered growth

Information desk:
Differentiation & Anaplasia-
 Differentiation refers to the extent to which neoplastic parenchymal cells resemble the corresponding
normal parenchymal cells, both morphologically and functionally.
 Anaplasia- Lack of differentiation. Anaplasia is considered a hallmark of malignancy. The term anaplasia
means “to form backward,” implying a reversal of differentiation to a more primitive level.

Features of anaplasia-
 Pleomorphism: Both the malignant cells and their nuclei characteristically display pleomorphism (i.e.
variation in size and shape).
 Abnormal nuclear morphology: The nuclei are hyper-chromatic and disproportionately large for the cell.
The nucleus to-
 Cytoplasm ratio may approach 1: 1 instead of the normal 1:4 or 1:6. The nuclear shape is also very
variable.
 Mitoses: Atypical, bizarre mitotic figures, sometimes producing tripolar, quadripolar or multipolar
spindles.
Loss of polarity: Architecture, organization and orientation of malignant cells are markedly disturbed.
Necrosis and haemorrhage: Commonly present.
 Other changes: Formation of tumour giant cells having only a single huge polymorphic nucleus and
two or more large hyper-chromatic nuclei.

[Ref: Robbin’s/10th/P-42 & Khaleque’s/2021]

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137. The malignant tumours of bone include the-
a) Osteoclastoma
b) Brown's tumour
c) Chondrosarcoma
d) Neuroblastoma
e) Meningioma
FFTFF
Explanation:
a+b) Benign
d) Malignant tumor of chest, adrenal gland, neck and spinal cord
[Ref: Robbin’s/10th/P-521, 1187]
138. Tumors metastasize into bone include-
a) Papillary thyroid carcinoma
b) Pulmonary adenocarcinoma Information desk:
c) Cervical squamous cell carcinoma Tumors metastasize into bone-
d) Renal cell carcinoma  Thyroid, Breast, Bronchus of lung, Kidney, Prostate.
e) Prostatic adenocarcinoma
FTFTT
Explanation:
a) Follicular thyroid carcinoma metastasized to bone but papillary carcinoma metastasized to lung only in minority
of patient.

139. Locally malignant tumors are-


a) Ameloblastoma Nice to know
b) Basal cell carcinoma
c) Marjolin's ulcer Avwg evmvq †h‡q Kvi Mjvq dzj gvjv †`e
d) Melanoma Avwg- Ameloblastoma
e) Ewing's sarcoma evmvq- Basal cell carcinoma
TTTFF ‡h‡q- Giant cell tumour of bone/ Osteoclastoma
Explanation: Kvi- Carcinoid tumour/ Cranio pharyngioma
c) Both locally malignant and precancerous (may leads Mjvq- Glioma (Astrocytoma, Oligodendroglioma
to SCC). dzj- Fibromotosis/ Desmoid tumour
gvjv- Mixed salivary/ Pleomorphic
†`e- Marjolin’s ulcer
140. Constituents of tobacco smoke that induce carcinogenesis include-
a) Nicotine
b) Nitrosamine
c) Carbon monoxide
d) Benzo[a]pyrene
e) Tar
FTFTT
Information desk:
Effects of selected tobacco smoke constituents-
Substance Effects
Tar Carcinogenesis
Polycyclic aromatic hydrocarbons Carcinogenesis
Nicotine Ganglionic stimulation and depression; tumour promotion
Phenol Tumour promotion; mucosal irritation
Benzo[a]pyrene Carcinogenesis
Carbon monoxide Impaired oxygen transport and utilization
Formaldehyde Toxicity to cilia; mucosal irritation
Nitrogen oxides Toxicity to cilia; mucosal irritation
Nitrosamine Carcinogenesis
[Ref: Robbin’s/10th/T-9.3 & Effects of Selected Tobacco Smoke Constituents]

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141. Widely used tumour markers for detecting hepatoblastoma in children-
a) HE4
b) Ferritin
c) CA19-9
d) AFP
e) CEA
FFFTF
Information desk:
Tumor markers Tumor types
Hormones
Human chorionic gonadotropin Trophoblastic tumors, nonseminomatous testicular tumors
Calcitonin Medullary carcinoma of thyroid
Catecholamine and metabolites Pheochromocytoma and related tumors
Ectopic hormones
Oncofetal antigens
Α-fetoprotein Liver cell cancer, nonseminomatous germ cell tumors of testis

Carcinoembryonic antigen Carcinomas of the colon, pancreas, lung, stomach, and heart
Isoenzymes
Prostatic acid phosphatase Prostate cancer
Neuron specific enolase Small cell cancer lung, neuroblastoma
Specific proteins
Immunoglobulins Multiple myeloma and their gammopathies
Prostate- specific antigen and prostate specific Prostate cancer
membrane antigen
Mucins and other glycoproteins
CA- 125 Ovarian cancer
CA- 19-9 Colon cancer, pancreatic cancer
CA- 15-3 Breast cancer
Cell-free DNA markers
TP53, APC, RAS Mutants in stool and serum Colon cancer
TP53, RAS Mutants in stool and serum Pancreatic cancer
TP53, RAS Mutants in sputum and serum Lung cancer
TP53 mutants in urine Bladder cancer
[Ref: Davidson’s/24th/B-7.4/P-136]
142. Fixatives used in pathology laboratory are-
a) Alcohol Information desk:
b) Formalin
Fixatives are-
c) Xylene
 10% formalin  95% ethanol
d) Liquid paraffin
 Glutaraldehyde  100% methanol
e) Glutaraldehyde
 Absolute alcohol
TTFFT

143. Histamine is released from-


a) Basophils
b) Endothelial cells
c) Macrophages
d) Mast cells
e) Platelets
TFFTT
[Ref: Robbin’s/10th/P-86 & Khaleque’s/2021/P-21]
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144. Red infarcts is/are seen in-
a) Heart
b) Spleen
c) Kidney
d) Lungs
e) Ovary
FFFTT

Information desk:
Infarct- Types of infarct-
 It is a localized area of ischemic necrosis in an organ or  Red infarct
tissue produced most often by sudden occlusion of its  White infarct
arterial supply or of its venous drainage e.g. MI.
Red infarcts example (LUSIBO) White infarcts example
1. Lung 4. Testes 1. Heart
2. Small intestine 5. Brain 2. Spleen
3. Ovary 3. Kidney
[Ref: Khaleque’s/2021/P-52-53]
145. Dysplasia-
a) Literally means disordered growth
b) May be reversible
c) Is necessarily progress to cancer
d) Is encountered in connective tissue only
e) Is often found in adjacent foci of invasive cancer
TTFFT
Explanation:
c) May progress to cancer, not necessarily
d) Encountered mainly in epithelium, also is connective tissue

Information desk:
Dysplasia-
 Dysplasia literally means disordered growth
 It occurs principally in epithelium but also in connective tissue.
 Characterized by loss in the uniformity of the individual cells as well as a loss in their architectural
orientation (loss of polarity).
 Shows considerable Pleomorphism.
 Hyper-erchromatic nuclei with a high nuclear-to-cytoplasmic ratio.
 Mitotic figures are more abundant than in the normal tissue.
 Dysplasia may be a precursor to malignant transformation, it does not always progress to cancer.
 Mild to moderate dysplasia may be completely reversible after removal of inciting stimulus.
 Precursor of ca.
[Ref: Robbin’s/10th/P-272]

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Faculty
146. Hyperopia is caused by-
a) Lens system that focuses the object behind retina
b) Uneven curvature of retina
c) Eyeball that is shorter than normal
d) Lens whose refractive power is more than normal
e) Lens whose accommodation power is more than normal
TFTFF
Explanation:
b) Astigmatism causes uneven curvature of cornea or lens
e) Power of the eye is less than 60D

147. Features of Argyl Robertson’s Pupil include-


a) Near reflex is present
b) Pupil is dilated
c) Pupil doesn’t react to light
d) The condition is due to syphilitic lesion
e) The lesion is in the pretectal nucleus
TFTTT

148. Halothane-
a) Increases GI tract motility
b) Increases cerebral blood flow
c) Increases intraoccular pressure
d) Is a strong analgesic
e) MAC is 0.8
FTFFT
Explanation:
e) Mac 0.75% at 80 years & 0.65% at 80 years.
[Ref: Smith/7th/P-56-57]
149. Hormone producing tumour/s of ovary-
a) Dysgerminoma Information desk:
b) Choriocarcinoma Hormone producing tumour-
c) Granulosa cell tumour 1. Granulosa cell tumour
d) Struma ovary 2. Sartoli leydig cell tumour
e) Brenner tumour 3. Hilus tumour
FFTTT 4. Struma ovary
Chorio carcinoma is not a tumour of ovary.
[Ref: DC Dutta/Gynae/8th/P-243-244 & 320-323]
150. Hypodense structures revealed in CT scan are-
a) Fat
b) Bone
c) Air
d) Fluid
e) Calcification
TFTTF
[Ref: Bailey & Love’s/28th/P-122-123]

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151. Cough impulse is positive in-
a) Saphena varix Information desk:
b) Hernia Defense mechanism of inguinal canal-
c) Varicocele 1. Obliquity of inguinal canal
d) Ectopic testis 2. Arching of conjoint tendon
e) Encysted hydrocele of the cord 3. Shutter mechanism of internal Oblique
TTTFF 4. Ball valve mechanism due to contraction of cremaster
muscle which plugs to superficial ring
5. Slit valve mechanism: When external oblique muscle
contracts, intercrural fibres of superficial ring approximate.
6. Hormones
[Ref: SRB’s/6th/P-744, 1065, 1068]
152. The intervertebral discs-
a) Are largely composed on hyaline cartilage
b) The annulus fibrosus is formed of elastic tissue
c) Contribute to one quarter of the length of the vertebral column
d) Are found in all regions of the vertebral column
e) May compress the spinal cord when injured
FFTFT
[Ref: BD/8th/V-1/P-233]
153. Transection of the spinal cord at C6 level will produce-
a) Immediate spastic paralysis of the extremities
b) Diaphragmatic breathing only
c) Urinary retention
d) Paralytic ileus
e) Exaggerated knee jerks
FFTFT
[Ref: Clinical Neuroanatomy/Snell/8th/P-168]
154. In acute appendicitis-
a) Age is not an important factor
b) Marked leukocytosis occur
c) Ultrasound study is necessary for all patients
d) Appendicectomy is the treatment of choice in all situations
e) Typhlitis is the differential diagnosis in both sex
FTFFT
[Ref: Bailey & Love’s/28th/P-1337-1339]
155. Non-absorbable suture materials are-
a) Nylon
b) Polydiaxonone (PDS)
c) Polyglactin 910
d) Polypropylene
e) Silk
TFFTT
[Ref: Bailey & Love’s/28th/T-7.1/P-106; SRB’s/6th/P-1154]
156. Marjolin's ulcer develops in-
a) Keloid
b) Persistent sinus
c) Chronic friction
d) Naevus
e) Long standing venous ulcer
FTTFT
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Information desk:
Marjolin's ulcer-
 It is a well-differentiated squamous cell carcinoma which occurs in chronic scars like burn scar, scar
of venous ulcer.
 As it develops in a scar due to chronic irritation and there are no lymphatics in scar tissue, it will
not spread to lymph nodes.
 As scar is relatively avascular it grows slowly. As scar does not contain nerves, it is painless.
Once it reaches the normal skin it may behave like any other squamous cell carcinoma, i.e. it will
spread to lymph nodes.
It occurs in unstable scar of long duration-
1. Chronic sinus tracts 5. Vaccination points
2. Pre- existing sinsus 6. Chronic inflamanation
3. Osteomyelitis 7. Immuro suppresion
4. Burns
[Ref: Bailey & Love’s/28th/P-593 & SRB’s/6th/P-301]
157. After major surgery there is-
a) Negative sodium balance
b) Potassium retention
c) Increased plasma cortisol level
d) Decreased tendency for clotting
e) Negative nitrogen balance
FFTFT
Explanation:
a) A positive sodium balance occurs due to aldosterone effect.
b) Potassium loss occurs due to aldosterone effect.
d) Trauma is a hypercoagulable state. Clotting tendency increases for 10 times.
e) Negative nitrogen balance due to muscle protein breakdown.
[Ref: Bailey & Love’s/28th/P-3-4, 9, 292]
158. Tuberculous otitis media is characterized by-
a) Earache Information desk:
b) Fever TB otitis media-
c) Multiple perforations in tympanic membrane  Fever
d) Pale granulation  Multiple perforation of TM
e) Thin odorless discharge  Pale granulation
FTTTF  Painless ear discharge (foul smelling)
[Ref: Dhingra/8th/P-91]
159. Factors associated with increased risk of aspiration during anaesthesia-
a) Recent oral intake
b) Distal bowel obstruction
c) Hypervolemia
d) H2 blocker injection during induction
e) Hiatus hernia
TTFFT
[Ref: Smith/7th/B-44.1/P- 821, 834]
160. Prenatal chromosome analysis can be done from-
a) Amniotic fluid
b) Chorionic villous tissue Explanation:
c) Fetal cord blood  Prenatal chromosomal analysis done from- amniotic
d) Maternal peripheral blood fluid, chorionic villous tissue, fetal cord blood.
e) Maternal skin fibroblasts
TTTFF
[Ref: DC Dutta/Obs./9th/P-102]
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161. Causes of tinnitus are-
a) Hypertension
b) Hypotension
c) Mastoiditis
d) Sinusitis
e) Cervical spondylosis
TTFFF
Information desk:
Causes of tinnitus
Subjective tinnitus Objective tinnitus
Otologic- Neurologic- Vascular- • Patulous eustachian
• Impacted wax • Head injury (labyrinthine • AV shunts tube
• Fluid in middle ear concussion) – Congenital AV • Palatal myoclonus
• Acute otitis media • Temporal bone fractures malformations • Idiopathic stapedial
• Chronic otitis media • Whiplash injury – Glomus tumour of or tensor tympani
• Ménière’s disease • Multiple sclerosis middle ear myoclonus
• Presbycusis • Postmeningitic • Arterial bruit • Dental
• Noise-induced hearing • Brain haemorrhage – Carotid aneurysm • Clicking of TM joint
loss • Brain infarct – Carotid stenosis
• Idiopathic sudden • Cardiovascular – Vascular loop pressing
SNHL • Hypertension on VIIIth nerve in internal
• Acoustic neuroma • Hypotension auditory canal
• Anaemia – High-riding carotid
Metabolic- • Cardiac arrhythmias artery
• Hypothyroidism • Arteriosclerosis – Persistent stapedial
• Hyperthyroidism artery
• Obesity Pharmacologic-
• Venous hum
• Hyperlipidaemia • Certain drugs used by the
– Dehiscent jugular bulb
• Vitamin deficiency patient
(e.g. B12) • All ototoxic drugs
Psychogenic-
• Anxiety
• Depression
[Ref: Dhingra/8th/P-130]
162. Medications associated with infertility are-
a) Calcium channel blockers Information desk:
b) Spironolactone Drug causing infertility-
c) Proton pump inhibitors  Antihypertensive drugs  Cytotoxic drugs
d) Cephalosporins  Antipsychotic drugs  Nitrofurantion
e) Cimetidine  Anticonvulsant drugs  Cimetidine
TTFFT  β-blockers  Radiation are lilely to hinder
spermatogenesis
[Ref: DC Dutta/Gynae/8th/P-189]
163. Polycystic ovary syndrome patients have-
a) Relatively low serum FSH
b) High serum LH
c) Low serum estrogen level
d) High serum leptin level
e) High level of serum testosterone
TTFTT
[Ref: DC Dutta/Gynae/8th/T-29.6, 29.7/P-388]

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164. Lignocaine is-
a) First synthetic amide local anesthetic
b) Used to treat supraventricular tachycardia
c) May cause methaemoglobimaenia
d) Produce tachyphylaxis
e] Crosses placenta
TFTFT
[Ref: Smith/7th/T-1.1/P-7; Morgan/6th/P-266, BRS Pharma/7th/P-117 & Katzung/15th/P-480-482]
165. Gangrene of gut can occur in-
a) Volvulus of sigmoid colon
b) Bacilliary dysentery
c) Ileocaecal intusussception
d) Mesenteric vascular occlusion
e) Paralytic ileus
TTFTF
[Ref: SRB/6th/P-932, 937-985]
166. The progesterone only pill-
a) Is Liable to cause amenorrhea
b) Is safe and effective in lactating women
c) Can be prescribed to women with a medical history of venous thromboembolic episode
d) Acts to suppress the adenohypophysis
e) Increases tubal motility
TTTFF

Information desk:
Progestogen-only contraception-
Progestogen-only contraception includes:
Oral: POPs
 Parenterals: DMPA, NET-EN, implants (Implanon)
 LNG–IUS
Progestin-only Pill (POP/Minipill)-
 Progestin-only pill is devoid of any estrogen compound. It contains very low dose of a progestin. It has to
be taken daily from the first day of the cycle. It has to be taken regularly and at the same time of the day.
There must be no break between the pack.
Mechanism of action-
 It works mainly by making cervical mucus thick and viscous, thereby prevents sperm penetration.
Endometrium becomes atrophic, so blastocyst implantation is also hindered.
Advantages-
a) Side effects attributed to estrogen in the combined pill are totally eliminated
b) No adverse effect on lactation and hence can be suitably prescribed in lactating women and as such it is
often called ‘Lactation Pill
c) Easy to take as there is no ‘On and off’ regime
d) It may be prescribed in patient having (medical disorders) hypertension, fibroid, diabetes, epilepsy,
smoking, and history of thromboembolism, HIV positive women
e) Reduces the risk of PID and endometrial cancer.
Disadvantages-
a) Acne, mastalgia, headache, breakthrough bleeding, or at times amenorrhea in about 20-30% cases;
b) Simple cysts of the ovary may be seen, but they do not require any surgery;
c) Failure rate is about 0.3-2 per 100 women years of use. Failure is more in young compared to women
over 40. Women using drugs that induce liver microsomal enzymes to alter a metabolism (mentioned
above) should avoid this method of contraception.
Contraindications-
a) Pregnancy d) Arterial disease
b) Unexplained vaginal bleeding e) Thromboembolic disease
c) Recent breast cancer f) Women taking anti-seizure drugs
[Ref: D.C. Dutta/Gynae/8th/P-410]
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167. Osteosarcoma-
a) Is a highly malignant bone tumor
b) Arise from osteocyte cell
c) Is more common in epiphyseal region
d) Is more common in 2nd decade
e) Is sensitive to usual chemo and radiotherapy
TFFTT
Explanation:
b) Arises from primitive transformed cells of mesenchymal origin
c) More common in metaphysis
d) 75% occurring before the age of 20 years
[Ref: Apley’s/10th/P-207, 747]
168. In the unconscious patient-
a) Absence of radial pulse indicates a cardiac arrest
b) Chest movement indicate breathing is present
c) Dilated pupils indicate brain damage has occurred
d) The airway should be checked for obstruction
e) The patient dentures should be removed
TTTTT

169. Complications of hemorrhoids include-


a) Strangulation and thrombosis
b) Malignant transformation
c) Ulceration
d) Complete rectal prolapse
e) Portal pyaemia
TFTFT
[Ref: Bailey & Love’s/28th/P-1356-1357]
170. Medications that can give raise to pigmentary changes of the macula include-
a) Chloroquine
b) Desferroxamine
c) Tamoxifen
d) Amiodarone
e) Chlorpromazine
TTTFF
Information desk:
Medications that can give raise to pigmentary changes of the macula include-
 Antimalarial- quinine, hydroxychloroquine  Ethambutol  Tamoxifen
 Digitalis  Indomethacin  Isotretinoin
 Phenothiazine  Desferroxamine  Sildenafil
[Ref: A.K. Khurana/7th/P-529; Shamsul/2nd/P-176, 240 & S.K. Basak/7th/P-350]
171. Causes of nasal bone destruction are-
a) Lichen planus
Information desk:
b) Syphilis
Causes of nasal bone destruction are-
c) Sarcoidosis
 Syphilis  Sarcoidosis
d) Leishmaniasis
 Tuberculosis  Trauma
e) Amyloidosis
 Leprosy  Tumour
FTTFF
 Actinomycosis
[Ref: Dhingra/8th/P-181-187]

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172. In subclinical hyperthyroidism-
a) TSH, FT, and FT3 are all increased
b) TSH, FT4 and FT3 are all decreased
c) TSH is suppressed but FT4 and FT rise within the reference range
d) TSH is suppressed but FT and FTz always raised
e) TSH receptor antibodies may be positive or negative
FFTFT

How to interpret thyroid function test results


TSH T4 T3 Most likely interpretation(s)
Undetectable Raised Raised Primary thyrotoxicosis
Undetectable or low Raised Normal Over-treatment of hypothyroidism with levothyroxine
Factitious thyrotoxicosis
Undetectable Normal1 Raised Primary T3 toxicosis
Undetectable Normal1 Normal1 Subclinical thyrotoxicosis
Undetectable or low Raised Low or Non-thyroidal illness
normal Amiodarone therapy
Undetectable or low Low Raised Over-treatment of hypothyroidism with liothyronine (T3)
Undetectable Low Low Secondary hypothyroidism4
Transient thyroiditis in evolution
2
Normal Low Low Secondary hypothyroidism4
2
Mildly elevated 5–20 mIU/L Low Low Primary hypothyroidism
Secondary hypothyroidism4
2
Elevated >20 mIU/L Low Low Primary hypothyroidism
Mildly elevated 5–20 mIU/L Normal3 Normal2 Subclinical hypothyroidism
Elevated 20–500 mIU/L Normal Normal Artefact
Heterophilic antibodies (host antibodies with affinity to
the animal antibodies used in TSH assays)
Elevated Raised Raised Non-adherence to levothyroxine replacement - recent
‘loading’ dose Secondary thyrotoxicosis4
Thyroid hormone resistance
1
Usually upper part of reference range. 2T3 is not a sensitive indicator of hypothyroidism and should not be
requested. 3Usually lower part of reference range. 4 i.e. Secondary to pituitary or hypothalamic disease.
Note that TSH assays may report detectable TSH. (TSH = thyroid-stimulating hormone)
[Ref: Davidson’s/24th/B-20.5/P-654]
173. Clinical features of constrictive pericarditis are-
a) Rapid and high volume pulse
b) Pulsus paradoxus
c) Normal JVP
d) Hepatomegaly
e) Kussmaul sign
FTFTT
Information desk:
Features of constrictive pericarditis
Symptoms-
 Dyspnoea, oedema and abdominal swelling due to ascites and hepatomegaly.
Signs-
 Small volume pulse and pulsus paradoxus.
 JVP is always elevated, usually very high with prominent ‘x’ and ‘y’ descents.
 The apex beat may be impalpable.
 Heart sounds are usually soft, and an early third sound
 Kussmaul sign
 The liver is commonly grossly enlarged, ascites is marked, and peripheral oedema is present.
[Ref: Bailey & Love’s/28th/P-973]

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174. Possible mechanisms of subfertility due to fibroid uterus are-
a) Gross distortion of uterine cavity
b) Increased vascularity of uterus Explanation:
c) Obstruction of tubal ostium by fibroid  Ovarian factor- Anovulation
d) Dysfuncional uterine contractility  Peritoneal- Endometriosis
e) Enhanced oestrogenic environment  Unknown- Majority
TFTTF
Information desk:
Infertility: Infertility (30%) may be a major complaint. The probable known attributing factors are-
Uterine- Tubal-
 Distortion and/ or elongation of the uterine cavity →  Cornual block due to position of the fibroid
difficult sperm ascent  Marked elongation of the tube over a big
 Preventing rhythmic uterine contraction due to fibroids fibroid
during intercourse → impaired sperm transport  Associated salpingitis with tubal block.
 Congestion and dilatation of the endometrial venous
plexuses → defective implantation
 Atrophy and ulceration of the endometrium over the
submucous fibroids → defective nidation
 Menorrhagia and dyspareunia
[Ref: DC Dutta/Gynae/8th/P-228]
175. Causes of secondary postpartum hemorrhage are-
a) Uterine atony
b) Infection
c) Retained bits of placenta
d) Following episiotomy
e) Uterine tear
FTTFF
[Ref: DC Dutta/Obs./10th/P-392]
176. Reactionary hemorrhage-
a) Is hemorrhage occuing within 24 hours
after operation Information desk:
b) Is usually caused by dislodgment of clot, Primary, reactionary and secondary haemorrhage-
increased blood pressure or slipage of ligature  Primary haemorrhage is haemorrhage occurring
c) Is associated with infection immediately as a result of an injury (or surgery).
d) Can be significant, regarding re-exploration Reactionary haemorrhage is delayed haemorrhage (within
e) Is usually severe 24 hours) and is usually due to dislodgement of a clot by
TTFTF resuscitation, normalisation of blood pressure and
Explanation: vasodilatation. Reactionary haemorrhage may also be due
c) Secondary hemorrhage is associated with to technical failure, such as slippage of a ligature.
infection.  Secondary haemorrhage is due to sloughing of the wall of
d) Reactionary hemorrhage is usually not severe, a vessel. It usually occurs 7–14 days after injury and is
but can be significant, regarding re-exploration. precipitated by factors such as infection, pressure necrosis
th
[Ref: Bailey & Love’s/28 /P-15] (such as from a drain) or malignancy.
177. Moist gangrene occurs in-
a) Buerger’s disease
Information desk:
b) Diabetic foot
Common sites of moist gangrene-
c) Raynaud’s disease
1. Intestine (Commonest site)
d) Strangulated bowel
2. Mouth (Carcinoma oris)
e) Testicular torsion
3. Bed sore
FFFTT
4. Other sites: Vulva, scrotum, testis, anterior
Explanation:
abdominal wall and thigh.
a+b+c) Dry gangrene

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178. Antibiotic prophylaxis is suggested for patients with history of-
a) Coronary bypass surgery
b) Atrial fibrillation
c) Artificial heart value replacement
d) Myocardial infraction
e) Rheumatic fever
TFTFT

179. Familial adenomatous polyposis-


a) Is an autosomal recessive disorder
b) Is known as Lynch syndrome
c) Leads to adenocarcinoma in untreated case
d) Is diagnosed by detection of 100 polyps in the colon
e) May develop due to new mutation in germline
FFTTT

Information desk:
Features of FAP-
 Autosomal dominant inherited disease due to mutations of the APC gene on the long arm of chromosome
5.
 FAP is consequently equally likely in men and women.
 Polyps are usually visible on sigmoidoscopy by the age of 15 years and will almost always be visible by the
age of 30 years.
 If the diagnosis is made during adolescence, surgery is usually deferred to the age of 17 or 18 years unless
symptoms develop.
 Malignant change is unusual before the age of 20 years.
 More than 100 colonic adenomas are diagnostic.
 Prophylactic surgery is indicated to prevent colorectal cancer.
 Polyps and malignant tumours can develop particularly around the duodenal ampulla.
[Ref: Bailey & Love’s/28th/P-1356-1357]
180. Causes of acute retention of urine are-
a) Hematuria
b) Diabetic cystopathy
c) Hypertensive nephropathy
d) Sacral cord (S2-4) injury
e) Pelvic fracture rupturing the urethra
FFFTT

Information desk:
The most frequent causes of acute retention
Male-
 Bladder outlet obstruction (the most common  Acute urethritis or prostatitis
cause)  Phimosis
 Urethral stricture
Female-
 Retroverted gravid uterus  Bladder neck obstruction (rare)
Both-
 Blood clot  Faecal impaction
 Urethral calculus  Anal pain (haemorrhoidectomy)
 Rupture of the urethra  Intensive postoperative analgesic treatment
 Neurogenic (injury or disease of the spinal cord)  Some drugs- anticholinergics, antidepressants
 Smooth muscle cell dysfunction associated with  Spinal anaesthesia
aging
[Ref: Bailey & Love’s/28th/P-1527]

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SBA
181. Which of the following is not branch of the int. carotid artery?
a) Ant. cerebral artery
b) Middle cerebral artery
c) Posterior cerebral artery
d) Posterior communicating artery
e) Ophthalmic artery
C
Explanation:
1. Post cerebral artery is the branch of basilar artery
[Ref: Vishram Singh/3rd/V-3/P-74]

182. Most constricted part of urogenital system?


a) Membraneus urethra
b) Bulbar urethra
c) Prostatic urethra
d) External urethral meatus
e) Navicular fossa
D
[Ref: Vishram Singh/2rd/V-2/P-250]

183. Most superficial and strongest dorsiflexor of the foot?


a) Tibialis anterior
b) EHL
c) Flexor halucis longus
d) Tibialis posterior
e) Extensor digitorum brevis
A
[Ref: Vishram Singh/2rd/V-2/P-399]

184. A 14-year-old girl presented to emergency with severe upper abdominal pain for one day. Her serum amylase
level is 2620 U/L and plasma appears milky. Lead in: Which of the following lipoprotein particles are most likely
responsible for the appearance of her plasma?
a) Chylomicrons
b) Very-low-density lipoproteins
c) Intermediate density lipoproteins
d) Low-density lipoproteins
e) High-density lipoproteins
A
Information desk:
 Plasma cholesterol and TGs are clinically important because they are major treatable risk factors for
cardiovascular disease, while severe hypertriglyceridaemia also predisposes to acute pancreatitis.
[Ref: Davidson’s/24th/P-635]
 CM & VLDL are TAG rich. LDL and HDL are cholesterol rich. Chylomicron (CM) is composed of lipid 98%
and apoprotein 2% and VLDL is composed of lipid 92% and apoprotein 8%.
 90% of lipid core of CM is TAG (Triacylglycerol or triglyceride) and 80% of lipid core of VLDL is TAG.
[Ref: ABC of Medical Biochemistry/8th/P-245-246]
* Plasma appears milky- this statement also gives us a clue that here in plasma chylous portion is more so
CM/chylomicrons is the suitable answer.

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185. A 65-year-old woman was admitted to the hospital with extensive third degree burns. Three days later, she
became febrile and there was pus on the dressing that had a blue-green color. Gram stain of the pus revealed
gram negative bacilli. Lead in: The most likely bacteria causing her burn wound infection is-
a) Escherichia coli
b) Proteus mirabilis
c) Pseudomonas aeruginosa
d) Streptococcus pyogenes
e) Staphylococcus aureus
C
Explanation:
 Pseudomonas aeruginosa
[Ref: Lange/17th/P-157]
186. HIV is a virus that attacks the body's immune system, specifically T cells (CD4 cell) and leads to AIDs. If left
untreated, HIV weakens the immune system, making the individual more susceptible to other infections and
diseases. Lead in: What will be the most common long-term complications of HIV infection?
a) HIV associated dementia
b) Bone loss and osteoporosis Information desk:
c) Opportunistic infection  HIV is a neurotropic virus & invades the CNS early
d) Cardiovascular disease during infection. HIV associated dementia is a
e) Mental health disturbance subcortical dementia characterised by impairment
A of executive function, psychomotor retardation. &
impaired memory. There is no diagnostic test for
Explanation: HIV associated dementia. CT or MRI shows diffuse
 HIV associated dementia cerebral atrophy out of keeping with age.
[Ref: Davidson’s/24th/P-362]
187. Lichen sclerosis is associated with which of the following neoplasm?
a) Mesothelioma
b) Colorectal carcinoma
c) Vulvar squamous cell carcinoma
d) MALT lymphoma
e) Pancreatic carcinoma
C
[Ref: Robbin’s/10th/P-281]
188. Parkinson’s disease is strongly associated with-
a) Nieman pick disease type A
b) Nieman pick disease type B
c) Tay sachs disease
d) Gaucher’s disease
e) Glycogen storage disease
D
[Ref: Robbin’s/10th/P-160]
189. An antibiotic resistant plasmid enters a Pseudomonas aeruginosa cell. This plasmid carries a β-lactamase
gene and an aminoglycoside phosphotransterase gene. Lead in: Which one of the following wound be an effective
antimicrobial agent against this bacterial cell?
a) Ampicillin
Information desk:
b) Cephalexin
c) Gentamicin There are specific agents for pseudomonal inf-
1. Penicillin- Carbenicillin, Ticarcillin, Azolocillin,
d) Neomycin
e) Tetracycline Meztocillin, Ureidopenicillin, Carboxy penicillin
C 2. Cephalosporin- Ceflazidim, Cefoperazone, Celepine,
Cefpirome (4th gen)
3. Carbapenem- Meropenem, Imiperem
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Explanation: 4. Amynoglycoside- Tobramicin, Amikacin, Gentamicin
 Gentamicin is an anti-pseudomonal agent. 5. Quinolone- Fluroquinolone
6. Colistin
190. Central vision is assessed by-
a) Snellen's chart
b) Ishihara chart
c) Perimeter
d) Tangent screen
e) Slit lamp
D
[Ref: Ganong/26th/Fig-10.1]
191. Stimuli that increase gastrin secretion-
a) VIP
b) Somatostatin
c) Calcium
d) GIP
e) Glucagon
C
[Ref: Ganong/26th/T-25.4]
192. During the depolarization of haircells in organ of Corti, all the following events occur. Lead in: Which one is
the leading event?
a) Ca+ influx Information desk:
b) K+ influx  The leading event during depolarization of hair cells in
c) Movement of myosin based molecular motor in the organ of Corti is the movement of myosin-based
taller stereocilia molecular motors in taller stereocilia, which causes the
d) Pushing of shorter stereocilia to the taller one stereocilia to pivot around their insertion points and
e) Releasing tension in the tip link results in the opening of mechanically gated ion
C channels. This event is responsible for initiating the
[Ref: Guyton’s/14th/P-667] transduction of mechanical signals into electrical
signals, which ultimately leads to the generation of
action potentials in the auditory nerve fibers. The other
events listed, such as Ca2+ influx, K+ influx, pushing of
shorter stereocilia to the taller one, and releasing
tension in the tip link, are all consequences of this initial
movement of the stereocilia.
193. Which of the following drug of choice of septic shock?
a) Adrenaline
b) Dopamine
c) Nor-adrenaline
d) Dobutmine
e) Digoxin
C
[Ref: Bailey & Love’s/27th/P-15]
194. A 34 years old lady presented to bleeding from posterior gastric ulcer. Which of the following origin bleed?
a) Gastroduodenal artery
b) Celiac trunk
c) Splenic artery
d) Common hepatic artery
e) Left gastric artery
C

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Explanation:
 Duodenal ulcer → Gastrodeudenal artery
 Post gastric → Splenic artery
[Ref: Bailey & Love’s/28th/P-1159]
195. Which of the following most common hematological indication of splenectomy?
a) Heriditary spherocytosis
b) IIP
c) Thalassaemia
d) Sickle cell anaemia
e) Hypersplenism
A
[Ref: Bailey & Love’s/28th/B-70.2./P-1229]
196. A 47 years old male attacked in left ant descending block. In CABG operation which of the following is the
choice of graft?
a) Great saphaneous vein
b) Short saphaneous vein
c) Radial artery
d) Int. thoracic artery
e) Femoral vein
D
[Ref: Bailey & Love’s/28th/P-950]
197. Rt. sided disc herniation at the level of L5/S1 may cause-
a) Left sided sciatica
b) Weak dorsiflexion of rt. Foot
c) Diminished ankle jerk
d) Decreased sensation over medial aspect of lt. foot
e) Difficult heel walk
C
[Ref: Davidson’s/24th/P-1140 & Netter/4th/P-62]
198. Most common site of impacted ureteric stone?
a) Uretero-pelvic junction
b) Crossing the illiac artery
c) Juxtraposition of VD or broad ligament
d) Vescico ureteric junction
e) Trigone of UB
D
[Ref: Bailey & Love’s/27th/B-76.10/P-1407]
199. Most common malignancy that metastasize to spine in female?
a) Prostate
b) Lung
c) Breast
d) Thyroid
e) Colon
C
[Ref: Bailey & Love’s/28th/B-37.10/P-516]
200. Most common site of ectopic testis?
a) Superficial perineal pouch
b) Superficial inguinal pouch
c) Root of penis
d) Femoral triangle
e) Under the skin of front of thigh
B
[Ref: SRB’s/6th/Fig-26.193/P-1068 & BD/8th/P-2]

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