Questions from Positive in AIIMS

Dear Doctors,

Greetings from POSITIVE. By this time the ‘AIIMS-Fever’ would have subsided. Successful guys would have settled by now in the prestigious institute. POSITIVE’S best wishes and congratulations to all those successful candidates.Guys who couldn’t make it, will be (must be) horning their skills for the next battle-ALL INDIA-2008.

At this juncture, we at POSITIVE, did a microscopic audit of the performance of POSITIVE this year, keeping AIIMS-NOV-2007 as the Gold standard.We were very pleased to know that around 150 questions from AIIMS-NOV-2007,has been discussed in the various programmes at POSITIVE,which by any yard stick is a decent performance. As Evidence based medicine is the current concept, we have provided the evidences for our claim.

A question from AIIMS-NOV-2007 will be followed by the evidence from POSITIVE-the programme in which the concerned question was discussed. We have divided POSITIVE’s programmes as follows-a)MKM-Must Know MCQS-direct,indirect(22) b)POSITIVE model examinations,pretest,PICU-POSITIVE Intensive Care UNIT(14) c)OPERATION HARRI (62),d)Consultant’s discussion(55),MKT-Must Know Table(9)

HAPPY NEW YEAR GREETINGS TO YOU AND YOUR FAMILY FROM THE ‘‘POSITIVE’’ FAMILY.

POSITIVE’s advanced congratulations for the candidates who are putting up a sincere effort for ALL INDIA-2008.

A POSITIVE request for the next few months from the candidates preparing for the entrance examinations-
  • EAT MCQ,
  • DRINK MCQ,
  • SLEEP MCQ.
With warm regards
POSITIVE


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‘POSITIVE REVIEW’ AIIMS NOV-2007

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MKT

12. Urothelium does not line: [AIIMS-NOV-2007]

a. Collecting ducts
b. Minor calyx
c. Ureter
d. Urinary bladder

MKT Session-1

(8-04-07 EMBRYOLOGY,HISTOLOGY

38. Which of the following is correctly matched: [AIIMS-NOV-2007]

a. B cells – Somatostain
b. D cells – Insulin
c. G cells – Gastrin
d. …..

MKT-Session-1 (8-04-07)

11. Principal enteroendocrine cells in the gastrointestinal tract.

Cell Type and Location

Hormone Produced

A-stomach

Glucagon

G-pylorus

Gastrin(AIIMS-NOV-2007***)

S-small intestine

Secretin

K-small intestine

Gastric inhibitory polypeptide

L-small intestine

Glucagon-like substance (glicentin)

I-small intestine

Cholecystokinin

D-pylorus, duodenum

Somatostatin

Mo-small intestine

Motilin

EC-digestive tract

Serotonin, substance P

D1-digestive tract

Vasoactive intestinal polypeptide




132. A patient presents with hyperparathyroidism. He has a family history of his siblings having pituitary involvement, thyroid nodules, pancreatic involvement, parathyroid hyperplasia and cutaneous angiofibromas. Most likely diagnosis: [AIIMS-NOV-2007]

a. MEN 1
b. MEN 2A
c. MEN 2B
d. MEN 2C

MKT-POSITIVE SESSION

(Also in OPERATION HRRI-P-2231)

2. Multiple endocrine neoplasia (MEN)

Type

Genetic locus

Gland affected

Men – 1

Chromo some 11

Parathyroid hyperplasia / adenoma

Pancreatic islet cell hyperplasia/adenoma/carcinoma

Pituitary hyperplasia/adenoma;rarely carcinoid,pheochromocytoma, lipomata

MEN II (also known as “MEN IIA”

Chromosome 10

Medullary thyroid carcinoma

Pheochromocytoma (bilateral in 50%)

Parathyroid hyperplasia/adenoma;rarely cutaneous lichen amyloidosis

MEN III (also known as ‘MEN IIB’

Chromosome 10

Medullary thyroid carcinoma

Pheochromocytoma (commonly bilateral)

Mucosal/gastrointestinal neuromas

Marfanoid features/thickened ‘bumpy’ lips

All syndromes display autosomal dominant inheritance. Genetic (DNA Polymorphism) testing identifies carriers of MEN II and MEN III with > 90% certainly

106. Hypercalcemia is caused by all except: [AIIMS-NOV-2007]

a. Loop diuretics
b. Lithium
c. Vitamin D intoxication
d. ..

MKT-POSITIVE SESSION

8. Causes of Hyper Calcaemia

With normal or elevated (i.e. inappropriate)PTH levels

K Primary or tertiary hyperparathyroidism

K Lithium-induced hyperparathyroidism

K Familial hypocalciuric hypercalcaemia

With low (i.e. suppressed)PTH levels

K Malignancy (e.g.lung, breast, renal, ovarian, colonic and thyroid carcinoma)

K Multiple myeloma

K Elevated 1, 25(OH)2 Vitamin D3 (e.g. intoxication or sarcoidosis)

K Thyrotoxicosis

K Paget’s disease with immobilisation

K Milk alkali syndrome

K Thiazide diuretics

K Addison’s disease

135. Fractional excretion of Na++ <>

a. Pre-renal azotemia
b. ATN
c. Intrinsic renal failure
d. Renal artery stenosis

MKT-POSITIVE SESSION

Urine chemistry in differential diagnosis of ARF

Urine

Prerenal acute renal failure*

Ischemic Intrinsic acute renal failure

Urine osmolality, Uosm (mOsm/kg H2O)

> 500

<>

Urine to plasma osmolality

> 1.5

<>

Urine specific gravity

> 1.018

<>

Plasma BUN : creatinine ratio

> 20

<>

Urinary urea nitrogen : plasma urea nitrogen ratio

> 8

<>

Urinary creatinine : plasma creatinine ratio

> 40

<>

Urinary Na+ concentration (mmol/L)

<>

> 20

Fractional excretion of Na+ (%)c(AIIMS-NOV-2007***)

<>

> 2

Renal failure index UNa/Ucr/Pcr

<1

>1

Urine sediment

Hyaline casts

Muddy brown granular casts

(Also in OPERATION HARRI)

71. SAFE strategy is recommended for: [AIIMS-NOV-2007]

a. Trachoma
b. Glaucoma
c. Diabetic retinopathy
d. Cataract

SAFE strategy for trachoma: MKT-POSITIVE-2007-OPHTHAL

- Surgery for trichiasis.
- Antibiotics
- Facial Cleanliness.
-Environmental improvement.

114. PAS does not stain: [AIIMS-NOV-2007]

a. Fungal cell wall
b. Basement membrane of bacteria
c. Glycogen
d. Lipids

MKT –POSITIVE SESSION

Table 5. Common Histochemical / Cytochemical Stains in Tumour Diagnosis.

SUBSTANCE

STAIN

1. Basement membrane lcollagen

* Periodic acid – Schiff (PAS)

* Reticulin

* Van Gieson

* Masson’s trichrome

2. Glycogen

* PAS with loss

3. Glycoproteins, glycolipids (epithelial origin)

* PAS with diastase persistence glycomucins

4. Acid mucin (mesenchymal origin)

* Alcian blue

5. Mucin (in general)

* Combined Alcian blue – PAS

6. Argyrophilic argentaffin granules

* Silver stains

7. Cross striations

* PTAH stain

8. Enzymes

* Myeloperoxidase

* Acid phosphatase

* Alkaline phosphatase

9. Nucleolar organizer regions (NORs)

* Colloidal silver stain

110. A 2-year old child presents with scattered lesions in the skull. Biopsy revealed Langerhans giant cells. Most commonly associated is: [AIIMS-NOV-2007]

a. CD1a
b. CD57
c. CD3
d. CD68

MKT - RADIOLOGY and ONCOLOGY

12. Leukocyte Differentiation Antigens (CDs)

CD

Hematolymphoid Cell Expressiona,b

Related functions or proteins

CD 1a,b,c

Thymomas, Langerhans cell histiocytosis(AIIMS NOV-2007****), Precursor T-LL/L (some)

Associated with b2- microglobulin

CD 2

Mastocytosis (some )

E rosette receptor LFA-3

CD 3

Mature T-cell neoplasms (many), Precursor T-LL/L(T-cell ALL); signal transduction

CD 4

Mature T-cell neoplasms (some)

HIV Gp 120 receptor; MHC-II receptor recognition

CD 5

CLL / SLL (many)

Mature T-cell neoplasms (many) Mantle cell lymphoma;

T proliferation, CD 72 ligand

CD 6

T activation

CD 7

Mature T-cell neoplasms (most), AML (Some)

IgM FcR; T and NK activation

CD 8

Mature T-cell neoplasms (some)

MHC-1 receptor

CD 9

Tetraspan, signal transduction

CD 10

Precursor B-LL/L (most); follicular lymphomas (most), Neutral endopeptidase

CD 11a

LFA – 1; mediates cell adhesion binds 1-CAM

CD 11b

C’3bi receptor, αM integrin chain of MAC – I complex

CD 11c

HCL ; Marginal zone B-cell lymphoma (some) AML (monoblastic & myelomonocytic)

C3bi, C3dg receptor; αX integrin chain, LFA α chain

CD w12

Unknown function

CD 13

Coronavirus receptor, inactivates peptides

CD 14

Lipopolysaccharide receptor Gp-1-linked

CD 15

HL

Lewisx, neutrophil adhesion and phagocytosis

CD 16a

Large granular lymphocyte proliferation (NK type)

Fcy R; signal transduction on NK and M

CD 16 b

Fcy R; Gp-1-linked; immune complex receptor

CDw17

Lactoceramide

CD 18

Integrin heterodimer with CD11, LFA-1

CD 19

Mature B-cell neoplasms (most), precursor B-LL/L

Modulates B responsiveness

CD 20

Mature B-cell neoplasms, Precursor B-LL/L (some);

HL (nodular lymphocyte predominance)

B activation and proliferation

CD 21

Follicular dendritic cell neoplasms (See CD 35);

C’ 3D RECEPTOR; EBV receptor; B activation/ proliferation

CD 22

Mature B-cell neoplasms

Mediates adhesion

CD 23

CLL/SLL (most)

Fc epsilon R; cytotoxicity by M & Eos

CD 24

Gp-1-linked; regulates B proliferation and differentiation

CD 25

HCL; HL (most) ALCL (most) Mastocytosis, adult T-cell leukemia/lymphoma; IL-2H

CD 30

ALCL ; HL

Ki-1 (Ber-H2) antigen; TNFR-like protein involved in T activation

CD 31

Platelet-endothelial cell adhesion molecule -1 (PECAM-1), Plat GpIIA

CD 32

Myeloid leukemias

Fcy R, regulates B

CD 33

AML (most) Precursor B – ll/l

Function unknown

CD 34

AML (most) Precursor B- & T-LL/L (some)

Possible role in stromal adhesion

CD 35

Follicular dendritic cell neoplasms

C’ 3b/C’4b receptor (see CD 21)

CD 36

Plat GpIIIb, Gp-IV; collagen, thrombospondin, and malaria receptor

CD 38

Plasma cell neoplasms, CLL/SLL

Leukocyte activation

CD 40

TNFR protein involved in B differentiation

CD 41

Acute megakaryoblastic leukemia

Plat Gp-IIb; fibrinogen & Von Willebrand’s factor receptor

CD 42 a–d

Gps IX, 1bα , 1bb , V respectively

C 43

Precursor & Mature T-cell neoplasms, CLL/SLL (some), Mantle cell lymphoma, AML

Leukocyte sialoglycoprotein, adhesion

CD 44

H-CAM, Lymphocyte homing receptor

CD 45

Leukocyte common antigen (LCA)

Signal transduction

CD 45 RA, RB, RC

45 RA:B – cell lymphomas, HL (nodular lymphocyte predominant):

Restricted LCA forms with exons A, B, or C

CD 45 RO

Mature T-cell neoplasms, B-cell lymphomas (some)

Restricted LCA forms without exons

CD 49

α Integrin chains; laminin, fibronectin & collagen receptors

CDw52

Campath-1:Target for C’-mediated lysis;

CD 54

--CAM-1: LFA ligand; rhinovirus & malaria receptor

CD 55

Decay accelerating factor; Gp-1-linked; deficiency leads to paroxysmal nocturnal hemoglobinuria (PNH)

CD 56

Subset of NK/T-cell lymphomas

N-CAM ; Gp-1-linked

CD 57

Subset of NK/T-cell lymphomas

CD 59

PNH (antigen lost in PNH)

Gp-1-linked ; bubds C8 abd C9, blocks membrane- attack comlex

CD 61

Acute megakaryoblastic leukemia

Plat GpIIb/IIIa; β3 integrin; dimer with CD 41 or CD 51

CD 66b,d

Carcinoembryonic antigen (CEA), biliary glycoprotein

CD 68

Histiocytes (most)(?-AIIMS-NOV-2007***) ; Mastocytosis

Endocytosis or lysosomal traffic

CD 72

CD 5 ligand, B-cell activation / proliferation

CD 77

Transmembrane signaling in apoptosis

CD 79a,b

CD 79a: Precursor B-LL/L, B-cell lymphomas, myeloma (some)

B-cell receptor complex signal transduction

CD 83

Marker for DC

CD 87

Urokinase plasminogen activator receptor

CD 88

Receptor for C’5a; cell activation, chemotaxis

CD 90

CD 34 proliferation inhibitor ; Gp-1-linked

CD 94

Regulates LFA-1 cytolytic activity

CD 96

CD7+ AML; T-activated increased late expression (TACTILE)

CD 99

Precursor B - & T- LL/L

Adhesion and signalling; erythrocyte rosetting

CD 100

Function unknown

CD 103

HCL; Enteropathy-type T-cell lymphoma

Human mucosal lymphocyte (HML-1)

CD 108

HL cell lines

CD 114 – 116

G-CSFR and GM-CSFR

CD 117

AML, Mastocytosis

Stem cell factor receptor ; c-kit protein

CD 121-132

IL – receptors

CD 138

Myeloma

Syndecan-1; extracellular matrix receptor

CD 140

Platelet-derived growth factor

CD 141

Thrombomodulin; down-regulates coagulation, thrombin receptor

CD 143

Angiotensin converting enzyme (ACE)

CD 148

Lost in carcinoma of breast bladder , liver

CD 154

TNF family; B cell help by T cells

CD 155

Polio virus receptor

CD 157

Bone marrow stromal antigen (BST-1)

CD 161

NK cell-mediated cytolytic activity

191. All of the following are causes of cicatrizing alopecia except: [AIIMS-NOV-2007]

a. Lichen planus
b. Discoid lupus erythematosus
c. Alopecia areata
d. Lupus vulgaris

MKT-POSITIVE –DERM SESSION

9. Simplified tool for the diagnosis of alopecia

Disease

Diffuse loss (non – scarring)

Telogen effluvium

Diffuse alopecia areata

Androgenic alopecia (men)

Androgenetic alopecia (women)

Systemic disease (thyroid, iron deficiency, systemic lupus erythematosus, dermatomyositis)

Patchy loss (scarring)

Lichen planopilaris

Discoid lupus erythematosus

Folliculitis decalvans

Pseudopelade

Follicular degeneration syndrome

Patchy loss (non-scarring)

Alopecia localized

Tinea capitis

Traction alopecia

Trichotillomania

Syphilis

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