1

Dear Colleagues
There is some problem in the hard copy of explanatory answer of Pathology Questions of subject wise
test held on 8/6/2014. It was the totally fault of the printer who committed in mistake by wrongly binding
the answer key. So here is the correct explanation of question 35 to 41 is there. Inconvenience caused is
highly regretted. Dr. Bhatia

Correct explanatory answers of pathology subject wise test held on 8/6/2014.
Question no 35 to 41

35. Ans. B.1t is bilateral and symmetrical (Ref. Robbins, 8th edition, page 733,734)
Malignant mesothelioma in thorax arises from either visceral or parietal pleura. Their is increased incidence among people with heavy
exposure to asbestos. There is a long latent period of 25 to 45 years so usually seen in late adulthood or middle age group.
Malignant mesothelioma is a diffuse lesion that spreads widely in pleural space & is usually associated with extensive pleural effusion &
direct invasion of thoracic structure hence it is more of diffuse nature rather being bilateral & symmetrical.
Microscopically Malignant mesothelioma may be epithelioid (60%),Sarcomatoid (20%) or can be mixed i.e biphasic histology seen.

36. Ans. D. Apoptosis (Ref. Robins 7th /27)
Apoptosis is a form of programmed cell death in multicellular organisms.
a. The activation of the caspase cascade is the most central step in apoptosis. Caspases can initiate apoptotic signals (caspases-8 and -9)
and execute the apoptotic program (caspases-3, 6, 7).
b. The fundamental event in apoptosis is the activation of enzymes called caspases (so named because they are cysteine proteases that
cleave proteins after aspartic residues).
c. Activated caspases cleave numerous targets, culminating in activation of nucleases that degrade DNA and other enzymes that
presumably destroy nucleoproteins and cytokeletal proteins.
d. The activation of caspases depends on a finely tuned balance between pro- and anti-apoptotic molecular pathways.
e. Two distinct pathways converge on caspase activation, called
i. the mitochondrial pathway and
ii. the death receptor pathway.
f. Although these pathways can interact, they are generally induced under different conditions, involve different molecules, and serve
distinct roles in physiology and disease
Bcl-2 is the prototype for a family of mammalian genes and the proteins they produce. They govern mitochondrial outer membrane
permeabilization (MOMP) and can be either pro-apoptotic (Bax, BAD, Bak and Bok among others) or anti-apoptotic (including Bcl-2 proper,
Bcl-xL, and Bcl-w, among an assortment of others). There are a total of 25 genes in the Bcl-2 family known to date. Bcl-2 derives its name
from B-cell lymphoma 2, as it is the second member of a range of proteins initially described as a reciprocal gene translocation in
chromosomes 14 and 18 in follicular lymphomas.
Caspases are essential in cells for apoptosis, one of the main types of programmed cell death in development and most other stages of
adult life, and have been termed "executioner" proteins for their roles in the cell.

37. Ans. A. PAS(Ref. Ananathanarayan microbiology 7th ed. 611)
FUNGAL STAINS
Gomori methenamine silver (GMS), Gridley's fungus (GF), and periodic acid-Schiff (PAS) are special for and very efficient to visualize the
fungi. Among these three, GMS is more advantageous since it stains old and nonviable fungal elements more efficiently than the other two.
Hematoxylin and eosin (H&E) stain, on the other hand, is very useful to visualize the host's response but is not a special fungal stain. It does
not stain most of the fungi, except the Aspergillus spp. and the zygomycetes. Thus, a combination of GMS and H&E is usually employed to
visualize both the tissue reaction and the infecting fungus.
Mucin stains, like Mayer's mucicarmine, Southgate's mucicarmine and Alcian blue, stain the mucopolysaccharide capsule of Cryptococcus
neoformans.
However, they are not specific for this particular fungus. Blastomyces dermatitidis and Rhinosporidium seeberi may also be stained with the
mucin stains.
2
The most reliable method of diagnosis is culture. Specimens are streaked on inhibitory mold agar or Sabouraud's agar containing
antibacterial antibiotics and incubated at 2530 C. The identification is confirmed by growth at 35 C and conversion to the yeast form.
a. Periodic acid-Schiff reactive (PAS) method or reaction: This method is principally used to demonstrate structures rich in
polysaccharides (glycogen), mucopolysaccharides (e.g., ground substance of connective tissues, basement membrane, and mucus),
glycoproteins (thyroglobulin), and glycolipids. It is also used as fungal stain in tissue biopsies.
b. Masson's trichrome method or stain: Bouin's is the recommended fixative, Orth's (formalin-Mller), Zenker's, or formalin in alcohol
may be used. Dyes and solutions used are hematoxylin, acid fuchsin, phosphotungstic acid, and light green. Several modifications of
this method are available. Nuclei stain dark blue / purple; cytoplasm and neuroglial fibers, red; collagen in connective tissue, green /
light blue.
c. Alizarin red S/ alizarin water-soluble red / sodium alizarin sulfonate: a yellow-brown or orange-yellow powder used as a stain in
microscopy, as a reagent for aluminum, as an acid-base indicator, and in the determination of fluorine

38. Ans. A. CD1a (Ref. Robins pathology 7th/Figure 25-18)
- At least five CD1 genes (CD1a, b, c, d, and e) are identified. CD1 is expressed on cortical thymocytes, Langerhans cells, and dendritic cells.
It is absent on mature peripheral blood T cells but intracytoplasmic expression is detected on activated T lymphocytes.
CD1 proteins have been demonstrated to restrict T-cell response to non-peptide lipid and glycolipid antigens and play a role in non-classical
antigen presentation.

PULMONARY HISTIOCYTOSISX
- It is also known as eosinophilic granuloma or pulmonary Langerhans' cell granulomatosis.
- It is an uncommon interstitial lung disease that primarily affects young adults between 20 to 40 years of age.
- The identification of Pentalaminar X bodies (Birbeck granules) is considered to be diagnostic.
- The natural history of PHX is quite variable, with some patients experiencing spontaneous remission of the symptoms and others
progressing to end-stage fibroting lung disease.
Surface 1-A molecules (i.e., murine MHC class II molecules; refs. 1 and 2), membrane-associated enzymatic activities to hydrolyze
extracellular ATP (ecto-ATPase), and rod/tennis racketshaped intracellular organelles (Birbeck granules) are important markers of LCs.
More specific markers, such as CD1a, E-cadherin, and langerin, are now known to distinguish LCs from other DC subsets.
Rx:
- Corticosteroid and cytotoxic agents are of limited value in the treatment of this disorder.
- High dose MTX can be useful.
- Lung transplant should be considered for patients who progress to end-stage lung fibrosis.

Immunohistochemical Stains Useful in detecting neoplasms
Tissue Marker Diagnosis
1 Estrogen and progesterone receptors Breast cancer
2 BRST-1 Breast cancer
3 Gross cystic disease fibrous protein-15 Breast cancer
4 Thyroid transcription factor 1 Lung and thyroid cancer
5 Thyroglobulin Thyroid cancer
6 Chromogranin, synaptophysin, neuron specific enolase Neuroendocrine cancer
7 CDX-2 Gastrointestinal cancer
8 Calretinin, mesothelin Mesothelioma
9 Leukocyte common antigen Lymphoma
10 S-100, HMB-45 Melanoma
11 URO-III, thrombomodulin Bladder cancer
12 -Fetoprotein Hepatocellular cancer,
Germ cell cancer,
Hepatoblastoma
13 -Human chronic gonadotropin Germ cell cancer
14 Prostate specific antigen Prostate cancer
15 Cytokeratin Carcinomas

3
39. Ans. C. Burkitt lymphoma (Ref. Robins pathology 7th/500; 677; TABLE 10-10; Table 12-8.)
Tumor Type Genetic Markers Other Diagnostically Useful
Features
Neuroblastoma 17q gain, * 1p deletion * Clinical elevation in level of urinary
catecholamines

Q
N-myc amplification * Neurosecretory granules by
electron microscopy

Q
DNA hyperdiploidy, near triploidy Neuron-specific enolase expression
t(11;22), t(21;22), t(7;22) MIC2 (CD99) gene expression
EWS-FLI1 or EWS-ERG fusion transcript
Rhabdomyosarcoma t(2;13), * t(1;13)alveolar rhabdomyosarcoma
(ARMS)
Myogenin and Myo D1 expression
(all subtypes)
11p15.5 deletionembryonal rhabdomyosarcoma
(ERMS)
Alternating thick and thin filaments
by electron microscopy
PAX3-FKHR and PAX7-FKHR fusion transcript (ARMS)
Burkitt lymphoma
Q
t(8;14) ------most common,
t(2;8),
t (8;22)
B-cell phenotype expressing CD19,
CD20, CD10, IgM
Q

Epstein-Barr virus latent infection
(endemic cases)
Lymphoblastic
lymphoma/ acute
lymphoblastic
leukemia
Hyperdiploidy (>50),
Hypodiploidy(<46) *
Terminal deoxynucleotidyl
transferase (TdT)+
Q

B-lineage: various translocations, including t(12;21)
(TEL-AML1), , t (9;22) (BCR-ABL, Philadelphia
chromosome), * t(4;11) (AF4-MLL) * , t (1;19) (PBX-
E2A) T-lineage: 1p32 abnormalities (TAL1 gene)
Various B- and T-lineage antigens
Wilms tumor 11p13 (WT1) deletion/mutation
Q

11p15.5 abnormalities of imprinting (e.g., IGF2, H19, p57KIP2 )
16q, * 1p, * 7p deletion
Retinoblastoma 13q14 (RB) deletion/mutation Retinal S antigen expression
Medulloblastoma 17p deletion Evidence of neuronal differentiation
(synaptophysin expression) or glial
differentiation (glial fibrillary acid
protein [GFAP] expression)

40. Ans. C. t(x ; 18 )
LIST OF THE MOST IMPORTANT TRANSLOCATIONSIN PECULIAR CONDITIONS:\
TRANSLOCATION SEEN IN
t (8 ; 14) Burkitts lymphoma
ALL FAB Type L3
Immunoblastic B cell lymphoma
t (11;14) Mantle cell lymphoma
CLL
Multiple myeloma
t (14;18) Follicular lymphoma and some B cell lymphomas
t (15;17) Promyelocytic leukemia M3
t (4;11) ALL FAB : L1, L2 =Pre B ALL
t (6;14) Cystadenocarcinoma of Ovary
4
t (3;8) Renal adenocarcinoma
Mixed parotid tumour
t (8;21) AML with maturation M2
t (11;22) Desmoplastic Small Round Cell Tumours (DSRCTs):
Classical Ewings sarcoma
PNET
Askins tumour
t (12;22) Clear cell sarcoma
Malignant melanoma of soft tissues
t (12;16) Myxoid liposarcoma
t (2;13) Alveolar rhabdomyosarcoma
t (x;18) Synovial cell sarcoma
t (11;18) MALToma
t (14;15) CLL / SLL
t (9;22) CML and Pre B ALL
t (9;22, t (4;11) and t (1;19) Pre B ALL
t (8;14), t (8;22) and t (2;8) B cell ALL
t (2;5) CD30 +ve Anaplastic large cell lymphoma
t (9;14) Lymphoplasmacytoid lymphoma
t (8;14) and t (10;14) T cell ALL
t (10;17) Papillary thyroid carcinoma

41. Ans. C. Glycosyl phosphatidyl inositol (GPI)
(Ref. Kumar & Clark 6th/452; Robbins pathology 6th ed. 636; Fig. 13-16; Harrison-17th -661; Harper 27th-440)
The underlying defect is an inability of PNH cells to make glycosylphosphatidylinosi tol (GPI), which anchors surface proteins such as decay
accelerating factor (DAF; CD55) and membrane inhibitor of reactive lysis (MIRL; CD59) to cell membranes. CD55 and CD59 and other
proteins are involved in complement degradation (at the C3 and C5 levels), and in their absence the haemolytic action of complement
continues. The molecular basis of PNH has been found to be mutations in the pig-A (phosphatidylinositol glycan protein A) gene responsible
for synthesis of the GPI anchor.