Which of the following is a peroxisomal free radical scavenger a. ...... Peptide binding cleft is formed by alpha 1 and
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m .c o DISCLAIMER
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The questions presented in this book is copyrighted to the Publisher and are based upon the topics which have been most frequently asked in Pre PG Medical entrance examinations throughout the world. We don’t claim the material and question present in this book to be the exactly same, duplicated or reproduced from any examination conducted by any Board or Authority, statutory or non statutory in India or outside India. We declare that this book is neither sponsored nor related to any board or authority of Government (statutory or non statutory). The questions in this book are purely the work of our team, however medical science is a generic knowledge and creating similar material by authors is not uncommon. Any resemblance to them is purely a coincidence and by chance. Copying and reproducing any of the material of this book in any form completely or partially is prohibited under copyright act and is binding by law.
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KALAM BOOKS
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© Publisher 2016 October 2016 First Edition
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ISBN 978 81 89477 33 2
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CONTENTS Anatomy Question & Answers
1
2.
Physiology Question & Answers
49
3.
Biochemistry Question & Answers
97
4.
Forensic Medicine Question & Answers
159
5.
Microbiology Question & Answers
183
6.
Pathology Question & Answers
255
7.
Pharmacology Question & Answers
8.
PSM Question & Answers
9.
ENT Question & Answers
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1.
327 359 395
10. Ophthalmology Question & Answers
421
11. Medicine Question & Answers
465
12. Surgery Question & Answers
515
13. Obstetrics & Gynaecology Question & Answers
555
14. Paediatrics Question & Answers
601
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15. Anaesthesia Question & Answers
659 693
17. Radiology Question & Answers
715
18. Orthopaedics Question & Answers
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16. Dermatology Question & Answers
19. Psychiatry Question & Answers
783
IMAGE Based Question & Answers
pg
20. Anatomy Image based Question & Answers
819
21. Physiology Image based Question & Answers
830
22. Biochemistry Image based Question & Answers
837
23. Forensic Medicine Image based Question & Answers
852
24. Microbiology Image based Question & Answers
858
25. Pathology Image based Question & Answers
870
26. Pharmacology Image based Question & Answers
896
27. PSM Image based Question & Answers
904
28. ENT Image based Question & Answers
913
29. Ophthalmology Image based Question & Answers
920
30. Medicine Image based Question & Answers
938
31. Surgery Image based Question & Answers
947
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32. Obstetrics & Gynaecology Image based Question & Answers
959
33. Paediatrics Image based Question & Answers
968
34. Anaesthesia Image based Question & Answers
973
35. Dermatology Image based Question & Answers
985
36. Radiology Image based Question & Answers
997 1005
38. Psychiatry Image based Question & Answers
1015
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37. Orthopaedics Image based Question & Answers
PATHOLOGY Pathology : Questions & Answers |
1.
Cause for caseous necrosis in TB is a. Hydrolytic enzymes b. Mycolic acid
c. High lipid content d. Hydrophobic changes by bacterial wall
Which of the following is a reversible procedure ? a. Pyknosis c. Karyolysis b. Karyorrhexis d. Swelling of endoplasmic reticulum
3.
Which of the following prevents memory B cells from apoptosis a. PDGF c. Insulin like growth factor b. Nerve growth factor d. Fibroblast growth factor
4.
Which of the following is an antiapoptotic gene a. BAX c. BCL-XL b. BAD d. BIM
5.
SMAC/DIAMBLO is a a. Anti apoptotic protein b. Induces necrosis
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c. Acts both as anti and pro apoptotic protein d. Pro-apoptotic protein
Which of the following is a peroxisomal free radical scavenger a. Superoxide dismutase c. Catalase b. Gluthathione peroxidise d. All of the above
7.
Organelle where H2O2 is produced and destroyed is a. Peroxisome c. Golgi body b. Lysosome d. Ribosome
8.
Integrin is associated with all except a. Rolling b. Adhesion
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9.
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c. Arrest d. Transmigration
Eosinophils secrete all of the following except a. Major basic protein c. Hydrolytic enzyme b. Eosinophilic chemotactic factor d. Reactive form of O2
10. Resolution of inflammation is caused by a. TNF alpha, IL-1 AND CRP c. TGF beta, IL-1 receptor antagonist and IL-10 b. TNF alpha, IL-6 AND CRP d. TNF – Gamma
11. Which of the following secretes histamine a. Eosinophil c. Neutrophil b. Basophil d. Monocyte
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12. Factor present in final common terminal complement pathway is a. C4 c. C3 b. C5 d. Protein B 13. Oval cells are seen in a. Skin b. Cornea
c. Liver d. Bone
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14. At what stage neutrophil appears in peripheral blood a. Myeoloblast c. Myelocyte b. Promyelocyte d. Band forms
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15. Which of the following does not secrete interleukin 1 alpha a. Lymphocyte c. Macrophage b. Monocyte d. Neutrophil 16. Which of the following is not required for wound healing a. Zinc c. Copper b. Calcium d. Vitamin C
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17. The process of wound healing includes all of the following except a. Coagulation c. Angiogenesis b. Matrix synthesis d. Fibrolysis
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18. The inheritance pattern of familial retinoblastoma is a. Autosomal recessive c. X – linked recessive b. Autosomal dominant d. X-linked dominant 19. The pattern of inheritance of Retinitis pigmentosa are all except a. Autosomal recessive c. X – linked recessive b. Autosomal dominant d. X-linked dominant
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20. Angleman syndrome is due to a. Digenic inheritance b. Inversions
c. Uniparental disomy d. Mitochondrial disorder
21. Karyotyping of fetus can be done by all except a. Chorionic villus sampling c. Amniocentesis b. Cordocentesis d. Fetal skin biopsy 22. Which is not the karyotype of turners syndrome a. 46,XX, i(Xq) c. 46 XX, i(Xp) b. 45 XO d. 46 XX, r(X) 23. Most severe form of Ehler Danlos syndrome is a. Type 1 c. Type 4 b. Type 8 d. Type 2
Pathology : Questions & Answers |
c. Collagen d. Elastin
25. Multifactorial inheritance is known in a. Neurofibroma b. Haemophilia
c. Cardiac septal defects d. Hypophosphatemic rickets
26. Feulgen reaction is used to test a. mRNA b. tRNA
c. DNA d. All of the above
27. Microarray is used to a. Study multiple genes b. Study disease
c. Study organism d. Study blood group
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28. NK cells express a. CD 15, CD55 b. CD 16, CD 56
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24. In marfans syndrome defect is in a. Fibrillin I b. Fibrillin II
c. CD 16, CD58 d. CD21, CD66
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29. Toll like receptors are expressed in all except a. Macrophages c. B cells b. Dendritic cells d. T cells
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30. HLA B 27 is not seen in a. SLE b. Ankylosing spondylitis
31. Preformed antibodies cause a. Hyperacute rejection b. Acute rejection
c. B lymphocytes d. T helper cells c. Chronic rejection d. Acute humoral rejection
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32. Which of the following is not seen in extraglandular Sjogren disease a. Rheumatoid arthirits c. Lymphoma b. Raynaud phenomenon d. Splenomegaly 33. HIV can be detected and confirmed by a. PCR b. Immunochromatography
c. Fourth generation ELISA d. Western blot
34. Raji cell assays are used to quantitate a. Complement levels b. Immune complexes
c. T cells d. IFN levels
35. Amyloidosis most commonly affects a. Liver b. Tongue
c. Colon d. Heart
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36. The most reliable investigation for amyloidosis is a. Abdominal fat pad aspirate c. Urine examination b. USG d. Kidney biopsy 37.
Polycythemia is associated with a. Stomach cancer b. Liver cancer
c. Prostrate cancer d. Renal cell cancer
c. Leiomyosarcoma d. Retinoblastoma
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39. Arbiskov cells are seen in a. Myelobalstoma b. Neuroblastoma
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38. Which of the following is not a carcinogenic virus ? a. Hepatitis B c. Molluscum Contagiosum b. Hepatitis C d. HPV
40. Ectopic rest of tissue is known as a. Choristoma b. Hamartoma
c. Pseudo tumour d. Lymphoma
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41. Which of the following is a metastasis suppressor gene in relation to prostate cancer a. KAI -1 c. KISS b. NM 23 d. p53
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42. Most common paraneoplastic syndrome associated with lung cancer a. SIADH c. Hypercalcemia b. Cushings syndrome d. Polycythemia 43. Sentinel node biopsy for Ca breast is for a. Early diagnosis of cancer b. For staging the tumours
c. Frozen section d. Occult disease detection
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44. Deficiency of Vitamin D increases the risk of a. Colon cancer c. Breast cancer b. Prostate cancer d. All of the above
45. S100 is a marker used in the diagnosis of a. Melanoma c. LCH b. Schwannoma d. All of the above 46. Retinoblastoma gene regulates a. G1-S phase b. G2- M phase
c. G0 – S phase d. S- G2 phase
47. BRAF mutation is seen in 60% of cancers of a. Malignant melanoma c. Squamous cell carcinoma b. Basal cell carcinoma d. Teratoma
Pathology : Questions & Answers | 48. BRCA 1 gene is located in chromosome a. 17p21 b. 17q21
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c. 13p21 d. 13q21
49. Common site of hematopoiesis in fetus is a. Liver c. Bone marrow b. Spleen d. Gut c. Band protein d. Glycophorin C
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50. Shape of RBC is biconcave due to a. Ankyrin b. Spectrin
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51. Which property of haemoglobin is affected in sickle cell anemia a. Stability c. Affinity b. Function d. Solubility 52. NESTROFT test is used in the screening of a. Thalassemia c. Aplastic anemia b. AIHA d. G6PD deficiency
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53. Which of the following is most common haemoglobinopathy a. Thalassemia c. Haemoglobin C b. Sickle cell anemia d. None of the above
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54. Anemia of chronic disease is characterised by a. Increased sideroblast c. Increased bone marrow iron b. Increased TIBC d. Increased protoporphyrin 55. Earliest manifestation of megaloblastic anemia is a. Macrocytosis c. Basophilic stippling b. Hypersegmented neutrophils d. Cabot ring
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56. Which is the most common red cell defect without Hb abnormality a. Elliptocytosis c. Poikilocytosis b. Spherocytosis d. Sickle cell disease
57. All of the following red cell abnormality provides protection against malaria except a. G6PD deficiency c. Sickle cell anemia b. Thalassemia d. Acanthocytosis
58. Lacunar cells are seen in a. Lymphocyte predomninat HL b. Lymphocyte depleted HL
c. Nodular sclerosis d. Mixed cellularity
59. Mantle cell lymphoma shows a. CD 5+, CD 25 – b. CD5+, CD 10+
c. CD5+, CD 23+ d. CD5+, CD 23 –
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60. Poor prognostic factor for ALL is a. Female sex b. Leukocyte factor < 50,000
c. Age greater than 1 year d. Hypodiploidy
61. Plasmacytoid lymphomas may be associated with increase in a. IgG c. IgA b. IgM d. IgE c. T(15,17) d. T(8,14)
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62. Chromosomal translocation in CML is a. T(2,8) b. T(9,22)
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63. All of the following NHL involve the white pulp of spleen except a. Hairy cell leukemia c. Follicular lymphoma b. Burkitt lymphoma d. Mantle cell lymphoma 64. What is the ratio of kappa and lambda free light chains normally a. 7:3 c. 4:6 b. 6:4 d. 3:7 c. Macrophages d. Plasma cells
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65. Russel bodies are seen in a. Lymphocytes b. Monocytes
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66. Birbeck granules are seen in the cytoplasm of a. Mast cells c. Thrombocytes b. Langerhans cells d. Myelocytes 67. Dohle bodies are seen in a. Multiple myeloma b. May-hegglin anamoly
c. Waldenstrom macroglobulinemia d. Lymphoma
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68. Most common extranodal site for non–hodgkin lymphoma is a. Stomach c. Intestine b. Brain d. Tonsils 69. College girl appearance of leukocytes are seen in a. CLL c. ALL b. CML d. Hodgnkin lymphoma 70. Atheromatous plaque do not contain a. Platelets b. Neutrophils
c. Smooth muscle fibres d. Monocytes
71. All of the following conditions are associated with raised ANCA except a. Wegener granulomatosus c. Microscopic polyangitis b. Polyarteritis nodosa d. Churg strauss syndrome
Pathology : Questions & Answers | 72. Which vasculitis affects both areterial and venous system a. Wegeners granulomatosus c. Behcets disease b. PAN d. Kawsaki disease 73. Post MI 10th day which of the following enzyme level is raised a. LDH c. Troponin b. CPK d. Myoglobin
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74. Smoking is most commonly associated with which type of lung cancer a. Small cell cancer c. Adenocarcinoma b. Squamous cell carcinoma d. Carcinoid tumour
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75. Laminated concretions of calcium and proteins are a. Schaumann bodies c. Asteroid bodies b. Ferruginous bodies d. Gamma gandy bodies
c. Empyema d. Brochogenic carcinoma
77. Best marker for GIST is a. CD117 b. DOG-1
c. CD34 d. CD43
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76. Alpha-1 antitrypsin deficiency occurs in a. Emphysema b. Bronchiectasis
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78. True regarding crohns disease is all except a. Scleroderma c. Cobble stone appearance b. Transmural involvement d. Skin involvement 79. Gluten sensitive enteropathy is most strongly associated with a. HLA – DQ2 c. HLA DQ3 b. HLA DR4 d. Blood group B c. Increased pulmonary pressure d. Decreased pulmonary pressure
81. Increased Ig A levels are seen in a. Alcoholic hepatitis b. Alcoholic cirrhosis
c. Microvescicular fatty change d. Macrovesicular fatty change
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80. Nutmeg liver is seen in a. Right sided heart failure b. Left sided heart failure
82. Collagen accumulated in space of disse in case of liver cirrhosis are a. 1 and 4 c. 1 and 3 b. 2 and 4 d. 2 and 3 83. Most common type of bladder cancer is a. Squamous cell carcinoma b. Urothelial carcinoma
c. Adenocarcinoma d. Carcinoid
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84. Michalis Gutmann bodies are seen in a. Xanthogranulomatous pyelonephritis b. Malakoplakia
c. Nail patella syndrome d. Chronic pyelonephritis
85. Most common variant of RCC is a. Clear cell b. Papillary
c. Chromophobe d. Collecting duct
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86. An emerging viral pathogen causing pyelonephritis in kidney allograft recipients is a. Marburg virus c. JC virus b. Polyoma virus d. Ebola virus
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87. Most common gene associated with renal cell carcinoma is a. WT 1 c. VHL b. BRCA 1 d. PATCH
88. Hobnail pattern is seen in which type of RCC a. Clear cell c. Chromophobe b. Papillary d. Collecting duct
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89. Hepatic fibrosis is associated with which of the following a. Medullary cystic kidney c. ARPKD b. ADPKD d. Nephronopthosis
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90. Chromosome associated with ADPKD is a. 14 and 16 b. 14 and 13
c. 16 and 4 d. 16 and 14
c. Barter syndrome d. Giltleman syndrome
92. Papillary necrosis is seen in all except a. NSAID’s b. DM
c. Sickle cell anemia d. Shock
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91. ENaC mutation is associated with a. Liddle syndrome b. Gordon syndrome
93. Characteristic feature of benign nephrosclerosis is a. Leather grain appearance c. Onion skin appearance b. Flea bitten kidney d. Hyperplastic arteriosclerosis
94. Nodular glomerulosclerosis seen in a. DM b. Malignant hypertension
c. Amyloidosis d. Multiple Myeloma
95. Collapsing variant of FSGS is seen in a. HIV b. Heroin abuse
c. NSAID’s d. CMV
Pathology : Questions & Answers | 96. Most common nephropathy in the world is a. IgA nephropathy c. Minimal change disease b. FSGS d. Adult PSGN 97. Most common cause of nephrotic syndrome in children is a. Membranous GN c. Minimal change disease b. PSGN d. RPGN
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99. Type I RPGN is seen in a. SLE b. IgA nephropathy
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98. In thin basement membrane disease the defect is in a. Alpha 1 and Alpha 2 chains of type IV collagen b. Alpha 3 and Alpha 4 chains of type IV collagen c. Alpha 1 and Alpha 2 chains of type VI collagen d. Alpha 3 and Alpha 4 chains of type VI collagen
c. Henoch Schonlein purpura d. Good pasture syndrome
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100. True regarding IgA nephropathy is a. Usually seen in children 80%) – Moderate degree fever – Otitis media & mastoiditis may be seen – CNS involvement due to contiguous spread – Hematologic findings: Pancytopenia – Bone marrow: Infiltration by histiocytes Mutlifocal LCH – Multiple lesion involving multiple systems – Prognosis better than disseminated LCH – Fever & rash – Involvement of posterior pituitary- Diabetes insipidus – Typical Hand- Schuller Christian disease= Triad of exopthalmus+ diabetes insipidus+ calvarial defect Unifocal LCH • Focal lytic lesion in bone
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Excellent prognosis
Answer: b. May- Hegglin anomaly • Döhle bodies are oval basophilic leucocyte inclusion located peripherally in the cytoplasm of neutrophils. They are dilated endoplasmic reticulum. Seen in burns, infections, physical trauma, neoplastic diseases, May-Hegglin anomaly etc. • Multiple myeloma and Waldenstroms macroglobulinemia- Both are plasma cells dyscrasias. These plasma cells may have intracytoplasmic inclusion called as Russel bodies and intra nuclear inclusions called as Dutcher bodies.
68.
Answer: a. Stomach • Lymphomas are divided broadly into Hodgkins and Non hodgkins lymphomas. • Two thirds of Non Hodgkins lymphoma present as generalized lymphadenopathy(Nodal sites). • One third of the cases present at extranodal site. • Extra nodal sites include gastrointestinal tract, upper aero digestive tract, salivary glands, eye, mediastinum, lung, pleura, heart, spleen, liver etc. • The most common extranodal site is gastrointestinal tract, in which stomach is involved most often.
69.
Answer: b. CML • College girl appearance also called as garden party appearance is used in identification of a slide of CML because of the various sizes and configurations of WBC’S. • Convent girl appearance is seen in Chronic lymphocytic leukemia, because of the lymphocytes of same sizes and configurations.
70.
Answer: b. Neutrophils Ref: Robbins 8/e p502 The main components of atherosclerotic plaques are 1. Cells: Smooth muscle cells, monocytes/macrophages, T cells 2. Extracellular matrix: Collagen, elastic fibres, proteoglycans 3. Intra and extra cellular lipids
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67.
71.
Answer: b. Polyarteritis nodosa Ref: Robbins 8/e p511 Classification of vasculitis Large vessel vasculitis • Giant cell (temporal) arteritis – seen in >50yrs of age • Takayasu arteritis – seen in 5mm
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140. Answer: c. CDKN2A Ref: Robbins 8/e p1171 Melanoma • Most commonly arise from skin; but may also be seen in oral mucosa, anogenital mucosa, meninges, esophagus and eye • Any change in colour, shape or size of an already existing pigmented lesion should raise suspicion • Warning signs : ABC of melanoma (Asymmetry, irregular Borders and variegated Colours ) • Local spread : Radial growth followed by vertical growth • The tumour types that occur due to radial growth : Lentigo maligna (Indolent lesion), Superficial spreading (most common type, affect sun exposed areas) and acral/mucosal lentiginous melanoma (affect non sun exposed areas) • Pathogenesis : o Light pigmented skin and sun exposed skin areas – are at higher risk o MC1R, ASIP and TYR gene mutation – Involved in melanin production o Mutations of RB gene, CDKN2A (p14, p15, p16), CDK4, NRAS, BRAF, PI-3K/AKT, PTEN and c-KIT.
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| PG NEXT • Prognosis : o Tumour depth (Breslow thickness-distance between epidermal granular cell layer and deepest intradermal tumour cells o Number of mitosis o Evidence of tumour regression o Tumour infiltrating lymphocytes o Gender and Location
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141. Answer: a. Neuron Ref: Robbins 9/e p814 • Brain is a highly oxygen dependent tissue that requires a continous supply of oxygen and glucose. • Among all the cells in brain, neurons are most susceptible to hypoxia • Pyramidal cells of hippocampus and neocortex and purkinje cells of cerebellum – most susceptible neurons
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142. Answer: b. Intracytoplasmic inclusions Ref: Robbins 8/e p 1330 CNS tumours/ Intracranial tumours: Intracranial tumours include : Tumours of brain and meningeal tumours Most common intracranial tumour- Metastatic tumours Common primary sites of metastatic tumours to brain: Lung > Breast > Skin (melanoma) > Kidney > GIT Meningeal carcinomatosis – seen in carcinoma of lung and breast A rare tumour with a high chance of brain metastasis- Choriocarcinoma A common tumour which almost never invade brain – Prostatic adenocarcinoma Cells comprising CNS : Neurons Neuroglia or Glia – Includes astrocytes, oligodendrocytes and ependymal cells Microglia – Modified macrophages Meninges Brain tumours : 3 types – Neuronal tumours, glioma, embryonal tumours High grade tumours are aggressive, with increased risk of recurrence and distant metastasis.
Pathology : Questions & Answers |
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Classification of neuronal tumours WHO grade
Gangioglioma
I/II According to glial elements
Gangliocytoma
I
Dysembroplastic neuroepithelial tumour
I
Salient points Common neuronal tumour Common site : Temporal lobe (Hence patient present with seizures)
Common age group: Childhood Common site : Temporal lobe (seizures) Histology: Multiple nodules Cortical dysplasia Neurons floating in myxoid areas
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Neurons
Tumour type
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Cell of origin (Tumour)
Central Neurocytoma II
Common site : Lateral or third ventricles
Tumour type
WHO grade
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Classification of glial tumours (glioma) Common primary brain tumour in adults and children – Infiltrating astrocytoma The term “Infiltrating astrocytoma” includes diffuse astrocytoma, anaplastic astrocytoma and gliobalstoma Common site for primary brain tumours : Adults – Cerebrum Children – Posterior fossa
Pilocytic astrocytoma
I
Age group : children and young adults Common site : Cerebellum Gross : often cystic Histology : Well circumscribed, bipolar cells. Intracytoplasmic inclusionslike Rosenthal fibres and eosinophilic granular bodies (Rosenthal fibres composed of intermediate filaments like glial fibrillary acidic protein) Microcystic pattern Vascular proliferation seen
Diffuse astrocytoma
II
Histology : Infiltration to adjacent normal brain tissues
Anaplastic astrocytoma
III
Histology : Infiltration + nuclear pleomorphism + high mitosis
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Astrocytes
Salient points
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Ependymal cells
Grade III features + vascular proliferation called glomeruloid body + pseudopalisading necrosis
Oligodendroglioma II
Common site : cerebrum (mainly white mater) Histology : Perinuclear halo, calcification & tumour cells around normal neurons (perineuronal satellitosis)
Anaplastic III Oligodendroglioma
Features of oligodendroglioma +Increased cellularity, nuclear atypia, mitosis and necrosis
Ependymoma
Common site : Children- Fourth ventricle Adults - Spinal cord Histology : Ependymal rosettes, perivascular pseudorosettes
Myxopapillary Ependymoma Subependymoma
I
Common site : Filum terminale of the spinal cord
I
III
Features of ependymoma +high cellularity, nuclear atypia, high mitosis, vascular proliferation and necrosis
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Anaplastic ependymoma
II
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Oligodendroglia
IV
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Medulloblastoma A type of embryonal tumour , WHO grade IV Common age group : Children Common site : Cerebellum (Tumours of similar histology in cerebrum – “Supratentorial primitive neuroectodermal tumour” ) Highly malignant tumour Treatment : surgical excision and radiation Primary CNS lymphoma Common CNS neoplasm in immunocompromised individuals Mostly associated with Epstein-barr virus infections Common histologic type : Diffuse large B cell lymphoma Common brain tumour mutations Low grade astrocytoma : p53 mutation High grade astrocytoma : RB and p16 mutation Primary glioblastoma : MDM 2 mutation Secondary gliobalstoma (Glioblastoma arising from a low grade astrocytoma) : p53 mutation Oligodendroglioma : Loss of heterozygosity for chromosomes 1p and 19q Medulloblastoma : Loss of material from chromosome 17p
Pathology : Questions & Answers | Atypical teratoid/ Rhabdoid tumours (an embryonal tumour) Meningioma : Loss of chromosome 22
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: Chromosome 22
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CNS tumours with CSF spread “ As a rule any tumour arising from or close to ventricular system will show CSF spread” In addition a few high grade tumours will also show CSF spread. 1. Ependymal tumours 2. Medulloblastoma 3. Metastatic tumours 4. CNS lymphomas 5. Germ cell tumours 6. Pineoblastoma Rule of “M” CNS tumours with Multifocality – Metastasis Malignant lymphoma Melanoma Medulloblastoma (late stage only)
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Meningioma Cell of origin : Arachnoid cap cells High grade tumours are aggressive, having worse prognosis with increased risk of recurrence and distant metastasis. • Grade I meningiomas - Meningothelial, fibroblastic, transitional (shares features of both meningothelial and fibroblastic), psammomatous, secretory and microcystic types. Psammoma bodies can also be seen in meningothelial meningioma • Grade II meningiomas - Atypical, clear cell and chordoid meningiomas
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Criteria for atypical meningioma 4 or more mitosis /10 highpower fields Or atleast 3 atypical features (high cellularity, small cells with high Nuclear cytoplasmic ratio, prominent nucleoli, patternless growth and necrosis) • Grade III meningiomas – Anaplastic, papillary and rhabdoid Criteria for anaplastic meningioma >20 mitosis / 10 highpower fields
143. Answer: c. GFAP (Refer Q 142) 144. Answer:
a. Metastatic tumours (Refer Q 142)
145. Answer: c. Fibroblast Ref: Robbins 8/e p 1282 Neuroglia includes 3 types of cells namely astrocytes, oligodendrocytes & ependymal cells. • Brain injury of any kind (infection, inflammation or infarction) will cause acute swelling due to CSF accumulation. Resolution of this swelling is the first sign of
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• • • • • • • •
patient improvement. Some of these diseases will form liquefactive necrosis which are surrounded by proliferated astrocytes which is called reactive gliosis. Astrocytes – Supporting cell of neurons, form a part of blood brain barrier, proliferate in any injury. Oligodendrocytes – Produce myelin for nerves in central nervous system (Schwann cells – Cells that produce myelin in peripheral nervous system) Ependymal cells – Line the ventricular system Microglial cells – Scavenger cells that remove cellular debris from site of injury Fibroblasts – In CNS, fibroblasts are seen only in blood vessels supplying brain tissue. In CNS, fibroblasts does not have any role in healing and repair. Hence no scar will be formed in the brain. Whereas outside CNS, fibroblasts produce collagen which forms a scar.
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146. Answer: a. Sabre shin Ref: Robbins 8/e p374 Syphilis • Caused by Treponema pallidum. Usual mode of spread- Sexual contact • Three clinical stages : Primary , Secondary and tertiary. Primary syphilis • Occur 3 weeks after contact with infected individual • First clinical presentation: Chancre (single firm non tender raised lesion at the site of bacterial entry) • Chancre contains plenty of bacteria and lesion resolve within 3-6 weeks even without treatment • Remember, bacteria would have enter systemic circulation before appearance of chancre Secondary syphilis • Occur within 2-10 weeks after primary chancre. This stage is followed by a latent period • Patient present with maculopapular rash, condyloma lata (raised plagues in moist areas), superficial erosions, fever, lymphadenopathy and weight loss Tertiary syphilis • Rare. Occurs after a latent period of 5 years • Three manifestations- Cardiosyphilis, Neurosyphilis,Benign tertiary syphilis • Cardiovascular syphilis- Aortitis, aortic valve insufficiency and aneurysm of proximal aorta • Neurosyphilis – Meningovascular, tabes dorsalis, general paresis. Congenital syphilis • Hutchinson triad – Late manifestations of congenital syphilis • The triad include eighth nerve deafness, interstitial keratitis and Hutchinson teeth (screwdriver like small incisors).
147. Answer: b. CMV Ref: Sternberg 8/e p 353 The term “ Owl eye appearance” is used in the following 1. CMV inclusions 2. Reed Sternberg cells in Hodgkin lymphoma
Pathology : Questions & Answers |
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3. Giardia lamblia trophozoites 4. Anitschkow cells of Aschoff bodies in rheumatic heart disease Viral inclusions in the CentralNervous System Cell types
Disease conditions Herpes simplex Herpes zoster
+
_
Rabies
_
+
Subacute sclerosing panencephalitis (SSPE)
+
_
Progressive multifocal leucoencephalopathy
+
_
SSPE
+
_
Cytomegalovirus infection
+
+
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Oligodendrocytes
Cytoplasm
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Neurons
Nucleus
Various cells (Endothelial cells, ependymal & glial cells)
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148. Answer: d. Spinal cord and optic nerve Ref: Robbins 8/e p1305 Progressive multifocal leukoencephalopathy • Causative organism : JC polyoma virus • Disease of white matter which specifically targets oligodendrocytes. • The disease exclusively occurs in immunosuppressed individuals
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149. Answer: d. Subcortical leukoencephalopathy Ref: Greenberg clinical neurology 5/e Binswanger’s disease otherwise called as subcortical arteriosclerotic leukoencephalopathy 150. Answer: b. Spongiform change in brain Ref: Harrison 17/e p2647, Robbins 8/e p1308 Prion diseases: • A neurodegenerative disorder caused by misfolded proteins which are infectious and transmissible. • Abnormal protein: β-pleated sheet isoform of PrP protein (Normal counterpart: α-helix isoform of PrP protein) • Prion in humans: Creutzfeldt-Jakob disease Gerstmann-Straussler-Scheinker syndrome Fatal familial insomnia Kuru • Clinical presentation: Dementia, Myoclonus • Creutzfeldt-Jakob disease
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| PG NEXT – Sporadic – Transmission: Corneal transplant, deep implantation electrodes, Growth hormone extracted from affected humans - Histology : Spongiform changes, reactive gliosis & cerebral atrophy (late finding) Kuru – Common site : Cerebellum – Histology : Extracellular amyloid deposits
•
Gerstmann-Straussler-Scheinker syndrome – Histology : Amyloid angiopathy
•
Fatal familial insomnia – Familial, Mutation of PRNP gene which encodes PrP protein – Histology : Only prion disease where spongiform changes are absent
• •
Diagnostic tests : Western blotting after partial digestion by proteinase K Decontamination : Autoclaving at 134OC for 5 hrs or treatment with 2N NaOH for many hrs
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151. Answer: a. Narrowing of ventricles Ref: Harrison 18/e p3306, Robbins 8/e p1313
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Alzheimer disease Most common cause of dementia in the elderly Common sites involved : Hippocampus, temporal cortex and nucleus basalis of meynert
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Pathology: Deposition of Amyloid Aβ in brain tissues The precursor protein to develop Amyloid Aβ is amyloid precursor protein (APP), a normal protein in brain which has 3 cleavage sites for 3 enzymes (α- Secretase, β- Secretase, γSecretase) APP cleavage by α- Secretase and γ- Secretase results in a fragment which is soluble and normal APP cleavage by β - Secretase and γ- Secretase results in a fragment called amyloid Aβ Gross : Cortical atrophy with compensatory ventricular enlargement Histology : Neuritic plaques- spherical collections of neuritic process +central amyloid core Diffuse plaques – Only amyloid. No neuritic process Neurofibrillary tangles – composed of tau, ubiquitin and MAP2 (microtubule associated protein) Cerebral amyloid angiopathy Granulovacuolar degeneration – intraneuronal cytoplasmic vacuoles Hirano bodies – Elongated, glassy, eosinophilic bodies
Pathology : Questions & Answers |
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152. Answer: c. Pick’s disease Ref: Robbins 8/e p1318 Pick’s disease (Lobar atrophy) • Localised atrophy involving only frontal and temporal lobes but sparing parietal and occipital lobes
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153. Answer: a. Neuroblastoma Ref: Robbins 8/e p1051
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Microscopic findings: • Knife-edge appearance – Severe atrophy leading to wafer thin gyri • Pick cells – Cytoplasmic swelling of the surviving neurons • Pick bodies- Filamentous cytoplasmic inclusions in surviving neurons stained with silver stain
Flexnerwintersteiner rosettes
True ependymal rosettes
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Homer wright rosettes
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Rosettes • Rosettes consist of a spoke wheel arrangement of cells surrounding central core. • The central core consists of an empty lumen, or a space filled cytoplasmic processes or blood vessels • The cytoplasm of these cells are wedge shaped with the apex facing the core • The nucleus of these cells are peripherally positioned forming a ring around the core Perivascular pseudorosettes
Pineocytomatous & Neurocytic rosettes
Core –Cytoplasmic extension of cells
Core –an empty lumen
Core – blood vessel
Similar to Homer wright, but core has larger and irregular neuropil
Neuroblastoma Medulloblastoma PNET Pineoblastoma
Retinoblastoma Pineoblastoma Medulloepithelioma
Ependymoma
Ependymoma Medulloblastoma PNET Central neurocytoma Glioblastoma Pilomyxoid astrocytoma
Pineocytomatous rosette in Pineocytoma Neurocytic rosette in central neurocytoma
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Core - neuropil
154. Answer: b. NF-2 (Refer:Q138)
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155. Answer:
a. Breast (Refer: Q142)
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156. Answer: a. Cerebral infarct Microscopic features of cerebral infarction : Three categories 1. Early change (within 12 to 24hrs) : Red neurons, pyknosis and karyorrhexis of neurons 2. Subacute change (24hrs to 2 wks) : Necrosis of tissue, macrophage infiltration, vascular proliferation and reactive gliosis 3. Repair ( after 2wks) : Removal of all necrotic debris All these events lead to neuronal loss with few preserved neurons and glial cells in between – This pattern is called “Pseudolaminar necrosis” b. CSF (Refer: Q 142)
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157. Answer:
158. Answer: c. Gamma rays Ref: Kawthalkar essentials of Hematology 2/e p491 Preparation
Prepared by removing most of plasma from one unit of whole blood by a refrigerated centrifuge
Red cells in additive solution
Plasma removed by centrifugation and in the remaining packed RBCs SAGM (saline, adenine, glucose and mannitol) is added
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Packed RBCs
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Leucocyte poor red Obtained by passing blood through a leucocyte depletion filter cells Red cell components Washed RBCs Packed RBCs washed with normal saline to remove plasma proteins Frozen RBCs
Glycerol (cryoprotective agent) is added and the sample frozen
Irradiated RBCs
Gamma radiation prevents replication of donor lymphocytes which were left in packed RBCs. Shelf life is 28days or less. By centrifugation (If multiple donors)
Granulocyte Granulocyte components concentrate
By centrifugation of leucopharesis
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Platelet concentrate Platelet components Platelet concentrate
Plasma components
By plateletpheresis (If single donor)
Fresh frozen plasma
Plasma separated from whole blood by centrifugation and rapidly frozen at -25oC. Contains all coagulation factors except factor V and VIII
Cryoprecipitate
Slowly thaw 1 unit of FFP at 4o to 6oC. Then centrifuge which separates plasma from sediment. Take sediment and suspend in 10-20mlof plasma. Contains FI, FVIII, FXIII, vWF and fibronectin
Pathology : Questions & Answers | 159. Answer:
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b. 28 days (Refer: Q 158 )
160. Answer: a. Ch1 Ref: Kawthalkar essentials of Hematology 2/e p456 Blood group systems There are 30 blood group systems according to “International society of Blood Transfusion”. Blood groups which are highly immunogenic in order : ABO > Rh> K > C
Approximate Indian frequency 27%
B
31%
AB
8%
O
34%
Bombay group
Antigens on red cells
Antibodies in plasma
AA or AO
A, H
Anti-B
BB or BO
B,H
Anti-A
AB
A,B, H
Nil
OO
H
Anti-A and Anti-B
No H genotype
Nil
Anti-H
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A
Genotype other than H
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Blood group
Rare
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ABO blood groups: • A and B antigens are encoded in chromosome 9 • People of any group inherit H gene which produce a protein called H substance. This H substance is necessary to produce A and B antigens.
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Bombay blood group: • These people will not inherit the H gene and thus cannot produce H substance . • Such persons may inherit A or B gene or both but cannot produce A and B antigens • Their red cell type as group O, however unlike group O individuals, bombay blood group individuals won’t have H antigen and hence anti-H antibodies • They can be transfused only with blood of another Bombay blood group individual.
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Rh system: • Rh genes (D genes) are encoded in chromosome 1 • In India, approximately 95% of the people express D antigens on their red cells • Complete absence of all Rh antigens on red cells is associated with stomatocytosis (red cells have a fish mouth like central pallor) and compensated hemolysis
161. Answer:
d. Chr 9 (Refer: Q 160)
162. Answer:
c. Anti A, Anti B, Anti H (Refer Q 160)
163. Answer: c. 3–5 days Ref: Kawthalkar essentials of Hematology 2/e p489
| PG NEXT Blood component
Volume of 1unit
Storage
Shelf life
One unit will
Whole blood
400ml
2–6OC
35 days
Raise Hb by 1g/dl, PCV by3%
Packed RBCs
250ml
2–6OC
35 days
Raise Hb by 1g/dl, PCV by3%
Platelet concentrate
50–60ml
20–24 OC with continous agitation
3–5 days
Raise plt count by 5000cells/μL
Fresh frozen plasma
200–300ml
-25 OC
1 year
Supplement all clotting factors except factor V and VIII
Cryoprecipitate
10–20ml
-25 OC
1 year
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Supplement factor I, VIII, XIII, vWF, Fibronectin
165. Answer:
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164. Answer: d. 1 x 1012 Ref: Williams Hematology 8/e Plateletpheresis (Single donor platelets) • A donor is connected to a blood cell separator machine in which whole blood is collected in an anticoagulant solution, platelets are separated and retained , and remaining components are returned back to the donor. • With this method, 2.5 to 14x1011 platelets can be obtained. b. 4 OC (Refer: Q 164)
166. Answer: b. FFP (Refer: Q 164)
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167. Answer: b. VWD Ref: Kawthalkar essentials of Hematology 2/e p487 Indications for transfusion • Whole blood : Acute massive blood loss, exchange transfusion, non-availability of packed cells • Packed cells : Anemia and acute massive blood loss • Platelets : Thrombocytopenia due to decreased platelet production and hereditary platelet function defect • Fresh frozen plasma : Multiple coagulation factor deficiencies (Liver disease, warfarin overdose), DIC and massive blood transfusion • Cryoprecipitate : Treatment of Von willebrand disease, Factor VIII deficiency, Factor XIII deficiency and hypofibrinogenaemia 168. Answer: d. All of the above (Refer Q 160) “Look, it is not RBCs transfusion but plasma that is given in the question” The idea is, you have to transfuse a plasma which does not contain any antibody that is absent in the recipient. O blood group recipients have both anti-A antibody and anti-B antibody already. So plasma from group A, B, AB and O donors will not cause any harm to O group recipients • Universal red cell donor type : O negative • Universal plasma donor : AB group
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PATHOLOGY Q u e stions 1.
In the following karyotype what is the abnormality seen. Shows 2 X-chromosomes and 1 Y-chromosome. b. Short stature with polydactyly c. Loose connective tissue at nape of neck
2.
The picture below was taken by attaching a camera to the microscope. Which of the following is the requirement for such a microscope a. Dark field condenser c. Dichroic mirror d. Cathode ray tube
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b. Phase shifter
10 year old boy with history of jaw swelling and lymphadenopathy. The lymph node biopsy shows the below. Diagnosis is
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3.
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d. High-pitched crying
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a. Gynecomastia with long thin limbs
a. ALL b. CLL
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c. Burkit lymphoma
d. Mantle cell lymphoma
4.
25 year old presents with generalised lymphadenopathy and fever. On examination there was mild hepatomegaly. The lymph node biopsy shows the below. Diagnosis is a. Mantle cell lymphoma b. Burkitt lymphoma c. Hodgkins lymphoma d. Hepatosplenic gamma delta lymphoma
Q & A—Pathology | 5.
871
Identify the cell shown in the below photograph a. Smudge cell b. Myeloblast c. Lymphoblast
6.
23 year old male presents with fever and cervical lymphadenopathy. The peripheral smear shows the following finding. Diagnosis is b. ALL c. Infectious mononucleosis d. None of the above
50 year old male presented with left upper quadrant pain. On examination, spleen was palpable 10 cm below left costal margin. Which of the following IHC is used for diagnosis of the condition. Peripheral smear is as below a. CD 23 b. CD21
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c. Annexin A1
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7.
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a. AML
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d. Atypical lymphocyte
d. Cyclin D1
30 years old male with history of heartburn. Endoscopy shows a lesion in the esophagus which on biopsy shows? Which special stain will you do ? What will you look for?
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8.
a. b. c. d.
9.
Esophagitis, mucin stain, erosions or ulceration Adenocarcinoma esophagus squamous cell Carcinoma, keratin stain Barrets esophagus, mucin stain, dysplasia
Cell growth checkpoint is at which stage of cell cycle – a. b. c. d.
End of M End of G1 End of S End of G2
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10. 17 yr old pt develops intussception for which he was operated and the segment showed multiple polyps, histopathological section of which is given below tubulovillous hamartomatous juvenile polyp adenocarcinoma
11. Schwannoma, marked area represents
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a. Myxoid tissue b. Antony A pattern – Verocay bodies c. Antony B pattern –Verucay bodies d. Antony C pattern
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a. b. c. d.
12. 30 year old male presents with fever and generalised lymphadenopathy. The lymph node shows features as below. Diagnosis is a. Hodgkin lymphoma c. ALCL d. ALL
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b. Burkitt lymphoma
echinococcus with 2 layers strongyloides with 2 layers paragonimus with 2 layers cysticercosis with 3 layers
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a. b. c. d.
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13. Cavitatory lesion in right lower lung with dyspnoea with following histopathological appearance. Most likely diagnosis:-
14. 25yrs old female came with complaints itching and vaginal discharge. Cytology smear is shown in the picture given below. What is the diagnosis..? a. b. c. d.
Candida albicans Trichomanas Doderline Bacilli. Gardenella
15. Identify this urinary crystal: a. b. c. d.
Calcium carbonate stone Ammonium phosphate stone uric acid Calcium oxalate stone
Q & A—Pathology | 16. 29 yr old athlete, suddenly collapsed and died during sport activity. Gross finding is shown below most likely diagnosis? a. HOCM b. RHD c. Coronary heart disease d. IHD
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17. A 30 year old female presents with thyroid enlargement for 2 years. FNAC shows the following features. Diagnosis is a. Papillary carcinoma c. Medullary carcinoma d. Anaplastic carcinoma
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b. Follicular carcinoma
18. This patient came with anemia. This peripheral smear shows ________ a. macrocytic anemia
b. spherocytes of autoimmune hemolytic anemia
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c. microcytic hypochromic anemia due to iron deficiency d. target cells of thalassemia
19. What is shown in the below peripheral smear
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a. Cabot ring
b. Ring sideroblast
c. Basophilic stippling
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d. None of the above
20. 8 year old boy comes with history of anemia. The following test was ordered for him. What is the test done for a. Thalassemia
b. Sickle cell anemia c. ALL
d. G6PD deficiency 21. The gross section of kidney depicts a. Renal Cell Carcinoma b. Hydatid cyst c. Polycystic kidney d. Medullary sponge kidney
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22. This 25 year old lady came with anemia, jaundice and joint pains. The following are True EXCEPT a. She can present with pulmonary syndrome b. Hydroxyurea would help her c. She may have retinopathy d. HbF and HbA2 will be undetectable
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23. 25 year old presented with fever with chills and rigor. Peripheral smear examination shows the following. Diagnosis is a. Plasmodium vivax
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b. Plasmodium falciparum c. Trypanosoma d. Babesia infection
24. 50 year old with pancytopenia and splenomegaly. Bone marrow biopsy is shown below. Which of the following is used to grade the lesion b. PAS c. Perls stain
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a. Reticulin stain
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d. Sudan Balck B stain
25. 30 year old presented with low grade fever and splenomegaly. Peripheral smear showed leukocytosis with 4 % blasts. What is the test done below which is useful for diagnosis a. Karyotyping
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b. FISH
c. RT-PCR
d. None of the above
26. 50 year old with a space occupying lesion in the temporal lobe. The histopathology picture is as that of below diagnosis is a. Glioblastoma multiforme b. Meningionma c. Oligodendroglioma d. Astrocytoma
Q & A—Pathology |
875
27. Identify the following cell a. Basket cell b. Sezary cell c. Lymphoblast d. Downey cell 28. Identify the below cell
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a. Lymphoblast b. Smudge cell d. Atypical lymphocyte
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c. Myeloblast
29. A 23 year old present with tense bulla over extremities. The histopathology is as below. Most probable diagnosis is a. P. vulgaris c. P. vegetans
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b. P. foliaceous d. Bullous pemphigoid
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30. 40 year old male, non hypertensive non diabetic presents with nephritic range proteinuria. The following is the kidney biopsy. Which special stain you will order a. PAS
b. Silver stain
c. Myoglobin stain
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d. Congo red
1.
A n s w e r s
Answer: a. Gynecomastia Ref: Robbins 8/e p165) Klinefelter syndrome Genetic mechanism: Due to nondysjunction of either maternal or paternal X gene during meiosis, the male fetus will inherit one Y chromosome and more than one X chromosome. Remember, the chance of getting an extra X chromosome from the father or the mother is equal. Karyotype: 47XXY (common). Mosaics like 46,XY/47,XXY and 47,XXY/48,XXY are also seen
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| PG NEXT Pathogenesis: Except one X chromosome in the fetus all the other X chromosomes bears an active androgen receptor (that is represented shortest CAG repeats). The shorter the CAG repeats, more active the receptor is. Since the X chromosomes were inactivated, the fetus develop “hypogonadism”
2.
Answer: c. Dichroic mirror
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Clinical features: (All these presentations are secondary to male hypogonadism) • Long lower limbs • Lower IQ level (But no mental retardation) • Gynecomastia • Atrophied testes, small penis, male infertility • Loss of secondary sexual characteristics like deep voice, beard and male distribution of pubic hair. Other associations: • Type 2 diabetes, metabolic syndrome and mitral valve prolapsed Lab findings: • FSH elevated, testosterone reduced and increased estradiol
Answer: c. Burkitt lymphoma Ref: Dennis diagnostic lymphnode pathology p88)
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3.
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Fluorescent microscope • An optical microscope that uses fluorescence to generate an image • The specimen is illuminated with light of a specific wavelength which is absorbed by fluorophores causing them to emit light of a longer wavelength. • Components of such microscope are light source (xenon arc, mercury vapour lamp, LED or lasers), excitation filter, dichroic mirror and emission filter • Clinical applications: o Direct immunofluorescence of skin and kidney biopsies o Indirect immunofluorescence to study ANA, ANCA, AMA, SMA etc
Burkitt lymphoma • A mature B cell neoplasm of germinal centre origin with a characteristic chromosomal translocation, t(8;14) between protooncogene c-Myc on chromosome 8 and heavy chain gene IgH on chromosome 14. • There are other translocation partners for c-myc like kappa light chain gene on chr2 and lamda light chain gene on chr22. • Different types of mutations seen in Burkitt lymphoma are: t(8;14), t(8;2) and t(8;22) • Clinical types: Endemic BL, sporadic BL and Immunodeficiency associated BL • Lymphnode morphology: o Monomorphic small round lymphoid cells with basophilic cytoplasm o Cytoplasm contains characteristic vacuoles which contain fat droplets (hence stained with oilred O or sudan black stain)
Q & A—Pathology |
877
Proliferation index (Ki67): nearly 100% Numerous apoptotic bodies seen. Starry sky appearance: Due to phagocytosis of apoptotic bodies by tangible body macrophages Immunohistochemistry: Positive for CD20, CD79a, BCL-6. Negative for BCL-2. o o o
•
Answer: c. Hodgkin lymphoma (Refer Q58)
5.
Answer: b. Myeloblast Ref: Williams hematology 8/e, Robbins 8/e p598, 599, 600) Lymphoblast
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Myeloblast
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4.
Nucleoli
Multiple
Single
Cytoplasm
Granular
Auer rods
Present
MPO
+
SBB
+
NSE
+ in M4, M5& M6
-
PAS
-
+ (block positivity)
Acid phosphatase
-
+ in T- ALL
Agranular
Absent -
xt
-
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Note: 1. LAP is increased in Chronic myeloid leukemia (CML) including blastic phase. 2. Tartarate resistant acid phosphatase (TRAP) is also a cytochemical stain which is typically positive in Hairy cell leukemia (HCL) 3. Acid phosphatase positivity in T-ALL indicates its early differentiation. AP also shows variable positivity in monocytes, esinophils, and platelets. In the bone marrow megakaryocytes, macrophages and plasma cells are positive.
6.
Answer: c. Infectious mononucleosis Ref: Iochim’s lymph node pathology p78
Infectious mononucleosis • Causative agent: Ebstein Barr virus (HHV-4) • Mode of transmission: Direct contact with human secretions, most often by saliva • Infected cells: Epithelial cells and B cells in oropharynx • EBV infects B cells through C3d complement receptor (CD21) for which the co-factor used is MHC-II. • By age of 3 years, about 100% of children have positive serological findings for EBV. But not all those infected individuals acquire disease.
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• • • • • • •
Answer: c. Annexin A1 Ref: Williams Hematology 8/e chapter 95)
Hairy cell leukemia • An uncommon chronic lymphoproliferative disorder of B lymphocytes • Clinical presentation: Massive splenomegaly, hepatomegaly and lymphadenopathy • Peripheral blood: Bicytopenia/Pancytopenia, absolute monocytopenia, absolute neutropenia, anemia and thrombocytopenia. • Cytopenia could be due to hypersplenism, hairy cell infiltration of marrow and TNF-α secreted by hairy cells. • Hairy cells are mononuclear cells with eccentric or central round, ovoid, reniform, or convoluted nuclei. Nuclear forms tend to have a reticular chromatin pattern. Hairy cells have variable amounts of cytoplasm that is blue–gray in appearance, exhibiting thin cytoplasmic projections • Bone marrow aspirate shows “dry tap” due to marrow fibrosis • Bone marrow biopsy shows hairy cells with “fried egg appearance” • Cytochemical stain: Positive for tartrate resistant acid phosphatase • Immunohistochemical stain: Positive for Annexin A1(specific for HCL), CD20, TRAP, DBA44, T-bet • And CD103 (Frozen section) • Flowcytometry: CD11c, CD22, CD25 and CD 103. Also positive for pan-B markers like CD19, CD20 and CD22. Newly identified CD200 marker shows expression only in hairy cell leukemia and chronic lymphocytic leukemia. • Treatment of choice: Cladribine
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7.
EBV replicates in B cells, inducing expression of viral capsid antigen (VCA), membrane antigen (MA), early antigen (EA), EBV nuclear antigens (EBNA), and lymphocytedetected membrane antigen (LYDMA). Antibodies formed against these antigens were called heterophil antibodies which play a role in containing infection Incubation period: 2 to 5 weeks Triad of symptoms: Fever, pharyngitis and cervical /generalized lymphadenopathy Peripheral blood: Shows atypical lymphocytes which are T cell type (however EBV affects B cells) with abundant paleblue cytoplasm, large nuclei and conspicuous nucleoli called Downey cells Paul bunnel test: Agglutination of sheep erythrocytes by patient’s serum. Beef erythrocytes (specific for infectious mononucleosis ) and guinea pig kidney are also used. Monospot test: Most sensitive test in which agglutination was formed between horse erythrocytes and patient’s serum. Serology: To detect EBV specific antibodies VCA (IgM), VCA (IgG),EA and EBNA.
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Q & A—Pathology | Parameters
HCL
HCL-Variant
879
Splenic Lymphoma with Villous Lymphocytes
Blood Morphology Ovoid, reniform
Round
Round
Chromatin
Reticular ± nucleolus
Coarse with central nucleolus
Coarse ± nucleolus
Cytoplasm
Blue-gray, abundant
Blue-gray, abundant
Basophilic, scant to moderate
Monocytopenia
+
–
–
TRAP stain
+++
±
Aspirated marrow*
–
Splenic involvement
Red pulp
Red pulp
White pulp
++
++
++
+
++
–
±
++
±
–
CD11c
+++
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+++
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8.
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CD22
CD103
±
+
Flow cytometry
CD25
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Nuclear shape
Answer: d. Barret’s esophagus, Mucin stain, Dysplasia Ref: Odze and goldblum Surgical pathology of GI tract, Liver, biliary tract and pancreas 2/e p260) Barret’s esophagus
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Definition:According to American college of Gastroenterology, Barret’s esophagus is defined as “an endoscopically recognizable columnar metaplasia of the esophageal mucosa that is confirmed pathologically to have intestinal metaplasia, the later defined by the presence of goblet cells” Etiology: Chronic GERD Progression: If left untreated it may progress to the development of dysplasia and adenocarcinoma. Endoscopic findings: Columnar metaplasia in tubular esophagus is identified endoscopically as “Salmon coloured mucosa” which should be present above the normal gastroesophageal junction. Once identified biopsies will be taken which include the lesion and the adjacent normal esophageal mucosa. Histological findings: The biopsy will show intestinal metaplasia in a background of columnar metaplasia. So what is the difference between intestinal metaplasia?
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Columnar metaplasia – Mucosa with tall columnar lining (like those in the stomach) Intestinal metaplasia – Goblet cells which are normally present only in small and large intestine. Goblet cells are cup shaped cells seen scattered in between the columnar cells which have an eccentrically placed compressed nucleus and abundant pale blue cytoplasm. Sometimes, the cytoplasm of columnar cells appear bulky and resembles goblet cells, which are called “pseudogoblet cells”. How to differentiate?
•
• •
Seen as linear array of cells
2
Nucleus appears compressed and eccentrically placed
Nucleus appear perpendicular to the basement membrane similar to other columnar cells
3
Blue tinged cytoplasm
4
Strongly positive for mucin stain (Alcian blue stain) at pH 2.5
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Seen as single cells.
Ground glass cytoplasm
Weak positive for mucin stain (Alcian blue stain) at pH 2.5
Diagnosing a case of Barret’s esophagus is sufficiently not enough. A thorough search for dysplasia becomes mandatory. And dysplasia could be low grade or high grade Dysplasia: Nuclear stratification with abrupt absence of goblet cells in the dysplastic cells, nuclear pleomorphism, slender perpendicularly oriented nucleus and prominent nucleoli . Low grade dysplasia: If the above findings seen only in the lower half of the crypts (Like shown in the picture) High grade dysplasia: If the above findings and increased mitosis seen lower half of crypts, upper half of crypts and surface epithelium.
Answer: d. End of G2 Ref: Robbins 8/e p285) • G1: The point at which cells become committed to entering the cell cycle • S: Synthesis of DNA • G2: Cell undergoes rapid growth and protein synthesis in preparation for mitosis in this stage • M: Mitosis
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9.
1
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•
Pseudogoblet cells
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•
Goblet cells
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880
10.
Answer: b. Hamartomatous Ref: Robbins 8/e p816) Hamartoma- Tumour like growths composed of mature tissues that are normally present at the site in which they develop. Hamartomatous polyps are juvenile polyps, peutz jeghers, Cronkite Canada syndrome and cowden syndrome.
Q & A—Pathology |
881
Patient has peutz jeghers polyp which is common in adolescent and present with intussception. Peutz Jeghers syndrome are autosomal dominant presentation at median age with multiple GI hamartomatous polyps and mucocutaneous pigmentation.
Answer: b. Antoni A –Verocay bodies Ref: Robbins 8/e p1340
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11.
xt
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m
Gastrointestinal polyposis syndrome
Schwannoma
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Well circumscribed, encapsulated masses that are attached to a nerve but can be separated from from it (Whereas neurofibromas are unencapsulated, ill circumscribed mass that present within the nerve and expanding them, hence the tumour cannot be separated from the nerve) Microscopic findings: Two patterns – Antoni A and Antoni B patterns Antoni A – Cellular with spindle cells showing nuclear palisades. There is an alternate array of nuclear palisades and nuclear-free zones were together called “Verocay bodies” Antoni B – Less densely cellular and consists of loose meshwork of cells, microcysts and myxoid stroma.
12.
Answer: c. ALCL Ref: Robbins 8/e p615) Anaplastic large cell lymphoma • A mature T cell lymphoma with characteristic genetic translocation t(2;5).
| PG NEXT • • • • • •
Answer: d. echinococcus with 2 layers Ref: Robbins 8/e p392)
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13.
Genes in chromosome 2 encodes ALK protein and chromosome 5 encodes NPM (Nucleophosmin) Involves lymphnodes, skin, gastrointestinal tract etc. Hallmark cells – Atypical lymphoid cells with voluminous cytoplasm and typical horse shoe shaped nuclei Doughnut cells – Lymphoid cells with pseudoinclusions formed by invaginated nuclear membrane Immunohistochemistry: Positive for ALK-1(nuclear positive), CD30 and EMA ALK positive ALCL have better prognosis than ALK negative ALCL
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882
Answer: b. Trichomonas Ref: The Bethesda system for reporting cervical cytology 2/e)
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14.
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Hydatid cysts • Causative organism: Echinococcus granulosus • Definitive host: Dogs • Usual intermediate host: Sheep • Accidental intermediate host: Humans • Common sites involved: Liver, lung, bone and brain • Microscopic findings: o Composed of inner endocyst and outer pericyst. o Endocyst formed by the parasite and pericyst formed by the host tissues and inflammatory cells o Endocyst contains outer non nucleated lamellated layer and inner nucleated germinative layer. Within the germinative layer there are brood capsules, daughter cysts and scolices. Hydatid fluid contains degenerated scolices which forms sand like sediment called “Hydatid storm”
Organisms seen in cervical cytology • Doderlain bacteria(Lactobacillus): Normal bacterial flora that present as tiny bacilli • Trichomonas vaginalis: Pear shaped, oval or round cyanophilic organism almost the size of a monocyte. Nucleus is pale, vesicular and eccentrically placed. Flagella seen only in liquid based preparations. Leptothrix (long filamentary organism) usually seen in association with trichomonas. • Candida: Eosinophilic pseudohyphae which on liquid based preparations show “Shishkebab appearance” • Gardenella: Dust like coccobacillus covering the squamous cells called as “Clue cells”. The disease is termed as “Bacterial vaginosis” • Actinomyces – Cotton ball like clusters of filamentous organisms in radiating manner • Herpes simplex: Squamous cells with “ground glass” like intranuclear pseudoinclusions.
Q & A—Pathology | 15.
883
Answer: d. Calcium oxalate crystals
Answer: a. HOCM Ref: Robbins 8/e p575)
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16.
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Crystals in urine • Calcium oxalate monohydrate: Envelope shaped • Calcium oxalate dehydrate: Dumb bell shaped • Triple phosphate (Ammonium phosphate ): Coffin –lid shaped • Uric acid: Variable shapes, most commonly pear shaped • Calcium carbonate: Cartwheel like appearance • Cysteine: Stacks of hexagonal crystals • Cholesterol crystals: Stacks of rectangular crystals with broken edges
The picture shows a ventricular septal hypertrophy which narrows the left ventricular cavity forming a banana shaped appearance. This finding is characteristically seen in HOCM.
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Hypertrophic obstructive cardiomyopathy • A genetic disorder of sarcomeric proteins in cardiac muscle • Present in post pubertal age group. • 400 types of mutations identified, common being β-myosin heavy chain • Characterised by myocardial hypertrophy, defective diastolic filling and ventricular outflow obstruction • Myocardial hypertrophy is predominantly septal causing narrowing of the ventricular cavity which appears like a banana on longitudinal section
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• Because of reduced ventricular cavity, the diastolic filling is reduced, hence myocardial ischemia and sudden death • Microscopic findings: Myocyte hypertrophy, myocyte disarray and interstitial fibrosis Answer: d. Papillary carcinoma
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17.
Picture show papillary fragments with a fibrovascular core.
18.
Answer: d. Macrocytic anemia Ref: Barbara J Bain Blood cells 4/e p311, Harrison 18/e p866, 17/e p645-646, Tejinder Singh 2/e p54–61)
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| PG NEXT MEGALOBLASTIC ANEMIA Megaloblastic anemia is due to inadequate RBC production CAUSES OF MEGALOBLASTIC ANEMIA Vitamin B12 deficiency
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B. Impaired absorption (Anemia occurs 3-4 months after poor absorption) Gastric: Intrinsic factor deficiency - Pernicious anemia - In post gastrectomy patients Intestinal - Fish tape worm infestations(Diphyllobothrium latum) - Small bowel bacterial growth - Malabsorption syndrome - Ileal resection - Ileocaecal TB - Crohns disease - Metformin drug
A. Decreased intake Dietery deficiency - Malnutrition - Elderly - Alcoholism & cirrhosis B. Impaired absorption Malabsorption syndrome - Gluten sensitive enteropathy/ celiac - Tropical sprue Anticonvulsant drugs Oral contraceptives
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A. Decreased intake Malnourishment Vegetarians
Folic acid deficiency
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C. Increased requirement Pregnancy Disseminated cancer
C. Increased requirement Pregnancy, infancy Malignancy D. Impaired utilization Foic acid antagonists Ex: Methotrexate, 6- Merceptopurine, cyclophosphamide
Q & A—Pathology |
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Absorption of Vitamin B12:
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Role of Vit. B12 in biosynthesis of DNA a. Vit. B12 is an essential cofactor for conversion of homocysteine to methionine and formation of tetrahydrofolate. Tetrahydrofolate is converted to polyglutamate and then into DNA. b. In Vit B12 deficiency methyl FH4 trap occurs. c. Vit. B12 is essential for conversion of Methyl malonyl CoA Succinyl CoA
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In B12 deficiency methylmalonyl CoA is not converted to succinyl CoA . So methylmalonyl CoA accumulates and forms abnormal fatty acids leading to improper myelin formation and hence neurological defects occur.
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| PG NEXT Role of folic acid in biosynthesis of DNA a. 5, 10 Methylene polyglutamate is required for conversion of d UMP to d TMP to DNA. Lack of folic acid hinders DNA synthesis. b. Histidine is metabolized to formiminoglutamic acid ( FIGLU) which combines with FH4 to formglutamate. In folate deficiency this conversion cannot occur so FIGLU accumulates and is excreted unchanged in urine. This can be measured to detect folate deficiency Histidine FIGLU Glutamate+ 5- formimino THF
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FH4
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Hematological findings
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Pathogenesis of anemia 1. Unbalanced cell growth: Due to retarted DNA synthesis nuclear maturation lags behind cytoplasmic maturation. 2. Ineffective erythropoiesis: Due to intramedullary death of intermediate and late megaloblasts. Sometimes due to defective DNA synthesis most of the precursors of all lineages undergo apoptosis in the marrow leading to pancytopenia. 3. Hemolytic component: Mild hemolytic component is present as late normoblasts die prematurely in bonemarrow.
Peripheral blood picture
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1. Macrocytosis (↑ MCV, MCH. Normal MCHC) 2. Peripheral smear Macroovalocytes Few nucleated RBCs Evidence of dyserythropoiesis like- Basophilic stippling - Cabot ring - Howell- Jolly bodies 3. ↓ Hb 4. ↓ Hematocrit 5. Reticulocyte count – Normal or mild decrease 6. White cells- Leucopenia 7. Hypersegmented neutrophils/ MacropolycytesFirst manifestation 8. ↓ Platelets 9. Pancytopenia (10-20%) Lab investigations: 10. Serum iron, ferritin - ↑ in pure VitB12/ Folate defect 11. Serum bilirubin & LDH ↑- due to hemolytic component 12. Schillings test: Used to assess status of intrinsic factor (IF) & Vit B12 to distinguish pernicious anemia from other causes of Vit.B12 deficiency.
Bone marrow picture
1. Moderate- marked hypercellularity 2. Erythroid hyperplasia 3. M:E ratio reversal 4. Erythropoiesis- Megaloblastic 5. Giant metamyelocytes 6. Mildly reduced megakaryocytes 7. BM iron moderately increased in pure Vit B12/ Folate defects.
Q & A—Pathology |
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Note: In schillings test, four stages are there Stage I: Two doses of vitamin B12 (cobalamin) given. First a small dose (a radioactive form of B12) orally. Followed by a larger dose intramuscularly 1 hour later. The urine sample for next 24 hours is collected and given to the lab. The urine is checked to see if vitamin B12 is absorbed normally or not. If Stage I is abnormal, Stage II may be done.
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Stage II: Radioactive B12 is given along with IF, which is a protein produced by parietal cells in the stomach. Stage II of the test can tell whether a low vitamin B12 level is caused by IF defects in stomach. If stage I and II are abnormal then it may be due to intestinal resection or malabsortion syndromes. Stage III test is done. Stage III: This test is done after taking antibiotics for 2 weeks. It can tell whether abnormal bacterial growth has caused the low vitamin B12 levels.
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Stage IV: This test determines whether low vitamin B12 levels are caused by problems with the pancreas. With this test, you take pancreatic enzymes for 3 days. You then take a radioactive dose of vitamin B12.
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19.
Answer: d. Cabot ring Ref: Williams hematology 8/e) Inclusions
Composition
Cell Type
Reticulocytes
Appearance on Wright-Stained Film Invisible
Artifactual aggregation of ribosomes
Howell-Jolly bodies
Reticulocytes; Nuclear fragment containing aberrant rarely erythrocytes chromosomes
Cabot rings
Spindle remnant or histone-rich and iron-rich “cytoplasmic currents”
Ring or figureReticulocytes; of-eight strand heavily stippled late intermediate stained purple megaloblasts
Basophilic stippling
Pathologic precipitation of ribosomes
Reticulocytes
Denatured hemoglobin
Erythrocytes; occasionally reticulocytes
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Hemoglobin H inclusions
Dense blue spherical granule(s)
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Heinz bodies
Erythrocytes; Denatured reticulocytes hemoglobin (induced in vitro by exposure to brilliant cresyl blue, methylene blue, new methylene blue)
Visible after supravital staining
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“Reticulofilamentous substance”
Comments
Visible in unstained cells Visible in some hemolytic states
Dispersed blue granulations Rarely visible
Refractile inclusions after staining with methylene or Nile blue dyes
Invisible
Gives “golf-ball” appearance to erythrocytes after incubation with appropriate supravital stains
Q & A—Pathology |
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Answer: a. Thalassemia Ref: Journal of Clinical and Diagnostic Research. 2013 Dec, Vol-7(12): 2784–87) • Normally, red cells in saline solution begin to lyse at a saline concentration of 0.4–0.5% and lysis is complete at 0.32%. • However, in beta thalassemia trait, due to alteration in osmotic resistance of the affected RBC’s due to high surface volume ratio, lysis begins at a saline concentration between 0.4–0.35% and it may not be completed even at 0.1% solution. NESTROFT is done at a saline concentration of 0.36% in which RBCs of thalassemic patients resist osmotic lysis. • In the picture given, there is a distilled water tube and 0.36% saline tube. RBCs in distilled water show 100% RBC lysis hence can able to see the line drawn behind. • Whereas thalassemic RBCs, remains intact in 0.36% saline, hence the line cannot be seen. • If the tubes were left undisturbed for 3 hrs, RBCs of thalassemic patients remain intact and form deposits which is not seen in distilled water tube.
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20.
HbH inclusions in brilliant cresyl blue
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Siderocytes
Basophilic stippling
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Howell Jolly bodies
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21.
Answer: c. Polycystic kidney (Refer: Q89)
22.
Answer: d. HbF and HbA2 will be undetectable Ref: Robbins 8/e p645, T. Singh 1/e p270) Sickle cell anemia • Sickle cell disease is a hereditary hemoglobinopathy with structurally abnormal hemoglobin
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Normal adult red cell contains 96% HbA (α2β2), 3% HbA2 (α2δ2), and 1% fetal Hb (HbF, α2γ2). Sickle cell disease is caused by point mutation in 6th codon of β-globin chain Occur primarily in African blacks (This high frequency stems from protection afforded by HbS against falciparum malaria) Heterozygotes for HbS is called as sickle cell trait (ααβsβ) Homozygous for Hbs is called as sickle cell disease HbS (ααβsβs)
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Pathogenesis:
The solubility of hemoglobin is altered/ affected in HbS Factors affecting rate of sickling Interaction of HbS with HbA2
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In heterozygotes
About 40% is HbS
About 60% is HbA2
Since % of HbS is less compared to HbA2, HbS polymerization is disturbed. 50% HbS is necessary for sickling So heterozygotes do not sickle unless they are subjected to profound hypoxic conditions Interaction of HbS with HbF HbF inhibits the polymerization of HbS So infants till they reach 5 or 6 months of age, do not sickle after which HbF falls and they become symptomatic
Q & A—Pathology |
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Interaction of HbS with HbC In HbSC= HbS (50%) + HbC (50%) In HbAS= HbS (40%) + HbA (60%) So chance of sickling is high in patients with HbSC. In addition HbSC red cells tend to lose water & salt – become dehydrated- intracellular HbS concentration rises- HbS polymerizes- Lead to sickling
High mean hemoglobin concentration
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Remember HbSC disease is milder than sickle cell disease
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High MCHC- Higher HbS concentration directly proportional to aggregation and polymerization when deoxygenation occurs Intracellular dehydration – Increases HbS- Increase sickling
In case of HbS with coexisting α thalaseemia the production of hemoglobin itself will be decreased so automatically HbS concentration will also be decreased. So these patients will have a milder disease.
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Intracellular pH
Decrease in pH – reduces oxygen affinity –so increased fraction of deoxygenated hemoglobin- tend to sickle
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Transit time of red cells through microvasculature
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Increased transit time- sufficient time for aggregation and sickling- microvascular occlusion
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| PG NEXT Clinical features 1. severe chronic hemolytic anemia 2. increased breakdown of heme pigments in spleen- increase in bilirubin, splenomegalylater autosplenectomy can occur 3. the microvascular obstruction- ischemia and infarction (affect any organ, including bones, liver, kidney, retina, brain, lung, and skin)
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2 crisis in sickle cell anemia 1. Vasoocclusive or pain crisis- due to tissue ishemia/infarction 2. Aplastic crisis- a sudden but temporary cessation of erythropoiesis, usually triggered by parvovirus infection of erythroblasts. Diagnosis
1. Peripheral blood smear – SICKLE CELLS, Target cells, reticulocytosis
Treatment
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2. Demonstration of sickle cells in smears by subjecting them to invitro deoxygenation 3. Hemoglobin electrophoresis to demonstrate HbS. One altered peptide of HbS migrates faster towards the cathode (–) than the corresponding peptide of HbA
Supportive care, Hydroxyurea
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Hydroxyurea inceases HbF thereby reducing sickling and pain.
Q & A—Pathology | Answer: b. Plasmodium falciparum Ref: Barbara bain’s Blood cells 4/e p143)
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23.
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894
24.
Answer: d. Reticulin stain Ref: Barbara Bain’s Bone marrow pathology 3/e p206) Chronic idiopathic myelofibrosis • Clinical presentation: Splenomegaly
Q & A—Pathology | •
Peripheral smear examination: Pancytopenia, leukoerythroblastic blood film and tear drop cells Bone marrow aspiration: There will be either “dry tap” or “bloody tap” Bone marrow biopsy: o Prefibrotic phase: Hypercellular marrow spaces, with abnormal megakaryocytes in the form of clusters, immature forms, dysplastic forms noted. o Fibrotic phase: Increased reticulin fibres with streaming of hematopoietic cells, hypocellular marrow spaces, dysplastic megakaryocytes and dilated sinusoids
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Answer: b. FISH Ref: WHO classification of Tumours of hematopoietic and lymphoid tissues p.24 ) • It was a case of myeloproliferative neoplasm, mostly likely chronic myelogeous leukemiachronic phase (Since the blast percentage is less than 5%). • The picture shows fusion signal in a metaphase preparation which could be BCR-ABL fusion.
26.
Answer: d. Glioblastoma multiforme (Refer: Q142.)
27.
Answer: b. Sezary cells Ref:Barbara bain’s bone marrow pathology 3/e p296) • Sezary cells are atypical lymphocytes seen in peripheral blood in a case of sezary syndrome • Sezary cells have high nuclear cytoplasmic ratio, cerebriform nuclei (show brain like convolutions) and scanty cytoplasm.
28.
Answer: b. Smudge cell Ref: Barbara bain’s bone marrow pathology 3/e p243)
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Smudge cells are seen in chronic lymphocytic leukemia. More the smudge cells, better the prognosis.
29.
Answer: d. Bullous pemphigoid Ref: Weedon’s skin pathology 3/e p156) • All vesiculobullous lesions starting with the word “pemphigus” show intraepidermal blisters which could be subcorneal, intraepidermal or suprabasal. • Among the pemphigus lesions, subcorneal blisters is seen in pemphigus foliaceus and suprabasal blisters seen in pemphigus vulgaris. • Bullous pemphigoid present with subepidermal blisters formed by the antibodies reaction against “bullous pemphigoid antigen” present in basement membrane.
30.
Answer: d. Congo red (Refer: Q35)
