20.6.2013(pathology)43 Flashcards

0
Q

Infraclavicular lesion of chronic pulmonary TB

A

Assman focus

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1
Q

Marker of naive T cells

A

CD45RA

CD45 RO are markers for memory T cells

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2
Q

Ghon complex

A

Parenchymal subpleural lesion
Draining lymphatics
Enlarged caseous lymphnodes

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3
Q

Segmental atelectasis secondary to bronchial compression due to TB

A

Epituberculosis

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4
Q

TB caseous foci in brain,meninges and spinal cord

A

Rich focus

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5
Q

Ranke complex

A

Healed lesion in lung parenchyma

Hilar lymphnodes undergoing calcification

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6
Q

Simon focus

A

Early hematogenous seedling in apex of lungs

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7
Q

Lesion at apex of lung in chronic TB

A

Puhl lesion

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8
Q

Normal urinary sediment

A

5-6 erythrocytes in 20 high power fields

3-5 leukocytes in 20 high power fields

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9
Q

Vessel wall changes in malignant hypertension

A

Onion skin
Hyperplastic arteriosclerosis
Fibrinoid necrosis

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10
Q

Cardiac polyp

A

Post mortem Fibrinous clot

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11
Q

Types of EB

A
EB simplex(AD)
Junctional EB(AR)
Dystrophic EB(AD,AR)
kindler syndrome
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12
Q

Mutations in EB simplex

A

Keratin 5 and 14

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13
Q

EB simplex+muscular dystrophy

A

Plectin mutation

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14
Q

Mutations in EB simplex

A
Keratin 5,14
Plectin
Integrin
Plakophilin
Desmoplakin
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16
Q

Lethal JEB

A

Central facial erosions
Tracheal and bronchiolar erosions
Dental defects
Nail dystrophy

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17
Q

Layers affected in EB

A

EB simplex intra epidermal
JEB lamina lucida
Dystrophic Sublamina densa

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18
Q

EB with increased risk of SCC

A

Dystrophic EB

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19
Q

Mutation in FERMT1 gene

A

Kindler syndrome

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20
Q

Kindler syndrome

A
Poikiloderma
Photosensitivity
Blistering in areas of trauma
Mucosal involvement
Anal stenosis
Phimosis
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21
Q

Prenatal diagnosis of EB

A

Fetoscopy with skin biopsy

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22
Q

In MI, time of onset of Loss of contraction

A

Less than 2min

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23
Q

ATP depletion in MI

A

Reduced to 50% of normal in 10min

Reduced to 10% of normal in 40min

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24
Q

In MI, time of onset of irreversible cell injury

A

20-40min

Microvascular injury occurs after 1 hour

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25
Q

EM changes in MI

A
Reversible change
   Relaxation of myofibrils
   Glycogen depletion
   Mitochondrial swelling
Irreversible change
  Disruption of sarcolemma
  Mitochondrial AMORPHOUS DENSITIES
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26
Q

First light microscopy finding of MI

A

Variable waviness of fibres at border(30min-4hours)

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27
Q

Earliest gross morphological finding of MI

A

Dark mottling(12-24hours)

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28
Q

Appearance of coagulation necrosis in MI

A

4-12hours

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29
Q

Changes in heart,1-3days after MI

A

Coagulation necrosis

Brisk interstitial neutrophil infiltrate

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30
Q

Phagocytosis of dead cells by macrophages in MI starts by

A

3-7 days

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31
Q

Appearance of granulation tissue in MI

A

7-10 days

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32
Q

Changes in heart,10-14 days after MI

A

Well established granulation tissue

Collagen deposistion

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33
Q

Dense collagenous scar forms after MI in

A

2 months

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34
Q

Most common nerve used for biopsy

A

Sural nerve

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35
Q

Causes of onion bulb

A

Chronic inflammatory demyelinating polyneuropathy
Refsum disease
Dejerine sottas disease
Charcot Marie tooth disease

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36
Q

Palpably enlarged peripheral nerves

A
Hereditary motor and sensory neuropathy
 CMT
 Dejerine sotos
Leprosy
Refsum disease
Amyloidosis
Acromegaly
Neurofibromatosis
37
Q

Orange tonsils

A

Tangier disease

38
Q

Antibodies in CIDP

A

Anti Po antibody

39
Q

CIDP is common in

A

Males

40
Q

MADSAM

A

Multifocal acquired demyelinating sensory and motor neuropathy
Lewis sumner syndrome

41
Q

CIDP

A

Both sensory and motor involvement
Areflexia
Both distal and proximal muscles involved(legs>arms)
Disease progression for more than 8 weeks or relapses

42
Q

Features of GBS but absent albumino cytological dissociation

A

HIV
leukemia
Lymphoma
Neurosarcoidosis

43
Q

CIDP is associated with

A

MGUS(25% cases)

44
Q

Rx of CIDP

A

Glucocorticoids
IVIG
plasmapheresis

45
Q

POEMS syndrome

A
Polyneuropathy
Organomegaly
Endocrinopathy
Monoclonal gammopathy
Skin changes
46
Q

Defect in brugada syndrome

A

Sodium channel 5A

47
Q

Bartter syndromes associated with chloride channel defects

A

Type3

Type4

48
Q

Mutation in CMT

A

Connexion(x linked)

49
Q

CLCN7 defect

A

Osteopetrosis

50
Q

Mutation in malignant hyperthermia

A

RYR1

CACNA1S

51
Q

RYR2 mutation

A

Arrythmogenic right ventricular dysplasia type 2

52
Q

Mutations in CACNA1S

A

Malignant hyperthermia

Hypokalemic periodic paralysis

53
Q

Autosomal recessive long QT syndrome with deafness

A

Jerveil Lange nielsen

54
Q

Autosomal dominant long QT syndrome

A

Romano ward

55
Q

Long QT syndrome with dysmorphic features

A

Anderson syndrome

56
Q

Subendocardial hemorrhages in autopsy

A

Mechanism of death is exanguinations or head injury

57
Q

$ Subendocardial hemorrhages are situated in

A

Left ventricle

58
Q

Sites of Subendocardial hemorrhages

A
  1. Middle 3rd of interventricular septum(common site)
  2. base of papillary muscle
  3. posterior wall
59
Q

Shape of Subendocardial hemorrhages

A

Flame shaped

Confluent

60
Q

Poisons causing Subendocardial hemorrhages

A

Cocaine

Arsenic

61
Q

Causes of Edema in nephrotic syndrome

A

Hypoalbuminemia

Sodium retention

62
Q

Prothrombin activator

A

Factor Va
Factor Xa
Calcium

63
Q

Normal thrombin time

A

Less than 15s

64
Q

Technical difficulties in conventional cytogenetics

A

Poor metaphase activity
Contamination of tumor by bacteria
Predominance of nonviable tumor(necrotic sample)

65
Q

Best markers for predicting future coronary events

A

Apo(a)

B100

66
Q

Imaging findings in PMFL

A

Non-enhancing lesions
Multifocal asymmetric white matter lesions located periventricularly
Increased intensity in T2 and FLAIR

67
Q

Presentation of PMFL

A

Homonymous hemianopia,conjugate gaze abnormalities(visual defects are the commonest symptoms)
Dementia
Hemi or monoparesis and ataxia
Seizures

68
Q

Renal lesion in wegener

A

Focal and segmental necrotising glomerulonephritis(early lesion)
RPGN(late lesion)

69
Q

Granulomas in wegener

A

Found only in lungs and URT

70
Q

Fibronectin glomerulopathy is a type of

A

Fibrillary glomerulopathy

71
Q

Mode of inheritance of Fibronectin glomerulopathy

A

AD

72
Q

EM finding in Fibronectin nephropathy

A

Massive mesangial and sub endothelial electron dense deposits

73
Q

Staining in Fibronectin nephropathy

A

PAS and Trichrome positive

Congo red negative

74
Q

Types of fibrillary glomerulopathy

A
Congo-red positive 
  Amyloid
Immunofluorescence positive(immunoglobulin derived)
  Cryoglobulinemia(mixed essential,MM,CLL)
   Monoclonal gammopathy
   Systemic lupus
   Immunotactoid glomerulopathy
Non immunoglobulin derived
   Diabetic fibrillosis
   Fibronectin nephropathy
75
Q

Genetic forms of iron deficiency anemia

A

DMT1 mutation
Atransferrinemia
Glutaredoxin5
Aceruloplasminemia

76
Q

Brain damage occurs in which genetic iron deficiency anemia

A

aceruloplasminemia

77
Q

Late onset genetic forms of iron deficiency anaemias

A

Atransferrinemia

Aceruloplasminemia

78
Q

genetic form of iron deficiency anemeia that presents at birth

A

DMT1 mutation

79
Q

High serum iron is seen in which genetic forms of iron deficiency anemeia

A

DMT1
Glutaredoxin5

Low serum iron in other two forms

80
Q

Low or normal ferritin is found in which genetic forms of iron deficiency anemeia

A

DMT1

Others have high serum ferritin

81
Q

Hepcidin levels are low in which genetic forms of iron deficiency anemeia

A

DMT1

Atransferrinemia

82
Q

Conditions that lower plasma ferritin Independant of iron levels

A

Ascorbate deficiency

Hypothyroidism

83
Q

Iron accumulation in basal ganglia

A

Hallovorden Spatz

aceruloplasminemia

84
Q

Basolateral iron transporter

A

Ferroportin

85
Q

Hepcidin inhibits iron absorption by

A

Causing internalisation and degradation of ferroportin

86
Q

Syndrome associated with clear cell pap ca

A

Mc cune Albright

87
Q

Syndrome associated with cribriform variant of pap ca

A

Familial adenomatosis polyposis

88
Q

Syndromes associated with thyroid carcinoma

A

Cowden

Wermer

91
Q

Diff btw EB simplex and junctional EB

A

Oral mucosa involvement in junctional EB