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
EM changes in MI
``` Reversible change Relaxation of myofibrils Glycogen depletion Mitochondrial swelling Irreversible change Disruption of sarcolemma Mitochondrial AMORPHOUS DENSITIES ```
26
First light microscopy finding of MI
Variable waviness of fibres at border(30min-4hours)
27
Earliest gross morphological finding of MI
Dark mottling(12-24hours)
28
Appearance of coagulation necrosis in MI
4-12hours
29
Changes in heart,1-3days after MI
Coagulation necrosis | Brisk interstitial neutrophil infiltrate
30
Phagocytosis of dead cells by macrophages in MI starts by
3-7 days
31
Appearance of granulation tissue in MI
7-10 days
32
Changes in heart,10-14 days after MI
Well established granulation tissue | Collagen deposistion
33
Dense collagenous scar forms after MI in
2 months
34
Most common nerve used for biopsy
Sural nerve
35
Causes of onion bulb
Chronic inflammatory demyelinating polyneuropathy Refsum disease Dejerine sottas disease Charcot Marie tooth disease
36
Palpably enlarged peripheral nerves
``` Hereditary motor and sensory neuropathy CMT Dejerine sotos Leprosy Refsum disease Amyloidosis Acromegaly Neurofibromatosis ```
37
Orange tonsils
Tangier disease
38
Antibodies in CIDP
Anti Po antibody
39
CIDP is common in
Males
40
MADSAM
Multifocal acquired demyelinating sensory and motor neuropathy Lewis sumner syndrome
41
CIDP
Both sensory and motor involvement Areflexia Both distal and proximal muscles involved(legs>arms) Disease progression for more than 8 weeks or relapses
42
Features of GBS but absent albumino cytological dissociation
HIV leukemia Lymphoma Neurosarcoidosis
43
CIDP is associated with
MGUS(25% cases)
44
Rx of CIDP
Glucocorticoids IVIG plasmapheresis
45
POEMS syndrome
``` Polyneuropathy Organomegaly Endocrinopathy Monoclonal gammopathy Skin changes ```
46
Defect in brugada syndrome
Sodium channel 5A
47
Bartter syndromes associated with chloride channel defects
Type3 | Type4
48
Mutation in CMT
Connexion(x linked)
49
CLCN7 defect
Osteopetrosis
50
Mutation in malignant hyperthermia
RYR1 | CACNA1S
51
RYR2 mutation
Arrythmogenic right ventricular dysplasia type 2
52
Mutations in CACNA1S
Malignant hyperthermia | Hypokalemic periodic paralysis
53
Autosomal recessive long QT syndrome with deafness
Jerveil Lange nielsen
54
Autosomal dominant long QT syndrome
Romano ward
55
Long QT syndrome with dysmorphic features
Anderson syndrome
56
Subendocardial hemorrhages in autopsy
Mechanism of death is exanguinations or head injury
57
$ Subendocardial hemorrhages are situated in
Left ventricle
58
Sites of Subendocardial hemorrhages
1. Middle 3rd of interventricular septum(common site) 2. base of papillary muscle 3. posterior wall
59
Shape of Subendocardial hemorrhages
Flame shaped | Confluent
60
Poisons causing Subendocardial hemorrhages
Cocaine | Arsenic
61
Causes of Edema in nephrotic syndrome
Hypoalbuminemia | Sodium retention
62
Prothrombin activator
Factor Va Factor Xa Calcium
63
Normal thrombin time
Less than 15s
64
Technical difficulties in conventional cytogenetics
Poor metaphase activity Contamination of tumor by bacteria Predominance of nonviable tumor(necrotic sample)
65
Best markers for predicting future coronary events
Apo(a) | B100
66
Imaging findings in PMFL
Non-enhancing lesions Multifocal asymmetric white matter lesions located periventricularly Increased intensity in T2 and FLAIR
67
Presentation of PMFL
Homonymous hemianopia,conjugate gaze abnormalities(visual defects are the commonest symptoms) Dementia Hemi or monoparesis and ataxia Seizures
68
Renal lesion in wegener
Focal and segmental necrotising glomerulonephritis(early lesion) RPGN(late lesion)
69
Granulomas in wegener
Found only in lungs and URT
70
Fibronectin glomerulopathy is a type of
Fibrillary glomerulopathy
71
Mode of inheritance of Fibronectin glomerulopathy
AD
72
EM finding in Fibronectin nephropathy
Massive mesangial and sub endothelial electron dense deposits
73
Staining in Fibronectin nephropathy
PAS and Trichrome positive | Congo red negative
74
Types of fibrillary glomerulopathy
``` 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
Genetic forms of iron deficiency anemia
DMT1 mutation Atransferrinemia Glutaredoxin5 Aceruloplasminemia
76
Brain damage occurs in which genetic iron deficiency anemia
aceruloplasminemia
77
Late onset genetic forms of iron deficiency anaemias
Atransferrinemia | Aceruloplasminemia
78
genetic form of iron deficiency anemeia that presents at birth
DMT1 mutation
79
High serum iron is seen in which genetic forms of iron deficiency anemeia
DMT1 Glutaredoxin5 Low serum iron in other two forms
80
Low or normal ferritin is found in which genetic forms of iron deficiency anemeia
DMT1 Others have high serum ferritin
81
Hepcidin levels are low in which genetic forms of iron deficiency anemeia
DMT1 | Atransferrinemia
82
Conditions that lower plasma ferritin Independant of iron levels
Ascorbate deficiency | Hypothyroidism
83
Iron accumulation in basal ganglia
Hallovorden Spatz | aceruloplasminemia
84
Basolateral iron transporter
Ferroportin
85
Hepcidin inhibits iron absorption by
Causing internalisation and degradation of ferroportin
86
Syndrome associated with clear cell pap ca
Mc cune Albright
87
Syndrome associated with cribriform variant of pap ca
Familial adenomatosis polyposis
88
Syndromes associated with thyroid carcinoma
Cowden | Wermer
91
Diff btw EB simplex and junctional EB
Oral mucosa involvement in junctional EB