histo renal Flashcards

1
Q

kawasaki disease sx

A

strawberry tongue/ mouth inflammation cervical LN fever >5 days hand s and sole desquamation conjunctivitis

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2
Q

who gets kawasaki disease

A

<5yo

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3
Q

complication of kawasaki disease

A

coronary artery aneurysm

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4
Q

who gets buergers disease

A

men <35yo who smoke

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5
Q

pathology of Buerger’s disease

A

inflammation of arteries supplying the extremities e.g. radial and tibial- occlusion

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6
Q

appearance of Buerger’s disease on angiography

A

corkscrew due to segmental occlusive lesions

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7
Q

what is the triad of wegeners granulomatosis

A

saddle nose pulmonary haemmorhage cresenteric glomerulonephritis

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8
Q

what are nasal sx of wegeners

A

epistaxis sinusitis saddle nose

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9
Q

what are the pulmonary symptoms of wegeners

A

cavitations pulmonary haemmorhage

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10
Q

what are the renal symptoms of wegeners

A

crescenteric glomerulonephritis

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11
Q

triad of churg strauss

A

eosinophilia asthma vasculitis

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12
Q

what autoantibody mediates churg strauss

A

p ANCA against MPO

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13
Q

symptoms of microscopic polyangitis

A

pulmonary haemmorhage withglomerulonephritis

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14
Q

autoantibody in microscopic polyangiits

A

pANCA against MPO

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15
Q

what antibody mediates henoch scheinlich purpura

A

IgA

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16
Q

what are the symptoms of Henoch scheinlich purpura

A

UTI that after 5 days is followed by a purpuric rash over lower limb extensors and buttocks glomerulonephritis colicky abdo pain arthritis orchiditis

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17
Q

autoantibody for wegeners

A

c ANCA against PR3

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18
Q

what renal diseases affect the glomerulus

A

nephrotic syndrome nephritic syndrome

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19
Q

what renal diseases affect the tubules and interstitium

A

acute tubular necrosis tubulointerstitial nephritis

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20
Q

what are the three subtypes of tubulointerstitial nephritis

A

acute pyelonephritis chronic pyelonephritis with reflux nephropathy interstitial nephritis

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21
Q

what renal disease affect the renla blood vessels

A

haemolytic uraemic sndrome thrombotic thrombocytopenic purpura

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22
Q

triad of nephrotic syndrome

A

proteinuria (>3g/24hrs) hypoalbuminaemia oedema (+hyperlipidaemia)

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23
Q

buzzwords for nephrotic syndrome

A

frothy urine facial oedema in kids peripheral oedema in adults

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24
Q

minimal change disease

A

primary cause of nephrotic syndrome paediatric condition

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25
Q

what is seen on light microscopy and electron microscopy of minimal change disease

A

no change on light microscopy loss of podocyte foot process on electron microscopy no immune deposits

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26
Q

treatment of minimal change disease

A

steroids very good prognosis

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27
Q

membrnous glomerular disease findings on light microscopy

A

diffuse glomerular basement membrane thickening

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28
Q

membranous glomerular disease findings on electron microscopy

A

loss of podocyte foot processes spikey subepithelial depositis

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29
Q

immunoflourescance findings on membranous glomerular disease

A

ig and complement in granular deposits along ENTIRE GBM

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30
Q

causes of membranous glomerular disease

A

SLE drugs malignancy

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31
Q

prognosis of membranous glomerular disease

A

pooor response to steroids 45% have ESRF after 2-20 years

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32
Q

causes of glomerulosclerosis

A

being afrocarribean HIV nephropathy secondary to obesity

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33
Q

findings on light microscopy in glomerulosclerosis

A

scarring and consolidation in ofcal areas of glomerulus hyalinosis

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34
Q

findings on electron microscopy in glomerulosclerosis

A

loss of podocyte foot processes

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35
Q

immunoflourescance findings in glomerulosclerosis

A

Ig and complement in scarred areas

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36
Q

prognosis in glomerulosclerosis

A

50% ESRF 50% respond to steroids

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37
Q

renal histological findings in diabetes

A

diffuse GBM thickening kimmenstial wilson nodules

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38
Q

what are kimmenstial wilson nodules

A

mesangial matrix nodules

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39
Q

pathology of kimmenstial wilson nodules

A

Nodules of pink hyaline material form in regions of glomerular capillary loops in the glomerulus. This is due to a marked increase in mesangial matrix from damage as a result of non-enzymatic glycosylation of proteins

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40
Q

definition of nephritic syndrome

A

inflammation of the glomerulus

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41
Q

buzzword for nephritic syndrome

A

coca cola urine

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42
Q

signs of nephritic syndrome

A

haematuria dysmorphic rbc/ rbc casts inurine proteinuria but not in nephrotic range raised urea and creatinine oliguria

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43
Q

causes of nephritic syndrome

A

opst infectious glomerulonephritis rapidly progessive crescenteric glomerulonephritis Buerger’s disease Alport’s syndrome beinign familial haematuria

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44
Q

acute post infectionous glomerulonephritis usual pathogen

A

group A alpha haemolytic strep strep pyogenes

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45
Q

findings in acute post infectious glomerulonephritis

A

haematuria proteinuria oedema hypertension

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46
Q

common infection preceding acute post infectious glomerulonephritis

A

strep throat or impetigo 1-3 weeks earlier

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47
Q

whatare the findings on blood in acute post infectious glomerulonephritis

A

reduced C3 raised ASOT titre

48
Q

light microscopy findings in acute post infectious glomerulonephritis

A

increased cellularity of glomeruli

49
Q

electron microscopy findings in acute post infectious glomerulonephritis

A

subendothelial humps

50
Q

flouresacanc emicroscopy findings for acute post infectious glomerulonephritis

A

C3 and IgG granular deposits in GBM

51
Q

Buerger disease alternative name

A

IgA nephropathy

52
Q

pathology of Buerger disease

A

IgA immune complexdeposition in glomeruli

53
Q

findings on biopsy of Buerger disease

A

IgA and complement in mesangium

54
Q

preceding sundrome for Buerger disease

A

URTI 3 days earlier

55
Q

symptoms of buerger disease

A

frank haemoaturia or peristent microsccopic haematuria

56
Q

complications of buerger disease

A

ESRF

57
Q

the three types of cresenteric glomerulonephritis

A
  1. anti-GBM antibody 2. Immune complex deposition 3. ANCA associated/ pauci immune
58
Q

type 1 cresenteric glomerulonephritis pathology

A

anti GBM antibod against COL4-A3

59
Q

causes of type 1 cresenteric glomerulonephritis

A

goodpastures syndrome HLADRB1 association

60
Q

findings in flourescance microscopy of type 1 cresenteric glomerulonephritis

A

linear IgG deposits

61
Q

causes of type 2 cresenteric glomerulonephritis

A

SLE IgA nephropathy post infectious GN

62
Q

microscopy of type 2 cresenteric GN

A

light: cresencts electrons: lumpy bumpy granular IgG deposits in GBM and mesangium

63
Q

causes of type 3 cresenteric glomerulonephritis

A

panca micrscopic polyangiits canca wegeners granulomatosis

64
Q

pathology of type 3cresenteric glomerulonephritis

A

pauci immune no ab anca mediated

65
Q

what is alports syndrome

A

hereditary nephritis

66
Q

inheritance of alports syndrome

A

x linked

67
Q

triad of alports syndrome

A

sensorineural deafness, eye disorders and nephritic syndrome

68
Q

presentation of alports disease

A

5-20yo nephritic syndrome that progresses to ESRF

69
Q

common eye disorders in alports syndrome

A

lens dislocation cataracts

70
Q

benign familial haematuria aka

A

thin basement membrane disease

71
Q

genetic defect in benign familial haematuria

A

colagen IV alpha 4 chain

72
Q

inheritance of benign familial haematuria

A

autosomal dominant

73
Q

symptoms of benign familial haematuria

A

persistant asymptomatic haematuria

74
Q

differentials for asymptomatic haematuria

A

benign familial haematuria Alport syndrome IgA nephropathy

75
Q

pathology of ATN

A

damage to tubulointerstitial cells blcokage of tubules by casts reduced flow haemodynamic changes renal failure

76
Q

histology of ATN

A

necrosis of short tubules

77
Q

causes of ATN

A

ischaemic: sepsis, burns nephrotoxins: NSAIDS, gentamycin, myoglobin, heavy metals, contrast

78
Q

acute pyelonephritis symptoms

A

renal angle tenderness fever dysuria haematuria flank pain leukocytic casts in urine

79
Q

CHRONIC pyelonephritis with reflux nephropathy pathogenesis

A

recurrent bacterial infection causing scarring of the parencyma may be due to obstruction e.g. calculi or urine reflux

80
Q

acute interstitial nephritis pathology

A

drug hypersensitivity reaction beginning days after exposure

81
Q

symptoms of acute interstitial nephritis

A

eosinophilia haemauria prtoteinuria rash fever

82
Q

another name for chronic interstiital nephritis

A

analgesic nephropathy

83
Q

symptoms of chronic interstitial nephritis

A

HTN haematuria proteinuria anaemia

84
Q

pathophysiology of renal thrombotic microangiopathy

A

formation of platelet and fibrin rich thrmbi these thrombi damage passing RBC and platelets results in platelet and RBC destruction

85
Q

HUS pathogen

A

O157:H7 E coli

86
Q

location of thrombi in HUS

A

confined to kidneys therefore results in renal failure

87
Q

TTP thrombi location

A

in circulation esp CNS

88
Q

extra sx in TTP in addition to MAHA and bleeding

A

neuro sx (headache, seizures, coma)

88
Q
A
89
Q

symptoms of thrombotic microangiopathies (renal)

A

reduced platelets: petechia, bleeding, haematemesis, melaena MAHA: pallor, jaundice

90
Q

how to diagnose thrombotic microangiopathy (renal)

A

reduced Hb, reduced plt Coombes test NEGATIVE signs of haemolysis: raised bilirubin, LDH, reticulocytes fragmented RBC on blood smear

91
Q

manifestions of renal failure

A

raised urea and serum creatinine

92
Q

complication of renal failure

A

metabolic acidosis hyperkalaemia uraemia hypocalcaemia fluid overload HTN

93
Q

prerenal causes of renal failure

A

hypoperfusion hypovolaemia- burns, pancreatitis, sepsis

94
Q

renalauses of renal failure

A

ATN acute glomerulonephritis toxins thrombotic microangiopathy

95
Q

post renal causes of renal failure

A

obstruction e.g. calculi or tumour

96
Q

chronic renal failure defnition

A

pregressive irreversible loss of renal function results in symptoms of uraemia: fatigue, itching and confsuion

97
Q

causes of chronic renal failure

A

DM HTN PKD chronic peylonephritis glomerulonephritis

98
Q

pathology of polycystic kidney disease

A

destroyed renal parenchyma multiple kidney cysts liver cysts berry aneurysms

99
Q

mutation in polycystic kidney disease

A

PKD1 on chr 16 PKD2 in chr 4

100
Q

defective protein in polycystic kidney disese

A

polycystin 1/2

101
Q

clinical features of polycystic kidney disease

A

flank pain haematuria UTI

102
Q

complication of polycystic kidney disease

A

cyst infection cyst rupture cyst hammorhage

103
Q

lupus nephritis

A

immune complex deposition in kidney may be asymptomtomatic, may cause nephrotic syndrome or renal failure deponding on how many glomeruli are involved

104
Q

how many classes of lupus nephritis are tehre

A

6

105
Q

class 1 lupus nephritis

A

immune complex deposition but no structural alteration

106
Q

class4 lupus nephritis

A

>50% glomeruli involved diffuse lupus nephritis

107
Q

class 6 lupus nephritis

A

advances sclerosing >90% of glomeruli

108
Q

renal cell carcinoma types

A

clear cell chromophobic papilliary

109
Q

clear cell renal carcinoma features

A

well differentiated

110
Q

papilliary cell renal carcinoma features

A

dialysis associated cystic disease

111
Q

chromophobic renal cell carcinoma

A

pale eossinophilic cells

112
Q

RF for renal cell carcinoma

A

smoking HTN unopposed oestrogen heavy metals CKD

113
Q

paraneoplastic syndromes assocated with renal cell carcinoma

A

HTN hypercalcaemia amyloidosis Cushing’s disease polycythaemia

114
Q

sx of renal cell carcinoma

A

costo-vertabralangle pain mass haematuria