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Bloc D - Renal > Jan11 M2,3-Pathology of glomerular diseases and renal tubules > Flashcards

Jan11 M2,3-Pathology of glomerular diseases and renal tubules Flashcards

1
Q

give 5 primary glomerular diseases

A
  • membranous nephropathy
  • MCD
  • FSGS
  • IgA nephropathy
  • Membranoproliferative GN
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2
Q

give 5 secondary or systemic diseases that affect the kidney (glomerulus)

A
  • DM
  • amyloidosis
  • SLE
  • drugs (NSAIDs)
  • infectious (HIV, hepB,C, syphilis)
  • malignancy + paraneoplastic
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3
Q

4 clinical presentations for glomerular disease

A

hematuria, proteinuria, mixed, renal failure

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4
Q

how to know if hematuria is due to a glomerular disease (and not something more downstream)

A

if glomerular disease, RBC casts present

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5
Q

RBC casts point to what syndrome

A

nephritic. no RBC casts in nephrotic syndrome

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6
Q

pure nephrotic is caused by what

A

problem in glomerular filtration barrier (GBM or other)

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7
Q

proteinuria qt in nephrotic

A

3-3.5g a day or more

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8
Q

2 types of proteinurias in nephrotic + def

A

selective: albumin only

non-selective: albumin + other prots too

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9
Q

5 charact of nephrotic syndrome (labs)

A
  • heavy proteinuria (3g a day)
  • hypoalbuminemia
  • hyperlipidemia
  • lipiduria
  • edema
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10
Q

nephrotic syndrome: urine sediment findings

A
  • protein cast/waxy cast
  • fatty casts
  • oval fat bodies (desquamated tubular cells filled with reabsorbed lipids)
  • RBCs but no cast
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11
Q

can you find RBCs in nephrotic syndrome urine sediment

A

yes but no RBC casts

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12
Q

nephrotic syndrome: 3 main primary diseases

A
  • MCD
  • FSGS
  • membranous nephropathy
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13
Q

nephrotic syndrome: 3 main secondary diseases/conditions that can cause it

A
  • DM
  • amyloidosis
  • pregnancy
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14
Q

nephrotic syndromes (2 primary and 2 secondary) that present with hematuria

A

primary: 1. membrano-proliferative GN 2. IgA nephropathy
secondary: 1. lupus nephritis 2. Henoch-Schonlein purprue (HSP)

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15
Q

most common PRIMARY nephrotic syndrome disease in children and most common PRIMARY in adult

A

children: MCD
adults: FSGS

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16
Q

most common SECONDARY nephrotic syndrome diseases in adults

A
  • DM
  • amyloidosis
  • SLE
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17
Q

MCD: proteinuria type and only thing seen on biopsy

A

selective

only see effacement of foot processes on EM (LM and IF negative)

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18
Q

MCD treatment

A

steroids

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19
Q

MCD recurrence and prognosis

A

2/3 recurrence

very good prognosis

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20
Q

patho characteristics seen in some nephritic but not nephrotic syndrome

A

crescents, proliferation, hypercell, necrosis, inflammation

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21
Q

why selective proteinuria in MCD (2)

A

swelling of podocytes and podocyte fusion = loss of negative charge

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22
Q

general pathological feature of DM

A

deposition of glycosylated molecules on BMs everywhere

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23
Q

pathophgy of FSGS

A

injury (toxic or immune or genetic) to podocytes and loss of negative charge (hematuria is non selective)

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24
Q

main causes of FSGS (cause of podocyte toxicity)

A

HIV, heroin, hyperfiltration (high BP), medication

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25
Q

what type of immune toxicity to podocytes in FSGS

A

immune dysregulation with cytokines/T cells but no immune complexes and no autoimmune rx

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26
Q

prognosis of FSGS

A

50% dev ESRD in 10 yrs

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27
Q

type of proteinuria in FSGS and hematuria or not

A

non-selective proteinuria.

hematuria is mild or moderate

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28
Q

FSGS (focal segmental glomerulosclerosis): sclerosis meaning

A

scarring (fibrosis). less 50% glomeruli and part of glomeruli

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29
Q

why is there a vicious circle in FSGS

A

hyperfiltration injury. more P in GCs that still function so hyperfiltration injury in the glomerulus and sclerosis of nephrons

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30
Q

FSGS sometimes associated with ____

A

htn

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31
Q

membranous nephropathy: pathogenesis

A

antibodies recognize self protein on glomerular epithelial cells (podocytes)

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32
Q

membranous nephropathy: antibody often present (antibody against what)

A

antibody against PLA2R (podocyte antigen phospholipase A2 receptor)

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33
Q

membranous nephropathy: how fast it progresses + prognosis

A

slowly

40% progress to renal failure

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34
Q

membranous nephropathy: usual primary cause

A

a pathology of the GBM (membranous nephropathy is a form of GN)

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35
Q

membranous nephropathy: usual secondary causes (4)

A
  • infections (hep, syph, mal)
  • cancer
  • autoimmune (SLE)
  • drugs,toxins
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36
Q

FSGS: LM, IF and EM findings

A

LM: sclerosis + loss of capillaries
EM: non specific deposits of IGM and C3 segmentally
EM: effacement of foot processes

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37
Q

membranous nephropathy: LM, IF and EM

A

LM: diffuse thickening of the glomerular capillary walls
IF: IgG granular along the GBM
EM: sub-epithelial deposits, spikes

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38
Q

Diabetic nephrotic syndrome: at what point is it nephrotic syndrome

A

when proteinuria goes beyond the usual diabetic proteinuria

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39
Q

diabetic nephrotic syndrome LM, IF and EM

A

LM: diffuse or nodular GS, increased mesengium (KW lesions), arteriosclerosis, arteriolosclerosis, hyalinosis
IF: non specific
EM: thickening of GBM

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40
Q

Kimmelstiel-Wilson (KW) lesions in what condition and what is it

A

diabetic nephrotic syndrome

mesengial matrix increase and mesengial nodules

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41
Q

proteinuria and pregnancy usually sign of what

A

hypertension/pre-eclampsia

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42
Q

which nephrotic syndrome diseases (primary and 2ndary) get a biopsy and which do not

A 
MCD: no
FSGS: yes
MN: yes
DM: no (or ?)
pregnancy: no
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43
Q

azotemia and uremia def

A

azotemia: high BUN
urea: high blood urea

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44
Q

nephritic syndrome typical findings (like the 5 of nephrotic but for nephritic)

A

hematuria, RBC casts, proteinuria, renal failure (azotemia), htn

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45
Q

3 most common primary nephritic syndrome diseases (primary GNs) + 1 that we have to remember

A
  • acute post-infectious GN
  • IgA nephropathy
  • membrano proliferative GN (MPGN)
  • RPGN
46
Q

4 most common secondary nephritic syndrome diseases

A
  • lupus nephritis
  • Henoch-Schonlein purpura (HSP)
  • anti-GBM (Goodpasture syndrome)
  • Vasculitis/ANCA related GN
47
Q

acute post infectious GN affects what pop typically

A

children

48
Q

acute post infectious GN: after what infections usually

A

beta hymolytic streptococcal infections or URT or skin.

other: staph, pneumococcus, viruses

49
Q

presentation in acute post infectious GN

A

tea/cola colored urine, RBC casts, proteinuria, hematuria

50
Q

acute post infectious GN: LM if ever take a biopsy (2-3 things)

A

diffuse global hypercellularity (prolif of glomerular cells) and infiltration of PMN leukocytes (exudative GN) (+ crescents sometimes)

51
Q

acute post infectious GN on IF if ever take a biopsy

A

large granular deposits

C3 and IgG along GBM specifically

52
Q

how IgG deposits in membranous nephropathy (or membranous GN) and acute post infectious GN differ

A

in MN, smaller deposits and look like a stream

in acute post infectious GN, granular and larger (but deposit on GBM in both cases)

53
Q

prognosis and dev to ESRD in acute post infectious GN

A

good prognosis
children mostly affected and 1% children ESRD
adults (rarely): but 15-50% ESRD

54
Q

labs in acute post infectious GN (2)

A
  • low C3 (bc massive deposition in the kidney

- positive ASOT (for strep infection)

55
Q

IgA nephropathy (Berger): when does it happen and who is affected

A

1-2 days after URTI

children and young adults

56
Q

IgA nephropathy (Berger): prognosis

A

25% ESRD in 10 yrs

57
Q

fix things (2) that are common to all IgA nephropathy (Berger) patients on biopsy

A
  • mesengial prolif

- IgA deposition on mesengium (IF)

58
Q

variable features of pathophgy of IgA nephropathy (Berger)

A

highly variable in inflammation, crescents, necrosis and scarring

59
Q

Henoch-Schonlein purpura (HSP) def

A

systemic form of IgA nephropathy with vasculitis

60
Q

Henoch-Schonlein purpura (HSP) presentation

A

gross hematuria, GI symptoms, palpable purpura (vasculitis)

61
Q

Henoch-Schonlein purpura (HSP) special thing about the biopsy + finding

A

can do it on the skin

find vasculitis with IgA deposits

62
Q

Henoch-Schonlein purpura (HSP) prognosis

A

even better than IgA nephropathy

63
Q

RPGN presentation

A

hematuria, htn, RBC casts, oliguria

64
Q

RPGN cause

A

no cause, it’s a syndrome/clinical presentation

65
Q

RPGN main feature

A

crescents on biopsy

66
Q

RPGN often associated with what cause

A

-lupus
-anti-GBM
-etc
or sometimes idiopathic

67
Q

treatment of RPGN

A

corticosteroids

68
Q

RPGN prognosis

A

(IF UNTREATED), death from renal failure in weeks to months

69
Q

crescents in acute vs chronic RPGN

A

acute: cellular crescent
chronic: fibrous crescent

70
Q

RPGN biopsy findings

A

inflam, necrosis, damage to GBM, proinflam mediators make the cells proliferate

71
Q

T/F: crescents are the cause of damage in RPGN

A

false. leakage of blood and prot

72
Q

3 main types of crescentic GNs

A
  1. anti-GBM
  2. immune complex mediated (SLE, IgA nephritis, MPGN, post-infectious
  3. pauci-immune (ANCA-related)
73
Q

anti-GBM: pathophgy

A

antibodies to the type IV collagen (NC1 domain of alpha 3 chain) in the GBM

74
Q

anti-GBM: when is called Goodpasture syndrome

A

when lung involvement too (type IV collagen also in the lungs)

75
Q

anti-GBM treatment

A

steroids and plasmapheresis

76
Q

anti-GBM labs

A

anti-GBM antibodies

77
Q

anti-GBM prognosis

A

WITH treatment, 60% ESRD

78
Q

anti-GBM: LM, IF and EM

A

LM: crescents and necrosis
IF: linear IgG deposits on GBM
EM: no deposits visible

79
Q

pauci-immune GN: what population + prognosis

A

older patients. with treatment, 30% reach ESRD in less than 2 years

80
Q

pauci-immune GN labs

A

ANCA (anti neutrophil cytoplasmic antibody)

81
Q

pauci-immune GN: LM, IF, EM

A

LM: crescents
EM: no deposits
IF: no deposits (or minimal)

82
Q

pauci-immune GN: amunt of immune involvement

A

small

83
Q

any disease with Ab-Ag immune complex deposition can lead to ________
give 3 examples of diseases

A

RPGN

lupus, IgA nephropathy, anti-GBM

84
Q

glomerular diseases with crescents (3)

A
  • immune mediated ones (APIGN, MPGN, SLE, IgA nephritis)
  • anti-GBM
  • ANCA (pauci-immune)
85
Q

glomerular diseases with inflammation involvement (exduate)

A

APIGN

86
Q

glomerular diseases with scarring (5)

A

FSGS, diabetes, IGAN (and HSP), RPGN

87
Q

glomerular diseases associated with htn

A

FSGS, diabetes, RPGN. Nephritic in general. htn = cause of nephrotic in adults

88
Q

glomerular diseases that have hypercellularity (2 main)

A

APIGN, IGAN (and HSP), RPGN and crescentic diseases

89
Q

what glomerular diseases have necrosis

A

IGAN (and HSP), anti-GBM

90
Q

what kidney diseases have RBC casts (has to be glomerular bc RBC cast = glomerular)

A

IgA nephropathy, post-infectious GN, lupus, vasculitis, anti-GBM
(remember cast = nephritic)

91
Q

what kidney diseases have RBC casts (has to be glomerular bc RBC cast = glomerular)

A

IgA nephropathy, post-infectious GN, lupus, vasculitis, anti-GBM
(remember cast = nephritic)

92
Q

5 tubulointerstitial diseases

A
  • acute pyelonephritis
  • chronic pyelonephritis
  • reflux nephropathy
  • drug induced interstitial nephritis
  • ATN (acute tubular injury)
93
Q

acute pyelonephritis cause

A

bacterial infection (from UTI or form blood)

94
Q

acute pyelonephritis symptoms

A

sudden onset, malaise, fever, chills, CVA pain, dysuria (painful whne urinate), urgency

95
Q

acute pyelonephritis risk factors

A

immunosuppresion, women (shorter urehtra), procedures, obstruction, diabetes

96
Q

pathology of acute pyelonephritis

A

bacterial involvement (one kidney), pus in interstitium, microabcesses and WBC in urine. pus in tubules.

97
Q

papillary necrosis def

A

form of acute pyelonephritis with ischemic necrosis of the pyramids’ papilla in context of diabetes, obstruction, analgesic abuse

98
Q

acute/drug-induced interstitial nephritis: causes

A

hypersensitivy/allergy/abnormal immune rx/direct toxicity from a medication (antibiotics, analgesics: penicillins, diuretics, NSAIDs)

99
Q

acute/drug-induced interstitial nephritis: symptoms + onset

A

2-40 days after taking the drug.

oliguria, azotemia, fever

100
Q

acute/drug-induced interstitial nephritis: UA

A

hematuria, leukocytes, NO RBC CAST, bit of proteinuria

101
Q

pathology of acute/drug-induced interstitial nephritis

A

interstitial edema and inflammation

102
Q

ATI/ATN three types

A

pre-renal, renal, post-renal

103
Q

ATI/ATN is the most common cause of __________

A

AKI

104
Q

ATI/ATN cause if pre-renal vs if post renal

A

pre-renal: ischemic damage

post-renal: obstruction by compression causes toxicity

105
Q

manifestations of ATI/ATN

A

oliguria/anuria, drop GFR, electrolyte imbalance, acidosis, fluid overload

106
Q

2 types of injuries to tubules in ATI/ATN

A

ischemic or toxic

107
Q

most affected tubules in ATI/ATN

A

PCT

108
Q

ATI/ATN biopsy findings

A

vacuolization of cytoplasm, apical blebbing, dilation of tubules, nuclear loss, denudation

109
Q

amount of inflammation in ATI/ATN

A

none

110
Q

diseases with hematuria

A

nephritic + acute pyelonephritis

Bloc D - Renal (32 decks)

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