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PBL 2.2.4 > Path 20: Kidney no make pee > Flashcards

Path 20: Kidney no make pee Flashcards

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1
Q

Post strep glomerulonephiritis timeline and IF/EM

A

1-4 weeks

Granular staining pattern for IgG and C3 humps of immune complexes

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2
Q

Renal tubular acidosis types

A

1: Distal renal
2: Proximal renal
4: Hyperkalemic

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3
Q

Distal renal tubular acidosis pathogenesis

A

Inability of α-intercalated cells to secrete H+

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4
Q

Distal renal tubular acidosis findings

A

Decreased serum K+.

Urine pH above 5.5

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5
Q

Renal tubular acidosi: what type of acidosis ?

A

Normal anion gap

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6
Q

Proximal renal tubular acidosis pathogenesis

A

PCT HCO3 reabsorption is impaired leading to increased urine HCO3

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7
Q

Hyperkalemic tubular acidosis pathogenesis

A

Hypoaldosterone or aldosterone resistance leads to hyperK. Leads to decreased NH4 excretion

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8
Q

Labs in type 4 tubular acidosis

A

Increased serum K+

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9
Q

Fanconi sx sumptoms

A

Generalized PCT reabsoroption defect. Leads to excretion of all PCT absorbed sunstances

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10
Q

Barter syndrome pathogenesis and findings

A

Na/+K+/2Cl- defect

Acts like lasix

Metabolic alkalosis, hypoK, hypercalciuria

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11
Q

Liddle syndrome caused by

A

Gain of function leads to decrease in Na+ degredation and increase in Na+ reabsorption in collecting tubule

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12
Q

RBC casts seen with

A

Glomerolonephritis, HTN

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13
Q

WBC casts seen in

A

Tubulointerstitial inflamation, pyelonephritis

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14
Q

Granular casts seen in ? and appearance

A

Acute tubular necrosis

“Muddy brown”

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15
Q

Fatty casts seen in and visual

A

Nephrotic syndrome

Maltese cross

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16
Q

Waxy casts seen in

A

ESRF

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17
Q

Neprhitic syndrome presentation

A

Hematuria, RBC casts, oligouria, HTN

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18
Q

Nephritic syndrome etiology

A

Glomerula inflammation leads to GBM damage

Leads to RBC loss and hematuria

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19
Q

Nephrotic syndrome etiology

A

Podocyte damage fucks with charge barrier leading to proteinuria

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20
Q

Nephrotic syndrome findings

A

Massive proteinuria with edema, frothy urine, hypercoagulable state

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21
Q

PSGN post strep pathology

A

2-4 weeks after strep infection. Type III hypersensitivity

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22
Q

PSGN light IF

A

Starry sky/ granular appearance.

IgG, IgM and C3 deposition in GBM and mesangium

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23
Q

PSGN Electron microscopy

A

Subepithelilial IC humps

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24
Q

RPGN features

A

Rapid deterioration, cresents

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25
Q

RPGN and linear IF:

A

Goodpasture syndrome (Type II hypersensitivity)

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26
Q

RPGN and negative IF:

A

Granulomatosis

C-ANCA, MPO-ANCA, p-ANCA

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27
Q

RPGN and Granular IF

A

diffuse proliferative glomerulonephritis

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28
Q

Diffuse proliferative glomerulonephitis seen with

A

Lupus

29
Q

Diffuse proliferative glomerulonephritis EM

A

Sub endothelial deposit

30
Q

IgA nepropathy aka

A

Berger dx

31
Q

Berger disease presentation

A

IGA vasculitis due to current GI/Resp infection

32
Q

IgA nepropathy IF

A

On mesangium, granular

33
Q

Alport syndrome pathogenesis

A

Type IV collagen mutation

Glomerular basement membrane loss of integrity

34
Q

Minimal change disease pathology

A

Nephrotic syndrome in children

Due to foot process effacement

35
Q

Focal segemental glomerulosclerosis LM/EM findings

A

LM: segemental sclerosis and hyalinosis

EM: effacement of foot processes

36
Q

Membranous nepropathy pathogenesis

A

Usually idiopathic GBM thickening

37
Q

Membranous nepropathy LM/IF/EM findings

A

IF: granular
LM: thick GBM and capillary
EM: spike and dome subepithelial

38
Q

Amylodisosis finding

A

Apple green birefringence

39
Q

Diabetic glomerulonephropathy pathology

A

Hyperglycemia leads to glycation of proteins

leads to increads GBM membrane. Causes hypterfiltration

40
Q

Drugs that help diabetic nephropathy

A

ACE inhibitor

41
Q

Calcium stone features

A

Radiopaque , can be calciuria,

42
Q

Ammonium magnesium phosphate stones aka ____ + features

A

Struvite

Radiopaque

Caused by infections that hydrolyze urea

Coffin cristal

43
Q

Elevated urine ph causes precipitation of

A

Calcium phosphate

Ammonium magnesium phosphate

44
Q

Hypocitriuria causes precipitation of

A

Calcium oxalate

45
Q

Decreased urine ph causes precipitation of

A

Uric acid
Cystine

46
Q

Uric acid stone features

A

Radiolucent

Rhomboid crystal

Seen in diseases with rapid cell turnover

47
Q

Cystine stone features

A

Seen in cystinuria, hexagonal crystals

48
Q

Staghorn caliculi stone types

A

Infections (struvite)

Cystine

49
Q

Chronic pyelonephritis pathology

A

Interstitial fifrosis, usually due to obstruction.

Atrophic tubules lead to thyrodization

50
Q

Prerenal azotemia due to

A

Hypovolemia

51
Q

Prerenal azotemia BUN/CR

A

More than 20

52
Q

Postrenal azotemia BUN:Cr

A

less than 15

53
Q

Acute interstitial nephritis pathology

A

Drug induced hypersensitivity to NSAIDs, PCN and diuretics

54
Q

Acute interstitial nephritis presentation

A

Oliguria, fever, rash. No pain.

Pyuria, azotemia

55
Q

Acute tubular necrosis presentation

A

Acute renal failure, hyperK, metabolic acidosis, uremia, increased FENA+, unconcentrated urine

56
Q

Renal papillary necrosis presentation

A

Gross hematuria and flank pain, often inciting event

57
Q

Renal failure consequences

A

Metabolic acidosis

HyperK

Sodium retention

58
Q

Autosomal dominant kidney disease presentation and gene

Cysts where

A

APKD1/2 gene mutation. Presents as young adult with HTN and renal failure

Cyts in medulla and cortex

59
Q

autosomal dominant PKD treatment

A

ACE inhibitors

ARBs

60
Q

Autosomal recessive PKD features

A

Potter seuqnece, congenital hepatic fibrosis, cysts in collecting ducts .

61
Q

Renal cell carcinoma presentation

A

Hematuria, papable mass, flank pain

Fever, weight loss, paraneoplastic syndrome

62
Q

Renal cell carcinoma gene progression

A

Loss of VHL gene (chromosome 3)

63
Q

Most common malignant renal tumor in kids

A

Wilms tumor (avg 3yo)

64
Q

Wilms tumor pahtology

A

Malignant tumor made of blastema (mesenchyme)

65
Q

Wilms tumor presentation

A

Palapable mass, hematuria, HTN

66
Q

Wilms tumor with no iris and malformed genitals

A

WAGR complex

67
Q

wilms tumor with WT1 deletion

A

WAGR

68
Q

Wilms tumor with hypoglycemia, hypertrophy of tongue and muscles (+gene)

A

Beckwith-Wiedman

WT2

69
Q

Membranous nepropathy caused by (virus)

A

HepB

PBL 2.2.4 (13 decks)

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