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STEP1 > Renal 3 > Flashcards

Renal 3 Flashcards

1
Q

What is the mechanism of action of acetazolamide?

A

Inhibits carbonic anhydrase –> increased excretion Na HCO3 + diuresis + decreased total body stores of HCO3

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2
Q

What are the clinical uses for acetazolamide? (5)

A
  1. glaucoma
  2. metabolic alkalosis
  3. altitude sickness
  4. urine alkalization
  5. pseudotumor cerebri
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3
Q

What are the toxicities of acetazolamide?

A

–hyperchloremic metabolic acidosis

–NH3 toxicity

–paresthesias

–sulfa allergy

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4
Q

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

A

Focal segmental glomerulosclerosis

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5
Q

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

A

Focal segmental glomerulosclerosis

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6
Q

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

A

Membranous nephropathy

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7
Q

Focal segmental glomerulosclerosis

What would we see on LM, IF, and EM?

A

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

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8
Q

What is the treatment for membranous nephropathy? What is the response to this treatment?

A

Steroids.

Poor response; my progress to chronic renal disease

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9
Q

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

A

Minimal change disease

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10
Q

What are the possible causes/triggers of minimal change disease?

A
  1. recent infection
  2. immunization
  3. immune stimulus
  4. may be associated with Hodgkin lymphoma
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11
Q

What disease process is the nephrotic presentation of SLE?

A

membranous nephropathy

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12
Q

What is the cause of the granular IF and “spike and dome” on EM for membranous nephropathy?

A

subepithelial immune complex deposition

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13
Q

LM: congo red stain shows apple-green birefringence under polarized light

Diagnosis?

A

amyloidosis

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14
Q

Briefly describe the pathophysiology of how systemic amyloidosis causes nephrotic syndrome.

A

amyloid deposition in the mesangium

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15
Q

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

A

membranoproliferative glomerulonephritis

Type 1

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16
Q

With what co-morbidities/disease is membranoproliferative glomerulonephritis Type 1 associated?

A

Hep b

Hep C

May also be idiopathic

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17
Q

With what co-morbidities/disease is membranoproliferative glomerulonephritis Type 2 associated?

A

Associated with C3 nephritic factor

(stabilizes C3 convertase –> decreased serum C3 levels)

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18
Q

Why do we see “tram-tracking” in membranoproliferative glomerulonephritis Type 1?

A

GBM splitting caused by mesangial growth.

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19
Q

LM: mesangial expansion, GBM thickening, eosinophilic glomerulosclerosis (Kimmelstiel-Wilson lesion)

Diagnosis?

A

Diabetic glomerulonephropathy

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20
Q

Membranous nephropathy

What would you see on LM, IF, and EM?

A

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

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21
Q

Minimal change disease

What would you see on LM, IF, and EM?

A

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

22
Q
  1. recent infection
  2. immunization
  3. immune stimulus
  4. may be associated with Hodgkin lymphoma

These are the potential triggers for which nephrotic syndrome?

A

What are the possible causes/triggers of minimal change disease?

23
Q

amyloidosis

What would you see on LM?

A

LM: congo red stain shows apple-green birefringence under polarized light

Diagnosis?

24
Q

membranoproliferative glomerulonephritis

Type 1

What would you see on LM and F?

A

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

25
Q

Diabetic glomerulonephropathy

What would you see on LM?

A

LM: mesangial expansion, GBM thickening, eosinophilic glomerulosclerosis (Kimmelstiel-Wilson lesion)

Diagnosis?

26
Q

How does diabetes lead to glomerulonephropathy?

A

nonenzymatic glycosylation of the GBM –> increased permeability and GBM thickening

nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion

27
Q

LM: mesangial proliferation

EM: mesangial immune complex deposits

IF: IgA immune complex deposits in mesangium

Diagnosis?

A

Ig A nephropathy

(Berger disease)

28
Q

How does IgA nephropathy usually present?

A

Often presents with URI or acute gastroenteritis

Episodic hematuria with RBC casts

29
Q

What is Alport syndrome?

A

A mutation in Type IV collagen –> thinning and splitting of the GBM.

Most commonly X-linked

30
Q

With what symptoms is Alport syndrome associated?

A

glomerulonephritis

deafness

less commonly, eye problems

31
Q

LM: wire-looping of capillaries

IF: granular

EM: subendothelial and sometimes intramembranous IgG immune complexes, often with C3 deposition

A

Diffuse proliferative glomerulonephritis

32
Q

What is the most common cause of death in patients with SLE?

A

diffuse proliferative glomerulonephritis

33
Q

What are the two most common causes of diffuse proliferative glomerulonephritis?

A

SLE

membranoproliferative glomerulonephritis

34
Q

Cresent formation in the Bowman’s space/glomerulus on H&E/LM is indicative of what disease process?

A

rapidly progressive glomerulonephritis

There are multiple causes of RPGN; the clinical picture and IF can help make the specific diagnosis

35
Q

H&E: cresent formation in the Bowman’s space

IF: linear

Diagnosis?

A

Goodpasture’s Syndrome

36
Q

What is the classic presentation of Goodpasture syndrome? What is the disease process?

A

In Goodpasture syndrome, antibodies are made against the collagen (type IV) in the glomerular and alveolar basement membranes

presents as hematuria and hemoptysis, classically in young, adult males.

37
Q

H&E: cresent formation in the Bowman’s space

IF: granular

Diagnosis?

A

post-streptococcal glomerulonephritis

diffuse proliferative glomerulonephritis

38
Q

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

Diagnosis?

A

Wegener granulomatosis

microscopic polyangiitis

Churg-Strauss syndrome

39
Q

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

c-ANCA positive

Diagnosis?

A

Wegener granulomatosis

40
Q

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

p-ANCA positive

granulomatous inflammation, eosinophilia, asthma

Diagnosis?

A

Churg-Strauss syndrome

41
Q

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

p-ANCA positive

No granulomatous inflammation, eosinophilia, or asthma

Diagnosis?

A

microscopic polyangiitis

42
Q

LM: glomeruli enlarged and hypercellular

IF: granular, lumpy-bumpy appearance (IgG, IGM, C3 deposition along GBM and mesangium)

EM: subepithelial humps (IC)

Diagnosis?

A

post-streptococcal glomerulonephritis

43
Q

What is the classic hx for post-streptococcal glomerulonephritis?

A

Peripheral and periorbital edema, dark urine, and hypertension approximately two weeks after group A ß-hemolytic streptococcal infection of the pharynx or skin (impetigo).

increased anti-DNase B titers and decreased complement levels.

44
Q

What are the classic symptoms in nephritic syndromes?

A

azotemia

oliguria

hypertension (due to salt retention)

proteinuria (<3.5g/day)

hematuria and RBC casts in the urine

45
Q

What are the symptoms of nephrolithiasis (kidney stones)?

A

Colicky pain that radiates to the groin

unilateral flank tenderness

hematuria

46
Q

Ig A nephropathy

(Berger disease)

What would we see on LM, IF, and EM?

A

LM: mesangial proliferation

EM: mesangial immune complex deposits

IF: IgA immune complex deposits in mesangium

Diagnosis?

47
Q

Diffuse proliferative glomerulonephritis

What would we see on LM, IF, and EM?

A

LM: wire-looping of capillaries

IF: granular

EM: subendothelial and sometimes intramembranous IgG immune complexes, often with C3 deposition

48
Q

Goodpasture’s Syndrome

What would we see on LM and IF?

A

H&E: cresent formation in the Bowman’s space

IF: linear

Diagnosis?

49
Q

Wegener granulomatosis

microscopic polyangiitis

Churg-Strauss syndrome

What would we see on LM and IF?

A

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

Diagnosis?

50
Q

Wegener granulomatosis

What would we see on LM and IF? How would you distinguish this diagnosis from microscopic polyangiitis or Churg-Strauss syndrome?

A

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

c-ANCA positive

Diagnosis?

51
Q

Churg-Strauss syndrome

What would you see on LM and IF?

How would you distninguish this from Wegener granulomatosis? How would you distninguish this from microscopic polyangiitis?

A

H&E: cresent formation in the Bowman’s space

IF: negative (pauci-immune)

p-ANCA positive

granulomatous inflammation, eosinophilia, asthma

Diagnosis?

STEP1 (53 decks)

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