Renal 3 Flashcards Preview

STEP1 > Renal 3 > Flashcards

Flashcards in Renal 3 Deck (51):
1

What is the mechanism of action of acetazolamide?

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

2

What are the clinical uses for acetazolamide? (5)

1. glaucoma

2. metabolic alkalosis

3. altitude sickness

4. urine alkalization

5. pseudotumor cerebri

3

What are the toxicities of acetazolamide?

--hyperchloremic metabolic acidosis

--NH3 toxicity

--paresthesias

--sulfa allergy

4

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

Focal segmental glomerulosclerosis

5

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

Focal segmental glomerulosclerosis

6

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

Membranous nephropathy

7

Focal segmental glomerulosclerosis

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

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

8

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

Steroids.

Poor response; my progress to chronic renal disease

9

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

Minimal change disease

10

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

1. recent infection

2. immunization

3. immune stimulus

4. may be associated with Hodgkin lymphoma

11

What disease process is the nephrotic presentation of SLE?

membranous nephropathy

12

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

subepithelial immune complex deposition 

13

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

Diagnosis?

amyloidosis

14

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

amyloid deposition in the mesangium

15

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

membranoproliferative glomerulonephritis

Type 1

16

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

Hep b

Hep C

May also be idiopathic

17

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

Associated with C3 nephritic factor

(stabilizes C3 convertase --> decreased serum C3 levels)

18

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

GBM splitting caused by mesangial growth.

19

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

Diagnosis?

Diabetic glomerulonephropathy

20

Membranous nephropathy

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

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

21

Minimal change disease

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

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

22

1. recent infection

2. immunization

3. immune stimulus

4. may be associated with Hodgkin lymphoma

These are the potential triggers for which nephrotic syndrome?

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

23

amyloidosis

What would you see on LM?

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

Diagnosis?

24

membranoproliferative glomerulonephritis

Type 1

What would you see on LM and F?

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

25

Diabetic glomerulonephropathy

What would you see on LM?

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

Diagnosis?

26

How does diabetes lead to glomerulonephropathy?

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

 

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

27

LM: mesangial proliferation

EM: mesangial immune complex deposits

IF: IgA immune complex deposits in mesangium

Diagnosis?

Ig A nephropathy

(Berger disease)

28

How does IgA nephropathy usually present?

Often presents with URI or acute gastroenteritis

Episodic hematuria with RBC casts

29

What is Alport syndrome?

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

Most commonly X-linked

30

With what symptoms is Alport syndrome associated?

glomerulonephritis

deafness

less commonly, eye problems

31

LM: wire-looping of capillaries

IF: granular

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

Diffuse proliferative glomerulonephritis

32

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

diffuse proliferative glomerulonephritis

33

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

SLE

membranoproliferative glomerulonephritis

34

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

rapidly progressive glomerulonephritis

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

35

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

IF: linear

Diagnosis?

Goodpasture's Syndrome

36

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

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

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

IF: granular

Diagnosis?

post-streptococcal glomerulonephritis

diffuse proliferative glomerulonephritis

38

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

IF: negative (pauci-immune)

Diagnosis?

Wegener granulomatosis

microscopic polyangiitis

Churg-Strauss syndrome

39

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

IF: negative (pauci-immune)

c-ANCA positive

Diagnosis?

Wegener granulomatosis

40

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

IF: negative (pauci-immune)

p-ANCA positive

granulomatous inflammation, eosinophilia, asthma

Diagnosis?

Churg-Strauss syndrome

41

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

IF: negative (pauci-immune)

p-ANCA positive

No granulomatous inflammation, eosinophilia, or asthma

Diagnosis?

microscopic polyangiitis

42

LM: glomeruli enlarged and hypercellular

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

EM: subepithelial humps (IC)

Diagnosis?

post-streptococcal glomerulonephritis

43

What is the classic hx for post-streptococcal glomerulonephritis?

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

What are the classic symptoms in nephritic syndromes?

azotemia

oliguria

hypertension (due to salt retention)

proteinuria (<3.5g/day)

hematuria and RBC casts in the urine

45

What are the symptoms of nephrolithiasis (kidney stones)?

Colicky pain that radiates to the groin

unilateral flank tenderness

hematuria

46

Ig A nephropathy

(Berger disease)

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

LM: mesangial proliferation

EM: mesangial immune complex deposits

IF: IgA immune complex deposits in mesangium

Diagnosis?

47

Diffuse proliferative glomerulonephritis

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

LM: wire-looping of capillaries

IF: granular

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

48

Goodpasture's Syndrome

What would we see on LM and IF?

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

IF: linear

Diagnosis?

49

Wegener granulomatosis

microscopic polyangiitis

Churg-Strauss syndrome

What would we see on LM and IF?

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

IF: negative (pauci-immune)

Diagnosis?

50

Wegener granulomatosis

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

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

IF: negative (pauci-immune)

c-ANCA positive

Diagnosis?

51

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?

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

IF: negative (pauci-immune)

p-ANCA positive

granulomatous inflammation, eosinophilia, asthma

Diagnosis?