SU2M - Glomerular Disease Flashcards

0
Q

Pathogenesis of nephritic v nephrotic syndrome?

A
  • nephrITIC= inflammation of glomeruli due to any cause of glomerularnephritis
  • nephrOTIC= abnormal glomerular permeability due to a number of conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

3 Causes of glomerular nephritis?

A
  1. Immune-mediated disease –> most common!
  2. Metabolic disturbance
  3. Hemodynamic disturbance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of nephritic v nephrotic syndrome?

A
  • nephrITIC = poststreptococcal glomerulonephritis is the most common cause (can be due to any cause of glomerularnephritis)
  • nephrOTIC = membranous glomerulonephritis is the most common cause in adults (other causes = DM, SLE, etc) and minimal change disease is the most common cause in children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Lab findings in nephritic (3) v nephrotic (3) syndrome?

A
  • nephrITIC:
    1. Hematuria
    2. AKI = azotemia, oliguria
    3. Protienuria –> if present, will be mild and NOT in the nephrotic range
  • nephrOTIC:
    1. Proteinuria >3.5 g/24hr
    2. Hypoalbuminemia
    3. Hyperlipidemia –> w/ fatty casts in the urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical findings of nephrITIC (2) v nephrOTIC (3) syndrome?

A
  • nephrITIC:
    1. HTN
    2. Edema
  • nephrOTIC:
    1. Edema
    2. Hypercoagulable state
    3. Increased risk of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glomerular disease v. Tubular dz: acute or chronic?

A
  • GD = chronic

- TD = acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glomerular v. Tubular disease: which is usually caused by toxins?

A

-TD!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Glomerular v. Tubular disease: which can cause nephrotic syndrome?

A

-GD!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Glomerular v. Tubular disease: require biopsy?

A

-ONLY GD!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Glomerular v. Tubular disease: steroids and/or immunosuppresive medications for tx?

A

-both steroids and immunosuppresive medications are used to tx GD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Who is minimal change disease typically seen in?

A
  • children

- also associated with hodgkin’s and non-hodgkin’s lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Minimal change’s disease: histology?

A
  • NONE seen with light microscope!

- see fusion of foot processes on EM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Minimal change disease: prognosis?

A
  • very responsive to steroid tx (4-8 wks)

- but relapses can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is most likely the cause of minimal change disease?

A

-T cell dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Focal segmental glomerulosclerosis: who is it most commonly seen in? What 2 ssx are often present?

A
  • most commonly seen in adults, esp blacks

- often seen with hematuria and HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Focal segmental glomerulosclerosis: prognosis

A
  • fair to poor prognosis
  • generally resistant to steroid tx
  • pts usually develop renal insufficiency w/in 5-10 yrs of diagnosis
  • progressive dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Focal segmental glomerulosclerosis: tx?

A
  • controversial

- cytotoxic agents, steroids, immunosuppressive agents, and ACEi/ARBs are all options

17
Q

Membranous glomerulonephritis: common presentation?

A
  • presents with nephrotic syndrome

- glomerular capillary walls are thickened

18
Q

Causes of primary and secondary membranous glomerulonephritis?

A
  • primary: usually idiopathic
  • secondary:
    1. Infection - hep C, hep B, malaria, syphilis
    2. Drugs - gold, captopril, penicillamine
    3. Neoplasm
    4. Lupus
19
Q

Membranous glomerulonephritis: prognosis?

A
  • fair to good
  • course can be variable
  • remission can happen in 40% of the cases
  • renal failure occurs in 33% of cases
  • steroid tx does not change survival rate
20
Q

How does IgA nephropathy usually present?

A
  • recurrent asymptomatic hematuria/mild proteinuria
  • or gross hematuria after URI (or exercise)
  • renal function is usually normal
  • *this is th most common cause of glomerular hematuria
21
Q

IgA nephropathy: histology?

A

-mesangial deposits of IgA and C3 seen on EM

22
Q

IgA neohropathy: prognosis?

A
  • good as long as renal fctn is preserved

- renal insufficiency can occur in 25% of cases

23
Q

IgA nephropathy: tx?

A
  • no tx has been proven to be effective

- steroids are sometimes used for unstable dz

24
Q

Hereditary nephritis: genetics?

A

-x-linked or autosomal-dominant with variable penetrance

25
Q

Hereditary nephritis: ssx?

A
  • AKA Alport’s syndrome
    1. Hematuria
    2. Pyuria
    3. Proteinuria
    4. High-freq hearing loss, w/out deafness
    5. Progressive renal failure
26
Q

Hereditary nephritis: tx?

A

-No effective tx

27
Q

Most common cause of end stage renal disease?

A

-diabetic nephropathy

28
Q

Membranoproliferative glomerulonephritis: causes

A
  • usually due to hep C

- other causes: hep B, syphilis, or lupus

29
Q

Membranoproliferative glomerulonephritis: prognosis?

A
  • prognosis is poor

- renal failure develops in 50% of pts

30
Q

Most common cause of nephritic syndrome?

A

-post streptococcal GN

31
Q

Poststeptococcal glomerulonephritis: who is it commonly seen in? When?

A
  • primarily seen in children

- 10-14 days after an infection with group A beta-hemolytic step infection of upper resp tract or skin (impetigo)

32
Q

Poststreptococcal GN: ssx (6)?

A
  1. Hematuria
  2. Edema
  3. HTN
  4. Low complement levels
  5. Proteinuria
  6. Elevated antistreptolysin-O
33
Q

Poststreptoccoal GN: tx?

A
  • usually supportive
  • antiHTNs
  • loop diuretics –> edema
  • antibiotics –> controversial
  • steroids –> can be helpful in severe cases
34
Q

Goodpasture’s syndrome: classic triad?

A
  1. Proliferative glomerulonephritis –> usually crescentic
  2. Pulmonary hemorrhage
  3. IgG anti-glomerular basement membrane antibody
35
Q

Goodpasture’s syndrome: clinical features (4)?

A
  1. Rapidly progressive renal failure
  2. Hemoptysis
  3. Cough
  4. Dyspnea
    * *lung disease usually precedes kidney disease by days to weeks
36
Q

Goodpasture’s syndrome: histology?

A

-renal biopsy shows linear immunofluorescence pattern

37
Q

Goodpasture’s syndrome: tx?

A
  • plasmaphresis –> remove circulating anti-IgG antibodies

- cyclophosphamide and steroids –> decrease the formation of new antibodies

38
Q

HIV nephropathy: ssx?

A
  1. Proteinuria
  2. Edema
  3. Hematuria
39
Q

HIV proteinuria: histopathology?

A

-looks like a collapsing form of focal segmental glomerulosclerosis

40
Q

HIV nephropathy: tx (3)?

A
  1. Prednisone
  2. ACEi
  3. Antiretroviral tx