Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal II > Nephritic and nephrotic sydnromes > Flashcards

Nephritic and nephrotic sydnromes Flashcards

1
Q

Enlarged, hypercellular glomeruli on light microscopy. Granular immune deposits of IgG, IgM, and C3 in the mesangium and along GBM on immunofluorescence. Electron microscopy shows subepithelial lumps.

A

Acute proliferative glomerulonephritis (post-strep or post-infectious)

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

Possible complication of acute proliferative glomerulonephritis

A

Rapid progressive glomerulonephritis

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

Glomeruli may appear normal or have mesangial widening on light microscopy. Mesangial deposits of IgA and C3 on immunofluorescence. Electron dense deposits in mesangium on electron microscopy. Young male pt with history of similar episodes in the past.

A

IgA nephropathy/Berger disease

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

Disease characterized by anti-GBM antibody with or without lung involvement. Linear IgG and C3 deposits on immunofluorescence.

A

Type 1 rapidly progressive glomerulonephritis

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

Disease characterizes by post-infectious glomerulonephritis. Granular Ag+Ab complexes in immunofluorescence.

A

Type II rapidly progressive glomerulonephritis

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

Disease characterized by pauci-immune and ANCA-associated glomerulonephritis. No immune deposits on immunofluorescence. Most have circulating c-ANCAs or p-ANCAs.

A

Type III rapidly progressive glomerulonephritis

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

Diseases associated with type III RPGN

A

Wegener
Microscopic polyangiitis

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

Disease associated with type II RPGN

A

Post-infectious glomerulonephropathy

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

Is RPGN nephritic or nephrotic?

A

Nephritic

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

Pathogenetic type of type I RPGN

A

Anti-GBM

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

Pathogenetic type of type II RPGN

A

Immune-complex

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

Pathogenetic type of type III RPGN

A

Pauci-immune

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

RPGN type with normal serum C3, positive for anti-GBM antibody, and negative for ANCAs.

A

Type I RPGN

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

RPGN type with low to normal C3 and negative for anti-GBM antibody and ANCA.

A

Type II RPGN

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

RPGN type with normal C3, negative for anti-GBM antibody, and positive for ANCA.

A

Type III RPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diseases associated with type I RPGN

A

Goodpasture’s syndrome
SLE
Vasculitis
Wegener’s granulomatosis
Henoch-Schonlein purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment for nephritic syndrome

A

Plasmapheresis
Steroids
Cytotoxic agents in Goodpasture’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Light microscopy shows renal changes dominated by crescents. Parietal epithelium with monocytes, macrophages, and fibrin strands. Obliteration of Bowman’s space and compression of glomeruli.

A

Nephritic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Features of nephritic syndrome

A

Hematuria
RBC casts
Moderate proteinuria
Variable HTN and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Constant finding on electron microscopy in nephritic syndrome

A

Rupture of GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Another name for hereditary nephritis

A

Alport syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Features of Alport syndrome

A

Hematuria with RBC casts
Nerve deafness (cochlea)
Lens dislocation, cataracts, corneal dystrophy
Proteinuria may develop later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the mutation in Alport syndrome?

A

Abnormal type IV collagen

24
Q

Irregular thickening of basement membrane alternating with thinning producing splitting and lamination of lamina densa (basket-weave) on electron microscopy. Leads to focal segmental GN and global glomerulosclerosis.

A

Alport syndrome - hereditary nephritis

25
Q

Features of nephrotic syndrome

A

Massive proteinuria
Hypoalbuminemia
Anasarca
Hyperlipidemia and lipiduria

26
Q

Generalized edema 2/2 increased capillary hydrostatic pressure

A

Nephrotic syndrome

27
Q

Why are those with nephrotic syndrome susceptible to thromboembolic phenomena

A

Loss of antithrombin III and renal V thrombosis

28
Q

Primary causes of nephrotic syndrome in children

A

Minimal change disease (lipoid nephrosis)
FSGS

29
Q

Drugs that can cause secondary nephrotic syndrome

A

Penicillamine
NSAIDs

30
Q

Infections that can cause secondary nephrotic syndrome

A

Malaria
Syphilis
HBV and HCV
HIV

31
Q

Miscellaneous causes of secondary nephrotic syndrome

A

Bee sting
Hereditary nephritis/Alport
Autoimmune thyroiditis

32
Q

Primary causes of nephrotic syndrome in adults

A

Membranous glomerulopathy
FSGS

33
Q

Autoimmune kidney disease characterized by M-type phospholipase A-2 receptor resulting in immune complexes along subepithelial aspect of the basement membrane

A

Primary membranous nephropathy

34
Q

Disease characterized by slow loss of GFR, normal serum creatinine, nonselective proteinuria, edema, hypoalbuminemia, and hyperlipidemia. Urine shows oval fat bodies and fatty casts. C3 and C4 are normal.

A

Membranous nephropathy

35
Q

Light microscopy of glomerulus shows diffuse, thickened capillary walls without an increase in the number of cells. Spikes on silver methenamine stain.

A

Membranous nephropathy

36
Q

Mechanism of light microscopy changes in membranous nephropaty

A

Direct action of C5b-C9 on epithelial and mesangial cells leads to capillary wall injury and protein leakage.

Accumulation of dense IgG containing deposits along subepithelial side of GBM

37
Q

Electron microscopy findings in membranous nephropathy

A

Electron dense deposits along the epithelial side of the basement membrane and effaced foot processes

38
Q

Progression of membranous nephropathy

A

Sclerosis of glomeruli
Rising serum creatinine
HTN

39
Q

Systemic T cell dysfunction results in the production of a glomerular permeability factor that directly affect the glomerular capillary wall resulting in marked proteinuria and foot process fusion

A

Minimal change disease

40
Q

Nephrotic syndrome associated with respiratory infections, immunizations, and atopic disorders.

A

Minimal change disease

41
Q

Treatment for minimal change disease

42
Q

Microscopy finding in minimal change disease

A

Diffuse effacement of foot processes of the podocytes.
Normal light microscopy and immunofluorescence.

43
Q

Nephrotic syndrome type with proximal tubule cells laden with lipid and protein.

A

Minimal change disease

44
Q

Slit diaphragm protein genes identified as possible sites of mutation in FSGS

A

NPHS1 - nephrin
NPHS2 - podocin
TRPC6 - Ca channel

45
Q

Focal and segmental sclerosis of glomeruli on PAS stain. Higher incidence of hematuria, decreased GFR, and HTN with massive proteinuria, non-selective

A

Focal segmental glomerulosclerosis

46
Q

Tubular changes in HIV associated nephropathy

A

Striking focal dilatation of tubules filled with proteinaceous material –> tubulo-reticular inclusions within endothelial cells on EM

47
Q

Microscopy with silver stain shows retraction of glomerular tuft, narrowing capillary lumens, proliferation and swelling of visceral epithelial cells, and accumulation of IC protein adsorption droplets in visceral epithelial cells.

A

HIV associated nephropathy (FSGS)

48
Q

Alteration of GBM with proliferation of mesangial and endothelial cells with leukocyte infiltration. Can be nephrotic, combined, or non-nephrotic.

A

Membranoproliferative glomerulo-nephropathy

49
Q

Secondary causes of MPGN

A

SLE
HBV and HCV
CCL
Lymphoma

50
Q

General pathogenesis of type I MPGN

A

Both classical and alternate complement pathways

51
Q

General pathogenesis of type II MPGN

A

Alternate complement pathway only

52
Q

Light microscopy shows enlarged, hypercellular glomeruli, lobular accentuation, tram track appearance of thickened GBM, and possibly crescents.

A

MPGN, both type I and II

53
Q

Electron microscopy findings in type I MPGN

A

Subendothelial electron dense deposits

54
Q

Immunofluorescence findings in type I MPGN

A

Granular IgG and C3 deposits

55
Q

Serum findings in type II MPGN

A

Low serum C3, factor B, and properdin

56
Q

Electron microscopy findings in type II MPGN

A

Deposition of dense material in the lamina densa of GBM

Renal II (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions