Brainscape's Knowledge GenomeTM

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


See full index

Nefrologia PT > ASN QBank Pearls - Glomerular and Vascular Disorders > Flashcards

ASN QBank Pearls - Glomerular and Vascular Disorders Flashcards

1
Q

have often been associated with increased risk for progression of diabetic
nephropathy

A

smoking and HTN

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

which genetic screening test is likely to detect a mutation in more than 5% of sporadic FSGS in adolescents?

A

mutations in NPHS2 (podocin) gene, including p.R229Q variant

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

possible kidney biopsy findings in MM nephropathy

A
  • fractured tubular casts
  • Congo red–positive glomerular and tubular deposits
  • acute tubular injury/necrosis
  • plasma cell infiltrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

amyloidosis fibril size

A

9 to 12 nm

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

cryoglobulinemic GN microtubule shape and size

A
  • curved
  • 25-35 nm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

immunotactoid glomerulopathy microtubule pattern and size

A
  • parallel arrays
  • > 30 nm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

fibrillary GN fibril pattern and size

A
  • RANDOM
  • 15-30 nm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

lupus nephritis IG pattern

A

“fingerprint”

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

treatment for idiopathic MCD

A
  • sodium and fluid restriction
  • furosemide
  • statins
  • ACEI
  • high-dose prednisone daily or on alternate days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

spontaneous remission rate of nephrotic syndrome in iMCD

A

1/3, but may take up to 2 years or more

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

treatment of steroid-resistant FSGS

A

cyclosporine A often in combination with low-dose prednisone

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

lesion associated with highest response rate to treatment with steroids and 
has the BEST prognosis in nephrotic patients with FSGS

A

tip lesion

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

has not been shown to be effective treatment in patients with idiopathic membranous glomerulonephritis (iMGN)

A

prednisone alone

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

multiple myeloma with acute cast nephropathy clues

A
  • very low anion gap
  • hypercalcemia
  • anemia
  • presence of trace urine protein by dipstick
  • elevated UPC on direct measurement
  • protein electrophoresis shows IgG kappa paraprotein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HIVAN

A

collapsing FSGS

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

hepatitis B–induced membranous GN is usually associated with

A

hepatitis BeAg immune complexes in the subEPIthelial space

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

hepatitis BsAg-induced MPGN is usually associated with

A

subENDOthelial deposits due to the different sizes of molecules

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

hepatitis C leads to what type of cryoglobulinemia

A

type 2

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

hepatitis C leads to what type of MPGN

A

type 1 MPGN

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

cryoglobulins activate which complement pathway

A

classical complement pathway

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

HIV directly infects renal tissue including the

A
  • podocytes
  • mesangial cells, and
  • renal tubular cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

associated renal lesion;
- hepatitis A

A

postinfectious GN (PIGN)

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

associated renal lesion;
- hepatitis C

A

MPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

associated renal lesion;
- hepatitis B

A

membranous GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HIVAN or collapsing FSGS is due to

A

active viral replication in the podocyte –> podocytes change to proliferative macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

treatment that may lead to an improvement in renal function and nephrotic syndrome in HIVAN

A
  • HAART
  • ACEI or ARB, and
  • steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

HIVAN predominantly diagnosed in patients of what race

A

black

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

HIVAN predominantly affects what sex

A

males > females

29
Q

HIVAN RUS findings

A

echogenic, occasionally large-sized kidneys

30
Q

treatment for crescentic type I membranoproliferative glomerulonephritis (MPGN) secondary to cryoglobulinemia with no evidence of chronicity

A
  • initiation of HCV antiviral therapy 

  • plasmapheresis 

  • corticosteroids, and
  • rituximab
31
Q

NSAID use, AKI, and nephrotic syndrome

A

AIN and MCD

32
Q

cause of leukocytoclastic skin lesions (can be on legs and ears), AKI, small vessel vasculitis

A

cocaine use

33
Q
  • leukocytoclastic rash
  • nephritis
  • and abnormal liver function tests
  • undetectable C4
  • low to normal C3
A

cryoglobulinemia

34
Q

timeline of hematuria from PIGN

A

2 weeks after onset of infection

35
Q

sacroiliitis is associated with

A

human leukocyte antibody B27 (HLAB27) and IgA nephropathy

36
Q

associated with a high risk of relapse in pauci-immune necrotizing and crescentic glomerulonephritis (MPO-ANCA)

A

presence of upper respiratory tract disease (such as nasal crusting)

37
Q

MOST likely to be decreased in MPGN, especially C3 glomerulopathy

A

factor H (normal inhibitor of the alternative complement pathway)

38
Q

SLE and TMA, think of

A

anti-phospholipid antibodies

39
Q

cryoglobulin is typically what immunoglobulin dominant

A

IgM

40
Q

cryoglobulin pattern

A

short vague substructure or is microtubular

41
Q

immunotactoid glomerulopathy (GP) pattern

A
  • clonal staining
  • microtubular substructure
42
Q

fibrillary glomerulonephritis (GN) pattern

A
  • polyclonal with proliferation
  • randomly arranged fibrils
43
Q

hallmarks of granulomatosis w/ polyangiitis

A
  • older age
  • sinusitis
  • intermittent otitis media
  • crusting in nose
  • nodule on CXR
  • dysmorphic rbcs
  • AKI
  • peripheral edema
  • normal complements
44
Q

auto-Ab in granulomatosis w/ polyangiitis

A

proteinase 3–positive anti–neutrophil cytoplasmic autoantibody

45
Q

strongly associated with AR mutations in APOL1 gene in individuals of African ancestry

A
  • FSGS 

  • HIVAN
  • collapsing glomerulosclerosis a/w SLE 

  • SCD-associated nephropathy
46
Q

best test with highest sensitivity and specificity to evaluate for IG-related disorders

A

nephelometric assay for serum free light chains

47
Q

serum protein electrophoresis will miss cases due to its lower sensitivity

A

monoclonal diseases

48
Q

serum immunofixation electrophoresis will miss diseases that only produce

A

lights chains

49
Q

urine protein/immunofixation electrophoresis is not as sensitive as serum tests for

A

monoclonal proteins

50
Q

bevacizumab MOA

A

MAB against VEGF (vascular endothelial growth factor)

51
Q

HTN in setting of bevacizumab, renin and aldosterone levels

A

LOW

52
Q

best treatment for HTN and proteinuria 2/2 bevacizumab as long as no TMA

A

dihydropyridine calcium channel blocker (CCB)

53
Q

what does pamidronate nephrotoxicity cause?

A

collapsing FSGS and acute tubular injury

54
Q

clinical scenario diagnostic of classical polyarteritis nodosa (PAN)

A
  • severe HA
  • visual changes
  • fatigue
  • unintentional weight loss
  • fever
  • HTN
  • schistocytes on PBS

renal arteriogram findings in classical polyarteritis nodosa (PAN):- multiple aneurysms

  • irregular constrictions in larger vessels
  • occlusion of smaller penetrating arteries
55
Q

clinical scenario consistent with TMA from gemcitabine

A
  • edema
  • livedo-like rash with erythematous ulcer
  • HTN
  • AKI
  • anemia
  • elevated LDH
  • proteinuria
  • hematuria
56
Q

cause of “anticoagulant nephropathy”

A

warfarin (glomerular bleeding)

57
Q
  • kappa light chains
  • nephrotic proteinuria
  • nodular glomerulus, and
  • granular deposition along BM and in nodule on EM are diagnostic of
A

LCDD

58
Q
  • lambda light chains
  • nephrotic proteinuria
  • nodular glomerulus, and
  • fibrillar deposition in the nodule on EM are diagnostic of
A

renal AL amyloidosis

59
Q
  • vasculitic skin rash
  • renal insufficiency
  • hematuria
  • nephrotic range proteinuria, and
  • low C4 complement are diagnostic of
A

cryoglobulinemia type 2 leading to MPGN with immune deposits

60
Q

diffuse podocyte effacement on EM and segmental scarring on light microscopy

A

FSGS

61
Q

diffuse podocyte effacement on EM and a normal light microscopy

A

MCD

62
Q

numerous subepithelial deposits on EM and spikes on silver stain

A

membranous nephropathy

63
Q

10 nm fibrils detected on EM and mesangial expansion with amorphous material on light microscopy

A

amyloid

64
Q

subendothelial deposits on EM and mesangial hypercellularity on light microscopy

A

membranoproliferative GN

65
Q
  • screening test for SLE w/ 95% sensitivity
  • not diagnostic w/o other Abs or clinical features
A

ANA

66
Q
  • high specificity for SLE
  • sensitivity 70%
A

anti-dsDNA Ab

67
Q
  • MOST specific Ab for SLE
  • sensitivity only 30-40%
A

anti-Smith Ab

68
Q
  • present in 15% of patients w/ SLE
  • seen w/ other connective tissue d/o’s, eg Sjogren syndrome
A

anti-Ro/SSA

Nefrologia PT (112 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions