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Renal > Glomerular diseases > Flashcards

Glomerular diseases Flashcards

1
Q

Presence of Cast in urine indicates that

A

hematuria/pyuria is of glemerular or renal tubular origin

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2
Q

causes of hematuria with no casts (2)

A
  1. Bladder cancer

2. kidney stones

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3
Q

causes of pyouria with no cast (1)

A

acute cystitis

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4
Q

Cast in urine - types

A
  1. RBC casts
  2. WBC casts
  3. Fatty casts (oval fat bodies)
  4. Granular (“muddy brown”) casts
  5. Waxy casts
  6. Hyaline casts
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5
Q

RBC casts - seen in

A
  1. glomerulonephritis

2. malignant hypertension

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6
Q

WBC cast - seen in

A
  1. tubulointerstitial inflammation
  2. acute pyelonephritis
  3. trasnplant rejection
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7
Q

Fatty casts (oval fat bodies) - seen in

A

Nephrotic syndrome

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8
Q

Fatty casts (oval fat bodies) - associated with

A

Maltese-cross sign under polarized light

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9
Q

Fatty casts contain

A

lipid (eg. cholesterol)

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10
Q

Granular (“muddy brown”) casts - seen in

A

acute tubular necrosis

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11
Q

Waxy casts - seen in

A

ens-stage renal failure/chronic renal disease

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12
Q

Granular (“muddy brown”) casts vs waxy according to cellular or acellular

A

both acellular

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13
Q

Hyaline casts - seen in

A

nonspecific, can be normal finding, often in concentrated urine samples

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14
Q

Hyaline casts contain

A

protein (acellula)

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15
Q

casts with Maltese cross sign

A

Fatty casts (oval fat bodies)

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16
Q

muddy brown casts?

A

granular casts (acute tubular necrosis)

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17
Q

Nomenclature of glomerular disorders - focal (characteristcs and example)

A
  • less than 50% of glumeri are involved

- ex. focal segmental glomerulosclerosis

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18
Q

Nomenclature of glomerular disorders - diffuse (characteristcs and example)

A
  • more than 50% of glumeri are involved

- ex. diffuse proliferative glumerulonephritis

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19
Q

Nomenclature of glomerular disorders - proliferative (characteristcs and example)

A
  • hypercellular glomeruli

- membranoproliferative glomerulonephritis

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20
Q

Nomenclature of glomerular disorders - membranous (characteristcs and example)

A
  • thickening of glomerular basement membrane (GBM)

- membranous nephropathy

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21
Q

Nomenclature of glomerular disorders - primary glomerular disease (characteristcs and example)

A
  • a 1ry disease of the kidney specifically impacting the glomeruli
    2- eg. Minimal change disease
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22
Q

Nomenclature of glomerular disorders - secondary disease (characteristcs and example)

A
  • a systemic disease or disase of another organ system that also impacts the glomeruli
  • SLE, diabetic nephropathy
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23
Q

glomerulula diseases - groups

A
  1. nephritic syndrome
  2. nephrotic syndrome
  3. Nephritic-nephrotic syndrome
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24
Q

Nephritic syndrome vs nephrotic syndrome according to mechanism

A

Nephritic syndrome –> GBM disruption

Nephrotic syndrome –> podocyte disruption –> barier impaired

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25
Q

Nephritic syndrome - symptoms and findings

A
  1. Hypertension (salt secretion and periorbital edema)
  2. increased BUN and creatinine
  3. oliguria
  4. hematuria (with RBCs in urine)
  5. Proteinuria in Subnehrotic range (in severe cases may be in nephrotic range)
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26
Q

Nephritic syndrome - diseases?

A
  1. acute poststreptococcal glomerulonephritis
  2. Rapidly progressive glomerulonephritis
  3. IgA nephropathy (Berger disease)
  4. Alport syndrome
  5. Membranoproliferative glomerulonephritis
  6. Diffuse proliferative glomerulonephritis
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27
Q

Nephrotic syndrome - symptoms and findings

A
  1. Massive proteinuria (>3.5g/day) with hypoalbuminemia (pitting edema in soft tissues)
  2. hyperlipidemia (frothy urine with fatty casts)
  3. edema
  4. hypogammaglobulinemia (increased risk of infection)
  5. loss of antithrombin III –> hypercoagulable state
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28
Q

Nephrotic syndrome - 1ry vs 2ry (according to mechanism)

A

1ry –> direct podocyte damage

2ry –> podocyte damage from systemic process (diabetes)

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29
Q

Nephrotic syndrome - diseases (and if 1ry or 2ry)

A
  1. focal segmental glomeulosclerosis (1ry or 2ry)
  2. minimal change disease (lipoid nephrosis) (1ry or 2ry)
  3. Membranous nephropathy (membranous glomerulonephritis) (1ry or 2ry)
  4. Amyloidosis (2ry)
  5. Diabetic glomerulonephropathy
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30
Q

Nephritic-nephrotic syndrome?

A

severe nephritic syndrome with profound GBM damage that may damages the glomerular filtration charge barrier (if damage to GBM is severe enougj to damage charger barrier)
–> nephrotic-range proteinuria (>3.5g.day) and concominant features of nephrotic syndrome

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31
Q

Causes of Nephritic-nephrotic syndrome

A

can occur with any form of nephritic syndrome, but is most common seen with

  1. diffuse proliferative glomerulonephritis
  2. Membranoproliferative glomerulonephritis
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32
Q

Nephritic vs nephrotic vs Nephritic-nephrotic syndrome according to protein excreted per day

A

nephritic: Proteinuria in Subnehrotic range (less than in severe casees may be in nephrotic range
nephrotic: Massive proteinuria (>3.5g/day) with hypoalbuminemia
Nephritic-nephrotic syndrome: nephrotic-range proteinuria (>3.5g.day)

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33
Q

Nephritic syndrome - symptoms and findings

A
  1. Hypertension (salt secretion and periorbital edema)
  2. increased BUN (azotemia) and creatinine
  3. oliguria
  4. hematuria (with RBCs in urine)
  5. Proteinuria in Subnehrotic range (less than in severe casees may be in nephrotic range
34
Q

Acute poststreptococcal glomerulonephritis - age

A

Most frequently seen in children (may also occur in adults)

35
Q

Acute poststreptococcal glomerulonephritis - mechanism

A

2-4 weeks after A streptococcal infection of of skin (impetigo) or pharynx–> immune complexes –> type III hypersensitivity reaction

36
Q

Acute poststreptococcal glomerulonephritis - treatment

A

resolves spontaneously

37
Q

Acute poststreptococcal glomerulonephritis - clinical presentation

A
  1. peripheral and periorbital edema
  2. cola-colored urine (hematuria)
  3. hypertension
  4. oliguria
38
Q

Acute poststreptococcal glomerulonephritis - lab

A
    • strep titers/serologies
  2. low complement levels due to consumption
  3. LM: glomeruli enlarged and hypecellular
  4. IF: (starry sky) granular appearance (lumpy-bumpy) due to IgG, IgM and C3 deposotio along GBM and mesangium
  5. EM: subepithelial immune complex (IC) humbs
39
Q

causes of Rapidly progressive (crescentic) glomerulonephritis

A

several diseases processes may result in this pattern

  1. Goodpasture - anti-GBM + anti alveolar BM
  2. Granulomatosis with polyangiitis (Wegener) - PR3-ANCA/c-ANCA
  3. Microscopic polyangitis, Churg strauus - MPO-ANCA/p-ANCA
  4. poststreptococcal glomerulonephritis
  5. Diffuse proliferative glomerulonephritis
40
Q

Rapidly progressive (crescentic) glomerulonephritis - image

A

LM: crescent moon shape –> consist of fibrin and plasma proetins (eg. C3b) with glomerular parietal cells, monocytes, macrophages
IF: a. Goodpasture –> linear b. wegener, Microscopic polyangitis –> negative IF (Pauci-immune –> no IG/C3 deposotion) c. if PSGN or Diffuse proliferative glomerulonephritis –> granular

41
Q

Rapidly progressive (crescentic) glomerulonephritis - prognosis

A

poor –> rapidly deteriorating renal function (days to weeks)

42
Q

Rapidly progressive (crescentic) glomerulonephritis - treatment

A

emergent plasmapheresis

43
Q

Nephritic syndrome of SLE

A

Diffuse proliferative glomerulonephritis

44
Q

Diffuse proliferative glomerulonephritis - mechanism

A

due to SLE or membranoproliferative glomerulonephritis

45
Q

Diffuse proliferative glomerulonephritis - image

A

LM - wire looping of capillaries
EM: subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposotion
IF: granular

46
Q

IgA nephrpathy (Berger disasee) -mechanism/presentation

A

episodic gross hematuria that occurs concurrently with respiratory or GI tract infection (IgA is secreted by mucosal linings) –> IgA complex
RENAL PATHOLOGY OF HENOCH-SCHONLEIN PURPURA

47
Q

Henoch-Schonlein purpura - classic triad

A
  1. Skin: palpable purpura on buttocks/legs
  2. Arthralgias
  3. GI: abdominal pain
48
Q

IgA nephrpathy (Berger disasee) - image

A

LM - mesangial proliferation
EM - mesangial IC depositis
IF - IgA-based IC deposits in mesangium

49
Q

Alport syndrome - mechanism

A

Mutation in type IV collagen –> thinning and splitting of glomerular basement membrane
MC X-linked dominant

50
Q

Alport syndrome - mode of inheritance

A

MC X-linked dominant

51
Q

Alport syndrome - manifestation

A
  1. Eye problem (eg. retinopathy, lens dislocation)
  2. glomerulonephritis –> isolated hematuria
  3. sensorineural deafness
52
Q

Alport syndrome - image

A

“Basket-weave” appearance on EM

53
Q

Mebranoproliferative glomerulonephritis (MPGN) - mechanism

A 
type 1 --> 2ry to hepatitis B or C infection, May also be idiopathic 
type 2 (dense deposit disease) --> associated with C3 nephritic factor (autoantibody that stabilize C3 convertase) --> low serum C3 levels
54
Q

Mebranoproliferative glomerulonephritis (MPGN) - prognosis

A

poor response to steroids –> progress to chronic renal failure

55
Q

Mebranoproliferative glomerulonephritis (MPGN) type I - image

A

subendothelial immune complex (IC) deposits with granular IF
tram track appearance on PAS stain and H&E stain due to GBM splitting caused by mesangial ingrowth

56
Q

Mebranoproliferative glomerulonephritis (MPGN) type I vs type to according to location of deposits

A

type 1 –> subendothelial

type 2 –> intramembranous

57
Q

Nephrotic syndrome - symptoms and findings

A
  1. Massive proteinuria (>3.5g/day) with hypoalbuminemia (pitting edema in soft tissues)
  2. hyperlipidemia (frothy urine with fatty casts)
  3. edema
  4. hypogammaglobulinemia (increased risk of infection)
  5. loss of antithrombin III –> hypercoagulable state
58
Q

MCC of nephrotic syndrome in children

A

Minimal change disease (lipoid nephrosis)

59
Q

Minimal change disease (lipoid nephrosis) - mechanism

A
  1. often 1ry (idiopathic) and my be triggered by recent infection, immunization, immune stimulus
  2. Rarely, may be secondary to lymphoma (eg. cytokine mediated damage
60
Q

primary minimal change disease can be triggered by

A
  1. recent infection
  2. immunization
  3. immune stimulus
61
Q

Minimal change disease (lipoid necrosis) - treatment

A

excellent response to corticosteroids

62
Q

Minimal change disease (lipoid necrosis) - image

A

LM - normal glomeruli, lipid may be seen in PCT cells
IF - normal
EM - effacement of foot process

63
Q

MCC of nephrotic syndrome in African and Hispanics

A

Focal segmental glomerulosclerosis

64
Q

causes of focal segmental glomerulosclerosis

A
  1. Can be 1ry (idiopathic)
  2. 2ry to other conditions –> a. HIV infection b. Sickle cell anemia c. heroin abuse d. massive obesity
    e. interferon treatment f. chronic kidney disease due to congenital malformations
65
Q

focal segmental glomerulosclerosis - course and treatment

A

may progress to chronic renal disease

1ry disease has incosistent response to steroids

66
Q

focal segmental glomerulosclerosis - image

A

LM - segmental sclerosis and hyalinosis
IF - often (-), but may be + for nonspecific focal deposits of IgM, C3, C1…
EF - effacement of ffot process similar to minimal change

67
Q

MC cause of 1ry nephrotic syndrome in Caucasian adults

A

Membranous nephropathy (membranous glomerulonephritis)

68
Q

causes of Membranous nephropathy (membranous glomerulonephritis)

A
  1. primary (antibodies to phospholypase A2 receptor)

2. 2ry to: a. drugs (eg. NSAIDs, penicillamine) b. infections (HBV, HCV) c. SLE d. solid tumors

69
Q

causes of Membranous nephropathy (membranous glomerulonephritis) - course and treatment

A

may progress to chronic renal disease

1ry disease has poor response to steroids

70
Q

Membranous nephropathy (membranous glomerulonephritis) - image

A

LM - diffuse capillary and BM thickenning
IF - granular (immune complex)
EM - “spike and done” appearance with subepithelial deposits

71
Q

the most commonly involved organ in amyloidosis

A

kidney

72
Q

amyloidosis - common types

A
  1. AL (primary) 2. AA (secondary) 3. dialysis-related
  2. heritable 5. age related (senile) systemic
  3. organ specific
73
Q

nephrotic syndrome - amyloidosis - image

A

LM - congo red stain shows apple green birefringence under polairzed light due to amyloid deposition in the mesangium

74
Q

MCC of end-stage renal disease in US

A

Diabetic glomerulonephropathy

75
Q

Diabetic glomerulonephropathy - mechanism

A

Nonenzymatic glycosylation of GBM –> increased permeability, thickening
Nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion

76
Q

Diabetic glomerulonephropathy - image

A

LM - mesangial expansion, GBM thickening, eosinphilic nodular glomerulosclerosis (Kimmelstiel-Willson)

77
Q

eosinphilic nodular glomerulosclerosis

A

Kimmelstiel-Willson

78
Q

HCV, HBV nephritis - types

A

nephrotic –> Membraous nephropathy (membranous glomerulonephritis)
nephritic –> membranoproliferative glomerulonephritis

79
Q

Lupus nephritis - types

A

nephritic - diffuse proliferative glomerulonephritis

nephrotic - membranous glomerulonephritis

80
Q

heroin nephritis

A

focal segmental glomerulosclerosis

81
Q

MC nephropathy worldwide

A

IgA nephropathy (Berger disease)

82
Q

glomerular disease with subepithelial deposits

A
  1. Acute poststreptococcal glomerulonephritis

2. Membranous nephropathy (membranous glomerulonephritis)

Renal (15 decks)

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