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Nephrology > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

What glomerular nephropathies are primarily pediatric diseases

A

minimal change disease and post-striptococcal muriel and nephritis

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2
Q

What are the histologic characteristics of minimal change disease

A

Normal glomerular membrane with lipoid nephrosis

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3
Q

collapsing glomerulo nephropathy is associated with what

A

Remember the 4-H’s: Hiv, heroin, hemonopathies, heavy

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4
Q

Compare and contrast the histologic characteristics of collapsing and idiopathic FSGS

A

collapsing: Very poor prognosis; Epithelioid hyperplasia
Idiopathic: Prognosis is variable; degeneration of the glomerular epithelium

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5
Q

What are common diseases and drugs that cause secondary Membranous nephropathies

A

Thrombotic vascular diseases; NSAIDs; penicillamine; carcinomas of the lung, colon, & melanoma

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6
Q

Describe the histological characteristics of FSGS

A

focal Sclerosis and hyalinosis With the destruction of potocytes

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7
Q

Describe the pathogenesis of minimal change disease

A

cell cytokine storm triggers damage to the foot processes of the potocytes

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8
Q

70% of Membranous neuropathies are associated with deposits of IgG immune complexes. What is the pathogenesis Of these IGG deposits?

A

Antibodies against phospholipase A2 receptors Activate compliment C5b-C9 Which triggers the deposition of IgG complexes in the sub endothelial layer of the glomerular membrane leading to membrane thickening

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9
Q

describe the histologic features of memberness nephropathy

A

granular deposits in a spike in dome pattern

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10
Q

What is the pathogenesis of diabetic glomerulonephropathy

A

Extensive glycosylation of the renal vessels Leads to arterial or membrane thickening; this increases the pressure within the glomeruli and expands the mesangium; this leads to subsequent sclerosis and glomerular hypertrophy

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11
Q

Describe the histologic characteristics of diabetic glomerulonephropathy

A

arterial hyalinosis; kimmelstiel-wilson nodules in mesangial matrix; Gbm thickening

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12
Q

diabetic glomerulonephroth also causes what complication

A

4 collagen microangiopathy

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13
Q

What are the unique histologic features of amyloidosis neuropathy

A

Amyloid deposits within the mesangium; Apple Green Bifringements with bence Jones proteins

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14
Q

Membranous neuropathy is a generic term That can be associated with any disease that causes what?

A

thickening of the glomerular membrane Isolated to the sub epithelial layer

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15
Q

What nephropathies are isolated to just the mesangium and not the glomerular membrane

A

Amyloidosis neuropathy And IgA nephropathy; Class I & II SLE nephritis

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16
Q

What nephropathies are isolated to just the glomerular membrane and do not affect the mesagnium

A

FSGS; Membranous Nephropathy; Alport syndrome And thin basement membrane nephropathy; Class V & VI SLE nephritis

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17
Q

Membrano proliferative comarial nephritis Can cause either a nephronic or nephrotic syndrome. What do Both subtypes of this disease have in common

A

Both produce a granular pattern along the GBM And mesangium; both will have low serum levels of C3

18
Q

What is the pathogenesis of type 1 Member no proliferative glomerulonephritis

A

strong association with hepatitis C; Immune complex deposits mediated by classical complement

19
Q

What is the pathogenesis of type 2 membrano proliferative glomerulonephritis

A

Antibody mediated by alternative compliment; Antibodies bind to C3 convertase preventing its degradation and Subsequently overactivating complement

20
Q

compare and contrast the histologic characteristics of type 1 and type 2 membrano proliferative glomerulonephritis

A

one: Deposits in the sub endothelial layer of the basement membrane and in the mesangianm
two: intra memberous deposits within the gbm in a ribbon like fashion

21
Q

Because biopsies are expensive and invasive, wood lab can be used to differentiate type 1 and type 2 membrano proliferative glomerulonephritis

A

C4 serum levels
Type 1: low
Type 2: normal

22
Q

Iga nephropathy typically becomes symptomatic in which decade of life

A

second and third decade

23
Q

Having a history of what diseases are strongly associated with IGA nephropathy AKA burger disease

A

Complicated respiratory infections; in stage liver and celiac disease

24
Q

Describe the pathogenesis of IGA nephropathy

A

Thought to be due to immunological stresses and insults in the 1st and 2nd decades of life:
Respiratory tract infections can activate expression of GD-IgA; This triggers an autoimmune response against IG-IgA isotypes Which deposit in the mesangium; Subsequent activation of alternative complement causes damage to the glomeruli

25
Q

What are the histologic features of IGA neuropathy

A

The sangrial cell hyperplasia And protein deposits within the mesangianm

26
Q

Describe the pathogenesis Of PSGN

A

virulent factor: M protein Allows s. pyogenes to persist and survive inside Lukiosites And cause reactivation of infection elsewhere in the body; When these leuke sites deposit and the kidney it activates complement And causes subsequent damage to the glomerulus and the mesandium

27
Q

describe the distinct histologic characteristics of psgn

A

PMN Hyperplasia in the mesangium; granular deposits along the eclomycular capillaries Creating a starry Sky Lumpy Bumpy appearance; +IgG & C3

28
Q

Compare and contrast the different clinical manifestations of good pastures disease and granulomatosis with polyingitis

A

good pastures is primarily isolated to the lungs and kidneys; Whereas granulomatosis with polyangitis is a vascular disease that affects multiple systems and patients will typically present with complaints of nasal congestion due to nasal septum defects; They also have different antibodies: ANCA for GMP and anit GM for GP

29
Q

GP Antibodies affect what Protein

A

alpha 3 chain of type 4 collagen; IgG Type 2 hypersensitivity

30
Q

For good pasteur syndrome what we’ll be seeing with immunofluorescence that will not be seen with PMG

A

linear deposits

31
Q

what are similarities between gp and gmp

A

Both will present with Crescent shaped glomerulo capillaries; hemoptysis
Both are categorized as subtypes of rapidly progressive glomerulonephritis

32
Q

What are hallmarks of PSGN

A

Peri orbital edema; Recent history of a upper respiratory infection; decreased serum levels of C3 and normal serum levels of C4

33
Q

lab work of Lupus Induced nephritis Low serum levels of both C3 and C4. Therefore which complement pathway has been activated

A

the classical pathway

34
Q

what classes of sle nephritis are associated with glomerular crescents

A

classes 3 and 4

35
Q

Describe the histologic characteristics of class 3 and 4 lupus induced nephritis

A

wire looping, crescents, mesangial and sub endothelial electron dense deposits

36
Q

What antibodies are associated with sle

A

anti-ANA and anti-dsDNA

37
Q

What is the pathogenesis of Alport syndrome?

A

X linked dominant inheritance pattern; mutation of the alpha 3 subtype of collagen 4

38
Q

what are the clinical manifestations associated with Alport syndrome

A

Symptomatic onset 5-20 yrs. of age; hearing loss; orbital anomalies

39
Q

what are the unique histologic characteristics Of Alport syndrome

A

Interstitial foam cells; Splitting and lamination of the lamina densa Giving a basket like appearance

40
Q

Thin basement membrane neuropathy pathogenesis is Very similar to that of Alport syndrome. Difference between the two

A

thin basement membrane nephropathy is not associated at all with the clinical manifestations of Alport syndrome and the prognosis is very very good in comparison

Nephrology (11 decks)

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