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Renal > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

What are the 3 mechanisms of glomerular disease?

A
  • Immunocomplex deposition
    • circulate the deposit in glomerulus
      • Eg DNA-anti-DNA complexes in Lupus
    • activates complement resulting in neutrophil chemotaxis
  • antibodies against GBM or glomerular antigens
  • cytokine production by inflammatory cells
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2
Q

What are the 3 ways by which glomerular disease presents?

A

Hematuria (quality)

Loss of GFR (temporal change)

Proteinuria (quantitity)

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3
Q

How do we name glomerular disease? diffuse vs focal

glocal vs segmental

A

How many glomeruli?

Diffuse (all), focal (some)

How much of a glomerulus

glocal (entire glomerulus), segmental (part of)

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4
Q

Nephrotic syndrome

A
  • proteinuria > 3.5 g/day
  • hypoalbuminemia
  • edema
    • loss of plasma oncotic pressure vs Na/H20 retention
  • hyperlipidemia
    • increased hepatic protein production
  • lipiduria
  • hypercoagulability
    • loss of proteins C and S
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5
Q

Nephritis

A
  • mild proteinuria
  • hematuria
    • RBCs, RBC casts, dysmorphic RBCs
  • hypertension
  • edema
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6
Q

What are the 3 main primary nephrotic syndromes?

A

minimal change disease

focal segmental glomerulosclerosis

membranous nephropathy

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7
Q

What are the causes of acute glomerulonephritis

A

IgA nephropathy

post-infectious GN

Anti GBM disease/ Goodpasture’s

small vessel vasculitis

lupus neprhitis

membranoproliferative GN

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8
Q

What is IgA Nephropathy

who gets it, what is the most prominent feature, when does it occur? what symptoms occur with it?

A
  • Most common GN worldwide
  • most patients begtween age 10-50
  • hematuria is most prominent feature
    • 50-60% episodic gross hematuria
    • 30% persistent microhematuria
    • 10% acute GN or nephrotic syndrome
  • Proteinuria, if present, is generally mild
  • many cases are subclinical
  • dysuria and loid pain may accompany hematuria
  • hematuria frequently occurs in conjunction with an upper respiratory infection (synpharyngitic hematuria)
  • HTN may be present in patients iwth more advanced disease
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9
Q

What is seen on Light microscopy(LM), electron microscopy (EM) and immunoflouresence (IF)?

A
  • LM: Variable mesangial hypercellularity
    • may see segmental proliferation, segmental sclerosis and necrosis with crescents
  • IF: Mesangial IgA deposition
  • EM: Mesangial electron dense deopsits (paramesangial)
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10
Q

What is the prognosis of IgA nephropathy? What kind of treatment is it?

A
  • serum creatinine, BP, and degree of proteinuria
    • 40% of patients will slowly develop chronic kidney disease
  • fish oil may slow progression of disease
  • ACE inhibitors used to control blood pressure
  • Corticosteroids, other immunosuppressants also may be used in progressive disease
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11
Q

What is henoch-schonlein purpura?

A
  • Nephritic
  • Systemic disorder characterized by IgA deposition in multiple organs
  • multiple manifestations
    • skin: characteristic non-blanching purpura on legs and buttocks
    • joints: transient arthralgias
    • GI tract: abdominal pain, vomiting, melena, hematochezia
    • kidney: hematuria, proteinuria. rarely progressive renal failure
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12
Q

What is Post infectious GN? What is the prognosis?

A

post-streptococcal GN-classic example

follows infection in nephritogenic strain of group A beta hemolytic streptococcus

occurs 7-14 days after pharyngitis; 14-28 days after skin infection (note this is not synpharyngetic which means simultaneous and is seen with IgA nephropathy)

95% of children will recover with conservatice management, 1% progress to renal failure

60% of adults will recover promptly

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13
Q

What are the causes of rapidly progressive GNs

A

classic nephritic syndrome with rapid progression (days to weeks) to renal failure

sometimes referred to as crescentic GN

causes:

  • Anti-GBM/Goodpasture’s
  • Immune complex GN
    • lupus nephritis
    • post-infectious
    • cryoglobulinemeia
  • ANCA associated GN (Pauci immune)
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14
Q

WHo gets Anti-GBM/ Goodpastures syndrome? How does it present?

A
  • males> females
  • may present as pulmonary-renal syndrome
    • hemoptysis
    • pulmonary ifiltrates
    • glomerulonephritis
      • GN alone in anti-GBM disease
  • due to circulating anti-GBM antibody
    • antigen is a3 chain of type V collagen
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15
Q

How do we diagnose and treat Anti-GBM/ Goodpasture syndrome?

A

diagnosis:

+ anti-GBM antibody in blood

Linear IgG and C3 on kidey biopsy IF

treatement:

plasmapheresis

prednisone

cytoxan

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16
Q

What is Pauci immune GN?

A

cresenteric GN with litte deposition of immune reactants

“pauci immune”

idiopathic or associated with antineutrophil cytoplasmic antibody (ANCA) vasculitis

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17
Q

What are 3 small vessel vasculitis?

A
  • microscopic polyangiitis
    • no granulomatous inflammation and no asthma
  • granulomatosis with polyangiitis (wegners)
    • necrotizing granulomatous inflammation; no asthma
  • eosinophilic granulomatosis with polyangiitis
    • necrotizing granulomatous inflammation, asthma, eosinophilia
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18
Q

What is granulomatosis with polyangiitis (GPA)? How does it present and what is seen on renal biopsy?

A
  • granulomatous vasculitis of medium to small arterioles
  • c-ANCA + in 80%
  • presentation
    • upper respiratory tract symptoms (sinusitis, nasal lesions, hemoptysis)
    • mononeuritis mulitplex
    • purpura
    • nephritis
  • renal biopsy: cresenteric GN without immune deposits
    *
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19
Q

Fill this in

A
20
Q

what are the 3 primary nephrotic renal diseases? in children 80% will have which one?

A

membranous nephropathy

focal segmental glomerulosclerosis (FSGS)

minimal change

21
Q

What are secondary causes of nephrotic syndrome?

A

systemic diseases:DM, SLE, amyloidosis

infections: HIV, Hepatitis B, Hepatitis C, syphyllis
drugs: classical examples include NSAIDs, gold, penicillamine

22
Q

what laboratory studies/techniqes are used to dignose nephrotic syndrome?

A
  • ANA, anti-ds-DNA, complement levels
  • serum and urine protein electrophoreses
  • HBV and HCV serologies
  • cryoglobulins
  • syphillis serology

renal biopsy is generally indicated

23
Q

what are teh treatments for all causes of nephrotic syndrome?

A

ACE inhibitor or Angiotensin II receptor blocker to lower intraglomerular pressure and reduce proteinuria

lipid lowering statin

diuretic, salt restriction to improve edema

24
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

25
Q

what is the peak incidence of mininmal change disease?

A

2-6

5% progress to rend stage renal disease

spontanneous remissions can occur

treatment with steroids often includes remission although relapses occur in about 75%

fewer relapses after puberty

26
Q

what causes Minimal change disease?

A

in adults, can be idiopathic or associated with:

  • drugs-NSAIDs
  • neoplasms-Hodgkin’s lymphoma, pancreatic, prostate, lung, colon and renal cell carcinomas, mesothelioma, oncocytoma
  • infections-syphyllis, HIV
27
Q

What do you see on LM, IF, EM for minimal change disease?

A

LM: Glomeruli, interstitium and tubules appear normal

IF: negative or mesangial IgM

EM: Podocyte foot process effacement (fusion)

28
Q

How do we treat minimal change disease?

A
  • children respond well to corticosteroids
  • majority of adults with minimal change disease respond to steroids
    • usually takes longer than in children
    • partial remissions may occur
29
Q

Who gets membranous nephropathy?

A
  • most common cause of nephrotic syndrome in caucasian adults
  • caused by antibodies to the podocyte antigens phospholipiase A2 receptor (70%) or thrombospondin type 1 domain containing 7A (10%)
30
Q

what are secondary causes of membranous nephropathy?

A
  • infections: HBV
  • connectivetissue diseases: SLE
  • Neoplasms-carcinoma of lung, colon, stomach, breast; non-Hodgkin’s lymphoma
    • consider age appropriate cancer screening
  • drugs-gold, penicillamine, mercury, NSAIDs, captopril
31
Q

What is the onset of membranous nephropathy like? how do patients present?

A
  • onset is insidious
  • patients usually present with heavy proteinuria and nephrotic syndorme
    • HTN and azotemia occur later
    • occult malignancies and infections may become evident later
    • renal vein thrombosis occurs in 20%
32
Q

What is seen on LM, IF, EM in membranous nephropathy?

A

LM: diffuse thickening of GBM, GBM “spike” on silver stain

IF: granular GBM deposits of IgG

EM: subepithelial deposits

**spikes are seen bc staning for the basement membreane so the complexes dont get stained

33
Q

where do immune deposits deposit in membranous nephropathy?

A

immune deposits form on the subepithelial aspect of glomerula basement membrane

34
Q

What is the rule of thirds for membranous nephropathy?

A

1/3 apontaneous remission

1/3 partial remission with stable function

1/3 slowly progressive loss of renal function

35
Q

How do we treat people with membranous nephropathy?

A

patients with poor prognostic factors might be managed conservatively with ACE and/or ARB and followed closely

otherwise steroids and or immunosuppressive drugs

36
Q

Who gets Focal Segmental glomerulosclerosis? What is seen with it?

A
  • most common cause of idiopathic nephrotic syndrome in African Americans
  • more aggressive than minimal change disease
    • HTN, hematuria more common
    • renal dysfunction is commonly progressive
    • ESRD occurs 5-20 yrs after presentation
37
Q

How does primary FSGS present?

Secondary? Heriditary?

A

Primary: usually presents with acute onset of nephrotic syndrome

secondary FSGS: usualyl manifests with slowly increasing renal insufficiency and proteinuria

herditary FSGS: mutations in proteins that make up the glomerular slit diaphragm

38
Q

what are the causes of secondary FSGS?

A

drugs-NSAIDs, heroin

infections- HIV

Massive obesity

healed previous glomerular injury

loss of functioning renal mass-unilateral agenesis, reflux nephropathy, etc.

39
Q

What is seen on LM, IF and EM for Focal Segmental Glomeruloscleosis?

A

LM: focal and segmental glomerular sclerosis with capillary collapse, hyaline and lipid deposition and adhesion to Bowman’s capsule

IF: negative of IGM and C3 in mesangium or in segmental scars

EM: podocyte foot process effacement; may see segmental sclerosis

**global sclerosis

40
Q

how do we treat FSGS?

A
  • prognosis correlates with degree of proteinuria-ACE inhibitors decrease proteinuria
  • corticosteroid can induce remission in some patients patients
  • treatment for steroid resistant patients and patients who relapse is problematic
    • immunosuppressives
  • progression to ESRD in 50% at 10 years

***black, HIV, obesity

41
Q

what is seen in membranoproliferative glomerulo-nephritis (MPGN)

A
  • proteinuria and hematuria commonly coexist
  • HTN occurs in 1/3
  • low C3 complement is a prominent feature
  • variable clinical presentation
    • 50% nephrtoic syndrome
    • 30% asymptomatic proteinuria +- hematuria
    • 20% acute Gn
42
Q

What are the 2 types of MPGN and what is seen?

A
  • Primary MPGN
  • Secondary MPGN
    • connective tissue diseases- SLE
      cryoglobulinemia
    • infections- Hepatitis C virus, HBV, endocarditis abscesses
    • neoplasms
43
Q

what is seen on LM, IF, EM for MPGN?

A

LM: hypercellular glomeruli, endocapillary cell proliferation, lobular appearing glomeruli

IF: granular C3 deposition

EM: subendothelial deposits

44
Q

what 3 things happen with systemic lupus erythematous (SLE)

A
  • a multisystem auto-immune disorder
    • abnormal autoantibody production
    • immune complex deposition
    • inflammatory cell infiltration
45
Q

What is lupus nephritis?

A
  • common cause of diffuse proliferative GN
  • 40% of patients develop overt nephritis
    • follow U/A in SLE patients
    • HTN suggests the presence of renal disease
  • man of the different clinical syndromes of renal disease can occur in the setting of SLE
  • renal biopsy is important to order considering the lesion in SLE
46
Q

treatment for lupus nephritis

A
  • general principles of management of any class of lupus nephritis
    • aggressive BP control
    • control of lipid levels
    • appropriate treatment od extrarenal involvement
  • classes III-V usually treated with corticosteroids + cytotoxic therapy
    • class IV: renal failure rate 25% by 5-10 yrs

Renal (7 decks)

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