Brainscape's Knowledge GenomeTM

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


See full index

FA17 Nephrology > Glomerulonephropathies 1 > Flashcards

Glomerulonephropathies 1 Flashcards

1
Q

acute glomerulonephritis

A

immunologic mechanisms triggers inflammation and proliferation of glomerular tissue

causes damage to kidney

thickening and proliferation in glomerulus

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

microalbuminuria

A

excretion of 30-300 mg of protein per day

sign of early renal disease

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

macroalbuminuria

A

excretion of >300 mg (3g) per day

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

nephritic syndrome

A

abrupt onset of proteinuria 1-3 g/day

+/- hematuria, RBC casts

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

nephritic syndrome is often accompanied by

A

HTN
Reduced GFR – oliguria, AKI
Edema/fluid overload

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

nephrotic syndrome

A

heavy proteinuria (>3g/day)

hypoalbuminemia, edema, hyperlipidemia

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

secondary causes of nephrotic syndrome

A

DM

lupus

amyloidosis

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

damage done in glomerulonephropathies

A

immune mediated inflammation and proliferation damages GBM, mesangium or capillary endothelium

deposition of immune complexes and complement in tissues of glomeruli PLUS invasion by PMNs and thickening of GBM

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

types of GN

A

focal (<50%)
diffuse (all glomeruli)
segmental (only part of tuft involved)
global (entire glomerular tuft)

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

GN pathology

A

thickening and cellular proliferation of glomerulus

GBM becomes leaky and lets proteins into ultra filtrate

persistent inflammation = fibrosis and scarring of GBM

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

rapid GN

A

> 50% loss of nephron function over WEEKS

can be permanent

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

prolonged GN

A

inflammatory changes over time persistent abnormalities

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

general clinical findings of GN

A

edema (decreased onchotic pressure)

weakness, fever, abdominal pain, malaise

HTN

urine is dark and volume reduced

evidence of renal failure

proteinuria, RBCs and RBC canes in U/A

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

pathognomonic GN finding

A

RBC casts in U/A

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

special lab work up to determine GN etiology (8)

A
  1. Complement - CH50, C3, C4 (low levels = GN)
  2. Anti GBM autoAbs
  3. ANA (SLE, autoimmune)
  4. anti-dsDNA (SLE, autoimmune)
  5. ANCA (vasculitides)
  6. HIV
  7. viral hepatitis panel
  8. anti-PLAR2 recetor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diagnostic study of choice in GN

A

renal biopsy looking for immune deposits

confirm diagnosis and type of GN

minimal, linear, granular

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

minimal deposits GN (3)

A
  1. pauci-immune GN (vasculitides)
  2. GPA/Wegener’s
  3. Eosinophillic granulomatosis (Churg-Strauss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

linear deposits GN (1)

A
  1. anti GBM GN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

granular deposits (8)

A
  1. PSGN
  2. IgA nephropathy
  3. HSP
  4. HIV
  5. HBV
  6. HCV GN
  7. cryoglobulinemia
  8. SLE/autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

general GN treatment

A

reduction fo HTN and fluid overload

treat underlying cause

salt and water restriction

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

post infectious GN (PSGN)

A

due to subtype of group A hemolytic strep, increased caused by staph infection

appears 1-4 WEEKS following impetigo, cellulitis, pharyngitis, UTI - also seen in other bacterial infections

uncommon in developed countries, 60+, 5-12 y/o, M>F

22
Q

PSGN mechanisms of damage (4)

A
  1. circulating immune complex deposits in GBM
  2. strep antigens deposit in GBM, cause immune reaction
  3. Abs against strep antigens react with glomerular proteins (molecular mimicry)
  4. nephritic strain of strep turns IgG against us
23
Q

s/s of pSGN

A

oliguria, edema , HTN

colca colored urine with RBCs, RBC casts, proteinuria <3 g/day

LOW serum complement + Strep (or other agent) titers HIGH

24
Q

diagnosing PSGN + tx

A

renal biopsy needed to r.o other causes

TX: ABX, salt and fluid restriction, diuretics, anti-HTN (CCB)

oliguiria/fluid retention spontaneously resolve - proteinuria and hematuria can take 6-12 months to resolve

25
Q

IgA Nephropathy

A

MC form of acute glomerulonephritis (particularly in asians and caucasians)

teens or young adults, M>F

IgA and C3 deposition in the glomerular mesangium

26
Q

cause of IgA Nephropathy

A

unknown- may develop with minimal/no symptoms

associated with hepatic cirrhosis, celiac dz, HIV

27
Q

IgA Nephropathy symptoms

A

episodes of gross hematuria (1-3 days) and associated with URI, GI, Flu illnesses

30-40% have microscopic hematuria and mild proteinuria on routine UA

RARE nephrotic syndrome or progressive GN with nephritic pic

28
Q

clinical course IgA Nephropathy

A

gross hematuria lasting 1-3 days associated with URI, GI, or fLU illness

urine: red-cola colored 1-3 DAYS after onset of associated illness

flank pain, low grade fever (mimic UTI)

29
Q

IgA Nephropathy lab findings

A

IgA levels increased
complement normal

renal biopsy: focal GN, diffuse mesangial IgA C3 deposits, proliferation of cells
- bx is persevered for severe/progressive disease

30
Q

tx of IgA Nephropathy

A

HTN or proteinuria = ACE/ARB

fish oil- anti inflammatory

corticosteroid (proteinuria 1-3 g)

immunosuppressant may be used

31
Q

prognosis fo IgA Nephropathy

A

most unfavorable prognostic indicator is proteinuria >1g/day

1/3 have remission, some have progressive insufficiency and ESRD, microscopic hematuria and stable GFR

32
Q

IgA Vasculitis

A

small vessel vasculitis of unknown cause

MC form of systemic vasculitis in children

MC in children, male predominance, self limited

occurs in fall, winter, spring, preceded by URI

33
Q

clinical features IgA Vasculitis

A
  1. palpable purpura (w/o thrombocytopenia or coagulopathy)
  2. arthritis (lg joints, swelling and tenderness)
  3. abdominal pain (colicky, worsen to GIB, intussception)
  4. renal disease
34
Q

distinguish IgA Vasculitis and IgA Nephropathy

A

identical lesions on renal biopsy

IgA Vasculitis is cutaneous, GI, Connective tissue

35
Q

diagnosis of IgA Vasculitis

A

low C3/C4, high IgA levels

made if classic clinical pic present - if not, bx skin or renal

managed outpatient (OTC meds)

most recover fully and no recurrence (some have recurrence in 4 months)

36
Q

rapidly progressing GN

A

anti-glomerular basement GN
connective tissue disorders
granulomatosis w/polyangiitis
hypersensitivity GN

37
Q

anti GBM GN

A

rare disease, bimodal epidemiology (males in 20-30s, female in 50-60)

auto-An to subtype of collagen found only in glomerulus and kidney

38
Q

goodpastures syndrome

A

AGBM GN

pulmonary hemorrhage mediated by anti-GBM abs and GN

can have HLA connection

39
Q

anti-GBM GN clinical findings

A 
URI 
HEMOPTYSIS 
Dyspnea 
HTN 
Edema
Nephritic proteinuria 
RBC cast
40
Q

renal biopsy in anti-GBM GN

A

ANCA - must distinguish between GPA and anti-GBM

crescentic GN and linear IgG deposits along glomerular capillaries (GPA = no complexes)

41
Q

ANCA

A

antibody in both GPA and Anti-GBM

autos directed against granules in cytoplasm of neutrophils and monocyte lysosomes

found in 30% of patients with AGBM, indicates positive finding

42
Q

anti-GBM GN tx

A 
plasmapheresis (remove Abs) 
immunosuppressive drugs (prevent formation of new Abs and control inflammation)

mortality improved but need to catch early

43
Q

connective tissue disorders RPGN

A

Type II

SLE, polyarteritis

glomerular inflammation caused by deposition of complexes in capillaries

44
Q

GPA RPGN

A

aka Wegener’s

pacui-immune necrotizing GN

45
Q

hypersensitivity vasculitis RPGN

A

rxn to drug or ag

causes widespread inflammation

MC: PTU, hydrazine, allopurinol, minocycline

46
Q

renal cysts

A

epithelium lined cavities filled with fluid/semi solid material

common to have one in normal population

must distinguish from abscess, PCKD, malignancy

benign still require periodic monitoring

47
Q

problematic renal cysts

A

scattered thru kidney

U/s, CT, surgical exploration

48
Q

dialysis cyst

A

commonly develops

can mask adenocarcinoma

can use arteriography to evaluate

49
Q

PCKD

A

autosomal dominate, multiple cysts

progress to ESRD

abdominal/flank pain, hematuria, HTN

large kidneys on exam, hepatic, splenic, pancreatic cysts

diagnosed with u/s

50
Q

PCKD complications

A
  1. abdominal or flank pain (lg size + infection, bleeding, stones)
  2. hematuria (fragile, stretched vessels rupture, - gross = cyst rupture, recurrent = CA)
  3. renal infection (fluroquinolones x14 days, fever + leukocytosis)
  4. HTN - RAAS activation 2/2 ischemia
  5. nephrolithiasis
  6. Cerebral aneurysm
  7. other
51
Q

poor prognosis indicators in PCKD

A 
lg kidneys 
multiple infxn/hematuria 
HTN
male sex 
AA ethnicity

FA17 Nephrology (13 decks)

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