Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
IgA Nephropathy
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
cause of IgA Nephropathy
unknown- may develop with minimal/no symptoms associated with hepatic cirrhosis, celiac dz, HIV
27
IgA Nephropathy symptoms
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
clinical course IgA Nephropathy
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
IgA Nephropathy lab findings
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
tx of IgA Nephropathy
HTN or proteinuria = ACE/ARB fish oil- anti inflammatory corticosteroid (proteinuria 1-3 g) immunosuppressant may be used
31
prognosis fo IgA Nephropathy
most unfavorable prognostic indicator is proteinuria >1g/day 1/3 have remission, some have progressive insufficiency and ESRD, microscopic hematuria and stable GFR
32
IgA Vasculitis
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
clinical features IgA Vasculitis
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
distinguish IgA Vasculitis and IgA Nephropathy
identical lesions on renal biopsy IgA Vasculitis is cutaneous, GI, Connective tissue
35
diagnosis of IgA Vasculitis
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
rapidly progressing GN
anti-glomerular basement GN connective tissue disorders granulomatosis w/polyangiitis hypersensitivity GN
37
anti GBM GN
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
goodpastures syndrome
AGBM GN pulmonary hemorrhage mediated by anti-GBM abs and GN can have HLA connection
39
anti-GBM GN clinical findings
``` URI HEMOPTYSIS Dyspnea HTN Edema Nephritic proteinuria RBC cast ```
40
renal biopsy in anti-GBM GN
ANCA - must distinguish between GPA and anti-GBM crescentic GN and linear IgG deposits along glomerular capillaries (GPA = no complexes)
41
ANCA
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
anti-GBM GN tx
``` plasmapheresis (remove Abs) immunosuppressive drugs (prevent formation of new Abs and control inflammation) ``` mortality improved but need to catch early
43
connective tissue disorders RPGN
Type II SLE, polyarteritis glomerular inflammation caused by deposition of complexes in capillaries
44
GPA RPGN
aka Wegener's pacui-immune necrotizing GN
45
hypersensitivity vasculitis RPGN
rxn to drug or ag causes widespread inflammation MC: PTU, hydrazine, allopurinol, minocycline
46
renal cysts
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
problematic renal cysts
scattered thru kidney | U/s, CT, surgical exploration
48
dialysis cyst
commonly develops can mask adenocarcinoma can use arteriography to evaluate
49
PCKD
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
PCKD complications
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
poor prognosis indicators in PCKD
``` 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.
© 2025 Bold Learning Solutions. Terms and Conditions