Renal Flashcards

1
Q

Crescentic GN depositions

A
  • RPGN crescents:
    • glomerular parietal cells
    • monocytes and macrophages
    • FIBRIN on deckkk
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2
Q

type 1 RPGN (Goodpasture syndrome) deposits

A

C3 and IgG-linear depositis seen on IF microscopy

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3
Q

Acute PSGN depositions

A
  • IF:
    • IgG, IgM, C3: lumpy bumpy
    • (will have DEC serum C3 levels)
  • EM: subepithelial IC
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4
Q

DPGN deposits

A
  • EM: (subendothelial, sometimes intramembranous)
    • IgG based IC + C3
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5
Q

MPGN deposits

A
  • Type 1: subendothelial IC +granular IF
  • Type 2: intramembranous IC (dense deposits)
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6
Q

FSGS deposits

A
  • IF: focal IgM, C1, C3
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7
Q

ACE inhibitors and bradykinin

A
  • ACE metabolizes brady=LESS brady
  • ACE inhibitors=less brady metab=MORE brady
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8
Q

TWO main causes of overflow incontinence

A
  1. impaired detrusor contractility
  2. bladder outlet obstruction (BOO)
    1. tumor obstructing the urethra

CP: involuntary+continuous urinary leakage when bladder is full

-incomplete emptying

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9
Q

what is the differential diagnosis for urinary incontinence

A
  1. stress
    1. loss of urethral support and abdo pressure>urethral sphincter pressure
    2. s/s: leaking with cough, sneeze,laugh, lift
  2. urge
    1. detrusor overactivity (PT with MS)
    2. s/s: sudden overwhelming or freq need to empty bladder
  3. overflow
    1. impaired detrusor contractility, BOO
    2. s/s: involuntry dribbling of urine, incomplete emptying
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10
Q

classifications for RP(crescentic)GN

A
  1. anti-GBM RPGN
    1. linear GBM of IgG and C3
    2. some: antiGBM in lungs (Goodpasture)
  2. immune-complex RPGN
    1. lumpy bumpy d/t IgA + IgG + complement
    2. d/t:
      1. PSGN
      2. SLE (serum anti-PHOSPHOLIPID Ab)
      3. IgA nepropathy
      4. HSP
  3. pauci-immune RPGN
    1. nada on BM
    2. ANCA in serum=
      1. granulomatosis with polyangiitis
      2. microscopic polyangiitis
      3. idiopathic
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11
Q

nephrotic syndrome and aldosterone

A
  • plasma oncotic pressure is DEC
  • net plasma filtration into interstitium
  • DEC effective circulating intravascular volume
  • compensatory INC in RAAS
  • elevated circulating aldosterone
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12
Q

CP MCD

A
  • 5yo boy w/ generalized edema after mild URI
  • UA: proteinuria, albumin + trace IgG
  • PP: loss of GBM anions=can no longer repell albumin=SELECTIVE albuminuria
    • d/t immune dysregulation, systemic T cell dysfunction= overproduce glomerular permeability factor (GPF)
    • GPF:
      • causes podocyte foot process fusion
      • DEC anionic properties of the glomerular basement membrane

**INC SELECTIVE FILTRATION OF PROTEINS**

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13
Q

Thrombotic microangiopathy

A
  • PENTAD for TTP (thrombocytopenic thrombotic purpura-HUS is a thrombotic microangiopathy-TMA)…all in the setting of a GI illness
    1. fever
    2. neuro symptoms (progressive lethargy)
    3. renal failure
    4. anemia
    5. thrombocytopenia
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14
Q

what are the shared common clinical and pathologic features of TMA syndromes (thrombotic microangiopathy)

A
  • platelet activation in arterioles and capillaries
  • diffuse micro-vascular thrombosis (most commonly affect: brain, kidneys, heart)
  • microangiopathic hemolytic anemia with schistocytes
  • thrombocytopenia
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15
Q

FSGS CP

A
  • (has a collapsing variant)
  • CP: heavy proteinuria
  • “collapse and sclerosis of glomerular tufts”
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16
Q

RP(crescentic)GN CP

A
  • macroscopic hematuria
  • HTN
  • progresive renal failure
  • three major classifications:
    1. anti-GBM (w/ hemoptysis in Goodpasture syndrome)
    2. immune-complex mediated (SLE)
    3. pauci-immune (w/ pulm, upper respiratory, and kidney involvement in granulomatosis with polyangiitis)
17
Q

PSGN CP

A
  • childhood dz
  • can follow strep pharyngitis and lead to coke-colored urine + periorbital edema
  • renal biopsy: diffuse proliferation and subepithelial Ig deposits
18
Q

HSP vs. IgA nepropathy CP/renal bx

A
  • HSP: childhood dz; NON-thrombocytopenic palpable purpura + arthritis
  • IgA nephropathy presents w/ recurrent hematuria and low-grade proteinuria after URTI
  • BOTH: IgA deposition in mesangium
19
Q

ATN renal biopsy

A

patchy necrosis of tubular epithelium and loss of basement membrane

20
Q

TMA renal bx

A

platelet-rich thrombi in glomeruli and arterioles

21
Q

What does BPH do to the kidneys

A
  • intermittent BOO + overflow incontinence
  • urinary retention=INC pressure in the urinary tract and resultant reflux nephropathy
  • ultimately: hydronephrosis and renal intersitial atrophy (“parenchymal pressure atrophy) and scarring
22
Q

diabetic nephrosclerosis termed

A

glomerular sclerosis and hyalinosis

23
Q

long-standing systemic HTN termed

A

hyperplastic arteriolar changes (intimal fibroelastosis)

-diagnostic of hypertensive nephropathy seen in pts with poorly controlled HTN

24
Q

terms for the causes of ITN

A
  • low-flow states: MI
  • systemic vasodilation: sepsis
  • s/s–INC sBUN & Cr: azotemia
25
Q

dysplasia termed precursor of malignancy

A
  • epithelial dysplasia=alteration in cell architecture
    • cells change shape, size (pleomorphic) and staining (hyperchromatic); nuclei enlarge
26
Q
A
27
Q

urate nephropathy termed

A
  • d/t tubular obstruction f/m urate crystal deposition
  • seen in indivs wih ACUTE HYPER-uricemia (tumor lysis syndrome)
  • CP: acute renal failure d/r chemo for a malignancy