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Pathoma > Renal > Flashcards

Renal Flashcards

1
Q

what vessel blocks a horseshoe kidney

A

IMA

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2
Q

unilateral agenesis

A

hypertrophy of other one

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3
Q

bilateral renal agenesis

A
  • oligohydramnios
  • leads to lung hyperplasia (no stretch
  • low set ears and limb defects (Potter sequence)
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4
Q

dysplastic kidney

A
  • congenital malformation, non inherited
  • cartilage and cyst
  • usually unilateral
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5
Q

adult polycystic kidney

A
  • bilateral
  • autosomal dominant
  • enlarged kidney
  • APKD1/2
  • associated with berry aneurysm, hepatic cysts and mitral valve prolapse
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6
Q

newborn polycystic kidney disease

A
  • recessive

- congenital hepatic fibrosis and hepatic cysts (portal hypertension)

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7
Q

medullary cystic kidney disease

A
  • cysts are in medullary collecting ducts
  • shrunken kidneys
  • autosomal dominant
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8
Q

hallmark of renal failure

A
  • azotemia and oliguria
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9
Q

prerenal failure (labs)

A
  • lower GFR, azotemia and oliguria
  • high BUN:Cr (reabsorption still works)
  • tubular function is intact - low FeNa
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10
Q

postrenal (labs)

A
  • decrease GFR and azotemia
  • early = high BUN:Cr and normal FENa
  • late = decrease BUN:Cr ratio, high FENa, unconcentrated urine
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11
Q

ATN

A
  • injury of tubules (detachment of cells from BM)
  • azotemia with low BUN:Cr, high FENa
  • muddy brown casts in urine
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12
Q

etiology of ATN

A

ischemia and nephrotoxicity

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13
Q

areas susceptible to ischemia

A

proximal tubule and medullary segment or thick ascending limb

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14
Q

causes of ATN

A

antibiotics, lead, crush, ethylene glycol, radiocontrast dye, urate (tumor lysis)

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15
Q

crystals in ethylene glycol poisoning

A

oxalate crystals

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16
Q

features of ATN

A
  • oliguria with muddy brown casts
  • high BUN and creatinine
  • hyperkalemia and metabolic acidosis
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17
Q

what happens post ATN

A

cells are stable, takes time to regenerate

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18
Q

acute interstitial nephritis

A
  • drugs including NSAIDs, PCN and diuretics
  • inflammation in interstitium
  • eosinophils in urine
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19
Q

renal papillary necrosis

A
  • gross hematuria and flank pain

- caused by aspirin, sickle cell

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20
Q

labs in nephrotic syndrome

A
  • hypoalbuminemia (albumin >3.5)
  • hypergammaglobulinemia
  • hypercoagulable state (lose ATIII)
  • hyperlipidemia and hypercholesterolemia (blood is thin so fat goes in blood)
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21
Q

minimal change disease

A
  • children
  • associated with Hodgkins lymphoma
  • loss of foot processes from cytokines
  • normal glomeruli with no immune complexes
  • no loss of immunobloblulin
  • good response to steroids
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22
Q

focal segmental glomerulosclerosis

A
  • can be associated with HIV, heroin or sickle cell
  • effacement of foot processes on EM
  • no immune complexes
  • progression of MCD
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23
Q

membranous nephropathy

A
  • associated with hepatitis B/C, SLE or drugs
  • thick glomerular basement membrane
  • immune complex deposition (granular)
  • spike and dome - subepithelial
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24
Q

membranoproliferative glomerulonephritis

A
  • thick capillary membranes with tram-track appearance
  • immune complex deposition (granular)
  • mesangial cell is proliferating
  • deposits can be anywhere
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25
Q

two types of membranoproliferative glomerulonephritis

A

type 1 - subendothelial (Hep B/C and tram tracks)

type 2 - within BM (antibody C3 nephritic factor - too much C3 convertase)

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26
Q

locations of immune complexes

A
  • subepithelial - membranous nephropathy
  • in BM - type 2 MPGN
  • subendothelial - type 1 MPGN
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27
Q

grouping of nephropathies

A
  1. MCD and FSGN - effacement of foot process by cytokines
  2. membranous and MPGN - membranes with immune complexes
  3. diabetes and amyloidosis (systemic disease)
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28
Q

diabetes nephropathy

A
  • high glucose leads to NEG of BM resulting in hyaline arteriolosclerosis
  • high GFR (hyperfiltration) leading to sclerosis
  • give ACE inhibitors to help
29
Q

amyloidosis

A
  • amyloid in mesangium

- apple green biregringence

30
Q

hallmark of diabetic nephropathy

A
  • sclerosis of mesangium and formation of Kimmelstiel-Wilson nodules
31
Q

labs in nephritis syndrome

A
  • limited proteinuria
  • oliguria and azotemia
  • salt retention and periorbital edema and hypertension
  • RBC casts
32
Q

pathophys of nephritis

A

immune complexes activating complement, C5a attracts neutrophils causing damage

33
Q

PSGN

A
  • after group A strep
  • either skin or pharynx
  • M protein
  • subepithelial humps (complexes pile up)
34
Q

findings in PSGN

A
  • cola urine
  • oliguria
  • edema
35
Q

RPGN (rapidly progressive glomerular nephritis)

A
  • nephritic syndrome that progresses to renal failure

- crescent

36
Q

crescent are made of…

A

macrophages and fibrin (inflammatory debris

37
Q

types of immunofluorescence

A
  1. linear (goodpasture)
  2. granular (PSGN)
  3. negative (vasculitis)
38
Q

goodpasture

A
  • antibodies to collagen 4 in BM
39
Q

renal disease in lupus

A

diffuse proliferative glomerulonephritis (nephritic) and membranous nephropathy (nephrotic)

40
Q

IgA nephropathy

A
  • in mesangium
  • RBC casts
  • after mucosal infections
  • complex deposition
  • can progress to renal failure
41
Q

Alport syndrome

A
  • defect in type 4 collagen
  • thinning and splitting of GBM
  • isolated hematuria, sensory hearing loss and ocular disturbances
42
Q

positive leukocyte esterase

A
  • pus in urine
43
Q

nitrites

A

bacteria in urine

44
Q

sterile pyuria

A

chlamydia and neisseria

45
Q

WBC casts

A

in pyelonephritis

46
Q

chronic pyelonephritis

A
  • malformation of valve from bladder to kidney
  • cortical scarring with blunted calyces
  • scarring at upper and lower poles
47
Q

histology in chronic pyelonephritis

A
  • thyroidization of tubules
  • atrophic tubules contain eosinophilic proteinaceous material
  • waxy casts
48
Q

calcium stone

A
  • have to exclude calcium causes
  • in Chrons disease (less absorption of oxalate)
  • treat with HCTZ
49
Q

ammonium magnesium phosphate

A
  • infection with urease positive organisms

- staghorn calculi that acts as a nidus

50
Q

Uric acid stone

A
  • radiolucent
  • in dry heat and acidic pH
  • in gout or myeloproliferative disorders
  • treat with alkalinization of urine
51
Q

cysteine stone

A
  • defect in tubules that decrease cysteine reabsorption

- staghorn calculi

52
Q

most common causes of renal failure

A

diabetes, HTN and glomerular disease

53
Q

EPO is produced by….

A

renal peritubular interstitial cells

54
Q

clinical findings in renal failure

A
  • hyperkalemia
  • acidemia
  • hypocalcemia (less vitamin D and can’t excrete phosphate)
  • renal osteodystrophy
55
Q

renal osteodystrophy

A
  • low calcium causes PTH to rise and hit bone
  • osteitis fibrosa cystica
  • osteomalacia (can’t mineralize new bone)
  • osteoporosis (metabolic acidosis)
56
Q

dialysis kidneys

A

shrunken with cysts

- risk for RCC

57
Q

angiomyolipoma

A
  • hamartoma of vessels, muscle and fat

- increase frequency in tuberous sclerosis

58
Q

renal cell carcinoma

A
  • epithelial tumor
  • hematuria, palpable mass and flank pain
  • fever, weight loss and paraneoplastic
  • presents with left sided varicocele
  • yellow mass
59
Q

pathogenesis of RCC

A
  • loss of VHL
  • increases IGF-1
  • increased HIF (VEGF and PDGF)
60
Q

two pathways of RCC

A

sporadic - smoking
RCC - yonger and bilateral
- both with VHL

61
Q

Von Hippel-Lindau disease

A
  • loss of VHL gene

- risk for hemangioblastoma and RCC

62
Q

Wilms tumor

A
  • in children
  • blastema, primitive glomeruli and tubules
  • large flank mass and hypertension
63
Q

syndromes with Wilms tumor

A 
WAGR (aniridia, genital problems and retardation)
Beckwith Wiedemann (hypoglycemia, hemihypertrophy and organomegaly)
64
Q

urothelial carcinoma

A
  • in bladder usually
  • cigarette smoke, naphthylamine, azo dyes, cyclophosphamide or phenacetin
  • painless
65
Q

two pathways of urothelial carcinoma

A
  1. flat - starts as high grade (early p53)

2. papillary - low grade to high grade to invasion

66
Q

field defect

A

all of urothelium has been hit, tumors are multifocal and recur

67
Q

risks of SCC

A

cystitis, schistosoma, low standing nephrolithiasis

68
Q

where does adenocarcinoma of bladder come from

A

urachal remnant (dome of bladder), cystitis glandularis, exstrophy (no caudal portion)

Pathoma (11 decks)

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