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Step 1 Flash Cards > Renal > Flashcards

Renal Flashcards

1
Q

most common site of obstruction in fetus

A

ureteropelvic junction

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2
Q

multicystic dysplastic kidney

A

due to abnormal interaction between ureteric bud and metanephric mesenchyme
- non functional kidney of cysts and connective tissue

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3
Q

glomerular filtration barrier

A
  • fenestrated capillaries provide size barrier
  • BM provides charge membrane (lost in nephrotic syndrome)
  • epithelial layer has podocytes
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4
Q

equations for GFR, RPF and FF

A 
GFR = Cinulin = Ui x V/Pi
RPF = RBF x (1-Hct)
FF = GFR / RPF = GFR /  (RBFx(1-Hct))
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5
Q

Hartnup disease

A

deficiency in neutral AA transporter, leading to dec tryptophan uptake

  • can lead to pellagra-like symptoms because niacin is derived from tryptophan
  • treat with high protein diet and nicotinic acid
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6
Q

early proximal convoluted tubule functions

A
  • reabsorb AA, glucose, and most H2O, Na, Cl, Phos, K
  • secretes NH3 (buffers H+)
  • PTH inhibits Na/phos transport, inc phos excretion
  • ATII increases Na/H exchange, inc Na, H2O and HCO2- absorption (permitting contraction alkalosis)
  • 65-80% of Na reabsorbed
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7
Q

thin descending loop of henle

A
  • water passively reabsorbed due to concentration gradient
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8
Q

thick ascending loop of henle

A
  • actively reabsorbs Na, K and Cl through Na/K/2Cl transporter
  • Mg and Ca reabsorbed paracellularly 2/2 K backleak
  • impermeable to H2O
  • 10-20% of Na reabsorbed
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9
Q

early distal convoluted tubule

A
  • actively reabsorbs Na, Cl
  • PTH inc Ca/Na exchange, inc Ca reabsorption
  • 5-10% of Na reabsorbed
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10
Q

collecting tubule

A

reabsorbs Na in exchange for K+ and H+ (mediated by aldosterone)

  • ADH acts on V2 receptor and inc insertion of aquaporins
  • 3-5% of Na reabsorbed
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11
Q

Fanconi syndrome

A
  • reabsorptive defect in the PCT
  • inc excretion of AA, glucose, HCO3- and phos
  • may result in metabolic acidosis
  • causes include hereditary defects (Wilson disease), ischemia and nephrotoxins/drugs
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12
Q

Bartter syndrome

A
  • reabsorptive defect in the thick ascending loop of Henle
  • AR, affects Ka/K/2Cl transporter
  • hypokalemia and metabolic alkalosis, hypercalciuria
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13
Q

Gitelman syndrome

A
  • reabsorptive defect of NaCl in DCT
  • AR
  • hypokalemia and metabolic alkalosis
  • NO hypercalciuria
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14
Q

Liddle syndrome

A
  • inc Na reabsorption in distal and collecting tubules
  • AD
  • results in hypertension, hypo K, metabolic alkalosis, low aldo
  • treat with amiloride
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15
Q

effects of Angiotensin II

A
  • acts on AT I receptors on vascular smooth muscle to constrict
  • constricts efferent arteriole to inc FF despite low volume state (compensatory Na reabsorption)
  • stimulates aldo (inc Na reabsorption)
  • stimulates ADH (inc H2O reabsorption)
  • stimulates prox tubule Na/H activity
  • stimulates hypothalamus (thirst)
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16
Q

juxtaglomerular apparatus function and B-blockers effect on it

A
  • JG cells (modified smooth muscle cells) sense dec renal blood flow and release renin
  • macula densa senses NaCl in the distal convoluted tubule –> renin
  • B1 sympathetic tone also increases renin release
  • b blockers block the B1 receptors on JGA, causing decreased renin release
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17
Q

Vit D in the kidney

A

proximal tubule cells convert 25-OH vit D to 1,-25 OH2 vit D via 1-alpha hydroxylase
- this enzyme is stimulated by PTH

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18
Q

NSAIDs

A
  • block the protective vasodilation of the afferent arteriole that usually would increase RBF
  • can constrict the afferent arteriole and dec RBF so much they cause acute renal failure
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19
Q

Winter’s formula

A

PCO2 = 1.5[HCO3-] + 8 +/- 2

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20
Q

causes of anion gap metabolic acidosis

A

MUDPILES

-methanol, uremia, DKA, propylene glycol, iron tablets or INH, lactic acidosis, ethylene glycol, salicylates

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21
Q

causes of non-anion gap metabolic acidosis

A

HARD ASS

- hyperalimentation, addisons, RTA, diarrhea, acetazolamide, spironolactone, saline infusion

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22
Q

metabolic alkalosis with low urine Cl

A
  • vomiting, NG aspiration, prior diuretic use
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23
Q

metabolic alkalosis with high urine Cl and hypo/euvolemia

A
  • diuretic use, Barter and Gittelman syndromes
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24
Q

metabolic alkalosis with high urine Cl and hypervolemia

A

excess mineralocorticoids (primary hyperaldo, cushing disease, ectopic ACTH prodcuction)

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25
Q

renal tubular acidosis

A

d/o of the renal tubules which leads to a non-anion gap hyperchloremic metabolic acidosis

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26
Q

RTA 1

A
  • pH > 5.5
  • defect in alpha intercalated cell’s ability to secrete H+ (no new HCO3- is generated)
  • associated with hypokalemia and inc risk for calcium phosphate stones
  • causes: amphotericin B, analgesic nephropathy, MM, congenital urinary anomalies
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27
Q

RTA 2

A
  • pH < 5.5
  • defect in prox tubule HCO3- reabsorption
  • associated with hypoK, inc risk for hypophosphatemic rickets
  • causes: Fanconi syndrome, chemicals toxic to prox tubules (lead, aminoglycosides), and carbonic anhydrase inhibitors
28
Q

RTA 4

A
  • pH < 5.5
  • hypoaldo, aldo resistance or K sparing diuretics
  • hyperkalemia impairs ammoniagenesis, dec H+ excretion into the urine
29
Q

RBC casts mean

A

glomerulonephritis, ischemia or malignant hypertension

30
Q

WBC casts mean

A

tubulointerstitial inflammation, acute pyelo, transplant rejection

31
Q

fatty casts (“oval fat bodies”) mean

A

nephrotic syndrome

32
Q

granular (“muddy brown”) casts mean

A

acute tubular necrosis

33
Q

waxy casts mean

A

advanced renal disease/chronic renal failure

34
Q

hyaline casts mean

A

nonspecific, can be norm esp in concentrated urine

35
Q

eosinophilic casts mean

A

MM, chronic pyelo

36
Q

nephritic syndromes

A

inflammatory process leading to hematuria and RBC casts in the urine

  • assoc with azotemia, oliguria, HTN and proteinuria (< 3.5mg/day)
  • acute poststrep glomerulonephritis, RPGN, IgA nephropathy, Alport syndrome
37
Q

nephtitic/nephrotic syndromes

A

-diffuse proliferative glomerulonephritis, membranoproliferative glomerulonephritis

38
Q

nephrotic syndromes

A
  • > 3.5 mg protein/day, hyperlipidemia, fatty casts, edema, hypercoaguability
  • FSGS, Membranous nephropathy, MCD, amyloidosis, diabetic glomerulonephropathy
39
Q

FSGS

A

LM - segmental sclerosis and hyalinosis
IF -ve
EM - effacement of foot process
- most common cause of nephrotic syndrome in hispanics and AA
- idiopathic or 2/2 HIV, sickle cell, heroin, obesity, interferon treatment, CKD
- inconsistent response to steroids

40
Q

membranous nephropathy microscope findings

A

LM - diffuse capillary and GBM thickening
IF - granular as a result of immune complex deposition. nephrotic presentation of SLE
EM - “spike and dome” appearance with subendothelial deposits

41
Q

membranous nephropathy epi/cause

A
  • most common cause of nephrotic syndrome in caucasian adults
  • can be due to Ab to phospholipase A2 receptor, drugs (NSAIDS), HBV/HCV, SLE or solid tumors
  • poor response to steroids
42
Q

MCD

A

LM normal, neg IF, EM - effacement of foot processes

  • most common in kids
  • triggered by recent infection, immunization, Hodgkins Lymphoma
  • excellent response to steroids
43
Q

amyloidosis

A
  • LM - congo red stain shows apple-green birefringence under polarized light
  • associate with chronic conditions (TB, MM, rheumatoid arthritis)
44
Q

Type I MPGN

A
  • subendothelial immune complex deposits with granular IF, “tram-track” appearance due to GBM splitting
  • nephritic/nephrotic syndrome
  • assoc with HBV, HCV
45
Q

Type II MPGN

A
  • inramembranous IC deposits, “dense deposits”

- assoc with C3 nephritic factor (stabilizes C3 convertase –> serum C3 levels)

46
Q

diabetic glomerulonephropathy

A

LM - mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

  • glycosylation of GBM – inc permeability and thickening
  • glycosylation of efferent arterioles inc GFR, leads to mesangial expansion
47
Q

acute poststreptococcal glomerulonephritis

A
  • LM - glomeruli enlarged and hypercellular
  • IF - “starry sky” granular appearance and “lumpy bumpy” due to IgG, IgM and C3 deposition along GBM and mesangium
  • EM - immune complex humps
  • 2 weeks after GAS pharyngitis or skin infection
  • Type III HS reaction that resolves spontaneously
  • coca-cola urine, ASO titer and low C3
48
Q

rapidly progressive (crescentic) glomerulonephritis

A
  • LM and IF - crescent moon shape (crescents consist of fibrin and plasma proteins with glomerular parietal cells, monocytes and macrophages)
  • 2/2 Goodpasture’s disease, Wegener’s, Microscopic polyangiitis
  • poor prognosis
49
Q

diffuse proliferative glomerulonephritis

A
  • due to SLE or MPGN
  • LM - “wire looping” of capillaries
  • EM - subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
  • IF - granular
  • most common cause of death from SLE
50
Q

IgA nephropathy (Berger disease)

A
  • LM - mesangial proliferation
  • EM - mesangial IC deposits
  • IF - IgA based IC deposits in the mesangium
    Seen with HSP.
  • often presents with a URI or acute gastroenteritis (“a few days after a flu-like illness”)
51
Q

alport syndrome

A
  • mutation of type IV collagen – thinning and splitting of the glomerular basement membrane. most commonly x linked
52
Q

calcium oxalate kidney stones

A
  • radioopque and envelope/dumbbell shaped
  • promoted by hypercalciuria
  • can result from ethylene glycol, vit C abuse, crohns
  • treat with thiazides and citrate (prevents precipitation)
53
Q

ammonium magnesium phosphate kidney stones

A
  • radioopaque and coffin lid shaped
  • caused by infection by urease + bugs, because they alkalinize the urine
  • treat infection, remove stones
54
Q

uric acid stones

A
  • radiolucent, rhomboid or rosettes
  • risk factors include decreased urine volume, arid climates and acidic pH
  • can be 2/2 gout or high cell turnover states (leukemia)
  • treat by alkalinizing urine
55
Q

cystine stones

A

radioopaque and hexagonal

  • sodium nitroprusside test +
  • treat by alkalinizing the urine and hydrating
56
Q

renal cell carcinoma

A
  • originates from the proximal tubule cells –> polygonal clear cells filled with accumulated lipids and carbs
  • hematuria, palpable mass, polycythemia, flank pain, fever, weight loss
  • invades renal vein/IVC and spreads hematogenously
  • golden yellow on macroscopic exam
  • resection and immunotherapy, resistant to chemo
57
Q

renal oncocytoma

A
  • benign epithelial cell tumor, well circumscibed with central scar
  • large eosinphilic cells with abundant mitochondria without perinuclear clearing
  • painless hematuria, flank pain, abdominal mass
58
Q

Wilms tumor

A
  • most common renal malignancy in kids (2-4)
  • large palpable flank mass and/or hematuria
  • “loss of function” mutations to tumor suppressor genes WT1 or WT2
  • assoc with VHL or WAGR complex (Wilms tumor, Aniridia, GU malformations, Retardation)
59
Q

Transitional Cell Carcinoma

A
  • painless hematuria with no casts

- associated with problems with your Pee SAC: phenacetin, smoking, aniline dyes, and Cyclophosphamide

60
Q

squamous cell carcinoma of the bladder

A
  • due to chronic iritation of the bladder –> squamous metaplasia and dysplasia
  • schistosomiasis, chronic cystitis, smoking, chronic nephrolithiasis
  • presents with painless hematuria
61
Q

acute infectious cystitis

A
  • causes: E. coli, s. saprophyticus (sexually active women), Klebs, Proteus, adenovirus (hemorrhagic cystitis)
  • sterile pyuria and neg urine cultures seen with gonorrhea and chlamydia
62
Q

acute pyelo

A
  • WBC casts in the urine

- complications include chronic pyelo, renal papillary necrosis, and perinephric abscess

63
Q

chronic pyelo

A

coarse asymmetric corticomedullary scarring, blunted calyx

- tubules contain eosinophilic casts resembling thyroid tissue (thyroidization of the kidney)

64
Q

ATN phases

A
  • inciting event
  • maintenance phase - oliguric, lasts 1-3 weeks with risk of hyperkalemia, met acidosis, volume overload, inc creat and BUN
  • recovery phase - polyuric, BUN and Cr fall, risk of hypoK, hypoMg, hypoPhos, hypoCa
  • can be ischemic (prox tubule/thick ascending limnb) or nephrotoxic (prox tubule)
65
Q

renal papillary necrosis

A
  • sloughing of renal papillae - gross hematuria and proteinuria
  • assoc with DM, acute pyelo, chronic phenacetin use, sickle cell
66
Q

prerenal/renal/postrenal

A

urine osmolarity - > 500, >40, >40
FeNa - 2%, >1-2%
BUN/Cr - >20, 15

67
Q

consequences of renal failure

A

MAD HUNGER

  • Metabolic Acidosis, Dyslipidemia, Hyperkalemia, Uremia, Na/H2O retention, Growth retard/DD in kids, EPO failure, Renal osteodystrophy
  • can’t excrete phos or reabsorp Ca –> low Phos, High Ca, inc PTH, subperiosteal thinning of bones

Step 1 Flash Cards (36 decks)

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