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USMLE Step 1 > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the divide of fluid compartments?

A

60 (TBW)-40 (ICF)-20 (ECF)-15 (interstitial)-5 (plasma)

% of total body weight

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2
Q

How is GFR estimated?

A 
With inulin (freely filtered, not absorbed, not secreted)
Estimate with creatinine (overestimate, secreted by tubules)
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3
Q

How is ERPF estimated?

A

With PAH (underestimate by 10%, both filtered and actively secreted, nearly all PAH entering kidney leaves first pass by excretion)

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4
Q

What effect do prostaglandins have on nephron?

A

Dilate afferent arteriole (increase RPF, GFR, FF stays constant)

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5
Q

What effect do NSAIDs have on nephron?

A

Inhibit prostaglandin production, prevent afferent arteriole dilation. Can induce acute renal failure.

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6
Q

What effect does angiotensin II have on nephron?

A

Constricts efferent arteriole (decreased RPF, increases GFR, FF increases)

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7
Q

What are some key roles of the PCT?

A

Brush border–carbonic anhydrase-bicarbonate recycling; reabsorbs all glucose/AAs/most ions; generates/secretes ammonia (buffer urine); 65-80% of Na reabsorbed

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8
Q

What are the hormones that act on the PCT? effects? Drugs?

A

PTH–inhibits Na/PO4 contransport–>phosphate excretion; Angiotensin II–stimultes Na/H exchange–>increases Na/H20/HCO3- reabsorption–>contraction alkalosis; Carbonic anhydrase inhibitors (acetazolamide) alkalinize urine.

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9
Q

What are some key roles of the thin descending loop of Henle?

A

Passive reabsorbs water via medullary hypertonicity. It is impermeable to Na+. Concentrating segment–>makes hypertonic urine.

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10
Q

What are some key roles of thick ascending loop of Henle?

A

Actively reabsorbs Na/K/Cl (via NaK2Cl transporter). Ion movement induces paracellular absorption of Mg and Ca (via K+ backleak). Impermeable to water–>dilutes urine as it ascends

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11
Q

What are drugs that act on thick ascending loop?

A

Loop diuretics (furosemide) act on NaK2Cl transporter.

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12
Q

What are some key roles of the early distal convoluted tubule?

A

Actively resorbs Na/Cl, makes urine hypotonic.

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13
Q

What hormones act on early distal convoluted tubule? What drugs?

A

PTH–increases Ca/Na exchange–>increasing Ca2+ reabsorption; Thiazide diuretics inhibit Na/Cl cotransporter

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14
Q

What are some key roles of the collecting tubule?

A

Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone). Principal cell respond to aldosterone and ADH to regulate amount of water re-absorbed. Alpha/Beta intercalated cells secrete acid/bicarbonate respectively.

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15
Q

What hormones act on collecting tubule? Drugs?

A

Aldosterone on principal cells (inserts Na channel on luminal side–>increased Na reabsorption/potassium excretion; ADH acts at V2 receptor–>insertion of aquaporins on luminal side. Amiloride/triamterene inhibit luminal Na channels. Spironolactone/epleronone are aldosterone antagonists.

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16
Q

Where do fanconi syndrome, bartter syndrome, gitelmans and liddle syndrome occur?

A

FABulous Glittering Liquid: Fanconi (PCT) Bartters (thick ascending loop) Gitelman (DCT) Liddle (collecting tubule)

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17
Q

Increased excretion of nearly all amino acids

A

Fanconi syndrome (PCT reabsorption defect) can result in metabolic acidosis (proximal RTA)

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18
Q

Renal tubular defect resulting in hypokalemia, metabolic alkalosis with hypercalciuria

A

Bartter Syndrome (reaborptive defect in thick ascending loop), autosomal recessive, affects NaK2Cl cotransporter/like being on furosemide

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19
Q

Renal tubular defect resulting in hypokalemia, metabolic alkalosis, hypocalciuria

A

Gitelman Syndrome (autosomal recessive, resorptive defect in early DCT in Na/Cl contransporter), like being on thiazide diuretic

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20
Q

Renal tubular defect resulting in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone

A

Liddle Syndrome (autosomal dominant, increased Na re-absorption in collecting duct-mutant epithelial Na channel)

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21
Q

What is Tx for liddle syndrome?

A

Amiloride–K sparing diuretic that inhibits epithelial Na channel in collecting duct.

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22
Q

In PCT, describe Cl vs Na reabsorption. Which is faster?

A

Na re-absorption is faster. Cl concentration slower–relative concentration increases then plateaus.

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23
Q

What is ANP? Where does it come from/What does it do/MoA

A

Released from atria in response to increased volume. “check” against RAAS; relaxes vascular smooth muscle via cGMP, causing increased GFR and decreased renin. Natriuresis with no compensation. Net sodium and volume loss.

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24
Q

What triggers RAAS?

A

Decreased BP (sensed by JG cells which release renin). Decreased Na delivery sensed by macula densa. Increased sympathetic tone (B1 receptors).

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25
Q

What shifts potassium out of cell causing hyperkalemia?

A

DO Insulin LAB: Digitalis, HyperOsmolarity, Insulin deficiency, Lysis cells, Acidosis, Beta-adrenergic antagonist

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26
Q

Nausea, malaise, stupor, coma

A

hyponatremia

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27
Q

irritability, stupor, coma

A

hypernatremia

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28
Q

U waves, flat T waves, arrhythmias, muscle weakness

A

hypokalemia

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29
Q

Wide QRS, peaked T waves, arrhythmias, muscle weakness

A

hyperkalemia

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30
Q

Tetany, seizures, QT prolongation

A

hypocalcemia

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31
Q

Tetany, torsades de pointes

A

hypomagnesmia

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32
Q

Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

A

hypermagnesemia

33
Q

Bone loss, osteomalacia

A

hypophosphatemia

34
Q

Renal stones, metastatic calcifications, hypocalcemia

A

hyperphosphatemia

35
Q

Defect in ability of alpha-intercalated cells to secrete H+

A

Type 1 RTA (distal, urine pH > 5.5); new HCO3 for plasma not generated–>nonAG metabolic acidosis. Hypokalemia. Increased risk for calcium phosphate kidney stones. Caused by amphotericin B toxicity, analgesic nephropathy, urinary tract congenital obstructions

36
Q

Defect in proximal tubule HCO3- reabsorption

A

Type 2 RTA (proximal, urine pH < 5.5); HCO3 excretion is acidified by distal alpha-intercalated cells. Hypokalemia. Increased risk for hypophosphatemic rickets. Caused by Fanconi syndrome (Wilson disease), lead, aminoglycosides, carbonic anhydrase inhibitors, multiple myeloma light chains

37
Q

Hypoaldosteronism, mild acidosis, hyperkalemia

A

Type 4 RTA (hyperkalemic, urine pH < 5.5); caused by hypoaldo/aldosterone resistance/K sparing diuretics. Hyperkalemia inhibits ammoniagenesis in PCT–>decreased buffering capacity and decreased ability to excrete H+ via urine.

38
Q

How can you distinguish between Type 1/2/4 RTA?

A

Type 1/2 are hypokalemia. Type 4 is hyperkalemia. Type 1 has high urine pH > 5.5 (too distal to be acidified) and has severe acidosis.

39
Q

Segmental sclerosis and hyalinosis, negative IF, effacement of foot process

A

Focal segmental glomerulosclerosis–most common cause of nephropathy in blacks and hispanics

40
Q

diffuse capillaryand GBM thickening, granular (IC) complex deposition on IF, spike and dome appearance with sub-epithelial deposits

A

Membranous nephropathy–most common cause in caucasion adults

41
Q

Normal glomeruli, negative IF, effacement of foot processes

A

Minimal change disease–most common in children

42
Q

Congo red stain showing apple-green birefringence under polarized light

A

Amyloidosis (kidney most common organ involved), associated w/ chronic conditions (multiple myeloma, TB, rheumatoid arthritis)

43
Q

subendothelial IC deposits with granular IF; “tram track” appearance due to GBM splitting caused by mesangial ingrowth

A

Mebranoproliferative glomerulonephritis Type 1. Ass with HBV, HCV, idiopathic.

44
Q

intramembranous IC deposits “dense deposits”

A

Membranoproliferative glomerulonephritis Type 2. Associated with C3 nephritic factor (stabilizes C3 convertase to decrease serum C3 levels)

45
Q

Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

A

Diabetic glomerulonephropathy (kimmelstiel wilson lesion). Nonenzymatic glycosylation of GBM increases permeability and thicking. Nonenzymatic glycosylation of efferent arterioles increases GFR–>mesangial expansion.

46
Q

Glomeruli enlarged and hypercellular. “Starry sky” granular appearance “lumpy bumpy” along GBM and mesangium. Subepithelial IC humps.

A

Acute post-streptococcal glomerulonephritis (IgG IgM C3 deposition along GBM/mensagium. Type 3 hypersensitivity.

47
Q

Crescent moon shape

A

RPGN. Crescents consist of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages. Goodpasture, Wegener, MPA.

48
Q

Goodpasture syndrome

A

Type 2 hypersensitivity, antibodies to GBM and alveolar basement membrane, linear IF

49
Q

Wegener (granulomatosis with polyangiitis)

A

PR3-ANCA/c-ANCA

50
Q

Microscopic polyangiitis

A

MPO-ANCA/p-ANCA

51
Q

Wire looping of capillaries, subendothelial and sometimes intramembranous ICs, granular IF appearance

A

Diffuse proliferative glomerulonephritis due to SLE or MPGN. Most common cause of death in SLE (nephrotic + nephritic). IgG, C3 deposition.

52
Q

Mesangial proliferation, mesangial IC deposits, IgA based IC deposits in mesangium

A

IgA nephropathy (Berger disease), seen with Henoch-Schonlein purpura, presents/flares with URI/gastroenteritis

53
Q

Thinning and splitting of glomerular basement membrane

A

Alport Syndrome–mutatation in Type 4 collage, X linked; glomerulonephritis/deafness/eye problems

54
Q

Calcium kidney stones. Precipitate pH/Appearance/Tx

A

calcium phosphate: increased pH/envelope or dumbellshaped/Thiazides and citrate; calcium oxalate/low pH/caused by ethylene glycol, vitamine C abuse, Crohn’s Disease

55
Q

Most common kidney stone presentation?

A

Patient with calcium oxalate stone; hypercalciuria, normocalcemia

56
Q

Ammonium magnesium phosphate kidney stones

A

Struvite. increased pH. Coffin lids. Infection with urease + bugs (Proteus, Staphylococcus, Klebsiella hydrolyze urea to ammonia and alkalinize urine), staghorn caliculi–>UTI nidus; Tx infection and remove stone

57
Q

Uric acid kidney stone

A

Radiolucent, decreased pH, rhomboid/rosettes; strong association with hyperuricemia (gout). Seen in leukemia, increased cell turnover. Tx by alkalinizing urine

58
Q

Cystine kidney stone

A

Decreased pH. Hexagonal. Cystinuria, staghorn caliculi. Sodium nitroprusside test positive. Tx by urine alkalinization and hydration.

59
Q

polygonal clear cells filled with accumulated lipids and carbohydrates

A

Renal cell carcinoma, proximal tubule cells, hematogenous spread to lung/bone, most common renal malignancy, Chromosome 3 deletion (VHL syndrome), paraneoplastic syndromes: EPO/ACTH/PTHrP; silent cancer often presents with mets

60
Q

Well circumscribed mass with a central scar and large eosinophilic cells with abundant mitochondria without perinuclear clearing

A

Renal oncocytoma. Benign epithelial cell tumor

61
Q

Wilms tumor

A

most common renal malignancy of early childhood, LOF mutations of tumor supressors WT1/2 on chromosome 11

62
Q

Wilms tumor, aniridia, genitourinary malformation, mental retardation

A

Beckwith Wiedemann syndrome (WAGR)

63
Q

Papillary growth lined by transitional epithelium with mild nuclear atypia and pleomorphism, painless hematuria

A

Transitional cell carcinoma, most common tumor of urinary tract, ass with Phenacetin/Smoking/Aniline dyes/Cyclophosphamide (Pee SAC)

64
Q

Chronic irritation of bladder, painless hematuria

A

Squamous cell carcinoma of bladder–RFs include schistosoma haematobium (middle east), chronic cystitis, smoking, chronic nephrolithiasis,

65
Q

Causes of cystitis? Most common? Sexually active young women? Ammonia scent? hemorrhagic?

A

E coli is most common. Staph saprophyticus in sexually active young women (e coli still more common). Proteus mirabilis has ammonia scent. Adenovirus has hemorrhagic.

66
Q

Nitrite positive urine

A

Gram-negative (E coli, Klebsiella, proteus) infection

67
Q

Sterile pyuria and negative urine cultures

A

urethritis by N gonorrhea or Chlamydia trachomatis

68
Q

White casts in urine, fever, CVAT, striated parenchymal enhancement on CT

A

acute pyelonephritis

69
Q

Lymphocytic infiltrate, eosinophilic casts within tubules

A

Chronic pyelonephritis caused by recurrent kidney stones, vesicoureteral reflux

70
Q

eosinophilic pyuria, azotemia

A

Drug induced interstitial nephritis (tubulointerstitial nephritis) caused by drugs that act like haptens–>hypersensitivity (Type 3). Typically 1-2 weeks after drug started (diuretics, penicillins, sulfonamides, rifampin) but can occur months later

71
Q

ARF after obstetric catastrophe (abruptio placentae) or septic shock

A

Diffuse cortical necrosis (combo of vasospasm and DIC)

72
Q

In ischemia, which parts of nephron are most susceptible to injury?

A

PCT and thick ascending limb.

73
Q

Causes of renal papillary necrosis

A

diabetes mellitus, acute pyelo, chronic acetaminophen use, sickle cell anemia/trait

74
Q

Consequences of renal failure

A

MAD HUNGER: Metabolic acidosis, Dyslipidemia, Hyperkalemia/Hyperphosphatemia, Uremia, Na/H2O retention, Growth retardation, EPO failure, Renal osteodystrophy

75
Q

ADPKD

A

PKD1 (ch16) PKD2 (ch4), death from CKD or hypertension. Berry aneurysms, mitral valve prolapse, benign hepatic cysts.

76
Q

ARPKD

A

autosomal recessive. Congenital hepatic fibrosis, can cause potter syndrome via in utero renal failure,

77
Q

Simple vs complex cyst

A

complex cyst is septated with solid components that require followup for risk of renal cell carcinoma

78
Q

shrunken kidneys on US, tubulointerstitial fibrosis

A

medullary cystic disease, progressive inability to concentrate urine,

USMLE Step 1 (36 decks)

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