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USMLE REVIEW > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

What fundamental problem creates Potter Sequence?

A

Oligohydromnios causes by bilateral renal agenesis (failure of ureteric buds to form)

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2
Q

What cells release renin?

A

Juxtaglomerular cells

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3
Q

3 stimuli to induce renin release

A

Decreased BP
Hypoosmolarity (low Na)
Catecholamines = B-adrenergic stimulation

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4
Q

Water distribution in water

A

60% body wt is water
2/3 of that is intracellular

1/3 is extracellular –1/4 of that is intravascular

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5
Q

At what blood glucose are all renal transporters saturated?

A

350 mg/dL

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6
Q

Vitamin deficiency resulting from Hartnup disease?

A

Hartnup = defective tryptophan transporter

Results in Niacin deficiency (B3) = pellegra

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7
Q

3 D’s of pellegra

A

Diarrhea
Dementia
Dermatitis

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8
Q

Which drugs inhibit the Na/Cl/K pump in thick ascending limb?

A

Loop Diuretics

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9
Q

Where are Ca and Mg reabsorbed in the kidney?

A

Thick ascending limb

More Ca+ absorbed in early distal tubule when PTH is present

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10
Q

Where does PTH act in the kidney?

A

Early distal convoluted tubule

Increases reabsorption of Ca+

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11
Q

What cells are located in the collect duct? what do they do?

A

Principle = reabsorb water and Na, secrete K

Alpha-intercalated = secrete H+

Beta-intercalated = secrete HCO3-

*Both intercalated reabsorb K+

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12
Q

What psych drug can block the function of aquaporins?

A

Lithium - can induce nephrogenic diabetes

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13
Q

What class of diuretic directly affects principle cells?

A

K+ sparing diuretics = spironolactone, eplerenone

*aldosterone antagonists

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14
Q

Treatment for acute altitude sickness?

A

Acetazolamide

Low partial pressure O2 at high altitude

So increase ventilation to oxygenate tissues

Blow off more CO2 causing Respiratory alkalosis

Compensate by getting rid of Bicarb… takes several days

Acetazolamide helps decrease bicarb and overcome alkalosis

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15
Q

Treatment for psueduotumor cerebri? (idiopathic intracranial HTN)

A

Acetazolamide

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16
Q

Which diuretics lose Ca+?

A

Loop Diuretics!

*Thiazides retain Ca+

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17
Q

Loop diuretic that is safe to give to a patient with a sulfa allergy?

A

Ethacrynic Acid

**Not a sulfonamide but has same action as furosemide

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18
Q

Common side effects of loop diuretics?

A 
Hypokalemia
Dehydration
Gout
Sulfa allergy
Ototoxicity
Nephrotoxicity
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19
Q

MOA of chlorthalidone

A

Thiazide diuretics

Inhibit NaCl reabsorption in early DCT

LOWERS Ca+ excretion!!

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20
Q

4 drugs used to treat HTN

A

Hydrochlorothiazide
ACE
ARB
Ca+ channel blocker

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21
Q

3 treatments to correct hyperkalemia

A

B-agonist (albuterol)
IV bicarbonate
IV insulin + dextrose

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22
Q

First treatment for severe hyperkalemia to prevent arrhythmias?

A

IV calcium

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23
Q

Correcting to rapidly may result in central pontine myelinolysis

A

Hyponatremia

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24
Q

Electrolyte imbalance causing peaked T waves

A

Hyperkalemia

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25
Q

Electrolyte imbalance causing tetany

A

Hypocalcemia, hypomagnesemia

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26
Q

Electrolyte imbalances causing arrhythmias

A

Hyperkalemia
Hypokalemia
Hypomagnesemia

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27
Q

Electrolyte imbalance causing decreased deep tendon reflexes

A

Hypermagnesemia

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28
Q

Electrolyte imbalance causing flattened T waves, and U waves on ECG

A

Hypokalemia

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29
Q

Treatment for nephrogenic DI

A

Thiazides
Indomethicin
Amiloride

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30
Q

Treatment for Lithium-induced nephrogenic DI

A

Amiloride

Li enters through ENA and blocks fusion of aquaporins with membrane

Amiloride blocks ENA so Li can’t even enter cell! Bang!

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31
Q

Differential for high anion gap acidosis

A

MUDPILES

Methanol
Uremia
DKA
Propylene glycol
Isoniazide/ Iron
Lactic Acidosis
Ethylene glycol
Salycilates

**adding acids

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32
Q

How do you determine an anion gap?

A

[Na+] - [Cl-] - [HCO3-]

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33
Q

Differential for non-anion gap acidosis?

A

HARD ASS

Hyperalimentation
Addison Disease
Renal Tubular Necrosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
34
Q 
EM = Subepithelial humps
LM = Hypercellular glomeruli
A

Post strep glomerulonephritis

35
Q

Decreased C3
High anti-streptolysin O
High anti-DNase B

A

Recent strep infection

36
Q

IgA based immune complex deposits in mesangium

Mesangial proliferation

A

IgA nephropathy = Berger Disease

37
Q

Thinning and splitting of basement membrane

Mutation in type IV collagen

A

Alport Syndrome

38
Q

Causes of rapidly progressive glomerulonephritis…

A

Goodpasture syndrome

Wegeners (Granulomatosis with polyangiitis)

Microscopic polyangiitis

39
Q

Wire loop appearance on LM - pronounced basement membrane

A

Lupus nephritis = diffuse proliferative glomerulonephritis

40
Q

Linear pattern of IgG deposition on IF

A

goodpasture

41
Q

Lumpy-bumpy deposits of IgG, IgM, and C3 in the mesangium

A

Post strep glomerulonephritis

Nephritic

42
Q

Deposits of IgA in the mesangium

A

Berger Disease = IgA nephropathy

Nephritic

43
Q

Anti-GBM antibodies, hematuria, hemoptysis

A

Goodpasture

44
Q

Crescent formation in the glomeruli

A

Rapidly Progressive Glomerulonephritis

Nephritic

45
Q

Defining features of nephrotic syndrome

A

Proteinuria > 3.5 mg/day
Hypoalbuminemia
Peripheral Edema

46
Q

Kimmelstiel-Wilson lesions

A

Diabetic glomerulonephropathy

Nephrotic

47
Q

Most common nephrotic syndrome in children

A

Minimal Change (Nephrotic)

48
Q

Most common nephrotic syndrome in adults?

A

Focal Segmental Glomerulosclerosis

Nephrotic

49
Q

Effacement of epithelial foot processes

A

Minimal Change

Nephrotic

50
Q

Nephrotic syndrome associated with Hep B

A

Membranoproliferative Glomerulonephritis

Both

51
Q

Subendothelial hump and tram track appearance

A

Membranoproliferative Glomerulonephritis

Both

52
Q

Segmental sclerosis and hyalinosis

Nephrotic

A

Focal segmental glomerulosclerosis

Nephrotic

53
Q

Spiking of the GBM due to electron dense subepithelial deposits

A

Membranous Nephropathy

54
Q

How can you distinguish prerenal azotemia from intrinsic renal failure?

A

Prerenal azotemia = increased Na+ retention and BUN reabsorption… thus decreased FeNa, and increased BUN/Creatinine ratio

Intrinsic RF = can’t reabsorb Na+ so FeNa is increased, can’t reabsorb BUN so decreased BUN/Creatinine ratio

55
Q

Muddy Brown/Granular Casts

A

Acute Tubular Necrosis

56
Q

Fever
Eosinophilis
Azotemia
Rash - diffuse maculopapular

A

Acute Interstitial Nephritis (aka Drug induced interstitial nephritis)

*Most common cause is DRUGS

57
Q

Hyaline cast

A

Concentrated urine

Not pathologic

58
Q

Red cell cast

A

Glomerular bleeding (glomerulonephritis, vasculitis)

59
Q

White cell casts

A

Acute pyelonephritis

60
Q

Epithelial cell casts

A

Acute Interstial Nephritis

61
Q

Fatty Cast

A

Nephrotic Syndrome

62
Q

Waxy Cast

A

End stage renal stage = further degeneration of granular casts

63
Q

HTN
Hepatic cysts
Intracranial aneurysms
Mitral Valve Prolapse

A

ADPKD

64
Q

urease-positive bacteria indicated in struvite stones? (Magnesium Phosphate stones)

A

Proteus Mirabils
Klebsiella
(S. sapro)

65
Q

Radio opaque
Enveloped shaped crystals
Most common

A

Calcium oxalate stone

*Tx = Thiazide diuretics (retain Ca+)

66
Q

Coffin lid crystals in urine

A

Struvite Stone
Radiopaque
Staghorn calculi

67
Q

Polycythemia
Anemia
Hypercalcemia

A

Renal Cell Carcinoma
Von Hippo Lindau
Chromosome 3

68
Q

Most common renal malignancy of early childhood

A

Wilms Tumor (nephroblastoma)

69
Q

Painless hematuria

A

Transitional cell carcinoma

70
Q

Risk Factors for transitional cell carcinoma

A

Phenacetin
Smoking
Aniline Dyes
Cyclophosphamide

71
Q

Approximation for GFR

A

Inulin = freely filtered, and not secreted or absorbed

72
Q

Approximation for RPF

A

PAH = is 100% excreted…. freely filtered and secreted

73
Q

Preferentially dilate afferent arteriole

A

Prostaglandins

Increased RPF
Increased GFR
FF is constant

74
Q

Preferentially constrict efferent arteriole?

A

Angiotensin II

Decreased RPF
Increased GFR
Therefore increased FF

75
Q

EPO secretion by kidney

A

Released by interstitial cells in peritubular capillary bed in response to hypoxia

76
Q

What cells hydroxylate vitamin D?

A

PCT

77
Q

How do you determine predicted CO2?

A

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

78
Q

Complication of hydronephrosis?

A

Possible atrophy of renal cortex and medulla

79
Q

Pre-renal azotemia

A

Increased BUN/Creatinine ratio (>20)
Decreased FENa

BUN retained in kidney because trying to increase volume

80
Q

Intrinsic Renal Failure

A

Decreased BUN/Creatinine ration because BUN reabsorption is impaired

Increased FENa

Generally due to acute tubular necrosis (muddy brown casts)

81
Q

When would you see post-renal azotemia?

A

Due to outflow obstruction

Develops only with bilateral obstruction

Stone, BPH, neoplasia, congenital anomalies

82
Q

Consequences of renal failure

A

MAD HUNGER

Metabolic Acidosis
Dyslipidemia
Hyperkalemia
Uremia
Na/H20 retention (HF, pulmonary edema, HTN)
Growth retardation/ developmental 
Erythoropoietin failure (anemia)
Renal osteodystrophy (damage to bone that occurs from renal failure)

USMLE REVIEW (25 decks)

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