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UWorld Medicine Ultra-HY > Renal/Electrolytes > Flashcards

Renal/Electrolytes Flashcards

1
Q

Paraneoplastic syndromes associated with renal cell carcinoma (4)

A
  1. Polycythemia (ectopic EPO)
  2. Hypercalcemia (bone mets, PTH-RP, and/or prostoglandins)
  3. Elevated platelets
  4. Secondary amyloidosis
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2
Q

Mechanism of bleeding risk in uremia?

Treatment?

A

Platelet dysfunction (PT, PTT, and platelet count all normal, but platelet function impaired so bleeding time prolonged)

Treatment: desmopressin (increases release of factor VIII-vWF multimers that activate platelets) and/or HD

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3
Q

Common side effect of IV EPO in ESRD

Rare but serious side effect

A

Common: Worsening hypertension

Rare but serious: Red cell aplasia

(Other common: headache, flu-like syndrome that responds to NSAIDs)

(Less common with subq EPO)

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4
Q

Two complications of nephrotic syndrome

A
  1. Atherosclerosis (hyperlipidemia from elevated liver synthesis of protein and lipids)
  2. Thrombosis (loss of antithrombin III) (Especially in nephrotic syndrome due to membranous glomerulopathy)
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5
Q

Cause of nephrotic syndrome associated with Hepatitis B

A

Membranous glomerulopathy

(Hep B also associated with membranoproliferative glomerulonephritis (MPGN) and polyarteritis nodosum (PAN), but these do not usually cause nephrotic syndrome)

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6
Q

Cause of nephrotic syndrome associated with Hodgkin lymphoma

A

MInimal change disease (also associated with NSAIDs)

Most common cause in kids, but less so in adults

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7
Q

Cause of nephrotic syndrome associated with HIV

A

Focal segmental glomerulosclerosis (also associated with AA-race and obesity)

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8
Q

Specific pathologic finding in diabetic nephropathy

A

Nodular sclerosis, with Kimmelstiel-Wilson nodules

DIffuse glomerulosclerosis is more common in diabetic nephropathy, but is non-specific

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9
Q

Mechanism of injury in membranous glomerulopathy

A

Immune complex deposition (so is membranoproliferative glomerulonephritis)

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10
Q

Mechanism of injury in membranoproliferative glomerulonephritis

A

Immune complex deposition (so is membranous glomerulopathy)

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11
Q

Glomerulonephritis associated with Hepatitis C

A

Memrbanoproliferative glomerulonephritis (MPGN)

Also less commonly associated with Hepatitis B

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12
Q

Renal disease with sterile pyuria and WBC casts

A

Tubuloinsterstitial nephritis

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13
Q

Disease with hemoptysis and nephritis/AKI

A

Goodpasture’s disease (anti-GBM)

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14
Q

Linear IgG deposition in the glomerulus

A

Goodpasture’s disease (anti-GBM)

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15
Q

What is a dangerous extrarenal complication of ADPKD?

A

Intracranial berry aneurysm (however, routine screening is not recommended in ADPKD patients)

(Can also have hepatic cysts, valvular heart disease, colonic diverticula, and hernias)

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16
Q

Hypertension with microhematuria and a palpable flank mass

A

Autosomal dominant polycystic kidney disease (ADPKD)

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17
Q

Cause of sudden generalized edema and hypertension

A

Acute nephritic syndrome (due to sudden decrease in GFR)

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18
Q

Two causes of glomerulonephritis after URI? Time course of each? Association with complement?

A

IgA nephropathy: within 5 days, normal complement (mesangial IgA deposits)

Post-infectious GN: delayed (10-21 days), low C3 (also elevated ASO / DNAse B antibodies)

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19
Q

Serologic association with post-infectious glomerulonpehritis

A

Anti-streptolyisin O (ASO) and anti-DNAse B antibodies

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20
Q

Muddy brown casts

A

Acute tubular necrosis

21
Q

WBC casts

A

Interstitial nephritis and pyelonephritis

22
Q

RBC cases

A

Glomerulonephritis

23
Q

Fatty casts

A

Nephrotic syndrome

24
Q

Broad, waxy casts

A

Chronic renal failure

25
Q

Hyaline casts

A

Nonspecific and not necessarily pathologic (can be seen in prerenal AKI but also just in concentrated urine)

26
Q

Electrolyte abnormality from vomiting

A

Hypochloremic, hypokalemia, metabolic alkalosis

27
Q

Electrolyte abnormality from diarrhea

A

Hyperchloremic metabolic acidosis

28
Q

Lab test to distinguish between saline responsive and saline resistant metabolic alkalosis

A

Urine chloride

Low (<20 mEq/L) in saline-responsive contraction alkalosis

High in saline-resistant metabolic alkalosis (e.g. due to hyperaldosteronism - these patients have volume overload and are excreting NaCl)

29
Q

One possible treatment for saline resistant metabolic alkalosis

A

Acetazolamide (blocks resorption of bicarb)

But causes hypokalemia, so use caution

30
Q

Causes of saline-resistant metabolic alkalosis

A
  1. Primary hyperaldosteronism
  2. Cushing syndrome
  3. Severe hypokalemia (<2 mEq/L)
31
Q

Normal anion gap?

A

Normal AG: 6-12 mEq/L

32
Q

Winter’s formula?

A

Expected PaCO2 = 1.5*bicarb + 8, +/- 2

33
Q

Causes of normal anion gap metabolic acidosis (2)

A
  1. Diarrhea (vast majority of cases)

2. Renal tubular acidosis

34
Q

Renal tubular acidosis associated with autoimmune disease?

Most common autoimmune disease in the association?

A

Type 1 RTA

Most commonly Sjogren’s syndrome (also seen in RA)

35
Q

Hyponatremia with high urine osmolarity and high urine sodium (>40)

A

SIADH

Retain free water due to inappropriate ADH, but excrete Na+ due to increased blood volume

36
Q

Cancer classically associated with SIADH

A

Small cell lung cancer

37
Q

Progression of EKG changes with hyperkalemia

A
  1. Peaked T waves, short QT
  2. Long PR, wide QRS
  3. Loss of P wave
  4. Conduction blocks, ectopic pacing, sine-wave patterns
38
Q

Electrolytes in hypomagnesemia

A
  1. Refractory hypokalemia (inhibits K+ resorption in kidney)

2. Hypocalcemia (reduces PTH)

39
Q

Electrolyte abnormalities in tumor lysis syndrome

A
  1. Hyperuricemia (from metabolized nucleic acids)
  2. Hyperkalemia
  3. Hyperphosphatemia
  4. Hypocalcemia (precipitates with phosphate)
40
Q

Pretreatment that can help prevent AKI in tumor lysis syndrome

A

IV fluids and allopurinol or rasburicase (to prevent hyperuricemia)

(Allopurinol: blocks xanthine oxidase and therefore uric acid production)
(Rasburicase: recombinant uric oxidase, breaks down uric acid)

41
Q

Infiltration that leads to hypoparathyroidism

A

Cancer, Wilson’s, hemochromatosis

42
Q

Effect of thiazides on calcium? Loop diuretics?

A

Thiazides: increase calcium reabsorption and therefore can lead to hypercalcemia.

Loop diuretics: increase calcium excretion and therefore can lead to hypocalcemia

43
Q

How do thiazides affect diabetes?

A

Worsen glucose intolerance by impairing insulin release and worsening glucose utilization

44
Q

AE of furosemide not linked to kidney effects

A

Ototoxicity (hearing loss, tinnitus)

45
Q

Three common types of nephrotoxic drugs that should be discontinued in AKI

A

NSAIDs, ACEIs, and aminoglycosides

46
Q

Most common drug-induced chronic renal failure?

Pathologic effects?

A

Analgesic nephropathy (usually combined analgesics, e.g. aspirin + naproxen)

Leads to papillary necrosis and chronic tubulointerstitial nephritis

47
Q

What presents with rash, arthralgias, hematuria, and WBC casts?

A

Interstitial nephritis

Make sure you don’t confuse with reactive arthritis, but the “can’t pee” there is urethritis/cervicitis, not renal

48
Q

Who is at risk for contrast-induced nephropathy?

What can be done to reduce this risk?

A

At-risk: Diabetics and baseline kidney disease

Prevention: hydration and acetylcysteine

UWorld Medicine Ultra-HY (13 decks)

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