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UWorld Medicine HY > Renal/Electrolytes > Flashcards

Renal/Electrolytes Flashcards

1
Q

Sign of uremic encephalopathy on exam?

Treatment?

A

Sign: asterexis (flapping hand tremor)

Treatment: Emergent HD

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2
Q

Classic triad of renal cell carcinoma

A
  1. Flank pain
  2. Hematuria (invasion of colelcting system)
  3. Palpable abdominal mass

(Rarely seen, indicates late stage disease)

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3
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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4
Q

Most common cause of death in dialysis patients

A

Cardiovascular disease (tend to have other risk factors, and ESRD is an independent risk factor)

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5
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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6
Q

When is EPO given in ESRD

A

If hemoglobin <10 after iron supplementation

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7
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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8
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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9
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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10
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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11
Q

Cause of nephrotic syndrome associated with HIV

A

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

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12
Q

What is the earliest sign of diabetic nephropathy?

A

Glomerular hyperfiltration

Leads to damage via to intraglomerular hypertension, ACEIs protect against this

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13
Q

Medications protective against diabetic nephropathy

A

ACEIs (reduce intraglomerular hypertension)

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14
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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15
Q

Early pathologic finding in hypertensive kidney disease? Later finding?

A

Early: benign nephrosclerosis (hypertropy and intimal medial fibrosis)

Late: glomerulosclerosis (loss of capillary surface area with glomerular and peritubular fibrosis)

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16
Q

Mechanism of injury in membranous glomerulopathy

A

Immune complex deposition

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17
Q

Mechanism of injury in mebranoproliferative glomerulonephritis

A

Immune complex deposition

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18
Q

Glomerulonephritis associated with Hepatitis C

A

Memrbanoproliferative glomerulonephritis (MPGN)

Also less commonly associated with Hepatitis B

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19
Q

Renal disease with sterile pyuria and WBC casts

A

Tubuloinsterstitial nephritis

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20
Q

Disease with hemoptysis and nephritis/AKI

A

Goodpasture’s disease (anti-GBM)

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21
Q

Linear IgG deposition in the glomerulus

A

Goodpasture’s disease (anti-GBM)

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22
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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23
Q

Hypertension with microhematuria and a palpable flank mass

A

Autosomal dominant polycystic kidney disease (ADPKD)

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24
Q

Cause of sudden generalized edema and hypertension

A

Acute nephritic syndrome (due to sudden decrease in GFR)

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25
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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26
Q

Serologic association with post-infectious glomerulonpehritis

A

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

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27
Q

First test in postoperative oliguria

A

Bladder scan (in cast of postoperative urinary retention, due to ineffective detrusor muscle)

(Straight cath is an alternative that is diagnostic and therapeutic)

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28
Q

Muddy brown casts

A

Acute tubular necrosis

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29
Q

WBC casts

A

Interstitial nephritis and pyelonephritis

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30
Q

RBC cases

A

Glomerulonephritis

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31
Q

Fatty casts

A

Nephrotic syndrome

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32
Q

Broad, waxy casts

A

Chronic renal failure

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33
Q

Hyaline casts

A

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

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34
Q

Electrolyte abnormality from vomiting

A

Hypochloremic, hypokalemia, metabolic alkalosis

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35
Q

Electrolyte abnormality from diarrhea

A

Hyperchloremic metabolic acidosis

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36
Q

Phases of metabolic alkalosis

A

Generation (excess bicarb production) and Maintenance (prevention of renal bicarb excretion)

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37
Q

What is a common reason for the maintenance of metabolic alkalosis?

A

Hypovolemia

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38
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)

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39
Q

One possible treatment for saline resistant metabolic alkalosis

A

Acetazolamide (blocks resorption of bicarb)

But causes hypokalemia, so use caution

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40
Q

Causes of saline-resistant metabolic alkalosis

A
  1. Primary hyperaldosteronism
  2. Cushing syndrome
  3. Severe hypokalemia (<2 mEq/L)
41
Q

Normal anion gap?

A

Normal AG: 6-12 mEq/L

42
Q

Winter’s formula?

A

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

43
Q

Causes of normal anion gap metabolic acidosis (2)

A
  1. Diarrhea (vast majority of cases)

2. Renal tubular acidosis

44
Q

Electrolyte abnormality in severe diarrhea

A

Hypokalemia with normal anion gap metabolic acidosis

45
Q

Types of renal tubular acidosis?
Urine pH in each
K+ level in each?

A

Type 1: Distal failure to excrete
Type 2: Proximal failure to resorb bicarb rare)
Type 4: Aldosterone resistance

Urine pH: Alkalotic with type 1 (unable to acidify) normally acidic in type 2 and 4

K+: Hypokalemia in type 1 and 2, hyperkalemia in type 4

46
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)

47
Q

Complications of methanol poisoning? Ethylene glycole poisoning?

A

Methanol: vision changes

Ethylene glycol: hypocalcemia and AKI (metabolized to oxalate, precipitates with calcium including in kidney)

48
Q

Metabolic acidosis with osmolar gap

A

Due to alcohols: ethanol, methanol, ethylene glycol

49
Q

Acid-base in salicylate toxicity

A
  1. Respiratory alkalosis early (stimulation of respiratory centers)
  2. Anion gap metabolic acidosis later
50
Q

Acid-base disorder with tinnitus

A

Salicylate poisoning

51
Q

Fluid replacement in hypernatremia

A

Unstable: volume replacement with normal saline
Stable: slow replacement with D5 1/2NS

52
Q

Most common causes of hypernatremia (2)

A
  1. Loss of hypotonic fluids

2. Decreased free water intake

53
Q

Hyponatremia without low osmolarity (2)

A
  1. Hyperglycemia

2. Advanced renal failure

54
Q

Hyponatremia with low urine osmolarity

A

Primary polydipsia

55
Q

Hyponatremia with low urine sodium (<25)

A

Resulting from intravascular hypervolemia leading to ADH secretion

56
Q

Hyponatremia with high urine sodium (>25)

A

SIADH, adrenal insufficiency, hypothyroidism

57
Q

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

A

SIADH

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

58
Q

Treatment of mild SIADH

Treatment of severely symptomatic SIADH

A

Mild: Water restriction, +/- salt tablets
Severe: Hyperstonic saline

59
Q

Interpretation of vasopressin suppression test in high urine output

A

Primary polydipsia: urine concentrated with free water restriction
Central DI: urine concentrates with vasopressin
Nephrogenic DI: urine remains dilute with vasopressin

60
Q

Treatment of nephrogenic DI

A
  1. Check for hypercalcemia, and correct if found
  2. If due to lithium, discontinue (but may not reverse fully)
  3. Otherwise, hydrochlorothiazide
61
Q

Cancer classically associated with SIADH

A

Small cell lung cancer

62
Q

Electrolyte abnormalities in primary adrenal failure

A

Hyperkalemia, hyponatremia, non-anion gap metabolic acidosis

63
Q

When does hyperkalemia require emergent treatment?

A
  1. Serum K+ >7
  2. Rapidly rising K+
  3. EKG changes
64
Q

Rapid treatment of severe hyperkalemia

A
  1. Calcium gluconate
  2. IV insulin + glucose
  3. Beta agonists (e.g. inhaled albuterol)
  4. Sodium bicarbonate
65
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
66
Q

Medications that can lead to hyperkalemia

A
  1. NSAIDs
  2. ACEIs/ARBs
  3. Beta blockers
  4. Digoxin
  5. K+-sparing diuretics
67
Q

Electrolytes in hypomagnesemia

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

2. Hypocalcemia (reduces PTH)

68
Q

Electrolyte abnormalities in tumor lysis syndrome

A
  1. Hyperuricemia (from metabolized nucleic acids)
  2. Hyperkalemia
  3. Hyperphosphatemia
  4. Hypocalcemia (precipitates with phosphate)
69
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)

70
Q

Total calcium correction with hypoalbuminemia

A

Corrected Ca = Measured Ca + 0.8*(4-albumin)

71
Q

Relationship between acid-base and free calcium

A

H+ and Ca2+ essentially compete for binding to albumin, so acidosis increases free Ca2+, and alkalosis decreases free Ca2+

72
Q

Infiltration that leads to hypoparathyroidism

A

Cancer, Wilson’s hemochromatosis

73
Q

Causes of hypocalcemia

A
  1. Hypoparathyroidism
  2. Metabolic causes: vitamin D deficiency, CKD
  3. Precipitation: pancreatitis, hyperphosphatemia, osteoblastic metastasis
74
Q

Symptoms of severe hypercalcemia

A
  1. Stones: kidney and gall stones
  2. Bones: bone pain
  3. Groans: abdominal pain, N/V, constipation
  4. Thrones: polyuria and dehydration
  5. Psychiatric overtones: depression, anxiety, cognitive dysfunction, insomnia, coma
75
Q

Short-term treatment of severe hypercalcemia?

Long-term hypercalcemia treatment?

A

Short-term: Calcitonin + NS

Long-term: Bisphosphonates

76
Q

Paraneoplastic syndrome associated with squamous cell cancer of the lung

A

Hypercalcemia due to PTHrp

SCa++mous

77
Q

Treatment of milk alkali syndrome

A

Isotonic saline and furosemide (causes Ca2+ excretion)

78
Q

Electrolyte abnormalities in milk alkali syndrome

A
  1. Hypercalcemia
  2. Metabolic alkalosis (alkali intake + renal dysfunction)
  3. Hypophosphatemia
  4. Hypomagnesemia
79
Q

Causes of hypercalcemia with elevated/normal PTH

A
  1. Primary hyperparathyroidism

2. Familial hypocalciuric hypercalcemia (genetic mutation in calcium sensor that inhibits PTH release)

80
Q

Complication of overly rapid correction of hyponatremia?

Overly rapid correction of hypernatremia?

A

Hyponatremia correction: Osmotic demyelination syndrome

Hypernatremia correction: cerebral edema

81
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

82
Q

How do thiazides affect diabetes?

A

Worsen glucose intolerance by impairing insulin release and worsening glucose utilization

83
Q

AE of furosemide not linked to kidney effects

A

Ototoxicity (hearing loss, tinnitus)

84
Q

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

A

NSAIDs, ACEIs, and aminoglycosides

85
Q

Effect of NSAIDs on renal arterioles?

ACEIs?

A

NSAIDs: constrict the afferent arteriole (preventing prostoglandins from dilating it)

ACEIs: dilates efferent arterioles more than afferent (angiotensin constricts efferent more than afferent)

(Both reduce GFR and can worsen pre-renal azotemia)

86
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

87
Q

Most common cause of interstitial nephritis

A

Drug-induced (70% of cases)

88
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

89
Q

Common triggers of drug-induced interstitial nephritis (7)

A
  1. Penicillins
  2. Cephalosporins
  3. Sulfonamides (e.g. TMP-SMX)
  4. Rifampin
  5. NSAIDs
  6. Phenytoin
  7. Allopurinol
90
Q

How can renal toxicity from acyclovir be prevented?

A

Aggressive hydration (toxicity is from acyclovir crystals forming in the urine)

91
Q

What electrolyte disturbance can result from TMP-SMX?

A

Hyperkalemia:

(Trimethroprim can block ENaC and lead to hyperkalemia, as you lose sodium and water but not potassium, mimics the K-sparing diuretic amiloride)

92
Q

What electrolyte disturbance can result from albuterol?

A

Hypokalemia (drives K+ into cells - goes for any beta agonist)

93
Q

One contraindication for metformin

A

Renal failure (creatinine >1.5 in men, >1.4 in women) due to risk of lactic acidosis

(FDA relaxed this CI but it is still a relative CI)

94
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 acetylcystein

95
Q

Common cause of drug-induced DI

A

Lithium

96
Q

Most common glomerulonephritis in adults

A

IgA nephropathy (can present within 5 days of URI or pharyngeal illness)

97
Q

First step in work-up of confirmed true hypercalcemia?

A

PTH level

98
Q

Primary causes of PTH-independent hypercalcemia

A
  1. PTHrp (humoral hypercalcemia of malignancy)
  2. Osteolytic malignancy (e.g. multiple myeloma, breast cancer)
  3. Hypervitaminosis D (e.g. granulomatous disease, lymphoma, supplementation)

UWorld Medicine HY (7 decks)

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