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CPR > Pharmacology: Hyperkalemia, Hypokalemia > Flashcards

Pharmacology: Hyperkalemia, Hypokalemia Flashcards

1
Q

describe the ECG changes with hypokalemia

A
  1. flattened T waves
  2. ST segment depression
  3. prolonged QT interval
  4. U waves
  5. atrial arrhythmias
  6. v tach, v fib
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2
Q

describe the ECG changes with hyperkalemia

A
  1. tall T waves
  2. prolonged PR interval
  3. widened QRS interval
  4. flattened P waves
  5. arrhythmias – bradycardia, v tach, v fib
  6. sinus arrest or nodal rhythm w/ possible asystole
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3
Q

name the K-sparing diuretics

A
  1. triamterene, amiloride (Na channel blockers)

2. spironolactone (aldosterone agonist)

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4
Q

name the K-wasting diuretics

A
  1. thiazides (NaCl cotransporter blockers)
  2. loop diuretics (NaK2Cl cotransporter blockers)
  3. carbonic anhydrase inhibitors (rarely used)
  4. osmotic diuretics (non-reabsorbable solutes)
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5
Q

name the site of action:

carbonic anhydrase inhibitors

A

PCT

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6
Q

name the site of action:

osmotic diuretics

A

PCT, thin descending limb

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7
Q

name the site of action:

loop diuretics

A

TAL

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8
Q

name the site of action:

thiazide diuretics

A

DCT

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9
Q

name the site of action:

Na-channel blockers

A

cortical CD

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10
Q

name the site of action:

vaptans

A

CD

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11
Q

furosemide MOA

A
  • directly inhibits reabsorption of Na and Cl in TAL via blocking NaK2Cl cotransporter (loop diuretic; K-wasting)
  • indirectly inhibits paracellular reabsorption of Ca and Mg by TAL d/t loss of K backleak responsible for lumen + transepithelial potential
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12
Q

furosemide effects

A

increased excretion: Na, H2O, K, Cl, Mg, Ca

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13
Q

furosemide applications

A
  • edema from CHF, hepatic disease, renal disease
  • acute pulmonary edema (decrease preload; rapid dyspnea relief)
  • HTN (alone or combo; will work in pts w/ low GFR*)
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14
Q

furosemide pharmacokinetics

A
  • onset: IV ~5 mins, PO and IM 30 mins
  • duration: 6-8 hrs oral, 2 hrs IV
  • half life: ~0.5-2 hrs, longer if low GFR
  • eliminated unchanged in urine
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15
Q

furosemide toxicities

A
  • hypo: K, Na, Ca, Mg
  • hypochloremic metabolic alkalosis
  • ototoxicity
  • sulfonamide, risk of HSN
  • hyperglycemia; hyperuricemia; hyperlipidemia
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16
Q

sulfonamide similar to furosemide w/ longer t1/2, better oral absorption and evidence of higher effectiveness in HF

A

torsemide

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17
Q

sulfonamide similar to furosemide w/ more predictable oral absorption

A

bumetanide

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18
Q

non-sulfonamide loop diuretic

A

ethacrynic acid

*reserved for those w/ sulfa allergy

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19
Q

hydrochlorothiazide MOA

A

inhibits Na reabsorption in DCT via blockade NaCl cotransporter (K-wasting)

20
Q

HCTZ effects

A

increases urinary excretion of Na and H2O; K, Mg

K-wasting

21
Q

HCTZ applications

A
  • HTN (alone, combo; not effective in pts w/ low GFR*)
  • edema
  • off-label: Ca nephrolithiasis, nephrogenic diabetes insipidus
22
Q

HCTZ pharmacokinetics

A
  • well absorbed via oral
  • peak action 2 hrs, duration 6-12 hrs
  • eliminated unchanged in urine (6-15 hr t1/2)
23
Q

HCTZ toxicities

A
  • hypo: K, Mg, Na, Ca
  • orthostatic HTN
  • sulfonamide
  • hypochloremic metabolic alkalosis
  • hyper: Ca, glycemia, uricemia
24
Q

similar to HCTZ, poor oral absorption

A

chlorothiazide

25
Q

similar to HCTZ, half-life 40-60 hrs

A

chlorthalidone

preferred by some HTN specialists

26
Q

similar to HCTZ, long-acting and a favorite of cardiologists for adjunct diuretic in CHF

A

metolazone

27
Q

is Mg loss greater with loop diuretics or thiazides?

A
  • thiazides

- note: Mg primarily reabsorbed in TAL/distal nephron

28
Q

in pts on thiazide diuretics, what is thought to be the primary mechanism for increased Ca reabsorption in PCT?

A

volume contraction

used to think it was TRPV5?

29
Q

amiloride MOA

A

blocks ENaC channels in CD (NaK exchange; connecting tubule); K-sparing diuretic

30
Q

amiloride effects

A
  • small increase in Na excretion
  • blocks major pathway for K elimination
  • H, Mg and Ca excretion decreased indirectly
31
Q

amiloride applications

A
  • counteracts K loss induced by other diuretics in treatment of HTN, CHF
  • off-label: ascites, pediatric HTN
32
Q

amiloride pharmacokinetics

A
  • oral, onset <2 hrs but small effects
  • t1/2 6-9 hrs, increased w/ low GFR
  • excreted unchanged in urine and feces
  • DDI: enhancing effects of other K-sparing drugs (ACEi, ARB) and exacerbating hypotensive effects
33
Q

amiloride toxicities

A
  • hyper: K (black box warning)
  • hypo: Na
  • hypochloremic metabolic alkalosis, hypovolemia
  • dizziness, fatigue, HA
  • NVD, bloating, constipation
34
Q

similar to amiloride for edema and off-label for HTN, rapidly absorbed, duration of action 6-9 hrs, eliminated as drug metabolites

A

triamterene

35
Q

spironolactone MOA

A
  • competitive antagonist of aldosterone receptors (K-sparing, CD)
  • partial agonist at androgen receptors (creates side effects)
36
Q

spironolactone effects

A

K-sparing, blunts ability of aldosterone to promote NaK exchanged in CDs

(decreased Na entry through luminal Na channels, decreased basolateral NaK-ATPase)

37
Q

spironolactone applications

A
  • counteracts K loss induced by other diuretics in treatment of HTN, CHF, ascites
  • treatment of primary hyperaldosteronism (Conn)
  • off-label: reduce fibrosis post-MI heart failure
  • off-label: hirsutism, treatment of androgenic alopecia in females
38
Q

spironolactone pharmacokinetics

A
  • t1/2 ~20 hrs
  • steroid effects slow on and slow off, single dose lasts 2-3 days
  • DDIs: enhancing effects of K-sparing drugs (ACEi, ARB) and exacerbating hypotensive effects of others
39
Q

spironolactone toxicities

A
  • hyperkalemia
  • amenorrhea, hirsutism, gynecomastia, impotence
  • tumorigen in chronic animal toxicity studies
40
Q

more selective aldosterone antagonist, approved for use post-MI heart failure and alone or in combo for treatment of HTN

A

eplerenone

41
Q

what component allows licorice to potentiate aldosterone effects in the kidney? also dose-dependently increases systolic BP

A

glycyrrhizic acid

42
Q

why must oral K be taken with water?

A

minimize GI irritation/laxative effect

43
Q

name the drugs for treatment of hypokalemia

A
  • KCl
  • KP (hypoK and hypoP)
  • KHCO3; or precursors, potassium citrate and potassium gluconate (acidosis)
44
Q

what is the typical rate for IV K in hypokalemia?

A

10-20 mEq/hr

45
Q

describe the three step treatment of hyperkalemia

A
  1. antagonize cardiac effects – IV Ca
  2. redistribute K into cells –
    - insulin and glucose (reliable)
    - B2-agonist albuterol
    - bicarbonate (not recommended)
  3. facilitate K excretion –
    - K-wasting diuretic
    - mineralocorticoid (if hypoaldosteronism)
    - cation exchange resin
    - dialysis
  4. monitor intake <60 mEq/day; abx can be hidden source

CPR (3 decks)

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