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Metabolism & Nutrition > K+ balance > Flashcards

K+ balance Flashcards

1
Q

Calcium gluconate (mechanism of action)

A

Antagonize adverse cardiac effects of hyperkalemia. Does not change plasma K+.

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2
Q

Effects of hyperkalemia in the body (i.e. heart, muscles, brain)

A
  1. Heart
    - Arrhythmias (heart slows down - slowed conduction of Na+ for depolarization, ultimately stops! Asystole)
  2. Skeletal muscle
    - Weakness, stiffness
  3. Brain
    - Protected by BBB so minimal effects
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3
Q

Effects of hypokalemia in the body (i.e. heart, muscles, kidney, brain)

A
  1. Heart
    - Speeds up (arrhythmias - ventricular premature beats, ventricular tachycardia & fibrillation)
  2. Skeletal muscle
    - Weakness, muscle breakdown.
  3. Kidney
    - Stimulates kidney to make more bicarbonate
  4. Brain
    - Protected by BBB
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4
Q

Cell membrane transporters relevant to K+ distribution (3)

A
  1. Na+-H+ antiporter - stimulated by insulin
  2. Na+, K+-ATPase stim. by Beta-2 adrenergy. Increase ICF [Na+]
  3. H+ enters cells (complex mech), K+ exits in exchange (and vice versa)
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5
Q

4 main causes of hyper/hypokalemia. Loss/excess of K+ in body

A
  1. Excess/insufficient K+ intake/IV - ~ not a significant factor
  2. Renal f(x): urine flow through CCD; factors affecting K+ secretion in CCD (i.e. aldosterone)
  3. Gut loss of K+: diarrhea, vomiting (bicarbonaturia)
  4. K+ entering/exiting cells
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6
Q

Factors altering distribution of K+ b/w cells & ECF (6) - effect on K+ in/out of cells

A
  1. Na/K+-ATPase - f(x) normally / inhibited by digoxin
  2. Adrenaline - Acts on Beta-2 receptor & stim. Na+/K+ ATPase / Beta-2 receptor blocked by beta-blocker
  3. Insulin acts on Na+/H+ anti porter / insulin is deficient.
  4. Acid-base status - Administer HCO3- to ECF (causes H+ to exit cells & K+ enters in exchange) / Add HCl to ECF (H+ enters cells, Cl- does not, so K+ exits). BUT metabolic acidosis w/ lactic acid. Some H+ enters cells w/ lactate –> K+ does not need to exit (same w/ ketoacidosis, methanol, ethylene glycol)
  5. Cells being built or dying - Cells being built (e.g. treat pernicious anemia w/ Vit B12) / Widespread death of cells (e.g. Leukemia, tumor lysis syndrome)
  6. Hyperglycemia - Osmotic removal of water from cells, K+ follows.
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7
Q

Factors altering distribution of K+ b/w cells & ECF.

A
  1. Na+/K+ ATPase
  2. Adrenaline
  3. Insulin
  4. Acid-base status
  5. Cells being built/dying
  6. Hyperglycemia
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8
Q

Mechanism of action of aldosterone

A

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9
Q

K+ sparing diuretics. Why?

A

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10
Q

Stimuli for aldosterone release

A
  1. Presence of K+

2. AngII

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11
Q

Causes of diminished renal excretion

A
  1. Decreased flow through CCD
    - Severe renal failure
    - Decreased excretion of osmoles (low salt/low protein diet)
  2. Decreased secretion of K+
    - Hypoaldosteronism
    - Antagonists of aldosterone
    - Tubular disease
  3. Tubular integrity
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12
Q

Causes of hypoaldosteronism

A
  1. Loss of signal for aldosterone release
    - Hyporeninemia (NSAIDs - since PGs increase renin)
    - ACE inhibitors / Ang receptor blockers
  2. Adrenal disease (Addison’s disease)
    - Autoimmune
    - Infection (tuberculosis, fungi, HIV)
    - Metastatic cancer
    - Some forms of congenital adrenal hyperplasia
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13
Q

Bicarbonaturia

A
  1. Vomiting out HCl causes addition of new HCO3- to blood. (H2O + CO2 –> H+ + HCO3-).
  2. Kidneys do not reabsorb all filtered HCO3-
  3. Increased flow through CCD as HCO3- drags Na+ and water with it.
  4. Increased K+ secretion in CCD. Luminal HCO3- makes lumen charge more -ve.
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14
Q

Things we can give to treat hyperkalemia - shifting K+ in/out of cells

A
  1. Na+/K+ ATPase pump - Beta 2 adrenergic receptor agonist. Give adrenaline.
  2. Give insulin
  3. Give NaHCO3
  4. Vit B12 to treat pernicious anemia - facilitate formation of RBCs
  5. Give glucose - hyperglycaemia
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15
Q

Things we can give to treat hypokalemia - shifting K+ in/out of cells

A
  1. Na+/K+ ATPase pump - Digoxin - blocks it
  2. No insulin
  5. 6.
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16
Q

Urinary ways to increase/decrease K+ secretion in hyperkalemia/hypokalemia

A 
Increase flow through CCD 
1. Osmotic diuresis (give glucose)
2. Bicarbonaturia (vomiting) 
3. Pharmacologic diuretics (K+ losing diuretics furosemide, hydrochlorothiazide) 
Increase K+ secretion in CCD
1. Bicarbonaturia (vomiting)
2. Hyperaldosteronism
17
Q

Rationale behind osmotic diuretics

A
  1. Extra particles excreted in urine (i.e. glucose, HCO3-) drag more water through CCD –> increased flow through CCD.
  2. Decreased ECF volume depletion –> increased RAS –> increased aldosterone system. Also, luminal HCO3- causes a -ve charge –> increased K+, Na+ to balance out charge.
18
Q

Causes of hyperaldosteronism

A
  1. Primary
    - Tumour of adrenal cortex makes aldosterone in an unregulated way.
  2. Secondary
    - Various causes (e.g. Renal artery stenosis)

Metabolism & Nutrition (5 decks)

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