Disorders of K Metabolism Flashcards

1
Q

Plasma K+ rises with ________ and falls with _______
(name that blood pH state)
↓↑→

A

acidemia, alkalemia

  • in acidemia, K+ moves from ICF → ECF
  • alkalemia increases K+ secretion
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2
Q

Effects of alkalosis on K+ secretion

A
  1. High pH causes movement of K+ into the all the cells from ECF
  2. enhances electrochemical gradient for K+ secretion
  3. Hypokalemic state

*note that alkalosis lowers H+ state, thus relieving their inhibitory effect on apical K channels→ faster flow of K+ into tubules

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3
Q

Difference between mild and severe acidosis on K+ secretion

A

Acidosis should normally ↓ K+ secretion due to:

  • inhibiting apical K+ channels
  • stimulate K+ movement from the cells into ECF (away from lumen)

Severe acidosis should normally ↑ K+ secretion due to:
- inhibiting Na+ R → inhibiting H2O R → increasing tubular flow → ↑ K+ secretion

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4
Q

Major determinants of urinary K+ excretion

A
  1. Normal distal tubule function
  2. Aldosterone activity
  3. Urinary flow rate
  4. Delivery of non-reabsorbed anions to distal nephron
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5
Q

Aldosterone stimulates the distal part of the nephron, stimulating K+ secretion or reabsorption?

A

aldosterone stimulates the distal nephron secretion of K+
(it upregulates Na reabsorption→ K into the cell → K+ out of the cell)

*absence of aldosterone increases body K and plasma K, which in turn increases aldosterone secretion

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6
Q

Increase in urinary flow rate does what to K+ excretion?

A

it should increase K+ excretion, by creating a favorable electrochemical gradient for tubular secretion

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7
Q

Delivery of non-reabsorbed anions to distal nephron does what to K+ excretion?

A

It should increase.

Anions should “drag” K+ along as an obligate cation.

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8
Q

Compare suddenly giving K+ to individuals who are maintained on a strictly low/moderate K+ intake vs giving low K+ diet with supplemental K+ .on the side

A

Low K+ diet + suddenly given K+ = severe hyperkalemia

Low K+ diet w/ supplemental K+ suddenly given K+ = harmless bc animal has adapted to high K+ loads and secrete K+ faster

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9
Q

why is hyperkalemia a problem in acute renal failure but not usually in chronic renal failure?

A

K+ adaptation, in contrast to Na+ reabsorption is a slow process to turn on/off.
Hyperkalemia is a bigger problem in ARF than CRF unless GFR is extremly depressed.

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10
Q

3 ways to evaluate ↓ Serum K+

A

Is the cause of low Serum K+ due to:

  1. Spurious (fake) causes
  2. Decreased TB K+
  3. Transcellular shift
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11
Q

Spurious(fake) causes of ↓ Serum K+

A

Extreme Leukocytosis WBC >100k

note that massively increased WBC also can lead to pseudohyperkalemia

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12
Q

Decreased TB K+ leading to ↓ Serum K+ are due to which 2 things?

A

Renal 101:

  1. decreased K+ intake
  2. increased K+ loss
    - Renal or extrarenally
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13
Q

Transcellular shifts leading to ↓ Serum K+ (5)

A
  1. alkalosis
  2. insulin excess (acute)
  3. B2 adrenergic agonist excess (acute)
  4. Hypokalemic periodic paralysis
  5. Hypothermia
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14
Q

Treatment of hypokalemia/K+ deficiency

A

Restore plasma and TB K+ to normal:

  • intravenously during emergency (cardiac arrythmia or paralysis)
  • orally
  • diuretics that are K+ sparing (spirinolactone, triamterone, amiloride)

(very limited, scary to treat, bc you have to do these slow)

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15
Q

Consequences of Hypokalemia/K+ deficiency

A
  1. Metabolic
  2. cardiovascular effects
  3. Neuromuscular effects
  4. Renal effects
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16
Q

Metabolic effects of Hypokalemia

A
  1. suppresses insulin release → glucose intolerance (high)
  2. retards growth
  3. intracellular acidosis
  4. increase renal ammonia production → make it worse
17
Q

what do you have to worry about in pts on digitalis?

A

hypokalemia can enhance development of atrial/ventricular arrythmias in pts on digitalis

18
Q

Both hyper and hypokalemia have which neuromuscular effects?

A

muscle weakness

paralysis

19
Q

renal effects of hypokalemia

A

increased thirst

renal concentration defect → polyuria

20
Q

Hyperkalemia progression on EKG

A

if pt has >6.0, do an EKG

peaked T waves → Wide QRS complex w. flattened P waves → sine waves (more severe)

21
Q

EKG of hypokalemia

A

u waves after repolarization of T waves → artia/ventricular arrythmias in pts on digitalis

22
Q

Types of hyperkalemia and their causes

A
  1. pseudohyperkalemia (spurious)
    - hemolysis of drawn blood (tight torniquet)
    - massively incrased WBC
  2. True hyperkalemia
    - transcellular shift from ICF to ECF
    - decreased excretion
    - increased input
23
Q

Causes of transcellular shifts that result in true hyperkalemia (5)

A

reversible shift from ICF to ECF

  • acidosis
  • digitalis intoxication
  • beta adrenergic blocker
  • alpha 2 adrenergic agonist
  • hyperglycemia!/hyperosmolar
24
Q

Causes of decreased excretion that result in true hyperkalemia

A

Acute renal failure
K+ sparing diuretics
hypoaldosteronism (low adrenal steroids)

25
Causes of increased input that result in true hyperkalemia
endogenous ( hemolysis, rhabdo) exogenous (K+ rich foods >300 mEq/d) (note that diabetes/inadequate insulin response can also cause acute hyperkalemia) - acute
26
Treatment of Hyperkalemia with ECG changes present
1. reverse the depolarization - stabilize membrane - calcium infusion 2. move K+ from ECF to ICF: - Sodium Bicarb - Glucose/insulin - beta agonist 3. remove K+ from body - diuretics - hemodialysis
27
insulin deficiency, acidosis, beta blockers may result in hyper or hypokalemia?
hyperkalemia | -
28
Vomiting, diarrhea, and anorexia could result in hyper or hypokalemia?
Hypokalemia (met acidosis) | - extrarenal cause
29
How does K+ affect insulin?
K+ is a stimulus for insulin secretion | - insulin moves K+ from ECF to ICF
30
What 3 hormones regulate internal K+ balance?
1. insulin 2. catecholamines 3. aldosterone
31
How do catecholamines regulate K+
it moves K+ from ECF to ICF (just like insulin does), especially during stress via B2 receptor
32
what plays key roles in regulating external K+ balance (very imp)
1. Kidney (reabsorption + SECRETION (unlike Na, water, ca, where there are just R) 2. Cortical collecting tubule 3. GFR (minor player)
33
Chronic hypokalemia what should you assess? What do you expect to find?
Look at urine K+ | - low (40 Meq/L) - renal
34
low urine K | could be due to what?
Met acidosis - diarrhea (GI losses) Low K+ intake
35
high Urine K (>40 Meq/L) - renal causes of hypokalemia
look at that cortical collecting duct K secretion no acid base disorder: Mg depletion metabolic alkalosis: aldosterone drives K+ and H+ secretion metabolic acidosis: DKA
36
What is the first test you would order in a pt with hyperkalemia?
repeat ECG - if normal: work up first, treat second - if not normal: treat now, work up second
37
Low aldosterone would cause hyper or Hypokalemia?
Hyper: leads to less Na+ R and thus less K+ excretion