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
Q

Causes of increased input that result in true hyperkalemia

A

endogenous ( hemolysis, rhabdo)
exogenous (K+ rich foods >300 mEq/d)
(note that diabetes/inadequate insulin response can also cause acute hyperkalemia) - acute

26
Q

Treatment of Hyperkalemia with ECG changes present

A
  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
Q

insulin deficiency, acidosis, beta blockers may result in hyper or hypokalemia?

A

hyperkalemia

-

28
Q

Vomiting, diarrhea, and anorexia could result in hyper or hypokalemia?

A

Hypokalemia (met acidosis)

- extrarenal cause

29
Q

How does K+ affect insulin?

A

K+ is a stimulus for insulin secretion

- insulin moves K+ from ECF to ICF

30
Q

What 3 hormones regulate internal K+ balance?

A
  1. insulin
  2. catecholamines
  3. aldosterone
31
Q

How do catecholamines regulate K+

A

it moves K+ from ECF to ICF (just like insulin does), especially during stress via B2 receptor

32
Q

what plays key roles in regulating external K+ balance (very imp)

A
  1. Kidney (reabsorption + SECRETION (unlike Na, water, ca, where there are just R)
  2. Cortical collecting tubule
  3. GFR (minor player)
33
Q

Chronic hypokalemia what should you assess? What do you expect to find?

A

Look at urine K+

- low (40 Meq/L) - renal

34
Q

low urine K

could be due to what?

A

Met acidosis
- diarrhea (GI losses)
Low K+ intake

35
Q

high Urine K (>40 Meq/L) - renal causes of hypokalemia

A

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
Q

What is the first test you would order in a pt with hyperkalemia?

A

repeat ECG

  • if normal: work up first, treat second
  • if not normal: treat now, work up second
37
Q

Low aldosterone would cause hyper or Hypokalemia?

A

Hyper: leads to less Na+ R and thus less K+ excretion