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Renal > Disorders of Potassium Balance > Flashcards

Disorders of Potassium Balance Flashcards

1
Q

What is the intracellular concentration of potassium in the body?

A

150 mEq/L

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2
Q

What maintains the large potassium gradient across the cell membrane?

A

Na+-K+-ATPase

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3
Q

What are the cutoffs for hyperkalemia and hypokalemia?

A

[K+] > 5 mEq/L is hyperkalemia

[K+] < 3.5 mEq/L is hypokalemia

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4
Q

What is the major effect of potassium imbalance?

A

hyperkalemia causes the membrane potential to become less negative

hypokalemia causes the membrane potential to become more negative

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5
Q

What is the normal range of potassium in the plasma?

A

3.5-4.9 nM

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6
Q

What hormones promote the uptake of K+ into cells?

A

epinephrine and insulin

increased uptake by stimulating the Na+-K+-ATPase pump

act within a few minutes

insulin is the most important

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7
Q

causes of hypokalemia

A

excess insulin - stimulates Na+/K+ ATPase

beta adrenergic agonists - stimulates Na+/K+ ATPase

acute illness (MI, head injury) - catecholamine stimulation of Na+/K+ ATPase

hypokalemic periodic paralysis - mutations in cation channels

alkalemia - stimulates Na+/K+ ATPase

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8
Q

major pathophysiologic factors influencing the distribution of K+ between the ICF and ECF

A

acid-base balance

plasma osmolality

cell lysis

exercise

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9
Q

How does acid-baes balance affect potassium distribution?

A

metabolic acidosis increases plasma K+

metabolic alkalosis decreases plasma K+

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10
Q

How does plasma osmolality affect potassium distribution?

A

increased osmolality increases K+ release by cells

decreased osmolality ddecreases K+ release by cells

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11
Q

How does exercise affect potassium distribution?

A

K+ is released from skeletal muscle

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12
Q

causes of hyperkalemia

A

beta adrenergic blockade - inhibits Na+/K+ ATPase

digitalis toxicity - inhibits Na+/K+ ATPase

intense exercise - activates K+ ATP channel

acidosis - inhibition of Na+/K+ ATPase and activation of K+ channels

hyperosmolality (hyperglycemia) - water rich in K+ exits the cells because of osmolar effect

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13
Q

What is the distribution of K+ reabsorption in the nephron?

A

67% reabsorbed in the PT

about 20% absorbed by the loop of Henle

reabsorption is a constant fraction of the amount filtered

10% to 50% in the DCT

5% to 30% in the CCD

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14
Q

What is the process of K+ transport in the distal tubule and collecting duct?

A

1) K+ uptake across the basolateral membrane by Na+-K+ ATPase
2) diffusion of K+ from the cell into the tubular fluid, operation of Na+-K+ ATPase pump creates a high tracellular [K+], which provides the chemical driving force for K+ exit across the apical membrane through K+ channels

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15
Q

What are the major factors that control the rate of K+ secretion by the distal renal tubule and the collecting duct?

A

the activity of the Na+-K+ ATPase in the collecting tubule

the driving force for K+ in the apical membrane, influenced by urine flow rate

the ability of K+ to cross the apical membrane via a K+ channel called RMK

the ability of Na+ channels to function, creating a favorable electrical gradient for potassium secretion

aldosterone which increases the activity of the Na+-K+ ATPase pump and opens the sodium channel

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16
Q

major physiologic regulators of K+ secretion

A

plasma [K+}

aldosterone

distal Na+ delivery

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17
Q

Describe the mechanisms in a principle cell for potassium excretion

A

ROMK K+ channels and ENaC Na+ channels on the apical membrane

Na+-K+ ATPase and K+ channels on the basolateral membranes

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18
Q

factors that perturb K+ secretion

A

levels of circulating aldosterone in pathological states such as excess (increased K+ secretion) or deficiency (decreased K+ secretion)

flow of tubular fluid and distal sodium delivery and urine flow

acid-base balance - alkaloses increases K+ secretion an dacidosis decreases K+ secretion

19
Q

amiloride

A

a diuretic that blocks sodium channels in the CCD

has the same effect as decreasing nluminal Na+

indirectly decreases K+ secretion

20
Q

ECG findings of hyperkalemia

A

P wave flattened

PR interval prolonged

QRS complex widens

ventricular fibrillation or aystole leading to cardiac arrest may occur at high levels

21
Q

extrarenal causes of hyperkalemia

A

tissue damage and factors that modify transcellular distribution of potassium and result in a shift of potassium from the intracellular to the extracellular fluid compartment

22
Q

renal causes of hyperkalemia

A

decreased GFR (reduced to less than 10 mL/minute) when the mechanisms fail

aldosterone deficiency - most commonly caused by diabetes and interstitial renal disease, drugs blocking RAAS and NSAIDs can also lead to this, as well as chronic heparin therapy

decreased distal Na delivery or blockade of Na channels in the cortical collecting tubule

distal Na delivery or blockade of Na channels in the cortical collecting tube - best characterized in patients with chronic obstructive nephropathy with damage to collecting duct cells interfering with both H+ and K+ secretion

potassium-sparing diuretics such as amiloride or triamterene also interfere with sodium transport and directly inhibit potassium secretion, spironolactone can cause it as well

23
Q

factors affecting adrenal aldosterone release

A

angiotensin II +++

K+ ++

ACTH +

ANP -

Dopamine -

24
Q

causes of selective aldosterone deficiency (normal cortisol)

A

low plasma renin activity - hyporeninemic hypoaldosteronism

normal plasma renin activity - normoreninemic hypoaldosteronism, cyclosporin A

25
Q

iatrogenic causes of renal hyperkalemia

A

NSAIDs

ACE inhibitors

ARBs

chronic heparin therapy

cyclosporin A

FK506 (tacrolimus)

spironolactone

26
Q

drugs that cause decreased distal Na+ delivery or blockade of Na+ channels in the CCT

A

amiloride

triamterene

trimethoprim

pentamidine

27
Q

acquired diseases that lead to problems with potassium excretion

A

chronic obstructive nephropathy - damage to CCD cells that impair H+ and K+

sickle cell disease

systemic lupus erythematosus

28
Q

What level of hypokalemia are symptoms usually seen at?

A

~2.5 mEq/L

plasma K may only be slightly reduced even with substantial body K+ depletion

29
Q

ECG changes associated with hypokalemia

A

increased AV conduction time

diminished QRS voltage

ST segment depression, widening, flattening

inversion of T waves

appearance of U waves

30
Q

depletional vs. nondepletional hypokalemia

A

depletional - low boy potassium from normal or extra renal losses

nondepletional - normal body potassium from transcellular redistribution

31
Q

What are some sources for extra renal loss of K+?

A

inadequate intake

copious sweat losses

GI tract losses such as vomiting, diarrhea, etc.

32
Q

reasons for renal losses of K+

A

mineralocorticoid excess

glucocorticoid excess

diuretics

Barter’s syndrome

Gitelman’s syndrome

renal tubular acidosis

33
Q

causes for hypokalemia associated with metabolic acidosis

A

diarrhea

renal tubular acidosis type I and II

ureteral diversions to the GI tract

34
Q

causes of hypokalemia associated with metabolic alkalosis

A

vomiting

diuretics

Berter’s syndrome

Gitelman’s syndrome

35
Q

causes of hypokalemia associated with normal or low blood pressure

A

diuretics (thiazide and loop diuretics)

proximal and distal tubular acidosis

Barter’s syndrome

Gitelman’s syndrome

hypomagnesemia

drug-induced (aminoglycosides, cisplatin)

36
Q

causes of hypokalemia associated with hypertension

A

primary and secondary hperaldosteronism

Cushing’s syndrome

pseudohyperaldosteronism

licorice

Liddle’s syndrome

37
Q

primary vs secondary hyperaldosteronism

A

primary - plasma renin low, plasma aldosterone high, secondary to adenoma, hyperplasia, and adrenal carcinoma

secondary - plasma renin and aldosterone high, secondary to renovascular disease

38
Q

Cushing’s syndrome

A

excess cortisol causes hypokalemia

39
Q

mechanism of licorice in hypokalemia

A

11 beta hydroxysteroid dehydrogenase deficiency

40
Q

Liddle’s syndrome

A

defect in Na+ channels in the DCT, where they are open more often

41
Q

features of Barter’s Syndrome

A

hypokalemia, urinary K+ wastage

metabolic alkalosis

normal or low BP

increased plasma renin and aldosterone

increased urinary prostaglandins

hyperplasia of juxtaglomerular apparatus

resistance to exogenous angiotensin II infusion

urinary calcium normal or increased

plasma Mg2+ normal or low

42
Q

features of Gitelman’s

A

milder phenotype compared to Barter’s

hypokalemia, urinary K+ wastage

metabolic alkalosis

normal or low BP

increased plasma renin and aldosterone

increased prostaglandins (?)

hyperplasia of JG apparatus (?)

resistance to exogenous angiotensin II infusion (?)

low serum Mg2+

low urinary Ca2+ excretion

43
Q

What distinguishes hypokalemia caused by vomiting?

A

low chloride

Renal (28 decks)

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