Hypokalemia Flashcards

0
Q

What are the 2 most important ways one can lose K+ from the body?

A

Through the GI tract and renally.

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1
Q

Roughly what percentage of K+ is stored outside cells?

corrected from “inside”… hopefully you recognized that was wrong, though.

A

About… 2%

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2
Q

Is it possible to get hypokalemia through inadequate intake?

A

Of course. But it’s not common.

It’s seen in remarkably bad diets, alcoholism, and anorexia nervosa.

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3
Q

Review: 2 types of drugs that promote transcellular shift of K+ into cells?

A

Beta-adrenergic agonists (epinephrine, bronchodilators).
Insulin.

These can be used to treat hyperkalemia, but they also can cause hypokalemia.

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4
Q

3 non-drug causes of transcellular shifts that cause hypokalemia?

A

Alkalosis.
Hypokalemic periodic paralysis. (rare… often precipitated by high carbohydrate load)
Rapid cell growth.

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5
Q

Diarrhea of any cause will lower K+.

A

Okay. (this can be bad, but sometimes also useful)

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6
Q

2 major factors what when increased will cause increased renal K+ loss?

A

Na+ and flow in the distal tubule.

Aldosterone.

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7
Q

If distal Na+/flow and aldosterone are the 2 major factors affecting renal K+ loss, what are 3 more minor factors? (not looking for etiologies here)

A

Presence of poorly absorbable anions (e.g. bicarb).
Acid-base balance (metabolic alkalosis, or RTA).
Hypomagnesemia.

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8
Q

3 ways diuretics can cause hypokalemia?

A
Increased distal Na+ and flow.
Secondary hyperaldosteronism (due to decreased volume).
Diuretic-induced metabolic acidosis.
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9
Q

What should you think if you seen hypokalemia + hypertension? (3 possibilities)

A

Primary hyperaldosteronism.
Apparent mineralocorticoid excess (cortisol not converted to cortisone).
“Increased mineralocorticoid effect” (high renin, GRA, Liddle’s)

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10
Q

What lab values would suggest that high aldosterone is coming from “primary” cause (eg. adrenal adenoma)?

A

High aldosterone with low renin.

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11
Q

If cortisol binds to the mineralocorticoid receptor (MR) quite well, why don’t we all have mineralocorticoid excess symptoms?

A

Cortisol is converted to cortisone, which doesn’t bind MR.

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12
Q

What enzyme converts cortisol to cortisone? What’s a natural inhibitor of this enzyme?

A
11 beta-hydroxysteroid dehydrogenase 2.
Glycyrrhizic acid (in licorice!) inhibits it.
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13
Q

If there’s renal artery stenosis causing ischemia, how will the kidney respond?

A

With increased renin.

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14
Q

What’s going on in glucocorticoid-remediable hyperaldosteronism (GRA)?

A

Unusually genetic translocation causes aldosterone to be produced in the zona fasciculata* in response to ACTH. Glucocorticoids suppress ACTH, and thus suppress the aldosterone production.

*recall that aldosterone is usually made in the zona glomerulosa.

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15
Q

Will Liddle’s syndrome respond to spironolactone?

A

No. In Liddle’s syndrome, ENaC is active without aldosterone, so antagonizing it won’t help.

16
Q

How does Liddle’s syndrome cause hypokalemia?

review, again: What cell is involved?

A

Increased Na+ reabsorption creates an electrochemical gradient that promotes K+ secretion/excretion (via principal cells).

17
Q

2 primary salt-wasting nephropathies? What drugs do they mimic?
What’s the attempted compensation for these?

A

Bartter’s syndrome: defect in NKCC2 (or ROMK, or basolateral Cl- channel), mimicking loop diuretics.
Gitelman’s syndrome: defect in Na/Cl cotransporter, mimicking thiazides.

Both of these lead to RAAS activation, but the compensation is unable to raise volume/BP.

18
Q

What’s the mechanism for hypomagnesemia causing hypokalemia?

A

Mg2+ binds ROMK and slows K+ from exiting into lumen.

If there’s less Mg2+, more K+ leaks out.

19
Q

3 typical “poorly absorbable anions” that can cause hypokalemia?

A

Bicarb (vomiting, metabolic akalosis, Type II RTA).
beta-hydroxybutyrate (from DKA).
Penicillin (and its relatives).

20
Q

What lab value most strongly suggests that a hypokalemia is caused by renal loss?

A

High urine K+.

21
Q

If you suspect a renal loss of K+, what value next helps you narrow the differential?

A

Is the BP high or low?
High: hyperaldosterone (or its mimics), high renin,
Normal BP: RTA, diuretics, nephropathies, vomiting

22
Q

How is (Type II) RTA different from other causes of hypokalemia?

A

RTA will have low serum bicarb.

Vomiting/NG tube and diuretics/nephropathies will have high serum bicarb.

23
Q

Most dangerous complication of hypokalemia?

A

Arrhythmias

24
Q

ECG changes in hypokalemia?

A

ST depression.
T wave flattening.
U waves

25
Q

How do muscles perform when there’s low K+?

A

Poorly. Smooth muscle of the gut doesn’t work well -> ileus, constipation.
Skeletal muscle gets weak.
Rhabdomyolysis can happen.

26
Q

Can hypokalemia cause…. polyuria/polydipsia, metabolic alkalosis, and chronic interstitial nephritis?

A

Yeah..

27
Q

How does hypokalemia cause “nephrogenic diabetes insipidus”?

A

Hypokalemia downregulates aquaporin-2, so ADH isn’t effective -> diabetes insipidus (excress free water loss).
This causes the polyuria. Compensatory increased ADH will (partly) cause excessive thirst.