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Flashcards in Hypokalemia Deck (28)
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Roughly what percentage of K+ is stored **outside** cells?
**corrected from "inside"... hopefully you recognized that was wrong, though.**

About... 2%


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

Through the GI tract and renally.


Is it possible to get hypokalemia through inadequate intake?

Of course. But it's not common.
It's seen in remarkably bad diets, alcoholism, and anorexia nervosa.


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

Beta-adrenergic agonists (epinephrine, bronchodilators).

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


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

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


Diarrhea of any cause will lower K+.

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


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

Na+ and flow in the distal tubule.


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)

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


3 ways diuretics can cause hypokalemia?

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


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

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


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

High aldosterone with low renin.


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

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


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

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


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

With increased renin.


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

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.


Will Liddle's syndrome respond to spironolactone?

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


How does Liddle's syndrome cause hypokalemia?
(review, again: What cell is involved?)

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


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

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.


What's the mechanism for hypomagnesemia causing hypokalemia?

Mg2+ binds ROMK and slows K+ from exiting into lumen.
If there's less Mg2+, more K+ leaks out.


3 typical "poorly absorbable anions" that can cause hypokalemia?

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


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

High urine K+.


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

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


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

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


Most dangerous complication of hypokalemia?



ECG changes in hypokalemia?

ST depression.
T wave flattening.
U waves


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

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


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



How does hypokalemia cause "nephrogenic diabetes insipidus"?

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.