K+ Balance Flashcards
Hyperkalemia
K+ leaving cells
Increased extcacellular K+
Hyperactive muscle reflexes
In heart, Ca2+ and Na+ channels inactivated so can’t generate normal sinus rhythm and ectopic foci take over –> v-fib or standstill; also membrane repolarization mayb be accelerated
Short QT interval, peaked T waves
Hypokalemia
K+ entering cells
Decreased extcacellular K+
Membrane hyperpolarized
In heart, delayed ventricular repolarization leads to v-tach
Prolonged refractory period on EKG
Inuslin and K+ balance
Insulin stimulates K+ uptake into cells by increasing activity of Na/K ATPase
After you eat, insulin takes K+ from food into cells so you don’t get hyperkalemic
In type I diabetes mellitus, have no insulin so can get hyperkalemia!
Acid-base abnormalities of the body and K+ balance
Alkalosis: have not enough H+ in blood, so H/K exchanger in cells puts out H+ and takes in K+ so you get hypokalemia
Acidosis: have too much H+ in blood, so H/K exchanger in cells takes in H+ and puts out K+ so you get hyperkalemia
Note: Respiratory alkalosis/acidosis do not change K+ concentrations because CO2 diffuses freely across cell membranes to maintain electroneutrality; Metabolic acidosis because of excess organic acid (ketoacids, lactic acid) doesn’t change K+ because lactate can just enter with H+
Adrenergic stimulation and K+ balance
Beta2 receptors: increase Na/K ATPase, take K+ into cells, hypokalemia
Alpha receptors: K+ out of cells, hyperkalemia
Hyperosmolarity and K+ balance
Hyperosmolarity causes shift of K+ out of cells
Increased osmolarity in ECF –> water flows out of cells –> intracellular K+ concentration increases –> K+ diffuses out of cells
Exercise and K+ balance
Decreased ATP –> K+ channels open and K+ released
Usually this is fine but if person on beta blockers (which also causes hyperkalemia), or has renal failure and can’t excrete K+, they can get hyperkalemia
Note: remember muscle metaboreceptors increase blood flow to exercising muscle, and K+ is one signal!
All non-renal determinants of K+ balance
Insulin
Acid/Base disturbances
Adrenergic receptors
Osmolarity
Cell lysis (hyperkalemia)
Exercise
In the kidney, where is normal K+ reabsorption and secretion?
Distal tubule and collecting duct
Alpha-intercalated cells reabsorb K+ (H/K ATPase exchanger)
Principal cells secrete K+ (Na/K ATPase in basolateral membrane and K+ channel out into lumen)
High and low K+ diet effects on K+ secretion/reabsorption
High K+ diet: K+ secretion by principal cells
Low K+ diet: decreased K+ secretion by principal cells AND increased K+ reabsorption by alpha intercalated cells
Aldosterone effect on K+ secretion
Aldosterone increases K+ secretion (hypokalemia)
Aldosterone inserts Na/K ATPase into basolateral membrane and Na+ channels into luminal membrane to bring more Na+ into cell –> more Na+ pumped into blood from Na/K ATPase means more K+ removed from blood at same time
Also, aldosterone directly inserts K+ channels onto luminal membrane to let K+ out
To correct problem, aldosterone increases H/K ATPase activity in alpha-intercalated cells to increase reabsorption and try to prevent hypokalemia (and decreased aldosterone decreases H/K ATPase activity)
High K+ plasma concentration directly stimulates aldosterone release, and low K+ plasma concentration inhibits aldosterone release
High Na+ diet (and diuretics) and K+ secretion
High Na+ diet causes increased K+ excretion (hypokalemia)
More Na+ goes into principal cells from lumen –> more Na+ reabsorbed (via Na/K ATPase) into blood (in addition to more excreted too) –> brings more K+ into cell from blood –> more K+ secretion
Note: diuretics cause SAME effect b/c they increase Na+ in filtrate before it gets to principal cells
K+ sparing diuretics
These diuretics act to inhibit aldosterone on principal cells –> no Na+ reabsorption in principal cells of collecting duct –> Na+ does NOT build up to increase K+ secretion in this case!
Used in combination with loop or thiazide diuretics to prevent hypokalemia
Luminal flow rate and K+ secretion
When flow rate through collecting duct is high, K+ secretion increases because:
1) High K+ conductance across to lumen and lower K+ concentration so more K+ carried away by filtrate
2) More water and Na+ in collecting duct reabsorbing more Na+ means secreting more K+ (b/c of Na/K ATPase)
6 factors affecting K+ secretion
1) Dietary intake of K+
2) Plasma [K+] directly
3) Luminal flow rate
4) Aldosterone
5) Luminal membrane potential/electrochemical gradient
6) Diuretics (K-sparing vs. K-wasting)
