V: Potassium Balance Flashcards
Postassium balance has to be kept
CONSTANT
% K+ in ICF
98%
% K+ in ECF
2%
Hyperkalemia values
K+ > 5meq/L
Hypokalemia values
K+ < 3.5meq/L
Consequences of hyperkalemia and hypokalemia
Weakness
Paralytic ileus
Cardiac arrythmia
Internal K+ balance depends on
Hormones
Drugs
Pathological state
External K+ balance is
Urinary K+ excretion = Dietary K+
What 3 hormones released after K+ ingestion
Insulin
Catecholamines
Aldosterone
Insulin effect
Stimulates K+ uptake through increase in Na+/KATPase
Sympathetic nervous system effect
Through B2 receptors, increase in Na+/K+ATPase
Increase in Na+/K+ATPase promote
K+ into the cell which can result in HYPOKALEMIA
On the other hand, a receptors cause
K+ to move out of cell and cause Hyperkalemia
Aldosterone effect
Increases Na+/K+ATPase
Not pathological situations where an alteration in extracellular K+ may occur due to disturbance in internal K+ balance
Exercise as K+ moves out of cells
Acid-base abnormalities, H+/K+ exchange. As H+ leaves the cell, K+ has to accompany it, leading to disturbance in external balance
During alkalemia pH [H+] blood H+ movement K+ movement
pH>7.45
[H+] decreased
H+ moves out of cells
K+ enters cells
During acidemia pH [H+] blood H+ movement K+ movement
pH<7.35
[H+] increased
H+ into cells
K+ leaves cells
K+ movement compared to H+
K+ follows the opposite movement from H+
Shift of K+ during hyperosmolarity
Hyperosmolarity is when there a decrease in H2O
H2O leaves the cell and drags K+ along with it
Cell lysis effect on K+
Releases K+ causing hyperkalemia
Agonist vs antagonist
Agonist is a drug that binds to its receptor to produce a similar response
Antagonist does not allow receptor to follow response
K+ shifts into cell: HYPOKALEMIA
Insulin B-2 Adrenergic agonist A-adrenergic antagonist Alkalosis Hyposmolarity (too much H2O)
K+ shifts out of cell: HYPERKALEMIA
Insulin deficit B-2 Adrenergic antagonist Acidosis Hyperosmolarity (decrease H2O) Cell lysis Exercise
Why are external balance mechanisms flexible
Because K+ varies a lot
K+ handled in nephron through
Filtration
Reabsorption
Secretion
in FILTRATION of K+
It is not bound to plasma so freely filters
In REABSORPTION of K+ in PCT and TAL
PCT absorbs 67% of filtered K+
TAL absorbs 20%
Which part of nephron is responsible for adjustments in K+ when dietary K+ changes
Distal tubules and collecting ducts
In a low K+ diet, which cells involved
K+ is reabsorbed (because there is not many so we want to reabsorb it all) by A-INTERCALATED CELLS
Urinary K+ excretion in a low K+ diet
<1%
On a high K+ diet, which cells are involved
K+ secreted by PRINCIPAL CELLS (K+ passes to renal tube from capillaries)
Urinary K+ excretion at high protein diets
As high as 110%
Reabsorption in proximal convoluted tubule and thick ascending limb is
CONSTANT under most conditions
Excretion in late distal tubule and collecting ducts is
VARIABLE because they perform fine-tuning of K+ excretion to maintain K+ balance
Type A cells function
During HYPOKALEMIA/ACIDOSIS
K+ reabsorption by a-intercalated cells
H+ secretion
Type B cells function
During HYPERKALEMIA/ALKALOSIS
H+ reabsorption
K+ secreted by B-intercalated cells
H+ and K+ secretion/reabsorption
Is the opposite
If H+ is reabsorbed (HYPERKALEMIA/ALKALOSIS) then K+ is secreted
Magnitude of K+ secretion determined by
Size of electrochemical gradient for K+
Aldosterone, acid-base disturbances, dietary K+ all increase
Impact secretion of K+
Dietary K+ process
Increase in intracellular K+ Increase in K+ in intercalated cells HYPERKALEMIA (Type B intercalated cells) K+ increased SECRETION Increased K+ in urine
Aldosterone effect on Na+
Increases Na+ reabsorption by inducing Na+/K+ATPase
Increased K+ secretion
What channels does an increase K+ impact (HYPERKALEMIA)
Na+/K+ATPase
ROMK channels
High Na+ diet impact on K+
Increase in Na+ to principal cells
Increase Na+ extruded from cell through Na+/K+ATPase pumps
Increase K+ into cell
Increase K+ excretion
What are diuretics
Pills that reduce Na+ and H2O
Block Na+ reabsorption
Impact of diuretics in K+
Diuretics block Na+ reabsorption
Increase K+ excretion
What do diuretics block
Aldosterone function (which is to increase Na+/K+ATPase)
Increase flow rate impact on K+ secretion
Increase flow rate increases K+ secretion
More flow = more diluted K+
During acidosis and alkalosis, impact on K+ flow
Acidosis (high H+ in blood) = K+ out of cell
Alkalosis (low H+ in blood) = K+ into cell
During acidosis, which pump is inhibited
Na+/K+ATPase so K+ leaves the cell to maintain neutrality = hypokalemia
During alkalosis, movement of H+ and K+
H+ leaves the cell for buffering
K+ enters to maintain electroneutrality which causes hypokalemia
Main external buffer systems
Bicarbonate and phosphate
In volume depletion, aldosterone stimulates
Na+ retention without K+ secretion
In hyperkalemia there is stimulation of
K+ secretion w/ salt retention
During hypovolemia, mechanism of AngiotensinII
In hypovolemia we want to increase Na+ reabsorption (bc H2O follows it) to increase extracellular volume
Angiotensin II –> Aldosterone
Aldosterone will increase ENaC, so more Na+ rebasorbed
Angiotensin II will promote Na+/Cl- cotransport
Angiotensin II will inhibit ROMK, K+ secretion
During hyperkalemia, aldosterone and angiotensin II effect
We want to decrease K+ in cell, so K+ excretion
Aldosterone will promote ENaC and ROMK, Na+ and K+ secretion
Angiotensin II will block Na+/Cl- cotransport
Where is the Na+/Cl- cotransporter
In early distal convoluted tubules
