Potassium Balance Flashcards
Where is ROMK (renal outer medullary potassium channel) found? and what’s its function?
K channel that allows the K+ that is reabsorbed to be recycled back across the luminal membrane into the tubule
- K that comes out increases the lumen positivity that causes passive paracellular transport of +ve charges such as K, Ca, Na, and Mg.
Where is K+ secreted?
Occurs in the principle cells of the Cortical DCT and Medullary DCT
- The K secretion is associated with Na reabsorption in the segment
What are the Mechanistic effects of aldosterone on Potassium secretion?
Aldosterone => stimulates the Na/K ATPase pump to move Na out of the cells and K into cells
=> synthesis of new Na and K channel for apical membrane.
- Na passively flows in through new apical channel (due to inc pump activity)
- K then flows out (secretion) to maintain the electroneutrality
Factors that effect K secretion in the principle cells?
- concentration gradient of K across the basolateral membrane – it depends upon serum K concentration
- electrical gradient across the luminal membrane – it depends upon the reabsorption of Na through the Na channels in the luminal membrane. Which in turn depends upon the Na concentration in the tubular lumen (distal delivery of Na)
- K permeability of the luminal membrane - that depends upon the number of open K channel on the luminal membrane. Which is affected by the aldosterone
What is the effect of aldosterone on K+ secretion?
Aldosterone => Potassium secretion
What happens to K+ secretion on a low potassium diet?
Constant low level secretion
- even with inc Na delivery to distal tubule
- happens because low K will remove stimulation of aldosterone secretion.
What happens to K+ secretion on a high potassium diet?
Enhanced secretion
- increases the serum K level which will increase the:
1. K concentration gradient between intracellular and extracellular K level
- Serum aldosterone level (“most potent stimulator” - wiki)
In what conditions would you see decreased potassium secretion?
- Renal failure
- Distal tubule dysfunction
- Decreased distal tubule flow
- Hypoaldosteronism (or if it’s action is blocked
What occurs if potassium secretion id decreased below normal?
K+ remains in plasma
=> hyperkalemia
In what conditions would you see increased potassium secretion?
A. Increased distal Na delivery
- Diuretics - loop and thiazides
- Bartter’s syndrome
- Gitelman’s syndrome
B. Hyperaldosteronism
i. ) Primary
ii. ) Secondary:
1. Vomiting and NasoGastric suction
How is the internal K+ balance maintained?
by regulating the K transport across the cell membrane via:
- Na/K ATPase pump
- passive K+ outflow channels
Factors that affect the internal balance of potassium (I.e. movement across the cell membrane)
- Plasma K concentration
- Insulin
- Epinephrine
- Acid-base disturbance
- Plasma tonicity (osmolarity)
- Cell lysis and proliferation
How does insulin effect the movement of K across the cell membrane?
Insulin moves K+ INSIDE the cells, but it does not directly work on Na/K pump
- Instead, insulin stimulates a NaH exchanger on the cell membrane that moves Na+ in and H+ out
- this intracellular Na than activate the NaKATPase pump and moves K INSIDE the cells.
How does epinephrine effect the movement of K across the cell membrane?
Activate the NaKATPase pump by stimulating beta receptor.
- Any other hormones or drugs that can stimulate beta receptor will stimulate NaKATPase pump.
- Examples:
1. Albuterol (beta receptor agonists and used in bronchial asthma)
2. Deficiency of insulin (as in diabetic patients)
3. Beta Blockers (Na/K-ATPase pump activity will be impaired w/ decrease movement of K from ECF to ICF. But the K channel which is not affected by the hormones will remain open and will continue to move K ICF to ECF which will result in elevated K in ECF)
How does the plasma K+ level affect movement across the cell membrane
Directly affects the K diffusion out of the cells
- If the serum K level is low then gradient will be high and so there will be more K coming out of the cells.
How do changes in Acid-base level affect the internal balance of potassium?
Changes in extracellular pH produce reciprocal shifts in H+ and K+ between extracellular and intracellular fluid compartments.
- Metabolic acid-base disturbances > respiratory disturbances
How do changes in plasma tonicity (osmolarity) affect the internal balance of potassium?
Elevated plasma osmolality or hypertonicity
=> water moving out of cells =>
- Solvent drag (K+ gets dragged w/ water)
- Inc. IC [K+] => inc. [K+] gradient between ECF and ICF => passive diffusion out of cells
How does cell lysis affect the internal balance of potassium? and when does this occur?
Intracellular K+ is released into the extracellular space yielding an increase in extracellular [K+] (hyperkalemia)
- Rhabdomyolysis (breakdown of muscle cells)
- Hemolysis (breakdown of RBCs)
How does cellular proliferation affect the internal balance of potassium?
K+ is rapidly taken up by proliferating cells => fall in extracellular potassium levels
- as seen in malignancy
Causes of hyperkalemia?
- Excessive intake
- Decreased Renal excretion
- Internal Redistribution (release from ICF)
Conditions that cause hyperkalemia via decreased renal excretion?
- Renal Failure (acute and chronic)
- Distal tubule dysfunction
- Hypoaldosteronism (primary or if it’s effect on tubule are blocked)
Conditions that cause hyperkalemia via internal redistribution?
- Insulin deficiency
- Beta-blockers
- Alpha receptor agonists
- Acidosis
- Hyperosmolarity
- Cell lysis
EKG changes with hyperkalemia in progressivly worsening order
- Tall T wave
- widening QRS
- Sine wave
Signs and symptoms of hyperkalemia
- Cardio toxicity manifesting as:
- EKG changes
- Cardiac conduction defects
- Arrhythmias -> bradycardia - Neuromuscular changes
- Ascending weakness, and paralysis
Tx of hyperkalemia?
- Stablization of cardiac muscle
- IV calcium - Lower K+ levels
a. ) Move K+ into cells
- insulin
- bicarbonate
- beta-agonists (albuterol)
b. ) remove K+ from body
- Diuretics
- dialysis
- cation exchange resin (kayexalate)
Causes of hypokalemia? (serum [K+]
- decreased intake
- Internal redistribution
- Increased renal/ GI excretion
Normotensive diseases that cause hypokalemia?
- Metabolic alkalosis (high bicarb)
- Diuretics
- Prolonged Vomiting, Nasogastic suction
- Bartter’s syndrome, Gitelman’s syndrome - Metabolic acidosis (low bicarb)
- Renal Tubular Acidosis (RTA)
- Ureteral diversion (Uretero-ileostomy, uretero-sigmoidostomy)
A dysfunction of which part of the nephron tubule would cause hypokalemia?
The proximal tubule
- primary location from K+ reabsorption
How does vomiting cause hypokalemia?
- Vomiting will cause loss of fluid, H+ and Cl. - Loss of fluid will decrease ECF volume, hypotension and release of hormone Aldosterone.
- Loss of H will result in elevated HCO3 level in blood (metabolic alkalosis)
- less Cl delivered to the distal tubule so Na will be delivered to distal tubule with negatively charged HCO3.
- Inc aldosterone in collecting tubule will cause reabsorption of Na which will increase electro negativity of the lumen resulting increased secretion of K and H.
hypertensive disorders that cause hypokalemia?
- hyperreininemia
- renal artery stenosis
- renin secreting tumor - Hyperaldosteronism (primary aka Conn’s)
- adrenal hyperplasia
- adrenal tumor - Cushing syndrome
- glucocorticoid excess
Basically anything with excess aldosterone
EKG changes in hypokalemia?
- absence of T wave
- prominent U-wave (wave after T- not P)
- ST-depression
Clinical manifestations of hypokalemia?
Most cases are asymptomatic, but:
A. Cardiac muscle:
- specific EKG changes, and arrythmias. (arrythmias with increased heart rate - tachyarrythmias)
B. Chronic hypokalemia
- elevated BP
- associated with ADH resistance and lead to nephrogenic Diabetes Insipidis
Tx of hypokalemia
- K+ replacement
- usually KCl (KPO4 if also have PO4 def.)
- IV K+ should be given slowly to avoid cardiac arrest w/ rapid infusion - Potassium sparing diuretics
What are the two different types of Potassium sparring diuretics? where do they work?
- Aldosterone receptor antagonists - act by preventing the binding of aldosterone
- ENa channel inhibitors - Inhibiting this channel will increase the +ve charges in the lumen, which in turn will prevent K secretion.
- both work in the CD
