Regulation of K, Ca, PO4, Mg Flashcards
What are two hallmark signs of hyperaldostronism?
Hypokalemia and metabolic alkalosis.
In a patient with hyperaldostronism, osmolarity doesn’t change, why?
With aldosterone, patient would reabsorb both Na and water proportionately, thus not affecting osmolarity.
In a patient with HYPOatdostronism, how does osmolarity change?
Osmolarity decreases. Without ADH, the body is not able to retain Na and so the patient will present with hyponatremia.
What happens to the resting membrane potential of a patient with hypokalemia?
The membrane potential increases and thus takes longer for a AP to occur. Patient would present with muscle weakness.
Normally, ECF concentration of K is 65 mmole. There was a disturbance where K had to move into cells. How will patient’s electrolyte balance, acid-base balance change?
patient will become hypokalmic and is at risk of acidosis.
Patients with acidosis are at risk of _?
hyperkalemia.
What are some factors that can cause K to move out of the cell and into the blood?
- Acidemia
- hyperosmolarity
- Ischemia (cell damage)
- heavy exercise.
- Hypokelemia
- a-adrenergic agonist
What are some factors that can cause K to move into the cell and out of the blood?
- Hyperkalemia
- Alkalemia
- b-adrenergic agonist
- insulin
Diabetics are at risk hyperkalemia, why?
Insulin is a way to move K out of the blood and into the cell. If the patient is insulin deficient or insulin does not work, the patient is not able to move K out of the blood when there’s too much K in the blood.
What percentage of K is reabsorbed in the PCT? TAL?
67% in the PCT
20% in TAL
How does K get reabsorbed in the TAL?
Via Na, K, 2Cl cotransporter
What are five factors that which affect K secretion in the collecting duct?
- EC K concentration
- Na reabsorption: negative luminal voltage attracts K via leak channels
- Luminal fluid flow rate
- EC pH: K and H exchange across cell membranes.
- Aldosterone: stimulates K secretion in collecting duct to maintain electroneutrality when na is reabsorbed.
Normally, excess K is excreted from the body without causing much problem. How is this balance changed in a person who is on a loop diuretic?
Patient will be at risk for developing hypokalemia and thus may require K supplements.
How sodium diet can cause _ 1_ K secretion, and thus may cause 2.
- less
2. Hyperkalemia.
How can you increase Na delivery to late distal tubule and collecting duct?
By using a diuretic.
One way to treat hyperkalemia is to secrete it in the DCT/Collecting duct. How can this be accomplished?
By using a diuretic which increasing downstream delivery of Na to the distal tubules/collecting ducts. This results in increased Na reabsorption and K secretion.
In the collecting duct principal cells can exchange which ions to increase K secretion and where (apical vs basolateral) is this exchanger located?
Na/K exchanger on the apical side.
Principal cells is also able to decrease K secretion by what mechanism?
Increased H causes H/K exchange which lowers IC K concentration and thus decreases K secretion.
How does K secretion change in an acidodic pt vs an alkolatic patient?
In acidodic pt K secretion is decreased (body is trying to secrete H instead)
In an alkalatic pt, K secretion increases.
What effect does increased plasma [K] have on aldosterone secretion?
increases aldosterone secretion
What is the mechanism by which aldosterone stimulates K secretion by the principal cells?
Aldosterone translocates to the nucleus and causes transcription of new Na/K ATPase which are then inserted at the basolateral membrane and increases their activity. It also transcribes new potassium channels and inserts them on the luminal side of the membrane for K to get secreted.
True or false : Aldosterone is more sensitive to K levels than it is to stimulation by Ang II
True.
What is Conn’s disease?
Primary hyperaldosteronism. Tumor on adrenal cortex causing inappropriate amount of aldoserone secretion.
What is the consequence of hyperaldosteronism?
Hypokalemia
