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Kidney Lect 11
Potassium Homeostasis and Disorders
| Question | Answer |
|---|---|
| What is the normal range for extracellular [K+]? | 3.5-100 meq/L |
| The large K + concentration gradient between the extracellular and intracellular compartments is maintained by the action of the plama membrane ... | Na + ,K + -ATPase, which transports 2 K + into the cell for every 3 Na + out of the cell. |
| Alterations in the transcellular potassium gradient may | o Alter the cell membrane resting potential o Impair neuromuscular excitability, e.g. cardiac pacemaker rhythmicity and cardiac conduction o Impair cell membrane transport processes |
| The regulation of total body potassium content through alterations in potassium intake and excretion | External Balance |
| The regulation of the distribution of potassium between the intracellular fluid (ICF) and extracellular fluid (ECF) compartments | Internal Balance: |
| Where is the majority of the body's potassium found? | In the INTRAcellular volume |
| A normal dietary K + intake is approximately ___ meq K + per day. | 50 - 150 |
| Potassium excretion | Kidneys (90%)--only one strickly regulated; remainder in stool and sweat |
| Describe renal potassium handling | 1) Freely filtered 2) 90% reabsorbed in proximal tube (65%) and loop of henle (thick ascending--25%) 3) Collecting duct both absorbs AND secretes K+ (highly regulated); proximal K+ handling PASSIVE and not regulated |
| The potassium-secretory cell in the collecting duct is the ____ | principal cell |
| What features allow the principal cell to handle K+? | -basolateral Na + ,K + -ATPase -apical (luminal) potassium channel (ROMK channel) -apical (luminal) epithelial sodium channel (ENaC channel) -high-resistance tight junctions between cells |
| How does the Na+K+Atpase pump regulate potassium secretion? | Na+ uptake through the apical sodium channel down the Na + gradient created by the Na + ,K + -ATPase-->electrical gradient across the apical membrane--> favors K+ secretion into the tubule lumen. |
| In the principal cell, These K + and Na + transport processes are stimulated by... | the hormone aldosterone |
| What are the major determinants of potassium secretion in a cell? | o K + concentration membrane gradient o K + permeability across the apical membrane (number of open K + channels) o Lumen-negative potential difference across the apical membrane |
| The potassium-absorbing cell in the collecting duct is the ____. | intercalated cell. |
| what is the intercalated cell responsible for? | K+ reabsorption and H+ secretion |
| What mediates K+ reabsorption? | Potassium reabsorption by the intercalated cell is an active process which is mediated by the apical membrane H + ,K + -ATPase |
| The regulation of renal potassium secretion occurs at the level of the... | distal nephron; Alterations in glomerular filtration rate and proximal tubular function have little direct effect on net potassium handling. |
| Peritubular factors that affect distal tubular potassium handling | (serum K + concentration, serum aldosterone, extracellular pH |
| Luminal factors that affect distal tubular potassium handling | distal tubular flow rate, distal tubular sodium delivery, luminal anion composition |
| How does increased K+ dietary intake affect K+ excretion? | Increases apical membrane Na + and K+ transport and activity of the Na + ,K + -ATPase-->acutely enhances K + secretion in part due to enhanced aldosterone secretion. However, aldosterone– independent mechanisms also underlie this effect. |
| potassium adaptation | Response to changes in dietary potassium (more gradual); potassium secretion will be higher in an individual on a high potassium diet as to compared to an individual on a normal or low potassium diet. |
| What adaptive changes in the kidney result due to increase K intake? | o Increased Na + ,K + -ATPase activity, increased apical membrane Na + and K + transport, morphological changes (increase in the area of the basolateral membrane) in principal cells o Decreased K + reabsorption by intercalated cells |
| During potassium deprivation, adaptive changes are seen in the ___ cell | intercalated |
| How do intercalated cells change to adapt to potassium deprivation? | (an increase in apical cell membrane area with a corresponding increase in apical potassium transporters) |
| How does aldosterone stimulate potassium secretion? | 1) binds to intracell receptor in collecting duct-->AIP production 2) increases NaKATPase activity, increasing K+ entry and creating Na+ gradient 3)increases # of apical membrane Na+ and K+ channels-->lumen negative electrical potential difference |
| How does chronic aldosterone activation affect Na+ excretion? K+ excretion? | Na+ excretion decreases after first couple of days but eventually returns to match sodium intake; K+ excretion in persistently high aldosterone levels remains elevated relative to K intake |
| aldosterone escape | Na+ excretion drops initially due to aldosterone but eventually rises again to match dietary intake (K+ does not have this mechanism) |
| How does acidemia affect [K+] handling? | decreases intracellular [K + ] in collecting duct cells and decreases potassium secretion. |
| How does alkalemia affect [K+] handling? | Conversely, alkalemia increases intracellular [K + ] in collecting duct cells and increases potassium secretion. Thus, renal potassium secretion increases with increasing plasma pH |
| How is [K+] handling affected by pH? | excretion DIRECTLY PROPORTIONAL to pH (low pH, low excretion) |
| How does distal tubular flow rate affect K+ secretion? | Increasing the tubular flow rate in the distal nephron STIMULATES potassium secretion (clears secreted K+), while decreasing the flow rate antagonizes potassium secretion |
| How does increasing distal tubular sodium delivery affect K+ handling? | Increasing distal tubular sodium delivery STIMULATES distal tubular Na + reabsorption resulting in the generation of a lumen-negative potential difference which stimulates K+ secretion. |
| How does distal tubular anion composition affect K excretion? Why? | Substitution of another anion for chloride stimulates potassium secretion; poorly reabsorbable ions add to lumen negative potential difference (Cl- does too, but more easily reabsorbed-->less gradient) |
| What factors are of the greatest importance in K excretion? | Distal tubular flow rate and aldosterone |
| transtubular potassium gradient (TTKG) | ratio of the estimated potassium concentration in the cortical collecting duct (CCD K ) to the plasma potassium concentration (P K ) |
| During potassium depletion: the TTKG should be... | < 2.5 (usually close to 1.0). |
| During potassium loading: the TTKG should be ... | > 10. |
| How do you calculate TTKG? | TTKG = (Uk/Pk)/(Uosm/Posm) |
| What organs regulate the internal balance of K+? | pancreas, liver, and muscle |
| How does the pancreas regulate K? | increased K+-->pancreas releases insulin, which stimulates cellular (liver and muscle) uptake of K (mediated by NaKATPase and is INDEPENDENT of glucose transport)-->reduce K+ levels |
| How do catecholamines affect K+ levels? | stimulate celullar uptake; mediated by Beta2 receptors; K uptake results in increased NaKATPase activity |
| How does aldosterone affect the internal K+ balance? | Aldosterone stimulates potassium uptake by cells. o This effect is much less than its effect on external potassium balance. |
| How do acid base distubances affect the INTERNAL balance of K? | Potassium ions shift in opposite direction of the hydrogen ion flux to maintain electroneutrality |
| How does [HCO3-] affect K+ internal balance? | * Increased [HCO 3-] under isohydric conditions causes potassium to shift into cells. * Decreased [HCO 3- ] under isohydric conditions causes potassium to shift out of cells |
| How would an increase in plasma tonicity affect K+ internal balance? | Increases in plasma tonicity result in fluid shifts from the intracellular to the extracellular compartments. Potassium exits the intracellular compartment via solvent drag |
| How does cell lysis affect K+ levels? | With cell lysis intracellular contents are released into the extracellular space. Since the ICF K + content is almost 2 orders of magnitude higher than ECF K + content, the extracellular [K + ] can rise abruptly. |
| How do proliferating cells affect K + cells? | In states of rapid cellular proliferation, potassium is rapidly taken up into the proliferating cells and extracellular potassium falls. |
| Hyperkalemic and hypokalemic periodic paralysis | disorders of skeletal muscle cell membrane ion channels which lead to flaccid paralysis and transmembrane potassium shifts. |
| The underlying defect in hyperkalemic periodic paralysis is ... | a skeletal muscle voltage-gated sodium channel mutation. |
| The primary defect in hypokalemic periodic paralysis appears to be a ... | skeletal muscle dihydropyridine-type calcium channel mutation. |
| Will excessive potassium intake lead to hyperkalemia? | Not unless there is impaired potassium excretion |
| What factors affecting external balance can lead to hyperkalemia? | Excessive potassium intake, decreased renal excretion (due to renal insufficiency or decreased distal tubular flow), mineralcorticoid deficiency, or distal tubular dysfunction |
| How will acute renal failure affect K+ excretion? | Will impair renal excretion of K (esp if oliguric) |
| In chronic renal failure, how is K+ excretion affected? | significant impairtment does not occur until GFR < 15-20 ml/min; above this level, distal tubule delivery sufficient to maintain K balance (due to adaptation, mainly due to aldosterone) |
| How does decreased distal tubular flow affect K+ excretion? | Decreased tubular flow significantly reduce renal capacity for potassium excretion |
| What (3) etiologies can cause decreased distal tubular flow? | volume depletion, reduced effective arterial blood volume, and medications (NSAIDs inhibit prostaglandins which keep afferent arterial flow; ACE inhibitors block AII in efferent arterioles, lowering GP) |
| What etiologies (5) can cause internal K balance to increase? | Insulin deficiency, beta-adrenergic blockade, hypertonicity, acidemia (metabolic>respiratory), cell lysis |
| Pseudohyperkalemia: definition | describe situations in which significant hyperkalemia is reported by the laboratory despite a normal plasma potassium concentration. |
| What suggests pseudohyperkalemia? | absence of hyperkalemic ECG changes |
| What things can explain pseudohyperkalemia? | incorrect phlebotomy technique (e.g., prolonged tourniquet application or muscle exercise producing local muscle K + release) or from in vitro K + release from cells, leukocytosis (WBC > 100,000/mm 3 )) |
| What ECG changes do you see with increasing serum K+? | peaked T-wave, wide QRS, shortened QT interval, prolonged PR interval, further widening of QRS complex + absent P wave; sine wave morphology (ventricular tachycardia) |
| What cells are most affected by hyperkalemia? | myocytes and neurons; hyperkalimea-->decrease in Na+ permeability-->net reduction in membrane excitability |
| How do you treat hyperkalemia (acute)? | Urgent: 1) place on ECG monitoring 2) give IV Ca++ 3) IV insulin (with glucose--NO bolus) 4) beta adrenergic agonists 5) IV sodium bicarbonate 6) diuretics, IV saline 7) GI resins 8) dyalisis (if needed) |
| How does IV calcium help hyperkalemia? | MEMBRANE STABILIZATION; raises threshold potential-->decreases cardiotoxic effects of hyperkalemia without affecting plasma K concentration |
| How does IV insulin help in hyperkalemia? | increases redistribution into cells |
| How do beta-adrenergic agonists help hyperkalemia? | β-agonists stimulate the cellular uptake of potassium due to increased Na+K+ATPase activity; albuterol works (inhaled) |
| How do you treat chronic hyperkalemia? | 1) treat underlying process 2) restrict K intake 3) stop offending drugs 4) enhance distal tubular sodium delivery and flow (liberal Na+ intake, diuretics), 5) mineralcorticoid replacement (rarely needed) |
| What mineralcorticoid replacement might help patients with hyperkalemia (chronic)? | fludrocortisone |
| What factors affect K+ external balance? | total body K deficiency may be due to inadequate K intake, from increased extrarenal K+ losesses, or increased renal K+ losses |
| What clinical settings contribute to inadequate intake of K+? | alcoholism and malnutrition |
| What etiologies result in increased external potassium loses? | GI losses (diarrhea, laxative abuse, vomiting, nasogastric suction/drainage); cutaneous losses (profuse sweating + burns) |
| How does gastric fluid loss lead to K+ wasting? | *Although potassium is lost directly in the gastric fluid during protracted vomiting or nasogastric drainage, majority of the L losses in this setting results from renal potassium wasting due to metabolic alkalosis and secondary hyperaldosteroni |
| What etiologies are responsible for increased renal potassium losses? | Can be linked to hypertension (due to mineralocorticoid excess); normotensive disorders may be caused by increased distal tubular flow rate, presence of poorly reabsobed anions, primary tubular dysfunction, an secondary hyperaldosteronism |
| What etiologies are associated with hypertensive hypokalemic disorders? | hyperreninemia (renal artery stenosis or renin secreting tumor); primary hyperaldosteronism (Conn's syndrome); Cushing's syndrome (exogenous steroid therapy, cortisol hypersecretion); congenital adrenal hyperplasia |
| What etiologies are associated with normotensive hypokalemic disorders? | diuretic therapy, osmotic diuresis, renal tubular acidosis, prolonged vomiting or nasogastric drainage, ureteral diversion |
| How does prolonged vomiting or nasogastric drainage lead to normotensive hypokalemic disorders? | Prolonged loss of gastric secretions results in a severe metabolic alkalosis. Renal potassium wasting results from increased delivery of bicarbonate (poorly reabsorbable anion) to the distal nephron and secondary hyperaldosteronism. |
| What factors affecting internal balance may contribute to hypokalemia? | insulin excess, catecholamine excess, alkalemia, cell proliferationhyperpolarization |
| Initially, hypokalemia results in membrane ___ due to the decrease in the extracellular:intracellular potassium concentration ratio. | hyperpolarization |
| More severe hypokalemia results in a secondary increase in sodium .... | conductance that results in membrane depolarization. |
| What changes are seen in ECG during hypokalemia? | flat t-wave, prominent U-wave, depressed ST segment |
| What renal manifestations are seen in patients with hypokalemia? | increased renal generation of ammonia and nephrogenic diabetes insipidus |
| Why does renal generation of ammonia increase in hypokalemia? | With hypokalemia intracellular K + shifts to the extracellular fluid compartment and hydrogen ion moves intracellularly to maintain electroneutrality. Increased intracellular H + ion concentration directly stimulates renal ammoniagenesis. |
| How does hypokalemia contribute to nephrogenic diabetes insipidus? | Nephrogenic diabetes insipidus results from a diminished responsiveness of the cortical collecting tubule to ADH. |
| How is hypokalemia treated? | consists of correction of the underlying disorder (if possible) and potassium replacement; K+ sparing diuretics |
| How can potassium be repleted? | oral route preferred; IV (caution), with max rate at 10 meq/hr; K+ requires finite time to enter cells; too rapid infusion may result in transient hyperkalemia (!) |
| What diuretics should you use in patients with hypoklaemia and: primary renal potassium wasting? hyperaldosteronism? | amiloride and triamterene; spironalctone |
Created by:
karkis77
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