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21 Cards in this Set
- Front
- Back
Describe the normal distribution of potassium in the body
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-96% in intracellular fluid
-2% in extracellular fluid |
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Describe the process of K intake
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-We eat cells and therefore out diet is rich in potassium
-The K is absorbed in the small intestine -Very little comes out in stool -It is dumped directly into the extracellular space -All cells have Na:K ATPase which pumps Na out of the cell in exchange for moving K in -This exchange process is heavily regulated and is affected by a number of factors including metabolism, pH, and hormones |
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Describe K efflux and influx in cells
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-Most cells are muscles so most K is in muscles
-There are many kinds of K channels -These channels and the Na:K ATPase are mediated by many factors -Efflux: Hypokalemia, acidosis, hyperosmolality, alpha-adrenergic agonists, strenuous exercise -Influx: Hyperkalemia, alkalosis, beta-adrenergic agonists, insulin, aldosterone(?) |
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What occurs to an ingested K load?
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Disposal occurs by redistribution and by urinary excretion
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Describe the effect of serum [H+] on K
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-Patients in acidosis have larger increases in serum K and a slower decline.
-Patients in alkalosis have a smaller increase and faster decline in serum K |
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Describe how diabetes affects serum [H+]
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-In untreated diabetes there is increased serum K and a slower decrease
-Once you give insulin, within a few seconds the K in the blood drops due to increased entry into cells |
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Describe how beta receptor agonists/antagonist affect serum [H+]
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-Epinephrin through the beta adrenergic receptors stimulates entry of K into the cells
-This is usually not very important, but if you have an asthmatic that takes lots of beta adrenergic antagonists they can develop hypokalemia. -Many patients on beta blockers develop hyperkalemia |
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Describe where K reabsorption and excretion occur
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-The major organ is regulation of K excretion is the kidney
-K is filtered and most is reabsorbed in the proximal tubule (65%) -Another 25% is absorbed in the thick ascending limb -By the time the urine comes to the collecting duct almost 100% of the K has been absorbed -K is excreted through a secretory process involving the principle cell in the collecting duct and the distal tubule |
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Describe K secretion in the collecting duct
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-Collecting duct can absorb Na and secrete K
-In rare conditions, it can absorb K (chronic K depletion) -Urine has low K conc, cell has K -There is a big gradient and 2 classes of channels in the apical membrane |
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Describe the driving forces in K secretion in the collecting duct
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-The lumen of the tubule is negative with respect to blood, so there is a big electrical driving force
-There is a chemical driving force from concentration differences |
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Describe the relationship between K secretion and tubule flow rate
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-The higher the urine flow rate, the greater the K secretion
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Describe the effect of K in diet on K secretion
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-High K diet results in increased K secretion through increase in aldosterone levels independent of angiotensin II
-Low K diet results in low K secretion -This is why diuretics are one of the major causes of hypokalemia -Low flow occurs in pre-renal azotemia and CHF |
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Describe the regulation of K secretion
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-K channel normally closed and opens occassionally
-Aldosterone regulates K channel -Increases activity of K channel -Increases activity of Na channel -Increases Na:K ATPase -Urine Flow rate -Brings in low K tubular fluid -Acid Base balance -Affects intracellular K -Low intracellular K lowers K excretion (hyperkalemia) -High intracellular K increases K excretion (hypokalemia) -Any condition associated with aldosterone has a tendency to cause increase K excretion provided that urine flow rate is reasonable |
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Describe what to consider in a patient with hypo/hyperkalemia
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1. Redistribution
Acid/Base status, insulin, catecholamines 2. Intake Dietary, IV 3. Renal Excretion Aldosterone, Urinary flow rate, Acid/Base status, Renal Failure (esp interstitial disease), Interstitial Disease 4. Non-Renal Loss GI (diarrhea), Sweat |
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Describe causes of hypokalemia
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-Redistribution
-Alkalosis, glucose/insulin, catecholamines -Increased excretion -Hyperaldosteronism -Primary: Cushing's syndrome -Secondary: CHF, volume depletion, cirrhosis, all from increased renin and angiotensin -Increased urine flow rate -Diuretics -Alkalosis -Drugs -Amphotericin B (for fungal infections) -Extra renal loss -Sweating, Diarrhea, Vomiting |
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Describe the clinical manifestions of hypokalemia
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-Muscle weakness
-Eventually paralysis -Occasionally rhabodomyolysis -This is because membrane potential is dependent on IC/EC K ratio -If EC K is very low and IC K is high, membrane hyperpolarized -Can't stimulate to contract -Cardiac Arrhythmias -Prolongation of QT -U waves -Heart will eventually stop in diastole -Effects on renal function -Inhibition urine concentration because Na:K ATPase requires K and Na reabsorptionin the kidney is dependent on Na:K ATPase -Increases HCO3 reabsorption -Increased NH3 production, enzymes that make ammonia are very sensitive to K |
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Describe what to consider in a hyperkalemic patient
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-Redistribution
-Acidosis, Diabetes, Beta blockers -Increased intake -Oral or IV (with renal failure) -Decreased Excretion (most common cause) -Low aldosterone -Cells that produce renin can atrophy in interstitial renal dease causing low renin and aldosterone -This is often seen in diabetes -Decreased flow rate -Acidosis -Drugs |
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Describe K levels in patients with chronic renal failure
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-Patients with chronic renal failure do not have low flow rate
-They often have polyuria because they cant concentrate and they cant dilute. Everything has to pass through the few nephrons that are still functioning. -Such nephrons excrete a lot of K. |
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Describe K levels in patients with acute renal failure
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-Oliguric acute renal failure is often associated with hyperkalemia
-Non-oliguric renal failure is not. -Diuretics that block Na channels in the collecting duct decrease the membrane potential and can lead to hyperkalemia. -Blockers of aldosterone receptors can produce hyperkalemia. |
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Describe the causes of hyperkalemia
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-Decreased excretion
-Hypoaldosteronism -Primary: Addison's disease -Secondary: Hyporeninemic hypoaldosteronism, ACE inhibitors -Decreased urine flow rate -Acute renal failure with oliguria -Acidosis -Drugs -K sparing diuretics -NSAIDs -Heparin (reduces aldosteron levels) |
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Describe the clinical manifestations of hyperkalemia
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-Cardiac arrhythmia
-T wave becomes very high -Eventually develop ventricular fibrillation -Can induce acidosis by inhibiting NH3 production in the nephron -Acidosis can produce hyperkalemia by increasing efflux of K from the cell. |