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21 Cards in this Set

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Describe the normal distribution of potassium in the body
-96% in intracellular fluid
-2% in extracellular fluid
Describe the process of K intake
-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
Describe K efflux and influx in cells
-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(?)
What occurs to an ingested K load?
Disposal occurs by redistribution and by urinary excretion
Describe the effect of serum [H+] on K
-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
Describe how diabetes affects serum [H+]
-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
Describe how beta receptor agonists/antagonist affect serum [H+]
-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
Describe where K reabsorption and excretion occur
-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
Describe K secretion in the collecting duct
-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
Describe the driving forces in K secretion in the collecting duct
-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
Describe the relationship between K secretion and tubule flow rate
-The higher the urine flow rate, the greater the K secretion
Describe the effect of K in diet on K secretion
-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
Describe the regulation of K secretion
-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
Describe what to consider in a patient with hypo/hyperkalemia
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
Describe causes of hypokalemia
-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
Describe the clinical manifestions of hypokalemia
-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
Describe what to consider in a hyperkalemic patient
-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
Describe K levels in patients with chronic renal failure
-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.
Describe K levels in patients with acute renal failure
-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.
Describe the causes of hyperkalemia
-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)
Describe the clinical manifestations of hyperkalemia
-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.