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44 Cards in this Set
- Front
- Back
___ plays a key role in generation of the resting membrane potential, which influences many biologic functions.
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Potassium
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Describe (in order) the EKG abnormalities we see in a hyperkalemic state, starting with a normal EKG and normal potassium concentration.
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1 - Normal EKG
2 - "Take your right hand and 'pinch' the T wave" (a T wave with a peak like a mountain) 3 - "Now take your left hand and smoosh the P wave flat." (flattened P wave) 4 - "Now move them apart" (QRS complex gets wider and wider from this point on as [K+] increases) |
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Surpluses or deficits of K+ predispose to ____ _______.
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cardiac arrhythmias
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Immediate/Short-Term/Quick changes in [K+] takes place via...
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exchange with the intracellular fluid (translocation into cells)
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Factors promoting K+ uptake into cells
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- [K+]p
- insulin*** (usually give some glucose with it) - epinepherine*** - metabolic alkalosis - aldosterone |
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The major way [K+] gets into the cell is via...
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Na+/K+ ATPase
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With INORGANIC metabolic acidosis (HCO3- loss or HCl gain), H+ moves ___ of cells and K+ moves ___ cells.
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H+ moves INTO; K+ moves OUT
Note: There is little shift in organic acidosis |
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In metabolic alkalosis, K+ moves ____ cells, and H+ moves ____ of cells.
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K+ moves INTO; H+ moves OUT
Note: There is little shift in respiratory alkalosis |
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_______ are in charge of long-term potassium balance.
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Kidneys (through increase/decrease of excretion)
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Factors promoting K+ excretion
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- Aldosterone***
- Distal flow of Na and water (providing Na for exchangers) - Plasma potassium concentration |
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Virtually all regulation of K+ occurs in the _____.
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CCD (Cortical collecting duct)
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Events controlling K+ excretion have the greatest impact in the _____.
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CCD (Cortical collecting duct)
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hyper-_____ and hypo-_____ are two major stimuli for aldosterone release.
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Hyperkalemia; Hypovolemia
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Factors contributing to ACUTE hyperkalemia
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- Increased load
- Impaired excretion - Release from cells (metabolic acidosis, cell lysis, rhabdomyolysis, beta blockade, insulin deficiency, exercise) |
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Factors contributing to CHRONIC hyperkalemia
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- Severe renal failure
- Hypoaldosteronism - Decreased distal flow and subsequent Na delivery - Drugs (K-sparing diuretics, NSAIDs, ACE inhibitors, trimethoprim) |
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T or F: A hyperkalemic patient usually has more than one reason for hyperkalemia
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TRUE
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Key questions in assessing the cause of a non-obvious case of hyper-/hypokalemia:
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1*** - Urine [K+] . . . (Normal is 80. If healthy kidney, hypokalemia excretion will be around 20, and hyperkalemia will be around 200)
2 - Is the problem in cortical collecting duct volume or [K+]? 3*** - Is aldosterone acting? (TTKG = ((U/P) for K+) / ((U/P) for Osm) . . . TTKG > 7 means aldo is acting and TTKG < 2 means aldo is NOT acting.) |
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Mechanism of K+ loss during vomiting
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K+ is lost via the URINE due to alkalosis, and increase aldosterone stimulation from hypovolemia.
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Correcting severe hypokalemia may need several hundred mmol of ___ given in the form of _____ unless the patient is acidemic.
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K+; KCl
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Licorice can cause an excess of ________ through the inhibition of _______.
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aldosterone; 11-Beta Hydroxysteroid Dehydrogenase
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Define primary hyperaldosteronism
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problems with the adrenal glands themselves producing too much aldosterone - either from a tumor, or some idiopathic etiology.
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Liddle syndrome
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aldosterone gain of function through a mutation, causing HTN, hypokalemia, and metabolic alkalosis. Treat with amiloride.
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Bartter and Gitelman Syndrome
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- Bartter: mimics loop diuretics, HYPERcalciuria ("Barter with my parents to go on the loop-de-loop roller coaster")
- Gitelman: mimics thiazide diuretics, HYPOcalciuria - Bartter occurs earlier in life ("Bartters in babies"), and Gitelman is more common overall. |
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All diuretics (except apironolactone) act on the ____-side of the nephron.
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LUMINAL-side
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All diuretics (except mannitol) get into the lumen via...
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SECRETION into the proximal tubule.
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Pharm: Mannitol
(MOA, Pharmacokinetics, Toxicity, Indications,Contraindications) |
1) Mechanism of action
-osmotic diuretic, acts as an osmole, pulling fluid into the tubule. 2) Pharmacokinetics -only given intravenously, t1/2 ~1 hr 3) Toxicity -from increased plasma osmolality 4)Indications -decrease CNS pressure 5)Contraindications -CHF, renal failure |
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Pharm: Acetazolamide
(MOA, Pharmacokinetics, Toxicity, Indications,Contraindications) |
1) MOA
- increase urinary bicarb, K+, and water excretion. (Won't work unless there's adequate biarb in the plamsa.) 2) Pharmacokinetics - weak diuretic, t1/2 ~ 13 hrs 3) Toxicity - metabolic acidosis from losing bibarb and hypokalemia 4) Indications - Glaucoma, CNS pressure, altitude sickness, urine alkalinization 5) contraindications - liver failure |
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Pharm: Loop diuretics (MOA)
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Mechanism of action: Inhibition of Na/K/2Cl co-transporters (AKA "furosemide-sensitive transporters")
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Pharm: Loop diuretics (Pharmacokinetics)
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Fast - acts in 20 minutes. Most potent of the diuretics. t1/2 ~ 1-2 hrs.
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Pharm: Loop diuretics (Toxicity)
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- hypokalemia
- volume contraction - Ca and Mg depletion |
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Pharm: Loop diuretics (Indications/Contraindications)
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Indication: HTN, acute diuresis needed, need more potent diuretic, hypercalcemia
Contraindication: susceptible to vomune depletion (i.e. the elderly), susceptible to hypokalemia (digitalis, hepatic cirrhosis) |
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Pharm: Thiazide diuretics (MOA)
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Mechanism of action: inhibits NaCl transport in the cortical thick ascending loop and distal tubule
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Pharm: Thiazide diuretics (Pharmakokinetics)
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well absorbed from gut, acts within 1 hr, lasts 6-48 HOURS
Note: these last longer than loop diuretics, thus, they're more likely to cause hypokalemia |
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Pharm: Thiazide diuretics (toxicity)
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hypokalemia, hyponatremia, hyperuricemia, and hypercalcemia
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Pharm: Metolazone
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same MOA as thiazides; given in addition to loop diuretics sometimes for extra "punch"; often given in more advanced renal insufficiency
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Pharm: K-Sparing Diuretics (MOA)
e.g. Spironolactone and Eplerenone |
MOA: competitive aldosterone antagonist. Inhibits the reabsorption of Na as well as K+/H+ secretion in the late distal tubule and collecting duct.
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Pharm: K-Sparing Diuretics (Pharmakokinetics)
e.g. Spironolactone and Eplerenone |
Takes up to 2 days to start working; spironolactone is the only diuretic to work on the "blood" side of the tubule; relatively weak diuretic
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Pharm: K-Sparing Diuretics (Toxicity)
e.g. Spironolactone and Eplerenone |
- Hyperkalemia
- Gynecomastia, and amenorrhea (spironolactone) |
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Pharm: K-Sparing Diuretics (Indications/Contraindications)
e.g. Spironolactone and Eplerenone |
Indications: Primary hyperaldosteronism, Secondary hyperaldosteronism (cirrhosis), Chronic heart failure (reduces mortality)
Contraindications: hyperkalemia |
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Pharm: amiloride (MOA)
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K+ sparing diuretic (so don't give to a hyperkalemic patient), inhibits the Na+ channels in the late tubule and collecting duct, and since the positively-charge Na isn't reabsorbed, the positively-charge K+ doesn't move out into the lumen to take its place, thus, it's potassium-sparing.
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Why don't diuretics work?
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- failure to treat the underlying/primary disorder
- high Na intake - noncompliance - volume depletion - NSAIDs (reducing renal blood flow) - metabolic acidosis (lowers efficacy of carbonic anhydrase inhibitors) |
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The two main substances the kidney uses to "deal with" (excrete) acids
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Ammonia (binds a H+ to turn into ammonium), Phosphate
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How to use urinary Cl- to treat metabolic alkalosis
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Urinary Cl- is < 10 = chloride RESPONSIVE = non-renal problem . . . give NaCl
Urinary Cl- is > 10 = chloride UNresponsive = kidney's fault . . . stop diuretics, and treat the problem. |
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Most important test to help you determine the cause of non-anion gap metabolic acidosis is:
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Urinary anion gap
= urinary (Na + K) - Cl |