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33 Cards in this Set
- Front
- Back
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What does digoxin do overall? |
Plays a role in modulating force and it is the main inhibitor of the Na+/K+ pump. |
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Where is is digoxin specific to? |
It's generally more specific to the heart, but it does work in other parts of the body to some small extent. |
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What happens to Na+ by using digoxin? |
Na+ concentration goes up in the cell. This effects the transporters that try to keep Ca++ in balance. During depolarization even more Na+ floods into the high concentrations of Na+ in the cell. Having high lvls can actually reverse the Na+/Ca++ exchanger so Na+ can move down its concentration gradient. |
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What are the different types of Ca++ transporters that help to removed Ca++? |
PMCA(high affinity, low capacity) -removes 5% (1/4 of the Ca++ leaving the cell) Na+/Ca++ Exchanger(low affinity, high capacity) -removes 15% (3/4 of Ca++ leaving the cell) |
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When is Ca++ removed in a normal situation? |
As soon as it enters the cell. But, on the action potential it's phase 2-3 |
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Due to the high concentration gradient of Na+ in the cell we can expect what to happen with Ca++? |
More Ca++ would come in during phase 1. Since more is coming in then the AP will be longer. |
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Due to the high concentration gradient of Na+ in the cell we can expect what to happen with the refractory periods? |
Both refractory periods would be longer |
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Is digoxin a temporary drug? What patient should you be mindful of not getting this drug? |
Nope, it is a drug that you don't really stop. Pt with bradycardia. |
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Where does digoxin work better? |
It works better in the ventricular tissue, than the atrial tissue. And, it does not effect nodal tissue very much. |
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What does Digoxin do to the charge of the cell? |
It makes the cell more positive, effectively messing with the resetting process. |
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What causes too much K out of the cell? |
-Digoxin/Sux/K+ sparing diuretics -Acidosis -Shock -Renal failure -Adrenal Failure -Widespread tissue Destruction -Decreased ventilation |
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How does digoxin cause hyperkalemia? |
inhibition of the Na+/K+ pump |
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How does acidosis cause hyperkalemia? |
Enzymes don't work too well, so Na+/K+ pump does not work well. The high concentration of H+ kicks K+ out of the cell. |
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How does widespread tissue destruction cause this hyperkalemia? |
The cells lyse and release their contents, which hold massive amounts of K+ |
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How does shock cause hyperkalemia? |
The heart not satisfying the metabolic needs of the body, allows for it to become ischemic. Decreases the Na+/K+ ATPase pump. |
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How does Renal failure cause hyperkalemia? |
Issue of getting rid of K+ The worse the renal failure, the worse the K+ problem. |
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How does Adrenal failure cause hyperkalemia? |
With increase K+ lvls, the body usually produces aldosterone to get rid of it. Because it is failing, it can't produce aldosterone, so it can't get rid of K+ |
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How does sux cause hyperkalemia? |
Holds N-ACh ion channels open. K+ leaks out because of depolarization. |
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How does K+ sparing duretics cause hyperkalemia? |
Doesn't get rid of K+ |
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How does hypoventilation cause hyperkalemia? |
the increase of CO2 is like the increase of H+, which boots K+ out of the cell. |
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What can help decrease K+ in those with hypoventilation? |
Hyperventilate a pt. By taking CO2 out of the equation, it favors the production of more CO2. |
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How does a beta agonist help with hyperkalemia? |
Increases the rate at which Na+/K+ ATPase runs. |
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How does the insulin receptor help with hyperkalemia? |
It is functionally tethered to Na+/K+ ATPase pumps. It needs to put GLUT transporters on the surface to activate the Na+/K+ ATPase. |
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How does kayexelate help with hyperkalemia? |
GI K+ absorber |
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How does non-K+ sparing diuretics help with hyperkalemia? |
Gets rid of K+, but this is temporary because there is a huge supply in the cells. |
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What can help decrease K+ in those with renal failure? |
Dialysis or CRRT |
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What can help increase K+ in those with adrenal failure? |
Supplemental adrenal compunds |
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What does a Ca++ bolus do for hyperkalemia? |
It helps to settle down the heart by blocking the release of Na+ since Ca++ plugs up Na+ channels. This encourages less K+ to leak out. |
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Increasing K+ does what? |
Increased resting membrane potential. |
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What is the threshold potential for fast tissue? |
-65 mV |
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What does mild hyperkalemia do? |
Brings resting membrane potential closer to threshold for fast Na+ channels. This magnitude of the deflection will be smaller because the Vrm is higher. There will be an increase in HR. |
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What does bad hyperkalemia do? |
Vrm is higher than threshold potential, so what is left is L-type Ca++ channels(these need to reach -40mV to depolarize). It will result in a weaker HR. The magnitude is much smaller and wave is shorter. But, as long as L-type can reset, we will have an AP. When the Vrm is greater than L-type Ca++ reset, then we have vfib cause the heart can't do anything. |
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What is the Acid-Base formula? |
H+ + HCO3- <-> H2CO3 <-> CO2 + H2O |
