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NBME 22 Answers

 +6  upvote downvote
submitted by โˆ—titanesxvi(106)
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hope this image help to understand it, the pumps don't work because lack of ATP

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an1  Dr.Sattar explains this really well. summary: Troponin outside the cell means that the membrane must have been damage (irreversible damage) for it to leak out. This leads to failure of the Na/K ATPase pump. Na builds up inside and water follows causing further cell swelling membrane damage. Ca also builds up inside. K will build up outside because its normally supposed to be pumped in but the pump is broken. Also, recall from FA that Hyperkalemia is seen with DO LABBSS; cell lysis +2



 +5  upvote downvote
submitted by โˆ—dodgerslakers15(22)
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In cellular ischemia, the Na+/K+ ATPase pump stops working due to decreased ATP levels. Consequently, sodium is not pumped out and potassium is not pumped into the cell, leading to an accumulation of sodium in the cell and potassium outside the cell. Furthermore, the sarcoplasmic reticulum Ca-ATPase pump fails, which leads to an increase in calcium in the cell.

Bottom line, ischemic tissue: there is a buildup of sodium and calcium in the cell.

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madamestep  I also like to remember this via the effects they cause. Low ATP โ†’ Na/K ATPase cant do its thing so you get Na left in the cell. Water follows Na โ†’ Cellular swelling. Ca2+ ATPase cant work during an MI, remember that you get contraction necrosis in a STEMI during hours 4-12. Contraction is from the increased Ca2+. +



 +1  upvote downvote
submitted by โˆ—oznefu(22)
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I get that the answer is correct for a reversible injury where there is cell swelling because of the increased intracellular Na+ and Ca2+ due to impaired Na/K and sarcoplasmic reticulum activity ...

But if there are increased cardiac enzymes in the blood indicating cell death and membrane damage, wouldnโ€™t the intracellular electrolytes be low since they are released into the blood?

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lord_voss  troponin = irreversible injury and membrane damage -> high extracellular concentration of Na+ and Ca++ causes both to move into cell through damaged membrane and high intracellular K+ leaves the cell +13
rogeliogs  Question is asking about the changes in the myocardiocytes and my second interpretation was that they are asking the changes before they "rupture" and liberate their content in the blood producing increase enzymes in the patient. Therefore because is a ischemic process = reduction of O2 = low ATP = impairment of Na/K ATPase = increase Na-decrease K intracellular = block Ca/Na exchanger = increase Ca intracellular. the same effect as digoxin +5
allodynia  What will happen to Na and ca conccentration when there is an irreversible injury? +
baja_blast  @allodynia Pathoma pg. 4 has a really good summary of this. In short, Na+ and Ca2+ both increase intracellularly in an irreversible injury. +



 +1  upvote downvote
submitted by delamj(3)
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I thought this was a pretty good summary from wikipedia.

Steps 1-4 explain the question:

  1. Lack of oxygen causes the [cardiomyocyte's] normal process for making ATP for energy to fail.
  2. The cell switches to anaerobic metabolism, producing lactic acid.
  3. ATP-reliant ion transport pumps fail, causing the cell to become depolarized, allowing ions, including calcium (Ca2+), to flow into the cell.
  4. The ion pumps can no longer transport calcium out of the cell, and intracellular calcium levels get too high.
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 +0  upvote downvote
submitted by โˆ—mtkilimanjaro(18)
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Another way to think about this is just that decreased O2 leads to dysfunction of the Na+/K+ ATPase as others have mentioned.

This is pretty much identical to the mechanism of digoxin, which blocks the Na/K ATPase and calcium accumulates in the cell because it cant be exchanged for extracellular Na+ (which is not intracellular due to defective Na/K ATPase)

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 -4  upvote downvote
submitted by โˆ—sbryant6(205)
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If you know the MOA of digoxin you should be able to get this question right.

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