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NBME 17 Answers

nbme17/Block 0/Question#0 (reveal difficulty score)
A 58-year-old woman is brought to the ...
Membrane lipid peroxidation ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
tags: pharm pathoma repeat

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 +35  upvote downvote
submitted by โˆ—cassdawg(1779)

I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.

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zalzale96  Created an account just to up vote this answer +5
cheesetouch  1998 journal via google " Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation" +
peteandplop  "Evidence suggests that reactive oxygen species (ROS) may play important roles in the pathogenesis in myocardial infarction [2]. Following ischemia, ROS are produced during reperfusion phase [3, 4]. ROS are capable of reacting with unsaturated lipids and of initiating the self-perpetuating chain reactions of lipid peroxidation in the membranes" ( +1
mittelschmerz  Honestly the wording got me on this one. Great answer +
acerj  Also, you can rule out a few of the options to help justify this. Post MI you expect necrosis, not apoptosis. Remember, apoptosis is suicide, and necrosis is MURDER! Cell swelling is a sign of cellular injury, not cell shrinkage. The heart will undergo coagulative necrosis, not liquefactive necrosis. Also, protease inactivation by cytoplasmic free calcium is kind of nonsensical to me. Free calcium is more likely to cause cell injury via caspases (a form of proteases amongst other things), which is why calcium is usually bound up inside healthy cells. +5
ownersucks  This question presentation is exactly how Sattar said in pathoma Ch2. Raise in cardiac enzyme following reperfusion +
amy  FA2020 305: Reperfusion injury: free radical and increased Ca influx--hypercontraction of myofibrils There is increased cytoplasmic free calcium ions, but it induces hypercontraction, no protease inactivation. +

 +4  upvote downvote
submitted by โˆ—j44n(141)

Dr. Sattar for the win, this is a reperfusion injury. The cells dont have ATP so they cant run reduction reactions when they get 02 again. Its like being bankrupt they cant "pay" for thing like glutathione system etc so they get a build up of free radicals and free radicals cause lipid peroxidation

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 +2  upvote downvote
submitted by โˆ—feochromocytoma(36)

As others have mentioned, this is necrosis of the cardiocytes, which lead to the increase in the biomarkers CK-MB and Troponin...

Signs of cell necrosis would be cellular swelling and leaking of the content. Due to the ROS generation from the O2 reperfusion -> causing peroxidation of the membrane lipids -> loss of cellular "barriers" -> leaking

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imgdoc  You're mixing up two concepts here. This isn't necrosis, there is no inflammation occurring here. This is irreversible cell injury secondary to free radical damage. Cellular swelling is associated with reversible cell injury and wouldn't cause leaking of cellular contents. +

 +1  upvote downvote
submitted by sennachan8059(1)

This patient has acute MI leads to coagulative necrosis of cardiac cell. A&B are not true because cell shrinkage, formation of apoptotic bodies are sign of apoptosis. C is not true because she had coagulative necrosis. E is not true because cytoplasmic free Ca leads to protease Activation not inactivation

So the answer is D. ROS from reperfusion injury leads to embrane lipid peroxidation and membrane damage which makes cardiac enzyme leak into circulation.

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 +0  upvote downvote
submitted by โˆ—namesthegame22(11)

Also Noteworthy:

In acetaminophen overdose, a saturation of phase II metabolic pathways leads to excess acetaminophen metabolized by CYP-mediated reactions to N-acetyl- benzoquinoneimine (NAPQI), which has strong oxidizing properties and is directly hepatotoxic. It's the reactive oxygen species that cause hepatotoxicity from acetaminophen overdose.

Oxidizing free radicals damage hepatocytes through peroxidation of lipids in cell membranes, oxidative damage to intracellular proteins, and strand breaks in DNA.

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