Prep for USMLEPrep for USMLE Forum
   Forum    Step 1  Step 2 CK Step 2 CS Step 3  Match  IMGs Resources Search






Previous Topic | Next Topic  nbme Q EXPLAINNNNNNNNNNN 




 
Kaplan Qbank USMLE



Author8 Posts
  #1

In acute coronary spasm, within seconds mitochondria swelling & depletion of glycogen grannules. Which event caused this?
a.accumulation of FFA
b. Decrease ATP
c. Degradation of membrane phospholipids
d. Efflux of K
e. Influx of Na



  #2

B

decrease in ATP causes decrease in ATPase, which transport 3 Na+ out and 2K+ in, resulting in swelling of cells.


___________________
The Key to Succeed is Patience.

  #3

B

  #4

thanks robin for the explanation. But why A is wrong?

  #5

I thought A was wrong since the FFA are being used up by the mitochondria to keep up the ATP reserves.

Agreed with B

  #6

You are right ATP is needed for efflux of Na, but at a mitochondrial level the disruption of its membrane causes the sweeling.

___________________
JL

  #7

Cell. 1997 Nov 28;91 (5):627-37 9393856 [Cited: 60]
Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria.
[My paper] M G Vander Heiden , N S Chandel , E K Williamson , P T Schumacker , C B Thompson
Mitochondrial physiology is disrupted in either apoptosis or necrosis. Here, we report that a wide variety of apoptotic and necrotic stimuli induce progressive mitochondrial swelling and outer mitochondrial membrane rupture. Discontinuity of the outer mitochondrial membrane results in cytochrome c redistribution from the intermembrane space to the cytosol followed by subsequent inner mitochondrial membrane depolarization. The mitochondrial membrane protein Bcl-xL can inhibit these changes in cells treated with apoptotic stimuli. In addition, Bcl-xL-expressing cells adapt to growth factor withdrawal or staurosporine treatment by maintaining a decreased mitochondrial membrane potential. Bcl-xL expression also prevents mitochondrial swelling in response to agents that inhibit oxidative phosphorylation. These data suggest that Bcl-xL promotes cell survival by regulating the electrical and osmotic homeostasis of mitochondria.
Mesh-terms: Anti-Bacterial Agents, pharmacology; Antimycin A, pharmacology; Apoptosis, physiology; B-Lymphocytes, chemistry; B-Lymphocytes, cytology; B-Lymphocytes, ultrastructure; Cytochrome c Group, metabolism; Flow Cytometry; Gene Expression, physiology; Homeostasis, physiology; Human; Intracellular Membranes, metabolism; Intracellular Membranes, pathology; Jurkat Cells, chemistry; Jurkat Cells, cytology; Jurkat Cells, ultrastructure; Membrane Potentials, physiology; Microscopy, Electron; Mitochondria, pathology; Mitochondria, physiology; Mitochondria, ultrastructure; Mitochondrial Swelling; Oxidative Phosphorylation, drug effects; Proto-Oncogene Proteins c-bcl-2, genetics; Support, U.S. Gov't, P.H.S.; Transfection;


___________________
JL

  #8

I AM SORRY BUT WHY WUD FFA ACCUMULATE? smiling face
think about it n u will know that its not the answer...

when there is ISCHEMIA the anareobic glycolysis takes over...FFA oxidation REQUIRES oxygen which doesnt occur ...secondly this switch takes time...I dun want to go into details of this but simply put... Na/K pump needs IMMEDIATE energy which is possible through anaerobic glycolysis and for that GLYCOGEN stores deplete...secondly when thats gone...mito swells up...needs Ca homeostatsis as well as sodium homeo to maintain the state...







You don't have permission to post.




Login or Register to post messages in this topic





















Contact | Leaders | Disclaimer | Privacy

Copyright @ Prep for USMLE. All rights reserved.