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A 37-year-old chemist with a 20-year history of bipolar disorder is rushed to the emergency department by his wife, who found him lying unconscious in the living room of their room. The man's skin is bright red, and he is breathing rapidly. Upon presentation, his breath smells like bitter almonds.
1. What is the most likely diagnosis?
2. What biochemical process is disrupted in this condition?
3. Does this patient have a greater-than-normal or lower-than normal proton concentration in the intermembrane space of his mitochondria?
4. What is the most appropriate treatment for this conditon?
5. What other substances inhibit the electron transport chain?
6. What additional substances disrupt oxidative phosphorylation?
MDiva
08-25-2006, 09:40 PM
1. cyanide poisoning
1. cyanide poisoning
Correct.. good job...MDiva...
2. What biochemical process is disrupted in this condition?
think about the 3 C's... carbon monoxide, cyanide, cytochrome oxidase... directly inhibit the electron transport chain (ETC)...is the first step;
3. Does this patient have a greater-than-normal or lower-than normal proton concentration in the intermembrane space of his mitochondria? So if cyanide inhibits the ETC.. means that there is less energy.. therefore lower proton concentration...
4. What is the most appropriate treatment for this conditon?
Amyl nitrate.. why? converts hgb to methb BUT is this not bad for us.. yes and no... methgb binds very strongly to the cyanide therefore stopping it from inhibiting the ETC..
5. What other substances inhibit the electron transport chain?
I named one above.. carbon monoxide; and to be honest with you.. when I answered this question.. that is the only one that I knew; others include: amytal, rotenone, antimycin A, azide;
6. What additional substances disrupt oxidative phosphorylation?
Again.. the only ones that I knew were the uncoupling agents that Goljan talks about in the book such as 2.4-DNP; others include ATPase inhibitors such as oligomycin which directly inhibit mitochondrial ATPase;
ZWobble
08-25-2006, 11:14 PM
What drugs result in inhibition of mitochondrial DNA synthesis, leading to a decrease of the total number mitochondria and reduced NADH oxidation in cells?
What would this result in?
What drugs result in inhibition of mitochondrial DNA synthesis, leading to a decrease of the total number mitochondria and reduced NADH oxidation in cells?
What would this result in?
you would ask a pharm question, knowing that this is my weakest subject :shock: :( :rolleyes: ... let's see what I have retained... am thinking these are the drugs that work in the different phases of the cell cycle... such as methotrexate (S-phase), 5-FU (S-phase), Pacitaxol (spelling might be wrong)--M-phase...
Is this right? or am I totally off... b/c I am guessing here..and hoping..:shock: :cry:
ZWobble
08-26-2006, 01:20 AM
Nucleoside analouges (cytosine, arabinoside, AZT etc)
It results in increased cystolic NADH, shunting of pyruvate to lactate (lactic acidosis), hyperglycemia due to increased gluconeogenesis and fatty liver due to inability to oxidize fatty acids.
MD your defo on the right track..this was such a random question anyways
thanks zwobble.. just PM'd you...
st_55
08-28-2006, 08:14 PM
all the inhibitors of the etc are:amytal, rotenone,malonate, antimycin d, cyanide, carbon monoxide. chlorophenicol, and oligomycin. I know u mentioned majority of these md...but there were some that i didnt see.
no problem.. thank you st 55...
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