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Kaplan Qbank USMLE



Author12 Posts
  #1

Q1. A 64 years old man came to the EM with severe chest pain, sweating and shortness of breath. The attending physician diagnosed it as acute myocardial infarction. In a an MI, hypoxia develops in the cardiac muscle. In such a condition, which of the following rate limiting enzyme of TCA cycle will be activated?

a.Succinyle dehydrogenase

b.Citrate symthase

c. Malate dehydrogenase

d.Alpha keto gluterate dehydrogenase

Q2. A 32 yaers old man is starving for the last 2 days. Which of the following enzymes will be activated in his body?

a. Glucokinase

b. Pyrovate dehydrogenase

c. Glycogen phosphorylase

d. Glucose 6 phosphatase

e.Methylmalonyl coa synthase

Q3.A 40 years old lady with aBMI of 34 has had a heavy meal about half an hour ago. Which rate limiting enzyme will be activated in her body now?

a.Hepatic glycogen phosphorylase

b.Muscle glycogen phosphorylase

c.Glycogen synthase

d. Phosphoenolpyrovate carboxy kinase

e. Fructose 1,6 bi phosphatase



Cheers

bd200004@yahoo.com




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bd200004@yahoo.com

  #2

Ahh, Rate Limiting enzymes.. I'll give it a shot.. Feel free to correct me if I am wrong.

Q1. I always thought isocitrate dehydrogenase was the RL enzyme for TCA cycle, but since ischemia is resulting in the MI I would assume that the patient must switch to anearobic means of producing ATP. Hence, i would guess malate dehydrogenase. The activation of malate dehydrog. would directly result in the start of gluconeogenisis. so C

Q2. Id say C, glycogen phosphorylase.. When the body begins to starve it needs to break down its glycogen reserves in order to neurish the body.

Q3. C, by process of elimination.. I am pretty sure all the other enzymes are involved in utilizing energy storage and/or gluconeogenisis. Meanwhile glycogen synthase builds glycogen stores after a meal.

Anyone got any other toughts?

  #3

Q1 D Alb I also always thought isocitrate dh is the rate limiting enayme, but thats not here. I am also aware that amp stimulates alphketo glutarate dh. and thus pick this one So D

Q2 C

Q3 C in the insulin world directly after a meal, insulin dephophorylates glycogen phophorylase which inactivates the enzyme, and dephophorylates glycogen synthase which activates it. Glucagon does the opposite via phophorylation and thus my answer for Q2.

The thing I worry about in q2 is that I thought glycogen stores would be depleted 12 -16hours after a fast. Still there might be someresidual amount snd it still might be activated (phoporylase) I cant seem to recall what process methmalonyl coa synthase is a part of.

Edited by Ancylostoma on 01/14/07 - 06:59 PM

  #4

Answer

1.b Citrate synthase is the rate limiting enzyme in TCA cycle. In Acute MI, there is ischaemia=>depletion of ATP=>activation of Citrate synthase to compensate the loss.

2.d Glucose 6 phosphatase. During starvation, body tries to utilise glucose at first that is depleted within hours. Then glucose is produced by glycogenolysis in liver and kindney.But that too is depleted within 24 hours. So, after 24 hours the main source of glucose is Gluconeogenesis, that is glucose is produced from non-carbohydrate sources like lactate, alanine, pyruvate.

3.c Glycogen synthase. Following the meal, there is an Insulin world. Insulin causes dephosphorylation of Glycogen synthase that is active form. Glycogen phosphorylase is also dephosphorylated but it is inactive.



I shall post some more questions for you soon.

Cheers mates.

Thanks,

bd200004@yahoo.com




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bd200004@yahoo.com

  #5

my answewrs are
1) B-citrate synthase
2)C-glycogen phosphorylase
3)C-glycogen synthase

  #6

I agree with bd 2005 answers.
Good explanation.

  #7

bd2005 wrote:
1.b Citrate synthase is the rate limiting enzyme in TCA cycle. In Acute MI, there is ischaemia=>depletion of ATP=>activation of Citrate synthase to compensate the loss.

Can u please explain how making citrate's gonna give us ATP in hypoxia?? raised eyebrow

According to me, in hypoxia, the whole TCA cycle's gonna shut down, and energy's gonna come frm anerobic glycolysis only
n there ll be low levels of acetyl CoA coz pyruvate is gonna be diverted to lactate to regenerate NAD.

And isocitrate dehydrogenase is the RATE LIMITING ENZYME in TCA cycle.nod

According to me, all the enzymes of TCA r gonna have decreased activity.

Edited by indidoc1 on 03/12/07 - 04:12 AM

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  #8

bd2005 wrote:

2.d Glucose 6 phosphatase. During starvation, body tries to utilise glucose at first that is depleted within hours. Then glucose is produced by glycogenolysis in liver and kindney.But that too is depleted within 24 hours. So, after 24 hours the main source of glucose is Gluconeogenesis, that is glucose is produced from non-carbohydrate sources like lactate, alanine, pyruvate.


Now during starvation, gluconeogenesis is stimulated in liver.. but thats not due to any change in the activation state of glucose 6 phosphatase.. The enzyme which is induced by glucagon and cortisol is PEPCK
on the other hand, glycogen phosphorylase is gonna be activated by glucagon.. whether glycogen is exhausted or not doesn't matter.. its happening bcoz of phosphorylation of the enzyme.

___________________
"Whether you think you can or whether you think you can't, you're right!" ~ Henry Ford

  #9

bd2005 wrote:

3.c Glycogen synthase. Following the meal, there is an Insulin world. Insulin causes dephosphorylation of Glycogen synthase that is active form. Glycogen phosphorylase is also dephosphorylated but it is inactive.

On this, i absolutely agree wth u.. nodnodnod

So given these Qs.. my answers r gonna be..

1-C i m choosing the lesser among all evils wink bcoz its a pathway in gluconeogenesis.. But gluconeogenesis occurs in liver only.. n i don't think MI will lead to gluconeogenesis in liver.
Also thinking abt D.
I still have the concept that all dehydrogenases except LDH r inhibited in hypoxia.

2-C
3-C

And may i plz know the source of thes Qs bd2005? raised eyebrow

Edited by indidoc1 on 03/12/07 - 04:49 AM

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"Whether you think you can or whether you think you can't, you're right!" ~ Henry Ford

  #10

NAAAAHHH.. ATP INHIBITS ,NADH, SUCCINYL COA ALL INHIBIT a ketogluterate dehydrogenase n citrate synthase and ADP ACTIVTES THEM.. CITRATE SYNTHASE IS THE MAJOR REGULATORY ENZ IN TCA CYCLE( FIRST AID).. obviously loss of inhibition durin ischmia wud increase their activity..

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  #11

NAAAAHHH.. ATP ,NADH, SUCCINYL COA ALL INHIBIT a ketogluterate dehydrogenase n citrate synthase and ADP ACTIVTES THEM.. CITRATE SYNTHASE IS THE MAJOR REGULATORY ENZ IN TCA CYCLE( FIRST AID).. obviously loss of inhibition durin ischmia wud increase their activity..

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  #12

secondly glcogen doesnt last beyond 24 hrs,.. not top talk of 48 hrs..

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