Prep for USMLEPrep for USMLE
         Forum      |     Resources New Posts   |   Register   |   Login





 skeletal muscle  



Post Reply  
  • 0/5
  • 1
  • 2
  • 3
  • 4
  • 5


Author12 Posts
  #1

Periodic hyperkalemic paralysis is characterized by high potassium concentration and muscle weakness. Which of the following is likely to cause muscle weakness as a result of increased extracellular potassium concentration?
A. Hyperpolarization of muscle cells
B. Inactivation of sodium channels in muscle cells
C. Increased release of neurotransmitters from alpha motoneurons
D. Decreased potassium conductance in muscle cells
E. Increased duration of action potentials produced by alpha motoneurons




  #2

b) Inactivation of sodium channels in muscle cells

How is the duration of the action potential determined (in regards to choice (E))? I've always been a bit unclear on this.


  #3

B. sakaki is correct

i may b wrong but i dont think that duration of action potential can be changed in skeletal muscle. In cardiac muscle, yes this is possible, but not in neurons or skeletal muscle. is i m wrong plz correct me


  #4

correct
answer is b)


Periodic hyperkalemic paralysis is produced by inactivation of the Na channels on the skeletal muscle membrane. Mechanism of action is unclear but is thought that the increased ECF K causes a mutation in the gene coding for the Na inactivation gate.


  #5

in my opinion increased ECF K decreases K efflux thru ungated K channels. this lead to depolarization due to retention of +vely charged ion. as long as membrane remain depolarized inactivation gates of Na channels remain closed. thats how Na channels are inactivated.


  #6

I agree that it should be a voltage-dependent inactivation of the Na+ channels rather than a "mutation in the gene."


  #7

canstep1 are u sure of what u wrote?


  #8

I read about it in an article from national institute of neurological disorders..

According to that,
The periodic paralyses are inherited disorders of voluntary muscle, characterized by intermittent attacks of weakness, during which affected muscles become slack, weak, and unable to contract. Between attacks, however, the affected muscles usually work normally. The two most common types of periodic paralyses are hypokalemic (caused by mutations in the calcium channel gene on chromosome 1) and hyperkalemic (caused by mutations in the sodium channel on chromosome 17).

I agree with canstep1...


  #9

sia can u explain how mutation in sodium channel lead to hyperkalemia and what is the consequenc eof mutation, i mean does it increase Na channel activity or dedcreases it?


  #10

From what I remember, potassium levels may or may not be high during the attacks in hyperkalemic periodic paralysis. Rather, it may be precipitated by hyperkalemia.

I found a nice mechanistic explanation in Brenner and Rector's The Kidney. The hyperkalemic periodic paralysis results from a mutation in the sodium channel, as sia stated.

K+ intake or exercise followed by rest---> increase in extracellular K+ ---> slight membrane depolarization ---> opening of Na+ channels and the switch of abnormal Na+ channels to non-inactivating mode ---> persistent inward Na+ current ---> sustained depolarization ---> efflux of K+ (which acts in a vicious cycle) as well as an inactivation of normal Na+ channels ---> loss of membrane excitability ---> paralytic attack

"Mild muscle depolarization (5 to 10 mV) in HYPP results in a persistent inward Na+ current through the mutant channel; the normal, allelic SCN4-encoded channels quickly recover from inactivation and can then be reactivated, resulting in myotonia. When muscle depolarization is stronger (i.e., 20 to 30 mV), all of the Na+ channels are inactivated, rendering the muscle inexcitable and causing weakness."

Therefore, the mutation causes the mutant Na+ channels to fail to inactivate, which leads to sustained depolarization, and all the normal Na+ channels inactivate under such (voltage-dependent) conditions, resulting in loss of electrical excitability and hence a paralytic attack.


  #11

My answer would be choice A

I have rather very simple explaination for the above condition.

High ECF K concentration will slow the K ion efflux through ungated K channels. Thus intracellular K ion concentration would increase slowly. This will lead to less negative membrane potential. Less negative membrane potential means less force on Na ions. Na ion conductance through voltage gated channels will reduce and will lead to slow depolariztion and muscle weakness. Isn't it that simple concept if not going through complex genetics???? As a matter of fact I don't know anything partaining to the genetics regarding this disease..

Please correct me if I am wrong


Edited by lungi on Oct 17, 2006 - 2:42 PM

  #12

lungi wrote:
This will lead to less negative membrane potential. Less negative membrane potential means less force on Na ions. Na ion conductance through voltage gated channels will reduce and will lead to slow depolariztion and muscle weakness.
Please correct me if I am wrong


Hi Lungi.
I think that your example illustrates the opposite - membrane becomes less negative. And option A is about hyperpolarization, i.e. more negative membrane.





Bookmark and Share



This thread is closed, so you cannot post a reply.



Login or Register to post messages








show Similar forum topics

skeletal muscle contraction
Skeletal Muscle Relaxant Question
Question about skeletal muscle
show Related resources









Advertise | Support | Premium | Contact