Jackofknives
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2. A 55 year old woman sees a neurologist bc of weakness in her legs that improves over the course of the day or with exercise. Extracellular electrical recordings from a single skeletal muscle fiber reveal normal miniature end plate potentials. Low-frequency electrical stimulation of the motor neuron, however, elicits an abnormally small depolarization of the muscle fibers. The amplitude of the depolarization is increased after exercise.
Whats the most like cause of her leg weakness?
(A) blockade of postsynaptic ACh receptors
(B) ACh esterase deficiency
(C) Reduced ACh synthesis
(D) Impaired presynaptic voltage-sensitive Ca2+ influx
(E) Inhibition of Ca2+ reuptake into the sacroplasmic reticulum
3. The molecular mechanism underlying these symptoms is most similar to which following?
(a) Botox
(b) Curare
(c) Neostigmine
(d) ACh
(e) Tetrodotoxin
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| drgho
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D.) Lambert-Eaton
E.) not sure....but tetrodotoxin is used in presynaptic Ca2+ channels experiment as some form of antagonists. i think this one is the closet.
Edited by drgho on 08/20/07 - 08:05 AM
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| hope4dabest
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for the 1st one shouldnt it be C...dont know about the 2nd q?
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| Jackofknives
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| hope4dabest
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lamber is due to insufficient release of NT ACH?? right
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| hope4dabest
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oh sorry the choice C says synthesis...didnt read properly
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| edie
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B, C
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| drgho
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B & C has similar mechanism but don't think congenital myasthenic (AChE deficiency) presents as movement improved after exercise.
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| Jackofknives
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Maybe you guys should reason instead of guessing. try to take everything in the question into consideration instead of only considering what you want to take into account and overlook the other equally relevant factors.
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| edie
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Ok. We need Ach to get into the extrcellular space, so we need Ca2+ to be released to activate the release of Ach. Need an AP to get us our Ca2+, Depolarization as a result of Ach release gets the EPP. AchE gets us back to resting potential. Exercise improves the amp of depolarization. In the vignette, it looks like a problem with Ca2+, can narrow down to D, E for first q. JOK, am I going in right direction? This is where I get blocked!
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| drgho
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Well. the patient is female 55, unlike congenital myasthenia. MEPP is normal meaning baseline ACh quantum release is ok..in other words ACh synthesis is normal and release is normal. so C is out. increment response on exercise...so not myasthenia...age also not support myasthenia( myasthenia gravis: 20's , 30's in female and fifties in male, congenital myasthenia: very young children). so A and B are out. with impaired Ca2+ pump at SR, the patient will get substained contraction 'cause it is the mechanism to lower the cytosolic calcium after contraction in muscle. E is false too. In Lambert_Eaton, age is 50's, present with lower limb weakness and increment response after the exercise. So, D. is the only possible answer.
Let's analyse the mechanism of D. when motor nerve is stimulated, the action potential generated due to opening of Na+ channels. when the action potential arrived nerve terminal, opens Ca2+ channels which in turn causes the release of ACh which act on postsynaptic nicotinic ACh receptor and terminated by ACh Esterase. Some ACh synapes have autoreceptors on presynaptic neuron and ACh in turns inhibit its own release. B and C act on postsynaptic and so false. A,D and E left and A is inhibitor of ACh release by inhibiting docking of ACh vesicles on nerve membrane. E. tetrodotoxin(neuronal Na+ channel blocker) can also inhibit the release of ACh by inhibiting nerve action potential. ACh can feedback inhibit its own release but mechanism is not clear. so must be among A, D and E but neither A or E directly inhibits the presynaptic Ca2+ channels and mechanism of D is not well-understood. A inhibits downstream event of that Ca2+ channels and E on upstream event of Ca2+ channels. So what is true depends on how the question-maker thinks.......Whichever from A, D or E is true, it is just a biased conclusion.
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| edie
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Thank you DrGho  Am clear about Lambert-Eaton. All eyes now on the queston maker...or Jack 
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| kiterunner
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The clinical picture and increased amplitude of the depolarization after exercise give away the diagnosis ~ Lambert Eaton`s. Now if I`m correct, presynaptic ca++ influx is impaired in Lambert Eaton`s possibly due to antibody against ca++ channels.
So my ans. is D for 2.
Similar mechanism ---- inhibition of Ach release from presynaptic vesicles ---- botox. Ans is A for 3.
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| po
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for 2=D
for second=may be curare it causes non depolarising block,not sure though.
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| Jackofknives
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D. the normal miniature end plate potentials indicate sufficient synthesis and packaging of ACh and the presence and normal function of ACh receptor channels. The most likely explanation for this pt’s symptoms is a presynaptic deficiency – in this case, an impairment of the voltage-sensitive Ca2+ channels responsible for the increase in cytosolic Ca2+ that triggers the release of ACh into the synapse. The increase in postsynaptic depolarization observed after exercise in indicative of an accumulation of Ca2+ in the presynatpic terminal after multiple action potentials have reached the nerve terminal.
A. Botox – blocks ACh transferase ( - synthesis); Curare – blocks nicotinic ACh receptors; Tetrodotoxin – blocks voltage sensitive Na+ channels; neostigmine is ACh resterase inhibitor.
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