doc_clotaire wrote:
4. Insulin resist
i second that
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| ssrpk
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increasing acetylcholine in the synaptic cleft or increasing insulin iun the bloodstream will overcome the resistance.
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| young_doc
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The question is asking about the pathophysiologic basis of the disease..
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| Jesussaves
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is it the autoimmune basis and so type 1 DM??.....not sure
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| cirus
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the ans is 4- Insulin resist
the explanation on kaplan Q Bank--> Myasthenia graves disease is an auto immune disease with antibodies against the acetyl choline that bind to the receptors & block the effect of acetyl choline, then they said that the only one in the list that shares the same pathophisiology is Insulin resistance as ANTIBODIES TO INSULIN BLOCK THE INSULIN RECEPTORS. I never new that insulin resist (Type 2 DM ) is due to an auto immune disease & there are antibodies
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| prathapdoctor
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i think insulin resistance in type2 diabetes is better option for this question.
both myasthenia and type 2 diabetes are associated with insensitivity of receptor or absence of receptor itself.
if we consider, type of autoimmune reaction, all the first 3 options come under type2 hypersensitivity like myasthenia.
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| young_doc
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Interesting...i never knew there that insulin resistance is due to Ab's. I mean you don't often hear of Insulin resitance being a Type 2 Hypersensitivity!
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| cirus
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that makes 2 of us!!
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| prathapdoctor
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but in type2 diabetes, there will not be destruction of receptors by antibodies.
but finally, in both the diseases(myasthenia and type2 diabetes) we see the absence or insensitivity of receptors
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| cirus
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prathapdoctor
but the kaplan explanat said that there are abs blocking the insulin recept..
can anyone explain that
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| prathapdoctor
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is it? interesting, i dont know that.
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| ssrpk
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antibodies bindiong to insulin receptors....surely i never heard that. maybe that was just an analogy to explain insensitivity.
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| dr in trouble
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In type 2 Diabetes, there is insensitivity to insulin not destruction of receptors.
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| dr_arc
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i think the similarity that they are trying to draw attention to is that in MG there is enough acetylcholine the problem is there are ab to the Ach receptor so Ach cannot act at its receptor
in insulin resistance there is enough insulin but there are antibodies to insulin so insulin cannot act at it's receptor.
also in both cases it is antibodies that prevent circulating substances from acting, the other three though type 2 are ab directed against tissue antigens and subsequent consequences. these two though, the pathophysiology is due to the inability of circulating substances to act either because there is an antibody against the receptor or in the second case against the substance itself which prevents the substance from getting attached to its receptor . in either case there is no substance receptor interaction
i think what they mean is the antibodies that develop to exogenous insulin in some people using one of the older less purified forms of insulin for a long time. i dont know for sure but remember reading something like that sometime.
Edited by dr_arc on 07/07/07 - 01:03 AM
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| dr in trouble
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In type 2 diabetes the problem is not antibodies but the downregulation of insulin receptors due to obesity and other causes like glucokinse receptors in pancreas not completely activated and result in decrease insulin secretion but u r right that the main problem is nonavailability of receptor in the precence of hormones.
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| dr_arc
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yup . agree abt step 2 path , but the question stem has no mention of type 2 DM.
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...But how about Type I DM---Type II HS?