beta blocker in diabetics

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cage92

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i know betablocker are contraindicated in mechanism since it block symp symptoms of hypoglycemia? but diabetic patient are hyperglycemic and other issue it is al contraindicated since it block hepatic gluconeoogeneis why i need gluconeogenesis in diabetic( since metformin treatmennt block gluconeogenes)
 
Consider a Type 1 Diabetic who has just taken NPH and fallen asleep. We've risked a hypoglycemic coma overnight by providing say propranolol, no?

Early adrenergic signs are critical to indicate to the patient that thye need sugar and to follow the e rule of 15's:15g of carbs to restore sugars checking every 15 minutes until it restores. it is not a method of ensuring blood-sugar control.
 
Consider a Type 1 Diabetic who has just taken NPH and fallen asleep. We've risked a hypoglycemic coma overnight by providing say propranolol, no?

Early adrenergic signs are critical to indicate to the patient that thye need sugar and to follow the e rule of 15's:15g of carbs to restore sugars checking every 15 minutes until it restores. it is not a method of ensuring blood-sugar control.
ah ok so its in case only if there are insulin inducer sever hypoglycemia
 
ah ok so its in case only if there are insulin inducer sever hypoglycemia

It only *has* to be insulin-induced for type 2. For a type 1 diabetes it wouldn't have to be insulin induced, since alpha cells of islets are destroyed as well. Say they haven't eaten anything in a while, and they start to get hypoglycemic. Normally they'd start having catecholamine-mediated tachycardia, diaphoresis, tremor--the beta blocker masks this response so they don't know they're hypoglycemic.
 
It only *has* to be insulin-induced for type 2. For a type 1 diabetes it wouldn't have to be insulin induced, since alpha cells of islets are destroyed as well. Say they haven't eaten anything in a while, and they start to get hypoglycemic. Normally they'd start having catecholamine-mediated tachycardia, diaphoresis, tremor--the beta blocker masks this response so they don't know they're hypoglycemic.

i mean by insuline induced(is that he take exogenous insuline) since its diabetic patient he shouldnt have hypoglycemia even on fasting or what?
 
why only type 1? since both lack the effect of insuline typ1 dont have islet cell and typ2 has insuline resistance

right, type 2 has insulin resistance, but the alpha cells are not destroyed in type 2, so gluconeogenesis/glycogenolysis are not deranged, and they won't have hypoglycemic episodes, only hyperglycemic episodes

that's the basis for why metformin is an effective treatment, as it inhibits gluconeogenesis, thus reducing blood glucose levels
 
right, type 2 has insulin resistance, but the alpha cells are not destroyed in type 2, so gluconeogenesis/glycogenolysis are not deranged, and they won't have hypoglycemic episodes

so by conclusion: type 1 face those sympathetic symptoms since he face hypoglycemia😀😀thank you
 
why only type 1? since both lack the effect of insuline typ1 dont have islet cell and typ2 has insuline resistance

Key difference and testable Step 1 difference: relative and resistance based insulin deficit (DM2) versus ABSOLUTE insulin deficit (DM1) which is still sensitive to exogenous insulin.

Giving an injection of insulin + beta blockade = bad news for the Type 1 diabetic. Or working out. On the other hand, the type 2 diabetic has less to worry about. Insulin resistance is aplenty, and their baseline blood sugars are likely higher. Sure, you still worry in a type 2. It just isn't as touch and go. For instance, we were taught that you advise the type 1s to increase food intake before exercise to avoid hypoglycemic events on the treadmill, but type 2 on say metformin + exenatide + sitagliptin wants to get on a treadmill? More power to em.

It's just a principal based on absolute and relative deficiencies, insulin resistance, and baseline blood sugars.
 
right, type 2 has insulin resistance, but the alpha cells are not destroyed in type 2, so gluconeogenesis/glycogenolysis are not deranged, and they won't have hypoglycemic episodes, only hyperglycemic episodes

that's the basis for why metformin is an effective treatment, as it inhibits gluconeogenesis, thus reducing blood glucose levels

so by conclusion: type 1 face those sympathetic symptoms since he face hypoglycemia😀😀thank you

Important to remember that Type 2 is viewed as a dual disease, of not only decreased insulin but increased glucagon...hence most of your type 2s are overweight where most of your type 1s are normal bmi or underweight.

I vaguely remember a question referring to this being on either an NBME or my actual test.
 
Important to remember that Type 2 is viewed as a dual disease, of not only decreased insulin but increased glucagon...hence most of your type 2s are overweight where most of your type 1s are normal bmi or underweight.

I vaguely remember a question referring to this being on either an NBME or my actual test.

One of the NBMEs addresses that insulin resistance is associated with hyperglucagonemia (naturally via arrows!!!) so well put.
 
Key difference and testable Step 1 difference: relative and resistance based insulin deficit (DM2) versus ABSOLUTE insulin deficit (DM1) which is still sensitive to exogenous insulin.

Giving an injection of insulin + beta blockade = bad news for the Type 1 diabetic. Or working out. On the other hand, the type 2 diabetic has less to worry about. Insulin resistance is aplenty, and their baseline blood sugars are likely higher. Sure, you still worry in a type 2. It just isn't as touch and go. For instance, we were taught that you advise the type 1s to increase food intake before exercise to avoid hypoglycemic events on the treadmill, but type 2 on say metformin + exenatide + sitagliptin wants to get on a treadmill? More power to em.

It's just a principal based on absolute and relative deficiencies, insulin resistance, and baseline blood sugars.
really thank you guys
 
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