Dm

[yalemd]

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1: DM screeing: One of the following:

a: Fasting Glucose>=126 on 2 occasions, or
b: Random Glu>200, or
c: HbA1c>6.5 on 2 occasions (what I know it is used for complaince, not screeing. But just in case it was int he options and no Fasting or random sugar mentioned, can we still choose HbA1c?

2: Screening in Preg is 1hour (75) OGTT, right?

3: Silent MI in DM is due to autonomic neurapathy or periphral neuropathy? Could anyone please explain why?

4: Down phenomenon in DM, could anyone please explain how does it happen?

Thanks a lot and appreciate your thoughts and time

 

[IHeartNerds]

A1C is endorsed for the diagnosis of DM by several professional organizations including the ADA. The cut-off is 6.5% and should be repeated. This is relatively new (within the last year) and I doubt will show up on the real Step2.

Screening for gestational DM is 1 hour 50g glucose tolerance at 24ish weeks. Positive is over 140 and mandates formal three-hour 100g testing.

Silent/atypical MI in DM is due to de-innervation of cardiac sympathetic afferent fibers, if i recall, so I suppose autonomic neuropathy is more correct, however, many patients with DM and atypical MI do not have other signs and symptoms of autonomic neuropathy such as orthostatic hypotension or gastroparesis.

 

[yalemd]

A1C is endorsed for the diagnosis of DM by several professional organizations. This is relatively new (within the last year) and I doubt will show up on the real Step2.

Screening for gestational DM is 1 hour 50g glucose tolerance at 24ish weeks. Positive is over 140 and mandates formal three-hour 100g testing.

Silent/atypical MI in DM is due to de-innervation of cardiac sympathetic afferent fibers, if i recall, so I suppose autonomic neuropathy is more correct, however, many patients with DM and atypical MI do not have other signs and symptoms of autonomic neuropathy such as orthostatic hypotension or gastroparesis.

Does that mean gastroparesis is because of autonomic, not periphral neurpathy?
Could you please list what complications are autonomic and what periphral cause it gets me confused.

Thanks for sharing

 

[IHeartNerds]

Does that mean gastroparesis is because of autonomic, not periphral neurpathy?
Could you please list what complications are autonomic and what periphral cause it gets me confused.

Thanks for sharing

Autonomic neuropathy = neuropathy of the autonomic NS
Peripheral neuropathy = neuropathy of the peripheral NS

That isn't meant to be snide, just a simple way to think of it.

What does the autonomic NS do? Regulate organs. What does autonomic neuropathy do? Disturb that organ regulation. Thus the orthostasis / gastroparesis / bladder dysfunction / erectile dysfunction.

What does the peripheral NS do? sense things and active muscle. What does peripheral neuropathy do? Disturb that. Thus the classic sensory loss. Although not thought of much, diabetic peripheral neuropathy does cause some muscle innervation loss and you can see wasting in the feet of some patients. This just makes their walking worse, as you might imagine.

 

[Mortal_Lessons]

To be precise, the autonomic nervous system is a part of the peripheral nervous system, making an autonomic neuropathy a subtype of peripheral neuropathy.

Autonomic neuropathy = neuropathy of the autonomic NS
Peripheral neuropathy = neuropathy of the peripheral NS

 

[Mortal_Lessons]

4: Down phenomenon in DM, could anyone please explain how does it happen?

Thanks a lot and appreciate your thoughts and time

I think it's named the Dawn (with an 'a') phenomenon because it's observed during dawn, the early morning hours. And it has to do with the natural morning boost of GH and cortisol, both of which help to increase plasma glucose. For the diabetic, this might make it particularly difficult to control early morning glucose levels.

 

[fergustsi]

1: DM screeing: One of the following:

a: Fasting Glucose>=126 on 2 occasions, or
b: Random Glu>200, or
c: HbA1c>6.5 on 2 occasions (what I know it is used for complaince, not screeing. But just in case it was int he options and no Fasting or random sugar mentioned, can we still choose HbA1c?

2: Screening in Preg is 1hour (75) OGTT, right?

3: Silent MI in DM is due to autonomic neurapathy or periphral neuropathy? Could anyone please explain why?

4: Down phenomenon in DM, could anyone please explain how does it happen?

Thanks a lot and appreciate your thoughts and time

to diagnose diabetes with a random glucose of greater than 200 you also have to have symptoms of DM.

 

[lakersbaby]

I think it's named the Dawn (with an 'a') phenomenon because it's observed during dawn, the early morning hours. And it has to do with the natural morning boost of GH and cortisol, both of which help to increase plasma glucose. For the diabetic, this might make it particularly difficult to control early morning glucose levels.

agreed just to add tho i think the question would want you to know that you would increase the evening insulin dose in the dawn effect as opposed to the somogyi effect which is caused by the marked hypoglycemia causing nocturnal release of catecholamines and cortisol which would require you to decrease the evening dose of insulin.

 

[OveractiveBrain]

If some one comes in with elevated morning glucose you must consider a 3Am glucose level.

if the 3 am level is LOW you have a Symogi effect (spelling); aka a rebound hyperglycemia. You gave too much insulin at the PM dose, and the patient goes hypoglycemic in the early am. In response, counterregulatory hormones are released which increase blood sugar, so when they wake up, they have a high bG/

if the 3 am level is HIGH you have the Dawn phenomena (it is with an a). You gave not enough insulin and gluconeogenesis from overnight fasting dominated the insulin you tried to give them. The counterregulatory hormones dominate in the absence of sufficient insulin. This is a blast back to Biochemistry. Gluconeogenesis and Glycolysis are tethered by hormones. Insulin causes glycolysis and uptake of insulin into the cells, while Cortisol, GH, and glucagon activate gluconeogenesis. Without enough insulin, and in the state of fasting, counterregulatory hormones predominate, gluconeogenesis predominates, and you get a hyperglycemia from hepatic glucose production.