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Flashcards in Type I Diabetes - Auble Deck (15):

Describe the pathogenesis of Type 1 diabetes.

Presentation of pancreatic antigen (GAD65) by APCs causes activation of Th1 and CD8+ cells to destroy the beta-cells/

The initial insult has not been conclusively identified.


Like most autoimmune diseases, T1DM results from a combination of genetic predisposition and environmental exposures & triggers.

What is the trigger in T1DM?

Unknown; it has been theorized to be a viral infection due to its prevalence in winter months, but this is unproven.


Describe 4 electrolyte imbalances SOMETIMES seen in untreated T1DM.

Hyponatremia (due to osmotic dilution of plasma)

Hypokalemia (due to diuresis, vomiting...)

Low bicarbonate due to consumption by acidosis

Hypophosphatemia due to phosphaturia and decreased intake.


T1DM primarily affects which gender?


What is the most common age of onset?

T1DM affects men and women equally.

Non-hispanic whites > African-american > Hispanic > Asian > Native American

Onset usually in adolescence (10-19), but can be seen as early as infancy.


What are the typical symptoms seen in untreated T1DM?

Polydipsia, polyuria with enuresis, weight loss yet increased appetite, fatigue.


What is the gold standard test to diagnose Diabetes Mellitus?

Oral glucose test; bolus of glucose is given orally to assess the insulin response; in DM it is absent.


Why would a bolus of IV glucose provoke a weaker immune response than an orally administered bolus?

Why might the insulin curve feature two peaks?

IV administration bypasses the GI tract, thus there is no potentiation of insulin secretion facilitated by incretins (GLP-1).

The peaks could correspond each to acute and chronic production of insulin (ie Preformed granules or synthesis-on-demand)


M1 Review: How are ketone bodies made?

Under what conditions are they made?

2 molecules of Acetyl-CoA are combined into acetoacetyl-CoA, which can in turn be transformed into acetoacetate (and beta-hydroxybutyrate, acetone)

Under conditions of fasting and starvation (ie when glucose is unavailable and more energy must be derived from fat stores.


Name the insulin that corresponds to the duration of effect.

1. 14 hours

2. 12-16 hours

3. 24 hours

4. 3-4 hours

5. 6-8 hours


1. 14hrs - Detemir

2. 12-16hrs - NPH

3. 24hrs - Glargine

4. 3-4hrs - Aspart/glulisine/lispro

5. 6-8hrs - Regular


Try to name 5 complications of diabetic ketoacidosis.

Increased ketoacids (given)

Severe hyperglycemia



Kussmaul breathing (respiratory compensation for acidosis)


What are the signs and symptoms of a mild insulin overdose?

What causes these effects?

How should it be treated?

Shakiness, dizziness, sweatiness, tachycardia, hunger, fatigue, and headaches.

Mostly adrenergic stimulation.

Oral sugars (juice, candy, glucose tablets)


What are the signs and symptoms of a moderate insulin overdose?

What causes these effects?

How should it be treated?

Confusion, combativeness, poor coordination, and slurred speech.

Mostly due to neuroglycopenia.

More oral sugars (frosting, sugar-gels)


What are the signs and symptoms of a severe insulin overdose?

How should it be treated?

Stupor, seizures, and coma.

Referral to emergency services and IM glucagon.


Given that different foods can have different effects on blood sugar levels, what foods are desirable in the context of maintenance of blood sugar in T1DM?

What is a glycemic index?

Avoidance of high sugar (too much to compensate, too fast) and high fat (too long to compensate) foods.

Glycemic index relates a food's effect on blood sugar level relative to a glucose index of 100. For example, gatorade may score 80 while barley scores only 30.


Describe the presentation and pathogenesis of latent T1DM in adults.

Some adults presenting with Diabetes Mellitus will demonstrate anti-islet antibodies; they often shortly (or already have) experienced destruction of the pancreatic beta cells. Be careful not to write off all adult diabetes as Type 2!

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