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GI2.17_Metabolic Syndrome and Diabetes_ABALI > Diabetes > Flashcards

Diabetes Flashcards

1
Q

The 3 main types of diabetes:

A
  1. T1: insulin dependent; autoimmune against β-cells.
  2. T2: insulin resistance.
  3. Gestational: during pregnancy only.
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2
Q

What types of glucose channels are located on the pancreas?

A

GLUT2 (do not respond to insulin).

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3
Q

Steps in insulin release from pancreatic beta cells:

A
  1. glucose enters beta cells via GLUT2.
  2. glucose undergoes glycolysis and TCA cycle to produce ATP.
  3. increased ATP activates ATP-sensitive K+ channels; depolarization.
  4. depolarization activates calcium channels.
  5. increased intracellular calcium activates cAMP.
  6. cAMP triggers insulin secretion.
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4
Q

What molecules cause insulin secretion through direct activation of cAMP in pancreatic beta cells?

A

incretins binding incretin receptors.

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5
Q

The three incretins and their overall function:

A
  • CCK, GLP1, GIP.
  • increase insulin secretion and inhibit glucagon secretion.
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6
Q

Common types of organ damage due to diabetes:

A
  • microvascular
    • retinopathy
    • nephropathy
    • neuropathy
  • macrovascualr
    • stroke
    • cardiovascular disease
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7
Q

The two causes of organ damage in diabetes:

A
  1. non-enzymatic glycosylation of proteins (alters activity).
  2. stimulation of polyol pathway (sorbitol accumulation).
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8
Q

What is HbA1C?

A
  • glycosylated hemoglobin due to hyperglycemia.
    • indicator of blood glucose status for past 120 days.
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9
Q

Steps in cellular damage due to sorbitol accumulation in hyperglycemia?

A
  1. glucose accumulates in tissues with insulin-independent glucose transporters.
  2. glucose converted to sorbitol via aldose reductase.
  3. sorbitol accumulaiton leads to the influx of water.
  4. cellular swelling causes damage.
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10
Q

Primary distinguishing features of T1 diabetes:

A
  1. young, sudden onset insulin deficiency and symptoms.
  2. ketoacidosis.
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11
Q

Cause of T1 diabetes:

A
  • Autoimmune attack against pancreatic β-cells.
  • insulin deficiency/absence.
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12
Q

Symptoms of T1 diabetes:

A
  • abrupt onset of 3 “P”s:
    • polyphagia (excessive hunger)
    • polydipsia (excessive thirst)
    • polyuria (frequent urination)
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13
Q

What leads to hypertriglyceridemia (chylomicrons, VLDL, and TAGs) in T1 diabetics?

A
  1. Lipoprotein lipase synthesis low due to insulin absence/deficiency.
  2. HPL activity increased due to glucagon and epinephrine.
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14
Q

What leads to hyperglycemia in T1 diabetics?

A
  1. increased gluconeogenesis (glucagon).
  2. decreased uptake of glucose by peripheral tissues (GLUT2; needs insulin) and liver (glucokinase inactive; needs insulin).
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15
Q

What leads to ketoacidosis in T1 diabetes?

A
  1. mobilization of FA from adipose tissue.
  2. increased hepatic β-oxidation and synthesis of ketone bodies.
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16
Q

Treatment for T1 diabetes:

A
  • insulin therapy to normalize blood glucose and prevent ketoacidosis.
17
Q

Why is ketoacidosis more common in T1 than T2 diabetes?

A
  • T1 has complete absence of insulin.
  • lipolysis is uninhibited; increased beta-oxidation.
  • liver forms ketone bodies (hydroxybutyrate) from excess acetyl CoA.
18
Q

Why is intensive insulin therapy contraindicted in children and elderly?

A
  • increased risk of hypoglycemia.
    • children: brain damage due to hypoglycemia.
    • elderly: stroke and MI due to hypoglycemia.
19
Q

HbA1C target level during standard insulin therapy:

A

8-9% (1-2 insulin shots a day).

20
Q

HbA1C target level during intensive insulin therapy:

A

7% (3-4 insulin shots a day).

21
Q

Symptoms of T2 diabetes:

A
  1. gradual onset of hyperglycemia and hypertriglyceridemia.
  2. NO KETOACIDOSIS.
22
Q

Primary cause of T2 diabetes:

A

insulin resistance.

23
Q

Which requires larger amounts of insulin to regulate glucose levels: obese or normal weight individuals?

A

obese

24
Q

Progression of T2 diabetes:

A
  1. insulin resistance leads to increased insulin secretion.
  2. blood glucose continues to rise; hyperinsulinemia.
  3. beta-cell dysfunction; insulin secretions fall.
  4. hyperglycemia worsens.
25
Q

Risk factors for insulin resistance:

A
  1. genetics (polygenetic)
  2. obesity
  3. sedentary lifestyle
  4. aging
26
Q

Higher levels of which blood marker are associated with a higher incidence of retinopathy?

A

HbA1C

27
Q

Main treatments for T2 diabetes:

A

diet, weight loss, exercise.

28
Q

The 5 drugs utilized for T2 diabetes treatment:

A
  1. abarcose
  2. sulfonylureas
  3. biguanides (metformin)
  4. incretin-DPP-4 inhibitors (Januvia)
  5. SGLT2 inhibitors
29
Q

Function of abarcose:

A
  1. inhibits alpha-glucosidases in intestinal lumen.
  2. decreases carbohydrate absorption.
30
Q

Function of sulfonylureas:

A
  • increases insulin secretion.
  • decreases serum glucagon.
31
Q

Steps in sulfonylureas function:

A
  1. inhibit ATP-sensitive K+ channels in pancreatic beta-cells.
  2. beta-cells depolarize due to increased intracellular K+.
  3. beta-cell calcium channel depolarization; insulin secretion increases.
32
Q

Function of biguanides (metformin):

A

inhibits gluconeogenesis

33
Q

Steps in metformin function:

A
  1. inhibits complex 1 of ETC.
  2. AMP levels increase; AMPK activated; glucose uptake.
  3. AMP inhibits glucagon receptors and decreases cAMP/PKA.
34
Q

What is DPP-4?

A

hydrolase that degrades incretins.

35
Q

Function in incretin-DPP-4 inhibitors (Januvia):

A
  • inhibit DPP-4 hydrolases that degrade incretins.
  • increased incretin activity and insulin secretion.
36
Q

Function of SGLT2 inhibitors?

A
  • block glucose reabsorption in kidney.
  • glucose excretion increases; lower blood glucose levels.
37
Q

Difference between age and nutritional status at time of onset in T1 versus T2 diabetes:

A
  • T1: childhood; malnourished appearance.
  • T2: after 35; obesity usually present.

GI2.17_Metabolic Syndrome and Diabetes_ABALI (2 decks)

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