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BMS150 Post-MT2 > Type II Diabetes Mellitus > Flashcards

Type II Diabetes Mellitus Flashcards

(49 cards)

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1
Q

In a diabetes diagnosis, _____ > 6.5%

A

HbA1c

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2
Q

Races at a higher risk for T2DM?

A

Indigenous, Hispanic, African ancestry

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3
Q

Autoimmune disease => pancreatic beta cell destruction, usually onset is in childhood but sometimes in early adulthood

A

Type 1 diabetes

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4
Q

Combination of peripheral resistance to insulin action and an inadequate secretory response by beta cells

A

Type 2 diabetes

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5
Q

Single-gene disorders or secondary to infection or pancreatic destruction by other means

A

Monogenic and secondary causes

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6
Q

Is type 1 or type 2 diabetes more common?

A

Type 2

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7
Q

Monozygotic twin concordance T2DM vs T1DM?

A

T2DM - 70-90%
T1DM - 30-50%

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8
Q

Each gene implicated in T2DM has the ability to increase the relative risk of expressing diabetes by what percentage?

A

5%

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9
Q

Notable genes implicated in T2DM?

A
  • TCF7L2 gene
  • PPAR receptor
  • IRS gene
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10
Q

Transcription factor that works on a wide variety of genes including the Wnt pathway genes?

A

TCF7L2

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11
Q

Transcription factor/nuclear receptor that binds FFAs and/or PGs?

A

PPAR receptor

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12
Q

Most important environmental risk factor?

A

Obesity (esp. central obesity)

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13
Q

Two step pathophysiology of T2DM?

A
  1. Impaired insulin action (sensitivity)
  2. Impaired insulin secretion
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14
Q

What happens with impaired insulin action?

A

Insulin resistance and abnormal fat and skeletal muscle metabolism

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15
Q

What is impaired insulin secretion usually accompanied by?

A

Imbalance in insulin/glucagon activity ratio => increased glucagon action

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16
Q

Pathophysiologic pearl?

A

To progress to overt T2DM, you need impaired insulin secretion, which seems to arise after a long history of insulin resistance

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17
Q

What are the 3 aspects of developing insulin resistance?

A
  1. Increased FFAs and adipocyte endocrine dysfunction
  2. Reduction of incretins
  3. INS-R desensitization
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18
Q

How does lack of insulin result in increased FFAs?

A

Results in excessive activity of lipoprotein lipase

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19
Q

What incretins are released by the GI tract in response to a meal?

A

GIP and GLP-1

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20
Q

What does incretin release do in a healthy person? (3)

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A
  • Decrease gastric emptying (satiety)
  • Increase insulin release
  • Reduce glucagon secretion
21
Q

Non-esterified fatty acids increase _______, and more are released from ________ than peripheral fat

Study These Flashcards
A

Insulin resistance; central fat

22
Q

What process are NEFAs released from adipose tissue through?

23
Q

When is NEFA release normally stimulated?

Study These Flashcards
A

When energy demand is high (fasting, exercise)

24
Q

What hormones stimulate NEFA release?

Study These Flashcards
A

Glucagon and adrenaline

25
What does increased intracellular [NEFA] cause?
Serine phosphorylation of insulin receptor (inactivates it)
26
What are adipokines and what do they do?
Protein hormones from fat cells - Increase sensitivity of insulin receptor - Increase enzymes that ox NEFAs
27
Increased NEFA oxidation is mediated by what?
AMP-K = protein kinase activated by metformin
28
Anti-hyperglycaemic adipokines? (2)
- Leptin - Adiponectin
29
Hyperglycaemic adipokines? (2)
- Resistin - Retinol-binding-protein 4
30
Pancreatic pathology: Reduction in the number and size of islets and leukocytic infiltrates in the islets (T-cells, mostly)?
Type 1
31
Pancreatic pathology: Reduction in islet cell mass as well as amyloid deposition around beta cells?
Type 2
32
What type of diabetes involves inflammation and reduction in islet size?
Type 1
33
What are advanced glycation end products (AGEs)?
Metabolic products of glucose non-enzymatically linked to amino groups of intra-and extracellular proteins
34
What do AGEs bind to?
R-AGE on macrophages, T-cells, smooth muscle cells and endothelial cells
35
What does R-AGE binding lead to? (4)
- Release of pro-inflam cytokines - Generation of ROS - Increased procoagulant activity - Prolif of vasc smooth muscle cells and ECM
36
AGEs cause cross-linking of matrix proteins and render them resistant to what?
Proteolysis
37
In the end, what do AGEs contribute to? (4)
- Decreased large artery elasticity - Narrowing of smaller arteries - Atherosclerotic plaques - Increased susceptibility to coagulation
38
Activation of what pathway by hyperglycemia leads to deposition of excess matrix, secretion of pro-inflammatory cytokines, and increased susceptibility to coagulation?
Protein kinase C
39
Endothelial dysfunction predisposes to what?
Atherosclerosis
40
What is a hallmark of diabetic macrovascular disease?
Accelerated atherosclerosis involving aorta and large and medium-sized arteries
41
Most common cause of death in diabetics?
MI caused by atherosclerosis of the coronary arteries
42
Vascular lesion associated with HTN more prevalent and more severe in diabetics?
Hyaline arteriolosclerosis
43
What does amorphous, hyaline thickening of wall of arteries cause?
Narrowing of the lumen
44
Diffuse thickening of basement membranes?
Diabetic microangiopathy
45
Where is diabetic microangiopathy prominent? (5)
- Capillaries of skin - Skeletal muscle - Retina - Renal glomeruli - Renal medulla
46
What does diabetic neuropathy cause the loss of?
- Pain sensation - Loss of vibration, proprioception, fine touch
47
What are some features of autonomic neuropathy? (3)
- Orthostatic hypotension - Incomplete bladder emptying = recurrent infection - Sexual dysfunction
48
Some chronic diabetics develop hyper-osmolar non-ketotic crises (HONK) - what does this result in? (3)
- Severe dehydration - Impaired level of consciousness - Hyper-osmolarity
49
What is an early sign of insulin resistance in some?
Acanthosis nigricans

BMS150 Post-MT2 (17 decks)

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