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BMS150 Post-MT2 > Type II Diabetes Mellitus > Flashcards

Type II Diabetes Mellitus Flashcards

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)

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

A

Insulin resistance; central fat

22
Q

What process are NEFAs released from adipose tissue through?

A

Lipolysis

23
Q

When is NEFA release normally stimulated?

A

When energy demand is high (fasting, exercise)

24
Q

What hormones stimulate NEFA release?

A

Glucagon and adrenaline

25
Q

What does increased intracellular [NEFA] cause?

A

Serine phosphorylation of insulin receptor (inactivates it)

26
Q

What are adipokines and what do they do?

A

Protein hormones from fat cells
- Increase sensitivity of insulin receptor
- Increase enzymes that ox NEFAs

27
Q

Increased NEFA oxidation is mediated by what?

A

AMP-K = protein kinase activated by metformin

28
Q

Anti-hyperglycaemic adipokines? (2)

A
  • Leptin
  • Adiponectin
29
Q

Hyperglycaemic adipokines? (2)

A
  • Resistin
  • Retinol-binding-protein 4
30
Q

Pancreatic pathology: Reduction in the number and size of islets and leukocytic infiltrates in the islets (T-cells, mostly)?

A

Type 1

31
Q

Pancreatic pathology: Reduction in islet cell mass as well as amyloid deposition around beta cells?

A

Type 2

32
Q

What type of diabetes involves inflammation and reduction in islet size?

A

Type 1

33
Q

What are advanced glycation end products (AGEs)?

A

Metabolic products of glucose non-enzymatically linked to amino groups of intra-and extracellular proteins

34
Q

What do AGEs bind to?

A

R-AGE on macrophages, T-cells, smooth muscle cells and endothelial cells

35
Q

What does R-AGE binding lead to? (4)

A
  • Release of pro-inflam cytokines
  • Generation of ROS
  • Increased procoagulant activity
  • Prolif of vasc smooth muscle cells and ECM
36
Q

AGEs cause cross-linking of matrix proteins and render them resistant to what?

A

Proteolysis

37
Q

In the end, what do AGEs contribute to? (4)

A
  • Decreased large artery elasticity
  • Narrowing of smaller arteries
  • Atherosclerotic plaques
  • Increased susceptibility to coagulation
38
Q

Activation of what pathway by hyperglycemia leads to deposition of excess matrix, secretion of pro-inflammatory cytokines, and increased susceptibility to coagulation?

A

Protein kinase C

39
Q

Endothelial dysfunction predisposes to what?

A

Atherosclerosis

40
Q

What is a hallmark of diabetic macrovascular disease?

A

Accelerated atherosclerosis involving aorta and large and medium-sized arteries

41
Q

Most common cause of death in diabetics?

A

MI caused by atherosclerosis of the coronary arteries

42
Q

Vascular lesion associated with HTN more prevalent and more severe in diabetics?

A

Hyaline arteriolosclerosis

43
Q

What does amorphous, hyaline thickening of wall of arteries cause?

A

Narrowing of the lumen

44
Q

Diffuse thickening of basement membranes?

A

Diabetic microangiopathy

45
Q

Where is diabetic microangiopathy prominent? (5)

A
  • Capillaries of skin
  • Skeletal muscle
  • Retina
  • Renal glomeruli
  • Renal medulla
46
Q

What does diabetic neuropathy cause the loss of?

A
  • Pain sensation
  • Loss of vibration, proprioception, fine touch
47
Q

What are some features of autonomic neuropathy? (3)

A
  • Orthostatic hypotension
  • Incomplete bladder emptying = recurrent infection
  • Sexual dysfunction
48
Q

Some chronic diabetics develop hyper-osmolar non-ketotic crises (HONK) - what does this result in? (3)

A
  • Severe dehydration
  • Impaired level of consciousness
  • Hyper-osmolarity
49
Q

What is an early sign of insulin resistance in some?

A

Acanthosis nigricans

BMS150 Post-MT2 (17 decks)

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