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(C) CM 1A: Heme/Onc/Endo > Lecture 24: DM Pathophysiology and Epidemiology > Flashcards

Lecture 24: DM Pathophysiology and Epidemiology Flashcards

1
Q

What is the usual fasting BG?

A

70-99 mg/dL

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2
Q

What are the two ways our body raises our BG?

A
  • Glycogenolysis
  • Gluconeogenesis
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3
Q

What kind of glycogenolysis cannot be used in the blood?

A

Skeletal muscle; it is only used by the muscle cells themselves.

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4
Q

What is the secondary source of energy for the brain when glucose is not available?

A

Fatty acids

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5
Q

What are the two forms of fat storage?

A
  • Glycerol
  • Fatty Acids
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6
Q

What happens to our excess proteins? What about if we are in a fasting state?

A

In excess, they get broken down into fatty acids, ketones, or glucose.

In fasting, AAs get broken down if we have insufficient glucose and insulin.

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7
Q

What are the two groups of cells in the pancreas?

A

Pancreatic acini: Digestive juices into duodenum
Islets of Langerhans: Hormone secretion

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8
Q

What secretes insulin? Glucagon?

A

Alpha cells: Glucagon
Beta cells: Insulin

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9
Q

What are the three forms of insulin?

A
  • Preproinsulin
  • Proinsulin (New A-B chain link, no signal peptide)
  • Insulin (C chain cleaved off, just A-B chain.)
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10
Q

How do we measure B-cell function?

A

C-peptide levels, which have long half-lives and are present only in endogenous insulin.

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11
Q

What is the primary regulator of beta cell secretion of insulin?

A

Blood Glucose

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12
Q

What are the primary GLUTs? Where are they found?

A
  • GLUT-2 and 1: Transport glucose into cells, including beta cells.
  • GLUT-4: Skeletal and adipose tissue. Inactive until stimulated by insulin.
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13
Q

What happens to glucose in a beta cell?

A
  1. Phosphorylation of glucose
  2. ATP generation
  3. Inhibition of ATP-sensitive K+ channel
  4. Sulfonylureas can bind to this channel
  5. Beta cell is depolarized, resulting in opening of the voltage-gated calcium channel
  6. Insulin is released.
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14
Q

When insulin is released from the beta cell, what else is released?

A
  • C peptide
  • IAPP (islet amyloid polypeptide)
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15
Q

What opposes the action of insulin in general?

A

Glucagon

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16
Q

What is the function of amylin?

A
  • Regulate plasma glucose concentration with insulin.
  • Decreased postprandial glucagon secretion
  • Slowed gastric emptying
  • Increased satiety
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17
Q

What secretes somatostatin and what is its function?

A

Delta cells in the Islets of Langerhans primarily.

Inhibits the release of insulin and glucagon.

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18
Q

What are incretins and their functions?

A

Gut-derived hormones that promote insulin release after oral nutrient load.

  • Generally accounts for 50% of postprandial insulin secretion.
  • Slowed gastric emptying and increased satiety
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19
Q

What is the effect of epi on glucose?

A

Keeps BG high when stressed.

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20
Q

What do corticosteroids, primarily cortisol, do to blood glucose?

A

Increases it via gluconeogenesis in the liver.

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21
Q

What is DM?

A

Disorder characterized by an imbalance between insulin availability and insulin need.

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22
Q

What cause of death is DM in the US?

A

Number 8!

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23
Q

What is the most common type of T1DM?

A

Type 1A DM (95%), autoimmune destruction of beta cells.

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24
Q

What is T2DM associated with?

A
  • Insulin resistance
  • Inadequate insulin secretion
  • Increased glucose production
25
Q

What is T3DM/other types of DM associated with?

A
  • Pancreatic destruction
  • Genetic defects in production of insulin or glucose
  • Gestational DM (7% of pregnancies)
26
Q

What is Type 1B DM?

A

Idiopathic, usually asian/african origin.

Lacks any associated autoantibodies

27
Q

What is the underlying pathophysiology of T1DM?

A

Insulinopenia.

28
Q

What is the overall treatment for T1DM?

A

Insulin, since they lack the ability to produce it.

29
Q

What are the etiologies that contribute to Type 1A DM?

A
  • 1/3 genetic (HLA genes primarily)
  • 2/3 environmental (milk, hygiene hypothesis, viruses)
30
Q

What is latent autoimmune diabetes in adults? (LADA)

A

Adults with extremely slow progressing T1A DM.

31
Q

How many beta cells need to be destroyed before a patient starts showing s/s of DM?

A

70-80% of beta cells.

32
Q

Describe the process of T1A DM.

A
  1. Islets of Langerhans become infiltrated by lymphocytes
  2. T cells (most likely) destroy beta cells specifically.
  3. No other cells are destroyed usually.
33
Q

What treatment is specifically shown to have poor efficacy in treating T1ADM?

A

Immunosuppressive therapy does NOT work.

34
Q

What autoantibodies tend to be positive for T1ADM?

A
  • Anti-GAD65 (MC)
  • Anti-ZnT8
  • Anti-IA2
  • Islet cell autoantibody (ICA)
  • Anti-insulin autoantibody (IAA)
35
Q

What might cause negative autoantibodies for all tests for someone with T1ADM?

A
  • It declines the longer they have had it.
  • Exogenous insulin use
  • Actually T2DM or gestational
36
Q

What characterizes T2DM?

A

Insensitivity/resistance of tissues to insulin leading to inadequate insulin secretion.

They generally only secrete enough insulin to prevent ketosis.

37
Q

What contributes to the development of T2DM?

A

Genetic: multiple loci associations, such as identical twins or parental hx.

Environmental: Obesity (visceral) is the #1 environmental factor.
Generally obesity, poor nutrition, and high or low birth weight

38
Q

What are the metabolic characteristics of T2DM?

A
  • Impaired insulin secretion and resistance
  • Excessive hepatic glucose production
  • Abnormal fat/lipid and muscle metabolism
39
Q

Early in T2DM, how does the body compensate?

A

Compensatory hyperinsulinemia

40
Q

Over time, what 2 prediabetic abnormalities can occur for prediabetic patients?

A
  • Impaired glucose tolerance due to impaired peripheral tissue uptake of glucose.
  • Impaired fasting glucose due to increased hepatic production of glucose
41
Q

What happens to insulin secretion and sensitivity as someone develops impaired glucose tolerance? (IGT)

A

As IGT progresses, both secretion and sensitivity decrease for insulin.

42
Q

What was the old diabetes triumvirate?

A
  • Abnormal insulin secretion
  • Increased hepatic glucose production
  • Decreased peripheral glucose uptake
43
Q

What is the new perspective regarding the pathophysiology of DM?

A

Ominous octet.

  1. Decreased insulin secretion
  2. Increased hepatic glucose production
  3. Decreased peripheral glucose uptake
  4. Increased lipolysis (increases insulin resistance overall)
  5. Decreased incretin effect (incretins promote insulin release)
  6. Increased glucagon secretion
  7. Increased renal glucose absorption (SLGT2)
  8. NT dysfunction (appetite normally suppressed by insulin)
44
Q

What are the main 2 incretins?

45
Q

What is gestational diabetes?

A

Insulin resistance due to metabolic changes in pregnancy as body prepares for fetus.

46
Q

What characterizes maturity-onset diabetes of the young?

A

Autosomal dominant that causes genetic impairments in the secretion of insulin.

47
Q

When does BG peak postprandial?

A

Generally around 2 hours is the peak BG before it drops down to normal.

48
Q

What are some of the ways we stage diabetes?

A
  • Fasting BG
  • 2h PG (post OGTT)
  • HbA1c
49
Q

What is metabolic syndrome sometimes called?

A

MetS or Syndrome X

50
Q

What does MetS increase the risk of?

A
  • Atherosclerosis
  • Heart disease
  • Stroke
  • Cancer
  • Dementia
  • T2DM
  • ED
51
Q

What is the criteria for MetS?

A

3+ of the following:

  • Waist circumference: > 40in for men, > 35 in for women.
  • Fasting TGs: > 150 or on medication.
  • HDL: < 40 men, < 50 women or on medication
  • BP: > 130 SBP or 85 DBP, or or no medication
  • Fasting BG: > 100 or on medication
52
Q

What are the risk factors of metabolic syndrome?

A
  • Overweight/Obesity
  • Physical inactivity
  • Aging
  • T2DM (75% of T2DM patients meet criteria)
  • CVD (50% of patients also meet criteria)
  • Lipodystrophy
53
Q

What is the primary contributor to metabolic derangements?

A

Insulin resistance.

This results in increased circulating FFAs which further reduces the antilipolytic effect of insulin.

Leptin resistance (secondary)

54
Q

How is HTN affected/caused by insulin resistance?

A

Insulin normally vasodilates without impacting its mild sodium retention.

Hyperuricemia also leads to HTN via RAAS.

55
Q

How do inflammatory cytokines lead to metabolic syndrome?

A

Proinflammatory cytokines increase due to increase in adipose tissue mass.

Anti-inflammatory cytokines like adiponectin decreases.

56
Q

What are some clinical manifestations of MetS?

A
  • Acanthosis Nigricans: velvety darkening of skin folds associated with insulin resistance.
  • Increased waist circumference
  • Hepatic enlargement if liver involvement. (NALFD/steatohepatitis)
  • PCOS
  • Hyperuricemia
  • Obstructive sleep apnea
57
Q

How do we treat MetS primarily?

A

Primary: Weight reduction via caloric restriction.

  • Diet resistriction by 500 kcals/day from their baseline
  • Physical activity 30 mins/day, preferably 60-90 for significant weight loss
  • Anti-obesity drugs
  • Bariatric Surgery
  • Support groups
58
Q

How do we treat other MetS criteria besides obesity?

A
  • Dyslipidemia: restrict dietary cholesterol and maybe statins/fibrates
  • HTN: sodium restriction, ACEI/ARB
  • Hyperglycemia: Restrict carb intake; TZDs or metformin

(C) CM 1A: Heme/Onc/Endo (28 decks)

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