Exam #4: Pathophysiology of DM Flashcards Preview

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Flashcards in Exam #4: Pathophysiology of DM Deck (15)
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1
Q

What are the distinguishing features between Type I and Type II DM related to B-cell function?

A

Type I= absolute beta cell destruction leading to beta cell destruction
- Decrease in beta-cell mass

Type II= insulin resistance followed by an insulin secretory defect
- Increase in beta-cell mass

*Note that there are 2x subtypes of DM-I, a & b. A= autoimmune, B= idiopathic–diagnosis is based on NOT finding autoantibodies

2
Q

What are the distinguishing features between Type I and Type II DM related to insulin sensitivity?

A
  • In type-II DM the body is NOT responding to insulin i.e. a decrease in insulin sensitivity, which initially results in an INCREASE in insulin secretion–a compensatory mechanism
  • Type I, the body simply is NOT producing insulin
3
Q

What are the distinguishing features between Type I and Type II DM related to blood glucose levels?

A

Generally, normal fasting blood glucose level is ~95 mg/dL

DM= higher fasting glucose, higher peak glucose, and longer time to return to normal

*Note that this is assuming some insulin activity i.e. DM-II, in DM-I, glucose levels simply continue to rise following glucose challenge.

4
Q

What are the distinguishing features between Type I and Type II DM related to ketone production?

A

Type I is more commonly associated with ketogenesis and the development of DKA

5
Q

Describe the significance of obesity, genetics, environment, and the immune system in the development of Type I DM.

A

Type 1= insulin-dependent DM

  • genetic predisposition
  • typically immune mediated i.e. autoantibodies to B-cells that are detectable PRIOR to the onset of symptoms
  • environmental trigger via a virus or toxin–antigenic exposure may play a role as well

*****Note that key genes associated with DM-I are located on the MHC the locus. Also, despite the presence of autoantibodies in DM-I, these do NOT destroy the pancreas; rather, INFILTRATION OF T-LYMPOCYTES causes destruction of B-cells

6
Q

Describe the significance of obesity, genetics, environment, and the immune system in the development of Type II DM.

A
  • There is a strong correlation between visceral adiposity and DM-II
  • However, there is also a genetic correlation related to B-cell function & turnover (e.g. twin studies–one twin has DM-II, the other has 90% chance of having it as well, which is HIGER than the same study in DM-I)
  • Environmental= low physical activity and high caloric/fat intake are major contributing environmental factors to the development of DM-II
7
Q

What are the signs and symptoms of Type I DM?

A
  • Osmotic diuresis leads to POLYURIA
  • POLYDIPSIA (thirst) due to a hyperosmolar state
  • Blurred vision due to hyperosmolar state
  • Weight loss
  • Weakness/ Dizziness
  • Paresthesias
  • Depressed level of consciousness that is more severe with rapid insulin deficiency
8
Q

What are the signs and symptoms of Type II DM?

A

1) Asymptomatic initially
2) Infections become more frequent b/c of the energy (glucose) source for microorganisms
3) Neuropathy
4) Classic severe insulin deficiency signs occurs late in the progression of symptoms
5) Obesity & metabolic syndrome

*****#4, note that type II DM becomes apparent when the Beta-cells are no longer able to compensate for increased resistance to insulin

9
Q

What are the metabolic changes that occur in patients in Type I DM?

A
  • Cells think that they’re starving b/c they don’t have glucose in the cell; thus, they try to mobilize energy, leading to…
  • Gluconeogenesis
  • Glycogenolysis
  • Ketogenesis
10
Q

What are the metabolic changes that occur in Type II DM patients?

A

Metabolic Syndrome:

1) Hyperinsulinemia
2) Dyslipidemia
3) HTN

11
Q

What are the therapeutic strategies employed & rationale for these strategies in treating Type I DM?

A

1) Diet i.e. balanced carbs, fat, and protein

2) Patient education on:
- Carb counting
- Insulin action
- Blood glucose targets

3) Insulin ABSOLUTELY required it must be non-PO route b/c insulin is a peptide that will be degraded in the GI tract

12
Q

What are the therapeutic strategies employed & rationale for these strategies in treating Type II DM?

A

First, remember that potential therapies for the DM may have a negative impact on the overall Metabolic Syndrome in DM-II, which presents a challenge to treating DM-II

1) Diet
2) Patient education
3) Pharmacologic strategies

*Insulin is used ONLY when other agents DO NOT allow for achievement of therapeutic goals

13
Q

What are the acute complications potentially experienced by DM patients? How are these addressed?

A

Hypoglycemia (e.g. insulin overdose)

  • Glucose
  • Glucagon

DKA

  • Restore plasma volume
  • Reduce blood glucose
  • Correct acidosis
  • Replenish electrolytes
14
Q

Outline the different pharmacological strategies that are used to treat DM-II.

A

1) Increase insulin secretion
2) Increase insulin action
3) Inhibit gluconeogenesis
4) Inhibit glucose digestion & absorption from the GI tract
5) Suppress glucagon secretion

15
Q

How can you pharmacologically increase insulin secretion in DM-II?

A
  • GLP1 analogs are used to activate GLP1 receptors to promote insulin secretion
  • DPP4 (enzymes that breaks down GLP1) inhibitors, which indirectly promote insulin secretion
  • Inhibition of ATP-sensitive K+ channels on B-cells to eventually cause insulin release

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