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Physiology > DM > Flashcards

DM Flashcards

1
Q

What is type Ia DM?

A

Immune mediated destruction of islet cells

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2
Q

What is type Ib DM?

A

idiopathic destruction of islet cells

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3
Q

What is the endocrinopathy that causes DM?

A

Somtatostatinoma

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4
Q

What are the diseases that can lead to DM?

A

Pancreatitis, CF, CA

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5
Q

What is the hormone that causes GDM?

A

Progesterone

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6
Q

What is the normal fasting plasma glucose levels?

A

<100 mg/dL

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7
Q

What is the normal plasma glucose level 2 hours after a meal?

A

<140 mg/dL

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8
Q

What is the diabetic fasting bg level?

A

> 126 mg/dL

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9
Q

What is the diabetic bg level 2 hours after glucose load?

A

> 200 mg /dL

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10
Q

What are the cells that are destroyed in DM I?

A

Beta cell destruction

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11
Q

True or false: any drop in beta cells will change bg levels?

A

False-there are more beta cells that needed to meet demand

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12
Q

What are the genes that are associated with DM I?

A

DQ and DR genes of the MHC class II

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13
Q

What are the two haplotypes that are associated with DM I?

A

DR3 and DR4

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14
Q

What are the antibodies that can be detected in DM I?

A

autoantibodies to islet cells, insulin, others

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15
Q

Are the antibodies responsible for the destruction of islet Beta cells?

A

no, infiltration of activated T lymphocytes in beta cells is.

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16
Q

What are the two possible triggers for DM I?

A

Toxins or viruses

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17
Q

What is the effect of breastfeeding on the development of DM I?

A

Decreases risk

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18
Q

What is the effect of living in first world countries on DM I?

A

Increases risk

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19
Q

How could viruses theoretically cause the development of DM I?

A

Molecular mimicry

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20
Q

What happens to gluconeogenesis in DM I?

A

increases

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21
Q

What happens to glycogenolysis in DM I?

A

Increases

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22
Q

What happens to glycolysis in DM I?

A

Decreases

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23
Q

What happens to lipolysis/ketone production in DM I?

A

Increases

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24
Q

What causes blurred vision seen in DM I?

A

Hyperosmolar state

25
Q

What causes the weight loss seen in DM I?

A

Depletion of water

Loss of muscle mass

26
Q

What causes the weakness/dizziness seen in DM I?

A

Postural hypotension

K loss and loss of muscle catabolism

27
Q

What causes the paresthesias seen in DM I?

A

Temporary peripheral sensory nerve dysfunction

28
Q

What causes LOC with DM I?

A

Dehydration of tissues

DKA

29
Q

What are the three ways to manage DM I?

A

Diet
Edu
Insulin

30
Q

Why can insulin not be given PO?

A

Peptide would be degraded by GI

31
Q

What are the two causes of DM II?

A

Insulin resistance or secretory defect (or both)

32
Q

What happens to Beta cell mass in DM II?

A

Increase since there is no uptake of glucose

33
Q

What happens to the insulin receptors in DM II?

A

Less of them OR decrease affinity to insulin

34
Q

What are the three adipokines?

A

Leptin
IL-6
TNF-alpha

35
Q

What is the effect of adipokines?

A

Recruits immune cells

36
Q

Can an increase in insulin and beta cell mass overcome insulin resistance?

A

Yes

37
Q

What causes the increased beta cell stress in DM II?

A

Increased ER stress
Adipokines
Ectopic fat deposition in islets

38
Q

What is metabolic syndrome?

A

Hyperglycemia associated with:

Hyperinsulinemia
Dyslipidemia
HTN

39
Q

Metabolic syndrome can lead to what?

A

CAD and Stroke

40
Q

What is the effect of insulin on Na retention?

A

Increases

41
Q

What is the effect of insulin on VLDL secretion?

A

Increases

42
Q

What is the effect of insulin on vascular smooth muscle cell proliferation? What does this result in?

A

Increases–results in atherosclerosis

43
Q

What is the significance of metabolic syndrome on management?

A

Changes therapeutic approach

44
Q

Which DM type has a higher concordance rate between monozygotic twins?

A

Type II

45
Q

What are the genes that predispose someone to DM II involved in?

A

Beta cell function

46
Q

Why are infections more common in DM II?

A

high sugar blood = good for bacteria

47
Q

What are the classic, severe signs/symptoms of DM II?

A

Polyuria, polydipsia, blurred vision, weakness

48
Q

What are the pharmacologic strategies toward DM II?

A
  1. Increase insulin secretion or action
  2. Inhibits gluconeogenesis
  3. Inhibit glucose digestion/absorption
  4. Suppress glucagon
49
Q

What is the effect of drugs that mimic GLP1 on treating DM II?

A

Promotes insulin secretion

50
Q

What is the effect of drugs that inhibit DDPP4 on treating DM II?

A

inhibits GLP1 degradation

51
Q

What is the effect of drugs that sulfonylurease and meglitinde analogs on treating DM II?

A

Inhibits that ATP sensitive K pump on beta cells which closes the channel and causes a depolarization

52
Q

What is the effect of drugs that thiazolidinediones on treating DM II?

A

Promote the expression of GLUT1 and GLUT4, and thus increase glucose uptake in peripheral tissues

53
Q

What are the symptoms of hypoglycemia?

A 
Tachycardia
Sweating
Tremors
Nausea
Hunger
54
Q

What are neuroglycopenia symptoms

A 
Irritability
Confusion
HA
Speech difficulty
Blurred vision
LOC
55
Q

What is the treatment for hypoglycemia?

A

Glucagon/glucose

56
Q

What causes DKA?

A

insulin deficiency causes lipolysis, causing acidification of the blood

57
Q

When is DKA seen in DM II pts?

A

Sepsis, trauma, or surgery

58
Q

What are the treatment goals of DKA?

A

Restore plasma volume
Reduces glucose
Correct acidosis
Replenish electrolytes

Physiology (75 decks)

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