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Endocrine Module > Diabetes Pathophysiology > Flashcards

Diabetes Pathophysiology Flashcards

1
Q

What are the sources of glucose (a primary energy source)?

A

Food, Glycogen Stores, and Liver

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2
Q

What is the primary macronutrient used for energy?

A

Carbohydrate CHO

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3
Q

What is catabolism of CHO?

A

Glycogenolysis

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4
Q

What is the synthesis of CHO called?

A

Gluconeogenesis or Glycogenesis, it synthesizes glucose during glucose deficiencies

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5
Q

Glycogenolysis is what?

A

Process of breaking down CHO for QUICK energy

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6
Q

Glycogenesis is what?

A

Converting CHO to glycogen for storage (skeletal muscle, liver, fat)

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7
Q

Protein synthesis is stimulated by what?

A

Insulin, because insulin moves glucose from blood into storage

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8
Q

B-Cells in the pancreas produce what?

A

Insulin and Amylin

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9
Q

A-Cells in the Pancreas produces what?

A

Glucagon

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10
Q

What hormones are utilized to decrease glycemia?

A

Insulin, incretin hormones, and amylin

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11
Q

What hormones are utilized to increase glycemia?

A

Glucagon, epinephrine, cortisol, and growth hormone

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12
Q

What is the incretin effect?

A

Orally administered glucose CHO, is the primary stimulus for insulin secretion

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13
Q

Where does insulin go first when secreted?

A

Liver

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14
Q

Basal Release is what?

A

Continuously secreted insulin from the pancreas

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15
Q

Bolus Release is broken into what?

A

First Phase and Second Phase

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16
Q

First Phase Bolus is:

A

Peak in insulin secretion in response to meals, shuts down hepatic glucose production

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17
Q

Second Phase Bolus is:

A

delayed, mostly used in periphery

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18
Q

What is the key action of insulin?

A

Insulin promotes glucose uptake, without it there is no glucose uptake

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19
Q

What are the 3 general actions of insulin?

A

Lowering of blood glucose, promotes storage of glucose, and promotes potassium intake

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20
Q

What are the effects of insulin in the liver?

A

Promote glucose uptake, stimulate glycogen storage, synthesis of triglycerides, and inhibits glycogenolysis

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21
Q

Insulin Action in Muscle and Adipose

A

Both have increase glucose uptake, muscle = AA, adipose = triglycerides

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22
Q

What is the major source of elimination for endogenous insulin?

A

Liver

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23
Q

What are the insulin requiring tissues?

A

Muscle and Adipose

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24
Q

What is GLP-1?

A

Glucagon Like Peptide that is released by L-cells in the intestine in response to glucose

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25
Q

What is the action of GLP-1?

A

Stimulates insulin secretion (glucose dependent)

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26
Q

How is GLP-1 metabolized?

A

Rapidly by DPP-4 (dipeptidyl peptidase 4)

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27
Q

What is GIP?

A

Glucose Dependent Insulinotropic Peptide, released from K cells in response to glucose/fat intake

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28
Q

What is the action of GIP?

A

Promote insulin biosynthesis, insulin secretion (glucose dependent)

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29
Q

How is GIP metabolized?

A

Rapidly by DPP-4

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30
Q

What is the role of Amylin?

A

Promotes lowering of glucose by: slow gastric empty, suppression of glucagon, increase satiety

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31
Q

When are GLP-1 and GIP released?

A

As you eat/glucose consumption

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32
Q

What are glucose levels in an normal prior to a meal?

A

70-99

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33
Q

What should glycemic levels be maintained at?

A

Fasting: less than 100
After Glycemic Load: Less than 140

34
Q

What happens during a meal?

A
  1. GLP-1 and GIP
  2. First Phase
  3. Second Phase
  4. Decrease in Counter Regulatory Hormones
35
Q

What are the counter regulatory hormones to insulin?

A

Glucagon, epinephrine, cortisol, and growth hormone

36
Q

Glucagon secreted from pancreatic alpha cells has what action?

A

Primary effect on the liver to stimulate glycogenolysis and gluconeogenesis

37
Q

In the presence of what is glucagon inhibited?

38
Q

What is the role of Epinephrine?

A

Stimulates hepatic glucose release via glyconeolysis and lipolysis

39
Q

What is the role of Cortisol?

A

Stimulates hepatic uptake of AA which can be used to produce glucose

40
Q

What is the role of Growth Hormone?

A

Stimulates lipolysis and inhibits glucose uptake in muscle and adipose tissue

41
Q

What happens when there is absence of insulin in the liver?

A

Increase glucose production, increase lipolysis and subsequent increase in ketone production

42
Q

What are the 3 main ketones produced?

A

Beta Hydroxybutyrate, Acetoacetic Acid, and Acetone

43
Q

What happens when there is a lack of insulin in Muscle and Adipose?

A

Muscle: protein breakdown to release AA for hepatic gluconeogenesis
Adipose: increased lipolysis to release free FA for hepatic gluconeogenesis and ketone

44
Q

What is Hemoglobin A1c?

A

Glucose binds hemoglobin A1, molecule in a concentration dependent manner
Marker of glycemia over 2-3 month period

45
Q

What is the goal A1c of a normal person?

46
Q

What is the goal A1c for diagnosed patient?

47
Q

What is the goal fasting/preprandial BS of a normal person?

A

<100 mg/dL

48
Q

What is the goal fasting/preprandial BS of a diagnosed patient?

A

80-130 mg/dL

49
Q

What is the goal postprandial BS of a normal person?

A

<140 mg/dL

50
Q

What is the goal postprandial BS of a diagnosed patient?

A

<180 mg/dL

51
Q

What is the goal bedtime range for a diagnosed person?

A

100-180 mg/dL

52
Q

What is the estimated correlated FSBS of an A1c of 10%?

53
Q

If you are estimating FSBS, if you drop 1% of A1c, what is average drop in BS?

A

30
aka 9% = (10%) 240-30 = 210

54
Q

When to monitor A1c with Diabetes?

A

Every 3 months when A1c not at goal
Every 6 months when at goal
Every 12 months when A1c within pre-diabetes range

55
Q

Screening A1c Recommendations

A

Risk Factors = Anytime
Age 35 and Every 3 years if normal

56
Q

Pre-Diabetes Definition

A

Blood glucose or A1c levels higher than normal but not high enough to be classified as diabetes

57
Q

What is IFG?

A

Fasting plasma glucose 100-125 mg/dL

58
Q

What is IGT?

A

OGTT result with 2 hour plasma glucose of 140-199 mg/dL

59
Q

What is classification of prediabetes?

A

Patients who meet IFG or IGT criteria
A1c 5.7-6.4%

60
Q

Diabetes Diagnostic Criteria

A

A1c >6.5% OR,
Fasting plasma glucose >126 mg/dL OR,
Symptoms of hyperglycemia and random plasma glucose >200 mg/dL OR,
OGTT with 2 hour plasma glucose >200 mg/dL

61
Q

Which type of diabetes produce antibodies to B-cells making it an autoimmune disorder, autoantibodies that begin to destroy B-Cells?

62
Q

What are the types of antibodies?

A

Glutamic Acid Decarboxylase 65 GAD65
Islet Cell Antibody ICA
Insulin Autoantibody IAA
Tyrosine Phosphatases Antibody IA-2

63
Q

What is the pathogenesis of Type 2 DM?

A

Early resistance to insulin resulting in pancreas compensating with hyperinsulinemia, but normal glycemia
Impaired glucose tolerance IGT
Impaired fasting tolerance IFT

64
Q

Diagnosis of Metabolic Syndrome (3 out of 5 required)

A

Abdominal Obesity (>40 M, >35 W)
Elevated triglycerides >150
Elevated BP >130/85 or on medication
Elevated fasting glucose >110
Low HDL <40 M, <50 W

65
Q

What are the implications of metabolic syndrome?

A

Inflammation, diabetic dyslipidemia, prothrombotic state, endothelial dysfunction/vascular, and increased risk for CV disease

66
Q

What is GAD and what does it indicate?

A

Glutamic Acid Decarboxylase Antibody GAD, may indicate LADA aka Type 1 and 1/2

67
Q

What are the laboratory markers of Type 1?

A

Low serum insulin, Low C-Peptide, Present autoantibodies, High blood glucose, Present glycosuria, High A1c, and Present ketones

68
Q

What are the risk factors for Type 2 DM?

A

BMI >25 or >23 in Asian Americans, history or impaired glucose tolerance, physical inactivity, family history of diabetes, high risk ethnicity, history of gestational diabetes, HTN, low HDL, triglycerides >250, polycystic ovary disease, other conditions associated w/insulin resistance, history of CV disease, and metabolic syndrome

69
Q

What are the laboratory markers of Type 2 DM?

A

Normal/Elevated serum insulin and C-Peptide, Absent autoantibodies, Elevated glycemia, Elevated A1c, Present glucosuria, Uncommon ketones, and Hyperglycemia hypersomolar syndrome

70
Q

What is DKA?

A

Diabetic Ketoacidosis, Type 1 Exacerbation

71
Q

What are S/S of DKA?

A

Abdominal pain, fruity breath, CNS depression, coma, tachycardia, dehydration, and tachypnea

72
Q

What is HHS?

A

Hyperglycemic Hyperosmolar State, Type 2 Exacerbation, NO ketones

73
Q

What are the S/S of HHS?

A

Hyperglycemia >1000 mg/dL, lethargy, confusion, hypotension, and tachycardia

74
Q

What are the causes of hyperglycemia?

A

Associated with suboptimal medication, excessive glucose release from the liver, excessive ingestion of CHO, and medications (steroids)

75
Q

What are symptoms of hyperglycemia?

A

Polyuria, serum glucose >180
Polyphagia
Polydipsia

76
Q

What are the causes of hypoglycemia?

A

Excessive quantity of medication, more than usual physical activity, and inadequate food intake

77
Q

What are the symptoms of hypoglycemia?

A

Autonomic: trembling, pounding heart, tachycardia, sweating
Neuroglycopenic: blurred vision, slurred speech, numbness, dizziness
Other: hunger, nausea, weakness, headache

78
Q

What is released resulting in most of the autonomic symptoms?

A

Epinephrine

79
Q

What is the treatment for mild hypoglycemia?

A

Consume 15-20 g of simple CHO
Recheck BS in 15-20 mins
Repeat treatment if necessary

80
Q

What do you administer during severe hypoglycemia, unresponsive?

81
Q

What are the risks for Gestational Diabetes GDM?

A

Macrosomia, excessive maternal weight gain >40 lbs, preeclampsia, still birth, neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia, respiratory distress syndrome,
Increased risk of baby developing DM2, obesity, or metabolic syndrome
Increased risk of maternal development of DM2

Endocrine Module (16 decks)

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