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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
What is the action of GLP-1?
Stimulates insulin secretion (glucose dependent)
26
How is GLP-1 metabolized?
Rapidly by DPP-4 (dipeptidyl peptidase 4)
27
What is GIP?
Glucose Dependent Insulinotropic Peptide, released from K cells in response to glucose/fat intake
28
What is the action of GIP?
Promote insulin biosynthesis, insulin secretion (glucose dependent)
29
How is GIP metabolized?
Rapidly by DPP-4
30
What is the role of Amylin?
Promotes lowering of glucose by: slow gastric empty, suppression of glucagon, increase satiety
31
When are GLP-1 and GIP released?
As you eat/glucose consumption
32
What are glucose levels in an normal prior to a meal?
70-99
33
What should glycemic levels be maintained at?
Fasting: less than 100 After Glycemic Load: Less than 140
34
What happens during a meal?
1. GLP-1 and GIP 2. First Phase 3. Second Phase 4. Decrease in Counter Regulatory Hormones
35
What are the counter regulatory hormones to insulin?
Glucagon, epinephrine, cortisol, and growth hormone
36
Glucagon secreted from pancreatic alpha cells has what action?
Primary effect on the liver to stimulate glycogenolysis and gluconeogenesis
37
In the presence of what is glucagon inhibited?
Glucose
38
What is the role of Epinephrine?
Stimulates hepatic glucose release via glyconeolysis and lipolysis
39
What is the role of Cortisol?
Stimulates hepatic uptake of AA which can be used to produce glucose
40
What is the role of Growth Hormone?
Stimulates lipolysis and inhibits glucose uptake in muscle and adipose tissue
41
What happens when there is absence of insulin in the liver?
Increase glucose production, increase lipolysis and subsequent increase in ketone production
42
What are the 3 main ketones produced?
Beta Hydroxybutyrate, Acetoacetic Acid, and Acetone
43
What happens when there is a lack of insulin in Muscle and Adipose?
Muscle: protein breakdown to release AA for hepatic gluconeogenesis Adipose: increased lipolysis to release free FA for hepatic gluconeogenesis and ketone
44
What is Hemoglobin A1c?
Glucose binds hemoglobin A1, molecule in a concentration dependent manner Marker of glycemia over 2-3 month period
45
What is the goal A1c of a normal person?
4-5.6%
46
What is the goal A1c for diagnosed patient?
<7%
47
What is the goal fasting/preprandial BS of a normal person?
<100 mg/dL
48
What is the goal fasting/preprandial BS of a diagnosed patient?
80-130 mg/dL
49
What is the goal postprandial BS of a normal person?
<140 mg/dL
50
What is the goal postprandial BS of a diagnosed patient?
<180 mg/dL
51
What is the goal bedtime range for a diagnosed person?
100-180 mg/dL
52
What is the estimated correlated FSBS of an A1c of 10%?
240
53
If you are estimating FSBS, if you drop 1% of A1c, what is average drop in BS?
30 aka 9% = (10%) 240-30 = 210
54
When to monitor A1c with Diabetes?
Every 3 months when A1c not at goal Every 6 months when at goal Every 12 months when A1c within pre-diabetes range
55
Screening A1c Recommendations
Risk Factors = Anytime Age 35 and Every 3 years if normal
56
Pre-Diabetes Definition
Blood glucose or A1c levels higher than normal but not high enough to be classified as diabetes
57
What is IFG?
Fasting plasma glucose 100-125 mg/dL
58
What is IGT?
OGTT result with 2 hour plasma glucose of 140-199 mg/dL
59
What is classification of prediabetes?
Patients who meet IFG or IGT criteria A1c 5.7-6.4%
60
Diabetes Diagnostic Criteria
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
Which type of diabetes produce antibodies to B-cells making it an autoimmune disorder, autoantibodies that begin to destroy B-Cells?
Type 1
62
What are the types of antibodies?
Glutamic Acid Decarboxylase 65 GAD65 Islet Cell Antibody ICA Insulin Autoantibody IAA Tyrosine Phosphatases Antibody IA-2
63
What is the pathogenesis of Type 2 DM?
Early resistance to insulin resulting in pancreas compensating with hyperinsulinemia, but normal glycemia Impaired glucose tolerance IGT Impaired fasting tolerance IFT
64
Diagnosis of Metabolic Syndrome (3 out of 5 required)
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
What are the implications of metabolic syndrome?
Inflammation, diabetic dyslipidemia, prothrombotic state, endothelial dysfunction/vascular, and increased risk for CV disease
66
What is GAD and what does it indicate?
Glutamic Acid Decarboxylase Antibody GAD, may indicate LADA aka Type 1 and 1/2
67
What are the laboratory markers of Type 1?
Low serum insulin, Low C-Peptide, Present autoantibodies, High blood glucose, Present glycosuria, High A1c, and Present ketones
68
What are the risk factors for Type 2 DM?
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
What are the laboratory markers of Type 2 DM?
Normal/Elevated serum insulin and C-Peptide, Absent autoantibodies, Elevated glycemia, Elevated A1c, Present glucosuria, Uncommon ketones, and Hyperglycemia hypersomolar syndrome
70
What is DKA?
Diabetic Ketoacidosis, Type 1 Exacerbation
71
What are S/S of DKA?
Abdominal pain, fruity breath, CNS depression, coma, tachycardia, dehydration, and tachypnea
72
What is HHS?
Hyperglycemic Hyperosmolar State, Type 2 Exacerbation, NO ketones
73
What are the S/S of HHS?
Hyperglycemia >1000 mg/dL, lethargy, confusion, hypotension, and tachycardia
74
What are the causes of hyperglycemia?
Associated with suboptimal medication, excessive glucose release from the liver, excessive ingestion of CHO, and medications (steroids)
75
What are symptoms of hyperglycemia?
Polyuria, serum glucose >180 Polyphagia Polydipsia
76
What are the causes of hypoglycemia?
Excessive quantity of medication, more than usual physical activity, and inadequate food intake
77
What are the symptoms of hypoglycemia?
Autonomic: trembling, pounding heart, tachycardia, sweating Neuroglycopenic: blurred vision, slurred speech, numbness, dizziness Other: hunger, nausea, weakness, headache
78
What is released resulting in most of the autonomic symptoms?
Epinephrine
79
What is the treatment for mild hypoglycemia?
Consume 15-20 g of simple CHO Recheck BS in 15-20 mins Repeat treatment if necessary
80
What do you administer during severe hypoglycemia, unresponsive?
Glucagon
81
What are the risks for Gestational Diabetes GDM?
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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