Diabetes #1 Flashcards

1
Q

List (3) examples of first and second generation Sulfonylureas, the medication activity, and the actions.

A

First generation:

  1. chlorpropamide (Diabinese)
  2. tolbutamide (Orinase)
  3. tolazamide (Tolinase)

Second generation:

  1. glipizide (Glucotrol)
  2. glimepiride (Amaryl)
  3. glyburide (Diabeta, Micronase)

Medication Activity:
Secretagogues (increases insulin secretion from the pancreas)

Action:

  • Stimulates insulin secretion
  • Decreases glycogenolysis
  • Improve insulin sensitivity
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2
Q

List (2) examples of Meglitinide analogues, the medication activity, and the actions.

A

Examples of Meglitinide analogues:

  1. repaglinide (Prandin)
  2. nateglinide (Starlix)

Medication activity:
Secretagogues (increases insulin production from pancreas)

Action:
Stimulates insulin secretion

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3
Q

List (2) examples of Alpha-glucosidase inhibitors, the medication activity, and the actions.

A

List (2) examples of Alpha-glucosidase inhibitors:

  1. acarbose (Precose)
  2. miglitol (Glyset)

Medication activity:
Starch blockers

Action:

  • Reduces rate of carbohydrate absorption
  • Slows the digestion of starch
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4
Q

List (1) example of a Biguanide, the medication activity, and the actions.

A

List (1) examples of a Biguanide:
1. metformin (Glucophage)

Medication activity:
Improves insulin effect

Action:

  • Reduces hepatic glycogenolysis
  • Reduces G.I. glucose absorption
  • Improve insulin sensitivity
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5
Q

List (2) examples of Thiazolidinediones (glitizones), the medication activity, and the actions.

A

List (2) examples of Thiazolidinediones:

  1. rosiglitazone maleate (Avandia)
  2. pioglitazone HCl (Actos)

Medication activity:
Improves insulin effect

Action:

  • Increase insulin sensitivity
  • Reduces hepatic glycogenolysis
  • Decreases appetite
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6
Q

List the medication activity and the action of DDP-4 Inhibitors.

A

Medication activity:
Improves action of incretins

Action:
Promotes insulin secretion and glucagon suppression and prolongs incretin actions.

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7
Q

What does a fasting blood glucose level (FBG) of 72-99 mg/dL indicate?

A

Normal FBG

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8
Q

What does a fasting blood glucose level (FBG) of 100-125 mg/dL indicate?

A

Impaired fasting blood glucose (pre-diabetes)

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9
Q

What does a fasting blood glucose level (FBG) of 126+ mg/dL (on more than one occasion) indicate?

A

Diabetes

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9
Q

On an oral glucose tolerance test (OGTT) sample drawn two hours after a 75 g glucose drink, what does a glucose level of 140-199 mg/dL indicate?

A

Impaired glucose tolerance (pre-diabetes)

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10
Q

On an oral glucose tolerance test (OGTT) sample drawn two hours after a 75 g glucose drink, what does a glucose level of < 140 mg/dL indicate?

A

Normal glucose tolerance

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12
Q

On an oral glucose tolerance test (OGTT) sample drawn two hours after a 75 g glucose drink, what does a glucose level of 200+ mg/dL indicate?

A

Diabetes

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13
Q

What are the 5 diagnostic criteria for metabolic syndrome?

How many of the 5 criteria are needed in order to make a diagnosis?

A

Three (3) of the following are required in order to be diagnosed with metabolic syndrome:

  1. Abdominal obesity males 40+ inches, females 35+ inches; both non-Asian)
  2. Triglycerides 150+ mg/ dL (or on medications for high triglycerides)
  3. Low HDL cholesterol (males 130/85 mmHg (or on antihypertensive medications)
  4. Fasting blood glucose >100 mg/dL (or on hypoglycemic medication)
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13
Q

What is the difference in BMI between obesity and being overweight?

A

Overweight: BMI 25-29.9
Obese: BMI >=30

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14
Q

List 3 risk factors for metabolic syndrome.

A
  1. Obesity
  2. Hypertension
  3. Insulin resistance
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16
Q

List 4 signs of insulin resistance.

A
  1. Acanthosis nigricans
  2. Fatigue
  3. Drowsiness after meals
  4. Dyslipidemia
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17
Q

List 2 signs of dyslipidemia.

A
  1. Arcus cornealis (thin gray-white arc at the edge of the cornea)
  2. Xanthelasma (yellowish raised skin plaques usually found along the nose, near the eyelids)
18
Q

Define Gluconeogenesis.

A

Breakdown of proteins/ fats to make glucose

breakdown of fats can lead to problems

19
Q

Define Glycogenolysis.

A

Break down glycogen to make glucose

20
Q

Where does Insulin come from?

A

Islets of Langerhans (beta cells) in pancreas

21
Q

List 5 effects that insulin has on the body.

A
  1. Promotes the intake of glucose movement into cells to be used as energy/ stores
  2. Promotes storage as glycogen
  3. Stops glycogenolysis
  4. Prevents gluconeogenesis
  5. Stimulates enzymes for energy production
22
Q

Name 3 things Glucagon does during fasting.

A
  1. Promotes glyconolysis
  2. Inhibits glycogen storage
  3. Stimulates gluconeogenesis
23
Q

List the secretion location and timing of Glucogon-like peptide 1 (GLP-1), its 6 actions, and the physiologic effects on glucose levels.

A
  1. Secreted by cells in the intestines (when nutrients in intestines)
  2. Actions of GLP-1:
    - Increases insulin secretion (glucose-dependent)
    - Decreases secretion of glucagon
    - Inhibit gastric acid secretion: digest food slower
    - Delay gastric emptying
    - Promote insulin sensitivity
    - Increase satiety
  3. Result: Glucose levels stay low, due to secreted insulin
24
Q

List the secretion location of Glucose dependent insulinotropic polypeptide (GIP), its action, its relative level in Type II diabetics, and the result.

A
  1. Secreted by duodenum & jejunum
  2. Action of GIP:
    Causes insulin secretion, decreasing blood sugar levels
  3. In T2DM, GIP is lower than normal
  4. Result: Body may not recognize insulin
25
List 4 actions of Amylin and its physiologic effect on glucose levels.
Actions: - Supplements action of insulin - Suppresses postprandial gluagon secretion - Regulates gastric emptying - Increases satiety 2. Result: Decreases blood glucose levels
26
Describe the action of Dipeptidyl pepdidase IV (DPD-IV), and the resulting physiologic effect on glucose levels.
1. Effects glucose metabolism by breaking down incretins | 2. Result of DPD-IV: Blood glucose levels rise because the blood sugar lowering effects of incretins would be lower
27
Describe Insulin issues in T1DM and T2DM. Fill in the blanks: in diabetics, the body thinks it’s ________, even though there is technically a lot of ______ available
1. Problems with production (Type I) or recognition (Type II) 2. In diabetics, the body thinks it’s starving, even though there is technically a lot of glucose available.
28
What are diabetic complications related to?
Hyperglycemia, as blood glucose continues to rise.
29
How does polyuria occur in diabetics?
Kidney still work, & as renal threshold is reached for glucose, excretion increased via osmotic diuresis [Sugar = high osmotic pressure, therefore a lot of H2O brought with it]
30
What are the 3 hallmark symptoms of DM and why do they occur?
Hallmark Symptoms of DM: 1. Polyuria 2. Polydipsia 3. Polyphagia
31
Describe polyphagia in diabetics.
Polyphagia: cells aren’t getting enough glucose, so hunger drives are heightened and client end up gaining weight.
32
When ______ is released, gluconeogenesis occurs in the diabetic client.
Glucagon
33
What is the result of gluconeogenesis?
When fats are broken down, FAs converted into ketones, client becomes acidotic
34
Describe the first correction attempt for diabetic ketoacidosis. Why might this correction potentially fail?
Sodium bicarbonate produced, but may not be enough sodium available (due to electrolyte imbalance from polyuria)
35
Describe the second correction attempt for diabetic ketoacidosis, its purpose, its s/sx, and a potential misinterpretation.
1. Breathing rate/ depth increased (“Kussmaul respirations”) 2. Purpose: blowing off acetone 3. S/sx: - Fruity-smelling breath - Gait problems 4. Misinterpretation: May be confused with alcohol problems, due to breath/ gait
36
Describe 3 Characteristics of T1DM.
1. Autoimmune disease 2. Insulin not produced 3. Progressive destruction of Beta cells
37
What is the effect of insulin secretion increasing oral meds on a client with T1DM? What do they require as medicinal therapy?
1. T1DM are not affected by oral insulin secretion increasing oral meds 2. Client would need insulin therapy for life
38
Describe genetic predisposition to T1DM and how the disease is thought to occur.
1. Not directly inheritable | 2. Response to beta-cell-like proteins, and then to beta cells themselves
39
Describe the blood test for T1DM. Does everyone receive it?
1. Looks for serum Islet Cell Antibodies (ICAs) [Is a predictor for Type I Diabetes, if elevated] 2. Not ordered on all patients
40
Describe the onset, requirements, and age of development of T1DM.
1. Acute onset: 3 hallmark symptoms develop quickly, may live with for a long time before reporting 2. Req insulin injections/ pump 3. Usually develops in child-YA, <30 y/o [Now Type II is becoming more common, due to obesity]
41
Remember your jingle for hyper- vs. hypoglycemia: "Hot & dry: ____ ______ Cold & Clammy: _____ _____ ______"
Hot & Dry: Sugar High | Cold & Clammy: Needs Some Candy
42
How many units per kilogram per day of insulin are generally given per day, for non-pregnant women?
0.5-0.7 | Start low, Move up if needed.