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Dental Pharm Exam 5 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Secretory Cells of Diabetes?

A

Acinar Cells

Islets cells of Langerhans

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2
Q

What are acinar cells?

A

Part of the exocrine pancreas that secretes digestive enzymes

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3
Q

What is the anatomy of Langerhans cells?

A

*Endocrine Pancreas
1. Islet Core
-Beta Cells: Insulin and Amylin Secreting
2. Islet Mantle
Alpha: Glucagon secreting
Delta: somatostatin
PP/F: pancreatic polypeptide
Epsilon: ghrelin

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4
Q

What is the role of the endocrine pancreas?

A
  1. Coordinate flow of glucose, FFA, and other substrate molecules
  2. Mobilization of stored fuels during fasting
  3. Delivery and storage of fuels during feeding
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5
Q

What happens in the pancreas with high blood glucose in a healthy person?

A
  1. High Blood Glucose acts on Pancreas to release insulin from Beta Cells
  2. Cells take up glucose from the blood, Liver produces glycogen
  3. Blood Glucose Falls
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6
Q

What happens in the pancreas w/ low blood glucose in a healthy person?

A
  1. Low blood glucose acts on pancrease to release glucagon form alpha cells
  2. Liver breaks down glycogen
  3. Blood glucose rises
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7
Q

How is glucose released from Beta Cells in the pancreas?

A
  1. Glucose Transported into cells via GLUT2
  2. Oxidative metabolism increases intracellular ATP
  3. Increased ATP inhibits K Channels
  4. Less K exit = depolarization
  5. Depol opens voltage dependent calcium channels
  6. Calcium promotes granular release of insulin into circulation
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8
Q

What are the cellular actions of insulin?

A
  1. Insulin binds and activates insulin receptors
  2. Sends a signal to effect gene expression/growth regulation as well as a signal to GLUT4
  3. GLUT 4 moves extracellular glucose intracellularly, which is then utilitzed by glycogen/lipid/protein synthesis
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9
Q

What 3 places is insulin used, what does not require insulin to utilitze glucose?

A
  1. Muscle, Liver, Fat

2. Brain

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10
Q

What happens to the brain, muscles, liver, and fat w/o insulin?

A
  1. Brain is ensured energy in the forms of glucose and ketone bodies
  2. No glucose uptake into skeletal muscle
  3. New glucose is synthesized and glycogen is broken down in the liver
  4. Fat is broken down to generate FFA, which are converted into ketone bodies in the liver
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11
Q

How does insulin regulate glucose?

A
  1. Promotes glucose utlilization
  2. Decreases Circulating Glucose
  3. Decreases Glucagon Secretion
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12
Q

What can upregulate glucose?

A
  1. Glucagon
  2. Epinephrine
  3. Glucocorticoids
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13
Q

How do glucagon/epi/glucocorticoids regulate glucose?

A
  • Opposite effects of glucose
    1. Increase Glucose Production
    2. Promote breakdown of glycogen
    3. Decrease insulin secretion/insulin receptor expression
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14
Q

What is hyperglycemia?

A

Unopposed mobilization of glucose

*stress-induced hormone secretion can work against insulin/anti-diabetic drug effects

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15
Q

What does diabetes mellitus refer to?

A
  • its a family of disorders in which nutrient metabolism is impaired as a consequence of impaired insulin production or responsiveness
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16
Q

What are the types of diabetes mellitus and what is the incidence?

A
  1. Type I insulin dependent DM (IDDM): 5%
  2. Type II noni-insulin dependent DM (NIDDM): >90%
    * Gestational DM (Type IV), Diabetes secondary to disease or drug admin (Type III)
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17
Q

What is the most predominant syptom of diabetes mellitus and what acute syptoms are related to it?

A 
1. Hyperglycemia: consequence of elevated circulating glucose level
Acute symptoms:
1. Fatigue
2. Increased Urination
3. Dehydration
4. Weight Loss
5. Blurred Vision
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18
Q

What type of diabetes is associated w/ ketoacidosis?

A

Type 1

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19
Q

What is hemoglobin A1c and what does it do?

A
  1. Glycated hemoglobin in RBC
  2. Serves as maker for avg blood glucose levels over the previous months prior to the measurement
    * Requires lab testing
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20
Q

Symptoms of controlled diabetes: chronic hyperglycemia

A
  1. Retinopathy, claucoma, catereacts
  2. High BP (HTN)
  3. Atherosclerosis/CHD
  4. Peripheral Neuropahty
  5. Kidney damage/failure
  6. Poor circulation/neuropathy in feet = ulcerations and infections
    * susceptibility to all types of infection
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21
Q

Facts and tx for Type 1 diabetes

A
  1. Aka juvinile onset
  2. Absolute insulin deficiency, emerges at young age, autoimmune destruction of pancreatic Beta cells
    Tx: insulin (can add synthetic amylin)
    Goal: maintain blood glucose w/in normal limits
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22
Q

What is the source and administration of insulin?

A
  1. Human insulin form recombinant DNA

2. Admin subccutneously as a solution or suspension: can’t be take orally

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23
Q

What are the preparations of insulin?

A
  1. Ultra-short acting: insulin lispro
  2. Short acting: regular insulin
  3. Intermediate acting: NPH insulin
  4. Long acting
    * Can use mixtures or multiple-dosing regimens
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24
Q

Insulin Lispro onset, peak, duration

A

15-30min
1-2 hr peak
4-6 hr duration
Mimics feeding

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25
Q

Insulin - onset/peak/duration

A

30-60min
2-3 hr peak
6-8 hr duration

26
Q

NPH insulin O/P/D?

A

2-4 hr onset
4-6 hr peak
14-18 hr Duration

27
Q

Long acting insulin drugs?

A
  1. Insulin Glargine
  2. Insulin Detemir
    Delayed onset (hours) sustained effect (24hrs)
28
Q

What is the standard mode of insulin delivery?

A

Subcutaneous injection

29
Q

What is the primary determinant of the effects of insulin that is injected subcutaneously?

A

The rate of subcutaneous blood flow

*increased BF = increased absorption and increased risk for insulin-induced hypoglycemia

30
Q

What is the most common complication of insulin therapy?

A

Hypoglycemia

31
Q

What are the common causes of hypoglycemia?

A
  1. Delay of a meal
  2. Exercise
  3. OD
32
Q

Signs of hypoglycemia?

A
  1. CNS/Behavior manifestations: confusion, bizzare behavior, coma
  2. Reflex autonomic hyperactivity: tachycardia, sweating
33
Q

TX of hypoglycemia

A
  1. Glucose admin: OJ, candy etc.. (if conscious), or IV glucose if unconscious
  2. Glucagon - mobilize sufficient glucose to resotre consciousness in cases of insulin-induced hypoglycemia
34
Q

What is Pramlintide and what does it do?

A
  1. Synthetic Amylin
  2. Fascilitates insulin induced reduction in blood glucose levels
  3. Can also promote insulin-induced hypoglycemia
35
Q

What are the affects of amylin?

A
  1. Decreases gastic emptying (slows intestinal glucose absorption)
  2. Reduces glucagon secretion
  3. Suppresses appetite
36
Q

How is pramlintide administered?

A
  1. Used as adjunts w/ insulin

2. Injected SC before meals

37
Q

Is insulin released in Type II diabetes?

A

Yes, but tissues are nonresponsive

38
Q

3 Phases of Type II Diabetes

A
  1. Insulin resistance and increased hepatic glucose production w/ normal insulin seretion
  2. Insulin resistance w/ compensatory increases in insulin secretion
  3. Insulin resistance w/ depleted insulin response (glucose tolerance)
39
Q

How are type I and type II symptoms different?

A

Similar syptoms except NO KETOACIDOSIS

40
Q

What are the risk factors of T2 Diabetes?

A
  1. Genetic

2. Obesity: 80% T2 are overweight

41
Q

Drug TX classes for T2 diabetes?

A
  1. Insulin Sensitizers
  2. Secretagogues
  3. Incretin-related drugs
  4. Insulin preparations
  5. Others
  6. Combotherapy
42
Q

What drugs are insulin sensitizers?

A
  1. Biguanides (metaformin)

2. Thiazolidinediones

43
Q

What drugs are secretagogues?

A
  1. Sulfonylureas

2. Meglitinides

44
Q

Incretin-Related Drugs

A
  1. GLP-1 Agonists

2. DPP-4 Inhibitors

45
Q

What drugs fall under the “other” category of T2 diabetes tx?

A
  1. Alpha Glucosidase Inhibitors

2. SGLT2 Inhibitors

46
Q

What is the first choice tx for most cases of T2 diabetes, what does it do?

A

Metaformin

  • Oral anti-diabetic, class biguanides
  • Sensitizing agent: promotes insulin’s actions
  • 20% reduction in blood glucose; also improves survival and morbidity
  • produces weight loss
47
Q

What is the MOA for Metformin?

A
  • Stimulates key metabolic regulator: AMPK (AMP activated protein kinase)
    1. Increased GLUT4 expression and glucose uptake = insulin-independent glucose uptake
    2. Inhibition of glucoeogenesis in liver
    3. Decreased mobilization of FFA
    4. Increased insulin sensitivity
48
Q

What are the key features of metformin? (7)

A
  1. Can be taken orally
  2. Restores insulin responsiveness
  3. Very effective (reduces mortality and morbidity)
  4. Produces weight loss
  5. Minimal risk for hypoglycemia (euglycemic)
  6. Relatively safe
  7. Cheap
49
Q

What are SE of metformin?

A
  • not tolerated by everyone
    1. GI (diarrhea, nausea, vomiting)
    2. Rare but fatal lactic acidosis in diabetics (avoid w/ impaired kidney/liver function and severe lung disease)
50
Q

What drugs are thiazolidinediones (TZDs)?

A

Rosiglitazone

Pioglitazone

51
Q

Facts about TZDs (5)

A
  1. Oral, 1x per day
  2. Sensitizing agent: promote insulins actions
  3. Regulate gene expression via intracellular PPAR-gamma: nuclear receptor expressed in muscle, fat, liver
  4. Precise mechanism of PPAR is not clear
  5. Effective at controlling glucose levels and minimal risk of hypoglycemia
52
Q

What are the adverse effects of TZDs?

A
  1. Liver toxicity
  2. Weight gain (due to edema)
  3. Increased LDL
  4. Increased bone fractures in post-menopausal women
  5. Macular edema
  6. Fluid retention = weight gain and increased risk for CHF (avoid in pt w/ CHF)
53
Q

What happened after a study with Rosiglitazone (Avandia)?

A
  1. Off european market altogether

2. Used as last resort in US

54
Q

What drug was recently shown to have a 2-3 fold risk of bladder cancer?

A

Pioglitazone

55
Q

How do secretagogue anti-diabetics work?

A

Increase insulin release from pancreatic beta cells

*can produce hypoglycemia

56
Q

What are the oral secretagogue medications?

A
  1. Sulfonylurease

2. Meglitinides: repaglinide, nateglinide

57
Q

Facts about sulfonylureases?

A

1 Oral secretagogue anti-diabetic
2. Only T2 Diabetes, first oral anti-diabetic med developed
3. 2nd line in most cases
Have 1st/2nd/3rd generations

58
Q

What are SE of sulfonylureases?

A
  1. Hypoglycemia and weight gain
  2. Teratogenic
  3. secondary beta cell failure w/ chronic use, resulting in lost 5-10% of patients each year
59
Q

What are the generations of sulfonylureases?

A

First gen: no longer used due to severe hypoglycemia risk
Second Gen: Glyburide: lower risk for hypoglycemia, BID admin
Third Gen: Glimepride: 1xday w/ lowest risk of hypoglycemia

60
Q

Meglitinide facts (5) and meds (2)

A
  1. Oral secretagogue
  2. Only for T2 Diabetes
  3. Short acting (t1/2 - 1 hour)
  4. Used in combo w/ other meds
  5. Take before a meal to manage mealtime increases in glucose
  6. Repaglinide
  7. Nateglinide
61
Q

SE of Meglitinides

A

Hypoglycemia

62
Q

MOA of Secretagogues

A

Block ATP-Gated K channels on pancreatic Beta Cells

Dental Pharm Exam 5 (3 decks)

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