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Pharmacology Exam 5 > Anti-Diabetes > Flashcards

Flashcards in Anti-Diabetes Deck (37)
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1
Q

Classification of Diabetes Mellitus

A

Type I-Insulin dependent (deficiency)

Type II-Insulin independent (resistance)

2
Q

What diabetes can cause

A

major cause of heart disease and stroke; 7th leading cause of death in United States.

3
Q

Macrovascular complications of diabetes

A

Coronary artery disease, cerebral vascular problem, peripheral vascular disease

4
Q

Microvascular complications of diabetes

A

Nephropathy, retinopathy and neuropathy

5
Q

Diagnostic Criteria for Diabetes

A
  • Fasting plasma glucose (FPG)
  • HbA1c level (also considering FPG results)
  • Glucose level 2 hrs after a 75 g glucose load (less used)
6
Q

Type I Diabetes

A
 Insulin dependent
 Juvenile onset
10%
 Inflammation of islets or antibodies to islet
 Prone to ketoacidosis
 HLA association
 No obesity
 Vascular complications*
7
Q

Type II Diabetes

A

 NOT Insulin dependent  Maturity onset
90%
 Inability of insulin action  Not prone
 No association with HLA
 Obesity is a common risk factor  Vascular complications*

8
Q

Model of insulin action on glucose transport in myocytes & adipocytes

A

Insulin binds to the α subunits of the insulin receptor and stimulates the tyrosine kinase activity of the β subunits. Glucose transport proteins are then activated and translocated from the cytoplasm to the cell membrane which stimulates glucose entry into the cell.

9
Q

Long-acting therapy

A

`Glargine

10
Q

Short-acting

A

Aspart/Lispro

Regular

11
Q

Insulin management schedules:

A

2 or 3 meals (+/-PM) considerations; single or mixed insulin preps

12
Q

Insulin Delivery Devices:

A

Syringes; Refillable/Prefilled Pens; Insulin Pumps

13
Q

Complications of Insulin

A

Hypoglycemia: relieved by glucose (food intake; i.v. injection, etc.), ketoacidosis, insulin allergy, or lipodystrophy at injection site.

14
Q

Pathophysiology of T2D

A

know how glucagon and insulin work

15
Q

Sulfonylureas(SFUs):

A

Glyburide

16
Q

Glyburide mode of action

A

Induce insulin release from pancreas (closing ATP-K+ channels)
Reduce serum glucagon levels
Potentiates action of insulin on its target tissues

17
Q

Adverse drug reactions of glyburide

A

Severe hypoglycemia; weight gain, nausea, vomiting, hypersensitivity reactions

18
Q

Indication for glyburide

A

T2D patients failed to achieve glycemic control with diet & life-style modifications; may be used in patients with kidney disease

19
Q

Biguanides:

A

Metformin, generally 1st choice therapy

20
Q

Metformin Mode of Action

A

↓ hepatic glucose production (HGP) (activates AMP-kinase)
↑ insulin action on peripheral muscle and fat tissues
Non-insulin-dependent effects, thus no hypoglycemia & no weight gain; No effect on release of growth hormone, glucagon.

21
Q

Contraindications of Metformin

A

Contraindicated in patients with renal impairment, hepatic diseases, heart problems, acidosis, blood infection, etc.

22
Q

Thiazolidinediones(TZDs)

A

Rosiglitazone and Pioglitazone

23
Q

Mode of Action of rosiglitazone and pioglitazone

A

Agonists for nuclear peroxisome proliferator-activated receptor-γ (PPAR γ) & activate insulin responsive genes that regulate carbohydrate and lipid metabolism
Promote glucose uptake to muscles/fat & decrease HGP
Require insulin presence for action

24
Q

Adverse drug reactions of rosiglitazone and pioglitazone

A

1st year liver function monitoring
Edema (fluid retention), weight gain
Rosiglitazone (FDA restricted access): risk of heart attack/MI;
Pioglitazone: common usage in the US

25
Q

Indications and other considerations for rosiglitazone and pioglitazone

A

Good for overweight/obese patients;

Slow onset: 4-6 wks to affect blood glucose (may even take 3-4mos)

26
Q

α-GlucosidaseInhibitors

A

Acarbose

27
Q

Mode of action of acarbose

A

Delays carbohydrate digestion and slows glucose absorption in the gut
No effect on insulin release

28
Q

Adverse drug reaction of acarbose

A

Dose related malabsorption, flatulence, nausea and diarrhea (No weight gain)

29
Q

Newer Anti-Diabetics

A

Two main gut incretins:
GIP and GLP-1 (diminished in T2D post-meal)
Exenatide- IV
DPP-4 inhibitors (oral): sitagliptin
Both GLP-1 and GIP are rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4).

30
Q

Incretins

A

are a group of GI hormones that increase insulin release from the beta cells of the islets of Langerhans after eating. Incretin levels become elevated even before blood glucose levels. They also slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. They also inhibit glucagon release from the alpha cells of the Islets.

31
Q

Glucagon-LikePeptide1(GLP-1)Agonists

A

Exenatide

32
Q

Mode of action of exenatide

A

Induces insulin release (glucose-dependent)
Reduces post-meal glucagon, and hence HGP Slows stomach emptying
Promotes satiety and inhibits appetite
Preserves beta cell mass

33
Q

Exenatide dosing regimens:

A

injected twice daily 1hr pre-meal; or ER (Extended Release) for once weekly

34
Q

Adverse drug reactions to exenatide

A

Nausea, vomiting, headache. Avoid in patients with severe kidney & GI problems

35
Q

InhibitorsofDipeptidePeptidase-4(DPP-4)

A

Sitagliptin

36
Q

Mode of action of sitagliptin

A

Inhibits degradation of incretins thus increasing GLP-1

Can be administered orally (once daily)

37
Q

Adverse reactions of sitagliptin

A

Headache, risk of infections

Caution in kidney problems and potential contraindications