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Pharm > Pancreatic Hormones & Diabetic Drugs > Flashcards

Pancreatic Hormones & Diabetic Drugs Flashcards

1
Q

Which diabetes has more of a genetic predisposition

A

Type II

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2
Q

Which diabetes has insulin deficiency

A

Type 1

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3
Q

Which diabetes has a loss of beta cells

A

Type 1

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4
Q

Which diabetes is more prone to ketoacidosis

A

Type 1

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5
Q

Which diabetes is prone to a non-ketototic hyperosmolar coma

A

Type II

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6
Q

K+/ATP and Insulin:

Open state of K+/ATP channel

A

hyperpolarize the cell by causing outflow of K+ and inhibit insulin release

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7
Q

K+/ATP and Insulin:

Closed state of K+/ATP channel

A

depolarize the cell and insulin released.

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8
Q

Insulin Receptor signaling:

A

insulin binding to alpha subunit regulates beta subunit activity –>

autophosphorylation of beta subunit –>

increase tyrosine kinase activity –>

phosphorylation of other substrates –>

activation of phosphoinositide 3-kinase

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9
Q

Effects of insulin on the liver

A

Stimulates:

  • glycogen synthesis
  • triglyceride synthesis

Inhibits:

  • glycogenolysis
  • ketogenesis
  • gluconeogenesis
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10
Q

Effects of insulin on skeletal muscle

A

Stimulates:

  • glucose uptake
  • protein synthesis
  • glycogen synthesis

Inhibits:

  • Protein degradation
  • Glycogenolysis
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11
Q

Effects of insulin on adipose tissue

A

Stimulates:

  • Glucose uptake
  • Triglyceride storage

Inhibits:
- lipolysis

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12
Q

Overall, insulin stimulates ____and inhibits ____

A

Promotes anabolic processes and

Inhibits catabolic processes

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13
Q

advantages to recombinant DNA insulin

A
  • Less insulin resistance
  • Less allergy
  • Less lipodystrophy
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14
Q

Rapid/ short-acting insulin:

onset and duration

A

Onset: 5-15 min
Duration: 3-5 h

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15
Q

Rapid insulin

A
  • Insulin lispro, aspart, glulisine given s.c
  • Inhaled human insulin - Indicated only in adults,
  • Contraindicated- children, asthma, bronchitis, smokers
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16
Q

short-acting insulin
• duration
• what? method given?
• use?

A
  • Duration: 5-8h
  • Regular insulin given s.c and i.v.
  • Use in diabetic ketoacidosis and other emergency situations
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17
Q 
intermediate-acting insulin:
•  onset
•  duration
•  what?
•
A
  • onset: 2-5h
  • duration: 4-12h
  • Lente insulin, NPH insulin (Neutral protamine Hagedorn or isophane) mixture of insulin with protamine (basic substance obtained from fish sperm)
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18
Q

Ultra-long acting insulin
• onset
• duration
• what?

A
  • onset: slow
  • duration: 20-24h
  • Ultra lente, Insulin glargine, Insulin detemir
  • Peakless, given once daily
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19
Q

Hypoglycemia
• S/Sx
• Tx

A
  • Sympathetic signs (tachycardia, sweating, palpitations, tremors) parasympathetic signs (nausea, hunger)
  • Treatment : Glucose or glucagon treatment
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20
Q

Allergy and resistance to insulin

A
  • Local cutaneous reactions or systemic

* Human insulin are less antigenic than insulin from animal sources

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21
Q

lipodystrophy

A
  • Atrophy of fatty tissue at the site of injection

* Never seen since the development of highly purified insulin

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22
Q

Treatment of Type II DM includes

A 
•  Diet
•  Exercise
•  Wt reduction
•  Step wise approach to drug treatment
•  Patient education 
➢ Oral drugs for reduction of blood glucose
•  Used only in the Rx of Type II DM
•  Oral medication is initiated when 2-3 months of diet and exercise alone are unable to achieve or maintain their optimal plasma glucose levels
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23
Q

Insulin secretogogues

A
  • Sulfonyureas

* Meglitinides

24
Q

Oral Hypoglycemics

A 
1.  Insulin secretogogues 
•  Sulfonyureas 
•  Meglitinides 
2.  Biguanides 
3.  Thiazolidinediones 
4.  Alpha glucosidase inhibitors
25
Q

First Generation Sulfonylurea

A
  • Chlorpropramide
  • Tolbutamide
  • Tolazamide
26
Q

2nd Generation Sulfonuylurea

A
  • Glipizide
  • Glyburide
  • Glimepiride
27
Q

Mechanism of action of Sulfonylurea

A
  • Block ATP sensitive K+ channels in pancreatic beta cells –> Inhibits the efflux of K+ resulting in depolarization
  • Opening of voltage gated Ca influx –> release of preformed insulin –>
  • Increase the sensitivity to insulin by increasing number of insulin Receptors
28
Q

Chloropropamide (Diabinese)

A
  • Long acting for 32 hours
  • Can cause prolonged hypoglycemia in elderly patients (contraindicated age)
  • Slowly metabolised in liver, so Contraindicated in patients with hepatic disease
29
Q

Tolbutamide (Orinase)

A
  • Rapidly metabolised in liver

* Short half life - safest SU in elderly

30
Q

2nd generation SU drugs:

A
  • glipizide (glucotrol)
  • glyburide (micronase, glynase prestab)
  • glimepiride

➢ Second generation drugs commonly prescribed agents because of fewer side effects and drug interactions

31
Q

glipizide (glucotrol)

A
  • 2nd generation SU drug.
  • commonly prescribed agents because of fewer side effects and drug interactions
  • Half-life - 2 to 4 hours
  • Potency – High (2.5 to 40 mg/d)
  • 90% is oxidized to inactive metabolites in liver
  • Contraindicated in patients with hepatic disease - can cause hypoglycemia
32
Q

Glyburide (Micronase, Glynase PresTab)

A
  • 2nd generation SU drug.
  • commonly prescribed agents because of fewer side effects and drug interactions
  • Half-life - 6 hours
33
Q

Glimepiride

A
  • Approved for once-daily use

* Potency – Highest (1 to 8 mg/d)

34
Q

Clinical uses of Sulfonylureas

A
  • Hypoglycemic agents for treatment of Type 2 DM
  • Act by increasing endogenous insulin secretion \ not indicated for Type 1
  • Most effective when ß cell function has not been severely compromised
  • Increased insulin secretion favors lipogenesis
  • Suitable drug in non obese diabetics
35
Q

A/E in Sulfonylureas

A
  • Severe hypoglycemia
  • Most common with glyburide and chlorpropramide in elderly patient
  • Weight gain
  • Erythema, skin reactions
  • Disulfiram like reaction with alcohol (chlorpropramide)
36
Q

Contraindications for Sulfonylureas

A
  • Pregnancy
  • Surgery, Severe infections
  • Severe stress or trauma
  • Severe hepatic or renal failure
  • Insulin therapy should be used in all of these
37
Q

Meglitinides:

A

Repaglinide and Nateglinide

38
Q 
Meglitinides 
•  MOA
•  DOA
•  use
•  a/e
A

➢ Insulin secretogogues….same as sulfonyl ureas
➢ Rapid onset and short duration of action
• Suitable for controlling postprandial hyperglycemia
➢ Approved for used alone or with biguanides
➢ Common adverse effect is Hypoglycemia

39
Q

Biguanides

A

Metformin

40
Q

Biguanides (Metformin) MOA

A

Antihyperglycemic:
• Increases peripheral insulin sensitivity
• Inhibits hepatic gluconeogenesis & glucose absorption from GI tract
• Reduction of plasma glucagon levels
• “Euglycemic”, no hypoglycemia. *
• Does not alter insulin secretion *

41
Q

Clinical use of Biguanides (Metformin)

A
  • They are Insulin sparing agents
  • Do not produce hypoglycemia
Secondary beneficial effects on lipids:
•  Reduced triglycerides
•  Reduced total cholesterol
•  Reduced LDL
•  Increased HDL
•  Does not increase Weight

Use:
• Appropriate for obese Type 2 diabetics
• Other use: Polycystic ovarian syndrome - lowers the serum androgens and restores normal mentrual cycles and ovulation

42
Q

used to control postprandial hyperglycemia

A

Meglitinides: Repaglinide and Nateglinide

43
Q

Metformin A/E and contraindications

A

Adverse effects:
• *Gastrointestinal – anorexia, nausea, vomiting, diarrhea
• Lactic acidosis (increased risk in alcoholics & in Pts with hepatic impairment)
• Vitamin B 12 defeciency

Contraindications:
• Alchoholism, renal and hepatic disease- risk of lactic acidosis

44
Q

Thiazolidinediones

A

Pioglitazone, Rosiglitazone

45
Q

Thiazolidinediones MOA

A

➢ Mechanism: Stimulate the nuclear peroxisome proliferator-activating receptors (PPAR’s) involved in transcription of insulin-responsive genes –> Increase the glucose uptake in muscle and adipose tissue & decreases hepatic gluconeogenesis
• They reduce plasma glucose and Triglycerides

46
Q

Thiazolidinediones A/E

A

Adverse effects:
• Do not cause hypoglycemic, earlier drugs were hepatotoxic (troglitazone)

➢ Adverse effects
• Troglitazone*:
• Hepatotoxicity- Withdrawn from market

  • Rosiglitazone, Pioglitazone*:
    • No evidence of drug-induced hepatotoxicity
    • Peripheral Edema, anemia
      • Are hepatic enzyme inducers
        • TZDs- euglycemics
47
Q

troglitazone

A

(Thiazolidinedione)

hepatotoxic–withdrawn from office

48
Q
  • Rosiglitazone, Pioglitazone*:
    • No evidence of drug-induced hepatotoxicity
    • Peripheral Edema, anemia
      • Are hepatic enzyme inducers
        • TZDs- euglycemics
A
  • No evidence of drug-induced hepatotoxicity
  • Peripheral Edema, anemia
  • Are hepatic enzyme inducers
  • TZDs- euglycemics
49
Q

Alpha glucosidase inhibitors

A

Acarbose, Miglitol

50
Q

Alpha glucosidase inhibitors MOA

A
  • Competitive and reversible inhibitors of a glucosidase in the small intestine
  • Delay carbohydrate digestion and absorption
  • Reduction in postprandial hyperglycemia
51
Q

Alpha glucosidase inhibitors clinical use

A
  • Individuals with significant postprandial hyperglycemia

* Monotherapy or in combination with other oral hypoglycemics

52
Q

Alpha glucosidase inhibitors A/E

A
  • Flatulence, Nausea, Diarrhea
  • Due to increased fermentation of unabsorbed carbohydrate by colonic bacteria
  • Do not produce hypoglycemia, lactic acidosis, or significant weight gain
53
Q

Pramlintide

A
  • Administered s.c
  • Synthetic analog of amylin, supress glucagon release
  • Targets post prandial blood sugar levels
54
Q

Exenatide

A

(1st incretin therapy to be approved for DM)

  • Administered s.c
  • Synthetic glucagon like polypeptide (GLP-1)
  • Potentiates insulin secretion
55
Q

Sitaglyptin

A

Inhibitor of dipeptidyl peptidase-4-enzyme that degrades GLP-1

56
Q

Glucagon effects

A

➢ The primary counter-regulatory hormone
• Effects are generally opposite those of insulin:
• Stimulates glycogenolysis, ketogenesis, and gluconeogenesis
• Inhibits glycogen synthesis and lipogenesis
• Increased hepatic glucose output
• Increased blood glucose level

➢ Other effects
• Inotropic and chronotropic effects on heart
• Relaxation of intestinal muscle

57
Q

Glucagon clinical uses

A
  • Severe hypoglycemia
  • Overshooting in insulin therapy
  • Hypoglycemia from long-acting oral agents
  • Relaxation of the GI tract for X-ray and magnetic resonance visualization
  • Inotropic effect on heart- can be used to reverse effects of ß-blocker overdose

Pharm (32 decks)

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