Pharmacology II Flashcards

1
Q

How is Diabetes Mellitus characterized?

A
  1. Hyperglycemia with derangedd secretion of insulin
  2. Thickening of basement membranes of capillaries
  3. Late complications involving tissues that DO NOT require insulin for glucose uptake (retina, glomerulus, and peripheral nerves resulting in blindness, renal failure, and neuropathy)
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2
Q

What is the difference between Type I and Type II DM?

A

Type I: lack of insulin release by B-cells

Type II: Insensitivity to insulin by receptive tissue (also sometimes low insulin release)

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3
Q

What is the treatment for Type I DM? What are the delayed preparations?

A

Insulin

Forms:
Insulin Lispro (rapid onset, but shorter duration)
Isophane (NPH)
Insulin glargine (maintains glucose at around 130mg/dl for ~20hr)
Insulin Zinc extended

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4
Q

What are the short acting insulin preparations?

A

Insulin Aspart

Insulin glulisine

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5
Q

What is the treatmet for Type II diabetes?

A
  • Diet and Exercise
  • Oral hypoglycemics (& euglycemics)
  • Insulin may be used
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6
Q

What are pharmacological treatments available to treat Type II DM? (think general groups)

A

Sulfonylureas

Metformin

Acarbose

Thiazolidinediones

Exenatide

SGLT2 Inhibitors

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7
Q

What are the different sulfonylureas?

A

Tolbutamide

Glyburide

Glipizide

Gliclazide

Glimepiride

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8
Q

What is the MOA of sulfonylureas in treating T2 DM?

A

Sulfonylureas bind to the same K+ channel on membrane of pancreatic beta-cells that is regulated by glucose metabolism

–> Leads to depolarization of cells and insulin release

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9
Q

What are side effectsof sulfonylureas?

A

Prolonged and severe hypoglycemia
(May be FATAL!)

Symptoms:
Sweating
Hunger
parasthesis
Tremor
Anxiety

Treat with fast acting glucose:
OJ
Coke
IV glucose

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10
Q

What is reaglinide?

A

Not a sulfonylurea, but act just like one

–> binds to K+ channels to cause depolarization and insulin release

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11
Q

What is metformin? MOA?

A

A Biguanide used to reduce hyperglycemia

–> Reduces hepatic glucose output by inhibiting gluconeogenesis

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12
Q

What are adverse effects of metformin? And what is the key positive effect?

A

Never causes hypoglycemia

Adverse Effects:
Lactic acidosis
(only seen in patients with renal failure or CHF)
Diarrhea

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13
Q

What is Acarbose? MOA?

A

An alpha-glucosidase inhibitor

–> Acts by inhibiting carbohydrate breakdown in the intestine

–> Reduces glucose uptake from intestine - reduces post-prandial spike in blood glucose

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14
Q

What are side effects of Acarbose?

A

Alone, will not cause hypoglycemia - but if taken with sulfonylurea & hypoglycemia occurs, must take glucose, not sucrose (patient should keep glucose tablets with them)

Abdominal bloating

diarrhea

flatulence

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15
Q

What are the thiazolidinediones? MOA?

A

Pioglitazone
rosiglitazone
ciglitazone

Selective PPAR-gamma agonists (peroxisome proliferator-activated recetpor-gamma)
–> Increases insulin sensitivity
Possibly by increasing GLUT4 in muscle and adipose
–> Decreases gluconeogenesis in liver

(aka ‘glitazones’)

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16
Q

What are some benefits of using glitazones?

A

No liver toxicity

Does NOT cause hypoglycemia alone

(aka thiazolidinediones)

17
Q

What is exenatide? MOA?

A

A synthetic peptide used to treat T2 DM

Mimics glucagon-like peptide-1 (GLP-1) released from the GI tract

–> Stimulates insulin release and inhibits glucagon release

18
Q

What is sitagliptin? MOA?

A

Orally active dipeptidyl peptidase-4 inhibitor

–> prevents the breakdown of endogenouse glucagon-like peptide-1 (GLP-1)

–> GLP-1 is a potent stimulator of insulin release in a glucose-dependent manner and inhibits glucagon release

–> significantly reduces Hemoglobin A1c

19
Q

What SGLT2 inhibitor is used to treat T2 DM? MOA?

A

Canagliflozin

Normally, in the kidney, glucose is filtered out of blood in glomerulus and 100% is reabsorbed back into the blood in the proximal tubule by the Na-glucose cotransporter-2 (SGLT2)

By inhibiting SGLT2, canagliflozin causes more glucose to be lost in urine