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Pharmacology > Metabolic Disorders > Flashcards

Metabolic Disorders Flashcards

1
Q

Natural Insulin

A
  • Unmodified human insulin
  • Rapid action(fast), short duration(9min)
  • Used in hyperglycemic emergencies
  • only insulin given by IV
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2
Q

Insulin Lispro

A
  • Humalog, reversal of 28 & 29 AA, Lys & Pro, prevents dimer

- 5-15 min(very fast), given before meal

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3
Q

Insulin Lente

A
  • longer acting(slow), mixed with zinc-> micro precipitates-> takes longer to absorb
  • Ultra-lente-> longest acting(very slow)
  • Only s.c. administration
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4
Q

NPH Insulin

A
  • Neutral Protamine Hagedorn, Protamine( large positively charged ion-> slow absorption)
  • Long acting(slow)
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5
Q

Insulin Glargine

A
  • Lantus, A21-> asparagine replaced by glycine, 2 arginines add to C-terminus of B-chain
  • Acid solution injected into subcutaneous tissue-> micro precipitates very slow release-> 24hr release w/ no peak
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6
Q

sulfonylureas mechanism of action

A
  • treat type 2
  • Beta cells, blocks K ATPase-> depolarization-> Ca influx-> insulin secretion
  • Increase insulin binding on target cells, reduce serum glucagon levels
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7
Q

Tolbutamide

A
  • Type 2, Sulfonylurea 1st gen, half-life 6-12hrs

- Chlorpropamide (no longer use), Tolazamide, Acetohexamide

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8
Q

Glimepiride

A
  • Type 2, Sulfonylurea 2nd gen, half-life 18-24hrs, 100x more potent
  • Glipizide, Glyburide
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9
Q

Glitazone mechanism of action

A
  • Increase insulin sensitivity of target cells

- PPARgamma agonist-> transcription of insulin receptor components and glocose transporters

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10
Q

Troglitazone

A
  • First gen glitazone

- hepatotoxic, no longer in use

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11
Q

Rosiglitazone

A
  • Second gen glitaone
  • Half-life 7 hrs
  • Metabolites active up to 150 hrs
  • Pioglitazone
  • Side effect hypoglycemia
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12
Q

Metformine

A
  • Only Biguanide
  • Increase glucose uptake, inhibit gluconeogenesis in liver, mechanism unknown
  • Appetite suppressant, Diarrhea, nasea
  • lowers LDL and VLDL
  • Does not cause hypoglycemia
  • Not for patients with liver or kidney disease
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13
Q

Alpha-Glucosidase Inhibitor mechanism

A
  • Inhibit intestinal enzyme Alpha-glucocidase in small intestine-> prevent the breakdown of complex carbohydrates
  • Utilize non absorbable saccharides thayt act as competitive inhibitors
  • Does not increase insulin levels, may be used in type 1 diabetes
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14
Q

Acarbose

A
  • Alpha-Glucosidase inhibitor
  • Also inhibits alpha-amylases
  • No absorption, no side systemic effects
  • Prevent postprandial(post meal) hyperglycemia
  • Diarrhea, Flatulence
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15
Q

Miglitol

A
  • Alpha-glucosidase inhibitor

- Systemically absorbed, no effect on alpha-amylases

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16
Q

Incretins

A
  • Gastrointestinal hormones:Glucagon-like peptide 1(GLP1), Gastric Inhibitory Peptide(GIP)
  • Inactivated by Dipeptidyl Peptidase 4(DPP4)
  • Causes insulin release before glucose levels elevated
  • Reduced gastric emptying-> slower carb absorption-> reduced food intake
  • Inhibit glucagon release
17
Q

Exenatide

A
  • Incretin memetic, Gila monster saliva
  • No effect if glucose levels normal-> No hypoglycemia
  • Long-term weight loss
  • S.Cc injection only
18
Q

Sitagliptin

A
  • DPP4 inhibitor-> increase incretins
  • No effect if glucose levels normal-> No hypoglycemia
  • Oral administration
  • Vildagliptin
19
Q

Amylin

A
  • Pancreatic hormone from B-Islet cells
  • Inhibit Glucagon release, Reduce gastric emptying
  • Promote satiety
20
Q

Pramlintide

A
  • Amylin memetic
  • Only drug other than insulin approved for type 1 diabetes
  • Used in combination with insulin
21
Q

Atherosclerosis initiating mechanism

A
  • Endothelial Cells(EC) bind LDL
  • When activated by injury, EC and attached macrophages produce ROS-> oxidize LDL->Lipid per oxidation-> destruction of LDL receptors which normally clear LDLs
  • Oxidized LDL phagocytosed by macrophages via scavenger receptors-> foam cells-> thickening of arterial walls
  • Lipoprotein a contains apoprotein a-> similar to plasminogen, plasminogen displaced on EC-> reduced production of fibrinolytic plasmin-> increased Fibrin->thombrosis
22
Q

HMG-CoA reductase inhibitor mechanism

A
  • HMG-CoA reductase is rate limiting enzyme in the production of cholesterol
  • Resembles HMG-CoA, reversible competitive inhibitor
  • Isolated Aspergillus sp.(mold)
  • Side effects: heptotoxicity, GI disturbances, myopathy
  • Statins accululate in the liver-> cholesterol production in the liver effected-> liver up regulates LDL receptors to take in LDL from the blood-> LDL in blood reduced
23
Q

Simvastatin

A
  • HMG-CoA reductase inhibitor
  • Precursor activated in the liver
  • Lactone ring hydrolyzed
  • Lovastatin
24
Q

Fluvastatin

A
  • HMG-CoA reductase inhibitor
  • Already in active form
  • Pravastatin
25
Q

Atorvastatin

A
  • Long-lasting inhibitor of HMG-CoA reductase

- Lipitor

26
Q

Fibrates

A
  • Fibric acid derivatives
  • PPARalpha agonists-> B-oxidation of fatty acids
  • stimulates lipoprotein lipase activity-> cellular uptake of free fatty acids from LDL and Chylomicrons
  • reduce VLDL production in the liver (little effect on LDL)
  • Increase HDL
  • Rare but severe Myositis(muscle inflammation)
27
Q

Clofibrate

A
  • Fibrate treatment for hyperlipidemia

- Bezafibrate, Fenofibrate, Ciprofibrate, Gemfibrozil

28
Q

Cholestyramine

A
  • Bile acid binding resin, Anion exchange resin prevents absorption and enterohepatic recirculation of bile acids-> increase LDL receptors in liver-> increase LDL uptake-> lower LDL levels in the blood
  • Side effects: Bloating, constipation, diarrhea
  • Interfere with drug absorption digitoxin and fat soluble vitamins
  • Not appetizing
  • Colestipol

Pharmacology (10 decks)

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