Diabetes Drugs (Sketchy Medical) – Flashcards
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Metformin (Biguanide)
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First Line drug for DM II
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Metformin (Biguanide)
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MOA: Modulates enzyme activity in the liver --> inhibiting gluconeogenesis Effects: decreases serum glucose, decreased intestinal glucose absorption, and increased peripheral uptake; increases insulin sensitivity
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Metformin (Biguanide)
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S/E: lactic acidosis esp in renal failure Benefit: moderate weight loss in obese patients
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RosiGLITAZONE, PioGLITAZONE (Thiazolidinediones)
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MOA: activate PPAR-gamma, an intracellular receptor that regulates gene transcription of adiponectin Upregulates GLUT4 in peripheral tissue Effect: increases insulin sensitivity and fatty acid oxidation; increases TG storage (decreases serum TG)
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RosiGLITAZONE, PioGLITAZONE (Thiazolidinediones)
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S/E: weight gain, peripheral edema, exacerbation of CHF, and decreased bone mineral density
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Pramlintide
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MOA: amylin analogue w/c is a peptide in insulin secretory granules that decreases glucagon, gastric emptying and appetite Used to control spikes in glucose postprandialy
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Acarbose & Miglitol
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MOA: competitively inhibits alpha-glucosidase enzymes to decrease conversion of disaccharides into absorbable monosaccarides --> delays carbohydrate absorption at brush border Used to control postprandial glucose spikes
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Acarbose & Miglitol
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S/E: Diarrhea, flatulence, abdominal pain
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CanagliFLOZIN & DapagliFLOZIN
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MOA: inhibits sodium-glucose cotransporter 2 (SGLT2) which normally reabsorbs glucose in proximal tubule Inhibition leads to urinary glucose lose
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CanagliFLOZIN & DapagliFLOZIN
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S/E: can cause UTIs and vaginal candidiasis due to increased glucose in urine; also causes hypotension due to osmotic diuresis Contraindicated: renal insufficiency
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insulin Glulisine, Aspart, & Lispro
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Rapid Acting, Short Duration Insulins Given SQ Control postprandial glucose spikes
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regular Insulin
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Use: only insulin that can be given IV; treats diabetic ketoacidosis whcih is due to LOW levels of insulin causing hyperglycemia and ketone production This drug can also treat hyperkalemia.
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NPH insulin
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a intermediate acting insulin given SQ
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Insulin Determir & Glargine
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long duration of action and provide steady background of insulin; shots given 1-2 times daily
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Glyburide & Glipizide
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Names of 1st Generation Sulfonylureas Can cause disulframe like reactions with alcohol
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Sulfonylureas: Glyburide & Glipizide, Tolbutamide, Chlorpromadine Meglitinides: Repaglinide and Neteglinide
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MOA: bind K+ channels --> close K+ channels --> depolarization --> influx of Ca2+ --> endogenous insulin release
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Tolbutamide, Chlorpromadine
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Names of 2nd Generation Sulfonylureas Can cause hypoglcemia; given in smaller doses, and have longer duration of action than 1st generation
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No sulfa hypersensitivty reactions
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Why might you use Meglitinides instead of Sulfonylureas?
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RepaGLINIDE & NeteGLINIDE
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Names of Meglitinides
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ExenaTIDE & LIragluTIDE
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MOA: activate glucagon-like peptide 1 (GLP-1) receptors: increase in insulin release & satiety, decrease in glucagon release and a decrease in gastric emptying
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ExenaTIDE & LIragluTIDE
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Diabetes Drugs that can cause pancreatitis
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SitaGLIPTIN, SaxaGLIPTIN, LinaGLITPAN
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MOA: Inhibit dipeptidyl peptidase 4 (DPP4) which prevents the breakdown of GLP-1 Will have same effects at GLP-1 Agonists: increase in insulin release & satiety, decrease in glucagon release and a decrease in gastric emptying
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SitaGLIPTIN, SaxaGLIPTIN, LinaGLITPAN
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DM II drug that has increased risk of nasopharyngitis and URIs
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Rapid Acting, Short Duration (glulisine, aspart, or lispro) for postprandial glucose spikes PLUS Long Acting (detemir or glargine) for steady background insulin
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Combination of Drugs you'd likely give for someone with type I diabetes:
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Beta cells for endogenous insulin release. They are functional at start of DM II, but will eventually die if DM II not controlled.
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Most of the diabetes II drugs require this to functional:
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Glucose --> increases ATP levels at Beta cells in pancrease --> ATP dependent-K+ channels close --> dec. in K+ efflux --> depolarization of Beta cells --> voltage gated Ca2+ channels open --> Ca2+ influx --> insulin release
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How does glucose cause insulin release?
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c-peptide
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What is also released along with endogenous insulin?
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Tyrosine Kinase: require conformational change to initiae downstream signaling pathways
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What kind of receptors are insulin receptors?
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1.) Liver: increase hepatic glycogen stores, increase glyogenesis and decrease glycogenolysis 2. Skeletal Muscle: increase glycogen stores, increase protein synthesis, increase K+ into cells (decreases serum K+) 3.) Adipoctypes: increase TG storage
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What are the effects of insulin on the 1.) liver 2.) skeletal m. 3.) adipoctyes?
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GLUT 4
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The binding of insulin to its receptor causes these to be inserted into the membranes of peripheral tissues (adipose and muscle) so that glucose can enter the cell?
