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USMLE - Pharm

Kaplan Section 7 - Endocrine 2

Diabetes Mellitus: Type 1 (IDDM) and Type 2 (NIDDM) -- Which is early onset and which is adult onset? IDDM is early onset; NIDDM is adult onset.
Diabetes Mellitus: Type 1 (IDDM) and Type 2 (NIDDM) -- Which has impaired response to insulin? NIDDM --> diet --> oral hypoglycemics +/- insulin
Diabetes Mellitus: Type 1 (IDDM) and Type 2 (NIDDM) -- Which has loss of pancreatic B cells? IDDM Type 1 --> absolute dependence on insulin (diet + insulin +/- oral agents)
Diabetes Mellitus: Type 1 (IDDM) and Type 2 (NIDDM) -- Which is ketoacidosis-prone? IDDM Type 1
Name 4 things that can increase insulin release 1. glucose, 2. sulfonylureas (anti-diabetic drugs for type 2 diabetes - inc insulin release from pancreatic B cells), 3. M-activators, 4. B2 agonists
What class of drugs decreases insulin release? alpha 2 agonists
Put these forms of INSULIN in increasing order of onset/peak effect/duration: Lente, Lispro, Regular, Ultralente Lispro < Regular < Lente < Ultralente
Which forms of insulin are used IV? Shortest acting forms: Lispro and Regular
What are the symptoms of diabetic ketoacidosis? 1. polyuria, 2. polydipsia, 3. nausea, 4. fatigue, 5. dehydration, 6. Kussmaul's breathing (deep and labored breathing --> blow off CO2 --> pCO2 low in blood), 7. fruity breath
What is the treatment for diabetic ketoacidosis? 1. regular insulin IV, 2. fluid and electrolyte replacement
What is DKA? diabetic ketoacidosis: hyPERblycemia, acidosis, and high levels of circulating ketone bodies.
What leads to DKA? no insulin production from B cells & no exogenous insulin --> starvation state --> break down fat to get energy --> production of ketone bodies --> brain switches from using glucose as fuel to ketone bodies --> ketone bodies lower pH
What cells do not need insulin in order to uptake glucose? erythrocytes, neurons, hepatocytes, some intestinal tissue, and pancreatic beta-cells.
Why do some cells require insulin to uptake glucose and most cells do not? Most cells have only GLUT-4: insulin --> 2nd messenber cascade --> GLUT4 to cell membrane -->uptake of glucose. Conversely, when insulin [ ] low, these transporters dissociate from membrane-->can't uptake glucose.
How do pancreatic B cells work? K+ efflux maintains hyperpolarization of membranes --> no depolarization --> no release of insulin (insulin released only upon depoarization)
How does glucose act on pancreatic B cells? increase intracellular ATP --> K+ efflux stops --> hyperpolarization not maintained --> membrane depolarization --> opens Ca2+ channels --> inc Ca2+ influx --> insulin released from granules
How do sulfonylureas work? block K+ channels --> K+ efflux stops --> hyperpolarization not maintained --> membrane depolarization --> opens Ca2+ channels --> inc Ca2+ influx --> insulin released from granules
Name 3 things that sulfonylureas do: 1. inc insulin release --> 2. dec glucagon release from pancreatic alpha cells, 3. continued use of sulfonylureas --> increased receptor sensitivity to insulin in tissues (receptors in tissues can respond to even lower levels of insulin)
Acetohexamide First generation sulfonylurea; makes an active metabolite
In what patient population should you decrease the dose of acetohexamide? Renal dysfxn pts
Tolbutamide First generation sulfonylurea
What is the advantage of Tolbutamide over Acetohexamide? Can use in pts with renal dysfxn
Chlorpropamide First generation sulfonylurea; long-acting
Should you give chlorpropamide to those with SIADH? Why or why not? SIADH - syndrome of inappropriate antidiuretic hormone --> more concentrated urine and hyponatremia due to inc volume; no because chlorpropamide stimulates even more ADH release and potentiates its anti-diuretic effects
What is one effect of drinking alcohol while on chlorpropamide? chlorpropamide causes disulfiram-like actions (inhibiting acetaldehyde dehydrogenase, which breaks acetaldehyde (from EtOH) down to acetic acid --> N&V, headache, hypotn, inactivates folate, dec avail of thiamine
Name the 3 first generation sulfonylureas 1. acetohexamide, 2. tolbutamide, 3. chlorpropamide
Name the 2 second generation sulfonylureas 1. glipizide, 2. glyburide
What should you do when prescribing glipizide in a patient with hepatic dysfxn? Decrease dose of glipizide (sulfonylurea)
When should you decrease the dose when prescribing glyburide? In pts with renal dysfxn. Glyburide forms an active metabolite.
What are two common adverse effects of taking sulfonylureas? 1. hypoglycemia (cause insulin release --> less sugar in blood), 2. weight gain
With sulfonylureas, there is heightened hypoglycemia if taken in conjunction with which drugs? CISS; cimetidine (H2 antag), insulin, salicylates (ASA), sulfonamides (antibacterials)
What are these symptoms of: lip/tongue tingling, lethargy, confusion, sweats, tremors, tachycardia, coma, seizures Hypoglycemia
How to treat hypoglycemia? 1. oral glucose, 2. IV dextrose if unconscious, 3. glucagon (inhale or IM)
What is Metformin? drug that decreases post-prandial glucose levels
What is the advantage of Metformin? doesn't cause hypoglycemia or weight gain
What is the mechanism of Metformin? 1. inc issue sensitivity to insulin, 2. dec hepatic gluconeogenesis
Should you or should you not prescribe metform in conjunction with a sulfonylurea? You should because metformin and sulfonylureas are synergistic.
What is the adverse effect of Metformin? lactic acidosis
What is acarbose? In GI tract: starch ---(a-glucosidase)---> glucose. Acarbose inhibits a-glucosidase --> dec formation of absorbable CHO's --> dec postprandialglucose --> dec demand for insulin
What is the advantage of acarbose? Doesn't cause hypoglycemia.
What are the adverse effect of Acarbose? discomfort, flatulence, diarrhea
What are pioglitazone and rosiglitazone? hypoglycemics that act similar to metformin. They 1. dec hepatic gluconeogenesis, 2. inc tissue sensitization to effects of insulin, 3. (not like metformin) upregulate number of insulin receptors on tissues
What are adverse effects of pioglitazone and rosiglitazone? weight gain and edema
What is repaglinide? stimulate insulin release from pancreatic beta cells
When would you use repaglinide? in diabetes type 2 --> just before meals due to short half life
What drug would you use to reverse a B-blocker overdose? Glucagon. Glucagon --> adenylyl cyclase --> + inotropy (contractility) and + chronotropy (HR)
What are bisphosphonates? 1. stabilize bone structure and 2. induce osteoblasts to secrete osteoclast inhibitors --> less bone resorption --> slow progression of osteoporosis
What would you use bisphosphonates for? 1. Paget dz (The bone breaks down more quickly, and when it grows again it is softer than normal bone), 2. post-menopausal osteoporosis
What is alendronate? a bisphosphonate used in 1. post-menopausal osteoporosis (with HRT, causes increases in bone mineral density), 2. DOC for steroid-induced osteoporosis
What are etidronate and pamidronate? bisphosphonates
Why would you want to avoid using etidronate and pamidronate? causes bone mineralization defects
What is an adverse effect of alendronate? Causes GI distress, including esophageal ulcers.
Created by: Missy Kratz Missy Kratz on 2008-03-27

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