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USMLE - Pharm
Kaplan Section 7 - Endocrine 2
| Question | Answer |
|---|---|
| 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:
christinapham
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