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EndoNut 2.5.13
| Question | Answer |
|---|---|
| What are the major effects of reduced insulin secretion in Type 2 DM? | hyperglycemia, significant glucose variability |
| What are some systemic effects of type 2 DM? | incr/inappropriate hepatic glucose production, insulin resistance in periphery, diminished incretin secretion, diminished amylin secretion |
| What cell is most affected in type 2 DM? | beta cells |
| What are incretins generally? | gut hormone that are release by enterointestinal cells after nutrient loading. overall: lower both fasting and prandial glucose |
| What are the effects of GLP 1 (incretin)? | augments insulin secretion, stimulates glucose dependent insulin release (incr uptake), surpresses glucagon secretion ( decr heptic production of glucose), slows gastric emptying, promotes beta cell mass and survival |
| What is amylin? What levels are seen in DM type 2? | AA produced by beta cell and stored with insulin, co-secreted in response to glucose and other ceta cell stimulating factors. deficient in DM |
| What is the mech of amylin? | reduces gastric emptying, regulation of glucagon and promotes satiety |
| What is the natural hx of DM type 2? | progressive, even if well managed, therapy usually needs to be amplified |
| What kills beta cells in DM type II? | high blood sugars kill them, also some lipidd (elevated FFA, TG) |
| What factors affect PPG (post prandial glucose) levels? | overall glycemic control, meal size and nutrient composition, time of day, insulin sensitivity, insulin secretion, pharmacodynamics of drug therapies |
| What are 2 major complications that must be tx aggresively in type 2 DM? | HTN and hyperlipidemia |
| What is Hyperosmolar hyperglycemic non-ketotic state (acute)? | little or no ketoacid accumulation, plasma glucose exceeds 1000mg, osm may reach 380, neuro abnormaliites frequently present |
| What are some common precipitation factors for HHNK? | pneumonia, UTI, stroke, drugs ( corticosteroids, higher dose of thiazide diuretics), hot weather and insufficienct water intake in elderly |
| What is the Tx for HHNK? | fluid loss usually about 8-10L, give fluids, electrolyte corrrections, insulin drip with glucose |
| What are the indications for the types of therapy in type 2 DM? | pharmocologic if HbA1C 6-7%, combination therapy if 7-10% and insulin if it's >10% |
| What classes of DM drugs act on the pancreas? | sulfonylureas, meglitinides, matiglinide |
| What classes of DM drugs act on the liver? | metformin>>thiazolidinediones |
| What classes of DM drugs act on the intestine? | alpha glucosodiase inhibitors, DPP-4 antagonists |
| What classes of SM drugs act on the fat and muscle? | thiazolidinediones>>metformin |
| What class is metformin and what is its action and coverage? | biguanides. surpression of hepatic glucose production, insulin sensitizing, basal coverage |
| What is checked to see if a pt needs metformin? | morning glucose |
| What is the major SE of metformin esp in kidney problems? | can cause lactic acidosis, rarely hypoglycemia, avoid in elderly and withhold at time of contrast dye study |
| What are the 2 classes of secreatogogues? | sulfonylureas, meglitinides |
| What is the action of secreatogogues? | stimulate the pancreas to secrete insulin |
| What are 3 sulfonylureas? | glipizide, glyburide, glimepiride |
| What are 2 meglitinides? | repaglinide, nateglinide |
| What are the major SE of sulfonylurease? | 15-20% wont respond, can have hypoglycemia, modest weight gain, no data to confirm worsening of heart disease |
| What are the actions of meglitinide? | stimulate insulin release with glucose, good for post prandial coverage |
| What are the major SE of meglitinide? | multiple daily doses, slight weight gain, mild hypoglycemia, reduced tittration in liver disease |
| What is the action of the thiazolidinediones? | insulin sensitizer, mild impact on hepatic glucsoe production |
| What is the class of rosiglitazone, pioglitazone? | thiazolidinediones |
| What are the major benefits of the thiazolidinediones? | incr Si at muscle and fat, decr HbA1c |
| What are the major SE of the thiazolidineodiones? | volume expansion with edema and weight gain, decr Hb, decr OCP, cardiac issues, bladder cancer |
| What is the action of alpha glucosidase inhibitors? | delay absorbtion of complex carbs |
| What is the class of acarbose, miglitol, voglibose? | alpha glucosidase inhibitors |
| What are the major nenefits to alpha glucosidase inhibitors? | no change in weight, decr GIP and incr GLP-1, no hypoglycemia |
| What are the major SE of alpha glucosidase inhibitors? | GI SE, limited post prandial lowering, start at low dose, no difference b/w acarbose and miglitol |
| What is the class of saxxagliptin, linagliptin, sitagliptin? | DPP-4 antagonists, blocks incretins, keeps native GLP -1 1 around short acting= very much preprandial |
| What are the major SE of DPP-4 antagonists? | wight neutral, adverse reactions similar to placebo |
| What is the class of exenatide, liraglutide? | injectable GLP-1 for prandial |
| What is the class of pramlintide? | synthetic amylin, used with prandial meals |
| What are the benefits of the GLP-1 Agonists? | incr insulin secretion, decr glucagon secretion, delays gastric emptying, weight loss |
| When should insulin be added to oral therapy for type 2 DM? | HbA1c is not at goal, preprandial or postpranidal glucose ranges not at goal, side effects, or in acute illness |
| What are 3 major acute complications of DM? | ketoacidosis (type 1), hyperosmpolar hyperglycemic state ( type II), hypoglycemia secondary to tx |
| What are 3 chronic microvascular complications of DM? | nephropathy, retinopathy, neuropathy |
| What are 3 major chronic macrovascular complications of DM? | CAD, cerebrovascular disease, peripheral vascular disease |
| Why does hyperglycemia cause harm? | eye, kidney, NS dont't require insulin to carry glucose into cell, when too much glucose, the glucose gets shunted to alternative pathways with cause incr in oxidative stress and possible apoptosis |
| What usually precedes diabetic nephropathy? | patients usually have preexisting retinopathy/neuropathy |
| What is used for BP control to prevent DM nephropathy? | RAS blockade (ACE I, ARB), goal is <130/80 for micoalbuminuria and 125/75 fo <1g proteinuria |
| What is seen in peripheral sensory polyneuropathy in DM?(PSPN) | affects distal lower extremities in a stocking and glove distrobution |
| What are some complications of PSPN? | ulcersm charcot arthropathy, amputation |
| What is the presentation of acute charcot deformity? | recent onset of unilateral warmth, rednmess, edema over foot and anle |
| What is the presentation of chronic charcot's foot? | insidious swelling over months or ears, leads to collapse of arch in midfoot, plantar bony prominences, and pressure ulceration |
| What is the Tx for charcot foot deformity? | acute: off loading until edema resolves, later is use specialized footweat to maintain a stable foot |
| What is seen in peripheral mononeuropathy in DM? | single nerve damage, wrist, foot drop |
| What is seen most commonly in cranial mononeuropathy in dM? | unilateral paiun near affected eye due to CN III being most commonly involved, pupil is spared |
| What is the tx for gastroparesis in DM? | small frequent meals, metoclopramide, erythromycin |
| How can DM lead to atherogenesis? | get hyperglycemia, exces FFA, insulin resitance which lead to alternative pathways and oxidative stress. this leads to endothelial dysfunction |
Created by:
tjs2123
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