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Pharm - EXAM 2
Diabetes
| Question | Answer |
|---|---|
| What ethnic group is DM most prevalent? | American Indian and Alaska natives |
| What ethnic group is 2nd most prevalent in getting DM? | Non-Hispanic Blacks |
| What vascular complications occur with DM? | Heart disease and stroke (leading cause of diabetic-related deaths; 2 - 4 x higher in DM; increase rate of atherosclerosis) |
| How does DM cause retinopathy? | DM causes abnormalities of the small blood vessels of the retina. |
| What other eye disorders are prevalent in DM patients? | Glaucoma, cataracts, corneal disease |
| What other complications are more prevalent in DM patients? | Hypertension, nephropathy, neuropathy, peripheral vascular disease, dental disease |
| How does poorly controlled diabetes affect pregnancy in the 1st trimester? | Leads to birth defects and spontaneous abortion. |
| How does poorly controlled diabetes affect pregnancy in the 2nd trimester? | Leads to high birth weight babies. |
| How are diabetic complications prevented? | Keep HbA1C < 7%; maintain BP < 125 - 130/75 - 80; maintain LDL < 70 - 100 |
| What antihypertensive class may decrease the progression of nephropathy? | ACE inhibitors (lower dose) |
| What is the diagnostic criteria for DM? | Symptoms (polyuria, polydipsia, polyphagia, weight loss, signs of complications) PLUS a random plasma glucose > 200 mg/dl. |
| Besides symptoms and glucose > 200, list 2 other criteria that is also considered diagnostic for DM. | 1. Fasting plasma glucose > 126 mg/dL or 2. two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test (not usually done unless pt is pregnant) |
| What is HgA1c? | It's a reflection of glucose levels over the last 6 weeks. |
| What is a normal HgA1c for a non-diabetic? | < 6% |
| What is a normal HgA1c for a diabetic? | < 7% |
| What other value can be calculated to show patients how HgA1c reflects what the average is of their actual glucose? | Estimated Average Daily Glucose (eAG) |
| Which diabetes is because of absolute insulin deficiency? | Type I - the pancreas doesn't make insulin |
| How is Type I diabetes treated? | Must replace the insulin that the body is unable to produce. |
| What causes type I diabetes? | Autoimmune destruction of pancreatic beta cells which may be triggered by environmental factors |
| What are the 4 main features of type I DM? | 1. Long preclinical period, 2. hyperglycemia after 80 - 90% of islet cells are destroyed in the pancreas, 3. transient remission with "honeymoon phase" and 4. established disease |
| Which diabetes is caused by insulin resistance? | Type II - insulin is being made, the body is just unable to use it correctly; relative insulin deficiency |
| What does insulin resistance lead to? | 1. lipolysis 2. free fatty acid production, 3. increase in hepatic glucose production (cells aren't using glucose correctly so it tells the liver that they need more), 4. decreased skeletal uptake of glucose |
| What causes type 2 DM? | Diabetogenic lifestyle (excessive calories, inadequate calorie expenditure, obesity) and genetic predisposition |
| True or False: The cardiovascular risk begins after the development of hyperglycemia. | False; the risk begins prior to the development of hyperglycemia. Some patients may have a vascular event before high sugars are detected. |
| List the other types of DM. | Gestational, genetic defects of insulin receptors or beta cells, pancreatic disease, drug-induced (corticosteroids) |
| What are the other names of Syndrome X? | Pre-diabetes, insulin resistance syndrome, metabolic syndrome, dysmetabolic syndrome. |
| What are the features of Syndrome X? | Insulin resistance, HTN, elevated fibrinogen and plasminogen activator inhibitor (markers of inflammation), and low HDL and high LDL |
| If Syndrome X is suspected, can precautions be taken to prevent the development of diabetes? | Yes; BP should be maintained WNLs, low HDLs and high LDLs should be treated, fibrinogen and plasminogen activator inhibitor should be lowered by figuring out what is causes them to be elevated. |
| What non-pharmacological treatments can be given for a diabetic patient? | Lifestyle modification, maintain weight, diet, and aerobic exercise. |
| What type of diet should a diebetic patient be on? | Caloric restriction to reach no more than 20% above IBW; low fat, low cholesterol; debate over carbohydrates |
| What kind of patient education is needed for a diabetic patient? | Effectiveness of prescribed therapy, disease teaching, diet teaching, medication teaching, self-glucose monitoring |
| What aspects of self-glucose monitoring should be taught? | Maintaining a diary of glucose levels and hypoglycemic episodes, syring technique |
| How is a patient's glucoses monitored? | Self monitoring, HgA1c, diary, have patient show you how they give themselves injections and how they use the meter. |
| What are the major classes of diabetic medication therapy? | Insulin, oral agents, incretin and amylin mimetics |
| What are the classes of oral agents used to treat diabetes? | Sulfonylureas, short acting secretogogues, biguanides, thiazolidinediones, alpha-glucosidase inhibitors, dipeptidyl peptidase-4 inhibitor |
| What are the anabolic physiologic effects of insulin? | glucose uptake in muscle, brain & organs; and putting down stores by glycogen synthesis, and lipogenesis |
| What are the anticatabolic (antibreakdown) physiologic effects of insulin? | Inhibits gluconeogenesis, inhibits glycogenolysis, inhibits lipolysis. These inhibit breakdown of sugar and lipids to keep sugar in teh blood consistent so it goes into the cells to be utilized. |
| For type 2 diabetes, how do medications help the cells secrete insulin? | 1. Some drugs act on insulin granules to put insulin out 2. some drugs act on calcium channel, 3. some drugs act on K channel and Na/K pump, and 4. some drugs act on Glut 2 receptors to help more insulin out of cell. |
| What are the sources of insulin that are no longer made in the U.S.? | Beef (differs from human by 3 amino acids), pork (differs from human by 1 amion acid), beef-pork mixture |
| What is the main source of insulin that is used? | Human made from recombinant technology. |
| Is human insulin preparations allergenic? | No. Should be non-allergenic. |
| What are the major insulin preparations? | Ultra-fast/ultra short-acting, short-acting, intermediate-acting, long-acting, and ultra long acting. |
| What are the symptoms of hypoglycemia? | Tachycardia, trmulousness, confusion, agitation, seizures, aphasia |
| How is hypoglycemia treated? | Oral glucose if possible; IV glucose (D50); glucagon 1 gm IM in thigh |
| What is lipohypertrophy? | An adverse effect of insulin that causes an increased fat mass at the injection site which delays absorption of insulin at the site. |
| What is lipoatrophy? | Antibody formation that causes destruction of fat and the injection site which changes the absorption of insulin at the site. |
| How is lipohypertrophy and lipoatrophy treated? | Rotation of injection sites. |
| What is the best site for insulin injection? | Abdomen |
| How does a hypoglycemic agent cause a drug-drug interaction? | Potentiation of the effect leading to hypoglycemia. |
| How does a diuretic agent cause a drug-drug interaction? | Increases blood glucose |
| How does a glucocorticoid cause a drug-drug interaction? | Increases blood glucose |
| How does phenytoin cause a drug-drug interaction? | Increase blood glucose |
| How do beta-blockers cause a drug-drug interaction? | Can increase or decrease blood glucose. Can also blunt the sx of hypoglycemia such as tachycardia and tremulousness so may not recognize a low BG the way they used to if they are on a beta-blocker. |
| What patient populations are at higher risk for hypoglycemic events while on sulfonylureas? | Elderly, renal insufficiency, and liver disease |
| What are some pearls for Type I DM's? | 1. Eating must be planned around peak insulin times. 2. No vigorous activity in limb that just received an insulin injection 3. Different sites have different absorption times. |
| What is the Somogyi Phenomenon? | A rebound hyperglycemic period following a hypoglycemic episode. |
| What causes the Somogyi Phenomenon? | When the body senses hypoglycemia, it releases counter-regulatory hormones to produce more glucose. However the body doesn't have the mechanisms to handle the extra sugar. |
| How is the Somogyi Phenomenon detected? | The patients wake up with hyperglycemia in the morning. Pts should wake themselves at 2 am to check their blood sugar and keep a diary. |
| How is the Somogyi Phenomenon avoided? | If patient's blood glucose is low in the middle of the night, the patient's nighttime insulin is decreased to avoid hypoglycmia during the night. |
Created by:
HJR
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