Pharm exam 3

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Pharm exam 3
2013-07-18 09:33:37

pharm exam 3
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  1. what are the microvascular complications of diabetes
    • retinopathy
    • neuropathy
    • nephropathy
  2. what are the macrovascular complications of diabetes
    • heart attacks
    • stroke
    • peripheral vascular disease
  3. what are the acute complications of diabetes
    • hypoglycemia
    • DKA
    • hyperosmolar nonketotic syndrome (HNKS)
  4. what are the risk factors for diabetes
    • physical inactivity
    • 1st degree relative with diabetes
    • high-risk ethnicity
    • women who delivered a baby >9lbs or dx with GDM
    • females with PCOS
    • HTN
    • history of CVD
    • HDL<35mg/dl and/or TG >250mg/dl
    • HbA1C ≥ 5.7%, IGT or IGF on previous tests
  5. what are the different classifications of diabetes
    • type 1
    • type 2
    • gestational
  6. screening is used performed to detect which type of diabetes
    type 2
  7. at which age do you begin testing for DM type 2 and if tests are normal, how often do you repeat the test
    • - begin at 45 y/o without risk factors
    • - consider in adults of any age who are obese or overweight and have one or more additional risk factors

    * if tests are normal, repeat at least every 3 years
  8. what are the diagnostic testing for DM
    • random plasma glucose
    • fasting plasma glucose
    • 75 gm oral glucose tolerance test
    • hemoglobin A1C (HbA1C)
  9. for a fasting plasma glucose, what are the normal levels and what are the abnormal readings with interpretation
    • normal: <100mg/dL
    • impaired fasting glucose: 100-125 mg/dL (reflects hepatic glucose output)
    • diabetes: ≥ 126 mg/dL
    • impaired glucose tolerance: 140-199 (reflects glucose uptake by peripheral tissues, ie tissue insensitivity)
    • diabetes: ≥ 200 mg/dL
  10. for an oral glucose tolerance test (2hr postload), what are the normal levels and what are the abnormal readings with interpretation
    • normal: <140mg/dL
    • impaired glucose tolerance: 140-199 mg/dL (reflects glucose uptake by peripheral tissues, ie insulin insensitivity)
    • diabetes: ≥ 200 mg/dL
  11. for a HbA1c test, what are the normal levels and what are the abnormal readings with interpretations
    • normal: <5%
    • increased risk for diabetes: 5.7-6.4%
    • diabetes: ≥ 6.5%
  12. what are the goals of therapy for DM
    • fasting plasma glucose: 70-130 mg/dL
    • post-prandial plasma glucose: <180 mg/dL
    • HbA1c: < 7%
    • BP: <130/80 (<125/75 mmHg if proteinuria)
    • LDL: <100 mg/dL (<70 mg/dL with overt CVD)
    • HDL: >40 (men) >50 (female)
    • TG: <150 mg/dL
  13. what are the lifestyle changes to help with diabetes prevention
    • weight loss of 7% body weight
    • moderate physical activity of at least 150 min/wk
  14. what are the medications use in diabetes prevention
    • - metformin 500-1700 mg/d*
    • - acarbose (precise) 300mg/d
    • - orlistat (xenical) 360 mg/day
    • - rosiglitazone (Avandia) 8 mg/d

    * consensus panel felt that metformin should be the only drug considered for prevention due to cost, S/E, and lack of a persistent effect seen with the other drugs
  15. what type of diabetes results from β-cell destruction, usually leading to an absolute insulin deficiency and what is the DOC
    type I

  16. what is the MOA of insulin
    • - replaces (type I) or supplements (type II) endogenous insulin
    • - facilitates the disappearance of glucose from the circulation into insulin-sensitive peripheral tissues & inhibits hepatic glucose output and glucagon secretion
  17. what are the adverse effects of insulin
    • hypoglycemia
    • weight gain
    • lipodystrophies
  18. dimpling at the skin at injection site due to fat breakdown is known as what
  19. a fat mass occurring at the injection site is known as what
  20. what are your bolus insulins (controls post-prandial hyperglycemia)
    • rapid-acting insulin
    • short-acting insulin
  21. what are your basal insulins (controls fasting hyperglycemia)
    • intermediate-acting insulin
    • long-acting insulin
  22. what are the names of your rapid-acting insulin
    • lispro (Humalog)
    • aspart (novolog)
    • glulisine (apidra)
  23. what is the name of your short-acting insulin
    regular (Humulin R) (novolin R)
  24. what is the name of your intermediate-acting insulin
    NPH (humulin N) (novolin N)
  25. what are the names of your long-acting insulin
    • glargine (lantus)
    • detemir (levemir)
  26. what are your NPH-regular combinations
    • humulin 70/30
    • novolin 70/30
  27. what are you insulin analog combinations
    • Humalog mix 75/25 (neutral protamine lispro/lispro)
    • Humalog mix 50/50 (neutral protamine lispro/lispro)
    • novolog mix 70/30 (aspart protamine suspension/ aspart)
  28. what are the factors that affect insulin pharmacokinetics
    • administration
    • clearance
    • absorption
  29. for the sites of injection for insulin, where is the most rapid to the least rapid absorption
    • abdominal fat
    • posterior upper arms
    • lateral thigh area
    • superior buttocks area
  30. which type of insulin is a highly concentrated form of human regular insulin, and is used in pts with severe insulin resistance (require insulin doses >200 units/day)
    U-500 insulin
  31. the ISMP recommends administration of insulin through which type of syringe
    tuberculin syringe
  32. if a U-100 syringe is used, how is the dosage measured for U-500
    U-100 unit markings = U-500 dose (actual units) x 0.2
  33. if a tuberculin syringe is used, how is the dosage measure for U-500
    tuberculin syringe vol = U-500 dose (actual units) x 0.002
  34. what is the non-insulin injectable for type I DM (controls post-prandial hyperglycemia)
    pramlintide (amylin)
  35. what is the onset, peak, duration, and maximum duration of aspart (novolog)
    • onset: 15-30 min
    • peak: 1-2 hours
    • duration: 3-5 hours
    • max duration: 5-6 hours
  36. what is the onset, peak, duration, and max duration of lispro (Humalog)
    • onset: 15-30 min
    • peaks: 1-2 hours
    • duration: 3-4 hours
    • max duration: 4-6 hours
  37. what is the onset, peak, duration, and max duration of glulisine (aspidra)
    • onset: 15-30 min
    • peak: 1-2 hours
    • duration: 3-4 hours
    • max duration: 5-6 hours
  38. what is the onset, peak, duration, and max duration of regular (humalin R/novolin R)
    • onset: 30-60 min
    • peak: 2-3 hours
    • duration: 4-6 hours
    • max duration: field was blank
  39. what is the onset, peak, duration, and max duration of NPH(humalin N/novolin N)
    • onset: 2-4 hours
    • peak: 4-8 hours
    • duration: 8-12 hours
    • max duration: 14-18 hours
  40. what is the onset, peak, duration, and max duration of detemir (levemir)
    • onset: 2 hours
    • peak: mild
    • duration: 14-24 hours
    • max duration: up to 24 hours

    * daily for type II; often BID for type I
  41. what is the onset, peak, duration, and max duration of glargine (lantus)
    • onset: 4-5 hours
    • peak: none
    • duration: 22-24 hours
    • max duration: 24 hours
  42. what is the correction factor for insulin when the pre-meal glucose is high
    • correction factor = 1500/TDD (regular insulin)
    • correction factor = 1800/TDD (rapid-acting insulin's)
  43. what is the equation to determine the correction dose of insulin
    (current BG - desired BG)/correction factor = correction dose
  44. when planning meals or counting CHOs, how is the insulin-to carbohydrate figured
    • 450/TDD = CHO coverage dose (regular insulin)
    • 500/TDD = CHO coverage dose (rapid-acting insulin's)
  45. insulin syringes measure what
  46. tuberculin syringes measure what
  47. how is the insulin dose adjusted if pre-breakfast blood glucose is high/low
    adjust the evening basal insulin dose
  48. how is the insulin dose adjusted if the pre-lunch blood glucose is high/low
    adjust breakfast rapid/reg insulin dose
  49. how is the insulin dose adjusted if the pre-supper blood glucose is high/low
    adjust morning basal insulin dose (and/or pre-lunch dose)
  50. how is the insulin dose adjusted if the pre-bedtime blood glucose is high/low
    adjust supper rapid/reg insulin dose
  51. how is the insulin dose adjusted if the 2-hr post prandial glucose is high/low
    adjust pre-meal rapid/reg insulin dose
  52. how is the insulin dose adjusted if the 0300 blood glucose is high/low
    adjust evening basal insulin dose
  53. how often are stable pts tested for HbA1c, and how often are pts not meeting goal tested
    • stable: twice a year
    • not meeting goal: quarterly/ or when changing dose
  54. how often is self- monitoring of blood glucose measured in type I and type II diabetics
    • type I: ideally 4-7x a day; at least 3 or more times daily
    • type II: often daily
  55. when are ketones tested for in diabetic pts
    • type I/II DM: when BG is consistently > 250/400 mgdL
    • GDM: during acute illnesses and when symptoms of ketoacidosis are present
  56. what are the common medications that affect glycemic control by increasing glucose levels
    • atypical (2d gen) antipsychotics
    • diuretics (thiazides)
    • glucocorticoids
    • niacin
    • oral contraceptives
    • phenytoin
    • sympathomimetics
  57. what are the common medications that affect glycemic controls by decreasing glucose levels
    • ACEI
    • alcohol
    • salicylates (high-dose)
  58. which type of diabetes is characterized by insulin resistance and a relative lack of insulin secretion over time, and have a progressive decline in β-cell function and insulin secretion
    type 2
  59. insulin resistance related to weight gain is proportional to what
    amount of visceral adipose tissue
  60. what improves insulin sensitivity and decreased with increasing obesity
  61. what medications are in the insulin secretagogue pharmacological class
    • sulfonylureas
    • metglitanides (repaglinide and nateglinide)
  62. what medication is in the biguanide pharmacological class
  63. what medications are in the A-glucosidae inhibitor pharmacological class
    • acrabose
    • miglitol
  64. what medication is in the thiazolidinediones pharmacological class
    • pioglitazone
    • rosiglitazone
  65. what medication is in the amylin analogue pharmacological class
  66. which medications are in the GLP-1 agonist pharmacological class
    • exantide
    • liraglutide
  67. which medications are in the DPP-4 inhibitor pharmacological class
    • sitagliptin
    • saxagliptin
  68. what is the medication in the bile acid sequestrants pharmacological class
  69. what is the medication in the dopamine agonist pharmacological class
  70. when HbA1c is low, what is the major contributor to overall hyperglycemia
    postprandial glucose
  71. when HbA1c is high, what is the major contributor to overall hyperglycemia
    fasting plasma glucose
  72. what is the average daily requirement of insulin
    ~0.5 units/kg
  73. what is the MOA of sulfonylureas
    binds to specific sulfonylurea receptor on the pancreatic β cell leading to enhancement of insulin secretion (2d phase)
  74. what are the adverse effects of sulfonylureas
    • hypoglycemia
    • weight gain
  75. what drug interactions occur with sulfonylureas
    • - protein displacement
    • - altered hepatic metabolism:↑ SU concentration (cimetidine- enzyme inhibitor)
    • ↓ SU concentration (rifampin- enzyme inducer)
    • - glyburide-bosentan (tracleer) CI
    • - GLP-1 agonist and DPP-4 inhibitors: consider ↓ing the sulfonylurea dose by 50% to ↓ the hyperglycemia risk
  76. which pharmacological classes target fasting and what is the typical HbA1c reduction
    • - human insulin & insulin analogs (basal)- as necessary to achieve goal
    • - insulin secretagogues (SU)- 1.5-2 %
    • - biguanide- 1.5-2%
    • - thiazolidinediones- ~1-1.5%
    • - bile acid sequestrants- ~0.4%
  77. which pharmacological classes target post-prandial glucose and what is the typical HbA1c reduction
    • - human insulin & insulin analogs (bolus): as necessary to achieve goal
    • - insulin secretagogues (non-SU)- 0.8-1%
    • - amylin analogue- 0.3-0.7%
    • - GLP-1 agonists- ~0.9-1.1%
    • - DPP-4 inhibitors- ~0.7-1%
  78. which pharmacological classes target both fasting and post-prandial glucose and what is the typical HbA1c reduction
    dopamine agonist- ~0.5-0.7%
  79. if a pt has an issue with insulin secretion, which class of drugs do you want to use
    • insulin
    • insulin secretagogues
    • GLP-1 agonist
    • DPP-4 inhibitors
  80. if a pt has an issue with insulin resistance, which class of drugs do you want to use
    • biguanides
    • thiazolidinediones
    • dopamine agonist
  81. what are your second generation sulfonylureas
    • glipizide (Glucotrol)
    • glipizide XL (Glucotrol XL)
    • glyburide (diabeta; micronase)
    • glyburide, micronized (glynase)
    • glimepiride (amaryl)
  82. what is the MOA for non-sulfonylurea secretagogues
    stimulate insulin secretion from the beta cells of the pancreas
  83. what are the adverse events of non-sulfonylurea secretagogues
    • hypoglycemia
    • weight gain
  84. what are the names of the non-sulfonylurea secretagogues
    • nateglinide (starlix)-- weight gain
    • repaglinide (prandin)-- weight gain
  85. which class of drugs do you want to consider for individuals who have a history of skipping meals or eat on an irregular schedule
  86. what is the MOA of Biguanide
    decreases hepatic glucose production, and increases insulin sensitivity of hepatic and peripheral (muscle) tissues
  87. what is the dosing of Biguanides
    • given with largest meals to minimize GI SE
    • only labeled oral agent for use in children (10-16 years)
  88. what is the only oral antihyperglycemic agent shown to reduce the risk of total mortality
    metformin (Glucophage)
  89. what are the adverse events of biguanides
    • diarrhea
    • metallic taste
    • decreases vit b12 absorption
    • CI if Scr >1.4 in females, 1.5 in males
    • CI if increased risk for lactic acidosis
  90. what are the situations when using biguanides that increase and reducing lactic acid
    • tissue hypoperfusion (increase)
    • liver disease and alcohol (removal in liver)
  91. what are the drug interactions with biguanide
    hold metformin if radiographic iodinated contrast media is given and resume 2-3 days later after normal renal function documented
  92. what are the names of the biguanides
    • Immediate release: metformin (Glucophage)
    • metformin (riomet)
    • Extended release: metformin XR (Glucophage XR)
    • metformin ER (Fortamet XR)
    • metformin (glumetza)
  93. when are a-glucosidase inhibitors taken
    doses are taken with 1st bite of meal and titrated slowly
  94. what are the AE of a-glucosidase inhibitors
    GI(gas, abdominal discomfort, diarrhea)
  95. if a pt is on either an a-glucosidase inhibitor and he becomes hypoglycemic, what should be given to the pt
    glucose or alternatively milk (lactose)
  96. what are the names of the a-glucosidase inhibitors
    • acarbose (precise)
    • miglitol (glyset)
  97. which medication class binds the peroxisome proliferator activator receptor-γ, enhancing insulin sensitivity at skeletal muscle, liver, and fat cells
    thiazolidinedione (TZDs)
  98. what are the negative outcomes of TZDs
    • fatal/non-fatal hepatoxicity (draw baseline LFTs and secondary any suspicion of liver disease)
    • lipids (increase LDL)
    • heart failure
    • MI
    • eye exams
  99. what are the adverse events with TDZs
    • fluid retention/edema
    • CI in NYHA class III/IV HF
    • weight gain
    • increased fracture rate
    • MI
    • macular edema
    • hepatic failure
  100. what are the names of the TDZs
    • pioglitazone (actos) (if used more than a year may be associated with increased risk of bladder CA)
    • rosiglitazone (Avandia)
  101. The transport triglycerides, cholesterol and phospholipids derived from the diet or synthesized in the intestine from the gut to the liver, adipose tissue and muscle
  102. These are formed mainly in the liver and some in the intestine, they transport endogenous triglycerides and cholesterol, the remnants are either converted into LDL or removed from the systemic circulation
  103. These are formed by VLDL catabolism, they transport cholesterol to the cells, and make the greatest contribution to the development of atherosclerosis
  104. These are formed in the liver and intestines, and they transport cholesterol from peripheral cells to the liver which is beneficial because cholesterol is removed from vasculature
  105. What are the major risk factors for atherosclerosis
    • Elevated cholesterol/LDL cholesterol
    • Smoking
    • Hypertension BP greater or equal to 140/90 or on antihypertensive medication
    • Low HDL cholesterol <40 mg/deciliter
    • Family history of premature CHD
    • Age (men > 45 years; women > 55 years)
  106. what are the optimal levels, near/above optimal, borderline high, high and very high levels of LDL cholesterol
    • <100 optimal
    • 100-129 near/above optimal
    • 130-159 borderline high
    • 160-189 high
    • ≥ 190 very high
  107. what are the readings for normal, borderline high, high, and very high for TG levels
    • <150 normal
    • 150-199 borderline high
    • 200-499 high
    • ≥ 500 very high
  108. what are the bad and good levels for HDL
    • <40 low (bad)
    • ≥60 high (good)
  109. what are the desirable, borderline high, high, and very high levels for total cholesterol
    • <200 desirable
    • 200-239 borderline high
    • >240 high
    • >280 very high
  110. for a pt with CHD or CHD risk equivalents, what should their LDL goal be, at what LDL level do you initiate therapeutic lifestyle changes, and at what LDL level do you consider drug therapy
    • goal <100
    • therapeutic lifestyle changes ≥100
    • consider drug therapy ≥130 (100-129;drug optional)
  111. if a pt has 2 risk factors for atherosclerosis, what is their LDL goal, the level to initiate therapeutic lifestyle changes, and level to consider drug therapy
    • goal <130
    • initiate therapeutic lifestyle changes ≥130
    • level to consider drug therapy 10 year risk 10-20% ;≥130; 10 year risk <10%; ≥160
  112. if a pt has 0-1 risk factors for atherosclerosis, what is their LDL goal, level to initiate therapeutic lifestyle changes, and when to consider drug therapy
    • goal <160
    • therapeutic lifestyle change ≥160
    • drug therapy ≥190 (160-189; LDL lowering drug option)
  113. what are some ways for the pt to reduce CVD risk
    • stop smoking
    • diet&exercise
    • control BP
    • daily low dose ASA
    • increase HDL cholesterol
  114. which drug class reduces major acute coronary events, CHD mortality, coronary procedures, stroke and total mortality, and is the most potent LDL lowering agent
    HMG-CoA reductase inhibitors
  115. what are the HMG-CoA reductase inhibitors (statins) place in therapy
    elevated LDL and/or VLDL
  116. what are the major side effects of statins (HMG-CoA reductase inhibitors)
    • myopathy and rhabdomyolysis
    • increased liver enzymes
  117. what are the CI of the statins
    • absolute: liver disease
    • relative: use with certain drugs that inhibit the P4503A4 enzyme system (macrolides, CCB, and azole antifungals)
  118. what are your drug names for the HMG-CoA reductase inhibitors (statins)
    • simvastatin (zocor)- pm dosing
    • atorvastatin (lipitor)- dose anytime
    • fluvastatin (lescol)- pm dosing (no food)
    • lovastatin (mevacor)- pm dosing with food
    • pravastatin (pravachol)- pm dosing (no food)
    • rosuvastatin (crestor)- dose anytime
  119. what are the statin drug/drug interactions
    • HMG-CoA reductase inhibitors and fibric acid derivatives- severe myopathy or rhabdomyolysis has been reported with lovastatin
    • HMG-CoA reductase inhibitors and nicotinic acid- concurrent administration increases risk of severe myopathy or rhabdomyolysis and liver toxicity
  120. the evening doses of statins is to coincide the drug with what
    with the nighttime upturn in endogenous cholesterol biosynthesis
  121. what are the most efficacious statins on the market
    atorvastatin and rosuvastatin
  122. which statins do not require adjustment for renal insufficiency
    atorvastatin and fluvastatin
  123. which statins have not been reported any serious interactions with cytochrome P450
    pravastatin and fluvastatin
  124. which statin is not highly protein bound
  125. What is the MOA of the bile acid sequestrants
    anion exchange resins that bind negatively charged bile acids and bile salts in the small intestine for excretion leading to more cholesterol being converted into bile acids
  126. what are the side effects of the bile acid sequestrants
    • GI stress/constipation
    • decreased absorption of other drugs, fat-soluble vitamins, folic and ascorbic acid.
    •    *** there should be a 4 hour window between these and other medications
  127. why do you want to use caution with bile acid sequestrants in pts with TG(especially >400mg/dl)
    the increase in hepatic cholesterol biosynthesis may result in increased VLDL production
  128. what are the names of the bile acid sequestrants
    • colestipol (colestid)
    • cholestyramine (questran)-power only, mix with fruit juice
    • colesevelam (welchol)
  129. what is the newest bile acid binding agent, it is more potent so pts take smaller doses and has fewer GI S/E and less interference with absorption of other drugs
    colesevelam (welchol)
  130. which cholesterol lowering meds are the only approved agents in pregnancy
    bile acid sequestrants
  131. which drug reduces the hepatic synthesis of VLDL by inhibiting lipolysis, a reduction in VLDL results in decreased plasma LDL
    nicotinic acid
  132. which cholesterol lowering medication is the best agent to increase HDL
    nicotinic acid
  133. what are the S/E of nicotinic acid
    • flushing and itching
    • hyperglycemia
    • hyperuricemia (caution in gout)
    • upper GI distress
    • hepatotoxicity
  134. what are the CI of nicotinic acid (niacin)
    • liver disease
    • active peptic ulcer hypersensitivities
  135. what can you do for a pt to help reduce the side effects of flushing and itching when taking nicotinic acid (niacin)
    • administer ASA 30 min prior
    • taking niacin with meals
    • titrating the dose upward slowly
    • using controlled release products
  136. what is the disadvantage of using nicotinic acid (niacin)
    difficult to get pt to a therapeutic dose
  137. which cholesterol lowering medication stimulates lipoprotein lipase activity which hastens the removal of chylomicrons and VLDL from the plasma (and subsequently decreases TG)
    fibric acids
  138. what is the primary place of fibric acids in therapy
  139. what are the S/E of fibric acids
    • GI disturbances
    • gallstones
    • GI malignancy
    • myopathy
    • muscle inflammation
  140. what are the CI of fibric acids
    • severe renal or hepatic disease
    • ** interacts with warfarin (must decrease warfarin dose)
  141. what are the drug names of the fibric acids
    • gemfibrozil (lopid)-- 30 min ac
    • fenofibrate (tricor, antara, lofibra) -- only one used for daily dosing
  142. what is your selective cholesterol absorption inhibitor
    ezetimibe (zetia)
  143. which lipid medication inhibits absorption of cholesterol at the brush border of the small intestine
    ezetimibe (zetia)
  144. which lipid medication is approved for children 10-18 years of age
    ezetimibe (zetia)
  145. what is the first choice of cholesterol medications to start a pt on

    ** if CI then alternatives are bile acid sequesterants or nicotinic acids)
  146. if after 6 weeks of therapy the LDL goal is not achieved, what is the progression of drug therapy
    • consider higher dose of statin or add a second drug
    • bile acid sequestrants are a good second choice with statins (watch TG)
  147. if after 6 weeks of adding on a second drug and the LDL goal is still not reached, what is the progression of drug therapy
    intensify drug therapy or refer to a lipid specialist
  148. how often is drug therapy for LDL monitored
    q 4-6 mo
  149. what are the approved medications for hypertriglyceridemia
    • niacin
    • fibrates
    • statins (atorvastatin is only one approved)
  150. which cholesterol medication should be avoided in diabetics
  151. which medication is a bulk forming laxative that does have some LDL lowering ability
    psyllium (Metamucil)
  152. what are the adverse effects of metamucil
    flatulence and bloating
  153. before selecting a HMG-CoA reductase inhibitor, what should be done
    LFTs before starting and at 6 and 12 weeks after starting and then about q 6 mos

    if levels go to 3 times the upper normal limits-- stop medication
  154. when should HMG-CoA reductase inhibitor therapy be evaluated
    6 weeks
  155. what controls the release of hormones from the anterior and posterior pituitary
  156. when is exogenous hypothalamic or pituitary hormone therapy applied
    • replacement therapy for hormone deficiency
    • antagonist for disease that result in excess production of pituitary hormones
    • diagnostic tools for endocrine disorders
  157. what inhibits the release of growth hormone, glucagon, insulin and gastrin
  158. what are the approved uses for GHIH
    • treatment for acromegaly
    • control of symptoms in pts with metastatic carcinoid and vasoactive intestinal peptide-secreting tumors (VIPomas)
  159. what are the endogenous and exogenous products of GHIH
    • endogenous- somatostatin
    • exogenous:
    • lanreotide (somatulin)- approved for acromegaly only)
    • octreotide (sandosatin)- more potent than somatostatin at inhibiting GH release
  160. which hormone is a diagnostic agent used to differentiate between pituitary (cushings disease) and ectopic production of ACTH
  161. administration of CRH in a pt with Cushing's will result in what
    additional ACTH and cortisol secretion
  162. when giving CRH, if a pt has an ectopic production of ACTH what will occur
    they will not respond with additional ACTH and cortisol secretion
  163. what is the medication name for CRH
    corticorelin (acthrel)
  164. what are the approved uses for GnRH
    • diagnostic agent (factrel)
    • primary hypothalamic amenorrhea (factrel)--pulse doses stimulate FSH and LH release
    • breast CA (zoladex)-- continuous doses→ medical castration)
    • prostate CA (zoladex, Lupron)-- continuous dose
    • endometriosis (zoladex, Lupron, synarel)-- continuous dose x 6 months only)
    • central precocious (before 8 in girls, 9 in boys) puberty (synarel)-- continuous dose
  165. what are the products of GnRH
    • gonadorelin (factrel for inj)
    • goserelin (zoladex)
    • leuprolide (Lupron, eligard, viadur)
    • nafarelin (synarel)
    • triporelin (telstar depot)
  166. what are the approved uses of dopamine agonists
    • tx of hyperprolactinemia
    • tx of prolactin-secreting ademoa
    • tx of acromegaly
  167. what are the dopamine agonist products
    • bromocriptine (parlodel)
    • cabergoline (dostinex)
  168. what are the clinical uses of GH in adults
    • HIV pts with wasting
    • replacement therapy for adults with GH deficiency
    • short bowel syndrome
  169. what are the GH products
    somatotropin (genotropin, humatrope, norditropin-ECF, nutropin, omnitrope, saizen, serostim, tev-tropin, zorbtive)
  170. what are the approved uses for GH antagonists
    tx of acromegaly resistant to or unable to tolerate other therapies
  171. what is the most effective agent at normalizing IGF-1 serum concentrations
    GH antagonist
  172. what is the GH antagonist agent
    pegvisomant (somavert)
  173. what are the approved uses for TSH (thyrotropin)
    diagnostic agent for detecting blood levels of the thyroglobulin to exclude the dx of residual or recurrent thyroid cancer following a thyroidectomy
  174. what are the TSH (thyrotropin) agents
    thyrotropin alfa (thyrogen)
  175. what are the approved uses for adrenocorticotropic hormone (ACTH)
    diagnostic agent used to differentiate between primary adrenal insufficiency (Addison's disease; adrenal gland disorder) and secondary adrenal insufficiency caused by inadequate ACTH secretion (pituitary disorder)
  176. what is the ACTH product
    cosyntropin (cortrosyn)
  177. what are the approved uses of FSH and LH
    • ovulation induction (FSH)
    • ovulation induction (LH) in infertile females with LH deficiency
    • spermatogenesis induction (FSH)
  178. what are the FSH and LH products
    • follitropin alfa (rFSH, gonal-f, gonal-f RFF)
    • follitropin beta (rFSH, follistim AQ)
    • urofollitropin (uFSH, bravelle)

    lutropin alfa (luveris)
  179. what are the approved uses for oxytocin
    • during labor
    • stimulate uterine contraction
    • post-partum
    • stimulate lactation
    • control post-partum bleeding
  180. what are the oxytocin products
    oxytocin (Pitocin) for inj
  181. which dopamine antagonist is also used (off label) to stimulate lactation
    metoclopramide (reglan)
  182. what are the approved uses of vasopressin (ADH, AVP)
    acts of the renal collecting ducts to conserve water; used in the diagnosis and tx of diabetes insipidus)

    - pressor (no cardiac properties) used in the ACLS algorithm for VF/pulseless VT
  183. what are the vasopressin products
    vasopressin (pitressin)
  184. what are the approved uses of desmopressin (DDVAP)
    • tx of DI (nasal DDAVP)
    • control bleeding associated with hemophilia A and von Willebrand's disease (nasal Stimate)
    • primary nocturnal enuresis (tablet DDVAP)
  185. what are the desmopressin products
    • desmopressin (DDVAP for inj, nasal, tab)
    • desmopressin (stimate nasal)
  186. circulating T3 and T4 are bound to what
    • thyroxine binding globulin (70%)
    • thyroxine-binding prealbumin (15%)
    • albumin (10-15%)
  187. what are the etiologies of primary hypothyroidism
    • hashimotos disease (most common in developed countries)
    • sx, radiation, or radioiodine induced (iatrogenic)
    • iodine deficiency (most common worldwide)
  188. what are etiologies of secondary hypothyroidism
    • hypothalamus or pituitary insufficiency (central hypothyroidism)
    • drug induced
  189. untreated hypothyroidism in infants and children results in what
  190. what are the treatment goals of hypothyroidism
    • provide exogenous thyroid hormone
    • normalize TSH and FT4 concentrations
    • - TSH: 0.4 - 4.2 microIU/dL
    • - FT4: 0.8 - 2.3 ng/dL
    • - FT3: 1.4 - 4.2
    • minimize the symptoms and long-term consequences of hypothyroidism
  191. what is the name of the synthetic T3 in thyroid replacement
    liothyronine (cytomel)
  192. what is the name of synthetic T4 in thyroid replacement
    levothyroxine (synthroid)
  193. what is the name of synthetic T4:T3 (4:1) in thyroid replacement
    liotrix (thyrolar)
  194. what is the name of the animal sources for thyroid replacement
    desiccated thyroid (armour thyroid)
  195. what is the drug of choice when giving a thyroid replacement medication
    levothyroxine (synthroid)
  196. what is the recommended dosing for thyroid replacement medications
    often recommended on an empty stomach on the AM to avoid episodes of insomnia, but can be given daily at bedtime
  197. what are the adverse events when giving a thyroid replacement med
    S/S of excessive thyroid (worsening cardiac function, decreased bone mineral density leading to osteopenia/osteoporosis)
  198. what are the drug interactions associated with thyroid replacement meds
    • decreased drug absorption: ferrous sulfate, bile acid sequestrants
    • increased drug clearance: phenytoin, carbamazepine, rifampin
    • decreased FT4: estrogens (by increasing thyroid binding globulin levels)
    • block conversion of T4 to T3: amiodarone, propanolol
    • inhibit synthesis and release of thyroid hormone: lithium
    • warfarin- inversely related to thyroid hormone balance
  199. what are the medication names of the thyroid replacement meds
    • desiccated thyroid (animal source)-- greater risk of hypersensitivity reactions
    • levothyroxine (T4, synthroid)-- DOC
    • liothyronine (T3, cytomel)
    • liotrix (T4:T3; 4:1)
  200. any state characterized by thyroid hormone excess, including ingestion of excess thyroid hormone and thyroiditis is known as what
  201. hyper-function of the thyroid is known as what
  202. what are the etiologies of hyperthyroidism
    • graves disease- most common
    • pituitary adenomas
    • toxic adenoma- least common
    • toxic multi-nodular adenoma
    • painful subacute thyroiditis
    • drug induced- 2nd most common cause
  203. what are the treatment goals of hyperthyroidism
    • eliminate excess thyroid hormone
    • normalize TSH and FT4 concentrations
    • minimize the symptoms and long-term consequences of hyperthyroidism
  204. what are the names of the thioamides (medications that block the synthesis of the thyroid hormones)
    • propylthiouracil (PTU)-- DOC for pregnancy, nursing, and thyroid storm
    • methimazole (tapazole)-- DOC secondary daily administration, less exceptions noted for PTU
  205. what are the names of the iodides (medications that block the release of the thyroid hormones)
    potassium iodide (SSKI, Lugol's solution)
  206. what is the radioactive isotope used in hyperthyroidism
  207. what are the adrenergic blockers that control the symptoms of hyperthyroidism
    Beta blockers
  208. what are the pharmacotherapy considerations for pts with hyperthyroidism
    • most useful in young pts with small glands and mild disease
    • non- invasive
  209. what are the radioactive iodine therapeutic considerations
    • treatment of choice for most pts>21 years with graves disease, multinodular goiter or toxic adenoma
    • CI in pregnant or nursing  females (defer 6-12 months)
  210. what are the surgery considerations for pts with hyperthyroidism
    • treatment of choice for very large glands, pts unwilling or unable to take anti-thyroid drugs or ¹³¹I
    • vast majority of pts will become hypothyroid following near total thyroidectomy
    • most invasive
  211. which hyperthyroid med inhibits thyroid perioxidase, thus blocking the organification and coupling (inhibits thyroid synthesis)
  212. what are the negative outcomes of the thioamides
    • fevers, chills, ST (check CBC w/diff ad d/c therapy-- look for agranulocytosis)
    • jaundice
  213. what are the adverse events associated with thioamides
    • rash
    • arthralgia, lupus like symptoms (D/C therapy)
    • leukopenia (continue therapy)
    • agranulocytosis (usually seen within first 3 mo's immediately D/C therapy)
    • hepatitis (PTU: first 6 mo's of therapy)
    • cholestatic jaundice
  214. what are the drug interactions associated with thioamides
    D/C either thioamide at least 3-5 days before administering ¹³¹I
  215. which thioamide only inhibits the peripheral conversion of T4 to T3
  216. when are relapses seen when using thioamides for hyperthyroidism
    generally seen 3 to 6 months after drug discontinuation, and occur more often in smokers and those with large goiters
  217. these hyperthyroidism meds in large doses inhibits thyroid perioxidase, resulting in decreased iodide organification (Wolff-Chaikoff block), coupling and hormone release. These meds also reduce the thyroid glands vascularity (thereby increasing firmness) and size prior to thyroidectomy
  218. what are the adverse events of the Iodides
    • rash
    • hypersalivation
    • swollen, sore gums/ulcers
    • metallic taste
    • itching
    • rhinitis
  219. what are the drug interactions associated with iodides
    • D/C at least 2 weeks before the use of ¹³¹I and not started until at least 3-7 days after ¹³¹I is administered
    • may increase lithium levels by decreasing secretion
  220. why is iodide suppression not useful in long term treatment of hyperthyroidism
    the effects of iodide suppression are overcome in ~1-2 weeks; the thyroid escapes the iodide inhibition resulting in a surge of T3 and T4 release
  221. which medication that treats hyperthyroidism rapidly accumulates in the thyroid and emits beta and gamma radiation (t1/2~ 5-8 days), thereby destroying thyroid tissue; full effects seen after 2-6 month period
    radioactive iodine (¹³¹I)
  222. what are the adverse events when using radioactive iodine (¹³¹I)
    • hypothyroidism
    • CI in pregnancy or nursing mothers
    • radiation precautions
  223. what are the drug interactions associated with radioactive iodine (¹³¹I)
    d/c iodine products at least 2 weeks and anti-thyroid medications at least 3 days before administering ¹³¹I
  224. which beta blockers, when treating hyperthyroid symptoms, may also block the peripheral conversion of T4 to T3
    propranolol and nadolol
  225. what are the adverse events when using beta blockers to treat symptoms of hyperthyroidism
    • bradycardia
    • bronchoconstriction
    • HoTN
    • caution in CHF, diabetes, and COPD
    • 1st degree heart block (increased PRI)
  226. what are the drug interactions associated with beta blockers when treating symptoms of hyperthyroidism
    • B2 agonists
    • non-DHP CCBs (verapamil, diltiazem)
  227. what are the beta blockers used in treatment of hyperthyroidism
    • propranolol- may decrease T3 levels by 20% by inhibiting peripheral conversion of T4 to T3
    • nadolol- may also inhibit peripheral conversion
    • metoprolol- B1 specific
    • esmolol- used in ICU for tx of severe thyrotoxicosis or thyroid storm
  228. which non-DHPs can be used to control tachycardia in pts whom are CI for use of beta blockers
    • verapamil
    • diltiazem
  229. end-state of untreated hypothyroidism is known as what (medical emergency)
    acute myxedema coma
  230. what is the treatment of choice for myxedema coma
    levothyroxine IV
  231. acute exacerbation of all the symptoms of thyrotoxicosis is known as what (life threatening)
    thyroid storm
  232. what are the precipitating causes for thyroid storm
    • trauma
    • infx
    • anti-thyroid agent withdrawl
  233. how is acute thyroid storm treated
    • propranolol or esmolol IV (if inpt)
    • PTU (prevents the synthesis of thyroid hormones)
    • SSKI (potassium iodide, prevents the release of thyroid hormones)
    • hydrocortisone (protects pt against shock and blocks the peripheral conversion of T4 to T3)
  234. what is virchows triad
    • stasis- alterations in normal blood flow
    • injuries to the vascular endothelium
    • hypercoagulability alterations in the constitution of blood
  235. the formation of an unwanted clot within the blood vessels or heart is known as what
  236. what is the most common abnormality of hemostasis
  237. a small part of a clot that breaks off and travels to another part of the vascular system is known as what
  238. which coag pathway is inhibited by warfarin which inhibits the hepatic synthesis of several clotting factors
  239. which coag pathway is inhibited by heparin which inhibits the activity of several clotting factor
  240. what decrease the formation or the action of chemical signals that promote platelet aggregation
    platelet aggregation inhibitors
  241. what irreversibly blocks TXA2 synthesis from arachidonic acid in platelets in inhibiting COX. This also inhibits prostacyclin activity in endothelial cells
  242. this medication is a noncompetitive platelet ADP antagonist, it inhibits platelet aggregation by selectively and irreversibly blocking ADP binding
    clopidogrel (Plavix)
  243. which medication can be used if a pt has is CI to ASA
    clopidogrel (plavix)
  244. which med used to be approved only for post MI, peripheral artery disease but is now approved for unstable angina
    clopidogrel (Plavix)
  245. which platelet aggregation inhibitor is a fragment of a monoclonal antibody that causes stearic hindrance near the active GP IIb/IIIa binding site preventing fibrinogen from binding to platelets
    abciximab (reopro)
  246. which platelet aggregation inhibitors are no monoclonal antibodies and are less immunogenic; they reversibly inhibit the binding of fibrinogen to the glycoprotein IIb/IIIa receptor (there duration of action is shorter than abciximab)
    • eptifibatide (integrilin)
    • tirofiban (aggrastat)
  247. what are the natural inhibitors of coagulation in the blood
    • protein C (destroys activated factors Va and VIIIa)
    • protein S (cofactor for protein C)
    • antithrombin III (inactivates IIa, VIIa, IXa, Xa)
  248. why would you want to use an anticoagulant
    • venous thrombosis (DVT or history of reoccurring DVTs)
    • artificial heart valves
    • atrial fibrillation
    • protein C and protein S deficiencies
    • prophylactic after sx
  249. what do anticoagulants limit
    the expansion of existing thrombi and reduce the chance of new clots forming, they do NOT break down clots
  250. which anticoagulant binds to AT-III and speeds its ability to inhibit thrombin
  251. what are the adverse events associated with heparin
    • bleeding
    • HIT
    • osteoporosis, hyperkalemia
  252. how is heparin monitored
    aPTT is used to monitor theraoy with 1.5 to 2.5 times the mean normal value being the standard value within 24 hours
  253. if a pt is given heparin and start to bleed uncontrollably, how is heparin reversed
    protamine- it forms an inactive complex with heparin
  254. how soon do you want to draw blood once heparin is given
    no earlier than 6 hrs after bolus or change in rate
  255. what are the advantages of using LMWH over heparin
    improved bioavailablity
  256. these anticoagulants have a lower affinity for antithrombin but maintain effect on factor Xa result is they do not affect aPTT time so this test is not necessary
  257. what are the names of the LMWH drugs
    • enoxaparin (lovenox)
    • dalteparin (fragmin)
    • ardeparin (normiflo)
    • tinzaparin (innohep)
  258. which anticoagulants can be used to treat and prevent DVTs and PE
  259. which anticoagulation med can be used in pregnancy because it does not cross the placenta
  260. this is a heparin antagonist, it is used to reverse heparin, but will not completely reverse LMWH
    protamine sulfate
  261. this anticoagulant inhibits vitamin K epoxide reductase which reduces available vitamin K needed by the vitamin K dependent clotting factors (factors II, VII, IX, and X)
    warfarin (coumdain)
  262. what is the reversing agent of warfarin (Coumadin)
    vitamin K
  263. how many days may it take for warfarin (Coumadin) to reach steady state
    5-7 days
  264. which type of medications do you want to avoid when using warfarin (Coumadin)
    NSAIDs for pain control due to increased GI bleed
  265. what are the adverse reactions of warfarin (Coumadin)
    • bleeding, bruising
    • rare- skin necrosis and purple toe syndrome
  266. what are the standard INR values for warfarin (Coumadin)
    • INR target of 2.5 (range 2-3) is standard
    • INR of 3 (range 2.5-3) in pts with mechanical heart valves and other high risk categories)
  267. what are the vitamin K products
    • mephyton (phytonadione) tablets
    • aquamephyton  (phytonadione) inj
  268. what medications directly inhibit thrombin; don't need a cofactor
    • lepirudin (refludan)
    • argatroban (acova)
    • bivalirudin (angiomax)
  269. which thrombin inhibitor is an anticoagulant for pts with HIT; irreversible thrombin inhibitor; IV weight based; aPTT 1.5-2.5x
    lepirudin (refludan)
  270. which thrombin inhibitor is an anticoagulant for pts with HIT; reversible thrombin inhibitor; IV weight based; aPTT is 1.5-3x initial
    argatroban (acova)
  271. which thrombin inhibitor is indicated for unstable angina (USA) with PTCA (percutaneous transluminal coronary angioplasty); is a reversible thrombin inhibitor; IV weight based; ACT monitored in renal pts
    bivalirudin (angiomax)
  272. this medication is a specific factor Xa inhibitor, has no cross-reactivity with heparin antibodies, is approved for prophylaxis of DVT in pts undergoing sx for hip fx, hip replacement, or knee replacement, and has also been used for treatment of PE and acute DVT
    fondaparinux (arixtra)
  273. these dissolve clots by activating the conversion of plasminogen to plasmin that hydrolyzes fibrin
  274. when is the greatest therapeutic window for giving thrombolytics
    within the first 3 hours
  275. what are the names of the thrombolytic enzymes
    • streptokinase (steptase)
    • urokinase (abbokinase)
  276. what are the names of the tissue plasminogen activators (TPAs)
    • alteplase (activase)
    • reteplase (retevase)
    • tenecteplase (TNkase)
  277. what are the names of the miscellaneous thrombolytic agents
    pentoxifylline (trental)
  278. which thrombolytic improves blood flow by decreasing the blood viscosity and improving erythrocyte flexibility
    pentoxifylline (trental)
  279. when is pentoxifylline (trental) indicated
    intermittent claudication-- chronic occlusive arterial disease of the limbs
  280. which thrombolytic inhibits phosphodiesterase activity and suppress degradation of cyclic adenosine monophosphate resulting in an increase in cAMP in platelets and blood vessels. It reversibly inihibits platelet aggregation induced by ADP
    cilostazol (pletal)
  281. what is a neurohormone co-secreted from the B-cells with insulin, is very low or absent in type 1 DM, and lower than normal in tyoe 2 DM
  282. what is the synthetic analog of amylin
  283. which drug in diabetes suppresses inappropriate high postprandial glucagon secretion, increases satiety, and slows gastric emptying
    amylin analog
  284. when should amylin be doses
    SQ immediately prior to a major meal in the abdomen or thigh
  285. what are the negative outcomes associated with amylin analogs
    hypoglycemia (esp in type 1's and usually within 3 hours of inj)
  286. what are the adverse events associated with amylin analogs
    • nausea
    • vomiting or anorexia
    • do not use in pts with gastroparesis or pts taking GI motility agents
    • recurrent hypoglycemia/hypoglycemia unawareness
    • pediatrics
    • HbA1c > 9% or pts that are non-compliant with insulin regimen or SMBG
  287. what are the names of the amylin analogs
    pramlintide (symlin)-- do not mix with other insulins (pH ~4); skip dose if meal is skipped; weight reduction
  288. this is defined as the greater insulin response to an oral glucose load than observed with a similar IV glucose challenge
    incretin effect
  289. what are the 2 incretin hormones
    • glucose-dependent insulintropic polypeptide
    • glucagon like peptide
  290. which increntin is secreted from the L-cells in the distal intestine in response to meals, and it also suppresses glucagon secretion, slows gastric emptying, and reduces food intake by increasing satiety
    GLP-1 glucagon-like peptide 1
  291. which incretin Is secreted by K-cells in the intestine, it does not affect glucagon secretion, gastric motility, or satiety, and has little effect on insulin secretions at glucose concentrations >140mg/dL
    GIP (glucose-dependent insulinotropic polypeptide
  292. which incretin enhances insulin secretion in a glucose-dependent manner, suppresses glucagon secretion, slows gastric emptying, and reduces food intake
    glucagon-like peptide 1 agonist
  293. what are the negative outcomes associated with GLP-1
    • hypoglycemia
    • amylase/lipase for suspected pancreatitis
    • difficulty swallowing, hoarseness, and neck masses for suspected thyoird cancer
  294. what are the adverse events associated with GLP-1
    • CI in type 1 DM
    • N/V/D, acute pancreatitis (exenatide)
    • nausea (exenatide ER)
    • N/V/D, acute pancreatitis, CI in pts with a personal or family history of medullary CA; pts with thyroid nodules or elevated serum calcitonin should be referred to an endocrinologist
  295. what are the drug interactions associated with GLP-1
    sulfonylurea- consider decreasing the SU dose by 50% to decrease the risk of hypoglycemia
  296. what are the agents for GLP-1
    • exenatide (byetta)- weight loss; 53% homology to human GLP-1
    • exenatide ER (bydureon)- administer weekly, pt must constitute, decreases HbA1c > byetta with less N
    • liraglutide (victoza)- weight loss; 97% homology to human GLP-1
  297. which incretin based therapy prolongs the t 1/2 of endogenous GLP-1 and GIP resulting in enhanced insulin secretion and glucagon suppression; no effect on gastric emptying and satiety
    dipeptidyl peptidase inhibitors
  298. what are the agents of dipeptidyl peptidase-4 inhibitors
    • sitagliptin (Januvia)- weight neutral
    • saxagliptin (onglyza)- weight neutral
    • linagliptin (trajenta)- dose adjustment not required for renal or hepatic impairment; most selective for DPP-4
  299. what are the adverse events associated with bile acid sequestrants
    • constipation
    • dyspepsia
    • do not use if TG are > 500 mg/dL
  300. what are the drug interactions associated with bile acid sequestrants
    • consider a dose reduction of the sulfonylurea if used in combo
    • caution re: drug-drug and fat soluble vitamin absorption interactions (take other medications 1 hr before or 4 hrs after)
  301. what are the agents of bile acid sequestrants
    colesevelam (welchol)- may also reduce LDL; weight neutral
  302. what are the combination products for DM
    • glipizide/metformin (metaglip)
    • glyburide/metformin (glucovance)
    • repaglinide/metformin (prandimet)
    • pioglitazone/metformin (actoplus met)
    • pioglitazone/glimepiride (duetact)
    • rosiglitazone/metformin (avandamet)
    • rosiglitazone/ glimepiride (avandaryl)
    • sitagliptin/metformin (janumet)
    • sitaglipti/simvastatin (juvisync)
    • linagliptin/metformin
  303. what are the acute complications of combination diabetic drugs
    • blood glucose ≤ 70 mg/dL
    • sympathetic symptoms; tachycardia, tremors, sweating, anxiety, hunger
    • neuroglycopenic symptoms; confusion, weakness, drowsiness, dizziness, blurred vision, difficulty speaking and concentrating
  304. this acute complications of DM is characterized by a triad of uncontrolled hyperglycemia, metabolic acidosis, and ketosis
    DKA (2/3 of cases have type 1DM)
  305. what are the low risks for GDM
    • age < 25
    • normal body weight pre-pregnancy
    • negative Fhx of DM
    • non-high-risk ethnicity for DM
    • no hx of abnormal glucose metabolism
    • no hx of poor obstetrical outcomes
  306. what are the high risks for GDM
    • marked obesity
    • hx of GDM or previous delivery of large for gestation age infant
    • strong Fhx of type 2 DM
    • PCOS
    • presence of glucosuria
  307. what is the DOC for GDM
    insulin (reg and NPH)
  308. what are the GDM treatment goals
    • FPG ≤95 mg/dL
    • 1 hr postprandial glucose ≤ 140 mg/dL
    • 2 hr postprandial glucose ≤ 120 mg/dL