Pharm Exam 3

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Pharm Exam 3
2011-11-14 02:51:29
Souter Pharm Exam

Souter Pharm Exam 3
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  1. -lasix
    -action: blocks reabsorption of sodium and chloride in ascending loop of henle
    -effects: hyponatremia, hypochloremia, dehydration, hypotension, hyperglycemia, hyperuricemia
    High-celing (loop) diuretics
  2. -action: promotes urine production by blocking reabsorption of sodium and chloride in early segment of distal convoluted tubule
    -effects: hyponatremia, hypochloremia, dehydration, hypokalemia, hyperglycemia, hyperuricemia
    thiazide diuretics
  3. what are the 2 groups potassium-sparing diuretics divide into?
    aldosterone antagonists and nonaldosterone antagonists
  4. where does the mechanism of action ofpotassium-sparing diuretics take place?
    late distal convoluted tubule and collecting duct (distal nephron)
  5. an example of nonaldosterone antagonist
  6. an example of aldosterone antagonist
  7. action: blocks actions of aldosterone in distal nephron, causes retention of potassium and increased excretion of sodium
    effects: hyperkalemia and endocrine effects
    direct inhibitor, by blockage of aldosterone
    aldosterone antagonist (potassium-sparing diuretic)
  8. action: disrupts soidum-potassium exchange in distal nephron like spironolactone; direct inhibitor; quicker response
    effect: hyperkalemia, N&V, leg cramps, dizziness
    nonaldosterone antagonist
  9. action: promotes diuresis by creating an osmotic force w/in lumen of nephron
    effects: edema, HA, N&V, F&E imbalance
    Mannitol (osmotic diuretics)
  10. prevent reabsorption of water, sodium and chloride
    increases urine flow
  11. study of movement of blood throughout the circulatory system
  12. receptor specificity:beta1, causes selective beta1-adrenergic receptors --> only indication of HR
    effect: tachycardia (effect)
  13. receptor specificity (dopamone, beta1, @high doses it is alpha1)
    -increases myocardial contractility, which in turn increases cardiac output
    effect: tachycardia, dysrythmias, anginal pain
    -shcok is a major indicator for use
    -increases cardiac output, therefore increases tissue perfusion
  14. indicated fr HF and control of dysrythmias, can reduce symptoms, increase exercise tolerance and decrease hospitalizations
    *exerts positive INOTROPIC action on the heart
  15. what does postive inotropic action mean?
    an increase of force of ventricular contraction, therefore produces an increased cardiac output
  16. myocardial contractility by inhibiting enzyme (Na+, K+-ATPase). K+ ions compete w/ digoxin for binding to Na+, K+-ATPase. B/c K+ competes w/ digoxin: decrease in K+, increase in binding digoxin + Na+, K+-ATPase. increase in this can produce excessive inhibition of Na+, K+-ATPase which results in toxicity.
    Inotropic action in relationship to potassium
  17. digoxin therapeutic range?
    what is the level at when there is a risk for toxicity?
    • 0.5-0.8 ng/mL
    • above 1 ng/mL
  18. symptoms of toxicity with digoxin?
    anorexia, N&V (most common), fatigue and visual disturbances
  19. how do you treat toxicity from digoxin?
    FAB antibody fragmants (DIGIBIND), cholesterol and activated charcoal
  20. digoxin's half-life?
    1.5 days
  21. indications for use of digoxin?
    HF and dysrhythmias
  22. normal range for potassium?
  23. hypokalemia + diuretics?
    there is a blockage of potassium reabsorption, therefore there is a decrease
  24. hypokalemia + digoxin?
    hypokalemia promotes dysrhythmias, and digoxin is used for dysrythmias and HF
  25. foods high in potassium?
    green leafy vegetables, bananas
  26. types of angina?
    chronic stable, angina, variant angina, and unstable angina
  27. type of angina triggered most often by physical activity. other causes are emotional excitement, large meals, and cold exposure. underlying cause is coronary artery disease (CAD) -- fatty plaque in arterial wall, blood flow reduce, angina result
    chronic angina
  28. type of angina that is caused by coronary artery spasm, therefore restricts blood fow to myocardium
    variant angina
  29. type of angina that is caused by severe CAD complicated by vasospasm, platelet aggregation and transient coronary thrmobi or emboli
    unstable angina
  30. what are the different ways nitrates can be administered?
    sublingual, SR oral capsule, transdermal, translingual spray, transmucosal (buccal) tablet, topical ointment and IV
  31. what are the side effects of nitrates?
    hypotension, HA, tachycardia
  32. what can happen if nitrates interact with hypotensive drugs?
    nitrate can intensify effects of other hypotensive agents, life-threatening hypotension can develop, and suppression of nitroglycerin -produce tachycardia can develop
  33. -vasodilator
    -a "cardioselective" agent, produces selective blockade of beta receptors in heart
    Metoprolol (lopressor)
  34. actions: blocks calcium access to cells therefore causing a decrease in heart contractility and conductivity and leading to a decrease in demand of oxygen
    varapamil, nifedipine, dilitazem
    calcium channel blockers
  35. assessment made by nurse for CCBs?
    • monitor VS, watche for low BP
    • monitor liver and renal function tests
    • weigh client (report any edema and weight gain)
  36. -an antidysryhthmias
    -class IB (sodium channel blocker), IV
    -therapeutic range: 1.5-5 mcg/mL
    -accelerates repolarization
    -used only for ventricular dysryhthmias (limited to ST therapy of ventricular dysryhthmias)
  37. -an antidysryhthmia
    -active against a variety of ventricular and superventricular dysrythmias
    -class IC agent (sodium channel blocker)
    -prodysrhythmic actions: can intensify exisiting dysryhthmias or provoke new ones
    -decreases cardiac conduction and increases effective refractory period
  38. -an antidysryhthmia
    -class IB agent (sodium channel blocker)
    -delays repolarization
    -produces dose-dependent decrease in sodium an potassium conduction, thereby a decrease in the excitability of myocardial cells
  39. -an antidysryhthmia
    - class III (potassium channel blocker)
    -delays repolarization
    -used only fr STtherapy for severe ventricular dysryhthmias
  40. -1st generation beta blocker (nonselective, blocks beta1&beta2)
    - 1st beta blocker to receive widespread clinical use and remains one of the most important beta-blocking agents
    - highly lipid soluble so it readily cross cell membrane
  41. action of propanalol?
    • beta drug. blocks beta 1 and beta 2 receptors.
    • action: beta1- suppression of secretion of renin; beta2- bronchoconstriction, vasoconstriction and reduced glycogenolysis
  42. propanalol uses (reasons to use it)?
    hypertension, angina pectoris, cardiac dysryhthmias and MI
  43. what are the effects of propanlol?
    bradycardia, AV heart block, HF, rebound cardiac excitation, bronchoconstriction, inhibition of glycogenolysis, CNS effects
  44. -a vasodilator
    -indications: hypertension
    -effects: excessive hyptension (HA, nausea, palpitations), cyanide poisoning, thiocyanate toxicity (disorientation, psychotic behavior and delirium)
  45. -close relative to thiazide diuretic but w/o the diuretic effects
    -indications: hypertension
    -effects: reflex tachycardia, hyperglycemia, hyperuricemia, GI effects, salt and water retention
  46. -ends in 'pril'
    -uses: indication is hypertension, HF, acute MI, L ventricular dysfunction, diabetic and nondiabetic nephropathy
    ACE inhibitors
  47. side effects of ACE inhibitors?
    COUGH , NEUTROPENIA, hyperkalemia, angioedema, renal failure, fetal injury, rash
  48. -action: cause dilation of aterioles and veins; decrease in release of aldosterone, increase in renal excretion of sodium and water
    -uses: hypertension, HF, diabetic nephropathy, MI, stroke prevention, migraine HA
    -effects: angioedema, fetal harm, renal failure
  49. anticoagulant, injection, inactivates both thrombin and factor Xa, effects begin and fade rapidly, aPTT, antidote: protamine
  50. anticoagulant, orally, inhibits synthesis ofclotting factors factor Xa, effects begin slowly and then persist several days, PT, antidote: vitamin K
    warfarin (coumadin)
  51. INR
  52. PT
    12 secs
  53. aPTT
    40 seconds
  54. -ends in 'ase'
    -removes thrombi that have already formed
    -action: promote conversion of plaminogen to plasmin
  55. major complication for thrombolytics?
  56. side effects of thrombolytics?
    bleeding, antibody production, hypotension, fever
  57. -a cholesterol reducing agent
    -lowers LDL and total cholestrol
    -action: inhibits HMG-CoA reductase hepatocytes synthesize more HMG-CoA reductase, then cholesterol synthesis is largely restored to premature levels
    -labs: LDL, VLDL, triglycerides, liver and renal tests
    -effects: uncommon; typically rash, HA
  58. -a cholesterol reducing agent
    -increases HDL levels
    -action: decreases production of VLDLs
    -effects: flushing, itching, gastric upset, N&V, diarrhea, liver injury, hyperglycemia
    -labs: liver function tests
  59. -a cholesterol reducing agent
    -decreases LDL cholesterol levels
    -action: absorbs and combines w/ bile acid to frm insoluble complex that is excreted through feces
    -labs: fasting LDL, HDL, total cholesterol, triglycerides, electrolytes
    -effects: constipation (main), bloating, indigestion, nausea, decrease in fat absorption
    bile-acid sequestrants
  60. -a cholesterol reducing agent
    - decreases triglyceride levels
    -actions: interacts w/ specific receptor subtype, increases syntehesis of LPL and decreases production of apolipoprotein C-III
    -labs: PTT
    -effects: gallstones, myopathy, liver injury
    fibric acid derivatives
  61. risk factors fr elevated cholesterol?
    age, total cholesterol, smoking status, HDL cholesterol, and systolic BP
  62. drugs for hypothyroidism?
    liotrix, levothyroxine (synthroid-main)
  63. drugs for hyperthyroidism?
    PTU and methimazole
  64. regular insulin (humulin R)
    • onset: 30-60 min
    • peak: 1-5 hr
    • duration: 6-10 hr
  65. Lispro (humalog, rapid acting)
    • onset: 15-30 mins
    • peak: 0.5-2.5 hrs
    • duration: 3-6.5 hrs
  66. NPH (intermediate, humulin N)
    • onset: 60-120 mins
    • peak: 6-14 hr
    • duration: 16-24 hr
  67. Glargine (lantus, long acting)
    • onset: 70 min
    • peak: same throughout day (none)
    • duration: 24 hours
  68. -an oral hypoglycemic
    -action: promotes insulin secretion by the pancreas; may alson increase tissue response to insulin
    -pt teaching: only for type 2
    sulfonylureas (glimepiride:glipizide:glyburide)
  69. -oral hypoglycemic
    -action: inhibits CHO digestion and absorption, thereby decreasing the postpradinal rise in blood glucose
    -pt teaching: type 2 w/ hyperglycemia that is not controlled
    Alpha-glucose inhibitors (acarbose)
  70. -oral hypoglycemic
    -action: decreases insulin resistance, and thereby increases glucose reuptake by muscle and decrease glucose production by the liver
    -pt teaching: only for type 2, can expand blood volume, causes edema, poses a risk for pts with HF
    thiazolidinediones (glitazones)