M6-7 part2

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TomWruble
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160895
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M6-7 part2
Updated:
2012-07-23 23:40:26
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nur119 mod7 cardiovascular ch42 ch43 ch44 ch45 ch46 exam3
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cardiovascular drugs
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  1. 1) When are cardiovascular drugs used?
    • → Arthereosclerosis
    • → CHF
    • → Cardiac arrythmias
    • → Angina
    • → HTN
    • → Shock
  2. 2) Review electrical conduction of the heart
    • → SA
    • → AV
    • → Bundle of HIS
    • → Bundle fibers
    • → Purkinje fibers

    Note: the whole heart is capable of pacemaking, but each part is slower than the previous in the "normal" circuit. Thus the SA sets the pace at 60-80, the AV at 40-60, and the ventricles at 30-40 BPM.
  3. 3) List 5 actions of cardiovascular drugs.
    • → Increase cardiac output - blood flow to the heart
    • → Decrease cordiac output, blood pressure, and heart rate
    • → Increase or decrease clotting
    • → Alter the quality of the blood
    • → Decrease cardiac chest pain
  4. 4) Do cardiac drugs alter the underlying disease?
    • NO
    • There are 2 broad cat of HD: CAD and HB (Heart Block - conduction issues). CAD is treated with bypass surgery
  5. 5) Name 2 inotropic effects of cardiac drugs.
    • → "positive" inotropics increase the force of contraction, like digoxin. They also reduce the ventricular rate.
    • → "negative" inotropics decrease contractility, thus decreasing workload, like beta blockers or calcium channel blockers.
  6. 6) Name 3 inotropic drugs
    • → Digoxin T1/2=36 hr and not to be confused with digitoxin, also a cardiac glycoside, but with a t1/2 of 4-9d and rarely Rx.
    • → Inocor, IV only
    • → Primacor, IV only
  7. Brain Natriuretic Peptide (BNP)?
    • → Best lab value to confirm HF, esp in Pts with dyspnea which may be from lung disease.
    • → Healthy value < 100 pg/mL
    • → "positive" (unhealthy) value > 100 pg/mL
    • → Increases with age so whil a 80-year-old woman may have a value of 160, if she had HF it would be 400.
  8. 8) Digoxin maintenance?
    • → 0.125 to 0.5 mg/d and in some Pt q2d
    • → Duration is 2-4d (5 half-lives) whether IV or PO, only the onset and peak are faster w/ IV
    • → Therapeutic Serum level (TSL) is 0.5 to 2 ng/mL @ 0.5 for HF and 2 for atrial flutter or fibrillation  
  9. Exaccerbation of Digoxin Toxicity?
    • → Thiazide diuretcis
    • → Loop diuretics
    • → Hypokalemia
    • → Hypomagnesemia
    • → Hypercalcemia
  10. Signs of Digoxin Toxicity?
    • Anorexia
    • → Diarrhea
    • → nausea
    • → Vomiting (together as N/V)
    • Bradycardia (< 60 BPM)
    • Visual illusions (white, green, yellow halos around objects)
  11. 7) What are 2 indications for Digoxin?
    • → Tachy heart
    • → CHF
  12. 9) Name 2 actions of digoxin (Lanoxin).
    • → 1) SLOWS THE RATE OF CONTRACTION
    • → Negative chronotropic
    • → Decreased conduction
    • → Stimulates the vagus nerve

    → 2) Positive inotropic - increases contraction efficiency, i.e. stroke volume

    → 3) Negative dromotropic - decreases conduction of heart cells (e.g. conduction speed in the AV node, and subsequently the rate of electrical impulses in the heart, leading to negative chronotropic
  13. Signs of left/right HF?
    • → Left, fluid backs up in lungs causing difficulty breathing
    • → Right, fluid backs up in peripheral tissue leading to edema
  14. 10) List contraindications for digoxin.
    • → Life-threatening arrythmia (ventricular dysrhythmias) 2nd or 3rd (complete block of AV node) degree heart block
    • → Low K or Mg
    • → High Ca 
  15. 11) What is digitalization?
    • → Rapid introduction of digoxin - 0.75-1.5 mg divided q6-8 over 24hr
    • → Higher risk of toxicity
    • → NOT for CHF, mainly tachy Pts
  16. Vagus Nerve & the Heart?
    • → Parasympathetic innervation of the heart is controlled by the vagus nerve. To be specific, the vagus nerve acts to lower the heart rate.
    • → Since NG tubes can stimulate the vagus nerve, putting one in can slow the HR.
  17. 12) How many half-lives docs it take Digoxin to reach steady state?
    5
  18. 13) Digoxin interventions
    • → Before admin, take apical P and if < 60, HOLD
    • → Drug has low therapeutic index - easy toxicity
    • → Cleared by Kidneys
  19. 14) What is Digibind?
    • → The antidote for digoxin toxicity
    • → Use for serum digoxin levels over 2ng/mL
  20. 15) What are Inocor and Primacor used for?
    • → These are both "first line" drugs vis a vis digoxin for acute HF in a hospital
    • → They are "IV only" wheras Dig is also PO
    • → Inocor may be prescribed when digoxin and diuretics have not been effective
    • → Primacor is used for short-term Tx of HF. It may be given before heart transplantation.
  21. 16) List 4 causes of congestive heart failure (HF).
    • Maddie: (CHF)
    • → HTN
    • → Ischemia to heart
    • → Hypoerthyroidism
    • → Excessive IV fluids
    • → Transfusions
    • → Drugs that decrease the force of contraction, i.e. beta adrenergic

    • Book: (HF)
    • → Chronic HTN
    • → NI
    • → CAD
    • → Valvular HD
    • → congenital HD
    • → Aging
  22. 17) Define preload and afterload.
    • → Preload is an excess of blood in the ventricle after diastolic, i.e. the ventricle is already preloaded for the next systol.
    • → Afterload is additional force on the ventricular wall caused by excess resistance in the aorta.
  23. How do heart drugs compensate for preload and afterload?
    • → Preload - dec flud returning to heart
    • → Afterload  - reduce pressure out

    → Morphine and Nitro both dec preload & afterload
  24. 18) How docs the heart compensate in patients with CHF?
    • → Increased heart rate & vasoconstriction
    • → Increased volume of blood, stretches the muscle fibers, causes ventricular hypertrophy
    • → Activation of the renin - angiotensin - aldosterone system → Vasoconstriction / increased reabsorption of sodium and water
    • → Eventually → CHF occurs
  25. 19) List 4 categories of drugs that are usedin CHF therapy.
    • → Cardiotonic - iotropic, e.g. digoxin
    • → Diuretics, e.g. HCTZ hydrochlorothyazide - to reduce fluid vol 
    • → Angiotensin - ACE (Angiotensin [a vasoconstrictor] Converting Enzyme) inhibitors
    • → Vasodilators to reduce fluid volume returning to heart
  26. 20) Review cardiac physiology.
    • → Stimulation from electrical impulses
    • → Transmission of impulse
    • → Contraction of atria/ventricles
    • → Relaxation of atria/ventricles
  27. 21) What is automaticity?
    The ability of the heart to generate its own impulse, e.g.

    • SA:               60-80 BPM
    • AV:               40-60 BPM
    • Ventricles: 30-40 BPM
  28. 22) What is automaticity dependent upon?
    • → Moving Na & Ca into myocardial cells
    • → Moving K out of myocardial cells
  29. What is Romazicon an atidote for?
    BENZODIAZEPINE

    How is this related to the heart? An O/D of benzodiazepine can cause bradycardia, which is treated with adrenalin (wrong cause) instead of romazicon (right cause)... 
  30. 23) What does sodium, calcium, and potassium do?
    They are required for proper conduction of impulses and contration of hear muscles.
  31. 24) What are 4 indications for antiarrhythmics?
    • → Rapid ventricular rate or VTAC
    • → PVC (Premature ventricular Contraction) ca lead to VTAC
    • → Fatal Arrythmias
    • → To maintain NSR (normal sinus rhythm) after conversion from atrial fibrillation
  32. 25) Sodium Channel Blockers?
    → Block movement of Na → decreasing rate of conduction

    • → Quinidine - t1/2 6 hr, low therapeutic index, give with food
    • → Lidocain

    → Neither are used much 
  33. Angina Tx Flowchart
    • → Nitrates
    • → plus beta-blockers
    • → plus calcium blockers
  34. 31) Antianginals - Short Acting
    • Nitrates
    • → Nitroglycerine
    • → Dose via short-acting patch or SL (sublingual)

    • → Decrease preload & afterload
    • → Dose: IV, PO, SL, topical
    • → Tolerance develops to nitrates - dose ONLY during waking hours - remove topical at HS
    • → Wx reflex tachy common
    • → Wx hypotension, headache
    • → When by IV (glass bottles very potent): FREQUENT BP (every few minurtes then every 5)
    • → When by SL: q5 min X 3 then ER
  35. Antianginals - Long Acting
    → Imdur
  36. Antianginals - Beta-Adrenergic Blockers
    • → Lopressor
    • → Tenormin: cardioselective block of b1 → Decreases HR & Reduces force of contraction
    • ineffective for vasospastic angina
  37. Antianginals - Calcium Channel Blockers
    • → Norvasc
    • → Cardizem
    • → nifedipine (Procardia)
    • → nisoldipine
    • → verapamil
  38. Calcium Channel Blockers: Uses?
    • → Reduce automaticity
    • → Slow conduction by vlocking calcium movement
    • → cardizem- slows heart rate
    • → verapamil - not used

    → Also used for antianginal
  39. Antidysrhythmics - Prolong Repolarization
    • K channel blockers
    • → Used for chronic, recurrent ventricular tachycardia

    • → adenosine (Adenocard) - restores NSR in Pts with PSVT (Paroxysmal supraventricular tachycardia) any rapid heart rhythm originating above the ventricular tissue, t1/2 < 10 seconds!!!!!! so must have RAPID IV injection
    • → amiodarone, long t1/2, Wx for hypotension and bradycardia
  40. Antidysrhythmics - Beta-Adrenergic Blockers
    • → Inderal - Pt w/ asthma should NOT use.
    • → Decrease conduction velocity and recovery time
    • → Block automaticity →  slow rate
    • → Contraindicated for CHF
  41. Antidysrhythmics - Sodium Channel Blockers 1B
    • → lidocaine (Xylocaine)
    • → slow conduction and shorten repolarization
  42. Antidysrhythmics - Sodium Channel Blockers 1A
    • → quinidine - not used much because it causes diarrhea
    • → slow conduction and prolong repolarization
  43. Magnesium sulfate???
    From notes: decreases irritability of the heart which can lead to life threatening arrhythmias
  44. Antidysrhythmics Nursing Considerations
    Always doc P & BP
  45. 27) What is Angina Pectoris
    • → Develops because of arterial plaque or spasms in coronary arteries
    • →non-pharm tx first: salt, weight, smoke

    • Typ Radiation pattern
    • → Male: to arm & jaw
    • → Female: to back 
  46. 26) What should the nurse check before any antiarrhythmics?
    P & BP
  47. 28) Review types of angina
    • → Classic: Oc with stress or exertion
    • → Unstable (preinfarction): Oc frequently w/ progressive severity unrelated to activity
    • → Variant (vasospastic): Oc during rest
  48. Cardiac Troponin
    • Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain or acute coronary syndrome. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood. This can also occur in patients with coronary vasospasm.
    • It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction.
  49. 31) Beta-Adrenergic Blockers
    • → Prevent sympathetic (as in SNS) stimulation
    • → Decrease angina
    • → Decrease need for NTG
    • → Improve exercise tolerance
    • → Prototype - INDERAL
    • → Used for exercise induced tachycardia which can cause chest pain

    Should NOT be abruptly stopped; the dose should be tappered down.
  50. 31) Calcium Channel Blockers
    • → Prevent movement of calcium into the cell
    • → Dilate arteries/decrease cardiac workload - decreasing BP
    • → Slows ventricular response
    • → PROTOTYPE - Cardizem  
    • Used for: Slow conduction velocity, decrease contractility (negative inotropic)

    • → Norvasc
    • → Cardizem
    • → Verapamil
  51. 32) How is shock defined? List signs and symptoms.
    • → Low PB
    • → High HR

    • → Confusion
    • → Cool Extremities
    • → Oliguria - low output of urine. It is clinically classified as an output below 300-500ml/day
  52. 36) Review the different types of shock.
    • Drug use to correct OK
    • → Cardiogenic
    • → Vasogenic
    • → Anaphylatic
    • → Neurogenic
    • → Septic
    • → Insulin

    • Do not use drugs to ty to correct:
    • Hypovolemic, use fluids or blood products
  53. 34) Which drug can be administered to increase cardiac output, treat hypotension, and increase urine output?
    • → Dopamine, or
    • → Dobutamine
    • → If either of above fail then Norepinephrine

    → Epindephrine is the drug of choice for anaphylactic shock @ 0.2 to 0.5 mg IM or subQ vis tuberculin syringe for accuracy (1:1000 solution)
  54. 35) How is this drug odministered? What is the expected therapeutic effect?
    • → Dopamine dose for (non-hypovolemic) shock 2-20 mcg/kg/min by 400-800mg in 250 mL D5W admin via electronic fusion pump.
    • → Therapeutic goal: Systolic of 80-100
  55. 38) How is hypertension defined?
    • → Systolic > 140 although the AHA wants 120
    • → Diastolic > 90
  56. 39) Briefly highlight effects of hypertension.
    • → Increased workload for heart
    • → Plaque buildup
    • → Narrows lumen increasing risk of thrombus
    • → necrotic areas develop & rupture
    • → Breaks off ...
  57. 40) How is hypertension treated?
    • Non-pharm
    • → Salt
    • → Tobacco
    • → Weight reduction
    • → Exercise (increases HDL)
    • → Stress-reduction
    • → Alcohol

    • Pharm (6 categories)
    • → Diuretics
    • → Sympatholytics
    • → Direct-acting ateriolar vasodilators
    • → ACE inhibitors
    • → Angiotensin II receptor blockers (ARBs)
    • → Calcium Channel blockers
  58. 41) ACE Inhibitors
    • → Block enzyme which converts angiotensin I to angiotensin II, a potent vasoconstrictor
    • → Decrease peripheral resistance by blocking the release of aldosterone, which then allows sodium and water to be excreted and K to be retained.

    • → CAPOTEN
    • → VASOTEC
    • → ZESTRIL
    • → ACCUPRIL
    •  
    • Monitor K levels (as it may get high)
    • Last about 24 hours
  59. 41) Angiotensin II receptor blockers (ARBs)
    • → Like ACE inhibitors these block the release of aldosteron leading to sodium and water excretion and K retention.
    • → Instead of blocking the creation of angiotensin II like and ACE would, ARBs block the angiotensin II from the AT1 recptor sites.
    • → Like to ACE they cause vasodilation and decreased peripheral resistance, but do not cause the constant ittitating cough that ACE inhibitors can.

    → Cozaar
  60. 41) Anti-adrenergics
    • → Block sympathetic nervous system
    • → Alpha & beta blockade
  61. 41) Vasodilators
    • → Decrease afterload
    • → Not used alone because of reflex tachycardia
    • → Act on arteries inc blood flow to brain & kidneys, reflex tachy can result from the vasodilation and accompanying dec BP, so beta blockers are jointly Rx to dec HR.

    • → Apresoline
    • → Nipride
    •  
    • Hypertensive emergency - Nipride (arterial and venous) & diazoxide (arterial only)

    Stop drug if: Thiocyanate toxicity: hypotension, tinnitus, dyspnea, blurred vision, metabolic acidosis

    Cautious lowering to avoid stroke, MI, acute renal failure!!

    → Nipride decomposes in light; container must be wrapped in Al foil. Good for 24 hr. Discard is red or blue. Can cause cyanide toxicity.
  62. Block the release of aldosteron leading to...
    Sodium and water excretion and K retention.
  63. What "test question" situation is related to ACE inhibitors and ARBs?
    • → Both block the release of aldosteron leading to sodium and water excretion and K retention.
    • Hyperkalemia can lead to kidney damage!
  64. 42) List considerations regarding edema.
    • → Symptom of many diseases
    • → Interferes with blood flow
    • → Dependent ancles & feet
  65. 43) What is anasarca?
    Generalized body swelling or edema
  66. 44) Review nonpharmacologic measures for edema.
    → Keep feet elevated
  67. 45) Name 3 indications for diuretic therapy.
    • → HTN
    • → Edema
    • → Dyspnea
  68. 46) How do diuretics work?
    Produce diuresis by inhibiting water and sodium retention by the kidneys.
  69. Thiazide Diuretics
    • → Prototype - Diuril
    • → HCTZ
    • → Vasodilation of arterioles
    • → Decrease sodium and water reabsorption
    • → Do not give after 6P
    • → Give in AM
    • → inc risk for digoxin toxicity
    • K-wasting along w/ sodium and magnesium, but promo calcium reabsorption
  70. Loop Diuretics
    • → Lasix - most preferred - need K supplement since K-wasting
    • → IV
    • → DRUG OF CHOICE FOR RAPID EFFECTS
    • → CAUTION IF PATIENT TAKING DISOXIN
    • → DECREASED K ca lead to digoxin toxicity
    • → Patients taking Prednisone will lose even more K!

    → Bumex - take this if sulfa allergy, which would be contraindicated for lasix
  71. Potassium Sparing Diuretics
    • → Aldactone
    • → aldosterone antagonist
    • → Not for renal patients
    • → Avoid salt substitutes which contain K, as it may lead to hyperkalemia with this diuretic.
  72. Osmotic Diuretics
    • → Produce rapid diuresis by increasing solute
    • → Water pulled from extravascular sites to blood

    → mannitol (Osmitrol) - Can be used to treat narrow-angle glaucoma to reduce IOP (Intraocular pressure); and Head Injuries
  73. Carbonic Anhydrase Inhibitors (diuretics)
    → Diamox

    → Blocks the acid-base enzyme: carbonic anhydrase → sodium, K, & bicarb excretion and eventually metabolic acidosis.

    → Used primarily to reduce IOP in open-angle (chronic) glaucoma, not narrow-angle (acute)
  74. 48) Discuss combination therapy.
    • → Moduretic: amiloride HCl & hydroclorothiazide
    • → Maxide: triamterene & hydroclorothiazide

    Combinations of K-sparing & K-wasting to prevent hypokalemia
  75. 49) Blood coagulation
    defense mechanism to prevent blood loss
  76. 49) Platelets
    Control bleeding and blood angulation; become sticky and adhere to vessselwall and to other platelets to make a clot
  77. 49) Thromboplastin
    Also functions to stop bleeding (it is released by disintegrating platelets)
  78. 50) Review blood coagulation phases:
    • → Release of thromboplastin
    • → Prothrombin to thrombin
    • → Fibrinogen to fibrin
  79. 51) Venous Thrombosis
    • → Become lodged and obstruct bloodflow
    • → Can impair blood flow by local congestion, edema, and inflammation.
    • → Usually occurs in veins (thrombophlebitis, DVT)
    • → Related to venous stasis - slow blood flow
    • → Detaches easily and can travel toother parts of the body.
  80. 51) Arterial Thrombosis
    • → Associated with artherosclerosis, HTN, turbulent blood flow
    • → If temporary, ischemia results
    • → If permanent, necrosis occurs
  81. 52) What ore risk factors for thromboembolism.
    • → Major illnesses
    • → Major abdominal & thorasic surgery
    • → History of PE or thromboembolism
    • → GYN surgery esp if estrogen or BCP's (birth control pills)
    • → Bed rest or limited activity for 5 days
  82. 53) Discuss anticoagulant therapy
    • → Anticoagulant therapy is more effective for venous thrombosis (DVT thromboplebitis), pulmonary embolism
    • → Prevents the formation of new clots & the extension of existing ones.
    • → DOES NOT DISSOLVE CLOTS!!!!!!!!!!

    • → HEPARIN - IV or subQ
    • → Coumadin - warfarin: PO
    • → Lovenox

    → INTERFERE WITH COAGULATION FACTORS.
  83. 56) What is the purpose of low dose SQ Heparin?
    Prevents or treats DVT
  84. 54) What are indications for Heparin?
    • → DIC (disseminated intravasular coagulation) these clots consume proteins and platelets which deplete clotting factors causing excess bleeding, and oddly enough the anticoagulant heparin can Tx this.
    • → Vascular surgery
    • → Hemodialysis
    • → DVT
    • → PE
    • → MI
    • → CVA (cerebrovascular accident - stroke)
    • → Venous disorders
    • → Coronary thrombosis
  85. 55) How is Heparin adjusted?
    • → Adjust via PTT (prothrombin time)
    • → Target 1.5X-2.5X the "control" or normal
    • → Normal 25-35 seconds
    • → Therapeutic level sought: 35-85 seconds

    Any injections for heparin Pts: pressure for 2 minutes and elevate
  86. 57) What is the antidote for Heparin?
    → Protamine sulfate

    • → Binds & neutralizes
    • → 1 mg/100 units hepatin; then 10-50mg in 10-15 minutes; max 100mg in 2 hr
  87. 62) What is Coumadin?
    • → Rodenticides
    • only oral anticoagulant
    • → Risk for HTN → bleed out brain
    • → Long term Tx
    • → Works by interfering with vitamin K
  88. 63) What are 2 ways Coumadin is regulated?
    • → PT (prothrombin time): normal 12 seconds, therapeutic target 1.5X or 18 seconds
    • → But to eliminate lab & reagent differences, the INR (international normalized ratio) is used.
    • → Normal INR 1.3-2
    • → warfaring therapeutic: 2-3
    • → Mechanical heart valves: 2.5-3.5, but may be as high as 4.5  
  89. 64) What is the antidote for Coumadin?
    • → Vitamin K, but it takes 24-48 hours to take effect
    • → Low dose vitamin K for INR > 5.5
    • → Excessive vitamin K → warfarin 1-2 weeks to become effective again
    • → Acute bleeding: fresh frozen plasma
  90. 65) How do antiplatelet drugs work?
    • → Prevent thrombosis by preventing platelet aggregation in arteries
    • → This is via interference w/ 1st phase of blood coagulation
    • → Note: heparin & warfaring prevent thrombosis in veins
  91. 66) Nome 3 common antiplatelet drugs.
    • → Plavix - bleeding may inc when taken w/ ASN
    • → Ticlid
    • → Aggrenox
  92. 67) Name indications for antiplatelet drugs.
    • → Prevention of MI or CVA in Pts with familial history
    • → Prevention of repeat MI or CVA
    • → Prevention of CVA for Pts having TIA

    Note: CVA & TIA have the same etiology, but unlike a stroke, the symptoms of a TIA can resolve within a few minutes or 24 hours. However, brain injury may still occur in a TIA lasting only a few minutes.
  93. Embolus
    any detached, traveling intravascular mass (solid, liquid, or gaseous) carried by circulation, which is capable of clogging arterial capillary beds (create an arterial occlusion) at a site distant from its point of origin.
  94. Thrombus
    • → blood clot, is the final product of the blood coagulation step in hemostasis
    • → via the aggregation of platelets that form a platelet plug, and the activation of the humoral coagulation system (i.e. clotting factors)
    • → is normal in cases of injury, but pathologic in instances of thrombosis.
  95. 68) How do thrombolytics work?
    • → Dissolves by converting plasminogen  to plasmin , which destroys the fibrin in the clot.
    • → Within 6 hours
    • → Reestablishes blood flow & limits tissue damage.
  96. 69) Name 3 thrombolytics.
    • → tPA (tissue plasminogen activator)
    • → streptokinase
    • → urokinase
  97. 70) When are thrombolytics used?
    • → Within 4 hours of a MI
    • → Within 3 hours of a CVA
    • → PE
    • → DVT
    • → Noncoronary arterial occlusion from acute thrombolembolism
  98. 71) What are nursing responsibilities related to thrombolytic therapy?
    • → Monitor VS
    • → Monitor EKG
    • → Teach safety: Wx urine bleeding
  99. 72) Why is the management of dyslipidemia important?
    → Greater risk of arthersclerotic plaques and heart disease
  100. 73) What is another term used for dyslipidemia?
    → Hyperlipidemia
  101. 74) Lipitor
    • → Antihyperlipidemic
    • → Decreases the production of cholesterol
    • → Take at bedtime.
    • → An adverse effect of statins is rabdomyalysis
    • → Statins are contraindicated in active liver disease because of potential hepatotoxicity
  102. 74) Lescol
    • → Antihyperlipidemic
    • → Decreases the production of cholesterol
    • → Take at bedtime, on an empty stomach.
    • → An adverse effect of statins is rabdomyalysis
    • → Statins are contraindicated in active liver disease because of potential hepatotoxicity
  103. Lopid
    • → Antihyperlipidemic
    • → Increase the oxidation of fatty acids resulting in decreased hepatic production of triglycerides.
    • Used for very high triglyceride levelslll
    • → Take on an empty stomach before breakfast and dinner.
  104. Niacin
    • → Antihyperlipidemic
    • → Decreases both Triglycerides and cholesterol
    • → Administer with meals.
    • → Hot Flashes are a side effect that should be reported to physician
  105. 75) What are peripheral vasodilators?
    • → Used to treat PAD or PVD (peripheral arterial/vasvula disease), which is:
    • → numbness & coolness of extremities and intermittant claudication (pain & weakness of the limb when walking but no symptoms at rest)
    • → Most drugs for PAD do not cure the health problem, but can aid in relieving symptoms
  106. Rabdomyalysis
    Painful muscles
  107. 76) Discuss therapy with Trental.
    • → For PAD
    • → decreases blood viscosity
    • → improves flexibility of erythrocytes
    • → Approved by FDA but
    • → one research study showed it to be no more effecive than a placebo

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