Pharm Exam Two - Lecture Two.txt

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Pharm Exam Two - Lecture Two.txt
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Pharm Exam Two Lecture
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Angina and CHF
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  1. Coronary Artery Disease, Myocardial Ischemia and Myocardial Infarction and continuums that do what?
    1. Impairs pumping ability of the heart by depriving the heart muscle of blood-borne oxygen and nutrients.
  2. Imbalances between supply and demand occur from what?
    • 1. Tachycardia
    • 2. Exercise
    • 3. HTN
    • 4. valvular disease
  3. Ischemic Heart Disease begins with CAD primarily from atherosclerosis, slide One:
    • 1. Dyslipidemia, HTN, Tobacco use, DM, Obesity, Sedentary lifestyle, nontraditional factors..
    • 2. Atherosclerotic plaques can grow to occlude blood flow (leads to stable angina or effort related) or can rupture/ulcerate leading to thrombus formation (acute coronary syndromes, unstable angina, myocardial infarction).
  4. Angina Pectoris; Determinant of myocardial oxygen demand what are they:
    • 1. Wall Stress from; (1) Intraventricular Pressure (2) Ventricular Radius (volume) (3) Wall Thickness
    • 2. Heart Rate
    • 3. Contractility
  5. Angina Pectrois; What are the Determinants of myocardial oxygen supply;
    • 1. Perfusion Pressure (AoDBP)
    • 2. Duration of diastole
  6. Angina Pectrois; What are the Determinants of vascular tone?
    • 1. cGMP (improves relaxation)
    • 2. Ca++ (modulates myosin light chain kinase)
    • 3. resting Membrane potential (at or below increases excitability)
    • 4. cAMP (improves relaxation/inactivity)
  7. What are the three class of treatment for Angina Pectoris?
    • 1. Organic Nitrates - (improve fuel flow, decrease demand)
    • 2. Calcium channel blockers - (Decrease Demand)
    • 3. Beta Blockers - (Decrease demand)
  8. What is the Pharmacokinetics of Nitrates / Nitrites?
    • 1. Liver
    • - Organic nitrate reductase
    • 2. Bioavailability
    • - Per oral route, only 10-20%
    • - Therefore, nitroglycerine and isosorbide dintrate given SL to bypass liver.
    • - Isosorbide mononitrate for oral use, 100% bioavialability
    • 3. Excretion
    • - After glucuronidation, largely by kidneys
  9. Pharmacodynamics; What is the mechanism of action in smooth muscle for Nitrates / Nitrites?
    • 1. Drug activated by release of nitric oxide via ALDH2
    • 2. Free nitrite ion released, converted to nitric oxide
    • 3. Combines with guanylyl cyclase, increases cGMP
    • 4. Increased cGMP increases smooth m. relaxation
  10. What are the organ system effects, vascular smooth muscle, of Nitrates / Nitrites?
    • 1. Arterial relaxation
    • 2. Venous relaxation
    • 3. Vein relaxation greater than arterial
    • 4. marked vein relaxation
    • 5. Increased venous capacitance
    • 6. Decreased Ventricular Load
    • 7. Studies suggest redistribution of coronary flow from normal to ischemic tissue
    • 8. Weak negative inotropic effect via nitric oxide
  11. What are the acute adverse effects of Nitrates / Nitrites?
    • 1. Orthostatic hypotension
    • 2. Tachycardia (Autonomic Response)
    • 3. HA (Nitrates contraindicated in increase ICP)
  12. Tolerance of nitrates / nitrites will cause what?
    • 1. Tachyphylaxis with long acting preparations (oral/TD)
    • May be result of decreased NO release
    • Systemic compensation (Sympathetic discharge, salt and water retention over (time)
  13. Mechanism of clinical effects: Nitrate effects in angina of effort is what?
    • 1. Nitrate effects in angina of effort
    • 2. Decreased venous return,
    • 3. decreased intracardiac volume,
    • 4. decreased wall tension=Decreased myocardial oxygen demand
  14. Mechanism of clinical effects: Nitrate effects in Variant Angina is what?
    • 1. Nitrate effects in Variant angina
    • 2. Relax smooth m. of epicardial coronary arteries,
    • 3. thus relieving CA spasm
  15. Mechanism of clinical effects: Nitrate effects in Unstable Angina is what?
    • 1. Nitrate effects of Unstable angina
    • 2. Thought to be from increased epicardial CA diameter and decreased myocardial oxygen demand
  16. Name some beneficial effects of nitrates in the treatment of angina
    • 1. Decreased ventricular volume
    • 2. Decreased arterial pressure
    • 3. Decreased ejection time
    • will all result in decreased myocardial oxygen requirement
    • 4. Vasodilation of epicardial coronary arteries
    • will result in relief of coronary artery spasm
    • 5. Increased collateral flow
    • will improve perfusion to ischemic myocardium
    • 6. Decreased left ventricular diastolic pressure
    • Will result in improved subendocardial perfusion
  17. Name some deleterious effects of nitrates in the treatment of angina
    • 1. Reflex tachycardia
    • will result in myocardial oxygen requirement
    • 2. reflex increase in contractility
    • 3. decreased diastolic perfusion time due to tachycardia
    • will result in decreased coronary perfusion
  18. What is the Pharacokinetics of calcium channel blockers?
    • 1. Orally active
    • 2. High first pass effect
    • 3. High plasma protein binding
    • 4. verapamil and diltiazem also used IV
  19. What is the mechanism of action for calcium channel blockers
    • 1. Bind to a1 subunits of L-type Ca++ channels. Allosteric difference b/n dihydropyridines and non dihydropyrodines
    • 2. Bind to open and inactive channels, inside cell membrane
    • 3. Can be affected by sympathomimetics (increase transmembrane flux of Ca++)
  20. What is the organ system effects of calcium channel blockers?
    • 1. Smooth m.: Relaxation. Vascular smooth m. more sensitive.
    • -Dihydropyridines more effective on vascular smooth m.
    • 2. Cardiac m.:
    • -Non dihydropyridines more effective on cardiac. Verpamil and diltiazem block tachycardias in SA and AV node more than dihydropyridines.
    • 3. Skeletal m.: Not depressed.
  21. What is the Toxicity of Calcium channel blockers?Direct effect of their therapeutic actions
    1. Cardiac depression (bradycardia, AV block, arrest, heart failure)
  22. 2. Nifedipine (immediate acting) associated with increased incidence of MI in HTN patients. Should be avoided.
  23. 3. Patients on β blockers more sensitive to cardiodepressant effects of Ca++ channel blockers.
  24. What are the mechanism of clinical effects for calcium channel blockers?
    • 1. Decrease contractility
    • 2. Decrease arterial and intra-ventricular pressure
    • 3. Decrease SA & AV node conduction with verapamil and diltiazem. Less reflex tachycardia noted with non dihydropyridines, so choice agents for control of angina.
  25. Beta Blockers: Although not vasodilators may be used for angina of effort because it?
    • 1. Decreased myocardial oxygen consumption
    • Therapeutic effects r/t hemodynamic effects-
    • -Decrease HR
    • -Decrease BP
    • -Decrease Contractility
  26. When treating Angina of effort what drugs may be used?
    • 1. Long acting nitraes
    • 2. Calcium channel blockers
    • 3. beta blockers
  27. Long-acting nitrates, Ca++ channel blockers, or β blockers may be chosen.
    • Choice depends on patient’s response.
    • 1. HTN patients: Use Ca++ chanel or β blockers
    • 2. Non HTN patients: long-acting nitrate appropriate
    • 3. If monotherapy ineffective, add drug from different class.
    • (See table 12-7)
  28. Nitates alone will:
    • 1. reflex increase heart rate
    • 2. decrease arterial pressure
    • 3. decrease end diastolic volume
    • 4. reflex increase contractility
    • 5. decrease ejection time
  29. Beta blockers or calcium channel blockers will:
    • 1. decrease increase heart rate
    • 2. decrease arterial pressure
    • 3. increase end diastolic volume
    • 4. decreasee contractility
    • 5. increase ejection time
  30. Combined Nitrates with Beta blockers or calcium channel blockers will:
    • 1. decrease increase heart rate
    • 2. decrease arterial pressure
    • 3. none or decreased end diastolic volume
    • 4. none contractility
    • 5. none ejection time
  31. What does positive inotropic mean?
    1. strengthens contraction
  32. what does negative inotropic mean?
    1. weakens contraction
  33. what does positive chronotropic mean?
    1. increase Heart rate
  34. What does negative chronotropic mean?
    1. decrease heart rate
  35. What is the definition of CHF?
    1. CO not sufficient to maintain tissue oxygen demands
  36. 2. 50% Mortality within the first 5 years
  37. 3. Systolic
    • -Decreased contractility
    • -Decreased ejection fraction
  38. 4. Diastolic
    • -Decreased elasticity
    • -Decreased filling
    • -Decreased stroke volume but can have a normal ejection fraction
  39. List the pathophysiologic mechanisms involved in CHF:
    • 1. Primary insult
    • 2. decreased cardiac performance
    • 3. neurohormonal stimulation
    • 4. release of renin/angiotensin, catecholamines, others
    • 5. Vasoconstriction and increased vascular volume - increased after load -decreased cardiac performance
    • 6. Increased preload
    • 7. heart failure symptoms
  40. What are the goals for treatment of CHF?
    • 1. Prevent further damage
    • 2. Promote optimal function
    • 3. Monitor closely for early intervention
    • 4. Minimize episodes of acute decompensation
  41. 5. Treat Co-morbid Exacerbating conditions
    • -HTN, Hyperlipidemia, DM
    • -Tobacco cessation
    • 6. Self Monitoring
    • -Nutrition
    • -Symptoms
  42. What drug groups are used in Heart failure? Chronic heart failure
    • 1. Diuretics
    • 2. Aldosterone receptor antagonists
    • 3. ACEI
    • 4. ARBs
    • 5. B Blockers
    • 6. Cardiac Glycosides
    • 7. Vasodilators
  43. What drug groups are used in Heart failure? Acute heart failure
    • 1. Diuretics
    • 2. Vasodilators
    • 3. Beta Agonists
    • 4. Bipyridines
    • 5. Natriuretic Peptide
  44. Pharmacologic treatment for CHF
    • 1. Diuretic
    • 2. Aldosterone Antagonists
    • 3. ACE Inhibitors
    • 4. ARB
    • 5. Beta Blockers
    • 6. Cardiac glycosides
    • 7. Vasodilators
    • 8. Bipyridines
    • 9. Natriuretic peptides
  45. Pharmacologic treatment for CHF: Diuretics, what is the purpose, specific meds and cautions?
    • 1. Decrease venous pressure and preload>decrease NaCl/H2O retention>decrease edema>remodeling> increase pump efficiency, esp. in systolic failure.
    • 2. Specific Meds:
    • -Furosemide drug of choice in acute heart failure.
    • -Spironolactone, Eplerenone with ACE I decrease Morbidity/Mortality with Severe Disease
    • -Start with Thiazide with mild disease, switching to loop as needed.
    • 3. Cautions:
    • -Monitor secondary K+ loss if concurrently taking digoxin
  46. Pharmacologic treatment for CHF: Ace Inhibitors, ARBs: Purpose
    • 1. Purpose
    • -Decrease Preload by decrease NaCl/H2O retention
    • -Decrease Afterload
    • -Decrease remodeling (thickening/dilation)
  47. 2. ACE = Use appears to lead to specific decrease in Morbidity and Mortality in moderate and severe disease
  48. 3. ACE = First line drug in LV disease with no edema
  49. 4. ACE = First line tx with diuretic for chronic CHF
    -NOT a substitute for digoxin
  50. 5. All ACE are equally effective
    6. If patient unable to tolerate ACEI, try ARB.
  51. Pharmacologic treatment for CHF: Beta Blocker:
    • 1. Meds
    • Studies show positive effect with use of bisoprolol, carvedilol and metoprolol
  52. 2. Mechanism of Action
    Used to prevent further injury by decreasing HR
  53. 3. May need to use for months prior to seeing an effect
    -Start low go slow
  54. Pharmacologic treatment for CHF: Cardiac Glycoside Digitalis-Digoxin
    • 1. Purpose
    • -Positive Inotropic
    • -Negative Chronotropic
    • 2. Pharmacodynamics/Mechanism of Action
    • Mechanical:
    • -Inhibit sodium pump (Na+/K+-ATPase transporter): Inc. intracellular Na+
    • -Reduce Ca++ expulsion from Inc. intracellular Na+. Ca++ sequestered in SR.
    • Electrical:
    • -Direct- Dec. SA node rate, Dec. AV node conduction velocity/Inc. refractory period, Slight Dec. in refractory period in Purkinje system.
    • -ECG: Increased PR interval and Decreased QT interval.
    • 3. Pharmacokinetics
    • -65-80% absorbed after po administration
    • -2/3rd excreted: Not extensively metabolized.
    • -Renal clearance proportional to Cr. clearance.
    • -Half life 36-40 hours
  55. Cardiac Glycoside Digitalis-Digoxin: Side effects and Contraindicatons/cautons
    • 1. Side effects
    • -HR must be > 60/min to give
    • -Arrhythmias with toxicity
    • -Bradycardia/tachycardia
    • 2. Contraindications/Cautions
    • -Hyperkalemia decreases effects of digitalis, esp. toxic effects.
    • -Hypercalcemia increases effect and risk of arrhythmia.
    • -Hypomagnesaemia increases digitalis effects.
    • -Take home message: Carefully evaluate serum electrolytes before/during digitalis therapy, monitor closely for digitalis-induced arrhythmias.
  56. Pharmacologic treatment for CHF: Vasodilators
    • 1. Venodilator
    • -Isosorbide
    • -Decreases preload ventricular stretch
    • -Antianginal
    • 2. Arteriolar
    • -Hydralazine
    • -Decreased mortality when used with Isosorbide
  57. Pharmacologic treatment for CHF: bipyridines
    • 1. Purpose
    • -Positive Inotropic
    • -Vasodilation
    • 2. Meds
    • -Inamrinone, milrinone – parenteral only
    • 3. Mechanism of Action
    • -Phosphodiesterase inhibitors, type 3.
    • -Decrease cAMP breakdown
    • -Moderate Ca++ flux
    • 4. Side effects
    • -Thrombocytopenia, hepatotoxic, arrhythmias
    • 5. Indications
    • -Emergency decompensation use only
  58. What is the treatment for Acute Decompensation Episodic Treatement?
    • 1. Direct Vasodilator
    • -Nitroprusside, nitroglycerin
    • 2. Beta Adrenoceptor agonist
    • -Dobutamine
    • -Positive Ionotropic effect
    • -Increase CO
    • -Dopamine
    • -Positive Ionotropic effect
    • -Increase BP
    • -Increase renal blood flow (?)
    • 3. Bipyridines
    • 4. Natriuretic Peptides
  59. Cardiac output =
    1. heart rate x stroke volume
  60. Blood pressure = cardiac output x resistance
  61. Tie it together:
    • 1. Cardiac Output = Heart Rate x Stroke Volume
    • 2. The Acutely Failing Heart:
    • Fix treatable cause if possible: AMI- PCI, thrombolytics, etc.
    • 3. IV TX:
    • -Unload: Diuretics- Furosemide
    • -Augment: Beta Agonists- Dobutamine, Dopamine
    • -Relax: Vasodilators- Na++ nitroprusside, nitroglycerin, nesiritide.
  62. Tie it together?
    • 1. Cardiac Output = Heart Rate x Stroke Volume
    • 2. The Chronically Failing Heart:
    • 3. Class A (Prefailure- risk factors)
    • -Control: Tx obesity, HTN, DM, hyperlipidemia
    • 4. Class B (Class I- Symptoms with severe exercise)
    • -Relax: ACEI/ARB
    • -Slow: B Blocker
    • -Unload: Diuretic
    • 5. Class C (II/III- Symptoms with marked or mild exercise)
    • -Same as B, Add:
    • -Remodel: Ald. Agonist
    • -Squeeze: Digoxin
    • -Mo’ Relax: Hydralazine, nitrate

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