HPRS Exam 4

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cotypatricia
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78553
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HPRS Exam 4
Updated:
2011-04-11 02:12:09
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Anticoagulants HTN Dyslipidemia Anemia Antiarrythmias Heart Failure CAD
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Pharmacology review for exam 4 covering drug therapies for Anticoagulants, HTN, Dyslipidemia, Anemia, Anticoagulants, Antiarrythmias, Heart Failure, CAD
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  1. Systolic B/P HTN
    • Heart pumps blood
    • Major risk factor for CVD's
    • Rise in systolic B/P continues through life (compared to diastolic)
    • Most common form of HTN*
  2. Diastolic B/P HTN
    • Heart relaxes and fills with blood
    • Diastolic B/P levels of over 50 yo
  3. Primary HTN
    • Cause is unknown, but risk factors include:
    • - family hx
    • - racial predisposition
    • - obesity
    • - stress
    • - smoking
    • - sedentary lifestyle
    • - high fat diet
  4. Secondary HTN
    • Specific etiology:
    • - renal disease
    • - pregnancy
    • - drug induced
  5. D.A.S.H.
    Dietary Approaches to Stop Hypertension
  6. Functions of Ion Exchange in Kidneys
    • Filtration: movement of substance from blood to nephron within the glomerus
    • (Tubular) Reabsorption: ions go from tubules to blood/vascular system
    • (Tubular) Secretion: ions go from the blood supply to the tubules
  7. Sites of Ion Echange in Kidneys
    • Proximal & Distal Tubules: sodium ions are reabsorbed in echange for hydrogen (secreted)
    • Loop of Henlee: chloride ions are reabsorbed in conjunction with sodium
    • Distal Tubule: Na/K (secreted) exchange occurs, controlled by aldosterone
    • Collecting Duct: water is reabsorbed under the influence of ADH (antidiuretic hormone) in the proximal tubules & collecting duct
  8. Drug Example of Thiazide Diuretics
    Hydrochlorothiazide (HCTZ)
  9. Drug Examples for Thiazide-like Diuretics
    • Hygroton (chlorthalidone)
    • Lozol (indapamide)
    • Zaroxolyn (metolazone)
  10. MOA of Thiazide Diuretics
    inhibits Na reabsorptions in the distal tubules causing and increased excretion of Na, water, K, & H
  11. Side Effects of Thiazide Diuretics
    • Sulfa Allergy
    • photosensitivity
    • Hypercalcemia
    • Hyperlipidemia
    • Hyperglycemia
    • Hyperuricemia
    • Hyperkalemia (sxs: leg cramps, m. weaknedd, constipation, arrythmia, lethargy, decreased mental alertness)
  12. Pt Counsling for Thiazide Diuretics
    • INCREASE INTAKE OF PATASSIUM RICH FOODS:
    • watermelon
    • apricots
    • bananas*
    • nuts
    • cantaloupe
    • oranges
    • dates
    • fish
  13. Drug Examples of Loop Diuretics
    • Bumetanide (Bumex)
    • Furosemide (Lasix)
    • Ethacrynic Acid
  14. MOA of Loop Diuretics
    inhibition of Na & Cl in the ascending Loop pof Henlee and distal tubules --> lose water, Na, Cl, Mg, & Ca
  15. Types of Duiretics
    • Thiazide/Thiazide-like Diuretics
    • Loop Diuretics
    • Potassium-Sparing Diuretics
  16. Drug Examples of Potassium Sparing Diuretics
    • Amiloride
    • Spironolactone (Aldactone)
    • Triamtrene (Dyrenium)
  17. MOA of Potassium Sparing Diuretics
    block the aldosterone receptor --> results in K retention
  18. (1) What is a Side Effect to the Potassium Sparing Diuretics, Spironaloactone?
    (2) What is the alternative?
    • (1) S.E.: causes breast development in men
    • (2) alternate drug: Eperolone
  19. Types of Sympatholytic Drug Classifications
    • Beta Blockers
    • Central Acting Alpha2 Agonists
    • Peripheral Alpha1 Antagonists (blockers)
  20. Name the Beta Blocker drug examples. (-olol)
    Which ones are selective and non-selective?
    • Tenormin (atenolol) - selective
    • Inderal (propranolol) - nonselective
    • Lopressor (metoprolol) - selective
  21. Name an additional indication for Potassium-Sparing Diuretics.
    also used to clear up Acne
  22. MOA for Beta Blockers
    Decrease Co through negative chronotropic & inotropic effects on the heart & inhibition of renin release from the kidneys
  23. Drug Example for Central Acting Alpha2 Agonists
    Catapress (clonidine)
  24. Side Effects of Central Acting Alpha2 Agonists
    • nightmares*
    • dry mouth
    • constipation
  25. Pt Education for of Central Acting Alpha2 Agonists
    • Don't stop abruptly
    • Decrease dosage slowly to prevent rebound HTN
  26. Drug Examples for Peripheral Alpha1 Antagonists (blockers)
    (-zosin)
    • Minipress (prazosin)
    • Hytrin (terazosin)
    • Cardura (doxazosin)
  27. Name an additional indication for Peripheral Alpha1 Antagonists (blockers)
    BPH
  28. Side Effects & corresponding Pt Counsling for Peripheral Alpha1 Antagonists (blockers)
    • S.E.: "first dose" phenomenon"
    • Counsling: take h.s.
  29. Drug Examples for Vasodilators
    • Apresoline (hydralazine)
    • Loniten (minoxidil)
  30. MOA for Vasodilators
    works directly on smooth muscle to cause relaxation --> leads to vasodilation & decreased B/P
  31. Side Effects for Vasodilators
    • fluid retention
    • tachycardia
    • dizziness/lightheadedness
    • syncope (fainting)
  32. Name the specific Side Effect for the Vasodilator, Loniten (minoxidil).
    What product uses this as the intended effect?
    • S.E.: hair growth
    • product: Rogain
  33. Hypertension (HTN)
    • defined by persistent elevation of arterial blood pressure
    • -50 million Americans w/HTN (2003)
    • "silent killer"
    • pt is usually symptomless
    • can lead to other complications (heart failure, kidney failure, stroke/cerebral hemorrhage)
  34. Renin-Angiotension-Aldosterone System (RAA or RAAS)
    • - decrease in renal perfusion (to kidneys) - increase of renin from Juxtaglomerular cells of kdney - angiotension - angiotension 1 (weak vasoconstriction) - combines with ACE (angiotension converting enzyme) - angiotension II (powerful vasocontrictor) - increase in Aldosterone release - increase in Na reabsorption & water - increase in blood volume
    • GOAL: increase in B/P
  35. Drug Examples of ACE Inhibitors
    (-pril)
    • Capoten (captopril)
    • Vasotec (enalapril)
    • Zestril/Ptinivil ( lisinopril)
    • Lotensin (benzapril)
    • Accupril (quinapril)
    • Altace (remipril)
  36. Indications of ACE Inhibitors
    • No Angiotensin II produced (in plasma)
    • Decrease in Aldosterone release
    • Decrease in Na reabsorption & water
    • Where does K go?
    • "ACE" = where drug works**
    • K+ levels increase in blood --> Hyperkalemia
    • Decrease in blood volume
    • GOAL: Decrease B/P
  37. Side Effects of Ace inhibitors
    • hyperkalemia
    • hypotension
    • coughing**
    • angiodema
    • metallic taste*
    • SEVERE: swelling of face
  38. Pt Cousling for ACE Inhibitors
    monitor intake of sodium and/or salt substitutes
  39. Drug Ecamples for Angiotensin II Receptor Antagonists (blockers) (ARBs)
    (-sartan)
    • Cozaar (losartan)
    • Diovan (valsartan)
    • Avapro (irbesartan)
    • Micardis (telmisartan)
  40. MOA for Angiotensin II Receptor Antagonists (blockers) (ARBs)
    block the AT II receptor directly (does not inhibit ACE or renin release) --> results in a decrease in Aldosterone release --> causes vasoldiltion effect
  41. What is the advantage of using Angiotensin II Receptor Antagonists (blockers) (ARBs) for HTN drug therapy?
    • it has little effect on the serum potassium
    • does not cause the side effect of angiodema
    • very little coughing spells
  42. Drug Example for Renin Inhibitors
    Tekturna (aliskiren)

    new tx*
  43. Clinical Indication for Renin Inhibitors
    tx of HTN alone OR as combination therapy
  44. MOA of Renin Inhibitors
    blockade of the conversion of angioteninogen to angiotensin 1
  45. Side Effects of Renin Inhibitors
    • Dizziness
    • Rash
    • Hyperkalcemia
  46. Function of Calcium Channels
    Calcium is responsible for the force of contraction, normal activity, & heart rate of the heart
  47. 2 Subclasses of Calcium Channel Blockers (CCBs)
    • (1) Dihydropyridines
    • (2) Non-Dihydropyridines
    • Similar in first 2 MOAs
    • differ in structure & 3rd MOA, with different affinities for different areas of the cardiovascular system
  48. Drug Examples of Dihydropyridine CCBs
    (-dipine)
    • Procardia/Adalat (nifedipine)
    • Norvasc (amlodipine)
    • Sular (nisoldipine)
  49. MOA of Dihydropyridines CCBs
    • produce mainly a vasodilarion effect, but can also decrease the oxygen demand by the heart
    • Block entry of the calcium in Cardiac Muscles --> allows for m. relaxation & vasodilation-->decreases ability of the heart to develop forceful contractions--> decrease O2 demand by the heart & B/P
  50. Drug Examples of Non-Dihydropyridines CCBs
    • Calan (verapamil)
    • Cardizem/Tiazac (Diltiazem)
  51. MOA of Non-Dihydropyridines CCBs
    • have important effect on the pacemaker cells of the heart (SA & AV nodes), where they block Calcium Channels --> decreases rate of SA node, decreasing heart rate slightly & decreasing the conduction velocity of the AV node
    • specifically affects rate - mainly treating tachyarrythmias **
  52. Side Effects & Counsling of Calcium Channel Blockers (CCBs)
    • HA
    • Facial Fluching
    • Dizziness
    • Hypotension
    • constipation
    • Xerostoma
    • Counsling: use with caution in CHF *
  53. What are two side effects specifically related with Dihydropyridine CCBs?
    • Reflex tachycardia - due to vasodilation effects
    • Peripheral Edema
  54. Combination Therapy
    • Usualy add in drug from different class
    • Problems occur with sensitivity to cold
  55. Clinical Trials: On Target Trail
    ongoing Temisartan alone & in combination with Ramipril - Global endpoint trial --> more adverse effects & no benefit when used together
  56. Clinical Trials: Accomplish Trail
    Avoiding Cardiovascular events through combination therapy in pts living with systolic HTN --> ACE inhibitor/Amlodipine netter than ACE inhibitor/HCTZ
  57. Major Lipids in Body
    • (1) Cholesterol, (2) triglycerides, & (3) phospholipids
    • trasnport lipoprotein complexes
    • Essential subtrates for cell membrane formation & hormone synthesis
  58. 3 Major Classes of Lipoproteins
    • (1) LDL
    • (2) VLDL (associated with TG)
    • (3) HDL
  59. Dyslipidemia = Hyperlipidemia
    • Increase in bad cholesterol
    • Decrease in good cholesterol
  60. Bad Cholesterol
    • TC: total cholesterol
    • TG: Triglycerides
    • LDL: Low density lipoproteins
  61. Good Cholesterol
    HFL: high density lipoproteins
  62. LDL Calculation
    TC (total cholesterol) - HDL (high density lipoproteins) - TG (triglycerides)/5
  63. Optimal LDL Cholesterol Levels
    Less than <100 (<70)
  64. Atherolsclerosis (hardening)
    • CAD
    • Angina
    • HF
    • MI
    • Stroke
    • PAD
  65. Optimal HDL Cholesterol Levels
    • men: above >40 mg/dl
    • women: above >50 mg/dl
  66. Optimal Triglyceride Cholesterol Levels
    less than <150 mg/dl
  67. Optimal Total Cholesterol Levels
    less that <200 mg/dl
  68. Risk Factors for Dyslipidemia
    • AGE
    • -- men: 45+ yo
    • --women: 55 + yo OR premature menopause w/o estrogen replacement therapy
    • Family hx of premature CHD (definite MI; sudden death before 55 yo in father OR 1st degree male relative & before 65 in mother OR 1st degree female relative)
    • Smoking
    • HTN (140/90 mmHg OR taking HTN meds)
    • Low LDL cholesterol (<40 mg/dL)
  69. 10 yr risk: >20%
    • Risk Category: CHD/CHD risk equivalent (DM, CHD, CVD)
    • LDL goal: <100 (<70)
  70. 10 yr risk: 10 - 20%
    • Risk Category: 2+ risk factors
    • LDL Goal: <130 (<100)
  71. 10 yr risk: <10%
    • Risk Category: 2+ risk factors
    • LDL Goal: <130
  72. Risk Category: 0 - 1 Risk Factors
    LDL Goal: <160
  73. Non-Drug Therapy for Dyslipidemia
    TLC = Therpeutic Lifestyle Change:
  74. "stains" = HMG-CoA Reductase Inhibitors
    • 1st drug of choice for tx of most pts at risk for coronary & other artherosclerotic vascular disease - HUGE class
    • These agents can decrease the incidence of major coronary events & death in such patients
    • Very potent at reducing TC & LDL
    • HMG-CoA = enzyme *
  75. Drug Examples of "Stains" (HMG-CoA Reductase Inhibitors)
    (-vastatin)
    • Lipitor (atorvastatin)
    • Lexol (fluvastatin)
    • Mevacor (lovastatin)
    • Pravachol (pravastatin)
    • Crestor (rosuvastatin)
    • Zocor (simvastatin)
    • Livalo (pitavastatin)
  76. MOA of of "Stains" (HMG-CoA Reductase Inhibitors)
    • interrupt the conversion of HMG-CoA (enzyme) to mevalonate --> reduces cholesteral biosynthesis
    • rate limiting step in cholesterol sythesis *
  77. Side Effects of "Stains" (HMG-CoA Reductase Inhibitors)
    • Mild GI distress
    • Headaches
    • Myalgia
    • Rhabdomyolysis --> leads to renal failuer (rare)
  78. Pt Counsling & Food/DDIs for "Stains" (HMG-CoA Reductase Inhibitors)
    • Counsling: Need to elevate liver fxn at baseline & 2 months after starting therapy
    • Food & DDI:
    • --Azoles
    • --CCBs
    • --Grapefruit Juice
  79. Drug Examples for Bile Acid Sequestrants
    • Welchol (coresevelam)
    • Colestid (colestipol)
    • Questran (cholestyramine)
  80. MOA of Bile Acid Sequestrants
    • Bind to bile acids to disrupt recirculation of bile acids
    • Stimulate bbile acid synthesis from cholesterol
  81. Side Effects & Pt Counsling for Bile Acid Sequestrants
    • S.E.: Constipation & bloating
    • --Fiber suppliment may reduce GI effects
    • Decrease absorptions of fat soluable vitamins
    • Decrease Absorption of other drugs
    • --Warfarin & Digoxin
  82. Niacin
    Vitamin B-3
  83. MOA of Niacin
    Reduces hepatic synthesis of VLDL (associated with triglycerides)
  84. Side Effect & Pt Counsling for Niacin
    • Skin Flushing & Puritis
    • GI distress
    • Hyperglygemia/
    • Hyperuricemia/
    • Hepatotoxicity
    • Acanthosis Nigricans
  85. Contraindications of Niacin
    • PUD
    • Liver disease
    • Severe Gout *
  86. Drug Examples of Fibric Acid Derivatives
    • Lopid (gemfibrozil)
    • Tricor/ Lofibra/ Trilipix (fenofibrate)
  87. MOA of Fibric Acid Derivatives
    Reduce the rate of lipogenesis in the liver
  88. Side Effects of Fibric Acid Derivatives
    • GI Distress (dyspepsia)
    • Gallstones
  89. DDI for Fibric Acid Derivatives
    Rhabdomyolysis is increased when combined with a "-vastatin" ("stain"/HMG-CoA Reductase Inhibitor)
  90. Drug Example of Cholesterol Absorption Inhibitors
    Zetia (zetimibe)
  91. MOA of Cholesterol Absorption Inhibitors
    Decreases absorption of cholesterol from the brush border of the intestine
  92. Side Effects of Cholesterol Absorption Inhibitors
    Mild GI Distress
  93. Drug Example of Fish Oil Supplementation
    Lovaza
  94. MOA of Fish Oil Supplementation
    • not completely understood
    • active components are DHA & EPA
  95. Indications & Dosing for Fish Oil Supplementation
    • Indicated for pts with increased TG (triglycerides)
    • Dosing: 4 g/d
  96. Side Effects of Fish Oil Supplementation
    • Increase bleeding time
    • Eructation (fishy)
    • Dyspepsia
  97. DDI of Fish Oil Supplementation
    Possible DDI with anticoagulants
  98. Hematopoiesis
    • The production of new blood cells
    • 3 essential nutrients (key players):
    • (1) iron
    • (2) vitamin B-12
    • (3) folic acid
  99. Anemia
    a deficiency in O2 carrying erythrocytes (RBCs)
  100. Populations with Iron Deficiency Anemia
    • Premature infants
    • children during rapid growth periods
    • pregant/lactating women
    • chronic kidney disease
    • pts with certain inabilities to absord iron
    • blood loss
    • Avg diet contains 10-15 mg of elemental iron - only 5-10% absorbed *
  101. Oral TX for Iron Deficiency Anemia
    • ferrous sulfate (ferrous Salts = most efficiently absorbed) *
    • gluconate
    • fumarate
  102. Side Effects of Oral TX for Iron Deficiency Anemia
    • Constipation
    • GI Upset
    • Black Stools
  103. Parental TX for Iron Deficiency Anemia
    • Iron Dexatran
    • -- IM = stains
    • -- IV = hurts
  104. Side Effects of Parental TX for Iron Deficiency Anemia
    • HA
    • light-headedness
    • fever
    • hypersensitivity - test dose
  105. Vitamin B-12 Deficiency Anemia
    • B-12 serves as cofactor for severl essential biochemical reactions
    • -- DNA sythesis
    • -- myelin sheath protection
    • "extrinsic factor": intrinsic factor is a protein secreted by the stomache to help uptake dietary Vitamin B-12
  106. Etiology of Vitamin B-12 Deficiency Anemia
    • inadequate dietary intake, decreased absorption, & inadequate utilization
    • Avg diet contains 5-30 mcg with only 1-5 mcg absorbed *
    • --sources: liver, eggs, dairy
  107. Symptoms of Vitamin B-12 Deficiency Anemia
    • Pallor
    • Icterus
    • Gastric Mucosal Atrophy
    • B-12 only: Neuropsychiatric abnormalities
    • -- Numbness
    • -- Parethesias
    • -- Irritability
  108. Name & Define the 2 Forms of Vitamin B-12 Deficiency Anemia
    • (1) Pernicious Anemia: lack the ability to synthesize intrinsic factor (inhibit B-12) dietary uptake)
    • (2) Megaloblastic Anemia: results from dificiency of cyanocobalamine
  109. TX for Vitamin B-12 Deficiency Anemia
    Cyanocobalamine
  110. Coagulation
    • Normal blood clot formation due to local tissue injury
    • Liquid to solid "plug"
  111. Thrombocytes
    • Platelets
    • cells in blood that migrate to tissue injury
    • necessary for clot formation
  112. Aggregation
    when platelets stick to each other
  113. Thrombus
    clot formation
  114. Thromboembolism
    • When clots are jammed in a blood vessel
    • i.e. "moving clot"
  115. Roles & Conditions related to Anticoagulation Therapy
    • Used against Clot formation when clotting mechanism becomes too active
    • Inhibit platelet aggregation OR interfere w/plasma clotting factors
    • (5) Cxs treated:
    • (1) Deep Vein Thrombosis
    • (2) Atrial fibrillation
    • (3) Stroke
    • (4) MI
    • (5) Pulmonary Embolus
  116. "Key Players" of Anticoagulation Therapy
    • (1) Adenosine diphosphate (ADP)
    • (2) Thrombin
    • (3) Antithrombin
  117. Adenosine Diphosphate (ADP)
    • Powerful inducer of platelet aggregation
    • 1 of 3 "key players" in anticoagulation therapy
  118. Thrombin
    • Central role in hemostasis
    • Allows fibrogen to form a fibrin clot
    • Activator of platelets & other clotting factors
    • 1 of 3 "key players" in anticoagulation therapy
  119. Antithrombin
    • Anticoagulant
    • 1 of 3 "key players" in anticoagulation therapy
  120. Drug Examples for Indirect Thrombin Inhibitors
    • Heparin
    • LMWH = Low Meolecule Weight Heparin:
    • -- Lovenox (enoxaparin)
    • Selective Anti-Xa inhibitor:
    • -- Arixtra (fondaparinux)
  121. Drug Examples for Direct Thrombin Inhibitors
    • Lepirudin
    • Dabigaran
  122. Precautions for Heparin
    • Administerd IV & Sub-Q
    • Never give IM or Orally
    • Close monitoring required
  123. Side Effect of Heparin
    Heparing-induced thrombocytopenia
  124. MOA of Heparin
    • interferes with Platelet aggregation
    • Inhibits Thromboplastin activity
    • Inhibits Thrombin Activity
    • Prevents fibrin to form clot
    • indirect thrombin inhibitor *
  125. Drug Example for Low Molecular Weight Heparin (LMWH)
    Lovenox (enoxaparin) - fragments of heparin
  126. MOA for Low Molecular Weight Heparin (LMWH)
    • Inhibits factor Xa
    • Indirect thrombin inhibitor *
  127. LMWH = Low Molecular Weight Heparin
    • More predictable
    • improved SC bioavailability
    • longer half life
    • less need for monitoring
  128. Drug Example & dosing of Selective Anti-Xa Inhibitors
    • Arixtra (fondaparinux)
    • Dosing: once daily, whereas Lovenox is 1- 2 x daily
  129. MOA of Selective Anti-Xa Inhibitors
    • Inhibits factor Xa --> interrupts the blood coagulation cascade & inhibits thrombin formation & thrombin development
    • indirect thrombin inhibitor *
  130. Lepirudin
    • Recombinant formulation of hirudin
    • Hirudin: thrombin inhibitor isolated from the saliva of leeches
    • Direct thrombin inhibitor *
  131. Pradaxa (dabigatran)
    • FDA approved on October 2010
    • "Prodrug"
    • BID dosing
    • direct thrombin inhibitor *
  132. Side Effects/Adverse Effect of Pradaxa (dabigatran)
    • Bleeding
    • Dyspepsia
    • GERD
  133. Advantages of Pradaxa (dabigatran)
    • no monitoring or dose adjustments
    • no known food-drug interactions
    • Pregnancy C
  134. DDI of Pradaxa (dabigatran)
    • Very little DDIs
    • -- rafampin
  135. Disadvantages of Pradaxa (dabigatran)
    • Lack of a way to monitor
    • No reversal agent to treat overdose
    • Cost $$
  136. Drug Examples of Anti-Platelets
    • ASA (Aspirin)
    • Plavix (clopidigrel)
    • Effient (prasuarel)
    • Dypridamole
  137. Drug Example for Anticoagulants
    Coumadin (Warfarin)
  138. MOA of Aspirin
    • Irreversibly inhibits the formation of thromboxane --> no platelet aggregation
    • Anti-Platelet *
  139. MOA of Plavix (clopidigrel) & Effient (prasuarel)
    • Block adenosine diphosphate binding to membrane receptors & preventing ADP activation of GP IIa/IIIb in coagulation cascade
    • Anti-Platelet
  140. Advantage vs Disadvantage of Effient (prasuarel)
    • Advantage: more beneficial compared to Plavix (clopidigrel) in reducing thrombic events
    • Disadvantage:bleeding seen more frequently with Effient (prasuarel)
  141. MOA of Dipyridamole
    • Reversibly interferes with the platelet aggregation by increasing adenosine (inhibitor of platelet reactivity)
    • Inhibits phosphodisterase within the platelets
    • Anti-platelet
  142. MOA of Wafarin (coumadin)
    • inhibits Vitamin K dependent clotting factors II, VII, IX, X
    • Prevents synthesis od normal clotting factors
    • Anti-Coagulant
  143. Benefits of Warfarin (coumadin)
    • Orally
    • Less side effects
    • inexpensive
  144. Side Effects/Adverse Effect of Warfarin (coumadin)
    • Skin Necrosis
    • Purple Toe Syndrome
    • "X" - pregnancy?
    • Easy Bruising
    • Thrombocytopenia
    • Bleeding/Prolonged Bleeding
    • -- in gums during brushing & shaving
    • -- hematuria & blood in stool
    • unexplained epistaxis
  145. What are some preventative measures for the adverse side effects of Warfarin (coumadin)?
    • gentle blowing of the nose
    • use electric razor
    • soft-bristle tooth brush
    • need ID card
    • Get counsling before taking OTC meds
  146. DDIs for Warfarin (coumadin)
    • Causing Increase Response = Bleeds (4 Gs):
    • -- Ginkgo
    • -- Ginseng
    • -- Garlic
    • -- Green Tea
    • Decrease Response = Clots:
    • -- chronic alcohol use
    • -- St. John's Wart
    • -- green leafy vegetables
  147. Antidote for Heparin
    • Protamine Sulfate
    • 1 mg of Protamine will neutralize: 90- 120 units of heparin, 1 mg of enoxaparin, or 100 IU of daltreparin
  148. Antidote for Coumadin (warfarin)
    • Vitamin K
    • Promote synthesis of prothrombin, factors XII, IX, & X
    • Phytonadione & menadione are fate soluable
    • Menadiol is water soluable
  149. Fibrinolytic/Thrombolytic Enzymes
    • "Clot Busters"
    • Must be administeres ASAP
  150. Drug Example of Fibrinolytic/Thrombolytic Enzymes
    Activase (alteplase-tPA)
  151. MOA of Fibrinolytic/Thrombolytic Enzymes
    to stimulate plasminogen to change into plasma --> causes firinolysis to occur --> dissolve preformed clots
  152. Adverse Side Effects of Fibrinolytic/Thrombolytic Enzymes
    • Activase (alteplase-tPA):
    • -- hemorrhage
    • -- allergic reaction
  153. Contraindication for Anti-coagulants & Fibrinolytic/Thrombolytic Enzymes
    • Active bleeding rendencies
    • uncontrolled HTN
    • Ulcers
    • Recent surgery on brain &/or spinal cord
  154. Drug Examples of Coagulants
    • Vitamin K (Aquamephyton)
    • Thrombin-powder
  155. Indications for Coagulants
    • neonates:
    • -- to help with clotting
    • -- whose mothers were on oral anti-coagulation therapy
    • control bleeding during a surgical procedure
    • Hemophiliac, missing clot factor VII
  156. Cardiac Electrophysiology: Myocardial Action Potential
    normal heart beat initiated by electrical signals
  157. Cardiac Electrophysiology: Phase 0
    Rapid Depolarization
  158. Cardiac Electrophysiology: Phase 1
    • notch
    • initial repolarization
  159. Cardiac Electrophysiology: Phase 2
    AP Plateau
  160. Cardiac Electrophysiology: Phase 3
    Final repolarization
  161. Cardiac Electrophysiology: Phase 4
    return to stable diastolic potential
  162. Conduction system of the Heart
    • S.A. node: "Pacemaker," maintains pumping
    • A.V. node
    • Bundle of His
    • Purkinje Fibers
    • Responsible for coordinating the contractions of the heart chambers
  163. EKG/ECG: P wave
    reflects atrial depolarization
  164. EKG/ECG: PR wave segment
    reflects how long it takes for nerve impulse to get from the S.A. node to the A.V. node
  165. EKG/ECG: QRS wave
    reflects ventricular depolarization
  166. EKG/ECG: ST segment
    • Plateau Phase
    • absolute refractory period
  167. EKG/ECG: T wave
    ventricular repolarization
  168. Absolute Refractory Period (ARP)
    • Phase 1, 2, 3
    • no stimulus, no matter how strong, will excite the nerve
  169. Relative Refractory Period (RRP)
    • End of Phase 3
    • Stronger than normal stimuli can cause excitation
  170. Arrythmias
    • An abnormality in either the rate and/or rythm of the heart
    • Loss of cardiac rythm, especially irregularity of heartbeat
  171. 2 Mechanisms that Result in Arrythmias
    • (1) "automatic": abnormality in impulse generation
    • (2) "reentrant": abnormality in impulse conduction
  172. Types of Arrythmias
    • Tachycardia
    • Atrial Flutter
    • Atrial Fibrillation (most common)
    • Ventricular Fibrillation (worse kind)
    • premature atria contraction
    • premature ventricular contraction
    • bradycardia
  173. How do Anti-Arrythmics Work to control Arrythmias?
    • Sodium blockade
    • Blockade of sympathetic autonomic effects in the heart
    • prolongationm of the refractory period
    • Calcium Channel Blockers
    • Goal: to convert arrythmias to a normal rhythm
  174. Vaughan Williams Classification
    • Class IA, IB, IC
    • Class II
    • Class III
    • Class IV
  175. MOA of Class I Anti-Arrythmics
    bloack sodium channels
  176. Drug Examples for Class IA Anti-Arrythmics
    • Quinidine (Quinaglute)
    • Procainamide (Pronestyl)
  177. Drug Example for Class IB Anti-Arrythmics
    Lidocaine (Xylocaine)
  178. Drug Example for Class IC Anti-Arrythmics
    Propafenome
  179. Drug Examples for Class II Anti-Arrythmic
    • Propranolol
    • Beta-Blockers
  180. MOA of Class II Anti-Arrythmics
    • Beta-Blockers
    • block conduction velocity
  181. Drug Examples for Class III Anti-Arrythmics
    • Bretylium (Bretylol)
    • Amiodarone (Cardarone)
  182. MOA of Class III Anti-Arrythmics
    blocks the potassium channels that results in prolongation of AP
  183. Drug Examples for Class IV Anti-Arrythmics
    • Nondihydropyridines ***
    • Verapamil
    • Diltiazrm
    • calcium channel blockers
  184. MOA of Class IV Anti-Arrythmics
    • Calcium Chyannel Blockers
    • inhibit calcium entry --> slow conduction
  185. MOA of Multaq (dronedarone)
    • All 4 MOAs:
    • (1) block sodium channels
    • (2) beta-blocker: block conduction velocity
    • (3) blocks potassium channels -->prolongation of AP
    • (4) Calcium Channel Blocker: inhibit calsium entry --> slow conduction
  186. Multaq (dronedarone) vs Amiodarone (Cardarone)
    "anything you can do...I can do better"
  187. Counsling for Multaq (dronedarone)
    Severe liver injury - monitor LFTs
  188. Heart Failure (HF)
    • Progressive Disorder - Pathophysiological state, caused by an event, in which the heart is unable to pump blood at a rate sufficient to meet the metabolic needs of the body
    • Interferes with heart's ability to contract &/or relax decreasing output
    • Acute onset = MI
    • Chronic onset = HTN
  189. Body's Compensatory Effects of Heart Failure (HF)
    • increased heart rate & contractability
    • vasoconstriction
    • (ventricular) remodling
    • increase reload --> increase cardiac output
  190. Clinical Presentation of Heart Failure
    • Edema - pulmonary OR peripheral
    • Tachypnea
    • Nocturnal dyspnea
    • exercise intolerance
    • orthopnea
    • dyspnea on exertion
    • Rales (crackling sounds) on auscultation
  191. Standard 1st Line Therapies for Heart Failure (HF)
    • ACE-inhibitors
    • Beta-Blockers
    • Diuretics
    • Digoxin
    • Aldosterone antagonists/blockers
    • Angiotensin II receptor Blockers (ARBs)
    • Nitrates & Hydralazine
  192. Indications for Cardiac Glycosides
    • HF
    • Arrythmias
    • -- Atrial Fibrillation
    • -- Supraventricular tachyarrythmias
  193. Administration of Cardiac Glycosides: Digitalizing Dose
    frequent & higher doses are given to acheive desired blood levels
  194. Administration of Cardiac Glycosides: Maintenance Dose
    Smaller regular doses given once a day to maintain blood levels
  195. Drug Example of Cardiac Glycoside
    Lanoxin (digoxin)
  196. MOA of Lanoxin (digoxin)
    • Cardiac Glycoside:
    • Inhibition of the Na/K ATPase pump which acts to increase the intracellular Na/Ca2+ exchange -->increase intracellular Ca
    • --> decrease heart rate
    • -->increase force of contraction
    • -->slow conduction thru AV node
  197. Lanoxin (digoxin) Theraputic Serum Concentration: Heart Failure
    0.5 to 0.8 ng/ml
  198. Lanoxin (digoxin) Theraputic Serum Concentration: Arrythmias
    0.8 to 2 ng/ml
  199. Lanoxin (digoxin) Toxic Serum Concentration
    >2.5 ng/ml
  200. Onset of Lanoxin (digoxin)
    • Enterohepatic circulation
    • -- rapid
    • -- long duration
  201. Monitoring Parameters for Lonoxin (digoxin)
    • Potassium (K)
    • Calcium (Ca)
  202. Side Effects of Lanoxin (digoxin)
    • N & V
    • HA
    • visual disturbances - halos around dark objects
    • rash
    • slow &/or irregular pulse
  203. Positive Inotropic Agents
    • Increase FOC
    • Ex: Cardiac Glycoside
  204. Negative Inotropic Agent
    • Decrease FOC
    • Ex:
    • -- Beta-Blocker
    • -- Calium Channel Blocker
  205. Positive Chronotropic Agent
    • Increase HR
    • Ex:
    • -- Epinephrine
    • -- Atropine
  206. Negative Chronotropic Agent
    • decrease HR
    • Ex: Cardiac Glycoside
  207. CAD: Ischemia
    decrease clood flow to heart muscle due to coronary artery blockage --> leads to O2 demand exceeding the O2 supply
  208. CAD: Arteriosclerosis
    • Due to aging
    • Hardening & narrowing of the arteries --> results in decrease blood flow
  209. CAD: Artherosclerosis
    • Fatty deposits accumulate in the walls of the arteries --> reduce blood supply
    • Most common form of Arteriosclerosis*
    • Linked to (1) high cholesterol, (2) increased B/P, & (3) smoking
  210. CAD: Angina
    • Due to arteriosclerosis OR artherosclerosis
    • Chest pain
  211. 3 types of Angina
    • (1) Stable Classic Angina
    • (2) Unstable Angina
    • (3) Vasospasm of coronary artery
  212. Tx of Angina
    • Rest
    • Anti-Anginal Drug:
    • -- Vasodilators (Nitrates)
    • -- Beta-blockers
    • -- Calcium Channel Blockers
    • -- Renexa (for chronic angina)
  213. Drug Examples for Nitrates
    • Nitroglycerin (NTG Sublingual tabs)
    • Isosorbide mononitrate
    • Isosorbide dinitrate
  214. MOA of Nitrates
    • Dilate Veins & Arteries
    • Cecrease B/P
    • Decrease work on the heart
    • Decrease Oxygen consumption
  215. Side Effects of Nitrates
    • Flushing
    • Headaches
    • Faintness
    • Dizziness
    • Tachycardia
    • Orthostatic HTN
  216. Pt Counsling (DDIs) for Nitrates
    • Avoid those drugs used to treat ED:
    • -- Sidenafil (24 hr)
    • -- Verdenafil (24 hr)
    • -- Tadalafil (48 hr)
  217. Indication for Ranex (ranolazine)
    tx for chronic angina
  218. MOA for Ranex (ranolazine)
    • Exerts anti-ischemia effects w/o changing heart rate OR B/P *
    • Inhibits the late phase of the inward sodium channel in ischemia cardiac cells during repolarization --> reduces intrcellular (Na) --> reduces calcium influx via Na/Ca2+ exchange --> results in decreased ventricular tension & myocardial O2 consumption
  219. Side Effects for Ranex (ranolazine)
    • Dizziness
    • Constipation
  220. Myocardial Infarction (MI)
    • Results from a sudden interruption of blood supply to an area of myocardium bc of complete (or near complete) occlusion of a coronary artery
    • heart cells do not receive adequate blood supply --> Necrosis (death) of the muscle cells
    • = "Heart Attack"
  221. What diseases can result from a Myocardial Infarction (MI)?
    • HF
    • Cardiac Arrythmias
  222. Clinical Presentation of Myocardial Infarction (MI)
    • Chest pain (angina)
    • Possible pain in arms/shoulders
    • Diaphoresis
    • Arm tingling/numbness
  223. Tx for Myocardial Infarction (MI)
    • Rest: heart healing process
    • *"MONA"*: Morphine, Oxygen, Nitrate, Aspirin
    • Prevention: life style modifications
    • Stool Softener
    • Treat Other complications: HTN
  224. Acanthosis Nigricans
    • skin disorder that results in velvety, light-brown-to-black markings in areas including the neck, armpits, groin, and under the breasts
    • commonly associated with obesity and hyperinsulinemia, diabetics, or pts of African descent
  225. Xerostomia
    Dry mouth due to lack of saliva

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