MCMP 408 Final

  1. decreased butyrylcholinesterase function causes
    increased serum succinyl choline leading to respiratory apnea
  2. Isoniazid in slow acetylators causes
    peripheral neuropathy
  3. Hydralazine slow acetylation causes
    auto immune disease
  4. MPTP is metabolized by _______ and taken up by _______ causing ________. Two drugs that would prevent this are:
    MAO-B; DAT; parkinsons like sx; MAO-B inhibitor or DAT inhibitor
  5. Acetaminophen is metabolized by _____ to _____
    2E1, a reactive intermediate which can bind cell components leading to hepatotoxicity
  6. Alcohol induces Cyp ____
  7. The antidote for APAP OD is
  8. Warfarin is metabolized by _____
    CYP 2C9
  9. Inducers of 2C9 are
    Barbiturates, carbamazepine, rifampin, griseofulvan
  10. Inhibitors of 2C9 are
    Azo antifungals, Metronidazole, sulfapyrazone
  11. Omeprazole is metabolized by
  12. Omeprazole induces
  13. induction of 1A1,2 leads to
    metabolism of procarcinogens to carcinogens
  14. Terfenadine is metabolized by _____, build up of terfenadine causes _______
    3A4; cardiotoxicity
  15. 3A4 inhibitors
    Erythromycin, ketoconazole
  16. Rerpine
    MOA, SE
    • blocks VMAT
    • diarrhea, cramps, acid secretion, sedation, nightmares, depression
  17. Clonidine
    MOA, SE
    • alpha 2 agonist at slpha 2 and imidazoline receptors
    • transient increase in BP
    • dry mouth, sedation, depression, withdrawal
  18. Methyldopa
    MOA, SE
    • alpha 2 agonist, PRODRUG
    • sedation, mental impairment, lactation, positive coombs test
  19. Guanabenz/Guanfacine
    MOA, SE
    • alpha 2 agonist at imidazole and alpha 2 receptor
    • Dry mouth, sedation, depression, withdrawal
  20. Prazosin, Terazosin, Doxazosin
    MOA, SE
    • alpha 1 antagonist
    • first dose effect (orthostatic hypotension)--> take at night, Na/H20 retention, relfex tachycardia
  21. Propranolol
    MOA, CI, SE
    • beta blocker
    • CI in diabetes, asthma, COPD, class 4 CHF
    • ^ VLDL, decrease HDL, inhibit lypolysis, glycogenolysis, glucose release, bronchile resistance, sedation
  22. Metoprolol, Atenolol
    MOA, SE
    • beta 1 blocker
    • less SE
  23. Labetalol
    MOA, compensatory response
    • beta block, alpha 1 block
    • no reflex tachycardia
  24. Carvediolol
    MOA, compensatory response
    • alpha 1 block, beta block
    • no reflex tachycardia
  25. Carbonic anhydrase inhibitors are located in the _____ and inhibit _____
    Proximal conveluted Tubule; carbonic anhydrase
  26. Carbonic anhydarse inhibitor
    name, SE
    • Acetazolamide
    • K wasting, hyperchloremic metabolic acidosis, paresthesia, drowsiness, renal stones
  27. Carbonic anhydase inhibitors
    Use, CI
    • acute mountain sickness, metabolic alkalosis, glaucoma, urine alkalinization
    • Hepatic Cirrosis
  28. Carbonic Anhydrase inhibtors
    Ion loss
    lose sodium/potassium and bicarb
  29. Loop Diuretics work in the _____ and inhibit ______
    thick ascending loop of henle; Na/K/2Cl transport
  30. Loop diuretics
    name, SE
    • Furosemide, Bumetanide, Ethacrinic Acid
    • K wasting, dehydration, hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesemia
  31. Loop diuretics
    use, ion effects
    • edema, hypercalcemia, hyperkalemia, renal fail, anion OD
    • Lose NA, K, Cl, Mg, Ca
  32. Thiazides inhibit _____ and act in the _______
    Na/Cl; distal conveluted tubule
  33. Thiazides
    K wasting, hypokalemic metabolic alkalosis, hyperuricemia, impaired carb tolerance, hyperlipidemia, hyponatremia
  34. Thiazides
    HTN, CHF, hypercalciuria, diabetes insipidus
  35. Thiazides
    Ion effect
    • Lose Na/Cl
    • Keep Ca
  36. Triamterene and amiloride work in the ______ and inhibit _______
    collecting tubule; Na channel
  37. Collecting tubule drugs
    SE, CI
    • kidney stones, hypokalemia, hyperchloric metabolic acidosis
    • K supplements, ACEi
  38. collecting tubule drugs
    maintains K
  39. Spironolactone, inspira work in the _____ and inhibit _____
    Collecting tubule; aldosterone
  40. spironolactone
    hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia, impotence, BPH
  41. Spironolactone
    HTN, CHF, mineralcorticoid excess, aldosteroneism
  42. Collecting tubule drugs
    Ion effects
    • Lose Na
    • Keep K
  43. Angiotensinogen is cleaved to angiotensin 1 by _____
  44. Angiotensin 1 is cleaved to angiotensin 2 by _____
  45. ANG 2 is converted to ANG 3 by ________
  46. ang 1 activity
    little to none
  47. ang 2 causes
    release of aldosterone and vasoconstriction
  48. Rapid pressor response of ANG 2
    increase in peripheral resistance due to direct vasoconstriction, enhanced NE action, increase sympathetic discharge, release of NE from adrenals
  49. Slow pressor of ANG 2
    Na reabsorption, synthesis/release of aldosterone, altered hemodynamics
  50. cardiovascular effects of ANG 2
    increased preload/afterload, increased cascular wall tension, increased expression of protooncogenes, growth factors and ECM proteins
  51. ANG 3
    same release of aldosterone but less vasoconstriction
  52. Can ang 1 be converted directly to ang 3
    yes by a work around pathway
  53. What three mechanisms control renin release
    • Macula densa
    • Blood pressure of pre-glomerular blood vessels
    • sympathetic activation of beta receptors
  54. ACEi MOA
    binds active site of ACE and inhibit it
  55. ACEi use
    htn, lv systolic dysfunction, MI, diabetic neuropathy
  56. ACEi tox
    hypotension, dry cough, hyperkalemia, acute renal failure, skin rash
  57. ACEi DDI
    antacids (decreased ba), NSAIDs (reduced effectiveness), k supplements, digoxin (^levels)
  58. ACEi CI
    2nd/3rd trimester, neutropenia in renal insufficient patients
  59. Captopril
    altered taste, rash
  60. Enalopril
    prodrug that requires cleavage to enalaprilat and is eliminated hepatically
  61. Lisinopril
    Lysine derivative of enaloprilat NOT prodrug
  62. Fosinopril
    Prodrug that rquires hepatic esterase activation and has extensive hepatic metabolism
  63. ARB MOA
    antagonize ang 1-3
  64. ARB use
    HTN, CHF, progressive renal impairment,
  65. ARB tox
    hypotension, hyperkalemia, teratogen
  66. ARBs
    Losartan, Valsartan, Irbesartan, Candesartan, Temisartan, Eprosartan
  67. Renin inhibitors
    tekturna, prevents formation of ANG 1-3
  68. Tekturna CI
  69. Vasoconstrictors 3 moa
    • voltage gated Ca channels
    • receptor activated Ca channels
    • pharmaco mechanical coupling
  70. Endothelin, angiotensin, vasopressin
    natural vasoconstrictors
  71. Bosentan and Ambrisentan
    antagonize endothelin causing vasodilation to treat pulmonary arterial hypertension
  72. mechanism of vasoconstriction
    ca channel activation, release of intracellular ca, ca binds calmodulin, MLCK phorphorylates MLC, myosin can interact with actin, contraction
  73. Vasoconstrictor uses
    HTN, control blood flow (procedures), shock, anesthesia, chronic orthostatic hypotension, hemostasis, decongestants
  74. Nasal decongestants
    phenylephrine, pseudophedrine, ephedrine, naphazoline, tetrahyrdocoline, oxymetazoline
  75. migraine is
    severe debilitating ha
  76. migraine triggers
    stress, decreased levels of estrogen, increased PGE
  77. migraine Sx
    aura, photophobia, hyperacusis, polyuria, diarrhea, mood appetite disturbances
  78. migraine patho
    initial vasoconstriction then vasodilation followed by edema and inflammation
  79. triptans MOA
    5-HT 1D agonist causing vasoconstriction and inhibiting release of inflammatory neuropeptides
  80. Sumatriptan
    • high incidence of reoccurence
    • MAO-A inhibitor
  81. Zolmitriptan
    CI in Wolff parkinson white syndrome
  82. Naratriptin
    • Slow onset, longer duration
    • CI in severe hepatic/renal impairment or peripheral vascular disease
  83. Rizatriptan
    CI in patients with PKU
  84. Triptans SE
    warmth/tingling, vertigo, malaise, fatigue, feelings of heaviness, sense of pressure in chest
  85. Ergots MOA
    5-HT 2A agonists
  86. Ergot SE
    diarrhea, nausea, vomiting, prolonges vasospasm, uterine contractions
  87. Ergot DDI
    beta blockers and macrolides increase ergot levels and may result in ischemia
  88. Ergots for prophylaxis
    ergonovine, methylergonovine, methylsergide
  89. Ergots for abortion
    ergotamine, dihydroergotamine
  90. Prophylactic migrain Tx
    ergots, beta blockers, CCB, antidepressents, antiseizures, melatonin, ACEi, NSAIDs
  91. K is high ___ side the cell
  92. Na is high ___ side of the cell
  93. Ca is high ____ side of the cell
    outside, wants to come in!
  94. Blocking of Ca channels leads to
    Decreased blood pressure and provides relief of angina pectoris as well as antiarrhthmic effects
  95. Dihydropyridines
    isradipine, felodipine, amlodipine, nifedipine, nislopidine, nicardipine, nimodipine
  96. Dihydropyridamines MOA
    binds to closed channels to prevent opening
  97. DHP selectivity
  98. DHP use
    reduce O2 demand in heart . effective to tx angina
  99. Phenylalkylamines MOA
    binds inside pore to prevent ion passage--> frequency dependent block
  100. PAA selectivity
  101. PAA use
    slows conduction through SA/AV nodes to decrease HR and force of contractility
  102. Benzothiacepines MOA
    some tonic block, some frequency dependent block
  103. BZP selectivity
    cardio and vaso
  104. BZP use
    slows conduction but less than PAA
  105. Nimodipine
    selective for cerebral arteries used to treat brain bleeds
  106. Amlodipine
    slow onset of action and long DOA, no reflex tachycardia
  107. PAA
  108. BZP
  109. DHP SE
    reflex tachycardia, facial flushing, ankle edema
  110. Diltiazem
    ankle edema
  111. verapamil se
    ankle edema, constipation
  112. Stable Angina
    predictable. Gets worse with exercise, exertion
  113. Varient Angina
    sudden transient constriction typically at night
  114. unstable angina
    new or sudden worsening of angina at rest
  115. Goals of treatment
    • dilate coronary arteries and increase perfusion to the heart
    • decrease oxygen demand of the heart
    • decrease afterload and preload
  116. Organic nitrates MOA
    increase NO which activates guanylate cyclase leading to relaxation dilating veins, minor artery dilation
  117. main effect of nitrates
    decreased preload
  118. GTN
    sublingial for acute attacks
  119. ISDN
    oral/transderm for prophylaxis
  120. 5-ISMN
    oral/transderm for prophylaxis
  121. nitrate tolerance
    occurs due to inhibition of aldehyde dehydrogenase which activates NO to dilate blood vessels
  122. Nitrates SE
    hypotension, flushing, HA
  123. Nitrate problem
    reflex tachycardia, decreased preload leads to decreased blood pressure causing the baroreceptors to increase HR
  124. CCB MOA
    decrease influx of Ca which causes contraction causing dilation of arteries (decreased afterload)
  125. CCB problem
    reflex tachycardia, decreased afterload leads to decreased blood pressure causing the baroreceptor to increase HR
  126. Beta blockers MOA
    Block epi stimulation of myocardium, decreasing the oxygen demand (decrease HR and force)
  127. Beta blocker problem
    can increase preload due to increase pr intercal and filling time which increases LV-EDV
  128. Which CCB should not be used in combo with beta blockers?
    verapamil--> too much depression of the heart
  129. Ranolazine
    Blocks Na channels responsible for Na overload (which leads to ca overload) to PREVENT angina
  130. PDE3 inhibitors
    PDE3 breaks down cAMP which causes contraction. PDE3 inhibitors will allow cAMP to stick around causing contraction of myocardium. In vessels it causes vasodilation by decreased MLCK
  131. PDE5 inhibitors
    PDE5 breaks down cGMP which causes relaxation. inhibitors allow sustained relaxation of smooth muscle allowing the CC to stay full of blood
  132. Human B type naturetic peptide
    causes dilation
  133. natrecor
    synthetic human type b naturetic peptide
  134. endothelin
    endogenous peptide vasoconstrictor
  135. K agonists
    open k chennels so potassium leaves resulting in hyperpolarization
  136. Arteriole selective
    k agonists, hydralazine
  137. Amrinone/milirone
    PDE3 for CHF
  138. Cialis
    longest onset, longest duration, more selective
  139. Levitra
    Shortest onset, shortest duration, most selective
  140. Viagra
    Medium onset, medium duration, least selective
  141. Bosentan
    blocks ETa and ETb for primary arterial hypertension
  142. Ambrisentan
    blocks ETa receptor for primary arterial hypertension
  143. Minoxidil
    prodrug k agonist for severe htn
  144. Diazoxide
    K agonist for acute htn
  145. hydralazine
    interferes with release of ca from er, can induce lupus
  146. Adenosine
    binds to the A1 receptor leading to increased camp and increase relaxation, Minimal clinical use as a vasodilator
  147. Ca ATPase
    pumps Ca out of cells
  148. SERCA
    pumps Ca into SR
  149. NCX
    major route of Ca clearance
  150. if Na/K pump is blocked
    more sodium is in the cell so the NCX pump works less so Ca will remain in cell. SERCA will pump more into the SR.
  151. Cardiac glycoside
  152. Dig tox
    delerium, fatigue, malaise, confusion, anorexia, N/V, ab pain, PROARRHTHMIC EVENTS
  153. Dig antidote
    digibind--> goes straight to untreated HF
  154. Drugs that decreease dig absorption
    neomycin, antacids, bran
  155. Drugs that increase dig absorption
    Erythromycin, omeprazole, tetracycline
  156. Dig and kaliuretics
    Potassium and dig compete for the same receptor. less potassium means glycosides are more able to bind --> TOX
  157. causes of CHF
    MI, HTN, genetic predisposition
  158. CHF
    inability of heart to pump out enough blood to support the body's O2 demand
  159. Diastolic failure
    heart cant fill with enough blood (cant expand adequatley, stiff walls)
  160. Systolic failure
    heart cant contract well enough
  161. Sx of CHF
    tachycardia, cardiomeglia, arrythmia, fatigue (heart tries to pump harder and faster), shortness of breath, pulmonary edema Cyanosis, orthopnea (decreased lung function due to pulmonary edema due to preload being large and leaking into the pulmonary interstitum)
  162. why does CHF get cyclically worse
    systemic vascular resistance causes increase contraction to compensate. heart needs more oxygen. doesnt get it. preload increases causing back up in lungs. blood is oxygenated less. gets worse and worse.
  163. Drugs that reduce preload will
    decrease oxygen demand and increase oxygen supply
  164. drugs that reduce preload
    diuretics (furosemide) , venodilators (nitrates), angiotensin inhibiotrs (ACEi, ARBs)
  165. reduced afterload will
    decrease MAP
  166. drugs that reduce afterload
    organic nitrates, hydralazine, ACEi, ARBs NOT CCB
  167. Stimulate contractiluty drugs
    glycosides, pde inhibitors, beta agonists (dobutamine, dopamine)
  168. Acute failure drugs
    Milirone and amirone, beta agonists
  169. Drugs that treat congestive symptoms
    diuretics, vasodilators
  170. drugs that increase CO
    inotropes and vasodilators
  171. ACEi
    FIRTS LINE reduce preload, reduce afterload, prevent/reverse remodeling
  172. Beta blockers
    desensitize baroreceptors, decrease remodeling
  173. reduce/reverse remodeling
    aldosterone antagonists, beta blockers, ACEi
  174. improve survival rates
    ACEi, beta blockers, aldosterone antagonists
  175. SA nide
    normal origin of AP
  176. P wave
    depolarization of atria
  177. QRS
    depolarization of ventricles
  178. T
    repolarization of ventricles
  179. Re-entry arrythmias
    • obstacle to conduction
    • unidirectional block
    • slow enough conduction time
  180. Phase 0
  181. Phase 1
    Na channels
  182. Phase 2
    Ca channels
  183. Phase 3
    K channels
  184. Phase 4
  185. Class 1
    Na channel blockers
  186. Class 2
    beta blockers
  187. Class 3
    potassium channel blockers
  188. Class 4
  189. AP in heart
    phase 4 (HCN/GIRK), 0(Ca, slow), 3(K)
  190. Beta blockers used
    esmolol, acebutolol, propranolol
  191. Class 1a
    • na and k mixed
    • procanamide, quinidine, disopyramide
    • lengthen QT, slow 0, prolonged AP, increase refractoryness
  192. Class 1b
    • Na
    • lidocaine, tocainide, mexilentine
    • NO ekg change
    • blocks bad
  193. 1c
    • na block
    • fleconide propfenone
    • marked slow 0
  194. class 3
    • K block
    • amiodrone, bretylium, sotalol, bronedorne, dofetilide
    • prolonged AP increased QT inverval
    • Can cause torsade de pointes
  195. Class 4
    • CCB
    • verapamil and diltiazem
    • slow 0, lengthen APD
  196. Class 2
    • beta blockers
    • esmolol acebutolol, propranlol
    • incresed PR interval
Card Set
MCMP 408 Final
MCMP 408 Final