GU Pharm Exam 1 Module 7

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  1. Name all the classes of anti-hypertensives
    (10)
    • 1. Diuretics
    • 2. B-antagonists (blockers)
    • 3. alpha1 antagonists
    • 4. alpha 2 agonists (centrally acting)
    • 5. Mixed alpha/beta antagonists
    • 6. ACE Inhibitors
    • 7. ARBs
    • 8. Direct Renin Inhibitors
    • 9. Ca+ Ch blockers
    • 10. Vasodilators
  2. What is the site of action of Thiazide diuretics?
    Distal tubule (where concentration of drug is higher than concentration in the blood)
  3. What is the MOA of Thiazide Diuretics? What do they promote?
    MOA: competitive antagonism of Na/Cl- cotransporter in DISTAL TUBULE- which inhibits Na/H2O reabsorption

    • -decrease intravascular volume
    • -direct vasodilatory effect
  4. What are 4 common AE's of Thiazides?
    • Hypokalemia (decreased reabsorption of K+
    • Hyperurecemia
    • Hyperglycemia
    • Dehydration
  5. When should Thiazides NOT be used?
    • 1. In renal failure or if CrCl is <30 ml/min
    • 2. In pts with Gout
  6. Name the prototypical Thiazide Diuretic?
    HCTZ: hydrochlorthiazide
  7. Name 3 Potassium-Sparing Diuretics?
    • Triamterene
    • Amiloride
    • Maxide (combo: HCTZ/TMT)
  8. Where is the site of action of K+ Sparing Diuretics?
    Renal collecting duct
  9. What is the MOA of K+ Sparing Diuretics? (2)
    • 1. Na+ channel blockade in collecting duct
    • 2. Increased reabsorption of K+
  10. Are K+ sparing diuretics commonly used as monotherapy?
    No. They are usually used in combo with HCTZ's. 

    ex. Maxide
  11. What is common AE of K+ Sparing Diuretics?
    Hyperkalemia
  12. Name 2 aldosterone antagonists used in heart failure?
    • Spirinolactone
    • eplerenone
  13. Name 3 Loop Diuretics?
    • Lasix (furosemide)
    • bumetanide
    • torsemide
  14. What is the MOA of Loop diuretics?
    MOA: inhibit Na+, K+, Cl- cotransporters in the Loop of Henle
  15. What 5 AE's can occur with Loop Diuretics?
    • Hypokalemia
    • Dose related ototoxicity
    • Hypomagnesemia
    • Hypocalcemia
    • "Sulfa" allergy
  16. What are the MOA's of aldosterone antagonists? (2)
    • 1. competitive antagonism at the aldosterone receptor
    • 2. Inhibition of mineralcorticoid receptors
  17. What AE can aldosterone receptor antagonists cause?
    Hyperkalemia
  18. How do B-Blockers work? (6 functions)
    • 1. antagonism of catecholamines at B-receptor, which prevents activation of alpha 1 receptor
    • 2. Decrease cardiac output via decrease of HR and contractility 
    • 3. Cause initial compensatory increase in PVR
    • 4. Long-term decrease in PVR by inhibition of B-receptors in the kidneys which decrease renin
    • 5. Produce resting bradycardia
    • 6. Reduce exercise-induced tachycardia
  19. What are common AE's of B-Blockers? (7)
    • Acute asthma, wheezing
    • Symptomatic bradycardia
    • Fatigue
    • Depression
    • Hypoglycemia
    • Sexual dysfunction
    • Lipid increases
  20. How should B-Blockers be stopped if necessary?
    Avoid abrupt stopping of B-Blockers!
  21. What are MOA's of non-selective B-Blockers?
    • 1. antagonize catecholamines at B1 and B2 receptors
    • 2. inhibit sympathetically induced renin secretion
  22. What are CI of non-selective B-Blockers?
    • 1. asthma
    • 2. drug interactions with other CYP2D6, 2C19 drugs
  23. Name a non-selective B-Blocker?
    Propranolol (Inderal)
  24. What are selective B-Blockers? What suffix do they end with?
    • Selective for B1 (end in "olol") have less CNS AE's
    • Metoprolol (Lopressor, Toprol XL, atenolol, bisoprolol, esmolol
  25. Name some partial B-Blockers? (suffix ending)
    • Acebutolol, carteolol, penbutololm pindolol
    • OLOL
  26. What is MOA of Partial B-Blockers?
    • ISA (intrinsic sympathomimetic activity
    • - less decrease in HR and CO
    • -agonism when sympathetic tone is low (less resting bradycardia)
    • -antagonism when sympathetic toneis high (still blocks exercise-induced tachycardia)
  27. Name some mixed alpha1/Beta 1, 2 Blockers?
    Labetolol and Carvedilol
  28. When is Labetolol (Normodyne, Trandate) used?
    • 1. Orall with 3:1 B to alpha antagonism
    • 2. IV to treat hypertensive crisis
  29. When is Carvedilol (Coreg) used?
    • Primarily in heart failure.
    • Non-selective B-blockade and an alpha blockade??
  30. What is the MOA of Apha-1 Blockers?
    Name 3.
    Inhibit peripheral vasomotor tone, reducing vasoconstriction and decreasing SVR and therefore BP

    Prazosin, Terazosin, Doxazosin
  31. What is a precaution with Alpha-1 blockers/antagonists? How are they dosed to prevent this?
    • "First dose effects" -postural hypotension
    • Dose at HS then titrate up slowly
  32. Which Alpha-1 antagonists are used for BPH?
    Terazosin, Doxazosin, Tamsulosin
  33. What is MOA of centrally acting Agents?
    • 1. agonize alpha 2 receptors in brain
    • 2. reduce sympathetic outflow from vasopressor centers in the brain
  34. What are 7 common AE's with Centrally acting agents?
    • sedation
    • impaired concentration
    • nightmares
    • depression
    • vertigo
    • EPS
    • lactation in men
  35. Which Central agent is used in pregnancy and why?
    • Methyldopa (Aldomet)
    • Renal blood flow is maintained- so good for renal insufficiency
  36. What are cautions for use of Clonidine?
    • 1. avoid abrupt cessation which can lead to rebound hypertension
    • 2. PO or transdermal available
    • 3. 50/50 hepatic metabolism and renal excretion
  37. Name some ACE inhibitors. What is the common suffix?
    "PRIL"

    Lisinopril, captopril, ramipril, enalapril, fosinopril, quinapril, benzapril
  38. What is the site of action and MOA of ACE Inhibitors?
    • ACE receptor in endothelium
    • MOA: block conversion of angiotensin 1 to angiotensin II; block inactivation of bradykinin
  39. Name some of the Pro-Drug ACEI?
    Ramipril, enalapril, benzepril, fosinopril
  40. Name a population particularly suited for ACEI
    Diabetics with proteinuria
  41. Name common AE's of ACEI?
    Hyperkalemia, angioedema, cough (due to bradykinin) (NSAIDS may impair effects by blocking bradykinin-mediated vasodilation)
  42. What are CI for ACEI?
    • Pregnancy
    • Renal artery stenosis
  43. Name some ARBs? Common suffix?
    "ARTAN"

    Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan
  44. What is the site of action of ARB's?
    Ang II receptor
  45. What is the MOA of ARB's? What makes them different from ACEI's
    • competitive binding of Ang II receptor results in decreased peripheral vasoconstriction;
    • no effect on ACE or bradykinin- thus no SE of cough or angioedema
  46. What are possible AE's of ARBs? CI's?
    • AE: hyperkalemia
    • CI: pregnancy
  47. Name a Direct Renin Inhibitor?
    SOA?
    MOA?
    CI's?
    • Aliskiren (Tekturna)
    • SOA: Renin binding pocket
    • MOA: prevents conversion of Angiotensinogen to Ang I by Renin
    • CI: pregnancy
  48. What are the 4 general MOAs of Anti-arrhythmics?
    • 1. Alter maximum diastolic potential in pacemaker cells and/or the resting membrane potential in ventricular cells
    • 2. Alter rate of phase 4 depolarization
    • 3. Alter threshold potential
    • 4. Alter the action potential duration
  49. Name the Class of Antiarrhythmics which affect Na+ Channels (subclasses)
    • Ia: Na and K+: 
    • Ib: Na
    • Ic: Na
  50. Which Class of Antiarrhythmics affect Beta-1 receptors?
    Class II.: Beta Blockers
  51. What Channel do Class III Antiarrhythmics affect?
    III: K+
  52. Which Channel does Class IV Antiarrhythmics affect?
    Class IV: Ca+: Ca+ Ch blockers
  53. Class Ia Antiarrhythmics block ___ and ____ Channels which have 3 effects on EKG.
    1. 
    2.
    3.
    • Ia block Na+ and K+
    • 1. Prolong repolarization
    • 2. Prolong QT interval → torsades de pointes (TdP)
    • 3. Decreases conduction velocity
  54. What AE's occur with Class Ia?
    What degree of affect do the following Class Ia drugs exhibit these AE's?
    (quinidine, procainamide, disopyramide)
    • Anti-cholinergic effects due to K+ blockade
    • (can't pee, can't spit, can't see)
    • Disopyramide>quinidine>>procainamide
  55. Name 3 specific facts about quinidine (Class Ia)
    AE's:
    Metabolism:
    DI:
    • AE: diarrhea, nausea, headache, dizziness
    • Met: CYP450
    • DI: increases Digoxin levels
  56. Name 3 specific facts about procainamide (Class Ia)
    • 1. AE: lupus-like syndrome, thrombocytopenia, neutropenia, anemia
    • 2. Requires renal and hepatic adjustments
    • 3. Active metabolite is NAPA
  57. Which of the 3 Class Ia agents is a Negative Inotrope with anti-cholinergic AE's? Which condition should it be avoided in?
    • disopyramide
    • Do not use in Heart Failure
  58. Class Ib Antiarrhythmics block____channels.
    Examples are ______ and ________
    Na+ (binds to both open and inactivated Na+ channels.

    Lidocaine and mexilitine
  59. How do Class Ib agents work?
    What condition are they used for?
    What condition are they ineffective for?
    Which enzyme are they metabolized by?
    • 1. Shorten repolarization and QT interval
    • 2. Used for ventricular arrythmias
    • 3. Not effective for supraventricular arrythmias
    • 4. Metabolized by CYP450
  60. What are the AE's possible for Class Ib agents?
    Neurological: paresthesias, agitation, slurred speech, somnolence, confusion, psychosis and seizure
  61. Class II Anti-arrhythmics are also known as __________
    Beta Blockers
  62. What is MOA of Class II agents? (4)
    • 1. Block sympathetic stimulation of B-1 receptors
    • 2. Slow SA node firing and conduction through AV node 
    • 3. Prolong repolarization
    • 4. Decrease the rate of repolarization
  63. AE's for Class II drugs?
    Excessive negative inotropic effects, heart block, bradycardia, bronchospasms and insomnia. (Off-target effects of B2 blockade)
  64. Of the Class I (a, b,c)  antiarrythmics, which is the most potent Na+ channel blocker?
    What are the effects on cardiac function?
    • Class Ic
    • Depressive effects on cardiac function
    • Pro-arrythmic effects
  65. What are AE's of Class Ic drugs?
    Sinus-node dysfunction, marked decrease in conduction velocity, conduction block, blurred vision, dizziness
  66. Name 3 Class Ic drugs
    Flecainide, propafenone, moricizine, encainide
  67. Class III antiarrhythmics block ____ channels which ________ repolarization.

    Name them:
    • K+
    • prolongs

    Ibutilide, dofetilide, sotalol, amiodarone, dronedarone
  68. ________ is a Class III drug which also blocks ______ receptors.
    Sotolol
  69. ___________ is a Class III drug which also blocks ___ and _____ and ______ receptors.

    This drug also has a ______ half-life (20-50 days)
    • Sotolol
    • Ca+ and N+ and Beta
    • Long
  70. _________ is a Class III drug which is similar to amiodarone but it is _______ and therefore has a shorter half-life and has_______ AE's.
    • Dronedarone
    • less lipophilic
    • fewer
  71. Class III drugs: Ibutilide and Dofetilide are used for _____________. Which one requires registration by providers and patients if Rx
    AE: they can cause ___________
    CI: K+ and Mg++ must be monitored
    • Atrial flutter/fibrillation and chemical cardioversion.
    • Torsades de Pointe
    • Dofetilide
  72. Amiodarone is used to treat _______ and _______.
    It has many potential AE's such as (9)
    • ventricular and atrial arrhythmias.
    • 1. Decrease AV/SA node fx: bradycardia
    • 2. Pneumonitis, pulmonary fibrosis
    • 3. Hyperthyroidism or hypothyroidism
    • 4. Elevated LFT's
    • 5. Optic neuritis, corneal microdeposits
    • 6. PEripheral neuropathy
    • 7. Skin discoloration, photosensitivity
    • 8. GI upset
    • 9. CYP450 drug interactions
  73. ____________ has a more favorable SE profile than Amiodarone. But it may cause __________ and should be used with caution in systolic HF.
    • Dronaderone
    • Hepatotoxicity
  74. Class IV drugs block ____channels. They ____ firing at the ____node and cause slowed conduction velocity through the ____ node. They have ___inotropic effect. They are used for treatment of ____________
    • Ca++ into cardiac muscle cells.
    • slow, SA, AV
    • negative
    • PSVTs and rate control for afib/aflutter.
  75. Class IV drugs are NOT used for_______.
    Examples of the 2 non-dihydropyridines are:
    • ventricular arrythmias. 
    • Verapamil and diltizem
  76. AE's for Class IV drugs are:
    • Bradycardia
    • Excessive AV block
    • Heart failure
    • Edema
    • Hypotension
    • Constipation, dizziness (Verapamil)
  77. Class IV Ca+ Ch blockers can be divided into __________ and _________.
    Dihydropyridines and Nondihydropyridines
  78. The dihydropyridines are selective for _____________. AE's associated with these drugs are____________.
    Names of drugs: Amlodipne, felodipine, nifedipine, nicardipine, nimodipine.
    • 1. Smooth muscle over cardiac muscle (skeletal muscle is unaffected since contraction is not dependent on extracellular Ca+.
    • 2. Reflex tachycardia, peripheral edema, flushing, HA, dizziness
  79. How do vasodilators work? 3 MOA
    • 1. NO formation
    • 2. K+ channel openers
    • 3. D1 stimulation
  80. _______ is a vasodilator which stimulates endogenous ____ to be produced which dilates arterioles only (no venous dilation). IT is rapidly metabolized by _________ and AE's include______________
    • hydralazine
    • NO
    • First-pass
    • SLE-like syndrome with higher doses
  81. ________ is a vasodilator which gives off NO itself and causes arterial AND venous dilation. ROA is __________. IT is used in __________. AE's include ____________.
    • Nitroprusside
    • IV only
    • Hypertensive crisis
    • Cyanide toxicity
  82. Fenoldopam is a vasodilator which is a _____ receptor agonist. IT decreases PVR and increases renal blood flow. AE's: SLE-like syndrome with high doses.
    D1.
  83. ________ is a K+ channel opener with AE of hypertrichosis when used topically.
    Minoxidil
  84. ACLS protocol (ABCD)
    • Circulation
    • Airway
    • Breathing
    • Defibrillation
  85. 2 pulseless shockable rhythms responsive to defibrillation
    • Rapid V-Tach
    • V-Fib
  86. 2 non-shockable states unresponsive to defibrillation
    • Asystole
    • Pulseless electrical activity (PEA)
  87. 5 Meds for tx of VT or VF
    • Epinephrine
    • Vasopressin
    • Amiodarone
    • Lidocaine
    • Magnesium
  88. What is epinephrine's MOA for VT/VF?
    Stimulates alpha, B1, B2 to increase cardiac output and BP. Benefits of Epi outweigh the risks in pulseless arrest.
  89. Vasopressin MOA?
    Direct vasoconstrictor, ADH. No inotropic effects.
  90. Acronym for tx of Stable Angina (ABCDEO)
    • A: ASA, anti-anginals
    • B: B-Blockers, BP
    • C: cholesterol, cigarettes
    • D: diet, DM
    • E: exercise, education
    • O: obesity

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epm49
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315494
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GU Pharm Exam 1 Module 7
Updated:
2016-02-09 21:33:48
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Anti hypertensives
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Module 7
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