Pharm Drugs - Even Lectures

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Pharm Drugs - Even Lectures
2013-05-01 11:45:38
Dental Pharmacology

UMN SOD Pharm Exam 4
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  1. ACE Inhibitors, AT1 receptor blockers, renin inhibitors
    • Lecture: Anti-HTN Drugs
    • Angiotensin System Blockers
    • Little or no increase in heart rate
    • Reduce maladaptive ventricular hypertrophy   
    • Side effects: cough, angioedema and rash 
    • Overall a very safe class of drugs
    • Contraindication: pregnancy
    • Prototype: Captopril (‘pril’ suffix signifies ACE inhibitor)
  2. Propanolol, metoprolol
    • Lecture: Anti-HTN
    • Beta-Blockers
    • Side effects: bronchoconstriction due to beta-2 receptor blockade (propanolol is a non-selective beta-antagonist)
    • Effects: decrease CO, reduce renin release, decrease TPR (after weeks), blunt reflexes caused by vasodilators (decrease baroreceptor induced reflex tachycardia)
  3. Amlodipine
    • Lecture: Anti-HTN drugs
    • Calcium Channel Entry Blockers (CCBs)
    • Bind receptors on Ca channels in cardiac and smooth muscle cells
    • Prevent Ca influx into smooth muscle --> decrease TPR
    • Prevent Ca influx into cardiac cells --> potential for decreased HR, slowed AV conduction and decreased inotropy
    • Mild side effects
    • Can cause reflex tachycardia in response to hypotension caused by vasodilation
    • May be combined with a beta-blocker
    • Act selectively on arterioles (not veins)
    • Postural hypotension is rare
    • Gingival hyperplasia side effect
  4. Thiazides, hydrochlorothiazide, chlorthalidone
    • Lecture: Anti-HTN drugs
    • Diuretics
    • First line drug
    • Natriuretic (discharge of Na through urine)
    • Acute effects: decrease plasma volume --> decrease CO
    • Chronic effect: decrease TPR
    • K "sparing" diuretics
  5. Nitric Oxide (NO)
    Lecture: Anti-HTN drugs

    • Endogenous Vasoactive Agents
    • Released from vessel intima (ECs)
    • Activates guanylyl cyclase
    • Drug target: Increase production of or supply NO
  6. Natriuretic peptides
    Lecture: Anti-HTN drugs

    Endogenous Vasoactive Agents
  7. Vasodilator prostaglandins
    • Lecture: Anti-HTN drugs
    • Endogenous Vasoactive Agents
    • Caution - administration of NSAIDs can potentially increase AP
  8. Kinins
    • Lecture: Anti-HTN drugs
    • Endogenous Vasoactive Agents
    • Contribute to ACE inhibitor effects
  9. Prazosin
    Lecture: Anti-HTN drugs

    • Alpha-1 Adrenergic Blockers
    • Causes both arterial and venous vasodilation
    • Side effects: Postural hypotension (drugs that dilate veins directly OR prevent release or action of NE) and reflex tachycardia
    • Usually taken with a diuretic
    • Beta-blockers should also be co-administered
  10. Minodoxidil
    Lecture: Anti-HTN drugs

    • Direct acting vasodilators
    • K channel agonist
    • Act directly on VSM
    • Little effect on veins so little orthostatic hypotension
    • Used for most refractory cases; only in combo with beta-blockers and usually with a diuretic
    • Side effects: reflex tachycardia and edema
  11. Hyralazine
    Lecture: Anti-HTN drugs

    • Direct acting vasodilators
    • Now used in combo with a nitrate
    • Act directly on VSM
    • Little effect on veins so little orthostatic hypotension
    • Used for most refractory cases; only in combo with beta-blockers and usually with a diuretic
    • Side effects: reflex tachycardia and edema
  12. Reserpine
    Lecture: Anti-HTN drugs

    • Peripherally Acting Sympathomimetics
    • Drugs that interfere with the storage and/or release of NE
    • Older drugs that have severe side effects and only rarely used now for HTN
    • Depletes stores of NE from neurons in both the CNS and PNS
    • Decreases in NE release from post-ganglionic SNS neurons reduces PR and dilates veins
    • Side effects: sedation, orthostatic hypotension, high incidence of depression
  13. Clonidine, a-methyl-DOPA
    Lecture: Anti-HTN drugs

    • Centrally Acting Alpha-2 Agonists
    • Advantage - dont cause postural hypotension
    • Decrease HR (lowering CO) and TPR --> decreased AP
    • Side effects: hypertensive rebound if there is an abrupt withdrawl of drug, dry mouth, sedation
    • Considered a second-line drug or for special cases (ie pregnant HTN pts)
    • Clonidine acts as a parent compound in CNS
    • a-methyl-DOPA converted to a-methyl NE
  14. Glyceryl Trinitrate (GTN)
    Lecture: Anti-anginal drugs

    • Organic nitrates
    • Overall effect: relaxation of most smooth muscle and decrease platelet aggregation
    • Mechanism: GTN --> increased NO in VSM
    • Directly acting vasodilators - nitrates increase NO synthesis within cells, nitroprusside releases NO
    • Nitrovasodilators increase VSM NO --> Activation of guanylate cyclase --> increase cGMP --> stimulation of a cGMP-dependent kinase --> decreased intracellular Ca, Ca desensitization, opening of K channels --> relaxation of VSM

    • Hemodynamics:
    • Decreased AP (due to decreased PR and CO)
    • LVEDP and thereby CO (due to venodilation)
    • Possibly increase HR and contractility
    • Total CBF usually not increased in pt with classical angina
    • Distribution of CBF: improved to ischemic areas

    Side effects: excessive decrease in AP with sildenafil use, orthostatic hypotension
  15. Anti-Anginal CCB
    • Do not dilate veins but useful for both classical and vasospastic angina
    • Dilate coronary vessels - therefore useful for vasospastic angina; also dilate collaterals
  16. Beta-adrenoceptor antagonists
    Lecture: Anti-anginal

    Reduce cardiac response to exercise, decrease sys BP, decrease HR, therefore decrease O2 demand

    • Useful effects in angina/role:
    • Prophylaxis
    • Improve survival post MI
    • Block reflex tachycardia
  17. Aspirin and clopidogrel
    Lecture: Anti-anginal drugs

    • Drugs for unstable angina
    • unstable angina may reflect a non-occlusive thrombus on a plaque; may be related to impending plaque rupture and MI
    • Clopidogrel (inhibits ADP mediated platelet aggregation), aspirin, CCB, GTN and anticoagulants used for unstable angina
    • Lowering of LDL-cholesterol is critical; endothelial function recovers and plaque is stabilized
  18. Ranolazine
    Lecture: anti-anginals

    • 1st new class of antianginal drug approved for decades
    • MOA is uncertain: change cardiac metabolism?
    • Decrease Ca overload
    • Decreases angina frequence and nitrate use
    • Increases exercise tolerance
    • Effective via oral route of administration
  19. Ivabradine
    Lecture: Anti-anginal

    • MOA is likely due to causing reduced HR
    • Selective inhibitor of inward Na and K current during phase 4 (ie pacemaker current)
    • Will decrease HR in excess of beta-ARX induced reduction
    • Helpful for patients that can't tolerate BARX