Pharmacology
Download
1 / 27

Pharmacology - PowerPoint PPT Presentation


  • 388 Views
  • Updated On :

Pharmacology. Goal of Pharmacology? Composed of: Pathology of conditions The physiologic & anatomic deviations from the normal that constitute the disease mechanisms of drugs effects of drugs on exercise and EKG’s individuality of patient and dose response

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about ' Pharmacology' - Roberta


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Pharmacology l.jpg
Pharmacology

  • Goal of Pharmacology?

  • Composed of:

    • Pathology of conditions

      • The physiologic & anatomic deviations from the normal that constitute the disease

    • mechanisms of drugs

    • effects of drugs on exercise and EKG’s

    • individuality of patient and dose response

  • Foundation of the drug therapy goal

    • rests on pharmacokinetics and dynamics


Pharmacokinetics l.jpg
Pharmacokinetics

  • Bioavailability

    • Enteral (taken by mouth)

    • Parenteral (bypass GI system)

  • Distribution of the drug by means of the circulatory system

    • General or restricted

  • Clearance: rate of elimination by all routes

  • Half-life: indicates length of time the effects will last (reduced by 50%)

  • All of the above determine the prescribed dosage


Pharmacodynamics l.jpg
Pharmacodynamics

  • An understanding of the critical role of drug receptors

  • Most common sites for cardiac drug receptor interactions are:

    • Autonomic Nervous System (ANS)

    • Kidneys

    • Vascular smooth muscle


Slide4 l.jpg

Autonomic Nervous System

Functional and Anatomical Divisions of ANS (most organs receive dual innervation)

I. Sympathetic autonomic nervous system

  • Tends to activate organ

    II. Parasympathetic autonomic nervous system

  • Tends to inactivate organ


Slide5 l.jpg

Thoracic region

Lumbar region


Slide6 l.jpg

Autonomic Nervous System

Vascular Smooth Muscle

Kidneys

Sympathetic NS

Parasympathetic NS

Adrenergic neurotransmitters

Cholinergic neurotransmitters

Alpha receptors

Beta receptors

Muscarinic

Nicotinic

β1

β2

Catecholamines

Decreased contractility and HR

Tachycardia & HTN

Contraction / Stimulation

Relaxation of VSM



Physiology of anti ischemic drugs l.jpg
Physiology of Anti-Ischemic Drugs

O2 supply is dependent on many factors:

  • coronary blood flow

  • O2 carrying capacity of blood

  • anatomy of coronary arteries (lumen size)

    O2 demand is affected by:

  • preload & afterload

  • wall thickness

  • contractility & heart rate

  • left ventricular volume and diameter


Anti ischemic drugs9 l.jpg
Anti-Ischemic Drugs

  • Pathophysiology

    • Inadequate coronary blood flow results in ischemia

    • O2 demand is increased under conditions that increase HR, BP,or both

    • Most common cause of decreased supply is coronary artery disease

      • atherosclerotic plaque causes reduced lumen size

  • Clinical Assessment (Myocardial VO2)

    • Rate-pressure product = HR x SBP

  • Pharmacologic Intervention

    • Reestablish a balance between myocardial O2supply and demand


Anti ischemic drugs11 l.jpg
Anti-Ischemic Drugs

Decreasing myocardial O2 demand

  • Beta Blockers

  • Nitrates

  • Calcium channel blockers

    Increasing myocardial O2 supply

  • Antiplatelet agents

  • Anticoagulants

  • Thrombolytic agents


Beta blockers l.jpg
BETA BLOCKERS

Treatment

  • Used to treat angina, hypertension, arrhythmias

  • Used in acute and post MI setting

    Pharmacodynamics

  • Exert their effects by competitively blocking the beta adrenergic receptors

  • ß1 blockers: Inhibit cardiac stimulation

    • “cardioselective” if they just work on β1 receptors

  • ß2 blockers: Inhibit relaxation of vascular system & bronchi


Beta blockers13 l.jpg
BETA BLOCKERS

Effect of Beta Blockers

  • Decrease heart rate at rest and with exercise (- chronotropic effect)

  • Decrease myocardial contractility at rest and with exercise (- inotropic effect)

  • Decrease blood pressure at rest and during exercise

  • End result => decreased VO2 demand

    • Diastolic filling time increases as HR decreases


Slide14 l.jpg

BETA BLOCKERS

  • Side effects

    • Excessive fatigue

    • Peripheral vasoconstriction

    • Bronchial spasm/constriction

    • Significant bradycardia

    • May worsen lipid profile

    • Rebound ectopy (with abrupt withdrawal)

  • Generic/Brand names of β-blockers


Nitrates l.jpg
NITRATES

Treatment

  • Used to treat hypertension & angina

    Pharmacodynamics

  • Directly relax vascular and coronary smooth muscle, thereby decreasing myocardial demand

    • Vasodilation on venous system (decrease venous return) => decreased volume/preload

    • Vasodilation of coronary arteries => decreased afterload


Nitrates16 l.jpg
NITRATES

  • Effect of Nitrates

    • Resting heart rate often increases

    • Decreased blood pressure at rest and during exercise

    • Increases coronary blood flow

    • No significant effects on exercise heart rate

    • patients are able to perform more exercise without developing symptoms


Nitrates17 l.jpg
NITRATES

Administration

  • May be given sublingual, pill, intravaneously, transdermally

    Side effects of Nitrates

  • Patients can develop tolerance to this nitrate (desensitization of receptors)

  • headaches, flashing sensations, nausea

  • Orthostatic hypotension (and dizziness after exercise)

    Generic/Brand names of Nitrates


Calcium channel blockers l.jpg
CALCIUM CHANNEL BLOCKERS

Treatment

  • Used to treat coronary vasospasm, angina, hypertension

    Pharmacodynamics

  • 2 sources of Ca++: intracellular (SR) and extracellular (plasma)


Calcium channel blockers20 l.jpg
CALCIUM CHANNEL BLOCKERS

Pharmacodynamics

  • 2 sources of Ca++: intracellular (SR) and extracellular (plasma)

  • Act by blocking various calcium-dependent process in vascular smooth muscle & myocardial cells

  • Action occurs through limiting Ca++ entry into cardiac and smooth cells


Calcium channel blockers21 l.jpg
CALCIUM CHANNEL BLOCKERS

Effect of Calcium Channel Blockers

  • Coronary arteries dilate (treat vasospasm)

  • Decreases blood pressure

  • arrhythmia control

  • Tend to decrease heart rate and blood pressure (thus, treatment of post MI angina)


Calcium channel blockers22 l.jpg
CALCIUM CHANNEL BLOCKERS

  • Side effects of Ca++ Channel Blockers

    • Headache

    • Flushing

    • Dizziness

    • Orthostatic hypotension

    • Syncope (fainting)

      Generic/Brand names of calcium channel blockers


Antiplatelet agents l.jpg
ANTIPLATELET AGENTS

Pharmacodynamics

  • Prevent thrombus formation by decreasing the platelets’ ability to adhere and aggregate at the site of the injury

    Effect of platelet aggregation antagonists

  • Acts as a ”blood thinner”

    Generic/Brand names of antiplatelet agents


Anticoagulants l.jpg
ANTICOAGULANTS

Pharmacodynamics

  • Inhibit the formation of thrombin and therefore negate the influence of thrombin on fibrinogen

    Effect of Anticoagulants

  • Prevent blood clot formation

    Generic/Brand names of anticoagulants


Thrombolytic agents l.jpg
THROMBOLYTIC AGENTS

Pharmacodynamics

  • Facilitates the conversion of plasminogen to plasmin

    Effect of Fibrinolytics

  • Purpose is to acutely destroy (lyse) or decrease the blood clot formation that occurs within the coronary artery at the time of the myocardial infarction.

  • 3-4 hours from the onset of ischemia (75% success) [6 hours?]


Thrombolytic agents26 l.jpg
THROMBOLYTIC AGENTS

Side Effects of Thrombolytic Agents

  • NOT tissue specific -->Blood clotting ability is markedly altered (avoid potential tissue trauma)

  • Cerebral vascular accidents

  • GI bleeding

    Generic/Brand names of Thrombolytics


General pharmacology l.jpg
General Pharmacology

  • Antianginals (used to reduce chest pain assoc. with angina)

    • Nitrates and Nitroglycerin

    • Beta Blockers

    • Calcium Channel Blockers

  • Antihypertensives (used to reduce BP)

    • Alpha blockers

    • ACE Inhibitors

    • Beta Blockers

    • Calcium channel blockers

    • diuretics

  • Antiarrhythmic (used to reduce/prevent devt. of cardiac arrhythmias)

    • Classified by their action on cardiac tissue


ad