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PathopharmA 2
CHAPTER 17,18,19 ANDRENERGIC AGONIST +ANTAGONIST
| Question | Answer |
|---|---|
| CHAPTER 17 WEEK 6, WE DID SOME QUESTION | NOREEPINEPHRINE DOESNT ACTIVATE BETA 2 RECEPTOR(BRONCHODILATION) |
| Adrenergic Agonists | Produce their effects by activating adrenergic receptors (mimic the effects of natural transmitters NE, epinephrine, and dopamine) Sympathomimetic-FIGHT OR FLIGHT Broad spectrum of applicationsCongestive heart failureAsthmaPreterm labor |
| Mechanisms of Adrenergic Receptor Activation | Direct receptor binding Promotion of norepinephrine (NE) release Inhibition of NE reuptake Inhibition of NE inactivation |
| Therapeutic Applications of Adrenergic Receptor Activation ALPHA 1 | Hemostasis•Arrests bleeding via vasoconstriction Nasal decongestion•Mucosal vasoconstriction Adjunct to local anesthesia •Delays absorption of local anestheticElevation BP•VasoconstrictionMydriasis•Dilation of the radial muscle of the iris |
| Adverse Effects of Adrenergic Receptor Activation | Vasoconstriction HypertensionNecrosis: Alpha1-blocking agent (eg, phentolamine)Bradycardia |
| Drugs capable of activating alpha1 receptors | EpinephrineNorepinephrinePhenylephrineDopamine |
| herapeutic Applications of Adrenergic Receptor Activation ALPHA 2 | Reduction of sympathetic outflow to the heart and the blood vessels Relief of severe pain |
| Therapeutic Applications of Adrenergic Receptor Activation BETA 1 | All of the clinically relevant responses to activation of beta1 receptors result from activating beta1 receptors in the heart GIVEN DUE TO RESPONSE Beta1 receptors can be activated by epinephrine, NE, isoproterenol, dopamine, dobutamine, and ephedrine |
| BETA 1 | increases HR and force of contractionIncreases cardiac output Improves tissue perfusion ShockProfound hypotension and greatly reduced tissue perfusionPrimary goal of treatment is to maintain blood flow to vital organs |
| BETA 1 | enhance impulse conduction through the AV node Atrioventricular (AV) heart block •Beta1 stimulants can help overcome AV block •Drugs are only a temporary form of treatment •Long-term management: Pacemaker |
| BETA1 initiate contraction in a heart that has stopped beating | Cardiac arrestDrugs are not the preferred treatment Initial management focuses on cardiopulmonary resuscitation, external pacing, or defibrillation as well as the identification and treatment of the underlying cause |
| ADR BETA1 | Dysrhythmias Angina pectoris: Because beta1 agonists increase cardiac oxygen demand by increasing the heart rate and the force of contraction, patients with compromised coronary circulation are at risk of an anginal attack |
| Clinical Consequences of Beta2 Activation BETA 2 | Applications of beta2 activation are limited to the following:LungsUterus Beta2 activating drugsEpinephrineIsoproterenolAlbuterol |
| Therapeutic Application of Beta2 Activation Activation of beta2 receptors in the uterusRelaxes uterine smooth muscle•Delay of preterm labor | Activate beta2 receptors in the lung to promote bronchodilationAsthma•Help relieve or prevent asthma attacks•Selective for beta2 receptors (such as albuterol) •Less selective agents (such as isoproterenol) |
| Adverse Effects of Beta In patients with normal pancreatic function, insulin release will maintain blood glucose at an appropriate level | HyperglycemiaActivation of beta2 receptors in the liver and the skeletal muscles Breakdown of glycogen into glucoseBeta2 agonists cause hyperglycemia only in patients with diabetes |
| Adverse Effects of Beta2 Activation | Tremor Tremor is the most common side effect of beta2agonistsTremor generally fades over time and can be minimized by initiating therapy at low doses |
| Clinical Consequences of Dopamine Receptor Activation | dilates the renal vasculature Used to treat shock: Dilation of the renal blood vessels reduces the risk of renal failureIncreases urinary output Enhances cardiac performance by activating beta1 receptors in the heart |
| Multiple Receptor Activation: Treatment of Anaphylactic Shock | Severe allergic responseHypotension, bronchoconstriction, and edema of the glottisTreatmentEpinephrine: Treatment of choice for anaphylactic shock |
| interactionsEpinephrine19 | Receptor specificityAlpha1Alpha2Beta1Beta2Chemical classificationCatecholamineMultiple drug interactions |
| Therapeutic uses | Delays absorption of local anesthetic Controls superficial bleeding Elevates blood pressure Overcomes AV block Restores cardiac function during arrest Causes bronchial dilation in patients with asthma Treatment of choice for anaphylactic shock |
| Pharmacokinetics | Absorption: Intramuscular (IM), subcutaneous (SQ), and intravenous (IV)Inactivation: Short half-life |
| Adverse effects | Hypertensive crisisDysrhythmiasAngina pectorisNecrosis after extravasationHyperglycemia |
| Norepinephrine | Receptor specificityAlpha1Alpha2Beta1Chemical classificationCatecholamine |
| Therapeutic uses | Hypotensive states Cardiac arrest Differs from epinephrine: Does not activate beta2receptorsDoes not promote hyperglycemia Necrosis with extravasation NO ORALLY |
| Drug interactions | MAO inhibitors (MAOIs), TCAs, general anesthetics, and adrenergic blocking agents |
| Isoproterenol | Receptor specificity: Beta1 and beta2Chemical classification: Catecholamine Therapeutic usesCardiovascular•AV heart block•Cardiac arrest •Increase cardiac output during shock FORMS=IV, IM, and intracardiac injections |
| Adverse effects | Fewer than those of NE and epinephrine (does not activate alpha-adrenergic receptors)Tachydysrhythmias and angina pectorisHyperglycemia in diabetes patients |
| Drug interactions | MAOIs, TCAs, and beta-adrenergic blockers |
| Dopamine | Low therapeutic dose: DopamineModerate therapeutic dose: Dopamine and beta1receptorsVery high dose: Alpha1 receptors, beta1 receptors, and dopamine |
| Therapeutic uses | Shock•Increases cardiac output•Increases renal perfusionHeart failure•Increases myocardial contractility |
| Adverse effects | Tachycardia, dysrhythmias, and anginal painNecrosis with extravasation |
| Drug interactions | MAOIs, TCAs, certain general anesthetics, and diuretics |
| PREPARATION | Dispensed in aqueous solutions Dosage: Must be dilutedAdministration: Administered by IV |
| After an intramuscular injection of penicillin, a patient develops severe difficulty breathing and a swollen tongue. Which medication should the nurse prepare to administer? | Epinephrine is the drug of choice for patients in anaphylactic shock. |
| A patient is receiving dopamine [Inotropin] for the treatment of shock. What would indicate to the nurse that the medication is effective? | Increased urine output Dopamine will dilaterenal blood vessels, improve renal perfusion, and increase urine output. |
| The nurse cares for a patient with asthma who uses an albuterol (Ventolin) metered-dose inhaler. The nurse is most concerned if the patient makes which of the following statements? | I can use the inhaler as often as needed.” activate beta1 receptors as well as beta2 receptors. not to NOT exceed the recommended dosage, =tachycardia by activating beta1 receptors in the heart. Tremor is a common adverse effect of this drug. |
| . | RECEPTOR- AGONIST- ANTIGONIST- ADR- S/S |
| CHAPTER 18 | |
| Adrenergic Antagonists | Cause direct blockade of adrenergic receptorsWith one exception, all produce reversible (competitive) blockade more selective Alpha-adrenergic blocking agents Beta-adrenergic blocking agents |
| Therapeutic Applications of Alpha Blockade | Essential hypertension causing vasodilation by blocking alpha1 receptors on arterioles and veins In response to venous dilation:•Return of blood to the heart decreases•Cardiac output decreases•Arterial pressure is reduced |
| Therapeutic Applications of Alpha Blockade ALPHA 1 receptors: Reduce the contraction of smooth muscle in the prostatic capsule and the bladder neck (trigone and sphincter) | Benign prostatic hyperplasia (BPH) Symptoms: Dysuria, increased frequency of daytime urination, nocturia, urinary hesitancy, urinary urgency, a sensation of incomplete voiding, and a reduction in the size and force of the urinary stream |
| Therapeutic Applications of Alpha Blockade | Raynaud’s disease Peripheral vascular disorderVasospasms in the toes and fingersSuppress symptoms by preventing alpha-mediated vasoconstriction Ineffective against other peripheral vascular disorders that involve inappropriate vasoconstriction |
| Adverse Effects of Alpha1 Blockade | Orthostatic hypo•Blockade of A1receptors on veins•Redcd muscle tone in the venous wall•Upon standing, blood pools in the veins•Return of blood to the heart is reduced•Cardiac output decreased: BP dropsReflex tachycardia•Reflex to increase HR via the ANS |
| Adverse Effects of Alpha1 Blockade Rduced BP promotes renal retention of NA and H20•combined W/ diuretic when used for HBP | Nasal cngstion•Dilates vessels of the nasal mucosaInhibition of ejaculation(NEEDS 4 ejaculation)•Impotence is reversible; resolves when drug is discontinued NA retention and inc. blood volume• |
| Adverse Effects of Alpha2 | Potentiation of reflex tachycardia |
| Alpha1-Adrenergic Antagonists PRAZOSIN | Selective competitive inhibitor of alpha1-adrenergic receptorsTreatment of hypertension (not approved for BPH but can benefit men with BPH) |
| Pharmacokinetics | Administered orallyPeak effects: Develop after 1 to 3 hoursHalf-life: 2-3 hours2-3 times/day dosing Extensive hepatic metabolismBiliary excretion FIRST DOSE EFFECT |
| Tamsulosin [Flomax] | Causes “selective” blockade of alpha1 receptors of the smooth muscle of the bladder neck (trigone and sphincter), the prostatic capsule, and the prostatic urethra •Blockade of vascular alpha1 receptors is weak•Approved only for BPH |
| Beta-Adrenergic Antagonists | Angina pectoris•a mainstay of antianginal therapy• By blocking beta1 receptors in the heart, these drugs decrease cardiac workload•Reduce oxygen demand by bringing it back into balance with oxygen supply•Prevention of ischemia and pain |
| Beta-Adrenergic Antagonists USE | Hypertension •Beta blockers were considered drugs of choice for hypertension Long-term use: Beta blockers reduce peripheral vascular resistance, which could account for much of their antihypertensive effect |
| Cardiac dysrhythmias• | Dysrhythmias =excssive electrical actvty in the sinus node +atria •Blockage of cardiac beta1 receptors = 1.Decrease sinus nodal rate discharge 2.Suppression of the cnductn of atrial impulses through the (AV) node =prevntng ventricles fromexcessive rate |
| Myocardial infarction (MI) | An MI is (necrosis) caused by the localized interruption of blood flow to the heart wall•Trt; with a B blocker can reduce pain, infarct size, mortality, and the risk of reinfarction• TTMT with a beta blocker must begin soon an MI has and contnue 4 years |
| Heart failure | Considered standard therapy for heart failure •Previously, heart failure was considered an absolute contraindication to the use of a beta blocker Carvedilol Bisoprolol Metoprolol |
| Hyperthyroidism | an increase in the sensitivity of the heart to catecholamines (eg, nor, epinephrine)•Normal levels of sympathetic activity to the heart can generate tachydysrhythmias and angina pectoris•Blockade of cardiac beta1 receptors suppresses these responses |
| Migraine prophylaxis | beta-adrenergic blocking agents can reduce the frequency and intensity of migraine attacks •Not able to abort a migraine headache once it has begun •Mechanism by which beta blockers prevent migraine is not known |
| Stage fright-PUBLIC SPEAKER | Prominent symptoms are tachycardia, tremors, and sweating brought on by generalized discharge of the sympathetic nervous system •Beta blockers help prevent stage fright by preventing beta1-mediated tachycardia |
| Pheochromocytoma | Pheochromocytomas secrete large amounts of catecholamines •Can cause excessive stimulation of the heart •Cardiac stimulation can be prevented by beta1 blockade |
| Glaucoma | Elevated intraocular pressure with subsequent injury to the optic nerve •Specific group of beta blockers are used for the treatment of glaucoma to lower intraocular pressure |
| Adverse effects of beta blockade | Therapeutic responses to beta blockers are due almost entirely to the blockade of beta1 receptors ADR IS DUE TO B1+B2 NONSELECTIVE B BLOCKER (DRUGS THAT BLOCK B1+B1) HAVE BROADER ADR THAN CARDIO SELECTIVE B1 BLOCKER DRUGS(BLOCK B1 RECEPTOR AT T. DOSE |
| Adverse effects of BETA1 blockade | The blockade of cardiac beta1 receptors can produce bradycardia (excessively slow heart rate) •The heart rate can be increased with the use of a beta-adrenergic agonist (eg, isoproterenol) and atropine, which is a muscarinic antagonist |
| Reduced cardiac output | reduce cardiac output by decreasing the heart rate and the force of myocardial contraction• GREAT caution in patients with heart failure or reduced cardiac reserve •Further decrease in cardiac output could result in insufficient tissue perfusion |
| Precipitation of heart failure | Suppression of cardiac function with a beta blocker can cause HEART FAILURE S/S:SOB, night coughs, swelling of the extremities) NOTIFY MD if these occur •Although beta blockers can precipitate heart failure, they are also used to treat heart failure |
| AV heart block | delay in the conduction of electrical impulses through the AV node blockade of cardiac beta1 receptors can suppress AV conduction, so the production of AV block is a ADR of beta-blocker therapy • B1B contraindicated 4 patients with preexisting AV block |
| Rebound cardiac excitation | The long-term use of beta blockers can sensitize the heart to catecholamines beta blocker withdrawn abruptly, anginal pain or ventricular dysrhythmias may develop TAPERING the dosage over a period of 1 to 2 weeks) TO MINIMIZED REBOUND CARDIAC EXCITATION |
| Bronchoconstriction BETA 2 BLOCKER | in the lung can cause constriction of the bronchi •resulting increase in airway resistance can be life threatening CONTRAINDICATED W/ ASTHMA PATIENTS These patients should be given an agent that is beta1selective (eg, metoprolol) |
| Hypoglycemia from inhibition of glycogenolysis | Epine, acting at B2 receptors in skeletal muscle and the liver, can stimulate glycogenolysis-(INHIBIT TIS PROCESS) PT W/ diabetes are especially dependent on B2-mediated glycogenolysis to overcome insulin-induced hypoglycemia B1 DRUGS 4 DIABTETIC PT |
| Adverse effects in neonates from beta1 and beta2 blockade | residual effects on the newborn infant (TE DURING PREGNANCY) LAST IN the circulation for several days after birth, so neonates may be at risk for bradycardia (from beta1 blockade), respiratory distress (from beta2 blockade), and hypoglycemia (from B2B) |
| Beta-Adrenergic Antagonists: Metoprolol | Pharmacologic effects Second-generation beta blocker Selective blockade of beta1 receptors in the heart Not likely to cause bronchoconstriction or hypoglycemia Preferred over the nonselective beta blockers for patients with asthma or diabetes |
| Pharmacokinetics | Very lipid soluble Well absorbed after oral administration Extensive metabolism on its first pass through the liver Elimination is by hepatic metabolism and renal excretionBeta-Adrenergic Antagonists: Metoprolol (Cont.) |
| Therapeutic uses | HypertensionAngina pectorisHeart failureMyocardial infarction |
| Adverse effects | Bradycardia Reduced cardiac output AV heart block Rebound cardiac excitation Minimal bronchoconstriction and interference with beta2glycogenesisBeta-Adrenergic Antagonists: Metoprolol (Cont.) |
| Precautions, warnings, and contraindications | Contraindicated IN PTS W/ sinus bradycardia and AV block greater than first degree Caution patients W/ heart failureSafer than propranolol for PTS W/ asthma, DIABETES or a HX of severe allergic reactionsWill mask common S/S OF hypoglycemia |
| patient is receiving a drug that blocks alpha1-adrenergic receptors. Which adverse effect, if experienced by the patient, is of most concern to the nurse? | Orthostatic hypotension is the most serious adverse response to alpha-adrenergic blockade. This hypotension can reduce blood flow to the brain, thereby causing dizziness, lightheadedness, and even syncope (fainting). |
| The nurse instructs a patient about doxazosin [Cardura]. Which statement by the patient to the nurse indicates an understanding of the instructions? | “The medication should be taken tonight before I go to bed.” Doxazosin can cause orthostatic hypotension, reflex tachycardia, and nasal congestion. As with prazosin and terazosin, the first dose can cause profound hypotension, GIVE AT HS |
| A patient with type 2 diabetes mellitus is diagnosed with stable angina. Which beta blocker, if prescribed by the physician, would the nurse question? | Nadolol [Corgard] Rationale: Nonselective beta blockers such as nadolol [Corgard] should be avoided when treating patients with diabetes mellitus. |
| The nurse prepares to administer metoprolol [Lopressor] to a patient with chronic stable angina. What is a priority assessment to make before the administration of this medication? | Heart rate nonselective agents CAUTION in patients with asthma, bronchospasm, diabetes, or a history of severe allergic reactions. Use all beta blockers with caution in patients with a history of depression and in those taking calcium channel blockers. |
| . | |
| CHAPTER 19 | |
| Indirect-Acting Antiadrenergic Agents | Prevent stimulation of peripheral adrenergic receptors Two groups Adrenergic neuron-blocking agents•Decrease norepinephrine release Centrally acting alpha2 agonists•Reduce impulses along the sympathetic nerves |
| Centrally Acting Alpha2 Agonists | Reduce the firing of sympathetic neurons Used primarily for hypertension Effects similar to those of the direct-acting adrenergic receptor blockers |
| Clonidine | Centrally acting alpha2 agonistHypertensionSevere painAttention-deficit/hyperactivity disorder |
| Mechanism of antihypertensive action | Selective activation of alpha2 receptors in the central nervous system (CNS)Reduces sympathetic outflow to the blood vessels and the heart |
| Pharmacologic effects | Bradycardia and a decrease in cardiac outputMinimal orthostatic hypotension |
| Pharmacokinetics | Lipid soluble Readily absorbed after oral administration |
| Therapeutic uses | Two approved applications •Hypertension •Severe pain Investigational•Managing opioid withdrawal•Facilitating smoking cessation•Tourette’s syndrome |
| Adverse effects | Drowsiness: 35% of patients Xerostomia(dry mouth): 40% of patientsRebound hypertension •Withdraw slowly over 2 to 4 days Use during pregnancy• Not recommended Abuse Other ADR •Constipation, impotence, gynecomastia, and adverse CNS effects |
| Adrenergic Neuron-Blocking Agents | Act presynaptically to reduce the release of norepinephrine from sympathetic neurons Very little effect on the release of epinephrine from the adrenal medullaReserpineAdrenergic Neuron-Blocking Agents |
| Reserpine | Mechanism of action Depletion of norepinephrine from postganglionic sympathetic neuronsClosely resembles alpha and beta blockadeCan cause depletion of transmitters (serotonin, catecholamines) |
| Pharmacologic effects | Peripheral effects •Slows heart rate and reduces cardiac output CNS effects•Sedation and state of indifference |
| Therapeutic uses | Principal indication: Hypertension (but not a preferred drug) |
| Adverse effects | Depression Bradycardia, orthostatic hypotension, and nasal congestionGastrointestinal involvement |
| A patient plans to stop taking prescribed clonidine [Catapres] to treat hypertension because of the side effect of dry mouth. Which action by the nurse is best? | Xerostomia (dry mouth) is common, occurring in about 40% of patients who are taking clonidine. PT advised that discomfort can be reduced by chewing gum, sucking hard candy, and taking frequent sips of fluids. |
| A patient is prescribed reserpine for hypertension. The nurse should monitor the patient for which adverse effect? DIARRHEA CAN OCCUR | Severe depression persist for months after the drug is withdrawn. Suicide has occurred. depletion of NOREPI from sympathetic neurons = bradycardia, orthostatic hypotension, and nasal congestn. can increase the secretion of gastric acid=ulcer formatn. |
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