Chapter 13 Adrenergic Drugs Affecting

SNS responses prepare body to react to potential threat Adrenergic drugs : adrenalin like and mimic involuntary bodily functions Affect cardiac, renal , resp, GI, reproductive, and ophthalmic targets In SNS – NOREPINEPHRINE (NE) is released from postganglionic nerve terminals at target organ (EXCEPTION IS SWEAT GLANDS) NE belongs to CATECHOLAMINES class Natural catecholamine- NE, epinephrine, dopamine – the 3 main neurotransmitters. ** Synthetic catecholamines- Isoproterenol, dobutamine Non catecholamine- ephedrine, phenylephrine, terbutaline All catecholamines bind to ADRENERGIC RECEPTORS ADRENERGIC RECEPTORS : alpha and beta Alpha 1, alpha 2 Beta 1, beta 2, beta 3 Some drugs only activate 1 receptor subtype → selective/specificity Some affect 1+ Some may start w 1 only and later affect >> NE is synthesized through chemical steps that require phenylalanine and tyrosine At the end of the cycle NE is stored in vesicles of presynaptic neuron , waits for action potential Action potential → releases NE into synaptic cleft NE binds to alpha or beta receptors Reuptake of NE ends action MAO- monoamine oxidase destroys NE enzymatically COMT- catechol-o-methyltransferase destroys NE in the synaptic cleft ACTION OF NE is TERMINATED by MAO & COMT ** Adrenal gland – site most responsible for release of epinephrine Adrenal medulla is part of the neural tissue destine to become the sympathetic nervous system → tissue splits → adrenal medulla becomes its own functional division. Outgoing neuron from the ventral spinal cord terminates onto the core of the adrenal gland and makes synaptic contact ACH is the neuro transmitter at that point and stimulates CHROMAFFIN CELLS(neuroendocrine cells_ of adrenal medulla to release epi directly into the bloodstream→ epi travels to target organs = SYMPATHETIC EFFECTS/ FIGHT OR FLIGHT S/S Action of epi is finished through HEPATIC METABOLISM , rather than through reuptake SYMPATHOMIMETICS/ADRENERGIC DRUGS (mimic the SNS) Aka adrenergic drugs, adrenergic agonists, or sympathomimetics. Stimulate the SYMPATHETIC NS → FIGHT OR FLIGHT S/S TX of shock and hypotension Produce many same s/e as anticholinergics (> everything) Remember sympathomimetics can be either catecholamines or noncatecholamines Catecholamines- have same biological structure as NE → SHORT DURATION OF ACTION and must be given PARENTERALLY . CANNOT BE GIVEN PO BECAUSE MAO AND COMT enzymes are HIGHLY active in INTESTINES !!! they will be absorbed and have no effect . ONLY PARANTERAL ADMIN or INHALATION ADMIN !!!! ** Non catecholamines- can be taken PO and have LONGER DURATION OF ACTIONS b/c they aren’t destroyed by MAO or COMT Can act INDIRECTLY or DIRECTLY (just like parasympathomimetics) CATECHOLAMINES (MAIN 3) → epinephrine, norepienephrine, dopamine – ACT DIRECTLY , bind to and activate adrenergic receptors DIRECTLY Meds that work INDIRECTLY- cause release of NE from vesicles w/in the presynaptic terminal or inhibt reuptake/destruction of NE. Ephedrine- acts INDIRECTLY & DIRECTLY * Remember 5 diff receptors have different actions→ MEMORIZE THEM Alpha 1- vasodilates eyes , constricts vessels Alpha 2 – inhibits NE release Beta 1- >HR(tachy), contraction and renin;kidneys Beta 2 – bronchodilates , relaxes everything (Bladder, eye muscle, smooth muscle , uterus), increased BS Beta 3- relaxes muscle of bladder, LYPOLYSIS , thermogenesis YOU WILL KNOW EFFECTS OF MEDS BY KNOWING THESE ^^ PHENYLEPHRINE (neo-synephrine) Nasal decongestant;mydriatic drug;antihypotensive/ adrenergic drug (sympathomimetic) Is a SELECTIVE ALPHA ADRENERGIC AGONIST - LACKS beta adrenergic agonist activity Available intranasal, ophthalmic, IM, SQ, IV Intranasal admit (Spray/drops) → < nasal congestion by constricting blood vessels in nasal mucosa (Yes, constricted blood vessels in the nasal mucosa can improve congestion and breathing. When a person exercises, adrenaline is released, which results in vasoconstriction, or squeezing of the blood vessels. This vasoconstriction shrinks the nasal membranes, the air passages open up and the patient breathes more easily1. Vasoconstrictors are used in cases of allergic rhinitis, sinusitis, colds, flu, seasonal allergies to dilate blood vessels in the nose. Then, using a nasal spray or drop will cause the blood vessels to constrict, thereby helping to relieve congestion because the airways in the nose have more space) Topical admin→ to eye, dilates without causing cyclopegia (paralysis of eye muscle) Parenteral admit: reverses acute hypotension d/t spinal anesthesia or vascular shock. >BP Few cardiac s/e + longer duration= advantages for tx of acute hypotension Parenteral admin can cause tissue injury; extravasation Eye drop admin can damage soft contact lenses s/e: not common via IN , topical route IN- buring of mucosa, rebound congestion if used long time Eye drop/ointment- can cause narrow angle glaucoma secondary to mydriatic effect (Dilation effect) - > doses can cause reflex BRADYCARDIA d/t > BP d/t stimulation of alpha 1 receptors Parenteral- use caution w pts w advance CAD, HTN, hyperthyroidism (BC remember its going to raise everything) Anxiety, restlessness and tremor may occur d/t stimulation of CNS. Hyperthyroidism pts- may have SEVERE increase in BMR → causing > BP and ventricular tachy BLACK BOX WARNING: severe reactions or death with IV infusion d/t rapid infusion. Don’t use IV , ONLY IF NO OTHER ROUTE IS FEASIBLE Should NOT be used/given to pts w acute pancreatitis, heart disease, hepatitis, narrow angle glaucoma Interact MAO inhibitos → cause HTN crisis (MAO inhibitors prevent destruction of NE at synapse= longer lasting effects) >effects w tricylic antidepressants, ergot alkaloids, oxytoxin Incompatible w Fe preps Cause dysrhythmias when taken w digoxin (>too high HR) OVERDOSE- can cause tachy and HTN Tx w alpha blocker such as phentolamine (regitine) to (EKG monitoring) , urine output for IV admin. Teach pt to report palpitations, sob, chest pain, > nervous, tremors, HA, urine retention (old ppl at risk d/t previous cardiac disease) Teach pt to avoid caffeine to avoid excess nervousness , insomnia, or tremors Monitor IV site for extravasation – if present , STOP infusion, notify MD ALWAYS use INFUSION PUMP for IV admin for PRECISE DOSING Meds that target B2 receptos → INCREASE BS (monitor diabetics, make adjustments to diabetic meds PRN) Monitor oral and nasal mucosa Inspect for irritation, runny nose , bleeding. PROLONGED USE OF intranasal admit can cause REBOUND CONGESTION and BURNING of nasal mucosa >fluid intake to moisten airways → assist in expectoration of mucus Don’t use IN sprays for > 3-5 days without MD order OTC saline nasal can help w dry/irritated nasal Eye comfort- dark room, sunglasses, soft cloth d/t mydriasis – watch out for photosensitivity;; eyedrop solutions can stain some lenses Make sure pt is UPRIGHT position for inhalation forms to properly aerolize and prevent overdose from large droplets Epi pen teaching , call 911 and MD after use Don’t share nasal sprays ADRENERGIC BLOCKING DRUGS /ANTAGONISTS Inhibit the sympathetic NS Produce rest and digest s/s Widely used for HTN ADRENERGIC ANTAGONISTS DIRECTLY block adrenergic receptors AKA SYMPATHOLYTICS (LYSE SNS effects) Alpha adrenergic antagonists used for effects on vascular smooth muscle EX: doxasozin (Cardura) causes vasodilation- urine output by relaxing smooth muscle of bladder, prostate and urethra MOST COMMON A/E OF ALPHA BLOCKERS → ortho hypotension. ---→ Reflex tachy, nasal congestion and impotence and s/e that can also occur Pheochromocytoma – rare catecholamine secreting tumor on the adrenal gland that causes life threatening HTN – Phentolamine (Regitine) helps in dx Phentolamine also used for HTN crisis Phentolamine is ANTIDOTE for catecholamine OVERDOSE – injected ID for catecholamine extravasation PHENTOLAMINE IS A ADRENERGIC BLOCKING DRUG !! STOPS ADRENERGIC RESPONSES Beta adrenergic antagonists – block either B1 or B2, or both Affect cardio system < HR and contraction , slow electrical conduction through AV node Drugs that are selective for B1 → CARDIOSELECTIVE (Ex: atenolol) ; have < s/e Beta blockers primarily used for HTN tx Beta blockers can also ease pain of migraines and angina Can tx dysrhythmias Can tx HF Can Tx narrow angle glaucoma A/E – can exacerbate HF , increase r/o HYPOTENSION, brady, bronchoconstriction , SOB , hypo/hyperglycemia , diarrhea, n/v, muscle cramps, rash, blurred vision, fatigue, depression, erection issues. DO NOT DC BETA ADRENERGICS ABRUPTLY – can cause resurgence of s/s >BP, Heart palpitations, chest pain. Etc. PRAZOSIN ( MINIPRESS) Antihypertensive/adrenergic blocking drug SELECTIVE ALPHA 1 ADRENERGIC antagonist that competes w NE at its receptors on vascular smooth muscle in arterioles and veins. Major action → RAPID < in peripheral resistance that < BP . Little effect on CO or HR Causes < REFLEX TACHY Tolerance to HTN effects may occur Commonly used in combo w beta blockers and diuretics- to tx HTN SHORT HALF LIFE – taken 2-3x/day Start w LOW DOSE to avoid severe hypotension s/e: ortho hypotension→ can cause unconsciousness 30 mins after 1st dose (that’s why 1st dose should be LOW and take and BEDTIME ) dizziness, drowsiness, lightheadedness reflex tachy can occur d/t rapid < in BP nasal congestion or inhibition of ejaculation used w other HTN meds → extremely < BP Over dose may cause HYPOTENSION Admin fluid expanders (NS, VASOPRESSORS- dopamine/dobutamine) to > BP Pharmacotherapy w adrenergic blocking drugs Monitor for therapeutic effects: VS WNL, dysrhythmias and palpitations relieved, ease in urination Monitor wt , VS,urinary output, CO, Report a/e : brady, hypotension, dysrhythmias, reflex tachy, dizziness, HA, < urine Drug toxicity S/S: severe hypotension, seizures, palpitations, dysrhythmias Pulse should be taken for 1 whole min BP taken standing, sitting, laying- for orhto static bp identification Don’t take med if BP <90/60 Monitor for s/s of dysuria- hesitancy in urination, retention, feelings of full bladder, difficulty starting urinary stream First dose should be given at bedtime !! d.t possibility of unconsciousness after the first dose Avoid driving 12-24 hrs after 1st dose or if/when dose is increased Monitor BS , adrenergic blocking can interfere w diabetic management Assess moods/mental stats – adrenergic blockers can cause depression or dysphoria ( feeling unhappy, dissatisfied, frustrated ) Eye comfort d/t MIOSIS . careful driving Do no stop meds abruptly & take at same time each day