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PathopharmA 2


CHAPTER 12 WHAT IS NEUROPHARMACOLOGY? is the study of drugs that alter processes controlled by the nervous system-CNS AND PNS
NEUROPHARMACOLOGIC DRUGS AFFECT Skeletal muscle contraction Cardiac output Vascular tone Respiration Gastrointestinal function Uterine motility Glandular secretion Ideation, mood, and perception of pain
DRUG AFFECTING Transmitter synthesis (Making the transmitter) WILL Increase transmitter synthesisDecrease transmitter synthesisCause synthesis of transmitter molecules
DRUG AFFECTING Transmitter storage (Hanging out until release) WILL Cause receptor activation to decrease TAKE PLACE IN THE VESSICLES —tiny packets present in the axon terminal. Each nerve terminal contains a large number of transmitter-filled vesicles.
DRUG AFFECTING Receptor binding WILL Cause activation Block activation Enhance activation
DRUG AFECTING Termination of transmission WILL Block transmitter reuptakeInhibit transmitter degradationBoth Increase transmitter availability and cause receptor activation to increase
SELECTIVITY CAN BOCK TARGETTED RECEPTORS Most desirable quality a drug can haveAble to alter a disease process while leaving other physiologic processes largely unaffected
Three types of information needed: ALPHA 1- found on vascular smooth muscle. determine arteriolar resistance and venous capacitance, NOREPINEPHRINE CONTRACTION I.E URINARY SPHINCTER ALPHA 2-they modulate sympathetic outflow. I,E CLONIDINE- EPINEPHRINE Type (or types) of receptor(s) through which the drug acts (eg, alpha1, alpha2, beta1) BETA 1-Increase the heart rate and increase the heart's strength of contraction or contractility-EPINEPHRINE
A patient is scheduled for a procedure that requires axon conduction blockade. The nurse anticipates that which medication will be used? A local anesthetic
A patient receives a medication that results in the activation of the acetylcholine receptors of the heart. The nurse should assess the patient for which intended effect? Decreased heart rate ACETYLCHOLINE MAKE HEART BEAT
The nurse teaches a student nurse about the action of an antagonist medication. The nurse determines that the teaching is successful if the student makes which statement? “Antagonist medications prevent receptor activation.”
A patient is prescribed a drug that causes the selective stimulation of beta2 receptors. The nurse should assess the patient for what Improved breathing Beta2 stimulation will result in improved breathing as a result of bronchial dilation.
BETA 2 RECEPTOR BETA 2-SMOOTH MUSCLE RELAXATION IN THE LUNGS=BRONCHODILTION-NOREPINEPHRINE smooth muscle ( bronchial, vascular, gastrointestinal, and uterine), skeletal muscle, the myocardium, and the liver. Stimulation of these receptors = relaxation, MAY result in peripheral vasodilation with subsequent hypotension and reflex tachycardia.
Central nervous system Brain and spinal cord
Peripheral nervous system Somatic motor system•
PNS=Autonomic nervous system (ANS) Parasympathetic SympathetiC Three principal functions Regulate the heartRegulate the secretory glands (salivary, gastric, sweat, and bronchial)Regulate the smooth muscles (bronchi, blood vessels, urogenital system, and GI tract)HELP CONTROL VISION, DECREASE CARDIAC
Sympathetic Nervous System Functions SENSATION OF COLD W/ FEAR=BLOOD IS SHUNTED AWAY FROM SKIN Three main functions 1.Regulation of the cardiovascular system •Maintaining blood flow to the brain•Redistributing blood •Compensating for the loss of blood , primarily by causing vasoconstriction
Sympathomimetic Drugs Primarily used for effects on the following areas:Heart and blood vessels• Hypertension, heart failure, and angina pectorisLungs• Primarily asthma
Parasympathetic Nervous System Seven regulatory functionsSlowing the heart rateIncreasing the gastric secretionsEmptying the bladderEmptying the bowelFocusing the eye for near vision Constricting the pupilContracting the bronchial smooth muscle
Parasympathetic nervous system drugs Digestion of foodExcretion of wasteControl of visionConservation of energy
Neurotransmitters of the Peripheral Nervous System Acetylcholine-Employed at most junctions of the peripheral nervous system Norepinephrine-Released by most postganglionic neurons Epinephrine-Released by the adrenal medulla
Functions of Cholinergic Receptor Subtypes Activation of nicotinicN (neuronal) receptors•Release of epinephrine from adrenal medulla Activation of nicotinicM (muscle) receptors•Contraction of skeletal muscle
Activation of muscarinic receptors •Increased glandular secretion (pulmonary, gastric, intestinal, sweat glands)•Contraction of smooth muscle in bronchi and GI tract•Slowing of heart rate•Pupil constriction and lens focuses•Dilation of blood vessels•Voiding of urinary bladder
Functions of AdrenergicReceptor Subtypes Alpha1VasoconstrictionEjaculationContraction of bladder neck and prostate Alpha2Located in presynaptic junctionMinimal clinical significance
Functions of AdrenergicReceptor Subtypes Beta1Heart•Increases:Heart rateForce of contractionVelocity of conduction in atrioventricular (AV) node(how fast impulse travel to av node)Kidney•Renin release
Functions of AdrenergicReceptor Subtypes Beta2Bronchial dilationRelaxation of uterine muscleVasodilationGlycogenolysisDopamineDilates renal blood vessels
Receptor Specificity of the Adrenergic Neurotransmitters Epinephrine can activate all alpha and beta receptors but not dopamine receptorsNorepinephrine can activate alpha1, alpha2, and beta receptors but not beta2 or dopamine receptorsDopamine can activate alpha1, beta1, and dopamine receptors
Neurotransmitter Life Cycles Life cycle of acetylcholineLife cycle of norepinephrineLife cycle of epinephrine
The nurse administers a medication to a patient that stimulates the function of the parasympathetic nervous system. The nurse should assess the patient for which intended effect? Improved bladder emptying
The nurse administers a medication to a patient that stimulates the sympathetic nervous system. The nurse should assess the patient for which intended effect? Stimulation of the sympathetic nervous system results in increased heart rate and blood pressure, shunting of blood from the skin and viscera into the skeletal muscle, dilation of the bronchi, dilation of the pupils, and mobilization of energy stores,
A nurse administers a medication that activates dopamine receptors. The nurse should assess the patient for which intended effect? Improved renal perfusion Activation of dopamine receptors dilates blood vessels in the kidney,
Cholinergic Drugs Agents that influence the activity of cholinergic receptorsMost mimic or block the actions of acetylcholine Cholinesterase inhibitors  Indirectly prevent the breakdown of acetylcholine
Tips for Understanding the Cholinergic Drugs Look at the receptors that the drug affectsLook at the normal responses to the activation of those receptorsLook at whether the drug in question increases or decreases receptor activation
Muscarinic Agonists and Antagonists Muscarinic agonistsBethanecholMuscarinic antagonists (anticholinergic drugs)Atropine Anticholinergic drugs for overactive bladder (urge incontinence)Other muscarinic antagonistsToxicology of muscarinic antagonists
Muscarinic Agonists Bethanechol “Parasympathomimetic agent”Selective agonist at muscarinic cholinergic receptorsHeart: BradycardiaSmooth muscle:•Lung: Constriction of the bronchi•Gastrointestinal system: Increased tone and motility•
Muscarinic Agonists Bladder: Contraction of detrusor muscle and relaxation of the trigone and sphincter Exocrine glands: Increased sweating, salivation, bronchial secretions, and secretion of gastric acid Eye: Miosis and contraction of the ciliary muscle
Therapeutic uses Urinary retention, investigational gastrointestinal uses, glaucoma, dry mouth ADR-Hypotension•: Increased tone and motility• Exacerbation of asthma •Dysrhythmias in patients with hyperthyroidism
Toxicology of muscarinic agonists Source: Ingestion of certain mushrooms, direct-acting muscarinic agonists, and cholinesterase inhibitors
Toxicology of muscarinic agonists Symptoms: Profuse salivation, lacrimation (tearing), visual disturbances, bronchospasm, diarrhea, bradycardia, and hypotension with possible cardiovascular collapse
Toxicology of muscarinic agonists Treatment: Atropine and supportive therapy
Principal structures affected by muscarinic activation BradycardiaExocrine glands: Increased sweating, salivation, bronchial secretions, and secretion of gastric acid
Principal structures affected by muscarinic activation Smooth muscles •Contraction in lung (constriction) •Gastrointestinal tract (increased tone/motility) •Bladder (contraction of detrusor) •Vascular (relaxation, vasodilation, and hypotension)•Eye (pupillary constriction and ciliary contraction)
Muscarinic Antagonists(Anticholinergic Drugs) arasympatholytic drugs, antimuscarinic drugs, muscarinic blockers, and anticholinergic drugs Competitively block the actions of acetylcholine at muscarinic receptors Anticholinergic drugs: Produce the selective blockade of muscarinic receptors (not all cholinergic receptors) USE CAUTION IF TAKING OTHER ANTICHOLENERGIC DRUGS OR ANTIHISTAMINE
DRUG OF CHOICE Atropine Best-known muscarinic antagonistMechanism of action:•No direct effect of its own•Muscarinic receptor blockade
Pharmacologic effects (receptor blockade) Increases heart rate•Decreases secretions•Relaxes the bronchi, decreases the tone of the urinary bladder detrusor, and decreases the tone and motility of the GI tract•Mydriasis (pupil dilation)• Mild excitation to hallucinations and delirium
Therapeutic uses Preanesthetic medication•Disorders of the eye•Bradycardia•Intestinal hypertonicity and hypermotility•Muscarinic agonist poisoning•Peptic ulcer disease•Asthma•Biliary colic
ADVERSE EFFECTS •Xerostomia (dry mouth)•Blurred vision and photophobia•Elevation of intraocular pressure•Urinary retention•Constipation•Anhidrosis•Tachycardia•Asthma
Drug interactions Preparations, dosage, and administration Avoid combining atropine with other drugs capable of causing muscarinic blockade . General systemic therapy•Cholinesterase inhibitor poisoning•Ophthalmology
Anticholinergic Drugs for Overactive Bladder Overactive bladder (OAB): Specific anticholinergic drugs for OAB:Oxybutynin [Ditropan XL, Oxytrol, Gelnique]•Anticholinergic side effects common •Syrup•Extended-release tablets•Transdermal patch and ge
Other Muscarinic Antagonists-PATCH PUT BEHIND EARS Scopolaminemuch like those of atropine Therapeutic doses of atropine produce mild central nervous system excitation; therapeutic doses of scopolamine produce sedation suppresses emesis and motion sickness, whereas atropine does not
Ipratropium bromide Used to treat asthma, COPD, and rhinitis caused by allergies or the common coldInhalation or nasal spray routes: Not associated with typical antimuscarinic side effects (dry mouth, blurred vision, urinary hesitancy, constipation)
Toxicology of Muscarinic Agonists Source of muscarinic poisoning Direct-acting muscarinic agonistsCholinesterase inhibitors SymptomsResult from the excessive activation of muscarinic receptorsTreatmentMuscarinic blocking agent, such as atropine
MUSCARINIC ANTIGONIST-ANTIDOTES Physostigmine [Antilirium] S/S-Dry mouthBlurred visionPhotophobiaHyperthermiaCentral nervous system effectsHot, dry, and flushed skin
The nurse teaches a patient about bethanechol [Urecholine]. Which statement by the patient requires an intervention by the nurse? “The medication should be taken with meals.” Administration with food can cause nausea and vomiting, so the drug should be administered 1 hour before meals or 2 hours after.
A patient is prescribed bethanechol [Urecholine] for urinary retention. If the patient exhibits signs of an overdose, such as increased salivation and sweating, bradycardia, or hypotension, which medication should the nurse administer? Atropine [AtroPen] MUSCARINIC POISONING=overdose of medications that promote muscarinic activation (eg, bethanechol, cholinesterase inhibitors) or from the ingestion of certain mushrooms.
A patient who takes oxybutynin [Ditropan] for an overactive bladder takes an over-the-counter antihistamine for hay fever symptoms. What symptoms should the nurse watch for that would indicate toxicity? Dry mouth, increased temperature, and blurred vision
A patient is brought to the emergency department with hallucinations related to a tricyclic antidepressant overdose. The patient has hot, flushed skin and an oral temperature of 103.8F (39.9C). an antidote? Physostigmine [Antilirium]
Neuromuscular Blockers Placenta: Minimal effects on fetus Prevent acetylcholine from activating nicotinic receptorsCause muscle relaxation (paralysis) USED IN surgery, endotracheal intubation, mechanical ventilation, and other procedures No oral formsIV ONLY Cannot cross: BBB(ONLY PARALYSIS) NOT SEDATION
Steps in muscle contraction: AcetylcholineNicotinicCalcium
Competitive Neuromuscular Blockers Mechanism of action Competes with acetylcholine for nicotinicM receptorsBlocks receptor activation of acetylcholine Pharmacologic effects Muscle relaxation: Flaccid paralysisHypotensionCentral nervous system: No effect
Pharmacokinetics Rapid onset of paralysisPeak effects persist 20 to 45 minutes and then declineComplete recovery in 1 hour Adverse effectsRespiratory arrestCardiovascular effects
Vecuronium [Norcuron] Analog of pancuronium ANTIDOTE: Neostigmine [Prostigmin] for muscle relaxation during intubation, general anesthesia, and mechanical ventilation NO ganglionic or vagal block and NO histamineCardio effects are less,Excreted primarily in the bileParalysis may be prolonged in PT W/ liver dysfunction OR OBESE
Depolarizing Neuromuscular Blockers: Succinylcholine SUCCS-NO NEED TO BE COMPLETELY MOBILE, AFTER SEDATION Ultrashort-acting Muscle relaxation: State of flaccid paralysisNo effect on central nervous system Eliminated by plasma cholinesterasesPeaks at 1 minute, fades after 4 to 10 minutes Therapeutic uses Muscle relaxation during intubation
Often used off-label to decrease the strength of muscle contractions during electroconvulsive therapyBrief duration-NOT GOOD FOR PROLONGED PROCEDURE Poorly suited for use during prolonged procedures
ADVERSE REACTION Prolonged apnea in patients with low pseudocholinesterase activity•Unable to degrade succinylcholine rapidly•Succinylcholine causes paralysis to persist for hours DUE TO PATIENT INABILITY TO GET RID OF SUCCINYLCHOLINE-DUE TO ADR REACTION, SUCCLASTING HRS
Malignant hyperthermia CAN BE FATAL GENETIC PREDISPOSITION can be triggered by succinylcholine Muscle rigidity associated with a profound elevation of body temperature, sometimes to as high as 43C 104F Cardiac dysrhythmias, unstable blood pressure, electrolyte derangements, and metabolic acidosis
TREATMENT OF MALIGNANT HYPERTERMIA Immediate discontinuation of succinylcholine Cooling the patient with external icepacks and IV infusion of cold salineAdministering IV dantrolene, which stops heat generation by acting directly on skeletal muscle to reduce its metabolic activity
Postoperative muscle pain Between 10% and 70% of patients receiving succinylcholine experience postoperative muscle pain •Pain is most common in the neck, shoulders, and back
Postoperative muscle pain Pain develops 12 to 24 hours after surgery and may persist for several hours or even days •The cause may be the muscle contractions that occur during the initial phase of succinylcholine action
Hyperkalemia Succinylcholine promotes the release of potassium from tissues Death from cardiac arrest has resulted•Significant hyperkalemia is most likely to occur in PT with major burns, multiple trauma, denervation of skeletal muscle, or upper motor neuron injury
Drug interactions Cholinesterase inhibitors: Potentiate the effects of succinylcholineAntibiotics: Aminoglycosides, tetracyclines, and certain other nonpenicillin antibiotics intensify the effect of succinylcholine
Toxicology Overdose can produce prolonged apnea No specific antidote to succinylcholine poisoningManagement is purely supportivePreparations, dosage, and administration
Therapeutic Uses of Neuromuscular Blockers Hearing not affectedPatient is fully awake and completely paralyzed-Ensure patient comfort at all times to prevent convulsive movements during electroshock therapy Endotracheal intubation: Suppresses gag reflex Facilitation of mechanical ventilation Suppress spontaneous respiratory movements Reduce resistance to ventilation
The physician orders a intravenous infusion of cisatracurium [Nimbex] for a patient receiving mechanical ventilation. It is most important for the nurse to take which action before starting the infusion Administer lorazepam [Ativan] intravenously. Sedative (eg, lorazepam) must be administered to conscious patients before theadministration of a neuromuscular blocking agent.
A patient receives vecuronium [Norcuron] to facilitate mechanical ventilation. Which medication would the nurse administer to reverse muscle paralysis? Neostigmine [Prostigmin] A cholinesterase inhibitor (eg, neostigmine) will reverse the neuromuscular blockade of nondepolarizing agents such as vecuronium.
A patient receives succinylcholine [Anectine] before endotracheal intubation. What would the nurse expect? Muscle paralysis for 5 to 10 minutes
The nurse identifies which patient as being most at risk for developing complications if succinylcholine [Nimbex] is used? (gentamicin, which is an aminoglycoside) may intensify the effects of neuromuscular blocking agents. A patient with full-thickness burns to the chest and legs Succinylcholine promotes the release of potassium from tissues. Significant hyperkalemia is most likely in patients with major burns =death from cardiac arrest. caution w/myasthenia gravis
Created by: Seka_nurse
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