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PathopharmA 2
CHAPTER 12,13,14,16 NEUROPHARMACOLOGY
Question | Answer |
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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 |
WHAT IS NEURON? | |
AXONAL CONDUCTION | NONSPECIFIC ACTION POTENTIAL DOWN THE AXON RELEASE OF |
SYNAPTIC CONDUCTION | HIGHLY SELECTIVE AFFECT RELEASE OF NEUROTRANSMITTER NEUROTRANSMTTERS-CARRIED INFO THROUGH GAP-BIND TO RECEPTOR-POSTSYNAPTIC CELL(COULD BE MUSCLE CELLS OR GLAND THE ACTION DEPENDS ON THE POSTSNAPTIC CELL (IF RECEPTOR NOT PRESENT, THERE IS NO BINDING) |
DRUG AFFECTING Transmitter synthesis (Making the transmitter) WILL | Increase transmitter synthesisDecrease transmitter synthesisCause 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 Transmitter release WILL | Promote or inhibit release RELEASE IS TRIGGERED BY ARRIVAL OF AN ACTION POTENTIAL AT THE AXON TERMINAL, WHICH INITIATEED THE PROCESS AND VESSICLES UNDERGO FUSION WITH THETRMINAL MEMBRANE, CAUSING RELEASE OF TRANSMITTERS |
DRUG AFFECTING Receptor binding WILL | Cause activation Block activation Enhance activation |
DRUG AFECTING Termination of transmission WILL | Block transmitter reuptakeInhibit transmitter degradationBoth Increase transmitter availability and cause receptor activation to increase |
SELECTIVITY | CAN BOCK TARGETTED RECEPTORS Most desirable quality a drug can haveAble 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. |
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CHAPTER 13 | |
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 heartRegulate 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 pectorisLungs• Primarily asthma |
Parasympathetic Nervous System | Seven regulatory functionsSlowing the heart rateIncreasing the gastric secretionsEmptying the bladderEmptying the bowelFocusing the eye for near vision Constricting the pupilContracting the bronchial smooth muscle |
Parasympathetic nervous system drugs | Digestion of foodExcretion of wasteControl of visionConservation 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 | Alpha1VasoconstrictionEjaculationContraction of bladder neck and prostate Alpha2Located in presynaptic junctionMinimal clinical significance |
Functions of AdrenergicReceptor Subtypes | Beta1Heart•Increases:Heart rateForce of contractionVelocity of conduction in atrioventricular (AV) node(how fast impulse travel to av node)Kidney•Renin release |
Functions of AdrenergicReceptor Subtypes | Beta2Bronchial dilationRelaxation of uterine muscleVasodilationGlycogenolysisDopamineDilates renal blood vessels |
Receptor Specificity of the Adrenergic Neurotransmitters | Epinephrine can activate all alpha and beta receptors but not dopamine receptorsNorepinephrine can activate alpha1, alpha2, and beta receptors but not beta2 or dopamine receptorsDopamine can activate alpha1, beta1, and dopamine receptors |
Neurotransmitter Life Cycles | Life cycle of acetylcholineLife cycle of norepinephrineLife 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, |
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CHAPTER 14 | MUSCARINIC-ALL ORGANS REGULATED BY THE PARASYMPATHETIC NERVOUS SYSTEM NOREPINEPHRINE=MUSCARINIC AGONIST MUSCARINIC ANTIGONIST-EPINEPHRINE |
Cholinergic Drugs | Agents that influence the activity of cholinergic receptorsMost 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 affectsLook at the normal responses to the activation of those receptorsLook at whether the drug in question increases or decreases receptor activation |
Muscarinic Agonists and Antagonists | Muscarinic agonistsBethanecholMuscarinic antagonists (anticholinergic drugs)Atropine Anticholinergic drugs for overactive bladder (urge incontinence)Other muscarinic antagonistsToxicology of muscarinic antagonists |
Muscarinic Agonists | Bethanechol “Parasympathomimetic agent”Selective agonist at muscarinic cholinergic receptorsHeart: BradycardiaSmooth 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 | BradycardiaExocrine 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 antagonistMechanism 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 | Scopolaminemuch 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 coldInhalation 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 agonistsCholinesterase inhibitors SymptomsResult from the excessive activation of muscarinic receptorsTreatmentMuscarinic blocking agent, such as atropine |
MUSCARINIC ANTIGONIST-ANTIDOTES | Physostigmine [Antilirium] S/S-Dry mouthBlurred visionPhotophobiaHyperthermiaCentral nervous system effectsHot, 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 103.8F (39.9C). an antidote? | Physostigmine [Antilirium] |
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CHAPTER 16 | |
Neuromuscular Blockers Placenta: Minimal effects on fetus | Prevent acetylcholine from activating nicotinic receptorsCause muscle relaxation (paralysis) USED IN surgery, endotracheal intubation, mechanical ventilation, and other procedures No oral formsIV ONLY Cannot cross: BBB(ONLY PARALYSIS) NOT SEDATION |
Steps in muscle contraction: | AcetylcholineNicotinicCalcium |
Competitive Neuromuscular Blockers | Mechanism of action Competes with acetylcholine for nicotinicM receptorsBlocks receptor activation of acetylcholine Pharmacologic effects Muscle relaxation: Flaccid paralysisHypotensionCentral nervous system: No effect |
Pharmacokinetics | Rapid onset of paralysisPeak effects persist 20 to 45 minutes and then declineComplete recovery in 1 hour Adverse effectsRespiratory arrestCardiovascular 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 histamineCardio effects are less,Excreted primarily in the bileParalysis 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 paralysisNo effect on central nervous system Eliminated by plasma cholinesterasesPeaks 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 therapyBrief 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 43C 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 salineAdministering 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 succinylcholineAntibiotics: Aminoglycosides, tetracyclines, and certain other nonpenicillin antibiotics intensify the effect of succinylcholine |
Toxicology | Overdose can produce prolonged apnea No specific antidote to succinylcholine poisoningManagement is purely supportivePreparations, dosage, and administration |
Therapeutic Uses of Neuromuscular Blockers Hearing not affectedPatient 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 |