⚡ Module 7 · Autonomic Nervous System

12 drugs · 9 concepts · tested on Exam 4

The classesConceptsDrugsPictures

💡 The big idea

This is the module that makes half of pharmacology make sense. Everything reduces to one 2x2: sympathetic (fight or flight) vs parasympathetic (rest and digest), crossed with agonist (turn it on) vs antagonist (turn it off). Once you know which receptor a drug hits — alpha-1, alpha-2, beta-1, beta-2, muscarinic, nicotinic — the therapeutic effects and the adverse effects are the same everywhere in the body.

🧠 How to think about this module

🏷️ The whole module in 9 classes

Learn these groups and the drug list stops being 12 separate names.

ClassWhat it doesExamplesWhat gets tested
Alpha-1 agonistsConstrict blood vessels: BP up, nasal mucosa dries, pupil dilates.phenylephrine, pseudoephedrine, midodrine, norepinephrine (partly)Reflex bradycardia and hypertension. IV vasoconstrictors cause tissue necrosis if they extravasate — check the site at least hourly; phentolamine is the antidote. Oral decongestants are contraindicated in uncontrolled hypertension.
Alpha-1 blockersRelax vascular smooth muscle and the bladder neck.prazosin, doxazosin, terazosin, tamsulosinFirst-dose phenomenon — severe orthostatic hypotension and syncope with the first dose. Give the first dose at bedtime and teach the client to sit on the edge of the bed before standing.
Central alpha-2 agonistsTell the brain to send LESS sympathetic outflow, so BP falls.clonidine, methyldopa, dexmedetomidineNever stop clonidine abruptly — severe rebound hypertension. Taper it. Sedation and dry mouth are expected; methyldopa is the classic safe antihypertensive in pregnancy.
Beta-1 agonists and catecholaminesSpeed and strengthen the heart; used in shock and cardiac arrest.dobutamine, dopamine, epinephrine, norepinephrine, isoproterenolContinuous cardiac monitoring and an arterial line; central access preferred. Titrate to MAP or blood pressure per protocol. Tachyarrhythmias and increased myocardial oxygen demand are the limiting effects.
Beta blockersSlow the heart, lower BP, reduce myocardial oxygen demand.metoprolol, atenolol, bisoprolol, esmolol (beta-1 selective); propranolol, nadolol, sotalol, timolol, carvedilol, labetalol (non-selective)Assess the apical pulse for a full minute before giving. If it is under 60, withhold the dose and call the provider unless other parameters were ordered. Non-selective agents cause bronchospasm in asthma and mask the tachycardia of hypoglycemia in diabetes.
Beta-2 agonistsRelax bronchial and uterine smooth muscle.albuterol, levalbuterol (short-acting); salmeterol, formoterol (long-acting); terbutalineTachycardia, tremor, nervousness, and hypokalemia. Needing a rescue inhaler more than 2 days a week means the control regimen has failed. Long-acting beta agonists are never rescue drugs.
Cholinergics (muscarinic agonists and cholinesterase inhibitors)Raise acetylcholine: wet everything, empty the bladder and bowel, strengthen weak muscle.bethanechol (urinary retention), pilocarpine (glaucoma); neostigmine, pyridostigmine, edrophonium, donepezilCholinergic crisis is the overdose picture — SLUDGE plus bradycardia, bronchospasm, and increasing muscle weakness. Atropine is the antidote. Support the airway first.
Anticholinergics (muscarinic antagonists)Dry everything, speed the heart, relax the bladder and bronchi.atropine, ipratropium, oxybutynin, scopolamine, benztropine, glycopyrrolate, diphenhydramineUrinary retention, constipation, blurred vision, dry mouth, heat intolerance, and confusion. Especially dangerous in older adults and contraindicated in narrow-angle glaucoma and significant BPH.
Neuromuscular blockersParalyze skeletal muscle at the nicotinic junction for intubation and surgery.succinylcholine (depolarizing); rocuronium, vecuronium, cisatracurium (non-depolarizing)These provide NO sedation and NO analgesia. A paralyzed client must also be sedated and treated for pain — they can hear and feel everything. Succinylcholine causes hyperkalemia and can trigger malignant hyperthermia.

⚖️ Depolarizing vs non-depolarizing neuromuscular blockers

Succinylcholine (depolarizing)Rocuronium / vecuronium (non-depolarizing)
Holds the receptor channel open — fasciculations first, then paralysisCompetitively blocks the receptor — no fasciculations
Onset roughly 30-60 seconds, duration about 5-10 minutes — the intubation drugSlower onset, duration 30 minutes or more — the maintenance drug
No reversal agent; you wait for it to wear offReversed by neostigmine with glycopyrrolate, or by sugammadex
Causes hyperkalemia; can trigger malignant hyperthermiaNo malignant hyperthermia risk
Avoid in burns, crush injury, and neuromuscular disease (lethal potassium release)Preferred when succinylcholine is contraindicated

🚨 Red flags DANGER

🧵 Exam traps ⭐ HIGH YIELD

🧠 Ways to remember it

🧠 The concepts 9

What are the adverse effects of beta-blockers?⭐ HIGH YIELD

Bradycardia and hypotension are the big ones. Also fatigue, dizziness, bronchospasm (non-selective agents in asthma or COPD), MASKED HYPOGLYCEMIA symptoms, erectile dysfunction, depression and vivid dreams, and worsening of acute decompensated heart failure. NEVER stop a beta blocker abruptly: rebound tachycardia, hypertension, angina, and MI.

Beta blockers SLOW the heart, MASK the low sugar, TIGHTEN the airway, and are never stopped cold.

What medications can be administered to increase blood pressure?⭐ HIGH YIELD

Vasopressors and inotropes: norepinephrine (first-line in septic shock), epinephrine, phenylephrine, dopamine, vasopressin, dobutamine (an inotrope), and oral midodrine for chronic orthostatic hypotension.

DrugMain actionBest use
Norepinephrine (Levophed)Strong alpha-1 vasoconstriction plus some beta-1First-line for septic and most distributive shock
EpinephrineAlpha-1, beta-1, and beta-2Anaphylaxis, cardiac arrest, refractory shock
PhenylephrinePure alpha-1 vasoconstrictionRaises BP without increasing heart rate; useful with tachyarrhythmia
DopamineDose-dependent: dopaminergic, then beta-1, then alpha-1Bradycardia with hypotension; causes more arrhythmias than norepinephrine
VasopressinV1 receptor, non-adrenergic vasoconstrictionAdd-on to norepinephrine in septic shock
DobutamineBeta-1 inotrope; can LOWER blood pressureCardiogenic shock and low cardiac output: increases contractility

Fluids first, then squeeze. Norepinephrine is first-line in septic shock.

What are the signs and symptoms of cholinergic overdose/crisis?🚨 DANGER

Cholinergic crisis is an excess of acetylcholine. Think SLUDGE plus the killer B's: Salivation, Lacrimation, Urination, Defecation and diarrhea, GI cramping, Emesis, plus Bradycardia, Bronchorrhea, and Bronchospasm. The secretions and respiratory muscle weakness are what kill.

SLUDGE plus the killer B's. Everything that can leak, leaks.

What are the pharmacological treatment options for cholinergic overdose/crisis?🚨 DANGER

ATROPINE is the antidote: an anticholinergic that dries secretions and reverses bradycardia. For organophosphate or nerve-agent poisoning, add PRALIDOXIME (2-PAM) to reactivate acetylcholinesterase, plus benzodiazepines for seizures and aggressive airway support.

Atropine DRIES the flood; pralidoxime UNSTICKS the enzyme.

What adverse effects are associated with anticholinergic medications?⭐ HIGH YIELD

Anticholinergics block acetylcholine at muscarinic receptors, producing dry mouth, blurred vision and photophobia from mydriasis, constipation, urinary retention, tachycardia, decreased sweating with hyperthermia, and confusion or delirium, especially in older adults.

Blind as a bat, dry as a bone, red as a beet, hot as a hare, mad as a hatter, and full as a flask.

What causes malignant hyperthermia?🚨 DANGER

Malignant hyperthermia is a genetic (autosomal dominant, usually an RYR1 ryanodine receptor mutation) hypermetabolic reaction triggered by VOLATILE INHALED ANESTHETICS (halothane, sevoflurane, desflurane, isoflurane) and the depolarizing paralytic SUCCINYLCHOLINE. Uncontrolled calcium release from the sarcoplasmic reticulum causes sustained muscle contraction.

Dantrolene DAMPENS the calcium. Fever is the LAST sign; the CO2 rises first.

Compare depolarizing and non-depolarizing neuromuscular blockers.🚨 DANGER

Depolarizing blockers (succinylcholine) act as acetylcholine AGONISTS: they depolarize the motor end plate, cause fasciculations, then sustained paralysis, and there is NO reversal agent. Non-depolarizing blockers (the -curium and -uronium drugs) are competitive ACh ANTAGONISTS: no fasciculations, longer acting, and reversible with neostigmine or sugammadex.

Depolarizing (succinylcholine)Non-depolarizing (rocuronium, vecuronium, cisatracurium)
Agonist that persistently depolarizes the end plateCompetitive antagonist that blocks ACh from binding
Muscle fasciculations first, then paralysisNo fasciculations, smooth onset of paralysis
Ultra-short, about 5 to 10 minutes; broken down by plasma pseudocholinesteraseIntermediate to long acting; renal and hepatic elimination
NO reversal agent, you must wait it outReversed by neostigmine with glycopyrrolate, or sugammadex for rocuronium and vecuronium
Used for rapid sequence intubationUsed for maintenance of surgical paralysis and in ventilated patients
Risks: malignant hyperthermia, HYPERKALEMIA, bradycardia, raised ICP and IOP, postop myalgiasRisks: prolonged paralysis, histamine release with older agents, residual weakness

SUX = short, sudden, no antidote. The '-uroniums' you can reverse.

What are the pharmacological treatment options for myasthenia gravis?⭐ HIGH YIELD

First-line is a cholinesterase inhibitor, PYRIDOSTIGMINE (Mestinon), which increases available acetylcholine at the neuromuscular junction. Add immunosuppression (corticosteroids, azathioprine, mycophenolate); for crisis use PLASMAPHERESIS or IVIG; thymectomy is used in selected patients.

Pyridostigmine 30 to 60 minutes before meals: strength for the fork.

Edrophonium⭐ HIGH YIELD

Edrophonium (Tensilon) is an ultra-SHORT-acting cholinesterase inhibitor used diagnostically, in the 'Tensilon test,' to distinguish myasthenic crisis from cholinergic crisis. Strength IMPROVES = myasthenic crisis (too little ACh). Weakness WORSENS with SLUDGE symptoms = cholinergic crisis (too much ACh).

Edrophonium is the QUESTION, not the treatment: better means myasthenic, worse means cholinergic. Atropine at the bedside.

💉 The drugs 12

💉 Albuterol

Bronchodilator, Adrenergic β2-agonist, sympathomimetic, bronchodilator

What it is for

Prevention of exercise-induced asthma, acute bronchospasm, bronchitis, emphysema, bronchiectasis, or other reversible airway obstruction Unlabeled: Hyperkalemia in dialysis patients, COPD, emphysema

How it works

Causes bronchodilation by action on β2 (pulmonary) receptors by increasing levels of cAMP

Watch for
Teaching
🔗 Full card in the drug guide

💉 ClonidineBLACK BOX

Antihypertensive, Central alpha-adrenergic agonist

What it is for

Mild to moderate hypertension, used alone or in combination; severe pain in cancer patients (epidural), attention-deficit/hyperactivity disorder (ADHD)

How it works

Inhibits sympathetic vasomotor center in CNS, which reduces impulses in sympathetic nervous system; B/P, pulse rate, cardiac output are decreased …

Watch for
Teaching

Antidote / reversal: 1

🔗 Full card in the drug guide

💉 EpinephrineHIGH ALERT

Bronchodilator nonselective adrenergic agonist, vasopressor, Catecholamine

What it is for

Acute asthmatic attacks, hemostasis, bronchospasm, anaphylaxis, allergic reactions, cardiac arrest, adjunct in anesthesia, shock

How it works

β1- and β2-agonist causing increased levels of cAMP, thereby producing bronchodilation, cardiac, and CNS stimulation; high doses cause vasoconstriction via alpha-receptors; low doses can cause vasodilation via β2-vascular receptors

Watch for
Teaching
🔗 Full card in the drug guide

💉 MetoprololHIGH ALERTBLACK BOX

Antihypertensive, antianginal, β1-Blocker

What it is for

Mild to moderate hypertension, acute MI to reduce cardiovascular mortality, angina pectoris, NYHA class II, III heart failure, cardiomyopathy

How it works

Lowers B/P by β-blocking effects; reduces elevated renin plasma levels; blocks β2-adrenergic receptors in bronchial, vascular smooth muscle only at high doses; negative chronotropic effect

Watch for
Teaching

Antidote / reversal: 1

🔗 Full card in the drug guide

💉 NorepinephrineHIGH ALERT

Vasopressor, α/ β-agonist

What it is for

Acute hypotension, shock

How it works

Causes increased contractility and heart rate by acting on β-receptors in heart; also acts on α-receptors, thereby causing vasoconstriction in blood vessels; B/P is elevated, coronary blood flow improves, and cardiac output increases

Watch for
Teaching
🔗 Full card in the drug guide

💉 Phenylephrine/pseudoephedrineHIGH ALERT

Vasopressor, nasal decongestant, mydriatic, Alpha-1 adrenergic agonist

What it is for

Clinically important hypotension from vasodilation, especially under anesthesia (IV); nasal congestion (spray); pupil dilation for eye exams (ophthalmic); hemorrhoids (topical). The oral form is sold for congestion but FDA has proposed removing it as ineffective.

How it works

An alpha-1 agonist with minimal to no beta activity. It squeezes blood vessels; it does not directly drive the heart. Pressure rises because the vessels tighten, and the vagus answers that rise by SLOWING the heart.

Watch for
Teaching

Antidote / reversal: 1

🔗 Full card in the drug guide

💉 Prazosin

Antihypertensive, α1-Adrenergic blocker, peripheral

What it is for

Hypertension, benign prostatic hypertrophy to decrease urine outflow obstruction

How it works

Blocks α-mediated vasoconstriction of adrenergic receptors, thereby inducing peripheral vasodilation

Watch for
Teaching
🔗 Full card in the drug guide

💉 TerbutalineBLACK BOX

Selective β2-agonist; bronchodilator, Catecholamine

What it is for

Bronchospasm Unlabeled: Premature labor

How it works

Relaxes bronchial smooth muscle by direct action on β2-adrenergic receptors through the accumulation of cAMP at β-adrenergic receptor sites; bronchodilation, diuresis, CNS, cardiac stimulation occur; relaxes uterine smooth muscle

Watch for
Teaching
🔗 Full card in the drug guide

💉 AtropineHIGH ALERT

Antidysrhythmic, anticholinergic parasympatholytic, antimuscarinic, Belladonna alkaloid

What it is for

Bradycardia <40-50 bpm, bradydysrhythmia, reversal of anticholinesterase agents, insecticide poisoning, blocking cardiac vagal reflexes, decreasing secretions before surgery, antispasmodic with GU, biliary surgery, bronchodilator …

How it works

Blocks acetylcholine at parasympathetic neuroeffector sites; increases cardiac output, heart rate by blocking vagal stimulation in heart; dries secretions by blocking vagus

Watch for
Teaching

Antidote / reversal: 1

🔗 Full card in the drug guide

💉 Bethanechol

Urinary tract stimulant, cholinergic, Synthetic choline ester

What it is for

Urinary retention (postoperative, postpartum), neurogenic atony of bladder with retention Unlabeled: Ileus, GERD, anticholinergic syndrome

How it works

Stimulates muscarinic ACH receptors directly; mimics effects of parasympathetic nervous system stimulation; stimulates gastric motility, micturition; increases lower esophageal sphincter pressure

Watch for
Teaching
🔗 Full card in the drug guide

💉 Oxybutynin

Anticholinergic, urinary antispasmodic, Synthetic tertiary amine

What it is for

Antispasmodic for neurogenic bladder, overactive bladder in females (OTC)

How it works

Relaxes smooth muscles in urinary tract by inhibiting acetylcholine at postganglionic sites

Watch for
Teaching
🔗 Full card in the drug guide

💉 Succinylcholine (How does the duration of action compare to other neuromuscular blockers?)HIGH ALERTBLACK BOX

Neuromuscular blocker (depolarizing, ultra short)

What it is for

Facilitation of endotracheal intubation, skeletal muscle relaxation during orthopedic manipulations

How it works

Inhibits transmission of nerve impulses by binding with cholinergic receptor sites, thus antagonizing action of acetylcholine; causes release of histamine

Watch for
Teaching
🔗 Full card in the drug guide
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Where this came from. The drug cards come from your own drug guide, fact-checked against FDA labeling. The explanations were written from your course textbook, Pharmacology (WTCS, 2e). If anything here contradicts your instructor, believe your instructor — they write the exam.
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