PNS function & Cholinergic and Anti-Cholinergic Drugs

Peripheral Muscarinic Effect on Lungs

-Bronchial muscle contraction -Stimulates mucus gland secretion

Cholinesterase Regenerator

-Pralidoxime

8. Which receptors below are considered adrenergic receptors? (Select all that apply.) -Alpha1 - Beta2 -Dopamine - Muscarinic1 - Beta1 - Alpha2

Adrenergic receptors can be divided into four major subtypes: alpha1, alpha2, beta1, and beta2 receptors. •Another type of adrenergic receptor, the dopamine receptor, does not respond to epinephrine or norepinephrine. Rather, it responds only to dopamine, a neurotransmitter found primarily in the central nervous system.

Muscarinic Receptor (M4)

Gi located in lungs

Muscarinic Receptors (M5)

Gq located in CNS

What are the six categories of cholinegic drugs?

Six categories: -Muscarine agonists -Muscarine antagonists -Ganglionic blocking agents -Ganglionic simulating agents -Neuromuscular blocking agents -Cholinesterase inhibitors

3. Which symptom is the most indicative of muscarinic poisoning? -Constipation -Heart rate of 140 beats per minute -Blood pressure of 180/110 mm Hg - Blurred vision

Symptoms: -Manifestations of muscarinic poisening result from excessive activation of muscarinic receptors. Prominent symptoms are profuse salivation, lacrimation (tearing), visual distrurbances, bronchospasm, diarrhea, bradycardia, hypotension. Severe poisoning can produce cardiovascular collapse!! Why are the wrong options...well, wrong?

Muscarinic Receptor (M1)

binding causes activation of Gq/PLC/IP3 --> depolarization of neurons located in nerves, nerve terminals, and some effector cells (exocrine glands, stomach)

Muscarinic Receptor (M2)

binding results in inhibition of adenylyl cyclase--> activation of K+ channels--> presynaptic inhibition--> slows heart rate and contractility of atria located in heart, nerves, smooth muscle, lung (vasculature, airway, gut)

1. A nurse is preparing to give bethanechol [Urecholine]. What is an expected outcome of this drug? -Nondistended bladder -Increased heart rate and blood pressure -Improved pulse oximetry reading -Relief of cardiac rhythm problems

-1st: What class is bethanechol? -->Muscarinic agonist-MOA? --->Selectively mimic the effects of acetylcholine at muscarinic receptors. -2nd: Common use of bethanechol? -->urinary retention by activating muscarinic receptors of the urinary tract.

Contraindications of Muscarinic Agonists

-Asthma -Coronary Insufficiency -GI ulcers -GI/Urinary Incontinence -GI/Urinary Obstruction

What drug represents the classification of muscarine agonists, and what are their MOA?

-Because nearly all muscarinic receptors are associated with the parasympathetic nervous system, responses to muscarinic agonists closely resemble those produced by stimulation of parasympathetic nerves. Accordingly, muscarinic agonists are also known as parasympathomimetic agents. • -The muscarinic agonists and antagonists produce their effects through direct interaction with muscarinic receptors. (mimic the effects of ACh) • The muscarinic agonists bind to muscarinic receptors, thereby causing receptor activation.

Peripheral Muscarinic Effects on Eye

-Decreased IOP -Sphincter contraction of pupil (miosis) -Ciliary muscle contraction for near vision

What would be a good pharmacokinetic fact to know about Bethanechol if given orally (usual route)?

-Effects beginin 30-60 minutes and persist for about 1 hr. Because Bethanechol is a quaternary ammonium compound the drug crosses membranes poorly. As a result, only a small fraction of each dose is absorbed.

Peripheral Muscarinic Effect on GI Tract

-Increased gastric motility -sphincter relaxation -stimulates secretion

Acetylcholinesterase

-enzyme produced by the effector cells -tethered to the outside surface of the cell -tetrameric-one active site per monomer -metabolizes acetycholine

Atropine and Scopolamine

-prototype drugs for anti-muscarinics -both natural plant products

Peripheral Muscarinic Effect on Glands

-stimulates secretions sweat (note: sympathetic) salivary lacrimal nasopharyngeal

9. Which receptors mediate responses to the neurotransmitter acetylcholine? (Select all that apply.) -Alpha1 -Beta2 -Dopamine -Nicotinic -Muscarinic

1. Acetylcholine is the transmitter released by (1) all preganglionic neurons of the parasympathetic NS, (2) all preganglionic neurons of the sympathetic nervous system, (3) all postganglionic neurons of the parasympathetic nervous system, (4) all motor neurons to skeletal muscles, and (5) most postganglionic neurons of the sympathetic nervous system that go to sweat glands. 2. Cholinergic receptors are receptors that mediate responses to acetylcholine. 3. Cholinergic receptors can be divided into three major subtypes: nicotinicN, nicotinicM, and muscarinic receptors.

Neuromuscular blockers (indirect-acting cholynolytics)

1. Dantrolene 2. Botulinum Toxin A

Organophosphates (Irreversible Anti-cholinesterase) (Indirect-acting Cholinomimetics)

1. Echothiophate 2. Parathion 3. Malathion 4. Sarin 5. VX series -typically very lipophilic--> absorbed by all routes of administration -WELL ABSORBED FROM SKIN -READILY ENTER CNS -COVALENTLY BINDS AchE & BuChE -direct covalent attachement to esteratic @ the serine hydroxyl--> once attached, bond hydrolyzes very slowly -If side group leaves after binding--> enzyme cannot be recovered except by synthesis of the new enzyme (process termed AGING) AGING RESULTS IN OVERDOSE -RECOVERY REQUIRES ENZYME SYNTHESIS (body must regenerate AchE) -Most have very little therapeutic value (only echothiophate-charged) MOSTLY TOXIC SUBSTANCES -Insecticides (parathion, malathion, diazinon) -nerve gasses (tabun, VX, sarin, soman)

Reversible Anti-cholinesterases (Indirect Cholinomimetics)

1. Edrophonium 2. Neostigmine 3. Pyridostigmine 4. Physostigmine 5. Donepezil Competitive Inhibitors -Edrophonium (short acting) -Demecarium (long acting) Carbamate Esters -covalent attachment to esteratic site (bond hydrolyzes min-hours) -Uncharged (CNS penetration) -Physostigmine -Charged -Neostigmine -Pyridostigmine

Drugs Augmenting Non-Depolarizing Neuromuscular blockers

1. Gaseous Anesthetics -decrease excitability of skeletal muscles 2. Aminoglycoside Antibiotics -decrease Ach release -decrease excitability of skeletal muscles 3. Tetracycline Antibiotics -decrease Ach release -decrease excitability of skeletal muscle 4. Calcium Channel Blockers -decrease Ach release -decrease calcium influx in muscle

Contraindications for Muscarinic Receptor Antagonists

1. Glaucoma (esp. acute) -relaxation of ciliary muscle -decreased outflow 2. Prostatic Hypertrophy -further impairs urination -decreased bladder contraction 3. GI tract atony -will further impair GI motility 4. Cardiac Arrhythmia -decreased vagal tone -greater SNS tone 5. Hyperthyroidism -may exacerbate elevated rate

Non-medical Organophosphates

1. Nerve Gases -Sarin- lethal by inhalation -VX- lethal by inhalation & skin contact 2. Pesticides -Malathion -Parathion

Medical Uses of Anti-muscarinics

1. Parkinsons Disease -decrease tremor/hypersalavation -Benztropine (in conjunction w/ L-dopa) 2. Prophylactic Motion Sickness (Scopolamine) 3. Mydriasis and Cycloplegia (Tropicamide-shortest acting) 4. Peptic Disease (P) and/or GI hypermotility (GI) -may be included in antidiarrheal preparations 5. Urinary Incontinence, overactive bladder (tolterodine-m2 selectivity- oral) 6. Respiratory Diseases -COPD -Asthma -inhaled to limit side effects 7. Poisoning with acetylcholinesterase inhibitors (atropine)

Treatment of Succinylcholine-induced Malignant Hyperthermia

1. Reduce temperature quickly 2. Give DANTROLENE (blocks release of activator calcium from T-tubular network)

Treatment: Organophosphate Poisoning

1. Remove toxin from patient -clothes -wash skin 2. Give PRALIDOXIME (2-PAM) as soon as possible after intoxication [12 HOUR WINDOW]

3. A patient with a history of hypertension experiences dizziness when standing. Which question is priority for the nurse to ask the patient?

Adrenergic blocking agents can be prescribed for hypertension and have side effects such as dizziness and syncope. Since the patient was recently diagnosed with hypertension, the patient has most likely been prescribed new medication, such as an adrenergic blocking agent. Assuming the patient has been drinking alcohol is not the most important and relevant question at this point. If the patient has been prescribed an adrenergic blocking medication, the sauna or excessive heat could exacerbate the symptoms of vasodilation. The nurse should first determine exactly what medications the patient is taking. Test-Taking Tip: Avoid taking a wild guess at an answer. However, should you feel insecure about a question, eliminate the alternatives that you believe are definitely incorrect, and reread the information given to make sure you understand the intent of the question. This approach increases your chances of randomly selecting the correct answer or getting a clearer understanding of what is being asked. Although there is no penalty for guessing, the subsequent question will be based, to an extent, on the response you give to the question at hand; that is, if you answer a question incorrectly, the computer will adapt the next question accordingly based on your knowledge and skill performance on the examination up to that point.

Muscarinic antagonists (anticholinergic drugs)

Atropine Competitively blocks muscarinic receptors.

10. Which statement is most appropriate for the nurse to include in the discharge teaching plan for a 30-year-old woman beginning a new prescription of clonidine [Catapres]? 1 "You will need to have your blood drawn regularly to check for anemia." 2 "This medication often is used to manage hypertension during pregnancy." 3 "Take this medication first thing in the morning to reduce nighttime wakefulness." 4 "If you stop taking this drug abruptly, your blood pressure might go up very high."

Rebound hypertension is a potential adverse effect of clonidine. Patients should be warned against abrupt withdrawal. Clonidine is not associated with anemia. It can cause drowsiness and usually is taken at night. Clonidine is not recommended for pregnant patients.

1. What is the primary effect of neuromuscular (NM) blockers?

The primary effect of neuromuscular (NM) blockers is relaxation of skeletal muscle, causing a state known as flaccid paralysis. Some neuromuscular blockers can lower blood pressure. Neuromuscular blockers do not diminish perception of pain or loss of consciousness—even when administered in doses that produce complete paralysis.

Edrophonium Test (AchE)

used for: A. Diagnosis of MG -will improve grip strength in patient w/ MG B. Optimization Dosage of anti-AchE -Overmedicated--> Cholinergic Crisis (inhibition of synaptic transmission @ NMJ) -Under-medicated-->Myasthenic Crisis--> patient becomes weak Test:: -ADMINISTER & CHECK GRIP STRENGTH =If improves--> increase medication =gets worse-> suggests over-medication

Cholinergic drug adverse effects acronym

~SLUDGEM~ -Salivation and sweating -Lacrimation -Urination -Defacation -GI cramps -Emesis (vomiting) -Miosis (pupil constriction) & Muscle spasm

Muscarine Antagonists (aka anticholinergic) -what is this classifications general MOA, and common drug prototype?

• Atropine, the prototype of the muscarinic antagonists, produces its effects through competitive blockade at muscarinic receptors. It (1) increases the heart rate; (2) reduces secretion from sweat, salivary, and bronchial glands and decreases secretion from acid-secreting cells of the stomach; (3) causes relaxation of the bronchi, decreased tone of the urinary bladder detrusor, and decreased tone and motility of the gastrointestinal tract; (4) acts in the eye to cause mydriasis and cycloplegia; and (5) acts in the central nervous system to produce excitation (at low doses) and delirium and hallucinations (at toxic doses). •

Atropine-therapeutic affects?

• Therapeutic applications of atropine include use as preanesthetic medication, aid in ophthalmic examinations, reversal of bradycardia, treatment of intestinal hypertonicity and hypermotility, and management of muscarinic agonist poisoning.

Acetylcholine

(Acetate Ester) -naturally ocurring neurotransmitter -primary neurotransmitter for all autonomic preganglionic neurons, PNS postganglionic neurons, and somatic nervous system -Limited Therapeutic Use -poor oral absorption -short duration of action -widespread effects because high affinity for ALL cholinergic receptors --rapidly hydrolyzed by acetycholinesterase and pseudocholinesterase --agonist at all nicotinic and muscarinic receptors (muscarinic responses predominate at low doses)

Cholinomimetics

(direct acting choline esters) Acetates (hydrolyzed by AchE) -Ach -Methacholine (slower metabolism) Carbamates (not metabolized by AchE) -Carbachol -Bethanechol --All compounds ar charged Alkaloids (natural plant products) (more selective for muscarinic receptors) -Muscarine -Pilocarpine(has peripheral and central effect) -Muscarine -Cevimeline (tx: dry mouth) ==activate all muscarinic subtypes

5. A nurse gives a medication that inhibits acetylcholinesterase. How would this drug affect autonomic activity? -Parasympathetic activity would increase. -Parasympathetic signals would be depressed. - Sympathetic activity would increase. -Respiratory centers would be depressed.

*Key word: autonomic. What does autonomic activity include? -Autonomic NS is divided into Parasympathetic division, and sympathetic division. --what do they do? Rational: *Upon dissociating from its receptors, ACh is destroyed almost instantaneously by acetylcholinesterase. *Acetylcholinesterase is an enzyme that metabolizes acetylcholine. When acetylcholine is not broken down, it continues to send its message. Acetylcholine is associated mostly with the parasympathetic nervous system; therefore, this system would be stimulated by acetylcholine-inhibiting drugs.

Contraindications for muscarinic agonist

--DO NOT USE IF OBSTRUCTION IS PRESENT--- MAY RESULT IN PERFORATION -DO NOT USE IF ULCERS PRESENT -AKA: make sure the retention is caused by the signals being messed up not by an actual internal obstruction:ie ---enlarged prostate ---kidney stone etc. Adverse effects: see ch. 13 for specifics (there's alot) ~~Think about where it is acting: Use your knowledge base of pathophysiology or normal physiology~~ -Cardioscular System: can cause hypotension (why?) -Gastrointestinal System: -->excessive salivation, increased secretion of gastric acid-->ulcers, abdominal cramps, and diarrhea-->involuntary defacation. Assess for hx of intestinal obstruction, surgery of bowel, gastric ulcers. -Urinary tract: -->increases pressure in urinary tract . Assess for hx of urinary tract obstruction (stones, enlarged prostate, cancer) -Exacerbation of Asthma: can cause bronchodilation. -Dysrythmias in Hyperthyroid patients: see text (p. 117) *Thinking about cardiovascular effects what kind of patients would you NOT give this to? --IF it slows heart rate....etc look up patho. The specifics for these adverse effects should be listed in any pharmacology book.

2. A nurse prepares to administer a new prescription for bethanechol [Urecholine]. Which information in the patient's history should prompt the nurse to consult with the prescriber before giving the drug? -Constipation -Hypertension -Psoriasis -Asthma

-1st: MOA because this tells you what other systems have similar receptors that a muscarinic agonist such as bethanechol would/could also effect/ adversely effect: - ~~Think about where it is acting: Use your knowledge base of pathophysiology or normal physiology~~ -Cardioscular System: can cause hypotension (why?) -Gastrointestinal System: -->excessive salivation, increased secretion of gastric acid-->ulcers, abdominal cramps, and diarrhea-->involuntary defacation. Assess for hx of intestinal obstruction, surgery of bowel, gastric ulcers. -Urinary tract: -->increases pressure in urinary tract . Assess for hx of urinary tract obstruction (stones, enlarged prostate, cancer) -Exacerbation of Asthma: can cause bronchodilation. -Dysrythmias in Hyperthyroid patients: see text (p. 117)

cholinesterase inhibitors

-Influence cholinergic receptors indirectly by preventing the breakdown of ACh. -Represented by: *Neostigmine *Physostigmine

Organophosphates

-Irreversible cholinesterase inhibitors -highly lipid soluble -readily enter the CNS AGING: -covalently bind AChE & BuChE -Recovery requires enzyme synthesis -Aging Prevention--> give 2-PAM (given to soldiers @ risk for nerve gas attack) -only useful organophosphate is Echothiophate for Glaucoma (if pilocarpine is insufficient)

Atropine- Adverse effects?

-Most adverse effects of atropine and other anticholinergic drugs are the direct result of muscarinic receptor blockade; they include: -Xerostomia (dry mouth): -Blurred vision and photophobia -Elevation of intraocular pressure -Urinary retention -Constipation -Anhidrosis (suppression of sweating) -Tachycardia -Asthma. • Dry mouth can impede swallowing and can promote tooth decay, gum problems, and oral infections. Patients experiencing dry mouth should be informed that dryness can be alleviated by sipping fluids, chewing sugar-free gum, treating the mouth with a saliva substitute, and using an alcohol-free mouthwash.

Functions of the Parasympathetic Nervous System (Remember in 4th grade terms-break it down to your patient)

-Movement and things we don't have to think about. Slowing of heart rate -Increased gastric secretion -Emptying of the bowel -Focusing the eye for near vision -Constricting the pupil -Contracting bronchial smooth muscle Certain poisons act on PNS: -insectisides -nerve gases -certain mushrooms and plants

Indirect-Acting Parasympathomimetics (cGMP phosphodiesterase Inhibitor)

-Sildenafil

Muscarinic Receptors

-activated by acetylcholine -located on effector cells: A. smooth muscle B. heart C. secretory glands -globular transmembrane proteins linked to G- proteins within the cell 5 subtypes (1-5) M1, M3, M5 (odd)- coupled to Gq/PLC M2, M4 (even) coupled through Gi

Myasthenia Gravis

-autoimmune diseases characterized by destruction of nicotinic acetylcholine receptors at the NMJ -results in poor transmission of information -skeletal muscle weakness/paralysis -rapid fatigue Tx: Anticholinesterases--> prevent breakdown of Ach in order to activate receptors Diagnosis 1. Test for anti-Ach Receptor Antibodies 2. EDROPHONIUM TEST: -will improve grip strength in patient with MG

Neuromuscular blockers (non-depolarizing agents)

-competitive antagonists of the nicotinic cholinergic receptors at the neuromuscular junction (Nm) -act to induce a flaccid paralysis without stimulating the muscle to contract -tubocurarine is the classical agent in this group (no longer used in US.) 1. Tubocurarine (classic side effects) 2. Pancuronium 3. Mivacurium 4. Rocuronium Adverse Effects: 1. Histamine Release -direct action of induction on mast cells -HYPOTENSION, reflex tachycardia -Bronchospasm, Bronchosecretion -GREATEST W/ TUBOCURARINE 2. Ganglionic Blockade -block in ganglia, adrenals -HYPOTENSION -GREATEST WITH TUBCURARINE 3. Respiratory Paralysis -TREAT W/ ARTIFICIAL RESP./O2 -REVERSE w/ EDROPHONIUM or NEOSTIGMINE Drug Interactions: -Augmented by gaseous anesthetics, aminoglycosides, tetracyclines, calcium channel blockers -Antagonized by Ach-E inhibitors and depolarizing NMJ blockers Diseases that alter drug's blocking effects 1. Myasthenia Gravis (inc.) 2. Liver/Kidney Disease/Aging (inc.) 3. Motor Nerve Damage (dec.) 4. Severe Burns (dec.)

Peripheral Muscarinic Effect on Urinary Bladder

-detrusor (body of bladder) contraction -Trigone & sphincter relaxatoin

Neuromuscular Drugs

-drugs that affect neuromuscular junction -somatic nervous system -no ganglia -neurons go straight into effecter striated skeletal muscle -site of Ach release--> binds nicotinic receptors (Nm)

Uses of Anticholinesterases

-drugs therapeutic for: 1. Glaucoma 2. Myasthenia Gravis 3. GI and Urinary Indications 4. Reversal of non-depolarizing neuromuscular blockade 5. Alzheimer's disease 6. Muscarinic Antagonist Overdose -compete by increasing Ach -also used as: 7. Insecticides 8. Nerve gas

Neuromuscular Junction

-found in somatic nervous system N -upon motor nerve stimulation, Ach is released via exocytosis -Ach diffuses across the synaptic cleft and binds to a nicotinic cholinergic receptors -High density of Nm receptors (surface) -Ach reaches receptor before AchE (deep in clefts) -Receptor consists of 5 or 6 transmembrane subunits ordered in a barrel arrangement (alpha, beta, gamma, delta, etc.) -Ach binds to each alpha subunit and induces a conformational change to open a central non-selective cation pore through the protein complex -depolarization of the muscle fiber occurs--> muscle contracts

Ganglionic Neurotransmission

-ganglion is an integration point for fine autonomic control of effector cells -stimulation o f nicotinic receptors is the PRIMARY site for information transfer -modulation--> WIDE RANGE OF EFFECTS -Other nerves innervate the ganglia and play a modulatory role -either increase/decrease the sensitivity of the ganglion to nicotinic receptor activatoin -primarily by depolarizing/ hyperopolarizing the cell -Nicotinic receptors become desensitized after continuous exposure to agonists. -Muscarinic and peptidergic receptors are present on postganglionic neurons -Activation leads to a slow depolarization of the cell Muscarinic receptor activation of interneurons results in the release of dopamine and activation of receptors on the postganglionic neuron Activation leads to hyperpolarizing the neuron

Acetylcholinesterase inhibitors (anticholinesterases)

-prevent the breakdown of Ach--> results in increased levels of Ach--> over-activation of receptors -Low doses--> mostly muscarinic -high doses--> muscarinic and nicotinic -prolong the life of acetylcholine -produce muscarinic effects -greatest effects in organs with continuous nerve stimulation (eye, GI, bladder) -may also elicit nicotinic effects and nicotinic blockade at high doses (cause the receptors to shut down with continuous stimulation)

Butyrylcholinesterase

-produced in the liver -secreted into plasma -can also produced by effector cells -has variable number of subunits -only known function is in DRUG METABOLISM: -Cocaine -succinylcholine -mivacurium

Muscarinic Receptor (M3)

-receptor binding results in activation of Gq/PLC/IP3 -smooth muscle contraction -induction of glandular secretion -nitric oxide release --> +guanylyl cyclase--> increased cGMP-->relaxation/vasodilation -located in smooth muscle, glands, vascular endothelium (widely distributed)

Cholinergic Agonists (Direct acting cholinomimetics)

1. Acetylcholine 2. Muscarine 3. Pilocarpine 4. Methacholine ~5. Bethanecol~ 6. Nicotine 7. Varenicline

Drugs that Antagonize Non-Depolarizing Neuromuscular Blockers

1. Anticholinesterases -reverse post-op NMJ block -pretreat with muscarinic antagonist 2. Depolarizing NMJ Blockers -Nm receptor agonists -only during phase I block

Effects of Pilocarpine on Eye in Glaucoma Treatment

1. Opens trabecular meshwork -contracts ciliary muscle (M3) -increases aqueous humor outflow -Prolonged decrease of IOP 2. Spasm of Accommodation -contracts ciliary muscle (M3) -lens rounds for near vision -transient effect (approx. 2 hours) 3. Miosis -contracts pupillary sphincter (M3) -transient increase in IOP -recovers in house Often used in conjunction with Ach-E inhibitor

Treatment: Carbamate Poisoning (Cholinesterase Inhibitor Poisoning)

1. Remove toxin from patient -clothes -wash skin (highly absorbed) 2. give ATROPINE (antagonist) to reverse cholinergic overstimulation; repeat if needed

Treatment of Respiratory Paralysis Caused by Neuromuscular blockers

1. Treat with artificial respiration/O2 2. Reverse withe IV edrophonium/neostigmine (AchE inhibitors--> competes w/ competitive inhibitor)

Nicotinic Receptor Antagonists (Direct-acting cholinolytics) (Ganglionic Blockers)

1. Trimethaphan 2. Mecamylamine Medical uses: -limited uses due to large number of side effects: 1. Blockes ALL autonomic ganglia 2. No longer used to treat chronic hypertension 3. Some use for hypertensive crisis A. Induce controlled hypotension for surgery of the head and neck/dissecting aortic aneurysm B. Treatment of autonomic hyperreflexia that can occur in some spinal injuries

Nicotinic (Nm) Receptor Antagonists (Direct-Acting Cholinolytics) (Neuromuscular Blockers)

1. Tubocurarine 2. Pancuronium 3. Mivacurium 4. Rocuronium 5. Succinylcholine 1-4 are non-depolarizing (Nm antagonist) (note cur- is compared with curare) 5-depolarizing (Nm agonist) Use: USED TO CAUSE PARALYSIS OF SKELETAL MUSCLE 1. used as adjunct to anesthesia -reduce stage of anesthesia that must be attained during surgery -lower doses of gen. anesthesia improve safety (reduce CV and respiratory. depression) 2.Abdominal/Orthopedic Surgery 3. Aid to Tracheal Intubation 4. Artificial Respiration -paralyze respiratory muscles 5. Control of Seizures (epilepsy, electroconvulsive therapy) Chemistry: -all are quaternary amines -IV only -no CNS effects -Diffusion to NMJ= Onset -concentration sets diffusion -most potent--> slow onset -long-acting often most potent -Elimination Sets Duration -Renal--> long duration (>80 min) -Hepatic --> medium duration (40 min) -Enzymatic--> short duration (20 min or less) Adverse Effects: -Histamine release--> hypotension -Ganglionic blockade--> hypotension -Respiratory Paralysis (tx w/ O2, & IV endrophonium/neostigmine)

Adverse Reactions of Succinylcholine

1. may induce MALIGNANT HYPERTHERMIA (genetic susceptibility)--> rapid rise in body temperature due to muscle contraction -Treatment: 1. Reduce temperature quickly 2. Give DANTROLENE (blocks release of activator calcium from T-tubular network) 2. Activation of ganglionic receptors -inc. BP & bradychardia -increased ocular, CSF, GI pressure -use with caution in patients with Glaucoma Brain Tumor After meals (increased intragastric pressure--> vomiting & aspiration) 3. Hyperkalemia (K+ released from muscle esp with burns/motor neuron damage--cardiac arrest) 4. Muscle Soreness (due muscle contractions) 5. Overdose can lead to respiratory failure -if use, have equipment ready to facilitate respiration.

Functions of the Sympathetic Nervous System

3 Main: *1. Regulating the cardiovascular system: -->Maintenance of blood flow to the brain -->Redistribution of blood flow during exercise -->Compensation for loss of blood, primarily by causing vasoconstriction. *2. REgulating body temperature: -->by regulating blood flow to the skin, sympathetic nerves can increase or decreased heat loss. -->Sympathetic nerves to sweat glands promote secretion of sweat, thereby helping the body cool. -->by inducing piloerection (erection of hair), sympathetic nerves can promote heat conservation. *3. Implementing the acute stress response (commonly called a "fight or flight" reaction).

8. The nurse is evaluating the teaching done with a patient who has a new prescription for transdermal clonidine [Catapres-TTS]. Which statement by the patient indicates understanding of the nurse's teaching? 1 "The patch will not cause any skin reaction." 2 "I need to apply the patch before my evening meal." 3 "I will need to apply a new patch once every 3 to 4 days." 4 "I will apply the patch to the hairless, intact skin area on my upper arm.

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17. Before administering an adrenergic agonist, what is the most important assessment for the nurse to complete? 1 Temperature 2 Skin integrity 3 Blood pressure 4 Respiratory rate

An adrenergic agonist causes vasoconstriction leading to high blood pressure. Temperature, skin integrity, and respiratory rate are not directly affected by adrenergic agonists. Blood pressure is the most important assessment because of the detrimental effects of high blood pressure, such as stroke, which can be life threatening.

Other Uses of Anticholinesterases

A. Atony of the gut without obstruction -Neostigmine (oral)-M3--> contraction B. Urinary retention without obstruction -Neostigmine (s.c.)- M3--> contraction C. Alzheimers -Donepezil: improves cognitive function in mild to moderate stages of disease -high affinity for CNS AchE -low affinity for PNS BuChE D. Non-depolarizing muscular blockade E. Glaucoma F. Myasthenia Gravis

Innervation of the Corpora Cavernosa

A. Endothelium: - activation of muscarinic receptors--> results in activation of endothelial nitric oxide synthase (eNOS)--> production of nitrous oxide--> diffuses over into smooth muscle--> activates Guanylyl cyclase--> increases production of cGMP--> +PKG--> relaxation B. Direct Neural input: -Parasympathetic: -Neural NO essential for erection -Ach nerves play indirect role -Sympathetic: dominant at rest

Diseases Altering Effects of Non-Depolarizing Blockers

A. Myasthenia gravis -decreased Ach receptors--> increased block (use lower dose) B. Liver/Kidney Disease/Aging -decreased metabolism--> increased block (use lower dose) C. Motor nerve Damage -increased receptors--> decrease block (greater dose to compete with increased number of receptors) D. Severe burns -increased receptors--> decreased block (greater dose needed to compete with increased number of receptors)

25. The patient is taking an adrenergic blocker drug. The nurse notes that the patient's weight has increased 2.5 pounds over the past 24 hours and lower extremities are swollen. Based on this information, which action will the nurse take? 1 Contact the prescribing healthcare provider. 2 Take no action; this is an expected side effect. 3 Monitor the patient closely for any additional symptoms. 4 Document this information, and notify the nursing supervisor

Although it is important to document the information and monitor the patient, this information should be called to the prescribing healthcare provider's attention since the patient may be developing edema as an adverse effect of the medication.

27. Antimuscarinic poisoning can result from overdose of antihistamines, phenothiazines, and tricyclic antidepressants. Differential diagnosis is important, because antimuscarinic poisoning resembles which other condition? 1 Epilepsy 2 Meningitis 3 Psychosis 4 Diabetic coma

Antimuscarinic poisoning often resembles psychosis and psychotic episodes. It is important to differentiate, because antipsychotic drugs have antimuscarinic properties and could intensify the symptoms of poisoning.

Peripheral Muscarinic Effect on Blood Vessels

Arteries -dilation (via NO) -direct effect is to contract vessels Veins -dilation (via NO) -direct effect is to constrict

21. The nurse is teaching the patient about atenolol [Tenormin]. Which statement by the patient indicates a correct understanding of the nurse's instruction? 1 "One missed dose will not affect my blood pressure." 2 "I may experience occasional chest pain and discomfort." 3 "I will need to wait for 6 months and then stop this medication." 4 "I will not stop taking this drug without the approval of my healthcare provider because my heart rate may beat very fast or could become irregular and out of rhythm."

Atenolol is a beta blocker and can cause rebound cardiac excitation if withdrawn abruptly. If abruptly withdrawn, the patient can have tachycardia (heart rate will beat very fast) and ventricular dysrhythmias (heart will be irregular and out of rhythm). To decrease the risk of rebound excitation, the dose should be tapered off over 1 or 2 weeks. Patients should carry an adequate supply when traveling.

26. Which statement made by the patient indicates understanding of teaching related to a new prescription for atenolol [Tenormin]? 1 "I will not stop taking this medication abruptly." 2 "I will increase my fluids to prevent constipation." 3 "I will take the first dose of this medicine at night." 4 "I will wear sunscreen and a hat when I work in the sun."

Atenolol is a beta blocker and can cause rebound cardiac excitation if withdrawn abruptly. Patients should carry an adequate supply when traveling. It does not commonly cause constipation, first-dose hypotension, or photosensitivity.

5. The nurse is caring for a patient receiving atropine. Which is a therapeutic indication for giving this drug? -Use as a preanesthesia medication -Treatment of tachycardias -Prevention of urinary retention -Reduction of intraocular pressure in glaucoma

Atropine therapeutic uses: 1. Preanesthetic medication 2. Disorders of the eyes 3. Bradycardia 4. Intestinal hypertonicity and hypermotility 5. Muscarinic agonist poisening **Why are the other options wrong?

20. The nurse determines that a postoperative patient has bladder atony. Which cholinergic drug should the nurse expect to be prescribed to the patient? 1 Donepezil [Aricept] 2 Cevimeline [Evoxac] 3 Bethanechol [Urecholine] 4 Succinylcholine [Anectine

Bethanechol [Urecholine] is a direct-acting cholinergic drug that is used to treat atony of the bladder. It is the only direct-acting cholinergic drug that is administered orally. Succinylcholine [Anectine], Donepezil [Aricept], and cevimeline [Evoxac] are not useful for treating atony of the bladder. Succinylcholine [Anectine] is used in general anesthesia as a neuromuscular blocker. Donepezil [Aricept] is an indirect-acting cholinergic drug that is used to treat Alzheimer's disease. Cevimeline [Evoxac] is a direct-acting cholinergic drug used in the treatment of xerostomia (dry mouth) due to Sjögren's syndrome.

5. The nurse is preparing to give bethanechol [Urecholine]. What is an expected outcome of this drug?

Bethanechol [Urecholine] is a muscarinic agonist and therefore activates muscarinic receptors. This can lead to relaxation of the urinary sphincter muscles and increased voiding pressure. It also can cause bradycardia and hypotension, bronchoconstriction, and dysrhythmias in hyperthyroid patients. Test-Taking Tip: If you are unable to answer a multiple-choice question immediately, eliminate the alternatives that you know are incorrect and proceed from that point. The same goes for a multiple-response question that requires you to choose two or more of the given alternatives. If a fill-in-the-blank question poses a problem, read the situation and essential information carefully and then formulate your response.

Effects of Neuromuscular drugs on NMJ

Botulinus toxin- blocks Ach Release Nondepolarizing blocker- blocks Ach binding to receptor Succinylcholine (cholinomimetic)- blocks endplate depolarization Dantroline- inhibits muscle contaction

Pancuronium

Class: -Neuromuscular Blocker (non-depolarizing) Receptors: -Nm antagonist Uses: -same tubocurarine Administration: -IV only -Slow Onset (4-6 minutes) -Long duration (120-180 min) Adverse Effects: 1. Vagal Blockade -little to no ganglionic blockade or histamine release

29. The nurse assesses a patient who is on cholinergic drug therapy. The nurse finds that the patient has diarrhea, abdominal cramps, and respiratory distress with a heart rate of 48 beats/min and blood pressure of 98/74 mm Hg. The patient does not have a history of coadminstering medications. What is the likely reason for the patient's condition? 1 The patient had a drug interaction. 2 The patient had consumed alcohol. 3 The patient had an allergic reaction. 4 The patient had an overdose of the drug

Cholinergic drugs mimic the effects of acetylcholine by binding to cholinergic receptors. An overdose of cholinergic drugs acts directly on the parasympathetic nervous system and activates the nicotinic receptors. An overdose of the drug shows its adverse effect in increased gastrointestinal secretions, which cause abdominal cramps. This drug reduces the heart rate considerably, thereby leading to hypotension. This may also cause atrioventricular block, leading to cardiac arrest. The patient has no history of coadministering medications; therefore a drug interaction is not the most likely scenario. Alcohol does not interact with cholinergic drugs.

12. A patient with myasthenia gravis was initially prescribed pyridostigmine [Mestinon]. After reviewing the medical history of the patient, the nurse informs the primary healthcare provider that the patient has asthma. What instruction should the nurse anticipate from the primary healthcare provider? 1 Elevate the patient's bed while sleeping. 2 Teach deep breathing exercises to the patient. 3 Discontinue administering pyridostigmine (Mestinon). 4 Administer pyridostigmine [Mestinon] intramuscularly.

Cholinergic drugs such as pyridostigmine [Mestinon] should not be administered to the patient with asthma because it will worsen the symptoms. Pyridostigmine [Mestinon] may cause muscle cramps and difficulty in breathing. Therefore, it should be discontinued in asthma patients. Deep breathing exercises and elevating the patient's bed may not help to prevent the adverse effects caused by pyridostigmine [Mestinon]. Administering pyridostigmine [Mestinon] worsens the symptoms of asthma, and the patient will face breathing difficulty. Therefore, the nurse should avoid administering pyridostigmine [Mestinon] intramuscularly.

Nicotine

Class -Mixed Receptor Agonist (Direct-acting) Receptors: Nn, Nm Therapeutic Uses: -tx of nicotine dependence (cessation) -oral (gum), nasal spray, dermal patch -Insecticides -depolarizing/desensitizing block Good oral absorption (tertiary amine) -readily absorbed by intestine and CNS Selective for nicotinic receptors (all autonomic ganglia and NMJ) Metabolized by the liver (resistant to cholinesterases) Toxicity: -very toxic at high concentrations -nausea vomiting, weakness, confusion -used as insecticide -2 cigarettes have enough nicotine to make sick and cause cardiopulmonary collapse if eaten (most nicotine is burned)

Pralidoxime (2-PAM)

Class: -Cholinesterase regenerator (highly nucleophilic) Target: -Binds to AchE/BuChe Therapeutic Use: -Cholinesterase regenerator for nerve gas exposure -breaks nerve gas binding to AchE/BuChE before "AGING" occurs TREATMENT OF ORGANOPHOSPHATE POISONING: 1. Remove toxin from patient -clothes -wash skin 2. Give PRALIDOXIME (2-PAM) as soon as possible after intoxication [12 HOUR WINDOW]

Methacholine

Class: -Direct Muscarinic Agonist Receptor: -M1-M5 Therapeutic Uses: -Diagnose bronchial hyperactivity -challenge test to test airway sensitivity (subcutaneous injection) -Slower metabolism by AChE (hydrolyzed more slowly than acetylcholine) -Primarily muscarinic agonist; weak nicotinic -Use limited by CV effects (M2)

Sarin & VX Series

Class: -Irreversible Anticholinesterases (indirect) Target: -AChE/BuChE Uses: -Nerve gas (2) Other: -RAPID DERMAL ABSORPTION -AGES VERY RAPIDLY Toxicity: (SLUDGE) CNS -nausea/vomiting -seizures, coma, respiratory arrest Autonomic Ganglia -stimulation--> blockade CV: -decreased CO -Hypotension Exocrine Glands -SEVERELY increased secretion Smooth Muscles -SEVERE contraction Skeletal Muscles -Muscle fasciculation -NMJ depolarizing/desensitizing block (diaphram) Toxicity Treatment: 1. Remove clothes, wash skin 2. Administer ATROPINE

Pilocarpine

Class: -Muscarinic Agonist (Direct) Receptor: -M1-M5 Therapeutic Uses --topical only-- 1. open/wide angle glaucoma A. opens trabecular meshwork B. spasm of accomodation C. miosis 2. Xerostomia (dry mouth) -treatment assumes functional salivary glands -relatively short acting; frequent adm. Potential side effects: -sweating, nausea, chills, dizziness Contraindications -ASTHMA -DRUG INTERACTIONS Orally effective (tertiary amine) -can enter CNS (stimulation) -acts on ALL muscarinic receptors -potent effects on sweat/salivary glands

Bethanecol MOA ( in audio). -Typical drug -MOA -Pharmacologic effects -Uses -Adverse effects (by system) -Other types of drugs

Class: -Muscarinic Agonist (Direct) -SELECTIVE Receptors: -M1-M5 Therapeutic Uses: 1. GI atony=decreased motility (oral) -Post-op ileus (following surgery) -congenital megacolon -spinal cord injury -reflux esophagitis 2. Urinary retention (sc, oral) Administration: GI--> orally Urinary--> subcutaneous DO NOT USE IF OBSTRUCTION IS PRESENT--- MAY RESULT IN PERFORATION -DO NOT USE IF ULCERS PRESENT Other: -High resistance to Ach-esterase -Orally effective -Long duration of action -selective for muscarinic receptors

Propantheline

Class: -Muscarinic Receptor Antagonist (quaternary amine) Receptor -M1-M5 Therapeutic Use: -Diarrhea Blocks receptors on GI mucosa

Ipratopium

Class: -Muscarinic Receptor Antagonist (quaternary amine) Receptor: -M1-M5 Therapeutic Uses: 1. Asthma 2. COPD Adm: Inhalant -Limits side effects

Tropicamide

Class: -Muscarinic Receptor Antagonist/Anti-muscarinic (tertiary amine) Receptor: -M1-M5 Therapeutic Use: 1. Briefer Mydriasis -routine eye examination 2. Cycloplegia Adm: -TOPICAL -effects last 4-6 hours Adverse Effects: -Drowsiness -Light sensitivity (pupil dilation) CONTRAINDICATION -GLAUCOMA -can increase IOP Note: -has shortest onset and shorter duration (good for routine eye exam)

Benztropine

Class: -Muscarinic Receptor Antagonist/Anti-muscarinic (tertiary amine) Receptor: -M1-M5 Therapeutic Use: 1. Parkinson's Disease -adjunct to L-DOPA therapy -decrease tremor -decrease hypersalivation

Scopalamine

Class: -Muscarinic Receptor Antagonist/Anti-muscarinic (tertiary amine) Receptor: -M1-M5 Therapeutic Use: (central and peripheral actions) 1. Motion Sickness (prophylactic only) Administration: -Oral -transdermal patches -IM Adverse Effects: -SIGNIFICANT SEDATION -causes amnesia, dreamless sleep in the absence of pain -during pain, causes hallucinations, nightmares -"truth serum of movies"

Tolterodine

Class: -Muscarinic Receptor Antagonist/Anti-muscarinic (tertiary amine) Receptor: -M3 Therapeutic Uses: 1. Overactive Bladder 2. Incontinence Administration: -Used ORALLY Adverse Effects: -M3 selectivity--> decreased side effects

Atropine

Class: -Muscarinic Receptor Antagonist/Anti-muscarinic (tertiary amine)--> competes with Ach at the receptor Receptor: -M1-M5 Therapeutic Use: (Peripheral Actions) 1. Cholinergic agonist Overdose 2. Long-lasting, mydriasis, cycloplegia 3. Acetylcholinesterase Inhibitor Poisoning (competes with Ach buildup) Administration: -good oral absorption -Low Dose--> paradoxically slowing HR -due to centrally mediated actions at low dose -High Dose--> elevate HR -due to direct antagonism of muscarinic receptors of the heart Adverse Effects CNS effects

Botulinum Toxin A

Class: -Neuromuscular Blocker Target: -Cholinergic nerve terminals MoA: -prevents release of Ach by blocking calcium influx--> inhibits muscle contractions for cosmetic and medical uses Therapeutic Uses: 1. IM or intradermal injections 2. Skeletal muscle disorders -Dystonias -Strabismus, Blepharospasm 3. Skin Disorders -Hyperhidrosis (palms, axillae) -Wrinkles 4. Spasms of esophagous/LES Adm: -IM or Intradermal (type A most common) Limitations: -REQUIRES REPEATED INJECTIONS (IV) -effects last 3-4 months up to 1 yr -10% develop antibodies (ineffective) -Variable Duration Due to: A. upregulation of Nm receptors B. Sprouting of nerve terminals C Presence of antibiodies -No response in 2-5% of patients

Succinylcholine

Class: -Neuromuscular Blocker (Depolarizing) Receptor: -Nm agonist and initially increases sensitivity of muscle to Ach--> DEPOLARIZES AND DESENSITIZES THE NMJ Therapeutic Use: -Rapid induction of paralysis -Rapid Onset (1-2 min) -Short Duration (approx 5 min) -rapidly metabolized by butyryl-cholinesterase (plasma cholinesterase) but resistant to acetylcholinesterase Notes: Phase I: Asynchronous Contractions -Agonistic actions: initial burst of action potentials--> twitch/fasciculations Phase II: maintenance of drug leads to muscle inability to activate--> becomes paralyzed and desensitized

Trimethaphan

Class: -Nicotinic Receptor Antagonist (Ganglionic Blocker) Receptor: -Nn (a3b4) Therapeutic Use: -Rapidly decreases BP --used in dissecting aortic aneurysm --spinal cord injury induced hypereflexia Administration: -ACUTE IV TREATMENT ONLY Side effects: loss of predominant tone (parasympathetic and sympathetic effects)

Mecamylamine

Class: -Nicotinic Receptor Antagonist (Ganglionic Blocker) Receptor: -Nn (a3b4) Therapeutic Uses: -Tourette's Syndrome Administration: -Oral treatment only Side effects: -loss of predominant autonomic tone (Symp & Parasym.)

Rocuronium

Class: -Non-depolarizing Neuromuscular Blocker Receptor: -Nm antagonist Therapeutic Use: -Rapid tracheal intubation Adm: -IV -Rapid onset (1-2 min) -Intermediate duration (30-40 min)

Mivacurium

Class: -Non-depolarizing Neuromuscular Blocker Receptor: -Nm antagonist Therapeutic Use: -Aid tracheal intubation Administration -IV -Intermediate onset (2-4 min) -Short duration (12-18 min) -quickly inactivated by hydrolysis (B-AchE)

Sildenafil

Class: -Parasympathomimetic (Indirect) Target: -inhibits cGMP-PDE (phosphodiesterase-5) -->maintains high levels of cGMP--> results in: A. Relaxation of Corpus Cavernosum B. Dilation of lung vasculature Therapeutic Uses: 1. Erectile Dysfunction (Viagra-1x daily) 2. Pulmonary hypertension (Revatio: 3x daily) Orally effective Onset: 1 hour Duration: 4-5 hours Note for ED A. Requires intact innervation B. Requires sexual arousal -use 1 hr. b/f intercourse -->only 1x daily Adverse effects: CV patients: -potentiates nitrates/NO drugs!!!! -LOW BLOOD PRESSURE -REFLEX TACHYCARDIA (huge increase in HR) -ANGINA & MI -Headaches/Flushing/Dyspepsia -Priaprism (>4 hours) -Visual Disturbances -bluish tint of vision -NAION (Non-arteritic ischemic optic neuropathy)

Neostigmine

Class: -Reversible Anticholinesterase Action: -Ach build-up--> stimulates all receptors Thx: 1. Tx of Myasthenia Gravis (oral) 2. Glaucoma (topical) 3. GI/Urinary atony (SC, oral) ( M3--> contraction) 4. Reversal of NMJ block (IV, IM) Other: -No CNS effects (quaternary amine) -Competitive inhibitor of AchE/BuCHE -duration of action: 4-6 hours -Carbamylated enzyme resists hydrolysis -AchE can actually clip this compound--> inactivation

Physostigmine

Class: -Reversible Anticholinesterase (Indirect) Action: -Ach-build-up stimulates all receptors Thx: 1. Glaucoma (topical) 2. Muscarinic antagonist OD (Hyperthermia+ Seizures) Administration: -IV/IM Other -tertiary amine--> enters the CNS -Use only for SEVERE MUSCARINIC ANTAGONIST OVERDOSE

Donepezil

Class: -Reversible Anticholinesterase (Indirect) Action: Ach build-up--> stimulates all receptors Thx: Alzheimer's Disease (Oral) -preferential inhibitor of CNS AchE -Note: improves cognition, DOES NOT PREVENT DEGENERATION Other: -Tertiary amine: enters CNS -Preferential inhibitor of CNS AchE -improves cognition only; no degeneration prevention

Dantrolene

Class: -Skeletal Muscle Relaxant Target: -Sarcoplasmic reticulum Calcium-Channels -Blocks Ca2+ release from sarcoplasmic reticulum in skeletal muscle--> prevents contractoin Therapeutic Use: 1. Treatment of malignant hyperthermia caused by succiylcholine/general anesthetics 2. Cerebral palsy/Stroke patients Side Effects: -Muscle weakness (due to dec. Ca2+) -Hepatic Toxicity

Pyridostigmine

Class: -Reversible Anticholinesterase (Indirect-Acting) Action: -Ach build-up--> stimulates all receptors Thx: 1. Myasthenia Gravis (oral) 2. Prophylaxis vs. Nerve Gas Administration: I.V. or I.M. Other: -No CNS effects (charged=quaternary amine) -Competitive inhibitor of AchE (covalent but is hydrolyzed) -Longer duration 6-8 hours

Echothiophate

Class: -Irreversible Anticholinesterase (indirect) Target: -AChE/BuChe Therapeutic Use: -Glaucoma -used if pilocarpine is insufficient Adverse Effects: -increased chance of ocular side effects 1. Miosis 2. Spasm of Accommodation 3. Cataract formation No CNS effects (quaternary amine) Stable in aqueous solution

Malathion & Parathion

Class: -Irreversible Anticholinesterases (indirect) Target: -AchE/BuChE Use: -Insecticide (2) Other: -stable in aqueous solution -Prodrugs: activated in liver -Safe with proper use TOXICITY: (SLUDGE) -TREAT WITH ATROPINE!!!!!! CNS -nausea/vomiting -seizures, coma, respiratory arrest Autonomic Ganglia -stimulation--> blockade CV: -decreased CO -Hypotension Exocrine Glands -SEVERELY increased secretion Smooth Muscles -SEVERE contraction Skeletal Muscles -Muscle fasciculation -NMJ depolarizing/desensitizing block (diaphram)

Muscarine

Class: -Muscarinic Agonist (Direct) Receptors -M1-M5 Therapeutic Use: -No current therapeutic uses Poor oral absorptions (quaternary amine) Acts on all muscarinic receptors

Tubocurarine

Class: -Neuromuscular Blocker (non-depolarizing) Receptor: -Nm antagonist Therapeutic Uses 1. Adjunct to general anesthesia 2. Abdominal/orthopedic surgery 3. Artificial respiration 4. Aid to tracheal intubation 5. Control of seizures Administration: -IV only -no CNS effects (quaternary amine) -Slow onset (4-6 minutes) -Long duration (80-120 min) Adverse Effects: SEVERE HYPOTENSION 1. Histamine Release 2. Ganglionic Blockade -NO CNS EFFECTS (no vagal blockade)

Edrophonium

Class: -Reversible Anticholinesterase (Indirect) Action: -competitive inhibitor of AchE-->interferes with binding to Ach to AchE-->ACh buildup--> stimulates all receptors Thx: 1. Diagnosis of Myasthenia Gravis 2. Evaluate treated myasethenics 3. Paroxysmal atrial tachycardia Administration: -I.V/I.M only Other: -No CNS effects (quaternary amine) -Competitive inhibitor of AchE/BuChE -Short duration of action- (10 minutes) -rapidly reversible

Varenicline

Class: -Synthetic Nicotinic Partial Agonist Receptor: -selective alpha4-beta2 partial agonist -stimulates DA terminals in CNS Therapeutic Use: -Tx nicotine dependence (oral) -blocks full agonist effect of nicotine -decreases severity of nicotine withdrawal A. Oral (gum, lozenge, inhalation) -# of units per day gradually decreased beginning 6-12 weeks after therapy begins B. Transdermal patch -sequential schedule -start with strongest patch -patch worn 16 hours a day Adverse Effects: -Nausea/vomiting -sleep disturbances -constipation -flatulence

26. Following the assessment of a patient with Alzheimer's disease, the nurse informs the primary healthcare provider that it is not safe to prescribe donepezil [Aricept] to the patient. Which assessment finding supports the nurse's conclusion? 1 The patient's heart rate was 55 beats/min. 2 The patient had reduced serum sodium levels. 3 The patient had reduced serum uric acid levels. 4 The patient's fasting blood glucose level was 80 mg/dL

Donepezil [Aricept] causes severe cardiovascular disorders. Therefore, it should be avoided in the patient who has bradycardia. A fasting blood glucose level of 80 mg/dL indicates that the patient has normal blood glucose levels; hence, this does not pose a safety concern. Donepezil [Aricept] is not contraindicated in the presence of low sodium and uric acid levels.

Toxic Reactions Muscarinic Receptor Antagonists

EFFECTS ARE DOSE DEPENDENT: -fever and flushed skin (sweating inhibition) -dry skin and mouth -dilated pupils, cycloplegia -tachycardia -agitation ("DRY AS A BONE, BLIND AS A BAT, RED AS A BEET, MAD AS A HATTER") -hypotension @ high doses (ganglionic block) -children more susceptible to poisoning

General Effects of Muscarinic Receptor Blockade

EYE -MYDRIASIS, CYCLOPLEGIA Mucus Glands -decreased secretion (xerostomia) SALIVARY GLANDS -DECREASED SECRETION (XEROSTOMIA) HEART -Low Dose-->slows HR (CNS effect) -High Dose--> increase HR Gut -decreases motility, -less effect on secretions (enteric NS) Urinary Tract -decreases micturition speed (bladder relaxation) Bronchial Muscle -Relaxation CNS -DROWSINESS -toxic doses can produce excitement, halucinations, coma NOTE THESE ARE FOR GENERAL INHIBITION OF ........

15. When the patient develops anaphylactic shock, which drug does the nurse expect to administer? 1 Ephedrine 2 Isoproterenol [Isuprel] 3 Epinephrine [Adrenalin] 4 Norepinephrine [Levophed

Epinephrine is administered in emergencies and is one of the primary vasoactive drugs used in anaphylactic shock emergencies. Norepinephrine [Levophed] is similar to epinephrine but it does not activate beta2 receptors. It is used in hypotensive states and cardiac arrest. Isoproterenol [Isuprel] acts only at beta-adrenergic receptors. It is used to manage atrioventricular (AV) heart block and to improve outcomes in cardiac arrest to increase cardiac output during shock. Ephedrine promotes beta2-mediated bronchodilation, so it is beneficial to asthma patients.

Epinephrine: Contraindications? -What patient hx would alarm you if you were getting ready to administer lidocaine with epinepthrine prior to surgery?

Epinephrine is an adrenergic agonist that causes vasonconstriction and raises blood pressure. The nurse should bring the patient's high blood pressure to the healthcare provider's attention so the provider can weigh the risks versus benefits of administration. Lidocaine with epinephrine is not an antibiotic. There is no chance of cross-sensitivity. Lidocaine with epinephrine should not be used for lesions at the end of digits or of the nose or penis; however, it may be used for scalp lesions. Recovering from a virus is not a contraindication to receiving lidocaine with epinephrine.

1. The nurse is preparing to give a drug that stimulates the parasympathetic nervous system. Which patient response is an expected outcome of this drug? -Wheezing decreases due to bronchodilation. -Heart rate decreases to 60 beats per minute. -Diarrhea stool count decreases. -Oxygenation improves because of bronchodilation.

Functions of the Parasympathetic Nervous System -Slowing of heart rate -Increased gastric secretion -Emptying of the bowel -Focusing the eye for near vision -Constricting the pupil -Contracting bronchial smooth muscle Certain poisons act on PNS: -insectisides -nerve gases -certain mushrooms and plants *Stimulation of the parasympathetic nervous system (PNS) causes slowing of the heart rate. The PNS does not regulate temperature. The PNS would facilitate peristalsis and thus would not decrease diarrhea. The PNS is associated with contraction of bronchial smooth muscle.

4. A patient with a new prescription for propanolol [Inderal] tells the nurse he has a history of asthma. The nurse's priority action is to:

Inderal is a nonselective beta blocker which can result in bronchoconstriction. The healthcare provider (HCP) needs to be notified about the patient's history of asthma. Teaching the patient how to take the blood pressure, to change positions slowly, and informing the patient to carry a rescue inhaler are all important; however, notifying the HCP is priority to ensure safety and prevent bronchoconstriction first.

28. The nurse prepares to administer the antidote to a patient in cholinergic crisis. What medication would the nurse anticipate the healthcare provider to order? 1 Atropine 2 Pralidoxime [DuoDote] 3 Dobutamine [Dobutrex] 4 Neostigmine [Prostigmin]

Intravenous atropine can alleviate the muscarinic effects of cholinesterase inhibition. Pralidoxime [DuoDote] is a specific antidote to poisoning by the irreversible (organophosphate) cholinesterase inhibitors; the drug is not effective against poisoning by reversible cholinesterase inhibitors.

Effector actions of Muscarinic receptors

M1- nerves, nerve terminals, some effector cells (exocrine glands, stomach) M2- heart, nerves, smooth muscle, lung M3- smooth muscle, glands, vascular endothelium M4- lung M5- CNS

2. The nurse in the cardiac care unit is caring for a patient receiving epinephrine. Which assessment criterion takes priority in monitoring for adverse effects of this drug?

Monitoring of the heart rhythm is essential to assess the patient for dysrhythmias. Epinephrine can cause a number of adverse effects, including hypertensive crisis, dysrhythmias, angina, tissue necrosis after extravasation, and hyperglycemia. Test-Taking Tip: Work with a study group to create and take practice tests. Think of the kinds of questions you would ask if you were composing the test. Consider what would be a good question, what would be the right answer, and what would be other answers that would appear right but would in fact be incorrect.

6. The nurse is caring for a group of patients who are all receiving anticholinergic drugs. In which patient is an anticholinergic drug contraindicated? A 60-year-old woman with an overactive bladder (OAB) A 72-year-old man with glaucoma A 45-year-old woman with peptic ulcer disease (PUD) A 26-year-old man being prepared for surgery today

Most adverse effects of atropine and other anticholinergic drugs are the direct result of muscarinic receptor blockade; they include dry mouth, blurred vision, photophobia, elevation of intraocular pressure, urinary retention, constipation, anhidrosis (suppression of sweating), tachycardia, and asthma.

Anticholinergic drugs aka muscarinic antagonists

Muscarinic antagonists competitively block the actions of acetylcholine at muscarinic receptors. • Because most muscarinic receptors are located on structures innervated by parasympathetic nerves, the muscarinic antagonists are also known as parasympatholytic drugs. • Other names for these agents are antimuscarinic drugs, muscarinic blockers, and anticholinergic drugs. • When a drug is characterized as anticholinergic, this means that it produces selective muscarinic blockade—not blockade of all cholinergic receptors.

6. The nurse is preparing to give a drug to stimulate activation of adrenergic receptors. Which effects indicate sympathetic stimulation? -Increase in heart rate -Constriction of pupils - Atrioventricular block - Sinus bradycardia

Must know: -What is the function of adrenergic receptors? -Where do adrenergic receptors reside in the ANS? **Activation of the adrenergic receptors stimulates the sympathetic nervous system and causes an increase in heart rate Rational: 1. Two basic categories of receptors are associated with the PNS: Cholinergic and Adrenergic receptors. 2. Adrenergic receptors are receptors that mediate responses to epinephrine (adrenaline) and norepinephrine. 3. Adrenergic receptors can be divided into four major subtypes: alpha1, alpha2, beta1, beta2 Activation of ocular alpha1 receptors leads to mydriasis (dilation of the pupil). • Activation of alpha1 receptors in blood vessels produces vasoconstriction. • Activation of alpha1 receptors in the sexual apparatus of males causes ejaculation. • Activation of alpha1 receptors in smooth muscle of the bladder (trigone and sphincter) and prostatic capsule causes contraction. • Drug effects resulting from activation of peripheral alpha2 receptors have minimal clinical significance. • Activation of cardiac beta1 receptors increases the heart rate, force of myocardial contraction, and conduction velocity through the atrioventricular node. • Activation of beta1 receptors in the kidneys causes release of renin into the blood. • Activation of beta2 receptors dilates the bronchi, relaxes uterine smooth muscle, increases glycogenolysis, enhances contraction of skeletal muscle, and dilates arterioles (in the heart, lungs, and skeletal muscle). 4. Neurotransmission at adrenergic junctions is terminated by reuptake of intact norepinephrine into nerve terminals. • After reuptake, norepinephrine may be stored in vesicles for reuse or destroyed by monoamine oxidase. • Epinephrine travels via the bloodstream to target organs throughout the body, where it can activate alpha1, alpha2, beta1, and beta2 receptors. • Termination of epinephrine's actions is accomplished primarily by hepatic metabolism, not by uptake of epinephrine into nerves.

Primary treatment for Myasthenia Gravis

Neostigmine & Pyridostigmine -no CNS effects -competitive inhibitors -long duration of action b/c they carbamylate the enzyme--> makes action longer

7. A patient is to be discharged home with a new prescription for prazosin [Minipress]. Which statement is most important for the nurse to include in the teaching plan? 1 "You should move slowly from a sitting to a standing position." 2 "You should increase your intake of fresh fruits and vegetables." 3 "Take your first dose of this medication first thing in the morning." 4 "Be sure to wear a Medic Alert bracelet while taking this medication.

Orthostatic hypotension is the most serious adverse effect of prazosin and other alpha1 blockers. Patients should be taught to move slowly when changing from a supine or sitting position to an upright position to avoid dizziness and prevent falls. Fresh fruits and vegetables are good to include in the dietary teaching, but this is not as important as preventing hypotension. A Medic Alert bracelet should not be needed for this drug. This drug causes significant first-dose hypotension. The initial dose should be taken at bedtime. Patients should avoid driving and other hazardous activities for 12 to 24 hours after the first dose. Test-Taking Tip: Pace yourself when taking practice quizzes. Because most nursing exams have specified time limits, you should pace yourself during the practice testing period accordingly. It is helpful to estimate the time that can be spent on each item and still complete the examination in the allotted time. You can obtain this figure by dividing the testing time by the number of items on the test. For example, a 1-hour (60-minute) testing period with 50 items averages 1.2 minutes per question. The NCLEX exam is not a timed test. Both the number of questions and the time to complete the test varies according to each candidate's performance. However, if the test taker uses the maximum of 5 hours to answer the maximum of 265 questions, each question equals 1.3 minutes.

14. The nurse is caring for a 60-year-old woman who has been prescribed oxybutynin [Ditropan] for the treatment of overactive bladder (OAB). Which statement by the nurse will be most helpful to include in the teaching plan? 1 "Ditropan is very effective. Most patients experience significant relief." 2 "You may experience a slower heart rate. Call your doctor if it is below 60." 3 "Sip on water and suck on hard candy to help with the problem of dry mouth." 4 "Antihistamines, such as Benadryl, can help with some of the side effects of Ditropan.

Oxybutynin [Ditropan] is an anticholinergic drug that commonly causes dry mouth. Other side effects include constipation, tachycardia, urinary hesitancy, urinary retention, and visual disturbances. Oxybutynin is only moderately effective (30% better than placebo). It should not be taken with other drugs with anticholinergic properties, such as antihistamines, because of the additive anticholinergic effects.

13. What is the pathophysiology for a myasthenic crisis? 1 Overdose with a cholinesterase inhibitor 2 Accidental ingestion of organophosphate insecticides 3 Insufficient acetylcholine at the neuromuscular juncture 4 Excessive acetylcholine at the neuromuscular juncture

Patients who are inadequately medicated may experience myasthenic crisis, a state characterized by extreme muscle weakness caused by insufficient acetylcholine at the neuromuscular juncture. A cholinesterase inhibitor (eg, neostigmine) is used to relieve the crisis. Accidental ingestion of organophosphate insecticides is a common source of poisoning.

9. The nurse has administered bethanechol to a patient with hypotonic bladder. After 45 minutes, the nurse finds that the patient is effectively responding to the medication. Which observation would support this conclusion? 1 The patient voided. 2 The patient's respiratory rate increased. 3 The patient has decreased bowel sounds. 4 The patient's blood pressure was reduced

Patients with hypotonic bladder have urinary retention. Therefore, to determine the efficacy of the drug, the nurse should reassess the patient after administering the medication. If the patient voids within 60 minutes of administering, it indicates that the patient is effectively responding to the drug. Hypotension is an adverse effect of cholinergic medications such as bethanechol [Duvoid]. Therefore, a reduction in blood pressure would indicate that the patient is having paradoxical effects of the drug. Cholinergic medications prevent constipation by increasing gastric motility. These drugs may cause an increase in the bowel sounds. Test-Taking Tip: Multiple-choice questions can be challenging, because students think that they will recognize the right answer when they see it or that the right answer will somehow stand out from the other choices. This is a dangerous misconception. The more carefully the question is constructed, the more each of the choices will seem like the correct response.

16. The nurse is caring for a patient with myasthenia gravis who is beginning a new prescription of neostigmine [Prostigmin], 75 mg PO twice daily. What is the most important initial nursing action? 1 Assess the patient's ability to swallow. 2 Teach the patient to wear a Medic Alert bracelet. 3 Check the patient's deep tendon reflexes (DTRs). 4 Obtain a measurement of the plasma level of neostigmin

Patients with myasthenia gravis have decreased muscle strength and may have impaired swallowing. If swallowing is insufficient, the medication must be given by the parenteral route. Plasma levels are not as important when beginning medication. Neostigmine typically is dosed to symptoms. The patient should be taught to wear a Medic Alert bracelet and may need to have deep tendon reflexes (DTRs) monitored, but assessing swallowing is a higher priority.

Direct Muscarinic Receptor Antagonists (Anti Muscarinics)

Quaternary Amines: (CHARGED) 1. Propantheline 2. Ipratropium Teritiary Amines: (UNCHARGED) 1. Atropine 2. Scopolamine 3. Tolterodine (M3 only) 4. Tropicamide 5. Benztropine competitive inhibitors -compete with Ach at the receptor -generally reversible -most agents are nonselective (M1-M5) -(Tolterodine is exception M3) also called Belladonna alkaloids ("beautiful lady"--put in eyes to dilate pupils) -Major Effects: -mydriasis, cycloplegia -decrease salivary secretion -Low dose: slow heart rate -High dose: increases heart rate -CNS drowsiness

4. A nurse is preparing to give a medication that stimulates the beta2 receptors. What response will the nurse expect from this drug? -Increased peristalsis - Constriction of the pupil -Hypoglycemia - Bronchodilation

Rational: *Activation of the Beta2 receptors: -Dilates the bronchi -Relaxes uterine smooth muscle -Increases glycogenolysis -Enhances contraction of skeletal muscle -Dilates aterioles -->Heart -->Lung -->skeletal muscle Activation of beta2 receptors leads to bronchodilation; decreased uterine contractions; hyperglycemia; and vasodilation of the heart, lungs, and skeletal muscle. It does not produce increased peristalsis, constriction of the pupil, or hypoglycemia.

4. Which label most aptly describes the drug atropine [Sal-Tropine]? -Cholinergic -Parasympatholytic -Muscarinic agonist -Parasympathomimetic

Rational: -Muscarinic antagonists competitively block the actions of ACh at muscarine receptors. Because the majority of muscarinic receptors are located on structures innervated by parasympathetic nerves, the muscarinic antagonists are also known as --parasympatholytic drugs

2. A patient is experiencing symptoms of the fight-or-flight response. Which autonomic process stimulates this response? -Sympathetic system -Predominant tone of the organs -Baroreceptor reflex -Parasympathetic system

Rational: -Stimulation of the sympathetic nervous system produces the fight-or-flight response. The baroreceptor reflex regulates blood pressure.

3. The nurse knows that which neurotransmitter is most commonly found at the synapses of the peripheral nervous system? - Norepinephrine - Epinephrine - Dopamine - Acetylcholine

Rational: The PNS employs three neurotransmitters: --ACh --Norepinephrine --Epinephrine --Perhaps Dopamine However: *Acetylcholine is the transmitter employed at most junctions of the PNS. *Norepinephrine, epinephrine, dopamine, and acetylcholine are neurotransmitters for the peripheral nervous system, but acetylcholine is the most abundant. It is released by all preganglionic neurons in the sympathetic and parasympathetic systems. It also is released by all postganglionic neurons of the parasympathetic nervous system.

Peripheral Muscarinic Effects on Heart

SA node -decrease in rate (negative chronotropy) Atria -decrease in contractile strength force (negative inotropy) -decrease in refractory period AV-Node -decreased conduction velocity (negative dromotropy) -increase in refractory period Ventricles -small decreases in contractile strength

Overdose/Adverse Effects of Muscarinic Agonists

SLUDGE -Salivation -Lacrimation -Urination -Diaphoresis -GI upset -Emesis Also hypotension, bradycardia, arrhythmia, miosis, respiratory difficulty (mucous and bronchial constriction)

23. Which direct-acting cholinergic drug is used as a general anesthetic? 1 Pilocarpine [Pilocar] 2 Carbachol [Carboptic] 3 Bethanechol [Urecholine] 4 Succinylcholine [Quelicin]

Succinylcholine [Quelicin] is a direct-acting cholinergic drug that is used as a general anesthetic. It acts as a neuromuscular blocker, resulting in the loss of sensation. Carbachol [Carboptic] and pilocarpine [Pilocar] are drugs used to reduce intraocular pressure in conditions such as glaucoma. Bethanechol [Urecholine] is used to treat atony of the bladder and the gastrointestinal tract.

22. Which condition is an indication for the use of succinylcholine [Anectine]? 1 Relief of status epilepticus 2 Pain relief after major surgery 3 Loss of consciousness during surgery 4 Facilitation of endotracheal intubation

Succinylcholine is an ultrashort-acting neuromuscular (NM) blocker used to facilitate insertion of an endotracheal tube for mechanical ventilation. Because an intact gag reflex can fight tube insertion past the glottis and into the trachea, reflexes can be suppressed temporarily by this short-acting agent. It is not indicated for the treatment of status epilepticus. It does not provide pain relief or loss of consciousness.

Anticholinesterase Toxicities

TOXICITY CNS -nausea/vomiting -seizures, coma, respiratory arrest Autonomic Ganglia -continuous stimulation--> blockade CV: -decreased CO -Hypotension Exocrine Glands -SEVERELY increased secretion (sludge) Smooth Muscles -SEVERE contraction Skeletal Muscles Initially: Muscle fasciculation Chronic--> NMJ depolarizing/desensitizing --> receptors shut down--> no longer responding -->block (diaphragm) -->respiratory arrest

24. The nurse assesses the peripheral intravenous infusion site of a patient receiving intravenous dopamine and suspects extravasation. What is the nurse's primary action? 1 Stop the infusion. 2 Pull the IV immediately. 3 Apply a cold pack to the site. 4 Elevate the patient's extremity

The nurse's first action is to stop the infusion followed by infusing phentolamine [Regitine] into the area to counteract the vasoconstrictive effects of the dopamine.

6. Which statement is true regarding the EpiPen? -The EpiPen can be stored in the patient's car. -The EpiPen auto-injector is a multi-use delivery system. -The EpiPen is available over the counter at any retail pharmacy. -The EpiPen is an epinephrine auto-injector indicated for emergency treatment of anaphylaxis

The only true statement is that the EpiPen is an epinephrine auto-injector indicated for emergency treatment of anaphylaxis. The EpiPen auto-injector is single-use only, not a multi-use delivery system. The EpiPen is sensitive to extreme heat and light, so the EpiPen should be stored at room temperature in a dark place and never stored in a car. The EpiPen is available only by prescription and not over the counter at any retail pharmacy. Test-Taking Tip: The night before the examination you may wish to review some key concepts that you believe need additional time, but then relax and get a good night's sleep. Remember to set your alarm, allowing yourself plenty of time to dress comfortably (preferably in layers, depending on the weather), have a good breakfast, and arrive at the testing site at least 15 to 30 minutes early.

7. Which organs are controlled primarily by the parasympathetic system? (Select all that apply.) -Gastrointestinal tract - Respiratory tract - Cardiovascular system -Skin -Salivary glands

The parasympathetic nervous system has seven regulatory functions relevant to pharmacology; it slows the heart rate, increases gastric secretion, empties the bladder and bowel, focuses the eye for near vision, constricts the pupil, and contracts bronchial smooth muscle. -Gastrointestinal tract- Correct - Respiratory tract- Correct -Cardiovascular system- Incorrect - Skin -Correct -Salivary glands- Correct **The sympathetic nervous system provides the predominant tone for the cardiovascular system.

25. The nurse is monitoring a patient prescribed reserpine for the treatment of hypertension. Which assessment parameter indicates that this medication is effective? 1 Decrease in diarrhea 2 Absence of bladder distention 3 Blood pressure of 118/72 mm Hg 4 Improved symptoms of depression

The primary indication of reserpine is to control hypertension. It has been used to treat psychosis, but more effective drugs now are available for that purpose. Adverse effects of reserpine include severe depression with suicide risk, gastric ulcer formation, and diarrhea. Reserpine is not used to treat urinary retention.

18. The patient is being treated with a dopamine intravenous drip. In order to monitor for infiltration of the site, what action is most important for the nurse to perform? 1 Apply a pressure dressing to the IV site. 2 Check the site every hour for evidence of swelling. 3 Encourage the patient to call if the site becomes painful. 4 Encourage the patient to keep the arm with the IV straight.

The site should be monitored every hour for evidence of infiltration to prevent extravasation.

What do cholinergic drugs do? -Direct -Indirect (see photo)

They affect the cholinergic receptor-needs ACh -blocks ACh -or mimics ACh

Nicotinic Receptor Blockers

Three mechanisms of action: 1. Competitive inhibitors -block Ach binding 2. Non-competitive inhibitors -block ion channel 3. Depolarizing drugs -initial stimulation then block Do not distinguish between parasympathetic and sympathetic ganglia -Inhibit general autonomic function -->Limited therapeutic use Effects on tissues/systems will depend on the predominant neural tone in that system

19. The nurse is teaching a patient with a history of anaphylaxis how to use an EpiPen. Which statement made by the patient indicates that he understands the proper use of this drug? 1 "I will jab this medication firmly into my outer thigh if needed." 2 "I will keep my medication in the refrigerator when I'm not using it." 3 "I must remove my pants before injecting the medication into the leg." 4 "I should take this medication within 30 minutes of the onset of symptoms."

To use the EpiPen, the patient should form a fist around the unit with the black tip pointing down, remove the activation cap, jab the device firmly into the outer thigh, wait 10 seconds, remove the unit, and massage the area for 10 seconds. The medication can be given directly through clothing if necessary.The EpiPen should be stored in a cool, dark place, but refrigeration can damage the injection mechanism. The medication should be taken at the first sign of symptoms. Anaphylaxis can develop within minutes after allergen exposure.

11. The nurse is reviewing drugs on the emergency cart with regard to their therapeutic action. Which medications can help initiate heart contraction during a cardiac arrest? 1 Inhaled albuterol 2 Topical phenylephrine 3 Intravenous epinephrine 4 Subcutaneous terbutaline

When beta1 receptors are activated, cardiac contraction is stimulated. When a beta1 agonist is indicated, epinephrine (given IV) is the preferred drug. Beta1 agonist drugs (eg, epinephrine), which are kept on the emergency cart, may be injected directly into the heart during an arrest. Alpha1 activation causes hemostasis, nasal decongestion, vasoconstriction, and mydriasis. Alpha2 activation reduces sympathetic outflow to the heart and blood vessels and relieves severe pain. Beta2 activation causes bronchodilation and relaxation of uterine smooth muscle. Topical phenylephrine (alpha 1 activation) is helpful for nasal congestion. Terbutaline (beta 2 activation) is indicated for preterm labor and/or asthma. Albuterol (beta2 activation) is indicated for asthma. Test-Taking Tip: Prepare for exams when and where you are most alert and able to concentrate. If you are most alert at night, study at night. If you are most alert at 2 am, study in the early morning hours. Study where you can focus your attention and avoid distractions. This may be in the library or in a quiet corner of your home. The key point is to keep on doing what is working for you. If you are distracted or falling asleep, you may want to change when and where you are studying.

Clinical Uses of Anticholinesterases (Glaucoma)

drugs: -cause miosis (pupil constriction) -ciliary muscle contraction -opening of trabecular meshwork--> allow outflow of aqueous humor A. Short acting: Physostigmine -temporary use for actue/closed angle until surgical intervention B. Chronic-long acting drugs: 1. Demecarium 2. Echothiophate -used in patient with chronic, wide-angle glaucoma when short acting treatments are ineffective ADVERSE EFFECTS: -Long-acting drugs associated with development of cataracts