Pharmacology Study Guide for NCLEX 2022 PDF

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Pharmacology Study Guide

A comprehensive study guide that will supplement your pharmacology lectures and readings

By: Barbara O. Instagram: @yournursingeducator E-mail: [email protected]

*Disclaimer: This PDF was created by cross referencing several resources. It is not meant to replace your pharmacology lecture/study notes or drug guid e book but is instead a supplementary resource to aid in studying. While all attempts were made to ensure accuracy, there is no guarantee of validity or accuracy. The purchaser of this guide assumes all responsibility for the use of this material.

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Table of Contents

General Pharmacology Information …………………………………………………………………………………… 3 Autonomic Nervous System Drugs ……………………………………………..……………………………………… 5 Neurological + Neuromuscular Drugs ………………………………………………………………………………. 10 Analgesics ………………………………………..………………………………………………………………………………. 16 Cardiovascular Drugs ……………………………….…………………………………………………………………….… 19 Respiratory Drugs ………………………………………………………………………………..…………………………… 27 Gastrointestinal Drugs ……………………………………………………………………………………………………… 30 Genitourinary Drug ………………………………………………………..………………………………………………… 35 Hematology Drug …………………………………………………………..………………………………………………… 38 Endocrine Drugs ………………………………………………………..…………………………………………………..… 41 Mental Health Drugs ……………………………………….………..…………………………………………………..… 44 Substances of Addiction …………………………………………………………………………………………………… 49 Immune, Antibiotic/Antiviral, & Anti-Inflammatory Drugs ……………………………………………..… 52 Fluids and Electrolytes …………………………………………..…..…………………………………………………..… 57 Quick Overview of Drugs………………………………………………………..…….………………………………..… 59 Common Medication Prefixes and Suffixes………………………………………………………………………. 64 Medication Calculation ………………………………………………………..………………………………………..… 65

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GENERAL PHARM PHARMACOLOGY ACOLOGY IN INFORMATION FORMATION Classi Classifications fications Therapeutic class: broad purpose of drug (e.g. antihypertensive is used for HTN) Pharmacologic class: specific pharmacological approach within the therapeutic class (e.g. beta blocker, calcium channel blocker, etc. are within the antihypertensive therapeutic class) Generic name: actual name of the drug (e.g. amlodipine) Trade name: the name that the drug is marketed under; several different ways to name the generic drug (e.g. Norvasc) FDA Pregnanc Pregnancyy Categories A: good studies show no risk of fetal abnormalities; good human research – no risk B: safe in animals but not adequate enough studies in humans OR adverse effect in animal studies but human studies do not show increased risk; safe in animals but no studies in humans or no harm in humans C: adverse effect in animals but no good studies in humans OR no animal studies and no human studies; no evidence of good or bad in humans D: risk to fetus but benefits may outweigh risk; evidence of harm in humans X: causes fetal abnormalities; should not be used during pregnancy Routes of Admi Administration nistration Enteral – through GI tract 1. Tablets/Capsules – some can be enteric coated (prevents digestion by stomach acids) 2. Sublingual/Buccal – drug goes directly into blood due to amount of blood vessels in this area 3. Nasogastric/Gastric (G-tube) Topical – applied to intended site of action 1. Transdermal 2. Ophthalmic 3. Otic 4. Nasal 5. Respiratory – administered via inhalation 6. Vaginal or rectal – suppositories, ointments, creams, gels; for irritation or infection Parenteral – involves needles penetrating skin 1. Intradermal – rapid absorption due to vasculature; local anaesthetics or allergy testing 2. Subcutaneous – insulin, heparin, vaccines; no more than 1 mL to be injected 3. Intramuscular – faster than ID or SC; proper landmarking needed; no more than 3 mL to be injected 4. Intravenous – very rapid onset; continuous infusion, intermittent infusion, IV push Pharmacokinetics Absorption → distribution → metabolism → excretion 1. Oral → Stomach/small intestine → Absorbed/Carried by Portal Vein/blood supply → Liver (Primary Site of metabolism in body) → Two possibilities: 1. Systemic Circulation → Tissue (Heart/Brain/Muscle/Kidney) 2. Excretion (Biliary) (Gall bladder/Bile ducts) → small-large intestines → Excretion (feces) 2. Parenteral/ Other routes → Directly absorbed into Systemic Circulation → Two possibilities: 1. Systemic Circulation → Tissue (Heart/Brain/Muscle/Kidney) 2. Excretion (Biliary) (Gall bladder/Bile ducts) → small-large intestines → Excretion (feces) Adverse Effects Unintended & undesired responses from drugs 1. Side effects • Secondary to main therapeutic effect of drug & are expected • Often occur at normal doses & are often unavoidable • Often due to poor specificity/selectivity of drug.

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E.g. antihistamines block H1 histamine receptors preventing allergy symptoms (runny nose, watery eyes). Side effects include drowsiness, dry mouth & urinary retention Drug toxicity: any severe adverse drug event • Often mediated by overdose • Reactions are often extensions of therapeutic effect o E.g. patient taking too much insulin = hypoglycemia Allergic Reactions: mediated by immune system • Requires prior sensitization where patient is exposed to allergen (ie. drug) • Upon subsequent exposure, an allergic reaction occurs → mast cells release chemical mediators such as histamine • Reactions can vary from itching rash to life threatening anaphylaxis (bronchospasm, edema, & severe hypotension) • Intensity is independent of dosage size (ie. small dose can produce severe allergy) Idiosyncratic Reaction: reactions that occur rarely & unpredictably • Genetic polymorphisms account for majority of idiosyncratic reactions • Examples of genetic polymorphisms that cause idiosyncratic reactions: ▪ CYP2C9: polymorphism decreasing metabolism (15% Caucasians) ▪ CYP2D6: poor metabolizers (10% African American/Caucasian). Patients do not experience pain relief when taking codeine (drug metabolized by CYP2D6 → morphine) ▪ Glucose 6-Phosphate dehydrogenase deficiency (G6PDH): enzyme important in red blood cell metabolism. Deficiency common in African/Middle-Eastern. Patients w/ deficiency may have red blood cell hemolysis w/ certain analgesics (ie. Aspirin) or anti-malarial drugs. Carcinogenic Effects: ability of a drug to cause cancer • Few drugs are carcinogenic • Diethylstilbestrol (DES) used to be given to prevent spontaneous abortion is high risk pregnancies. Years later → female offspring = vaginal/uterine cancer Mutagenic Effects: changes DNA & often carcinogenic or teratogenic • Drugs that aren’t carcinogenic or teratogenic may receive approval for use from regulatory agencies if there is sufficient evidence of safety from preclinical studies Teratogenic Effects: produce birth defects or impair fertility • Defects include behavioural & metabolic defects • Sensitivity to teratogens changes during development. • Gross malformation typically occurs in the 1st trimester • Exposure during 2nd + 3rd trimesters usually disrupts function as opposed to gross anatomy • Drug transfer across placenta is greatest in 3rd trimester (surface area for transfer between maternal & fetal circulation increases as placenta develops) o

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Main Neurotransmitters to Know Acetylcholine (Ach) – found throughout nervous system; sends + received information between the motor neurons and voluntary muscles (muscles you have conscious control over). Every movement you make depends on the release of Ach from your motor neurons to your muscles Dopamine (DA) – used by neurons to make voluntary movements + movements in response to emotion. Also plays role in pleasure/reward system in brain. Also crucial in focus + memory Norepinephrine (NE) – regulates mood + arousal (known as the stress hormone); Used in fight or flight - NE increases O2 to brain, increases HR and BP when needed, shuts down metabolic processes in stressful events to preserve energy, etc. Serotonin – plays large role in mood, sleep, wakefulness, and eating behaviours GABA + Glutamate – These 2 are the most plentiful neurotransmitters in the brain. GABA produces an inhibitory postsynaptic potential; it decreases the likelihood that a neuron will fire an action potential. Inhibitory = allows for us to stay calm/not overwhelm ourselves Glutamate produces an excitatory postsynaptic potential; it increases the likelihood that a neuron will fire an action potential. Excitatory = contributes to learning + memory

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AUTO AUTONOMIC NOMIC NERVOUS SSYSTEM YSTEM DRUGS Autonomic nervous system (ANS) regulates involuntary functions including heart rate, respiratory rate, and digestion by balancing sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) Choli Cholinergic nergic drugs Promotes action of neurotransmitter acetylcholine (Ach) = increase in Ach Stimulates PNS – rest & relaxation 1. Cholinergic agonist • Mechanism of Action (M OA): stimulates cholinergic receptors (mimics action of Ach) → allows body to ‘rest & relax’ • Produces these effects: salivation, bradycardia, dilated blood vessels, constriction of bronchioles, increased GI activity, increased contraction of bladder muscles, and constriction of pupils • Used for: weak bladder, abdominal distention, constriction of pupils/high eye pressure, and hypofunction of salivary gland • Side effects: nausea (N)/vomiting (V)/diarrhea (D), blurred vision, bradycardia, hypotension, SOB, urinary frequency, increased salivation, diaphoresis, corneal clouding, abdo pain/cramps, and flushing • Rarely administered by IV/IM route due to immediate breakdown by cholinesterase and due to potential of cholinergic crisis (extreme muscle weakness + possible paralysis of respiratory muscles) Drug Acetylcholine → Miochol E Bethanechol → Urecholine Carbachol → Miostat Pilocarpine → Isopto Carpine, Pilocar

Ch Cholinergic olinergic drugs Indica Indication tion Nursing Constriction of pupil during ocular Instill into anterior chamber of eye surgery Urinary retention Potential for influx infection if the sphincter doesn’t relax Glaucoma, inhibition of Instill to anterior chamber of eye. perioperative intraocular pressure Contraindicated in inflammation of anterior chamber Xerostomia (dry mouth) Inform pt that blurred vision can impair driving, particularly @ night

2. Anticholinesterase drugs • MOA: normally, Ach is broken down by the enzyme acetylcholinesterase. By destroying this enzyme, more Ach accumulates → allows body to ‘rest & relax’ • Used to: decrease eye pressure, increase bladder tone, improve peristalsis, promote contraction in myasthenia gravis, diagnose myasthenia gravis, and temporarily improve dementia • Side effects: arrhythmias, N/V/D, seizures, headache, anorexia, pruritius, urinary frequency, induction of preterm labor, SOB • Build-up of Ach can precipitate cholinergic crisis (S/S: abdo cramps, N/V/D, pupillary miosis, hypotension, increased secretions/salivation/perspiration, bronchospasm, bradycardia) • When quick effect is needed = use IV/IM route Drug Donepezil → Aricept

Anticholine Anticholinesterase sterase drugs Indica Indication tion Nursing Alzheimer’s Disease Important to take daily at same time (usually before bed)

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Edrophonium → Enlon Galantamine → Razadyne Neostigmine →Prostigmin Pyridostigmine → Mestinon Rivastigmine → Exelon Tacrine → Cognex

Diagnosing Myasthenia Gravis (MG), reversing a nondepolarizing neuromuscular blocker Alzheimer’s disease Myasthenia Gravis, post-op distention or urinary retention Myasthenia Gravis, reversal of muscle relaxants Alzheimer’s disease Alzheimer’s disease

If muscle weakness occurs during MG diagnosis test, discontinue drug and give atropine IV Administer twice daily (morning and evening) with food Contraindicated in peritonitis or mechanical GI obstruction Contraindicated in mechanical GI or urinary obstruction Take at regular intervals. Remind pt that drug can cause dizziness; avoid driving Can cause hepatic impairment – monitor LFTs

Anticholinerg Anticholinergic ic d drugs rugs Also known as cholinergic blockers Interrupt PNS impulses; prevent Ach from stimulating cholinergic receptors = decrease in Ach These drugs will do the OPPOSITE of above cholinergic drugs • MOA: Competitively inhibits the action of Ach • Used to: treat nausea, treat Parkinson’s, relax the GI and GU system, manage headaches, dilate the lungs, dilate the eye, and increase heart rate • Side effects: dry mouth, dry eyes, dry nasal passage, blurred vision, urinary hesitancy or retention, constipation, tachycardia • Contraindicated in: narrow angle glaucoma, hemorrhage, tachycardia, and myasthenia gravis Anticholine Anticholinerrgic gicss Drug Atropine

Ipratropium → Atrovent

Scopolamine → Scopace Glycopyrrolate → Robinul Benztropine → Cogentin

Dicyclomine → Bentyl Oxybutynin → Ditropan XL

Indica Indications tions Symptomatic sinus bradycardia

Nursing Monitor ECG and heart rate (can cause increased HR and ventricular ectopy). Also monitor intake + output due to possible retention COPD, acute asthma exacerbation Administered via nebulizer or inhaler. If administered with other inhalers, administer adrenergic bronchodilators first, followed by ipratropium, then corticosteroids. Wait 5 min between each Nausea, vomiting, motion sickness Administered via transdermal patch, IV, IM, or prophylaxis, chemotherapy induced N & V SC. Contraindicated in closed angle glaucoma Pre- and post- op reduction of saliva, drooling May increase GI lesions in patients taking oral potassium chloride tablets. Monitor intake + output – can cause retention Parkinsonism, drug-induced extrapyramidal PO dose to be taken with food. Therapeutic disorders (S/S: restlessness, rigidity, tremors, effects seen in 2-3 days. Frequent rinsing of pill rolling, masklike face, shuffling gait, muscle mouth will decrease dryness. spasms, twisting motions, difficulty speaking, loss of balance) Irritable bowel syndrome (IBS) Administer 30 mins before meals and at bedtime. Monitor intake + output due to possible retention. Monitor for drowsiness Overactive bladder (incontinence, frequency, Administered PO, transdermal patch, or urgency) transdermal gel. Contraindicated in glaucoma, intestinal obstruction, and urinary retention

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Tolterodine → Detrol

Overactive bladder (urge incontinence)

Assess for rash during therapy; can cause Stevens-Johnson syndrome. Stop medication if accompanied with fever, general malaise, fatigue, muscle or joint aches, blisters, oral lesions, conjunctivitis, or hepatitis. High doses can cause prolonged QT complex

Adrenergi Adrenergicc drugs Also called sympathomimetic drugs Produce effects similar to SNS – fight or flight = increase in norepinephrine (NE) • MOA: direct acting adrenergic = the drug directly stimulates adrenergic receptors. Indirect acting adrenergic = drug stimulates the release of norepinephrine from nerve endings • Receptor sites: o Alpha1 adrenergic receptors = cause vasoconstriction, papillary dilation, closure of sphincter and bladder o Alpha2 adrenergic receptors = cause decreased SNS activity, reduced NE release, insulin release o Beta1 adrenergic receptors = located in heart; cause increased HR and increased force of contraction o Beta2 adrenergic receptors = cause vasodilation, bronchodilation, increased release of glucagon o Dopamine receptors 1. Catecholamines • Primarily direct-acting adrenergics • Produce these effects: constrict blood vessels, increase heart rate, increase blood pressure, and dilate bronchi • Catecholamines are positive inotropes (make heart contract more forcefully) and positive chronotropes (make heart beat faster) • These drugs aren’t taken PO due to quick destruction by digestive enzymes • Side effects: dry mouth, N/V, CNS stimulation, appetite suppression, increased HR, bronchodilation, decreased blood flow to GI, pupil dilation, increased glucose levels • Contraindicated: uncorrected tachyarrhythmias Drug Dobutamine → Dobutrex Dopamine

Epinephrine → Adrenalin, Epi-Pen

Catecholamines Indica Indication tion Nursing Cardiac decompensation, low cardiac Stimulates beta1 receptors. Administer drug output into large vein; monitor site for inflammation + pain. Perform independent double check Hypotension, low cardiac output, poor Stimulates dopaminergic and beta1 perfusion of vital organs receptors. Administer drug into large vein; Low dose: increases urine output + renal monitor site for inflammation + pain. blood flow Perform independent double check. Medium dose: increases renal blood flow, cardiac output, heart rate, and heart contractility High dose: increases BP, potential risk of tachyarrhythmias Cardiac arrest, hypotension due to septic Stimulates beta1 and beta2 receptor. Can shock, anaphylaxis, symptomatic cause paradoxical bronchospasm (wheezing) bradycardia, management of asthma and with overuse of inhaler. Teach pt using COPD autoinjector about proper placement (into

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thigh @ right angle to leg, hold for 10 sec). Perform independent double check. Stimulates alpha receptors mostly; minor beta activity. Overdose can result in severe peripheral vasoconstriction with resultant ischemia and necrosis of peripheral tissue Stimulates beta1 and beta2 receptors.

Norepinephrine Acute hypotension, cardiac arrest, septic → Levophed shock

Isoproterenol hydrochloride

Shock, bronchospasm during anesthesia

2. Noncatecholamines • Can be direct-acting, indirect-acing, or dual-acting • Produce these effects: local or systemic vessel constriction, nasal/eye decongestion, dilation of bronchi, and smooth muscle relaxation • Can be taken orally, and have longer half life • Contraindicated: Monoamine oxidase inhibitors (can cause severe hypertension), tricyclic antidepressants (can cause hypertension + arrhythmias) • Side effects: headache, irritability, trembling, seizures, hypertension, palpitations, tachycardia, arrhythmias, flushing, angina Noncatechola Noncatecholamines mines Drug Indica Indication tion Phenylephrine Severe hypotension/shock

Albuterol → Ventolin

Bronchospasm

Salmeterol → Serevent Diskus

Asthma prevention and maintenance, COPD maintenance, prevention of exercise induced asthma

Terbutaline

Bronchospasm, pre-term labor (this drug will stop contractions)

Nursing Stimulates alpha receptors. Can cause severe bradycardia + decreased cardiac output due to increase in afterload Stimulates beta2 receptor. Can cause paradoxical bronchospasm with excessive inhaler use Stimulates beta2 receptor. Do not use to treat acute symptoms. Should only be used for patients not adequately controlled on other asthma controller medications; long term use can increase risk of asthma-related death Stimulates beta2 receptor. Should not be used in pregnancy for the prevention of prolonged treatment (48-72 hr) of preterm labor

Adrenergi Adrenergicc blocking drugs Also called sympatholytic drugs Block the effects of SNS = decrease in NE 1. Alpha adrenergic blockers (alpha blockers) • Interrupts action of epinephrine (E) and NE at alpha receptors • MOA: blocks the synthesis/storage/release/reuptake of NE, or the drug will antagonize E, NE, or adrenergic drug at alpha receptor site • Produces: relaxed/dilated blood vessels, decreased BP • Side effects: orthostatic hypotension, reflex tachycardia, nasal congestion Alpha Blockers Drug Doxazosin → Cardura

Indica Indication tion Hyperten...