Ch.1 – Intro to pharm
Pharmacology: the study of medicines
Pharmacotherapy: The application of drugs for prevention of treatment
Role of the nurse:
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... [Show More] �� Initial Assessment –Do you even need this drug?
• Intervention – administering drugs
• Reassessment – Did the drug help?
Pharmacokinetics: what the body does to the drugs after administered.
Pharmacodynamics: what the drug does to the body
Therapeutic classification: what is being treated by the drug – the disease.
Ex: anticoagulants, antihypertensive, antihyperlipidemics
Pharmacologic classification: How the drug acts – how it works
Ex: Diuretic, Calcium channel blocker, vasodilator, adrenergic antagonist (blocker)
*Drugs have chemical, generic, and trade names (Only 1 generic name but many trade names)
Ch. 2 – Drug regulations
Bioavailability: the % of the drug that makes it to the action site.
Drug Approval: Regulated by the FDA
• Preclinical research – lab setting (test tubes, bottles, animals)
• Phase 1 Clinical – 20-80 healthy people (mainly looking for safety)
• Phase 2 Clinical – 100’s of people that have disease, Placebo and Experimental group (looking for safety and advocacy – does drug work)
• Phase 3 Clinical – 1000’s people (looking for safety and variations – multicenter)
• Postmarketing surveillance – Adverse event report system implemented, possibly millions taking drug (looking for safety)
Drug Schedule: 5 classes
• Class 1 – Highest (Heroin, marijuana) – no prescriptions written
• Class 2 – High (Potent opioids, fentanyl, methodone, morphine) – monitored carefully and usually no refills given
• Class 3 – Moderate (low dose codeine, low dose hydrocodone, anabolic steroids) – 5 refills allowed within 6 months
• Class 4 – Low (Benzodiazepines, tramadol, barbiturates) 5 refills allowed in 6 mo
• Class 5 – Lowest (cough medicines, anti-diarrheal) – refills allowed
Ch. 3 – Pharmacokinetics
Process of pharmacokinetics: use diffusion and active transport to cross plasma membranes. Movement of a chemical from higher concentration to lower concentration
Factors: Size of drug molecule (small can penetrate), Ionization of molecule (non-ionized can penetrate), Lipid solubility (lipophilic can penetrate)
Drug ionization: most drugs are charged or uncharged (acid absorbed in acid= non-ionized. Base absorbed in base=ionized)
Drug interactions: drug-drug or drug-food, can affect absorption, high fat slows motility
*Higher doses produce faster, greater response to drugs, greater concentration gradient for diffusion.
Absorption: Movement from site of administration to the bloodstream.
Primary site is small intestine (due to large surface area)
Presence of food slows absorption
Where blood flow is high=drugs absorbed faster
Route of administration:
• Enteral – Drugs delivered to the GI tract (oral, NG tube, or G tube)
• Tablets and capsules – must dissolve before drug is avail for absorption, slow onset time. Oral liquid – absorbed faster
Enteric-coated – hard, way coating to resist stomach acid (Do not crush)
Extended release – dissolve slowly for longer duration of action.
(Do not crush them) more gentle on the body
• Oral disintegrating tablets or oral soluble films
• Sublingual and buccal routes – not subjected to stomach acid or first pass effect, meds kept in mouth
• NG and G tubes – liquid form administered thru devices. (Do not use sustained release medications)
*If multiple meds are ordered, give oral meds first then administer sublingual meds.
First pass effect – Body has its own mechanism to destroy meds. Drugs absorbed from the stomach and small intestine, travel to liver, where they may be inactivated before reaching target organ.
• Topical – applied to skin, mucous membranes, local effects, can have slow release
• Transdermal patches (expensive) – specified amt of med., rate of delivery can vary. Slow release or generalized relief
• Ophthalmic – local conditions of eye, surrounding structures
• Otic – ear drops – meds should be room temp.
• Intranasal – nasal spray – great place for drug delivery but mucus secretion unpredictable
• Vaginal – local conditions for birth control (IUD)
• Rectal – local or systemic, safe & effective for coma pts., avoids first pass effect – suppository or enema
• Parenteral – intradermal (shallow) or subcutaneous (deeper) – dermis contains more blood vessels – given via injection into the skin
• Intramuscular – delivered into muscles, more rapid onset of action, muscles can receive larger volume of drug (insulin, heparin, vitamins, vaccines)
• Intravenous – directly into bloodstream, fastest onset of action but most dangerous
Distribution: how drugs are transported throughout the body
Primary site is Protein
Factors: blood flow to tissues, drug solubility, tissue storage, drug protein binding
Drug Protein binding:Drug-protein complexes cant cross capillary membranes, can bypass stomach
o Only unbound drugs reach target tissues
o If person has high protein in body, they have less free drug and lots of drug-protein complexes which alters penetration = needing a higher dose drug
o If person has low protein in body, they have more free drug and less complexes which allows for more penetration = needing a lower dose drug Normal albumin levels (3.5 – 5.0)
Blood Brain Barrier: No pores, protects brain from pathogens and toxins, lipid soluble drugs can cross, inflammation can cause increased permeability.
Fetal-placental barrier: keeps harmful substances from getting to fetus via mothers bloodstream.
Metabolism: process that changes the activity of the drug and makes it more likely to be excreted. Alters structure and function of drugs, nutrients, vitamins, and minerals. Functional changes alter pharmacological activity.
Primary site of metabolism is Liver(run hepatic panel for liver function)
Prodrugs (drug + inactive component): meds that require metabolism to produce therapeutic effect. Therapeutic – not pharmacologic
Liver diseases – cant metabolize drugs so they need a lower dose
Hepatic microsomal enzymes: Cytochrome P450 (CYP) – enzyme that metabolizes many drugs – contribute largely to drug-drug interactions
Drugs as substrates – drugs metabolized by CYP enzyme
Drugs as enzyme inhibitors – shuts down enzymes, can lead to toxicity
Drugs as enzyme inducers – speeds up enzymes, activates the metabolism of specific enzymes, drug levels may decrease rapidly
CYP 450 inhibitor: Result- inhibitor slowed down metabolism creating more absorbed med leading to overdose of drug
CYP 450 inducer: Result – inducer sped up metabolism creating less absorbed med.
*Note: enzyme activity slowed in elderly, decreased metabolism with liver impairment – elderly need lower dose drugs
Excretion: the removal of drugs in the body
Primary site is kidney
Some drugs undergo reabsorption, can manipulate pH of kidney filtrate
Phases:
• Renal – dose reduction indicated in renal impairment
• Pulmonary – gases and volatile liquid, most excreted unmetabolized, affected by resp. rate and blood flow
• Glandular – Saliva, sweat, breast milk, taste and smell of some drugs
• Fecal and biliary – feces, bile, enterohepatic recirculation (may recirculate drugs, metabolites, and prolong action
*When pt has kidney failure – they can’t rid the body of meds so the drug builds up creating toxicity. Run eGFR blood test to check for kidney function. Test determines how fast kidney filters blood to produce urine.
• > 60 – normal
• 50-60 – stage 1 renal failure
• 40-49 – stage 2
• 30-39 – stage 3
• 20-29 – stage 4
• < 20 – transplant needed
Time-Response Relationships: the therapeutic response of most drugs depends on their concentration in the plasma.Also, the drug half-life estimating the duration of action for most medications. Repeated dosing allows a plateau drug level to be reached
Minimum effective concentration: amt of drug required to produce a therapeutic effect
Therapeutic range: the range where the drug produces a desired effect
Toxic concentration: level of drug that results in serious adverse effects – toxicity
Ex: 12-46 – daily labs can show the peak and trough
If 5 is shown – they need more drug, if 50 is shown, they need less drug
Drug half –life: Provides estimate of duration of action, plasma half-life (t½)
• Short half-life – drug given more frequently
• Long half-life – drug given less frequently
• Approx. 4 (½) until excretion – most of the drug is out of the body
Peak and trough levels – peak is highest, trough is lowest – used for monitoring safety for drug
Loading dose: higher amt given to “prime” bloodstream
• Ex: Z-pack
Maintenance dose: to keep concentration within therapeutic range
Ch. 4: Pharmacodynamics
Median effective dose (ED50) – Desired drug response in 50% of pts.
• Avg dose predicts therapeutic response in 50%
Median lethal dose (LD50) – lethal to 50% of test pts.
Therapeutic Index – describes the drug’s margin of safety – ratio of drugs (LD50) to its (ED50)
• Drug A – LD50/ED50 = 40/10 = 4 (2 pills will save you 4 pills will kill you) – less dangerous
• Drug B – LD50/ED50 = 20/10 = 2 (1 pill will save you, 2 pills will kill you) – more dangerous
• Higher the medication, the less dangerous it is
Median toxicity dose – produces toxicity in 50% of pts.
Margin of Safety (MOS) – the amt of drug that is lethal to 1% of animals divided by amt of drug that produces a therapeutic effect in 99% of animals
Dose-response relationship – how the actions of a drug change with increasing dose
• Phase 1: lowest doses – often doesn’t work
• Phase 2: most desirable range
• Phase 3: plateau reached – more saturated, increasing dose could cause toxicity
Receptor Theory: most drugs produce their actions by activating or inhibiting specific, cellular receptors
• Receptor – cellular molecule to which a medication binds to produce its effects
• Intrinsic activity – when the drug has the ability to bind to the receptor and produce strong action
Agonist: (full) – mimic action of endogenous substances (mimic exactly) – may be greater response than the original action (partial) – produce weaker action than endogenous substances, doesn’t mimic exactly but partially mimics it.
Antagonists: Prevents action of endogenous substances, may compete with agonists, useful in blocking excess endogenous activity, and may reverse adverse effects of overdose. Does NOT have intrinsic activity (cant bind to the receptor to produce strong action). Your body doesn’t make antagonists.
Ch. 5 - Adverse Drug effects
Adverse Effects: undesirable, potentially harmful
Side effects: are predictable, can occur at therapeutic doses for most people
Serious side effects: Can result in death, can cause congenital abnormalities, can cause life threatening events, require interventions, and require report by nurse
Prevention of side effects: watch carefully, obtain past medical history, prevent med. Errors, and know all drugs taken by patient. Question unusual orders, be prepared
*Always check med because different Dr’s can prescribe diff. drugs – also watch for dosage orders.
Allergic reactions: caused by a hyper-response of the immune system, are non-specific to drug. Anaphylaxis has same symptoms for all drugs (airway swelling, stop breathing)
• Common allergic drugs: Penicillin and related antibiotics, Insulin, Radiologic contrast media with iodine, NSAID’s, Chemotherapy, preservatives
Idiosyncratic reactions: unusual drug responses caused by genetic differences among pts., unusual or unexpected responses, rare, unpredictable, unrelated to action of drug
*People can be allergic to the inactive components of generic brands versus real brand
Risk-benefit ratio: drug benefit outweighs long term risk (i.e. cancer drugs)
Carcinogenic drugs: Damage DNA-leads to mutation, effects may not be seen for yrs. (drugs that have cancer risk: Antineoplastic, immunosuppressant’s, hormone and hormone antagonists)
Teratogens: causes birth defects (ex: anti-seizure & epileptic drugs)
Adverse Effects by system:
• Nephrotoxicity – majority of drugs excreted thru kidneys. (Symptoms: dehydration, abnormal lab values, history of renal impairment)
o Ex: -myacin drugs and long term use of diuretics (look at eGFR test)
• Neurotoxicity – BBB controls access, brain very sensitive, (Symptoms: Drowsiness, seizure activity, coma)
o Note changes in behavior, seizures, delirium
o Ototoxicity – hearing impairment due to damage of acoustic nerve #8
• Hepatotoxicity – Liver detoxifies majority of drugs, monitor liver function tests (panel), signs can be vague and can cause toxic drug levels
o Ex: Cholesterol meds can cause liver toxicity
• Dermatologic – very predictable, common (symptoms: rash with pruritus, Urticaria can lead to anaphylaxis, photosensitivity, Steven-Johnson syndrome (death of skin cells-rare)
• Cardiotoxicity – Prolongation of QT interval on ECG, EKG is common way to check
o Ex: Antineoplastic meds – can cause rare type of ventricular tachycardia which causes sudden death.
• Skeletal muscle and tendon toxicity – Monitor CK (creatinine kinase) – should be low or none – if elevated muscles can be toxic due to breakdown of muscle that leaks into bloodstream, monitor ECG’s, unexplained muscle pain
o Ex: statin and cholesterol meds
Drug Interactions: Drug-drug, drug-food, often go unnoticed, may or may not be harmful
• Mechanisms: effect on drug
o Inhibition: decreases therapeutic action
o Enhancement: provides greater therapeutic response
Pharmacokinetic Variable Type of Interaction Potential Drug Effect
Presence of food Decreased
Alteration of pH Variable
Absorption Drug-Drug binding Decreased
Increased peristalsis Variable
Slowed gastric emptying Variable
Displacement of drug
Distribution from plasma protein Increased
binding site
Stimulation of CYP enzyme Decreased
Induction
Metabolism
Inhibition of CYP enzyme Increased
inhibition
Increased Excretion Decreased
Excretion
Decreased Excretion Increased
• Food-drug interactions: Absorption and bioavailability affected
o Ex: Grapefruit juice and CYP3A4 enzyme
o MAOI – not compatible with any drugs (Nardil – antidepressant)
*Never give an agonist and an antagonist for the same receptor (giving a drug that constipates and one that causes diarrhea
Ch. 10 – Pharmacotherapy of the Geriatric patient
Polypharmacy: use of multiple meds (very common in the elderly) – increases risk of drug interactions
*ASK the pt to disclose ALL medications and supplements
*the elderly – everything slows down
• GI-system – decreased motility, pH and blood flow decreases, absorption decreases
• Cardiovascular – Heart muscle weakens, cardiac output decreases, B/P increases
• CNS: brain mass decreases, quantity of neurons decrease, BBB easily penetrated
• Renal system: Blood flow decreases. Fewer functional nephrons, renal function declines (Glomerular filtration rate decreases – results in prolonged exposure to certain meds) Excretion decreases
• Metabolism – liver function declines, decreased drug binding to plasma proteins
*Fewer receptors due to aging so they may not respond to the meds. Give them a lower dose of a more potent med to reach therapeutic level
Adherence (Compliance): regimen is a challenge for the elderly
• Potential barriers – Visual, hearing, functional impairment, cognitive dysfunction
• Drug misuse – overuse, underuse, erratic use – may be accidental or deliberate, self adjusting dose is common, splitting doses to make expensive med last longer
Medications may cause:
• Sudden change in mental status, rapid weight loss, dehydration, restlessness, Anorexia, changes in bowel habits and fluid balance, retention, functional status change in any systems
Ch. 41 – Pharmacotherapy of Inflammation and Fever
Inflammation: the response to agents that could damage tissues, it’s a symptom, usually self-limiting (acute), treat the underlying cause
• Acute: Lasts 1 week – 2 months, Immediate onset, caused by influx of neutrophils, pain and edema (most of the time is localized) result.
• Chronic: may last years, scar tissue can result, slow onset, caused by lymphocytes and macrophages
• Both types may have febrile response: Body temp over 102F, pulse over 90bpm, WBC count over 12,000
• Nonspecific inflammation: treated with NSAID’s and Corticosteroids, Fever: treated with antipyretics
NSAID’s: 3 major classes (Salicylates, Ibuprofen, COX-2 inhibitors) – Mild to moderate pain
Salicylates (Aspirin) – works by suppressing synthesis of prostaglandins by inhibiting COX (suppresses – antagonist)
Ibuprofen (Motrin, Advil) – inhibits COX-1 and COX-2, which block prostaglandin synthesis and modulate T-cell function, Inhibits cell chemotaxis
COX – 2 (Celebrex): primarily for inflammation – 2nd generation anti-inflammatory, Selectively inhibits the enzyme COX-2 (inhibits COX-1 (primarily in stomach, gastro protection) just a little
For NCLEX purposes Acetaminophen (Tylenol) listed as an NSAID: Inhibits COX-2 (very little COX-1), inhibits chemical mediators for pain, Direct action on the heat regulating hypothalamus.
Ch. 44 – Asthmas and other pulmonary disorders
Resp. system: involves 2 main processes – perfusion(O2 entering bloodstream, CO2 exiting bloodstream) and ventilation (air moving in and out of lungs).
Respiration:O2 is brought into the body and CO2 is removed
Pulmonary perfusion: blood flow thru the lung (Note: for a ventilator to work, pt must have some perfusion, if a person is blue they have poor or no perfusion)
• Alveoli: sacs at end of bronchial tree – responsible for gas exchange
• Bronchioles: elastic tubes leading from outside of alveoli
Nervous system controls ventilation
• Sympathetic – bronchiolar muscles relax and bronchodilation occurs
o Give an agonist
• Parasympathetic – bronchiolar muscles contract and bronchoconstriction occurs
o Give an antagonist
o Bronchospasm – airway makes smooth muscle hyperresponsive to stimuli drugs targeted to relax smooth muscle
o Thick, viscous secretions block the airway – drugs involve antibiotics or mucolytic (Musinex)
o Edema – engorgement of pulmonary blood vessels – drugs include diuretics and drugs to enhance cardiac function
o Less free space for the O2 to travel
Asthma: chronic inflammation resulting in airway edema, increased mucous secretions
• Status asthmaticus: emergency situation which asthma is unresponsive to drug treatment – can lead to respiratory failure – intubate the pt. with ventilator
Inhalation drugs: Aerosol therapy – delivers drugs directly to the site of action thru particles suspended in gas
• Delivery route
o Metered-dose inhaler (MDI), Dry powder inhaler (DPI), Nebulizer
• Two simple classes of asthma drugs
o Abortive – Quick relief medications (beta2 – agonist)
Only Beta2 agonist can be used for abortive therapy
o Preventative – long term control medications
Stepwise approach to managing asthma: (step 1- mild attack thru step 6 – severe attack) Treatment range from:
• ICS ( inhaled corticosteroid)
• LABA (long-acting beta2 agonist) – Serevent: bronchospasm in COPD
• LTRA (leukotriene receptor antagonist)
• SABA (inhaled short acting beta2 agonist) – Albuterol: Acute asthma
Beta2 adrenergic agonists – activate the sympathetic nervous system, causing bronchodilation
• Listen to lung sounds before and after treatment
Beta Blockers antagonists – closes bronchial tubes.
• Are used for high blood pressure, anxiety, and migraine headache
• Do not give to asthma pts
Inhaled anticholinergics antagonists – are used for preventing bronchospasm
• Opens up bronchial tubes but works on the parasympathetic system
• Atrovent (inhaler) – Blocks cholinergic receptors in bronchial smooth muscle
• Tiotropium (Spiriva) – long duration of action, can reverse progression of asthma (preventative use only)
Inhaled corticosteroids – most effective for long term control, preventative only- suppresses inflammation w/o major adverse effects
• Beclomethasone (Beconase AQ, OVAR)
o Nursing responsibilities – always give water for pt to rinse mouth out after
o Can cause fungal infection (Candidiasis)
• Fluticasone (Flovent)
o Intranasal (allergic rhinitis)
o Oral inhalation (asthma, COPD)
Leukotriene modifiers – primarily used for prophylaxis – reduce inflammation by either blocking enzyme that controls leukotriene synthesis or by blocking leukotriene receptors
• Delayed onset – oral pill, not inhaler
• Montelukast (Singulair)
Methylxanthines– rarely prescribed for asthma, used for long term management of persistent asthma that is unresponsive to beta agonists or inhaled corticosteroids, Risk for toxicity
• Theophylline (TheoDur) – bronchodilator – very narrow margin of safety
o Check serum levels regularly
COPD- progressive pulmonary disorder – chronic and recurrent obstruction of airflow
• Chronic Bronchitis – Excess mucus produced in lower resp tract
• Emphysema – loss of bronchiolar elasticity and destruction of alveolar walls
• Treatment – Mucolytics and Long term Oxygen therapy
• All asthma meds can be used to treat COPD
Ch. 45 – Pharmacotherapy of Allergic Rhinitis and the Common cold
Common cold – caused by a viral infection of upper resp tract – self limiting
Pathology of Allergic Rhinitis
• Exposure to pollen – Plasma cells release IgE antibodies – IgE antibodies bind to mast cells – Pollen binds to IgE antibodies and causes histamine release – histamine causes allergy symptoms
• Preventors – used for prophylaxis
o Antihistamines – H1 receptor antagonists block main histamine receptors
Fexofenadine (Allegra) second generation H1 receptor antagonist
Cetirizine (Zyrtec) second generation
Desloratadine (Clarinex) second generation
Diphenhydramine (Benadryl) first generation (drowsiness)
o Intranasal corticosteroids – applied directly to nasal mucosa – prevent or reduce symptoms
Fluticasone (Flonase)
• Relievers – used for acute symptom relief
Oral
Singulair – blocks leukotriene receptors
o Decongestants – constricts blood vessels causing airway to open relieving nasal congestion
Intranasal sympathomimetic – immediate relief – habit forming
Oral sympathomimetic – eliminates rebound effect
Pseudoephedrine (Sudafed)
Antussives – drugs used to suppress the cough reflex
• Dextromethorpan (Robitussin DM, Delsym)
• Benzonatate (Tessalon) – pearls – suppresses cough reflex by anesthetizing stretch receptors in lungs
Expectorants and Mucolytics – to treat thick bronchial secretions
• Guaifenesin (Mucinex) – Expectorant
• Acetylcysteine (Mucomyst) – Mucolytic
Ch. 12 Neurotransmitters and the Autonomic Nervous system
Nervous Systems – CNS (Brain and spinal cord), PNS (somatic – voluntary & autonomic (ANS) – involuntary – nerves that carry messages to and from the CNS)
• Neurons (Sensory and motor)
Autonomic Nervous System (ANS)
• Sympathetic – fight or flight*
• Parasympathetic – rest or digest*
*Both systems are active at the same time – Can give agonist or antagonist for both systems (4 classes)
Homeostasis* – achieved by changing one or both branches (Autonomic tone)
• Increasing the firing of sympathetic nerves *Body will achieve this
• Decreasing the firing of parasympathetic nerves naturally
Neurotransmitters – the more released, the more intense and longer lasting the response
• Once done can either diffuse or can be recycled back through the reuptake mechanism (pump) into the 1st preganglionic neuron
• Also can be terminated by enzymes for metabolism that degrade the neurotransmitter
Synaptic transmission – allows info to be communicated between 2 nerves to muscles and glands
• Two neuron chain (preganglionic – 1st neuron, postganglionic – 2nd neuron)
• Synapse – space between 2 neurons where neurotransmitters travel
• Neuroeffector junction – specialized synapse where postganglionic neuron can terminate
Classifying Autonomic Drugs – Four possible actions
• 1. Stimulation of sympathetic nervous system
o Sympathomimetics
o Adrenergic-agonists
• 2. Stimulation of parasympathetic nervous system
o Parasympathomimetics
o Muscarinic agonists
• 3. Inhibition of sympathetic nervous system
o Adrenergic antagonists or blockers
• 4. Inhibition of parasympathetic nervous system
o Anticholinergics
o Parasympatholytics
o Muscarinic blockers
Two primary ANS neurotransmitters – made in advance – stored in vesicles – when needed vesicles burst and release chemicals
• Norepinephrine (NE) – blood pressure
o Adrenergic transmission – receptors at end of postganglionic sympathetic neurons, secreted by adrenal medulla in adrenal gland
o Adrenergic Agonists – activate sympathetic system to produce fight or flight
Directly – binds to and activates adrenergic receptors
Indirectly – increases amt of NE, available at adrenergic synapses
Catecholamines– short duration, given parenterally or inhalation, no BBB
Noncatecholamines– by mouth, crosses BBB, lasts longer
NonSelective– activate both alpha and beta receptors – treat bronchospasm, cardiac arrest, hypotension
1. Epinephrine (adrenalin) – stimulates both alpha and beta – nonselective catecholamine
2. Dopamine (dopastat) – nonselective – noncatecholamine
3. Droxidopa (Northera) pill- nonselective – noncatecholamine (treats orthostatic hypotension)
Alpha1– excitatory effects – intense vasoconstrictive effect leading to hypertension
Drugs used for hypotension, nasal congestion
Topical for the eye
1. Phenylephrine (Neosynephrine) – selective
2. Midrodrine (ProAmatine) – selective - noncatecholamine
Alpha2 - inhibitory effects – act in CNS to decrease sympathetic activity
Inhibits NE release, treat hypertension
Beta1– receptors – critical care drugs (heart attack, failure)
heart, coronary vessels, kidneys – increase HR and force of contraction of heart
Beta2 - receptors – treat asthma
GI tract, lungs, arterioles
1. Isoproterenol (Isuprel) – bronchodilator
2. Albuterol (Ventolin)
o Adrenergic antagonists – blocks the effects of NE at adrenergic receptors – lower BP
Alpha1 – blocker – blocks vasoconstriction in veins, relax smooth muscle of bladder and prostrate, used to treat hypotension and BPH
1. Tamsulosin (Flomax) – BPH - selective
2. Prazosin (Minipress) – HTN - selective
3. Doxazosin – antihypertensive & BPH - selective
Alpha2 – blocker
Beta1 – blocker
1. Propanolol (Inderol) – anti hypertensive – nonselective
2. Metoprolol (Lopressor) – anti hypertensive - selective
Beta2 – blocker
o Terminated by Reuptake pump and enzymes MAO and COMT
o Pheochromocytoma – adrenal gland caner which causes an abundance of NE and epi. To be made (BP rises very high – run blood test to check epi levels and check urine to see if it overflowed into urine)
• Acetylcholine (Ach) – muscles
o Cholinergic transmission – Ach is the neurotransmitter released by cholinergic receptors
o Cholinergic agonists – drugs that increase action of Ach at cholinergic receptors, promoting rest and digest responses
Direct cholinergic agonists – releases Ach into the synaptic cleft, drug binds to Ach receptors, enhancing action potential – drug inactivated by AchE
Indirect cholinergic agonists – drug binds AchE, preventing Ach from being destroyed, AchE inhibitors
Muscarinic agonist – stimulates cholinergic receptors (Location: parasympathetic target, organs except heart – stimulation of smooth muscle and gland secretions, decreased H/R and force of contraction)
Bethanechol (Urecholine)direct acting– urinary system
Pyridostigmine (Mestinon) – indirect acting – Myasthenia Gravis
Myasthenia Gravis – progressive, grave muscular weakness, difficulty in chewing, swallowing, speech, and vision (Diagnosed by anti-acetylcholine receptor antibody test. If unclear, edrophonium test – give mestinon via IV, wait a few min., have them walk, if they can – its +)
Nicotinic agonist – activates Ach receptors at the ganglia – smoking (Location: postganglionic neurons and neuromuscular junctions of skeletal muscle – stimulation of smooth muscle and gland secretions)
Used primarily in nicotine replacement therapy – tobacco cessation
o Terminated by Acetylcholinesterase (AchE) – destroys Ach
o Cholinergic Antagonists – block the effects of Ach at muscarinic or nicotinic receptors, inhibit the action of Ach
Muscarinic antagonists – block receptors in the parasympathetic nervous system (anticholinergics, cholinergic blockers)
atropine (Atropen) – helps start heart and deal with bradycardia
Nicotinic antagonists – neuromuscular blockers – inhibit transmission at neuromuscular junctions in skeletal muscle – produce muscle paralysis
**Vecuronium (Norcuron) – used for short term procedures – Paralysis of pt.
Ch. 21 – pharmacotherapy of degenerative diseases of the CNS
• Parkinson Disease – abnormal motor movement, fatigue, slow movement, tremors, muscle rigidity, bradykinesia (slowness of voluntary movement and speech, difficulty chewing, swallowing, speaking, shuffling gait) – insufficient amounts of dopamine
*when dopamine is depleted, Ach becomes dominant which stimulates the muscles which cause tremors.
o Treatment: Dopamine agonist, Anticholinergic drugs (rarely used)
o Wearing off effect – loss of drug effect during prolonged course of therapy
o On-off syndrome – alternating between symptom free periods and when drugs stop working
o Levodopa combined with carbidopa (Sinemet) – inhibits the enzyme that destroys Levodopa – most effective therapy
o Pramipexole (Mirapex) – partial dopamine agonist
o Ropinirole (Requip)– monotherapy early with levodopa in advanced disease
o Rotigotine (Neupro) – early and late stage PD & RLS
Catechol-O-methyltransferase (COMT) inhibitors – breaks down dopamine
Monoamine oxidase-B inhibitors (MAOI)
o Selegiline (Eldepryl) – clinically proven to slow progression of PD
• Alzheimer Disease – Dementia – chronic degenerative disorder – memory loss, confusion, inability to think or communicate effectively – Ach in the brain responsible for memory is depleted – loss of neurons and neuron function
o Donepezil (Aricept) – raises Ach concentrations in brain
o Memantine (Namenda) – prevents cell death
o Galantamine (Razadyne) – rarely used
o Rivastigmine (Exelon) – mild to moderate symptoms of AD
Ch. 22 Pharmacotherapy of Seizures
Epilepsy – disruption of neuronal activity of brain characterized by 2 or more seizures
Seizures – disturbance of the brains electrical activity – may result in loss of consciousness, sensation alteration in motor activity.
• Convulsions – involuntary, violent spasms of large skeletal muscles of face, neck, arms, and legs
• Idiopathic – family history of epilepsy
o Febrile – caused by high fevers- last 1-2 minutes
• Acquired - injury to brain
• Older adults – associated with comorbid conditions (CV disease, esp. CVA(stroke), Alzheimer, subdural hematoma, CNS infection, brain tumors, polypharmacy)
• Generalized onset – multiple foci that spread abnormal discharges across both hemispheres of the brain simultaneously – loss of consciousness and reoccurrence
o Tonic-Clonic – preceded by aura, intense muscle contraction, hoarse cry at onset, loss of bladder control, shallow breathing – convulsions
o Absence – common in children, staring and transient loss of consciousness, eyelid fluttering, muscular jerking movement
o Atonic – less common, characterized by stumbling or falling
o Myoclonic – Common, large jerking body movements, quick contractions, no loss of consciousness, frequent at night
• Partial (focal) onset – when one area of brain shows abnormal brain waves, subtle symptoms –
o Simple partial seizure - can progress to generalized seizure – wide array of symptoms, may begin small (motor cortex – jerky movements) – no loss of consciousness
o Complex partial seizures – psychomotor or temporal lobe seizures, alter levels of consciousness, involves sensory, motor, and autonomic symptoms, aura precedes, no memory of seizures
• Status epilepticus – medical emergency, seizures continue for 30 min or more and 2 can occur concurrently – common with generalized tonic-clonic seizures, continuous muscle contractions – “Gran-Mal” – airway compromised
• AED medication – dependent on type of seizure, never skip dose or stop taking it – stress management and ketogenic diet can help
o Suppress neuron discharges
o Control electrolyte movement
Inhibit influx of sodium and calcium neurons
o Neurotransmitter balance
Increase in activity of GABA in brain (GABA is 1- charge)
Blocking of glutamate receptors in brain
• Antiseizure drugs – ALL are harmful to the fetus and ALL could cause depression
o Benzodiazepines – work in the CNS – not first choice of drug
o Diazepam (Valium)
o Lorazepam (Ativan) – emergency IV push
o Barbituates (Phenobarbital) – long term management
o Primidone (Mysoline) – doesn’t work on absence seizures
o Hydantoins– effective in management of most types of seizures – delay influx of sodium ions
Phenytoin (Dilantin) – used for focal onset
o Carbamazepine (Tegretol) – used for focal onset – inhibit sodium channels – first choice for tonic-clonic and partial seizures
o Gabapentin (Neurotin) – very weak, works good for nerve pain
o Valproic acid (Depakote) – good for generalized onset
Ch. 25 – pharmacotherapy of severe pain and migraines
General principles of pain management – to reduce pain to a level that allows pt to perform ADL’s
• Pharmacologic therapies
o Nonopioids – NSAID’s & acetaminophen – mild to moderate pain
o Opium – extracted from unripe poppy plant seeds
o Opiates – natural substances obtained from opium
o Opioid agonists– man made synthetic drug (Narcotics)
Morphine sulfate – activates mu and kappa receptors
Hydrocodone – effective antitussive
Hydromorphone (Dilaudid) – 5x’s more powerful than morphine
Oxycodone (Oxycontin) – long acting
Codeine – stronger antitussive action
Fentanyl – for breakthrough pain already on opioid meds
o Opioid antagonists - blocks mu and kappa receptors (treat opioid overdose)
Nalozone (Narcan) – used to treat withdrawals - rescue med when pt is in resp. distress
o Adjuvant analgesics – used to treat nerve pain
*Assess pt (resp. rate, pain level, B/P): document, administer drug, reassess pt (resp. rate, pain level, B/P): document – make sure you monitor and document
• PCA – pump – infusion pump allows pt to self administer
Migraines – throbbing, pulsating pain, preceded by aura, neurotransmitter serotonin plays a key role, unilateral or bilateral, lasts 4-72 hrs, moderate to severe pain
• Triggered by hormonal changes in women, stress, bright or flickering lights, change in weather or altitude
• Foods: alcohol, aged cheese, chocolate, caffeine, pickled or fermented foods, aspartame, MSG
• Symptoms: preceded by aura, nausea, vomiting, photophobia, phonophobia
• Goals: terminate acute migraine (abortive), prevent frequency of them
o Mild Migraines
NSAID’s, acetaminophen, caffeine
o Moderate migraines
Triptans (abortive therapy) – constrict certain intracranial vessels
Sumatriptan (Imitrex) – cranial vessel constriction
*Note: Almotriptan (Axert), Eletriptan (Relpax), Frovatriptan (Frova), Naratriptan (Amerge), Rizatriptan (Maxalt), Zolmitriptan (Zomig) – all are used to target menstrual migraines – last 6 days
• Migraine prevention therapy
o AED – antizeizure meds
o Beta-blockers (-olol) – can cause depression
o Tricyclic antidepressants
o Calcium channel blockers – blood pressure control [Show Less]