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Adv Rx Test 1

WillWallace Adv RX Ch 1 2 3 11 12

QuestionAnswer
*Anticholinergic drugs block M receptors, <SLUD, atropine is prototype and is used to <secretions before anesthesia can also be called antimuscarinic, atropinic, antiparasypathetic and parasympatholytic
Anticholinergic action blocks M causing decrease SLUD
Calculating dose mg equals mL x % x 10 example how many mg’s are there in 2cc of a 20% solution? mg eq 2 x 20 x 10 or mg eq 400mg caution-do not move decimal.
Find the solution mg equals mL x % x 10 example if there are 30 mg in 2cc of a drug, what percent solution is this- 30
How many mg of Alupent are in .5ml of a 1:200 concentration 1:200 is g/mL*100 eq .5%, mg eq .5*.5%*10 answer is 2.5mg
How many mg per ml are in a 2.25% solution mg eq ml*%*10 so mg eq 1ml*2.25%*10 or 22.5
MDI technique shake, hold 1" from mouth, exhale normally, squeeze MDI at beginning of slow deep inhalation, inhale fully and hold for 10 seconds, exhale-wait 15-30 sec (for SABA, none for other meds) and repeat.
*Sympathomimetic bronchodilator method of action aka adrenergic agonist, stimulate production of cAMP causing bronchodilation
*Adrenergic agonist method of action stimulates G protein in bronchial smooth muscle, G protein makes cAMP and cAMP equals bronchodilation (sympathomimetic)
*Sympathomimetic bronchodilator drugs terbuterline, albuterol, isoproterenol levelbuterol (adrenergic)
Atropine and method of action aka anticholinergic, aka antimuscarinic, blocks ACH receptor site (M), causes <SLUD by blocking ACH, competitive antagonist for M
*Parasympatholytic (<M) vs. parasympathetic (>M) patholytic is anti or against, parasympatholytic is anticholinergic (blocks M), parasympathetic is cholinergic (>M-causes bronchoconstriction)
*Cholinergic indirectly acts or mimics parasympathetic action (bronchoconstriction, SLUD), includes choline esters (>M recept), anticholinesterases(blocks ACHase)
Routes of administration PO aka oral (most common and safest), parenteral aka IM or IV, topical aka svn
Agonists drugs that combine with specific receptors to cause a drug action, drugs that stimulate action
Antagonists aka blocker, drugs that combine with a specific receptor and cause no action
Competitive antagonism antagonists and agonists compete for same receptor, example is antihistamine which competes for receptor with histamine, by reducing the binding of histamine, effects of histamine are reduced. Gum in keyhole
*ACH regulation 1. Metabolized by enzyme ACHase aka acetylcholinesterase 2. ACH blockers like atropine, Ipratropium or Tiotropium
*NE regulation at synapse 1 Reuptake via active transport, 2 MOA and COMT enzymes
*NE regulation at cells cells regulate NE by increasing cAMP or blocking phosphodiesterase (enzyme that breaks up cAMP)
*Alpha receptor a, adrenergic(sympathomimetic) receptor, located in most arteries and veins, NE is neurotransmitter, action is vasoconstriction. Epi (adrenal gland) action is vasoconstriction-<bleeding, <swelling, >BP
*B1 receptor adrenergic (sympathomimetic) receptor located in the heart, NE is neurotransmitter, action is moderate >HR and moderate > contractility, Epi action is greater > in HR and contractility
*B2 Receptor adrenergic(sympathomimetic) receptor located in bronchiolar smooth muscle, uterus and skeletal muscle blood vessels. NE is neurotransmitter but has no action, Epi action is bronchodilation, uterus relaxation and skeletal muscle vessel vasodilation.
Factors that alter drug effects pt compliance, placebo effect, pathological state, time of admin, sex, age, genetic variations, drug interactions
*Un-ionized un-ionized are very water and lipid soluble and absorb quickly, because they are able to pass easily through plasma membrane, non-charged, neutral
*Muscarinic receptor site of ACH, parasympathetic, class of drugs that stimulate ACH, action is decreased HR, bronchoconstriction and vasodilation
Potentiation special case of synergism where one has no effect but can increase the effectiveness of the other 1+0 eq 2
*NE norepinephrine, neurotransmitter of sympathetic nervous system, neuroeffector sites are smooth muscle and cardiac muscle, receptor are a, B1 and B2
*NE effects (fight or flight) vasoconstriction, >HR, >contractility of heart, <GI activity, pupil dilation, bronchodilation, bladder relaxation, urinary sphincter constriction
*ACH effects (rest & digest) <HR and contractility, >GI activity, pupil constriction, bronchoconstriction, bladder constriction, urinary sphincter relaxation. SLUD
*a action vasoconstriction, increased BP, stops bleeding, decreases swelling,
*B1 action increased HR, increased contractility, increased cardiac output
*B2 action smooth muscle relax, bronchodilation
Metabolism liver * alphabetically e and k come first in alphabet fallowed by l and m, so excretion- kidney and liver-metabolism
*Excretion kidneys * alphabetically e and k come first in alphabet fallowed by l and m, so excretion equal kidney and liver equals metabolism, excretions also takes place in lungs and GI tract
*ACHase acetylcholinesterase aka ACHE, enzyme that metabolizes excess ACH
*Drug absorption many membranes; stomach, capillaries and tissues-3 factors, transport mechanism, lipid solubility and drug ionization (un-ionized)
ACH aka acetylcholine, aka cholinergic, neurotransmitter of parasympathetic, receptor site M, action < HR, < BP, bronchoconstriction, neuroeffector site is smooth muscle, cardiac muscle and glands.
Potency more physiological effect with smaller dose, more potent-more toxic, lower the effective dose-more potent
Parenteral injectable aka IM, IV
Entral GI tract, pills caplets, suppository, elixir, suspension (most common)
Topical transdermal, cream patch ointment, inhaled, MDI, DPI, SVN, USN, atomized, vaporized
*Adrenergic aka sympathomimetic, term meaning a drug that mimics the action of the sympathetic nervous system. Stimulate receptor sites example
Pharmacokinetics quantifies the time required for drug absorption, distribution, metabolism and method of excretion
sympathomimetic aka adrenergic-drug that mimics action of sympathetic ns
*drug distribution plasma protein binding, tissue affinity and blood flow
*drug transport passive diffusion (most common) moves from high to low, filtration, and active transport
prototype "a drug that acts like" i.e. atropine is prototype anticholinergic and epinephrine is prototype adrenergic
Therapeutic dose recommended amount of a drug that should be used to obtain the desired clinical effect.
sympathetic nervous system fight or flight aka adrenergic, more dominant side of ANS, effector site neurotransmitter is Ne. >HR, >BP, vasoconstriction, bronchodilation, contractility
LD 50 median lethal dose
*TI Therapeutic Index, ratio of LD50 to ED50 indicates drugs safety, lower TI is the more toxic the drug, higher the TI, the safer the drug. TI eq LD50/ED50
Teratogens drugs that are known to cause birth defects
Carcinogens drugs that cause malignant neoplasms (cancer)
Antimuscarinic specifically blocks m receptor sites
*Competitive antagonist competes for receptor site, blocks but has no effect
*Functional antagonist effects of two drugs cancel each other out
ED50 effective dose, dose at which 50 percent of test animals show desired effects
Idiosyncrasy unexplained or unpredictable susceptibility to a drugs action
Tachyphylaxis rapidly developing tolerance to a drug
*Anticholinesterase blocks ACHase enzyme, allowing >ACH and increasing bronchoconstriction and SLUD
*COMP & MOA enzymes that metabolize excess Ne, can be injected or inhaled-never swallowed
Pharmacology study of drugs and their origin plants animals and minerals
Epinephrine not a neurotransmitter, released by adrenal gland in response to sympathetic activation
Ceiling effect response increases with dose until dosage increase does not increase effect-used to check relative potency of 2 or more drugs. Note; once ceiling effect is reached, increasing dose has no advantage and may be toxic.
*Phosphodiesterase enzyme that breaks up cAMP
Choline esters action stimulate m receptors and mimic effects of ACH, causes bronchoconstriction and SLUD
SLUD salivation, lacrimation, urination, defecation; to much ACH to much SLUD, to much SLUD → death
*Antagonist categories competitive (affinity but no effect), functional (effects of 2 cancel each other), chemical (physically chemically binds in blood stream)
Additive effect two drugs act on receptors to have a combined effect that is the sum of the two drugs effect 1+1 eq 2
Drug info USP, NF, PDR
*Synergistic response aka synergism when two drugs are combined and the effect is greater than the sum, 1+1 eq 3
*Parasympathetic aka cholinergic, rest and digest, neurotransmitter is ACH, receptor sites are Muscarinic and nicotinic, blocker is atropine, does not function as a unit
MDI on Mechanical Vent medial to pt on circuit, actuate at end expiration adjust dosage as needed, minimum 8 puffs may go to 20, 15 seconds between puffs
*High dosing Albuterol effective ceiling is 15 mg, heart neb for continuous, hazard is hypovolemia, decreased k+, increased glucose
Aerosol advantages immediate onset of action at site, reduced systemic side effects, smaller doses, pt can be taught to self admin, convenient and rapidly effective while minimizing side effects
Aerosol disadvantages exact dose is unknown, only 10-20% is deposited, breathing pattern effects airway deposit, 2/3 exhaled, much swallowed, wrong neb or flow effects delivery
*Nebulizer flow rates 6-7 L/min * however since neb can run at 10 L/min and not 4 L/min appropriate answer on test is 7-10 L/min
*SVN delivery factors inspiratory hold (3-5 seconds) is most important for distribution and retention of meds-slow deep breath, 6 L/min flow for 1-5 micron particles, 2.5-4 mL’s solution, inspiration only
MDI advantages convenient, inexpensive, no prep, new MDIs are patent actuated and assures proper aspiratory flow and pattern
MDI disadvantages requires pt coordination, pharyngeal deposits, abuse risks, cfc’s, 75% of pt’s and 50% of medical workers don’t know how to use them
Mech vent and SVN meds tend to stick to tube or baffle, 1.5 to 3% make it to airway, SVN should be distal to pt in circuit (close to flow source) often requires double dose
*SVN particle size 1-5 microns
Direct installation giving meds directly down ET tube or trach, 3-5 ml normal dose, no guarantee of dose, most often used for mucus plugging. Disadvantage, violent cough and systemic side effects
Direct installation drugs Epi-cardiac arrest, NS-sputum sample, B2, mucomyst, surfactant in preemies.
*Combivent Ventolen(albuterol) + atrovent combination sympathomimetic and anticholinergic, best with copd’er
Bronchodilator categories sympathomimetic (increase cAMP), anticholinergic (block ACH), Xanthines (inhibit Phosphodiesterase increasing cAMP)
Xanthines aka theophylline, caffeine, thrombromine & theophylline, Phosphodiesterase inhibiter, used in treating neonate apnea and bradycardia, long term COPD, last resort in asthma, rare use, bad side effects.
Finding desired dose desired dose/dose on hand equals amount/X example morphine in 10 mg/5mL vial, need 4 mg.....10/5 eq 4/X so 10X/10 eq 20/10 so x eq 2 mg
*Anticholinergic bronchodilators blocks ACH-blocks SLUD, causes <secretions, >HR, bronchodilation, prototype is atropine (bad side effects) Ipratropium is safer alternative, good choice for bronchospasm in COPD with B2 agonist
*Swelling & edema treatment alpha (racemic epi) + steroids. Steroids also treats secretions, treat swelling and secretions will go down too.
what is Bronchoconstriction REDUCED AIRWAY LUMEN, caused by smooth muscle bronchospasm, swelling and edema, excess secretions
*the anticholinergic bronchodilators drugs are atropine (prototype), ipratropium (Atrovent) tiatropium (Spiriva) glycopyrrolate (Robinol-used for bronchorrhea in CHI)
*Albuterol dosage SD 2.5 mg/3mL or .5mL in 2.5cc NS q4-8, Exacerbation 2.5-5mg 20mins x 3 or 10-15mg/hr cont
*Xopenex/levalbuterol dosage SINGLE ISOMER SD .63mg/3mL, q4-6, exacerbation-adult 1.25-2.25mg 20 mins x3 then same q1-4 no cont neb (need to double ck max),
*Ipratropium dosage Atrovent, anticholinergic, parasympatholitic,(compet agonist) blocks cAMP, very safe, can mix with albuterol, for exacerbation .5mg 20mins x 3 then as need, STANDARD DOSE .2 qid
Prednisone dosage for asthma exacerbation child 1mg/kg 2 dose max/day(max 30mg) until PEF or FEV1 at 70%, adult 40-80 mg/day 1-2 doses until PEF or FEV1 at 70%, out pt burst 3-10 days
*Salmeterol dosage LABA, >5yrs DPI-50mcg/blister, 1 blister q12
Catecholamines bronchodilators naturally produced in the body in response to stress, epinephrine, receptor is a, B1, B2, metabolized by MAO & COMP (sympathetic, adrenergic, cholinergic)
Catecholamine drugs first synthetic adrenergic drug, strong a, B1, and B2 drugs, cannot be taken orally, (because of stomach MAO & COMT), very short duration 1- 3 hrs, epi, racemic epi (Vaponephrine), isoproterenal (Isuprel)
Finding desired dose desired dose/dose on hand equals amount/X example; bottle of Demerol has 50mg/5cc, how much do we need to deliver 25mg of Demerol? 50/5 eq 25/x so 125/50x reduce to 2.5/x or x equals 2.5cc
*resorcinol drugs are modified catecholamines, no a, B1, B2, some resistance to MAO and COMT, terbuterline (stops contractions) and metaproterenol (not used now because of B1 side effects, hard on heart) 4hrs
*Saligenin drugs modified catecholamines, SABA-short acting B2 agonist, last 6hrs, B2 preferential, very little B1, albuterol
*R-Isomer or single isomer drugs levelbuteral (Xopenex), also a saligenin but has no B1, and considered a LABA long acting beta agonist
*saligenin drugs are albuterol, levalbuterol, (Xopenex) and salmeterol (Serevent)
strong a, B1, B2 drugs epinephrine and racemic epinephrine (Vaponephrine)
Strong B2 agonist drugs levalbuterol (Xopenex) is the only single isomer B2 agonist drug, all others have some B1 effects
Strong B2, strong B1 agonist are isoproterenol (Isuprel)
Dose-response curve graphic representation of the relationship between dose in mg and the response to or effect of the drug.
Antitusuve anti cough
Expectorants increase fluid in resp tract and stimulate cough
SSKI potassium iodine-expectorant for asthma and bronchitis (no longer used)
*Bronchorrhea condition associated with excess thin watery pulmonary secretions, most often with head injury, drug of choice- glycopyrrolate (Robinal), hazard is mucus plugging
*Mucomyst n-acetylcysteine, mucolytic, breaks down disulfide bonds
Mucus molecule mucopolysaccaride chain, strands of amino acids and amino sugars connected by disulfide bonds
Mucolytics drugs dornase alfa (Pulmozyme), n-acetylcysteine (Mucomyst), sodium bicarb
*Dornase Alfa aka Pulmozyme, mucolytic, lyces bacteria and cellular debri DNA, most often used with CF & bronchiectisis, never mix with other drugs, need special jet neb (maint drug)
*Sodium Bicarb mucolytic, alters PH to disrupt amino acid chain, very rare alternative to mucomyst, asthma pt with thick secretions (done is 2% or 4.2%)
*The most effective method of mucolysis is aerosolized mucolytics
*Side effects of N-acetylcysteine (Mucomyst) bronchospasm, acute airway obstruction, oropharyngeal irritation
*Side effects of dornase alfa (Pulmozyme) pharygitis, laryngitis and voice alteration
*What are the contraindications for the use of Mucomyst administration without a bronchodilator, administration to semicomatose pt without suction equip and monitoring
*When should RT use sterile distilled water as dilute instead of NS with bronchodilator with pt is like Kay and has a salt restriction
mucolytic indicators thick inspissated secretions, aerosol - able to cooperate & deep breath, trach or endotrach by direct instillation
*Bland aerosol aerosols that do not have a direct effect on mucus molecule and usually no side effects. Normal saline (.9%NaCl), hypo (.45%NaCl) and hypertonic saline (5%NaCl), and sterile distilled water
Secretion patients CF, bronchiectisis and chronic bronchitis
increased secretion indicators tactile fremitise (you can feel it), rhonchi (low pitch rumble), caused by ineffective cough and muscle fatigue
Mucolytics agents that disrupt mucus molecule so that secretions can be removed (coughed or suction), cause mucolysis (breaking apart)
*Sterile distilled water most common solution in LVN for humidification of airway, also used as a dilute in SVN-TRACH PTS
Sputum induction used when pt has dry non-productive cough, hypertonic saline (5% to 10%) not to exceed 1500 mg/day
Hypotonic osmotic pressure is less than body fluid, most common is .45% NaCl (1/2 NS), used in LVN when pt cannot tolerate distilled water and as dilute in SVN for pt with severe salt restriction
*Hypertonic osmotic pressure is greater than body fluid, used for sputum production, most common 5-10% NaCl (hygroscopic droplets attract humidity and grow larger) NEVER TO ASTHMATIC
NS normal Saline, osmotic pressure is same as body fluid (0.9% NaCl), most common bronchodilator dilute, unlikely to cause bronchospasm, but can increase sodium
*Pulmozyme dose unit dose 2.5 mL, contain 1 mg dornase alfa/mL solution (1mg is 2.5 mL), use separate neb, q1 or q2, (refrig and protect from light)
Bland aerosol indicators pt who require humidity of resp tract, intubated or trach. As thinning agent prior to postural drainage and chest percussion, sputum induction. (continuous jet, Babington or USN)
*n-acetylcysteine aka Mucomyst, indicated for pt with excessive purulent thick or inspissated secretions, breaks disulfide bond, also used in acetaminophen (Tylenol) OD & renal protection, 10-20 % solution, bad smell, max 72 hrs
Mucomyst dose unit dose 10% or 20% solution, 20% solution can be mixed 1:1 with distilled water or NS if needed, refrig extra, date and discard after 4 days, 3-4mL/tx q4h with bronchodilator.
budesonide aka Pulmacort, aerosol corticosteroid (only SVN steroid) needs a specific jet neb
aerosol corticosteroid fluticasone-Flovent,flunisolide-Aerobid,triamcinolone-Azmacort
*Asthma attack anatomy mast cell exposed to allergen (antigen-antibody), mast cell degranulates releasing histamines (edema, mucus, constriction), cytokines (recruiters-cause late stage) and leukotrines (inflammatory mediator)
Bronchial asthma most common chronic lung disease, 4% of population and increasing, symptoms, dyspnea, diffuse wheezing, airway obstruction from bronchospasm, edema and mucus.
*S&S of serious asthma exacerbation marked breathless, short phrases only, use of accessory muscles, drowsiness, PEF 50-70% predicted use quick relief, PEF <50% ED
ED TX for mild-mod exacerbation >40%, O2 to achieve 90%SaO2, SABA up to 3x/hr, oral corticosteroid if not resp to SABA
ED TX for severe exacerbation <40% O2 to achieve 90% SaO2, high dose SABA + Ipratropium (20 mins or continuous), oral corticosteroids
TX for impending or actual resp arrest intubate and mech vent on 100%, SVN SABA and Ipratropium, IV Corticosteroids, consider adjunct therapies, admit to ICU, hourly SABA
Asthma mucus thickened & viscid (sticky) with eosinophils
What drug stabilizes the mast cell Intal aka cromolyn sodium
how often can we give Vaponephrine every hour
*advantages of steroids by aerosol rapid absorption at site of action with reduced systemic side effects
what is the only inhaled steroid available for svn budesonide
*the most effective method for mobilizing and improving mucokinetics is adequate hydration and fluid intake
Mucosal edema accumulation of fluid in the mucosal membrane, caused by infection, trauma, disease, or conditions like anaphylaxis or allergic reaction (most often treated with alpha racemic epi
*Asthma attack progression coughing, exp wheezes, I:E wheezes, insp wheeze (air trapping), vent failure (intubate)
Anti-asthmatic drug classes mast cell stabilizers & leukotriene blockers
Aerosol steroid advantage decreased systemic side effects, no addiction, no cushings
Aerosol steroid disadvantage increased expense, not for status asthmaticus, increased risk of superinfection, horseness, cough, requires pt effort and coordination
*CNS additive effects especially true with depressant drugs, alcohol and barbs will result in synergistic effect of both
*Antagonism of CNS drugs stimulants and depressants antagonism is variable, often unpredictable and extremely variable
Depressant drugs and excitation some may cause a brief period of excitation prior to depressant stage, example is general anesthetic
Acute or chronic excitation is often followed by what? depression,long term amphetamines or convulsive state, depression usually follows
Drug induced (chronic) depression is usually followed by what? period of excitation, usually following termination of chronic use of narcotics or barbs
*Sedative calming effect, decrease CNS activity and drowsiness
*Hypnotic drowsiness, facilitates onset of sleep
*Anti-anxiety agent (anxiolytic) reduces anxiousness, particularly incapacitating or inappropriate anxiety
*Barbiturates prototype of sedatives and hypnotics, very powerful, no analgesic properties, little cardio effect, redistribution, very addictive, can cause life threatening withdrawals, not normal REM
Sedation and hypnotic are related how? by dose, >sedation can cause sleep, <hypnotic can cause sedation
*Barb uses today induction agent in general anesthesia, anticonvulsants in treating epilepsy, backup sedative hypnotic agents
*Barbiturate drugs thiopental, pentobarbital and Phenobarbital (Luminal)-long acting anticonvulsant
*Benzodiazepines most widely used sedative hypnotic and anti-anxiety, replaced barbs, enhance GABA neurotransmitters in the brain, few side effects, rare OD
*Benzo drugs (>gaba) midazolam (Versed) short duration, amnesia
Alcohol ethyl alcohol, CNS depressant, side effects-cardio, GI, fetal development
*Tricyclic antidepressants TCA’s, most often used antidepressants, least side effects
*Monoamine oxidase inhibitors MAOI’s, antidepressant, greater toxicity and interact with some foods and drugs
*TCA’s & MAOI’s action increase levels of norepinephrine and/or serotonin in the brain tissue, CAUSE HYPERTENSION
Psychostimulant drugs amphetamines and methylphenidate, stimulants, paradoxical they are used in ADHD
*Anti-anxiety meds barbs, nonbarb sedative hypnotics, alcohol and benzos, benzos are the mainstay
*Epilepsy paroxysmal (sudden onset) increase in CNS activity that is recurrent, has stereotypic clinical characteristics and associated massive discharge of elec activity that is self limiting
*Partial seizures SIMPLE-local discharge without loss of Consciousness or COMPLEX-loss of consciousness with many ANS behavior (most difficult to diagnose)
*Primary generalized seizures PETIT MAL (absence)-rapid onset, loss of consciousness and mild rhythmic movement or GRAND MAL (tonic-clonic) 4-10% of seizures, asleep or awake, can be caused by lack of sleep, alcohol, fatigue
Anticonvulsant/anti-epileptic drugs break up a seizure, Phenobarbital (Luminal), valium and aderian????????
*Parkinsonism middle age and progressive, lack of dopamine-containing neurons in the substantia nigra area of one of the cerebral nuclei (in CNS), causes lack of balance in excitatory and inhibitory neurons
Symptoms of Parkinsonism develop slow at first, gradual become chronic, tremor, rigidity, akinesia(loss of movement), bradykinesia(slow move) and loss of balance, idiopathic (unknown) cause
*TX of Parkinsonism increase dopamine, Levodopa-passes blood brain barrier
*General anesthetics drug that induces the absence of all sensation
Anesthesia Stage I Analgesia aka twilight, midbrain and some spinal cord
Anesthesia Stage II Excitation via IV, amnesia
*Anesthesia Stage III Surgical Anesthesia via inhalation, intubation, for surgery, 4 planes (only seen when using ether)
Anesthesia Stage IV Medullary Supression effects respiratory and cardio, causes apnea, coma, and death
N*itrous Oxide low risk, gas, most widely used general anesthetic, especially as adjunct with general anesthetics to <need for more potent agents, rapid, good analgesic, metabolized in lung instead of liver, little cardio effect
Inhaled general anesthetics are gases-nitrous oxide and cyclopropane(no longer used), Volatile liquids-ether, halothane, methoxyflurane
*Fluothane halothane, volatile liquid delivered as vapor particularly in peds, also potent bronchodilator-last resort for status asthmaticus
*Thane or rane in drug name inhaled general anesthetics ie halothane methoxyflurane
*Anesthetic delivery generals are for body core, IV and IV nerve blocks are for peripheral
Fentanyl high dose narcotic, used with versed for conscious sedation, profound analgesia, also used as preanesthetic to create sedation
Propofol aka diprivan, high dose narcotic (will need intubated), used for anesthetic induction and maintenance
*Preanesthetic medications fentanyl, to create sedation and Atropine, to decrease salivary and bronchial secretions
*Narcotic analgesics drugs that decrease pain without loss of consciousness, aka opioid, used to treat visceral pain (severe pain)
B endorphins morphine-line substances
Dymorphines more recent group of narcotics
*Morphine prototype narcotic, oldest naturally occurring analgesic and best understood, standard for which others are compared, high addiction, high resp suppression, side effect constipation, dose-10mg
*Morphine effects on respiratory powerful depressant, <RR & <VT causing >CO2, can cause bronchospasm-caution with asthmatics
Classifications of narcotic analgesics agonist (stimulates opioid receptors), agonist-antagonist (stimulates some and blocks some opioid receptors) and antagonist (blocks receptors)
*Agonist narcotic drugs morphine (opium), hydromorphone (Dilaudid) and hydrocodone (Vicodin) (both are semisynthetic derivatives of morphine and codeine), meperidine (Demerol) synthetic derivative of morph and code
Agonist-antagonist drugs none we need to know
*Antagonist narcotic drugs naloxone (Narcan) treat opioid OD
Meperidine synthetic agonist narcotic, 1/10 to 1/5 as potent as morphine, dose 50-100 mg, mod-high addiction, high resp suppression, few side effects
Codeine 1/6 as potent as morphine, dose 60 mg, low addiction, low resp sup, few side effects
*Non-narcotic analgesics Salicylates,
*Salicylates acetylsalicylic acid (ASA; Aspirin), non-narcotic analgesia for mild to mod pain, antipyresis (<body temp), anti-inflammatory in joints and ligaments, anticoagulation
*Salicylate side effects GI(ulcers), Hypersensitivity (allergy) including bronchospasm, anticoagulant effect
*Acetaminophen Tylenol, nonsalicylate non-narcotic, analgesic, antipyresis, not an anti-inflammatory
*Non steroid anti-inflammatory Salicylates like aspirin and ibuprofen like Advil and Motrin (ibuprofen is also analgesic, antipyresis)
*CNS drugs can alter effects of neurotransmitters on CNS by antagonism, increased or decreased synthesis of neurotransmitter
*Can a sedative drug become hypnotic by increasing the dose? yes
*True Benzo statements have few side effects compared to barbs, main clinical use is TX of anxiety with some Tx of sedation, action is stimulate GABA neurotransmitters, can create additive effect w/alcohol or other depressants
*TCA’s and MAO inhibitors are antidepressants
*The major side effect of TCA’s and MAO inhibitors that is of greatest concern is hypertension
*Which antidepressants causes worse hypertension MAO's
*The mainstay drug for Parkinsonism is Levodopa
*What is the caution with morphine with COPD reduced resp of morphine can cause death in copd’er with normal dose
*RACEMIC EPI NOT A BRONCHODILATOR, <K, >GLUCOSE, METABOLIC ADRENERGIC
*Sympathomymetics are fight or flight they do not <BP
Catecholamine duration short 1-3 hrs and cannot take orally
MUCOMYST DYSULFIDE BONDS
PULMOZYME LYCES DNA
SERUM THEOPHYLLINE LEVELS INCREASE WITH WHAT LIVER DISEASE AND ALCHOLISM
SIDE EFFECTS OF N-ACETYCYSTEINE BRONCHOSPASM
Created by: williamwallace