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Adv Rx Test 1
WillWallace Adv RX Ch 1 2 3 11 12
| Question | Answer |
|---|---|
| *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
Popular Respiratory Therapy sets