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WWall RX test 1

wwall RX Review Ch 1,2,10&11 6/08

Anticholenergic action blocks ACH causing bronchodilation
calculating dose mg=mL x % x 10
powder aerosols activated by pt breath, advantage is pt must breath correctly for device to work, no propellant
Checking MDI contents full=fully submerged and upside down in water, 1/2 full= upside down but not fully submerged, empty, canister will float on side
MDI technique hold 1" from mouth, exhale normally, squeeze MDI at beginning of slow deep inhalation, inhale fully and hold for 5 seconds, exhale-wait 2 mins and repeat.
sympathomimetic bronchodilators method of action 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
atropine and method of action aka anticholinergic, aka antimuscarinic, blocks ACH receptor sites, causes bronchodilation by blocking ACH, competitive antagonist for M receptor
Cholinergic indirect acting, drug that acts or mimics parasympathetic action, stimulates M receptor
ACH regulation 1. metabolized by enzyme ACHase aka acetylcholinesterase 2. ACH blockers like atropine, Ipratropium or Tiotropium
NE regulation at synapse 1. re-uptake 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)
Un-ionized un-ionized are very water and lipid soluble and absorb quickly, because they are able to pass easily through plasma membrane
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=2
Ne norepinephrine, neurotransmitter of sympathetic nervous system, receptors sites are a, B1 and B2
a action vasoconstriction, increased BP, stops bleeding,decrease 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, aka parasympathetic, receptor site M, action decreased HR, decreased BP, bronchoconstriction
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 receptor site of Sympathetic NS aka adrenomimetic, receptors sites are a, B1 and B2
Pharmacokinetics quantifies the time required for drug absorption, distribution, metabolism and method of excretion
tid 3 times per day
q4h every 4 hours
qid 4 times daily
bid 2 times daily
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
pharmacodynamics studies the actions of drugs on the body, how drugs work
sympathetic nervous system fight or flight aka adrenergic, more dominant side of ANS, functions as a unit, effector site neurotransmitter is Ne. increases HR, increases 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.
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
Idiosyncrasy unexplained or unpredictable susceptibility to a drugs action
Tachyphylaxis rapidly developing tolerance to a drug
Anticholinesterase blocks ACHase enzyme
COMP & MOA enzymes that metabolize excess Ne, can be injected or inhaled
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
Phosphodiesterase enzyme that breaks up cAMP
Choline esters action stimulate m receptors and mimic effects of ACH
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+1-2
Drug info USP, NF, PDR
drug class that includes Albuterol that cause bronchodilation adenergic B-agonist
Synergistic response aka synergism when two drugs are combined and the effect is greater than the sum, 1+1-3
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 MDI’s 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
Spacer reservoir, improves med delivery, holds in suspension
Bronchodilator side effects tachycardia and shakiness
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 premies.
Combivent ventolen + atrovent combination sympathomimetic and anticholinergic, best with copd’er
Finding active ingrediance mg-mL* % * 10
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. Bad side effects.
Finding desired dose desired dose/dose on hand=amount/X example morphine in 10 mg/5mL vial, need 4 mg.....10/5=4/X.....10X/10=20/10.....X=2 vials
Anticholinergic bronchodilators blocks ACH-blocks SLUD, causes decreased secretions, increased 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)
Combovent albuterol + ipratropium (Ventolen + Atrovent), B2 agonist plus anticholinergic
Albuterol dosage .5% mL or 2.5 mg (.5mL+2.5mL NS), MDI 2 puffs 3-4 hrs, rapid onset=5 mins, effective 4-6 hrs aka Provental or Ventolen,
Xopenex dosage aka levalbuteral, single isomer albuterol with no side effects, but very expensive, standard dose .63 mg, max 1.25 every 4-6 hrs
what are catecholamines and what are their actions? strong a, B1, and B2 drugs, cannot be taken orally, (because of stomach MAO & COMT), very short duration 1- 3 hrs, epi, racemic epi (Vapoenephrine), isoproterenal (Isuprel)
the recorcinol drugs are modified catecholamines, resistant to MAO and COMT, terbuterline (stops contractions) and metaproterenol (not used now because of B1 side effects, hard on heart)
the 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)
strong B2, mild B1 agonist are bitolterol (Tornalate), albuterol, (Provental, Ventolen), pirbuterol (Maxair), salmeterol (Serevent) terbutaline, metaproterenol (Alupent)
Created by: annabannana
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