Upgrade to remove ads
Busy. Please wait.
Log in with Clever
or

show password
Forgot Password?

Don't have an account?  Sign up 
Sign up using Clever
or

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
Your email address is only used to allow you to reset your password. See our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

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

        Help!  

Question
Answer
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)  
🗑


   

Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
 
To hide a column, click on the column name.
 
To hide the entire table, click on the "Hide All" button.
 
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
 
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.

 
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how
Created by: annabannana
Popular Respiratory Therapy sets