| Flap 1 | Flap 2 |
| Anticholenergic action | blocks ACH causing bronchodilation |
| what is bronchoconstriction | smooth muscle bronchospasm, swelling and edema, increased secretion production=reduced airway lumen |
| treating secretions | treat swelling=treating secretions |
| 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 | remove cap and shake, open mouth-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 |
| metric conversion for lbs | 1 lbs=2.2 kilograms |
| Adrenergic agonist method of action | stimulates G protein in bronchial smooth muscle, G protein makes cAMP and cAMP equals bronchodilation |
| what is atropine and what is the 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 |
| Fluid mosaic | cell membrane structure of the plasma membrane, a phospholipids bilayer filled with moving proteins |
| 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) |
