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Adv Rx Test 2

WillWallace Adv RX Test 2 Ch 5,10,14,16

QuestionAnswer
*Advantages of aerosol drug delivery immediate onset of drug action at the desired site, reduced side systemic side effects, smaller doses of potent drugs (b-agonists), pt may be taught to self-administration
Main advantages of aerosols convenient and rapidly effective while minimizing side effects
Types of aerosols bronchodilators, decongestants, antibiotics, anti-inflammatory agents, mucolytics, wetting agents, surface active agents (ethyl alcohol) and anti-asthmatics (cromolyn sodium)
Disadvantages of aerosols inability to determine the absolute amount of drug deposited in lung (10% or less), uncooperative or uncoordinated pt-little drug to smaller airways and periphery, wrong neb-wrong particle size metabolized-no effect
*Single most important variable in effective aerosol administration pt breathing pattern-BREATH HOLD
*Selection criteria for effective aerosol administration is 1.willingness to cooperate, 2.slow deep breaths with 3-5 sec. hold at end-inspiration, 3. Responsiveness of pt pulm disease to drug being used
*Therapeutic range of aerosolized meds is 1-5 microns
Technique for SVN treatment 1. 2.5-4 mL solution, 2. Flow rate of 6-8 L/min, 3. Nebulization on inspiration only (Y or thumb port), 4. Inhale slowly and deeply (2xnormal) and hold at end-insp for 3-5 seconds
The most important factor in SVN treatment technique is Inhale slowly and deeply (2xnormal) and hold at end-insp for 3-5 seconds
What is the standard bronchodilator delivery method pre and post PFT’s MDI’s
*Calculating dose mg eq mL x % x 10
powder aerosols activated by pt breath, advantage is pt must breath correctly for device to work so better deposition of aerosol is likely, no propellant
*Checking MDI contents COUNT PUFFS USED
*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 15-30 seconds and repeat.
*Spacers/chambers improve med deliver for MDI’s by holding aerosol in suspension for a longer period, FOR BETTER DISTRIBUTION
Multiple MDI meds, which one should pt take first always take bronchodilator first, wait 1-2 mins then steroids (always rinse mouth to avoid fungus or oral infections)
tid 3 times per day
q4h every 4 hours
qid 4 times daily
bid 2 times daily
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
*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
Bronchodilator side effects tachycardia and shakiness
*SVN particle size 1-5 microns
Direct installation giving meds directly down ET tube or trach, (1 bolus) 3-5 ml normal dose, no guarantee of dose, most often used for mucus plugging.
Disadvantage of direct installation violent cough, bronchospasm and systemic side effects
Direct installation drugs Epi-cardiac arrest, NS-sputum sample, B2, mucomyst, surfactant in preemies.
*Finding active ingredients mg eq mL* % * 10
Finding desired dose desired dose/dose on hand eq amount/X example morphine in 10 mg/5mL vial, need 4 mg..10/5 eq 4/X so 10X/10 eq 20/10.....X eq 2 vials
How many mg are in 1 gram 1000
How many mg are in .7 grams .7 x 1000 eq 700mg
How many mg of salt are in 3mL of NS? NS is 9% so 1 mL is eq to .9g/100mL or 900mg/100mL reduce to 9mg/1mL eq 9mg, 9mg x 3mL eq 27mg of salt in 3mL’s of NS
*Doctor orders 3mL of 10% mucomyst but is only available in 20% find the mg’s in 3mL of 10% and then solve for mL in 20%, so mg eq 3mL x 10% x 10 eq 300mg, so 300mg eq ?mL x 20% x 10 ?ml is equal to 1.5mL
Isopreterenol comes in a 1:200 solution. you need a 1mg dose, how much of the solution is needed to deliver this dose 1:200 is 1/5x100 or .5% so solve for mL, 1mg eq ?ml x .5% x 10 eq .2mL
A bottle of morphine is labeled morphine 10mg/mL, how many mL are need to deliver 3 mgs? mg/mL eq mg/x so 10mg/1mL eq 3mg/x solve for x, cross multiply 3/10 answer is .3mL
Aerosolized drugs that reduce inflammation and selling in the airways are anti-inflammatory and anti-asthmatics
Uses for anti-inflammatory and anti-asthmatics are acute inhalation injuries (poison, fumes, steam), laryngeal trauma (intubation/extubation) or infection/viral (croup), severe allergic reactions (anaphylaxis), acute and chronic asthma
Asthma management 1st line drug-albuterol, 2nd line drug-steroids/anti-inflammatory, 3rd line drug-increase 1 and 2, 4line drugs-xanthines (Theophylline)
Management protocol for sever/acute asthma 1-O2, 2-albuterol 5mg + atropent .5mg q20mins x 3, 3-steroid IV Solumedrol *takes 30 to 60 mins to kick in, 4-last resort to prevent intubation-epi every 30 mins to 3hrs (max is 2xeach hour), 5-resp failure intubate and mech vent
Asthma attack progression coughing, exp wheezes, I:E wheezes, insp wheeze (air trapping), vent failure (intubate)
*Corticosteroids anti-inflammatory, steroids produced by the adrenal cortex (on top of kidney)
Glucocorticoids corticosteroids that decrease swelling
Regulation of steroids in the body pituitary release of hormones cause adrenal cortex to release steroids (continuous up and down)
When are steroids at their peak in the body 8am
What are the effects of long term use of steroids adrenal atropy, steroid dependant
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)
beclamethasone Vanceril, high dose topical corticosteroid, low systemic, rapid metabolism, MDI, 2 puff 400ug, qid or qit, 5-10mg
triamcinolone Asthmacort, 2 puffs qid, corticosteroid
flunisolide Aerobid, 2puffs bid, corticosteroid
*fluticasone Flovent (aka Flonase-up the nose) rapid onset long lasting, corticosteroid FOR CHRONIC AIRWAY INFLAMMATION
budesonide Pulmacort .5mg/2mL daily, max dose 1mg/day, can be split for bid (only steroid available in SVN)
*salmeterol + fluticasone Advair, CHRONIC ASTHMA MAINT, B2 agonist (bronchodilator) + anti-inflammatory (corticosteroid) (1+1 EQ 3) POTENTIATE
*Anti-asthmatic drug classes mast cell stabilizers & leukotriene blockers
*Mast cell stabilizers prophylactic-prevent extrinsic asthma by stabilizing mast cell wall so it will not burst, Intal aka cromolyn sodium and Tilade aka nedocromil sodium
*leukotrine blockers competitive antagonist for leukotrines receptors, Accolade aka zafirlukast, Singular (5YR OLD W/rad) aka montelukast, Zyflo aka zileutin
*Singular montelukast, available down to 12 months age (RAD), chronic, exercise and very safe, leukotrine blocker, competitive antagonist
Mechanism of action for leukotriene blockers stops arcodonic from becoming leukotrines
zafirlukast aka AccolaTe, anti-asthmatic, selective and competitive antagonist of leukotriene receptors, hazard is renal failure, can’t be taken with food, so poor pt compliance
*budesonide aka Pulmacort, aerosol corticosteroid (only SVN steroid) needs a specific jet neb
fluticasone aka Flovent, aerosol corticosteroid,
flunisolide aka Aerobid, aerosol corticosteroid
triamcinolone aka Azmacort, aerosol corticosteroid intermediate duration 5-10 days ramp up
*SVN steroid budesonide aka Pulmacort
*Bronchoscopy drugs are lidocaine aka Xylocaine, 4-7 mL of 2-4% solution, local anesthetic/antitusive onset is fast 30 sec peak is 2-3 mins, lasts 1 hour, instill or SVN. Epi if needed for bleeding
Adverse effects of lidocaine (Xylocaine) suppresses stress related arrhythmias, in extreme cases may cause seizures
*Bronchial provocation/challenge drugs are metholine chloride (Provocholine), cholinergic aka parasympathomymetic, used in asthma differencial diagnosis, never take bronchodilators or histamines prior
*Blood supply of the heart O2 rich from left ventricle to aorta branches to coronary artery and is dependent on the force of contractions of myocardium
CO 70mL per stroke x 80 HR is equal to CO of 5.6L/min
Conduction system of the heart SA node depolarizes and spreads to atria and down to AV node, AV node sends impulse to bundle of his, to left and right bundled branches and into purkinje fibers causing depolarization of ventricles
*Positive chronotropic effect increased HR from sympathic NE
*Positive inotropic effect increased force of contractions (contractility) from sympathic NE causes increased stroke volume
*Negative chronotropic effect decreased HR from acetylcholine from parasympathetic (beta blockers)
*Negative inotopic effect decreased contractions (contractility) from acetylcholine from parasympathetic, causes decreased stroke volume.
Pwave atrial depolarization
QRS complex depolarization of the vents
T wave repolarization of the atria
Most common heart diseases CHF and coronary artery disease
CHF loss of contractility causes inefficient pump causes enlarged heart and loss of blood to organs and fluid accumulation (pulm edema) 3rd spacing
CAD-coronary artery disease decreased blood flow to coronary circulation, caused by arteriosclerosis (narrowing) or atherosclerosis (hardening), both lead to decreased blood flow and decreased efficiency
Angina pectoris chest pain, caused by lack of blood flow to heart from lack of o2 (ischemia) for contractions-early warning
Static angina predictable, caused by exercise, stress, excitement, or digestion of heavy metal, usually relieved by rest
Variant type angina caused by vasospasm of the coronary arteries-unpredictable and unstable, no pain fibers in heart, makes pain referred
*Nitrates and nitrites drugs that improve flow of O2 to myocardium, cause peripheral and coronary vasodilation by relaxing entire vasculature, <cardiac work so <need for O2 so <pain and <BP. In variant type the drugs relieve vasospasm and increase blood flow.
Normal BP <140/90
Secondary hypertension 10% of cases where cause is know, kidney disease, CHF etc
Diastolic resting pressure, most important number >130 is med emergency
Peripheral resistance vasoconstriction-tone or diameter of blood vessels
Increased BP bottom line >blood volume along with >vasoconstriction, 10-15% of population has it, leading cause of heart attack, stroke and kidney disease.
Calculating BP COxPR, where CO is HRxSV
Myocardial infarction heart attack, occlusion of blood supply to cardiac muscle, large enough-dead, tissue distal to blockage dies
*Cardiac glycosides Digitalis (prototype), very strong, positive inatrope (>contractility) increases CO and >perfusion, increase renal to <edema. Works by increasing ++Ca (calcium), <peripheral vascular resistance and >renal function, IV ONLY (FOXGLOVE)
*What is digitalis used to treat primarily CHF, but also atrial fib and flutter, TI is low and toxicity is very high, CARDIAC GLYCOSIDE
Digitalis and Digitoxin digitalis is IV only and digitoxin is by PO, once loading dose is found, cut to ¼ dose for maintenance
30% of strokes are caused by untreated atrial fib, blood pools in atria and coagulates, move to brain and causes clot
Sign of arrhythmias originating in the atria is aka supraventricular arrhythmias, narrow QRS, flutter RR 200-350, fib RR 350
Reasons for converting arrhythmias include warning of potential problem or problem has occurred, extreme anxiety or fear, infarction has occurred, greatly decrease efficiency of heart, decrease o2 deliver to heart (cause of PVC’s)
Causes of arrhythmias 1.ischemia (lack of O2), occlusion and infarction, 2 dehydration, 3 electrolyte imbalance, 4 drugs (digitalis) 5 congenital and idiopathic causes
Classes of anti-arrhythmic drugs group I-block sodium channels to prevent depolarization, < cardiac irritability, Group II-beta blockers to <HR, Group III-neuronal blockers, Group IV-calcium channel blockers (antagonist)
*Group I anti-arrhythmic drug lidocaine (Xylocaine), sodium channel blocker, used in ventricular irritability, <contractibility
*Group II anti-arrhythmic drug propranolol (Inderal), Beta blocker, used to treat supraventricular tachycardia, <HR
*Group III anti-arrhythmic drug Amiodarone, a-adrenergic neuronal blocker, used for tx of V-tach, side effect is lung damage
*Group IV anti-arrhythmic drug verpamil (Calan), calcium channel blocker, used in advanced life support, calcium antagonist
*Hypertension is caused by <kidney perfusion causes release of rennin causes BLA BLA then ANGIOTENSIN II to form which causes vasoconstriction and hypertension
Hypertension TX diuretics, Beta-blockers, ace inhibiters aka Ace-I’s (a antagonists)
*What is the side effect of Ace-I’s DRY COUGH
*Lasix loop diuretic, most potent hypertension diuretic, cause loss of Na+ and K+, need careful monitoring of chloride and potassium
*Thiazides diuretic, FIRST LINE W/B-AGONIST used in mgmt of hypertension, inhibits reabsorbtion of sodium (K+)
Osmotic diuretics work by osmotic pressure
What are the most popular diuretics osmotic and thiazides
Chronic atrial fib causes blood clots that lead to stroke, treat with anticoagulants
Anticoagulants clot preventers, anti-platelets and heparin
Anti-platelets are aspirin, plavix and fish omega 3
Heparin (prototype) IV only inhibits thrombin, and Coumarin (oral) inhibits prothombin
Clot busters/THROMBOLYTICS AKA TOA streptocanase and urocanase (MOST COMMON)
Hyperlipidemic agents drugs that lower fat, triglycerides and cholesterol in the blood
What is the most common arrhythmia atrial fib
All of the following statements about cardiac glycosides are true >intracellular calcium, >force of contraction, >stroke volume and cardiac output, <peripheral edema
An arrhythmia can cause symptoms ranging from mild palpitations to cardiac arrest T or F True
Anti-arrhythmic drugs are calcium channel blockers, beta blockers, adrenergic neuronal blockers, sodium channel blockers
INDICATION OF B-BLOCKERS HYPERTENSION, ANGINA AND CHF (not asthma)
WHAT CAUSES RELEASE OF RENIN <BLOOD FLOW TO KIDNEYS
HYPERTENSION BP>140/90
NEUROTRANSMITTER FOR PARASYMPATHOMIMETIC ACH
4 MG TAB QID, MED COMES IN 2MG TABS, HOW MANY TABS FOR ONE DOSE 2 TABS
DRUG IS AVAIL IN 250MG/10ML SOLUTION, WHAT % STRENGTH IS THIS? 2.5%, MG EQS MLx%x10, so 250 eq 10mlx%x10, so 250mg eqs 100%, solve for %, 250/100 eqs 100%/100 so 2.5 eqs % or 2.5%
DRUG COMES IN 5MG/ML WHAT % STRENGTH IS THIS .5%, 5mg eqs 1ml x % x 10, so 5mg eqs 10%, solve for %, 5/10 eqs 10%/10 so .5 eqs %, or .5%
WHAT % OF MED IS DEPOSITED ON MUCOSAL SURFACE DURING SVN 10-20%
WHAT HORMONE IS A POTENT VASOACTIVE CHEMICAL CAUSING HYPERTENSION ANGIOTENSIN II
FIRST LINE TX FOR HYPERTENSION IS THIAZIDE DIURETICS AND B-BLOCKERS
HOW DO ACE-I WORK BY BLOCKING ANGIOTENSIN I FROM BECOMING ANGIOTENSIN II
Created by: williamwallace