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Adv Rx Test 2
WillWallace Adv RX Test 2 Ch 5,10,14,16
| Question | Answer |
|---|---|
| *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
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