1) Know nasal decongestants, main category of decongestants used routinely, common names, side effects, advantage of nasal vs oral

decongestants, nursing assessment when using decongestants, when to discontinue inhaled decongestants and after how many days: Sympathomimetics like pseudoephedrine or pheylephrinework on the A1 receptors and constrict the arterioles in the nose, reducing the thickness of the mucosa layer, and thus widening the airway to allow more air to enter. Watch out w/ DM b/c it increases the breakdown of glycogen (raises blood sugar). There are local & systemic decongestant, systemic drugs have the most side fx (dysrhythmias & hypertension), oral decongestants are not good for ppl w/ high BP (due to sympathetic fx). Inhaled (afrin) should be taken 3-5 days max or else pt can have rebound congestion, pt should use inhaled steroid if over 3-5 days 2) Know antihistamines, common antihistamines used for allergies, First generation and second generation, difference between these two groups, difference in receptors from histamine receptors found in the stomach, common side effects of antihistamines, nursing teaching, monitoring and contraindications: Antihistamines works to block histamine 1 receptors, [*H2 receptors are related to your stomach]. They tend to create anticholinergic side fx, cant pee, dry mouth, blurred vision, arrhythmias. Diphenhydramine (Benadryl) (1st generation antihistamine). 2nd genrn antihistamines cause less drowsiness but more expensive. Dont mix antihistamines w/ alcohol. Important teaching about antihistamines (think about what youd teach a pt about an anticholinergic): high fiber diet, lots of fluids, arrhythmias. Common drugs include Fexofenadine (Allegra), Claritin, Zyrtec, Clarinex 3) Know inhaled anticholinergics used in asthma and COPD, names discussed during class, uses, side effects, and contraindications: ipratropium (Atrovent), does not cause as much bronchodilation as sympathomimetic. If pt complains of dry mouth, offer a lozenge or piece of ice (not necessarily increasing fluids b/c the pt may have COPD or CHF), but the pt does not need to immediately stop taking the medication. Dry mouth is a common side effect of anticholinergic drugs. Not used for acute asthma attack. Never use w/ glaucoma! 4) Pseudoephedrine and reason for being placed behind the counter in pharmacies: used for meth production 5) Know asthma, treatment, goals of therapy, medications used to treat asthma acute attack vs prevention. Know common drugs discussed during lecture (SABAs, LABAs, Inhaled steroids, leukotriene modifiers, mast cells stabilizers, Xanthines), when to use one over another. Which ones are contraindicated for acute episodes, chronic, etc, mechanism of action of different categories discussed in class. 6) Know basic mechanism of action of antitussives: Dextromethorphan and opioids are antitussives. They suppress the cough reflex, dont give for a productive cough unless pt is having trouble sleeping at night 7) Know theophylline, when it is used in asthma treatment, therapeutic level and major side effects: No caffeine b/c this med behaves similar to caffeine, it is a sympathomimetic. Narrow safety margin; watch out for arrhythmias and Sz. Used prophylactically, not for acute asthma attack. Often used in other countries, not so much in the US, except when pt is unresponsive to the traditional therapies. 8) Know when a patient is taking an inhaled steroid and a SABA which one should be used first to enhance the effects of the medication (consider their mechm of axn): Take SABA first. The SABA will open up the airways in order for the steroid to enter & be effective. So take SABA, wait 5-10min for it to work and then take steroid 9) Mucolytics and their mechanism of action. Acetylcysteine (Mucomyst), works at a microscopic level to break the chemical bonds of the mucous and loosen it, thinning it out. 10) Know clinical picture of a patient in severe respiratory distress secondary to asthma and which medications to use in the acute exacerbation: ALWAYS Assess PEAK FLOW and RESP SOUNDS b4 and after admin of meds. If you here wheezing upon exhalation then they have asthma, wheezing upon inhale and

exhalation is getting bad and no breath sounds is an emergency b/c no air movement in or out, pt may need respiratory ventilation. Paradoxical breathing is when the pt takes a deep breath their belly goes up but the chest doesnt move (like a baby); it means the air is not getting into the lungs and its pushing down into the abdomen. A sign of resp failure is that w/ deep breathing their skin retracts into IC spaces. Asthma attack=hype-responsiveness to an allergen that increases smooth muscle constriction, mucous production and decreased air movement (mostly going out) causing hyperinflation of the alveoli. There is no cure. Airway edema is reversible but w/ recurrent exacerbations can cause lung remodeling. Asthma is caused by both genetic and environmental factors i.e. dust, smoke, environmental, even GERD, meds, exercise. Main goals of managing asthma: is PREVENTION, reducing the frequency of acute attacks and terminating acute bronchospasm when they occur, decrease the disability r/t the dz, decrease # of sick days, decrease nighttime symptoms, decrease lung remodeling, decrease use of short acting beta adrenergic agonists (SABA), and avoid triggers. Blacks and black children, then Hispanics, esp Puerto Ricans have the highest rates of asthma. Hyperinflation of alveoli significantly decreases the surface area and thus causes SOB & decr oxygenn. Dx through assessing Peak Flow, (measures how much air is expelled in 1 second ). 11) Know teaching with inhaled steroids and how to decrease side effects when taking this group of medications: Inhaled steroids have less side fx but take longer to work (5 days up to several weeks) than systemic steroids. Prolonged and improper use can cause steroid build up in your body same s/s for Cushings. Oral steroids, taken longer than 7-10 days, must be tapered off (dont want to get adrenal insufficiency). Steroids are for maintenance and inflammation, not for acute exacerbation, use SABAs. Fluticasone & Budesonide are both intranasal (inhaled) steroids. Steroids work by decreasing the secretion of inflammatory mediators, reducing tissue edema, and causing mild vasoconstriction. Steroids are dz-modifying drugs 12) Lipids, HDL, LDL, phospholipids, triglycerides and their role in the human body. Know which ones are healthy and which one increases the risk of coronary disease. Know normal and ideal levels and which patients are at higher risk of developing a heart attack. Know main classes of medications used to treat hyperlipidemia and their different mechanisms of action. Know first line medication to treat hypercholesterolemia and main side/adverse reactions, nurse monitoring with this group of medications and what to report to MD/NP, know which clients complaints should raise a red flag and which labs may be affected when developing adverse reaction. Know medications contraindicated with statins and what happens when you mix them. Know niacin and how to decrease a common side effect of this medication.

13) Know hypertension, components that affect blood pressure in the body, main organs affected by chronic HTN, different stages of HTN, different medications used according to stage and what is the first line drug for the treatment of HTN. Know mechanism of action of main groups of medications used for HTN, side effects and nursing monitoring. (diuretics, beta blockers, ACE inhibitors, ARBS, calcium channel blockers and alternative medications like direct vasodilators and alpha meds). Know labs to monitor with diuretics like HCTZ and loop diuretics, know which electrolyte can increase dig toxicity, know normal level of electrolytes monitored when patients are taking diuretics, diet that should be supplemented or encouraged, what foods should be avoided. Know beta blockers, mechanism of action, nursing monitoring before and after giving, how to stop these medications and rationale behind it. 14) Know beta blockers, selective vs non selective, know names of selective and non selective discussed in class. Know which group of patients can develop life threatening side effects. Nursing monitoring when administering beta blockers, mechanism of action etc. 15) Know digoxin, what effect does it have in the heart, main pharmacological uses, early sign and symptoms of toxicity, normal therapeutic range, reversal agent, and monitoring before administering. Know which electrolyte imbalance can increase dig toxicity.

16) Know heart failure, right vs left. Know first line drug for compensated heart failure, reason for using this medication. Know common side effects of ace inhibitors, know adverse reactions, and be able to identify drugs that are ace inhibitors. Know the difference in mechanism of action of ace vs ARBs. Know role of beta blockers in heart failure. Know which drugs affect mortality of patients with CHF by reversing remodeling vs symptom improvement like digoxin. 17) Know basic treatment of chest pain (cardiac in origin). MONA and reason for using this. 18) Know Nitroglycerin, uses, Mechanism of action, contraindications, drug interactions, patient teaching and common side effects. Know how many times patients can take SL nitro and time period between doses of sublingual nitro. Know what to do after 3rd nitro taken and no improvement of symptoms. 19) Know printzmetal angina and main medications used to treat it. Know medications name of this category discussed in class. Selective vs non selective. Know common side effects and what effect do they have on the RAAS system. How would this effect in the RAAS system show during your nursing assessment of the client? Review notes from wed, 3/21/12 review session Dobutamine is specifically for ppl w/ heart failure, it increases contractility but not the HR; should be used instead of dopamine w/ heart failure. You can tell dopamine, doputamine or any kind of vasocompressor is working when there is an increased in urine output, b/c by increasing the BP the pt will have increased kidney perfusion and thus incr urine output Anticholinergics (Atrovent) for asthma has few systemic sfx b/c its inhaled. The main thing you worry about with any anticholinergic is Glaucoma, then some other ones are BPH, tachycardia For acute exacerbations of asthma give SABA. Anaphylaxis: first drug to give is always epi. For allergic rxn the first line drug is Benadryl, it works faster than Zyrtec or other 2nd genrn drugs. Acute Asthma attack, take bronchodilator first (SABA) then after 5min once the bronchodilator works to open airways then you can take the inhaled steroid otherwise the steroid wont even reach where its supposed to go moNa: When a pt presents w/ chest pain you give moNa. Give oxygen first! Morphine will relax & vasodilate, nitroglycide is a preload reducer and its also gonna vasodilate the coronary arteries and then aspirin will prevent platelet aggregation (at least until fibrin takes over and wraps around the platelets) Selective Ca+ blocker (eg amlodipine/Norvasc) works only on the vessel. Nonselective works on the heart and the vessel used for Prinzmetal angina (spastic angina is not diet related or cholesterol, its just spasms, can happen to healthy ppl). Interaction w/ the RAAS: when you have dilation, blood pools (causes decr renal perfusion), this activates the RAAS system. Indications of water retention: edema, weight gain. Aldosterone cascade causes water retention (weight gaining) Mast cell stabilizers, leukotrienes, LABAs, and inhaled steroids are not used for acute asthma. SABAs are (and in practice anticholinergic nebulizers are too). Theophylline is used when everything else fails (level is 1020mcg). ***Digoxin therapeutic level 0.8-2.0, watch K+ w/ Digoxin. Low K=Dig tox. Important note for pts on diuretics, other than K+ sparing. Normal K+ levels: 3.5-5.0

Which diuretics causes low K+: Loop diuretics and TZD diuretics Hypokalemia is less dangerous than hyper b/c its less deadly and easier for pt to fix at home. Thiazides are given first line b/c they dont cause hyperkalemia like K+ sparing and they dont make you pee constantly as much that Loops (Lasix) does. Take diuretics in the morning not at night b/c of constant urination. The loop diuretic will cause more sever hypokalemia and hypotension than thiazides. JNC-7 stages of hypertension: below 120/80 is fine, Pre-HTN is 120-140/80-90, Stage I HTN is 140-160/90-100, Stage II HTN is 160+/100+. JNC-7 recommends thiazide diuretic as the initial drug for mild to moderate HTN (Stage I), but you may consider ACEI, ARBS, CCBs, or BBs on a case by case. For stage II the pt medn will depend on the other comorbidities, the pt cant leave the hosp w/o being on a BP medn If pt is taking a b-blocker and an ACE Inhibitor is added. What will happen? BBs decr HR & BBs decr HR & force, ACEs inhibit cr8n of Ang II causing vasodilatn (lowered systemic resistance) and also prevent secretion of aldosterone (lowered fluid volume) so together these drugs will be VERY effective at lowering BP, can cause excess hypotension (weak, dizzy, syncopal episodes). [If a test ever asks which med is likely to give syncopal episodes look for a BP medn as the correct answer]

Cut off HR to hold digoxin or b-blockers is 60bpm Statins used to treat hypercholesterolemia. Dont give erythromyocin/arithromyocin, azoles, and niacin cuz they increase the statin level in the blood by 40% which causes rhabdomyolysis and statins already put pt at risk for rhabdomyolysis. Hepatoxicity both AST & ALT will be elevated but AST will be more. Rhabdomyolysis: the big issue is myoglobinuria causing renal failure. Main Tx w/ rhabdo is increase fluids to help kidneys deal. Lab test for Rhabdo: Increased serum transaminase and cpk. Increased K+ b/c K+ lives in cells and muscle cells are lysing. Increased metabolic acidosis. Myoglobinuria. The test will come back positive for hematuria (b/c the test cant differentiate btwn the hemo- & myo- globins) but when the sample is viewed microscopically it turns out that there is no RBCs, it is not hematuria, it is myoglobinuria. Theophylline s/fx has a lot of cardiac probs, extreme tachy. It is used as a maintenance drug but it is outdated and rarely used. Cant take w/ caffeine b/c it is similar to caffeine. 3 types of lipids: triglycerides, phospholipids and steroids. Cholesterol is a major steroid in the body. Cholesterol is needed to make plasma membrane of the cell and serves as a building block for a # of essential biochemicals (vitamin D, bile aids, estrogen, testosterone, cortisol). However, cholesterol is needed in minute amounts and the liver can synthesize its own aka not needed in the diet. Lipids are not water soluble, so in order to move through the blood stream they use lipoproteins which is a ball of cholesterol, triglycerides, and phospholipids along with a protein carrier called apoprotein in order to move through the blood stream. The 3 common lipoproteins are: LDL, HDL, and VLDL LDL (think lethal): takes cholesterol to the sites or to the actual vessels for storage in the intimal layeratherosclerosis; level should be <130 but ideal is 100 HDL (think healthy): bring cholesterol into the liver in order to make bile or excrete it; level should be >40 and ideal is 60 VLDL: eventually turns into the LDL b/c it drops the triglycerides to the cells and then becomes LDL and goes to the vessels and deposits cholesterol

Triglycerides: level should be <150, 150-200 is borderline high, and 200-500 is very high. Triglycerides are an energy source, main drug to tx hypertriglyceridemia is fibric acid derivatives (look for fibr in the name) Aspirin: main drugs to prevent stroke & heart attack, prevents the coagulation cascade, prevents platelets from aggregating Nicotinic acids/niacin: dont worry about mech of action, but what it does is decr VLDL & therefore LDL and increases HDL. Has many s/fx and pts dont tolerate well at all (flushing must take w/ aspirin to reduce the release of prostaglandins) Absolute contraindication for nitroglycerin: Taking male enhancements (Viagra, Cialis, levetra). If pt has taken Viagra w/in the last 72 hrs they cannot have nitro. Can cause priapism/prolonged erection (you must drain the blood) and give alpha 1 blocker/enhancer??? Nitro and Viagra will cause hypotension & cardiovascular collapse Difference in drugs given for right sided HF (inferior wall MI), you would avoid nitro b/c of the hypotension. When pts are given nitro they must be given fluids when they have right sided HF. Nitro is more of a venous dilator than a coronary artery dilator, doesnt work on other arteries. Most med that dilate the arteries work at the level of the arterioles; it doesnt actually dilate the artery it works on the arterioles. For left-sided HF you would just give meds that are going to reduce the afterload (reduce peripheral resistance), e.g. BBs, Ace I, ARBs Pt w/ left sided heart failure will present w/ prob of the LUNGS (so think Left=lung) and right periphery. Left sided HF can cause right sided HF indirectly and eventually b/c the fluid from the left ventricle builds up in the lungs consequently increasing the amount of pressure in the lungs, increasing the workload of the Right Ventricle. Cor Pulmonale is right sided HF 2ndary to pulmonary HTN, they will present w/ preripheral sysmptoms i.e. JVD, ascites. Benadryl s/fx sleepiness, dry nose and throat, dry mouth (increase fluids, if pt has fluid restrxns then suck on candy, ice chips, lemon lozenge, stimulate salivary glands), constipation, dec urination