NURSING 3365 COURSE MAP Exam 2 (GRADED A) Questions and Answers | 100% GUARANTEED PASS.

NURSING 3365 COURSE MAP Exam 2 (GRADED A) Questions and Answers COURSE MAP: Exam 2 4. Antihypertensives a. What are the goals of therapy? To get the BP down and ease work of heart. We use BB and Alpha Blockers but Ace and ARB to open the peripheral resistance and reduce afterload so heart can do work easier. b. What is the relationship of CO to blood pressure? i. Orthostasis with first few doses c. Beta blockers prototype –propranolol i. Non-cardioselective- what does that mean? Doesn’t decide- affects lungs ii. What is the difference between propranolol and atenolol Look back at the sympathetic nervous system d. Alpha 1 Blockers see above e. Alpha 2 agonist see above f. Ace inhibitors Prototype lisinopril (Zestril) (angiotensin converting enzyme inhibitors) (See the Blackboard animation) pril- tells me its an ACE inhibitor. i. Hyperkalemia ii. Contraindicated in pregnancy / breast feeding iii. Angioedema iv. Dry cough – change to ARB g. ARBs Prototype losartan (Cozaar) (angiotensin II receptor blockers)–how do they differ from ACE inhibitors? Prevent to action Can they cause hyperkalemia? Yes and cause angioedema and airway can close airway (anaphylaxis) h. Calcium channel blockers i. Dihydropyridines versus D= Dilate Prototype: nifedipine (Procardia)- treats HTN ii. Nondihydropyidines N=Nodes Prototype: verapamil (Calan) diltiziazem(Cardizem) Slows heart rate and treats HTN i. What are the major side effects of each? Can get super constipated and need to be told need fluid and stool softener. Can get gingival hyperplasia 12. Diuretics a. What is the danger of diuretics with lithium? Don’t worry about Lithium b. What assessments are required for all diuretics? Well, number 1 allergies, known about weight, 2.2 grams per pound, know the 3 type, if they are pregnant, which is gentle or powerful. A bit if sulfur in all these diuretics and be aware of it ( doesn’t mean if someone has a sulfur allergy but be aware) c. Three different classes 1. Loops- Prototype - furosemide (Lasix) Given by oral if the gut works, patients get IV in hospital since blood supply to GI tract isn’t reliable and we want rapid and complete response. Never given fast and can cause ototoxicity like ringing in the ear. i. What are the indications for Lasix? ii. IV administration- never given fast – causes ototoxicity iii. Recognition of side effects- powerful and waste K and people can be hypokalemia and need for nerve conduction in heart and for muscle contraction so side effects will be: palpitation, skipped beats, feel weak, and muscle weakness. Ex: cardiac – conduction dysrhythmias - related to hypo or hyperkalemia musculoskeletal- hypokalemia –weakness, twitching ii. What’s the effect of diuresis from loop diuretics on serum creatinine? iii. ***If you measure daily weight, output and output for accurate dosage and diuresis and fluid. 2. Thiazides- Prototype- hydrochlorothiazide (HCTZ) (gentle and at low can be used alone or with another medicine for HTN affect) (reduction in preload and waste K so hypokalemia) a. Low doses – used for treatment hypertension b. Higher doses – diuretic effect c. Side Effects: Potassium wasting (hypokalemia) i. What’s the effect on serum creatinine? ii. Skin rash – why? Sulfur allergy and can also cause increase in uric acid and can cause gout. iii. Hyperuricemia- what does that cause? iv. Hyperglycemia v. Hypercalcemia 3. Potassium sparing Diuretics a. Two Pototype drugs-spironalactone (Aldactone) triamterene (Dyrenium) b. Potassium-sparing- prevent potassium loss c. What are the side effects common to both? GI upset, and in men is gynocomastia and in woman has abnormal periods and triamterene messes with folic acid. d. What is a specific side effect of spironolactone in men? Gynocomastia e. What is the anemia caused by triamterene? Listed above 4. Hypokalemia a. Replacement- what is preferred route of administration- oral (or through a gastric tube) b. How is it administered intravenously? Slowly over hours not minutes c. What is the risk for patient taking digoxin and diuretics if they develop hypokalemia? Go to BB and look at animation and calcium channel and look at digoxin and the pump and when blood level K low- more digoxin and can bind to gain entry so it does its thing (it allows cell to release calcium which increases force of contraction and slow HR) Hypokalemia=predispose to digoxin toxicity BUT sever toxicity can keep K in blood too much meaning Hyperkalemia 13. Drugs for heart failure and atrial fibrillation: A. Antihypertensives as above B. Digoxin a. Is it used in compensated or uncompensated heart failure? Is it the first drug chosen? Used when nothing else works. The rule is we listen to apical HR 1 minute and then less than 60 hold the dose and call prescriber. b. What is the mechanism of action of digoxin? (see Blackboard animation) 1. How does it affect cardiac muscle contractility? (positive inotrope) 2. What effect does it have on AV node conduction? (negative dromotropic) 3. What effect does it have on heart rate (negative chronotropic) 4. How does hypokalemia predispose to digoxin toxicity (see Blackboard animation). Watch it over and over until you get it. Discussed above 5. How does digoxin toxicity predispose to hyperkalemia? Discussed above c. Narrow therapeutic index drug (0.5-2 mg/ ml) d. Bioavailability issue Capsules vs tablets vs IV- are they all equivalent? Can patients switch between formulations safely? Shouldn’t be switching between formulations because they have different extents that they can be absorbed. Given IV and very slowly- like extremely slow otherwise we change the electron gradient across cell membrane and produce dysrhythmias. e. Long half-life – so how frequently is it given? Long half life- can be given daily but not with food due to binding up and pooping up. NO high fiber FOOD WITH medicine f. IV administration- very slowly due to electron gradient g. Drug interactions- many h. Toxicity i. Recognition- early vs late signs 1. Early signs and symptoms- malaise, GI upset (anorexia, nausea, vomiting) cardiac (abnormal rhythms - pt may complain of palpitations or skipped beats) musculoskeletal (muscle weakness- may be related to hypokalemia) 2. Late signs and symptoms- visual color changes happen late j. How is digoxin toxicity treated? 1. Mild- drug is held. – if its 2.2 (that’s barely above upper level) 2. Severe -Digibind: What is this and when is it used? This is also called Digifab and is super expensive. This is people who have a level of 6 and the K level is similar you would use this. k. Potassium -what’s the big deal with patients on digoxin? Do k+ and digoxin compete for the same binding site on the cell? (Look at the animation in Bbd). l. Suspect toxicity with loop diuretics –why? Watch the labs because diuretics also cause hypokalemia as well. m. Before administering drug check apical heart rate for one minute. When do you hold the drug and call the prescriber? When it is below 60. n. Check Lab results: serum Creatinine and Serum Potassium o. Patient Teaching 1How to take their pulse 2 What to report p. How do you know the drug is working? What symptoms and or signs should improve?**More urine output, less swelling and less preload and can feel pulse in feet and ankle, extremities warmer to touch and more energy and SOB will decrease. 14. Angina drugs:-Prototype nitroglycerine 57:02 A. Acute coronary syndrome versus stable angina. B. What is the goal of anti-anginal therapy? 1. Nitroglycerine a. Mechanism action – Converted to nitric oxide by sulphydrly groups – leads to vasodilation b. Short-acting versus long-acting nitrates i. What are each used for? ii. What drug formulations are short, which are long? iii. Why is a Nitrate-free interval necessary? (those sulfhydryl groups have to be regenerated overnight) We convert and we need sulphhydrol groups to do so and we tell patients to take patch off at night so 8-12 hour interval or if pills, don’t take anything after 5pm. This gives us enough time to generate more. iv. Sexual performance enhancement drugs (Viagra, Cialis) and dangers with Nitrates –especially IV nitroglycerine (they are both powerful vasodilators) c. Treatment of acute chest pain at home with sublingual nitroglycerine- How many? – at what interval? -and when to call 911? They need to put one under tongue and lay or sit down since it causes huge vasodilation and a buzz under the tongue and pain should subside 1 or 2 minutes and if that doesn’t happen, need to call 911. Can take a total of 3 at 5 minutes apart. d. Treatment of acute chest pain in hospital- when is it safe to give the second sublingual nitroglycerin? We go in and take vital signs and give sublingual nitroglycerin and now the systolic is below 90, do you give second dose? NO! They are vasodilator and it is below 90. e. Why wear gloves when applying nitroglycerin ointment? Comes in a tube and there is a grid and you squeeze in line and out it one clean skin and leave on for 12 hours. Take off old patch and rotate site and wear gloves to do so. f. IV nitrates – when and why? Male patient is asked if they have taken erectile dysfunction drugs because they work on different MOA- both can drop BP and that can be dangerous C. Patient teaching- for nitroglycerin tablets (safe drug storage and administration, and side effects). How will the patient know the drug is still good (potent)? Store in dark bottle and no high heat. 15. Lipid-lowering drugs- Look at Key Concepts on this a. Lipids: LDL, HDL, and triglycerides. Which drug classes work best on lowering LDL cholesterol? Statins and the lab test is a Lipid panel and looking at the LDL b. Side effects: i. Myalgias (muscle pain) (rare) ii. Rhabdomyolysis- rare but can be serious (muscle break down, leads to release of myoglobin which blocks renal tubules and leads to renal failure) c. Drug interactions with grapefruit and other CYP inhibitors- what happens to the free drug level and what can that lead to? This can increase the effect of the drug for predispose you to toxicity. d. Therapeutic effects of statins Prototype: atorvastatin (Lipitor ) reduced LDL cholesterol and triglycerides and increased HDL e. Pertinent labs Fasting lipid panel (to assess decrease in LDL cholesterol) i. Fibrates – Gemfibrozil (not recommended) decreases triglycerides (No longer recommended by the FDA). Can cause increased toxicity if given with statins. j. Niacin – mixed hyperlipidemia- not used much any more Used with High cholestol and high triclycerides and can cause flushing and itching so we tell them to take aspirin 30 minutes before to relieve that 1. Side effects: Flushing, burning, and itching (prevented with aspirin 30 minutes before Niacin) k. Bile acid sequestrants 1. Local effect only 2. Many drug-drug interactions 3. Increase fluid intake 4. Don't take other meds at same time 16. Parkinson’s drugs A. Parkinson’s disease is a progressive neurological disorder caused by loss of function of cells of basal ganglia. Reduced dopamine. Imbalance of dopamine and acetylcholine 1. Dopaminergic drugs- Prototype: Levodopa- Carbidopa pro-drug which is converted to dopamine. Why can't dopamine itself be given as a treatment for Parkinson's? a. What is the on and off versus end of dose phenomenon? KNOW THIS b. How do MAOIs help in Parkinson's disease? c. Why are MAO -B inhibitors preferred in Parkinson's? d. What is the "cheese effect"? e. Which antiviral agent was found to have anti-parkinson's effects- amantadine l. Anticholinergic drugs in this disease- Benadryl and Cogentin Used for EPS symptoms. 17. CNS drugs A. Stimulants a. Triptans for Migraine headaches (these drugs will be mentioned briefly) 1. Serotonin syndrome 2. Avoid in patients with heart disease b. ADHD medications- Prototype: methylphenidate (Ritalin) 1. Abuse potential in those without ADHD 2. Monitoring of desired outcomes: stable mood, improved concentration and grades in school and stable appetite and weight. 3. Adverse effects: decreased appetite, weight loss. c. Some stimulants still used in weight loss drugs (phentermine now combined with the antiepileptic drug topiramate to for Qsmia FYI not a prototype). Stimulants by themselves don’t work very long. Patient develops tolerance. d. What is the concern for M.I. with Cocaine abuse? Think about the stimulant sympathomimetic effect on arteries especially the coronary arteries. VERY powerful vasoconstrictor- ask drug history if they have had cociaine B. Depressants 1Alcohol- CNS depressants a. Metabolism chronic alcohol ingestion- CYP 450 inducer- reduces effect of other drugs 2. Withdrawal- prevention and treatment in the hospital- add a benzodiazepine like Prototype: lorazepam Ativan 3. Alcohol poisoning- can lead to temperature loss, respiratory depression coma and death a. Antabuse is used in hard-core alcoholics who are abstinent. It is considered an aversive agent because of the disulphram type reaction that will occur if they take a drink. They won’t die but they wish they would. This reaction can occur with very small amounts of alcohol. You will see it again with the antibiotic metronidazole(Flagyl). 4. Narcotics: Opioids 5. Marijuana 6. Combining CNS depressant drugs can cause severe respiratory depression and death 18. Anemia A. Iron deficiency- focus on this and when to give iron and when not too a. Prevention vs treatment (not all vitamin supplements contain iron- prenatal vitamins do contain iron) b. Patient teaching- we want drug to be absorbed properly 3. Administration of iron PO 4. Improving absorption- take with vitamin C – orange juice 5. Side effects of iron therapy- GI discomfort and black stools (expected outcome) c. Monitoring- CBC (Hemoglobin Hematocrit) and Iron studies we can give PO and occasionally give IV and there are precautions. B. Vitamin B12 deficiency versus folic acid deficiency- need both for making RBC a. Alcoholics - b. Malnutrition c. What is the role of folic acid supplementation in pregnancy- because lack of this can be linked to spina bifita and enechepholy. Shouldn’t be given folic acid until we know the cause of the anemia and folic acid is contraindicated in anemia. V12 given my I Muscular injection but other forms now C. Anemia of chronic renal insufficiency- Kidney produces erythropetin the hormone that stimulates the bone marrow to make RBCs. This is decreased in chronic kidney disease. If you have an insufficiency, you will develop anemia and get shot called Procrit to help bone marrow make RBC. We need to remember that they are procoagulants and can cause with uncontrolled HTN produce MI or stroke. ( if they have high BP or uncontrolled or if noncompliant) SO HTN is contraindication. a. use of ESAs ( erythrocyte stimulating agents) Prototype Erythropoetin alpha (Procrit) or darbopoetin alpha (Aranesp) c. Monitoring: These drugs can increase blood pressure and are procoagulants d. When would you hold these drugs? 19. Thyroid drugs A. Drugs for hypothyroidism a. Most commonly prescribed drug Prototype: levothyroxine (Synthroid) Show Less