Nursing 320 EXAM 2 STUDY GUIDE Complete
Nursing 320 EXAM 2 STUDY GUIDE Complete In preparation for the exam next week: Have a solid grasp on drug classes and names. Feel confident in interchanging a drug between its “class name” vs the actual generic name. Know when and why a drug might be used. Focus on your nursing considerations (intended and unintended outcomes). Exam 1 was split between concepts and drugs, now we are 100% testing on drug therapies. 1 ) Go through the study guide 2) Review your quizzes + assignments 3) Practice the cases at the end of each chapter 4) I am going to work on a small practice exam and will let you know when I post it 5) If you have time, ATI provides some extra practice questions via Pharmacology Made Easy. Go to MY ATI - Learn Tutorial is called Pharmacology Made Easy 3.0 1) The Cardiovascular System (ignore anything we didn’t discuss like dysrhythmia drugs) 2) Endocrine (ignore all the oral diabetes meds) 3) Respiratory (decent amount of questions here) A few helpful tips: • SLEEP WELL before the exam- numerous studies have shown the importance of sleep and its formation, storage and recall of memories. As a side note, some sleep experts (Dr. Matthew Walker -being the leading voice in my opinion) argue drowsy driving is more dangerous than drunk driving. Let that one sink in. • The exam is 60 questions, 90 minutes • Exam questions consist of multiple choice and select all that apply***** • There is no back tracking (SON policy) • No food/drinks are allowed (NCLEX policy) • You CAN write on the attestation form o Feel free to write down any concerns/comments about an exam question on this form as we do read your comments after the exam o If you have a question- write out the entire question, don’t just write the question #, everyone’s exams are randomized • We utilize Examsoft, our IT team is typically around for the first 10 minutes of exam time in case any problems arise. • The exam is open for review IMMEDIATELY after completion of the exam. Review your exam so you understand any questions should you have answered incorrectly. • I will review the item analysis of each exam ALONG with your attestation form comments and implement corrective measures should they be needed. • GOOD LUCK! WEEK 4- RESPIRATORY 1. Respiratory Drugs a. Pathophysiology Review i. Asthma/COPD 1. Acute vs.Chronic a. Acute inflammation: Type I hypersensitivity, reversible i. Inhaled allergen – activation of cells (IgE) ii. Rapid activations – mast cells, neutrophils and eosinophils, inflammatory soup iii. Bronchoconstriction (smooth muscle contraction) iv. Musous secretion, vasodilation, edema v. GOAL: stop acute inflammation, it will lead to chronic inflammation which can cause fibrosis and scarring COPD b. Chronic Inflammation – COPD, irreversible i. Airway remodeling ii. Pathological changes sub-epithelial fibrosis iii. Excessive secretions iv. Smooth muscle hypertrophy v. Emphysema – alveola wall damage, surface area where gas exchange occurs is reduced and effective respiration is impaired 2. Intrinsic vs. Extrinsic a. Drug Induced i. NSAIDS – inhibit cox enzyme, which cause excessive arachidonic acid, causing leukotrienes to react. b. Allergens – inhaled allergens – activation of IgE c. Pathophysiology i. Antibody- IgE ii. WBCs- Mast Cell iii. Inflammatory Soup 1. Leukotrienes 2. Histamine b. Lower Respiratory Drugs 1. Bronchodilators a. Administration Essentials i. Administration of Inhalers ii. Time Between Doses 1. 1-2 minutes between puffs as a general rule 2. When using different inhalers: wait 2-5 minutes iii. Time Between Different Inhalers iv. Inhaler hierarchy 1. FIRST: albuterol (SABA) because it works immediately 2. Then, if you want a steroid, the lungs are dilated and it will absorb better 3. Use the SABA before an ICS 4. SABAs are RESCUE 5. Long acting are meant for CHRONIC use b. Short acting Beta 2 agonists (SABA) i. Albuterol/levalbuterol 1. Used to Treat: a. Drug of choice for acute asthma exacerbation and prevention of exercise induced bronchospasm b. PRN to stop an attack or prevent one from occurring c. Off label for hyperkalemia (there are other, better options for this) 2. Albuterol is 50/50 R/S enantiomers 3. Isolated R-albuterol is called levalbuterol 4. MOA: Activation of beta 2 receptors activates cyclic adenosine monophosphate (cAMP), which relaxes smooth muscle in the airway and results in bronchial dilation and increased airflow 5. Adverse effects: a. Tachycardia/palpitations, angina b. Tremors (skeletal muscle), excitability/nervousness c. Throat irritation/hoarseness – ALL INHALERS d. Rarely hypokalemia 6. Nursing Considerations: this is a rescue inhaler – keep it wither you! a. Exhale first, deep slow inhale 3-5 seconds, getting full amount deep into lungs, hold breath for 5-10 seconds to allow drug to be deposited into lungs b. Report any heart related effects c. Intended outcomes – relief of wheezing, bronchodilation, decreased cough c. Long acting Beta 2 agonists (LABA) i. Arformoterol/salmeterol 1. Used to treat: a. Chronic usage, never PRN b. Asthma and COPD 2. MOA – Same as SABA, just long acting a. By activating beta 2 receptors in lung smooth muscle, this promotes bronchodilation 3. Adverse a. Tachy/palpitations, tremors (skeletal muscle), angina, nervousness/excitability b. Throat irritation/hoarseness c. QTc prolongation d. Hypokalemia e. BOXED WARNING – increased risk for asthma related death when used as a monotherapy – ALWAYS combine with another drug – often inhaled corticoid steroid 4. Nursing considerations a. Patients must be educated that this is NOT a rescue inhaler b. Not fast acting c. Does not treat asthma attack d. PREVENTS asthma attacks d. Short acting Muscarinic antagonists (SAMA) i. Ipratropium 1. Used to treat: a. FDA approved for bronchospasm with COPD b. Commonly used for bronchospasm with Asthma c. Alternative use for patients who can’t tolerate a SABA 2. MOA – block muscarinic cholinergic receptors found in the bronchi, preventing bronchoconstriction…not quite as fast acting as albuterol 3. Adverse effects a. Most common is dry mouth - Xerostomia b. Throat irritation/hoarseness c. This drug is rarely absorbed systemically: i. Constipation/urinary retention/nausea ii. Rarely – increase HR, anticholinergic A/Es iii. Disease states to watch out: GLAUCOMA, BPH e. Long acting Muscarinic antagonists (LAMA) i. Tiotropium 1. Used to Treat: long acting for COPD/Asthma, takes time to see the full effects 2. MOA – block muscarinic cholinergic receptors found in the bronchi, preventing bronchoconstriction 3. Spiriva – put pill inside inhaler – powdered – do not swallow pill! 4. HFA – shake before use - aerosolized 5. Adverse: Same as SAMAs a. Most common is dry mouth – stay hydrated – sugar free gum b. Throat irritation/hoarseness c. This drug is very rarely absorbed systemically d. Rarely – increased heart rate e. Anticholinergic adverse effects? f. Glaucoma/BPH 6. Nursing Considerations (Same as SAMA) a. Don’t swallow the pill! It is crushed and inhaled f. Xanthine Derivatives – first in the class – caffeine. Methylxanthine i. Theophylline 1. Used to treat: Chronic COPD/Asthma, not for mild cases 2. MOA: 2 parts a. 1 – acts like caffeine b. Causes bronchodilation c. Increases alertness (may help with respiratory alertness in brain) d. 2 – Inhibits PDE-4 phosphodiesterase – 4, cleaving enzyme. This normally destroys cAMP, means longer duration of bronchodilation e. Theophylline antagonist at adenosine receptor 3. Adverse effects – the body converts theophylline to caffeine a. N/V, anorexia, headache, dizziness b. Increased urination c. Palpitations, tachy, dysrhythmias d. Seizures e. Narrow therapeutic drug 4. Nursing considerations a. Know the RANGE – 10-20 mcg/ml b. Don’t take any caffeine with the drug c. Metabolism is easily influenced by other drugs, be careful d. Old drug, not used as much anymore 2. Anti-Inflammatory Drugs a. Leukotriene Modifiers i. Montelukast 1. Used to treat: a. Prevention of exercise induced bronchoconstriction b. Asthma 2. MOA – blocks leukotriene receptors located in the lungs…reducing risk of asthma attack 3. Adverse – headaches a. Neuropsychiatric events such as depression, anxiety, sleep disorders b. Nursing considerations b. Inhaled Corticosteroids ICS i. Fluticasone i. Educate about the potential for neuropsychiatric events ii. It’s a pill, not fast! iii. Take in the evenings iv. Take 2 hours prior to exercise c. Upper Respiratory Drugs 1. Used to treat – Common: inhaled – chronic COPD/Asthma a. We used IV versions for immediate acute attacks b. We use oral versions for a few days after the acute attacks 2. MOA – corticosteroid with anti-inflammatory activity (inhibits mast cells, histamine, leukotriene, many ‘phils,’ prostaglandins a. 20-25% of gene expressions are changed when you use steroids – suppress immune system 3. Adverse – oral Candidiasis “thrush” a. Throat irritation b. Reflex cough/bronchospasm c. Minimal systemic absorption, but still potential for adrenal suppression d. Systemic: i. Delayed growth in children ii. Bone mineral density loss iii. Hyperglycemia iv. Fluid/electrolyte imbalance – retain fluid v. GI ulcers vi. Immune system suppression 4. Nursing considerations a. Always use your fast-acting inhaler first b. Wash out mouth! c. Monitor for the systemic absorption d. Taper off oral/IV regimens 1. Antihistamines – drugs that directly compete with histamine for specific receptor sites (H1-H4). Two histamine receptors (H1-lungs, blood vessels and H2-Stomach, GI lecture) a. Histamine i. Constriction of smooth muscle – lungs H1 ii. Increase in body secretions – stomach acid H@, mucous H1 iii. Pruritus H1 iv. Sneezing H1 v. Vasodilation and increased capillary permeability H1 – fluid out of the blood vessels – BP/edema b. Antihistamines have several properties i. Antihistaminic ii. Anticholinergic iii. Sedative c. 1st Generation – antihistamine + anticholinergic, will sedate you i. Diphenhydramine 1. Used to treat: allergies, insomnia, motion sickness 2. MOA – blocks histamine receptors found centrally and peripherally in the body 3. Adverse – CNS sedation (dangerous with other drugs) a. Weight gain b. Blocking of histamine receptors in brain, also somewhat blocks acetylcholine receptors in the brain c. Anticholinergic effects – can’t see can’t pee can’t spit can’t shit 4. Nursing considerations a. Reduce inflammation and itching b. Concerns with other diseases: Geriatrics/Urinary Retention/Glaucoma c. Concerns with other drugs: opioids/EtOH, Benzodiazepines, Barbiturates d. 2nd Generation i. Loratadine Claritin 1. Used to treat: allergies 2. MOA – blocks histamine receptors found peripherally ONLY 3. Adverse – same as Benadryl, but NON sedating 4. Nursing consideration a. Geriatrics/urinary retention/glaucoma, still need to be aware 2. Decongestants i. Pseudoephedrine 1. Used to treat: primarily for nasal congestion 2. MOA – adrenergic agonists (primarily alpha) a. Goal is to constrict nasal blood vessel, secretions can now drain better 3. Adverse – increased HR, increased BP, arrhythmias – anxiety insomnia, tremor a. rebound congestion – no more than 3 days 4. Contraindications: known hypertension, heart disease a. Other mediations that can increase BP b. Glaucoma 5. Nursing considerations a. Educate patients that they should limit dosing- risk for systemic adverse effects 3. Cough Suppressants a. Opioid i. Codeine b. Don’t use for more than 3 days - hypercongestion c. Screen patients for contra-indications: heart disease/HTN, Glaucoma b. Non-opioid 1. Suppress the cough reflex by direct action on the cough center in the medulla 2. Works on cough reflex in the brain i. Benzonatate 1. Suppress the cough reflex by numbing the stretch receptors in the respiratory tract and preventing the cough reflex from being stimulated 2. Don’t chew, can numb the mouth! c. Opioid-Derived i. Dextromethorphan (+guaifenesin) 1. Suppress the cough reflex by direct action on the cough center in the medulla 2. Hallucinogen at extremely high doses (like ketamine) 3. Don’t give with MAO-I’s 4. Not controlled – sold OTC 5. Patients should report effectiveness of drug 6. Also acts as NMDA receptor antagonist 4. Expectorants a. Guaifenesin i. Reduces the viscosity of respiratory mucus ii. No common adverse effects iii. Take with a full glass of water! iv. No better than placebo 5. Mucolytics a. Hypertonic saline – helps with thinning of the viscosity of the mucus b. Acetylcysteine WEEK 5- HYPERTENSION, DIURETICS, DYSLIPIDEMIA 1. Hypertension Drugs – BP = CO X SVR a. Pathophysiology Review i. Sympathetic Nervous System: over activity, systems are set at high, enhanced sodium retention, insulin resistance, baroreceptor dysfunction ii. RAAS – excessive release of one of the en
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Subjects
- musous secretion
- vasodilation
- acute inflammation
- bronchodilators
- inhaler
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bronchoconstriction smooth muscle contraction
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pathological changes sub epithelial fibrosis
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emphysema – alveola wall damage