Pharmacology Test 2

NUR2474 Test # 2 Review Please review general tips from Quiz review document (test taking strategies, select all that apply questions, etc.). The test will utilize Respondus browser and monitor (using webcam). No notes or textbook allowed on the test. Calculator will be enabled in the browser. General tips for studying: 1. Memorize names of medication categories from the presentation 2. Memorize key drugs from categories above (there are many questions with specific drug names) 3. Use generic names 4. When reviewing particular drugs note category, indications, common side effects, toxicity signs (if applicable), reversal agents, mechanism of action (e.g. agonizing or antagonizing which receptors) 5. Read question instructions (there will be ‘select all that apply’ questions) Topics to review: 1. Educating patients on how to use metered dose inhalers (wait 1 min between puffs, etc.). a. Metered dose inhaler: (MDI) handheld device delivering a measured dose of a drug with each actuation i. Dosing is usually accomplished with 1-2 inhalations ii. When 2 inhalations are needed, 1-minute interval is needed in between iii. Begin inhalation before activating device iv. Even with optimal use, only about 10% of the drug reaches the lungs, 80% is swallowed, and 10% is left in the device or exhaled. v. Spacers- attach directly to MDI to increased delivery of drugs to the lungs vi. After inhaler use rinse mouth and gurgle, especially with glucocorticoids (steroid), can cause the steroid to be absorbed through membrane 2. Know the difference between short and long term treatments for asthma and COPD a. Long term treatments i. Anti-inflammatory drugs (Glucocorticoids: inhaled or oral, leukotriene modifiers, cromolyn, omalizumab) 1. Corticosteroid 2. Minimize systemic effects ii. Bronchodilators (Long acting beta2 agonists, theophylline) iii. Drugs are taken daily for long term control iv. Glucocorticoids for long term prophylaxis (prednisone) b. Short term treatments i. bronchodilators (short acting beta2 agonists, anticholinergics: Tiotropium) 1. albuterol ii. Provide symptomatic relief but do not alter the underlying disease process (inflammation) iii. Asthma patients taking bronchodilators should also be taking glucocorticoids for long-term suppression of inflammation 3. Know classifications for respiratory drugs (what’s used as a rescue inhaler, and what is for long term management) a. Rescue inhaler i. Bronchodilator-beta 2adrenergic agonist 1. Albuterol (Proventil, Ventolin) 2. Terbutaline sulfate (brethine) 3. Indicated for acute exacerbations of asthma, relief of bronchoconstriction due to bronchitis and emphysema and longterm control of chronic airway disease. 4. Effects start within minutes and last for 2-4 hours. b. Long-term treatment i. Corticosteroids (glucocorticoids) –long term and prophylaxis 1. Fluticasone (flonase) 2. Budesonide (Pulmicort, rhinocort) 3. Prednisone (deltasone) 4. Methylprednisolone (solu-medrol) ii. Bronchodilators (antileukotriene-leukotriene receptor antagonists) 1. Montelukast (singulair) 2. Zafirlukast (accolate) 4. Treatment of acute asthma i. may have to give IV corticosteroid glucocorticoid short term; and give rescue inhaler. 1. May need to add albuterol, nebulizer treatment, oxygen, or ipratropium ii. Bronchodilators: beta2 adrenergic agonist 1. Action: activation of beta2 receptors in the smooth muscle of the lungs, promotes bronchodilation, relieving bronchospasm a. Beta2 agonist have a limited role in suppressing histamine release in the lung and increasing ciliary motility iii. Use: asthma and COPD 1. Inhaled short acting beta2 agonists (SABAs) a. Taken PRN to abort an ongoing attack b. EIB: taken before exercise to prevent an attack c. Hospitalized patients undergoing a severe acute attacknebulized SABA in the traditional treatment of choice d. Delivery with an MDI in the outpatient setting may be equally effective 2. Inhaled long acting beta2 agonist (LABAs) a. Long term control of patients who experience frequent attacks b. Dosing in not PRN. It is on a fixed schedule c. Effective in treating stable COPD d. When used for asthma, must be combined with glucocorticoids e. Use alone in asthma is contraindicated 3. Adverse effects: a. Inhaled- systemic effects: tachycardia, angina, tremor b. Oral- excessive dosage: angina pectoris, tachydysrhythmias, tremor 4. Other treatments of acute asthma a. Nebulizer (Albuterol), ipotropium, oxygen, IV glucocorticoids 5. Administration of glucocorticoids (IV vs inhaled, nursing interventions, pt. education) a. Anti-inflammatory drugs: Glucocorticoids (long term treatment for asthma) b. Mechanism of action: most effective antiasthma drugs i. Prophylaxis to prevent exacerbations with opioid use, there is a good chance they will develop constipation ii. Docusate is a good option. iii. Gentle softener to help them with constipation iv. Prophylaxis until they do develop severe constipation, then go for more intense treatment options v. Decrease synthesis and release of inflammatory mediators vi. Reduce infiltration and activity of inflammation cells vii. Decrease edema of the airway mucosa caused by beta2 agonists viii. Usually administered by inhalation, but emergency situation- IV/oral routes also available c. Side effects: d. e. f. g. h. i. Can slow growth in children/adolescents. However, does not decrease adult height ii. Promotion of bone loss iii. Increased risk for cataracts iv. Increased risk for glaucoma Discontinuing medication: must be done slowly i. Recovery of adrenocortical function may take months ii. Dosage of exogenous sources must be reduced gradually iii. Must be given supplemental oral or IV glucocorticoids at times of severe stress Use: not a PRN (as needed) medication i. Prophylaxis of chronic asthma ii. Not used to abort an ongoing attack because beneficial effects develop slowly Inhaled use i. First line therapy for management of inflammatory component of asthma ii. Those with persistent asthma should use these drugs daily iii. Inhaled glucocorticoids are very effective and much safer than systemic glucocorticoids iv. Adverse effects: adrenal suppression (prevents the body from producing glucocorticoids on its own), oropharyngeal candidiasis(infection), dysphonia (rough voice changes) IV use i. Compensating for adrenal insufficiency ii. Patients on prolonged glucocorticoid therapy have a decrease endogenous production of glucocorticoids iii. If use is stopped suddenly or when switching from oral to IV therapy, the patient can die iv. During times of severe physical stress when the body would normally produce high levels of glucocorticoids, if the dose is not increased to meet the needs, the patient can die v. IV glucocorticoids are given at times of severe stress to compensate for adrenal insufficiency Oral use i. For those with moderate to severe persistent asthma or for management of acute exacerbations of asthma or COPD ii. Potential for toxicity; should be used only when symptoms cannot be controlled with safer medications (inhaled glucocorticoids, inhaled beta 2 agonist) iii. Treatment should be as brief as possible iv. Adverse effects: short term therapy, long term therapy, adrenal suppression, osteoporosis, hyperglycemia, peptic ulcer disease, growth suppression in young i. Patient education i. To minimize adverse effects patients should rinse mouth with water and gargle after each administration or use a spacer ii. To prevent bone loss patients should ensure adequate intake of calcium, vitamin D, and participate in weight bearing exercises 6. Tiotropium administration, onset, and therapeutic level timeframes a. Anticholinergic b. Long acting, inhaled agents approved for maintenance therapy of bronchospasm associated with COPD c. Not approved for asthma d. Action: relieves bronchospasms by blocking muscarinic receptors in the lungs e. Therapeutic levels: therapeutic effects begin about 30 minutes after inhalation, peaks in 3 hours, and persists about 24 hours i. With subsequent doses: bronchodilation continues to improve, reaching a plateau after 8 consecutive doses (8 days) ii. Adherence is very important f. Adverse effects: dry mouth (eating hard candy may help), minimal anticholinergic effects 7. Treatment principles of cold symptoms in children (treat individual symptoms) a. When treating pediatric upper respiratory infection, colds, allergies etc. avoid combination medications. Treat individual symptoms. b. One medication at a time for once symptom at a time, no combination drugs. i. If child has a cough, give med that is only used to treat cough. c. Avoid OTC cold remedies in children younger than 4-6 years d. Use only products labeled for pediatric label e. Avoid the use of antihistamine containing products to sedate children 8. Ulcer prevention with chronic NSAID use (identify specific med class) a. Most common cause of peptic ulcer- H. pylori bacteria. 2nd is NSAIDs b. Ulcer prevention with chronic NSAID use i. Drugs act in 3 basic ways to promote ulcer healing/prevent reoccurrence: (1) eradicate H. Pylori, (2) reduce gastric acidity, and (3) enhance mucosal defenses ii. NSAID-induced ulcers can be treated with any ulcer medication. However, histamine2 receptor blockers and proton pump inhibitors are preferred. c. Antiulcer drugs i. Antibiotics 1. Amoxiciilin (Amoxil), Busmuth (pepto-bismol), Calrithromycin (Biaxin), Metronidazole (Flagyl), Tetracycline, Tinidazole (Tindamax) 2. Action: eradicate H.Pylori d. Antisecretory agents i. H2 receptor antagonists: Cimetidine (Tagamet), Famotidine (Pepcid), Nizatidine (Axid), Ranitidine (Zantac) ii. Action: suppress acid secretion by blocking H2 receptors on parietal cells iii. Proton pump inhibitors (PPIs): Dexlansoprazole (Dexilant), Esomeprazole (Nexium), Landoprazole (Prevacid), Omeprazole (Prilosac, Zegerid, Lodsec), Pantoprazole (Protonix, Pantaloc), Rabeprazole (Aciphex, Pariet) iv. Action: suppress acid secretion by inhibiting H+, k+ -ATPase, the enzyme that makes gastric acid; minimize secretion of gastric acid e. Mucosal protectant i. Sucralfate (Carafate) ii. Acute ulcer maintenance therapy iii. Action: forms a barrier over the ulcer crater that protects against acid and pepsin for up to 6 hours iv. Adverse effects: constipation (only 2% of patients) v. Drug interactions: antacids may interfere with effects of sucralfate f. Antisecretory agent that enhances mucosal defenses i. Misoprostol (Cytotec) ii. Action: protects against NSAID induced ulcers by stimulating secretion of mucus and bicarbonate maintaining submucosal blood flow and suppression secretion of gastric acid iii. Only approved GI indication is prevention of gastric ulcers by long-term NSAID therapy iv. Adverse effects: dose related diarrhea and abdominal pain v. Contraindicated: pregnancy g. Antacids i. Auminum hydroxide, calcium carbonate, Magnesium hydroxide ii. Action: react with gastric acid to form neutral salts iii. Side effects: constipation, diarrhea, sodium loading iv. Drug interactions: cimetidine. Take 1 hour apart v. Contraindications: use with caution in patients with renal impairment h. Antacid: Magnesium hydroxide (milk of magnesia) i. Adverse effects: diarrhea. Usually taken in combination with aluminum hydroxide, an antacid that promotes constipation ii. Avoided in patients with undiagnosed abdominal pain iii. Frequently used as a laxative iv. Use with caution in patients with renal failure 9. Antacids and Cimetidine (patient education) a. Antacids can reduce absorption of cimetidine: should be administered at least 1 hour apart b. Acid suppressants (antacids): prevent ulcers, interact with other medications. Consult doctor before taking. c. Cimetidine prevents GERD and prevent ulcers d. Food decreases rate of absorption but not the extent. i. Hence, if cimetidine is taken with meals, absorption will be slowed and beneficial effects prolonged. e. Most of each dose is eliminated intact in the urine f. Half-life is relatively short (about 2-3 hours) but increases in patients with renal impairment. i. Dosage should be reduced in these patients g. Adverse effects i. antiandrogenic affects ii. CNS effects (difficulty crossing blood brain barrier) iii. Pneumonia iv. IV bolus (can cause hypotension and dysrhythmias) h. Drug interactions i. Warfarin ii. Phenytoin iii. Theophylline iv. Lidocaine 10. General GERD treatment principles a. With severe GERD if patient is already taking histamine antagonist we may add long term treatment of omeprazole. (Proton Pump Inhibitors, PPI) i. Dexlansoprazole (Dexilant) is used for symptomatic GERD (heartburn) ii. Pantoprazole (protonix) b. Treat with drugs or surgery i. Pepcid 20-40 mg bid ii. Prescription-strength nizatidine 150 mg capsules bid c. 3 goals for treatment i. Relief of symptoms ii. Promotion of healing iii. Prevention of complications d. Lifestyle changes can compliment drug therapy but should not be substituted for drugs i. Smoking cessation, weight loss, avoidance of alcohol or late-night meals, and sleeping with an elevated head. 11. PPI’s side effects a. Although generally safe, PPIs can increase the risk of fractures, PNA, and hypomagnesemia and can cause acid rebound when treatment stops. b. Proton pump inhibitors: most effective drugs for suppressing secretion of gastric acid and preventing ulcers (prophylaxis) i. Prophylactically given to patients in hospital ii. Therapeutic use- short term iii. Gastric/duodenal ulcers iv. GERD c. Adverse effects: i. Fractures ii. Pneumonia iii. Acid rebound iv. possible intestinal infection with Clostridium Difficile (cdiff) d. Omeprazole (Prilosec) first available PPI i. Mechanism of Action 1. inhibits gastric secretions, short half-life, short term therapy ii. Ulcer prophylaxis is indicated only for patients in ICU, and only if they have an additional risk factors such as multiple trauma, spinal cord injury, or prolonged mechanical ventilation (longer than 48 hours) iii. Treatment can be lifelong iv. Adverse effects: 1. Headache 2. GI 3. Pneumonia 4. Fractures 5. Hypomagnesemia 6. Rebound acid hypersecretion 7. Diarrhea (most common) 8. C. diff infection 9. Gastric cancer 10. Bone demineralization leading to osteoporosis e. Pantoprazole i. Adverse effects 1. Oral admin a. Diarrhea b. Headache c. Dizziness 2. IV admin a. Diarrhea b. Headache c. Nausea d. Dyspepsia e. Injection-site reactions i. Thrombophlebitis and abscess 3. Long term use a. Hypomagnesemia b. Osteoporosis c. Fractures f. PPIs and older adults i. PPIs are associated with an increase in the risk of fractures from osteoporosis. ii. PPIs can also cause medication interactions and vitamin or mineral deficiencies. iii. There should be a clear indication for prescribing these medications in this older population. 12. Sucralfate (mechanism of action, interactions) a. Acute ulcer maintenance therapy b. Does not affect acid levels. IS NOT AN ANTACID. c. Action: forms a barrier over the ulcer crater that protects against acid and pepsin for up to 6 hours d. Adverse effects: constipation (only 2% of patients) e. Drug interactions: antacids may interfere with effects of sucralfate; do not mix with ciprofloxacin f. Fairly safe but can cause systemic S/E (rarely) g. Space out over a few hours 13. General principles of treating constipation a. IF THERE ARE NO BOWEL SOUNDS, DO NOT GIVE LAXATIVES. Instead do an x-ray. b. Constipation: one of the most common GI disorders i. Defined as: hard stool, infrequent stools, excessive straining, prolonged effort, sense of incomplete evacuation, unsuccessful defecation c. Treatment i. Dietary fiber 1. Bran is best source 2. Absorbs water- softens feces and increases size 3. Can be digested by colonic bacteria, whose growth increases feces mass 4. Low fiber diet- frequent cause of constipation ii. Laxative effect 1. Production of soft, formed stool over 1 or more days. relatively mild iii. Catharsis 1. Prompt, fluid evacuation of the bowel. Fast and intense. “Violent” d. Classification of laxatives i. Bulk-forming laxatives – Psyllium (Metamucil) 1. Function similarly to dietary fiber: swell with water to form a gel that softens and increases fecal mass (take with large glass of water) 2. Preferred temporary treatment of constipation 3. Used for diverticulosis and irritable bowel syndrome ii. Surfactant laxatives – Docusate sodium (Colace) 1. Produce a soft stool several days after onset of treatment 2. Alter stool consistency by lowering surface tension, which facilitates penetration of water into feces 3. May also act on intestinal wall to inhibit fluid absorption and stimulate secretion and water and electrolytes into intestinal lumen. 4. Resemble stimulant laxatives 5. Straining can lead to vasovagal response, can pass out and/or die iii. Stimulant laxatives – (Bisacodyl (Dulcolax) 1. Stimulate intestinal motility 2. Increase amount of water and electrolytes in the intestinal lumen 3. Widely used and abused 4. Used for opioid-induced constipation and for constipation from slow intestinal transit iv. Osmotic laxatives – milk of magnesia or magnesium hydroxide (MOM) 1. Laxative salts: poorly absorbed salts that draw water into intestinal lumen, fecal mass softens and swells, wall stretches, and peristalsis is stimulated 2. Low doses: results in 6-12 hours 3. High doses: results in 2-6 hours 4. Adverse effects: dehydration, acute renal failure, sodium retention (exacerbated heart failure, hypertension, edema) e. Bowel-cleansing products for colonoscopy (intense) i. Sodium phosphate (osmotic laxative) 1. Hypertonic with body fluids 2. Adverse effects: dehydration, electrolyte disturbance, nausea, abdominal discomfort, kidney damage, hyperphosphatemia- can cause acute reversible renal damage and possibly chronic, irreversible renal damage ii. Polyethylene glycol (PEG) plus electrolytes (ELS) 1. Isotonic with body fluids 2. Requires ingestion of large volume of bad-tasting liquid 3. Combination of sodium picosulfate, magnesium oxide, and citric acid f. Other laxatives i. Lubiprostone: selective chloride channel activator 1. Promotes secretion of chloride-rich fluid into the intestine and enhances motility in the small intestine and colon 2. Result is spontaneous evacuation of a semisoft stool, usually within 24 hours ii. Mineral oil 1. Mixture of indigestible and poorly absorbed hydrocarbons. Laxative action is produced by lubrication. Mineral oil is useful when administered by enema to treat fecal impaction 2. Adverse effects: lipid pneumonia, anal leakage, deposition of mineral oil in the liver iii. Glycerin suppository: osmotic agent that softens and lubricates hardened, impacted feces 1. May also stimulate rectal contraction 2. Evacuation occurs about 30 minutes after insertion 3. Useful for reestablishing normal bowel function after termination of chronic laxative use 14. Bulk forming laxatives administration principles a. Bulk-forming laxatives i. Make sure it’s taken with plenty of water. Full glass of water to eliminate adverse effect. ii. Function similarly to dietary fiber: swell with water to form a gel that softens and increases fecal mass iii. Preferred temporary treatment of constipation iv. Used for diverticulosis and irritable bowel syndrome v. Adverse effects: minimal. Esophageal obstruction 15. Opiate use related constipation and treatment a. With opioid use, there is a good chance they will develop constipation b. Docusate sodium is a good option. i. Gentle softener to help them with constipation c. Prophylaxis until they do develop severe constipation, then go for more intense treatment options d. After surgery, administer laxative to prevent straining. 16. Senna side effects a. Turns urine yellow/brown (expected finding. No concern) 17. Ondansetron (Zofran) a. Antiemetic; serotonin receptor antagonist i. Blocks 3 types of serotonin receptors on afferent vagal nerve ii. More effective when used with dexamethasone b. Uses i. Approved for chemotherapy-induced nausea and vomiting (CINV) 1. Prevents N/V associated with radiotherapy and anesthesia c. Side effects i. Headache ii. Diarrhea iii. Dizziness iv. Prolonged QT interval v. Risk of torsades de pointes 18. Concurrent use of Digoxin and Furosemide (monitoring, interactions) a. Digoxin should not be administered with diuretics such as furosemide! b. May require more frequent evaluation of digoxin, potassium, and magnesium levels 19. Digoxin a. Mechanism of action i. Increases myocardial contractility, increases cardiac output ii. Treats dysrhythmias AND can cause dysrhythmias b. Monitoring i. Monitor potassium ii. Monitor digoxin serum level for therapeutic range (0.5-0.8 mg/mL) iii. Monitor kidney function 1. Renal disease c. Interactions i. Diuretics ii. ACE inhibitors and ARBs iii. Sympathomimetics iv. Quinidine v. Verapamil vi. Grapefruit juice! d. Toxicity i. Therapeutic range: 0.5-0.8 mg/mL ii. Toxicity greater than 2 mg/ml iii. Nausea iv. Anorexia v. Diarrhea vi. Visual disturbances 1. Patients may report a yellow haze over visual field (halo) vii. Arrythmias viii. Generalized malaise ix. hypokalemia e. Administration i. Give once a day because half-life is 1.5 days 20. Furosemide a. Monitoring i. Monitor blood sugar levels ii. Monitor electrolytes iii. EKG iv. Dehydration v. Fall risk due to hypotension vi. Kidney function of patients on all diuretics! 1. Creatinine a. 0.84 to 1.21 mg/dl 2. Creatinine clearance: a. Men—110 to 150 ml/min b. Women—100 to 130 ml/min 3. Bun a. 10-20 mg/dl b. Interactions i. Digoxin ii. Ototoxic drugs iii. Potassium-sparing diuretics iv. Lithium v. Antihypertensive agents vi. NSAIDs vii. Gentamicin c. Indications for use i. Pulmonary edema ii. Peripheral edema iii. HF iv. Hypertension v. Acute hypercalcemia vi. Anion overdose 21. Concurrent use of Furosemide and gentamycin a. Furosemide and gentamicin (antibiotic) should not be mixed due to acoustic damage—tinnitus 22. Potassium wasting vs potassium sparing antibiotic use (specific med examples from each) a. Monitor electrolytes with all kinds of diuretics! b. Potassium wasting i. Help you get rid of excess fluid, fluid in the lungs. ii. Used to treat 1. Pulmonary, edematous states (swollen from fluid), hypertension. iii. Interacts with potassium sparing diuretics because loop diuretics make you lose potassium and potassium sparing diuretics make you save potassium. iv. Must give potassium to patient on potassium wasting diuretics. 1. Furosemide c. Potassium sparing i. Aldosterone antagonist 1. Spironolactone a. Mechanism of action i. Blocks aldosterone in the distal nephron ii. Retention of potassium iii. Increased excretion of sodium b. Uses i. Hypertension ii. Edematous states iii. HF (decreases mortality in severe failure) iv. Primary hyperaldosteronism v. Premenstrual syndrome vi. Polycystic ovary syndrome vii. Acne in young women c. Adverse effects i. Hyperkalemia ii. Benign and malignant tumors iii. Endocrine effects d. Drug interactions i. Thiazide and loop diuretics ii. Agents that raise potassium levels ii. Non-aldosterone antagonists 1. Triamterene a. Mechanism of action i. Disrupts sodium-potassium exchange in the distal nephron ii. Direct inhibitor of the exchange mechanism iii. Decreases sodium reuptake iv. Inhibits ion transport b. Therapeutic uses i. Hypertension ii. Edema c. Adverse effects i. Hyperkalemia ii. Leg cramps iii. N/V iv. Dizziness v. Body dyscrasias (rare) 2. Amiloride a. Mechanism of action i. Blocks sodium-potassium exchange in the distal nephron b. Therapeutic uses i. Counteract potassium loss caused by more powerful diuretics c. Adverse effects i. Hyperkalemia d. Drug interaction i. ACE inhibitors; other drugs with hyperkalemia 23. Angioedema (common meds that cause it, interventions) a. Potentially life-threatening—become an ICU patient b. Edema to tongue, lips, eyes c. Common meds that cause it i. Angiotensin-converting enzyme (ACE) inhibitors ii. Angiotensin II receptor blockers iii. Direct renin inhibitors 1. Intervention a. Emergency care should be sought immediately b. Patient must never take ACE inhibitors again! 24. ACE inhibitors (side effects, interventions, patient education) a. Side Effects i. First-dose hypotension 1. Change position slowly 2. Ask for assistance ii. Fetal injury—do not give to pregnant women iii. Dry cough 1. Patients that can no tolerate ACE inhibitors due to the DRY COUGH may need to switch to ARBs (Angiotensin 2 Receptor Blockers). ARBs do not have the coughing symptom. iv. Angioedema 1. Potentially life-threatening—become an ICU patient 2. Edema to tongue, lips, eyes 3. Patient should never take ace inhibitor again! v. Hyperkalemia 1. Should not be mixed with potassium-sparing diuretics vi. Renal failure 1. Limit blood flow to kidneys vii. Neutropenia b. Patient education i. All ACE inhibitors (except enalaprilat) are administered orally ii. All are available in single-drug formulations iii. All oral formulations (except captopril and moexipril) may be administered without regard to meals. iv. Do not use with pregnancy, can cause fetal injury. c. Drug interactions i. Diuretics ii. Antihypertensive agents iii. Drugs that raise potassium levels iv. Lithium v. NSAIDs d. Monitor/assess i. Electrolytes 25. Nifedipine and metoprolol (betablocker) concurrent use a. Combined with beta-blocker to prevent reflex tachycardia i. Beta blockers decrease the adverse cardiac effects of nifedipine but can intensify the adverse cardiac effects of verapamil and diltiazem. 26. Beta blockers a. Mechanism of action i. Decrease cardiac oxygen demand b. Contraindications i. Vasospastic angina ii. Do not use with verapamil or diltiazem iii. Bradycardia iv. Bronchospasm, Bronchodilators, bronchitis v. AV block vi. Asthma vii. Acute/uncontrolled heart failure viii. Hypotension c. Monitor/assess i. Electrolytes 27. Treatment of HTN in diabetes a. Goal is BP less than 130/80 mmHg b. Use ACE inhibitor for treatment 28. Amiodarone (side effects) a. Effects on the heart i. Reduced automaticity in SA node ii. Reduced contractility iii. Reduced conduction in velocity iv. QRS widening v. Prolongation of PR and QT intervals b. Adverse Effects i. Protracted half-life ii. Pulmonary toxicity iii. Cardiotoxicity iv. Toxicity in pregnancy and breast-feeding v. Corneal microdeposits vi. Optic neuropathy c. Can produce itching, malaise 29. Magnesium elimination in the body a. magnesium hydroxide is given for constipation, heartburn, laxative, and antacid b. use with caution in patients with renal failure c. most prominent adverse effect is diarrhea d. avoided in patients with undiagnosed abdominal pain. i. When you have patient, who is constipated and has a distended stomach with abdominal pain. Could be constipation. But it could also be something else. TAKE AN X-Ray FIRST. 30. HMG-COA reductase inhibitors (statins)—cholesterol meds a. Timeframes for administration i. Administer at night! ii. Once daily, in the evening to mimic natural body processes b. Max effect i. Takes a few weeks to take full effect, then recheck cholesterol levels 31. Lovastatin (HMG-COA Reductase inhibitors) a. patient education i. Take the medication with the evening meal to increase absorption; cholesterol synthesis normally increases during the night; statins are most effective given in the evening. b. Drug interactions i. Most other lipid-lowering drugs (except bile-acid sequestrants) ii. Drugs that inhibit CYP3A4 iii. Use in pregnancy 32. Concurrent use of Colesevelam and Insulin a. May cause hypoglycemia, increased risk for diabetes. i. Monitor sugar levels 33. Cholesterol lowering agents a. HMG-CoA Reductase inhibitors—Statins lower LDL i. Help to increase HDL cholesterol. Reduce LDL most effectively. Increase bone formation. 1. Give statins at night. All of these drugs end in ‘statin’ 2. Side & Adverse effects: Headache, rash, GI disturbance, rhabdomyolysis, myopathy, hepatotoxicity, cataracts, new onset diabetes. 3. Interactions: Other lipid lowering drugs, don’t use during pregnancy, drugs that inhibit CYP3A4. b. Fibric-acid derivatives lower TG levels i. Fibric Acid Derivatives (Fibrates): can increase risk of bleeds for patients taking warfarin. 1. Side Effects: rash, gallstones, myopathy, liver injury, gastrointestinal upset. c. Nicotinic acid reduces LDL and TG levels i. Nicotinic Acid (Niacin): if someone has gout probably should not give niacin. Reduces LDL and TG levels. Increase HDL more effectively than other drugs. 1. Adverse effects: rash, itching, hepatoxicity, hyperglycemia, gouty arthritis, gastrointestinal upset, can raise blood levels of uric acid. d. Bile-acid sequestrants (cholestyramine, colestipol, colesevelam)- Reduces LDL i. Used in adjunct to statins. come as a powder can be mixed with any liquid. Form complexes with bile salts trapping cholesterol making you secret cholesterol. Prevents reabsorption of bile acids. Reduces LDL. Increased VLDL in some people. 1. Side effects: constipation, abdominal bloating, abdominal discomfort. e. Patient education i. only use drugs when modifiable lifestyle changes fail. ii. HDL is often called good cholesterol or healthy cholesterol because it seems to protect against atherosclerosis. iii. LDL promotes atherosclerosis which makes it “bad cholesterol” f. Cholesterol levels i. Total cholesterol level: 1. Acceptable: <170 2. Borderline: 170-199 3. Elevated: 200+ ii. LDL 1. Acceptable: <110 2. Borderline: 110-129 3. Elevated: 130+ iii. HDL 1. Females: 35-80mg/dl 2. Males: 35-65mg/dl 3. Should be greater than or equal to 35 mg/dL iv. Triglycerides 1. <150mg/dl in people with heart disease 34. Nitroglycerin a. Mechanism of action i. Anti-ischemic therapy ii. Mechanism of action 1. Vasodilator 2. Acts directly on vascular smooth muscles to promote vasodilation 3. Dilates arteries=more blood flow to heart b. Administration i. 3 doses sublingually every 5 minutes (tablet or spray) followed by IV therapy if persistent ischemia or hypertension occurs ii. Preparations 1. Sublingual 2. Sustained-release oral capsules 3. Transdermal/Topical ointment a. Take off for 8 hours every day to prevent tolerance buildup. 4. Translingual spray 5. IV infusion iii. Handle with gloves only as it can dissolve through membranes of the skin c. Patient education i. not to chew tab ii. change positions slowly iii. chest pain is common iv. adequate rest not to overwork heart v. Chronic stable angina 1. Take medication before you know the heart will be overworked. 2. Take prophylactically: before pain starts then go to ER! d. Indications i. Stable angina ii. Variant angina 1. Relaxes or prevents spasms in coronary arteries, increases O2 supply, does not reduce O2 demand iii. Sustained chest pain iv. IV for preoperative control of BP and treatment of HF with MI, unstable angina and uncontrolled exacerbations of chronic angina. e. Side/Adverse Effects i. Severe headache ii. Orthostatic hypotension iii. Reflex tachycardia f. Monitoring i. Check VS between doses 1. Hold medication if BP is <90 systolic or <60 diastolic 2. Hold medication if HR is <60 ii. Withdrawal long-acting preparations slowly! g. Food/drug interactions i. Phosphodiesterase type 5 inhibitors (Viagra, Cialis) 1. Unconscious, severe hypotension, cardiovascular collapse ii. Hypotensive drugs iii. Beta-blockers, verapamil, diltiazem h. Storage instructions i. Dark/cool/dry place, original container 1. No heat or light exposure ii. Once opened, only good for 30 days 35. Hemophilia treatment a. General principles i. bleeding disorder; failure of hemostasis; decreased clotting factors; a platelet plug is not formed; therefore, fibrin production does not proceed normally. ii. Primarily seen in males iii. Prognosis is usually good. iv. 1mg of iron is excreted each day. v. Minimize activities that can cause injury/bleeding vi. NSAIDs are avoided! Prevent clotting! b. Medications i. Desmopressin (DDAVP, Stimate) 1. Stops or prevents bleeding ii. Antifibrinolytic agents 1. Prevents recurrent bleeding 2. Less useful to stop ongoing bleeding 36. Factor VIII concentrate (hemophilia A) -- Factor IX (hemophilia B) a. Production methods and product safety i. Plasma-derived factor VIII ii. Recombinant factor VIII b. Administration i. On-demand therapy ii. Prophylactic therapy c. Side effects i. Mild allergic reactions 1. Rash 2. Hives 3. Dyspnea 4. Facial swelling d. Education i. Mild allergic reactions are common and treatment with Benadryl is recommended 37. Heparin a. Mechanism of action i. Enhances antithrombin ii. Rapid-acting anticoagulant iii. Suppresses coagulation by helping antithrombin inactivate clotting factors (thrombin and factor Xa) b. Indication i. DVT- short, rapid response- heparin is first choice treatment c. Monitoring lab (know levels) i. aPTT: 60-80s ii. platelets 1. thrombocytopenia a. Thrombocytopenia: if patients platelet counts are too low, medication should be lowered or stopped to prevent bleeding out. d. VS in bleeding patient i. Signs: 1. Urine, stool 2. Uncontrollable bleeding, wont stop 3. Petechiae, bruising, pallor, weakness, bloody noses, bleeding around mouth, eyes, ears ii. Vitals 1. Tachycardia 2. Tachypnea 3. Decreased systolic BP 4. Narrowed pulse pressure (immeasurable diastolic pressure) 5. Little to no urinary output 6. Decreased mental status/LOC 7. Cold/pale skin e. Antidote for Heparin i. Protamine sulfate 38. Warfarin a. Mechanism of action i. Anticoagulant ii. Suppresses coagulation by decreasing production of four clotting factors, namely iii. Blocks biosynthesis of factors VII, IX, X, and prothrombin (vitamin Kdependent factors) iv. Vitamin K antagonist v. Oldest oral anticoagulant (delayed onset) 1. Works later and takes longer to work. Better for long-term use b. Therapeutic levels i. INR: 2-3 ii. PT: 16-31s c. Lab values i. INR ii. PT iii. Hematocrit iv. Hemoglobin d. Antidote i. Vitamin K 39. Iron therapy a. Iron deficiency i. Most common nutritional deficiency and cause of nutritional-related anemia ii. Result from and imbalance of iron uptake and iron demand b. Oral iron preparations I: Iron salts i. Ferrous sulfate (drug of choice) ii. Prophylactic therapy 1. Adverse effects a. GI disturbances b. Staining of teeth c. Toxicity (may lead to death) i. N/V, diarrhea, and shock, followed by acidosis, gastric necrosis, hepatic failure, pulmonary edema, and vasomotor collapse 2. Drug interactions a. Antacids b. Tetracycline (antibiotic) c. Ascorbic acid (vitamin C) c. Parenteral iron preparations i. Iron dextran 1. Used for patients who have experienced intolerable or ineffective oral dosing 2. Adverse effects a. Anaphylactic reaction b. Hypotension c. Headache, fever, urticaria, and arthralgia d. Persistent pain with IM injections ii. Iron sucrose 1. Parenteral form of iron indicated for iron deficiency anemia in patients with CKD a. Broader range of CKD patients 2. Adverse effects a. Hypotension b. Cramps c. HF d. Sepsis e. Taste perversion iii. Ferumoxytol 1. Indicated for iron deficiency anemia in all patients with CKD, whether or not they are on dialysis or using erythropoietin a. Much more convenient b. Generally well tolerated 2. Most common adverse effects a. Nausea b. Dizziness c. Hypotension d. Headache e. Vomiting f. Edema d. Patient education i. Parenteral deferoxamine (desferal) may be administered to absorb iron and thereby prevent toxic effects. ii. To reduce the risk of pediatric poisoning, iron should be stored in childproof containers and kept out of reach. iii. Iron-containing products are the leading cause of poisoning fatalities in young children. 40. Anemia a. Lab values to monitor for bleeding i. Hemoglobin 1. Female: 12.0-15.5 g/dL 2. Male: 13.5-17.5 g/dL 3. Causes for low values a. iron, vitamin b12, or folate deficiency, bone marrow damage i. menarche, people on blood thinners, kidney failure, anemia ii. Hematocrit 1. Female: 35.5%-44.9% 2. Male: 40.7%-50.3% or 38.3%-48.6% 3. Causes for low values a. iron, vitamin b12, or folate deficiency, bone marrow damage b. anemia, vitamin/mineral deficiency, leukemia, lymphoma, blood loss, overhydration 41. Filgrastim a. Mechanism of action i. Granulocyte colony-stimulating factor 1. Leukopoietic growth factor (neutrophil counts increase; neutropenia <15000). ii. Produces dose-dependent increase in circulating neutrophils iii. Reduces the incidence of, need for hospitalization, and need for intravenous antibiotics b. Uses i. Cancer ii. Severe chronic neutropenia iii. Investigational uses c. Side effects i. Bone pain ii. Leukocytosis 42. Dabigatran a. Anticoagulant; Direct thrombin inhibitors (affects thrombin directly) b. Does not require monitoring of anticoagulation; has little risk of adverse interactions. c. Administration i. Same dose can be used for all patients regardless of age or weight ii. Take a couple times a day d. Side effects i. Bleeding ii. GI disturbances e. Patient education i. Do not crush or chew capsule; take whole ii. No specific antidote to reverse dabigatran-related bleeding iii. Usually take on an empty stomach 1. But can be taken with food to reduce GI disturbances