Pharm I Final Outline PDF

Pharm I Final 1. What is a common side effect of ace inhibitors? a. Cough b. Why do ACE inhibitors cause a cough? i. ACE inhibitors cause a cough due to the accumulation of bradykinin, a peptide normally broken down by the angiotensin-converting enzyme...

Pharm I Final 1. What is a common side effect of ace inhibitors? a. Cough b. Why do ACE inhibitors cause a cough? i. ACE inhibitors cause a cough due to the accumulation of bradykinin, a peptide normally broken down by the angiotensin-converting enzyme. Elevated bradykinin levels stimulate sensory nerves in the respiratory tract and promote mild airway inflammation, leading to a persistent dry cough in some patients. Switching to angiotensin receptor blockers (ARBs), which do not affect bradykinin, may alleviate this side effect. 2. What are some side effects of vasodilators? Vasodilators cause arterial smooth muscle relaxation leading to decreased BP. c. Reflex tachycardia d. Fluid retention e. Headache, dizziness, weakness, fatigue (due to sudden decrease of BP) 3. What is the mechanism of action of spironolactone? f. Blocks receptors of aldosterone. Retains potassium while excreting Na and water. Smaller degree of diuresis causing modest hypotensive effects. 4. What is an x-waiver for prescribing medication? What law allows NPs to prescribe medication without an x-waiver? g. X-waiver was a special authorization required for healthcare providers to prescribe buprenorphine to treat opioid use disorder (OUD). This waiver, mandated by the Drug Addiction Treatment Act of 2000 (DATA 2000), necessitated additional training and certification for providers. h. Section 1262 of the Consolidated Appropriations Act of 2023 removed the federal requirement for practitioners to have x-waiver to prescribe medications. 5. What is the process of obtaining a furnishing license in California for a nurse practitioner? i. Complete an accredited pharmacology course j. Hold an active furnishing number k. Register with the DEA to obtain a DEA number l. Furnish in accordance with a standardized procedure or protocol 6. What are the DEA requirements for controlled substances prescriptions? m. Patient Information: Full name, address. n. Prescriber information: Full name, address, DEA \# o. Drug information: Name, strength, dosage form, quantity (written in words and numbers), directions for use p. Date q. Signature r. Optional: ii. Refills: Schedule II -- No refills; Schedule III and IV: up to five refills within six months; Schedule V -- refill rules depend on prescriber's instructions. 7. Standardized policies and procedures in California: California AB 890 (signed in 2020) expands nurse practitioner (NP) practice authority by creating two categories: s. 103 NP: Allows NPs to practice independently without standardized procedures in group settings (e.g., clinics, hospitals) after completing a transition to practice (TTP) of 3 years (4,600 hours) under supervision in California. t. 104 NP: Grants full practice authority, allowing independent practice outside of group settings, after 3 years of practicing as a 103 NP (available starting January 1, 2026). 8. What is CURES (Controlled substance utilization review and evaluation system) u. California prescription drug monitoring program v. CURES is a critical tool for combating the opioid epidemic and ensuring controlled substances are prescribed responsibly in California. w. Helps healthcare providers identify and prevent prescription drug abuse. x. Providers must consult CURES before prescribing Schedule II--IV drugs for the first time and every 4 months for ongoing treatment. 9. What are some scheduled II controlled substances? y. Opioids: Dilaudid, morphine, oxycodone, hydrocodone, fentanyl z. Stimulants: Adderal, Ritalin, methamphetamine 10. What are common side effects of opioid use? a. CNS: sedation, drowsiness b. GI: Nausea, constipation c. Respiratory: respiratory depression d. Cardiovascular: hypotension e. Dermatological: pruritic, sweating f. GU: urinary retention 11. What is the difference between HDL cholesterol and LDL cholesterol? g. LDL cholesterol: only 50% is absorbed by liver, rest goes to peripheral cells. h. HDL cholesterol: produced in liver and intestine with function to remove LDL cholesterol from peripheral cells. 12. When to start screening pediatric patients for hyperlipidemia? i. At risk children and adolescents: between 2 and 8 years iii. Family history of HLD or heart disease iv. Unknown family history v. Personal risk factors: obesity, DM, hypertension j. All children between ages 9 and 11 and another screening ages 18 and 21 years 13. What is the mechanism of action of statins? k. Statins block the enzyme HMG-CoA reductase, reducing cholesterol production in the liver. l. Decreases intracellular cholesterol levels, leading to increased uptake of LDL from the bloodstream. m. Reduces triglycerides and slightly increases HDL levels. 14. What are the common side effects of statins? n. GI disturbances o. Headaches p. Myalgia, possibly myopathy q. Hepatotoxicity 15. What anti-cholesterol medication is contraindicated in pregnancy? r. Statins are contraindicated in pregnant women. These drugs inhibit HMG-CoA reductase, an enzyme crucial for cholesterol synthesis, which is essential for fetal growth. 16. What is the mechanism of action of nitroglycerin? s. Dilates peripheral arteries, veins, and coronary arteries. t. Veins return less blood to heart, reducing preload which results in reduced cardiac workload. u. Coronary arterial dilation increases blood flow and oxygen supply to myocardium. 17. What is BNP and why is it measured? v. BNP (B-Type Natriuretic Peptide): A polypeptide secreted by the heart\'s ventricles in response to excessive stretching or wall tension, often due to worsening heart failure. w. Provides an objective measure of cardiac function and is a strong predictor of risk for death and cardiovascular events in heart failure patients. x. Normal range: \ i. Requires urgent reversal: Hold warfarin, Consider Vitamin K 2.5 mg PO ii. Life threatening bleeding: Hold warfarin, Vitamin K 10mg IV, 4U FFP f. INR 4.5 -- 10: vii. No bleeding: Hold warfarin, Consider Vitamin K 2.5 mg PO viii. Requires urgent reversal: Hold warfarin, Vitamin K 2.5 mg PO or 1mg IV ix. Life threatening bleeding: Hold warfarin, Vitamin K 10mg IV, 4U FFP g. INR \ 10: x. No bleeding: Hold warfarin, Vitamin K 2.5mg PO or 1-2mg IV, repeat vitamin K every 24 hours as required xi. Requires urgent reversal: Hold warfarin, Vitamin K 1-2 mg IV over 30 min. Repeat every 6-24h as required xii. Life threatening bleeding: Hold warfarin, Vitamin K 10mg IV, 4U FFP 21. For newer anticoagulants, Pradaxa, Xarelto, Eliquis: h. Baseline and Periodic Labs: xiii. Renal Function: Creatinine, eGFR (dose adjustments needed for renal impairment). xiv. Hepatic Function: ALT, AST, bilirubin (important for rivaroxaban and apixaban). xv. CBC: Monitor for anemia or thrombocytopenia. i. Not Needed: xvi. Routine INR/PT or aPTT monitoring, as these medications have predictable effects and do not require frequent adjustment. Half-life is also shorter 5-12 hours. 22. What are the common side effects of heparin? j. Bleeding k. Hypersensitivity l. Thrombocytopenia m. Osteoporosis n. Alopecia o. Hyperkalemia 23. Which lab test is used to monitor therapeutic levels of heparin? p. aPTT: The activated partial thromboplastin time (aPTT) is the primary test used to monitor therapeutic levels of heparin. 24. Which anticoagulant is most appropriate as the first-line treatment for the following conditions? q. Pulmonary Embolism (PE) / Deep Vein Thrombosis (DVT): Heparin (followed by oral anticoagulants like warfarin or DOACs for long-term management). r. Transient Ischemic Attack (TIA): Aspirin (antiplatelet therapy is preferred for TIA). s. Atrial Fibrillation (A-fib) (to prevent stroke): Warfarin or Apixaban (or other DOACs for A-fib stroke prevention). t. Myocardial Infarction (MI): Aspirin and Clopidogrel (antiplatelet therapy is first-line for MI). 25. What are the classic signs of thalassemia? What does the blood smear look like? u. Classic signs: fatigue, weakness, pallor, shortness of breath v. Blood smear findings: microcytic, hypochromia, target cell and acanthocytes (cell with irregularly spaced bulbous projections) 26. What are the classic signs of B12 deficiency (pernicious) anemia? w. Gastric mucosal atrophy, neurologic changes (paranoia, dementia, confusion, delirium), yellow-blue color blindness, fatigue, weakness. 27. What are the differences between positive and negative inotropic and chronotropic medications and their effects on cardiac contractility? x. Inotropic Medications: Affect cardiac contractility. xvii. Positive Inotropes: Increase contractility (e.g., Digoxin, Dobutamine); used in heart failure. xviii. Negative Inotropes: Decrease contractility (e.g., Beta-blockers, Verapamil); used in hypertension and arrhythmias. y. Chronotropic Medications: Affect heart rate. xix. Positive Chronotropes: Increase heart rate (e.g., Atropine, Epinephrine); used in bradycardia. xx. Negative Chronotropes: Decrease heart rate (e.g., Beta-blockers, Verapamil); used in tachycardia and atrial fibrillation. 28. What is a hallmark side effect associated with amiodarone regarding skin that may concern patients? z. Blue-gray skin discoloration 29. What happens at each phase in the phases of action potential in a myocardial cell? a. Phase 0: Rapid depolarization from sodium influx b. Phase 1: initial repolarization caused by transient potassium efflux. c. Phase 2: Plateau phase where calcium influx balances potassium efflux, sustaining contraction. d. Phase 3: Repolarization caused by potassium efflux e. Phase 4: Resting phase where the membrane potential is maintained by the sodium-potassium pump 30. How do nitrates reduce cardiac workload and improve symptoms in patients with angina? f. Nitrates are converted to nitric oxide, which causes vasodilation. This reduces preload (venous return to the heart) and afterload (arterial resistance), lowering cardiac workload and oxygen demand. This mechanism helps relieve angina symptoms. 31. What are the modifiable and non-modifiable risk factors for hyperlipidemia? g. Modifiable Risk Factors: Include lifestyle factors such as poor diet, physical inactivity, obesity, and smoking, which can be changed to manage hyperlipidemia. h. Non-modifiable Risk Factors: Include age, race, gender, and family history of hyperlipidemia or early cardiovascular disease, which cannot be altered 32. What are the adverse effects of Fibric Acid Derivatives? i. GI disturbances, gallstones, myopathy. 33. What risk factors are used when calculating a 10 year ASCVD risk assessment score? j. The 10-year ASCVD Risk Score uses factors such as [age], [gender], [race], [total] [cholesterol], [HDL cholesterol], [blood pressure] (treated or untreated), [diabetes] status, and [smoking] status to estimate the likelihood of a cardiovascular event in the next 10 years. 34. What is the mechanism of action of digoxin? k. Digoxin inhibits the sodium-potassium ATPase pump. Indirectly leads to accumulation of intracellular calcium, causing increased myocardial contractility. 35. What is the mechanism of action of aspirin on the blood? l. Aspirin inhibits platelet activation through irreversible enzyme antagonism to block prostaglandin synthesis. 36. What is the clinical presentation of aplastic anemia, and how is it treated? m. Aplastic anemia is caused by bone marrow failure, often due to autoimmune mechanisms, chemo/radiation, infections, or medications. It presents with fatigue, infections, bleeding, and pancytopenia (on CBC). n. Aplastic anemia treatments: Mild cases treated with supportive care. RBC transfusions and platelets given as necessary. 37. What are the different types of pain receptors and how do they work? o. Thermal Nociceptors: xxi. Function: Respond to extreme temperatures (heat \>45°C or cold \30) 43. What is the mechanism of action of beta blockers? o. Beta blockers slow the heart rate (negative chronotropic) and decrease strength of heart contraction (negative inotropic). Decreases myocardial oxygen demand. 44. What is the mechanism of action of ARBs? How do angiotensin receptor blockers work? p. ARBs work by blocking the binding of angiotensin II (AT2) receptors in the blood vessels producing decreased afterload and preload on the heart. 45. What is the mechanism of action for calcium channel blockers? q. Blocks the influx of calcium cells in smooth muscle cells which causes relaxation of smooth muscle cells and dilation of arterioles. 46. What is the mechanism of action of bile acid resins? r. Bile acid resins bind with bile acids in the intestines, preventing their reabsorption and is excreted in the stool therefore lowering LDL. 47. What is the mechanism of action of fibric acid derivatives? s. Fibric acid derivatives reduce the production of triglycerides and cholesterol in the liver. They also increase the breakdown of fats in the blood by stimulating lipoprotein lipase enzymes. They are more effective at lowering triglycerides and raising HDL, yet slightly lowering LDL. 48. Which of the following risk assessment tools would be used to assess a patient for opioid abuse/misuse? (SISAP) t. Opioid Risk Tool (ORT): xxvii. Type: 5-item, patient-administered. xxviii. Purpose: Predict risk of aberrant drug-related behavior. xxix. Focus: Alcohol/drug abuse history, psychological disorders, and risk factors. xxx. Risk Levels: Categorizes patients as low, medium, or high risk. u. Screener and Opioid Assessment for Patients with Pain-Revised (SOAPP-R): xxxi. Type: 24-item, patient-administered. xxxii. Purpose: Assess risk of aberrant behaviors. xxxiii. Focus: History of alcohol/substance use, psychological status, mood, cravings, and stress. xxxiv. Use: Guides monitoring intensity based on risk level. v. Screening Instrument for Substance Abuse Potential (SISAP): xxxv. Type: 5-item, self-administered. xxxvi. Purpose: Predict opioid misuse risk. xxxvii. Focus: History of alcohol/substance abuse. xxxviii. Use: Improve pain management by focusing on appropriate opioid use and monitoring high-risk patients.