Pharm Exam 2 Questions with Answers Perfectly Solved Updates, Exams of Pharmacology

Download Pharm Exam 2 Questions with Answers Perfectly Solved Updates and more Exams Pharmacology in PDF only on Docsity! 1 / Pharm Exam 2 Questions with Answers Perfectly Solved Updates 1. What local anesthetics are the "amides"? 2. What local anesthetics are the "esters"? 3. Why is epinephrine often added to a local anesthet- ic? 4. What is bicarb added to a local anesthetic? 5. Where are amides metab- olized? 6. The more lipophilic the lo- cal anesthetic ... 7. What are the water solu- ble anesthetics? 8. What are the lipid soluble anesthetics? 9. Where are esters metabo- lized? lidocaine (xylocaine) bupivacaine (marcaine) benzocaine (hurricaine gel) epi reduces the absorption of LA by 20- 50% (bc epi is a vasoconstrictor), depending on the site of injection and the LA reduces pain on admin (lidocaine often burns on entry); it neutralizes the acidity of lidocaine liver - amides may accumulate in hepatic dis- ease or reduced hepatic perfusion ... the greater the potency, the more rapidly it will achieve therapeutic neuronal concentration, and the longer that interaction will last lidocaine, procaine, and mepivacaine (LiMP) tetracaine, bupivacaine and ropivacaine; these have a longer duration of action In plasma by cholinesterase 10. What is tachyphylaxis? decrease in duration, segmental spread or in- tensity of a regional block after repeated doses of equal size; to maintain a given level of effect, the dose has to be 2 / Pharm Exam 2 Questions with Answers Perfectly Solved Updates increased 11. What should you do pri- or to the start of a proce- dure? estimate the length of the procedure and choose a local anesthetic with a duration sufficient to last throughout the procedure 12. - decreased ambulation after sx - limit ability of pregnant patient to cooperate 5 / Pharm Exam 2 Questions with Answers Perfectly Solved Updates 23. What is B:G partition co- efficient? 24. What is a major ADE of inhaled anesthesia? 25. What is the cause of ma- lignant hyperthermia? 26. What are the signs of ma- lignant hyperthermia? 27. What is the treatment for malignant hyperthermia? 28. What is the preferred choice for IV anesthesia? 29. Why is etomidate not used as long term infu- sion? 30. What are some effects of ketamine? 31. What is a possible ADE of dexmedetomidine? 6 / Pharm Exam 2 Questions with Answers Perfectly Solved Updates how much drug needs to be in the alveoli to produce anesthesia in 50% of the population; the lower the MAC the more potent the agent!!!!! - blood:gas solubility in blood - higher B:G = slower onset - lower B:G = faster onset - faster onset = shorter duration malignant hyperthermia hereditary mutation in ryanodine receptors lead- ing to excess Ca2+ release from SR --> muscle contraction --> body heat, muscle breakdown --> acidosis, rigidity, rhabdomyolysis - tachypnea - tachycardia - rigidity - acidosis - rhabdomyolysis - h yperthermia dantrolene propofol because the half-life is relatively short inhibits cortisol synthesis - strong analgesia - potent bronchodilator = good in asthma - emergence delirium (hallucination, confusion) bradycardia, hypotension 7 / 32. What are the actions of leukotrienes? prostglad- in F2alpa? prostacyclin? thromboxane A2? 33. Which outcome is most likely to occur in suscep- tible patients who COX is inhibited? 34. What is the effect of PGI2? 35. How does PGE2 affect the kidney and vasculature? 36. What are the effects of PG on the GI tract? 37. What is alprostadil used for? 38. What is misoprostol used for? 39. What is misoprostol con- traindicated in? 40. What is Lubiprostone contraindicated in? 41. What is an use of dinopro- stone? 10 / 51. What is Reye Syndrome? - acute non-inflammatory encephalopathy - occurs in patients < 18 y/o after aspirin expo- sure during viral illness (varicella or influenza A or B) 11 / 52. What are the signs and symptoms of Reye Syn- drome? 53. What is a cardinal sign of salicylate overdose? 54. What is the normal range of anion gap? 55. What happens when you add an NSAID to an ACE-I? 56. What is a risk for Ketoro- lac (Toradol)? 57. What are the contraindi- cations for NSAIDs? 58. What are the effects of ac- etaminophen? 59. What is stage I aceta- minophen toxicity? 60. What is stage II aceta- minophen toxicity? - protracted vomiting - delirium progressing to coma - seizures - decerebrate posturing - hyperventilation - hepatomegaly - acidosis, hyerammonemia, elevated LFTs, de- creased glucose tinnitus and wide anion gap acidosis 8-16 mEq/L; it is widened with an excess of unmeasured anions is present in the blood decreased perfusion pressure highest risk of GI ulceration - use is limited to no more than 5 consecutive days - active GI bleed - diminished renal function (Crcl < 30) - risk of thrombosis - esp avoid COX2 selective - caution in patients with HTN or cardiac disease - antipyretic - central analgesia - NOT anti-inflammatory 0.1-24 hrs post ingestion anorexia, N/V, malaise, diaphoresis 12 / 24-72 hrs post ingestion resolution of stage I symptoms RUQ tenderness, oliguria, pancreatitis, inc AST/ALT, PT, BUN, SCr, bilirubin 15 / 72. What is the site of action for benzodiazepines? 73. What is the site of action for baclofen? GABAa GABAb agonist 74. What is baclofen? GABAb agonist; spasmolytic with less sedation than bennzos; also inhibits release of substance P to reduce pain 75. What are the ADE of ti- zanidine? 76. What is the first line agent for acute low back pain? 77. What are the ADE of cy- clobenzaprine? hypotension, bradycardia NSAIDs; skeletal muscle relaxants are an alter- nate treatment option - sedation - antimuscarinic - arrhythmia - serotonin syndrome 78. Mu receptor responsible for analgesia, euphoria, respiratory depression and physical dependence; most use- ful analgesic drugs are mu agonists 79. Delta receptor analgesic potential, with less respiratory depres- sion 80. Kappa receptor limited analgesic potential and are thought to be responsible for dysphoric and neurotoxic events (seizures) 81. Opioid partial agonists should not be combined with full agonists, or 16 / used in patients who have opioid dependence - may cause withdrawal!!! 82. In opioid overdose, what is usually the cause of death? respiratory shutdown 17 / 83. What are opioid actions on the GI tract? 84. Can you develop toler- ance to opioid induced constipation? 85. What are the uses of opi- oids? 86. What are schedule II drugs? - N/V - constipation (patient on stimulant laxative + stool softener at initiation) no - analgesia - antitussive - anesthesia very high abuse potential; prescriptions cannot be refilled; opioid full agonist approved for use in USA are class II 87. Opioid tolerance tolerance develops to analgesic, respiratory and sedating effects, but NOT constipation or miosis 88. What are symptoms of opioid withdrawal? 89. What are the treatment options for opioid over- dose? 90. What important patient education goes along with fentanyl patches? - increased pain - dysphoria - diarrhea, cramping - yawning - mydriasis - piloerection, diaphoresis (cold turkey) option 1 - intubate and let them sleep it off option 2 - titrate naloxone drip so pt I breathing well but still sleeping option 3 - naloxone push (angry patient) patients should fold patch with sticky side in- ward when discarding to prevent toxicity in chil- dren/pets 91. What is meperidine? "strong opioid" do not use in chronic pain, caution in renal failure due to toxic metabolic normeperidine anticholinergic (causes 20 / - malignancy - infection = vaccinate prior to initiation, no live vaccines - short term: hyperglycemia - long term: hyperglycemia, addisonian crisis upon withdrawal 21 / 103. Why do you have to care- ful with azathioprine? 104. What is the use of methotrexate? 105. What type of cells does MTX affect? may cause hyperuricemia and tumor lysis syn- drome; use of allopurinol or febuxostat can cause fatal accumulation of 6-MP if dose of aza- thioprine/6-MP is not reduced severe psoriasis, RA, Crohn's rapidly proliferating cells (diarrhea, stomati- tis, bone marrow suppression, erythema/rash, alopecia) 106. What is the ADE of MTX? - macrocytic anemia - hyperuricemia - teratogenic 107. What is the MOA of tofac- itinib? selective inhibitor of JAK3 (lymphocytes and dendritic cells) to block activation activation of STAT --> dec IL2, IL17, IFN- gamma, TNF-alpha 108. What are the ADE of tofac- infection (no live vaccines) and neoplasia itinib? 109. What do you need to mon- itor when you put a pa- tient is on tofacitinib? baseline TB test (PPD or interferon gamma as- say) 110. What are the causes of ex- - overproduction (cytotoxic drugs-cell death) cess urate? 111. What are some of the risk factors for gout? - under secretion (drugs - diuretics TZDs) - diuretic use - alcohol intake - HTN - BMI 22 / - sweetened beverage consumption - fructose intake - seafood - meat consumption - dairy 25 / 122. What are some of the modifiable risk factors for harm with pain manage- ment? 123. At what MME is there a risk for continued opioid use? 124. Which medication or medication combo has been demonstrated to provide the greatest relief of acute pain in multiple head to head trials? 125. When measures are tak- en to reduce prescrip- tion opiate abuse over- dose deaths from heroin increase. True or False? - LA/ER - time scheduled - methadone - high dose - co prescribing with benzodiazepines - multiple prescribers/pharmacies >/= 700 MME ibuprofen + acetaminophen False 126. What is allodynia? painful response to stimulus that is normally not noxious 127. What is hyperalgesia? increased sensitivity to pain 128. What pathways do opi- oids work on? 129. What does the CDC rec- ommend regarding opi- oids for chronic pain? opioids inhibit afferent transduction and activate descending inhibitory pathways - avoid ER/LA formulations when starting opi- oids - prescribe the lowest effective dose 26 / - eval <3 mo; at lest every 90 days - avoid prescribing opioids and benzodiazepines concurrently 130. morphine 27 / What is the metabolite of codeine? 131. What is the metabolite of hydrocodone? 132. What is the metabolite of oxycodone? 133. What is the goal for pain relief with chronic pain? 134. If you are prescribing >/= 50 MME per day what should you do? 135. How should you pre- scribe opiates for acute pain? 136. What MME should you avoid prescribing? 137. When tapering opioids down how should you start? 138. How should you rotate opioids? hydromorpho ne oxymorphone 30% improvement in pain; NOT to eliminate pain increase follow up frequency and consider offer- ing naloxone for overdose risk prescribe < 3 day supply; more than 7 days will rarely be required avoid > 90 MME/day, consider specialist to sup- port management of higher doses a decrease of 10% of the original dose per week is a reasonable starting point reduce by 25-50% to allow for incomplete cross tolerance