Pharmacology Exam 2 Questions and Answers: A Comprehensive Guide, Exams of Pharmacology

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PHARMACOLOGY EXAM 2 QUESTIONS

AND ANSWERS 100% CORRECT1!!!

what is pain - ANSWER -whatever the experiencing person says it is

• unpleasant sensory and emotional experience associated with actual or potential tissue damage
• pain is the primary reason people seek healthcare

effects of pain on metabolism, cardiac, respiratory, GU, GI, cognition - ANSWER metabolic- glucose intolerance cardiac-increased HR and cardiac workload, hypertension respiratory- decreased lung volumes, atelectasis, cough] GU- urinary retention, fluid overload GI- decreased mobility (constipation) cognitive- insomnia, confusion, decreased cognitive function

nurse's role when patient is in pain - ANSWER A assess, assure, advocate. assure patients that you are committed to relieve their pain B believe them when they report C check comfort levels and pain scale D demonstrate empathy E ease, dont make judgements or assumptions

Pain assessment 7 variables - ANSWER O- onset L-location D- duration C- character/severity A- aggravating/relieving factors R- radiating T- timing

What is the fifth vital sign? when do you do this? - ANSWER pain assessment -assess pain before intervention

• 30-60 mins after intervention
• assess as appropriate

• post op might need pain assessed more frequently than every 4 hours

assess before, after, and in between interventions

acute pain - ANSWER rapid onset, intense, usually subsides when treated

IM - ANSWER intramuscular lasts longer than IV but less than PO

IV - ANSWER intravenous immediately post op

transdermal - ANSWER Transdermal-requires absorption to achieve effects

topical - ANSWER Topical-Treats acute and chronic pain, immediate relief but just at application site (lidocaine cream before an IV start)

Epidural - ANSWER Epidural-requires placement of epidural catheter (by CRNA or physician), bolus or continuous dosing, Increased risk for infection

Patient-controlled analgesia (PCA) - ANSWER PCA-Patient controlled analgesia, set dose at set time. Benefit=pt feels pain and knows how much analgesic will relieve it. Pt is only one to dose self.

categories of pain- nociceptive and neuropathic - ANSWER nociceptive- due to injury to tissues dull or sharp aching pain usually responds well to treatment ex: spraining ankle, arthritis

neuropathic- due to injury to nervous system sharp, intense, shocking, or shooting pain does not respond well to treatment diabetic neuropathy, pain after spinal cord injury

non pharmacologic pain meds - ANSWER Few or no side effects Used in place of or as an adjunct to pain meds Lower doses of pain medication may be needed

TENS unit - ANSWER Applies electrical impulses to the nerve endings and blocks transmission of pain signals.

Delta - ANSWER Opioids do not interact well with Delta receptors. Therefore, consider the medications that do, to "counter-act" the effects of opioid medications. These would be your antagonist medications such as naloxone (Narcan).

agonist - ANSWER drug that activates certain receptors in the brain

antagonist - ANSWER a drug that neutralizes or counteracts the effects of another drug

Morphine sulfate - ANSWER -opioid agonist

• pharmacologic action- depressant of CNS, decreases pain
• Pharmacokinetics- inactivated by hepatic metabolism. 0.5 gone with first pass -routes of admin: PO, IV, IM, SQ, PR, epidural
• adverse affects: sedation, decreased GI motility, respiratory depression, urinary retention
• contraindications: liver disease, patient's with biliary surgery, preemie -drug/food interactions: dont give with other CNS depressants, antihistamines. Do not give if respiratory rate is below 12 breaths per min or to patients with bladder distention. Can cause orthostatic hypotension.

Nursing considerations of morphine sulfate - ANSWER administration- baseline vital signs including pain scale hold if respirations are less than 12 reversal agent ( ) and resuscitation equipment available at bedside

effectiveness- is pain better? is cough better? is diarrhea better?

naxolone (Narcan) - ANSWER antidote for opioids (opioid antagonist), blocks kappa and mu indications-reversal of CNS and respiratory depression bc of opioid abuse or alcohol abuse pharmacokinetics: immediate effects, 1/2 life 30-60 mins, frequent dosing q 1 hr action- blocks effects of opioids, including CNS snd respiratory depression without producing any opioid-like effects

• routes of administration: IV, SQ, I'm, IN, ETT -adverse effects: tachycardia, tachypnea, abstinence syndrome, pulmonary edema
• contraindication: opioid dependence
• monitor respiratory rate, rhythm, and depth, assess for baseline
• assess for opioid dependence before administering
• titrate dose -resuscitation equipment available at bedside

Mu receptors - ANSWER Opioids produce high activation of these receptors. Effects are analgesia, resp. depression, euphoria, and sedation. Also, causes physical dependence and decreased GI motility (constipation). A medication example is morphine or meperidine.

Kappa - ANSWER Kappa receptors are also selective by opioid medications. Examples are butorphanol and buprenorphine. They do not cause as much "depressive" action as the MU selective medications. Analgesia, sedation, and decreased GI motility occur.

antiheadache meds may be used in 2 ways - ANSWER - to abort an ongoing attack -to prevent an attack from coming

Drugs that abort a migraine attack Drugs that prevent attacks from occurring - ANSWER abort- nonspecific analgesics (aspirin-like drugs and opioid analgesics), migraine-specific drugs (ergot alkaloids and triptans) -begin treatment ASAP -drug selection depends on seriousness of attack

prevent- beta blockers (propranolol) tricyclic antidepressants (amitriptyline) anti epileptic drugs- (divalproex)

Ergot alkaloids (ergotamine) - ANSWER -pharmacologic action: Exact action unknown Alters transmission at serotonergic, dopaminergic, and alpha-adrenergic junctions Antimigraine effects seem to be related to agonist activity at subtypes of serotonin receptors Blocks inflammation associated with the trigeminal vascular system In cranial arteries - acts directly to promote constriction and reduce the amplitude of pulsations Depresses the vasomotor center affects blood flow Pharmacokinetics Oral, SL, or rectal Bioavailability with oral and SL low; rectal higher Half-life is 2 hours, but effects may be seen for 24 hrs Metabolized in the liver, excreted in the bile

Therapeutic Uses Stopping an ongoing migraine attack

Adverse Effects Well tolerated at usual therapeutic doses N/V in 10% of clients Weakness in the legs Myalgia - muscle pain Numbness and tingling in the fingers and toes Angina-like pain Tachycardia or bradycardia

Drug Interactions Triptans - a prolonged vasospastic reaction could occur CYP3A4 inhibitors - intense vasospasm, cerebral and/or peripheral ischemia HIV protease inhibitors Azole antifungal drugs Macrolide inhibitors Grapefruit juice - less potent inhibitor

Contraindications Hepatic or renal impairment Sepsis Coronary artery disease (CAD) Peripheral vascular disease (PVD) Clients taking potent inhibitors of CYP3A Pregnancy Risk Category X

Triptans - ANSWER First-line drugs for terminating a migraine attack

Relieve pain by constricting intracranial blood vessels and suppressing the release of inflammatory neuropeptides

Sumatriptan - ANSWER Pharmacologic Action & Pharmacokinetics -Causes selective activation of 5-HT1B and 5-HT1D receptors (5-HT1B/1D receptors) -Binding to these receptors on intracranial blood vessels causes -vasoconstriction -Binding to these receptors on sensory nerves of the trigeminal -vascular system suppresses release of CGRT -Reduces release of inflammatory neuropeptides -> diminishes perivascular inflammation -Oral, nasal, or SQ

Beta blocker (propranolol) Antiepileptic drugs (divalproex) Tricyclic antidepressants (amitriptyline

preventing resistance-limiting drug to organism targeted and dosing - ANSWER -limit drug to organism targeted:Culture and Sensitivity Avoid abx in viral illnesses Do not share antibiotics Do not stored unused antibiotics

Dosing: appropriate dose/duration critical concentration maintain therapeutic level take as prescribed dont stop when symptoms improve complete entire course

All meds are ____________ when given at toxic dose. - ANSWER poison

adverse reactions to anti-infective therapy - ANSWER kidney damage GI tract toxicity neurotoxicity hypersensitivity reactions superinfections

peak and trough levels - ANSWER

Beta blockers used to inhibit arterial dilation related to migraine pain. Antiepileptic drugs decrease the cranial nerves excitability. Antidepressants work by effecting levels of serotonin and other chemicals in the brain.

what are we aiming for in drug distribution? - ANSWER - reduce population of invading organism

• anti-infectives vary in effectiveness against invading organisms -some are selective only for a few organisms -Sometimes, we administer antimicrobials to decrease the risk of developing an infection (example: during surgical procedures). This is called prophylactic treatment.

bactericidal - ANSWER kill the cell

bacteriostatic - ANSWER prevent reproduction of the cell

Narrow spectrum of activity - ANSWER Effective against only a few microorganisms with a very specific metabolic pathway or enzyme

broad spectrum of activity - ANSWER Useful in treating a wide variety of infections Most adverse effects and risks

selectivity - ANSWER the ability to affect a specific organism

synergistic effect - ANSWER We may combine more than one drug or give drugs together to have a greater effect that when giving one by itself - this is called a synergistic effect.

Therapeutic Uses Abort an ongoing migraine attack Relieves headache and associated symptoms (nausea, neck pain, photophobia, phonophobia) Beneficial effects begin about 15 minutes after SQ or intranasal dosing and 30- minutes after oral dosing

Adverse Effects Most side effects are transient and mild Coronary vasospasm = biggest concern Chest symptoms - "heavy arms" and "chest pressure" Teratogenesis - should be avoided during pregnancy Vertigo, malaise, fatigue, and tingling sensations

Drug Interactions Ergot alkaloids and other triptans - excessive and prolonged vasospasm MAO inhibitors - can cause toxicity SSRIs and SNRIs - serotonin syndrome

Contraindications Ischemic heart disease Prior MI Uncontrolled hypertension Hepatic impairment