Pain and Inflammation Medications - Practice Flashcards

These practice flashcards cover key concepts from the lecture on pain and inflammation, including mechanisms, drug classes (NSAIDs, acetaminophen, tramadol, opioids, mixed agonist-antagonists), antidotes, side effects, monitoring, and patient education.

What are the three main opioid receptor types discussed, and which one is primarily responsible for strong analgesia?

Mu, kappa, and delta receptors; mu receptors are primarily responsible for strong analgesia but activation can cause respiratory depression, sedation, urinary retention, and constipation.

What triggers the body's natural pain relief (endogenous opioids) in response to a noxious stimulus?

The brain releases endorphins that bind to opioid receptors to help decrease the perceived pain.

What is the difference between peripheral-acting analgesics (like NSAIDs) and central-acting opioids in terms of mechanism?

NSAIDs inhibit prostaglandin synthesis in the peripheral nervous system by blocking COX enzymes, reducing pain and inflammation; opioids bind to central mu receptors in the brain/spinal cord to alter pain perception.

What does COX stand for and what are the roles of COX-1 vs COX-2 in pain and safety?

COX stands for cyclooxygenase. COX-1 protects gastric mucosa, supports platelet aggregation, and maintains kidney function; COX-2 drives pain and inflammation. Inhibiting both (first generation) reduces pain but can cause gastric/renal/bleeding risks, while targeting COX-2 (second generation) reduces GI risk but may raise cardiovascular risk.

What characterizes first-generation NSAIDs and what are their typical side effects?

Nonselective COX inhibitors that block both COX-1 and COX-2; side effects include gastric ulcers/bleeding, kidney dysfunction, and anticoagulation effects.

What characterizes second-generation NSAIDs and their trade-offs?

Selective COX-2 inhibitors with fewer GI side effects but higher risk of cardiovascular and cerebrovascular events; prototype is celecoxib (Celebrex).

Which NSAIDs are prototype first generation, and what is a unique use of aspirin?

Aspirin and ibuprofen are common first-generation NSAIDs; aspirin has a stronger anticoagulation effect and is often used for cardiac prophylaxis, but should not be given to children due to Reye syndrome.

What is the maximum daily dose of acetaminophen and what is the major risk and antidote?

Maximum 4 grams per day; major risk is liver damage; antidote is acetylcysteine (N-acetylcysteine).

What is the mechanism and typical use of acetaminophen compared with NSAIDs?

Acetaminophen is a central-acting analgesic/antipyretic with minimal anti-inflammatory effects; used for pain and fever; unlike NSAIDs, it lacks GI and anticoagulation effects.

What is tramadol, and what are its key precautions and side effects?

A centrally acting non-opioid (dual mechanism) analgesic with weak opioid receptor activity and serotonin/norepinephrine reuptake inhibition; used for moderate to severe pain not controlled by NSAIDs; side effects include dizziness, nausea, urinary retention; can cause seizures; avoid driving until you know its effects; dose should be the smallest effective dose.

What is the prototype opioid for moderate-to-severe pain and its major risks?

Morphine; strong mu-receptor agonist providing powerful analgesia but with risks such as respiratory depression, constipation, urinary retention, sedation; also suppresses cough reflex; use with caution in opioid-naïve and elderly patients.

What is naloxone (Narcan), and why is it important in opioid management?

Naloxone is an opioid antagonist that reverses mu receptor effects; may require repeated dosing due to short half-life; can precipitate withdrawal in dependent patients; monitor for return of pain and prepare patient if awake.

What is a mixed opioid receptor agonist-antagonist, and what are its clinical implications?

A drug that stimulates kappa receptors and blocks mu receptors (e.g., certain agents used around anesthesia); provides pain relief with less euphoria and respiratory depression but can precipitate withdrawal in opioid-dependent patients and is contraindicated in patients with a history of myocardial infarction.

What is allopurinol used for, and what are key hydration and monitoring considerations?

Used for long-term management of gout by reducing uric acid production; hydration (at least ~3 liters/day) helps prevent uric acid deposition in kidneys; monitor for hypersensitivity syndrome (rash, fever, low urine output, abdominal pain); may cause metallic taste and rare cataracts with long-term therapy.

What is prednisone, and what are its major side effects and safety considerations?

A synthetic corticosteroid that mimics cortisol, providing potent anti-inflammatory and immunosuppressive effects; side effects include hyperglycemia, osteoporosis, GI ulcers, and Cushing's syndrome; should be tapered slowly to prevent adrenal insufficiency and taken with food; monitor for high blood sugar and infections.

Why is tapering prednisone important?

To prevent adrenal insufficiency due to hypothalamic-pituitary-adrenal axis suppression; abrupt cessation can lead to nausea, fatigue, low blood pressure, and other symptoms.

How should pain assessment be used to evaluate analgesic effectiveness?

Use a patient-reported pain scale before and after medication; corroborate with other signs such as vital signs and behavior (e.g., reduced heart rate or agitation) to assess effectiveness.

What are common signs of NSAID-related kidney dysfunction to teach patients to watch for?

Weight gain, decreased urine output, swelling; monitor kidney function tests like BUN and creatinine.

What should patients know about NSAID-related GI side effects and when to seek help?

Be aware of GI upset and potential bleeding; watch for abnormal bruising, petechiae, black tarry stools, or coffee-ground emesis; seek medical care if these occur.

What role do prostaglandins and edema play in inflammation, and how does the body attempt to limit inflammation?

Inflammation involves prostaglandins and other mediators; white blood cells increase vascular permeability causing edema; cortisol (endogenous steroid) helps suppress inflammation via negative feedback mechanisms.

What is the relationship between fever and inflammation?

Fever is typically a systemic response to inflammation; local inflammation may not cause fever.

What education is important about OTC products containing acetaminophen?

Read labels carefully to avoid taking multiple products with acetaminophen; ensure total daily dose stays within 4 g; excessive use risks severe liver injury.