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NSAIDs and Pain
Pharmacology: NSAIDs, Pain, Controlled Substances (Summer Exam 1)
| Term | Definition |
|---|---|
| T/F: Food changes bioavailability of of NSAIDs, so you don't want to eat when taking them | False! Doesn't change bioavailability so you are encouraged to eat them to prevent GI side effects |
| Route of excretion with NSAIDs? | Renal; shouldn't take them if patients are in renal failure |
| Involved in tissue homeostasis and responsible for production of prostaglandins (gastric cytoprotection, platelet aggregation, renal flow autoregulation); adverse GI effects result w/ inhibition of this | COX-1 |
| Induced in activated inflammatory cells esp pain causing mediators | COX-2 |
| Exists in cerebral cortex and aorta..inhibited by NSAIDs and acetaminophen | COX-3 |
| T/F: All drugs affect COX enzymes reversibly | False, aspirin binds irreversibly, inactivating COX-1 (basis for aspirin's long-lasting effects on platelets) |
| NSAIDs reduce: | 1) Vasodilation/edema 2) Pain |
| T/F: Normal body temperature in humans is not affected by NSAIDs or APAP, only when the body temperature is raised in disease | True |
| How do NSAIDs and APAP exert antipyretic action? | Inhibiting prostaglandin production by blocking COX-III in the hypothalamus |
| _______ may take effect early but the ___________ effects may take up to 3 weeks (in regards to NSAIDS) | Pain relief, anti-inflammatory |
| What two toxicities/adverse effects do all NSAIDs have? | GI and renal toxicity |
| 2 mechanisms of GI adverse of NSAIDs (what is the specific adverse?) | Specific: GI ulceration; 1) local erosion from NSAIDs 2) Inhibition of cytoprotective prostaglandins |
| 2 mechanisms of renal toxicity with NSAIDs | 1) interactions w/ ACEI -> acute renal failure 2) NSAIDs by themselves inducing renal failure (often w/ pre-existing renal impairment) |
| T/F: Ibuprofen and Naproxen are in the same family | True (proprionic acid deriatives); Same family, but different effects/risk factors |
| Problem w/ COX-2 selective agents? Benefits of COX-2 selective agents? | P: Myocardial and coronary prostacyclin inhibition occurs at a high rate with these agents, resulting in enhanced platelet aggregation and constriction of vascular smooth muscle. B: Less GI Sx so works well w/ people prone to those |
| Why is Meloxicam Dr. Compton's favorite NSAID? | Keeps GI Sx under control and is only taken once a day |
| What order of kinetics is aspirin? | Low doses: first order but at a high dose: zero order (like alcohol). |
| Does aspirin have an anti-inflammatory effect? | Yes, but only at mega high doses (4-5 grams/day) |
| What is the risk of consuming alcohol with aspirin? | GI bleeding as alcohol washes the mucus through. |
| What other drug interactions of aspirin? (2 main things) | 1) Competes w/ penicillin for secretion (raising penicillin blood levels, which can be a good thing) 2) Displaces drugs from plasma proteins like warfarin, oral hypoglycemic agents and methotrexate. |
| Why do we avoid aspirin use in those under 18? | Reye’s syndrome – viral and genetically linked mitochondrial dysfunction and altered (lose) lipid metabolism (severe illness characterized by cytokine release, acute encephalopathy, impaired (lowered) gluconeogenesis, ammonia retention, and fatty liver) |
| T/F: It is recommended to combine NSAID w/ aspirin for additional coverage | FALSE, combining NSAIDs w/ aspirin raises risk of GI adverse |
| T/F: NSAIDs are CONTRA in pregnancy | True: can prevent uterine contractions (why they are good with dysmenorrhea or cramping) |
| What can people who are in renal failure take that inhibits COX receptors? | Acetaminophen! (as long as hepatic function is okay) |
| What COX receptor(s) does acetaminophen inhibit? What does this do? | Weak COX-1 and COX-2 inhibitor; mainly inhibits COX-3 in the CNS for anti-pyresis and analgesia. |
| Morning stiffness, Arthritis of 3 or more joints, Arthritis of hand joints, Symmetric arthritis, Rheumatoid nodules, Serum rheumatoid factor, Radiographic changes; Requires 4/7 for Dx | Rheumatoid arthritis |
| What does DMARD stand for? | Disease Modifying Antirheumatic Drugs |
| Why is it so important to start DMARD therapy as soon as possible? | Early DMARD treatment suppresses the inflammatory response and appears to reset the rate of progression for years to come |
| When is only having a RA patient on NSAIDs acceptable? | When transitioning from one DMARD to another |
| T/F: DMARDs have slight analgesic effects | False: NSAID or narcotic should be given w/ DMARD for analgesic effects |
| Preferred DMARD? What should be taken with it? Adverse? | Methotrexate (MTX); folate supplement; marrow suppression, liver cirrhosis (HEPATIC), hair loss, lung fibrosis (ESSENTIALLY HAS NEGATIVE IMPACT ON RAPIDLY DIVIDING CELLS) |
| Can't tolerate MTX? This anti-rheumatic agent interfers w/antigen processing in macrophages. Adverse: maculopathy ("BULLS EYE" macular lesion pathognomonic), most common in those who take high doses for long periods, 60 yo+, or have renal disease. | Hydroxychloroquine (originally an anti-malarial drug) |
| Drug also used in inflammatory bowel disease w/ unknown MOA in RA but reduces inflammatory eicosanoids and cytokines. Adverse include skin rash, hemolytic anemia w/ G6PD, | Sulfasalazine (SSZ) |
| Has placed some RA pts into permanent remission. Thought to inhibit lymphocyte proliferation. First DMARD! Adverse: decreased appetite, renal damage, marrow suppression, rash | "GOOOOOOOOLLLLD" |
| Prevents collagen cross-linking and chelates metals so metalloproteinases cannot work; Adverse: renal failure and skin rash | D-Penicillamine (3-mercapto-D-valine) |
| New DMARD and a pro-drug binding to inhibit pyrimidine synthesis stopping division of T-lymphocytes; Serious Adverse including lung fibrosis, hepatic damage, myelosuppression, Stevens-Johnson; last resort | Leflunominde |
| 1st biologic agent approved for RA; monotherapy for RA; MOA: produces a continuous protein "fusing" of the TNF receptor to a section of a human antibody | Etanercept |
| Biologic monoclonal antibody works developed in mice by blocking tumor necrosis factor alpha (TNFa) by preventing its binding to receptor of the cell. Approved for concammitant use w/ methotrexate. Adverse? | Infliximab; associated w/ hepatic damage and development of antibodies against patients own cells |
| First fully humanized monoclonal IgG antibody designed to bind TNFα. Excellent results when combined w/ methotrexate | Adalimumab |
| Once a month subcu injection in combo w/ methotrexate that works even when other TNFa antagonists have been ineffective | Golimumab |
| T/F: No evidence any biologic DMARD is more effective than another | True |
| All pts should be screened for ________ before beginning TNFa blocker therapy. What two major things should they be monitored for? Which is more important? | Tuberculosis; 1) Infections 2) Malignancy; Infections are the bigger worry |
| What is important about vaccines when using TNF inhibitors? | NO LIVE VACCINES: risk of disseminated infx (must give weeks/months before biologics) |
| Competitive inhibitor of IL-1 (mediator of inflammation), modifying biologic response to stimuli. Adverse: may increase incidence of lymphomas/solid tumors, infxs of URTs; NOT a DMARD | Anakinra |
| Monoclonal antibody against protein CD20, binding and initiating lysis. Used in those failing to respond to TNFa blockade. Adverse: cardiac arrest has occurred during first dose administration, progressive multi-focal leukoencephalopathy (PML); l | Rituximab |
| Fusion protein that inhibits T cell activation. Adverse: way larger increased cancer risk with a variety of tumors; later resort | Abatacept |
| 4 biggest CONTRAs of biologics | Immunosuppressed, pregnancy, cardiomyopathy, infection |
| Tx combo for early RA when there is high disease activity: | TNF blocker and methotrexate |
| Moderate to high disease RA disease activity: | Methotrexate and hydroxychloroquine |
| Most commonly used for acute gout attack for Sx (what kind of drug is it) | Indomethacin (Indocin), taken w/ food resolves redness and tenderness (it is an NSAID) |
| Blocks inflammatory response to deposited crystals. Does not affect renal excretion of uric acid, alter plasma solubility of uric acid, or change serum uric acid levels. Given until inflammation has resolved, or GI side effects prevent further use. | Colchicine |
| Given in those who cannot tolerate NSAIDs or failed Tx. Improvement seen over 24 hours. Best method? | Corticosteroids: intra-articular injections are very beneficial in those that have 1 or 2 large joints affected or who need to prevent systemic effects. |
| Indication for prophylaxis? What can you take? How about if you are hypertensive? | frequent acute gout attacks (>3/year); Can take colchicine once a day or allopurinol. If hypertensive: Losartan (an ARB) promoting urate diuresis. |
| 6 drugs that contribute to hyperuricemia | thiazides, loops, low dose ASA, niacin, cyclosporine, ethambutol |
| Allopurinol: Fn, MOA, Adverse? | lowers serum and urine uric acid levels by preventing hypoxanthine from converting into uric acid, thereby raising levels. If ANY sign of rash, take off immediately (-> TEN) |
| Chemically distinct from allopurinol, but same MOA. Adverse? Benefits vs allopurinol? | Febuxostat; Higher rate of CV thromboembolic events (must screen and counsel pts), but a lower level of hypersensitivity rxns |
| Blocks tubular reabsorption of uric acid and enhances urine uric acid excretion. Increases urine uric acid level and decreases serum uric acid. Benefit? Adverse? | Probenecid; Benefit is slows release of penicillin into urine, raising serum levels which is good for infx Tx. Adverse: increased risk of nephrolithiasis w/ urate stones |
| First line Tx for osteoarthritis | NSAIDs or acetaminophen and exercise of the joint (generates more synovial fluid) |
| Non-first line options for osteoarthritis: (3) | 1) Viscosupplementation (injection of gel-like substances into joint) 2) Glucosamine w/ chondroitin 3) topical capsaicin |
| 3 pathophysiologies of pain | 1) Nociceptive 2) Neuropathic 3) Mixed |
| 2 mechanisms of pathophysiology of chronic pain | 1) Nerves become hypersensitive to pain 2) Nerves become resistant to anti-nociceptive signals |
| What can occur w/ chronic pain? | Pain continues after injury resolves or body removed (phantom pain) |
| T/F: Phantom pain is psychiatric | False, neurologic |
| What is the physiological significance of pain signals in chronic pain? In acute pain? | CP: There are none. AP: initiated in response to stimulus. |
| 4 descriptors of nociceptive pain. What types of neurons do these affect? Two subtypes? | 1) Aching 2) Squeezing (as in myocardial pain) 3) Stabbing 4) Throbbing; Affect afferent neurons (C fibers); Subs: Somatic and Visceral |
| Usual characterization of neuropathic pain (how else may it present?) Two subtypes? | Usual: burning or SHOOTING like an electrical quality. Also may present as aching, throbbing, or sharp. Subs: central vs peripheral generator |
| What is causalgia? | Presence of hypersensitivity along w/ severe burning pain associated w/ abrupt tissue trauma such as crushing or stabbing. Also called post-traumatic pain syndrome. |
| Percentage who fail to attain adequate relief from pain | 50% |
| Three factors that impede chronic pain treatment? | 1) Provider related (fear of regulatory scrutiny) 2) Patient-related (stoicism, fear of addiction) 3) System-related (limits on narcotics etc.) |
| Highest rate of drug overdose of any group: | European Americans |
| What is the pain faces scale good for? | Children, dementia, or patients w/ reading problems |
| Most commonly prescribed/first-line medication for neuropathic pain. What is the mechanism, class and effect? | Gabapentin; Increases GABA and has a sedating, calming effect. It is an anti-convulsant. |
| What other class of medications is used heavily with neuropathic pain? What type of pain are they preferred for? | Anti-depressants; Preferred for dysesthesias |
| Which anti-depressants are best tolerated? Which are considered the best? Why aren't they used all the time? | SSRIs best tolerated while evidence shows tricyclics are the best. Problem is they have lots of anti-cholinergic effects |
| What improves pain, especially neuropathic pain, appetite, nausea, and malaise? What special population is it for? | Corticosteroids, used in the cancer population; Prednisone and dexamethasone usually employed |
| Non-specific analgesic effects with many pain syndromes including as an epidural during neuropathic cancer pain. Adverse? Class? | Clonidine; Sedating; a-2 adrenergic agonist |
| Better tolerated a-2 adrenergic agonist than clonidine | Tizanidine |
| 3 NMDA receptor antagonist used for neuropathic pain | 1) Ketamine 2) Dextromethorphan 3) Amantadine |
| T/F: No ceiling dose for pure-agonist opioids. Whether true or false, what does this mean? | True, means tolerance will occur. |
| T/F: Can double up on chronic opioid pain meds. | False, like asthma! Need a rescue medication for breakthrough pain |
| What are the 4 As we monitor during opioid therapy? | 1) Analgesia 2) ADLs 3) Adverse 4) Aberrant drug-taking/Addiction |
| 2 anesthetic approaches to chronic pain management | 1) Neuraxial drug administration (epidural or intrathecal infusion in the spine) 2) Neural blockade (temporary or permanent) |
| Neurostimulatory approach examples | Acupuncture, Dorsal column stimulation (stimulates muscle weakness until hyperexcitable) |
| Absolute last resort for chronic pain? | Surgical procedures |
| Psychologic Txs: | Behavioral Txs and biofeedback |
| Predictors of addiction (4) | 1) Hx of abuse 2) age 3) personality 4) family dynamic and social factors |
| 2 step monitoring approach to monitoring aberrant behaviors | Step 1: Are there aberrant drug-related aberrant behaviors? Step 2: If yes, are these behaviors best explained by the existence of an addiction disorder? |
| What is pseudoaddiction? | when pts don't get adequate Tx, causing them to request more, making them appear like an addict |
| More or less predictive of addiction: Requesting specific drugs | Less |
| More or less predictive of addiction: Borrowing drug from another person | More |
| More or less predictive of addiction: Multiple dose escalations despite warning | More |
| More or less predictive of addiction: Occasional impairment | Less |
| More or less predictive of addiction: Drug hoarding when Sx milder | Less |
| Great proactive strategy for addressing drug-related behavior: | Treatment Contract |
| Best step if pt develops substance use disorder | Impatient w/ detox and pharmacotherapy followed by maintaince monitoring |
| T/F: Gradually tapering off opioids for withdrawal purposes isn't effective. | True (>90% 1 year relapse rate) |
| Antagonist Tx used for blocking opiate agonist effects. Poor acceptance by pts as it has no other effects other than _________. What groups is it effective in? | Naltrexone; taking away cravings; effective in motivated individuals |
| Most widely used pharmacotherapy for opioid dependence. Must be in specialized Tx program and providers must watch you take it. What is an effect? | Methadone; induces tolerance to acute dose of opioid |
| What is the drug only DEA waivered physicians can provide (no PAs or NPs). Schedule III drug | Buprenorphine |
| Boo | Ya! |
| Major establishments of the Federal Controlled Substances Act of 1970 (2) | 1) Controlled substances can only be used for accepted medical use (no off-label). 2) A "closed" system of distribution was implemented (DEA registration, record keeping, etc.) |
| T/F: NC has a separate state licence requirement in addition to the DEA. | False, just DEA requirement |
| Exemption to requiring a DEA ID # on every prescription | If hospital is registered, individual DEA number not required for impatient use (INDIVIDUAL DEA NUMBER STILL REQUIRED FOR THOSE GOING HOME) |
| General class and specific drugs (4) for ADHD, sedation, narcolepsy, depression, wt loss. Adverse? | Stimulants; Ritalin (esp for depression), Concerta, Dextroamphetamine Sulfate (a Compton favorite), Adderall; Adverse: psychosis, aggression, seizures, anxiety |
| Sx of stimulant withdrawal (3 big ones) | low energy, depression, irritability |
| Drugs for anxiety, sleep induction, PTSD, alcohol/drug withdrawal. MOA? 4 types of specific drugs? Adverse? | Sedative hypnotics; enhance GABA activity; 1) Benzos 2) Barbs 3) Sleep meds 4) Miscellaneous like Soma/carisoprodol. A: essentially, intoxication. |
| Major effects of sedative hypnotic withdrawal? | CV and CNS arousal including: increased pulse and blood pressure and seizures. |
| 3 aspects of Mu agonists (what makes this different from Delta or Kappa?) | 1) supra-spinal and spinal analgesia 2) respiratory depression 3) physical dependence. Mu is the only opioid receptor that induces euphoria |
| Examples of pure mu opioid agonists | morphine, codeine, fentanyl (synthetic) |
| Example of partial mu agonist | tramadol (ultram) |
| What is the difference between mixed agonist/antagonist, and pure mu agonists? | pure has no ceiling where the mixed do (antagonist overwhelms agonist) |
| Two major adverse of opioids? Withdrawal? | 1) Psychological reward 2) physical dependence; W: flu-like syndrome (aches and pain; not as risky as sedative withdrawal) |
| Most likely controlled substance schedule to be abused | Schedule II |
| Cannot be prescribed (what schedule?) | Schedule I |
| Low potential for abuse that may lead to limited dependence (ex: tranquilizers, xanax | Schedule IV |
| Less potential for abuse that may lead to moderate dependence (ex: meds w/ codeine) | Schedule III |
| T/F: hydrocodone preparations are schedule III drugs | False; turned to schedule II this year |
| Who gets a schedule II pain med? What is the reality of this judgement and process? | Person w/ intractable pain "which no relief found after reasonable effort"; Reality is waiting to give pain med compromises patient interaction and care |
| T/F: May not issue a prescription of schedule II for general dispensing to patient | True, all Rx must be written for a specific patient |
| Process in which, during a strict emergency, a schedule II can be called in? | Can call it in, but must follow up w/ a written Rx to the pharmacy w/in 7 days or be reported to the DEA |
| T/F: Refills of schedule II drugs are only permitted by a physician | False, prohibited to all. |
| Guideline for refills of schedule III-IV drugs? | 5 monthly refills permitted (require a new Rx after 6 months total) |
| Guidelines of schedule V refills? | Judgment of prescriber and pharmacist |
| How much time do patients have to pick up remainder quantities of drugs when the pharmacist is unable to supply the full quantity? How long is a Rx valid for? | 72 hours; 60 days |
| T/F: Provider can provide withdrawal/detox medications for patients. | True, but not whole story. MUST have a separate registration w/ the DEA as a narcotic treatment program. |
| T/F: It is okay to prescribe narcotics to the narcotic addicted in order to alleviate pain | True |
| T/F: Issuing more than 1 Rx for the same schedule II med on the same day is okay if you post-date it correctly | False, Cannot issue more than 1 Rx the same date for the same schedule II drug, and NEVER POSTDATE. |
| Restrictions for PAs | Cannot exceed a 30 day supply and physician must possess same schedules for DEA registration |
| Biggest misuse we think of: | Diversion for profit |
| Where do most patients get extra drugs? | Free from a friend or relative |
| Personality of a drug seeker | chatty or irritable/pushy, rude to staff but not you, like a sales person |
| History of a drug seeker | Often can name DOC but has no old records or can't remember old providers name |
| What to look for and document in drug seeking patients, generally and w/ specific examples (stimulants, Benzos, narcotics) | Generally: too happy or sedated; Stims: wt loss, anxiety; Benzos/Barbs: mood depression/HypoTN; Narcs: N/V/pruritis |
| Important note about old records | Never prescribe refills for controlled substances until you have seen the old records or have looked on the controlled substance database |
| NOT A QUESTION, just remember: | Their inconvenience < your license. AND all controlled Rxs you write are recorded |
Created by:
crward88
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