Drugs Used to Treat Acute Pain Flashcards
Opiates are CONTRAINDICATED for patients who have which of the following?
- Severe head injury
- Bronchial asthma
- Renal dysfunction
- Acute myocardial infarction
Severe head injury
Of the following agents which one will provide the greatest relief of pain and affect the gastric mucosa and the LEAST?
- Aspirin and codeine (Empirin #3)
- Flurbiprofen (Ansaid)
- Acetaminophen (Tylenol)
- Acetaminophen and oxycodone (tylox)
Acetaminophen and oxycodone (tylox)
Aspirin is contraindicated with which of the following drugs
- Coumadin
- Triazolam
- Barbiturates
- Pentobarbital
- Methylprednisolone
Coumadin
What can the pharmacological control of pain be directed at?
- Initiation
- Propagation
- Perception
Signs of inflammation
- Edema (tumor)
- Redness (rubor)
- Heat (calor)
- Pain (dolor)
- Loss of function
Aspirin
Class: NSAID; analgesic
Mechanism of action: Irreversibly inhibits COX by acetylating serine 530 in the active site; this mechanism makes aspirin more effective but also more unsafe
Indication:
- Anticoagulation post MI (81-325 mg/day)
- Prevention of MI in males over 40 (81mg/day)
- Prevention of stroke in females over 40 (81 mg/day)
- Acute pain, 325-650 mg q4h; max = 4 G/day
Pharmacological effects:
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
-Same as NSAIDs
-Effects on the platelets
-Bleeding: occult bleeding from both inhibition of PGs and thromboxanes; inhibits platelet aggregation
oContraindicated drugs:
- Same as NSAIDs
- Warfarin: increase likelihood of bleeding
- Drugs for gout: decreased uricosuric effects; exacerbates gout
- Insulin, sulfonylureas: enhanced hypoglycemic effect
oContraindications:
- Same as NSAIDs
- Reye’s syndrome (influenza in children)
- Salicylate intolerance (asthma)
- Gouty arthritis
- Hypo-coagulation states
- GI and renal (like other NSAIDs)
oWhich analgesic can the patient take:
NSAIDs (Ibuprofen)
Class: NSAID, analgesic
Mechanism of action: Competitive cyclooxygenase inhibition
Indication:
- Acute Pain:clinically significant analgesia within 1 hour
- Inflammation:clinically significant anti-inflammatory effects take several days or weeks (this refers to chronic inflammation)
- Chronic Inflammatory diseases: rheumatoid arthritis, lupus, osteoarthritis
- Fever
Pharmacological effects:
- Ceiling effect
- Pre-medicate
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
-GI upset
-Renal function
oContraindicated drugs:
- Increased toxicity: Lithium (seizures), Digoxin, Cyclosporine, Methotrexate (chemo), oral hypoglycemic
- Increased risk of GI bleeding: Alcohol
- Increased risk of bleeding: SSRIs, Anticoagulants
- Antihypertensive drugs whose actions depend on renal PGs; no more than 4 days of treatment of the NSAID: ACE inhibitors, Diuretics, Beta-blockers
oContraindications:
- Ulcers or gastroesophageal reflux disease (GERD)
- Impaired renal function or renal disease
- Pregnancy: doubles risk for miscarriage in early pregnancy
- Allergy to salicylates or NSAIDs: ASA induced asthma, nasal polyps, angioedema
oWhich analgesic can the patient take:
What effect does aspirin have on platelets?
- COX enzyme is completely inhibited because of the covalent bond mechanism of PG inhibition
- PGs=precursors of thromboxane A2
- Thromboxane A2 is an inducer of platelet aggregation
- Platelets–>have no nucleus, so they cannot synthesize TA2 for their entire 10 day lifetime
What are the adverse effects of NSAIDs?
- GI upset: COX1 PGs that are involved in the production of mucous protective barrier against stomach acid (protons); 1-5% of patient/year experience peptic ulcers, GI bleeding, or GI perforations
- Renal function: COX1 and COX2 PGs reduce water and Na reabsorption at the ascending loop of Henle and maintain dilation of the renal vasculature; acute renal failure is more likely to develop in patients with pre-existing renal insufficiency, congestive heart failure, dehydration, or on angiotensin-converting enzyme (ACE) inhibitors (the lack of angiotensin II weakens reactive constriction of teh afferent arteriole, a normal protective response when renal blood flow is low)
ASA and NSAIDs interaction
- Low dose ASA therapy for the anti-platelet effect: competitive inhibition of the acetylation site of COX in the platelet
- Ibuprofen interferes with ASA binding: ibuprofen leaves the site, but ASA will be excreted because of its short half-life
- FDA recommends acetaminophen instead of NSAIDs when treating patient for pain who use ASA for anti-platelet effect
What causes the drug interactions between NSAIDs and antihypertensive drugs whose actions depend on renal PGs?
- Due to modulation of renin release
- Vasoconstriction and Na retention
- Cleaves angiotensinogen to angiotensin I
- Angiotensin I cleaved to angiotensin II bt angiotensin converting enzyme (ACE)
- You don’t want to interfere with renin release from the kidney because a lot of the drugs depend on renin release for their efficacy
What is the ceiling effect of NSAIDs?
- There is a maximal effect of NSAIDs because PGs are not the only mediators of inflammation (substance P, glutamate, nitrous oxide)
- Doses above the daily limits lead to renal damage and impairment
What are the therapeutics of NSAIDs?
- PGs are NOT stored; they are released as needed
- Pre-medication before dental appointment to prevent release and therefore patient has less pain and inflammation during appointment and after
Acetaminophen (Tylenol)
Class: Analgesic, antipyretic (NOT anti-inflammatory)
Mechanism of action:
- Possibly an inhibitor of CNS cyclooxygenase (most likely)
- Maybe activation of spinal serotonergic pathways
- Maybe inhibition of nitric oxide synthase
Indication:
- Analgesic of choice in patients that cannot take/tolerate ASA or NSAIDs
- Ulcer
- Asthma
- Diabetes
- Gout
- Children under 16
- Hypo coagulation states
Pharmacological effects:
- Metabolism of acetaminophen
- Hepatotoxicity at doses greater than 4g/day
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
oContraindicated drugs:
- Drugs that induce liver enzymes increase toxicity of acetaminophen
- Increased hepatotoxicity: EtOH, Isoniazid (Nydrazid), Phenytoin (Dilantin), Carbamazepine (Tegretol)
- Zidovudine (Retrovir): drug used for AIDS that reduces zidovudine metabolism, resulting in increased bone marrow toxicity
oContraindications:
- Liver disease: proteins are already compromised
- Hepatitis: inflammation
- Alcoholism: typically have less glutathione (source of electrons for body)
- If using tylenol, maximum dose is 2g/day
oWhich analgesic can the patient take:
Describe the metabolism of acetaminophen
- Normally, it gets conjugated to acetaminophen glucuronide or acetaminophen sulfate
- If there is too much, it can get metabolized into NAPQI by P450 enzyme, which leads to hepatoxicity (from free radical)
- NAC is used to get rid of the free radical by turning into glutathione, which donates an electron and allows excretion
