NBDHE Pharmacology in Dental Hygiene 2 — Questions and Answers

Question 1: Which analgesic should be avoided in a patient with aspirin-exacerbated respiratory disease (AERD/Samter's triad)?

Ibuprofen and all NSAIDs (including aspirin) (Correct answer)
Acetaminophen (paracetamol)
Codeine
Tramadol

Correct answer: Ibuprofen and all NSAIDs (including aspirin)

Patients with AERD (Samter's triad: asthma, nasal polyps, aspirin sensitivity) experience bronchospasm with all NSAIDs that inhibit COX-1, including ibuprofen; acetaminophen is generally safe.

Aspirin-exacerbated respiratory disease (AERD), also called Samter's triad, consists of chronic rhinosinusitis with nasal polyps, asthma, and exquisite sensitivity to aspirin and all COX-1-inhibiting NSAIDs. The mechanism involves COX-1 inhibition redirecting arachidonic acid toward the 5-lipoxygenase pathway, generating excess leukotrienes (LTC4, LTD4) that cause bronchospasm and rhinorrhea. Dental hygienists must avoid prescribing or recommending NSAIDs (ibuprofen, naproxen, ketorolac, aspirin) in these patients. Acetaminophen (which weakly inhibits COX-1 at therapeutic doses) is generally safe if given at doses ≤650 mg. Celecoxib (selective COX-2 inhibitor) may be tolerated but is not routinely recommended without specialist guidance.

Question 2: The opioid analgesic codeine exerts its analgesic effect by being converted to:

Morphine via hepatic CYP2D6 enzyme (Correct answer)
Oxycodone directly
Hydromorphone peripherally
Fentanyl in the CNS

Correct answer: Morphine via hepatic CYP2D6 enzyme

Codeine is a prodrug that undergoes O-demethylation by hepatic CYP2D6 to morphine (about 10% conversion), which provides most of its analgesic effect.

Codeine itself has minimal affinity for opioid receptors; approximately 10% is converted to morphine by cytochrome P450 CYP2D6 in the liver, which provides its analgesic efficacy. Genetic polymorphisms in CYP2D6 create clinical variability: (1) Poor metabolizers (PM) — 7% of Caucasians — receive little analgesia from codeine; (2) Ultra-rapid metabolizers (UM) — convert codeine to morphine rapidly, risking dangerous respiratory depression and death (especially in nursing mothers and children after tonsillectomy — FDA Black Box Warning). The FDA advises against codeine in children, nursing mothers, and post-tonsillectomy/adenoidectomy patients. CYP2D6 interactions (fluoxetine inhibits CYP2D6) further affect codeine efficacy.

Question 3: A patient is taking warfarin (Coumadin) for atrial fibrillation. If the dental hygienist recommends ibuprofen for post-procedural pain, what is the primary drug interaction concern?

NSAIDs inhibit platelet aggregation and may displace warfarin from plasma proteins, increasing bleeding risk (Correct answer)
Ibuprofen enhances warfarin's metabolism, reducing its anticoagulant effect
NSAIDs directly counteract warfarin at the receptor level
There is no clinically significant interaction

Correct answer: NSAIDs inhibit platelet aggregation and may displace warfarin from plasma proteins, increasing bleeding risk

NSAIDs inhibit platelet function (GI mucosal protection) and may compete with warfarin for protein binding sites, potentially raising free warfarin levels and increasing hemorrhagic risk.

The warfarin-NSAID interaction is clinically significant for multiple reasons: (1) NSAIDs inhibit platelet aggregation via COX-1 inhibition, impairing primary hemostasis independently; (2) Some NSAIDs (e.g., phenylbutazone) displace warfarin from albumin binding, transiently increasing free warfarin concentration; (3) NSAIDs can cause GI mucosal damage and erosion, creating a bleeding site compounded by warfarin's anticoagulant effect; (4) Selective NSAIDs may affect CYP2C9 (warfarin metabolism). Acetaminophen (≤2 g/day short-term) is the recommended analgesic for warfarin patients. The patient's current INR should be checked before any invasive dental procedure; INR ≤3.5 is generally acceptable for routine scaling.

Question 4: Which antihypertensive drug class is MOST likely to cause gingival enlargement?

Calcium channel blockers (particularly nifedipine) (Correct answer)
Beta-blockers
ACE inhibitors
Diuretics (thiazides)

Correct answer: Calcium channel blockers (particularly nifedipine)

Calcium channel blockers, especially nifedipine (and to a lesser extent amlodipine and diltiazem), are well-known causes of drug-influenced gingival enlargement.

Drug-influenced gingival enlargement (DIGE) is caused by three main drug classes: (1) Calcium channel blockers — nifedipine (most common, ~30% of users), amlodipine, diltiazem, verapamil; mechanism involves altered calcium metabolism in gingival fibroblasts, increasing collagen synthesis; (2) Anticonvulsants — phenytoin (original DIGE drug, ~50% of users); (3) Immunosuppressants — cyclosporine A (transplant patients, ~30% of users). ACE inhibitors (captopril, lisinopril) cause a persistent dry cough (bradykinin accumulation) and may cause angioedema but not gingival enlargement. Beta-blockers can cause xerostomia. For warfarin patients, NSAIDs are contraindicated; acetaminophen is preferred.

Question 5: Nitrous oxide-oxygen sedation (N2O/O2) used in dental hygiene is classified as which level of sedation?

Minimal sedation (anxiolysis) — patient fully conscious and responsive (Correct answer)
Moderate sedation (conscious sedation) — patient depressed but arousable
Deep sedation — patient barely arousable
General anesthesia — patient unconscious

Correct answer: Minimal sedation (anxiolysis) — patient fully conscious and responsive

At the concentrations used in dentistry (up to 50% N2O), nitrous oxide provides minimal sedation (anxiolysis) only — the patient remains fully conscious, maintains their own airway, and responds normally to verbal communication.

The American Society of Anesthesiologists (ASA) continuum of sedation: (1) Minimal sedation (anxiolysis) — normal cognition but reduced anxiety; airway maintained; no cardiovascular depression; (2) Moderate sedation — purposeful response to stimulation; airway and ventilation maintained; (3) Deep sedation — barely arousable; may need airway support; (4) General anesthesia — unconscious, requires airway management. Nitrous oxide at ≤50% produces minimal sedation/anxiolysis in most patients. Contraindications: COPD (patients dependent on hypoxic drive), first trimester pregnancy, severe psychiatric conditions, recent ear surgery (gas expansion), MTHFR enzyme deficiency. Proper titration, 100% oxygen at the end, and N2O recovery time are required.

Question 6: A patient taking selective serotonin reuptake inhibitors (SSRIs) for depression is at increased risk for which dental treatment complication?

Increased bleeding tendency due to impaired platelet serotonin uptake and aggregation (Correct answer)
Reduced local anesthetic efficacy
Malignant hyperthermia with epinephrine
Bradycardia with vasoconstrictors

Correct answer: Increased bleeding tendency due to impaired platelet serotonin uptake and aggregation

SSRIs block serotonin reuptake in platelets (which rely on serotonin for activation), impairing platelet aggregation and increasing bleeding tendency, particularly when combined with NSAIDs.

Platelets normally take up serotonin via SERT (serotonin transporter) and release it during activation to amplify aggregation. SSRIs block SERT in platelets, depleting platelet serotonin stores and impairing the platelet release reaction. The clinical result is a mild but measurable increase in bleeding time, particularly with surgical procedures. This effect is amplified significantly when SSRIs are combined with NSAIDs or aspirin. Dental hygienists should: (1) Avoid recommending NSAIDs for SSRI patients (use acetaminophen); (2) Be prepared for increased bleeding during scaling; (3) Apply appropriate local hemostasis. SSRIs do not significantly affect local anesthetic efficacy or interact dangerously with epinephrine.

NBDHE Pharmacology in Dental Hygiene 2

Which analgesic should be avoided in a patient with aspirin-exacerbated respiratory disease (AERD/Samter's triad)?