NEET MDS Dental Pharmacology Syllabus

Which local anesthetic is unique in containing both an ester and amide linkage, and what is its significance?

Articaine — it has an amide link plus an ester group (thiophene ring), allowing rapid plasma hydrolysis, a short half-life (~20 min), and good tissue diffusion.

Why are ester local anesthetics more likely to cause allergic reactions than amides?

Esters are metabolized by plasma cholinesterase to PABA (para-aminobenzoic acid), a known allergen. True amide allergy is rare.

Describe the mechanism of action of local anesthetics.

They reversibly block voltage-gated sodium channels on the internal surface of the nerve membrane, preventing Na+ influx, depolarization, and propagation of the action potential.

Why do local anesthetics work poorly in inflamed/infected (acidic) tissue?

Low pH shifts equilibrium toward the ionized (charged) form, reducing the lipid-soluble unionized fraction that crosses the nerve membrane, so less drug reaches its intracellular site of action.

Why is epinephrine added to local anesthetic solutions?

Vasoconstriction reduces systemic absorption, prolongs duration, deepens anesthesia, reduces toxicity, and decreases bleeding at the surgical site.

What is the maximum recommended dose of lidocaine with epinephrine?

Approximately 7 mg/kg (up to ~500 mg) with epinephrine; about 4.4 mg/kg (up to ~300 mg) without epinephrine.

Which local anesthetic carries a risk of methemoglobinemia, and which two are most implicated?

Prilocaine and benzocaine are most associated with methemoglobinemia, especially at high doses.

What is the mechanism of action of non-opioid analgesics such as NSAIDs?

They inhibit cyclooxygenase (COX-1 and COX-2) enzymes, reducing prostaglandin synthesis, thereby decreasing pain, inflammation, and fever.

How does the mechanism of acetaminophen (paracetamol) differ from NSAIDs?

Acetaminophen acts mainly centrally (weak central COX inhibition) with analgesic and antipyretic effects but little peripheral anti-inflammatory action and no significant antiplatelet effect.

Why is aspirin contraindicated before oral surgery in many cases?

Aspirin irreversibly acetylates COX-1 in platelets, inhibiting thromboxane A2 and platelet aggregation for the platelet's lifespan (~7–10 days), increasing bleeding risk.

What is the maximum safe daily dose of acetaminophen in adults, and the danger of overdose?

Generally up to 3–4 g/day. Overdose causes hepatotoxicity via the toxic metabolite NAPQI; the antidote is N-acetylcysteine.

Why are selective COX-2 inhibitors (e.g., celecoxib) used, and what is their main risk?

They reduce inflammation/pain with less GI ulceration (sparing COX-1 gastric protection), but carry an increased cardiovascular thrombotic risk.

Describe the mechanism of action of opioid analgesics.

They bind mu (μ), kappa (κ), and delta (δ) opioid receptors (mainly μ), inhibiting ascending pain transmission and activating descending inhibitory pathways, producing analgesia, sedation, and euphoria.

List four common adverse effects of opioids.

Respiratory depression, constipation, nausea/vomiting, sedation, miosis (pinpoint pupils), and physical dependence/tolerance.

What is the antidote for opioid overdose and its mechanism?

Naloxone — a competitive opioid receptor antagonist that rapidly reverses respiratory depression and sedation; it has a short half-life so repeat dosing may be needed.

What is codeine and why is its analgesic effect variable?

Codeine is a weak opioid prodrug metabolized by CYP2D6 to morphine; poor metabolizers get little analgesia while ultra-rapid metabolizers risk toxicity.

Define adjuvant analgesics and give two examples used in pain management.

Drugs whose primary indication is not pain but which relieve pain in certain conditions (especially neuropathic). Examples: anticonvulsants (gabapentin, carbamazepine) and tricyclic antidepressants (amitriptyline).

Which adjuvant analgesic is first-line for trigeminal neuralgia?

Carbamazepine — an anticonvulsant that stabilizes sodium channels and reduces neuronal firing.

What is the WHO analgesic ladder and how does it apply to dental pain?

A stepwise approach: Step 1 non-opioids (NSAIDs/acetaminophen) ± adjuvants; Step 2 weak opioids; Step 3 strong opioids. Most dental pain is managed at Step 1, often NSAID-based.

Why is the NSAID + acetaminophen combination favored for acute dental pain?

They act by different mechanisms, giving additive/synergistic analgesia superior to either alone, while allowing lower opioid use.

Name the major classes of antibiotics by mechanism of action.

Cell wall synthesis inhibitors (beta-lactams, glycopeptides); protein synthesis inhibitors (macrolides, tetracyclines, aminoglycosides, clindamycin); nucleic acid inhibitors (fluoroquinolones, metronidazole); folate synthesis inhibitors (sulfonamides).

What is the mechanism of action of penicillins?

Beta-lactams bind penicillin-binding proteins (transpeptidases), inhibiting bacterial cell wall peptidoglycan cross-linking, leading to cell lysis (bactericidal).

Which antibiotic is first-line for most odontogenic infections, and what is the alternative for penicillin-allergic patients?

Amoxicillin (often with metronidazole for anaerobes) is first-line. Clindamycin is the common alternative in penicillin-allergic patients.

What is the mechanism of action and dental role of metronidazole?

It is reduced intracellularly to form reactive species that damage anaerobic bacterial DNA; it is highly effective against anaerobes in periodontal and odontogenic infections. Patients must avoid alcohol (disulfiram-like reaction).

Why are tetracyclines avoided in children under 8 and in pregnancy?

They chelate calcium and deposit in developing teeth and bones, causing permanent intrinsic tooth discoloration and enamel hypoplasia.

What is the recommended antibiotic prophylaxis regimen for high-risk infective endocarditis before invasive dental procedures?

Amoxicillin 2 g orally (50 mg/kg in children) 30–60 minutes before the procedure; clindamycin or azithromycin/cephalexin for penicillin-allergic patients.

What is the mechanism of action of the azole antifungals (e.g., fluconazole, miconazole)?

They inhibit fungal cytochrome P450 enzyme 14-alpha-demethylase, blocking ergosterol synthesis and disrupting the fungal cell membrane.

What is nystatin and its clinical use in dentistry?

A polyene antifungal that binds ergosterol, forming membrane pores. Used topically (suspension/pastilles) for oral candidiasis (thrush); it is not absorbed systemically.

Which antiviral is used for herpes labialis/herpetic gingivostomatitis and its mechanism?

Acyclovir — a guanosine analog phosphorylated by viral thymidine kinase that inhibits viral DNA polymerase, halting herpes simplex virus DNA replication.

Describe the mechanism of action of benzodiazepines used for dental sedation.

They bind the GABA-A receptor at a site distinct from GABA, increasing the frequency of chloride channel opening, enhancing GABA's inhibitory effect to produce sedation, anxiolysis, amnesia, and muscle relaxation.

Which benzodiazepine is preferred for IV conscious sedation in dentistry, and what is its reversal agent?

Midazolam (rapid onset, short duration, water-soluble, amnesic). Its reversal agent is flumazenil, a competitive benzodiazepine-receptor antagonist.

What is nitrous oxide and its role as a non-benzodiazepine sedative in dentistry?

An inhaled inorganic gas providing rapid-onset, rapidly reversible minimal/moderate sedation and analgesia, titrated with oxygen; patient stays conscious and recovers quickly.

What are the key monitoring requirements during conscious (moderate) sedation in dentistry?

Continuous monitoring of consciousness/responsiveness, oxygen saturation (pulse oximetry), heart rate, blood pressure, and respiration, with resuscitation equipment and supplemental oxygen available.

What is the immediate management of vasovagal syncope (fainting) in the dental chair?

Place the patient supine with legs elevated (Trendelenburg), ensure a patent airway, give oxygen, loosen tight clothing, and monitor vital signs; recovery is usually rapid.

What is the first-line drug and dose for anaphylaxis in the dental office?

Intramuscular epinephrine 0.3–0.5 mg (1:1000) in the mid-outer thigh, repeated every 5–15 minutes as needed, with airway support, oxygen, and call for emergency help.

Differentiate a mild allergic reaction from anaphylaxis and their drug management.

Mild (urticaria, itching) is managed with an antihistamine (e.g., diphenhydramine). Anaphylaxis (airway compromise, hypotension, bronchospasm) requires immediate IM epinephrine first, then antihistamines, corticosteroids, oxygen, and fluids.

What is the emergency management of an acute asthma attack/bronchospasm in the dental chair?

Stop the procedure, sit the patient upright, give a short-acting beta-2 agonist inhaler (salbutamol/albuterol), administer oxygen, and give epinephrine plus call for help if severe or unresponsive.

What drug is given for suspected angina/myocardial ischemia during dental treatment, and how?

Sublingual glyceryl trinitrate (nitroglycerin) spray/tablet, which dilates coronary vessels; give oxygen, stop treatment, and if pain persists beyond ~15–20 min or MI is suspected, give aspirin and activate emergency services.

What is the role of aspirin in a suspected myocardial infarction in the dental office?

Have the conscious patient chew 162–325 mg aspirin to inhibit platelet aggregation and limit clot growth, while giving oxygen, nitroglycerin, and activating emergency medical services.