PH5.1-2 | Respiratory Pharmacology — Graded Quiz

Correct. Mild intermittent asthma (Step 1) is managed with as-needed SABA only. When symptoms exceed 2 days/week (or awakenings >2/month, or SABA use ≥2 days/week), the diagnosis shifts to mild persistent asthma (Step 2) — and a low-dose ICS controller is required. This classification-to-treatment mapping is the foundation of GINA step therapy.

GINA Step 1 = mild intermittent (symptoms ≤2 days/week); Step 2 = mild persistent (symptoms >2 days/week) → low-dose ICS controller. Knowing the threshold matters clinically.

GINA 2023 updated some low-dose ICS-formoterol recommendations, but the threshold for adding a controller remains tied to the persistent vs intermittent distinction. Symptoms occurring >2 days/week define mild persistent asthma — the GINA Step 2 trigger for adding a low-dose ICS.

Correct. Formoterol is unique among LABAs for having both rapid onset (1-3 minutes, comparable to salbutamol) and long duration (12 hours). This enables the MART (Maintenance And Reliever Therapy) strategy, where a low-dose ICS-formoterol combination serves as both the daily maintenance inhaler and the as-needed rescue inhaler. Salmeterol's slow onset (15-30 min) confines it to maintenance use only.

Formoterol has rapid onset (1-3 min) + 12-hour duration, enabling the MART strategy (Maintenance And Reliever Therapy with ICS-formoterol). Salmeterol has slow onset (15-30 min) — maintenance only.

Both formoterol and salmeterol are 12-hour LABAs — duration is the same. The key distinguishing property is onset: formoterol acts within 1-3 minutes (rapid), salmeterol within 15-30 minutes (slow). This difference drives the MART strategy eligibility.

Correct. GOLD 2023 guidelines recommend adding ICS to LABA+LAMA for COPD patients with blood eosinophils ≥300 cells/μL (indicating steroid-responsive eosinophilic inflammation) or those with ≥2 moderate or ≥1 severe (hospitalisation) exacerbations per year despite optimised dual bronchodilation. FEV1 threshold alone is no longer a sufficient indication.

ICS in COPD is indicated for the eosinophilic/exacerbation phenotype: eosinophils ≥300 cells/μL or ≥2 moderate exacerbations/year. FEV1 alone does not trigger ICS addition per GOLD 2023.

FEV1 < 50% was an older (GOLD 2011) threshold that has been replaced. Current GOLD 2023 bases the ICS-add decision on the exacerbation history and eosinophil phenotype, not spirometry alone. Productive cough and LTOT are not triggers for ICS addition.

Correct. In acute exacerbations, the short duration of ipratropium (4-6 hours) allows reassessment and re-dosing at appropriate intervals. The acute care team can titrate based on response. Tiotropium's 24-hour duration makes dose-titration impractical and risks prolonged anticholinergic effects if the patient's status changes. Ipratropium nebulisation is combined with salbutamol in acute asthma/COPD exacerbations (triple bronchodilation strategy).

Ipratropium = SAMA (onset 15-30 min, duration 4-6 h) — suitable for acute/ED setting with repeated doses. Tiotropium = LAMA (24-h duration), suitable for stable COPD maintenance, not acute titration.

Both ipratropium and tiotropium block M3 receptors — tiotropium actually has higher affinity. The key distinction in the acute setting is pharmacokinetics: duration matters for dose titration during a dynamic emergency.

Correct. When tiotropium (or ipratropium) aerosol inadvertently reaches the eye — particularly through poorly fitted nebuliser masks or incorrect inhaler technique (angled toward the eye) — local anticholinergic action causes mydriasis (pupil dilation) and ciliary muscle relaxation. In eyes predisposed to narrow angles, this increases resistance to aqueous outflow through the trabecular meshwork, precipitating acute angle-closure glaucoma. Counselling on correct inhaler technique and nebuliser mask fit is essential.

LAMA inhalers can precipitate acute angle-closure glaucoma if the aerosol reaches the eye (through poor inhaler technique or mask fitting). The local anticholinergic action dilates the pupil, blocking the trabecular meshwork in susceptible eyes.

Systemic absorption of inhaled tiotropium is minimal; it would cause anticholinergic mydriasis systemically only at toxic doses. Beta-2 agonists and theophylline do not have a clinically established mechanism for precipitating acute angle-closure glaucoma.

Correct. The widely used ICS equivalence table (GINA) places BDP 400 mcg/day and budesonide 400 mcg/day at equivalent medium doses. Fluticasone propionate is approximately twice as potent as BDP (FP 200 mcg ≈ BDP 400 mcg). Ciclesonide 160 mcg is also roughly equivalent to BDP 400 mcg (it is a prodrug activated in the lungs). Getting ICS dose equivalences right matters for safe switching between inhalers.

ICS potency equivalence: BDP 400 mcg ≈ Budesonide 400 mcg (both 'medium-dose') ≈ Fluticasone propionate 200 mcg (≈2× potency of BDP) ≈ Ciclesonide 160 mcg.

Fluticasone propionate is about twice as potent as BDP or budesonide by inhaled dose. FP 400 mcg/day is a HIGH-dose equivalent (double the BDP 400 mcg medium dose). Knowing these equivalences prevents inadvertent doubling or halving of effective ICS dose during brand switches.

Correct. Codeine acts centrally as a mu-opioid agonist in the medullary cough centre, suppressing the cough reflex. Its principal adverse effects in outpatient use are opioid-class effects: constipation (OIC — opioid-induced constipation from mu-opioid receptors in enteric nervous system), sedation, and risk of dependence/misuse. It is also converted to morphine by CYP2D6 — ultra-rapid metabolisers can experience morphine toxicity.

Codeine = central antitussive (mu-opioid agonism in medullary cough centre); adverse effects include constipation, sedation, dependence, and risk of neonatal opioid withdrawal syndrome if used in pregnancy.

Codeine is not a peripheral antitussive (that is benzonatate), not an expectorant (that is guaifenesin), and not an antihistamine. Central vs peripheral classification, and identifying the key adverse effect, are standard exam points.

Correct. ACE (angiotensin-converting enzyme) is identical to kininase II, which degrades bradykinin. ACE inhibition therefore causes bradykinin accumulation in airway tissues. Bradykinin stimulates bradykinin B2 receptors on pulmonary C-fibres, triggering cough. Additionally, bradykinin induces prostaglandin synthesis which further sensitises airway afferents. This dry, persistent, tickling cough occurs in 10-15% of Caucasians and up to 30-40% of South Asian (including Indian) patients, making it highly relevant clinically.

ACE inhibitor cough: ACE (kininase II) normally degrades bradykinin. When ACE is inhibited, bradykinin accumulates in the airways, stimulating C-fibre afferents and triggering cough. This occurs in ~10-20% of South Asian patients (higher than in Caucasians).

ACE inhibitors do not block beta-1 receptors (beta-blockers do). They do not have methacholine-like muscarinic activity. While prostaglandins are downstream of bradykinin accumulation, the primary trigger is bradykinin itself. This is the mechanism tested in pharmacology examinations.

Correct. Guaifenesin (the most widely used OTC expectorant) is thought to act primarily by irritating the gastric mucosa, which stimulates vagal afferents that reflexly drive increased tracheobronchial secretions via the gastrobronchial reflex. The increased secretion dilutes existing mucus, reducing its viscosity. This reflex mechanism explains why adequate hydration and correct dosing (with a full glass of water) enhances guaifenesin's effect.

Guaifenesin acts by reflex: gastric irritation → vagal stimulation → increased bronchial gland secretion → thinning of mucus. Ambroxol/bromhexine stimulate serous gland secretion directly. Acetylcysteine cleaves disulphide bonds.

Acetylcysteine is a mucolytic (direct disulphide bond cleavage). Ambroxol (active metabolite of bromhexine) directly stimulates serous mucus gland secretion and surfactant production in type II pneumocytes. Potassium iodide is an older expectorant (gastric reflex + direct stimulation) with a narrower therapeutic window and more adverse effects.

Correct. In a child with productive cough due to bacterial pneumonia, the cough reflex is clearing infected secretions from the lower airways. Suppressing this reflex — with any antitussive, including the 'safer' dextromethorphan — risks retaining infected secretions that could progress to empyema, lung abscess, or respiratory failure. The WHO has discouraged cough and cold medications in children under 6. Treatment: appropriate antibiotics, adequate hydration, postural drainage if tolerated, and parental education.

Antitussives (including dextromethorphan) are contraindicated in productive cough at any age. In children with bacterial pneumonia, cough clearance is life-critical. Treat the infection (antibiotics). WHO guidance: no cough suppressants in productive cough in children.

Dextromethorphan is not indicated in productive cough regardless of its better safety profile compared to codeine. Guaifenesin (expectorant) is a reasonable adjunct but not the primary management — and its evidence in children with pneumonia is limited. Intranasal steroids address post-nasal drip, not lower respiratory tract infection.