Respo – Pharma

This patient’s history is classic for Aspirin-Exacerbated Respiratory Disease (AERD), also known as Samter’s triad, which includes:

1. Asthma

2. Nasal polyps / chronic rhinosinusitis

3. Sensitivity to aspirin and other NSAIDs

Pathophysiology:

• Aspirin and other nonselective NSAIDs inhibit cyclooxygenase-1 (COX-1).

• This shunts arachidonic acid metabolism toward the 5-lipoxygenase pathway, increasing production of leukotrienes (LTC4, LTD4, LTE4).

• Leukotrienes are potent bronchoconstrictors, leading to asthma attacks, nasal congestion, and urticaria.

Thus, the most likely cause of his asthma attacks is aspirin-induced leukotriene-mediated bronchospasm.

❌ Explanation of Incorrect Options:

Nasal polyps and rhinitis predispose her to necrotizing bronchial infections
❌ Wrong — While nasal polyps may contribute to chronic sinus infections, they do not directly cause asthma attacks in this scenario.

Polyps in her nose also cause her to have polyps in her lungs
❌ Wrong — Nasal polyps do not form in the lungs; lung pathology in AERD is due to airway inflammation and leukotriene-mediated bronchoconstriction, not actual polyps.

Aspirin damages her distal airways causing them to dilate
❌ Wrong — Aspirin does not dilate airways; it triggers bronchospasm in sensitive individuals.

She most likely has a positive family history for asthma
❌ Wrong — While family history may increase risk, it does not explain the acute trigger; her attacks are clearly aspirin-induced.

✅ Correct answer: Respiratory acidosis

⸻

Step-by-step reasoning:

•Morphine is an opioid analgesic that depresses the respiratory center in the medulla.

•This leads to hypoventilation (slow breathing) — in this case, respiratory rate = 8/min, which is very low.

•When a person hypoventilates, CO₂ accumulates in the blood because it’s not being exhaled efficiently.

•↑ pCO₂ → ↓ pH → Respiratory acidosis.

⸻

Summary of mechanism:

•↓ Respiratory rate → ↓ CO₂ elimination → ↑ pCO₂ → ↓ pH → Respiratory acidosis

⸻

Why the others are incorrect:

•Respiratory alkalosis: Would occur with hyperventilation (e.g., anxiety, panic attacks), not hypoventilation.

•Metabolic acidosis: Caused by renal failure, diabetic ketoacidosis, or lactic acid buildup, not morphine.

•Hyperkalemia / Hypokalemia: Possible secondary effects in acid-base imbalance, but not the primary disorder here.

✅ Correct answer: Isoniazid

Explanation:

Isoniazid (INH) interferes with the metabolism of vitamin B6 (pyridoxine) by:

• Increasing its urinary excretion, and
• Forming inactive complexes with pyridoxal phosphate.

This leads to pyridoxine deficiency, which manifests as peripheral neuropathy, seizures, or sideroblastic anemia.

💊 Therefore, pyridoxine is given as an antidote or prophylaxis with INH to prevent neurotoxicity.

Why others are incorrect:

• Streptomycin → ❌ Causes ototoxicity and nephrotoxicity, not prevented by pyridoxine.
• Pyrazinamide → ❌ Can cause hyperuricemia and hepatotoxicity, no role for pyridoxine.
• Ethambutol → ❌ Causes optic neuritis (red-green color blindness), not pyridoxine-related.
• Rifampin → ❌ Causes orange-red discoloration of body fluids and hepatitis, unrelated to pyridoxine.

✅ Correct answer: Peripheral neuropathy

Explanation:

Isoniazid (INH) is a first-line antitubercular drug.

A prominent and characteristic side effect of INH therapy is peripheral neuropathy, caused by pyridoxine (vitamin B6) deficiency.

Isoniazid increases urinary excretion and decreases the activation of pyridoxine, which is essential for neurotransmitter synthesis.

→ This results in tingling, numbness, and burning sensations in hands and feet.

Prevention: Give vitamin B6 (10–50 mg/day) along with INH.

Why others are incorrect:

• Vision problems → ❌ Caused by Ethambutol (optic neuritis).
• Black stools → ❌ Seen with GI bleeding or iron therapy, not INH.
• Diarrhea → ❌ Non-specific; not a classic INH effect.
• Gout → ❌ Seen with Pyrazinamide or Ethambutol (↑ uric acid).

Asthma is characterized by bronchial hyperreactivity, airway inflammation, and smooth muscle constriction. One therapeutic approach is the use of antimuscarinic bronchodilators (e.g., ipratropium, tiotropium).

These drugs block muscarinic (M₃) receptors on bronchial smooth muscle and submucosal glands, preventing acetylcholine-induced bronchoconstriction and mucus secretion. The result is airway relaxation and improved airflow, alleviating asthma symptoms.

❌ Why the Other Options Are Incorrect

• Beta-2 adrenergic: Agonists at beta-2 receptors cause bronchodilation, not inhibition; they are not blocked by bronchodilator drugs.

• Beta-3 adrenergic: Found mainly in adipose tissue; irrelevant to airway tone.

• Beta-1 adrenergic: Located in the heart; blocking them would slow heart rate, not affect bronchial smooth muscle.

• Nicotinic: Present in autonomic ganglia and neuromuscular junctions; blocking them would affect muscle contraction but not directly relax bronchial smooth muscle.

Inhaled short-acting beta-agonists (SABA)

Explanation:

Inhaled short-acting beta-agonists (e.g., Salbutamol/Albuterol) are the first-line therapy for acute asthma attacks because they:

• Act within minutes to relax bronchial smooth muscles
• Provide rapid relief from bronchoconstriction and wheezing
• Are administered via inhalers or nebulizers for direct airway action

They target the β₂-adrenergic receptors, leading to bronchodilation.

❌

Incorrect Options Explained:

• Inhaled long-acting beta-agonists (LABA):
  ❌ Used for maintenance therapy, not for acute attacks, as they act slowly (e.g., Salmeterol, Formoterol).
• Leukotriene receptor antagonists:
  ❌ Drugs like Montelukast are for chronic control, not immediate relief.
• Inhaled corticosteroids:
  ❌ Reduce airway inflammation but take hours to days — used for long-term control, not emergencies.
• Oral antihistamines:
  ❌ Used for allergic rhinitis, not asthma; they do not relieve bronchospasm.

Bronchodilators work by relaxing bronchial smooth muscle, improving airflow.

• Levalbuterol → β₂-adrenergic agonist, causes bronchodilation

• Epinephrine → non-selective adrenergic agonist, bronchodilates via β₂ receptors

• Anti-adrenergic drugs → block α/β receptors in some contexts, leading to relaxation

• Anti-histamines → prevent histamine-induced bronchoconstriction

Acetylcholine, however, is a parasympathetic neurotransmitter:

• Acts on muscarinic receptors in bronchi → bronchoconstriction

• Not a bronchodilator; it’s actually the opposite.

Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their action by inhibiting cyclooxygenase (COX) enzymes, which catalyze the conversion of arachidonic acid → prostaglandins and thromboxanes.
By blocking this pathway, NSAIDs reduce:

• Inflammation

• Pain

• Fever

• Platelet aggregation (for some NSAIDs like aspirin)

Other options:

• Helps in formation of prostaglandins → opposite effect

• Helps metabolizing arachidonic acid → not the mechanism

• Formation of steroids → unrelated; corticosteroids act differently

• Inhibits lipoxygenase pathway → leukotriene pathway, target of specific drugs (e.g., zileuton)

Rifampin acts by blocking bacterial DNA-dependent RNA polymerase, preventing transcription and thereby halting RNA and protein synthesis.
It’s bactericidal and especially important in tuberculosis, leprosy, and prophylaxis for meningococcal exposure.

Other options:

• RNA-dependent DNA polymerase → inhibited by reverse transcriptase inhibitors (antivirals, not anti-TB).

• Arabinogalactan synthesis → target of Ethambutol.

• Mycolic acid synthesis → inhibited by Isoniazid.

• Glycosylation → not a target of anti-TB drugs.

❌ Inappropriately Matched

Pyrazinamide – Hypoglycemia → ❌ incorrect

It should be Pyrazinamide – Hyperuricemia, not hypoglycemia.

In asthma management, drugs are classified as:

1. Relievers (short-term control) → relieve acute bronchoconstriction

   • e.g. Salbutamol (short-acting β₂ agonist)

2. Controllers (long-term control) → reduce airway inflammation and hyperresponsiveness

   • e.g. Inhaled corticosteroids (ICS) such as Beclomethasone, Budesonide, Fluticasone

Beclomethasone is a glucocorticoid that works by:

• Decreasing airway inflammation

• Reducing eosinophil and mast cell infiltration

• Enhancing β₂-receptor sensitivity

• Decreasing mucus secretion

It is not for acute attacks, but for long-term prophylactic therapy to prevent exacerbations.

⚖️ Why the Other Options Are Incorrect:

✅ Correct Answer: Zileuton

Explanation:

Zileuton is an orally active inhibitor of the 5-lipoxygenase enzyme, which is responsible for converting arachidonic acid into leukotrienes (LTB₄, LTC₄, LTD₄, and LTE₄).

By inhibiting this pathway, Zileuton:

• Reduces leukotriene-mediated bronchoconstriction,
• Decreases airway inflammation, and
• Prevents edema and mucus secretion.

It is especially useful in chronic asthma management, particularly when inhaled medications are difficult to administer (e.g., in children).

❌ Aminophylline – A methylxanthine derivative that works by inhibiting phosphodiesterase, increasing cAMP, and causing bronchodilation. It does not inhibit leukotriene synthesis.

❌ Ipratropium – A muscarinic receptor antagonist (anticholinergic) that causes bronchodilation by blocking vagal tone, mainly used in COPD or acute asthma exacerbations, not as a leukotriene inhibitor.

❌ Montelukast – A leukotriene receptor antagonist (LTRA), not a 5-lipoxygenase inhibitor. It blocks leukotriene receptors (CysLT₁) rather than stopping their synthesis.

❌ Albuterol – A short-acting β₂-agonist (SABA) used for rapid relief of bronchospasm; it acts via bronchodilation, not on the leukotriene pathway.

Asthma is a chronic inflammatory disorder of the airways characterized by bronchial hyperreactivity, airway inflammation, and reversible airflow obstruction.
While bronchodilators (like β₂-agonists) provide rapid symptomatic relief, they do not address the underlying inflammation.
Hence, inhaled corticosteroids (ICS) such as beclomethasone are the cornerstone of long-term asthma management because they:

• Inhibit inflammatory cell activation (e.g., eosinophils, mast cells)

• Decrease cytokine production

• Reduce airway edema and mucus secretion

ICS must be taken regularly, even when the patient is asymptomatic, to maintain airway stability and prevent exacerbations.

✅ Correct Option: Beclomethasone

Beclomethasone is an inhaled corticosteroid that prevents airway inflammation by suppressing immune and inflammatory mediators.

• Used regularly for maintenance therapy

• Not for acute asthma attacks

• Reduces airway hyperresponsiveness over time

❌ Incorrect Options:

Salbutamol:
A short-acting β₂-agonist (SABA) used for immediate relief of bronchospasm, not for inflammation control.

Tiotropium:
A long-acting muscarinic antagonist (LAMA) mainly used in COPD; sometimes added in severe asthma, but it’s not anti-inflammatory.

Salmeterol:
A long-acting β₂-agonist (LABA) that provides bronchodilation, but must always be combined with corticosteroids; using it alone increases mortality risk.

Albuterol:
Same as salbutamol (different regional names). It’s a rescue medication, not for regular anti-inflammatory therapy.

Non-steroidal anti-inflammatory drugs (NSAIDs)—such as aspirin, ibuprofen, and naproxen—work primarily by inhibiting the cyclooxygenase (COX) enzymes, which are critical in the prostaglandin synthesis pathway.

Pathway overview:

• Arachidonic acid, released from membrane phospholipids by phospholipase A₂, can be metabolized by two main enzymatic routes:

  1. Cyclooxygenase (COX) pathway → produces prostaglandins, prostacyclin (PGI₂), and thromboxane A₂ (TXA₂).

  2. Lipoxygenase (LOX) pathway → produces leukotrienes.

There are two major isoforms of COX:

• COX-1: Constitutive enzyme; maintains physiological functions (gastric protection, platelet aggregation).

• COX-2: Inducible enzyme; expressed during inflammation and pain.

NSAIDs block both (non-selectively in most cases), thereby reducing prostaglandin synthesis → decreasing inflammation, pain, and fever.

❌ Why Other Options Are Incorrect:

• Lipooxygenase pathway: Not inhibited by NSAIDs; it produces leukotrienes, which are involved in asthma and allergic inflammation (targeted by anti-leukotriene drugs like montelukast).

• Thromboxane A₂: Its production depends on COX, but NSAIDs inhibit it indirectly by blocking the COX pathway, not specifically targeting thromboxane alone.

• Prostaglandins: Again, NSAIDs reduce prostaglandin synthesis but by inhibiting COX, not prostaglandins directly.

• Leukotrienes: Synthesized via lipoxygenase, so unaffected by NSAIDs.

✅ Correct Answer:

Nadolol

Nadolol is a non-selective β-blocker, meaning it blocks both β₁ receptors (in the heart) and β₂ receptors (in the bronchi, blood vessels, and other tissues).
Because of this, it reduces heart rate and contractility but can also cause bronchoconstriction, so it is contraindicated in asthma and COPD.

❌ Incorrect Options:

• Salbutamol — ❌ A β₂ agonist, not an antagonist; it dilates bronchi, used in asthma.

• Metoprolol — ❌ A β₁-selective blocker (cardioselective), safer in airway disease.

• Bisoprolol — ❌ Also β₁-selective, mainly acts on the heart.

• Atenolol — ❌ Another β₁-selective blocker with little to no effect on β₂ receptors.

✅ Correct Answer:

Nadolol

Nadolol is a non-selective β-adrenergic antagonist (β-blocker), meaning it blocks both β₁ (cardiac) and β₂ (bronchial, vascular, and metabolic) receptors.
Because of this non-selectivity, it can reduce heart rate and contractility (β₁ effect) but may also cause bronchoconstriction (β₂ effect), making it contraindicated in asthma and COPD.

It is used for:

• Hypertension

• Angina pectoris

• Long-term control of arrhythmias

❌ Incorrect Options:

• Bisoprolol — ❌ A β₁-selective blocker (cardioselective), primarily affecting the heart.

• Metoprolol — ❌ Also β₁-selective, safer in patients with mild airway disease.

• Salbutamol — ❌ A β₂-agonist, not an antagonist; it relaxes bronchial smooth muscle (used in asthma).

• Atenolol — ❌ Another β₁-selective blocker with minimal β₂ effect.

Beta agonists are the main class of bronchodilators used in conditions such as asthma and chronic obstructive pulmonary disease (COPD).
They act by stimulating β₂-adrenergic receptors in the bronchial smooth muscle, leading to increased cAMP and smooth muscle relaxation, which results in bronchodilation.

Types of β₂-agonists:

• Short-acting (SABA): Salbutamol (albuterol), Terbutaline — used for acute relief of bronchospasm.

• Long-acting (LABA): Salmeterol, Formoterol — used for maintenance therapy alongside corticosteroids.

They also decrease airway resistance and improve mucociliary clearance, making breathing easier.

❌ Why the Other Options Are Incorrect:

• Adrenergic agonists:
  This term is too broad — it includes both alpha and beta agonists. Alpha agonists mainly cause vasoconstriction, not bronchodilation. Only β₂-adrenergic agonists specifically dilate bronchi.

• Anti-leukotriene:
  These drugs (e.g., montelukast) reduce inflammation and prevent bronchoconstriction, but they do not directly relax smooth muscle to cause bronchodilation.

• Corticosteroids:
  These are anti-inflammatory, not direct bronchodilators. They reduce airway inflammation and edema but work over hours or days, not immediately.

• Anti-histamine:
  Used in allergic reactions, they block H₁ receptors to reduce mucus secretion and swelling but do not dilate bronchi significantly.

🩺 Clinical Connection:
In acute asthma attacks, short-acting β₂-agonists (like salbutamol) are the first-line treatment for rapid bronchodilation.
In contrast, long-acting β₂-agonists are used for maintenance, but always in combination with inhaled corticosteroids to prevent tolerance and control inflammation.

Atropine is a competitive antagonist of muscarinic acetylcholine receptors (M₁, M₂, and M₃).
When it blocks M₃ receptors in the bronchial smooth muscle, it prevents acetylcholine-induced bronchoconstriction and reduces mucus secretion—thereby promoting bronchodilation.

Mechanism summary:

• Normal M₃ activation: Acetylcholine binds → smooth muscle contraction → bronchoconstriction and increased secretions.

• With atropine: M₃ receptor blocked → smooth muscle relaxation → bronchodilation and dry airways.

❌ Why the Other Options Are Incorrect:

• Acetylcholine:
  It stimulates M₃ receptors, causing bronchoconstriction and increased glandular secretion — opposite of inhibition.

• Bethanechol:
  A muscarinic agonist, not an antagonist. It activates M₃ receptors, mainly used for urinary retention and intestinal atony, not for respiratory dilation.

• Salbutamol:
  A β₂-adrenergic agonist, which causes bronchodilation via sympathetic stimulation — not by blocking M₃ receptors.

• Propranolol:
  A non-selective β-blocker, which can actually worsen bronchoconstriction by blocking β₂ receptors — contraindicated in asthma and COPD.

🩺 Clinical Connection:
In COPD, muscarinic antagonists (like ipratropium and tiotropium, derived from atropine) help keep airways open by blocking M₃-mediated bronchospasm, improving airflow and reducing symptoms.

Epinephrine (adrenaline) is the drug of choice in anaphylactic shock, a severe systemic allergic reaction characterized by:

• Bronchoconstriction → airway obstruction

• Vasodilation → hypotension and shock

• Increased vascular permeability → edema

Epinephrine acts rapidly by stimulating α and β adrenergic receptors:

• α₁ receptors: cause vasoconstriction, raising blood pressure and reducing mucosal edema.

• β₁ receptors: increase heart rate and contractility, improving cardiac output.

• β₂ receptors: induce bronchodilation, relieving airway obstruction.

This combined action makes epinephrine life-saving in anaphylaxis.

❌ Why the Other Options Are Incorrect:

• Corticosteroids:
  Reduce inflammation but act slowly (hours later). Used as adjuncts, not for immediate life-saving effects.

• Norepinephrine / Noradrenaline:
  Strong α₁ and β₁ agonist, but weak β₂ activity → causes vasoconstriction and increases cardiac output but does not relieve bronchospasm.

• Aspirin:
  An antiplatelet and NSAID — contraindicated, as it may worsen allergic reactions in some patients (aspirin-induced asthma).

Montelukast is a leukotriene receptor antagonist (LTRA) used primarily in the management of asthma and allergic rhinitis.

🔹 Mechanism of Action:

• Leukotrienes (especially LTC₄, LTD₄, and LTE₄) are potent inflammatory mediators derived from arachidonic acid through the 5-lipoxygenase pathway.

• These leukotrienes bind toreceptors in the airway, causing bronchoconstriction, increased mucus secretion, and airway edema.

• Montelukast blocks these receptors (CysLT₁), preventing the effects of leukotrienes and resulting in bronchodilation and reduced inflammation.

🔹 Clinical Use:

• Prophylaxis and chronic treatment of asthma, especially in exercise- or allergen-induced cases.

• Allergic rhinitis (reduces nasal congestion and sneezing).

• Not useful for acute asthma attacks, since it doesn’t act immediately on bronchial smooth muscle.

❌ Why the Other Options Are Incorrect:

• Paracetamol:
  An analgesic and antipyretic that inhibits central prostaglandin synthesis; it has no action on leukotrienes or their receptors.

• Propranolol:
  A non-selective β-blocker, used in hypertension and arrhythmias; unrelated to leukotriene pathways.

• Zileuton:
  A 5-lipoxygenase inhibitor, meaning it inhibits leukotriene synthesis, not receptor binding. So while related to the same pathway, it acts earlier than Montelukast.

• Aspirin:
  A cyclooxygenase (COX) inhibitor, which decreases prostaglandin synthesis, not leukotrienes. In fact, aspirin can worsen asthma in some patients by diverting arachidonic acid metabolism toward leukotriene production.

Phenylephrine is a selective α₁-adrenergic receptor agonist that causes contraction of the radial (dilator) muscle of the iris, leading to mydriasis (pupil dilation).

🔹 Mechanism of Action:

• Activation of α₁ receptors → contraction of radial fibers in the iris.

• This widens the pupil without affecting the ciliary muscle, so accommodation remains intact (unlike anticholinergics such as tropicamide).

🔹 Clinical Uses:

• Used in eye examinations to dilate the pupil.

• Helps in reducing redness (as a vasoconstrictor).

❌ Why the Other Options Are Incorrect:

• None of these:
  Incorrect, since Phenylephrine is a well-known α₁ agonist that clearly causes mydriasis.

• Methyldopa:
  A centrally acting α₂ agonist used in hypertension, especially during pregnancy; it does not cause mydriasis.

• Guanfacine:
  Another central α₂ agonist, mainly used for ADHD and hypertension, causing sedation and bradycardia, not pupil dilation.

• Clonidine:
  Also an α₂ agonist, reduces sympathetic outflow from the CNS and thus tends to cause miosis (pupil constriction) rather than dilation.

Timolol is a non-selective β-adrenergic blocker commonly used in ophthalmology, particularly in conditions like glaucoma and during retinal surgeries to manage intraocular pressure (IOP).

🔹 Mechanism of Action:

• It blocks β1 and β2 receptors in the ciliary epithelium of the eye.

• This reduces aqueous humor production, thereby lowering IOP.

• Maintaining optimal IOP is crucial during retinal procedures to prevent retinal detachment and optic nerve damage.

Unlike mydriatic drugs (which dilate the pupil), Timolol does not affect the pupil size or accommodation — making it ideal for use during delicate retinal or glaucoma-related surgeries.

❌ Why the Other Options Are Incorrect:

• None of these:
  Incorrect, because Timolol is indeed the correct and well-established drug used to manage IOP in retinal surgeries.

• Tropicamide:
  A muscarinic antagonist used to dilate the pupil for eye examinations, not to control IOP or during retinal surgery.

• Propranolol:
  A systemic β-blocker used for hypertension, anxiety, and arrhythmias; not used topically in ophthalmology due to systemic effects.

• Albuterol:
  A β2-adrenergic agonist, which would increase aqueous humor production and potentially raise IOP — the opposite of the desired effect.

✅ Correct Answer: Bronchospasms

Explanation:

Non-selective beta-blockers (like propranolol) block both β₁-receptors (in the heart) and β₂-receptors (in the bronchi and blood vessels).

In asthmatic patients, blocking β₂-receptors prevents bronchodilation, which leads to bronchoconstriction (bronchospasm) — a dangerous narrowing of the airways that can worsen or trigger an asthma attack.

Why the other options are wrong:

• Postural hypotension ❌ – More common with alpha-blockers, not beta-blockers.
• Hypotension ❌ – Can occur, but it’s not the main contraindication in asthma; the respiratory effect is the critical issue.
• Bradycardia ❌ – Caused by β₁ blockade in the heart, but this effect is not unique to asthmatics and is often therapeutically desired.
• Tachycardia ❌ – Beta-blockers actually reduce heart rate, not increase it.

✅ Correct Answer:

Propranolol

Propranolol is a non-selective β-blocker, meaning it blocks both β₁ (cardiac) and β₂ (bronchial) adrenergic receptors.
Blocking β₂ receptors in the bronchi leads to bronchoconstriction, which can worsen asthma and COPD by reducing airflow and triggering bronchospasm.

Therefore, propranolol is contraindicated in patients with bronchial asthma or chronic obstructive pulmonary disease, as it can precipitate severe respiratory distress.

❌ Incorrect Options:

• Salbutamol — ❌ A β₂-agonist, not a blocker. It relieves bronchospasm in asthma rather than worsening it.

• Metoprolol — ❌ A β₁-selective blocker, primarily affects the heart with minimal bronchial effects, thus safer in mild asthma or COPD.

• Atenolol — ❌ Also β₁-selective, making it cardioselective and generally safer for patients with reactive airway disease.

• Esmolol — ❌ A short-acting β₁-selective blocker used intravenously in acute cardiac conditions, not known to cause bronchospasm.

✅ Correct Answer:

Rifampin

Rifampin, one of the first-line anti-tubercular drugs, can occasionally cause transient memory loss or confusion due to its effects on the central nervous system. These neuropsychiatric symptoms are uncommon but recognized, especially in patients on long-term therapy. The symptoms usually resolve once the drug is discontinued or the body adjusts.

❌ Incorrect Options:

• Streptomycin — ❌ Causes ototoxicity (hearing loss and balance issues) and nephrotoxicity, not cognitive impairment.

• Pyrazinamide — ❌ Known for hepatotoxicity, hyperuricemia, and joint pain, not neurological side effects.

• Ethambutol — ❌ Causes optic neuritis leading to vision and color perception issues, not memory problems.

• Isoniazid — ❌ Leads to peripheral neuropathy and vitamin B6 deficiency, but not transient memory loss.

Mifepristone is a progesterone receptor antagonist that blocks the action of progesterone on the uterus.

• Progesterone normally maintains uterine quiescence (prevents contractions) and keeps the cervix firm.

• By inhibiting progesterone, mifepristone leads to cervical ripening (softening and dilation) and increases uterine sensitivity to prostaglandins and oxytocin, facilitating labor induction or medical termination of pregnancy.

❌ Natural progesterone

• Maintains pregnancy by relaxing uterine muscles and keeping the cervix firm — opposite of inducing labor.

❌ Levonorgestrel

• A synthetic progestin used in contraception (morning-after pill), not for labor induction.

❌ Raloxifene

• A selective estrogen receptor modulator (SERM) used for osteoporosis and breast cancer prevention, not pregnancy-related actions.

❌ Tamoxifen

• Another SERM, primarily used in estrogen receptor-positive breast cancer, with no role in labor induction.

In the respiratory system, β₂-adrenergic receptors are found predominantly in bronchial smooth muscles. When these receptors are stimulated (for example, by β₂ agonists like salbutamol), they cause bronchodilation — widening of the airways and easing airflow.

In contrast, inhibiting or blocking β₂ receptors leads to bronchoconstriction. This principle becomes important in the treatment of glaucoma, where β₂ receptor inhibition reduces aqueous humor production in the ciliary body of the eye, thereby lowering intraocular pressure.

However, this same inhibition can have undesirable effects on the lungs — namely, airway narrowing. That’s why non-selective beta-blockers (which block both β₁ and β₂ receptors) can worsen asthma or COPD by triggering bronchospasm.

Thus, while β₂ inhibition is useful in glaucoma, it can be harmful in respiratory conditions, making this a key example of how pharmacologic receptor targets in one organ system can have significant effects in another.

❌ Why the Other Options Are Incorrect:

• Alpha-2:
  These receptors primarily reduce sympathetic outflow when activated. Their inhibition doesn’t significantly affect aqueous humor or airway tone.

• Alpha-1:
  Found in vascular smooth muscle; their blockade causes vasodilation, not a change in intraocular pressure or bronchodilation.

• Beta-1:
  Located mainly in the heart. Inhibition reduces heart rate and contractility but has minimal respiratory or ocular effect.

• Beta-3:
  Found mostly in adipose tissue; associated with lipolysis and thermogenesis, not relevant to eye or airway physiology.

Aminophylline is a phosphodiesterase (PDE) inhibitor and a derivative of theophylline, both of which belong to the methylxanthine class of bronchodilators.

It is sometimes used as an adjunct therapy in chronic obstructive pulmonary disease (COPD) and asthma, especially when other drugs fail to provide adequate control.

🔹 Mechanism of Action:

• Inhibition of phosphodiesterase (PDE)
• Adenosine receptor antagonism
• Anti-inflammatory effects
• Improves diaphragmatic contractility

⚠️ Clinical Considerations:

• Toxicity signs: nausea, vomiting, seizures, and arrhythmias.

• Drug interactions: metabolism affected by smoking, macrolides, and certain anticonvulsants.

❌ Why the Other Options Are Incorrect:

• Long-acting corticosteroid

  • Example: Fluticasone or Budesonide.

  • These are anti-inflammatory, not bronchodilators.

  • They work by suppressing airway inflammation, not by inhibiting PDE.

• Tiotropium

  • A long-acting muscarinic antagonist.

  • Blocks M3 receptors to cause bronchodilation.

  • No effect on phosphodiesterase.

• Albuterol (Salbutamol)

  • A short-acting β₂-adrenergic agonist.

  • Stimulates β₂ receptors → increases cAMP → bronchodilation.

  • However, this occurs through receptor activation, not PDE inhibition.

• Zileuton

  • A 5-lipoxygenase inhibitor used in asthma, not COPD.

  • Decreases leukotriene synthesis → reduces inflammation and bronchoconstriction.

  • No action on phosphodiesterase.

Tiotropium is a long-acting muscarinic antagonist used as a maintenance therapy for chronic obstructive pulmonary disease (COPD) and sometimes for severe asthma.

It works by blocking M3 muscarinic receptors in the airway smooth muscle, preventing acetylcholine-mediated bronchoconstriction.

Unlike short-acting antimuscarinics such as ipratropium, tiotropium dissociates very slowly from M3 receptors, resulting in 24-hour bronchodilation with once-daily dosing.

This makes it ideal for long-term management of COPD, a condition characterized by persistent airflow limitation and chronic bronchoconstriction.

🔬 Mechanism of Action:

1. Antagonizes M3 receptors → inhibits bronchial smooth muscle contraction.
2. Reduces mucus secretion and airway hyperreactivity.
3. Improves airflow and reduces COPD exacerbations.

❌ Why the Other Options Are Incorrect:

• Ipratropium

  • Also an antimuscarinic bronchodilator, but short-acting.

  • Used mainly for acute symptom relief or in combination with β₂-agonists.

  • Duration: 4–6 hours, not suitable for long-term control like tiotropium.

• Terbinafine

  • An antifungal agent (inhibits squalene epoxidase).

  • Used for dermatophytosis (tinea infections), not respiratory diseases.

  • No bronchodilator activity.

• Salbutamol (Albuterol)

  • A short-acting β₂-adrenergic agonist.

  • Provides rapid bronchodilation — useful for acute asthma attacks, not long-term COPD maintenance.

  • Duration: 4–6 hours only.

• Prednisone

  • A systemic corticosteroid used for anti-inflammatory effects in acute exacerbations of asthma or COPD.

  • Not a bronchodilator and not used chronically due to systemic side effects (immunosuppression, hyperglycemia, osteoporosis).

What Tropicamide does and why it’s used in eye exams
Tropicamide is an antimuscarinic (parasympatholytic) agent used topically in the eye. It blocks muscarinic receptors on the iris sphincter and the ciliary muscle. The functional consequences are:

• Temporary loss of sphincter activity → the circular smooth muscle that would normally constrict is inhibited, so the aperture of the eye becomes larger and allows better visualization of internal structures.

• Temporary paralysis of accommodation → the ciliary muscle relaxes, which helps in some parts of the exam (e.g., refraction in children, fundus view).

Clinical properties that make it ideal for routine exams

• Rapid onset: Works within minutes.

• Short duration: Effects typically wear off within a few hours (commonly around 4–6 hours), so normal vision returns the same day.

• Well tolerated for diagnostic use: Side effects are usually transient (photophobia, blurred near vision) but generally acceptable for brief diagnostic procedures.

Practical use

• Widely used by ophthalmologists and optometrists for funduscopy, retinal exam, slit-lamp exam when dilation is needed, and sometimes for refraction when temporary cycloplegia helps.

• Because the effect is short, patients don’t have to miss much time or endure prolonged visual disability.

❌ Why the Other Options Are Incorrect:

Ipratropium

• Class & use: An inhaled antimuscarinic bronchodilator used for obstructive airway disease (COPD/asthma).
• Why not: It is formulated and delivered for the respiratory tract, not the eye. It is not used as a diagnostic in routine ophthalmic exams.

Propranolol

• Class & use: A non-selective beta-blocker used for hypertension, arrhythmias, migraine prophylaxis, etc.
• Why not: It does not induce the temporary change needed for ocular visualization. (Topical beta-blockers like timolol are used to reduce intraocular pressure in glaucoma — that’s a therapeutic use, not for dilation during an exam.)

Atropine

• Class & use: A potent antimuscarinic that does produce dilation and cycloplegia.
• Why not for routine exam: Duration is the problem. Atropine’s ocular effects are very long-lasting (days to a week or more), causing prolonged blurred vision and light sensitivity. Because of this prolonged impairment, atropine is reserved for specific therapeutic purposes (e.g., treating uveitis, inducing prolonged cycloplegia in amblyopia therapy), not for routine diagnostic dilation.

Opioids

• Class & use: μ-opioid receptor agonists used for analgesia.
• Why not: Opioids typically cause pupil constriction (miosis), the opposite of what’s needed to allow an examiner a wider view of internal eye structures. They are not used to facilitate eye exams.

Anaphylactic shock is a life-threatening condition caused by massive histamine release leading to hypotension, bronchospasm, and airway edema.

• Epinephrine is the drug of choice because it works on α1, β1, and β2 receptors.

  • α1 agonism: Vasoconstriction → raises BP, reduces mucosal swelling.

  • β1 agonism: Increases heart rate and contractility → improves cardiac output.

  • β2 agonism: Causes bronchodilation and inhibits further mediator release from mast cells.
    This multi-receptor action is exactly what makes epinephrine lifesaving in anaphylaxis.

❌ Why the other options are incorrect:

• Norepinephrine: Strong α1 and β1, but weak β2 → helps BP but not bronchospasm.

• Phenylephrine: Pure α1 agonist → only vasoconstriction, no airway effect.

• Phentolamine: α-blocker → worsens hypotension, contraindicated.

• Dobutamine: β1 agonist → supports heart but no effect on airway or mast cell stabilization

✅ Correct Answer: 

Zileuton

• Zileuton directly inhibits the 5-lipoxygenase enzyme, which converts arachidonic acid into leukotrienes.
• By blocking this step, it prevents the synthesis of LTB₄, LTC₄, LTD₄, and LTE₄.
• This decreases bronchoconstriction, inflammation, and mucus secretion.

❌ Why the Other Options Are Wrong

• All of these → Incorrect, because only Zileuton acts on the 5-lipoxygenase enzyme; the others act elsewhere.
• Montelukast → Blocks cysteinyl leukotriene receptors (LTD₄ receptor antagonist), not the enzyme itself.
• Salbutamol → Short-acting β₂ agonist (SABA), causes bronchodilation via cAMP, no effect on leukotrienes.
• Albuterol → Same as salbutamol (different naming, US vs UK), β₂ agonist, no leukotriene effect.

Correct Answer:
✅ Inhibits DNA dependent RNA polymerase

• Explanation: Rifampin (rifampicin) works by inhibiting bacterial DNA-dependent RNA polymerase, thereby blocking transcription and halting bacterial RNA synthesis. This bactericidal action makes it a key first-line drug in the treatment of tuberculosis, as well as prophylaxis for Neisseria meningitidis and Haemophilus influenzae type b exposure.

Incorrect Options:

❌ Inhibits synthesis of arabinogalactan

• This is the mechanism of Ethambutol, which inhibits arabinosyl transferase and disrupts mycobacterial cell wall synthesis.

❌ Inhibits RNA dependent DNA polymerase

• This is the mechanism of reverse transcriptase inhibitors (antiretrovirals for HIV), not rifampin.

❌ Inhibits mycolic acid synthesis

• This is the mechanism of Isoniazid, which blocks mycolic acid synthesis in mycobacteria.

❌ None of these

• Incorrect, because rifampin’s exact mechanism is clearly described by the first option.

Correct Answer:
✅ Pyrazinamide

• Explanation: Pyrazinamide is one of the first-line anti-tubercular drugs and its most important side effects include hyperuricemia (by decreasing uric acid excretion) and hepatotoxicity. This can precipitate gout attacks in susceptible patients.

Incorrect Options:

❌ Streptomycin

• Causes ototoxicity and nephrotoxicity (as it is an aminoglycoside), not hyperuricemia.

❌ Ethambutol

• Known for causing optic neuritis with red-green color blindness, not uric acid elevation.

❌ Isoniazid

• Can cause peripheral neuropathy, hepatotoxicity, and lupus-like syndrome, but not hyperuricemia.

❌ Rifampin

• Causes hepatotoxicity and red-orange discoloration of body fluids, not hyperuricemia.

Correct Answer:
✅ Isoniazid

• Explanation: Isoniazid (INH) can cause peripheral neuropathy as a side effect because it increases the excretion of vitamin B6 (pyridoxine) and interferes with its metabolism. Supplementing patients on isoniazid therapy with pyridoxine (10–50 mg/day) prevents this neurotoxicity.

Incorrect Options:

❌ Pyrazinamide

• Main adverse effects: hyperuricemia (gout) and hepatotoxicity, not neuropathy.

❌ Streptomycin

• An aminoglycoside; main adverse effect is ototoxicity (hearing loss, vestibular damage).

❌ Ethambutol

• Causes optic neuritis (red-green color blindness), not prevented by pyridoxine.

❌ Rifampin

• Causes hepatotoxicity and red-orange discoloration of body fluids, no role for pyridoxine supplementation.

Correct Answer:
✅ Pyrazinamide → hypoglycemia

• Explanation: Pyrazinamide is an anti-TB drug that can cause hyperuricemia (leading to gout) and hepatotoxicity, but it is not associated with hypoglycemia. This makes this pair incorrectly matched.

Incorrect Options:

❌ Isoniazid → peripheral neurotoxicity

• Correct match. Isoniazid can cause peripheral neuropathy due to vitamin B6 (pyridoxine) deficiency. Supplementation with pyridoxine is recommended.

❌ Rifampin → harmless red urine color

• Correct match. Rifampin causes red-orange discoloration of urine, sweat, tears, which is benign but important to warn patients about.

❌ Ethambutol → optic neuritis

• Correct match. Ethambutol can cause optic neuritis, leading to red-green color blindness and decreased visual acuity.

❌ Streptomycin → ototoxicity

• Correct match. Streptomycin, an aminoglycoside, can cause ototoxicity (hearing loss, vestibular dysfunction).

✅ Correct Answer:

Isoniazid

• Isoniazid (INH), a first-line anti-tuberculosis drug, can cause neurotoxicity due to pyridoxine (Vitamin B6) deficiency.
• Neurological side effects include peripheral neuropathy, seizures, irritability, and memory disturbances (including transient memory loss).
• Supplementation with pyridoxine helps prevent these effects.

❌ Why the Other Options Are Wrong

• Streptomycin → An aminoglycoside; main side effects: ototoxicity (hearing loss, vertigo) and nephrotoxicity, not memory loss.
• Pyrazinamide → Causes hyperuricemia (gout attacks) and hepatotoxicity, not neurological side effects.
• Ethambutol → Side effect is optic neuritis (red-green color blindness), not memory loss.
• Rifampin → Causes orange-red discoloration of body fluids and hepatotoxicity; no effect on memory.

✅ Correct Answer:

Montelukast

• Montelukast is a cysteinyl leukotriene receptor antagonist (LTRA).
• It blocks the binding of LTC₄, LTD₄, and LTE₄ to their receptors on bronchial smooth muscle.
• This prevents bronchoconstriction, mucus secretion, and airway inflammation.
• Clinically important in asthma prophylaxis and aspirin-induced asthma.

❌ Why the Other Options Are Wrong

• Metaproterenol → β₂-adrenergic agonist → bronchodilator, not related to leukotrienes.
• Terbutaline → β₂ agonist → used in asthma and sometimes preterm labor, does not inhibit leukotrienes.
• Albuterol → Short-acting β₂ agonist (SABA), first-line in acute asthma, no leukotriene action.
• Zileuton → Inhibits 5-lipoxygenase enzyme, blocking leukotriene synthesis (not the receptor). So it reduces production but doesn’t directly inhibit cysteinyl leukotrienes at the receptor level.

✅ Correct Answer:

Tachycardia

• Non-specific beta-agonists (e.g., isoproterenol) stimulate both β1 (heart) and β2 (bronchi, vessels, uterus) receptors.
• β1 activation → increased heart rate and contractility → tachycardia is the most common and essential side effect.
• Tachycardia can also predispose to arrhythmias.

❌ Why the Other Options Are Wrong

• Myocardial infarction → Rare, may occur only in predisposed patients with coronary artery disease due to increased oxygen demand, but not the essential or typical adverse effect.
• Cardiac failure → Can be worsened in chronic cases but not the primary/essential effect.
• All of these → Incorrect because not all listed are essential; tachycardia is the key one.
• Bradycardia → Opposite effect; β1 stimulation increases, not decreases, heart rate.

✅ Correct Answer:

Diarrhea

• Atropine blocks muscarinic receptors, inhibiting parasympathetic (cholinergic) activity.
• In the GI tract, this causes decreased motility and constipation, not diarrhea.
• Therefore, diarrhea is not consistent with atropine’s effects.

❌ Why the Other Options Are Wrong

• Blurred vision → due to mydriasis (pupil dilation) and cycloplegia (loss of accommodation).
• Hallucinations → from atropine’s central anticholinergic effects at high doses.
• Restlessness → another CNS effect, especially in toxicity.
• Delirium → part of the severe anticholinergic syndrome (“mad as a hatter”).

✅ Correct Answer:

Inhaled corticosteroid

• Inhaled corticosteroids (e.g., budesonide, fluticasone) are the mainstay of long-term asthma management.
• They reduce airway inflammation, decrease hyperresponsiveness, and lower the frequency of exacerbations.
• Because they act locally in the lungs, systemic side effects are much less than with oral corticosteroids.

❌ Oral corticosteroid

• Oral corticosteroids (e.g., prednisone) are used only for severe acute exacerbations or poorly controlled asthma, not for regular maintenance because of significant systemic side effects.
• So, not the “main” drug of choice.

❌ None of these

• Incorrect, because inhaled corticosteroids are clearly effective and widely used for asthma.

❌ Pilocarpine

• Pilocarpine is a muscarinic agonist.
• It increases bronchoconstriction and secretions → worsens asthma instead of treating it.

❌ Sildenafil

• Sildenafil is a PDE-5 inhibitor used in erectile dysfunction and pulmonary hypertension, not in asthma.

✅ Correct Answer:

Increase heart contraction

• At low doses, epinephrine predominantly stimulates β₁-adrenergic receptors in the heart.
• This leads to:
  • ↑ Heart rate (positive chronotropy)
  • ↑ Force of contraction (positive inotropy)
• These β effects dominate at low concentrations before α₁-mediated effects (like vasoconstriction and pupil dilation) take over at higher doses.

❌ Increased gut motility

• Epinephrine actually decreases gut motility (sympathetic effect) through α and β receptor activation.
• The sympathetic nervous system slows digestion, not enhances it.

❌ Pupil constriction

• Pupil constriction (miosis) is a parasympathetic action via the oculomotor nerve (CN III).
• Epinephrine, being adrenergic, does the opposite.

❌ Salivary secretion

• Parasympathetic activity causes watery salivation.
• Epinephrine may produce thicker, viscous secretions, but it is not the main effect at low doses.

❌ Pupil dilation

• Epinephrine causes mydriasis (pupil dilation) through α₁ receptor stimulation.
• However, this is more evident at higher doses, not at low doses where β effects dominate.

✅ Correct Answer:

Pilocarpine

• Pilocarpine is a direct-acting cholinergic agonist (muscarinic receptor agonist).
• It mimics acetylcholine by binding directly to muscarinic receptors.
• Clinically, it is used in glaucoma (contracts ciliary muscle, increases aqueous humor outflow) and xerostomia (dry mouth) because it stimulates salivation.
• Key: Direct-acting agents bind to cholinergic receptors themselves, unlike indirect-acting drugs that inhibit acetylcholinesterase.

❌ Organophosphorous

• These are irreversible acetylcholinesterase inhibitors.
• They prevent breakdown of acetylcholine, causing excessive stimulation of cholinergic receptors.
• Thus, they are indirect-acting, not direct-acting.

❌ Physostigmine

• A reversible acetylcholinesterase inhibitor.
• Increases acetylcholine at synapses → indirect-acting.
• Used in atropine poisoning and glaucoma.

❌ None of these

• Wrong, because a valid direct-acting agonist (pilocarpine) is listed.

❌ Neostigmine

• Another reversible acetylcholinesterase inhibitor.
• Indirect-acting, used in myasthenia gravis and to reverse neuromuscular blockade.

Correct Answer:
✅ Pilocarpine

• Explanation: Pilocarpine is a muscarinic cholinergic agonist, meaning it stimulates parasympathetic activity (rest-and-digest), not sympathetic. It is used clinically in the treatment of glaucoma and xerostomia because it increases salivation and causes pupillary constriction (miosis).

Incorrect Options:

❌ Norepinephrine

• Primary neurotransmitter of the sympathetic nervous system; increases heart rate, blood pressure, and causes vasoconstriction.

❌ None of these

• Incorrect, because one option (pilocarpine) clearly does not increase sympathetic activity.

❌ Phenylephrine

• A selective α1-adrenergic agonist; increases sympathetic activity by causing vasoconstriction and raising blood pressure.

❌ Epinephrine

• Secreted by the adrenal medulla, it stimulates both α- and β-adrenergic receptors, strongly increasing sympathetic effects (increased HR, bronchodilation, vasoconstriction/vasodilation depending on receptor).

✅ Risk factors include <5 and >65 age

🧠 Explanation (Why this is correct):

Community-acquired pneumonia (CAP) is an infection of the lung parenchyma acquired outside of a hospital setting. Certain populations are at higher risk:

• Extremes of age: Children under 5 years and adults over 65 years have weaker or compromised immune systems.

• Other risk factors include chronic diseases (COPD, diabetes), smoking, and immunosuppression.

Thus, the statement about age-based risk factors is the most accurate.

❌ Explanation of Incorrect Options:

The most frequently identified organisms are gram-negative
❌ Wrong — In CAP, the most common organisms are Gram-positive:

• Streptococcus pneumoniae is the leading cause.

• Gram-negative organisms (e.g., Klebsiella) are less common and often seen in hospital-acquired cases.

It mostly presents like bronchopneumonia
❌ Wrong — CAP can present as lobar pneumonia or bronchopneumonia, but lobar pneumonia is classically more common in adults. Saying “mostly bronchopneumonia” is inaccurate.

Symptoms always include hemoptysis
❌ Wrong — Hemoptysis is uncommon in CAP and is not a required symptom. Most patients present with cough, fever, sputum production, and dyspnea.

Symptoms always include pleurisy
❌ Wrong — Pleuritic chest pain occurs in some patients but is not universal.

Lung diseases are broadly divided into obstructive and restrictive patterns based on pulmonary function tests (PFTs).

• Obstructive Lung Diseases (e.g., asthma, COPD, bronchiectasis, chronic bronchitis) involve increased airway resistance → making it hard to exhale air.

  • 🔹 Key Feature: Limitation to airflow, especially during expiration.

  • 🔹 PFT finding: ↓ FEV₁, ↓ FEV₁/FVC ratio (<70%).

• Restrictive Lung Diseases (e.g., pulmonary fibrosis, sarcoidosis, interstitial lung disease) involve reduced lung compliance or expansion, leading to reduced lung volumes.

  • 🔹 Key Feature: Reduced total lung capacity (TLC).

  • 🔹 PFT finding: ↓ FVC, normal or increased FEV₁/FVC ratio.

❌ Incorrect Options Explained:

• Restrictive lung diseases are characterized by reduced expansion of the lung → ✅ Partly true, but not the best choice when the question asks “about the lung diseases” in general, because airflow limitation defines obstructive diseases more specifically.

• Obstructive lung diseases are characterized by reduced expansion of the lung → ❌ Expansion is normal or even increased (hyperinflation).

• Restrictive lung diseases are characterized by reduced expiratory flow rate → ❌ Expiratory flow may be proportionately normal.

• Restrictive lung diseases are characterized by limitation to air flow → ❌ Airflow is usually normal; the problem is volume reduction.

✅ Increase in IgG immunoglobulins

🧠 Explanation (Why this is correct):

Asthma is a chronic inflammatory disease of the airways characterized by immune-mediated hypersensitivity. The key immunologic and pathophysiologic features include:

• Eosinophilic infiltration → eosinophils release cytotoxic proteins that contribute to airway inflammation.

• Mast cell activation and degranulation → release histamine, leukotrienes, and prostaglandins, causing bronchoconstriction and inflammation.

• Increased mucus production → goblet cell hyperplasia leads to airway obstruction.

• Airway hyperresponsiveness → the airways constrict excessively in response to triggers.

IgE, not IgG, is the primary immunoglobulin involved in asthma. IgE binds to allergens and triggers mast cell degranulation. IgG levels are not typically elevated and do not play a central role in the pathogenesis of asthma.

✅ Therefore, “Increase in IgG immunoglobulins” is the least characteristic feature of asthma.

❌ Explanation of Incorrect Options:

Infiltration of eosinophils in the airway
❌ Wrong — This is a hallmark of allergic asthma and contributes directly to airway inflammation.

Mast cell activation and degranulation
❌ Wrong — Central to the early phase of asthma attacks, causing bronchoconstriction and mediator release.

Increased mucus production
❌ Wrong — A key feature, leading to airway obstruction and wheezing.

Airway hyperresponsiveness
❌ Wrong — Characteristic of asthma; it underlies bronchospasm triggered by allergens or irritants.