Nokea
The pathophysiology of Asthma differs from COPD as:
- A. It is characterised by airflow limitation.
- B. There is abnormal inflammatory response to exposure to noxious particles or gases.
- C. The airflow limitation is reversible.
- D. It is considered an obstructive lung disease.
Correct Answer: C
Rationale: Asthma and COPD both feature airflow obstruction, but their pathophysiology diverges critically. Both have limitation, but asthma's is intermittent and reversible with bronchodilators due to bronchial hyperresponsiveness and inflammation (e.g., eosinophilic), per Farrell (2017). COPD's abnormal inflammatory response to noxious stimuli (e.g., smoking) causes progressive, irreversible damage (e.g., neutrophilic, emphysema), not asthma's profile. Reversibility defines asthma spirometry normalizes post-treatment unlike COPD's fixed obstruction (FEVâ‚/FVC <0.7 persists). Both are obstructive diseases, but this isn't the distinguishing feature. Asthma's reversible limitation stems from smooth muscle spasm and mucosal edema, responsive to therapy, contrasting COPD's structural loss (alveolar destruction), making this the key differential in clinical management and prognosis.
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Mr Yee, 45 years old, reports three recent gout attacks in the ankle or knee. You notice a small tophus over his left elbow. He says that two years ago he took allopurinol 100 mg for one month followed by 200 mg OM for one month, but stopped as it 'did not help his gout and there was no improvement'. When you probe, he states that he was not very adherent to allopurinol either then as it was some years ago. He says he took it likely 'once or twice a week'. He states that he did not experience any rashes or other side effects to it then. He did not go back to see his previous GP as he has moved house and your clinic is nearer to his home. He does not drink alcohol except one glass of wine once or twice a year on special occasions. Two weeks ago, he was admitted to the hospital for a gout flare. He had blood tests done, which returned the results below. He is asking you to give him Arcoxia standby as it usually works for his gout flare. Uric acid 620 mmol/L, Creatinine 96 umol/L, eGFR >90 mL/min, BP 144/94 mmHg. He has HTN on HCTZ long-term. Which is incorrect advice?
- A. Offer to restart allopurinol and explain that it does not work immediately. You may wish to discuss HLA B5801 testing particularly as it is unclear how frequent and for how long he was taking allopurinol previously
- B. Advise that he will need stepwise up-titration of a urate lowering agent to reach uric acid target. Regular blood tests will allow this to be done safely
- C. Advice that colchicine prophylaxis is helpful to prevent gout attacks, as it takes time for a urate lowering agent to reach uric acid target
- D. Advise him that allopurinol is ineffective. Offer to initiate febuxostat or probenecid immediately
Correct Answer: D
Rationale: Tophus and 620 uric acid yell chronic gout allopurinol's not bunk; past spotty use tanked it, not the drug. Restarting with titration, colchicine cover, and allergy watch fits; HLA testing flags risk. Swapping to febuxostat or probenecid skips allopurinol's shot wrong call when adherence, not efficacy, flopped. Clinicians correct this, steering chronic control right.
Certain drug classes may cause harm in patients with symptomatic (NYHA classes II-IV) reduced ejection Heart failure (HFrEF), and thus should be avoided. If they are strongly indicated, they are to be used with caution, and with close monitoring. Such drugs include all of the following except:
- A. Thiazolidinediones (glitazones, e.g., pioglitazone, rosiglitazone)
- B. Nonsteroidal anti-inflammatory drugs and COX-2 inhibitors
- C. Nutritional supplements (e.g., coenzyme Q10, carnitine, taurine, and antioxidants)
- D. Non-dihydropyridine calcium-channel blockers (verapamil, diltiazem)
Correct Answer: C
Rationale: HFrEF hates fluid and strain glitazones swell, NSAIDs tank kidneys, verapamil/diltiazem slow too much, trastuzumab trashes hearts. Supplements like CoQ10? Neutral or helpful, not harmful, a safe outlier. Clinicians dodge the rest, easing chronic pump woes, not this add-on.
Which of the following is NOT an early warning symptom of hypoglycaemia?
- A. Tremors
- B. Palpitations
- C. Diaphoresis
- D. Giddiness, drowsiness
Correct Answer: D
Rationale: Hypo's early buzz tremors, palpitations, sweat, anxiety screams adrenaline, waking patients to act. Giddiness and drowsiness lag, hitting as brain sugar drops, a later neuroglycopenic fade, not the first alarm. Clinicians teach this split, pushing quick carbs at the front signs, a chronic drill to dodge the haze.
What is the cut-off of blood pressure for the diagnosis of hypertension that is recommended by MOH Clinical Practice Guideline?
- A. 120/70 mmHg
- B. 125/75 mmHg
- C. 130/70 mmHg
- D. 140/90 mmHg
Correct Answer: D
Rationale: MOH guidelines hold hypertension at 140/90 mmHg, a conventional cutoff balancing sensitivity and specificity for diagnosis in primary care, aligning with global norms like WHO. Lower thresholds 120/70, 125/75, 130/70, 135/80 catch prehypertension or align with newer AHA standards, but MOH sticks to 140/90 for actionable clarity, triggering treatment to curb stroke or heart risks. This higher bar avoids overdiagnosis in resource-stretched settings, ensuring focus on clear disease, a practical call for managing chronic vascular load.
Which of the following is NOT part of the histology of non-alcoholic steatohepatitis?
- A. Fatty infiltration in liver
- B. Fibrosis of liver
- C. Inflammatory infiltrates in lobules
- D. Cirrhosis
Correct Answer: D
Rationale: NASH histology includes steatosis (fatty infiltration), lobular inflammation, and fibrosis, per pathology definitions. Mallory bodies (intracellular inclusions) are classic but not universal. Cirrhosis is an advanced NAFLD outcome, not a defining NASH feature progression, not initial histology. This distinction aids physicians in staging chronic liver disease accurately.