You are seeing Mr Yee two months later. At your last visit, he did not want colchicine prophylaxis as he did not want to take 'too many tablets'. He has started and is adherent to his urate lowering agent. Last month, his uric acid had decreased to 390 mmol/L. He had a gout flare last week. Hence, he came to your clinic today to ask about colchicine prophylaxis. Which is INCORRECT advice regarding colchicine prophylaxis?
- A. Offer to start colchicine at 500 mcg once daily or alternate days as gout prophylaxis as his renal function is normal
- B. Colchicine can help to reduce the frequency of flares, especially during the first six months of Urate lowering therapy
- C. Tell him that if he is started on NEW medications, he should inform his doctor or pharmacist that he is on colchicine regularly as colchicine can have drug interactions. If unsure and he needs to take NEW medications, such as a short course of antibiotics, he is to omit colchicine until the new medication is completed
- D. Regular colchicine prophylaxis in someone with normal renal function and regular monitoring can lead to renal failure
Correct Answer: D
Rationale: Colchicine curbs flares 500 mcg fits normal kidneys, cuts attacks in urate-lowering's rocky start, and needs drug interaction flags or skips with gut upset. But renal failure from regular use with monitoring? False colchicine's safe there, not a kidney killer. Clinicians nix this myth, grounding chronic gout aid in truth.
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Patients on insulin therapy should receive essential education on the following EXCEPT:
- A. Insulin injection technique
- B. Stopping all oral hypoglycaemic agents
- C. Recognition and self-management of hypoglycaemia
- D. Sick day management
Correct Answer: B
Rationale: Insulin therapy education for diabetes patients covers injection technique, hypoglycemia recognition and management, sick day rules, and safe driving, per diabetes care standards. However, stopping all oral hypoglycemic agents isn't universally essential many patients continue agents like metformin or SGLT-2 inhibitors alongside insulin for synergistic effects, depending on glycemic control needs. Assuming cessation oversimplifies treatment plans, potentially reducing efficacy. Education must tailor to individual regimens, not mandate stopping orals, making this the exception. Physicians ensure comprehensive teaching to enhance adherence and safety, critical in chronic disease management.
In patients who are awake during craniotomy, appropriate statements include:
- A. For a temporal lesion, neurosurgeons are likely to require the sitting position.
- B. A tracheal tube is likely to be used.
- C. A urinary catheter is likely to be inserted.
- D. Intraoperative seizures are likely to occur during cortical mapping.
Correct Answer: C
Rationale: Awake craniotomy allows functional mapping and patient cooperation. The sitting position is rare due to air embolism risks and is not specific to temporal lesions; supine or lateral positions are standard. A tracheal tube is avoided to maintain airway control via less invasive means (e.g., nasal cannula), as patients must remain responsive. A urinary catheter is routine for longer procedures to manage fluid balance and patient comfort, given immobility and duration. Patient anxiety is common but manageable, not an absolute contraindication. Seizures can occur during cortical mapping due to electrical stimulation, but likely' overstates frequency; they're a risk, not a certainty. The urinary catheter's inclusion reflects practical perioperative care, ensuring monitoring and comfort without interrupting the procedure's focus on brain function preservation.
The definition of Chronic Heart Failure is:
- A. Failure of the heart to adequately pump blood to the body
- B. Long-term inability of the heart to meet metabolic demands required to maintain homeostasis
- C. Prolonged enlargement of the left ventricle impacting on the contractility of the muscle
- D. Long term fluid build-up, causing increase in blood volume and reducing the ability of the heart to maintain blood flow
Correct Answer: B
Rationale: Chronic heart failure's essence long-term pump lag can't match body's metabolic needs, a homeostasis bust. Simple pump fail's vague; LV growth or fluid traps are bits, not the whole. Nurses grasp this, a chronic ticker's root.
A 58-year-old man with a known history of heart failure from cardiomyopathy, with an ejection fraction of 30 percent returns for a 3-week follow-up visit after being started on frusemide 40 mg od for increasing symptoms of dyspnea. Since starting frusemide, his symptoms have returned to baseline and he has lost 3 kg. He is maintained on guideline-directed medical therapy for heart failure including sacubitril/valsartan 97 mg/103 mg BD, carvedilol 12.5 mg BD, Simvastatin 40 mg ON, and aspirin 81 mg OD. His physical examination reveals: blood pressure of 128/80 mmHg, regular heart rate of 78 bpm, respiratory rate of 18 breaths/min, and room air oxygen saturation of 96 percent with no saturation decrease with hallway ambulation. He has no peripheral edema. A clinic electrocardiogram reveals a left bundle branch block with a QRS duration of >150 msec. What would be the most appropriate next step in management?
- A. Refer him to an electrophysiologist
- B. Discontinue the sacubitril/valsartan 97 mg/103 mg BD
- C. Change his diuretic to spironolactone 25 mg OD
- D. Increase the frusemide to 40 mg BD
Correct Answer: A
Rationale: HFrEF at 30% EF with LBBB >150 msec stabilized on meds hints at dyssynchrony, ripe for cardiac resynchronization therapy, so an electrophysiologist's next. Ditching sacubitril/valsartan or swapping diuretics lacks cause; upping frusemide or re-echoing waits. Clinicians tap this referral, boosting chronic pump sync, a guideline nod.
Animal experiments have shown that destruction of the ventromedial nuclei of the hypothalamus leads to unrestrained eating, because a specific structure is lost. Question: Which structure is lost?
- A. The amygdala
- B. The vagus nerve
- C. The satiety centre
- D. The feeding centre
Correct Answer: C
Rationale: Ventromedial zap satiety centre dies, eating runs wild, not amygdala's fear, vagus' gut, or feeding's drive. Nurses link this, a chronic overeat switch.