34 34. A 51‐year‐old woman presents to the emergency department with cellulitis of her left lower leg and epigastric discomfort after being on oral antibiotics for three days. She is otherwise well and has no other symptoms and ECG is normal. She is known to have autosomal dominant polycystic kidney disease with a serum creatinine of 86 μmol/L [60–110]. A serum high‐sensitivity troponin (hs‐cTn) is requested and the result is 40 ng/L [<29].What is the best interpretation of this result in terms of the likelihood of acute coronary syndrome?Likely because the specificity of hs‐cTn is high.Likely because the pre‐test probability is high.Unlikely because the specificity of hs‐cTn is low.Unlikely because the pre‐test probability is low.
35 35. A 78‐year‐old woman is admitted to the Acute Medical Unit with severe community acquired pneumonia. Her BP is 90/60 mmHg and oxygen saturation is 90% on 4 L of oxygen. Her other medical history includes type 2 diabetes, stage 3B CKD, and hypertension. A central venous line is inserted because of difficult venous access. She complains of increased dyspnoea. A bedside ECG is taken and shown below. Troponin level is 289 ng/L [<29].Which one of the following is the most likely diagnosis?Type 1 myocardial infarction.Type 2 myocardial infarction.Type 3 myocardial infarction.Type 4 myocardial infarction.
36 36. A 55‐year‐man presents with a 2‐hour history of palpitations and chest discomfort. He had a similar episode one year ago. He is known to have ankylosing spondylitis, diet‐controlled type 2 diabetes, and asthma. He uses a salbutamol inhaler two to three times a week. On examination, he is alert and orientated, BP is 110/60 mmHg, pulse rate is 150 bpm, SaO2 on room air is 95%. There is scattered expiratory wheeze. There is no heart murmur. His current ECG is shown in Figure 1.1A, while Figure 1.1B shows an ECG taken 1‐year ago during an infective exacerbation of asthma. His biochemistry results and troponin T are within normal reference range.Figure 1.1AFigure 1.1BThe most appropriate treatment for rate control is:Intravenous adenosine.Intravenous digoxin.Intravenous flecainide.Intravenous verapamil.
QUESTIONS (37–43) REFER TO THE FOLLOWING INFORMATION
Match the following blood pressure lowering agents to their mechanism of action.
1 Decreased renin secretion and decreased heart rate.
2 Decreased central synthesis of catecholamines.
3 Decreasing degradation of circulating natriuretic peptides.
4 Relaxation of smooth muscle through opening KATP channels.
5 Blocking the angiotensin I binding site on angiotensin converting enzyme (ACE).
6 Interfering with Ca2+ release on the sarcoplasmic reticulum.
7 Increased guanylyl cyclase activity.
1 37. Minoxidil
2 38. Sacubitril
3 39. Moxonidine
4 40. Captopril
5 41. Glyceryl trinitrate
6 42. Nebivolol
7 43. Hydralazine.
QUESTIONS (44–51) REFER TO THE FOLLOWING INFORMATION
Match the clinical features listed below to the most likely type of congenital heart disease or clinical syndrome found in patients.
1 Atrial septal defect (ASD).
2 Ventricular septal defect (VSD).
3 Patent ductus arteriosus (PDA).
4 Coarctation of the aorta (CoA).
5 Eisenmenger's syndrome.
6 Marfan's syndrome.
7 Tetralogy of Fallot.
8 Transposition of the great arteries.
44. Cyanosis, clubbing, polycythaemia, an elevated JVP with a dominant a wave pattern, right ventricular heave, palpable pulmonary component of the second heart sound (P2), loud P2, fourth heart sound, pulmonary ejection click, and pulmonary regurgitation on auscultation.
45. Cyanosis, clubbing, polycythaemia, right ventricular heave, a thrill at the left sternal edge, a single second heart sound (A2) and short pulmonary ejection murmur on auscultation, a boot shape heart, right ventricular enlargement, and decreased vascularity of lung vessels on CXR.
46. A better developed upper body in comparison with the lower limbs, radiofemoral delay, and hypertension in the upper limbs only, midsystolic murmur over the precordium and back, hypertensive changes in the fundi, a small aortic knuckle and rib notching on CXR.
47. Fixed splitting of the second heart sound (S2), pulmonary systolic ejection murmur (increasing on inspiration), signs of pulmonary hypertension.
48. A thrill and a harsh pansystolic murmur to the left sternal edge, mitral regurgitation.
49. Arachnodactyly, joint hypermobility, long, thin limbs, a long and narrow face, lens dislocation, blue sclerae, a high‐arched palate, pectus excavatum, aortic regurgitation, mitral valve prolapse, kyphoscoliosis, and arm span exceeding overall height.
50. A continuous murmur along the left sternal border, ECG shows left ventricular hypertrophy, CXR shows increased pulmonary vasculature.
Answers
1. Answer: C
An aneurysm is an artery that has enlarged to greater than 1.5 times the expected diameter. In the infrarenal aorta, the threshold diameter is accepted as 3.0 cm. Abdominal aortic aneurysm (AAA) affects approximately 4–7% of men and 1–2% of women over the age of 65 years.
Medical therapy options remain limited and no aneurysm‐specific pharmacotherapy is currently available. Medical management of AAA generally involves cardiovascular risk reduction, including antiplatelet, statin, and antihypertensive therapy. The best medical management is generally not intended to limit expansion or reduce the size of the AAA. However, managing cardiovascular risk factors is crucial for improving the overall survival of patients and the outcomes of future AAA repair.
Australian national driving regulations stipulate that untreated atherosclerotic aortic aneurysms >5.5 cm disqualify patients from an unconditional driver's licence, except with the approval of a treating vascular surgeon.
Patients with large aneurysms (men >5.5 cm; women >5.0 cm) should be considered for elective aneurysm repair. The optimal management of small AAAs (4.0–5.5 cm) has been clarified by several large, randomised control trials which demonstrate no long‐term survival benefit with open or endovascular repair.
Most AAAs detected with screening or as an incidental finding are below the threshold for elective repair. The risk of AAA rupture increases with AAA diameter (Table 1.1). The surveillance interval for asymptomatic AAA also depends on AAA diameter (Table 1.2).
Table 1.1 Annual AAA rupture risk by diameter.
| AAA diameter (cm) | Rupture risk (%/year) |
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|