People’s College of Medical Sciences & Research Centre
Bhanpur, Bhopal (M.P.) – 462037
MD – 2011 BATCH
3rd Internal ASSESSMENT exam
APRIL 5, 2014
Subject : medicine
Paper - 4
Time: 3 hours Max. Marks – 100
Note: All Questions are compulsory.
Diagrams are welcome.
Section A:
Question 1:
A 45-year-old previously healthy man presented to our hospital with first episode of palpitations associated with dizziness. These symptoms were followed by severe central chest pain which prompted his visit to the emergency room. Physical examination in the emergency room revealed a well built man, in mild distress. His blood pressure was 150/90 mm Hg and heart rate 90 bpm. His general physical, cardiac and rest of the clinical examination were normal. ECG revealed rsr’ in V1 and V2 and saddle-back pattern of ST elevation in V2:
His cardiac enzymes were normal. His hospital course was complicated by telemetry monitor showing multiple episodes of asymptomatic non-sustained polymorphic ventricular tachycardia (VT), 110–120 bpm.
After administration of a sodium channel blocker (Ajmaline), ECG showed coved ST-segment elevation in V2, rsr′ pattern in V1 and V2. On further history one of his brothers seemed to have died all of a sudden 10 years back.
What is your diagnosis? (5 Marks)
What are the differential-diagnoses? (5 Marks)
What is the mode of inheritance, male-female ratio, mean age of diagnosis, precipitating factors and risk factors in this disorder? (10 Marks)
What are the further management options to prevent sudden cardiac death in this patient? (5 marks)
Hint: This diagnosis has now become a commonly recognized global cause for sudden cardiac death (4%) since its first case report in 1992 by an Asian.
ANSWER 1:
What is your diagnosis? (5 Marks)
Brugada syndrome
What are the differential-diagnoses? (5 Marks)
· Pulmonary embolism· Acute right ventricular (RV) myocardial infarction
· Acute pericarditis/myopericarditis
· Arrhythmogenic RV cardiomyopathy
What is the mode of inheritance, male-female ratio, mean age of diagnosis, precipitating factors and risk factors in this disorder? (10 Marks)
BS is an autosomal dominant inherited disorder, accounting for 4% of all causes of SCD. It has variable penetrance, predominantly affecting men (80% of patients) more than women, with a ratio 9:1 and mean age at diagnosis is between 40 and 45 years.
What are the further management options to prevent sudden cardiac death SCD in this patient? (5 marks)
Genetic testing, ECG screening for family members and avoidance of provoking factors.The only proven treatment that decreases the risk of SCD in patients with BS is an AICD. Studies are ongoing to explore the effectiveness of quinidine and other pharmacological agents that might decrease arrhythmic risk in patients with BS. Isoproterenol (which increases the L-type calcium (ICaL) current), might be useful for treating electrical storm in BS
http://casereports.bmj.com/content/2013/bcr-2013-009918.full?sid=dd804c85-2f41-4e65-bd1a-9ace002728ae#ref-1
Question 2:
A 40-year-old woman was brought to the emergency department following a collapse. She was found pulseless by her cousin (who also happened to be a cardiac critical care nurse) and cardiopulmonary resuscitation was performed for approximately 2 min before emergency medical services (EMS) arrived. Initial rhythm was VF and she was shocked once with 200 J with successful conversion to sinus tachycardia. She was intubated in the field by EMS, but was combative after the shock and self-extubated, before reaching the hospital. On arrival, she was hemodynamically stable, maintained her respiration and remained in sinus rhythm.
Her EKG is below:
Pulmonary artery pressure was 48 mm Hg and ejection fraction was normal. Cardiac catheterisation showed no significant coronary artery disease, but has showed significant diastolic dysfunction.
Her Cardiac Cath data is below:
It shows a decrease in arterial pressure after a premature ventricular contraction (PVC) .
aa) What is the diagnosis? Mention one important differential diagnosis for this condition and discuss how you would distinguish between the two? (5 marks)
bb) What are the ‘major’ as well as ‘possible’ risk factors and mention one modifiable risk factor for ‘sudden cardiac death’ in individuals with the above disease? (2.5 marks)
c c) Name the above described cardiac cath sign originally named after the clinicians who reported the first case of this disease. (
ad) What are the further management options to prevent sudden cardiac death in this patient? (5 marks)
ANSWER 2:
a a) What is the differential diagnosis (after echocardiography) for this condition and how would you distinguish between the two? (10 Marks)
Athlete's heart—LV hypertrophy associated with athletic training.
· Positive genetic test results in athletes can resolve the issue, but due to the vast number of genes it is difficult to know what to test for unless you have an index family member (who has already been diagnosed with HCM). “Negative result can be non-diagnostic since only about half of the genes responsible for HCM have been identified,” says Edvardsen.
· Sex differences need to be taken into account since female athletes who have undergone high levels of training rarely show left ventricular wall thicknesses within the grey zone. Female athletes with borderline left ventricular wall thickness are most likely to have HCM.
· It is important to take a medical history to see whether athletes have experienced symptoms such as palpitations or arrhythmias and whether any other relatives have these symptoms. It is also helpful to obtain detailed knowledge of what an individual’s training actually involves. “Athletes following endurance sports, such as rowing and cycling, are more likely to be affected than those doing power sports such as weightlifting or wrestling,” says Edvardsen. An athlete who predominately does power sports in the grey zone is more likely to have HCM.
· Other echocardiographic parameters, such as LV end-diastolic capacity enlargement can provide useful information. An enlarged left ventricular end-diastolic cavity dimension (>55 mm) is present in more than one third of highly trained elite male athletes, while the diastolic cavity is small, usually <45 mm in most patients with HCM. The cavity only becomes larger (>55 mm) in patients who have evolved to the end-stage phase of the disease with progressive heart failure and systolic dysfunction.
· Most HCM patients show abnormal pulsed or tissue Doppler diastolic indexes of LV filling, independent of whether heart failure or outflow obstruction is present. Typically, the early peak of transmitral flow velocity (E) is decreased and deceleration time of the early peak prolonged (Edec), and atrial filling (A) is increased, thereby inverting the normal E/A ratio.
· Forced detraining can provide a useful approach, with elite athletes with LV hypertrophy known to show reductions in wall thickness (of about 2-5 mm) over deconditioning periods of around three months. No such changes occur with HCM patients.
http://www.escardio.org/congresses/euroecho2012/congress-to-you/Pages/hypertrophic-cardiomyopathy.aspx
a b) What are the ‘major’ as well as ‘possible’ risk factors and mention one modifiable risk factor for ‘sudden cardiac death’ in individuals with the above disease? ( Marks 5)
The major risk factors include prior cardiac arrest, spontaneous sustained VT, spontaneous or exercise-induced non-sustained VT, family history of SCD, unexplained syncope, LV thickness ≥30 mm, and an abnormal blood pressure response to exercise. This consensus document also noted possible risk factors, which include LVOT obstruction (resting gradient >30 mm Hg), high-risk cmutations, LV apical aneurysm and late gadolinium enhancement (LGE) on cardiovascular MRI (CMRI). The severity of other symptoms, such as dyspnoea, chest pain and effort intolerance have not been correlated with an increased risk of SCD. http://www.ncbi.nlm.nih.gov/pubmed/22093712?dopt=Abstract
b c) What are the further management options to prevent sudden cardiac death in this patient?
· Any patient with HCM identified, to have one or more major risk factors should be carefully evaluated for implantable cardioverter defibrillator (ICD) implantation for primary prevention of SCD.
· All HCM patients can be offered ICD as a secondary prevention after cardiac arrest or a documented ventricular fibrillation or a haemodynamically significant VT.
· The majority of asymptomatic patients with HCM have a relatively benign course. However, risk stratification needs to be done in each patient diagnosed with HCM.
· Patients not considered candidates for ICD, should have periodic (12–24 months) SCD risk stratification using ECG, transthoracic echocardiography, Holter monitors, exercise testing and clinical assessments.
· Screening of first-degree relative of patients with HCM, familial inheritance and genetic counselling is recommended. Genetic testing is recommended in first-degree relatives of index patients, who have been identified to carry a high-risk mutation.
3) Write a short note on Platypnoea Orthodeoxia syndrome. (10 marks)
Platypnea orthodeoxia syndrome (P-OS) is a rare syndrome characterized by clinically observable dyspnea and oxygen desaturation accompanying a change to a sitting or standing posture from a recumbent position, and it is resolved when the patient is supine.
Terms ‘platypnea’ and ‘orthodeoxia’ were accepted in 1969 and 1976 to describe the manifestations of this syndrome. (1,2)
Till now more than 188 cases(3) have been described in literature after this syndrome, first reported in 1949 by Burchell et al. (4) It may result from several cardiopulmonary processes with interatrial communications being the most common aetiology (5- 7) and some isolated case reports of various etiologies. Interatrial communication is so common etiology that now it is also regarded as “Platypnea Orthodeoxia Disease.” ( 3)
The precise mechanism for both the platypnea and orthodeoxia is still unknown even after more than 60 years of this entity first reported. In different isolated case reports, various mechanisms are often postulated to whatever special features were found in those particular patients. Three primary mechanisms have been postulated for this rare clinical phenomenon: intra-cardiac shunting, anatomic pulmonary vascular shunting, and ventilation-perfusion mismatching/pulmonary parenchymal shunts (2,5, 8) with inter-atrial communications being the most common etiologic association.(6, 9, 10)
1. Altman M, Robin ED: Platypnea (diffuse zone I phenomenon?).N Engl J Med 1969, 281:1347-8. 
2. Robin ED, Lamon D, Horn BR, Theodore J: Platypnea related to orthodeoxia caused by true vascular lung shunts.N Engl J Med 1976, 294:941-3.
3. Rodrigues P, Palma P, Sousa-Pereira L: Platypnea-orthodeoxia syndrome in review: defining a new disease? Cardiology. 2012;123(1):15-23.
4. Burchell HB, Hemholz HF Jr, Wood EH: Reflect orthostatic dyspnea associated with pulmonary hypotension. Am J Physiol 1949, 159:563-4.
5. Seward JB, Hayes DL, Smith HC, Williams DE, Piehler JM, Tajik AJ: Platypnea-orthodeoxia: clinical profile, diagnostic workup, management and report of seven cases.Mayo Clin Proc 1984, 59(4):221-31.
6. Robin ED, McCauley F: An analysis of platypnea-orthodeoxia syndrome including a "new" therapeutic approach.Chest 1997, 112:1449-51.
7. Gobart F, Rey C: Platypnea-orthodeoxia syndrome: a probably underestimated syndrome?Chest 2001, 119:1624-5.
8. Kennedy TC, Knudson RJ: Exercise -aggravated hypoxemia and orthodeoxia in cirrhosis. Chest 72: 1977,305–9.
9. Cheng TO: Mechanisms of platypnea-orthodeoxia: what causes water to flow uphill?Circulation 2002, 105(6):47.
10. Hagen PT, Scholz DG, Edwards WD: Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts.Mayo Clin Proc 1984, 59:17-20.
End of Section A
Deposit your Section A answer sheet and go to next question paper labelled as Section B, which requires use of internet. Collect your personal information/internet access device (smart phone/tab) from the invigilator. The total time provided to answer section A and B is divided equally in the overall duration of this paper."
Go to next page for Section B (requires use of internet)
People’s College of Medical Sciences & Research Centre
Bhanpur, Bhopal (M.P.) – 462037
MD – 2011 BATCH
3rd Internal ASSESSMENT exam
APRIL 5, 2014
Subject : medicine
Paper - 4
Time: 3 hours Max. Marks – 50
Note: All Questions are compulsory.
Diagrams are welcome.
Section B: Candidates can use the internet to answer this section
Question 3: (25 Marks)
a) a) Benefits of thrombolysis vs placebo in terms of absolute and relative risk reduction of patient outcomes such as mortality in subgroups such as patients with different times taken to begin thrombolysis, nature of thrombolytic agent (tPA vs stk), nature of ECG changes (such as STEMI vs non STEMI or bundle branch block or anterior wall vs inferior wall).
b) b) Harms of thrombolysis vs placebo with respect to bleeding and stroke
c) c) Please discuss in simple words the meaning of the terms absolute and relative risk reduction as well as ‘confidence interval.’ Also describe them in simple terms while you discuss the trial results (in answers to a and b) so that typical statements such as “Thrombolysis significantly reduced mortality at day 35 compared with placebo (Absolute risk reduction of 7820 out of 79,315 [x%] patients on thrombolysis versus 7357 of 79,285 [y%] patients on placebo; Relative Risk of 0.82, 95% CI (Confidence interval of 0.77 to 0.87)” can be appreciated even by your patient’s relatives when you advice them about the need for thrombolysis in a given patient.
ANSWER 3:
Answer a): One non-systematic review of large RCTs (9 RCTs, 58,600 people with suspected acute MI) comparing thrombolysis versus placebo found that thrombolysis significantly reduced mortality at day 35 compared with placebo (AR 2820/29,315 [9.6%] with thrombolysis v 3357/29,285 [11.5%] with placebo; RR 0.82, 95% CI 0.77 to 0.87).
The ARR absolute risk reduction or RD risk difference) was (11.5-9.6= 1.9) means if 100 people were treated with thrombolysis, around 2 people would be prevented from developing bad outcomes. Another way of expressing this is the number needed to treat (NNT). If 2 people out of 100 benefit from treatment, the NNT for one person to benefit is about 50 (100 ÷ 2) = 50). When the RR is less than 1, the risk of a bad outcome is decreased, meaning that the treatment is likely to do good. In this case the RR is 0.82 mentioned above, calculated by AR in intervened group divided by AR in placebo group i e 9.6/11.5=0.83
Relative risk reduction (RRR) indicates by how much the treatment reduced the risk of bad outcomes relative to the control group who did not have the treatment.
In this case, 1-0.83=0.17 or 17%.
Answer b) Harms of Thrombolysis versus placebo: Stroke/intracerebral haemorrhage
The above mentioned non-systematic review found that thrombolytic treatment significantly increased the risk of stroke compared with control at days 0 to 35 (340/29,315 [1.2%] with thrombolysis v 224/29,285 [0.8%] with control; P <0.0001
The non-systematic review found that thrombolytic treatment significantly increased the risk of major bleeding compared with placebo (ARI 0.7%, 95% CI 0.6% to 0.9%; NNH 143, 95% CI 111 to 166
http://bestpractice.bmj.com/best-practice/monograph/1013/treatment/evidence/intervention/0202/0/sr-0202-i2.html
4) 4) A 70 year old man, comatose after a stroke requires enteral nutrition (on Ryles tube) and is unable to afford costly formula foods. Discuss after an internet search the most cost effective way to ensure that he receives 50 g of protein and 2000 Kcals daily. (15 marks)
Search words used: cost effective ryles tube feed milk india
Answer: 1.5 litres of milk given as 200 ml every 3 hours in 24 hours. The concentration of protein in milk varies from 3.0 to 4.0% (30-40 grams per liter). The percentage varies with the breed of the cow and in proportion to the amount of fat in the milk. There is a close relationship between the amount of fat and the amount of protein in milk—the higher the fat, the higher the protein. 1 liter of milk would have approximately 600 to 700 Kcals and it can be further supplemented by adding sugar. http://babcock.wisc.edu/sites/default/files/de/en/de_19.en.pdf
4) 5) A 30 year old man with incidentally detected and asymptomatic mitral stenosis with a childhood history of rheumatic fever has come to you with gastric reflux symptoms. What will be your approach to rheumatic fever prophylaxis in this man? Carry out an internet search to find out relevant studies that may help you to decide the duration of rheumatic prophylaxis in patients and explain in the context of available study results how you may (or may not) individualize the duration of prophylaxis. (10 Marks)
Answer. No prophylaxis required in this 30 year old man. Search words: rheumatic fever prophylaxis duration india
The Consensus Guidelines on Pediatric Acute Rheumatic Fever and Rheumatic Heart Disease formulated in 2007 states regarding duration of secondary prophylaxis(i) If No carditis: Then prophylaxis for 5 years or till 18yrs of age, whichever is longer. (ii) If Mild to moderate carditis and healed carditis: Then prophylaxis for 10 yrs/25 yrs of age, whichever is longer.
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