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Student Discussions: 2017: February 26th to July 20th

For discussion during this semester
1. A patient has diabetes, hypertension and chronic kidney disease. His serum alanine transaminase is noted to be persistently high at 127U/L (about three times the upper limit of normal) for over 3 months. The other parameters of his liver function test are normal. He is negative for Hep B surface antigen and antibodies to Hep C. His total cholesterol and LDL cholesterol are both high at 8mmol/L and 5mmol/L respectively. His triglyceride level is also high at 2.6mmol/L. With this information, suggest possible reasons for his abnormal ALT value.

Response: Possible causes of raised ALT:
1)Non-Alcoholic Fatty Liver Disease
2)Alcoholic liver disease
3)Medication induced
4)Viral hepatitis
5)Autoimmune hepatitis
7)Extrahepatic (thyroid disorder, celiac disease, hemolysis, muscle disorder)

2. A man with chronic kidney disease has mild anemia with a hemoglobin of 10.2mg/dL. His serum iron is 9.9umol/L (normal 10.7 to 32.2) and his total iron binding capacity is 74umol/L (normal 38.5 to 85.9). Is his anemia due to iron deficiency?

Response: Iron deficiency anaemia classically shows low serum iron with high TIBC. In this case, TIBC is still within the normal range. In a man with chronic kidney disease, it is likely that his anaemia is due to anaemia of chronic disease. Management-wise, I would like to start him on haematinics (elemental iron, folic acid and vitamin B12) with Vitamin C supplement to help with absorption of iron. Elemental iron is for replacement of iron store whereas folic acid and vitamin B12 are provided because in the event of increased erythropoiesis following increased iron store, these two may become depleted.

3. A woman is being treated for hypothyroidism with Tab Thyroxine 75 ug OD. Her serum T4 is 13.73pmol/L (normal) and her serum TSH is 11.22mIU/L (high). She is clinically euthyroid. Is any dose adjustment of Thyroxine necessary?

From her thyroid function test, her serum T4 is normal while her serum TSH is high. This indicates subclinical hypothyroidism. Although she is asymptomatic and clinically euthyroid, there is a necessity to increase her dose of thyroxine. Dosage should be adjusted to maintain normal TSH levels as the aim of thyroxine in subclinical hypothyroidism is to make the patient clinically and biochemically euthyroid.

4. A 67 year old man developed pulmonary edema in April 2012. He had AF at that time. His echocardiogram showed severe mitral regurgitation and cardiomegaly with dilatation of all four chambers. The anterior mitral valve leaflet was noted to be flail. His coronary angiogram was normal and he underwent mitral valve replacement three days later. What do you think is the cause of his mitral regurgitation?

the cause is most likely due to dilated cardiomyopathy. When the left ventricle dilates, the papillary muscles and the cordae tendinae (supports of mitral valve) stretches which eventually causes mitral valve incompetence, mitral regurgitation. The mitral regurgitation is most likely the cause of the atrial fibrillation in this case. The patient also presented with pulmonary oedema, which shows that he most probably is in heart failure. Other causes may include, infective endocarditis, rheumatic heart disease or a previous MI.

5. Look at this report (question 5). It is a coronary angiogram report and it shows significant 3 - vessel disease. Currently, 2 years after this angiogram was done, the patient reports feeling well with no chest pain on exertion. He remains on medical therapy and did not undergo any revascularisation procedure. How will you explain his lack of cardiac symptoms?

His lack of cardiac symptoms could potentially be the result of his adherence to his medications which comprises of nitrates, antiplatelet, statin, ACE-inhibitor, and trimetazadine. It was not mentioned as to the TIMI grading of the coronary blood flow, as asymptomatic patients may have a normal TIMI Grade 3 flow despite the 3 vessel disease. That being said, the mechanism of why some individuals experience chest pain and some are symptom-free, is not fully understood. There have been proposals such as : 1) Higher pain threshold in ischemic episodes 2) Shorter duration and less severe ischemic episodes 3) Generalized defective perception of painful stimuli 4) Defective anginal warning system 5) Higher beta-endorphin levels 6) Higher production of anti-inflammatory cytokines, which may block pain transmission pathways and increase the threshold for nerve activation

6. The patient shown in this picture (Question 6 had undergone a procedure to insert a therapeutic device in the left infraclavicular region. This therapeutic procedure was done after he suffered loss of consciousness and was noted to have bradycardia. What is the therapeutic device and what do you think was the diagnosis at the time he suffered syncope?

The device inserted is an artificial, permanent pacemaker. Possible diagnoses include: slow AF/ 3rd degree Heartblock/ ischemic heart disease/ sick sinus syndrome.

7. A patient has the following arterial blood gas results: pH (7.28); PaCO2 (42.3mm Hg); PaO2 (84.4mm Hg); HCO3 (20mmol/L); What kind of acid base disorder does this patient have? Also, does this ABG show any evidence of a pulmonary diffusion defect or ventilation-perfusion imbalance?

The result of ABG shows metabolic acidosis in view of an acidotic ph (7.28) and low HCO3 (20mmol/l). In the case of metabolic acidosis, patients are suppose to have respiratory alkalosis (high pH, and low Co2) as a compensatory mechanism. But the Co2 remains at the upper limit of the normal value, which means to say the patient is not breathing well to wash out the carbon dioxide levels in his blood, could be due to a lung pathology or any condition that interferes with the ability of oxygen get to the alveoli or anything that prevents blood flow to the capillaries. The likely cause for his ABG is due to a V/Q mismatch, where there is some areas in the lungs are better perfused by blood and some areas are better ventilated than perfused. Likely cause of v/q mismatch is due to hypoxia.

8. A 55 year old woman had a vasovagal syncope in December 2016. Physical examination and all investigations including ECG were normal at that time. She had an ECHO done in March 2017. It showed dilated right atrium and tricuspid regurgitation. Both ventricles were normal size and LVEF was 55%. Is there a link between the ECHO findings and her syncope?

There is the possibility that the tricuspid regurgitation caused a decreased supply of oxygen rich blood which led to the brain undergoing cerebral hypoxia which caused the syncope. However, this would indicate a severe disease process, and hence biventricular hypertrophy would be expected. In this instance, a transient arrhythmia would be suspected. If there is no evidence of an arrhythmia and no ventricular hypertrophy, this ECHO findings and syncope are most likely unrelated.

9. A patient with DM, HPT and CKD has a hemoglobin of 9.9gm%. Her serum creatinine is 188umol/L and her serum K is 5.5mmol/L. She takes insulin, atorvastatin, aspirin, perindopril and felodipine. How will you decide whether the elevated serum K is significant enough for her to be admitted in the hospital? What changes in her current treatment will you make?

This patient has mild hyperkalemia with raised creatinine. In this case, the most probable cause of hyperkalemia is due to reduced potassium excretion. Common causes would include renal failure and medications that interfere with potassium excretion, namely potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, and non-steroidal anti-inflammatory drugs. She is currently on perindopril and aspirin which can affect potassium excretion. This patient need not be admitted into the hospital and can be treated as outpatient. Her medication should be re-evaluated and changed, and her potassium and creatinine should be monitored for laboratory signs of severe hyperkalemia and acute worsening of renal function, which requires hospitalization.

10. A 50 year old woman underwent surgery for atrial septal defect when she was 30 years old. She was admitted for congestive cardiac failure in January 2017. In March 2017, she is feeling better even though she has breathlessness on walking fast. On examination she has central cyanosis and atrial fibrillation without any evidence of heart failure. Her ECHO showed dilated LA, dilated RA, with a normal LV ejection fraction. Why does she have central cyanosis? Why are her atria dilated?

1) it was a failed correction. 2) she developed pulmonary hypertension with right to left shunting in lungs and masked left ventricular restriction 3) during surgical repair, inferior vena cava return to the left atrium by inclusion of Eustachian valve

11. A 49 year old man has been on antithyroid drugs for past 10 years for toxic nodular goitre. Currently he is on Tab Carbimazole and his serum T4 and TSH are both normal. He is reluctant to stop Carbimazole because of recurrence of hyperthyoidism on every occasion when he stopped it in the past. What is the appropriate advice for him regarding his thyroid disease?

for this patient, I would suggest him to go for radioiodine or surgery. This is because even after being on tablet carbimazole for 10 years, it seems that there is no remission……Thyrotropin-receptor antibodies level should also be checked as those with persistently high level after one or more years of treatment are unlikely to remain euthyroid after carbimazole is stopped.

12. A 33 year old woman has unexplained persistent hypokalemia. She was admitted twice in the past with fatigue and muscle weakness. What will you suspect if her blood pressure was high? What will you suspect if her blood pressure is normal?

Response awaited

13. A 55 year old woman is diagnosed as chronic Hepatitis B carrier. How is this diagnosis made?

HBsAg positive; Anti-HBs negative; HBeAg negative; Anti-HBe positive; Anti-HBc positive; IgM anti-HBc negative; ALT normal

14. A 69 year old man has breathlessness on exertion. There are fine crepitations heard in both lungs on auscultation of the back of the chest. He does not have cardiac failure. His spirometry shows reduced FEV1 and reduced FVC but normal FEV1/FVC ratio. What type of disease can explain his breathlessness?

The reduced FEV1 and FVC indicates restrictive ventilator defect. The reduction of lung volumes can be caused by intrinsic lung diseases (e.g: interstitial lung disease, acute pneumonitis), mechanical compression on the lungs that limits lung expansion (e.g: chest wall/pleural disorder) and neuromuscular disorders which decrease the ability of respiratory muscle to inflate and deflate the lungs. since the reduction of FEV1 and FVC in ILD are in proportion to the decreased lung volume, the FEV1/FVC ratio is normal.

15. A 62 year old woman was diagnosed as bronchial asthma and congestive cardiac failure with atrial fibrillation two years ago. Now, her ECHO shows mitral stenosis, mitral regurgitation. Explain what you think about the diagnosis offered to her two years ago and what kind of heart disease she has.

I think the diagnosis made 2 years ago is unlikely. Symptoms of AF, CCF, bronchial asthma can happen in both MS and MR. Bronchial asthma may be misdiagnosed due to the presence of bronchial obstruction secondary to enlarged LA. Secondly, it is very rarely that bronchial asthma is diagnosed at old age. In short, the presence of both MS and MR suggests that she may have rheumatic heart disease. CCF symptoms are due to enlarged LA pressure and subsequent pulmonary congestion and cor pulmonale.

16. A 69 year old man has breathlessness. His spirometry showed FEV1 to be 0.91 Litres (which is 31% of predicted value 2.95 L) and FVC to be 1.37 Litres (which is 44% of predicted value 3.08 L). What do you think is the cause of his breathlessness?

Both his FEV1 and FVC is decreased and his FEV1/FVC ratio is 0.66 which indicates that he might have an obstructive lung disease such as asthma, COPD or bronchiectasis.

Exercises in writing diagnoses and clinical summaries for Semester 10 students

Dr Velayudhan Menon, MD
Clinical Associate Professor of Medicine
International Medical University, Malaysia

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