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For discussion with final year medical students (March to July 2015)

A. Student initiated discussions Weeks 1 and 2
B. Student initiated discussions Weeks 3 and 4
C. Questions and Answers - March 2015
D. Student initiated discussions - Group A


June 2015

How do we create a good bedside presentation? (Based on a submission by Yap Wei Xian)

Original draft:

Mr TKH is a 58 year old Chinese gentleman with underlying diabetes mellitus and hypertension
for the past 10 years, right below knee amputation 2 years ago and diabetic retinopathy with
four times of bilateral laser intervention in the past year, currently presented with progressively
worsening abdominal distension and discomfort for the past 2 months. This was associated with
on and off bilateral lower limbs and scrotal swelling for the past 1 year. Unintentional weight and
appetite loss were also noted, moreover there is a strong family history of hepatocellular
carcinoma due to hepatitis B and Mr TKH is worried he might be affected in the same way. An
USG HBS scan performed in a local private hospital one day prior to admission showed liver
cirrhosis with portal hypertension and possibility of hepatoma. There were no identifiable risk
factors in him and he has no history of receiving blood transfusions. Otherwise patient did not provide complaints of shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, periorbital edema and frothy urine. Mr TKH is compliant to his medications (T Glucovance 500/5 od, T Amlodipine 10mg od, T Simvastatin 20mg ON and T Hydrochlorothiazide 12.5mg od) and follow-ups at Klinik Kesihatan Parit Yaani.

On examination, Mr TKH is alert, conscious and well-orientated. Vital signs are normal and random capillary blood glucose reads 4.0mmol/L at admission. There is bilateral pitting pedal edema up to mid-shin level and tinge of scleral icterus was noted. There is no digital clubbing. Besides that, peripheral stigmata of chronic liver disease are present. Abdomen is grossly distended with positive shifting dullness and fluid thrills. Examination of cardiovascular and respiratory systems showed no abnormal findings. Investigations wise, liver function test upon admission reveals low serum albumin (21g/L), raised total serum bilirubin (36.1µmol/L) and liver transaminases (ALT : 156mmol/L, AST : 146mmol/L). Coagulation profile is normal. Renal profile : Urea 9.1mmol/L; Sodium 132mmol/L; Potassium 3.6mmol/L; Creatinine 104µmol/L. Electrocardiography showed sinus rhythm with T wave inversion over leads II, III, aVF (i.e. inferior wall ischemia), and Echocardiography documented ejection fraction of 65-70%. Other investigations such as Serology screening (for Hepatitis B/C and retroviral disease) and tumour markers (α-fetoprotein, CEA and CA-125) are pending. We are treating this patient for 1) Decompensated liver cirrhosis (Child-Pugh class B) for investigation of cause; 2) Possible Hepatocellular carcinoma; 2) DM and HPT with underlying right BKA and bilateral diabetic retinopathy. His T Glucovance was withheld in view of the low random capillary blood glucose at admission and we also advocate GM pre-meals and pre-bed for 1 day. T Frusemide 40mg stat and od was initiated. Therapeutic paracentesis of 1.5L of serous fluid was performed on first day of admission without complications and it was consistent with a transudative picture (SAAG of 19g/L). Mr TKH was placed on Nil by mouth order for a repeat USG HBS scan today. A 24-hour urinary collection for total protein was ordered too. He was also planned for SOPD referral for OGDS surveillance and initiation of propranolol prophylaxis upon discharge later.

Step 1: From the original draft, extract the main elements of the story without any adjectives and unnecessary descriptions

58 year old Chinese gentleman - diabetes mellitus and hypertension - - right below knee amputation - diabetic retinopathy - abdominal distension for 2 months -bilateral lower limbs and scrotal swelling - weight and appetite loss - strong family history of hepatocellular carcinoma due to hepatitis B - USG scan showed liver cirrhosis with portal hypertension and possibility of hepatoma - On examination, alert, conscious and well-orientated - Vital signs are normal - random capillary blood glucose 4.0mmol/L - icterus present. - peripheral stigmata of chronic liver disease seen – Ascites present - liver function test -low serum albumin - raised total serum bilirubin - raised liver transaminases – renal profile normal - T wave inversion in inferior ECG leads –Provisional diagnoses -Decompensated liver cirrhosis (Child-Pugh class B) and Possible Hepatocellular carcinoma; with DM and HPT with underlying right BKA and bilateral diabetic retinopathy. T Glucovance stopped - T Frusemide initiated. Therapeutic paracentesis of 1.5L of serous fluid was performed – Ascites transudate - Decision to stop Glucovance - Decision to start Frusemide - Work up for Chronic hepatitis B and hepatic carcinoma.

Step 2: Make a narrative from the main elements after you have seen the big picture.

This 58 year old man with diabetes and hypertension presented to us with abdominal distension due to ascites. Clinical examination and an ultrasound of the abdomen have confirmed that he has cirrhosis liver with portal hypertension. As he has a strong family history of Hepatitis B infection, we are now investigating him for Hepatitis B and for hepatocellular carcinoma. His diabetic control is very good with a fasting plasma glucose of 4mmol/L. Since this degree of tight control represents a risk of hypoglycemia for him, we have decided to stop the Tab Glucovance that he is on for the time being. His blood pressure is normal. We did an abdominal paracentesis for him and removed 1.5 litres of fluid. The ascitic fluid was a transudate. We have also started him on oral frusemide. His LFT shows elevated liver enzymes which raises the suspicion of progressive and on-going liver inflammation. In addition to all these problems, I wish to point out that he has complications due to diabetes - retinopathy for which he has undergone laser therapy. He has also undergone a right below knee amputation for reasons I am not yet clear but which appears to be due to diabetic complications.


Questions based on a submission by Amanda Chang

1. A 78 year old man, a chronic smoker of 58-pack years, with Chronic Obstructive Airway Disease for the past 3 years, presented currently with progressively worsening shortness of breath for the past three days. What will you consider as the most likely reason for this breathlessness at this point?

2. He had low grade fever, productive cough with whitish sputum and pleuritic chest pain during the past one week. What physical finding is typically associated with pleuritic chest pain?

3. He is a known case on COPD for the past three years, on MDI Salbutamol II/II PRN and MDI Ipratropium bromide II/II tds under Medical Outpatient Department follow-up. Why is he receiving two types of bronchodilators – salbutamol and ipratropium?

4. This patient also has underlying hypertension, stage III chronic kidney disease (baseline creatinine on April 2015 was 136µmol/L), dyslipidemia, Benign Prostatic Hypertrophy and may have Parkinson disease. Based on the illnesses that he has, what should be considered as a cause of his chronic kidney disease?

5. His current medications are T Atenolol 80mg bd, T Simvastatin 20mg ON, MDI Salbutamol II/II PRN, MDI Ipratropium II/II tds, T HCTZ 25mg od, T Terazosin 4mg ON, T Amlodipine 10mg od. No history of allergies to medications are noted. What is obviously an error in the information given here?

6. Chest x-ray taken showed increased opacity over right lower lung zone and evidence of hyperinflation. Full Blood count (24/6/2015) : Hb 7.7g/dL, platelet 390 x 109/L, TWBC 7.06 x 109/L . RP (24/6/2015) : Urea 13.9 mmol/L/ Creatinine 226 umol/L. A working diagnosis of acute exacerbation of COAD secondary to Community Acquired Pneumonia was made. Name two other conditions that should be included in the diagnosis at this stage.

7. He was on started on IV Augmentin 1.2 g TDs and tablet Doxycycline 100 mg BD and nebulizer AVN 2:1:1 every 4 hourly. He was also referred for chest physiotherapy. In view of the high blood pressure, he was also given T. Amlodipine 10 mg stat. Patient was also planned for blood transfusion. The patient continues to remain anemic in spite of being treated for H.pylori infection. What should be the next investigation to be done for finding out the reason for his persistent anemia?


Managing diabetes during the Muslim fasting month of Ramadan


A few things about strokes

1. We invariably consider the possibility of a cerebellar stroke when patients have acute onset ataxia of gait or limb incoordination. Can you deduce which artery is involved (based on additional neurological signs) in this cerebellar stroke presentation: The patient has nausea, vertigo, dysphagia and dysarthria, loss of pain and temperature sensations on one side of the face and opposite side of the body?
Options are: A. Superior cerebellar artery. B. Posterior cerebral artery. C. Posterior inferior cerebellar artery.

2. What do you suspect when a patient has had a stroke but presents with paraplegia or quadriplegia and has loss of sensations in both affected limbs, incontinence of bowel and bladder and pain in the back and limbs with no cranial nerve involvement?
Options are: A. Spinal cord stroke. B. Brain stem stroke. C. Subcortical white matter stroke

3. Which of the following are directly related to patients who have had a subarachnoid hemorrhage? (More than one answer is possible).
Options are:
A. Nimodipine
B. Beta blockers
C. Xanthochromia of CSF
D. Endovascular coiling
E. Hypothermia

4. Which one of the following can be a cause of intracerebral hemorrhage in elderly patients?
Options are: A. Cortical vein thrombosis. B. Cerebral amyloid angiopathy. C. Cirrhosis liver.

5. In which type of stroke do we use heparin even though the stroke is associated with evidence of minor bleeding?
Options are: A. Cortical vein thrombosis. B. Cerebral amyloid angiopathy. C. Brain stem stroke

6. When will you start antihypertensive treatment in a patient with a stroke due to bleeding into the brain?
Options are:
A. When the BP is more than 220mm Hg systolic
B. When the BP is more than 200mm Hg systolic
C. When the BP is more than 180mm Hg systolic
D. When the BP is more than 160mm Hg systolic

7. Thrombolytic therapy with Alteplase (recombinant tissue type plasminogen activator) is recommended for ischemic strokes within 4.5 hours of onset. In which of the following situations will you prefer NOT to use rtPA? More than one answer is acceptable.
Options are:
A. When the patient is more than 80 years old
B. When the patient has a residual disability due to a previous stroke many years ago.
C. When the patient had suffered a stroke within the past 3 months

8. When does the cerebral edema that occurs after a cerebral hemorrhage reach its peak?
Options are: A. On the first day. B. On the fifth day. C. On the fourteenth day.

9. When patients who are on warfarin develop a cerebral hemorrhage, we give them Vitamin K and fresh frozen plasma to reduce the volume of bleeding. What can we give to reduce the volume of bleeding in patients with cerebral hemorrhage who are not on warfarin?
Options are:
A. Activated Factor VII
B. Activated Factor VIII
C. Activated Factor X

10. Dysphagia is a common problem after stroke. When is it usually appropriate to insert a nasogastric tube for feeding after a stroke?
Options are: A. After 2 hours. B. After 36 hours. C. After 72 hours.

11. Regarding recovery after a stroke, which of the following statements are correct?
Options are:
A. Proximal movements recover better than distal movements
B. Distal movements recover better than proximal movements
C. Lower limbs recover better than upper limbs
D. Upper limbs recover better than lower limbs

Compare your answers with mine

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

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