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2. (a) Read the following case report and answer the questions :                             1x5=5

A 60 years old male presented with epigastric pain radiating to back for 3 months. Weight loss for two months, dark urine and clay coulred stools for one week.

Ictrus present on investigation:

Serum bilirubin: total=12 mg/dl, Direct = 11.5 mg/dl

Indirect =0.5 mg/dl, Urine bilirubin = + ve

Serum ALT, AST and alkaline phosphatase – report awaited radiological investigations revealed presence of tumor in head of pancreas and dilated biliary canaliculi and duct.

Questions:

1. What kind of jaundice he is suffering from? Justify your diagnosis,
2. What do you understand by direct and indirect bilirubin? Where and how indirect bilirubin is converted to direct bilirubin?
3. Will bile salt be present in urine of this patient? Which test can be performed to detect the presence of bile salts in urine?
4. What will be the status of serum AST,ALT and alkaline phosphatase in this patient? Can we differentiate different types of jaundice on the basis of serum enzymes?

***

A 70 years old man presented with back pain, loss of weight and breathlessness. On examination, he was anemic.

Investigations showed:

Hb- 8 gm/dl, serum total proteins- 10.5 gm/dl, albumin – 3gm/dl, urea- 50 mg/dl, serum creatinine-2.3 mg/dl. Serum protein electrophoresis showed M band in gamma region. In urine, Bence Jones proteins were present. Radiological examination showed punched out lytic lesion in lumber vertebrae, ribs and pelvis.

1.     What is the likely diagnosis ? Name various other condition which alter A:G Ratio.

2.     What is the principle of electrophoresis?

3.     What is the normal pattern of serum proteins in electrophoresis?

4.     How are paraproteins (Myeloma proteins) different from normal immunoglobulin molecules?

5.      What are the Bence Jones proteins?  Hoe are they detected in urine?

***

A 45 years old male was admitted to hospital with severe abdominal pain. On examination-he had shock (B.P.90/60 mmHg), abdomen distended, breathing was fast and shallow (respiratory rate- 48/min). Blood investigation revealed the following report.

 

Blood parameter	Result	Reference range
pH Pco2 Bicarbonates Lactate K Na Chloride	7.05 30 mmHg 16 mmoles/l 4.5 mmoles/l 6.1 mmoles/l 140 mmoles/l 98 mmoles/l	7.35-7.45 36-46 mmHg 21-28 mmoles/l 0.4-1.4 mmoles/l 3.5-5.5 mmoles/l 135-155 mmoles/l 96-106 mmoles/l

Q.1 What is the disturbance present in this patient?

Q.2 Why Pco2 is decreased and K⁺ is increased?

Q.3 How much is the anion gap in this patients?

Q.4 What are the various causes of high anion gap acidosis  and normal anion gap acidosis?

Q.5 How pH is regulated by kidney?

***

A 17 years old boy was admitted to emergency department in unconscious state, he had frequency of micturation for six months. There was profound loss of body muscle mass. His breath was fruity in order. His random blood glucose was 150 mg/dl in his urine ketone bodies were found. After 3 days of insulin treatment his plasma glucose was 150 mg/dl. Diagnosis of diabetes mellitus with ketoacidosis was made. 

Questions:

1.     How much is the cut off value fasting plasma glucose to diagnose a person diabetic?

2.     Name the ketoacids here, those are causing acidosis?

3.     In acidosis what changes you expect in serum potassium value?

4.     Insulin is synthesized by which organ?

5.     Name one organ in which glucose entry is insulin independent?

A school going child was brought to the hospital with puffy face and oedema of lower limbs. Urine showed +++ for albumin and plasma albumin was low. His A/G ratio was reversed. The child was provisionally diagnosed as suffering from “nephrotic syndrome”  

Questions:

1.     In which organ albumin is synthesized?

2.     Why pitting oedema is associated with low blood albumin level?

3.     Name a test by which albumin is detected qualitatively in urine?

4.     Why A/G ratio is reversed in this case?

5.     What is the cut off value of serum albumin below which pitting oedema is found clinically?

***

A 3 years boy was brought to pediatric OPD by his mother with complaint of low body weight, diarrhea and difficulty of vision at night. During examination the boy was malnourished and bitot’s spots were found on eyes. Biochemical parameter reveals serum total protein 5 gm/dl(normal 6-8 gm/dl). The case was diagnosed as malnutrition with vitamin A deficiency.

Questions:

1.     Which is the earliest symptom of vitamin A deficiency?

2.     What is the possible biochemical reason of finding malnutrition and vitamin A deficiency together?

3.     Which isomer of retinal is necessary for vision?

4.     What is the role of retinoic acid in our body?

5.     Mention two good sources of vitamin A?

***

A young boy was admitted in hospital in a state of coma. On taking history from his mother, it was revealed that for several days before hospitalization he had been complaining of undue thirst and increased frequency of urination. On the day of hospitalization, he had started to vomit and had become chowsy. On examination: dehydrated, skin cold, kussmaul’s respiration, fruity odour of breath. Laboratory findings – blood sugar 540 mg/dl. Arterial blood pH =7.25, bicarbonate 5 mmole/l, urine glucose +++,ketone bodies +++

  Questions:

1. What is the diagnosis of this patient? Justify your diagnosis.

2. What is the cause of development of ketoacidosis in the patient? Patients of which type of diabetes mellitus are more prone to develop ketoacidosis and why?

3. What is the cause of increased thirst and urination in this patient? Write in brief the effect of hormones on blood glucose regulation.

4. What type of acid base disorder, this patient is suffering from? Why there is kussmaul’s respiration?

***

A young boy on returning from his school trip developed fever, nausea vomiting, generalized malaise and loss of appetite. On examination – Ictrus  present, liver slightly enlarged.

Investigations:

Serum AST=650µ/l, ALT=840µ/l, ALP=90µ/l, serum bilirubin: total =3 mg/dl, direct=0.6 mg/dl, indirect =2.4 mg/dl. Urine bilirubin-negative, Hay’s sulphur test= negative.

  Questions:

1.     What type of jaundice the boy is suffering from? What do you think is its possible cause?

2.     Justify the changes in values of biochemical test, giving their normal values?

3.     How and where is unconjugated bilirubin formed?

4.     What is the difference between direct and indirect bilirubin? 

***

A 55 years old male presented in emergency department with severe chest pain. ECG showed changes suggestive of myocardial infarction. Immediately blood sample was sent for cardiac marker enzymes. His lipid profile showed – total cholesterol = 410 mg/dl, LDL = 32 mg/dl, HDL = 38 mg/dl, Triglycerides = 200 mg/dl, VLDL = 40 mg/dl.  

Questions:

1. Is the lipid profile of this patient normal? If not, what are the desired values?
2. Which type of primary hyperlipidemia this patient is suffering from and what is the underlying biochemical defect?
3. Which serum enzyme should be estimated in this patient?
4. Give the pattern of serum enzyme changes following myocardial infarction.
5. What are the various risk factors for coronary artery disease and myocardial infarction?

***

A 3 years old boy was admitted to pediatric ward of a government hospital due to pain in abdomen. He had severe palor of skin, which prompted pediatrician to order his hemoglobin estimation in the laboratory. It was 3 gm%. Considering his tribal origin, possibility of sickle cell diseases was suspected. Laboratory was requested to test his blood for the possibility of sickle cell diseases. Patient’s hemoglobin was found insoluble in low oxygen solution. Electrophoresis showed that patient had only Hbs, while both parents had HbS and HbA.

1. Write primary structural defect in the patients hemoglobin.
2. Why the patient has anemia?
3. Why the patient hemoglobin was not soluble in low oxygen solution?
4. Why HbS move slower towards anode during electrophoresis at pH 8.6.
5. Why the patient did not suffer from anemia right from the birth?

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