1

MBBS : Stage 1A , 2005 / 06

STUDENT HANDBOOK
METABOLISM SYSTEM
Stage 2

Convenor : Dr. David Burleigh (d.e.burleigh@qmul.ac.uk )

Administrators : Robert Sprott & Kusum Roache

Part 2 MBBS Degree : Autumn Term 2010

© School of Medicine & Dentistry, QMUL, 2010

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METABOLISM 2 MODULE

STUDENT HANDBOOK

CONTENTS

SECTION PAGE

Contents ………………………………………………………………………… 2

Introduction and Overview……………………………………………………. 3

Lecture titles……………………………………………………….................... 4

Lectures objectives ....................................................................………….. 5 - 12

Clinical Demonstrations – learning objectives…......................................... 13

Learning Centre - objectives & instructions…………………………………. 14

Microanatomy –aims & objectives...........................................................… 15

PBL scenarios ………………………………………………………………. … 16 – 19

Recommended reading………………………………………………………… 20

Assessment …………………………………………………………………….. 21

Appendix 1 - Lecture handouts : …………………………………………….. 22

Kidney – functional histology……………………………………………………

Thyroid gland……………………………………………………………………..
Steroids……………………………………………………………………………
Diuretics…………………………………………………………………………..
Micturition…………………………………………………………………………

BRING THIS GUIDE TO ALL TEACHING SESSIONS

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INTRODUCTION & OVERVIEW

INTRODUCTION

The Metabolism Modules bring together elements from the Alimentary, Endocrine &
Renal systems. They also deal with aspects of biochemistry and Human Nutrition.

The Alimentary ( gastrointestinal ) system absorbs nutrients, primarily derived from

digestion of carbohydrates, proteins and fats.. Such nutrients are converted by
biochemical processes ( metabolism ) to provide the energy, growth and repair
requirements of the body. Hormones have a marked influence on such processes.
Finally waste products of metabolism, together with water and electrolytes, are excreted
by the kidneys.

OVERVIEW:

METABOLISM 1 MODULE ( YEAR 1 )

To describe how food provides nutrients through digestion and absorption and to
illustrate the links between gastro-intestinal structure and function.
To describe the metabolic processes involved in nutrient and fuel handling and cellular
energy production and utilisation.
To define and describe the function and structure of the liver and biliary system.

METABOLISM 2 MODULE ( YEAR 2 )

To consider some fundamentals of nutrition and how nutrient intake can determine
health and disease.
To further define and describe the function and structure of the liver and biliary system
in health and some common disorders.

To describe the role and sources of ‘ non-reproductive ‘ hormones and to understand

the pathophysiology of some common endocrine disorders.

To define and describe the function and structure of the kidney with particular reference
to excretory function and salt & water handling in health and some common disorders.

FOR PRACTICAL SESSIONS ATTEND AT THE TIMES ON YOUR TIMETABLE .

THIS KEEPS GROUPS TO A MANAGABLE SIZE AND ALLOWS TIME FOR
LECTURERS TO GUIDE AND INSTRUCT YOU .

LECTURE TITLES

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Week 1
1. Nutritional assessment and energy balance
2. Clinical skills ( abdomen )
3. Endocrine anatomy
4. Micronutrients
5. Malnutrition & eating disorders
6. Nutrition in medicine
7. Obesity

Week 2
8. Liver anatomy
9. Nutritional epidemiology of CHD
10. Kidney – functional histology
11. Liver disease
12. Imaging & Endoscopy
13. Renal anatomy

Week 3
14. Endocrine pancreas
15. Diabetes
16. Hypothalamus & pituitary
17. Adrenals
18. Steroids
19. Clinical skills ( thyroid )
20. Calcium

Week 4
21. Thyroid
22. Body fluid compartments and water balance
23 Renal function 1
24 Diuretics
25 Renal function 2
26 Acid / Base regulation
27 Acid / Base – Clinical concepts
28 Acid / Base workshop

Week 5
29 Advances in neuroendocrinology
30 Micturition

Formative assessment – Endocrine system

Formative assessment – Renal system

LECTURE OBJECTIVES

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Lecture 1: Nutritional assessment & Energy balance – Dr. Mark Holness

1. Define energy balance and state how energy requirements are calculated.
2. Define basal ( resting ) metabolic rate ( BMR ) .
3. Recall the thermogenic effects of physical activity and food.
4. Outline the role of uncoupling proteins.
5. Outline the special nutritional requirements of children.
6. Outline the nutritional requirements of the elderly.
7. Outline the nutritional needs of hospitalised patients

Lecture 2: Clinical skills - Dr. Adam Feather

1. The anatomical basis of the abdominal examination

2. How to gain consent to examine a person / patient’s abdomen
3. How to position a patient / person correctly prior to examining their abdomen
4. How to identify the common clinical signs that signal a patient with abdominal
disease is unwell.
5. How to systematically observe a patient from the end of the bed using the 'feet to
face' principle, identifying some common abnormalities of abdominal disease
6. How to perform a systematic examination of a patient with abdominal disease
including some peripheral and central clinical signs.
7. (and be able to demonstrate) the appropriate techniques required to perform a
holistic clinical examination of a patient with abdominal disease.
8. The associated clinical examination and investigations required to complete a clinical
assessment of a patient with abdominal disease.

Lecture 3: Endocrine & Biliary anatomy - Dr Catherine Molyneux

1. Describe the structural and functional relationships between the

hypothalamus and the pituitary gland
2. Understand the position and relations of the thyroid gland, the pancreas
and adrenal glands
3. Describe the components, course and relations of the biliary tree, and the
termination of the bile and pancreatic ducts

Lecture 4: Micronutrients – Dr. Mark Holness

1. List the principal causes of vitamin deficiencies in developed countries.

2. Give examples of the fat-soluble vitamins and describe their function within the
context of clinical features of their deficiencies.
3. Give examples of water-soluble vitamins and list the principal function common to B
vitamins.
4. Describe the clinical syndromes associated with deficiencies of the water-soluble
vitamins B1 (thiamin), B6, B12 and folate.
5. Give examples of important trace elements present in the diet within the context of
clinical features of their deficiencies.
6. Discuss the role of vitamins (and trace elements) as antioxidants.

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Lecture 5: Malnutrition and eating disorders – Dr. Mark Holness

1. Outline the prevalence and significance of protein-energy malnutrition

2. Define wasting and stunting
3. Outline the long-term effects of fasting and malnutrition on body composition and
metabolism.
4. Outline the impact of common micronutrient deficiencies on health.
5. Understand possible adverse consequences of rapid refeeding after malnutrition
6. Recall the salient features of anorexia and bulimia.

Lecture 6: Nutrition in medicine - Dr Penny Neild

1. Explain the prevalence and causes of malnutrition in UK

2. Describe how to identify those at risk of malnutrition.
3. Describe the physical and psychological consequences of undernutrition.
4. Describe the different methods of nutritional assessment
5. Outline the role of doctors and other health professionals in identification of
undernutrition and delivery of nutrition support
6. Describe briefly the ethical and medico-legal aspects of artificial nutrition support

Lecture 7: Obesity : prevalence , pathophysiology and treatment – Dr Simon

Coppack

1. Describe the prevalence of obesity in the UK and its relationship with the
population’s intake of fat and carbohydrate and trends in physical exercise.
2. Discuss the pathological and psychosocial consequences of obesity.
3. Explain the links between obesity, insulin resistance and diabetes.
4. List the treatment options for obesity.

Lecture 8 : Liver anatomy - Dr. Catherine Molyneux

tba

Lecture 9: Nutritional epidemiology of coronary heart disease – Dr Mark Holness

1. List the major risk factors for cardiovascular disease.

2. Be aware of key epidemiological studies of risk factors for cardiovascular disease.
3. Review the main dietary factors that influence the development of coronary heart
disease and hypertension.
4. Differentiate between types of lipids in relation to protection from and contribution to
cardiovascular disease.
5. Understand how salt and alcohol influence cardiovascular function.
6. Outline evidence that the risk of cardiovascular disease may be modified by
environmental influences in early life.

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Lecture 10: Structure & functions of the kidney – Dr. Greg Michael

1. Outline the general organisation of the urinary system including the kidney, ureter,
bladder and urethra.
2. Identify the parts of the nephron and describe the role of each component in the
physiologic processes involved in urine production.
3. Describe the vasculature of the kidney, relating its unique features to the physiology
of urine production and nourishment of the nephron.
4. Identify the components of the juxtaglomerular apparatus and describe its role in
regulation of blood and urine volumes and renal homeostasis.
5. Outline the structural components of the urinary passageways and bladder and
describe how micturition is controlled.

Lecture 11: Liver disease– Professor Parveen Kumar

1. To identify the important cause of chronic liver disease.

2. To appreciate the difference between liver failure, portal hypertension and cirrhosis.
3. To understand the different effects of alcohol on the liver.
4. To appreciate the importance of hepatotrophic viruses as a cause of chronic liver
disease and to understand the natural history of hepatitis B and C.
5. To recognise the features of biliary tract obstruction.

Lecture 12: Imaging & endoscopy – Professor Chris Fowler & Dr Andrea Rockall

1. Define endoscopy
2. Outline requirements for a successful endoscopic system
3. Give examples of the use of endoscopy in diagnosis and therapy

Lecture13: Renal & urinary anatomy – Dr. Catherine Molyneux

1. Describe the gross anatomy of the urinary system and relations of kidneys and
adrenal glands;
2. Understand the blood supply to the kidneys and adrenals and the
distribution of the arteries within the kidney
3. Describe the course of the ureters and the position and relations of the urinary
bladder in both sexes.
4. Discuss the structure, position and importance of urinary sphincter muscles

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Lcture14: Endocrine functions of the pancreas – Professor Mary Sugden

1. Describe the structure of the pancreatic islet of Langerhans; list the major cell types
and the hormones that they secrete.
2. Describe the main structural features of the insulin molecule.
3. Outline how insulin secretion is regulated.
4. List the major metabolic actions of insulin on glucose and lipid metabolism in the
postprandial state. 
5. Describe the actions of glucagon on glucose and lipid metabolism in the post
absorptive and fasting states.
6. Define the terms glucose tolerance and insulin resistance in relation to type 1 and
type 2 diabetes mellitus 
7. Summarise the effects of inadequate insulin secretion or action upon carbohydrate
and fat metabolism, including the etiology of diabetic ketoacidosis.

Lecture 15: Diabetes Mellitus – Professor Mary Sugden

1. Outline the potential abnormalities of glucose homeostasis in diabetes.
2. Outline the influence of the liver on circulating insulin levels.
3. Describe the principal forms of diabetes mellitus.
4. Outline the changes in glucose and insulin during an oral glucose tolerance test in
normal and diabetic subjects.
5. Describe the acute effects of insulin deficiency or glucagon excess.
6. Outline the consequences of ketoacidosis
7. List the long-term complications of diabetes mellitus.
8. Outline the macrovascular complications of diabetes mellitus.

Lecture 16: Hypothalamus and pituitary – Professor Joy Hinson

1. Describe the structure and origins of the pituitary gland and explain the relationship
between the hypothalamus and both the anterior and posterior pituitary.
2. List the hormones secreted by both the anterior and posterior pituitary and in each
case explain the role of the hypothalamus in regulating their secretion.
3. Use the concept of negative feedback to explain the principles underlying clinical
tests for pituitary hormone secretion.
4. Briefly outline the actions of the hormones of the posterior and anterior pituitary.

Lecture 17: Adrenals - Professor Joy Hinson

1. Describe the structure of the adrenal gland and relate the zones to production of
hormones.
2. Describe the regulation of hormone secretion by each zone
3. Describe the physiological actions of the adrenal hormones
4. Explain the effects of both excess and deficiency of adrenal hormones

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Lecture 18: Steroids – Dr. David Burleigh

1. Describe the mechanisms of action contributing to anti-inflammatory and

immunosuppressive effects of corticosteroids.
2. Clinical uses of corticosteroids.
3. Explain how long-term corticosteroid therapy disrupts endogenous corticosteroid
secretion
4. Describe other unwanted effects arising from long-term therapy with glucocorticoids.
5. List some synthetic steroids with mainly glucocorticoid activity. Explain the reason
for the development of such compounds.

Lecture 19 : Clinical skills ( thyroid ) Dr Nigel Yeatman

tba
Lecture 20: Calcium – Professor Joy Hinson

1. Explain the relationship between the various forms of circulating calcium in blood.
2. Recognise the structure of vitamin D 3 and describe the sources of this vitamin in the
body.
3. Describe the transformation of vitamin D 3 into an active hormone and explain how
this is regulated.
4. Describe the source of parathyroid hormone and explain how its secretion is
regulated.
5. Describe the actions of parathyroid hormone and 1,25-dihydroxyvitamin D 3 and
account for the effects of vitamin D3 deficiency, and for hypo- and hyper-secretion of
parathyroid hormone.
6. Outline the source and actions of calcitonin and explain its role in calcium
metabolism.
7. Briefly explain how the body excretes excess calcium.
8. Briefly explain the relationship between calcium and phosphate metabolism.

Lecture 21 : Thyroid – Dr. David Burleigh

1. Outline the synthesis, storage and release of thyroid hormones

2. Describe the effects of thyroid stimulating hormone on the thyroid gland
3. Outline the actions of thyroid hormones
4. Briefly explain the pathophysiology of hypo- and hyperthyroidism.
5. List the effects of excess and deficiency of thyroid hormones
6. Describe the detection and treatment of hyperthyroidism and hypothyroidism

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Lecture 22: Body fluid compartments and water balance – Dr Gurdip Hunjan
1. Distinguish between the terms ‘osmolarity’ and ‘osmolality’ and between the terms
‘isosmotic’ and ‘isotonic’. State a normal value for plasma osmolality.
2. Name the main fluid compartments of the body, commenting on their volumes and
predominant cations.
3. Explain how total body water and total body sodium are regulated by mechanisms
that are sensitive to plasma volume and plasma osmolality.
4. Quantify the factors that contribute to the water balance of the body.
5. By means of labelled diagrams, show the changes in volume and osmolality of
tubular fluid along the length of the nephron, in the presence or absence of anti-
diuretic hormone (ADH).
6. Explain how the thick-walled, ascending limb of the loop of Henle plays a key role (in
conjunction with ADH) in the production of either dilute or concentrated urine to meet
the requirements of water balance.
7. State the source, nature and mechanisms of release of ADH. Describe the stimuli
for the release of ADH and explain how ADH controls urine volume and osmolality.
8. Distinguish between the terms ‘water diuresis’, ‘osmotic diuresis’, ‘diabetes insipidus’
and ‘diabetes mellitus’. State typical values (and normal ranges) for the osmolality
and of urine and daily urine production.

Lectures 23 & 25 : Renal function – Dr. Gurdip Hunjan

1. Describe, and quantify, the forces acting in the glomerular capillary and in the fluid of
Bowman's capsule which are responsible for the production of glomerular filtrate.
2. Show, graphically, the effects of molecular size and charge on the composition of
glomerular filtrate.
3. Explain the ‘clearance concept’ and how this is used to measure glomerular filtration
rate (GFR). State the properties of suitable marker substances and show how
clearance, and hence GFR, are calculated. State normal values for the GFR.
4. Briefly describe the autoregulation of GFR under normal circumstances and the
significance of a reduced GFR.
5. Define the terms: filtration;reabsorption;secretion;excretion, as applied to the kidney.
6. Outline renal handling of important electrolytes.
7. Compare the reabsorption of sodium, glucose, amino acids and hydrogen carbonate
in the proximal tubule of the nephron.
8. Comment briefly on differences in sodium reabsorption in the proximal tubule, the
thick-walled, ascending limb of the loop of Henle and the distal tubule, noting the
significance of sodium reabsorption in these regions.
9. Explain the action of the counter-current exchange multiplier, in generating a
concentration gradient.
10. By reference to the renal reabsorption of glucose,define the terms:‘renal threshold’
and‘transport maximum’. What may be the effects of glucose presence in the final
urine?

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Lecture 24: Diuretics – Dr. David Burleigh

1. Show, by means of a labelled diagram, the proportions of sodium reabsorbed from

tubular fluid in: the proximal tubule; the loop of Henle; the distal tubule; the
collecting duct.
2. Compare the different mechanisms for sodium reabsorption found in different parts
of the nephron.
3. Describe the actions of aldosterone on the distal tubule and collecting duct which
maintain the sodium balance of the body. State the fraction of the total sodium
reabsorption which is subject to regulation by aldosterone.
4. List the major clinical indications of the uses of a diuretic.
5. Give the primary sites of action of thiazide, loop diuretics, and spironolactone, and
rank them in order of their efficacy.
6. Explain why diuretics increase potassium excretion, and how this may be reduced.
7. Explain the use of mannitol as a ‘diuretic ‘.

Lecture 26: Acid / Base regulation – Dr Gurdip Hunjan

1. Define ‘pH’ and state the normal range for arterial pH and the range compatible with
life. Comment on the differences between normal arterial and mixed venous pH
values.
2. List the sources of bodily acid and comment on the ways in which acid is removed
from the body, noting the relative importance of lungs and kidneys.
3. List the principal buffer systems in plasma, extra- and intra-cellular fluid and bone.
4. State the Henderson-Hasselbalch equation for the hydrogen carbonate / carbonic
acid buffer system and give normal values for each component. Explain why the
hydrogen carbonate / carbonic acid buffer system is important.
5. In terms of the ratio of base to acid and of absolute values of base and acid, explain
the processes of buffering, compensation and correction in acid-base disturbance.
6. Define the terms ‘acidosis’, ‘alkalosis’, ‘acidaemia’ and ‘alkalaemia’. Outline how a
sample of arterial blood may be used to determine the acid-base status of a patient.
7. Outline the role of hydrogen carbonate, phosphate and ammonium ions in the renal
excretion of acid, noting the relationship between tubular pCO 2, hydrogen carbonate
reabsorption and proton excretion.
8. Name the FOUR simple classes of acid-base disturbance, stating the primary
disturbance and the form of compensation for each class. Comment on the time
scale for renal as compared with respiratory compensation and give ONE clinical
cause for each class of disturbance.

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Lecture 27: Acid / Base , Clinical aspects – Pofessor Alistair Chesser

1. To know the methods available for the assessment of acid-base balance in patients.
2. To understand the pathogenesis and common causes of: a) respiratory acidosis,
b) respiratory alkalosis, c) metabolic acidosis,d) metabolic alkalosis
3. To recognise the biochemical changes associated with the above disorders and how
the body attempts to compensate.

Lecture 28 : Acid / Base workshop – Dr Gurdip Hunjan

Revision session on principles

Lecture 29 : Advances in neuroendocrinology - Professor Ashley Grossman

1.To understand the position and function of the pituitary.

2.To relate anatomy to specific tumoral secretory syndromes.
3.To understand the rationale and mode of action of somatostatin analogues in
acromegaly.
4.To understand the genetic basis of familial acromegaly.
5.To be able to relate diagnostic tests for Cushing's disease to normal
physiology.
6.To see the role of different therapeutic interventions in Cushing's
disease and their rationale.

Lecture 30 : Micturition – Dr David Burleigh

1. Describe the anatomy of the bladder, prostate and urethra.
2. Describe the reservoir and emptying functions of the bladder and outline the
neurological control of each.
3. Distinguish between urge incontinence, stress incontinence, overflow incontinence
and leak incontinence.
4. Explain the most common causes for each of the above.
5. Outline the investigations available to distinguish the cause of incontinence in an
individual.
6. Describe treatments available for disorders of micturition.

Formative Assessment : Endocrine system – Professor Joy Hinson

Formative Assessment : Renal system – Dr Gurdip Hunjan

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CLINICAL DEMONSTRATIONS

Clinical Demonstration 1: Nutrition & diet ( Mr Rhys White )

Clinical Demonstration 2: Obesity ( Dr Simon Coppack )

1. Discuss the important problems in obtaining a reliable nutritional history from obese
patients.
2. Enumerate the clinical signs which are relevant to the aetiology or complications of
obesity
3. Describe the physical, psychological social and emotional problems which may
confront obese patients.
4. Discuss the possible approaches to the treatment of obesity.

Clinical Demonstration 3: Liver Disease ( Professor Parveen Kumar )

Clinical Demonstration 4 : Type 1 diabetes ( IDDM ) ( Dr Simon Coppack )

Clinical Demonstration 5 :Acromegaly ( Professor Shern Chew)

1. Anatomical relations of the pituitary gland and the surgical anatomy of a pituitary
mass
2. Effect of a pituitary mass on normal pituitary physiology.
3. Physiology of the growth hormone axis and the pathophysiology of over-secretion
of growth hormone.
4. Origin and natural history of pituitary adenomas.
5. Signs and symptoms of acromegaly (consequences of growth hormone over-
secretion).
6. Principles of diagnostic endocrine and radiological tests.
7. Principles, benefits and risks of medical, surgical and radiotherapy treatments.
8. Social and emotional impact of pituitary disease.

Clinical demonstration 6 : Renal dialysis ( Dr Raj Thuraisingham )

1. Understand the principles and practical aspects of peritoneal dialysis in its many
forms.
2. Be aware of the limitations, advantages and disadvantages of peritoneal dialysis.
3. Understand the principles and practical aspects of haemodialysis.
4. Be aware of the limitations, advantages and disadvantages of haaemodialysis.

Clinical demonstration 7 : Renal transplantation ( Dr Raj Thuraisingham )

1. Describe the basic principles of tissue typing and lymphocytotoxic cross matching.
2. Be aware of the prognosis, advantages and disadvantages of transplantation.
3. Describe the complications associated with antirejection therapy.

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LEARNING CENTRE OBJECTIVES - Dr Catherine Molyneux

Urinary System
1. List the components of the urinary system.
2. Describe the position and relations of the kidneys.
3. Describe the blood supply to the kidneys and recognise on CT/MRI.
4. Describe the structure of the kidney.
5. Describe the course of the ureters.
6. Describe the anatomical relationships of the urinary bladder in both genders.
7. Describe the course of the urethra in both genders.
8. Demonstrate the anatomy of kidneys, ureters and bladder using radiological
imaging – CT MRI and IV pyelograms.
.

Endocrine System
1. Describe the position and anatomical relationships of the thyroid gland.
2. Describe the blood supply to the thyroid gland.
3. Describe the position and anatomical relationships of the pituitary gland
4. Understand the cavernous sinus and its contents
5. Describe the position and anatomical relationships of the pancreas.
6. Compare the position and anatomical relationships of the suprarenal glands.

Liver and biliary tract

1. Describe the components, course and relations of the biliary tree (tract).
2. Describe the termination of the bile duct and pancreatic duct.
3. Revise the normal structure and blood supply of the liver.
4. Describe some important pathologies of the liver.

LEARNING CENTRE SESSIONS

 YOU MUST BRING A WHITE COAT AND YOUR STUDENT GUIDE

 THE SESSIONS WILL START PROMPTLY AT THE TIMES INDICATED

 ACCESS TO THE LEARNING CENTRE IS BY ID CARD

 YOU WILL NEED TO REVISIT THE LEARNING CENTRE, IN YOUR OWN TIME,
FOR REVISION PURPOSES.

 YOU MUST ATTEND THE CORRECT TIMETABLED SESSION AND NOT JOIN
IN WITH ANOTHER GROUP. YOU MUST WEAR THE CORRECT COLOUR -
CODED BADGE . CHECKS WILL BE MADE TO ENFORCE THIS REQUEST.

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MICROANATOMY : Aims & objectives Dr. Greg Michael & Dr Cathy Baker

Whereas during Metabolism Stage 1 sessions in microanatomy and histopathology

dealt exclusively with the basic structure of the alimentary tract. Stage 2 will focus on
three areas not yet covered in depth: the urinary and endocrine systems and the liver.
These will be covered through short introductory descriptions accompanied by
explanatory diagrams and photomicrographs. Students should be able to identify
important features in the photomicrographs. In addition, case histories covering specific
disorders affecting each of these organs or systems will be presented. Skills of visual
recognition of pathological features as well as understanding of underlying disease
processes should be developed and may be examined in practical and written
assessments.

Objectives:

The Urinary System

1. Describe the basic structural organisation of the kidney, including its vasculature.
2. Describe the structure of the nephron.
3. Relate the structure of the glomerulus to its role in the filtration of blood.
4. List the causes of impaired glomerular filtration and the clinical consequences of this.
5. Describe the structure and microanatomy of the urinary tract, including the bladder.
6. Discuss the pathology of mass lesions of the urinary tract.

The Endocrine System

1. Describe the general organisation of endocrine tissues in the pituitary gland, thyroid
and parathyroid glands, adrenal gland and Islets of Langerhans of the pancreas.
2. Recognise and name the cell types found in these endocrine tissues.
3. Describe the blood supply to the pituitary gland and its relevance to anterior pituitary
function.
4. Describe the blood supply to the adrenal gland and the functional relationship
between the adrenal medulla and the nervous system.
5. Recognise and describe specific disease processes that affect the glands of the
endocrine system.

The Liver

1. Describe the architecture and blood supply of the liver.

2. Recognise and name the cell types found in normal liver.
3. Recognise and describe specific disease processes that affect the liver.
4. Understand how liver disease affects the function of the liver and/or other systems.

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PBL scenarios

PBL 1 - Malnutrition and metabolism

You are finishing an elective at a refugee camp run by a charity on the border of Sudathopia, a
sub-Saharan country which has suffered repeated famines. The harvest this year has been the
worst for 10 years. New residents come into the camp every day, all seriously thin and some on
the verge of dying ‘of malnutrition’, according to the resident camp doctor. Infants are especially
suffering, presenting with Marasmus or Kwashiorkor. In the UK you have seen lots of patients
who have been slimming for various reasons, and you have done an SSC on the Atkins Diet.
A new elective student (from St Elsewhere’s Medical School) arrives at the camp complaining
of the awful teaching he has received on these topics. He does not understand the key role of the
liver in maintaining glucose levels, and its ability to generate alternative energy supplies from
fats that the brain can adapt to use. He wonders if the people in the camp have the
same metabolism as people who go on diets for cosmetic purposes. When he learns that you are
from Barts and The London, he realises that you will be able to explain the metabolic changes in
these different situations.
 
PBL 2 –An overweight office worker
A 34-year old man visits his family GP, as he is worried about his increasing weight gain and
reports in the press linking obesity to Type 2 diabetes. The patient has gained 10 kg since
suffering a sports injury two years ago, and is now finding routine activities, such as climbing
stairs, difficult. He was active in competitive sports while at college and after, but did not
continue with organised sporting activity since injuring his knee. He works in a telephone call
centre and spends most of his time sitting at a desk. He has to put in a lot of overtime to make
ends meet, and admits to having a poor diet while working (containing a lot of saturated & trans
fats, simple sugars and salt).
Examination shows he has a blood pressure of 130 / 85, a weight of 87kg, height 1.7 m and
waistline measurement of 105cm. Laboratory analysis of a fasting blood sample subsequently
provided the following values (maximum target levels shown in brackets, except for HDL
cholesterol where minimum value shown):
Fasting blood glucose 5.9 mmol/L ( < 5.5 mmol /L )
Cholesterol 6.0 mmol/L ( < 5.2 mmol/L )
Triglycerides 2.0 mmol/L ( < 1.7 mmol/L for ♂ )
HDL cholesterol 0.95 mmol/L ( >1.03 mmol/L for ♂ )
As he left the surgery, the doctor reflected on the obesity epidemic and its causes. He
considered what existing treatments were available and wondered why reported future potential
therapeutic approaches aimed at suppressing appetite had not become clinically available.

PBL 3 –The alcoholic publican

A 44 year old publican was seen in the Accident and Emergency Department with a 2- week
history of feeling unwell and vomiting. Over the last four weeks his abdomen had become
swollen. He also had a tremor which resulted in spilling the customers’ drinks. He admitted to
drinking 1–2 bottles of whisky per day. On examination, his breath smelt of alcohol and his
speech was slurred. He looked jaundiced and his clothes had evidence of vomiting. There were
spider naevi on his neck and upper chest/back, and his breasts were slightly swollen.

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His palms were red over the thenar and hypothenar eminences, and the palmar fascia was
thickened. It was difficult to palpate his abdomen, but there was an enlarged spleen and liver.
The abdomen was dull to percussion, especially in the flanks, and 'shifting dullness' could be
elicited when he rolled onto his side. He had pitting oedema of his legs.
He had blood taken for full blood count, liver function tests and liver biochemistry:
Haemoglobin (Hb) 12 g/dl (normal 14-17.7 g/dl for males)
Mean corpuscular volume (MCV) 108 fl (normal 80-96 fl)
White cell count 3.8 x 109 /L (normal 4.5 – 10.5 x 109 /L)
Platelets 90 x 109 /L (normal 150 – 350 x 109 / L)
Liver function:
INR (prothrombin ratio) 1.6 (normal ~ 1 )
Albumin 25 g/L (normal 36-53 g/L)
Liver biochemistry:
Bilirubin 56 µmol/L (normal < 17 µmol/L)
Alkaline phosphatase (ALP) 200 Units/L (normal 25-110 U/L)
Aspartate aminotransferase (AST) 95 Units/L (normal 7-40 U/L)
Alanine aminotransferase (ALT) 100 Units/L (normal 5-40 U/L)
-Glutamyl transpeptidase (GGT) 120 Units/L (normal 11-50 U/L)
He was admitted and an i.v. infusion of glucose-saline established. He was given intravenous
thiamine. After a diagnostic tap of the ascites, he was managed with diuretics and weighed
daily. On admission his weight was 72kg [height 1.78m], and by the time of discharge after
successful treatment, his weight was 58kg, giving a BMI change from 23 to 18.

PBL 4 - Understanding your illness

Miss KP was a 24-year-old hospital cleaner with diabetes mellitus, which she had developed at
the age of 18. Her usual treatment was Actrapid insulin, 8 units 3 times daily 30 minutes before
meals, and Actraphane insulin, 16 units at bedtime. On the day of admission to hospital she had
presented to the A & E department with a three- day history of dysuria, loin pain and feeling
feverish. She felt unwell, had lost her appetite, and because she was not eating she had not taken
any insulin for 24 hours.
In A & E the casualty officer noted that she was disorientated in time and space, she had
Kussmaul’s respiration and he could smell ketones on her breath. He diagnosed a urinary tract
infection and arranged some blood tests and a dipstix urine test, which showed:
Plasma:
glucose 28 mmol/l (normal fasting 3.9 to 6.1)
Na+ 145 mmol/l (normal range 136 to 146)
K+ 3.4 mmol/l (normal range 3.5 to 5.1)

Urine: Ketones ++++ Blood ++ Protein ++

Arterial blood:
pH 7.1 (normal range 7.38 to 7.42 )
HCO3- 8.0 mmol/L (normal range 22-29)
pO2 13.0 kPa (normal range 10 to 13.4)
pCO2 3.6 kPa (normal range 5 to 5.5)

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She remained in hospital for 5 days receiving treatment, which included monitoring of
potassium levels as well as re-hydration and insulin administration. Although she usually
attended the Diabetic Clinic regularly, prior to discharge from hospital she had a further
education session with the diabetes specialist nurses.

PBL 5 - Abrupt withdrawal of steroid therapy

Mr A.B., a 38-year old divorced warehouse manager, has suffered from severe asthma since
childhood. He has been taking prednisolone, 30 mg orally daily for the last 18 months. His
sister was alarmed when, during a weekend visit, he told her that he had become worried after
reading about the side-effects of steroids, and had stopped taking the prednisolone tablets 1 week
previously. Ten days later he called her from home to say he felt very unwell. She went round
to his flat to visit him and immediately called in the GP. On arrival, the GP found Mr A.B. to be
pale, disorientated and suffering from nausea and vomiting. Pulse was 120 /min, blood pressure
was 80 / 40 lying and unrecordable on standing. An ambulance was called and Mr A.B. rushed
to the nearest A & E department. On arrival, blood was taken and the following plasma
concentrations of urea and electrolytes (U&Es) obtained:

Na+ 135 mmol/l (normal range 136 to 146 mmol/l)

K+ 5.2 mmol/l, (normal range 3.5 to 5.1 mmol/l)
Urea 12.2.mmol/l (normal range 2.5 to 6.4 mmol/l)
The next morning, blood was taken at 8am and the following values obtained:
Cortisol <50 nmol/l (normal range 150-650),
Adrenocorticotropin (ACTH) <2 ng/l (normal range 10-80)

Mr A.B. was treated with intravenous fluids and steroids, and made a rapid recovery. Before
discharge the side-effects of steroids were discussed, and Mr A.B. was counselled about the
dangers of stopping steroids abruptly.

PBL 6 – A swelling in the neck

Mrs Patel, a 38-year old schoolteacher, went to see her doctor because she was worried about a
swelling in her neck. It had been present since she was a child growing up in Africa, but had
changed over the previous few months, becoming very tender. Mrs Patel described how she had
been feeling very down and miserable recently. She felt that she had much less energy than
normal and always seemed to feel cold. It was a warm day when Mrs Patel went to see the
doctor, but she was wearing a thick sweater and warm boots. Mrs Patel had gained weight since
she last saw her doctor, although she told the GP that she had very little appetite and wasn’t
enjoying food as she used to.
She was worried that the swelling in her neck was cancer and that she was going to die. She
was also worried that she would lose her job because she didn’t have the energy for teaching.
The GP took a blood sample for an endocrine test. The following result was obtained:
TSH 92 mU/L (normal 0.4 to 5 mU/L)
On the basis of this result the GP reassured Mrs Patel that the swelling in her neck was not
cancer and that she was not likely to die from it. The GP started Mrs Patel on 50g thyroxine per
day and she was stabilised on g/day.
Within a month Mrs Patel was feeling much better, and after three months was back to her ‘old
self’, full of energy, back to her usual weight and enjoying life again.

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PBL 7 – A gymnastic mishap

An 18-year old female gymnast completely misjudged her manoeuvre on the uneven
(asymmetric) bars. As a consequence she received a sharp, heavy blow to her left upper
abdomen. Severely winded, she managed to reach the changing room, but after 30 minutes
became light-headed, confused, and reported difficulty in seeing properly. She then fainted, and
her concerned trainer drove her straight to the Accident and Emergency department.
On examination, she is pale, sweaty and shocked. The abdominal muscles feel rigid. Blood
pressure was recorded at 75 / 45, and pulse was 130 beats per minute. Investigations showed the
following:
Hb 9.6g/dL (normal 11.5 - 16 g/dL, ♀ )
serum urea 21 mmol/L (normal 2.5 – 6.5 mmol/L)
serum creatinine 153 µmol/L ( normal 60 – 110 µmol/L)
Urine analysis:
sodium < 10 mmol/L (normal 60 – 80 mmol/L)
blood - negative
protein - negative
Ultrasound of kidney was normal

In A & E, blood was sent for grouping and cross-matching. She was given plasma expanders
intravenously. Her blood pressure remained low, she had an emergency laparotomy, and a
ruptured spleen was removed. She passed only 100ml of urine during the operation and 100ml
more during the first four hours post-operatively. During this period she was also transfused 4
units of blood, and gradually over the next 8 hours started passing more urine. 24 hours after her
initial presentation, she was passing 100ml/hour; her serum urea was 7.2 mmol/l and serum
creatinine 78 µmol/l.
A detailed knowledge of anatomy & physiology of the spleen is not required for this PBL.

PBL 8 - The sugary kidney

A 72-year old man is referred to a renal clinic by his general practitioner because, on a
screening visit to the practice, he has protein found in his urine. He was diagnosed with type 2
diabetes 9 years previously, when he suffered with excessive thirst and was found to have
glycosuria. He attends regular appointments at an ophthalmology clinic for poor vision, and says
he has had laser treatment to his retina for diabetic complications.
Investigations provided by his GP indicate a serum creatinine of 132 mol/L (normal range 60-
110), giving him an estimated GFR (eGFR) of 49 ml/min using the MDRD (Modification of Diet
and Renal Disease study) formula; and his urine albumin : creatinine ratio (ACR) is 342. His
blood pressure in clinic is 172 / 93.
The consultant in clinic suggests carrying out a 24-hour urine collection to further document his
renal function and protein losses. She tells the patient that he has diabetic nephropathy, and that
his management will consist of good control of blood pressure and glycaemia.

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RECOMMENDED READING

Human Anatomy and Physiology.

Marieb and Hoehn [8th Ed. 2010 ]

Wheater’s Functional Histology.

Young et al [ 5th Ed. 2006 ]

Rang & Dale’s Pharmacology.

Rang et al [ 6th Ed. 2007 ]

Textbook of Medical Physiology.

Guyton and Hall [ 11th Ed. 2006 ]

Clinical Medicine.
Kumar and Clark [7th Ed. 2009 ]

Medical Sciences
Naish, Revest & Syndercombe Court [ 1st Ed. 2009]

Nutrition

Useful information can be found in :

Clinical Medicine , Kumar & Clark ; Chapt 5 – Nutrition.

Medical biochemistry , Baynes & Dominiczak ; Chapt 10 – Vitamins, minerals and nutrition.

Metabolism System Pt2: 2010 Student Handbook © School of Medicine & Dentistry, QMUL, 2010
 21

ASSESSMENT

1. PBL assessment
There will be two components of PBL assessment: write-up of a PBL, and attendance at
PBL tutorials.
You are required to undertake a worked write-up of one PBL from EITHER this module
OR the Cardiorespiratory module. The write-up title will be allocated to you by the PBL
tutor in the Metabolism module on Thursday 18 th November and must be submitted to
the same tutor on Thursday 25th November.
Late submissions will be penalized .

Write-up of a PBL The write-up should be between 1500 (min.) and 2000 (max.)
words, typed and using diagrams and tabulations where appropriate. This will be graded
taking the following into account:

Learning objectives: all stated and addressed.

Presentation: understandable, clarity of explanation, IT skills (word-processing,
diagrams, tables, layout).
Content: relevance and focus of content.
Resources: the range, relevance, suitability and format of listed resources used (and
correctly cited).

ALL PBL WRITE-UPS MUST BE SUBMITTED TO THE ‘TURNITIN’ SERVICE FOR

PLAGIARISM. IF THE WRITE-UP IS NOT SUBMITTED IN THIS WAY, A ZERO
MARK WILL BE ASSIGNED.

Attendance You are expected to attend all the PBL sessions. If you miss sessions,
you lose marks. If for whatever reason you cannot attend a PBL tutorial, your tutor will
expect you to give a reason, complete the relevant form and catch up with up the work
done by the rest of the group.

2. In-Course Assessment
There will be an In-Course Assessment exam based on the Cardiorespiratory and
Metabolism modules. This will be a single examination of 2½ hours’ duration held at
the end of the Metabolism System module. It will consist of short-answer questions and
extended-matching questions. There will also be a ‘Spotter’ examination.
The date of the examination is Friday 3rd December 2010. More details will be given
nearer the time.

3. Formative short-answer questions

In most PBL tutorials you will answer a 10 min SAQ , under exam conditions, based on
the previous PBL completed. Marks awarded and feedback given are for you to gauge
your knowledge and understanding of that PBL. The marks do not count towards the
Paper A total, ie it is a formative assessment .

Metabolism System Pt2: 2010 Student Handbook © School of Medicine & Dentistry, QMUL, 2010
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Metabolism System Pt2: 2010 Student Handbook © School of Medicine & Dentistry, QMUL, 2010