Year 6 Clerkship - Welcome & Curriculum Class 2020 (Revised 25.04.2019)

THE UNIVERSITY OF THE WEST INDIES
FACULTY OF MEDICAL SCIENCES

DEPARTMENT OF CLINICAL MEDICAL SCIENCES
Welcome Class of 2020

MB BS Internal Medicine Year 5
This is ONE unit of the MB.BS Medicine Program
MB.BS Medicine Course Code: MEDC 5300
Our Motto is: All for the patient
Tell me………I forget

Teach me ……I remember
Involve me....…I learn
- Benjamin Franklin
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Adult Medicine Unit / UWI & Dept. Medicine / POSGH
Contents:
● Welcome and Objectives of Clerkship 3
● Ward Work 4
● Your assessment 8
● Core Curriculum 9
● Structure of Training 11
●Medical Emergencies 12
●Phlebotomy Procedure - Venipuncture 13

● Radiology 14
● Pathology-In-Medicine 15
10. Student Lead Ward Rounds 16

11. The Case Historyin Medicine 17
12. Procedures in Medicine 18

Recording a Procedure in the medicalnotes 19
Report Writing – A communication skill 21
Guidelines in writing a prescription 22
Appendix:
Detailed Curricula:
I. Post-Exposure Prophylaxis
II. Procedures Following Exposure
III. Dermatology
IV. HIV
V. Pulmonology
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WELCOME TO FINAL YEAR INTERNAL (ADULT) MEDICINE
It is hoped that your relatively short time in final year medicine will be a useful learning
experience and that you will obtain a good grounding in internal medicine.
This is a busy clerkship and the volume of work can at times be overwhelming. Do not
hesitate to seek advice should you be unsure about any aspect of patient management or if
you have any personal problems that may preclude a good performance in this clerkship.
WE ARE INTERESTED IN YOU and we want YOU TO BE the best doctor that you can
be.
Adult Medicine Unit

The Adult Medicine Unit is one of 4 units in the Department of Clinical Medical Sciences.
The full time members of the unit are:

Professor S. Teelucksingh, Professor of Medicine
Dr. R. Ali, Lecturer in Medicine, DM Adult Medicine Coordinator & Head of the Unit
Dr. S. Sakhamuri, Lecturer in Medicine Year 4 coordinator
Dr. Sherry Sandy, Lecturer in Medicine, Year 5 coordinator
Dr. Naveen Seecharan, Lecturer in Medicine
Dr. Stanley Giddings, Lecturer in Medicine
Dr. Anil Ramlakhansingh, Lecturer in Medicine
There are several associate lecturers in the various hospitals and their names are included in
the abbreviated curriculum for year 4 and year 5.
CONTACTS
Year 5
Secretary: Ms. Heather-Joy Stephen
Office (POSGH) direct line 623 4030, 623 2951 Ext 2585
FAX 627-5184
Year 4
Secretary: Ms. Janelle Timothy
Office (EWMSC) Phone/Fax 663 4332 or 645 2640 ext 2926
EMAIL : Adult Medicine Unit, EWMSC
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THE OBJECTIVES OF THE MEDICINE CLERKSHIPS
1. To develop the skills of history taking and examination of all systems in the adult.
2. To participate in and learn from a multi-disciplinary approach to patient care.
3. To recognize and respond to the needs of your patients: - medical, social and
psychological.
4. To learn and demonstrate efficient and thorough medical documentation.
5. To demonstrate knowledge of patients’ rights and understand the basic tenets of
medical jurisprudence.
6. To communicate effectively with colleagues, patients and relatives.
In brief, we teach through service AND you learn through service. At the end
of the FINAL CLERKSHIP the student should have the proficiency level of an
intern.
Here are some guidelines which you will find useful.
WARD WORK
1. Working conditions: The focus in year 5 is on an apprenticeship system
● We consider that it is your privilege to see our patients and our honor to have you
on our unit. This final year is an apprenticeship year, use it wisely.
● At least one student to each ward (male/female) for each medical unit.
● Daily rounds with the unit doctors.
● You are to be punctual in reporting to your respective ward at the start of each day
and remain available from 0800 to 1600 hours.
● The unit must be covered from 0800 to 1600 hours on weekdays and on post call
days including weekends
● Units run best when they operate as a team. If you complete your ward work early
then you are expected to help out on the other ward.
● At the start of each day you should ascertain from the nurse in charge of the ward
whether there are any patients on outlying wards.
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● On call:
o Students to remain with the on call unit until 8.00 PM.
o you are expected to clerk patients per on call
o where possible, you should choose patients with differing conditions
o On the post call ward round and including weekends where you are on call
or posstcall, you are expected to remain with your unit until completion of
jobs.
● Absence from work: you are expected to call the consultant, registrar, co-ordinator
and the clerkship secretary well in advance if you are unable to turn up to work on
any one day. You must then provide an explanation in writing stating the days taken
off work on the first day of your return to work and leave this in the academic
office. Failure to follow this guideline may result a clerkship grade of “F” or other
similar penalty.
● Absence from any examination: According to University Regulations, if you are
absent for an examination component, you must have your sick leave validated by
the Health office in Main Campus. Failure to do so will result in your absence
counting as failed opportunity of the examination.
2. Clinical responsibilities:
● You are not allowed to document in patients’ notes as this is not medico-legally
acceptable.
● Clerking of Admissions: You are expected to clerk patients on call in accordance
with your training and as shown in the case history books: ALL SYSTEMS MUST
BE EXAMINED FOR EACH ADMISSION (General condition, skin, chest, CVS,
ABD, CNS).
● Students must submit 10 case histories (5 from each hospital) which are assessed by
a Lecturer, Consultant, Registrar or a DM resident in Medicine Department or
Medicine units. One of the case histories must be presented to a designated full-
time lecturer, which will be weighted high (25% of all case histories) than the
remaining.
o Reflexes must be recorded in the case notes as follows:
B T S K A Pl
RHS
LHS
- = no reflex, + = hyporeflexive
++ = normal, +++ = hyperreflexive
↑, →, ↓ = for the plantar responses
● Post call ward rounds supersede teaching sessions.

● All blood results must be retrieved before the ward rounds, signed and filed in the
notes and appropriate action taken.
● Blood results must be checked before you leave for the day
● Drug charts must be checked every day and if patients are not receiving their
medication, the reason must be ascertained
● Regular prescriptions must be written for patients so that their drugs will be
obtained from the hospital pharmacy in a timely manner
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● Please take time to document adequately.
● Follow up note-keeping for in-patients: Follow-up notes should be recorded using
the problem-based format:
Problem List: the problem list is dynamic and may be changed as new
information arises
S (subjective i.e. symptoms)
O (objective i.e. signs; pathology results, radiology results)
A (your assessment of progress and any new problems)
P (plan)
● Handover of critical cases on call: there must always be a handover of critical cases
between students (and of course between doctors) when on call. This will usually
take the form of a verbal discussion followed by a review of the notes and patient.
● Consultations – asking another unit for advice:
o Can only be authorized and signed by the registrar or consultant
o There must be verbal as well as written communication with the unit from
whom we are requesting advice.
o The name of the doctor and the unit consultant with you have communicated
must be recorded in the patient’s notes.
● All deaths must be reported to the consultant and a note drafted to the Medical
Chief of staff
3. Teaching of Junior Doctors and Students
● Formal teaching sessions for students are noted on the timetable.

● Your personal timetable consists of the teaching time table added to the time table
of activities of your assigned unit.
● When students have a teaching session they must let their team know where they
will be.
● Medical grand rounds are compulsory
● Consultant based ward rounds are teaching rounds and the students and junior
doctor is expected to keep herself/himself up-to-date by reading relevant clinical
material so as to supplement and make meaningful the arranged Consultant-led
teaching sessions
● This is a teaching unit and the junior doctors are expected to assign clinical
responsibilities to the students attached to the unit.
● The residents on this unit will have ONE teaching session per week with all
students in the clerkship.
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4. Role of Students in the Department of Medicine
● To attend all consultant led ward rounds
● To attend all post call and on call ward rounds and to present patients they have
clerked. On the on call days and post call days’ attendance at these ward rounds
will supersede any formal teaching sessions.
● Students should lead the ward rounds.
● To follow up on their admissions and to keep daily records of the performance
of their patients as outlined above.
● To undertake such responsibilities as are assigned by the junior doctor in charge
of the ward and this should include: investigations, results of investigations,
keeping the patient notes updated with results, checking on therapy given.
● Whatever you do MUST contribute to improving patient care and it is this that
will determine your ward-based assessment.
● When students are involved in patient care on the medical wards they must be
supervised by the junior or senior medical staff who must be present on the
wards while students are doing their jobs.
5. Communication skills
● In the final year you are expected to have a reasonable ability to communicate
with patients and staff. Your skills in this area will continue to develop after
graduation therefore you should not expect too much of yourself.
● Communication with patients and family : if you are in doubt it is best to leave
this to doctors BUT you MUST observe how this is done.
o You should never attempt to break bad news for the first time to patients
or family unless a registered medical practitioner approves this AND is
present during the interview.
o You must explain to patients any test you are going to do e.g. a blood
test
o You are expected to retrieve test results from the laboratory or radiology
departments but this must always be done in a professional manner
o You must be able to communicate with the various categories of nursing
staff and ward assistants always being careful to explain what you are
doing.
o The NURSE-IN-CHARGE is the senior nurse managing the ward. You
must always report to her and your supervising junior or senior doctor
when you first arrive on the ward during the day. You should always
seek the nurse’s advice before seeing patients you do not know.
o Always examine patients, especially female patients in the presence of a
nurse or student colleague who will be a witness to your professional
approach and who will constructively critique what you have done in an
appropriate manner.
● Kindly note that communication here refers to this in all its forms and includes
written and oral communication between doctors.
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6. Procedures performed
● Any procedure performed on a patient requires consent. Consent may be written

or verbal, formal or implied. Written informed consent is always preferred.
● The procedures performed in internal medicine and which require written
consent include: ABG, pleural tap, lumbar puncture, ascitic tap and drain.
● Or ANY procedure performed on a patient the following must be stated in the
medical notes of that patient:
Procedure: Name of procedure e.g. arterial blood gas

Indication: Why the procedure need to be done?
Consent: how was consent obtained?
Assistant: whoever assisted with the procedure
Methods: description of what was done
Findings: description of what was observed during the procedure
Plan: post procedure management of patient with what test were done on
the sample
7. Professional Conduct: all staff
● Your prime responsibility is to our patients to whom you are expected to display
concern, empathy, to whom you have a duty of care and for whom you are
expected always to do your very best.
● You are expected to maintain cordial and mutually respectful relationships with
all ward and laboratory staff.
● The dress code is:
● Female medical staff – white coats at all times, arms to be bare below
the elbow, no slippers, no exposed midriffs, no jeans, no jewelry on
hands or wrists with the exception of wedding rings/ bands.
● Male medical staff – shirt jac, no T-shirts or polo shirts, no tie, no jeans,
no slippers, no jewelry on hands or wrists with the exception of wedding
rings/ bands.
● Video/audio recording or photographing the teaching sessions without
permission is forbidden.
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1. YOUR ASSESSMENT: Year 5
● May be modified by the Department or Adult Medical Unit at any time but
generally will include the following. [The weighting of each component may vary
from time to time as determined at short notice by the Department, though where
possible adequate notice will be given.]
o You may be assessed on any of the items mentioned in this booklet and the
accompanying rubric-based booklet
o An end of clerkship written exam including MCQs, EMQs, IRQs Report
writing (E.g. prescription, death certificate, discharge form, medical report
etc.) and OSCE (80%)
o IRQs consist of a series of MCQs about a pathology result including ECG or
Chest X-ray or CT scan or a lab test report which is shown as part of the
question
o Ward work assessment, which includes professional behaviors, team
working, communication and history taking, relations with patients, clinical
knowledge and reasoning, time and stress management (about 10%)
o Presentations, projects, self-assessments and other observations (about 2%).
Continuous Assessment Component Weightage

Ward Work 10% (5+5)
Presentations & Projects – self assessment 2%
Case History Reports (10) 8%
Total 20%
End of Clerkship Assessment Component Weightage

OSCE 40%
Written stations 40%
Total 80%
Criteria for successful completion of clerkship assessment:
o All students must show adequate attendance in their ward work including call and
postcall and teaching sessions to successfully complete the clerkship. An attendance
record is created by the Group leader for each class and all students are to sign and
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have this co-signed by the senior doctor/tutor. Failure to achieve 75% attendance
will result in the clerkship having to be repeated; the examinations cannot be taken
if 75% is not achieved.
o All students must pass both end of clerkship OSCE, WRITTEN and overall
assessment to successfully complete the Adult Medicine course in Year 5.
o If a student fail in the overall clerkship assessment or both the OSCE and written,
the student need to approach the Deputy Dean’s office to repeat the whole clerkship
for eight weeks.
o If a student fail in OSCE/WRITTEN alone and scored 50% or more in the overall
assessment, then the student will be allowed to re-sit the OSCE/WRITTEN with the
next group or as decided by the Deputy Dean.
a) If the repeat OSCE/WRITTEN score is 50% or more, then the overall
clerkship mark will be considered as 50%. The student will receive a Grade
C and 2.0 GPA quality points.
b) Whereas if the repeat OSCE score is less than 50%, the student will be
required to approach the Deputy Dean’s office to repeat the whole clerkship
for eight weeks.
Grading system. The grading system for Adult Medicine clerkship is as follows:
o After a successful completion of eight week rotation and clerkship

assessment in Year 5 Adult Medicine the students will receive 6 credits.
Their Grades and GPA points will be measured as mentioned below.
Letter Grade Numeric Score QPs

A+ 90-100 4.3
A 80-89 4.0
A- 75-79 3.7
B+ 70-74 3.3
B 65-69 3.0
B- 60-64 2.7
C+ 55-59 2.3
C 50-54 2.0
F <50 0.0
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FOURTH AND FIFTH YEAR CORE CURRICULUM
Year 4 Year 5
CARDIOVASCULAR CARDIOVASCULAR
(Dr. R. Ali/ Dr. N. Seecharan) (Dr. R. Ali/ Dr. N. Seecharan)
1. Coronary artery disease including ACS Increased knowledge of therapeutics
2. Hypertension Increased knowledge of therapeutics
3. Valvular Heart Disease Cardiac Failure
4. Cath Lab orientation
RESPIRATORY RESPIRATORY
(Dr. S Sakhamuri) (Dr. S. Sakhamuri)
Asthma, COPD & Bronchiectasis Tuberculosis & other Infectious Lung Diseases
Pleural Diseases Pulmonary Vascular Diseases
Spirometry & other Pulmonary Function tests Interstitial Lung Diseases
Pneumonias Lung Cancer
Respiratory Failure
ARDS & Mechanical Ventilation
Chest X-ray, Chest CT and ABG interpretation
ENDOCRINOLOGY ENDOCRINOLOGY
(Prof. Teelucksingh) (Prof. S. Teelucksingh/ Dr. C. Lalla)
DM/hypoglycaemia Increased knowledge of management
Metabolic syndrome Increased knowledge of management
Thyroid disease Increased knowledge of management
Hypercalaemia, hypocalaemia
Hyponatraemia
NEUROLOGY NEUROLOGY
(Dr. S. Sandy ) (Dr. Sandy/Dr Ramlackhansingh/Dr. Esack)
1. CVA/TIA 1. Headache
2. Meningitis 2. Parkinson’s Disease
3. Cerebral Abscess 3. Upper Motor Neuron Diseases
4. Lumbar Puncture 4. Lower Motor Neuron Diseases
5. Patients with Dizziness
6. Subarachnoid Haemorrhage
FUNDUSCOPY FUNDUSCOPY
(Optometry School) (Dr. S. Sandy/ Optholmology Clinic)
1. Hypertensive Retinopathy Increased knowledge of management
2. Diabetic Retinopathy
3. Papilledema
4. Optic atrophy
DERMATOLOGY DERMATOLOGY
( Dr. N. Hallai) ( Dr. A. Cumberbatch)
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Please see Dermatology Curriculum Please see Dermatology Curriculum
INFECTIOUS DISEASES INFECTIOUS DISEASES

(Dr. S. Giddings/ Dr. Sakhamuri) (Dr. S. Giddings/ Dr. Sakhamuri)
1. HIV/AIDS & STDs 1. HIV/AIDS & STDs
2. Dengue & Chickungunya Fevers 2. Pneumonias
3. Leptospirosis 3. TB & other Lung Infections
4. Meningitis
5. Infective Endocarditis
6. GI & UTIs
GASTROINTESTINAL GASTROINTESTINAL
(Dr. M. Rahman)
1. GI Bleed Increased knowledge of management
2. IBD Increased knowledge of management
3. Liver disease/liver failure Increased knowledge of management
4. Pancreatic Diseases Increased knowledge of management
RENAL RENAL
(Dr. B. Mohammed/ (Dr. E. Mohammed)
Dr. L. Roberts)
1. Acute Renal Failure Nephrotic Syndrome
2. Chronic renal failure Nephritic Syndrome
3. HIV nephropathy Acute Gomerular Nephritis
Anuria & ESRD
RHEUMATOLOGY RHEUMATOLOGY
(Dr. H. Dyaanand - SFGH) ( - St. James Medical Complex)
1. RA 1. RA
2. SLE 2. SLE
3. Gout 3. Gout
4. OA 4. OA
5. MCTD 5. MCTD
6. Spondarthritides 6. Spondarthritides
HAEMATOLOGY
(Dr. Charles)
1. Nutritional Anaemia
2. Blood film
3. Thalassaemia
4. Sickle Cell Disease
5. Iron Deficiency Anaemia
6. Anticoagulation
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STRUCTURE OF TRAINING IN INTERNAL MEDICINE DURING YEAR 4 & 5
OF THE MB.BS PROGRAMME
The rotation will be as follows and involving all three major hospitals (POSGH,
EWMSC, SFGH), Sangre Grande Hospital (SGGH) and Tobago Regional Hospital
(TRH).
Training in internal medicine will last 16 weeks over the final two years of the MB.BS
programme, with eight (8) weeks in each of years 4 and 5.
The start hospital will be determined in Year 4 such that ALL hospitals have an
approximately equal number of students with FOUR (4) weeks being spent in training
in any one institution and another four (4) weeks in a second institution as determined
by the rotation schedule shown below.
The clerkship exam (COSCE) will be held in weeks 6 through 8 of any clerkship. These
dates will be stated in advance but may be altered by the adult medicine unit at short
notice depending on the availability of examiners. Students will always be advised of
such changes in advance.
Week 1 2
Year 4 Weeks 1 - 4 POSGH or SFGH or SGGH EWMSC
or TRH
▼ ▼ ▼
Year 4 Weeks 5-8 EWMSC POSGH or SFGH or SGGH
or TRH
Year 5 Weeks 1 - 4 EWMSC or SFGH POSGH

▼ ▼ ▼
Year 5 Weeks 5 - 8 POSGH SFGH or EWMSC
▼ ▼ ▼
End of Internal Medicine
Training END END
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MEDICAL EMERGENCIES
THE STUDENT IS EXPECTED TO BE ABLE TO INITIATE TREATMENT (and

seek help when indicated) FOR THE FOLLOWING EMERGENCIES.
1. Gastrointestinal bleeding
2. Resuscitation and life support / cardiac arrest / respiratory arrest
3. Acute asthma / status asthmaticus
4. Status epilepticus
5. Shock
6. Left ventricular failure
7. Diabetic Ketoacidosis / non-ketotic hyperglycemic coma
8. Hypoglycemia
9. Acute renal failure
10. Acute liver failure
11. Subarachnoid haemorrhage / Cerebrovascular accidents
12. Acute myocardial infarction
13. Hypertensive encephalopathy / severe uncontrolled hypertension
14. Coma
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PHLEBOTOMY PROCEDURE – VENIPUNCTURE
PHLEBOTOMY PROCEDURE- VENIPUNCTURE
MATERIALS
● Safety needles 22G (grey)
● Syringe
● Appropriate blood collection tubes
● Laboratory forms
● Tourniquet (rubber gloves may be used)
● Alcohol swab
● Dry swab
● Tray (to hold all materials)
PROCEDURE
✔ Collect all materials
✔ Label forms and blood tubes at nurses station from patient’s file for ONE patient
at a time, just before going to the bedside of that patient
At bedside:
✔ Ask patient to identify his/ her name and date of birth and cross check information
written on forms and blood tubes
*If patient incapable of confirming information, consult nurse or relative (if by
bedside)
✔ Explain procedure and its indication to patient
Venipuncture:
✔ Select an appropriate vein
✔ Apply tourniquet
*Ensure no running IV fluids on this hand
✔ Palpate selected vein (to ensure it’s not sclerosed)
✔ Clean area in a circular motion- starting centre going outwards
✔ Allow skin to dry
✔ Perform venipuncture
✔ Remove tourniquet
✔ On withdrawal of needle apply pressure to puncture site with dry swab
✔ THANK PATIENT
✔ Remove all materials from bedside
✔ Place sharps in sharps bin
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RADIOLOGY-IN-MEDICINE MODULE
At the end of the clerkship, the student should be familiar with:
1. CXR
2. CT of Chest
3. CNS Radiology
4. Abdominal X-ray and ultra sound
5. CT – Abdomen
6. MRI: CNS
7. Doppler studies
8. Assessment as part of the End of Clerkship OSCE in which x-rays shown will be
given to the students with a short case history.
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STUDENT-LEAD WARD ROUNDS
o At POSGH - under supervision of Dr. S. Sandy
o The goal may be summarized as follows: you are the doctor
o The student is expected to present a critical summary of the case
o The student should then discuss the major problems being managed at present and
how they are being resolved
o The student should also relate the discharge plan for the patient
o The student should be prepared to demonstrate key signs of medical illness
o The student should in the presentation show how pathology results are being used in
diagnosis and treatment of the patient’s underlying disease process
o Issues of communication need to be dealt with during this ward round
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THE CASE HISTORY IN MEDICINE
The cases that you clerk when on call are to be presented on the post call ward round OR
in clinic where possible. You are required to do atleast 10 histories one of which must be
marked by a University Lecturer. The latter will account for 25% of your history marks.
Histories can only be presented to persons involved in the patient’s care. Only consultants,
registrars and part 2 DM students will be allowed to correct your history. You are required
to present five histories in your first half of the rotation and a further 5 in the second half.
You will receive a grade: A, B+, B, C, F. The criteria for keeping an acceptable medical
record are as follows;
1. Note before: The case history is only valid if written CONTEMPORANEOUSLY
2. Each page is headed; Name, age, Hosp. Number.
3. Date in the top left hand corner of EVERY page
4. History: PC, HPC, PMH, PSH, DH, allergy history, FH, SH (please include
activities of daily living for elderly patients; smoking history. Alcohol use) and
where appropriate, occupational history
5. Examination: all systems (please see your text)
6. Differential diagnosis arranged in probabilistic order
7. Plan
8. Results of investigations and how they modify your management
9. A prescription written as for the pharmacy
The Minimum Criteria for achieving a grade of C in a case history is validity of both
criteria below:
(a) Adherence to each of the above criteria
(b) Absence of any major error in the recorded history
(c) You do not necessarily have to get the right diagnosis as it is understood
that the student is here to learn
Higher grades than ‘C’ necessarily require greater degrees of appropriate differential
diagnosis and details of management with demonstration of appropriate responses to
results of investigation.
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PROCEDURES IN MEDICINE
You must know:

1. Indications for procedure
2. Preparation for procedure
3. Contraindications to procedure
4. Sensitivity / specificity of the intended procedure
5. Possible adverse consequences
Procedure Date Signature
DIABETES & ENDOCRINILOGY
O Thyroid scintigram
O Treatment of thyroid disease with radioiodine
O Radionuclide scan
O CT scan of brain
O Fine needle aspiration of thyroid
O Blood glucose measurement with glucometer
O Urinalysis
O Setting up intravenous lines
RESPIRATORY
O Arterial Blood Gas
O Thoracocentesis
O Spirometry
O Chest tube insertion
O Bronchoscopy
CARDIOLOGY
O ECG: set and interpretation
O Stress Test
O Echocardiogram
O Radionuclide cardiac evaluation
O Cardiac catheterization / angiography
O Pacemaker insertion
GASTROENTEROLOGY
O Upper GI endoscopy
O Lower GI endoscopy
O Use of proctoscope
O Barium enema
O Barium meal / swallow
O Liver Biopsy
NEUROLOGY
O EMG
O EEG
O VEP
O CT scan
O AEP
O Lumbar puncture
NEPHROLOGY
O Ultrasound kidneys
O IVA / retrograde pyelography
O Kidney biopsy
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HAEMATOLOGY
O Use of blood counting machines
O Bone marrow aspiration and trephine
O Hemoglobin electrophoresis
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Recording a Procedure in the Medical Notes of Your Patient
The Following must be shown in order:
Date and Time of Procedure :

Name of Procedure :
Consent :How was consent obtained: verbal, written
(preferred)
Indication for procedure :
Doctor Carrying put procedure :
Assistants :Nurse, other doctor
Method (in point form)
Observations During Procedure (include any complications)
Assessment : whether the procedure was uneventful or had

complications
Plan – your follow up plan for the patient including any post procedure precautions
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Example
Date and Time of Procedure : 15th May 2010, 0900 hrs
Name of Procedure : Arterial Blood Gas
Consent :Verbal, pros and cons explained and rationale for test
Indication for procedure : Respiratory distress
Doctor Carrying put procedure : Dr. T ABGH (House officer)
Assistants : Medical Students GHTD, FGEQ, DFTY
Method (in point form)

1. Right radial arterial identified at the wrist
2. Allen’s test applied
3. 1 ml lidocaine 1%, infiltrated intradermal and subcutaneous without arterial
puncture and wait 2 mins
4. Syringe preheparinized with low concentration heparin followed by rapid
expulsion of fluid
5. 22G needle to syringe into right radial artery at about angle of 45 degrees to
skin.
6. 1ml of blood aspirated with negative pressure
7. Needle withdrawn and pressure applied for 2 mins by assistant
Observations During Procedure (include any complications)

1. Allen’s test showed that ulnar artery was patent, palmar
erythema with 5 secs
2. No pain during procedure
3. Patient on room air during procedure
Assessment: ABG taken, uneventful
Plan –
1. Bandage to wound
2. Blood sample to ABG machine in ice immediately.
Signature
Name
Designation
15th May 2010, 0930 Hrs: Interpretation of ABG

ABG on room air
Ph 7.47, PO2 60.2, PCO2 30 mmHg, HCO3 22, SaO2 90%
Interpretation: uncompensated respiratory alkalosis with hypoxia (acute Type I respiratory
failure)
Probable cause: consistent with underlying diagnosis of acute PE
Signature
Name
Designation
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REPORT WRITING – A COMMUNICATION SKILL
At the end of your two years in the clinical school, you should be able to communicate with
medical and paramedical colleagues in writing in any of the following ways. You should be
able to
1. Fill out a death certificate.
2. Request a consultation from another specialty.
3. Request a post – mortem examination.
4. Fill out a cremation form.
5. Write up a prescription.
6. Request a radiological examination.
7. Request a laboratory test.
8. Write a report to a doctor who has referred a patient to your care.
9. Write up a discharge summary.
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GUIDELINES IN WRITING PRESCRIPTIONS
COMPONENTS OF WRITTEN PRESCRIPTIONS
The body of a prescription is the same regardless of the field or specialty of medicine the
prescription comes from. Pharmacists require certain information be included on a
prescription and a prescription is not legally allowed to be altered by any person, even a
physician after it is written. If a doctor makes a mistake, he is required to re-write the
prescription from a new page.
Some of the information contained on a prescription pad must be put in place by the pad
manufacturer, such as:
● The name, address, and phone number of the practitioner (for private practice)
● Lines for the patient name, age, address and the current date
● Line for refill amount
● Line for the physicians signature
● The letters Rx (not always included)
All other information will be handwritten:
● The patients name, address, phone number and date of birth.

● The date the prescription is written.
● The name of the medication. This usually consists of the brand name of generic name
of a medication, however occasional the antigen or compound is used when in doubt.
● Whether the brand name medication is medically required. If it is not required the
doctor puts nothing and a generic is always used in place of a brand name.
● The dosage of a medication. For example a birth control pill might be 20
micrograms.
● How many doses can be taken at one time i.e., Take two every two hours.
● How the medicine will be taken. Orally, rectally, injections, etc.
● How many times a day the medication should be taken.
● What time of day the medication should be taken. Morning, on an empty stomach, with
food, etc.
● How much medication at once. i.e. one month worth, three months worth, etc.
● Number of refills. Narcotics, by law, cannot be refilled, a doctor must write a
prescription every time.
● Doctor’s signature.
27
SAMPLE OF HOSPITAL PRESCRIPTION
Hospital Reg. No._P268914_________________________
Clinic/Ward___62___________ D.O.B. _6/19/63_____
Name of Patient _ Priscilla Promiscuous_____________
124 Red Light Lane, Motown_____
Prescription:
RX Doxycycline 100 mg
Disp #14
Sig: Take 1 capsule bid x 7 days
Signature_ Molly Moral_____________________ M.C.

Date _8/14/98________________
Hospital Stamp and Clerk’s signature on other side.
G.P., TR./TO.-R. 2159-2,000 Pads - /01
28
OBJECTIVES:
● Understand the importance of properly written prescriptions

● Understand the correct format for writing prescription medications
● Understand proper procedures for writing controlled substance prescriptions
● Understand methods for avoiding prescription writing errors.
COMMON ERRORS IN PRESCRIPTION WRITING:
Omissions:
a) DAW (Dispense as written)
b) Refill quantity
c) Dosage form
d) Length of therapy/quantity
e) Patient allergies
f) Date
g) Route
h) Signature
Dose or Directions:
a) Dose significantly different from normal standards
b) Error in dose
c) Prescriptions for unavailable dosage forms/strengths
d) Misleading, incomplete or confusing directions
e) Take as directed
f) PRN directions or refills
g) Unclear dose based on a concentration
h) Sustained release dosage forms
Legal Requirements:
a) Omissions of patient's address
b) Prescriptions refills for drugs such as codeine, morphine, methadone etc.
c) Partial fillings of drugs such as codeine, morphine, methadone etc.
d) Generic prescribing for unavailable or inappropriate prescriptions
Quantity:
a) Unclear amount
b) Odd amount
c) Prescription for an amount that doesn't exist
29
Duration of Therapy:
a) Prescriptions for a duration that is substantially different from normal standards
b) Not specified
TIPS FOR AVOIDING PRESCRIBING ERRORS
How to avoid forged prescriptions:

a) Keep all blank prescription pads in a safe place
b) Minimize the number of prescription pads in use
c) Write in ink
d) Write out the amount prescribed in addition to the numerical number
e) Avoid large quantities
f) Only use prescription pads for prescriptions
g) Don't sign prescriptions in advance
h) Put only one prescription on a blank prescription form
Controlled or Unscheduled Medications:

a) Put the patient's diagnosis or the purpose of therapy on the prescription
b) Print
c) Include the patient's age and weight if relevant on the prescription
d) Use the metric system unless dealing with units
e) Avoid uncommon abbreviations
f) Be consistent
g) Sign your own prescriptions
h) Inform patient about medications
i) Never leave a decimal point naked
30
APPENDIX i
INFECTION PREVENTION AND CONTROL UNIT
GENERAL HOSPITAL, PORT OF SPAIN
Post Exposure Prophylaxis Policy (Revised July, 2005)
Exposure to Blood Borne Pathogens in the work place

31
If you have had an injury with a needle or any other sharp instrument, or have come in
contact with splashes of blood or body substances or human bites, follow these steps.
1. Wash thoroughly with soap under running water. Note the source of the exposure.
2. Report to Head Nurse/Nurse in charge
3. Have two blood samples taken from the source patient (with consent) and label
them properly:-
i. A purple top tube with 5-7mls of blood for Microbiology laboratory ,
POSGH for ELISA and/or Rapid HIV test
ii. A purple top tube with 5mls of blood for TPHL/CAREC for HIV and
HBV tests
4. Report to Infection Prevention & Control Nurse during the hours of 8.00a.m. –
4.00p.m. from Monday to Friday. Report to Nursing Supervisor in the Night
Sister’s office during the house of 4..00p.m. to 8.00a.m. from Monday to Friday
and 8.00am. – 8.00a.m. on Weekends and Public Holidays. Unique I.D. is
formatted and will then be given to the exposed person.
5. The Nursing Supervisor or the Infection Prevention & Control Nurse will authorize
the Laboratory Technician to do a Rapid Test on a blood sample from the source
patient
6. Take the 5mls blood sample to the Laboratory for the Rapid Test to be done.
(Bacteriology Lab. 8.00a.m. to 4.00p.m. from Monday to Friday and
Biochemistry Lab. From 4.00p.m. to 8.00a.m. and during weekends and Public
Holidays)
7. Report to the Head Nurse or Nurse in Charge in the Accident & Emergency
Department who will arrange for the exposed person to be seen by the Accident &
Emergency Doctor.
8. a. Consent to be signed by exposed person, to have blood taken for

investigations and Anti-Retroviral Therapy (ART)
b. A blood sample will be taken from the exposed person immediately after
exposure and properly labeled with the Unique ID: e.g. John Doe 29th June,
1945 will be DJ 450629 I.e. last name initial, first name initial, year, month and
day of birth
c. Collection and signing of blood samples must be submitted by the HCW’s
immediate supervisor
d. Rapid HIV test must be performed on the exposed person, if source patient is
positive, before start of ART
32
9. Immediate HBV/HIV counseling must be done by A&E doctors. A STAT DOSE
of the Anti-Retroviral therapy is given to the exposed person at the A&E
Department WITHIN TWO HOURS OF EXPOSURE after outlining the possible
risks, toxicity and the rationale for the use of prophylaxis. The exposed person is
asked about any medication he/she is on and the doctor outlines the various drug
interactions with the drug regime.
10. The blood sample from the exposed person is sent to Microbiology Lab for baseline
HIV status-ELISA test, and a 5ml sample from the source must be placed in the
CAREC REFRIGERATOR. This sample will be taken to TPHL for HBV testing
11. The Rapid test on the source patient must be done within two hours of exposure.
The Report will be given to the Nursing Supervisor/Infection Prevention & Control
Nurse who will immediately contact the exposed person. The exposed person
should leave information with the Infection Prevention & Control Nurse or the
Nursing Supervisor as to where he/she can be contacted.
Availability and Use of Medication
If the Rapid test of the source patient is positive and the exposed person is negative, he/she
is advised to take the Anti-Retroviral Medication for 28 days.
Post Exposure prophylaxis (PEP) with Anti-Retroviral therapy (ART) is most

effective when started immediately (at least within 72 hours).
In Low Risk Situations i.e. Exposure to body fluids or secretions from a potential source
of HIV infection without any muco-cutaneous penetration, and also when the source is HIV
negative.
▪ Counseling and follow up for four weeks
▪ No ART
▪ Re-evaluate for HIV antibodies after six weeks, three months and six months.
In Medium and High Risk Situations i.e. Exposure to moderate or large quantities of
blood or body fluids or secretions from a potential source of HIV infection with muco-
cutaneous penetration e.g. – Needle stick injuries, other sharp objects etc.
● If source is HIV negative

- No ART
- Re-evaluate for HIV antibodies after six weeks, three months and six
months with continued counseling
● If source is HIV positive and the exposed person is HIV negative
- Start ART
- Refer to Medical Research Foundation for further counseling and
33
management
● If both source and exposed person are HIV positive
- Refer to Medical Research Foundation for further management
Anti Retroviral Therapy (ART)

Medium Risk Zidovudine (AZT) 300 mg bid}
+ } Daily for four weeks
Lamivudine (3TC) 150mg bid }
High Risk AZT 300MG BID + 3tc 150MG BID + Nelfinavir (Viracept)
1250mg bid daily for four weeks
OR
AZT 300mg bid + 3TC 150mg bid + Indinavir (Crixivan) 800mg

Tid daily for four weeks
OR
AZT 300mg bid + 3TC 150mg bid + Efavirenz (Sustiva) 600mg

At bedtime daily for four weeks
When the pharmacy is closed, sufficient doses of the Anti-Retroviral Therapy medication
will be given to exposed in the Accident and Emergency department until such time that a
prescription can be filled.
The exposed person’s prescription must be filled immediately by the Pharmacist.
OTHER BLOOD INVESTIGATIONS AND FOLLOW UP CARE
● A complete Blood Count, Liver Function Tests and Kidney Function Tests must be
done on the exposed person at the beginning of the prophylaxis, two weeks after
start of treatment and one week after completion of prophylaxis. This is done at the
Medical Research Foundation
● The HIV-ELISA test for the exposed person is repeated at six weeks, three months
and six months irrespective of whether the source patient is positive or negative.
This is done at the Infection Prevention and Control Unit
34
● Any side effects of the medication must be reported to your doctor immediately
● Do not discontinue prophylaxis without Doctor’s advice
● Confidentiality must be maintained at all time
Hepatits B Virus (HBV) Follow Up
All exposed persons assessed
If unvaccinated – to receive vaccine series at staff clinic
If source is HBV positive, then if exposed person is
● Unvaccinated – to receive Vaccine series and HBIG (Hepatitis B immunoglobulin)

● Vaccinated – test for antibody to HbsAg, then receive one dose of vaccine and
HBIG, if antibody level is inadequate
Precautions during testing period (i.e. six months) after possible exposure
REFRAIN FROM:
2. Donating blood, plasma, body organs, sperms or other tissue
3. Sharing toothbrushes, razors, needles etc.
4. Breastfeeding
5. Unsafe sexual practices
Responsibility of The Infection Prevention and Control Nurse
● Counseling is done as soon as possible

● Appropriate accident forms are filled out in duplicate as soon as possible in the
Infection Prevention and Control Office
● The Original copy of the accident form must be posted out to the National
Surveillance Unit
● The carbon copy of the Accident form must be kept on the file in the Infection
Prevention and Control Office
● Dates for follow up investigations must be given
● Inform the HCW of the ELISA results as soon as it is received
35
Revised and viewed by
Signed
Signed
Dr. Madhura Manjunath Val R. Tobias RN

Clinical Microbiologist IPCU Nurse
General Hospital, PoS General Hospital, PoS
July, 2005
Approved by
Signed
Mr. Winston Welch

Medical Chief of Staff
General Hospital, PoS
36
APPENDIX ii
INFECTION PREVENTION & CONTROL UNIT POSGH JULY 2005
PROCEDURES FOLLOWING EXPOSURE TO
BLOOD-BORNE
PATHOGENS IN THE WORKPLACE
EXPOSURE INCIDENT
IMMEDIATE ACTION
▪ Wash exposed skin with soap and water.
▪ Flush mucous membranes (mouth, eyes, and nose) with
water.
▪ Remove soiled garments
▪ Note time of incident
▪ Report to Head nurse/Nurse in charge
Report to Infection Prevention and Control Unit

Junior Matron/Night Sister
Consent from source patient.

Exposed person reports/taken to A&E
Take 2 samples of blood from source counselling for HIV/HBV done
Consent form signed for blood & ART
Antiretroviral therapy
5ml to CAREC for HIV and HBV testing Blood sample sent to POSGH lab
5ml to POSGH lab for HIV rapid test
for baseline HIV status
(Get report within 2 hours)
Negative
Positive
Report to Infection Prevention
- Rapid HIV test done on exposed
And Control Unit
person before starting ART

- Continue PEP with ART for 28 days
37
- Check with Infection Prevention
Control Unit re policy
- Follow up with clinical monitoring
at Medical Research Foundation
Precautions during testing period to be followed

ART to be started within two hours of injury
HEPATITIS B VIRUS (HBV) FOLLOW UP
Exposed person assessed. If unvaccinated-to receive vaccine series at staff clinic.

If source is positive, then exposed person
If unvaccinated to receive vaccine series and HBIG

If unvaccinated-test for antibody HbsAg then receive one dose vaccine and HBIG if
antibody level is inadequate
Revised and reviewed by Approved by
Signed Signed Signed
Dr. Madhura Manjunath Val R. Tobias RN Mr. Winston Welch

Clinical Microbiologist IPCU Nurse Medical Chief of Staff
38
APPENDIX iii
DERMATOLOGY CURRICULUM
For Year 5 Medical Students (Clinical)
It is impossible to cover all important topics in dermatology during a short clerkship.
The idea is not to make you dermatologists but to help you to make sensible decisions
about immediate therapy to relieve the patients’ distress, to help you to manage to the stage
of resolution the more common and uncomplicated disorders and to assist you in deciding
when to refer for further investigation and management.
Medical students should have a working knowledge of:-
a. Basic anatomy, physiology and pathology of normal skin and common disorders
such as eczema, psoriasis, urticaria.
b. The approach to the patient with skin disease so as to come to a reasonable
differential diagnosis at the end of the inquiry and examination.
c. Descriptive terms used for skin lesions e.g. macules, papules, hyperkeratosis,
lichenification.
d. The basic clinical features, aetiology and pathogenesis as well as baseline
management of the following:
(i) Eczema (dermatitis) – endogenous forms such as atopic and seborrhoeic

eczema; exogenous forms such as contact irritant and allergic eczema.
(ii) Erythematosquamous eruptions

● psoriasis
● lichen planus
● pityriasis rosea
(iii) Inflammatory disorders of the pilosebaceous units – acne vulgaris
(iv) Erythematous eruptions

● urticaria
● erythema nodosum
● drug eruptions
(v) Bacterial skin diseases

● impetigo
● folliculitis
● syphilis
● Hansen’s disease
39
(vi) Viral skin diseases
● Herpes simplex
● Herpes zoster
● Viral warts – common and genital
● Molluscum contagiosum
(vii) Fungal skin diseases

● Pityriasis versicolor
● Dermatophyte infection of skin, hair and nails (tineas)
(viii) Infestations
● scabies
● lice
(ix) Auto immune disorders

● Systemic lupus erythematosus
● Cutaneous lupus erythematosus (chronic discoid)
● Dermatomyositis
● Scleroderma
●
(x) Disorders of immunological origin
● Alopecia areata
● Vitiligo
(xi) Common growths in skin e.g.

● Sebaceous cysts
● Haemangiomas
● Lipomas
● Melanocytic naevi
● Keloids
● Seborrhoeic warts and neoplamsm such as
o Melanoma
o Basal cell carcinoma
o Squamous cell carcinoma
(xii) Bullous disorders

● erythema multiforme
● pemphigus
● pemphigoid
40
(xiii) Common skin manifestations of systemic disease
▪ Renal disease
▪ Hepatic disease
▪ Internal malignancy
▪ Thyroid disease
▪ Diabetes
▪ Haematological disorders including malignancy, iron deficiency
Anaemia, pernicious anaemia
▪ Drug allergy
(xiv) Nail disorders

● Tinea unguium
● Chronic paronychia
● Changes with systemic disease
e. Basic pharmacology and applications of drugs used in dermatology e.g.

corticosteroids, tetracycline
RECOMMENDED TEXT BOOKS:

1. Lecture notes on Dermatology
Robin Graham Brown and Tony Burns
2. Clinical Dermatologhy
Rona Mackie
REFERENCES:
1. Textbook of Dermatology
Champion, Burton, Ebling
2. Dermatology in General Medicine

Fitzpatrick
41
APPENDIX iv
HIV CIRICULUM
HIV in Adult Medicine Curriculum:
Years 4 & 5 Undergraduate Medicine
Course description
Title: HIV Disease in Adult Medicine: Years 4 & 5 Undergraduate Medicine
Overview
This course is designed to complete the training of the medical undergraduate student in
HIV/AIDS medicine within the context of general internal medicine over two rotating 8
weeks clerkships.
Prerequisite
A pass in the MB: BS Phase 1 examination.
Organization of the Course

The course is taught in two modules
1. Year 4 – at the Eric Williams Medical Sciences Complex (EWMSC), and San
Fernando General Hospital.
2. Year 5 – at Port of Spain General Hospital
Depending on availability of personnel and consistent with the service commitment of the
medical teachers involved.
Integration within the Undergraduate Programme in Medical Sciences
Integration of the HIV teaching already occurs within the undergraduate curriculum but it
has now become a disease of national significance to this country and the Caribbean islands.
For this reasons it is being taught as a separate component of undergraduate adult medical
training. Training in HIV medicine will be closely related with other sub specialties
including Pulmonology, Gastroenterology, Urology, Cardiology, endocrinology, Venereal
Diseases, Nephrology and dermatology.
Over the course of the final to years of graduate training, students are expected to become
familiar with the management of HIV- associated conditions within and across these
specialties
42
Purpose of the Course
The course covers the broad spectrum of medical conditions associated with HIV infection
in adult medicine. Students would be expected to elicit signs within each of the major
systems of the body and to integrate these with the history into a final clinical diagnosis.
This course is designed for students during the final 2 clinical years of undergraduate
medicine.
By the end of the course, the student will be expected to diagnose and initiate treatment of
the following major common HIV-associated conditions: PCP, TB, Oesophageal
candidiasis, chronic cryptosporidial diarrhoea, non-typhi salmonella septicaemia, CMV
retinitis, progressive multifocal leucoencephalopathy, cerebral toxoplasmosis, cerebral
lymphoma, chronic mucocutaneous herpes simplex, Kaposi’s Sarcoma, Non-Hodgkin’s
lymphoma, primary cerebral lymphoma. Students should be expected to understand the
differential diagnosis of these conditions and how to differentiate between these and other
medical conditions by laboratory and radiological investigations.
Instructor Information
Co-ordinator for HIV teaching in Adult Medicine: Dr. S. Giddings

Course Tutors: Dr. S. Sakhamuri, Dr. N Bhagwandass and Professor S. Teelucksingh.
Office: Department of Medicine, Faculty of Medical Sciences, 2nd floor, building 67,
EWMSC, Mount Hope.
Contact Phone: Department of Medicine EWMSC 663 4332 or ext 2926
POSGH 623 4030 or ext 2585
Letter to the student:
This course spans two years of your training; the course content will be covered during your
year 4 and year 5 adult medicine clerkships as part of the already existing teaching program.
HIV disease is now a common condition as seen worldwide and also in the West Indies.
We hope that you will use this course to become familiar with the protean manifestations of
this condition and that you will be able to treat the various syndromes referred to with
confidence as an intern.
General Objectives: The objective of including HIV/AIDS-related education in the Medical school
curriculum is to produce a doctor with:
1. Understanding how to elicit a history of HIV-related diseases.

2. Knowledge about the history of the HIV virus, and how it is spread.
3. Competence to diagnose and manage persons with HIV infection and HIV- related
disease.
4. Knowledge of the extent of problems due to HIV/AIDS at global and regional levels, and
its impact on health.
5. Knowledge of the psychosocial and behavioral aspects of HIV/ AIDS infection.
. Communication skills and the ability to counsel persons with HIV/AIDS, as well as their
43
families.
7. The ability to plan and execute appropriate preventive measures against HIV infection in
the hospital, workplace and community.
8. Understanding the importance of team approach and cooperation for utilization of
resources.
9. Compassion for individuals living with HIV/AIDS.
10. An awareness of medical ethics; human rights issues, and costs of medical care.
Specific Objectives:
At the end of the course you will be able to
1. Define the signs and symptoms of HIV-related diseases.

2. State a differential diagnosis for each disease.
3. Know the causes of HIV associated disease.
4. Define each of the major diseases in this syllabus.
5. Integrate the signs and symptoms of HIV disease with the underlining cause.
6. Differentiate between the different conditions using the history, examination and
investigations discussed during this course.
7. Differentiate between diseases presenting with similar symptoms.
8. State the treatment of AIDS related acute Illnesses (PCP, esophageal candidiasis,
cryptococcal meningitis).
9. Discuss the treatment of pulmonary diseases associated with HIV.
10. Be able to diagnose and manage TB in HIV patients.
11. Integrate results of Mantoux testing with management of TB in HIV patients.
12. Be able to diagnose and manage HIV related diarrhoeal illnesses.
13. Integrate results of stool testing with management of HIV-related diarrhea
illness.
Assignments
1. The student will be expected to clerk at least 1 patient with HIV infection.
Clerking of a patient will involve:
a. Presenting complaint
b. Complete history
c. Examination of all systems of the patients
d. A description of what investigations that were done and should be done
with details of results where applicable
e. Treatment and response to treatment
f. Follow up plan for the patient including discharge
2. Students may be given a short project
44
Timeline of important events in the evolution of the
global HIV/AIDS epidemic in the last century
1981
First cases of new immunodeficiency disease in gay men in US
1982
Same immunodeficiency disease diagnosed in Europe
Disease named AIDS by the CDC in US, and SIDA in France and Spain
1983
Heterosexual spread of AIDS documented
1984
Retrovirus isolated by Montagnier group at Pasteur Institute in France, shown to be the
cause of AIDS by Robert Gallo laboratory
7,700 AIDS cases reported in US and 762 cases in Europe
1985
Blood test for HIV licensed by FDA
Ryan White, a 13-year-old hemophiliac with AIDS, is banned from school

Rock Hudson dies of AIDS
1986
LAV and HTLV-III renamed HIV
“Slim” disease (AIDS) widely recognized in Africa
1987
AZT introduced as first anti-HIV medication
AIDS Memorial Quilt displayed on the mall in Washington DC

HIV-infected persons barred from entering US
1988
First World AIDS Day held on December 1
1989
ddI made available as part of expanded access program as second HIV drug.
1990
Ryan White dies and Ryan White CARE Act becomes law
45
8–10 million HIV-infected persons worldwide
1991
Red ribbon becomes an international symbol of AIDS awareness
ddC approved AZTand ddC used in combination for first time
1992
India funds National AIDS Control project with >15% of its health budget
1993
Transmission of AZT-resistant virus documented
3TC approved for clinical use
1994
AZT shown to reduce mother to child transmission of HIV
1995
First HIV protease inhibitor approved
AIDS named leading cause of death in US of persons25–44 of age
1996
First use of HAART with dramatic clinical responses
1997
Deaths from AIDS in developed world begin to drop due to HAART
1998
Glaxo-Wellcome cuts price of AZT by 75% due to evidence that the drug reduces mother-
to-child transmission in developing world
Content
Clinical presentation of HIV diseases
a. Primary infection: fever, mucocutaneous skin rash, fatigue, fever, pharyngitis,

cervical lymphadenitis, myalgia, headache, oral ulceration. But also aseptic
meningitis, encephalitis and other neurological manifestations.
b. Asymptomatic infection: PGL
c. Mildly symptomatic infection: AIDS – related complex – chronic weight loss,
fever, diarrhoea, oral or vaginal candidiasis, oral hairy leukoplakia, zoster,
severe PID, bacillary angiomatosis, cervical dysplasia, ITP.
d. Acquired immunodeficiency syndrome: AIDS-defining illnesses.
e. The immune reconstitution inflammatory syndrome.
HIV testing and monitoring.
∙ Rapid Tests
46
∙ ELISA
∙ Western Blot (WB)
∙ PCR (viral load)
∙ CD4 count
INITIAL APPROACH TO HIV ⊕ PT
Document HIV infection
History and physical
Laboratory evaluation: CD4 count, viral loan, CBC with diff, U&E, LFT’s, fasting
glucose, PPD, syphilis, toxoplasmosis, CMV, fasting lipids, hepatitis serologies, baseline
CXR, Pap smear in women.
Antiretroviral Drugs:
NRTI, NNRTI, PI and FI.
Know:
When to start therapy
When to change therapy
Common Combinations used
Common combinations to avoid
When to start therapy
When to change therapy
Common drug interactions
Common side effects
COMPLICATIONS OF HIV/AIDS
1. Chest Medicine
a. PCP Infection/Pneumocystis jiroveci

- Aetiology
- Relationship to CD4 count (<200)
- Clinical presentation (dyspnoea, fever, non productive cough and chest
pains)
- Investigation: CXR, CT, ABG, BAL/Bronchial washings A-a gradient
and LDH gallium scan
- Treatment
- Primary and Secondary Prophylaxis
b. Histoplasmosis
- Aetiology
- Relationship to CD4 count
- Clinical presentation: hepatosplenomegaly, lymphadenopathy, cough,
47
chest pain( CNS, GI, cutaneous manifestations smaller%)
- Investigations: histoplasma antigen (resp secretion, blood, urine), biopsy of
involved tissue
- Prevention
- Prophylaxis
- Treatment; IV Amphotericin B followed by oral Itraconazole
c. Tuberculosis
- Aetiology
- Clinical presentation; LTBI-asymptomatic, Active TB-is influenced by
the degree of immunodeficiency.
- Diagnosis of latent TB infection (LTBI)
- Diagnosis of active TB infection
- When to start treatment
- What treatment to start
- Monitoring active TB disease
- Management of common adverse events-GI reaction, skin rash
- ART in the mgt of TB
- Optimal timing of imitation of ART
- Immune Reconstitution and Paradoxical Reaction-exaggerated
inflammatory response-fever, worsening of resp. status break through
meningitis.
- Management of treatment failure
- (see pulmonary medicine syllabus)
d. MAC
-Aetiology
-Clinical presentation: fever night sweats, weight loss, pancytopenia
-Investigations: sputum/AFB, alkaline phosphates, blood culture, CXR
-Treatment: Clarithromycin +Ethambutol
-Prophylaxis: Azithromycin or Clarithromycin
e. Cryptococcus
- Aetiology
- Clinical presentations (asymptomatic/symptomatic with/without
dissemination)
- Investigations
-Treatment
f. Pneumonia
- Aetiology
- Clinical presentation: similar to HIV negative patients
g. MAI Infection
- Mode Transmission
- Prior to HAART, occurred in 35% of all patients
- Relation to CD4 count (<50)
- Clinical presentation: fever, sweats, weight loss, chronic diarrhoea,
vomiting and abdominal pain.
48
- Findings: multi-systemic
- Diagnosis: ABF + ve, culture, blood cultures (to check for dissemination)
- Treatment
- Prophylaxis
h. Kaposi Sarcoma
i. Lymphoma
j. Cor pulmonale
2. Gastrointestinal
a. Oral
-Aphthous ulcers
-Thrush (oral candidiasis) associated with burning or pain
-Oral hairy leukoplakia
-Kaposi’s Sarcoma
b. Esophagitis
-Candidiasis: Clinical presentations, painful dysphagia,
Treatment - fluconazole
-CMV: confirmation-biopsy-“owl’s eye inclusions”
-HSV, apthous ulcers, pill-induced
c. Enterocolitis
-Bacterial (usually acute): Salmonella, Shigella, Compylobacter, Yersinia, C.
difficile
-Protozoal (usually cronic): Giardia, Entamoeba, Cryptosporidium, Isospora,
Microsporidium, Cyclospora
-Viral (CMV, adenovirus)
-Fungal (histopplasmosis): MAC; AIDS enteropathy
d. GI Bleeding
-CMV
-Kaposi’s sarcoma
-Lymphoma
e. Proctitis :HSV, CMV, Chlamydia, gonococcal

- Presentation,
- Treatment
- Monitoring of adverse SE
- Management of treatment failure
- Prevention
f. Hepatitis Band C
-Incidence in HIV infected individuals
-Mode of acquisition and carriage rate
-Treatment
-Management of treatment failure
49
-Prevention
g. Wasting
-Definition: Loss of > 10% body weight without obvious cause
-Geographical distribution: developing world mainly
-Peripheral fat loss (fat redistribution syndrome) associated with HAART.
3. Ophthalmologic
- CMV retinitis (CD4 count <50)

- Clinical presentation: floaters, flashing lights, fundoscopy (haemorrhagic
exudates)
- Differential diagnosis: toxo, acute retinal necrosis due to VZV, HIV-related soft
exudates, PORN (prog. Outer ret. Necrosis), syphilis, pneumocystis.
- Confirmation – biopsy- ‘owl’s eye inclusions.
4. Cutaneous
a. Seborrheic Dermatitis, HSV and VZV infections, Scabies etc

b. Dermatophyte infections
c. Molluscum Contagiousum (poxvirus)
d. Kaposi’s Sarcoma
e. Bacillary angiomatosis
f. Warts (HPV infection)
- Clinical features
- Treatment
- Prevention
5. Cardiac Disease
a. Cardiomyopathy
b. HIV related dilated cardiomyopathy common but not usually symptomatic
c. Drug induced.
d. Ischaemec Heart Disease and protease inhibitor related dyslipidaemias
e. Pericaardial effusion
- Clinical presentation
- Investigation-CXR, ECHO, ECG, lipid profile
- Management
6. Endocrine Disease
a. Hypoadrenalism
b. Hypopituitarism (rare)
c. Adrenal inefficiency (CMV adrenalitis)
50
7. Renal Disease
a. HIVAN (HIV associated nephropathy)

- Nephrotic syndrome or chronic renal failure
b. Acute renal failure.
- ATN (drug induced)- indinavir, pentamidine, cidofovir, co-trimoxazole,
aminoglycosides and amphotericin
c. Hypopituitarism (rare)
8. Neurological Diseases
a. Meningitis: cryptococcus, bacterial, viral (HSV, CMV), TB, history

Cryptococcal Meningitis
- Aetiology and spread
- Clinical presentation: insidious fever, headache, and malaise.
- Cryptococcal pneumonia may be concurrent
- Diagnosis and treatment
- CD4 count< 100
- Treatment: Induction and consolidation-Amphotericin & Flucytosine
then fluconazole, maintenance-fluconazole
b. Intra Cerebral Space Occupying lesion

∙ PML
- Aetiology
- Clinical presentation; insidious onset- hemi paresis, ataxia, aphasia, with a
clear sensorium
- Investigation: CT or MRI brain, PCR for JC virus
freatment: start ART immediately, if on ART and +drug resistance change
to effective regimen.
∙ Cerebral Toxoplasmosis
- Clinical presentation- Short history of fever
confusion, seizures and focal signs follow
raised intraccranial pressure as a common complication
- Investigations CT or MRI-ring enhanced lesion, toxoplasma IgG Antibody,
sterotacticCT guided needle biopsy
-Differential diagnosis: CNS lymphoma, mycobacterial infection (esp TB),
fungal infection (cryptococcus), bacterial abscess, chagas disease, rarely PML
-Treatment: pyrimethamine and sulfadiazine or clindamycin
- Prophylaxis-TMP-SMX.
∙ Primary CNS lymphoma (PCNSL)

Three main types
Grade III or IV immunoblastic
Burkitt’s lymphoma
Primary CNS lymphoma
- Clinical presentation: depends on site of tumor, focal seizures 80% extrnodal
51
disease
- Investigation: cytology +ve in only 25%, EBV DNA in CSF has high sensitivity
and specificity for PCNSL, CT scan, sterotactic brain biopsy
- Treatment: standard intensive regimens have been abandoned due to low
response rate.
c. AIDS dementia complex: memory loss and gait disorder
d. Myelopathy: infection (CMV, HSV), cord compression (epidurial absess,

lymphoma)
e. Peripherial neuropathy: medication induced, HIV, CMV
The year 4 & 5 HIV medicine module consists of the following sessions:
1. The pre-test and post-test counseling

2. Clinical presentation of HIV diseases
3. Reliability of HIV testing
4. Respiratory Diseases
5. GI diseases
6. CNS
7. Other Diseases
8. Evaluation and assessment
Assessment/Evaluation:
Your examination will be part of the assessment within Internal medicine.

Your assessment will take the following forms
1. A written examination based on structured questions or MCQs
2. Evaluation of a project
3. Grading of cases clerked
Teaching Strategies:
The department of medicine employs several teaching strategies, which will include
1. Guided lectures
2. Bedside teaching
3. Small group teaching
4. Non lecture strategies (projects, group discussions and co-operative learning
Resources:
1. Do not forget that the ward patients are your most valuable resource.
2. Patients in the medical outpatients’ clinics.
52
Readings:
1. Davidson’s Principles and Practice of Medicine.

2. Centers for Disease Control and prevention (CDC) and the HIV Medicine
Association of the Infectious diseases Society of America (HIVMA/IDSA),
guidelines for prevention. June 18, 2008.
3. Gladstone Institute of Virology and Immunology, University of California, San
Francisco, CA, USA. 2007.37:S 94-102
Course Calendar:
(please see content list above)
Year 4:
HIV testing and monitoring

Clinical manifestation of HIV
Neurological disease manifestations of HIV infection
Cardiac disease
Endocrine disease
Year 5:
Chest disease
Renal disease
Eye disease
GI disease
How to study for this course:

The most important study technique that we can suggest to you is to clerk as many patients
as possible with the various disease processes described above
Grading System:
As for year 4& 5 Internal Medicine course please follow internal medicine syllabus
53
APPENDIX v
PULMONMARY MEDICINE MODULE:
CURRICULUM: YEAR 4 & 5 UNDERGRADUATE MEDICINE
Course description
Title: Pulmonary Medicine: Year 4&5 Undergraduate Medicine
Overview
pulmonary medicine within the context of general internal medicine over two rotating 8
weeks clerkships.
Prerequisite
A pass in the MB:BS Phase 1 examination.
Organisation of the Course

1. Year 4 - at the Eric Williams Medical Sciences Complex (EWMSC)
2. Year 5 - at the Eric Williams Medical Sciences Complex (EWMSC) and Port of
Spain General Hospital
depending on availability of personnel and consistent with the service commitment of the
Pulmonary medicine is one of several components of general internal medicine with which
the student is expected to become familiar over the two final years of undergraduate
training in the Faculty of Medical Sciences and integrates closely with other sub-specialties
including cardiology, cardiothoracic surgery and intensive care medicine. Over the course
of the final 2 years of undergraduate training, students are expected to become familiar
with the management of pulmonary diseases within and across these specialties.
54
Pulmonary Medicine as a Discipline within Internal Medicine
The Department of Clinical Medical Sciences is comprised of four units: Adult Medicine
(General Internal Medicine), Paediatrics and Radiology. Pulmonary medicine is one of
several disciplines within internal medicine.
The course covers diseases of the chest or respiratory system and is also called
pulmonology, respirology, respiratory medicine, and pulmonary medicine or chest
medicine. Students would be expected to have been exposed to the rudiments of the chest
examination and history during Phase I training. This course is designed for students
during the final two clinical years of undergraduate medicine.
At the end of the course, the student will be expected to diagnose and treat the following
major common pulmonary conditions: asthma, COPD, lung cancer, pneumonia, pleural
effusion, tuberculosis, pulmonary embolism. The student will also be expected to
understand the differential diagnosis of these conditions and how to differentiate
between these and other medical conditions by laboratory and radiological
investigations.
Letter to the Student

Welcome to the Pulmonary Medicine component of the Internal Medicine Programme. We
hope that you will see this course as an extension of the learning initiated during your first
three years of training. Whereas in the first year of internal medicine (year 4
undergraduate) we emphasised knowledge of the underlying disease processes and the
acquisition of an accurate history and examination, our emphasis in the final year is on
diagnostic skill, investigation and treatment of common pulmonary diseases and their
differentiation from other diseases. The best advice we can give you is that learning is
patient-centred and not text-book centred, though your text books will provide a useful
resource. We hope you enjoy your brief time with us in this exciting field.
Contact Information
Tutors: EWMSC - Dr. S. Sakhamuri, Dr.Bahall, Prof. S. Teelucksingh and Associate
Lecturers from Thoracic Medicine Unit.
Port of Spain General Hospital – Associate Lecturers from the Department of
Medicine at POSGH
Office: Department of Clinical Medical Sciences, Faculty of Medical Sciences, 2nd Floor,
Building 67, EWMSC, Mount Hope
Contact Phone: Department of Medicine EWMSC 663 4332;
POSGH 623-4030 or ext 2585
Content
Clinical presentation of pulmonary diseases
Dyspnoea, cough, sputum, haemoptysis, wheeze, chest pain, fatigue, sleep disturbance,
excessive snoring, confusion, ankle oedema, hoarseness, night sweats.
55
The student is expected to characterize each of these symptoms by onset (where, when
how), duration and evolution. Common causes of each of these symptoms.
Symptom severity:
Dyspnoea: MRC dyspnoea scale, New York Heart Scale,
Sputum: volume and purulence
Haemoptysis: clinical significance and management of massive haemoptysis. Causes of
haemoptysis – PE, LRTI, Tb, lung cancer, bronchiectasis, aspergillosis
Chest pain: severity, location of pain in relation to cause, pleuritic chest pain
Chest History
Past Medical History: importance of comorbidites eg cardiac, diabetes
Drug History: importance of retrospective diagnosis of lung disease from the drug history.
Adverse effects on the lung – ACEIs, beta-blockers, NSAIDs, drugs causing pulmonary
fibrosis
Allergy history and relation to chest diseases esp. asthma, angioedema
Smoking – definition of a pack year as a measure of smoking burden
Family – genetic basis of some lung diseases – cystic fibrosis, alpha-1 antitrypsin
deficiency, familial diseases
Occupational lung disease: occupational asthma, dusts and COPD, air pollutants and
cardiopulmonary diseases eg. effect on heart rate variability
Social: disease and socio-economic status eg. Tb, COPD, compliance
Pet history: pet related lung diseases: asthma, extrinsic allergic alveolitis
Signs of Pulmonary Disease

(a) The following signs are of special importance in pulmonary medicine- cyanosis -
definition, detection, causes
clubbing. – definition, causes, HPOA
flapping tremor and respiratory failure
(b) Examination of the skin, pulse, joints,
JVP - characteristics of the JVP, differentiation from carotid pulse,
relationship to SVC obstruction, cardiac tamponade, tricuspid
incompetence
Lymphatic system - causes of lymph node enlargement
(c) Inspection, palpation, percussion and auscultation of the chest. Interpretation and
reporting of these signs will be emphasized.
Investigation of Pulmonary Diseases

I. Chest radiograph: characteristics of the various chest diseases in this syllabus
56
Spirometry:
Definition: FEV1, FVC, IC, FEV1/FVC ratio, PEFR, FEF25-75
Measurement of variables
Indications
II. Arterial blood gases:

Technique of taking ABG, technique of local anesthetic, Allen’s sign,
Interpretation of ABG and the Henderson-Hasselbach Equation,
Biochemistry of measurement of pH, CO2, O2, HCO3.
A-aDO2 gradient.
III. Bronchoscopy and bronchial biopsy

Indications, procedure, complications, risks, sedation, recovery, type
of sampling of the lower airway: mucosal biopsy, TBLB, Washings,
BAL
IV. Thoracentesis: indications, procedure, complications.
V. Pleural biopsy: indications, contraindication, risks, positioning of the patient, site
selection, technique, use of Abram’s needle,
VI. CT Scanning and CT guided biopsy
VII. Static lung volumes: definition, indications, VC, TLC, RV, FRC, factors affecting
each, body plethysmograph, anatomic dead space, RAW,
VIII. Gas transfer: indications, definition, DLCO, alveolar volume, KCO, factors affecting
each, methods of measurement.
IX. Lung Tissue analysis: Bronchoscopic biopsy (mucosal, TBLB), percutaneous biopsy,
thoracoscopic biopsy, open lung biopsy. Indications and complications of each.
Special emphasis will be placed on investigations I, II, III, VI above.
Specific Diseases of the Lung

In the final year several further diseases will be discussed in addition to those studies
during the fourth year:
(1) through (5) – Year 4; All topics in Year 5
(1) Asthma
a. Definition and prevalence
b. Aetiology: genetics, triggers:- smoke, pollutants, allergens.
c. Clinical presentation: acute severe asthma, episodic asthma, chronic
(persistent) asthma
d. Specific points in the history: family history, atopy, effects of aspirin,
NSAID or beta-blocker use, allergens
e. Objective measurements of lung function as PEFR, FEV1, FVC: (i) diurnal
variation, (ii) after use of beta-2 agonist inhalers or nebulisers or steroid
treatment (iii) after exercise. ABG and SaO2 measurements – indications
and interpretation.
f. Subtypes of asthma: allergic, exercise, occupational
g. Differential diagnosis
h. The management of acute severe asthma: Nebulisers, steroids, IV drugs,
57
role of arterial blood gas analysis[respiratory alkalosis, the asthmatic with a
normal or elevated PCO2], indications for a chest radiograph
i. Ward management: When to discharge, PEFR monitoring, training in use
of inhaled medications.
j. Intensive care: indications, discharge.
k. Community management of asthma: PEFR monitoring, grades of asthma
severity, GINA guidelines. Goals in treatment of asthma in the community:
abolition of symptoms, prevention of asthmatic exacerbations, life style
issues.
l. Asthma Therapeutics:
Delivery devices – spacers, MDIs, Dry powder devices
Reliever medications - beta-2 agonists short and long acting
Preventer medications: long acting beta-2 agonists, inhaled
steroids, LTRAs, PDE inhibitors, Omalizumab
Avoidance measures: Allergens, smoking, dampness,
Pollutants, respiratory viruses
(2) COPD
a. Prevalence. Definition – role of spirometry
b. Aetiology: active smoking, smoking burden, genetics
c. Clinical presentation: cough and sputum, dyspnoea, acute exacerbation
d. Signs: hyperinflation, weight loss, signs of respiratory failure (central
cyanosis, flapping tremor, bounding pulse), pedal oedema, signs of
pulmonary hypertension (raised JVP, loud P2, tricuspid regurgitation)
e. Differential diagnosis
f. Investigations: spirometry, static lung volumes (air trapping), reversibility
testing, chest radiograph, arterial blood gas analysis (normal, acute
respiratory acidosis, compensated type 2 respiratory failure), ECG, FBC
g. Treatment of Acute Exacerbations of COPD: nebulisers, steroids,
antibiotics, controlled oxygen therapy, diuretics, physiotherapy, non-
invasive ventilation
h. Treatment of COPD in the community: goals in treatment, smoking
cessation strategies, beta-2 agonists, anticholinergics, theophyllines, inhaled
steroids, PDE inhibitors. Other: exercise, nutrition, vaccination, ambulatory
oxygen, pulmonary rehabilitation.
(3) Pneumonia
a. Definitions of pneumonia in the community and in hospital
b. Classification of pneumonias: CAP, Nosocomial, aspiration, relapsing,
pneumonia in the immunocompromised, geographical
c. Pathogens
d. Incidence and mortality
e. Clinical presentation
58
f. Signs
g. Differential diagnosis: asthma, CCF, IHD, pneumothorax, pleural effusion
h. Investigations
i. FBC, U&E, LFTs, CRP, ESR, ABG
ii. sputum, blood cultures, urine tests
iii. serology
iv. Radiology
i. Prognostic factors: age, comorbidity etc
j. Complications: lung abscess, Empyema, screening for lung cancer
k. Treatment of community acquired and nosocomial pneumonia
i. treated in the community
ii. admitted to hospital: nursing care, drugs, fluids,
l. Follow-up management: CXR, lung function. When are they indicated?
(4) Pleural Effusion

a. Overview of diseases of the pleura: effusions, mesothelioma, pleural
thickening, pleural secondaries
b. Definition
c. Aetiology
d. Clinical presentation
e. Signs
f. Differential diagnosis
g. Investigations:
Radiology: characteristics of the CXR, indications for CT scanning
Thoracentesis: Diagnostic implications of appearance of fluid
Microbiology, cytology,
biochemistry - protein, LDH, pH, other depending on
suspected cause. LIGHT’S CRITERIA.
Need to compare with blood values
Needle biopsy – see above
Thoracoscopy, thoracotomy
h. Transudate vs. exudate and their causes
i. Tube drainage
j. Treatment of an empyema
(5) Lung Cancer

a. Bronchogenic carcinoma
i. Definition
ii. Incidence, aetiology and risk factors: sex, genetics, active and
passive smoking and pollutants, radiation, occupational exposures
{asbestos, nickel, arsenic, silica, radiation, hydrocarbons}
iii. Clinical presentation

iv. Signs
v. Non-metastatic extra-pulmonary manifestations
vi. Investigation: sputum, CXR, CT Scan,
59
vii. Investigation – bronchoscopy: (washings, brushings, biopsy),
Indications: Persistent cough, Dyspnoea, Haemoptysis,
Abnormal CXR, Inhalation of a foreign
object, Dx of asthma, lung ca, bronchitis, lung
inf, examine a congenital deformity
Contraindications: Unstable low BP, Arrythmias, Recent
heart attack or heart disease, Bleeding
problems, Allergy to lidocaine, Unstable
asthma, Restricted TMJ
Major Complications (0.5%): Respiratory depression,
Pneumonia, Pneumothorax, Airway
obstruction, Cardiorespiratory distress,
Arrhythmias, Pulmonary oedema, major
haemorrhage
Minor Complications : Vasovagal Reactions, Fever,

Arrhythmias, Haemorrhage, Airway
obstruction, Pnuemothorax, nausea and
vomiting
viii. Surgical biopsy
ix. Histologic classification of bronchogenic carcinoma
x. Staging of large and small cell tumours
b. Other tumours - clinical presentation, diagnosis and outline of management

strategies:
i. other primary lung tumours including alveolar cell carcinoma,
adenocarcinoma
ii. secondary tumours of lung,
iii. mesothelioma,
iv. mediastinal tumours
(6) Venous thromboembolism: Pulmonary embolism, DVT

a. Incidence and aetiology, risk factors
b. Clinical Presentation: acute massive PE, submassive PE, acute PE
c. Differential diagnosis
d. Investigation: CXR, ABG, V:Q Scan, CT-pulmonary angiogram
e. Treatment of acute PE and massive PE
Anticoagulation: heparins: unfractionated heparin, LMWH,
duration of heparin, treatment, overlap with
warfarin. Adverse effects including
thrombocytopaenia
Warfarin: indications, adverse effects, duration of therapy,
monitoring, drug interactions
Early discharge management plans
f. DVT: diagnosis and treatment
60
(7) Tuberculosis
a. Definition
b. Clinical epidemiology of TB: West Indies, world-wide, why TB is an
important public Health problem. The five most common causes of death
world-wide.
c. Clinical presentation of tuberculosis; pulmonary TB, extra pulmonary
manifestations: lymph node TB, tuberculous meningitis, other.
d. Risk factors: diabetes, immunodeficient states including AIDS/HIV –
tuberculosis as an AIDS defining illness.
e. Diagnosis: may be clinical but importance of bacteriological diagnosis.
Sputum, bronchial specimens, gastric lavage (children), biopsy
f. Clinical descriptions of TB cases: ‘smear positive’ and ‘sputum smear
positive’ TB.
g. Differential diagnosis
h. Notification and Public Health Law
i. Organisation of TB services
j. TB treatment: drug sensitivity is always required, use of 4 drugs,
interactions, drug resistant TB, DOT
k. Prevention and Control of TB: control of TB in hospitals, Contact tracing
and examination of contacts: Mantoux, Heaf tests, Chest radiograph. BCG
vaccination and chemoprophylaxis.
l. Bovine TB, opportunistic mycobacterial infection eg MAI
(8) Other Granulomatous lung diseases: sarcoidosis, Wegener’s, Goodpasteur’s,

fungal infection, other.
(9) Diffuse parenchymal lung disease – basic investigative strategies. Treatment of

IPF:
a. Acute disease: infection, allergy, ARDS
b. Episodic: pulmonary haemorrhage, Churg-Strauss, EAA, COP
c. Chronic disease: Occupational, drugs (amiodarone, bleomycin,
methotrexate, paraquat), systemic disease (SLE, Sjogren’s, RA,
lymphangitic carcinoma), cryptogenic fibrosing alveolitis (idiopathic
pulmonary fibrosis - IPF), chronic aspiration, pulmonary veno-occlusive
disease. Classification of IPF.
(10) Other diseases of the pleura and chest wall

a. Spontaneous Pneumothorax: Treatment options, tension pneumothorax
b. Mesothelioma: asbestosis exposure
c. Kyphoscoliosis as a cause of respiratory failure
d. Ankylosing spondylitis
(11) Sleep disturbances

a. Definition and differential diagnosis of persistent sleepiness
b. Apnoeas: central vs obstructive
c. Clinical presentation of OSA, Epworth Scale
d. Risk factors. Relationship to the metabolic syndrome.
61
e. Diagnosis of OSA
f. Treatment: behaviour modification, nCPAP, surgery and oral devices,
tracheostomy. Pharmacotherapy- modafinil.
(12) Respiratory Failure

a. Definition and types of respiratory failure
b. Causes and treatment of Type I respiratory failure
c. Causes and treatment of acute Type II respiratory failure.
d. Acute on chronic Type II respiratory Failure
1. Definition
2. Causes
3. Assessment and treatment
e. Oxygen Therapy
1. What is FIO2?
2. Natural of chronic hypoxaemia (rationale of treatment)
3. Adverse effects of oxygen
4. Methods of administration
f. Ventilation:
1. Definition
2. Invasive vs non-invasive: advantages and indications
In the study of each of these diseases, the principles of history taking and examination will
be emphasized.
Students will be expected to be able to describe the investigation of these diseases and the
principles of management and knowledge of drugs used where applicable.
Specific details of management including doses of drugs used will be required for acute
severe asthma and acute pulmonary embolism. The role of the intensive care unit in the
management of acutely decompensate pulmonary diseases will be discussed.
Goals/Aims
The knowledge base developed during the year 4 training in internal medicine will be
expanded in year 5. All diseases discussed during year 4 will be reviewed during bedside
sessions and a few other pulmonary diseases will be discussed.
Seven very common pulmonary diseases have been chosen for the core pulmonary
medicine in your syllabus. Patients with these diseases should be easily clerked on the
medical wards of San Fernando General Hospital and Port of Spain General Hospital or
chest wards at the EWMSC. These diseases of the lungs will be discussed in terms of
disorders of the airways, lung parenchyma or pleura in order to illustrate a simple model of
understanding pulmonary diseases.
Students will be expected to attend the Medical Grand rounds at the POSGH during their
training at POSGH and to answer simple questions about the cases discussed during these
sessions.
62
Students are expected to be aware of the latest therapeutic strategies employing evidence-
based medicine. This information may be accessed via the various approved websites.
By the end of their 2 years’ training in pulmonary medicine, students will expect to have
reached an internationally accepted standard in their knowledge and management of
pulmonary diseases within general internal medicine.
General Objectives
At the end of the course you will be expected to

1. understand how to elicit a history of pulmonary diseases
2. be able to elicit the signs of pulmonary diseases
3. state a differential diagnosis for each symptom of pulmonary disease
4. know the causes of clubbing and cyanosis and the differential diagnosis of
cyanosis
5. demonstrate time management within the program
6. demonstrate empathy and caring toward your patients
7. submit a short project
Structure of the course: teaching vs bedside learning

The years 4 & 5 pulmonary medicine module consists of 1 session per week for 8 weeks
either at POSGH or at EWMSC. You will be provided with a sessional timetable at the
start of the course.
Specific Objectives
1. define the symptoms and signs of pulmonary disease
2. state common causes (pulmonary and non-pulmonary) of each
symptom or sign mentioned above
3. define each of the major diseases in this syllabus
4. integrate the symptoms and signs of pulmonary disease with the
clinical presentation of each of the pulmonary diseases studied in
this course
5. differentiate between the different conditions using the history,
examination and investigations discussed during this course
6. state the treatment of acute asthma and acute PE
7. discuss treatment options of pulmonary diseases
8. differentiate between tuberculous infection and tuberculous disease
in clinical presentation and management
9. discriminate between different arterial blood gas results and their
causes
10. use abnormal spirometric results in the differential diagnosis of
chest diseases
63
Assignments
1. The student will expected to clerk at least 1 patient with each of the first 7
pulmonary diseases described in the content section above and to present and discuss
each case with any instructor. Clerking of a patient will involve
a. Presenting compliant
b. Complete history
c. Examination of all systems of the patients with special
emphasis on the chest examination
d. A description of what investigations were done and should be
done with details of results where applicable
f. Follow-up plan for the patient including discharge
Assessment/ Evaluation
The purpose of the assessment would be to help you to appreciate where you have reached
in attaining the goals set out in this syllabus and to stimulate you to continue to study
internal and pulmonary medicine.
(1) A written examination based on structured questions or MCQs
(2) Evaluation of a project and coursework
(3) Grading of cases clerked
Teaching Strategies
The Department of medicine employs several teaching strategies which will include
1. guided lectures,
2. bed side teaching,
3. small group teaching,
4. non-lecture strategies: projects, group discussions, role play, co-operative learning
Resources
1. Patients on the medical and surgical wards, POSGH, are our most valuable
Resource.
Readings
1. Davidson’s Principles and Practice of Medicine: respiratory medicine chapter.
2. Kumar and Clarke: respiratory medicine chapter.
3. West JB. Respiratory physiology – the essentials.
4. Approved Websites: ATS (Amer Thoracic Society), ACCP (Am College of Chest
Physicians), NIH (Nat. Institute of Health USA), NICE (Nat. Institute of Clinical
Excellence), SIGN (Scottish Intercollegiate Guidelines Network), BTS (Brit
64
Thoracic Society), ERS (Eur Resp Soc), PUBMED.
Other websites should be discussed with the instructor before use.
APPENDIX vi
NEPHROLOGY MODULE
Course description
Title: Nephrology: Year 4&5 Undergraduate Medicine
Overview
This course is designed to complete the training of the medical undergraduate student in nephrology
within the context of general internal medicine over two rotating 8 weeks clerkships.
Prerequisite

3. Year 4 - at the Eric Williams Medical Sciences Complex (EWMSC), and San Fernando
General Hospital (SFGH)
65
4. Year 5 - at Port of Spain General Hospital (POSGH)
Depending on availability of personnel and consistent with the service commitment of the medical
teachers involved.

Nephrology is one of several components of general internal medicine with which the student is
expected to become familiar over the two final years of undergraduate training in the Faculty of
Medical Sciences and integrates closely with other sub-specialties including cardiology,
cardiothoracic surgery and intensive care medicine. Over the course of the final 2 years of
undergraduate training, students are expected to become familiar with the management of kidney
and urinary diseases within and across these specialties.
Nephrology as a Discipline within Internal Medicine

The Department of Clinical Medical Sciences is comprised of four units: Adult Medicine (General
Internal Medicine), Paediatrics, Radiology and Psychiatry. Nephrology is one of several disciplines
within internal medicine.
The course covers diseases of the kidneys and the urinary system and is often called nephrology,
when the focus is on internal medicine and urology when the focus is on surgery. Students would be
expected to have been exposed to the rudiments of the examination of the kidneys and history during
Phase I training. This course is designed for students during the final two clinical years of
undergraduate medicine.
At the end of the course, the student will be expected to diagnose and treat the following major
common renal conditions: Acute and chronic renal failure, anuria, interstitial nephritis,
rhabdomyolysis, hepatorenal syndrome, acute upper urinary tract infections, renal stones and
renovascular diseases. The student will also be expected to understand the differential diagnosis
of these conditions and how to differentiate between these and other medical conditions by
laboratory and other investigations.
Welcome to the Nephrology component of the Internal Medicine Programme. We hope that you
will see this course as an extension of the learning initiated during your first three years of training.
In the first year of internal medicine (year 4 undergraduate) we emphasize knowledge of the
underlying disease processes and the acquisition of an accurate history and examination. In the final
year our emphasis is on diagnostic skill, investigation and treatment of common renal diseases and
their differentiation from other diseases. The best advice we can give you is that learning is patient-
centred and not text-book centred, though your text books will provide a useful resource. We hope
you enjoy your brief time with us in this exciting field.
Contact Information
Tutors: please general syllabus above
66
Content
Signs and Clinical presentation of renal diseases

General observation: Pallor and tiredness, dyspnoea, hydration, bruising, itching and scratch marks,
malaise, confusion, seizure or coma, nausea, anorexia or vomiting.
Hands: nail pigmentation with ‘brown line’.
Pulse and blood pressure: Hypertension.
Face: Yellow complexion and pallor.
Eyes: Hypertensive and diabetic retinopathy.
Lungs: Crackles in fluid overload
Heart: Extra heart sounds, pericardial friction rub.
Abdomen: Inspect scar, palpation of kidney and bladder, sacral oedema. Auscultation of renal
arterial bruits, rectal examination, prostate enlargement. Ballottement of the kidneys.
Legs: Oedema and peripheral neuropathy.
The student is expected to characterize each of these symptoms by onset (where, when how),
duration and evolution. Common causes of each of these symptoms.
Symptom severity:
Cardiac: Cardiac failure, ECG, pericardial fremitus or murmur, hypertension
Dyspnoea: MRC dyspnoea scale, New York Heart Scale, respiration type
Consciousness: Glasgow Coma Scale
Temperature: With or without peripheral contraction.
Back pain: severity, location of pain in relation to probable cause but even pain elsewhere.
Urine: Haematuria, protenuria.
Skin: Bruising, itching, scratch mark.
Renal History
Past Medical History: importance of comorbidites eg anaemia, cerebrovascular incidences,
hypertension and/or cardiac problems, diabetes, liver problems, dyspnoea, skin and even recurrent
infections.
Intake/output: Importance of amount of fluid intake and loss. Eating habits.
Passing urine: How is it best described? Dysuria, strangury, urgency and frequency, polyuria,
nocturia, oliguria/anuria, incontinence, urge or stress incontinence, nocturnal enuresis
Drug History: Drug abuse, importance of retrospective diagnosis of renal disease from the drug
history. Adverse effects– ACEIs, Angiotensin receptor antagonists, NSAIDs. Kidney toxic,
Aminoglycosides, amphotericin, lithium, ciclosporin and tacrolimus, and in overdose paracetamol.
Drug for HIV disease.
Allergy history all aspects.
Smoking – definition of a pack year as a measure of smoking burden
Family – genetic basis of some kidney diseases – polycystic kidney disease. Familial diseases in
general.
Social and occupational history: living or working in hot environment. Exposure to organic solvents,
working with aniline dye. Socio-economic status.
Ethnic or geographical situation: Nephropathia epidemica (hanta virus) mainly in Europe and
Russia. Balkan nephropathy. Systemic lupus erythematous with nephritis in the far east, severe
hypertension or diabetes mellitus with renal failure more common in patients of African origin.
Investigation of Kidney Diseases
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I. Urine analysis:
Macroscopic examination: appearance, odour, volume
Biochemical examination: Gravity, pH, glucose, ketones, proteinuria, haematuria, bilirubin
and urobilinogen, nitrite.
Microscopic examination: Cells (red, white, epithelial cells or malignant cells). Casts
(hyaline, granular, red cells, white cells, crystals
Microbiological examination: Morphological assessment of pathogens
II. Biochemical assessment of renal function. Urea and creatinine, sodium and potassium,
bicarbonate, calcium, protein and albumin, phosphate, urate and haematological status.
Immunological screening.
III. Radiological investigation of renal system:

Ultrasound: Kidney size/shape?position: evidence of obstruction, renal cysts or solid lesions:
stones; gross abnormality of bladder and post-micturition residual volume, guided kidney
biopsy.
Dobler ultrasound: Reduced or absent renal or venous blood flow.
IV Urography: Renal uretic or bladder stones, cysts, tumors, hydronephrosis, other diseases.
Renal angiography: Renal artery stenosis; possibly proceed to angioplasty and/or stending.
Magnetic resonance imaging angiography: Renal artery stenosis.
Renal istotope scanning: Renal uptake and excretion of radio-labelled chemicals.
Abdominal CT scan: Renal, retroperitoneal or other tumour masses or fibrosis.
IV. Biopsy: Indicated in the diagnosis and assessment of parenchymal renal disease. Low
complications rate.
V. Chest radiograph: Fluid (overload) estimation, position of the diaphragm and to exclude lung
infiltrations.
VI. Arterial blood gases: Technique of taking ABG, technique of local anaesthetic, Allen’s sign,
Interpretation of ABG and the Henderson-Hasselbach Equation, Biochemistry of
measurement of pH, CO2, O2, HCO3. To distinguish the degree of metabolic acidosis versus
the decreased ventilation due to interstitial lung oedema.
Specific Diseases/Syndromes of the kidneys

● Renal disease:
o Glomerulonephritis: primary and secondary, the immunopathogenisis of the major
glomerulopathies (with and without association with systemic disease), treatment
options including role and complications of immunosuppression
o Nephrotic and nephritic syndromes: aetiology, complications and management
o Diabetic nephropathy: incidence, stages, microalbuminuria, management-early and
late
o Analgesic nephropathy: aetiology, incidence, clinical manifestations, and treatment.
o Hypertensive renal disease and renovascular disease: incidence, natural history,
diagnosis, and management (including pharmacological and non pharmacological
treatment of hypertension)
o Inherited renal disease, e.g. polycystic kidney disease, Alport's disease: genetics,
diagnosis/screening, and complications
o Reflux nephropathy: aetiology, clinical manifestations, and therapy
o Tubulo-interstitial diseases of the kidney (including acute and chronic interstitial
nephritis): aetiology, clinical manifestations, and therapy.
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● Acute and chronic renal failure:
o Definition, differentiation between 'prerenal', 'renal' and 'postrenal' causes of acute
renal failure; knowledge of common causes of acute and chronic renal failure;
knowledge of symptoms and signs of uraemia; assessment of severity; non dialytic
therapy including principles of managing calcium phosphate balance
o Effect of common drugs on renal function and principles of dose modification of
drugs in renal failure.
● Urinary infections, nephrolithiasis and obstructive nephropathy:
o Urinary tract infections: clinical manifestations, microbiology, diagnosis,
investigation, management (including pyelonephritis, cystitis, prostatitis, and
recurrent urinary tract infections)
o Renal stone disease: incidence, aetiology, clinical manifestations, prevention, drug
therapy, urological principles
o Obstructive nephropathy: diagnosis and management including indications for
emergency nephrostomy; knowledge and understanding of acute urinary retention.
In the 4th year the main focus is on the principles of history taking and examination. Students will be
expected to be able to describe the investigation of these diseases and the principles of management
and knowledge of drugs used where applicable.
In the 5th year focus is on the medical and integrated treatment not least the pharmacological and non
invasive treatment .
Goals/ Aims
The knowledge base developed during the year 4 training in internal medicine will be expanded in
year 5. All diseases discussed during year 4 will be reviewed during bedside sessions and a few
other renal diseases will be discussed.
Patients with kidney failure diseases should be easily clerked on the medical wards of San Fernando
General Hospital, Port of Spain General Hospital or the EWMSC. These diseases will be discussed
in terms of pathophysiology in order to illustrate a simple model of understanding kidney diseases.
Collection and presenting findings fitted to the SOAP format will be emphasized.
Students will be expected to attend the Medical Grand rounds at the EWMSC and POSGH during
their training at EWMSC respectively POSGH and to answer simple questions about the cases
discussed during these sessions.
Students are expected to be aware of the latest therapeutic strategies employing evidence-based
medicine. This information may be accessed via the various approved websites.
By the end of their 2 years’ training in nephrology, students will expect to have reached an
internationally accepted standard in their knowledge and management of renal diseases within
general internal medicine.
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General Objectives
1. At the end of the course you will be expected to

1. Understand how to elicit a history of renal diseases
2. Be able to elicit the signs of kidney failure
3. State a differential diagnosis for each symptom of renal disease
4. Know the causes of each symptom of kidney failure
5. Demonstrate time management within the program
6. Demonstrate empathy and caring toward your patients
7. Submit a short project
The years 4 & 5 nephrology module consists of 1 session per week for 8 weeks (each year) either at
POSGH or at EWMSC. You will be provided with a seasonal timetable at the start of the course.
Specific Objectives
1. Define the symptoms and signs of uraemia

2. State common causes (Pre-, inter-, and post-renal) of each symptom or sign
mentioned above
3. Define each of the major diseases in this syllabus
4. Integrate the symptoms and signs of kidney failure with the clinical
presentation of each of the kidney diseases studied in this course
5. Differentiate between the different conditions using the history, examination
and investigations discussed during this course
6. State the treatment of renal emergencies:
❑ Acute renal failure.
❑ Anuria.
❑ Interstitial nephritis.
❑ Rhabdomyolysis.
❑ Hepatorenal syndrome.
❑ Acute upper urinary tract infections.
❑ Renal colic and renal stones.
❑ Haematuria.
❑ Renovascular disease.
❑ Cholesterol embolism.
❑ Contrast nephropathy.
7. Discuss treatment options of renal diseases.
8. Differentiate between chronic and acute renal failure in clinical presentation
and management.
9. Discriminate between different clinical chemistry results including arterial
blood gas results and their causes.
Lay out short treatment plan (until patient can be seen by nephrologists) based on published
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guidelines (= evidence based).
Assignments
1. The student will expected to clerk at least 5 patients with renal diseases described in the
content section above and to present and discuss each case with any instructor. Clerking of a
patient will involve
b. Complete history
c. Examination of all systems of the patients with special
emphasis on the renal examination
d. A description of which investigations that have already
been done with details of results where applicable and which
investigations are planned.
f. Follow-up plan for the patient including discharge
The purpose of the assessment would be to help you to appreciate where you have reached in
attaining the goals set out in this syllabus and to stimulate you to continue to study internal medicine
and nephrology.
Teaching Strategies
1. guided lectures,
Resources
1. Patients on the medical and surgical wards are our most valuable resource.
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Readings
1. Davidson’s Principles and Practice of Medicine: Renal chapter.

2. Kumar and Clarke: Renal chapter.
3. Chapter 20 ‘HIV and Renal Function’ in ‘HIV Medicine 2006’. Can be
downloaded free of charge from http://www.hivmedicine.com/
4. Some Recommended Websites: The American Society of Nephrology, BioMed-Nephrology,
Nephrology Rounds, Hypertension, Dialysis & Clinical Nephrology (HDCN), American Society of
Hypertension, American Society of Transplant Surgeons, International Society of Nephrology,
European renal association, National Kidney Foundation
The student should use sound judgment when searching information from various other websites.
If the student has doubts on the validity of a site, the student is encouraged to discuss the
information with the instructor.
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APPENDIX vii
ONCOLOGY CURRICULUM: Years 4 & 5
Objectives
Area Objective Topic
Public health
1.1 The role of cancer in population health and illness
1.2 Cancers – epidemiology, risk factors
1.3 Prevention, screening, and family risk
Cancer biology
2.1 Functional anatomy
2.2 Physiology
2.3 Pathology
2.4 Molecular biology
Patient management
3.1 Patient management including referral and multidisciplinary management
3.2 Quality of life, therapeutic ratio and resource costs
3.3 Uncertainty and information management
Diagnosis
4.1 Clinical examination
4.2 The diagnostic process
Treatment
5.1 General principles of treatment
5.2 Principles of surgery
5.3 Principles of radiotherapy
5.4 Principles of systemic therapy
5.5 Principles of palliative care
5.6 Follow-up and relapse
Communication skills
6.1 Psychosocial and cultural significance of cancer
6.2 Communication and counselling
6.3 Education of patients
6.4 Family and community support
Ethics
7 Ethics and professionalism
Clinical experience
8 Five essential cancer clinical experiences
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Area: Public Health
Objective 1.1
Appreciate the significance of cancer as a health problem in Australia and throughout the
world.
Objective 1.2
The role of cancer in population health and illness
Appreciate the significance of cancer as a health problem in Australia and throughout the
world.
Cancers – epidemiology and risk factors
a) Describe the epidemiological concepts of morbidity (incidence and prevalence),
mortality, relative risk and survival in relation to common cancers.
b) Discuss the role of statistical information, including surveillance and monitoring data,
and understanding the medical practitioner’s need to be able to access numerical
information.
c) Discuss the purpose of cancer registries.
d) Describe risk factors for various malignancies – genetic and non-genetic.
e) List the most frequently diagnosed malignancies and the most common causes of
cancer death in Australia; describe in a general way how these are different in different
parts of the world.
f) Describe the differential rates of cancers and their outcome in Indigenous and non-
Indigenous Australians and the reasons behind them.
g) Describe the differing outcomes of cancers, in general, between rural and urban
populations and the reasons behind them.
✔ Prerequisite knowledge
■ Statistical concepts of relative and absolute values.
■ Inherited and acquired risk factors.
■ DNA structure and function.
■ Mendelian genetics.
1.2 Representative questions that suggest the required depth of knowledge
1. Describe the role of epidemiology in establishing causes of cancer and identifying risk
factors for cancer. Give examples of causes of cancer and risk factors for cancer and
explain the differences between them.
Essential in answer
■ Concept of risk – definitions, relative v absolute risk
■ Concept of causation.
■ Understanding of data collection.
2. Answer, in language you would use, the question from 45 year-old Mabel Jones: "What
caused my bowel cancer doctor? And what are the risks that other members of my
family will get cancer?"
Essential in answer
■ Knowledge of risk factors for colorectal cancers.
■ Knowledge of genetics of colorectal cancers.
3. What proportion of breast cancer patients have an identifiable genetic cause?
(a) 1%
(b) < 5%
(c) 5-10%
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(d) 30%
Answer: (c)
4. Which conditions are associated with an increased risk of colon cancer?
Essential in answer
■ Ulcerative colitis.
■ Crohn’s disease.
■ Familial polyposis.
■ Other familial conditions including hereditary non-polyposis coli syndrome
(HNPCC).
■ Benign polyps of the bowel.
■ Previous colon cancer.
11
Objective 1.3
Prevention, screening and family risk
a) Describe methods for the primary and secondary prevention of cancer, including
measures that employ a public health approach, as well as those depending on
individuals and their doctors.
b) Describe the methods of screening for cancer and pre-malignant conditions.
c) Demonstrate an understanding of the scientific evidence for the utility of screening, the
difference between population-based screening and surveillance of individuals, and
cost-effectiveness issues.
d) Discuss environmental control and behavioural and chemical approaches to the
prevention of cancer.
e) Demonstrate an understanding of the psychosocial impact of screening and staging
investigations on the patient.
f) Demonstrate ability to take family history.
■ Basic epidemiological concepts including: prevalence; incidence; specificity;
sensitivity; predictive value; screening v diagnosis; cost-benefit analysis; and
prevention strategies.
IDEAL ONCOLOGY CURRICULUM FOR MEDICAL SCHOOLS
12
1. Elizabeth Smith, a 54 year-old long-standing patient is seeing you in a follow-up visit for
a settling U.T.I. You decide it is time she had a mammogram and suggest this to her.
She replies: "Why should I do that and what good would it do me?" What is your
answer?
Essential in answer
■ Mammographic screening of women over 50 years of age has been shown to
improve survival and produce better outcomes in populations that are screened.
2. John Smith, the 54 year-old husband of Elizabeth is seeing you for a routine insurance
check-up. During the course of the visit he asks you about cancer. He smokes 10
cigarettes a day, drinks "socially", is modestly overweight and has a younger brother
with colorectal cancer. He then specifically asks for a PSA test, as he is worried about
prostate cancer. What course of action and relevant explanations would you offer to
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him?
Essential in answer
■ Knowledge of environmental and lifestyle risk factors.
■ Knowledge of the genetics of colorectal cancer.
■ Knowledge of the controversy regarding PSA screening.
■ Recognition that smoking, overweight and familial risks are, on balance, more
significant issues than PSA levels for this patient.
3. With respect to screening for common cancers in Australia, select the best answer:
(a) Mammography has been advocated in Australia for asymptomatic women aged
<40 years.
(b) Pap smears can be discontinued when the woman ceases regular sexual activity.
(c) A normal result for prostate specific antigen (PSA) excludes a diagnosis of prostate
cancer.
(d) A family history of familial adenomatous polyposis increases the probability of
malignancy in an anxious 27 year-old female who reports altered bowel habit.
Answer: (d)
13
Objective 2.1
Functional Anatomy
Demonstrate an understanding of the anatomical basis of cancer assessment such as:
vascular supply (eg. liver); lymphatic drainage patterns (eg. breast); and anatomical
relationships of relevance to oncology (eg. pelvis).
■ General anatomy.
1. Describe the modes of potential spread of breast cancer in the upper outer quadrant
of the left breast.
Essential in answer
■ Direct extension – skin, chest wall.
■ Lymphatic spread – axillary nodes, internal mammary nodes, supraclavicular nodes.
■ Haematogenous spread – bone marrow, lung, liver, brain.
2. A patient has a squamous cell carcinoma of the apex of the left lung (Pancoast
tumour).
Describe the possible structures involved in local progression, and their effects.
Essential in answer
■ Brachial plexus (lower roots; C8/T1) – pain, weakness in small muscles of hand.
■ Cervical ganglion (sympathetic nerve) – Horner’s Syndrome.
■ Chest wall invasion – pain, mass.
■ Supraclavicular extension – pain, mass.
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Area: Cancer biology
14
Objective 2.2
Physiology
Describe the principles of handling of chemicals (by cells): drug metabolism, handling of
carcinogens.
■ Cell biology.
■ Organ function.
■ Normal physiology.
1. What is the blood/brain barrier?
Essential in answer
■ Concept of sanctuary sites.
■ Knowledge of mechanisms of fat solubility and molecular size.
2. In a cancer patient with renal impairment, chemotherapy doses should be (select the
best answer):
(a) Decreased.
(b) Increased.
(c) Unchanged.
(d) Reviewed.
Answer: (d)
15
Objective 2.3
Pathology
a) Describe the concept of carcinogenesis.
b) For the common cancers, demonstrate an understanding of microscopic and
macroscopic findings, including pathological features from pre-malignant to
malignant stages of cancer.
c) Describe patterns of spread of common cancers.
d) Demonstrate an understanding of the role and purpose of molecular pathology
particularly the prognostic and/or predictive values of receptors and other targets.
■ Cell biology.

16
1. Explain the patho-physiological mechanism(s) whereby a tumour may grow in
lines of diverse differentiation (“tumour heterogeneity”).
77
Essential in answer
■ Knowledge of mutation/genetic instability.
2. What are the roles of Tumour Angiogenesis Factor and Tumour Necrosis Factor in
neoplasia?
Essential in answer
■ Knowledge of new blood vessel formation.
■ Knowledge of abnormal cytokine production.
3. A 65 year-old man has been diagnosed with rectal cancer. Describe possible
Methods of cancer spread.
Essential in answer
■ Vascular and lymphatic systems.
■ Direct spread.
■ Trans-coelomic spread.
■ Implantation.
4. Describe how knowledge of ER PR and HER2 status in breast cancer will dictate
prognosis and treatment?
Essential in answer
■ Hormone responsiveness.
■ Role of hormonal treatment.
■ Role of Herceptin.
5. With respect to cancer spread, the most common site of extralymphatic

dissemination is from (select the best answer):
(a) Colon to lung.
(b) Breast to contralateral breast.
(c) Prostate to liver.
(d) Lung to brain.
Answer: (d)

17
Objective 2.4
Molecular biology
a) Demonstrate an understanding of the molecular genetics of cancer: role of
protooncogenes; tumour suppressor genes; DNA and RNA viruses; controls of
apoptosis and angiogenesis; and elements of molecular genetic techniques.
b) Demonstrate an understanding of the molecular correlates of the pathological
progression of cancer in a model system.
c) Describe hormonal influences and tumour markers relevant to tumour type and
prognosis.
d) Identify important familial cancer syndromes and demonstrate an understanding of
their molecular basis, mode of inheritance, associated risk of disease and implications
for family counselling.
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■ Biochemistry.
■ Functional anatomy.
■ Genetics.
■ Oncological physiology.
■ Pathology.

18
1. Discuss oncogenes and their normal counterparts.
Essential in answer
■ Normal functions of proto-oncogenes in the mitogenic cascade.
■ Oncogenes as mutations of proto-oncogenes resulting in gain of function
(dominant) characteristics.
■ Examples of classes of normal functions (growth factors, their receptors etc).
■ Examples of mutating events (point mutation, amplification, translocation etc).
2. Approximately 70% of patients with retinoblastoma have unilateral disease and 30%
have bilateral or multifocal disease. Explain the mechanisms for unilateral and
bilateral disease. What is the risk of recurrence in family members?
Essential in answer
■ Concept of RB1 as a tumour suppressor gene.
■ Familial and sporadic cancers and the Knudson (two hit) hypothesis - in familial
retinoblastoma the first hit is either inherited or a new mutation in a gamete.
■ Penetrance issues in familial cancers (bilateral disease always involves a germ-line
mutation; unilateral disease may be familial so parents of an apparently sporadic
case must be examined for evidence of healed retinoblastoma).
■ Familial cancers typically exhibit dominant inheritance with variable penetrance.
3. A young woman consults you because she is anxious about her family history of
breast cancer. Her mother died recently aged 53 of ovarian cancer following a history
of breast cancer. She had two second-degree relatives with breast cancer, an aunt who
died in her 40s and another aunt who died in her early 60s. Tissue is not available
from any of the deceased relatives.
What is this woman’s risk of cancer? What is your management rationale and why?
Essential in answer
If the diagnoses are correct and the deceased relatives are genetically related her risk
of breast and ovarian +/- colorectal cancer is high (involvement of BRCA1 or 2
possible). Referral to a clinical geneticist or familial cancer clinic is desirable. The
rationale for referral is to obtain risk assessment and management strategies which
would include:
■ Counselling: about risk and attitudes to genetic testing and information about its
limitations (currently not available in Australia without DNA from an affected
family member; false negatives).
■ Increased surveillance in the absence of testing or if gene mutation is detected.
■ Identification of other family members at risk.

19
79
4. Relate the following investigation findings to the appropriate tumour type:
(1) ovarian cancer
(2) breast cancer
(3) colorectal cancer
(4) prostate cancer
(5) hepatocellular cancer
(a) CA 15.3
(b) CA 19.9
(c) CA 125
(d) Prostate specific antigen (PSA)
(e) Carcinoembryonic antigen (CEA)
(f) Alpha fetoprotein (AFP)
Answer 1c, 2a, 3e, 4d, 5f

20
Objective 3.1
Patient management including referral and multidisciplinary management
a) Demonstrate awareness of clinical practice guidelines, where available, for appropriate
referral patterns - understand the need for evidence based medicine.
b) Identify effective means of communication to enhance the clinical management of
patients with cancer.
c) Demonstrate an understanding of the need to recognise, address and manage
psychological distress in the patient.
d) Recognise the importance of coordinated care in optimising overall management of
patients.
e) Recognise their own clinical limitations and understand that help from those with
better specialist knowledge can be sought.
f) Demonstrate an ability to seek help at an appropriate level of urgency, using
appropriate methods of communication, from appropriate sources.
g) Demonstrate an attitude of accepting responsibility for ensuring continuity of care for
patients over the long-term, and at all hours.
h) Describe the integration of treatment modalities.
i) Survey treatment options available to the patient, including a knowledge of
unproven/experimental therapies, as distinct from alternative therapies.
j) Demonstrate an understanding of the range of medical and non-medical health
professionals involved in cancer care.
k) Demonstrate an understanding of the effective use of a multidisciplinary management
team.
■ Basic understanding of how the health care system works.
Area: Patient management
21
1. Write a referral letter from a general practitioner to a specialist about a patient who you
suspect has a lung cancer (develop hypothetical case data). Include all the information
you consider relevant for the specialist to manage the case in conjunction with the
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patient’s GP (yourself).
Essential in answer
■ History taking.
■ Examination.
■ Succinct communication and relevance.
2. You have referred Mrs Briggs, a 47 year-old woman, to a general surgeon who you
went to university with because she has a suspicious lump in her left breast. Mrs
Briggs asks you about the multidisciplinary clinic that she has read about in the
National Health and Medical Research Council consumer guide. How do you respond?
Essential in answer
■ Knowledge of multidisciplinary management of cancer.
■ Knowledge of specialist v non-specialist management of cancer.
■ Ability to review management in light of evidence.
3. Write a submission to a hospital administration justifying the establishment of a
multidisciplinary breast clinic in your large teaching hospital.
Essential in answer
■ Knowledge of the different disciplines that contribute to successful cancer
management.
■ Knowledge of models that integrate disciplines.
■ Understanding of cost-benefits.

22
Objective 3.2
Quality of life, therapeutic ratio and resource costs
a) Understand how quality of life is assessed.
b) Appreciate the balance of risks and benefits of treatment as a key consideration in
making treatment decisions.
c) Demonstrate an understanding of the concepts of cost effectiveness, cost benefits and
opportunity costs.
d) Demonstrate an understanding of the principles of measurement of quality of life.
e) Demonstrate an understanding of the concept of therapeutic ratio.
f) Assess the effects of clinical decisions about treatment on the patient, their family and
the health care system in terms of: quality of life; burden of treatment; effect on the
disease process; and financial and other costs, including costs to the patient and family
associated with patient location v treatment location.
g) Incorporate measurements of quality of life in assessment of performance status.
h) Demonstrate an awareness of supportive care networks and how to access and utilise
them.
1. If two cancer treatments such as surgery and radiotherapy give the same survival
results for a given cancer, what other issues would you consider in advising which
treatment is the better?
Essential in answer
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■ Knowledge of how side-effects and quality of life impact on the therapeutic ratio.
■ Knowledge of costs/cost benefits/opportunity costs.
2. Discuss the common instruments used to measure quality of life.
Essential in answer
■ Definition of quality of life.
■ General knowledge of SF36, FL1C and the Rotterdam Symptom Checklist.
3. How does the general quality of a patient’s health impact on their probability of survival
when cancer is diagnosed?
Essential in answer
■ Understanding of measurement of performance status.
■ Understanding of impact of performance status on survival.
■ Understanding of side-effects.

23
Objective 3.3
Uncertainty and information management
a) Describe the importance of evidence based medical practice.
b) Demonstrate an understanding of the need to be able to critically appraise evidence.
c) Appraise information from patients and other subjective sources critically, and record in
a way that allows the information to be retrieved and communicated effectively for
optimal management.
d) Critically appraise the available information guiding the management of common
cancers and be able to distinguish different levels of evidence.
e) Locate published high quality evidence and guidelines for practitioners and patients
using electronic literature searches, both locally and from overseas.
f) Adapt and apply information to the management of individual cases and to the
formulation of management options in the absence of definitive information (tolerating
uncertainty).
g) Demonstrate an understanding of clinical trials and their importance; explain their value
to patients and encourage patients to participate in trials.
h) Describe basic elements of clinical trials, cohort studies and case control studies.
i) Appraise studies of treatment, prevention, diagnosis, prognosis, causation and harm,
systematic reviews, clinical practice guidelines and cost-effectiveness studies.
j) Demonstrate an understanding of the limits of evidence, its broad application and its
advancement over time.
k) Discuss unproven or alternative/complementary cancer therapies in a way that
encourages patients to appraise their claimed benefits and their costs in a critical manner.
■ Basic understanding of clinical epidemiology.
■ Ability to describe and utilise clinical epidemiological terms such as sensitivity and
specificity.
■ Understanding of processes of critical appraisal.
■ Ability to locate available evidence based medicine and guideline information by
Manual and electronic literature searches, including the internet and Cochrane
Collaboration databases.
82
■ Ability to describe basic elements of research methods: randomised control trials;
cohort and case control studies.
■ Understanding the relative value of evidence provided by such different research
methods and how they are quantified.
■ Understanding the role of qualitative research findings in guiding clinical decision
making.
■ Understanding the principles of evidence based medicine and levels of evidence.
■ Understanding the strengths and weaknesses of different study designs.

24
1. Mr Cathari, a 58 year-old man with metastatic colon cancer, visits you in your
General practice. He has some mild lethargy but is otherwise well. He wants advice
about alternative/complementary treatments for his cancer. What do you tell him?
Essential in answer
■ Concept of unproven as opposed to alternative therapy.
■ Critical appraisal of cost benefits.
■ Knowledge of guidelines.
2. A patient who has breast cancer comes to you with some information on breast
cancer from the internet. She is very worried and has a lot of difficulty knowing what
to believe. What do you tell her about retrieving useful information from the internet?
Essential in answer
■ Critical appraisal.
■ Knowledge of useful websites.
■ Encouragement of use of well written evidence based literature in addition to
web-based information.
■ Awareness of other sources of information such as breast cancer support services
and the Lymphoedema Association.
3. “Clinical practice guidelines are a waste of time” – discuss.

Essential in answer
■ Levels of evidence.
■ Variation in practice.
■ Limits to knowledge.
■ Accountability.
■ Individualising care.
4. A randomised phase III trial was performed between drug X and Docetaxel as second
line
therapy for metastatic non-small cell lung cancer. Fifty patients were randomised to
each arm and when comparing objective response rates no significant difference was
found between the two arms p>0.05. Discuss the possible meanings of this result.
Essential in answer
The numbers may not provide sufficient power to detect a clinically meaningful
difference so it is not necessarily a negative study, but an indeterminate result. Is
objective response rate the best endpoint in this situation?
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25

Objective 4.1
Clinical examination
a) Discuss clinical manifestations of cancer, considering broad aspects of:
(i) functional anatomy (vascular supply, lymphatic drainage, oncological anatomical
relationships);
(ii) oncological pathophysiology;
(iii) pathology.
b) Demonstrate an understanding of the components of the clinical examination of

common cancers.
c) Demonstrate effective clinical examination relevant to common cancers.
d) Describe the results of clinical examination.
e) Accurately describe the physical signs of cancer.
■ Anatomy of common cancer sites.
■ Clinical examination framework and skills.
Area: Diagnosis

26
1. What are the potential areas of spread of a breast cancer recently treated by surgery,
radiotherapy and chemotherapy? How would you detect them? Is early detection of
recurrence or metastasis worth while?
Essential in answer
■ Knowledge of organ/local/distant cancer spread.
■ Knowledge of clinical examination techniques.
■ Appropriate clinical examination reasoning.
2. Select two commonly occurring cancers (eg. breast and rectal) and discuss how your
examination of a patient is determined by your knowledge of the anatomical spread of
those cancers? Briefly describe the clinical techniques used for each aspect of the
examination of each organ or body part relevant to the examination for each cancer
type.
Essential in answer
■ Knowledge of organ/local/distant cancer spread.
■ Knowledge of clinical examination techniques.
■ Knowledge of how to self educate patients.
■ Appropriate clinical examination reasoning.
3. A 55 year-old male presents with his first episode of bright bleeding per rectum.
There is no past history of bowel problems. If no other personal history is
forthcoming, what investigation would be most appropriate?
(a) Faecal occult blood testing x3.
(b) CEA.
(c) Colonoscopy.
84
Answer: (c)

27
Objective 4.2
The diagnostic process
a) Demonstrate an understanding of the wide range of potential presentations of cancer,
and be open to unusual presentations.
b) Take history and conduct a physical examination, tailoring the latter to natural history
and patterns of spread of common cancers.
c) Assess performance status.
d) Discuss the differential diagnosis of common cancers based on specific oncological
findings.
e) Describe how to establish a diagnosis of cancer: outcome overview; diagnostic tools
(biopsy, surgery, cytology, imaging, endoscopy); genetic/biochemical/molecular
markers.
f) Demonstrate an understanding of the histopathological classification and staging of
cancers, including the concept of TNM and the implications of staging for prognosis
and treatment.
g) Recognise common complications of malignant disease, eg. superior vena cava
obstruction, spinal cord compression, bone involvement.
h) Evaluate critically the cost effectiveness of investigations.
■ Sufficient basic scientific knowledge of tumours, benign and malignant processes, the
principles of ‘cure’ of cancer (including epidemiological concepts such as five-year
survival).

28
1. Explain performance status.
Essential in answer
■ Knowledge of ECOG and Karnofsky Performance Scales and how performance
status affects outcomes.
2. Describe the diagnostic process for a woman presenting with a breast lump. If
malignant, what further investigations should you perform?
Essential in answer
■ Physical examination, mammography, ultrasound, fine needle aspiration.
■ If malignant assess pathology report and metastatic spread.
3. What is the purpose of staging tumours?
Essential in answer
■ Prognosis.
■ Treatment decisions.
■ Comparison with other data sets.
4. A 60 year-old female smoker presents with a one month history of worsening back
pain and a history of work-related back pain over 12 years. What are the potential
85
causes and how would you establish a diagnosis?
Essential in answer
■ Metastatic lung cancer.
■ Non-malignant causes.
■ Establish diagnosis – plain X-Ray films, bone scan, CT, biopsy.

29
Objective 5.1
General principles of treatment
a) Demonstrate a recognition of the importance of the patient in the decision-making
process and the influences that affect their choices.
b) Describe the principles of treatment with intent to cure and palliate.
c) Describe the role of multidisciplinary management of the patient.
d) Demonstrate an understanding that tailoring of standard treatment protocols may be an
appropriate component of patient focused care.
e) Demonstrate awareness of the process and outcome measures including concepts of
self audit and quality assurance to minimise deviation from best practice.
f) Outline how the treatment of malignancies by different modalities of treatment is
guided by the natural history of the malignancy and the findings of staging evaluations.
g) Demonstrate an understanding of the unique features of the management of cancer in
children and adolescents and cancer in the elderly.
h) Demonstrate an understanding of the management of potential complications of
cancer treatments eg. febrile neutropenia, mucositis, radiation skin injury.
i) Demonstrate an understanding of the management of common oncological
emergencies eg. spinal cord compression, hypercalcaemia.
j) Demonstrate an understanding of the patho-physiology of oncology emergencies and
their management eg. compressive, obstructive, coagulation and metabolic
syndromes.

1. List the possible causes of confusion in a patient with metastatic lung cancer.
Essential in answer
■ CNS – brain metastases.
■ Metabolic – hypercalcaemia, renal failure.
■ Iatrogenic – drugs eg. morphine, steroids.
2. How does the therapeutic ratio change when surgery is used for the palliation of lung
cancer rather than for cure?
Essential in answer
■ Shorter survival prospects of patients.
■ Reduced acceptability of side-effects.
Area: Treatment
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30
Objective 5.2
Principles of surgery
a) Describe the aims of surgical treatment of cancers and the general principles of
common procedures.
b) Demonstrate an understanding of the range of surgical options and the ways these are
affected by the integration into multi-modality care.
c) Recognise clinical indications for surgery of common cancers.
d) Evaluate the outcomes of surgery, including efficacy, short and long-term side-effects,
financial costs and quality of life.
e) Describe the general and specific pre-operative factors that influence surgical decision
making.
f) Discuss the effect surgery may have on body image, including the role of
reconstructive surgery.
g) Recognise the common complications of cancer surgery and understand their
management.
h) Discuss interactions with other modalities of therapy, both pre and post-operatively.
■ Principles of pre-operative assessment.
■ Principles of post-operative management including pain control.
■ General complications of anaesthesia and surgery eg. deep venous thrombosis,
lymphoedema, pneumonia.
31
1. Your patient is a fit 65 year-old man with prostate cancer. You are discussing radical
(not nerve sparing) prostatectomy as a treatment. What probability would you quote
him of these significant side-effects occurring after surgery?
Impotence occurs:
(a) < 5%
(b) 20%
(c) 50%
(d) 80%
Answer: (d)
2. A common management of early breast cancer is wide excision. What are the aims of
this treatment?
Essential in answer
■ Adequate pathological margin around invasive and intraductal cancer.
■ Breast conservation.
■ Good cosmetic outcome.
3. Radiation treatment to the breast after wide excision of cancer reduces the local
recurrence rate at five years to:
(a) 0
(b) 5 - 10%
(c) 10 - 20%
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(d) 40%
Answer: (b)
4. Discuss why different surgeons may have different local recurrence rates after
surgical resection of rectal cancer.
Essential in answer
■ Experience.
■ Training.
■ Number of cases per year.
■ Type of cases referred.
5. What are the long-term effects of lymph-node dissection for melanoma of the leg?
Essential in answer
■ Lymphoedema.
■ Infection risk.

32
Objective 5.3
Principles of radiotherapy
a) Describe the principles of radiobiology.
b) Discuss the principles of radiotherapy: loco-regional treatment with either curative or
palliative intent; when administered with curative intent it might be primary therapy or
adjuvant to the primary modality.
c) Describe the salient features of delivering radiation treatment using equipment such as
linear accelerators and brachytherapy machines. This should include a general
description of treatment simulators, bunkers and the treatment planning departments.
d) Describe the general features of brachytherapy treatment, including the use of
different isotopes placed with a variety of techniques in various anatomic sites, most
prominently for ca cervix and ca prostate.
e) Recognise the clinical indications for radiotherapy.
f) Evaluate the outcomes of radiotherapy including: efficacy, short and long-term side
effects, costs and quality of life.
g) Recognise the common complications of radiotherapy and understand their
management.
h) Discuss the integration of radiotherapy with other modalities.
i) Demonstrate an understanding of the access problems associated with radiotherapy
and how this may affect patient choice.

a. List the symptoms that may effectively be palliated by radiotherapy for patients with
metastatic malignant diseases.
Essential in answer
■ Bone pain, and other pains, particularly neuropathic.
■ Bleeding from ulcerated tumours.
■ Symptoms of brain metastases.
■ Symptoms of cord compression.
■ Dysphagia.
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■ Shortness of breath due to compressive lung tumours.
■ Haemoptysis.
■ Compressive symptoms from tumour masses.
■ Haematuria from bladder or prostate tumours.

33
b. In what ways would the delivery of palliative radiotherapy for patients with metastatic
disease differ from that of the delivery of radical or curative radiotherapy for patients
with more localised cancer?
Essential in answer
■ Fewer treatments.
■ Fewer acute side-effects and fewer late side-effects.
■ Less complex treatments.
■ Less demanding of the patient.
c. If a surgeon has successfully excised a carcinoma from the breast of a woman and
dissected the lymph nodes out of the axilla, is there any place for postoperative
radiotherapy to the breast, and if so, for what reason and for what benefit?
Essential in answer
■ Yes, there is a place for postoperative radiotherapy.
■ When high risk of local recurrence eg. large primary tumours, positive axillary lymph
nodes, high grade of tumour, positive margin, lymphovascular invasion.
■ To reduce local recurrence.
■ Possibly to improve survival.
d. A man in his early 60s has undergone a resection for a rectal carcinoma and is being
recommended to undergo a postoperative course of adjuvant radiotherapy to the pelvis
in conjunction with chemotherapy. What information should that patient be given in
order to help him make an informed decision before he consents to the therapy
proposed?
Essential in answer
■ Potential benefit in terms of relative reduction and risk of local regional recurrence.
■ Acute toxicity of treatment and late toxicity of treatment.
■ Logistics of the details of treatment delivery, including planning on a “simulator”,
planning beam arrangements and brief daily treatments in a specialist radiotherapy
centre on a “linear accelerator” over the course of more than a month.
■ Cost to the patient.

34
Objective 5.4
Principles of systemic therapy
a) Outline the principles of systemic therapy including chemotherapy, hormone and
immunotherapy biological therapies (including immunomodulators, signal transduction
inhibitors and monoclonal antibodies) and (prospectively) gene therapy.
b) Recognise clinical indications for use of systemic therapy in early and advanced
disease.
c) Evaluate the outcomes of systemic therapy including efficacy, short and long-term side
effects,financial costs and quality of life.
d) Demonstrate ability to assess response to systemic therapy both clinically and
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radiologically.
e) Recognise the common complications of systemic therapy and understand their
management.
f) Demonstrate ability to manage toxicities and adverse reactions to systemic therapy
eg emesis, febrile neutropenia.
g) Discuss the integration of systemic therapy with other modalities.

1. Describe some of the important toxicities associated with a course of systemic
chemotherapy for lymphoma (support your answer with possible mechanisms).
Essential in answer
■ Haematological (bone marrow toxicity) – Ø WCC (impaired immunity, risk of
secondary infection), Ø Hb, Ø platelets.
■ Hair loss – hair follicle synchronisation.
■ Nausea and vomiting.
■ Cardiomyopathy – anthracycline toxicity after certain dose levels.
2. What are the aims of systemic adjuvant therapy (treatment given after definitive
surgery) in breast cancer and what are some of the recognised indications for
consideration of such therapy?
Essential in answer
■ Aims – to reduce risk of death or recurrence or to delay these events in women
with breast cancer.
■ Indications – node positive BC, large primary tumours, women considered at
“high” risk of recurrence.
More detail than this would be considered of greater than required standard
(ie. high-grade tumours, pre-menopausal, vascular invasion).
35
Objective 5.5
Principles of palliative care
a) Demonstrate an understanding of the importance of the patient in decision making
processes and the influences that affect their choices.
b) Explain the role and structure of palliative and supportive care in the multidisciplinary
management of advanced cancer.
c) Explain considerations of when and how palliative care should be introduced.
d) Demonstrate the assessment of pain and other symptoms, including nausea, fatigue,
confusion, drowsiness and cachexia.
e) Discuss principles of both pharmacological and non-pharmacological pain relief and
the palliative management of other symptoms.
f) Demonstrate an understanding of "end of life" issues that confront patient, family and
physician:
■ Physical effects of advanced cancer;
■ Psychosocial aspects of terminal cancer, support (religious, cultural, spiritual,
existential), loss and bereavement;
■ Ethical aspects of “end of life” decision-making.
g) Demonstrate understanding of the Palliative Care Act(s).
h) Demonstrate appreciation of cultural aspects of end of life care.
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i) Demonstrate adequate communication skills, including breaking bad news and
discussion of end of life care.
j) Demonstrate understanding of utility of procedures to relieve symptoms eg. ascitic and
pleural taps.
■ History of palliative care in the health care system (1950 to present).

36
1. Discuss who would be appropriate members of a palliative care team at an acute
hospital.
Essential in answer
Palliative care doctor (liaison with hospice), palliative care nurse, social worker,
psychiatrist, oncologist, nursing liaison (community liaison), pastoral care worker.
Mention should be made of the multi-disciplinary nature of care.
2. During regular use of morphine for chronic pain control, what is the oral equivalent to
10mg of subcutaneous morphine sulphate?
(a) 60mg?
(b) 30mg?
(c) 10mg?
(d) 3.3mg?
Answer: (b)
The answer requires an understanding that oral morphine has only about one third of
the bioavailability of parenteral morphine when used regularly ie. three times the dose
is required. The required oral dose for a one-off dose is six times.

37
Objective 5.6
Follow-up and relapse
a) Demonstrate an understanding of the aims of follow-up including:
(i) recognition and management of local and distant recurrence;
(ii) complications of treatment;
(iii) detection of new primaries.
b) Describe manifestations of recurrence of common cancers.
c) Describe the management of recurrences, including aims, treatments and outcomes.
d) Demonstrate an understanding of the psychosocial impact of expected and
unexpected recurrences.
e) Demonstrate an understanding of the limitations and cost effectiveness of follow-up
itself.
f) Recognise recurrence patterns of common cancers.
1. For which cancers are there effective salvage treatment for recurrent disease that
offers a >25% chance of cure? (select the best answer/s, more than one may be
correct)
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(a) Hodgkin’s disease.
(b) Rectal cancer.
(c) Breast cancer initially treated by lumpectomy and radiotherapy.
(d) Lung cancer.
(e) Glioblastoma multiforme.
Answer: (a and c)
2. What would you tell a patient about the purpose and limitations of follow-up after
conservative treatment of colon cancer?
Essential in answer
■ To detect manageable recurrence.
■ To document treatment-related toxicity.
■ To establish outcomes including but not exclusively survival.
■ Recognition of non-clinical incentives that may drive the desire for follow-up
(financial, medico-legal, patient related).

38
Objective 6.1
Psychosocial and cultural significance of cancer
a) Discuss cultural and psychosocial factors influencing presentation for screening and
diagnosis.
b) Discuss the psychosocial impact of cancer diagnosis and treatment on the patient
and their family, and how they adjust in the short and long-term.
c) Discuss the economic impact of cancer on the patient and family.
d) Demonstrate an understanding of the impact of cancer on sexuality and fertility.
e) Be aware of significant cultural and religious differences in the population that
frame the challenge of breaking of bad news effectively.
f) Demonstrate understanding of resources offering appropriate and reliable patient
support information.
g) Demonstrate ability to assess the psychosocial state.
h) Demonstrate awareness of significant cultural and spiritual (rather than religious)
differences within the society.
■ Understanding of the doctor-patient relationship.
■ Patient-centred communication skills.
Area: Communication skills

39
1. Why is it important to have a carer present when you convey news about cancer?
Essential in answer
■ Retention of information is incomplete.
■ Communication should involve a number of formats at a number of different times,
ideally to the patient as well as a number of different support people.
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2. Discuss different cultural attitudes to death and dying.
Essential in answer
■ Knowledge of the “western” society model v Indigenous v Asian etc.
■ Part of continuum v major event.
3. Discuss the importance of body image in breast cancer management.

Essential in answer
■ Mastectomy v conservation v reconstruction.
■ Overall cosmetic outcome.
■ Effects on sexuality.
■ Effects of premature menopause caused by chemotherapy.
4. What are the two major side-effects which should be discussed with a man who is
about to undergo radical surgery for prostate cancer and how would you discuss
their management.
Essential in answer
■ Impotence and incontinence. In the management of impotence, pharmacological
and mechanical treatments can be discussed and counselling for the man and his
partner may be necessary.

40
Objective 6.2
Communication and counselling
a) Illustrate an ability to communicate the bad news of a diagnosis of cancer to a
patient, their family and “significant others” in a sensitive manner, addressing
concerns, fears and expectations, while making sure a realistic prognosis is
explained and ensuring that appropriate confidentiality is observed.
b) Be aware that the impact of receiving bad news interferes with patients’ ability to
comprehend fully the important information being presented to them. Illustrate the
ability to assess a patient’s realistic understanding of their situation and to
individually tailor verbal and written information provided according to patient
preferences and understanding.
c) Provide supportive counselling for the patient and carers, both personally and by
referral to expert help.
d) Demonstrate an understanding of how to explain the risks and benefits of options
for management to the patient and their significant others, so that active
participation in the management process is encouraged.
e) Facilitate informed consent for participation in clinical trials.
■ Basic counselling and communication skills, including eliciting the patient’s
agenda in relation to the doctor’s agenda; being able to listen.
■ Patient-centred counselling skills, including the importance of appropriate
location and the amount of time devoted to the task.
■ Knowledge of the process of grief and loss.
■ Knowledge of support groups (physical and internet).
41
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1. At the consultation in which you must tell a patient a diagnosis of cancer
(select the best answer/s):
(a) The most important thing is to cover all important aspects of management and
prognosis in the initial interview, to give a comprehensive statement about the
patient’s condition.
(b) Due to the need for confidentiality, the information is best given to the patient
on his/her own.
(c) Patient autonomy dictates that all management options should be presented
immediately to achieve informed consent.
(d) Most details of the discussion will be lost once the patient hears the diagnosis
and will need repetition at a later date.
Answer: (d)
2. In patients who require an interpreter to fully understand and contribute to

discussions about cancer management (select the most appropriate answer/s):
(a) A family member is always best at interpreting medical language and
transmitting information.
(b) An external interpreter is usually more impartial and transmits information more
consistently.
(c) Written material (in the patient’s native language) is often very helpful to aid
understanding.
(d) Family members and friends interpreting for the patient may filter (remove parts
of) medical information told to them by the treating doctor.
Answer: (b, c and d)

42
Objective 6.3
Education of patients
a) Demonstrate an understanding of the principles of educating patients to be
actively involved in their care.
b) Demonstrate an understanding of resources available to patients and the public
(eg. Cancer Councils, cancer support groups, books, brochures, internet,
Medline, search engines, clinical alerts, databases, chatlines, commercial
helpdesks, media, family, friends etc) and the limitations of these (ie. peer
reviewed journals vs popular press).
c) Discuss the doctor's role in patient education about self-examination and
worrying signs.
d) Promote preventive medicine and appropriate early detection practices and
encourage patients to educate others about these aspects.
e) Develop a partnership approach to cancer care and information acquisition
(eg. willingness to learn from all sources including patients).
f) Demonstrate an understanding of the benefits to ongoing patient education and
care that result from utilising a multidisciplinary team including health
professionals and others.
g) Demonstrate ability to provide patient education relating to general effects of
94
cancer treatment (symptom management and recognition of symptoms that
require medical review).
■ Information technology skills.
■ Introduction to screening of populations and case-finding in individuals.
■ Patient-centred communication skills.

1. Briefly outline how you would educate a patient concerning the six most
common cancers (in Australia or New Zealand) supposing he/she had recently
been diagnosed with each type of cancer. Describe the types of resources
available to patients giving some examples of the strengths and weaknesses of
each. Given that a metachronous second primary cancer is not uncommon (7-
10% lifetime risk), demonstrate your ability to educate a patient on preventive
measures and screening methods.
Essential in answer
■ Knowledge of the most common types of cancer in Australia (or NZ).
■ Knowledge of what resources exist.
■ Knowledge of benefits/limitations of resources.
■ Knowledge of preventive health care and screening.
■ Demonstration of a partnership approach to patient care.
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Objective 6.4
Family and community support
a) Discuss the role of psychosocial, physical, financial and information supports
available for patients and their families.
b) Identify available information resources, community resources, financial
resources and other physical supports.
c) Demonstrate an understanding of the means by which doctors can facilitate the
provision of these services.
d) Identify the impact on the family of a shift to home care.
■ Understanding of physical and psychosocial issues and the importance of
Personal support for the person with chronic ill health.

What are the available community supports for patients with cancer, and their
families?
Essential in answer
■ Treating doctor (surgeon, radiation or medical oncologist, haematologist), local
doctor, domiciliary nursing.
■ Cancer Councils (literature, education programs, phone-in support).
■ Home care programs (hospice associated; hospital in the home – for home
treatment) and specific support groups (eg. brain tumours, Laryngectomee
Associations, CanTeen).
■ Isolated patient transit schemes, pastoral care and bereavement services.
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44
Objective 7
Ethics and professionalism
a) Demonstrate an understanding of the effects on health professionals of caring
for patients with cancer and of the ways in which the stresses of this work can
be managed appropriately.
b) Discuss the bioethics of issues such as access, equity and resource allocation, as
well as medical care at the end of life.
c) Identify the key medico-legal issues in diagnosis, screening/early detection,
management, evidence-based guidelines, defensive medicine, commutative
justice, distributive justice, social justice, physician-assisted suicide, euthanasia.
d) Discuss principles, elements and role of informed consent in patient decision
making.
■ Understanding of broad medico-legal principles, patient consent, autonomy and
privacy.
7 Representative questions that suggest the required depth of knowledge

1. You are a GP in a five-doctor practice. A colleague is chronically unwell and a
number of patient complaints have called into question his competence. What do
you need to consider in resolving this problem?
Essential in answer
■ Direct approach to colleague.
■ Medical defence aspects.
■ “Sick doctor” counselling.
■ Defining clear outcomes-based plan.
2. Why is eliciting a patient’s agreement to proceed with cancer treatment a

complex problem?
Essential in answer
■ Differences in knowledge base.
■ Language:
– English as a second language, or inability to understand English at all;
– Lay usage v medical jargon.
■ Necessity to allocate sufficient time.
■ Repeat visits.
■ Oral v written v tape/video.
■ Problems in defining risk - benefit and probability of benefit.
Area: Ethics
45
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Objective 8
Clinical experience
Many important clinical skills must be learnt by experience. The five cancer clinical
experiences that medical students need before they graduate include:
a) Talking with and examining people affected by all stages of cancer.
b) Talking with and examining people affected by all common cancers.
c) Observing all components of multidisciplinary cancer care.
d) Seeing shared decision-making between people with cancer and their doctors.
e) Talking with and examining dying people.
Definitions:
■ Examine – experienced the salient features (eg. seen, felt).
■ Talk with – discuss symptoms, effects, plans and reflections.
■ All stages of cancer – early, locally advanced, locally recurrent and advanced.
■ All common cancers – breast, prostate, lung, colorectal, melanoma, gynaecologic,
lymphoma and leukaemia.
■ All components of multidisciplinary cancer care – includes people preparing for,
undergoing and having had cancer surgery, chemotherapy, radiation therapy,
palliative care and other supportive care.
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APPENDIX viii
METABOLIC MEDICINE MODULE

CURRICULUM : YEAR 4 & 5 UNDERGRADUATE MEDICINE
Course Description
Title
Metabolic Diseases: Year 4 & 5 Undergraduate Medicine
Overview
metabolic medicine within the context of general internal medicine over two rotating 8
weeks clerkships.
Prerequisite
A pass in the MBBS Phase 1 examination.
This course is taught in two modules:
1. Year 4 – at the Eric Williams Medical Sciences Complex (EWMSC),

San Fernando and Sangre Grande General Hospitals
2. Year 5 – at Port-of-Spain General Hospital
Metabolic medicine can be defined as a group of overlapping areas of clinical

practice with a common dependence on detailed understanding of basic
biochemistry and metabolism.
A metabolic disease is classified as either congenital (due to inherited enzyme abnormality)
or acquired (due to failure of a metabolic important organ or biochemical reaction) disorder
resulting from an abnormal metabolic process.
Metabolic diseases fall within the areas of expertise of both physicians and
chemical pathologists. This course is designed to integrate the foundation
knowledge learnt in Pre-Clinical years in the basic sciences of Biochemistry and
the Chemical Pathology clerkship with clinical practice.
The purpose of this course is for students to understand the pathophysiology of

metabolic disease, to be able to identify various presentations of metabolic illness and to
manage patients accordingly.
At the end of the course, the student will be expected to identify and manage clinical
presentations of electrolyte and fluid imbalances, disorders of nutrition, disorders of
98
lipid, protein and carbohydrate metabolism, disorders of calcium metabolism, bone
disorders and inborn errors of metabolism.
Contact Information
Tutors: EWMSC - Professor T. Seemungal, Professor S. Teelucksingh, Dr. S. Sakhamuri

and Associate Lecturers from Internal Medicine Unit.
Port of Spain General Hospital – Prof. T. Seemungal, Prof. S. Teelucksingh and
Associate Lecturers from the Department of Medicine at POSGH
Contact Phone: Department of Medicine EWMSC 663-4332;
POSGH 623-4030 or ext 2585
E-mail: terence.seemungal@sta.uwi.edu
Content
▪ Clinical Presentation of Metabolic Diseases
▪ History Taking
▪ Physical Examination
▪ Signs & Symptoms
▪ Investigations
▪ Specific Metabolic Diseases
o Disorders of Carbohydrate Metabolism
▪ Diabetes Mellitus
o Disorders of Lipid Metabolism
▪ Dyslipidaemia
o Disorders of Nutrition
▪ Obesity
▪ Vitamin & Mineral Deficiency
o Disorders of Protein Metabolism
o Calcium & Bone Disorders
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o Fluid & Electrolyte Imbalance
o Inborn Errors of Metabolism
o Other Metabolic Diseases
▪ Metabolic myopathies
▪ Metabolic polymyopathy
▪ Metabolic polyneuropathy
▪ Metabolic Emergencies
Structure of the Course: Teaching vs. Bedside Learning
The clinical Metabolic Medicine course is based primarily in formal or semi-formal

patient-based learning on the ward and in Diabetic/Endocrine clinics during your 4 th and 5th
years. Metabolic emergencies and clinical presentations of electrolyte imbalance,
dehydration, dyslipidaemia, diabetes, etc. are frequently encountered in the hospital.
Patients are your primary resource for learning in metabolic medicine.
Clinical Presentation of Metabolic Diseases
Symptoms:
Nonspecific – Exercise intolerance, Weight loss, Poor wound healing, Fatigue, Chills
CNS– Seizures, Neuropathic ulcers, Visual Disturbances, Dizziness
CVS– Palpitations, Diaphoresis
RS – Dyspnoea, Tachypnea
GIT– Vomiting, Diarrhoea, Nocturnal diarrhoea, Jaundice, Polyphagia, Dry mouth
GUS / Reproductive – Polyuria, Polydipsia, Impotence, Urinary Retention
MSS – Ataxia, Growth Problems, Muscle (pain, wasting, weakness, cramping), Bone
abnormalities, Problems with movement
Hair & Skin – Rash, Alopecia, Skin thinning, Lipodystrophy, Abnormal pigmentation
Signs:
▪ Signs of Dehydration – Sunken eyes, Decreased skin turgor, Hypotension,
Tachycardia
▪ Respiration – Tachypnea, Accessory muscles of Respiration, Nasal flaring,
Breathing pattern – eg. Kussmaul (metabolic acidosis), Cheyne-Stokes (acompanies
brain damage, heart failure, uremia, and respiratory depression)
▪ Cardiac – Arrythmias, Tachycardia
▪ BMI – Obesity, Underweight, Fat distribution
▪ Cutaneous – Acanthosis nigricans, Xanthelasma, Dermatological and
Rheumatological manifestations of Autoimmune disease
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Metabolic Disease History:
Past Medical History – Renal disease, Liver disease Contraindications

Drug History – Drug interactions, Indications, Contraindications
Family History – Diabates mellitus, renal disease, renal calculi, metabolic disease,
autoimmune disease, obstetric complications eg. Polyhydramnios, recurrent miscarriages,
large-for-gestational-age babies.
Physical Examination:
▪ General
o Vital Signs – BP, P, R, T, Blood Glucose, Sp02
o Calculate BMI using the equation
▪ BMI = Weight (kg)

( kg/m² ) Height² (m²)
▪ Obesity is defined as BMI > 30 kg/m2
o Cutaneous Manifestations – Acanthosis nigricans, Xanthelasma, etc.
o Assessment of hydration status (heart rate, blood pressure, mucous

membranes, skin perfusion)
▪ Examination of ALL the systems of the patients

▪ Complete Neurological Examination – Including Mental State Exam
Investigation of Metabolic Diseases:

▪ Electrolytes
o Sodium, Potassium, Chloride, Bicarbonate, Calcium, Magnesium,
Phosphate
▪ Renal Impairment, Hepatic Impairment
▪ Arterial Blood Gas Sampling
o Metabolic/Respiratory Acidosis/Alkalosis
▪ OGTT / HbA1c
▪ Water Deprivation Test
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Specific Objectives
1. Disorders of Carbohydrate Metabolism

▪ Classification:
o Glycogen Storage Disease
o Mucopolysaccharidosis eg. Hunter/Hurler’s Syndrome
o G6PD deficiency
o Diabetes Mellitus
Diabetes mellitus
▪ Diagnose diabetes and glucose intolerance disorders
o OGTT
o HbA1c >6.5%
▪ Interpretation of Oral Glucose Tolerance Test Results:
▪ Recommended Targets for Glycaemic Control:
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International Diabetes Foundation Global Guideline for Type 2 Diabetes. 2005.
▪ Features of Type 1 Diabetes:
▪ Type 1 DM vs. Type 2 DM
International Diabetes Foundation (IDF) 2005
▪ Classification:
o Insulin-dependent diabetes mellitus
o Non-insulin-dependent diabetes mellitus
o Maturity Onset Diabetes Mellitus of the Young (MODY)
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o Gestational Diabetes
o Other
▪ Signs of Insulin Resistance e.g. Acanthosis nigricans
A quantitative scale of acanthosis nigricans. J P Burke et al. Diabetes Care

October 1999 22:1655-1659.
▪ Give basic dietary advice, emphasizing its importance as first line therapy in Type 2
patients
▪ In the event of dietary failure institute appropriate therapy
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▪ Recognize the need for insulin treatment in diabetic patients
▪ Institute insulin therapy
▪ Educate patients in the use of insulin syringes, injection pens, home blood glucose
monitoring and urinalysis
▪ Give advice about the insulin dose adjustment
▪ Provide life style advice with regard to employment, driving, exercise, weight control
and smoking
▪ Advise with regard to avoidance of complications in the eye, kidney, peripheral
nerve, foot and cardiovascular systems
▪ Screening for, prevention and treatment of microvascular, macrovascular,
neurological and other complications to optimise the intermediate and final
outcomes of diabetes
▪ Signs of peripheral neuropathy eg. Glove-Stocking distribution of neuropathy,
Neuropathic ulcers, Slipping Slipper Sign
▪ Pharmacology of Oral hypoglycaemic agents [5 Commandments – Class of Drug,
Mechanism of Action, Indications, Contraindications, Side Effects]
▪ Insulin resistance altering therapies
▪ Glycaemic control in type 1 and 2 diabetic patients in a way that minimises the
impact on health and optimises long-term disease outcomes
▪ Have a working knowledge of the management of diabetic metabolic emergencies eg.
Diabetic Ketoacidosis
▪ Ability to educate diabetic patients about self-care, monitoring of glycaemic control
and prevention of complications
▪ The Metabolic Syndrome (epidemiology and definition)
2. Lipid metabolism and cardiovascular risk assessment
▪ Diagnosis and assessment of genetic and acquired hyperlipidaemia and other

dyslipidaemias
▪ Overall assessment of cardiovascular risk in primary and secondary prevention
settings
▪ Evaluate cardiovascular risk in genetic and acquired hyperlipidaemia
▪ Assess cardiovascular risk due to non-lipid factors eg. hyperhomocysteinaemia,
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fibrinogen, smoking
▪ Identify Vascular Complications Of Hyperlipidaemia
▪ Recognise Cutaneous And Other Signs Of Hyperlipidaemia
▪ Identify clinical features of genetic dyslipidaemias (xanthelasma, xanthoma-
tendinous, eruptive and planar, corneal arcus, lipaemia retinalis) and evidence of
macro- and micro-vascular disease.
▪ Give basic dietary advice to patients with hyperlipidaemia
▪ Interpret and critically appraise biochemical and genetic investigations for
dyslipidaemia
Lipoproteins
1. Very low-density lipoprotein (VLDL)
▪ Synthesised continuously by liver
▪ Carries 60% triglycerides and some cholesterol
▪ Enzymic degradation to intermediate density lipoprotein (IDL) and then LDL
2. Low-density lipoprotein (LDL)
▪ Formed from IDL by hepatic lipase
▪ Major carrier of cholesterol
▪ Binds to, and levels regulated by feedback on to, hepatic LDL
receptor
3. High-density lipoprotein (HDL)
▪ Synthesised in gut wall and liver
▪ Carries cholesterol from periphery to liver
▪ Inverse association with ischaemic heart disease
4. Chylomicrons
▪ Carry dietary lipid from gut to liver
▪ Broken down by lipoprotein lipase in portal vessels to free fatty
acids
Hyperlipidaemias
1. Can be primary or secondary
2. Atherosclerotic disease associated with high total cholesterol and LDL
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3. HDL protective
Primary disorders
1. Familial hypercholesterolaemia
▪ Autosomal dominant
(i) Heterozygotes ≈1:500
(ii) Homozygotes very rare
▪ Around 400+ defects in LDL receptor known
▪ Defect in the receptor means half-life of LDL in plasma is prolonged, leading to
increased serum levels
▪ Heterozygotes
(i) Total cholesterol 9–15 mmol/l
(ii) 6–8 times increased risk of IHD (MI at young age)
(iii) Xanthelasma and tendon xanthoma
▪ Homozygotes
(i) Xanthomas in early childhood
(ii) MI as child
▪ Treat with diet and statins
2. Familial triglyceridaemia
▪ Autosomal Dominant
▪ Plasma turbid
▪ Associated with eruptive xanthomata, pancreatitis, retinal vein
thrombosis, hepatosplenomegaly, lipaemia retinalis
▪ Treat with diet and fibrates
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3. Lipoprotein lipase deficiency
▪ Rare
▪ Autosomal Recessive
▪ Failure to break down chylomicrons
▪ Raised triglycerides
4. Familial combined hyperlipidaemia

▪ Elevated cholesterol and triglycerides
▪ Prevalence 1:200
▪ Main feature is atherosclerosis
Causes of secondary hyperlipidaemia
1. Mainly raised cholesterol

o Hypothyroidism
o Cholestasis
o Nephrotic syndrome
o Renal transplant
2. Mainly raised triglycerides

o Obesity
o Chronic alcohol excess
o Insulin resistance and diabetes
o Chronic liver disease
o Thiazide diuretics
o High-dose oestrogens
▪ The provision of dietary advice to patients with hyperlipidaemia to optimise long-

108
term outcome
▪ Institute appropriate drug therapy for the management of dyslipidaemia
▪ Know the pharmacology (5 Commandments) of drugs used in the management of
dyslipidaemia [Class, Mechanism of Action, Indications, Contraindications, Side
Effects]
3. Disorders of Nutrition
▪ Overnutrition (Obesity)
o Diagnosis of obesity
Classification BMI(kg/m2)
Principal cut-off
Additional cut-off points
points
<18.
Underweight <18.50
50
Severe thinness <16.00 <16.00
Moderate thinness 16.00 - 16.99 16.00 - 16.99
Mild thinness 17.00 - 18.49 17.00 - 18.49
18.50 - 22.99
Normal range 18.50 - 24.99
23.00 - 24.99
Overweight ≥25.00 ≥25.00
25.00 - 27.49
Pre-obese 25.00 - 29.99
27.50 - 29.99
Obese ≥30.00 ≥30.00
30.00 - 32.49
Obese class I 30.00 - 34-99
32.50 - 34.99
35.00 - 37.49
Obese class II 35.00 - 39.99
37.50 - 39.99
Obese class III ≥40.00 ≥40.00
The International Classification of adult underweight, overweight and obesity

according to BMI
o Basic dietary and exercise advice

o Initiating drug therapy
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o Measure skinfold thickness, bioimpedance
o Referral of patients appropriately for surgical treatment
o Managing the complications of obesity – diabetes, hypertension,
hyperlipidaemia
▪ Undernutritition (Disease-related malnutrition)

o Assessment of protein energy nutritional status
▪ Deficiencies
▪ Protein–energy malnutrition
o Undernutrition
▪ Weight 60–80% of standard for age, no oedema
o Marasmus
▪ Deficient in protein and calories
o Weight < 60% of standard, no oedema
▪ Kwashiorkor
o Solely due to protein deficiency
o Weight 60–80% of standard, oedema present
▪ Fatty liver often seen
o Assessment of vitamin and mineral status

▪ Vitamin A deficiency
▪ Thiamine deficiency
▪ Niacin deficiency (pellagra)
▪ Deficiency of other B group vitamins
▪ Ascorbic acid deficiency
▪ Vitamin D deficiency
110
▪ Dietary calcium deficiency
▪ Dietary selenium deficiency
▪ Dietary zinc deficiency
▪ Deficiency of other nutrient elements
▪ Other nutritional deficiencies
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o Assessment of nutritional requirements of patients
▪ With acute disease eg. Cerebrovascular Accident
▪ With chronic disease eg. Inflammatory Bowel Disease, CVA,
Malabsorption
4. Disorders of Calcium Metabolism and Bone
▪ The Bone Cycle
▪ Identify and Define common disorders of calcium metabolism and bone

o Osteoporosis
o Osteomalacia
o Rickets
o Vitamin D Metabolism
o Paget’s Disease
o Renal Calculi
o Defects of Renal Tubular Function
o Genetic Disorders of Parathyroid Function
o Hypo- and Hypercalcaemia
o Hypo- and Hyperphosphataemia
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▪ Vitamin D
o Mostly made in skin by action of UV light
o 25 – hydroxylated in liver
o Hydroxylated again to 1,25-OH D (calcitriol) in kidney
Hypercalcaemia
▪ Causes
o Primary hyperparathyroidism (adenoma of parathyroid gland)
o Malignancy – PTH-related protein and bone metastases,
▪ Commonly breast, kidney, thyroid, squamous cell tumours
▪ Calcium intake (and milk-alkali syndrome)
▪ Vitamin D
▪ Tertiary hyperparathyroidism
▪ Hyperthyroidism
▪ Sarcoid – macrophages in lesions produce 1,25 vitamin D3
▪ Thiazides
▪ Lithium
▪ Addison’s
▪ Theophylline toxicity
▪ Phaeochromocytoma
▪ Familial hypocalciuric hypercalcaemia
Features
▪ As underlying condition, plus
▪ Lethargy, malaise and depression
▪ Polyuria and polydipsia
▪ Weakness
▪ Confusion and psychosis
▪ Constipation
▪ Peptic ulceration
▪ Nausea
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▪ Renal stones
▪ Nephrocalcinosis
▪ Pseudogout
▪ Proximal myopathy
▪ Diabetes insipidus
▪ Pancreatitis
Treatment
▪ Aggressive rehydration
▪ Bisphosphonate (pamidronate)
▪ Frusemide
▪ Steroids
Hyperparathyroidism
▪ Primary
o Single adenoma in > 80%
o Multiple in around 5%
o Commonest in women aged 40–60
o Carcinoma very rare
o Results in ↑PTH, ↑serum and urinary calcium, ↑alkaline
phosphatase and ↓serum phosphate
o Causes increased osteoblasts and osteoclasts with woven
osteoid and osteatitis fibrosa cystica
▪ Secondary
o Due to hypertrophy of glands in response to chronic
hypocalcaemia (eg. in renal failure)
▪ Tertiary
o Consequence of long-standing secondary hyperparathyroidism.
Further gland hyperplasia raises calcium levels. Treatment is parathyroidectomy.
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Hypocalcaemia
Causes
o Hypoparathyroidism (including pseudohypoparathyroidism)
o Chronic renal failure
o Low levels of vitamin D3
o Hyperphosphataemia
o Hypomagnesaemia
o Sepsis
o Respiratory alkalosis
o Calcium deposition (eg acute pancreatitis)
o Carcinoma of prostate
Features
▪ Muscle weakness
▪ Neuromuscular excitability
▪ Confusion, seizures
▪ Tetany
▪ Alopecia
▪ Brittle nails
▪ Cataracts
▪ Dental hypoplasia
Treatment
▪ Supplementation of calcium, vitamin D3
Hypoparathyroidism
Causes
▪ Parathyroidectomy (intentional and accidental)
▪ Autoimmune
115
▪ Receptor defect (pseudohyperparathyroidism)
▪ Di George syndrome
Diagnosis (hypoparathyroidism)
▪ ↓Calcium, ↓PTH
▪ Pseudohypoparathyroidism
Receptor defect leading to resistance of target tissues to PTH
X-linked dominant
↓Calcium, ↑PTH
Clinical features
▪ Short stature
▪ Round face
▪ Short neck
▪ Shortening of the metacarpals and metatarsals
Disorders of Phosphate Metabolism
Causes of hyperphosphataemia
▪ Renal failure
▪ Hypoparathyroidism
▪ Acromegaly
▪ Vitamin D excess
▪ Overintake of phosphate
▪ Tumour lysis syndrome
Causes of hypophosphataemia
▪ Intravenous glucose
▪ Deficiency during parenteral feeding
▪ Recovery phase of DKA
▪ Primary hyperparathyroidism
116
▪ Renal tubular disease
▪ Vitamin D deficiency
▪ Alcohol withdrawal
Osteomalacia/rickets
▪ Decreased mineralisation of osteoid
Causes
o Calciopenic
Vitamin D deficiency
Impaired calcium metabolism
o Phosphopenic
Proximal renal tubular disease
Clinical features
▪ Pain
▪ Deformity
▪ Fractures
▪ Proximal myopathy
▪ Raised alkaline phosphatase
Paget’s disease
▪ Increased bone turnover with abnormal new bone turnover
▪ Causes pain, deformity, arthritis, nerve compression, fractures, sarcoma
▪ ↑↑ALP
▪ Calcium only raised with immobility
▪ Diagnosis – clinical, typical X rays or bone scan
▪ Treatment: analgesia and bisphosphonates
▪ Know the range of therapeutic drugs which have a role in altering bone turnover.
▪ Direct and interpret range of radiological and biochemical tests to assess bone
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disease.
▪ Choice of drugs and assessment of their effectiveness.
▪ The range of osteogenesis imperfecta and how it influences adult life.
▪ Renal osteodystrophy.
▪ Understand bone turnover and different biochemical bone markers.
Inborn Errors of Metabolism
▪ Inherited Metabolic Diseases

▪ Most are due to a single gene defect
▪ Classification:
o Disorders of carbohydrate metabolism eg. Glycogen storage disease
o Disorders of amino acid metabolism ef. Phenylketonuria, maple syrup urine
disease
o Disorders of organic acid metabolism (organic acidurias) eg. alcaptonuria
o Disorders of fatty acid oxidation and mitochondrial metabolism
o Disorders of porphyrin metabolism
● Porphyrias
Hereditary defects of enzymes involved in haem synthesis pathway
Overproduction of intermediates – porphyrins
Several different types; most important are
Acute intermittent porphyria
● Autosomal dominant
● Rare, commoner in females
● Due to low levels of porphobilinogen deaminase in liver
● Presents in youth
● Increased urinary porphobilinogen in attack; urine turns dark red
after standing
● Clinical features
(i) Severe abdominal pain
(ii) Neuropsychiatric symptoms
(iii) Vomiting
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(iv) Hypertension
(v) Tachycardia
(vi) Motor polyneuropathy
● Commonly precipitated by hepatic enzyme-inducing drugs, eg
alcohol, phenytoin, oral contraceptives, sulphonamides,
rifampicin, benzodiazepines
● Treatment of attacks
(i) High-carbohydrate diet
(ii) Haematin
(iii) Opiate analgesia
(iv) Fluid restriction for hyponatraemia
(v) Conservative management of seizures, as antiepileptics can
precipitate attacks
Porphyria cutanea tarda

● Chronic hepatic condition
● Many patients drink excessive alcohol
● Autosomal dominant and acquired
● Reduced hepatic uroporphyrinogen decarboxylase
● Accumulation of uroporphyrinogen (raised in urine)
● Many have evidence of iron overload and require venesection
● Photosensitive bullous rash main feature
o Disorders of purine or pyramidine metabolism

o Disorders of steroid metabolism
o Disorders of mitochondrial function
o Disorders of peroxisomal function
o Lysosomal Storage Disorders
▪ Adult impact of common IEMs especially
o Phenylketonuria
o Galactosaemia
119
o Homocysteinuria
Disorders of Electrolyte Imbalance

▪ Symptoms, Causes, Treatment and Complications of:
o Hypo- and Hypernatraemia
o Hypo- and Hyperkalaemia
o Hypo- and Hypercalcaemia
Causes of hyponatraemia – with normal extracellular water
▪ Pseudohyponatraemia
▪ Hyperlipidaemia
▪ Hyperproteinaemia
▪ Abnormal ADH release
▪ Hypothyroidism
▪ Severe potassium depletion
ADH-like substances
▪ Oxytocin
▪ DDAVP
Unmeasured osmotically active substances stimulating osmotic ADH
release
▪ Glucose
▪ Alcohol
▪ Mannitol
▪ Syndrome of inappropriate ADH secretion (SIADH)*
▪ Stress
▪ Surgery
▪ Nausea
Causes of hyponatraemia – with decreased extracellular volume

Renal
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▪ Osmotic diuresis (hyperglycaemia, severe uraemia)
▪ Diuretics
▪ Adrenocortical insufficiency
▪ Tubulointerstitial disease
▪ Unilateral renal artery stenosis
▪ Recovery post ATN
Gastrointestinal
▪ Vomiting
▪ Diarrhoea
▪ Haemorrhage
▪ Fistula
▪ Obstruction
Causes of hyponatraemia – with increased extracellular volume

▪ Oliguric renal failure
▪ Heart failure
▪ Liver failure
▪ Hypoalbuminaemia
Causes of hypernatraemia
▪ Dehydration
▪ Iatrogenic (administration of hypertonic sodium solution)
▪ Diabetes insipidus
▪ Osmotic diuresis
(a) Total parenteral nutrition
(b) Hyperosmolar diabetic coma
Causes of SIADH
Malignancy
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▪ Bronchus, bladder, prostate, pancreas
▪ Lymphoma
▪ Ewing’s sarcoma
▪ Mesothelioma
▪ Thymoma
Pulmonary disorders
▪ Pneumonia
▪ Abscess
▪ TB
▪ PEEP
▪ Asthma
Central nervous system
▪ Encephalitis
▪ Meningitis
▪ Trauma
▪ Subarachnoid haemorrhage
▪ Guillain-Barré syndrome
▪ Hydrocephalus
▪ Acute psychosis
▪ Acute intermittent porphyria
Drugs
▪ Opiates
▪ Carbamazepine
▪ Oxytocin
▪ Chlorpropamide
▪ Phenothiazines
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▪ TCAs
▪ Cytotoxics (vincristine, cyclophosphamide)
▪ Rifampicin
▪ Porphyria (drug induced)
Causes of diabetes insipidus
Cranial (reduced secretion of ADH)

▪ Idiopathic
▪ Familial (eg DIDMOAD syndrome)
▪ Craniopharyngioma
▪ Infiltrative processes of hypothalamus
o Sarcoidosis
o Histiocytosis X
● Trauma
● Pituitary surgery
● Lymphocytic hypophysitis
● Dysgerminomas
Nephrogenic (reduced action of ADH)
▪ Primary
o Childhood onset
o X-linked/dominant
o Tubular receptor abnormality
▪ Secondary
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o Hypercalcaemia
o Hypokalaemia
o Renal disease
o Chronic pyelonephritis
o APKD
o Post obstruction
o Sarcoidosis
o Drugs: Lithium
Demeclocycline (used to treat SIADH)
Amphotericin
Glibenclamide
Causes of polyuria
1. Excessive intake
▪ Alcohol
▪ Primary polydipsia (lesion of hypothalamus)
▪ Psychogenic polydipsia
2. Osmotic diuresis
▪ Diabetes mellitus
▪ CRF
▪ ARF (diuretic phase)
▪ Diuretics
▪ Diabetes insipidus (cranial and nephrogenic)
3. Hypokalaemia
4. Hypercalcaemia
5. Obstructive uropathy
6. Tubulointerstitial disease
Investigation of polyuria
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-Record fluid intake
-Record urine volume (if ,3l/24 hrs and normal biochemistry excludes
significant abnormality)
-Blood glucose, U&E, calcium
-Urinalysis
-Early morning urine osmolality
-Water deprivation test
(a) To identify the cause of polyuria and/or polydipsia
(b) Hourly urine and plasma osmolality measured until 3% of bodyweight lost
(c) Injection of DDAVP (synthetic ADH)
Interpretation of the Water Deprivation Test
Potassium Metabolism
▪ Potassium is the major intracellular ion. Excretion of potassium is increased by
aldosterone.
▪ Causes of hypokalaemia
Decreased intake
▪ Oral (uncommon except in starvation)
▪ Parenteral
Redistribution into cells
125
▪ Metabolic alkalosis
▪ Insulin
▪ Alpha-adrenergic antagonists
▪ Beta-adrenergic agonists
▪ Vitamin B12or folic acid when correcting megaloblastic anaemia
▪ Total parenteral nutrition (TPN)
▪ Hypokalaemic periodic paralysis
▪ Pseudohypokalaemia
▪ Hypothermia
Increased excretion
Gastrointestinal
▪ Purgative abuse
▪ Vomiting
▪ Villous adenoma
▪ Severe diarrhoea
▪ Ileostomy/uterosigmoidostomy
▪ Fistulae
Renal
▪ Thiazide diuretics
▪ Loop diuretics
▪ Renal tubular damage
▪ Mineralocorticoid excess
▪ Primary hyperaldosteronism (Conn’s)

▪ Secondary hyperaldosteronism
126
▪ Apparent mineralocorticoid excess
(a) Liquorice
(b) Carbenoxolone
▪ Cushing’s syndrome
▪ Bartter’s syndrome
▪ Renal tubular acidosis type 1 and 2
Hyperkalaemia
Causes
▪ Spurious
o Haemolysis
o Delayed separation of serum
o Contamination
o Excessive intake (parenteral, oral)
▪ Decreased excretion
o Acute oliguric renal failure
o Chronic renal failure
o (Mineralocorticoid deficiency (Addison’s disease)
o Hypoaldosteronism
o Drugs
▪ Spironolactone
▪ Amiloride
▪ Triamterene
▪ ACE inhibitors
▪ NSAIDs
▪ Ciclosporin
▪ Redistribution
o Acidosis
o Rhabdomyolysis
o Tumour lysis syndrome
127
o Digoxin poisoning
▪ ECG changes
o Tenting of T waves
o Reduction in size of P waves
o Increase in PR interval
o Widening QRS complexes
o Disappearance of P waves
o Further QRS widening
o Sinusoidal waveform
▪ Treatment
o IV calcium gluconate (stabilises cardiac membranes)
o IV insulin and dextrose
o Calcium resonium
o Frusemide
o Salbutamol nebulisers
o Dialysis
Magnesium
Hypomagnesaemia
1. Usually associated with low Ca2+and low K+
2. Associated with ventricular arrhythmias, fits, tetany and paraesthesiae
Causes
▪ Renal loss
o Loop/thiazide diuretics
o Alcohol
o DKA
o Volume expansion
o Hypercalcaemia
▪ Loop of Henle disorder

128
o Acute tubular necrosis
o Post obstruction diuresis
o Renal transplant
▪ Nephrotoxic drugs
o Aminoglycosides
o Cisplatin
o Ciclosporin
o Amphotericin
▪ GI loss
o High-volume diarrhoea
o Malabsorption
o Other small bowel disease
o Acute pancreatitis
o
▪ Primary renal magnesium wasting
o Rare familial condition
Hypermagnesaemia
Causes
(a) Magnesium infusion
(b) Magnesium enema
(c) Oral magnesium overdose
(d) Renal failure
(e) Adrenal insufficiency
(f) Milk-alkali syndrome
(g) Theophylline toxicity
(h) Lithium
Treat with iv calcium if symptomatic
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Acid-Base Homeostasis
▪ Metabolic Acidosis
▪ Metabolic Alkalosis
▪ With or without Respiratory compensation
▪ Other disorders of fluid, electrolyte and acid-base balance
Metabolic acidosis
Normal anion gap
(a) Direct loss of bicarbonate (↑chloride)
(i) Diarrhoea
(ii) Pancreatic fistulae
(iii) Ureterosigmoidostomy
(iv) RTA
(v) Acetazolamide
(b) Ingestion of acidifying agents
(i) Ammonium chloride
130
High anion gap
(a) DKA
(b) Lactic acidosis
(c) Renal failure
(d) Salicylate poisoning
(e) Methanol poisoning
(f) Ethylene glycol poisoning
Respiratory acidosis
- Hypoventilation leading to increased CO2and acidosis
- Causes
(a) COPD
(b) Severe asthma
(c) Obesity
(d) Neuromuscular disorders leading to hypoventilation
(i) Guillain–Barré
(ii) MND
(iii) Myasthenia gravis
(iv) Muscular dystrophy
(v) Flail chest
(vi) Severe kyphoscoliosis
(e) Muscle relaxants
Respiratory alkalosis
Hyperventilation leading to low CO2levels and alkalosis
Causes
(a) Psychogenic
(b) Pulmonary disease
(c) Altitude
(d) Right to left shunt
(e) CO poisoning
(f) Salicylates
131
(g) Acute liver failure
Metabolic alkalosis
o Vomiting
o Potassium depletion
o Hyperaldosteronism
o Rapid diuresis
o Fulminant hepatic failure
o Milk-alkali syndrome
o Forced alkaline diuresis
Lactic acidosis
Type A
(a) Poor tissue perfusion with or without hypoxia
(i) Exercise
(ii) Post epileptic seizure
(iii) Shock
(iv) Severe hypoxia
Type B
(a) Administration of drugs or metabolic disturbance leading to increased production
of lactate
(i) Metformin
(ii) Alcohol
(iii) Recovery from DKA
(iv) Liver failure
(v) Paracetamol poisoning
(vi) Thiamine deficiency
Osmolar gap
▪ Normally gap between serum osmolality and calculated osmolality is < 10
▪ If the value is greater then this suggests another osmotically active substance in the
132
blood
Calculated with formula
2(Na+ + K+) + urea + glucose
Causes of raised osmolar gap
▪ Methanol
▪ Ethylene glycol
▪ Diethylene glycol
▪ Ethanol
Other metabolic disorders

▪ Disorders of purine and pyrimidine metabolism
▪ Disorders of porphyrin and bilirubin metabolism
▪ Cystic fibrosis
▪ Amyloidosis
▪ Volume depletion
▪ Iron overload – Haemochromatosis
Iron
o 4 g in normal human body, two-thirds in haemoglobin
o 20 mg/day in normal diet; only 10% absorbed
o Fe2+more readily absorbed than Fe3+
o Transferrin one-third saturated normal
o Ferritin increased in iron overload (NB: acute-phase protein), decreased in deficiency
o Plasma iron varies ++
Haemochromatosis
o Autosomal recessive
o Commoner, more severe in men
o Gene on chromosome 6
o Features: micronodular cirrhosis chondrocalcinosis, pseudogout, skin bronzing,
diabetes, cardiomyopathy, arrhythmias
o Diagnosis: raised serum iron and ferritin. Transferrin > 45% saturated. Liver biopsy
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o Treatment: venesection, desferrioxamine
Causes of secondary iron overload

o Multiple transfusions
o Alcoholic cirrhosis
o Chronic hepatitis B/C
o Beta-thalassaemia
o Aplastic anaemia
o Sideroblastic anaemia
▪ Disorders in Copper metabolism

Copper
o 50% of amount ingested is absorbed
o Transported to liver by albumin
o Binds with globulin to form caeruloplasmin
Wilson’s disease
o Autosomal recessive
o Gene on chromosome 13
o Abnormality of caeruloplasmin formation, hence accumulation of copper in body
o Features: acute/chronic hepatitis, cirrhosis, Kayser–Fleischer rings, CNS symptoms,
arthropathy, RTA.
o Diagnosis: low caeruloplasmin, high urinary copper, liver biopsy, KF rings
o Treatment: penicillamine (copper chelator), liver transplant
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135
Metabolic Emergencies
▪ Diabetic Ketoacidosis (DKA)
o Mortality Rate <5%
o Precipitated by infection, CVA, alcohol, MI, Trauma, Drugs eg.

corticosteroids, onset of type 1 or first presentation of unrecognized T2DM,
discontinuation of or inadequate insulin doses, stress, DM
o Signs: Kussmaul’s breathing, restlessness, smells of ketones in the breath,
abdominal pains, ketonuria
Mild Moderate Severe

Plasma Glucose >250 >250 >250
mg/dL
Arterial pH 7.25 – 7.30 7.00 – 7.24 < 7.00
Bicarbonate 15 - 18 10 - 15 < 10
mEq/L
Urine Ketones Positive Positive Positive
Serum Ketones Positive Positive Positive
Serum Osmolality Variable Variable Variable
mOsm/kg
Anion Gap > 10 > 12 > 12
Sensorium Alert Alert/Drowsy Stupor/Coma
▪ Hyperosmolar Hyperglycemic State (HHS)

o Mortality rate ~ 15%
o Signs: Severe dehydration, glycosuria, varying degrees of coma
o Investigations: RBS, BUN/Creatinine, Electrolytes, Urine ketones/glucose,

ABG, FBC, Cheat X-ray, ECG, Urine M/C/S, Blood culture
Plasma Glucose mg/dL > 600

Arterial pH > 7.30
Serum Bicarbonate mEq/L > 15
Urine Ketones Small
Serum Ketones Small
Serum Osmolality mOsm/kg > 320
Anion Gap Variable
Sensorium Altered mental state/Stupor/Coma
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Treatment
▪ Fluid Replacement
o Usual deficit ~6L in DKA and ~9L in HHS
o Start with 1L Normal Saline in 30 mins
o 2nd L over 1 hour
o 3rd L over 2 hours
o 1L every 4 hours thereafter
o Choice of fluid guided by presenting clinical and biochemical parameters
o IV insulin
▪ Lactic Acidosis
o Patient may be comatose, ill looking but not dehydrated
o ° Acetone/ketone breath
Plasma Bicarbonate < 22

pH < 7.2
Lactic acid mmol/L > 5.0
o Causes include T2DM treatment with metformin
o Treatment: IV Sodium bicarbonate + Insulin + Glucose +/- Sodium

dichloroacetate
▪ Hypoglycaemia
o RBG < 50 mg/dL
o Altered mental state, coma, seizures
o Causes include treatment of T2DM with sulfonylurea
o Treatment: IV glucose infusion
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Guidelines for Common Medical Emergencies: T. Seemungal et al
At the end of the course you will be able to:

▪ Identify disturbances in fluid and electrolyte balance
▪ Integrate the symptoms and signs of common metabolic diseases with the clinical
presentation of each group of metabolic disorders
▪ Define the common metabolic diseases
▪ Distinguish between inborn or acquired errors of metabolism
▪ Know how to investigate patients in both in-patient and out-patient settings
▪ Know how to manage patients in both in-patient and out-patient settings
▪ Be able to identify and treat common metabolic emergencies
Resources
1. Patients on the medical and surgical wards, POSGH, are our most valuable resource

Readings
1. Guidelines for Common Medical Emergencies: T. Seemungal et al
2. Davidson’s Principles and Practice of Medicine: Metabolic Diseases.
3. Kumar and Clarke: Metabolic Diseases.
4. Oxford Textbook of Medicine
5. Harrison’s Principles of Internal Medicine
6. Royal College of Physicians Curriculum for Higher Specialist Training in Metabolic
Medicine
7. Royal College of Chemical Pathologists Training Board
8. Approved Websites:
International Diabetes Federation http://www.idf.org/
American Diabetes Association http://www.diabetes.org/
http://www.diabetesjournals.org/
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APPENDIX ix
ENDOCRINOLOGY MODULE:
Course description
Title: Endocrinology Medicine: Year 4&5 Undergraduate Medicine
Overview
endocrinology medicine within the context of general internal medicine over two rotating 8 weeks
clerkships. It is more inclined to appreciate the diseases of high prevalence in Trinidad and Tobago.
Prerequisite
A pass in the MBBS: Phase 1 examination.

5. Year 4 - at the Eric Williams Medical Sciences Complex (EWMSC), and San Fernando
General Hospital.
6. Year 5 - at Port of Spain General Hospital.
This depends on the availability of personnel and is consistent with the service commitment of the
Endocrinology is one of several components of general internal medicine with which the student is
expected to become familiar over the two final years of undergraduate training in the Faculty of
Medical Sciences. It integrates closely with other sub-specialties including Metabolic disorders, in
particular Diabetes. Over the course of the final 2 years of undergraduate training, students are
expected to become familiar with the management of Endocrine Diseases within and across these
specialties.
Endocrinology as a Discipline within Internal Medicine
The Department of Clinical Medical Sciences is comprised of four units: Adult Medicine (General
Internal Medicine), Paediatrics and Radiology. Endocrinology is one of several disciplines within
internal medicine.
139
The course covers diseases of the endocrine system. Students would be expected to have been
exposed to the rudiments of examination and history during Phase I training. This course is
designed for students during the final two clinical years of undergraduate medicine.

Welcome to the Endocrine Medicine component of the Internal Medicine Programme. We hope that
you will see this course as an extension of the learning initiated during your first three years of
training. Whereas in the first year of internal medicine (year 4 undergraduate) we emphasised
knowledge of the underlying disease processes and the acquisition of an accurate history and
examination, our emphasis in the final year is on diagnostic skill, investigation and treatment of
common endocrine diseases and their differentiation from other diseases. The best advice we can
give you is that learning is patient-centred and not text-book centred, though your text books will
provide a useful resource. We hope you enjoy your brief time with us in this exciting field.
Contact Information
Tutors: EWMSC - Professor S. Teelucksingh ,
Port of Spain General Hospital – Prof. T. Seemungal
Office: Department of Clinical Medical Sciences, Faculty of Medical Sciences, 2nd Floor, Building
67, EWMSC, Mount Hope
POSGH 623-4030 or ext 2585
E-mail: tseemungal@aol.com
Content
Clinical presentation of endocrine diseases
A list of common symptoms associated with endocrine diseases are as follows:
Major symptoms Differential Diagnoses
● Appetite and weight changes ↑appetite; weight loss: Thyrotoxicosis,

Uncontrolled DM.
↑appetite; weight gain: Cushing’s Syndrome,

hypoglcaemia, hypothalamic disease.
↓appetite; weight loss: Adrenal insufficiency,

Anorexia Nervosa, GI disease (particularly
malignancy)
↓appetite, weight gain: Hypothyroidism
● Changes in bowel habit/ Disturbed

Diarrhoea: Hyperthyroidism, Adrenal Insufficiency.
defaecation
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Constipation: Hypothyroidism, Hypocalcaemia.
● Changes in sweating ↑ Sweating: Hyperthyroidism,

Phaeochromocytoma, Hypoglycaemia,
Acromegaly, anxiety states and menopause.
● Changes in Hair distribution Hirsutism: PCOS, Adrenal Causes, Ovarian Causes,

Drugs
Absence of facial hair in a ♂: Hypogonadism
Temporal recession of scalp hair in ♀: Androgen

excess.
Loss of axillary and pubic hair in both sexes:

Hypogonadism or adrenal insufficiency.
● Lethargy Endocrine causes: Hypothyroidism, Addison’s

Disease, DM.
Anaemia
Connective Tissue Diseases (CTD)
Chronic Infection: HIV, infective endocarditis.
Drugs: Sedatives, diuretics causing electrolyte

disturbances.
Chronic Liver Disease
Renal Failure
Occult Malignancy
Depression
● Skin Changes Coarse, pale, dry skin: Hypothyroidism
Dry and scaly: Hypoparathyroidism
Flushing of the skin of the face and neck: Carcinoid

syndrome
Soft tissue overgrowth and skin tags in the axillae

(Molluscum Fibrinosum): Acromegaly
Acanthosis Nigricans: Acromegaly, DM, PCOS and

Cushing’s Syndrome.
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Xanthelasma: DM, Hypothyroidism
● Changes in Skin Pigmentation ↑Pigmentation: Primary Adrenal Insufficiency
↓Pigmentation: Hypopituitarism
Localized depigmentation (vitiligo): Hashimoto’s

Disease with hypothyroidism, Addison’s
Disease with adrenal insufficiency.
● Changes in stature Tall Stature: GH excess(gigantism), Gonadotrophin

Deficiency, Klinefelter’s Syndrome,
Marfan’s Syndrome, Generalised
Lipodystrophy.
Short stature: Turner’s Syndrome, Down

Syndrome, Rickets, Achondroplasia.
● Impotence Primary or Secondary Hypogonadism secondary to

hyperprolactinaemia.
Others: Emotional disorders, vascular disease,

autonomic neuropathy (DM or alcoholism),
Spinal Cord disease or testicular atrophy.
● Menstruation Primary or secondary amenorrhoea
● Polyuria(> 3L/dy) DM, Diabetes Insipidus, Primary polydypsia,

hypercalcaemia, tubulointerstitial or cystic
renal disease.
● Lump in the throat( Goitre) Thyroid Disease.
SYNDROMAL SYMPTOMATOLOGY
It is important to remember that hormones control so many aspects of body function
that the manifestations of endocrine disease are protean and it is sometimes easier to
identify the symptoms as belonging to a syndrome!!!
● Thyrotoxicosis Preference for cooler weather, weight loss,

increased appetite (polyphagia),
palpitations, increased sweating,
nervousness, irritability, diarrhoea,
amenorrhoea, proximal muscle weakness,
exertional dyspnoea.
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● Hypothyroidism(myxoedema) Preference for warmer weather, lethargy,
swelling of the eyelids (oedema), hoarse
voice, constipation, coarse skin,
hypercarotenaemia.
● Diabetes Mellitus Polyuria, polydypsia, polyphagia,

unexplained weight loss or weight gain,
blurred vision, weakness, infections, groin
itch, rash (pruritus vulvae, balanitis),
weight loss, tiredness, lethargy and
disturbance of conscious state.
● Hypoglycaemia Morning headaches, weight gain, seizures,

sweating.
● Primary Adrenal Insufficiency Pigmentation, tiredness, loss of weight,

anorexia, nausea, diarrhoea, nocturia,
mental changes, seizures (hypotension,
hypoglcaemia).
● Acromegaly Fatigue, weakness, increased sweating,

heat intolerance, weight gain, enlargening
hands and feet, enlarged and coarsened
facial features, headaches, decreased
vision, voice change, decreased libido,
impotence.
The student is expected to characterize each of these symptoms by onset, duration,

timing, and evolution. The student will also be expected to understand the differential
diagnosis of these symptoms and how to differentiate between these and other medical
conditions by clinical evaluation, laboratory and radiological investigations.
Endocrinology History
A previous history of any endocrine condition must be uncovered.

Past Medical History: importance of comorbidites
● Hypertension (may be due to an endocrine cause eg. Phaeochromocytoma, Cushing’s
Syndrome or Conn’s Syndrome),
● IHD
● Diabetes Mellitus- It is important to determine how well the patient understands the
condition and whether he/she understands the principles of a diabetic diet and adheres to it.
Find out how the blood sugar levels are monitored and whether or not the patient adjusts the
insulin dose. Special patient education of care of the feet and yearly visits to the
ophthalmologists to prevent any complications.
● Epilepsy- Seizures could be secondary to primary adrenal insufficiency
( hypotension, hypoglycaemia)
● Asthma
● Blood Dyscriasis
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● Cancer
Past Gynaecological History

● Does the patient have a history of gestational diabetes? Hyperglycemia? Delivery of an
infant weighing >9 lb (4.1 kg)? Toxemia? Stillbirth? Other complications of pregnancy?
Drug History: importance of retrospective diagnosis of endocrine disease from the drug history. A
dosage schedule and a side effects profile should be noted for any drug in use!!
● Previous use of any antithyroid drugs, thyroid hormone or any radio-iodine (131I) treatment
can→ Hypothyroidism.
● Any Radiation therapy for carcinoma? → Hypothyroidism
● Any steroid or mineralocorticoid replacement for eg. In hypopituitarism or hypoadrenalism?
Allergy History
Past Surgical History: It is important to obtain knowledge of any

● Thyroid Surgery: A partial thyroidectomy →Hypothyroidism or hypoparathyroidism
(Surgical damage to the parathyroid glands).
● Adrenal Surgery: ↓ adrenal or pituitary function
Family History: Important to note in

● Thyroid conditions
● Diabetes Mellitus
● Multiple Endocrine Neoplasia(MEN) syndrome: Rare autosomal conditions inclusive of
pituitary tumors, medullary carcinoma of the thyroid, hyperparathyroidism,
phaechromocytoma and pancreatic tumors.
Social History
● What is the patient’s alcohol intake?
● Does the patient smoke?
● Many of these conditions are chronic and carry with them serious complications. You need
to determine how well the patient is coping and ask about conditions at home and work as
these will have an important impact on the success of treatment.
Signs of Endocrine Disease

The pathophysiology and causes of each of these conditions along with the interpretation and
reporting of each sign is essential for proper diagnosis and should be emphasized.
THYROID DISEASE
Thyrotoxicosis Hypothyroidism
General ● Signs of weight loss and anxiety ● Signs of obvious mental and
Inspection physical sluggishness.
● Frightened facies
● Evidence of ‘Myxoedema
Madness’.
Legs ● Pedal oedema (pitting) - Sign of ● Non-pitting oedema
CCF which may be precipitated by
thyrotoxicosis in the elderly. ● Signs of peripheral
(Apathetic Hyperthyroidism) neuropathy
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● Pretibial Myxoedema- bilateral
pink,brown, or skin colored ● Uncommon neurological
elevated dermal nodules and abnormalities associated
plaques. with hypothyroidism:
✔ Carpal (Phalen’s sign)
● Proximal myopathy- on squatting? and Tarsal tunnel
syndrome.
● Hyperreflexia ✔ Delayed ankle jerks.
✔ Muscle cramps
Hands ● Fine tremor ● Peripheral cyanosis (↓CO)
● Onycholysis (Plummer’s nails) ● Cool dry peripheries
● Thyroid Acropachy ● Hypercarotenaemia of the

palms (↓ metabolism of
● Palmar erythema carotene)
● Palmar crease pallor –

● Warm sweaty palms anemia secondary to
✔ Chronic Disease
● Pulse- Sinus Tachycardia or Atrial ✔ Folate deficiency
Fibrillation secondary to bacterial
(Irregularly irregular). overgrowth
✔ Vitamin B12 deficiency
● Collapsing Pulse associated with
pernicious anemia
✔ Iron deficiency secondary
to anemia
Arms ● Proximal Myopathy- Raise the ● Proximal Myopathy- Raise
hands above the head. the hands above the head.
● Arm Reflexes- Abnormal briskness
Facies ● Thyroid Stare -Frightened ● Generally thickened skin

expression with a yellowish
discoloration secondary to
hypercarotenaemia
● Alopecia
● Vitiligo( Asociated with

autoimmune disease)
● Palpate for coolness and

dryness of skin and hair
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Eyes ● Exopthalmos ● Periorbital oedema
● Complications of proptosis: ● Loss/ thinning of the oute

✔ Chemosis one third of the eyebrows
✔ Conjuctivitis
✔ Corneal ulceration
✔ Optic Atrophy ● Xanthelasma
✔ Opthalmoplegia ( Associated hypercholesterolaemia)
● Lid retraction (sclera visible above

the iris).
● Lid lag- descent of the upper lid

lags behind descent of the eyeball.
● Ptosis? Rule out Myasthenia Gravis

which could be part of an
autoimmune polyglandular
syndrome.
Ears ● Test for bilateral nerve
deafness ( may occur in
endemic or congenital
hypothyroidism)
Mouth ● Swollen tongue?
● Ask person to speak- Listen

for coarse, croaking, slow
speech.
Neck Ex of Thyroid gland: Ex of the thyroid

● Inspect- ● ( as for thyrotoxicosis)
✔ Swelling?
✔ Moves on swallowing?
✔ Shape on swallowing?
✔ Any noted inferior border?
✔ Thyroidectomy scars?
✔ Dilated chest wall veins?
→Retrosternal Goitre→
Thoracic Inlet Obstruction
✔ Reddened gland? →
Suppurative thyroiditis
● Palpate (from behind) -

✔ Size
✔ Shape
✔ Consistency
✔ Tenderness
✔ Mobility
● Percussion-
✔ Change from resonant to
dull may indicate a
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retrosternal goitre (not a
very reliable sign)
● Auscultation-
✔ Any Bruits?
Chest ● Gynaecomastia ● Heart: Pericardial effusions

( occasionally)
● Lung- pleural effusions→
● Flow murmurs ( ↑ CO) stony dullness on
percussion, crepitations on
● Signs of CCF (Apathetic auscultation.
Hyperthyroidism)
PITUITARY DISEASE
Panhypopituitarism Acromegaly
General inspection ● Short stature( Failure ● Characteristic face and
of GH secretion body habitus as
before closure of the described below.
epiphyseal plates)
● Pallor of the skin

( anemia or ACTH
deficiency→ loss of
MSH activity)
● Fine wrinkled skin

and lack of body hair
( Gonadotrophin
deficiency)
● Complete absence of
secondary sexual
characteristics (if
Gonadotrophin failure
occurred before
puberty)
Lower Limbs ● Signs of osteoarthritis

in the hips and knees
● Psuedogout
● Foot drop secondary to

peroneal nerve
entrapment
Genital Region ● Loss of pubic hair in

both sexes
● Testicular atrophy
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in♂- small, firm
testes.
Hands ● Wide spade like shape

( soft tissue and bony
enlargement)
● Warm sweaty palms (↑

metabolic rate)
● Thickened skin
● Osteoarthritic
changes(skeletal
overgrowth)
● Carpal tunnel
syndrome secondary to
soft tissue overgrowth
(Phalen’s sign)
Arms ● Proximal myopathy
● Palpate behind the

medial epicondyle for
ulnar nerve thickening.
Axilla ● Loss of axillary hair ● Inspect for

in ♂ ✔ Non-tender skin
coloured
protrusions/skin
tags called
molluscum
fibrosum
✔ Acanthosis
nigricans
● Palpate for
✔ greasy skin
Face ● Multiple skin Large supraorbital ridge→

wrinkles around the frontal bossing
eyes (Gonadotrophin
deficiency)
● Transfrontal scars? →
Hypophysectomy
scars
● Loss of facial hair
over the bearded
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area?
→Gonadotrophin
deficiency
Eyes ● Assess for visual field ● Assess for visual field
defects eg. defects
Bitemporal
hemianopia ● Funduscopy
secondary to an ✔ Optic atrophy
enlargening pituitary ✔ Papilloedema (↑
tumour compressing ICP secondary to
the optic chiasm. extensive tumor)
✔ Angioid streaks
● Perform funduscopy: (red, brown or grey
Ex for optic atrophy streaks ×3-×5 the
(optic nerve size of a retinal
compression from a vein; appearing to
pituitary tumor). emanate from the
optic disc)
● Assess III, IV, V1, ✔ Note any
and VI secondary to hypertensive or
extrapituitary diabetic retinopathy
expansion into the
cavernous sinus.
Mouth ● Enlarged tongue which

cannot fit neatly
between the teeth
● Splayed teeth
● Lower jaw is square

and firm
● Prognathism-
protrusion of the jaw
● Hoarse voice
Neck ● Thyroid may be

diffusely enlarged or
multinodular
Chest ● Skin pallor ● Coarse body hair

● ↓ in nipple ● Gynaecomastia
pigmentation
● ↓in chest hair in the ♂ ● Full CVS Ex: signs of
arrhythmias,
● Secondary breast cardiomegaly and CCF
atrophy in♀ secondary to IHD,
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HTN and
Cardiomyopathy which
are all common in
acromegaly
Abdomen ● Hepatomegaly
● Spleenomegaly
● Renal enlargement
Back ● Inspect for kyphosis
Other ● Urinalysis- glycosuria

(GH is diabetogenic in
25% of cases)
● BP
ADRENAL DISEASE
Cushing’s Syndrome Addison’s Disease
General inspection Standing: Observe front, back Look for
and sides ● Vitiligo
● Moon like facies ● Cachexia
● Fat Distribution: ● Pigmentation in the

Gross truncal/central obesity. ✔ Palmar creases
Limbs appear thin in ✔ Elbows
comparison ✔ Gums
✔ Buccal Mucosa
● Bruising ( loss of ✔ Genital areas
perivascular supporting ✔ In scars
tissue secondary to (this is due to
protein catabolism) compensatory
ACTH
● Excessive pigmentation hypersecretion
on the extensor surfaces when there is
an adrenal
cause)
Legs ● Proximal myopathy

secondary to
mobilization of muscle
tissue or excessive
urinary K+ loss - Ask
the patient to squat.
● Pedal oedema ( salt and
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water retention)
● Bruising and poor

wound healing
Lower limbs ● Look for purple striae

between the thighs.
Arms ● Purple striae near the

upper arms
Axilla ● Purple striae
Face and neck ● Moon like face
● Plethora +/-
polycythaemia
● Acne
● Hirsutism in the ♀( in
the presence of
androgen excess)
● Telangiectasia
● Supraclavicular fat pads
Eyes ● Check the visual fields

for signs of a pituitary
tumor.
● Funduscopy-
✔ visual field defects
✔ optic atrophy
✔ papilloedema
✔ Hypertensive
changes
✔ Diabetic changes
Chest ● Gynaecomastia in the ♂
Abdomen Lay the patient in bed on one

pillow.
● Inspect for
✔ purple striae
(weakening and
disruption of the
fibres in the dermis
leading to exposure
of the vascular
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subcutaneous tissues)
● Palpate for
✔ Adrenal masses ( a
large adrenal
carcinoma will be
palpable over the
adrenal area)
✔ Hepatomegaly
secondary to fat
deposition.
Back ● Buffalo Hump (fat

deposition over the
interscapular region)
● Palpate for:
Bony tenderness of the vertebral
bodies ( ← crush
fractures from
osteoporosis secondary
to an anti-vitamin D
effect and ↑ urinary
calcium excretion which
both affect the bone
matrix)
Other ● Excessive pigmentation ● Take the BP to test

on the extensor surfaces for Postural
(MSH activity in the hypotension
ACTH molecule)
● Urinalysis- test the urine
for glucose since
steroids are
diabetogenic (↑ in
hepatic gluconeogenesis
together with an anti
insulin effect on the
peripheral tissues).
● Check BP- Salt and
water retention
(Aldosterone effect), ↑
angiotensin secretion
can result in
hypertension.
NB.
● Cushing’s disease is specifically pituitary ACTH overproduction while,
Cushing’s Syndrome could be secondary to excessive steroid hormone production from any
cause.
● Sometimes Ex of a patient with Cushing’s syndrome is difficult since they may be

suffering from steroid psychosis and refuse to do anything you ask.
152
● Signs suggesting that adrenal carcinoma may be the underlying cause include:
1. A palpable spleen
2. Signs of virilization in the ♀
3. Gynaecomastia in the ♂
● Signs that suggest that ectopic ACTH production may be the cause include:
1. Absence of the Cushingoid body habitus
2. More prominent oedema and hypertension
3. Marked muscle weakness
● Significance of hyperpigmentation:
1. An extra adrenal tumor
2. Enlargement of an ACTH- secreting pituitary adenoma following
adrenalectomy ( Nelson’s Syndrome)
● ADDISON’S DISEASE
This can be part of an autoimmune polyglandular syndrome:
Type I
1. Chronic Mucocutaneous Candidiasis
2. Hypoparathyroidism
3. Addison’s Disease.
Type II
1. IDDM
2. Autoimmune thyroid Disease
3. Addison’s Disease
4. Myasthenia Gravis
CALCIUM METABOLISM
Primary Hyperparathyroidism Hypoparathyroidism
✔ ‘stones’ (renal stones) → neuromuscular tetany
✔ ‘bones’ (osteopenia and
psuedogout)
✔ ‘abdominal groans’
( constipation, peptic ulcer
and pancreatitis)
✔ ‘psychological moans’
(confusion)
General ● Note the mental state ● Trousseau’s sign

Inspection of the patient: This is elicited with a blood
Coma? pressure cuff placed
Convulsions? on the arm with the
pressure raised
● Assess hydration above the patient’s
( polyuria from systolic blood
hypercalcaemia can pressure. Within 2
cause dehydration) minutes the thumb
becomes strongly
● Palpate shoulders, adducted and the
sternum, ribs, spine, fingers are extended
and hips for bony except at the
153
tenderness, metacarpophalangeal
deformity or joints.
evidence of previous
fractures. ● Chvostek’s sign-
Tap gently over the
facial nerve under
the ear. A brisk
neuromuscular
twitch occurs
● Hyperreflexia
● Dry skin
Legs ● Proximal Myopathy
Hands ● Fragile nails.
● Monilial infectionof
the nails?
Eyes ● Band Keratopathy ● Cataracts

(rare)
● Papilloedema
Mouth ● Deformity of the

teeth
Other ● Check BP ↑?
General Inspection ● Look for any evidence of dehydration- osmotic

diuresis (glycosuria) can → massive fluid loss.
● Note obesity ( associated with NIDDM) or signs

of recent weight loss ( uncontrolled glycosuria)
● Note any abnormal endocrine facies eg.

Cushing’s syndrome or acromegaly.
● Note any ↑ pigmentation (bronze diabetes)

secondary to haemochromatosis.
● Comatosis secondary to dehydration, acidosis or

plasma hyperosmolality.
● Kussmaul’s breathing (‘air hunger’) in DKA
154
since fat metabolism is ↑ to compensate for the
lack of availability of glucose; excess Acetyl-
CoA is produced and converted to ketone bodies
by the liver.
Lower Limbs Inspect for vascular and neurological abnormalities of the
feet.
● The skin of the feet may be hairless and atrophied

due to small vessel vascular disease and resultant
ischaemia.
● Leg ulcers- particularly on the toes or any area

that is exposed to pressure. These are usually due
to a combination of ischaemia and peripheral
neuropathy ( there’s glycosylation of neural
proteins)
● Superficial skin infections which are more

common because of high tissue glucose levels
and ischaemia providing a favourable
environment for growth of organisms:
✔ Boils
✔ Cellulitis
✔ Fungal infections
● Diabetic dermopathy: pigmented scars/small

rounded plaques with raised borders lying in a
linear fashion over the shins
● Necrobiosis lipoidica diabeticorum (rare) - a

central yellow scarred area surrounded by a red
margin when the condition is active.
● Thighs- Insulin injection sites → fat atrophy? Fat

hypertrophy? PALPATE!!!
● Quadriceps muscle wasting? ← Femoral nerve

mononeuropathy
● Knees- Charcots joints?
● PAPLATE the feet: Peripheral pulses? Temp?

Capillary return? Absent peripheral pulses, cool
peripheries and ↓ capillary return are all evidence
of PVD.
● Neurological Ex: Assess for peripheral

neuropathy, tap the reflexes, test for proximal
muscle power( diabetic Amyotrophy)
155
Genital Region ● ♂ can sometimes present with a balanitis
Upper Limbs ● Nails- Candida infection
● Injection sites? INSPECT and PALPATE
● BP- lying and standing because diabetic

autonomic neuropathy can cause postural
hypotension
Axilla ● Inspect for acanthosis nigricans
Face
Eyes ● Visual Acuity? – Retinal disease?
Any change in the shape of the lenses?
● Funduscopy:
1. Rubeosis- new blood vessel formation over the
iris that can→ glaucoma.
2. Cataracts- sorbitol deposition in the lens.
3. Non- proliferative retinal changes?
Haemorrhages- Dot (inner retinal layers) and blot (in the
superficial nerve fibre layer).
Microaneurysms- vessel wall damage
Exudates- Hard or soft ( cotton wool spots with a fluffy
appearance)
4. Proliferative changes? Changes in the blood
vessels in response to ischaemia
New vessel formation? → vitreal haemorrhage? →
Retinal detachment?
Any laser scars (small brown or yellow spots) secondary
to photocoagulation of new vessels by laser
therapy.
● Assess for CN III, IV and VI palsies.
Ears Observe for any evidence of infection:

● Malignant otitis externa ( Psuedomonas
Aeruginosa)
- a mound of granulation tissue in the
external canal
- a Facial nerve palsy in 50% of the cases
Mouth ● Candida infection
Neck ● Inspect for Acanthosis Nigricans
● Auscultate for carotid artery stenosis
156
Abdomen ● PALPATE for hepatomegaly secondary to fatty
infiltration or haemochromatosis.
Other ● Urinalysis: Test for

✔ Glucose
✔ Protein ( Diabetic Nephropathy secondary to
glomerulonephritis, renal artery disease or
pyelonephritis)
✔ Nitrites or blood ( Asymptomatic UTI)
Investigation of Endocrinological Diseases
In the interpretation of the results of endocrinological investigations the normal range of values for
the following hormones should be known
ACTH 09:00 10-80ng/L
Aldosterone (recumbent) 100-500pmol/L

AFP <10kU/L
Cortisol 09:00 140-680 nmol/L

24:00 <100nmol/L
FSH ♂ 2-10 U/L

♀ follicular 2-8U/L
♀ post menopausal >15 U/L
GH Post glucose load < 2mU/L

Stress >20mU/L
Insulin Fasting 3-15mU/L

Hypoglycaemia <3mU/L
LH ♂ 2-10 U/L
♀ follicular 2-10U/L
♀ post menopausal > 20 U/L
PTH 10-65 ng/L
Prolactin 50-400 mU/L
Renin 13-114 mU/L
Testosterone ♂ 9-30 nmol/L

♀ <2.5nmol/L
TSH 0.3- 4.0 mU/L
FT4 9-26 pmol/L
157
FT3 3.0-8.8 pmol/
Students need to be familiar with the strategy of investigation of patients with

1. PITUITARY AND HYPOTHALAMIC DISEASE:
(I) Identify hypopituitarism
ACTH deficiency
✔ Short acting synacthen test: know its uses, dose of admistration of
synacthen, specific timing of blood samples (0 and 30 mins) and
interpretation of results( normal 30 minute reading > 550nmol/L)
✔ Only if uncertain in the interpretation then the insulin tolerance test is used:
know its uses, contraindications, dose, aim, and timing of blood samples and
interpretation of results.
LH and FSH deficiency

✔ ♂: measure random serum testosterone
✔ ♀ premenopausal: Ask if she has regular menses
✔ ♀ post menopausal: Measure random serum LH and FSH ( normally
>30mU/L)
TSH deficiency
✔ Measure random serum thyroxine
✔ Note that TSH is often detectable in pituitary disease, due to inactive
isoforms in the body
GH deficiency
The student should know that this should only be investigated if GH replacement therapy is
being contemplated. Know that GH levels are commonly undetectable, so a choice
from a range of stimulation tests is required:
✔ 1 hour after going to sleep
✔ Frequent sampling during sleep
✔ Post-exercise
✔ Insulin induced hypoglcaemia
✔ Clonidine
✔ arginine
✔ glucagon
Cranial Diabetes Insipidus

( The student should know that this should only be investigated if the patient complains of
polyuria/polydypsia, which may be masked by ACTH or TSH deficiency)
✔ Exclude other causes with blood glucose, potassium and calcium
measurements.
✔ Water deprivation test: Know its use, protocol and interpretation.
✔ Or 5% saline infusion test.
(II) Identify hormone excesses

✔ Measure random serum prolactin
✔ Investigate for acromegaly (glucose tolerance test)
✔ Investigate for Cushing’s syndrome, of which there are a large number of
tests available reflecting that no single test is infallible. The student should
know the protocol and interpretation of each: Urine free cortisol, overnight
dexamethasone suppression test, Diurnal rhthym of plasma cortisol, low
dose dexamethasone suppression test, insulin tolerance test, high dose
158
dexamethasone suppression test, corticotrophin-releasing hormone test,
inferior petrosal sinus sampling.
(III) Establish the Anatomy and Diagnosis

✔ Consider visual field testing
✔ Image the pituitary and hypothalamus by MRI or CT
2. THYROID DISEASE
Hyperthyroidism
✔ Serum T3: ↑ (particularly in T3 thyrotoxicosis).
✔ Serum T4:↑ but in the upper part of the normal range.
✔ TSH: < 0.1 mU/L.
✔ 131I uptake and TRAb are of diagnostic value in Graves when exopthalmos, goitre
and pretibial myxoedema are not present.
✔ LFTs: slightly ↑ bilirubin, alanine aminotransferase and GGT; ↑ ALP from bone and
liver
✔ U&E’s: Mild hypercalcemia
✔ Urinalysis: Associated diabetes mellitus and ‘lag storage’
Hypothyroidism
✔ TFTs: serum T4↓ and TSH ↑ (>20mU/L)
✔ Non-specific tests-CE’s: ↑ LH and CK
▪ Lipid Profile:↑ cholesterol and TGs
▪ U&E’s: ↓Na+
✔ ECG- sinus bradycardia
Low voltage complexes
ST/T wave abnormalities
Simple Goitres and Soilitary Thyroid Nodules

The student should know the method, indications and contraindications of
✔ Thyroid isotope scanning
✔ Fine Needle Aspiration
3. PARATHYROID DISEASE
Students should know that before interpretation of any of the following values the total calcium
measurements need to be corrected if serum albumin is ↓.
✔ PTH measurements
Urinary calcium
✔ U&E’s: Ca, PO34-
✔ Alkaline phosphatase
4. ADRENAL DISEASE
Investigations for Cushing’s syndrome have been discussed.
Addison’s disease
✔ Cortisol levels.
✔ Synacthen test.
✔ U&E’s: ↓Na+,↑K+
✔ Renin and aldosterone measurements in a recumbent position
✔ Blood glucose
✔ TFTs
✔ CBC (pernicious anemia)
✔ Full autoantibody screen ( Abs against adrenals, gonads, thyroid, pancreatic beta
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cells and parietal cells)
✔ CXR to rule out Tuberculosis ( causes adrenal calcification)
5. DIABETES ( this would be considered in greater detail in both the specific objectives and
the metabolic curriculum)
Specific Diseases of the Endocrine System

In the final year several further diseases will be discussed in addition to those studies during the
fourth year:
Objectives:
1. Diabetes mellitus:
• Recognize differences in the pathogenesis and clinical presentation of type 1 and 2

diabetes. Develop the skills to diagnose and treat acute complications of diabetes such as
diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar syndrome (HHS) and
hypoglycemia. Recognize different pathophysiology of Insulin Resistance Syndrome
including various components of this syndrome and how to treat each one.
• Recognize the important recent studies and various treatment modalities for prevention of
diabetes including lifestyle modification and medical therapy and their rationale.
• Recognize various treatment modalities for therapy for type 2 diabetes utilizing
sulfunylurias, biguanides, a-glucosidase inhibitors, and thiozolidinediones, and the site
of action of each agent in the pathogenesis of type 2 diabetes.
• Recognize the importance of recent clinical trials on the use of Ace inhibitors and
angiotensin receptor blockers in prevention of deterioration of nephropathy in diabetes
as well as their role in prevention of type 2 diabetes in those patients with impaired
glucose tolerance.
2. Thyroid disorders:
• Interpret thyroid function tests for various forms of thyroid pathology.
• Evaluate how various aspects of thyroid function may affect cardiac function and the
theory behind such actions.
• Apply the knowledge from clinical trials for treatment of thyroid cancer and measurement
of the outcome of such therapies.
• Evaluate thyroid storm and Myxedema coma and their etiopathology and treatment.
• Evaluate theories behind alteration of lipid metabolism in various forms of thyroid

disorders.
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3.Hypertension:
• Recognize various endocrine organs dysfunction that leads to the development of

hypertension and the pathogenesis of each etiologic factor.
• Use the latest advances and diagnostic maneuvers to differentiate between hypertension
due hyperaldosteronism, Cushing's, and pheochromocytoma as well as hypercalcemia
and hyperthyroidism.
4. Calcium:
• Distinguish between hypercalcemia of neoplastic origin versus hypercalcemia associated

with parathyroid adenoma.
• Diagnose by imaging method between hyperparathyroid and thyroid disease; the medical
versus surgical management; and theory behind each method.
• Describe the management of hyper and hypocalcemic crises and the theory behind such
therapies.
5. Adrenal disorders:
• Recognize the physiology and pathophysiology of adrenal disorders as well as the

hypothalamic pituitary adrenal axis disturbances resulting in the over-activity or the
under-activity of the adrenal in Cushing's and Addison's.
• Diagnose and manage Cushing's syndrome and adrenal insufficiency

• Describe how to utilize radiological methods to distinguish and locate the site of the tumor.
• Describe how to recognize and manage Addisonian crisis.
• Describe methods to distinguish between primary and secondary hyperaldosteronism and

bilateral adrenal hyperplasia
• Describe the clinical signs and differential diagnosis of pheochromocytoma and the
pathogenesis of this tumor in multiple endocrine adenomatosis (MEA).
• Describe the latest advancements in the understanding of the metabolic pathway of

adrenomedullary hormones and various metabolites.
• Describe how various medicines may interfere with urinary tests in the work-up of
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pheochromocytoma and what may be done to avoid these problems.
6. Pituitary disorders:
• Recognize the clinical symptoms and signs of hypopituitarism and hyperpituitarism

(acromegaly, Cushing's disease, prolactinoma), and be able to distinguish the
etiopathologic pathways for development of each.
• Describe the pathogenic pathways for the development of Cushing' s disease and how to
diagnose by use of radiological manipulation.
• Be able to tell the percent surgical success for the major pituitary tumors (acromegaly,
Cushing's, and prolactinoma).
• Describe the alternative methods to surgical procedures in the above-mentioned pituitary

tumors. Distinguish between a pituitary apoplexy and empty Sella and propose a work-
up for each.
9. Gonadal dysfunction:
• Diagnose male hypogonadism and prevalence in the general population verses individuals
with type 2 diabetes.
• Diagnose and treat impotency and anorgasmia.
• Diagnose hypogonadism in the female including primary and secondary amenorrhea and
how to distinguish, diagnose, and treat such conditions.
• Explain the latest theory regarding the evolution of the polycystic ovary syndrome (PCOS)
and the effect of insulin on the evolution of such a syndrome.
• Explain the role of PCOS in the development of metabolic syndrome and the latest theory
on managing such patients by medical intervention.
10. Other Aspects of Endocrine and Metabolic Disease Management:
• Recognize the controversy regarding hormone replacement therapy and the data presented
to justify or discourage the use of such hormones in different populations.
• Describe the use of appropriate medications in regard to efficacy, cost, and side effects in
various endocrine disorders.
In the study of each of these diseases, the principles of history taking and examination will be
emphasized.
Students will be expected to be able to describe the investigation of these diseases and the principles
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of management and knowledge of drugs used where applicable.
Goals/ Aims
The knowledge base developed during the year 4 training in internal medicine will be expanded in
year 5. All diseases discussed during year 4 will be reviewed during bedside sessions and a few other
pulmonary diseases will be discussed.
The common endocrine diseases have been chosen for the core endocrine medicine in your syllabus.
Patients with these diseases should be easily clerked on the medical wards of San Fernando General
Hospital and Port of Spain General Hospital or chest wards at the EWMSC.
Students will be expected to attend the Medical Grand rounds at the POSGH during their training at
POSGH and to answer simple questions about the cases discussed during these sessions.
Students are expected to be aware of the latest therapeutic strategies employing evidence-based
medicine. This information may be accessed via the various approved websites.
By the end of their 2 years’ training in endocrine medicine, students will expect to have reached an
internationally accepted standard in their knowledge and management of endocrine diseases within
general internal medicine.
General Objectives

1. HISTORY TAKING
● Demonstrate the ability to obtain and accurate and complete history from a
patient, caretaker or family member. Specific historical areas include
✔ Symptoms of DM and complications,
✔ Symptoms of hypo and hyperthyroidism and hypercalcaemia,
✔ Use of diabetic monitoring equipment and
✔ Risk factors for DM.
● The student should be able to deal effectively with compliance /adherence
issues and openly explain to a patient the consequences of non-compliance.
2. PHYSICAL Ex
● The student should be able to perform a routine
✔ Screening thyroid Ex,
✔ Screening diabetic foot Ex with the use of the monofilament,
✔ Cardiovascular Ex for evidence of CCF and atherosclerosis,
✔ Neurological Ex for evidence of stocking glove neuropathy,
✔ Screening Ex for kyphosis
● While attempting to characterize abnormalitites egs
✔ Thyromegaly and thyroid nodules,
✔ Diabetic ulcers,
✔ Other diabetic neuropathies ( mononeuritis, mylopathy), recognize
evidence of diabetic neuropathy or prior laser therapy to the retina.
3. MEDICAL DECISIONS
● The student should reliably recognize critical illness and seek appropriate
assistance.
● Writes progress notes that identify important data and demonstrate
thoughtful problem based assessment and plan.
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●Recognize and initiates management for, and outlines therapeutic goals for:
✔ Uncontrolled Dm (Hyperosmolar states, DKA and Aasymptomatic
Hyperglycaemia)
✔ New onset Diabetes in an outpatient with monotherapy
✔ Dyslipidaemia
✔ Hypothyroidism in the young and the elderly
✔ Hypertension and Dyslipidaemia in the Diabetic patient
● The student should also be able to recognize and appreciate the management
of:
✔ Hyperthyroidism and the thyroid storm
✔ Adrenal insufficiency
✔ Hyperparathyroidism
✔ DM required combined therapy
● The student should also be able to appreciate the iniation of diagnostic
strategies in the management of
✔ Adrenal disorders
✔ Pituitary disorders
4. PROCEDURAL SKILLS
● Masters the cognitive, counseling and technical skills for
✔ Monofilament Ex
● Interpret the results of
✔ Fasting and post prandial glucose
✔ Cholesterol panel
✔ TSH determinations used for screening
✔ Microalbumin
✔ Thyroid hormone panels in sick hospitalized patients( euthyroid sick
patient)
✔ Thyroid uptake scan for Grave’s Disease, Factitious hyperthyroidism
✔ Calcium and phosphate labs
● Understands the indications for and begins to try to interpret the findings of
✔ Thyroid USS
✔ Thyroid uptake scan
✔ Bone density scans
✔ Pheochromocytoma screens
✔ MRI of the pituitary
✔ Visual field testing
✔ FNA of the thyroid
5.MEDICAL KNOWLEDGE
● Applies relevant clinical and basic science knowledge of the following medical
conditions
✔ Uncontrolled diabetes
✔ Chronic Diabetes Mellitus
✔ Thyroid Disease
✔ Adrenal insufficiency
✔ Hypercalcaemia
✔ Cushing’s Syndrome
● The student should begin to demonstrate a progression in the content knowledge
and analytical thinking with well formulated differential diagnoses and
management plans.
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6. INTERPERSONAL SKILLS AND COMMUNICATION
● Effectively establishes rapport with patients and family
● Demonstrate empathy and caring toward your patients
● Communicates well with primary referring team and other consultants
● Presents on rounds in an organized and articulate fashion
● Functions as an effective team member
● Provides timely and thorough documentation of patient care.
● Demonstrate time management within the program
.
7. PROFESSIONALISM
● Strives for patient care and knowledge excellence
● Reliably accomplishes assigned tasks
● Demonstrates integrity, respect for others, honesty and compassion
● Demonstrates timely completion of administrative tasks and documentation
● Sets a tone of respect and collegiality for the team
● Acts as a role model for patient care and professional behaviour
8. PRACTICE EVIDENCE BASED LEARNING AND IMPROVEMENT

● Seeks and accepts feedback from team about patient care, organization and
presentations.
● Learns basic EBM principles and article review.

The years 4 & 5 endocrine medicine module consists of 1 session per week (normally a clinic
session) for 8 weeks either at POSGH or at EWMSC. You will be provided with a sessional
timetable at the start of the course.
Specific Objectives
• Learn inpatient consultation management and efficient outpatient management of patients with
endocrine disorders
• Learn inpatient and outpatient management of patients with diabetes mellitus, including
ketoacidosis, non-ketotic hyperosmolar coma, simple glycemic control, management and prevention
of diabetic complications, and adjusting insulin and/or oral hypoglycemic therapy for procedures or
surgery.
• Recognize and treat life threatening endocrine disorders such as thyroid storm, myxedema coma,
hypertensive crises from pheochromocytoma, and adrenal crisis.
• Efficiently evaluate the endocrine systems of acutely and chronically ill patients, including the role
of stimulation and suppression testing and imaging studies
Assignments
1. The student will expected to clerk at least 1 patient with any of the
Endocrine diseases described in the content section above and to present and
discuss each case with any instructor. Clerking of a patient will involve
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g. Complete history
h. Examination of all systems of the patients with special emphasis on
the chest examination
i. A description of what investigations were done and should be done
with details of results where applicable
j. Treatment and response to treatment
k. Follow-up plan for the patient including discharge
The purpose of the assessment would be to help you to appreciate where you have reached in
attaining the goals set out in this syllabus and to stimulate you to continue to study internal and
pulmonary medicine.
Teaching Strategies
1. guided lectures,
3. small group teaching
Resources
1. Patients on the medical and surgical wards, POSGH, are our most valuable Resource.
Readings
1. Davidson’s Principles and Practice of Medicine: respiratory medicine chapter.

2. Kumar and Clarke: respiratory medicine chapter.
3. The Endocrine System at a Glance, 3rd ed
4. Clinical Examination 5th ed by Talley O’Connor
5. Approved Websites:
The Endocrine Society (http://www.endo-society.org/)
The American Association of Clinical Endocrinologists
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NIH (Nat. Institute of Health USA)
NICE (Nat. Institute of Clinical Excellence)
PUBMED
Other website should be discussed with the instructor before use.
APPENDIX x
NEUROLOGY MODULE:
Course description
Title: Neurology: Year 4&5 Undergraduate Medicine
Overview
neurology within the context of general internal medicine over two rotating 8 weeks
clerkships.
Prerequisite
A pass in the MBBS Phase 1 examination.

7. Year 4 - at the Eric Williams Medical Sciences Complex (EWMSC), and San
Fernando General Hospital
8. Year 5 - at Port of Spain General Hospital
depending on availability of personnel and consistent with the service commitment of the

Neurology is one of several components of general internal medicine with which the
student is expected to become familiar over the two final years of undergraduate training in
the Faculty of Medical Sciences and integrates closely with other sub-specialties including
cardiology, endocrinology and emergency and intensive care medicine. Over the course of
the final 2 years of undergraduate training, students are expected to become familiar with
the management of neurological diseases within and across these specialties.
Neurology as a Discipline within Internal Medicine

(General Internal Medicine), Paediatrics and Radiology. Neurology is one of several
disciplines within internal medicine.
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The course covers disorders of the nervous system. Students would be expected to have
been exposed to the rudiments of the neurologic examination and history during Phase I
training. This course is designed for students during the final two clinical years of
undergraduate medicine.
major common disorders of the nervous system: headaches, raised intracranial pressure,
syncope, epilepsy, head injury, stroke, dementia, meningitis and encephalitis, brain tumour,
parkinsonism and movement disorders, multiple sclerosis, spinal cord and root dysfunction,
peripheral neuropathy and neuromuscular disorders. The student will also be expected to
understand the differential diagnosis of these conditions and how to differentiate between
these and other medical conditions by laboratory and radiological investigations.
Welcome to the Neurology component of the Internal Medicine Programme. We hope

that you will see this course as an extension of the learning initiated during your first three
years of training. Whereas in the first year of internal medicine (year 4 undergraduate) we
emphasised knowledge of the underlying disease processes and the acquisition of an
accurate history and examination, our emphasis in the final year is on diagnostic skill,
investigation and treatment of common disorders of the nervous system and their
differentiation from other diseases. The best advice we can give you is that learning is
patient-centred and not text-book centred, though your text books will provide a useful
resource. We hope you enjoy your brief time with us in this exciting field.
Contact Information
Tutors: EWMSC - Prof. S. Teelucksingh, Dr A. Ramlackhansingh and Associate Lecturers

(Dr Esack and Dr Panday from Neurology Unit.
Port of Spain General Hospital – Dr. Sandy, Dr. A. Ramlackhansingh and Associate
Lecturers from the Department of Medicine at POSGH
POSGH 623-4030 or ext 2585
Content
Clinical presentation of disorders of the nervous system
1. Headaches
2. Blackouts & loss of consciousness
3. Dizziness & vertigo
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4. Weakness, altered sensation
5. Coma and brain death
6. Disordered cognition
7. Mood and behavior
8. Visual problems
9. Speech problems
10. Breathing and swallowing disorders
11. Incontinence
The student is expected to characterise each of these symptoms by;
a. onset (where, when how)
b. duration
c. evolution
And to know the i. nature
ii. mechanism
iii. common causes of EACH of these symptoms.
Neurologic History
Past Medical History: importance of comorbidites eg hypertension, diabetes, hyperlipidaemia,
atrial fibrillation, bacterial endocarditis, myocardial infarction (emboli), haematological disease.
Drug History: analgesic overuse, caffeine withdrawal, carbon monoxide, hormones (eg, estrogen),
nitrates, proton pump inhibitors, antiepileptics.
Family History: hx of stroke, migraine and many metabolic, muscle, nerve, and inherited
neurodegenerative disorders
Social History: smoking, occupational, and travel history provides information about unusual
infections and exposure to toxins and parasites
Signs of Neurologic Disease

All medical students should be able to perform the following parts of the neurologic
examination.
A. Mental Status
1. Level of alertness
2. Language function (fluency, comprehension, repetition, and naming)
3. Memory (short-term and long-term)
4. Calculation
5. Visuospatial processing
6. Abstract reasoning
B. Cranial Nerves
1. Vision (visual fields, visual acuity, and funduscopic examination)
2. Pupillary light reflex
3. Eye movements
4. Facial sensation
5. Facial strength (muscles of facial expression and muscles of facial expression)
6. Hearing
7. Palatal movement
8. Speech
9. Neck movements (head rotation, shoulder elevation)
10. Tongue movement
C. Motor Function
1. Gait (casual, on toes, on heels, and tandem gait)
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2. Coordination (fine finger movements, rapid alternating movements, finger-to-nose,
and heel-to-shin)
3. Involuntary movements
4. Pronator Drift
5. Tone (resistance to passive manipulation)
6. Bulk
7. Strength (shoulder abduction, elbow flexion/extension, wrist flexion/extension, finger
flexion/extension/abduction, hip flexion/extension, knee flexion/extension, ankle
dorsiflexion/plantar flexion)
D. Reflexes
1. Deep tendon reflexes (biceps, triceps, brachioradialis, patellar, Achilles)
2. Plantar responses
E. Sensation
1. Light touch
2. Pain or temperature
3. Proprioception
4. Vibration
Interpretation and reporting of positive signs will be emphasised.
Investigation of Neurologic Disease
The student should be aware that diagnostic procedures should not be used for preliminary
screening, except perhaps in emergencies when a complete neurologic evaluation is impossible.
Evidence uncovered during the history and physical examination should guide testing.
1. Lumbar puncture (spinal tap)

Indications, procedure, relative contraindications, complications, risks,
recovery and common side effects, cerebrospinal fluid abnormalities in various disorders.
2. CT Scanning
Indications, limitations, acute vs chronic changes, contrast and non-contrast
Images
3. Magnetic Resonance Imaging

Advantages, contraindications, plain vs contrast, MRA and MRV usefulness
4. Electroencephalogram
Usefulness especially in seizure disorders
5. Electromyography and nerve conduction velocity studies

Principles and diagnostic usefulness
6. Duplex Doppler ultrasonography

Use in assessing carotid bifurcation disease
Special emphasis will be placed on investigations 1, 2 and 3 above.
Specific Disorders of the nervous system

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In the final year several further diseases will be discussed in addition to those studies
during the fourth year:
(1) Headaches (acute new headache, migraine, tension type headaches)

a. Pathophysiology and etiology
b. Characteristics of headache disorders by cause

c. Primary headache disorders including; migraine, cluster and tension-type headaches.
d. Secondary headache disorders including; acute narrow-angle glaucoma, encephalitis,
giant cell arteritis, idiopathic intracranial hypertension, intracerebral hemorrhage,
meningitis, sinusitis, subarachnoid hemorrhage, subdural hematoma (chronic), tumor or
mass
e. Evaluation and Interpretation of findings - focuses on determining whether a secondary

cause is present. If no cause is identified, focuses on diagnosing primary headache
disorders.
f. Findings that are of particular concern including; neurologic symptoms or signs,
immunosuppression or cancer, meningismus, onset of headache after age 50,
thunderclap headache, symptoms of giant cell arteritis, systemic symptoms, red eye and
halos around lights.
g. Testing- major aspects of diagnosis should be clinical, understand indications and

urgency of need for CT (or MRI) depending on the acuity and seriousness of findings
and suspected causes, ESR if giant cell arteritis suggested, CT of the paranasal sinuses,
lumbar puncture.
h. Treatment as directed by the cause.
(2) Epilepsy (including status epilepticus)

a. Definitons of; epilepsy, non-epileptic seizures, symptomatic seizures, psychogenic
seizures
b. Common causes of seizures
c. Classification of seizures into i. generalized- infantile, absence, tonic-clonic,
atonic, myoclonic and ii. partial- simple, complex
d. Symptoms and signs of seizures (including status epilepticus)
e. Diagnosis including; history- including risk factors, physical examination-
including clinical characteristics, testing including CT, MRI, EEG,
neuropsychologic testing.
f. Prognosis
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g. Treatment of i. Acute seizures and status epilepticus
ii. Posttraumatic seizures
and principles of long term treatment including drug choice, adverse drug effects,
surgery and vagus nerve stiulation.
(3) Stroke (including subarachnoid haemorrhage)

a. Definition of cerebrovascular accident (CVA) and transient ischaemic attack (TIA)
b. Basic understanding of the vasculature of the brain
c. Risk Factors
d. Symptoms and signs including neurologic deficits and evolution of these with time.
e. Complications (including those related to being bedridden)
f. Evaluation including, immediate neuroimaging to differentiate hemorrhagic from
ischemic stroke, intracerebral from subarachnoid haemorrhage and to detect signs of
increased intracranial pressure, the advantages of CT vs MRI
g. Treatment including stabilization and supportive measures and treatment of
complication
(4) Meningitis and encephalitis

a. Definition including; acute bacterial and asceptic (with basic knowledge of organisms)
b. Symptoms and signs
c. Diagnosis including; blood DNA PCR for bacterial pathogens and blood culture, *CSF
analysis and indications for CT before lumbar puncture (with signs of intracranial mass
lesion)
*Specific knowledge of the CSF abnormalities in various infections is emphasised.
d. Treatment including; empiric and choice of antibiotic
(5) Parkinsonism and movement disorders

a. Classification of movement disorders including hyper and hypokinesias
b. Definition and Etiology of Parkinson’s Disease (PD)
c. Symptoms and signs of PD
d. Diagnosis, with focus on clinical aspect and role of neuroimaging
e. Treatment; i. oral antiparkinsonians including: - Dopamine precursors
- Antiviral drug (amantdine)
- Dopamine agonists
- Anticholinergics
- Monoamine oxidase-B (MAO-B)
inhibitors
- Catechol O-methyltransferase
(COMT) inhibitor
ii. Surgery
iii. Physical measures
f. Differentiation of Parkinson’s disease from Parkinsonism and the diagnosis and
treatment of Parkinsonism
(6) Peripheral neuropathy (including Guillain-Barré syndrome & common mononeuropathies)

a. Definition
b. Mononeuropathy including symptoms and signs and common presentations including;
i. Ulnar nerve palsy
ii. Carpal tunnel syndrome
iii. Peroneal nerve palsy
iv. Radial nerve palsy
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and their diagnosis and treatment
c. Polyneuropathy including symptoms and signs and classification by pathophysiology
including; i. Myelin dysfunction – due to Guillain-Barré syndrome,
ii.Vasa nervorum compromise – due to Chronic arteriosclerotic ischemia,
vasculitis, and hypercoagulable states
iii. Axonopathy – due to Diabetes mellitus, Chronic renal insufficiency, nutritional
deficiencies and toxic-metabolic disorders
d. Diagnosis including; i. Clinical evaluation
ii. Electrodiagnostic testing
iii. CSF analysis
e. Treatment; focus on correcting cause when possible, note usefulness of;
i. plasmapheresis or IV immune globulin for acute myelin dysfunction
ii. corticosteroids or antimetabolite drugs for chronic myelin dysfunction
(7) Head injury (including common complications)

a. Define the common types of traumatic brain injury including their pathophysiology,
clinical findings and diagnosis;
i. acute subdural haematoma
ii. basilar skull fracture
iii. brain contusion
iv. concussion
v. chronic subdural haematoma
vi. diffuse axonal injury
vii. epidural haematoma
viii. subarachnoid haemorrhage
b. Diagnosis including initial assessment and the use of the Glasgow coma scale,
complete neurological exam and the appropriate use of neuroimaging.
c. Prognosis, especially with regard to GCS.
d. Management of traumatic brain injury based on severity of injury and GCS score
e. The principles of management of severe injury including;
i. Immediate stabilization (airway, breathing, circulation)
ii. Supportive measures, including, when necessary, control of ICP
iii. Admission to an ICU
iv. Treatment of underlying disorder
- Knowledge of the approach to trauma patients is emphasized
(8) Neuromuscular disorders ( including myasthenia gravis)

a. Definition and pathophysiology including;
i. Presynaptic release of acetylcholine – as in botulism, Eaton-Lambert
syndrome
ii. Breakdown of acetylcholine within the synapse – as in cholinergic drugs and
organophosphate insecticides
iii. Postsynaptic receptors – as in myasthenia gravis
b. Symptoms and signs
c. Diagnosis and principles of management
(9) Raised intracranial pressure

a. Definition and pathophysiology of intracranial hypertension and hydrocephalus with
basic understanding of the Monro-Kellie Hypothesis, Mean arterial pressure and
cerebral perfusion pressure
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b. Stages of intracranial hypertension including risk of brain herniation
c. Causes of intracranial hypertension
d. Signs and symptoms of intracranial hypertension (including Cushing’s triad)
e. Treatment specific to aetiology but including general principles of controlling raised
intracranial pressure including; sedation, hyperventilation, hydration, diuretics, BP
control, corticosteroids, pentobarbital coma and decompressive craniotomy.
(10) Syncope, coma, brain death

a. Definition and pathophysiology of syncope
b. Common causes of syncope
c. Differentiation between cardiac and CNS causes of syncope through appropriate
investigation.
d. Acute management of syncopal episode
e. Definition and pathophysiology of coma
f. Symptoms and signs of coma and impaired consciousness
g. Common causes of coma and impaired consciousness
h. Diagnosis of cause of coma or impaired consciousness with special focus on
history, general physical examination, neurologic examination, eye
examination, respiratory pattern and investigation; including bedside
investigations, blood investigations and the appropriate use of CT, MRI and
lumbar puncture.
i. The use of the Glasgow coma scale in monitoring of patients
j. The principles of management including;
i. Immediate stabilization (airway, breathing, circulation)
ii. Supportive measures, including, when necessary, control of ICP
iii. Admission to an ICU
iv. Treatment of underlying disorder
k. Definition of brain death
l. Diagnosis of brain death including guidelines for determination of
m. Prognosis
(11) Dementia
a. Definition, classification into Alzheimer’s and non-Alzheimer’s type and different
pathophysiologies
b. Signs and symptoms (early, late and severe)
c. Differentiation of dementia from delirium with knowledge of common causes of
delirium
d. Differentiation of vascular dementia from Alzheimer’s disease (Hachinski score)
e. Diagnosis including clinical criteria, laboratory testing, neuroimaging and
neuropsychologic testing
f. Prognosis
g. Treatment including principles of patient safety, environmental measures, drugs
(cholinesterase inhibitors, NMDA (N-methyl-D-aspartate) antagonist, SSRI), caregiver
assistance and end of life issues.
(12) Brain tumour

a. Classification of common intracranial tumours by age.
b. Pathophysiology
c. Symptoms and signs
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d. Diagnosis (CT or MRI)
e. Treatment principles for advanced disease including; airway protection, dexamethasone
for increased intracranial pressure, mannitol for herniation and definitive therapy with
excision, radiation therapy, chemotherapy or a combination
(13) Multiple sclerosis

a. Definition and pathophysiology
b. Symptoms and signs including; cranial nerves, motor, cerebellar, sensory, spinal cord
symptoms
c. Diagnosis including clinical criteria, brain and spinal MRI or CT, CSF for IgG levels
d. Prognosis
e. Principles of treatment including corticosteroids, immunomodulators, muscle
relaxants, gabapentin or tricyclic antidepressants and supportive care
(14) Spinal cord and root dysfunction (including spinal cord compression)
a. Basic anatomy of spinal cord and its roots.
b. Effects of spinal cord dysfunction by segmental level
c. Symptoms , signs and cause of the following spinal cord syndromes;
- Anterior cord syndrome
- Brown-Séquard syndrome
- Central cord syndrome
- Conus medullaris syndrome
- Transverse myelopathy
- *Cauda equina syndrome (not a spinal cord syndrome- nerve root
dysfunction)
d. Classification of spinal cord compression as acute, subacute and chronic and their
symptoms and signs
e. Diagnosis using MRI vs CT in the elective vs emergency setting
f. Prognosis
g. Treatment principles including, immobilization, maintenance of oxygenation and
perfusion, supportive care, sometimes surgical stabilization,
possibly methylprednisolone for blunt injuries, long-term symptomatic care and
rehabilitation
(15) Functional symptoms as presentation of psychological disorder

a. Definition of a conversion disorder
b. Presentation
c. Diagnosis by; i. Excluding neurological disease
ii. Exclusion of feigning
iii. Establishing a psychological mechanism
d. Treatment principles including psychotherapy and cognitive behavioural therapy
In the study of each of these diseases, the principles of history taking and examination
will be emphasised.
Goals/ Aims
175
The knowledge base developed during the year 4 training in internal medicine will be
expanded in year 5. All diseases discussed during year 4 will be reviewed during bedside
sessions and a few other neurologic diseases will be discussed.
Seven very common neurologic diseases have been chosen for the core neurology module
in your syllabus. Patients with these diseases should be easily clerked on the medical or
neurology wards of San Fernando General Hospital, Port of Spain General Hospital and
EWMSC. These disorders of the nervous system will be discussed in terms of lesions of the
central nervous system and autonomic & somatic nervous systems with focus on basic
neuroanatomy in order to illustrate a simple model of understanding of disorders of
neurology.
Students will be expected to attend the Medical Grand rounds at the POSGH during their
training at POSGH and to answer simple questions about the cases discussed during these
sessions.
Students are expected to be aware of the latest therapeutic strategies employing evidence-
based medicine. This information may be accessed via the various approved websites.
By the end of their 2 years’ training in neurology, students will expect to have reached an
internationally accepted standard in their knowledge and management of disorders of the
nervous system within general internal medicine.
General Objectives

8. understand how to elicit a history of neurologic disease
9. be able to elicit the signs of neurologic diseases
10. state a differential diagnosis for each symptom of disease
11. demonstrate time management within the program
12. demonstrate empathy and caring toward your patients
13. submit a short project
The years 4& 5 neurology module consists of 2 sessions per week for 8 weeks either at
POSGH or at EWMSC. You will be provided with a sessional timetable at the start of the
course.
Specific Objectives

1. define the symptoms and signs of neurologic disease
2. state common causes (neurologic and non-neurologic) of each
symptom or sign mentioned above
176
3. define each of the major diseases in this syllabus
4. integrate the symptoms and signs of neurologic disease with the
clinical presentation of each of the neurologic diseases studied in this
course
5. differentiate between the different conditions using the history,
examination and investigations discussed during this course
6. discuss treatment options of neurologic diseases
7. discriminate between cerebrospinal fluid abnormalities in various
disorders
8. use abnormal CT Scan results in the differential diagnosis of
neurologic diseases
Assignments
3. The student will expected to clerk at least 1 patient with each of the first 7
neurologic diseases described in the content section above and to present and
discuss each case with any instructor. Clerking of a patient will involve
l. Complete history
m. Examination of all systems of the patients with special
emphasis on the neurologic examination
n. A description of what investigations were done and should be
done with details of results where applicable
o. Treatment and response to treatment
p. Follow-up plan for the patient including discharge
The purpose of the assessment would be to help you to appreciate where you have reached
in attaining the goals set out in this syllabus and to stimulate you to continue to study
internal medicine and neurology.
Your assessment will take the following forms:
Teaching Strategies
1. guided lectures,
Resources
177
1. Patients on the medical and surgical wards, POSGH, are our most valuable
resource.
Readings
1. Davidson’s Principles and Practice of Medicine: neurology chapter.

2. Kumar and Clarke: neurology chapter.
3. Macleod's Clinical Examination: neurology chapter
4. Approved Websites: AAN (American Association of Neurologists), NIH (Nat. Institute of
Health USA), NICE (Nat. Institute of Clinical Excellence), SIGN (Scottish Intercollegiate
Guidelines Network), BAN (British Association of Neurologists), ENS (European
Neurological Society), PUBMED.
Other websites should be discussed with the instructor before use
APPENDIX xi
CARDIAC MEDICINE MODULE:
Course description
Title: Cardiac Medicine: Year 4&5 Undergraduate Medicine
Overview
pulmonary medicine within the context of general internal medicine over two rotating 8 weeks
clerkships.
Prerequisite

The course is taught in two modules depending on availability of personnel and consistent
with the service commitment of the medical teachers involved.
9. Year 4
10. Year 5
178
Cardiac medicine is one of several components of general internal medicine with which the
student is expected to become familiar over the two final years of undergraduate training in
the Faculty of Medical Sciences and integrates closely with other sub-specialties including
pulmonary medicine, cardiothoracic surgery and intensive care medicine. Over the course of
the final 2 years of undergraduate training, students are expected to become familiar with the
management of cardiac diseases within and across these specialties.
Cardiac Medicine as a Discipline within Internal Medicine
(General Internal Medicine), Paediatrics and Radiology. Cardiac medicine is one of several
disciplines within internal medicine.
The course covers diseases of the heart or cardiovascular system and is also called
cardiology or cardiac medicine. Students would be expected to have been exposed to the
rudiments of the cardiovascular examination and history during Phase I training. This course
is designed for students during the final two clinical years of undergraduate medicine.
major common cardiac conditions: acute coronary syndromes (ACS), arrhythmias,
pulmonary arterial hypertension, valvular heart diseases and heart failure as well as
predisposing conditions. The student will also be expected to understand the differential
diagnosis of these conditions and how to differentiate between these and other medical
conditions by laboratory and radiological investigations.
Why do this course?
● According to the World Health Organization (WHO), cardiovascular disease

is responsible for one-third of all global deaths (about 17 million people each year.
(2006, Heart Institute of the Caribbean)
● 85% of the global mortality and disease burden from cardiovascular disease
(including an estimated 32 million heart attacks and strokes yearly) is borne by
developing countries. (2006, Heart Institute of the Caribbean)
● WHO forecasts indicate that the number of deaths in the region (Latin America and
179
the Caribbean) attributed to cardiovascular disease will increase by more than 60%
between 2000 and 2020, unless preventive measures are introduced. During the same
period, mortality from cardiovascular disease will only increase by 5% in the
developed world. (The Lancet, Volume 368, Issue 9536, Pages 625 - 626, 19 August 2006)
● According to the WHO, “undetected billions are at high cardiovascular risk ... due to
hypertension, diabetes, high lipids, tobacco use, physical inactivity and unhealthy
diet". (2006, Heart Institute of the Caribbean)
● In Jamaica and most of the Caribbean, cardiovascular disease is a leading cause of
death, disability and hospitalization and accounts for a major portion of local and
overseas health care spending. (2006, Heart Institute of the Caribbean)
● The societal costs of diabetes in Latin America and the Caribbean were estimated at
$US65 billion in 2000. (2009, Caribbean Community (CARICOM) Secretariat: Summit on Chronic
Non-communicable diseases [CNCDs])

Welcome to the Cardiac Medicine component of the Internal Medicine Programme. We hope
that you will see this course as an extension of the learning initiated during your first three
years of training. Whereas in the first year of internal medicine (year 4 undergraduate) we
emphasised knowledge of the underlying disease processes and the acquisition of an accurate
history and examination, our emphasis in the final year is on diagnostic skill, investigation and
treatment of common cardiovascular diseases and their differentiation from other diseases.
Some advice:
Learning is patient-centred and not text-book centred, though your text books will provide a
useful resource. “He who studies medicine without books sails an uncharted sea, but he who
studies medicine without patients does not go to sea at all.” (Sir William Osler)
Also, we do not ask questions enough. Asking questions are a vital component of the learning
process. Use it! “The important thing is not to stop questioning. Curiosity has its own reason
for existing.” (Albert Einstein)
We do hope you enjoy your brief time with us in this exciting field.
Contact Information
Tutors: EWMSC – Dr. R. Ali, Dr N. Seecheran
Port of Spain General Hospital – Prof. T. Seemungal
POSGH 623-4030 or ext 2585
180
Content:
Clinical presentation of cardiac diseases-
Chest pain, Shortness of breath (SOB), orthopnoea, paroxysmal nocturnal dyspnoea,

palpitations, syncope/pre-syncope/dizziness, fatigue.
The student is expected to characterize each of these symptoms by onset (where, when, how),
duration and evolution and have a knowledge of common causes of each of these symptoms.
History-
Past Medical history- previous ischaemic heart disease, hypercholesterolaemia, hypertension,

diabetes mellitus, history of dental decay or infection, history of rheumatic fever.
Drug history
Social history- smoking, physical activity
Family history- family history of coronary artery disease, DM, HTN
Signs of Cardiac disease-

● cardiac cachexia in severe cardiac failure
● syndromes associated with specific cardiac disease (Marfan’s syndrome- aortic
regurgitation, Down’s syndrome- congenital heart disease, Turner’s syndrome-
coarctation of the aorta)
● clubbing (cyanotic congenital heart disease, infective endocarditis)
● splinter haemorrhages, Osler’s nodes, Janeway lesions (infective endocarditis)
● xanthomata
● pulse (causes of bradycardia, tachycardia and variations in rhythm, character, volume,
radio-radial and radio-femoral delay)
● xanthelasmata
● high-arched palate
● Jugular venous pressure- pulsation (assessment of height and character)
● Skeletal and ‘surgical’ abnormalities
● Apex beat (displacement, character)
● Heart sounds (including murmurs- timing, location, levine’s grade, radiation)
● Basal crepitations
Investigation of Cardiac Diseases
1. CXR (cardiomegaly, features of CCF)
2. 12 lead ECG (recordings in acute MI, atrial fibrillation, sinus tachycardia, sinus
bradycardia, heart block- 1st, 2nd and 3rd degree, bundle branch block)
3. Non- invasive Imaging modalities:

● Echocardiography- evaluating cardiomyopathies, valvular morphology and
function, congenital heart disease
181
● Cardiac Computed Tomography- evaluating CAD
● Nuclear Imaging- evaluating myocardial perfusion, ejection fraction, shunts
4. Invasive Imaging modalities:

● Cardiac Catheterisation
● Angiography
Outline indications for each and possible complications (hypotension, heart failure,
arrhythmias, myocardial ischaemia, contrast reaction, cholesterol embolism.
5. Pericardiocentesis- diagnostic and therapeutic indications.
Clinical Pharmacology
For the following classes of drugs, consider:

● Mode of action
● Pharmacokinetics
● Indications
● Adverse effects and toxicity
● Contraindications
● Interactions
Drugs-
a. ACE inhibitors
b. Angiotensin receptor blockers
c. Antiarrythmic drugs
d. Anticoagulants
e. Antiplatelet agents
f. Β- blockers
g. Calcium channel blockers
h. Digitalis
i. Diuretics
j. Inotropic drugs
k. Nitrates
l. Statins and other lipid-lowering agents
Cardiovascular Disease Prevention
a. Hypertension
- Definition (essential & secondary)
- Pathophysiology
- Diagnosis
- Classification- JNC 7/8
- Treatment options- dietary, lifestyle, pharmacological
b. Dyslipidaemia
182
- Definition
- Diagnosis
- Complications and consequences
- Treatment options- dietary, lipid lowering drugs
c. Diabetes Mellitus
- Definition
- Classification
- Diagnosis (American Diabetes Association)
- Cardiovascular complications
- Treatment options
Specific Diseases of the Heart
(1) Acute Coronary Syndromes

a. Definition (including STEMI, Non-STEMI, unstable angina).
b. Outline pathophysiology: Role of risk factors (age, sex, dyslipidaemia, DM, HTN,
homocysteine, cigarette smoking, physical inactivity, obesity, diet).
c. History taking:
Major symptoms- chest pain/heaviness, dyspnoea, orthopnoea, paroxysmal nocturnal
dyspnoea, ankle swelling, palpitations, fatigue
Risk factors- hypercholesterolaemia, DM, HTN, obesity, physical inactivity
Past history- Hx of IHD
Social history- smoking
Family history- CAD, HTN, DM
d. Examination:
Diaphoresis, tachycardia and/or hypotension (25% with anterior infarction), bradycardia
and/or hypotension (up to 50% inferior infarction), other arrhythmias, JVP, apex
beat, auscultation.
e. Silent ischaemia and infarction.
f. Investigations:
Cardiac biomarkers (CK, Troponin)
ECG changes in various types of infarction (inferior wall, inferolateral, septal, lateral) and
artery affected.
g. Criteria for diagnosis.
h. Treatment options: Pharmacological (anticoagulants, β-blockers, cholesterol-
lowering drugs etc.), Percutaneous coronary intervention (PCI), Coronary artery
bypass grafting (CABG).
i. Monitoring: Complications
(2) Myocardial Diseases- Cardiomyopathy

a. Definition
b. Classification (European Society of Cardiology)- Hypertrophic, Dilated,
Restrictive, Arrythmogenic right ventricular cardiomopathy and Unclassified)
c. Diagnosis- clinical features and investigations
183
d. Complications
e. Management options
Myocardial Diseases- Myocarditis

a. Viral
- aetiology (enterovirus, parvovirus, adenovirus, echovirus)
- clinical features (fever, chest pains, flu-like symptoms, lymphadenopathy, arrhythmias,
cardiomegaly, pulmonary oedema, pericardial friction rub, heart failure)
- diagnostic procedures ( laboratory findings, ECG, echocardiography, chest
XRay)
- treatment options
b. Non-viral
- Lyme carditis, toxoplasma gondii, chagas’ disease, rheumatic carditis
c. Non infective myocarditis

- Churg-Strauss myocarditis
(3) Pericardial disease

a. Classify and define acute pericarditis (infective, idiopathic or neoplastic), chronic
pericarditis and constrictive pericarditis.
b. Aetiology (constrictive- idiopathic, postviral, tuberculous, rheumatoid etc)
c. Pathophysiology
d. Investigations- invasive and non invasive (including ECG abnormalities)
e. Differentiate constrictive pericarditis from restrictive cardiomyopathy
f. Related complications: pericardial effusion, cardiac tamponade and constriction.
g. Management
(4) Congenital (Adult) Heart disease
Clinical manifestations:
● Presenting symptoms- pulmonary venous congestion, congestive heart failure,
cyanosis, collapse, hypoxic spells, haemoptysis, cerebral and pulmonary
complications, and arrhythmias.
● Systemic manifestions- growth retardation, respiratory infections, cerebral
complications, pulmonary vascular disease.
● Physical examination- upper-lower extremities perfusion and pulse, splitting of heart
sounds, thrills, murmurs.
Outline the pathology, diagnosis (with the aid of changes in heart sounds, ECG,
echocardiography, chest x-ray and catheterisation) and management of the following:
a. Atrial Septal defects
b. Atrioventricular septal defects
c. Ventricular septal defects
184
d. Pulmonary stenosis
e. Aortic stenosis
f. Patent ductus arteriosus
g. Coarctation of the aorta
h. Tricuspid atresia
i. Ebstein’s anomaly of the tricuspid valve
j. Tetralogy of Fallot
k. Complete transposition of the great arteries
l. Common arterial trunk
m. Pulmonary atresia
(5) Valvular Heart Diseases
Outline the aetiology/pathophysiology, diagnosis (history, examination, investigations),

complications and management of each of the following:
a. Aortic stenosis
b. Aortic regurgitation
c. Mitral valve stenosis (include role of acute rheumatic fever)
d. Mitral valve regurgitation- role of rheumatic disease (include mitral valve
prolapsed)
e. Tricuspid stenosis
f. Tricuspid regurgitation
g. Acquired pulmonary valve disease
(6) Infective Endocarditis
a. Describe pathogenesis and microbiology of infective endocarditis (bacteria, fungi)

and predisposing lesions (loss of integrity of the endothelial lining, traumatic
procedures, intravenous drug abuse, thrombus formation, rheumatic heart disease,
congenital heart disease and intracardiac prosthetic materials).
b. Recognise the clinical features (flu-like symptoms, signs and symptoms of heart
failure, petechiae, splinter haemorrhages, osler’s nodes, regurgitant murmurs,
pulmonary oedema, acute MI).
c. Laboratory investigations (including blood cultures, ESR, CRP)
d. ECG (conduction abnormalities).
e. Cardiac imaging
f. Management
(7) Heart Failure (HF)
a. Definition
b. Clinical models of heart failure (systolic and diastolic HF, left and right sided HF,
high-output vs low-output HF)
c. Aetiology (myocardial disease, valve disease, pericardial disease)
d. New York Heart Association (NYHA) functional classification
185
e. Symptoms (breathlessness, fatigue, weakness, cough)
f. Examination (oedema, heart rate and rhythm, arterial and venous pulses, BP,
palpation of precordium, heart sounds)
g. Diagnostic tests (CBC, serum lipids, renal and hepatic function, BNP, CXR, ECG,
Echo, Stress testing, nuclear cardiology, MRI, angiography)
h. Management of acute and chronic HF
(8) Pulmonary Arterial Hypertension (PAH)
a. Definition
b. Clinical classification of pulmonary hypertension (Evian classification: Group 1
consists of PAH)
c. Primary & secondary PAH
d. Functional Classification
e. Clinical features (progressive exertional dyspnoea, angina of effort, syncope, right
heart failure, oedema, ascites, sudden death).
f. Investigations (arterial blood gases, CXR, ECG, Echo, MRI, pulmonary function
test, ventilation-perfusion lung scan, pulmonary angiography)
g. Diagnosis (including exclusion of secondary causes of PAH)
h. Management
(9) Arrhythmias
a. Classify and define:

- Bradycardias (sick sinus syndrome, AV conduction abnormalities,
intraventricular conduction disturbances)
- Tachycardias- Supraventricular arrhythmias
Ventricular arrhythmias (narrow and broad QRS
complexes)
- Ventricular fibrillation
- Atrial fibrillation (acute, paroxysmal, chronic), embolic
complications (assessment risk and prevention strategies)
b. Clinical features of each
c. Management (including anti-arrhythmic drugs)
(10)Sudden Cardiac Death and Resuscitation
a. Define - sudden cardiac death

- cardiac arrest
- cardiovascular collapse
b. Causes of each
c. Clinical characteristics
d. Management (including CPR)
186
(11)Cardiac manifestations of systemic disease
Diabetes mellitus CAD, atypical angina, CMP, systolic or diastolic CHF

Thiamine deficiency High-output failure, dilated CMP
Hyperhomocysteinemia Premature atherosclerosis
Obesity CMP, systolic or diastolic CHF
Hyperthyroidism Palpitations, SVT, atrial fibrillation, hypertension
Hypothyroidism Hypotension, bradycardia, dilated CMP, CHF, pericardial effusion
Phaeochromocytoma Hypertension, palpitations, CHF
Acromegaly Systolic or diastolic heart failure
Rheumatoid arthritis Pericarditis, pericardial effusions, coronary arteritis, myocarditis, valvulitis
Seronegative arthropathies Aortitis, aortic and mitral insufficiency, conduction abnormalities
Systemic lupus Pericarditis, Libman-Sacks endocarditis, myocarditis, arterial and venous
erythematosus thrombosis
HIV Myocarditis, dilated CMP, pericardial effusion
Amyloidosis CHF, restrictive CMP, valvular regurgitation, pericardial effusion
Sarcoidosis CHF, dilated or restrictive CMP, ventricular arrhythmias, heart block
Haemochromatosis CHF, arrhythmias, heart block
Marfan syndrome Aortic aneurysm and dissection, aortic insufficiency, mitral valve prolapse
Ehlers-Danlos syndrome Aortic and coronary aneurysms, mitral and tricuspid valve prolapse
Resources:
● Patients- wards/clinics
● Davidson’s Principles and Practice of Medicine
● Kumar and Clark
● Clinical Examination- Macleod
● Oxford Handbook of Clinical Medicine
● Websites- European Society of Cardiology, American College of Cardiology,
American Heart Association, International Diabetes Federation
References
1. Caribbean Community (CARICOM) Secretariat: Summit on Chronic Non-

communicable diseases (CNCDs), 2009
2. European Society of Cardiology Core Syllabus
187
3. European Society of Cardiology Core Curriculum
4. Harrison’s Principles of Internal Medicine: Cardiac manifestations of systemic

disease. 17th edition, 2008
5. Heart Institute of the Caribbean, 2006
6. Talley N. Clinical Examination: A systemic guide to physical diagnosis. 5 th

edition, 2005.
7. The Lancet. 2006, August; 368 (9536): 625 - 626
APPENDIX xii
Sample of Medical History:

18TH November 2010
Mrs. M C
Age 48 years
Known diabetic for 6 years
Presenting complaint:
Chest pains x 1/7
}
Pain in left forearm and
hand Headaches
Jitteriness x 3/52
188
History of presenting complaint:
Mrs. Cauldero was diagnosed with gestational diabetes 22 years ago during her 2 nd
pregnancy, and again during her 3rd pregnancy.
She was diagnosed with diabetes mellitus approximately 6 years ago.
Her last clinic visit was 3/52 ago.
Today, she complains that despite being consistent with diet and exercise routines, her
fasting blood glucose levels measured at home have been consistently high for the past 3/52.
She has also been experiencing chest pains for the past 1/52, as well as pain in her left
forearm and hand, headaches, jitteriness and fatigue for the past 3/52.
Her chest pain
● Is usually felt on the left side of the chest, with occasional radiation to the back;
does not radiate to neck or arms
● Described as gripping in nature and severe
● Begins suddenly when she is at rest
● Lasts less than five minutes
● Not associated with cold sweats/ nausea/ palpitations/dyspnoea
● No aggravating or relieving factors identified
● Occasionally occurs several times per day
The pain in her left forearm and hand

● Described as tingling, sometimes cramping
● Begins suddenly; not associated with any particular activity or time of day
● Episodes last less than five seconds
● Multiple episodes occur throughout the day
● No aggravating or relieving factors identified
Review of systems:
GENERAL: generally well but fatigued ºchange in sleep pattern, appetite or weight
CNS: headaches paraesthesia in left forearm and hand ºdizziness ºsyncope ºseizures
√ √
ºdiplopia ºblurry vision

CVS: chest pain palpitations orthopnoea
√ √ √
pedal oedema ºparoxysmal nocturnal
√
dyspnoea ºexertional dyspnoea

RESP: unremarkable
18TH November 2010
Mrs. M C
Age 48 years
GIT: dyspepsia nausea heartburn ºhaematemesis ºmelaena ºdysphagia constipation

√ √ √ √
√
polydipsia ºpolyphagia
GU: √
occasional dysuria and increased frequency ºhaematuria vaginal pruritus
√
ºabnormal vaginal discharge

MS / skin: unremarkable
Past medical history:

● Known diabetic x 6 years
● Gestational diabetes in 2nd and 3rd pregnancies
189
● Endometriosis x 13 years
● Left sided diffuse goitre detected 1 year ago
º hypertension ºasthma ºsickle cell anaemia ºepilepsy
Past surgical history:

● Removal of right-sided calcaneal spur x 6 years ago at EWMSC
● Total hysterectomy x 10 years ago at Mt. Hope Women’s Hospital
● Appendectomy x 27 years ago
● Tonsillectomy x 35 years ago
Past drug history:

● Danazol (used before pregnancy)
● Premarin 1.25mg po die x 10 years – discontinued for the past 2/12
● Black Cohosh
● Enalapril 5mg po die
Allergies: Nil known
Family and social history:

Mrs. Cauldero, a music teacher, is married and has three children, ages 26 to 18. She lives
with her husband and children in Sande Grande in a 2-storey house with all basic
amenities.
She has never smoked cigarettes and does not drink alcohol.
Her father died at age 55 years due to MI; her mother is 78 years old and hypertensive; her
brother has been diagnosed with hypercholesterolaemia.
Mrs. Cauldero is comfortable and believes that her illness has not adversely affected the
quality of her life.
Her main concerns are to maintain good vision and renal function.
Summary:
Mrs. Cauldero, a 48-year-old female, is a known diabetic for 6 years who has been
managed non-pharmacologically, and presents with a one-week history of chest pains and a
three-week history of headaches, pain in left forearm and jitteriness.
190

Year 6 Clerkship - Welcome & Curriculum Class 2020 (Revised 25.04.2019)

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THE UNIVERSITY OF THE WEST INDIES

FACULTY OF MEDICAL SCIENCES

Welcome Class of 2020

Our Motto is: All for the patient

Tell me………I forget

●Phlebotomy Procedure - Venipuncture 13

10. Student Lead Ward Rounds 16

12. Procedures in Medicine 18

II. Procedures Following Exposure

Adult Medicine Unit

The full time members of the unit are:

2. To participate in and learn from a multi-disciplinary approach to patient care.

4. To learn and demonstrate efficient and thorough medical documentation.

5. To demonstrate knowledge of patients’ rights and understand the basic tenets of

6. To communicate effectively with colleagues, patients and relatives.

Here are some guidelines which you will find useful.

1. Working conditions: The focus in year 5 is on an apprenticeship system

● Post call ward rounds supersede teaching sessions.

3. Teaching of Junior Doctors and Students

● Formal teaching sessions for students are noted on the timetable.

● Any procedure performed on a patient requires consent. Consent may be written

Procedure: Name of procedure e.g. arterial blood gas

7. Professional Conduct: all staff

Continuous Assessment Component Weightage

End of Clerkship Assessment Component Weightage

Criteria for successful completion of clerkship assessment:

o After a successful completion of eight week rotation and clerkship

Letter Grade Numeric Score QPs

INFECTIOUS DISEASES INFECTIOUS DISEASES

Year 5 Weeks 1 - 4 EWMSC or SFGH POSGH

THE STUDENT IS EXPECTED TO BE ABLE TO INITIATE TREATMENT (and

2. Resuscitation and life support / cardiac arrest / respiratory arrest

3. Acute asthma / status asthmaticus

6. Left ventricular failure

7. Diabetic Ketoacidosis / non-ketotic hyperglycemic coma

9. Acute renal failure

10. Acute liver failure

11. Subarachnoid haemorrhage / Cerebrovascular accidents

12. Acute myocardial infarction

13. Hypertensive encephalopathy / severe uncontrolled hypertension

PHLEBOTOMY PROCEDURE- VENIPUNCTURE

At the end of the clerkship, the student should be familiar with:

4. Abdominal X-ray and ultra sound

o At POSGH - under supervision of Dr. S. Sandy

o The goal may be summarized as follows: you are the doctor

o The student is expected to present a critical summary of the case

how they are being resolved

o The student should be prepared to demonstrate key signs of medical illness

diagnosis and treatment of the patient’s underlying disease process

o Issues of communication need to be dealt with during this ward round

1. Note before: The case history is only valid if written CONTEMPORANEOUSLY

2. Each page is headed; Name, age, Hosp. Number.

3. Date in the top left hand corner of EVERY page

5. Examination: all systems (please see your text)

6. Differential diagnosis arranged in probabilistic order

8. Results of investigations and how they modify your management

9. A prescription written as for the pharmacy

(a) Adherence to each of the above criteria

(b) Absence of any major error in the recorded history

You must know:

The Following must be shown in order:

Date and Time of Procedure :

Method (in point form)

Clinic/Ward_62_________ D.O.B. _6/19/63_____