Student Case Assigned Case To Review: Online General Practice Casebook

UNSW Primary Care 2012
Online General Practice Casebook
Student Case assigned Case to review
Azar, Rita 1 3
Chan, Ada 2 4
Chan, Enoch 3 5
Chia, Jie Yu 4 6
Chia, T-Yunn 5 7
Chong, Oi Fong 6 8
Dower, Ashraf 7 9
Gill, Manpreet 8 10
Go, Christopher 9 11
Gunalan, Shamini 10 12
Gunawardane, Udara 11 13
Hilvert-Bruce, Zita 12 14
Hou, Minsheng 13 15
Huang, Beatrice 14 16
Kam, Jonathan 15 16
Lee, Grace 16 17
Liang, Derek 16 18
Lim, Jonathan 17 19
Lim, Veronica Formosa 18 20
Liu, Jenny 19 21
Mohan, Rahul 20 22
Nayyar, Dhruv 21 23
Purnamasari, Dian 22 24
Sacks, Peta-Lee 23 25
Solomons, Haylee 24 26
Tai, Yee Shyn 25 1
Tsao, Jim 26 2
UNSW Primary Care

Online General Practice
Casebook
Adapted from the “General Practice Tutorial Casebook” by Dr Alexander McColl and
Ms Julianne Weatherley of the UNSW Rural Clinical School, Port Macquarie
Dr Alexander (Sandy) McColl, Head of Campus, Port Macquarie Rural Clinical School
Original Author and Reviewer
Julianne Weatherley, Admin assistant & timetable coordinator, Port Macquarie Rural
Clinical School
Design and Layout
Dr Michael Tam, Lecturer in Primary Care

Online Design and Adaptation
Dr Joel Rhee, Senior Lecturer and Convenor of Primary Care

Online Design and Adaptation
UNSW Primary Care

Learning outcomes
By the end of this learning activity you should be able to:
1. Outline the assessment and management of common clinical presentations in general

practice.
2. Collaborate with peers to create and review a quality document that can be used for Phase
3 Examination preparation.
3. Use evidence-based resources and guidelines to answer clinical questions.
Introduction
General practice is a clinical discipline with a wide base of both knowledge and skill. It differs
considerably from hospital-based medicine. General practice attempts to provide comprehensive
and continuing medical care for the patient.
For the vast majority of people, their initial contact in the Australian health system is via general
practice. For many patients, the general practitioner may be the sole provider of health care.
The purpose of this term is to expose you to the world of general practice and, consequently, to a
range of clinical conditions and skills which are both common and important. However, the
breadth of general practice means that it is unlikely that you will encounter the full spectrum of
general practice in your short rotation.
This casebook contains a sample of common clinical scenarios that you will encounter in your
clinical placement. It is designed not to replace clinical experience but to complement it. You will
learn the most by seeing real patients.
In this online document you will find a number of scenarios each with several clinical questions. In
pairs or groups of three you will need to accomplish three main tasks:
1. Work up a case and answer all the questions using evidence-based literature and clinical
guidelines. This task is due on Friday of week 6.
2. Critically review another case (as assigned) and leave constructive feedback and comments
for the benefit of your peers. This task is due by Friday of week 7.
3. Respond appropriately to the feedback on your case provided by your peers and modify
your answers as necessary. This task needs to be completed before Friday of week 8.
Expectations
● Your answers need to be accurate and of a standard expected for exam preparation.
● Your answers should be properly referenced and where possible you should provide
hyperlinks.
● This activity requires effective teamwork. You will need to collaborate with your partner(s)
in both working up your case and in reviewing another group’s case.
● Be critical when doing a review but ensure that your feedback is constructive and specific.
Give an honest mark (F to P+).
● DO NOT present any information that could be used to identify actual patients.
● Show respect for other students. Do not edit or vandalise other people’s answers.
● To leave comments, either use the “Insert → Comment” function or leave your comments
in specified boxes.
● Remember, an “easy” case means greater expectations of clinical competence in an

examination setting!
Important dates
Weeks 1-6: work on your case. Please finish by Friday week 6 to give adequate time for the
reviewers.
Week 7: review of cases. Please finish all reviews by Friday week 7 to provide an opportunity for
the feedback to be noted and the cases modified as appropriate.
Week 8: the Case Book will be reviewed and discussed on Friday week 8 after the student
presentations.
Case 1
Headache
Molly Hatcher is a 36-year-old lady.
"Doctor, I got home from work on Monday and I had this terrible headache."
On further questioning, she notes a bilateral frontal headache. She notes nausea without vomiting. She
notes mild photophobia.
Clinical assessment and diagnosis

What is your differential diagnosis?
provisional: tension headache. Differentials: migraine, sinusitis, Caffeine withdrawal, hangover (from
alcohol). Unlikely but important differentials include meningitis, stroke, subarachnoid haemorrhage, giant
cell arteritis.
What further questions may help differentiate the different types of headache pain?
A complete and thorough history of presenting complaint- (Site, onset, characteristics, radiation,
associated symptoms, timing, exacerbations/relieving factors, severity) should highlight key features that
may identify diagnosis. Eg. tight band around head for tension headache, unilateral with nausea,
vomiting or aura for migraine, excessive alcohol the prior night for a hangover etc.
Past History- any cardiovascular disease, neurological conditions, or previous episodes of headaches.
Family History- Migraines may have familial links
Medications- some medications may cause headaches e.g combined oral contraceptive pill. Allergies are
also important for allergic sinusitis and other allergic responses which usually involve headaches.
Social History- especially important for tension headaches- associated with stress/burden. ask about
financial, occupational or home-life stressors.
Menstrual history: headaches may be associated with PMS
What are the pertinent positive and negative findings on physical exam in relation to your differential
diagnosis?
vitals(BP, HR, temperature, Pupils (fixed or reactive)) and general appearance (degree of photophobia, ?
neck stiffness (meningism), irritability, rash/skin changes
neurological signs (raised ICP)
cardiovascular- especially carotid bruits, heart sounds, AF
e.g fever and purpuric rash ---> ?meningitis
no significant positives, no stiffness, no n+v,bilateral headache ---> ?tension headache
Questions
Compare and contrast the presenting signs and symptoms of migraine versus tension-type headaches.
Migraine: Aura (may or may not be present): precedes headache (minutes) and may be concurrent with it.
Distortion of images, lines, dots and zigzags or even hemianopia.
8% auras are associated with dysphasia or paraphasia.
Diagnostic criteria (without aura): at least 5 headaches of 4-72hr duration with nausea/vomiting or
photo/phonophobia. As well as at least two of the following:
unilateral pain, pulsating, interferes with function, worsened by routine activity.
can be triggered by cheese, caffeine (and its withdrawal), travel, exercise, oral contraceptive, alcohol,
anxiety or others (50% are unknown).
Tension Headache: bilateral, non pulsatile headache with or without scalp tenderness. no vomiting or
sensitivity to head movements are present. Most commonly patient is stressed by financial, occupational
or lifestyle situations and may have other signs of stress (tension in musculature, anxiety, irritation).
Discuss the warning signs of intracerebral bleed and elevated intracranial pressure.
Typically worse on waking, lying down for periods of time, coughing or bending forward (situations which
further increase ICP). Vomiting, papilloedema, fits or behavioural changes are also signs of raised ICP.
Furthermore, a history of trauma (blunt > sharp force), decreased visual acuity (peripheral field loss),
drowsiness, seizures, LOC, Cheyne-Stokes respiration.
Cushings response i.e. falling pulse and rising blood pressure
What treatments (non-pharmacological and pharmacological) are available for migraine headaches?
Non Pharmacological: warm/cold packs on head, rebreathing through paper bag, spinal manipulation,
acute management: rest in a quiet dark room and avoid movement.
if trigger is identified, highly recommended to avoid.
Pharmacological: Aspirin, diclofenac and ibuprofen, or paracetamol.
Ketoprofen may also be used, if management is not achieved with the above mentioned.
if frequency is more than twice a month, prophylaxis should be considered. propanolol or amitriptyline. It
is also important to have co-morbidities well managed, as they may trigger migraines independent of
prophylactic measures.
Self-Directed Question
Generate one self-directed question
Put answer here
References
eTG Complete [online] Migraine (2011). Therapeutic Guidelines Limited.
Longmore M, Wilkinson IB, Davidsone EH, Foulkes A & Mafi AR (2010). Oxford Handbook of Clinical
Medicine (8ed). Headaches p.460-463.
Boon NA, Colledge NR & Walker BR (2006). Davidson's principles and practice of medicine (20ed).
Headaches p1160-1164
Reviewer 1 comments
Reviewer 1 to put critical comments here
Note: try to be constructive! The goal is the help your colleague improve the overall quality of this
document.
Reviewer 2 comments
document.
Open comments and primary care term experiences

Any student can add comments and experiences in this section. Have you observed a clinical scenario
that is relevant? Share your thoughts with everyone in the box below!
Put additional comments here.

Case 2
Pharyngitis
Richard Betts is a 14-year-old boy. He presents to your office with his mother. She states "He's just been
so tired and run down these past few days. He also says he has a sore throat and he's achy all over."
On further questioning, Richard is a previously healthy 14-year-old boy with normal growth and
development. He is otherwise well.

What is your differential diagnosis?
Bacterial sore throat (i.e. group a strep, diptheriae, N. gonorrhoea, H. influenzae), Viral sore throat
(adenovirus, rhinovirus, parainfluenza virus, HSV, CMV, EBV)
How would you differentiate the causes of pharyngitis and fatigue in this young man?
- Perform throat +/- nasopharyngeal swab for culture

- Examine oropharynx to look for tonsillar exudates, erythema, post-nasal drip
- Palpate for lymphadenopathy, hepatomegaly, splenomegaly
Differentiating features
- Group A strep: positive rapid strep antigen test, unlikely with a history of cough, tonsillar exudates
- Viral: coryza, rash, hoarseness, cough, diarrhea, conjunctivitis more suggests of viral cause
- EBV: Monospot test
- CMV: CMV serology
Questions
Discuss the microbiology of pharyngitis – remember that not all infections are bacterial.
Most pharyngitis is due to a viral cause (up to 70% of acute sore throats). Pharyngitis (sore throat) arises
due to direct infection of overlying mucosa by invading pathogen and also as a result of inflammatory and
immune response to the pathogen.
Discuss Epstein-Barr virus – include clinical presentation and laboratory assessment.
Clinical presentation
History
- Syndrome of fatigue, malaise, and sore throat
- Temperature: (adults) high temperatures, may rise to39.4°C and gradually fall over a variable period of
7–10 days; (child) usually low-grade fever or may be afebrile.
Exam
- Fever, lymphadenopathy, pharyngitis
- Palatal petechiae
- Hepatosplenomegaly
- Tender lymphadenopathy (cervical nodes are most commonly enlarged)

- Rash on trunk and upper arms with occasional involvement of face and forearms
- myalgia
Lab assessment
- FBC: lymphocytosis (at least 50% of leukocytes) and atypical lymphocytosis (>10%)
- Monospot test: for heterophile antibodies
- Serology for EBV-specific antibodies (more sensitive than heterophile test)
Discuss the treatment of glandular fever/infectious mononucleosis – include patient precautions.
Nil specific treatment/Supportive care:

- hydration, antipyretics and analgesics
E.g. Paracetammol - (adult) 500-1000mg q. 4-6h, max 4000mg/d; (child) 10-15mg/kg q 4-6h, max
90mg/kg/d
For serious cases:

- corticosteroids: for upper airway obstruction or hemolytic anaemia
E.g. Prednisolone - (adult) 30-60mg/d for 5-7d; (child) - 1-2mg/kg/d for 5-7d
- IVIg: for thrombocytopenia
E.g. IVIG - (adult) 1g/kg/d for 1-2d; (child) 0.8-1g/kg single does
Precautions:
Due to possibility of splenic rupture due to splenomegaly, patients should be advised to avoid strenuous
physical activity for 3-4wks.
Why are antivirals not routinely prescribed as treatment?

- no benefit in resolution of symptoms or lowering rates of complications
References
Bisno, A. L. (2001). Acute pharyngitis. New England Journal of Medicine, 344(3), 205-211.
Domino, F. J., Baldor, R. A., Grimes, J. A. & Taylor, J.S. (2011). The 5-Minute Clinical Consult 2012 (20ed).
p.456-457, 991.
Best Practice - Infective Mononucleosis (iPad app)
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 3
Diane Krall is a 30-year-old lady who presents saying "Doctor, I've been really tired over the last couple of
months. I just want to lie down all the time."

What is your differential diagnosis for her fatigue?
Put answer here
Using clinical history and physical examination, how would you differentiate some of the diagnoses in
your differential?
Put answer here
Using laboratory assessment, how would you differentiate the diagnoses in your differential?
Put answer here
Questions
Discuss the clinical symptoms of both hypo- and hyperthyroidism.
Put answer here
Discuss the investigation of a thyroid nodule.
Put answer here
Put answer here
References
List references here
Note: use appropriate citation format (e.g., Vancouver) and include hyperlinks if available. If using clinical
guidelines, try to use contemporaneous Australian guidelines. Finding recent publications on the topic
(e.g., systematic reviews, primary research) is valuable. Textbooks and online resources like Best Practice
and eMedicine should be used as topic guides, but not as primary references.
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 4
Heart check
Duane Allman is a 54-year-old man.
"Doctor, I've been putting this off but I think that with my family history I need to get my heart checked."

What will you ask this patient to better understand his risk of coronary artery disease?
Ask about the modifiable and non-modifiable risk factors for coronary heart disease
Non-modifiable factors:
● (known) - male, age 54 y.o
● family history
○ of heart disease, cerebrovascular disease - which family members are affected
○ of cardiovascular risk factors - diabetes, hypertension, hyperlipidaemia
● past history of heart disease - eg. angina requiring stenting, abnormal cardiac function on tests,
etc.
Modifiable factors:
● diabetes
● hypertension
● hypercholesterolaemia
● obesity
● physical activity
● smoking history
Current symptoms
● chest pain
● shortness of breath on exertion
● paroxysmal nocturnal dyspnoea
● peripheral edema
Calculate absolute cardiovascular risk based on above
What other preventive health measures will you consider discussing with this patient?
For this age group of 50-59 years-old, the following preventative activities are recommended by the
RACGP Red Book and should be discussed with this patient
● issues of smoking, nutrition, alcohol and physical activity (SNAP) and readiness to change (where
applicable)
● assess risk of diabetes
● discuss about risk of skin cancer, especially if of Anglo-saxon heritage and importance of skin
checks
● discuss need for basic examination and investigations - for screening and baseline
○ weight, height, BMI, waist circumference; BP
○ blood test - fasting lipids and BSL
○ urinalysis for protein
● if at high risk of respiratory tract infections, consider vaccination
● colorectal cancer screening with FOBT
Questions
Discuss the major risk factors for coronary artery disease.
The pathogenesis of coronary artery disease (CAD) involves atherosclerosis - responsible for virtually all
cases of coronary heart disease. The established risk factors for CAD are thus the same factors
contributing to the process of atherosclerosis.
Age: In general, older individuals are at greater risk of CAD. Age interacts with other factors to predict risk
of CAD; at different ages different factors become important as best predictors for risk - e.g. diastolic BP
best predictor for <50 year-olds and pulse pressure for >60 year-olds.
Gender: The male gender is at greater risk. However, similarly, gender interacts with other factors to
confer risk - e.g. heavy smoking puts women at greater risk of CAD than men compared to non-smokers
Family history: An independent risk factor. A significant family history refers to CAD +/- death in first-
degree relative prior to age 50 in males and 60 in females.
Hypertension: Isolated systolic hypertension (high SBP) has been established as a major risk factor for
CAD. In addition, diastolic blood pressure and pulse pressure are reliable predictors too.
Lipids: High serum total cholesterol and LDL-cholesterol are the main variables used. However, other
components of lipid profile are associated with increased CAD risk too, for instance, low HDL-cholesterol
and hypertriglyceridemia.
Cigarette smoking: There is a dose-response relationship between risk of CAD and tobacco consumption.
Smoking is a reversible risk factor of CAD and smoking cessation is known to decrease risk regardless of
extent of smoking history.
Diabetes: Type II diabetes mellitus is an atherogenic disease. In addition, it is associated with other risk
factors like obesity and hyperlipidaemia
Physical Activity: Exercise has a protective effect against CAD as it is associated with reducing other risk
factors like lowering BP, elevating HDL-cholesterol, improving insulin sensitivity and increasing weight
loss. Cardiovascular fitness decreases risk of CAD and mortality from it.
Obesity: Measured by BMI and waist circumference. Associated with a number of other risk factors like
hypertension, insulin resistance, reduced HDL-cholesterol, etc.
Psychosocial factors: Correlation found between psychologic stress and atherosclerosis, which may be
both direct (endothelial damage) and indirect (exacerbation of other risk factors like hypertension,
smoking, etc)
Discuss the clinical presentation of stable angina versus unstable angina and acute coronary syndromes.
Stable angina
● chest discomfort in the setting of exertion or emotional stress
● associated symptoms - dyspnoea, nausea, vomiting, diaphoresis, fatigue, light-headedness
● atypical presentations - pain in epigastrium, jaw, neck or arms; particularly in women, older
people, diabetics
Acute coronary syndrome and unstable angina

● presentation - chest pain in 50%
○ may be localised or with radiation to arms, jaw, etc
○ pain reproducible by exertion, cold, emotional stress;
○ associated symptoms - abdominal pain, syncope, dyspnoea, diaphoresis, etc
○ symptoms typically lasts 30min or more
● comprises a spectrum - unstable angina, NSTEMI and STEMI
● classification is based on ECG findings
● unstable angina
○ classifications - prolonged angina (>20min) at rest; new onset of severe angina; increasing
angina (in frequency, longer in duration, or lower in threshold); angina that occurs after
recent episode of MI
○ absence of biochemical evidence of myocardial damage
Discuss the treatment of acute coronary syndrome in the family medicine clinic.
First-line management of ACS, pre-hospitalisation

● aspirin 300mg - unless already taken or contraindicated; preferably given early
● glyceryl trinitrate 300mcg, sublingual - as required
● morphine 1mg/min via IV until pain relief achieved (up to 15mg) - as required
● oxygen supplementation (optional) via face mask
○ only in patients who are dyspnoeic, hypoxaemic or have signs of heart failure or shock
○ monitor with pulse oximetry - maintain saturations >90%
● 12-lead ECG
● defibrillator at hand to avoid early cardiac death from reversible arrhythmias
● arrange for ambulance and hospitalisation
Homocysteine levels in CAD - point of intervention?
Circulating homocysteine levels have been found by observational studies to be associated with increased
risk of cardiovascular disease. Theories on pathogenesis have been established - immune response to N-
homocysteinylated proteins have been implicated in the enhancement of thrombosis; as well, there is
generation of an inflammatory response by endothelial cells with the release of cytokines, which are pro-
atherogenic events. The normal level for homocysteine is about 10umol/L. Studies have cited that every
5umol/L increase elevates CVD risk by 20%, independent of traditional CHD factors; and that up to 10% of
CAD events may be attributable to elevated circulating levels of homocysteine.
Given the strong association of homocysteine levels with CAD, it is a logical target for intervention. The
metabolism pathway of homocysteine is known: B-complex vitamins of B12, B9 and B6 are required for
the transformation and/or excretion steps. Indeed, supplementation with B-complex vitamins have shown
to lower homocysteine levels; however, critical review of completed trials have not shown significant
benefit in terms of incidence of cardiovascular events and it is a field of current research with several trials
under way. Hence, the use of B vitamin supplementation is the treating physician’s decision; if anything,
patients have reported improved energy levels while on B supplements
References
ACS Guidelines Working Group (2006) Guidelines for the management of acute coronary syndromes 2006
[Electronic Version] The Medical Journal of Australia, 184(8), S1-30
BMJ BestPractice (2012) Overview of ACS. Retrieved 25th October 2012 from:
http://bestpractice.bmj.com/best-practice/monograph/152/overview/introduction.html
BMJ BestPractice (2012) Stable Angina. Retrieved 25th October 2012 from:
http://bestpractice.bmj.com/best-practice/monograph/148.html
BMJ BestPractice (2012) Unstable Angina. Retrieved 25th October 2012 from:
http://bestpractice.bmj.com/best-practice/monograph/149.html
Kones, R (2011) Primary prevention of coronary heart disease: integration of new data, evolving views,
revised goals, and role of rosuvastatin in management. A comprehensive survey [Electronic Version] Drug
design, development and therapy, 5, 325-380
Marti-Carvajal, AJ., Sola, I., Lathyris, D., Salanti, G. (2009) Homocysteine lowering interventions for
preventing cardiovascular events [Electronic Version] Cochrane Database of Systematic Reviews, Issue 4,
Art. No.: CD006612
Mehta, SB. and Wen, CW. (2005) Management of Coronary Heart Disease: Stable angina,
Murtagh, John (2007) John Murtagh's general practice 4th ed. McGraw-Hill Australia Pty Ltd
RACGP (2012) Guidelines for preventive activities in general practice (8th edition). Retrieved, 25th
October 2012 from: http://www.racgp.org.au/download/Documents/Guidelines/Redbook8/redbook8.pdf
Walters, DL. and Cunningham, C. (2011) Managing acute coronary syndromes in the prehospital and
emergency setting: New guidelines from the Australian Resuscitation Council and New Zealand
Resuscitation Council [Electronic Version] Emergency Medicine Australasia, 23(3), 240-243
Wilson, PWF., Cannon, CP., Downey, BC. (2011) Overview of the risk equivalents and established risk
factors for cardiovascular disase. UpToDate 19.3
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 5
Ear pain in a child

Jimmy Jay is a three-year-old boy. He is brought in by his mother who states "Jimmy was up all night with
a painful left ear. He's had the sniffles for the past week."

What further information do we want from mum?
-More in-depth history of presenting illness

● Duration of ear pain, any discharge from the ear, is he pulling his ear, any problems with hearing,
past history of ear infections
● Other associated symptoms such as fever., lethargy, rhinorrhea, irritability, vomiting, decreased
appetite , cough and presence of sputum, shortness of breath
● any medications taken to ease the symptoms
-Past medical history

● e.g: any asthma etc
-Any medications (including over the counter) and allergies
-Immunisation status
-Family and social history

● Any other siblings, any family member currently ill
● Does the child attend day care
● Any smoking by household member
● recent travel
What symptoms and signs would suggest that Jimmy is critically unwell?
-SIgns of respiratory distress

● tachypnoea
● tracheal tug/sternal recession
● stridor/wheeze
● supraclavicular accessory muscle usage
● intercostal recession
- Consider his alertness and arousal

● any poor response to stimulation
● irritability/agitation
● drowsiness
- Consider circulation
● cold skin temperature (i.e: cold peripheries, mottled skin)
● palmar pallor
● poor capillary refill
● poor urine output
● Hypotension (late sign)
- any signs of skin manifestations such as petechiae
- any diarrhoea or billous vomiting. in this case you would also be concern about signs and symptoms of
dehydration such as sunken eyes, abnormal skin turgor etc
Questions
Discuss the microbiology and treatment options for otitis media.
Microbiology
Organisms involved in acute otitis media include

1) Bacteria
● Streptococcus pneumoniae (most common)
● Haemophilus Influenzae
● Moraxella catarrhalis
● Group A Strep
● Staph aureus
2) Viruses (coinfection with bacteria present in more than 40% of children with viral induced acute OM
● RSV
● Adenovirus
● rhinovirus
● influenzae virus
3) Others (rare)
● Candidiasis
● Aspergillosis
● Blastocytosis
● Mycoplasma Pneumoniae
Treatment Options
-Treatment goals include symptom resolution and reduction of recurrence.
Pain management
● Paracetamol 15mg per kg every 4-6 hours
● NSAIDS such as nurofen /ibuprofen (10mg per kg every 6 hours)
Antibiotics
● Amoxicilin 80-90mg per kg daily, given orally in 2 divided doses. for 10 days (First line drug)
● Cefuroxime 30mg per kg daily, given orally in 2 divided doses. (for patients with penicillin allergy
excluding those with type 1 sensitivity)
● Clarithromycin 15mg per kg per day, given orally in 3 divided doses (for patients with penicillin
allergy (type 1 hypersensitivity)
● Azithromycin 30mg per kg, given orally (used in patients with penicillin allergy)
● Amoxicilin/clavulanate (Augmentin) - 90mg of amoxicillin per kg daily, 6.4mg of clavulanate per kg
per day -- used in children with recurrent or persistent acute OM
Topical agents can also be used

● Ciprofloxacin/hydrocortisone drops - 3 drops twice daily
● Hydrocortisone/neomycin/polymyxin B ( 4 drops 3-4 times daily)
Tympanocentesis
● relieve pressure in the middle ear space and provide relief of pain
● beneficial for patients who have persistent disease unresponsive to antimicrobial therapy or
those in need of immediate pain relief.
Discuss the microbiology and treatment options for otitis externa.
Microbiology
Mainly bacterial (most common, up to 90%) and fungal. fungal infection is typically the result of prolong
treatment of bacterial, although fungus can also be the primary pathogen especially in areas of excessive
moisture or heat.
Organisms involved in OE include:

1) Bacteria (more common)
● Pseudomonas aeruginosa
● Staphylococcus aureus
2) Fungal
● Aspergillus (80-90%)
● Candidal
Treatment
Main goals of treatment is to control pain, cure the infection and prevent occurrence.
Pain management
● Paracetamol 15mg per kg every 4-6 hours
● NSAIDS such as nurofen /ibuprofen (10mg per kg every 6 hours)
For bacterial OE, always cleanse the ear as much as possible. if swelling is severe, consider inserting a
wick. first line treatment is a topical antibacterial agent.
● 2% Acetic acid
● Neomycin, polymycin B - 3-4 drops, 4 times daily
● Quinolone containing (ciprofloxacin and ofloxacin) - 3-4 drops, twice daily
Consider oral antibiotics only when OE is persistent, or have signs of necrotising OE, and in patients who
are immunosuppressed.
For fungal OE, Cleansing of the ear canal is a principle treatment, , which is used complementary with
topical agent such as
● acidifying agents 3-4 times daily for 5-7 days

● if acidifying agents fail, antifungal agents such as ketoconazole, clotrimazole etc can be used 3-4
times twice daily for 7 days
Briefly describe the two recent randomised trials by Hoberman et al. (2011) and Tahtinen et al. (2011)
published in the New England Journal of Medicine. What implications do these results have for
Australian practice?
Both trials appear to support the use of antibiotics (in this case, amoxicilin-clavulanate ) to treat acute OM
in children of age approx 6 months - 35 months. it has been shown to have a much better outcome in
terms of reducing symptoms and complications from this condition., although in Hoberman et al. (2011),
it has shown a worse side effect profile as compared to placebos.
The main challenge that these 2 trials have for Australia would be preventing excessive use of this
antibiotic. With the positive findings , it is possible that doctors will be more willing to prescribe this
medication to young children who show signs of a possible AOM. AOM is typically a clinical diagnosis and
it could be over diagnosed sometimes.However, it is important to ensure the appropriate use of
antibiotics , in order to reduce the development of resistant bacteria . Thus it is essential to correctly
identify individuals who truly require antibiotic treatment and this might require some costly tests such
as tympanometry or acoustic reflectometry, and bacterial cultures.
What are some ways to prevent Otitis Media in children?
-Clean ears frequently

- avoid giving them small objects which can be accidentally placed into the ear (foreign body )
-avoid exposure to cigarette smoke
- always ensure the child is fed with the head elevated
- Enforcing heptavalent pneumococcal conjugate /influenzae vaccine can have an effect on the incidence
of AOM
- use of xylitol ( a sugar alcohol) as prevention as it is thought to inhibit the growth of Streptococcus
pneumoniae and inhibits attachment of bacterial cells to the nasopharyngeal cells.
References
Ramakrisnan, K., Sparks,R.A., Berryhill, W.E. (2007). Diagnosis and treatment of Otitis media. American
Family Physician 76(1), 1650-1658
Hendley, J.O., Armengol, C.E. (2012)). Otitis media. Retrieved 26th Oct, from bestpractice.bmj.com
Sander, R. (2001). Otitis Externa: A Practical Guide to Treatment and prevention. American Family
Physician 63(1), 927-937
Ghossaini,S. (2012). Otitis Externa. Retrieved 26th Oct, from bestpractice.bmj.com

O Klein, J., Pelton, S. (2012). Acute otitis media in children: prevention of recurrence. Retrieved 26th Pct
from www.uptodate.com
Uhari, M., Tapiainen, T. & Kontiokari, T. (2000). Xylitol in preventing acute otitis media. Vaccine 19(S1),
S144-147/
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 6
Jaundice
James Beam is a 52-year-old accountant.
He states "You know Doc, I was looking in the mirror and I swear my eyes are light yellow."

What is your differential diagnosis for jaundice – both paediatric and adult?
Adult
 Pre-hepatic: haemolytic anaemia (sickle cell anaemia, thalassemia, hereditary spherocytosis,
G6PD deficiency), Gilbert’s syndrome
 Hepatic: viral/ alcoholic/ autoimmune/ drug induced hepatitis, cirrhosis, primary biliary cirrhosis,
parasite infections
 Post-hepatic: cholelithiasis, pancreatic carcinoma, cholangiocarcinoma, PSC, pancreatitis
Paediatric
 Unconjugated hyperbilirubinaemia:
Increased RBC production- ABO/ Rh, hereditary spherocytosis, G6PD deficiency
Decreased bilirubin clearance – Gilbert’s syndrome, Crigler Naijar syndrome, congenital hypothyroidism
Increased enterohepatic circulation- breast milk jaundice
 Conjugated hyperbilirubinaemia:
Structural abnormalities – biliary atresia, choledochal cyst
Genetic/metabolic- alpha-1 anti-trypsin deficiency, CF, galactosemia
Infections- CMV, Hep B, Rubella, Syphilis
What questions would you ask to assess for at-risk drinking and alcohol use disorders?
1. Quantity-frequency estimates of alcohol consumption

Quantitative alcohol history: daily average consumption (standard drinks/day), number of drinking days
per week pattern of drinking
Alcohol dependence
2. Screening questionnaires
Alcohol Use Disorders Identification Test (AUDIT): screen for range of drinking problems using 4
conceptual domains of alcohol consumption, drinking behavior, adverse reactions and alcohol-related
problems (>8 are risk drinkers)
CAGE questions (shortened)
3. Physical examination for intoxication or signs of harmful use of alcohol

Hypertension, pattern of accidents, dilated facial capillaries, blood shot eyes, hand or tongue tremor, Hx
of GI disorders, duodenal ulcers, cognitive deficits
Other conditions: liver cirrhosis, pancreatitis
Job, financial, marriage and relationship problems, insomnia, depression, anxiety, domestic violence
4. Biological markers of excessive alcohol consumption

Alcohol concentrations in breath, blood, urine, LFTs
What laboratory investigations are used to assess jaundice and chronic liver disease?
Urinary bilirubin and urobilinogen (presence of conjugated bilirubin- obstructive)

LFTs – ALT, AST (hepatocellular necrosis), GGT, ALP (bile stasis), Bilirubin, Albumin
FBC (haemolysis)
ESR (PBC)
LDH (haemolysis)
Coags
Hepatitis serology
Abd U/S (gallstones)
CT scan (carcinoma)
Questions
Discuss the toxic effects of alcohol in the various organ systems – remember lifestyle effects.
GI: alcoholic hepatitis, liver cirrhosis, peptic ulcers, pancreatitis, oesophageal varices
Neuro: Hepatic encephalopathy (sleep disturbance, mood and personality changes, reduced attention,
coma), Peripheral neuropathy
Cardiac: Alcoholic cardiomyopathy, HTN, arrhythmia
Resp: infections
Renal: calculi, UTI, acute renal failure due to sepsis
Reproductive: breast enlargement, menstrual irregularity, testicular atrophy, impotence
Discuss strategies for cessation of alcohol including medication.
5 As
Ask: Alcohol use status
Advise: Clear, strong and personalized style to encourage patient to quit
Assess: Patient is ready to make an attempt to quit
Assist: Provide counseling and pharmacotherapy to help
Arrange: Schedule follow-up contact
Pharmacotherapy:
Acamprosate – GABA analogue, reduce neuronal hyperexcitability in alcohol withdrawal, reduce
symptoms of withdrawal
Naltrexone – opoid receptor antagonist, prevent activation of dopaminergic pathway, reduce cravings
Dilsulfarim – inhibit alcohol dehydrogenase, lead to accumulation of acetaldehyde which cause
unpleasant effects e.g. flushing, headache, palpitations, chest pain, respiratory difficulties, nausea,
vomiting
Spectrum of liver disease associated with alcohol abuse

-Hepatocellular steatosis: lipid accumulation in hepatocytes, mainly centrilobular
-Alcoholic hepatitis: hepatocyte necrosis
-Alcoholic cirrhosis: bridging fibrosis and regenerative nodules
-Hepatocelluar carcinoma
References
Aertgeerts, B, Buntinx F, Ansoms S et al. 2001, Screening properties of questionnaires and laboratory tests
for the detection of alcohol abuse or dependence in a general practice population. Br J Gen Pract 51(464):
206- 217.
Gilmore, I and Garvey, C. 2002, Investigation of Jaundice. Medicine 30 (11): 11-13.
Longabaugh, R, Woolard RE, Nirenberg TD et al. 2001, Evaluating the effects of a brief motivational
intervention for injured drinkers in the emergency department. J Stud Alcohol 62(6): 806-816.
NHMRC 2001, Australian Alcohol Guidelines: Health Risks and Benefits. Canberra: National Health &
Medical Research Council.
Reviewer 1 comments
- good systematic way to categorise the differentials for jaundice; shows that thought processes differ in
adult vs paediatric population
- (minor) under ‘questions to ask’, the social repercussions of alcoholism are mentioned, but should come
under a ‘history’ section; i suppose this should also go into the ‘lifestyle effects’ of the next question?
collateral history may be helpful
- additional strategies for cessation may include information on help-lines and self-help groups like
‘alcoholics anonymous’; also, perhaps a short discussion on the pharmacological options with regards to
preferred choices and patient compliance
- an image may help for ‘spectrum of liver disease’, there’s one in Robbins
- great work! :)
Reviewer 2 comments
document.


Case 7
Skin lesion
James Taylor is a 42-year-old man.
He states "My wife wanted you to look at this spot on my back. I can't really see it and she was
concerned."

What questions would you ask this man in relation to skin lesions?
With regards to pigmented skin lesions the main diagnosis to exclude is a melanoma and hence the
questions related to this condition shall relate to melanoma.
It is important to ask about risk factors for the development of melanoma;
● Age of the patient; typically 30-50 years of age is when melanoma’s appear
● Ethnicity; Higher incidence in Caucasions
● Fair-skinned/Light-coloured eyes
● Previous melanoma or pre-malignant or non-melanomatous skin cancer;
● Number of common and dysplastic naevi (moles) a person may have; dysplastic naevus = poorly
defined border, >5mm in size, variagated colour and presence of erythema
● Family history of melanoma
● Sun exposure; occupation, time out in the mid-day sun
● Use of sun-block
Onset/Timing; When did you first notice the lump? (a lump present for years is unlikely to be a melanoma)
Evolution of the skin lesion; Melanomas are evolving lesions. Has there been any recent changes in the
following characteristics of the lesion
● size
● border
● colour
● shape
Associated bleeding?
Associated itching?
Any other surrounding lesions that have developed recently - Satellite lesions
Any lumps of bumps - Lymph node involvement
What is the differential diagnosis of pigmented skin lesions?
There is a broad differential for pigmented skin lesions with the majority being of a benign type;
Non-melanocytic pigmented skin lesions;
● Pigmented Basal Cell carcinoma
● Seborrhoiec Keratosis
● Solar keratosis
● Dermatofibroma
● Pyogenic Granuloma
● Foreign body granuloma
● Talon noir
● Tinea nigra
● Becker’s naevus
Melanocytic pigmented skin lesions;
● freckles
● lentigines
● Naevi;
○ congenital
○ acquired;
■ junctional naevus
■ compound naevus
■ intradermal naevus
● Melanoma
What are the criteria used to evaluate pigmented skin lesions?
ABCDE criteria is used to determine whether a lesion has an increased chance of being a melanoma;
● A - Asymmetry in size, shape,colour or thickness
● B - Border irregularity;
● C - Colour; pigmented lesions are more likely to be malignant
● D - Diameter>6mm
● E - Evolving; changing size, shape, contour, border of the lesion makes it more likely to be a
melanoma
If there is clinical suspicion of a melanoma then an excisional biopsy is performed to confirm the
diagnosis.
Questions
Discuss the warning signs for malignant melanoma.
● spontaneous ulceration or bleeding of a pigmented lesion

● itchiness of the lesion
● lesion begins to not resemble surrounding lesions (“ugly duckling”)
● constitutional symptoms of malignancy; weight-loss, fatigue, fever, night-sweats.
● symptoms of metastases; cough, shortness of breath, headache
● regional lymphadenopathy
Discuss the four types of malignant melanoma and their prognosis.
Superficial Spreading melanoma;

● 70% of melanomas
● Grows laterally through the epidermal-dermal junction rather than in an invasive manner; hence
it typically appears as a flat irregular lesion growing more than 2cm
● Arises from a dysplastic naevus
● Has a striking colour variation
Lentigo Maligna Melanoma;
● 4-10% of melanomas
● arises from a precursor lesion, Lentigo maligna, which is an intraepidermal growth of
melanocytes.
● Arises in sunexposed areas
● Flat, tan and often greater than 3cm in size
Nodular Melanoma;
● 15-30% of melanomas
● grow in a vertical/invasive direction and have no radial growth phase
● found on the trunk and limbs of young male patients
● ABCDE criteria does not apply; instead use EFG (E - Elevated, F - firm, G - growth for more than 1
month)
● may arise without a precursor lesion
● often blue/black but may be not pigmented
Acral Lentiginous Melanoma;
● appear on the palms, soles, distal phalanges
● more common in darker races
● worse prognosis
● may ulcerate in the later stages
Determinants of Prognosis;
● Thickness of tumour; breslow classification
● Depth of Invasion
● Stage
● Age
● Ulceration
● Sex (worse for men)
References
● Australian Cancer Network Melanoma Guidelines Revision Working Party. Clinical Practice
Guidelines for the Management of Melanoma in Australia and New Zealand. Cancer Council
Australia and Australian Cancer Network, Sydney and New Zealand Guidelines Group, Wellington
(2008)
● Murtagh, John (2007) John Murtagh's general practice 4th ed. McGraw-Hill Australia Pty Ltd
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 8
Leg ulcer
Molly Malone is a 70-year-old lady.
She is brought in by a daughter who notes an ulcer on the lower leg.

What questions would you ask Molly and her daughter about the aetiology of this ulcer?
Put answer here
What would you determine on physical exam?
Put answer here
Questions
Discuss the various types of wound dressings.
Put answer here
Discuss the type of wound that would benefit from the main types of dressings.
Put answer here
Discuss the microbiology of lower limb ulcers – diabetic and non-diabetic. Discuss suitable antibiotic
therapy.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 9
Wrist injury
Jeffrey Beck is a 10-year-old boy.
He is brought in by his mother who says "He was playing soccer and fell onto his right arm.
He says it's really sore and won't let anyone touch his right wrist."

Discuss the differential of tenderness at the radial aspect of the right wrist.
My provisional diagnosis given the trauma and tenderness will be a scaphoid fracture as it is
usually caused by a fall on an outstretched hand with dorsiflexion of the wrist and compression to
the radial side of the hand.
My DDx will include damage to any of the anatomical structure in the area, these include:
● - Scapholunate instability / ligament tear
● - Fracture of other carpal or metacarpal bones
● - Rupture of Flexi Carpi Radialis tendon
● - Radial Styloid Fracture
● - Extensor carpi radialis Longus / Brevis avulsion
● De Quervain’s disease
● Nerve Injury
Discuss how you will differentiate on physical exam and imaging.
Examination
A musculo-skeletal examination should be performed bilaterally of the wrist which would include
examining joints before and after (e.g. hands and elbows).
The approach of “look feel move” should be used.
Look: erythema, swelling, scars, deformities, skin changes, etc
Feel: temperature, swelling (synovitis, effusions, osteophytes), tenderness
Move: assess range of motion and strength in each joint as well as assess function
Special Tests
Scaphoid fracture
Anatomic snuffbox tenderness
Tenderness of scaphoid tubercle (pressure application to tuberosity at proximal wrist crease
during write extension)
Highly sensitive signs but not very specific
Scaphoid fracture unlikely if both tenderness are absent
Scapholunate ligament injury
Scaphoid shift test (palpable clunk over scaphoid tuberosity when wrist is deviated from ulnar to
radial position)
Triangular fibrocartilage complex damage

Ulnocarpal stress test (pain or clicking while compression load to a ulnar-deviated wrist)
Distal Radioulnar Joint Injury
Piano Key Sign (ulnar head springing back when depressed while supporting the forearm in
pronation)
Imaging
X-Ray
X-ray is a cost-effective way to assess the existence of a scaphoid fracture. Multiple views are
usually required to make a diagnosis (AP, lateral, oblique). Sometimes radiographers may order a
“scaphoid” view to aid diagnosis. However, non-displaced scaphoid may not always be visible on
radiography. In these instances, patients are casted for 1-2 weeks before a repeated X-ray
MRI
Not usually indicated due to cost associated with MRI. However, may be useful if fracture is not
detected on radiography.
US
Not usually indicated but high spatial resolution ultrasonography has been shown to be reliable
and accurate in identifying fracture. (operator dependent)
Bone Scintigraphy
Cochrane review showed that it is a cost-effective and accurate method for assessing occult
scaphoid fractures and is comparable with MRI in identifying fractures.
Questions
Discuss the approach to suspected scaphoid fractures.
Scaphoid fractures are divided into displace or non-displaced fracture. This division usually
dictates whether a surgical or non-surgical treatment is commenced. However, scaphoid fracture is
not always detected at presentation. Therefore, if it is not radiologically confirmed but clinically
suspected, a short-arm cast is placed to prevent further worsening of the condition. A 2 week
follow up radiograph or bone scintigraphy will be needed to confirm diagnosis. In non-displaced
scaphoid fractures, no surgical intervention is required for an optimal recovery provided that
immobilisation is established with a cast. Symptomatic treatment such as analgesic is also
required. A cast should be left on for 6 weeks and repeated x-ray to demonstrate complete
recovery of the damage. Note that damage closer to the thumb tends to recover quicker due to
better blood supply.
However, surgical treatment is warranted in fracture with even small amounts of displacement due
to the risk of non-union.
Discuss advice to patients after completing splint or cast.
After completing splint or cast, further damage must be prevented. Some of the advices may
include: avoid heavy lifting or strain in the area, avoid participating in contact sports, avoid
activities that may lead to a fall (e.g. iceskating, trampoline, etc)
Physical therapy is also important as full finger motion should be maintained throughout the
recovery period to avoid stiffness with precautions to the affected joint. Exercise will also
decreased the level of oedema in the damaged area. Elevation may also help to decrease level of
oedema. Exercise program may also be used to restore function and strength.
Describe how you would systematically review a hand/wrist x-ray.
Similar to all x-ray interpretation, begin by checking patient’s details as well as the date of X-ray
to ensure the most recent x-ray on the correct patient is being viewed. As mentioned, a hand/wrist
x-ray usually include an AP, lateral and oblique view.
Approach each film individually. General principles include tracing out the cortex to identify any
fractures as well as examining the joint space to identify any cartilage or ligament damage.
Smooth articular surfaces should also be identified. Identify abnormalities by thoroughly viewing
proximally to distally and inspect each phalanx individually.
AP Film
Distal radius and ulna should not overlap at their distal articulation
Scaphoid may appear shortened from its normal elongated shape in fracture or ligament
disruption
Lateral Film
Used to determine carpal alignment and degree of fracture angulation
Radius and ulnar should completely overlap one another
Oblique Film
Obtained in either partial pronation or supination
Cone down AP view of the scaphoid in ulnar deviation
May detect subtle fractures
What are some of the common locations of lesions on the ulnar aspect of the wrist?
Extensor Carpi Ulnaris sublaxation

Flexor Carpi Ulnaris tendinitis
Ulnar Head subluxaion-dislocation
Distal radioulnar joint arthritis
Pisiform subluxation-fracture
Pisotriquetral degeneration
Triangular fibrocartilage complex traumatic lesions
Ulnar styloid lesion
Lunate/triquetrum lesion
Lunotriquetral instability
Midcarpal instability
Capitates/hamate avascular necrosis
Carpometacarpal arthritis
References
American Academy of Orthopaedic Surgeons (2010) Scaphoid Fracture of the Wrist
Bethel, J. (2009) Scaphoid fracture: Diagnosis and Management. Emergency Nurse, 17(4), 24-29.
Duke Orthopaedics (2012) Wheeless’ Textbook of Orthopaedics
Forman, A., Forman, S., Rose, N. (2005) A Clinical Approach to Diagnosing Wrist Pain,
American Family Physician, 72, 1753-1758.
Krasin, E., Goldwirth, M., Gold, A. & Goodwin, D.R. (2001). Review of the current methods in
the diagnosis and treatment of scaphoid fractures. Postgraduate Medical Journal, 77, 235-237
Phillips, T., Reibach, A., Slomiany, W. (2004) Diagnosis and Management of Scaphoid Fractures,
American Family Physician, 70, 879-84.
Schubert, H. (2000) Scaphoid Fracture: Review of diagnostic tests and treatment. Canadian Family
Physician, 46, 1825-1832.
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 10
Richard Derringer is a 65-year-old man who has noted bright red blood on the toilet paper over the past
two weeks.

What further questions will you ask on history?
Put answer here
What is the most likely cause of small volume bright red blood per rectum?
Put answer here
What is the most likely cause of large volume bright red blood per rectum?
Put answer here
What further conditions are on the differential diagnosis of blood per rectum?
Put answer here
Questions
Outline an approach for the investigation of gastrointestinal bleed.
Put answer here
Discuss the risk factors for colorectal cancer.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 11
Peggy Lee is a 58-year-old lady with peripheral joint pain [wrist and hands] and neck pain.
She is on no medication.
She states "Doctor, my neck and hands are so sore. I need something for pain relief."

What further questions will you ask on history?
Put answer here
What are the differential diagnoses for this lady's pain?
Put answer here
Questions
Discuss the differences between rheumatoid arthritis and osteoarthritis. [Note features on history and
physical, laboratory investigations and diagnostic imaging.]
Put answer here
Discuss the diagnostic criteria of lupus [SLE]
Put answer here
Discuss an approach to treatment for osteoarthritis – include Allied healthcare providers.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 12
Knee pain
James Brown is a 50-year-old man with right knee pain.
He has been an active man all his life.
He states "Doc, my knee is getting to me. It's been aching off and on for the past two years. But this
month it's got real bad.

What is your differential diagnosis for this man's knee pain – remember both patellofemoral and
femoral-tibial joints?
Knee pain can result from trauma, overuse, internal derangement, osteoarthritis, inflammatory arthritis.
Knee pain can also be due to vascular or neurological conditions. Hip disease may also radiate to the knee
Provision Diagnosis based on age – osteoarthritis
DDx
- Radiation from back; osteoarthritis, loose bodies, degenerative meniscal tears
- Gout or pseudogout
- Trauma;
o Anterior cruciate ligament,
o Meniscal tears,
o Ligament sprains,
o Collateral ligament tears
- Arthritis;
o Inflammatory
o Degenerative
o Septic
o Haemarthrosis
o Reactive/fever
- Arterial occlusion
- Patellar tenopathy
- Patellarofemoral pain syndrome
- Fat pad syndrome
- Bursitis
- Lateral knee pain – relate to osteoarthritis
- Illiotibial band syndrome
- Knee pain + swelling
o Popliteal cyst
o Prepatellar bursitis
o Meniscal cysts
What is your differential diagnosis for knee pain in a 12-year-old; 18-year-old; 28-year-old male?
Children and adolescents (12 & 18 year-old)

· Patellar subluxation (more common in females)
· Tibial apophysitis (Osgood-Schlatter lesion)
· Jumper's knee (patellar tendonitis)
· Referred pain: slipped capital femoral epiphysis, others
· Osteochondritis dissecans
· Juvenile Rheumatoid Arthritis
Malignancies; osteosarcomas
Adults (28 year-old)

· Patellofemoral pain syndrome (chondromalacia patellae/runner’s knee)
· Medial plica syndrome
· Pes anserine bursitis
· Trauma: ligamentous sprains (anterior cruciate, medial collateral, lateral collateral) meniscal
tear
· Inflammatory arthropathy: Rheumatoid arthritis, Reiter's syndrome
Questions
Discuss your approach to investigation for this man's knee pain.
- Clinical assessment; history, onset, timing of pain, exacerbating and relieving symptoms
- XRAY; new bone formation, joint space narrowing, subchondral sclerosis and cysts
- Serum crp and esr
- Rheumatoid factor?
- Arthrocentesis?
- Uric acid levels ?
Discuss your approach to investigation of the acutely hot, swollen, painful knee joint in the 28-year-old
male.
-- Traumatic vs non traumatic

- Trauma; ligament sprains, anterior cruciate, collateral ligaments
- Non traumatic; inflammatory arthropathy, RA, septic arthritis, illiotibial band syndrome
Xray if
- Inability to bear weight
- Isolated tenderness at patellar or fibular head
- Active flexion of knee < 90
Serum ESR, CRP, FBC, Rh factor, anti CCP – rule out septic arthritis before commencing therapy
Put answer here
Discuss your approach to investigation of the acutely hot, swollen, painful ankle joint in the 48-year-old
male.
Put answer here
Put answer here
References
eTG complete [Internet].(2012a), Knee Pain, Melbourne: Therapeutic Guidelines Limited;
Accessed 2012 October 2012 http://etg.tg.com.au.wwwproxy0.library.unsw.edu.au/ip/
RACGP 2009.Best practice management of musculoskeletal conditions in general practice.
Retrieved from: http://www.racgp.org.au/guidelines/musculoskeletaldiseases
RACGP 2009. Guideline for the non-surgical management of hip and knee osteoarthritis.
Retrieved from .http://www.racgp.org.au/guidelines/osteoarthritis
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 13
Lower back pain

John Winter is a 70-year-old man with a four-day history of low back pain following a lifting and twisting
incident while working in the garden.
He states "Doc, I've never had back pain before. But this is really bothering me."

What is your differential diagnosis for low back pain in a 70-year-old man?
Main differentials given his age group and history include:

* mechanical e.g. strain/sprain, prolapsed/herniated disc
* degenerative causes e.g. lumbar canal stenosis, spondylosis
* metabolic e.g. paget’s, osteoporosis (primary or secondary e.g. medications, endocrinologic conditions)
resulting in atraumatic fracture
* neoplastic - more likely to be secondary malignancy (metastasis of prostate/lung/thyroid/renal cancer)
or haematological malignancy (e.g. multiple myeloma) than primary (e.g. osteosarcoma in younger
patients <30 yo)
Other causes of back pain are listed below:
Degenerative/mechanical: intervertebral foraminal narrowing, lumbar spinal stenosis with neurogenic

claudication, arthritis, spondylosis, prolapsed disc
Tumour
- benign or malignant (primary or secondary)
- e.g. osteosarcoma, secondary metastasis to vertebrae
- haematological malignancy e.g. leukemia, multiple myeloma
Vascular
- AAA
Infection / inflammation
- septic disc (discitis)
- osteomyelitis
- spinal epidural abscess
- autoimmune e.g. ankylosing spondylitis, reactive arthritis
Trauma
- strain or sprain
- whiplash injury
Fractures
- traumatic (e.g. falls, motor vehicle accidents)
- atraumatic (e.g. osteoporosis, neoplastic infiltration, steroids)
Metabolic
- paget’s disease
- osteoporosis (primary and secondary causes)
Others
- referred pain from visceral disease
- psychiatric
What are the "red flags" for low back pain of non-musculoskeletal origin?
mainly associated with malignancy, neurological compromise, infection and autoimmune and metabolic
complications
● nocturnal pain
● history of malignancy
● neurological disturbance
● sphincter disturbance
● leg claudication (spinal canal stenosis)
● current or recent infection
● immunosuppression e.g. steroids/HIV
● Abdominal mass
● Thoracic back pain
● history of chronic renal failure
● age <20 or >55
● acute onset in elderly people
● constant or progressive pain
● increase pain on being supine
● morning stiffness
● constitutional symptoms e.g. fever, night sweats, weight loss
Questions
Discuss a plan for diagnosis and treatment for this man.
- Acute musculoskeletal lower back pain is a clinical diagnosis

- tests are only needed if red flags are present
- If performed, these tests might include: FBC and ESR (chronic inflammation, multiple myeloma or other
malignancies, infection), EUC and ALP (for metabolic bone disease such as Paget’s), serum/urine
electrophoresis (myeloma), PSA (prostate cancer)
- Normal WBC in FBC would suggest that active infections are less likely
- Normal ESR means that active infections e.g. osteomyelitis, active rheumatological disease or neoplasia
is less likely; if elevated, further work-up is necessary
- CRP - if elevated, further work-up is necessary
- Urinalysis and culture - if normal, suggests active pyelonephritis (as a less likely cause of this man’s back
pain) is less likely
- Blood cultures - negative blood culture suggests osteomyelitis is less likely
- Need for imaging is discussed below

Treatment
In acute lower back pain less than 4 weeks duration, first line treatment consists of:
- Patient education + return to normal activity
- educate on high likelihood of good prognosis but warn about risk of frequent recurrences
- advised to limit bed rest and stay active as these are associated with reduced pain and better
functional outcomes
- even if non-specific backpain is severe, bedrest should be limited to < 48h
- self-care temperature treatments (ice, heat packs)
- moderate evidence to support use of heat wrap therapy for short term relief - Evidence level B
- RCT - showed electric blanket showed statistically favourable improvement in pain scores while
those with wool blanket showed no change in pain level
- ice - limited benefit/ poor quality studies (Evidence level C)
- However, empirical evidence showed that ice is useful for first few days of pain onset and should
be a first-line treatment
- Pharmacological
- analgesics - NSAIDS e.g. ibuprofen, naproxen, celecoxib - effective for improving acute LBP
(evidence C) with not much difference between various NSAIDS (Evidence A)
- Give NSAIDS for short duration only to prevent gastric, renal and CVS comorbidities (Evidence B)
- Paracetamol (evidence C)
- strong opioids e.g. oxycodone for severe non-specific LBP - Studies have shown similar efficacy to
NSAIDS or paracetamol in terms of return to work and symptom relief
- Muscle relaxants e.g. cyclobenzapine, tizanidine, metaxalone - Evidence level C for effectiveness
of providing increased pain relief compared to placebo + good evidence for effectiveness of
combination of muscle relaxants with NSAIDS or paracetamol
- Physiotherapy / Lumbar spine manipulation
- manipulation shown to be more effective than usual care (i.e. routine care by GP consisting of
analgesic, exercise , physiotherapy - Evidence C
- Systematic Review suggests that manipulation superior in terms of reduced pain and improved
function but only in the short term, not in the intermediate or long term
Discuss the role of imaging for this man's low back pain – when and preferred imaging modality
- Imaging is not required for MSK low back pain lasting < 4 weeks, in the absence of red-flag features or
suspicion of an underlying disease or alternate diagnosis
- Lumbar spine X-ray
- Lumbar spine X - ray will show degenerative changes in given age group and given his likely
diagnosis of MSK back pain
- X rays may be sufficient for the initial evaluation of patients who: have recent significant trauma,
osteoporosis, or age >70 years
- X rays can eliminate fracture, spondylolisthesis, or tumour diagnoses
- reasonable to order Xray if red-flag symptoms are present, although MRI is preferred
- X rays should not be ordered for non-specific LBP of <6 weeks duration as it has no effect on
outcomes
- Lumbar spine MRI
- Best test for complicated LBP
- if performed in uncomplicated LBP, will allow visualisation of scar tissues and degenerative
changes
- Can eliminate fracture, spondylolisthesis, and tumour/abscess diagnoses
- MRI should be ordered in the following circumstances: suspect radiculopathy or spinal stenosis
in potential candidates for surgery; suspect cauda equina; post-surgical LBP; unexplained weight
loss; immunosuppression; hx cancer; IV drug use; prolonged use of corticosteroids; or persistent
pain >4 to 6 weeks' duration
- MRI is of limited diagnostic value in acute non-specific LBP
- Studies have revealed disc protrusions, degenerative changes, and spinal stenosis in
asymptomatic patients who should not undergo any intervention
- Lumbar spine CT
- Not as useful as MRI for depicting disc protrusions
- Better than MRI for identifying bony pathology
- CT should be ordered in the following circumstances: if MRI contraindicated; need to depict
details of spondylolysis, pseudoarthrosis, or scoliosis; or detailed view of surgical fusion,
instrumentation, or bone graft integrity is needed
- Myelography
- Disadvantages include requirement for contrast and lumbar puncture, thus seldom used.
- Sensitivity of spinal stenosis using myelography (67% to 78%) is lower than with CT and MR
- Radionuclide bone scan

- Negative technetium polyphosphate test can rule out the diagnosis of osteomyelitis. In general,
the test is only necessary if radiographic results are ambiguous
Discuss the difference between hard and soft neurologic signs.
Hard neuro signs in the context of back pain are physical, concrete evidence of pathology and include 1)
loss of sensation in lower limbs 2) loss of motor function not due to pain and 3) muscle wasting . HArd
signs can be a medical emergency, and it is only where hard neurological signs fail to respond to
conservative treatment that one should consider surgery.
Soft signs are behavioural or clinical observations that may indicate the presence of pathology and can
include e.g. radiating pain, parasthesiae, lost reflexes - and they are not in themselves a medical
emergency.
e.g. Sciatic pain with soft signs: some sensory changes, mild or no reflex change, normal muscle strength,
normal bowel and bladder function. Whereas Sciatic pain with hard signs: sensory and reflex changes, and
muscle weakness caused by repeated, chronic, or acute condition; may have abnormal bowel and bladder
function.
Discuss the significance of pain radiating down the leg.
● Typically, musculoskeletal LBP does not radiate to the legs, but if it does, it does not travel beyond
the knee
● If pain is located below the knee, it cannot solely be attributed to musculoskeletal LBP and the
differential broadens to include pathology such as radiculopathy, spinal stenosis, peripheral

neuropathy, vascular claudication, and pathology of the lower extremities
● Pain radiating down the leg is likely to represent a nerve root syndrome characterized by radicular
pain arising from nerve root impingement most likely due to herniated discs
● Impingement pain tends to be sharp, well localized, and can be associated with paresthesia.
Impingement is associated with a positive straight leg raising sign (ie, shooting pain down
contralateral leg with leg raising), Neurologic deficits and pain radiation below the knee are most
commonly found with impingement
● The cause of impingement syndrome is most commonly herniated discs, but it may also be caused
by spinal stenosis, spinal degeneration, or cauda equina syndrome.
Discuss sociocultural risk factors (Yellow flags) for the development of chronic back pain and its
management in the context of general practice
References
BMJ. (2011). Musculoskeletal lower back pain BMJ Best Practice from
http://bestpractice.bmj.com.wwwproxy0.library.unsw.edu.au/best-
practice/monograph/778/diagnosis/tests.html
Perina, D., & Kulkarni, R. (2012). Mechanical Back Pain Workup. eMedicine Medscape Reference, 2012
from http://emedicine.medscape.com/article/822462-workup#showall
Chou R, Qaseem A, Owens DK, et al. Diagnostic imaging for low back pain: advice for high-value health
care from the American College of Physicians. 2011;154:181-189
Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in
people without back pain. N Engl J Med. 1994;331:69-73.
Roelofs PDDM, Deyo RA, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain.
Cochrane Database Syst Rev. 2008;(1):CD000396
Dagenais S, Gay RE, Tricco AC, et al. NASS Contemporary Concepts in Spine Care: spinal manipulation
therapy for acute low back pain. Spine J. 2010 Oct;10:918-40.
Longmore, M., Wilkinson, I., Turmezei, T. & Cheung, C. (2007) Oxford Handbook of Clinical Medicine 7th
Edition. Oxford University Press.

Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 14
Pap smear changes

Sarah McLachlan is a 35-year-old lady with abnormalities on a recent Pap smear. Her previous Pap
smears have been unremarkable.
She is quite concerned and seeking to understand what these abnormalities mean for her.
Questions
Discuss abnormalities of Pap smears – atypical squamous cells, HPV related change, CIN1-3 and the
relationship of these changes to squamous cell carcinoma of the cervix.
In Australia, Pap smear abnormalities of the cervix are reported via the Australian Modified Bethesda
System (2004) which correlates with other international systems of classifications being used in clinical
trials in the investigation of optimal management of these cases. The classification system is as follows:
Squamous abnormalities
· Possible low-grade squamous intraepithelial lesion
o Changes in squamous cells that may represent a low-grade squamous intraepithelial
lesion, but are not clear-cut
· Low-grade squamous cell intraepithelial lesion (LSIL)
o Morphologically correlates with productive viral (HPV) infection
o Changes observed would correlate with previous terminology such as ‘HPV effect’ or
‘CIN I’ (mild dysplasia)
· Possible high-grade squamous lesion
o Changes observed suspected to be presence of a high-grade squamous abnormality,
such as possible CIN 2, CIN 3 or squamous cell carcinoma (SCC), but insufficient to justify a
confident cytological prediction of a high-grade lesion
o Corresponds to previous terminology ‘inconclusive possible high-grade squamous
abnormality’
· High-grade squamous intraepithelial lesion (HSIL)
o Morphologically correlates with true preneoplastic changes in squamous cells as result
of HPV infection
o Changes observed correlates with previous terminology such as CIN 2 or CIN 3, or ‘high
grade squamous epithelial abnormality’
· Squamous cell carcinoma
Glandular abnormalities
· Atypical endocervical cells of undetermined significance
· Atypical glandular cells of undetermined significance
o These categories include glandular cell changes that the pathologist believes is beyond
the scope of a definite reactive process. Since HPV infection does not exist in glandular
cells, there is no glandular correlate with low-grade squamous abnormality.

· Possible high-grade glandular lesion
o Where there is suspicion of high-grade glandular abnormality such as possible
adenocarcinoma in situ (AIS), possible endocervical adenocarcinoma or possible
endometrial adenocarcinoma.
o Corresponds to ‘inconclusive possible high-grade glandular
abnormality’Adenocarcinoma
· Endocervical adenocarcinoma in situ
· Adenocarcinoma
Nearly all invasive cervical squamous cell carcinomas arise from precursor epithelial changes, referred to
as cervical intraepithelial neoplasia (CIN). CIN is graded as follows:
CIN I: Mild dysplasia

CIN II: Moderate dysplasia
CIN III: Severe dysplasia and carcinoma in situ
Not all CIN cases will progress to invasive cancer, however, and can persist without change or even
regress.
Likelihood Likelihood Likelihood

of of of
regression persistenc progressio
e n to
cervical
cancer
CIN I 50-60% 30% -
CIN II - - 5%
CIN III 33% - 12%
Discuss management of these various cervical changes.
Management of Recommend for repeat Pap test in 12 months – regardless of whether

women with abnormality is possible or definite
LSIL/possible LSIL
cytology Exception: women >30 years with no history of negative cytology in last 2-3
years – either early colposcopy or repeat cytology in 5 months is
recommended to detect occult HSIL/cancer.
Subsequent 12 month cytology result:

management High-grade changes – Refer for colposcopy

LSIL – Refer for colposcopy
Normal – Repeat Pap test in 12 months
Fluctuating Refer for colposcopy if two LSIL/possible LSIL reports (at least 12 months
abnormality in repeat apart) within 3-year timeframe, regardless of intervening normal cytology
Pap test results reports
Management of Refer to a gynaecologist for colposcopic assessment and targeted biopsy

women with possible where indicated
high-grade squamous
lesion
Management of Refer to a gynaecologist for colposcopic assessment and targeted biopsy

women with high- where indicated
grade squamous
intra-epithelial lesion
(HSIL)
Management of Refer to a gynaecologist for colposcopic evaluation of suspected

women with high- gynaecological malignancies or to a gynaecological oncologist, ideally within 2
grade squamous weeks.
intra-epithelial lesion
(HSIL) with additional Management & Treatment:
features suggestive of Treat CIN 2 or 3 to reduce risk of developing invasive cervical carcinoma
an invasive Fertility sparing treatments:
component 1. Ablative (Using CO2, laser, cold coagulation, radical diathermy or
cryotherapy;)
- The cervix must have been assessed by an experienced colposcopist
- Targeted biopsy has confirmed diagnosis
- No evidence of invasive cancer on cytology/colposcopy/biopsy
- Entire cervical transformation zone has been visualised
- No evidence of glandular lesion on cytology/biopsy
- If these conditions not fulfilled, excisional procedure is indicated
2. Excisional
- Includes ‘cold knife’ cone biopxy, laser, loop electro-excisional
procedure (LEEP) or other diathermy techniques
3. Cone biopsy
Used when:
- -Failure to visualise upper limit of cervical transformation zone in
woman with high-grade squamous abnormality on her referral
cervical smear
- Suspicion of an early invasive cancer on cytology/biopsy/colposcopy
- Suspected presence of an additional significant glandular abnormality
(AIS) on cytology/biopsy
4. Hysterectomy
Squamous cell Refer to a gynaecological oncologist or to a gynaecological oncology unit for

carcinoma (SCC) of urgent evaluation, ideally within 2 weeks.

the cervix
Management of Endometrial origin: refer to gynaecologist with expertise in colposcopic

women with Pap test evaluation of suspected malignancies or to a gynaecological oncologist.
reports of Endocervical, extrauterine or unspecified origin: refer to a gynaecological
adenocarcinoma oncologist or a gynaecological oncology unit.
Management of Refer to a gynaecologist with expertise in the colposcopic evaluation of

women with Pap test suspected malignancies or to a gynaecological oncologist.
reports of
endocervical - If invasive carcinoma is not identified -> cone biopsy
adenocarcinoma in - If overt cancer visualised -> target biopsy
situ (AIS)
Management of Refer to a gynaecologist with expertise in colposcopic evaluation of suspected

women with Pap test malignancies or to a gynaecological oncologist.
reports of possible
high-grade glandular
lesions
Management of Refer to a gynaecologist with expertise in colposcopic evaluation of suspected

women with Pap test malignancies.
reports of atypical
glandular or - Normal TZ: Cone or Observe + repeat Pap in 3 months + Colposcopy
endocervical cells of - TZ not visible: Cone biopsy
undetermined - Abnormal TZ:
significance
High grade intraepithelial abnormality -> Cone biopsy
Overt cancer -> Biopsy
Management of Refer to a gynaecological oncologist or a gynaecological oncology unit for

women with subsequent management.
adenocarcinoma on
cone or punch biopsy
What is the ThinPrep Pap Test? Discuss how it fits into cervical cancer screening.
The ThinPrep Pap test is a form of cervical cancer screening with liquid-based cytology, an alterative to the
conventional Papanicolaou smear. It was developed as an alternative to the Pap smear to improve
specimen adequacy in the hopes of improving test sensitivity for cervical abnormalities. The test involves
collection of cervical cells with the traditional sampling device (cervical broom or spatula and cytobrush)
but instead of smearing the sample on a slide, the device is rinsed into a vial with preservation solution
(swirled vigorously 10 times to release the specimen and then discarded). The sample is then sent to the
pathology laboratory, where it is processed to produce a monolayer of cells. The ThinPrep Imager system
is a computerised system that is used in some laboratories, which identifies 22 fields of interest most
likely to contain abnormal cells, which are then examined by a cytologist.
ThinPrep liquid based cytology has not been approved for government funding in Australia. It is
sometimes used as an additional test within a split sample specimen, where leftover sample from a
conventional cytology slide is used. Over 80% of cervical cytology done is for screening purposes, and the
rest for diagnosis.
Describe the current Australian guidelines on cervical cancer screening. Briefly contrast and compare
this to cervical screening in the United States and the United Kingdom.
Cervical Cancer Screening in Australia

Current Australian cervical cancer screening guidelines promotes routine screening with Pap smears every
two years for women between the ages of 18 (or two years after first sexual intercourse, whichever occurs
later – there is no evidence supporting screening women under 18 years of age routinely), and 69 years.
This is a part of the National Cervical Screening Program Renewal, which has seen the incidence of cervical
cancer and cervical cancer mortality decrease by approximately 50 per cent since implementation 20
years ago.
Cervical Cancer Screening in the US

Cervical cancer screening guidelines in the United States is recommended by the American Cancer Society
and American Society of Clinical Pathology, which now recommend screening in woman from age 21 to 65
years. If cytology (i.e. Pap smear) alone is used, screening should be done every 3 years. For women aged
30 to 65 years, screening interval can be lengthened to every 5 years if both cytology and HPV testing are
utilised.
· Unsatisfactory Pap tests should be repeated in 2 to 4 months.

· If Pap smear is negative and HPV test is positive, both tests are to be repeated at 12 months.
o If both tests are negative then, they can return to routine screening.
o If HPV test remains positive, they should be referred for colposcopy.
· For women with an abnormal Pap smear, regardless of HPV status, appropriate evaluation should
be done.
· Pap smear screening should continue even if immunised for HPV.
Cervical Cancer Screening in the UK

Cervical screening is conducted as part of the NHS Cervical Screening Programme. Liquid based cytology
testing is made available to women between ages 25 and 64 for free, every three to five years. The
screening intervals differ according to age, with the aim of providing a more targeted and effective
programme. Screening intervals are as follows:
Age group (years) Frequency of screening

25 First invitation
25-49 3 yearly
50-64 5 yearly
65+ Only screen those who have not been screened since age
50 or have had recent abnormal tests
It also incorporates the use of the NHS call and recall system for women who are registered with a GP to
be invited for screening, to keep track of follow-up investigation, and to recall women for screening in
three or five years time.
A 60 year old woman who has had a hysterectomy presents to her GP to enquire about whether she
needs to have a Pap smear done. Discuss how you would assess whether she needs a Pap smear and what
you would tell her as her GP.
References
Bekker-Grob, E.W., Kok, Inge., Bulten, J., van Rosmalen, J., Vedder, J.E.M., Arbyn, M., Klinkhamer, P.J.J.M.,
Siebers, A.G., and van Ballengooijen, M. (2012). Cancer Causes Control, 23; 1323-1331.
Davey, E., d’Assuncao, J., Irwig, L., Macaskill, P., Chan, S.F., Richards, A., and Farnsworth, A. (2006).
Accuracy of reading liquid based cytology slides using the ThinPrep Imager compared with conventional
cytology: prospective study. British Medical Journal.
Hoffman B.L., Schorge J.O., Schaffer J.I., Halvorson L.M., Bradshaw K.D., Cunningham F.G., Calver L.E.
(2012). Chapter 29. Preinvasive Lesions of the Lower Genital Tract. In B.L. Hoffman, J.O. Schorge, J.I.
Schaffer, L.M. Halvorson, K.D. Bradshaw, F.G. Cunningham, L.E. Calver (Eds), Williams Gynecology, 2e.
Retrieved October 28, 2012 from
http://www.accessmedicine.com.wwwproxy0.library.unsw.edu.au/content.aspx?aID=56710348.
Karjane, N.W., and Chelmow, D. (2012). Pap smear. Retrieved from

http://emedicine.medscape.com/article/1947979-overview#a30
Rosa, M., Pragasam, P., Saremian, J., Aoalin, A., Graf, W., and Mohammadi, A. (2012). The Unsatisfactory
ThinPrep Pap Test: Analysis of Technical Aspects, Most Common Causes, and Recommendations for
Improvement. Diagnostic Cytopathology.
2006 Consensus Guidelines for the Management of Women with Abnormal Cervical Cancer Screening
Tests. American Journal of Obstetrics and Gynecology, 197(4):346-355).
NHS Cervical Screening. (2012). Retrieved from http://www.cancerscreening.nhs.uk/cervical/about-

cervical-screening.html
National Health and Medical Research Council. (2005). Screening to prevent cervical cancer: guidelines for
the management of asymptomatic women with screen detected abnormalities. Retrieved from
http://www.nhmrc.gov.au/publications/synopses/wh39syn.htm
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 15
Breast lump
Bonnie Raitt is a 50-year-old lady who presents saying "I think I felt a lump under my left breast."

Discuss the differential diagnosis of breast lumps.
- Breast Carcinoma: Classically (particularly with advanced disease) is a hard lump which is tethered to the
underlying pectoralis muscle and is associated with peau d’ orange (thickening of the hair follicles due to
lymphoedema) and tethering of the skin (due to involvement of the suspensory lig./Cooper’s ligament).
Axillary lymphadenopathy is often present (as 80% of breast carcinoma are found in the outer 2 quadrants
of the breast which drain into the axilla). However, it can mimic a “benign”breast lump particularly in its
early stage as a single isolated nodule.
- Fibroadenoma: more common in 20-30 y/o, solitary lump and described as a “breast mouse” due to it
being highly mobile and difficult to catch between the fingers. Size varies with the menstrual cycle. While
often described as a benign neoplasm most of these lesions have been shown to be polyclonal
(hyperplastic) and in those which are truly neoplastic, it is the stromal component which is monoclonal
rather than the ductal epithelium.
- Fibrocystic change: onset 20-30s and is an exaggeration of normal breast architecture in response to the
menstrual cycle. This gives the breast a progressively more “lumpy” feel, but over time a defined breast
lump (mimicking breast carcinoma) can occur if there is a focal area where fibrous proliferation is greater
than in other areas.
NOTE: Breast carcinoma can arise on the background of fibrocystic change (typically the proliferating
type) and thus breast lumps should always be investigated
- Mastitis/breast abscess: occurs typically during breast feeding where trauma to the nipple and areola
lead to fissuring of the skin and infection by microorganisms
- Traumatic fat necrosis: occurs after trauma to the breast (eg after surgery)
- Phyllodes tumour: benign lesion which results in”leaf-like” architecture with papillary projections. May
grow to be very large and painful
- Sclerosing adenosis: non-neoplastic lesion characterised by proliferation of the terminal duct lobular unit
with associated stromal proliferation (giving rise to a breast lump)
Discuss clinical features of benign versus malignant breast lumps.

Malignant Benign
Age 75% of breast adenocarcinoma presents Occurs in younger patients,

in patients >50 though can occur at any age
Size Progressively gets larger, may have May expand and regress in
some response to the menstrual cycle relation to the menstrual cycle.
Progression is generally slower
Lump Typically harder and less well defined

due to the desmoplastic response
Breast signs - Peau d’orange :thickening of the hair - Additional breast signs are rare
follicles due to lymphoedema- from - Fibrocystic change may present
lymphatic obstruction by the carcinoma with a generalised “lumpy”
-Tethering of the skin: due to breast
involvement of the suspensory
(Cooper’s) ligament
- Tethering to underlying mm: due to
involvement of the underlying
pectoralis muscle
Lymph node involvement Can be involved due to reactive Can be involved due to reactive
hyperplasia or sinus histiocytosis in the hyperplasia or sinus histiocytosis
draining lymph nodes (lymph node is in the draining lymph nodes
firm, non-tethered). If metastatic (lymph node is firm, non-
involvement occurs then lymph node tethered). It does not become
can become very hard (due to the tethered to surrounding
desmoplastic response) and tethered to structures
surrounding structures
Involvement of other Can occur with metastatic disease. The Does not typically occur
organs most common sites of involvement are
- bone: osteolytic lesions resulting in
tenderness and pathological fractures
and hypercalcaemia
- Liver: hepatomegaly, metabolic
disturbances
- Brain: headache, focal neurological
signs, changes in behaviour, raised ICP
and herniation syndromes
- Lung: obstruction of bronchi leading to
segmental collapse and pneumonia.
Pleural effusions
-Adrenal glands: secondary addison’s
disease
Questions
Describe the current Australian guidelines on breast cancer screening.
Women at average risk (50-69 y/o):

- Screening mammogram every 2 years
- Breast check (self and by doctor)- Note: there is no current evidence that clinical breast exam provides
additional benefit for patients who attend regular mammogram screening
Women at moderately-high risk:

- Screening mammogram at LEAST every 2 years
- Regular breast checks
- Consider referral to family cancer clinic for assessment
- Generate an individualised surveillance program based on patients risk and assessment
Discuss the investigation and management of a solitary breast lump.
Triple test: History/PEx, Imaging and Biopsy

Imaging:
1. Diagnostic mammogram (note this is different to screening mammograms). These are particularly good
for calcified lesions. Disadvantages: can result in false negatives and cannot differentiate benign from
malignant lesions
2. Consider U/S in younger patients, or those with dense breasts. Cannot detect calcification
Biopsy- several modalities:

1. FNAB: least invasive, only provides cytology and no histology
2. Core Biopsy
3. Incisional biopsy
4. Excisional biopsy- may also be therapeutic if margins are acceptable
Discuss BRCA1 and BRCA2.
BRCA1 and 2 are tumour suppressor genes which produce a protein involved in the repair of damaged
DNA.
BRCA1 is also associated with an increased risk of Uterine tube carcinoma, Male breast carcinoma and
pancreatic carcinoma
BRCA2 is associated with Fanconi anaemia (which is itself associated with leukaemia), ovarian carcinoma,
prostate carcinoma, Uterine tube carcinoma, Male breast carcinoma and pancreatic carcinoma
These are uncommon familial syndromes which are found more commonly in minority groups such as the
Ashkenazi Jews
Briefly discuss the concept of “overdiagnosis” and describe the current debate of how this pertains to
breast cancer screening programs.
Overdiagnosis refers to the situation where people get a diagnosis even though their disease would never
have caused them harm. In breast cancer this refers to patients who receive a diagnosis of breast cancer
and undergo treatment, even though their cancer would not have resulted in death or illness.
1 cochrane study and 1 recent norwegian study both found that breast screening leads to a reduction in
breast cancer mortality by 15% but to 30% overdiagnosis and overtreatment. In terms of NNT and NNH, in
a 10 year screening program, for every 2,000 women screened, 1 women would have her life prolonged.
Conversely, 10 healthy women would otherwise have not been diagnosed as breast cancer and
undergone treatment unnecessarily. Additionally 200 patients will experience psychological distress for
several months due to false positive findings at screening.
What factors are known to increase the risk of breast carcinoma
- Female (125x risk of male)

- Age: >75% are diagnosed >50y/o, with a median age of diagnosis ~60y/o
- FHx: particularly with 1st degree relatives
- Familial syndromes: BRCA1 and BRCA2 mutations
- Increased oestrogen exposure: early menarche, late menopause, nulliparity or late age for first born
child,
- Risk associated with OCP and HRT is controversial
-Previous benign breast lumps: eg fibrocystic change (particularly if proliferative type with cellular atypia
was present), LCIS (not a pre-cancerous lesion, but increases risk of breast carcinoma in both breasts-not
just the one the LCIS was present in)
- Geographic factors: Increased risk in US/Europe vs. Asia
References
Gøtzsche PC, Nielsen M, (2011) Screening for breast cancer with mammography, Cochrane Reviews
Kalager M, Adami H,Bretthauer M,Tamimi R (2012) Overdiagnosis of Invasive Breast Cancer Due to
Mammography Screening: Results From the Norwegian Screening Program. Annals of Internal Medicine.
156(7)
National Institute of Health (2007), BRCA1 Genetics Home reference (Last updated Sept 24 2012).
Retrieved from http://ghr.nlm.nih.gov/gene/BRCA1
National Institute of Health (2007), BRCA2 Genetics Home reference (Last updated Sept 24 2012).
retrieved from http://ghr.nlm.nih.gov/gene/BRCA2
RACGP (2009), Guidelines for preventive activities in general practice (The Red Book) 7th Edition
Reviewer 1 comments
- excellent! perhaps for question 1, can try to categorise differentials into e.g. inflammatory/ Benign and
Malignant for neater presentation/easier to remember
- For breast cancer screening, perhaps can include guidelines for those with significant family history who
may not fall into aforementioned categories
- Are there circumstances where women younger than 50 years old are also recommended to go for
breast investigation?
- Do all breast lesions detected on self/clinical breast examination have to be investigated, regardless of
patient’s age?
- Perhaps can also include more info on specific features that one might find on history / physical
examination, ultrasound/ mammogram for a malignant breast lump
- Thank you Jon. Kam!
Reviewer 2 comments
document.


Case 16
Stephen Winwood is a 60-year-old man who has heard about the PSA test.
He states "Doc, I had a friend who was recently diagnosed with prostate cancer. It got me worried."

What are the signs and symptoms of obstructive and irritative uropathy?
Put answer here
What are the signs and symptoms of carcinoma of the prostate?
Put answer here
Questions
Discuss an approach to treatment for benign prostatic hyperplasia.
Put answer here
Compare and contrast the screening recommendations of the Royal Australian College of General
Practitioners, the Urological Society of Australia and New Zealand, the Royal College of Pathologists of
Australasia, and the US Preventive Services Task Force.
Put answer here
List and very briefly describe the findings of the recent major randomised trials on prostate cancer
screening (the USPSTF website will be helpful in identifying these trials).
Put answer here
Discuss the pros and cons of PSA testing.
Put answer here
Put answer here

References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 17
Stephen Raymond Vaughan is a 72-year-old man who presents saying "Doc, I've been feeling a bit dizzy.
I think my heart is beating a little fast." He is otherwise well.

What investigations are pertinent for someone who complains of palpitations/irregular heartbeat?
Put answer here
What are the potential triggers of a first episode of atrial fibrillation?
Put answer here
What features of atrial fibrillation on history, physical and clinical investigation would trigger a referral
to the emergency department?
Put answer here
Questions
Discuss the treatment rationale for atrial fibrillation.
Put answer here
Discuss prevention of complications – "who gets warfarin; who gets aspirin; who gets nothing."
Put answer here
Who do we refer for cardioversion?
Put answer here
Briefly describe the new oral anticoagulants.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 18
Elizabeth Finn is a 60-year-old lady with a two month history of dizziness.
She states "Doctor, whenever I get up from lying down I feel like everything is spinning".

What is the difference between dizziness and vertigo?
Put answer here
What is the differential diagnosis for dizziness?
Put answer here
What is the differential diagnosis for vertigo?
Put answer here
Questions
Discuss a plan of investigation for dizziness.
Put answer here
Discuss a plan of investigation for vertigo.
Put answer here
Discuss the treatment of benign positional vertigo.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 19
GORD
James Hendrix is a 50-year-old overweight man.
He states "Doc, I am feeling full and gassy all the time. I get a little regurgitation when I lie down."

Discuss investigation for Helicobacter pylori.
- Carbon 13 urea breath test: Based upon detection of products created when urea is split by H.pylori
urease. Can be used in patients 55yrs or younger without alarm features. However PPIs, bismuth and
antibiotics can interfere with the test resulting in false negatives.
- Upper GI endoscopy and biopsy urease testing: most specific and sensitive test for diagnosis of
pathology PUD in the setting of suspected H. pylori, and H pylori testing of mucosal biopsy urease testing
is done routinely when ulcers are present. Allows simultaneous assessment of histopathological changes
and to rule out malignancy. Used when the patient has alarm symptoms or is >55yrs age.
- H pylori serology: has >90% specificity and sensitivity based on quantitation of IgG against H pylori using
ELISA. Useful for detecting a newly infected patient but not a good test for follow up of treated patients
because the results do not indicate present infection and the IgG titre may remain elevated for a long
period of time after eradication.
- H pylori fecal antigen test: a novel rapid test based on monclonal antibody immunochromatography of
stool samples. Can be used in the initial stages of infection and to detect eradication after treatment.
Discuss the differences in presentation between GORD and PUD.
GORD typically presents with a history of heartburn, regurgitation and dysphagia. Heartburn is felt as a
retrosternal sensation of burning/discomfort that is worse after eating or when lying supine or bending
over. Dysphagia is present in 33% of patients with a sensation that food is stuck and solids is worse than
liquids. Occaisonally patients may report coughing (especially nocturnal cough), chest pain and wheezing.
PUD typically presents with epigastric pain (lower down than the pain OF GORD) characterised by gnawing
or burning sensation that occurs after meals. Pain that radiates to the back is suggestive of a posterior
penetrating gastric ulcer complicated by pancreatitis. Food/antacids relieve the pain of duodenal ulcers
but provide minimal relief of gastric ulcer pain. Regurgitation or dysphagia is uncommon. Other symtpoms
include hematemasis or melena from GI bleeding and symptoms consistent with anaemia (SOB, fatigue).
What are the “red flags” symptoms of gastro-oesophageal reflux?
Red flags of GORD indicate the need for further evaluation (endoscopy)
- dysphagia: assess for Barrett’s esophagus
- odynophagia: assess for esophageal ulcer

- significant weight loSS (>10% in 6 months)
- early satiety or vomiting
- aspiration
- wheezing or cough
- GI bleeding
- unexplained iron deficiency anaemia
- high risk patients (e.g. male >45yrs with longstanding symptoms or elderly patient with reflux)
Questions
Discuss the complications of persistent untreated GORD.
- Barrett’s esophagus: 10-20% incidence, due to intestinal type metaplasia of squamous mucosal
epithelium of the distal oesophagus to intestinal type columnar epithelium with mucus-secreting goblet
cells due to recurrent exposure and injury of the distal esophagus to gastric acid. Predisposes to the
development of oesophageal adenocarcinoma
- Oesophageal stricture: recurrent acid exposure leads to inflammation and fibrosis narrowing the
oesophagus and leading to mechanical dysphagia from stricture formation.
- Asthma (chronic cough, wheeze): due to aspiration or reflex vagal activation leading to
bronchoconstriction during acute episodes of GORD.
- Aspiration and airways disease
- Chest pain (and associated investigation for MI)
- Laryngeal injury and increased risk of laryngeal cancer
- Vocal cord polyps and hoarseness
- Subglottic stenosis
Discuss treatment options for GORD – when do we refer these people?
Treatment of GORD is based upon 1) lifestyle modification and 2) control of gastric acid secretion through
medical therapy with PPIs with adjunctive antacids/H2 antagonists. According to Best Practice (BMJ)
Guidelines:
--> In patients with initial symptoms less than once/week lifestyle change plus antacids are first line
(especially for pregnant women).
--> If symptoms are 2-3/week or more frequently PPI plus lifestyle changes are indicated.
--> If symtpoms are 2-3/week or more and incomplete response to PPI is found (even after dose
escalation) further testing and consideration for fundoplication is indicated.
1) Lifestyle modification:
Recommended for all patients regardless of severity of GORD - advise patient to lose weight (if
overweight), avoid alcohol, citrus, coffee, chocolate), have smaller meals, eating at least 3hrs before lying
down/sleeping, elevating the head of the bed.
2) Pharmacological treatment:
PPIs are highly potent for treating GORD, provides rapid symptom relief (80% of pts) and healing of
oesophagitis (78% of patients), more effective than H2 antagonists. Initial course is 4-8 weeks but most
patients will need ongoing therapy e.g. omeprazole 20mg PO, esomeprazole 20-40mg PO. Mechanism is
by inhibition of the H/K ATPase pump on parietal cell membranes hence decreasing acid secretion.
H2 receptor antagonists are indicated for mild-moderate symptoms and low grade oesophagitis. e.g.
Ranitidine (Zantac) 150mg PO Bd. Mechanism is by antagonism of histamine on parietal cells and thus it
reduces gastric acid secretion, promotes healing and reduces mucosal injury but not as effective as PPIs
for reducing the risk of persistent oesophagitis. NB: patients can develop tolerance TO h2 antagonists and
symptom relief may be decreased over long-term use.
Antacids e.g. aluminium hydroxide/magnesium hydroxide are symptom relievers that are used to relieve
acute attacks of heartburn and regurgitation. Works within minutes with a fast onset of action and
patients can self-administer as required. However patients needing continuous treatment or with
unresponsive symptoms need further diagnostic testing and evaluation. Antacids do not treat erosive
esophagitis.
In the presence of red flag symptoms referral to a gastroenterologist for endoscopic evaluation is required
as discussed above. In refractory cases or when complications related to reflux disease are identifieD 9as
above) surgical treatment (fundoplication) is necessary and referral to GI surgeon is required.
Discuss the role of eradication therapy for Helicobacter pylori.
H pylori is involved in the pathogenesis of PUD as well as gastric cancer and MALTomas. H pylori is
implicated in the majority of duodenal ulcers due to chronic hypersecretion of gastric acid stimulated by
chronic Hp infection. The bacterium impairs the secretion of somatostatin which normally inhibits gastric
acid secretion. In gastric ulcers, longstanding Hp infection accompanied by severe inflammation results in
gastric mucin degradation, disruption of tight junctions between epithelial cells and induction of epithelial
apoptosis. Hence treatment of h pylori is essential for the prevention and resolution of ulcers.
Rx involves triple therapy: Omeprazole 20mg BD + amoxycillin 1g BD + clarithromycin 500mg BD for 14

days is first line for H pylori eradication. Check for eradication 1 month after the end of therapy.
Describe the potential problems of long-term PPI therapy.
PPIs have proven to be safe over a long time, although use over >20yrs has not been examined. Initial
concerns about the development of enterochromaffin-like tumours has not be confirmed in clinical
studies. Fundic gland polyps of the gastric mucosa can occur with long-term acid suppression but are not
dangerous clinically. In patients with h pylori long term PPI can accelerate gastric atrophy and intestinal
metaplasia hence eradication of H pylori is indicated in patients on long-term PPI therapy.
The rate of pneumonia appears to be increased in patients with lonG_TERM ppi use (RR 20 and it is also
associated with a modest increased risk of bacterial gastroenteritis. Clostridium difficile infection causing
colitis has been linked to PPI use (RR4). PPIs are also associated with an increased risk of fracture and
osteoporosis and may reduce calcium absorption but there is no link between PPI and BMD in prospective
studies.
Although patients need to be aware of potential arms, the absolute level of risk from long-term PPi use is
very low.
Compare and contrast the step-up vs step-down approaches to GORD management
Traditionally, it was recommended that treatment of GORD involved starting with an antacid and working
up to H2 antagonist and PPI if there was inadequate control of symptoms. Outcomes of the step-up
approach include weeks before symptoms are controlled, slower healing of oesophagitis and overall
higher total drug costs and consultation/investigation fees. In contrast, current recommendations have
recommended a step-down approach whereby patients who fulfil criteria for reflux disease are treated
with PPI as the initial therapeutic intervention at optimal therapeutic doses. Aggressive therapy is then
reduced to maintenance doses, trial of withdrawal of therapy or subsequently to H2 antagonists or
antacids if the symptoms are very mild or intermittent. The step-down approach has been associated with
faster symptom control (within one week), rapid healing of oesophagitis, lower total drug cost and
consultation/investigations.
References
Chey WD, Wong BC. (2007) American College of Gastroenterology guideline on the management of
Helicobacter pylori infection. Am J Gastroenterol. 102(8):1808-25
Ramakrishnan K, Salinas RC. (2007) Peptic ulcer disease. Am Fam Physician.76(7):1005-12
Piterman L, Nelson, M. (2004) Gastro-oesophageal reflux disease. Current concepts in management.
Australian Family Physician. 33(12): 987-91
Therapeutic Guidelines eTG, (2005) Proton Pump Inhibitors. Therapeutic guidelines limited. nth Melbourne,
Vic.
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 20
James page is a 58-year-old man. He has recently undergone a coronary artery bypass graft.
He has a number of questions concerning cardiac risk factors, cardiac medications and lifestyle issues
following surgery.

Compare and contrast the presentations of various coronary syndromes: “stable” angina, “unstable”
angina and acute myocardial infarction.
Put answer here
Describe the ECG changes seen in myocardial ischaemia, and acute myocardial infarction.
Put answer here
Questions
Discuss cardiac risk factors and preventive care for this patient.
Put answer here
Discuss the standard medical regimen including both pharmacological and non-pharmacological therapy
for a patient with established coronary artery disease.
Put answer here
What is the recommended ongoing follow up that James should receive?
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 21
Vincent Gil is a 10-year-old boy with a recent history of nighttime cough and fatigue.
His mother states "He has an older brother with asthma. Do you think he has asthma too?"

Discuss findings on history and physical exam which would point towards a diagnosis of asthma.
Put answer here
Discuss the classic findings on spirometry.
Put answer here
Questions
Discuss the protocol for initiating treatment of a 10-year-old boy with asthma.
Put answer here
Discuss the Asthma Action Plan
Put answer here
Discuss the emergency investigation and treatment of asthma.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 22
William Wyman is a 60-year-old man with a 50 pack year smoking history.
He states "Doc, I feel lousy. I am short of breath and my cough has got a lot worse."

How do patients with undiagnosed COPD commonly present?
Patients with undiagnosed COPD commonly present with dyspnoea, cough, poor exercise tolerance and
sputum production.
What are the diagnostic criteria of COPD?
Formal diagnosis of COPD needs to be made using spirometry. The diagnostic criteria is FEV1/FVC < 70%.
Compare and contrast “chronic bronchitis” and “emphysema”.
Chronic bronchitis is defined clinically as the presence of chronic productive cough for 3 months in 2
consecutive years (and other causes of cough having been ruled out). However, emphysema is caused by
an abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, together with
destruction of the walls and without fibrosis.
The mechanism of airflow limitation is also different. The loss of elastic recoil and decrease in airway
tethering causes airflow limitation in emphysema, but airflow limitation in chronic bronchitis is due to
narrowing of airway caliber and increase in airway resistance.
They are similar in that they cause worsening dyspnoea as the COPD progresses.
Questions
Describe the non-pharmacological and pharmacological management of COPD.
The aim of management of COPD is to optimise function, prevent deterioration, manage exacerbations
and develop support networks and self management skills.
Discuss strategies for smoking cessation.
Put answer here
What is the microbiology of acute exacerbation of chronic bronchitis in the community setting?
Put answer here

Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 23
Joan Jett is a 30-year-old woman with irritative voiding symptoms.

What are irritative voiding symptoms?
Put answer here
What are the warning signs for progression to pyelonephritis?
Put answer here
Questions
Discuss the microbiology and treatment of common urinary tract infection.
Put answer here
What are the side-effects and contraindications to the antibiotics commonly used for empirical
therapy?
Put answer here
Discuss preventive measures for avoiding urinary tract infection.
Put answer here
Put answer here
References
Reviewer 1 comments

document.
Reviewer 2 comments
document.


Case 24
Lita Ford is a 52-year-old lady with a recent history of vaginal spotting and bleeding.
She states "I haven't had a period in seven years. I am really concerned."

What are the differential diagnoses of dysfunctional uterine bleeding in the woman?
Any postmenopausal bleeding is irregular.

DDx: Atrophic vaginitis (30% cases) - thin-walled epithelium sensitive to traumatic injury/inflamation
Exogenous hormones (30% cases)- un-opposed oestrogens (HRT/obesity) build up endometrium, which
them sloughs off.
Endometrial cancer (15%) Cervical cancer, other cancer.
Endometrial/cervical polyps/fibriods (10% cases)
How would this be different if Lita was 29-years-old?
She wouldn’t normally be post-menopausal at 29yo.

DDx: Irregular menstruation, pregnancy, breakthrough bleed (on OCP), fibroids, Uterine/Cervical cancer,
Infection/inflammation of cervix/vagina/uterus.
Questions
Outline the investigation of dysfunctional uterine bleeding.
History and bimanual exam with speculum. Ensure it is indeed vaginal bleeding and not PR/urethral
bleeding.
Transvaginal ultrasound (for masses and thickness of endometrial wall. In post-menopausal women,
should be <5mm)
Endometrial biopsy to pathology (rule out endometrial cancer. This can be done via aspiration in a clinical
setting)
NOTE: Pap smears are poorly sensitive for endometrial cancer (only detects 50% cases). Useless in this
situation.
If abnormal results from U/S and biopsy, CT (for further imaging/staging), hysteroscopy and curettage can
be performed.
What are the indications and contraindications for hormone replacement therapy?
Indications: relief of symptoms of menopause and protection against osteoporosis and cardiovascular
disease in women at increased risk.
Contra-indications: Oestrogen-dependant cancers (endometrium and breast), recent thromboembilic

disease.
What forms of hormone replacement therapy are currently available in Australia?
Oestrogen therapy:
Oestrogen therapy may be given orally (tablet), transdermally (patch), transvaginally (cream) or by
subcutaneous implant (pellet).
Progestogen therapy:
Must be given in an adequate dose for at least 12 days a month to counteract the proliferative effect of
oestrogen on the endometrium
Continuous combined therapy:

Both progestogen and oestrogen combined.
Put answer here
References
Palmer, D (1994) ‘Prescribing and the menopause: Regimens for hormone replacement therapy’ Aust
Prescr. 17:13-6
http://www.australianprescriber.com/magazine/17/1/13/6/
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 25
Sarah Miles is a 20-year-old lady with questions concerning contraception and sexually-transmitted
diseases.

Discuss the questions involved in taking a sexual history from this lady.
Put answer here
Discuss the microbiology of common sexually-transmitted illnesses in Australia
Put answer here
Questions
If Sarah has had no unprotected intercourse, and no other risk factors, what STI screening should be
performed?
Put answer here
Describe how this would change if she were in a different risk category.
Put answer here
Discuss the various methods of contraception including benefits and side effects of each.
Put answer here
Describe the contraindications to the combined oral contraceptive pill.
Put answer here
Put answer here
References
Reviewer 1 comments
document.
Reviewer 2 comments
document.


Case 26
Diabetes review
John Baldy is a 54-year-old man with type 2 diabetes.
He presents for yearly review.

What history, examination, and office tests should be performed from the perspective of John’s
diabetes review?
Annual Review (RACGP Guidelines, 2011/2012)

Goals
● review goals of management
● check for diabetic complications
● update immunisation schedule
● consider specialist review
History
● general wellbeing, complaints
○ chest pain
● review medications/changes
● management review (medications, specialist follow ups, diet, exercise)
● diabetic complications
○ chest pain
○ changes in vision
○ changes in voiding urine (frothy, proteinaceous urine?)
○ changes in sensation (neuropathy)
● SNAP risks
● immunisations
● family history and update
Examination
● anthropometric measurements (BMI, WC)
● blood pressure, pulse
● cardiovascular system
● eyes (fundoscopy, visual acuity)
● feet (ulcers, pulses, monofilament check)
Investigations
● bloods
○ blood glucose level
○ glycemic control (HbA1c)
○ lipids (cholesterol, triglycerides, HDL-C, LDL-C)

○ renal (microalbuminuria, plasma creatinine for eGFR)
● urinalysis
Other
● immunisations to consider
○ influenza once a year
○ pneumococcal
○ tetanus
Specialist Referrals to consider

● ophthalmologist/optometrist
● diabetes educator/clinic
● dietician
● podiatrist
● pharmacist (home medicine review)
● dentist
Describe the appropriate routine follow up investigations for type 2 diabetes.
● general
○ anthropometric measurements
○ glycemic control (HbA1c)
○ lipids
○ urinalysis
○ vision check
○ peripheral vascular health
○ evidence of neuropathy
● cardiovascular
○ exercise stress test
○ ECG
○ +/- echo
● endocrine
○ pre- and post- prandial blood glucose
○ urine microalbumin levels
○ plasma creatinine (eGFR)
Questions
Describe the non-pharmacological treatments for type 2 diabetes.
Weight reduction
● diet (low calorie, low fat, high complex carbohydrates)
● surgical therapy
Exercise (aerobic 60-70% age-maximal for 30mins+ 3/4 times a week)
Psychotherapy (stress from self-care responsibilities, concurrent depression)
Describe the oral pharmacological treatment options and their mode of action.
Biguanide (Metformin)
● phosphorylates AMP activated protein kinase (AMPK), a major cellular regulator of glucose and lipid
metabolism
● liver
○ suppresses gluconeogenesis gene expression (CRTC2)
○ suppresses lipogenesis gene expression (SREBF1)
○ suppresses fatty acid and triglyceride synthesis
○ inactivates HMG-CoA reductase → reduces cholesterol synthesis
○ increases fatty acid β-oxidation
● muscle
○ ↑GLUT4 translocation and glucose uptake
Sulphonylureas
● binds ATP-dependent K+ channels → ↓tonic efflux of K+ → opens VG-Ca++ channels → ↑intracellular
calcium → exocytosis insulin granules
● pancreas
○ ↑pancreatic insulin release
Thiazolidinediones (glitazones)
● lipid
○ binds to adipocyte PPAR𝛾 nuclear receptor, forms dimer with retenoid X receptor (RXR), dimer binds
to DNA to regulate transcription and translation
○ ultimately leads to ↑adipogenesis and fatty acid uptake in non-visceral, peripheral adipocytes
○ has 'lipid-steal' phenomenon, reduces triglycerides in liver and muscle → enhanced glucose
utilisation in liver and m → ↑insulin sensitivity
● adipokines
○ ↑adiponectin (↑fat oxidation)
○ ↓TNF-α and resistin (they normally impair insulin action)
Meglitinides
● same mechanism of action as sulphonylureas except binds to a different site on the ATP-dependent K+
channels
α-glucosidase inhibitors
● GI absorption
○ saccharides that act as competitive inhibitors of membrane bound α-glucosidase enzymes on small
intestine brush border
○ α-glucosidase normally converts carbohydrates (oligosaccharides) into glucose
○ Acarbose also inhibits pancreatic α-amylase activity, which normally breaks complex carbohydrates
into oligosaccharides
Dipeptidylpeptidase-4 inhibitors (DPP-4)
● inhibits DPP-4 breakdown of incretins GLP-1 and GIP (GLP-1 increases insulin, decreases glucagon, GIP
delays gastric emptying)
Incretin mimetics (exenatide)

● GLP-1/GIP analogue
Who is on your treatment team for type 2 diabetes? Discuss the role of each of these team members.
GP
● Coordinates team based care as per RACGP guidelines. Perform regular reviews of patient health status, management
outcomes, complications and medication review. Liases with specialists and provides referrals when necessary
Cardiologist
● Conduct annual exercise stress test, every two yearly ECGs, lipid, hypertension control and anthropometric
measurements
Endocrinologist
● Review of potential complications: microalbuminuria, eGFR, BSL, HbA1c, lipids, anthropometric measurements
Ophthalmologist
● Early detection of retinopathy, glaucoma or any changes in vision
Dietician
● Provides education on achieving a healthy diet with high fibre, low GI, low fat intake to help achieve glycemic control
Diabetes Clinic/Educator
● Provide general education on DM, physical activity, BSL self-monitoring, medication usage, foot care
Podiatrist
● reviews for evidence of peripheral neuropathy, educates on proper foot care
Pharmacist
● Dispenses prescription medications and provides useful advice on medication usage, especially new medications, and
potential ADRs
Physiotherapist
● Initiates appropriate exercise routine or program, can be part of Medicare Chronic Disease Management Plan Team
Care Arrangement
Dentist
● reviews for dental or periodontal problems, can be part of Medicare Chronic Disease Management Plan Team Care
Arrangement
Hospital ED Team
● Management of acute or life-threatening complications
Pathology Lab
● Takes blood for analysis. Also handles urgent ECGs.
Briefly discuss the role of, and controversy surrounding the newer long-acting insulin analogues in the
management of type 2 diabetes.
Use of long-acting insuline glargine (Lantus), an analogue of human insulin, have been implicated in
associations with increased cancer risks (Colhoun 2009; Currie, Poole et al. 2009; Hemkens, Grouven et al.
2009; Jonasson, Ljung et al. 2009). FDA review in January 2011 (FDA 2011), however, have showed
● duration evaluate cancer risk
● limited information in patient use of lantus
● other methodological flaws control of variables
No conclusive trials have so far identified a clear link between use of long-term insulin glargine analogue
and increased cancer risks. Current recommendations are to continue use if already on lantus unless
otherwise recommended by a medical professional or if patient wishes to change medications.
Periodontal complications of Diabetes

Periodontal disease is an often overlooked dental complication associated with diabetes (Loe 1993).
Studies show a higher prevalence of periodontal disease occurring in diabetic patients than the healthy
control population (Firatli 1997). Periodontal parameters affected include attachment loss, bleeding
scores, probing depths and missing teeth (Grossi, Zambon et al. 1994; Bridges, Anderson et al. 1996).
Clinical implications: dental problems should be monitored too in addition to traditional cardiovascular,
endocrinological, neurological complication reviews. Those with periodontal disease should be referred
early on for dental consultation. This can be done by a GP under the Medicare Chronic Disease
Management Team Care Arrangement Plan.
References
Bridges, R. B., J. W. Anderson, et al. (1996). "Periodontal status of diabetic and non-diabetic men: effects of smoking,
glycemic control, and socioeconomic factors." J Periodontol 67(11): 1185-1192.
Colhoun, H. M. (2009). "Use of insulin glargine and cancer incidence in Scotland: a study from the Scottish Diabetes
Research Network Epidemiology Group." Diabetologia 52(9): 1755-1765.
Currie, C. J., C. D. Poole, et al. (2009). "The influence of glucose-lowering therapies on cancer risk in type 2 diabetes."
Diabetologia 52(9): 1766-1777.
FDA (2011). FDA Drug Safety Communication: Update to ongoing safety review of Lantus (insulin glargine) and possible
risk of cancer.
Firatli, E. (1997). "The relationship between clinical periodontal status and insulin-dependent diabetes mellitus. Results
after 5 years." J Periodontol 68(2): 136-140.
Grossi, S. G., J. J. Zambon, et al. (1994). "Assessment of risk for periodontal disease. I. Risk indicators for attachment loss."
J Periodontol 65(3): 260-267.
Hemkens, L. G., U. Grouven, et al. (2009). "Risk of malignancies in patients with diabetes treated with human insulin or
insulin analogues: a cohort study." Diabetologia 52(9): 1732-1744.
Jonasson, J. M., R. Ljung, et al. (2009). "Insulin glargine use and short-term incidence of malignancies-a population-based
follow-up study in Sweden." Diabetologia 52(9): 1745-1754.
Loe, H. (1993). "Periodontal disease. The sixth complication of diabetes mellitus." Diabetes Care 16(1): 329-334.
RACGP (2011/2012). Diabetes Management in General Practice: Guidelines for Type 2 Diabetes.
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document.
Reviewer 2 comments
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UNSW Primary Care 2012

Online General Practice Casebook

Student Case assigned Case to review

Lim, Veronica Formosa 18 20

Tai, Yee Shyn 25 1

UNSW Primary Care

Dr Michael Tam, Lecturer in Primary Care

Dr Joel Rhee, Senior Lecturer and Convenor of Primary Care

UNSW Primary Care

By the end of this learning activity you should be able to:

1. Outline the assessment and management of common clinical presentations in general

3. Use evidence-based resources and guidelines to answer clinical questions.

● Remember, an “easy” case means greater expectations of clinical competence in an

Clinical assessment and diagnosis

Put answer here

Open comments and primary care term experiences

Put additional comments here.

Clinical assessment and diagnosis

- Perform throat +/- nasopharyngeal swab for culture

Discuss Epstein-Barr virus – include clinical presentation and laboratory assessment.

- Tender lymphadenopathy (cervical nodes are most commonly enlarged)

Discuss the treatment of glandular fever/infectious mononucleosis – include patient precautions.

Nil specific treatment/Supportive care:

For serious cases:

Why are antivirals not routinely prescribed as treatment?

Open comments and primary care term experiences

Put additional comments here.

Clinical assessment and diagnosis

Put answer here

Put answer here

Put answer here

Put answer here

Discuss the investigation of a thyroid nodule.

Put answer here

Put answer here

Open comments and primary care term experiences

Put additional comments here.

Clinical assessment and diagnosis

Calculate absolute cardiovascular risk based on above

Acute coronary syndrome and unstable angina

First-line management of ACS, pre-hospitalisation

Resuscitation Council [Electronic Version] Emergency Medicine Australasia, 23(3), 240-243

Open comments and primary care term experiences

Put additional comments here.

Ear pain in a child

Clinical assessment and diagnosis

-More in-depth history of presenting illness

-Past medical history

-Any medications (including over the counter) and allergies

-Family and social history

-SIgns of respiratory distress

- Consider his alertness and arousal

Organisms involved in acute otitis media include

-Treatment goals include symptom resolution and reduction of recurrence.

Topical agents can also be used

Discuss the microbiology and treatment options for otitis externa.

Organisms involved in OE include:

● acidifying agents 3-4 times daily for 5-7 days

-Clean ears frequently

Ghossaini,S. (2012). Otitis Externa. Retrieved 26th Oct, from bestpractice.bmj.com

Open comments and primary care term experiences

Put additional comments here.