Examination Medicine: A Guide to Physician Training (68 page)

3. 
It should also be established whether the patient has concurrent sexually transmitted disease (syphilis serology, hepatitis B serology) or tuberculosis (tuberculin test), and whether he or she is at risk of activation of latent infection (CMV, toxoplasma serology).

4. 
Renal and liver function should be checked prior to commencing antiviral drugs.

MONITORING

The key investigations for monitoring progress are the HIV plasma viral load and the CD4
⁺
T cell count. Serial full blood counts and biochemistry will help assess any complications of disease or therapy.

Treatment (
Table 13.8
)

Table 13.8

Longer term management considerations for HIV patients

1. 
Candidates will be expected to know the clinical features and general treatment options for common complications of HIV infection, especially opportunistic infection and malignancy. This list would include
P. jiroveci
(
carinii
) pneumonia, Kaposi’s sarcoma, cerebral toxoplasmosis, CMV infection,
Mycobacterium avium
complex (MAC) infection, diarrhoeal syndromes and cryptococcal meningitis.

2. 
Prophylaxis for
P. jirovecci
with cotrimoxazole or pentamidine (if CD4
⁺
count <200 cells/μL) and MAC with azithromycin (if CD4
⁺
count <50 cells/μL) is an important consideration. If the CD4
⁺
count is >200 cells/μL for three months, prophylaxis can be ceased. Pneumococcal vaccination is routine even when the CD4
⁺
count remains >300 cells/μL.

3. 
Herpes simplex prophylaxis with acyclovir and
Candida
prophylaxis with fluconazole or ketoconazole are appropriate for prevention after one episode has occurred.

4. 
Multiple antiretroviral agents are now available for the treatment of HIV (see
Table 13.5
). Known as HAART (highly active antiretroviral therapy), these drugs in combination have dramatically improved quality of life and life expectancy in HIV disease.

5. 
Some doubt remains as to the optimal time to commence therapy. It is clear that symptomatic patients, or those with an increasing viral load (>20 000 copies/mL) or a falling CD4
⁺
count (<350 cells/μL) are definite indications, but many clinicians prefer to commence treatment before this. Pregnancy, HIV-associated nephropathy and co-infection with hepatitis B are other indications. Drugs should be used only in combination to prevent emergence of resistance and most regimens contain three or more drugs. Treatment is not curative and must be continued indefinitely.

6. 
Regimens can be changed if there is evidence of disease progression. HAART reduces the risk of vertical transmission and probably also the risk of seroconversion following occupational exposure (e.g. needlestick injury), if given promptly.

7. 
Resistance testing is indicated for the treatment of the naive patient, or if treatment is failing and will be changed.

8. 
In pregnancy, the aim of therapy is to make the patient’s viral load undetectable. If the HIV RNA is more than 1000 copies, recommend caesarean section. Treat the mother with zidovudine as an infusion during labour, and treat the infant for 6 weeks.

9. 
Patients co-infected with HBV should have anti-viral treatment that is also effective for that (e.g. lamivudine, emtracitabine). Surveillance for the development of hepatic carcinoma is also indicated for these patients. For patients with HCV, wait until CD4 < 200 to avoid flares. Special care with drug monitoring is necessary if the patient has cirrhosis; zidovudine and didanosine should be avoided.

10. 
Patients whose disease is well controlled by antiviral agents are more likely to die of cardiovascular disease than infection. This is partly as a result of their drug treatment (e.g. with protease inhibitors). Aggresive control of cardiovascular risk factors is indicated. Hyperlipidaemia should be treated with pravastatin (which has less interaction with antiviral drugs).

CHAPTER 14

Think like a physician, think like an examiner – an approach with long case examples

I should have liked to be asked to say what I knew. They always tried to ask what I did not know. When I would have willingly displayed my knowledge, they sought to expose my ignorance. This sort of treatment had only one result: I did not do well in examinations.

Winston Churchill

The cases set out below are examples of typical and realistic long case patients. We have framed the case outlines from an examination perspective, including typical points likely to be raised in the discussion and clinical traps candidates may fall into. Think about how you would cope with them and what sorts of questions you might predict.

Only the most important parts of the history are summarised, as might be obtained by the examiners (not how you would present the case).

CASE 1

Mrs AB 3 is an outpatient and former hospital nurse. She has been unable to work for some years because of her illness.

In 2007, 2 weeks after the birth of her third child, she developed joint pains and swelling of the hands and feet. She had not had any rashes.

Investigations at the time led to a diagnosis of SLE.

She was treated with prednisone doses varying from 10 to 30 mg.

Steroid sparing agents such as azathioprine and mycophenalate were tried, but led to side-effects, but she is not sure what these were. Methotrexate caused febrile neutropenia. Diclofenac and hydroxychloroquine were not very effective.

In 2008 she had an episode of pleuritic chest pain, was diagnosed with pericarditis, admitted to hospital and treated with prednisone, starting with 40 mg. Her symptoms resolved over a few days.

In 2009 she had sudden loss of vision in one eye and retinal vein thrombosis was found. She was then diagnosed with anti-phospholipid syndrome and began treatment with warfarin.

In 2009–10 she had recurrent nocardia infections – skin, muscles (calf) and brain. There was no neurological deficit, but she had severe headache. This was treated successfully with cotrimoxazole.

In 2010 she developed left-sided paraesthesiae and vertigo. A TIA was diagnosed. A CT of the brain and carotid Dopplers were normal. Aspirin was added to her treatment.

In 2011 a pruritic rash developed on her legs and cotrimoxazole was stopped.

Her steroid use was associated with a number of problems: weight gain from 65 to 95 kgs; her BMI is now 35; she developed gestational diabetes needing insulin, but is now taking metformin. She is unsure of her current BSL; she checks it every 4 days or so. She has not had a hypoglycaemic episode; she doesn’t know her HbA1c.

She smokes 15/day and her husband smokes.

She looks after her 3 children at home; once a week she rides a bike with them, but her joints become very sore afterwards.

Joint symptoms and muscle weakness limit household work, e.g. putting out washing. Her husband works 6 × 12-hour days. She gets some support from her family at home.

She has an IUD for contraception and PV bleeding has improved with a progesterone device.

There have been no other rashes.

She has no kidney disease as far as she knows. There has not been a problem with hypertension.

Her last INR was 1.4. She has monthly tests.

Her eyes are reviewed regularly.

She is keen to work again as a nurse or clerk, but has been told this is not possible by her doctors.

She sees her main problem as her inability to work and exercise.

Examination

On the day of the exam the important examination findings were:

1. 
She was Cushingoid.

2. 
There was swelling without deformity involving the hands and wrists.

3. 
She had a healing rash on the legs (likely cotrimoxazole associated).

4. 
Her BP was 130/90 mmHg.

5. 
There was mild prox muscle weakness – she could stand with effort from chair without using her arms.

6. 
The left fundus was pale with 6/12 vision.

Discussion

First examiner

1. 
SLE

a. 
Serology and diagnosis and role of follow-up blood tests

b. 
Management of joint symptoms: drugs, exercise, physiotherapy

c. 
Steroids and doses

d. 
Future complications of SLE; especially kidneys

e. 
Nocardia prophylaxis

2. 
Diabetes:

a. 
routine discussion: how diagnosed, family history

b. 
vascular risk

c. 
renal risk

d. 
role of ACEI

e. 
BSL measurements

f. 
weight loss

g. 
smoking cessation strategies

h. 
patient’s understanding of prognosis.

3. 
Warfarin – INR monitoring and use of aspirin for anti-phospholipid syndrome.

Second examiner

1. 
Contraception issues.

2. 
Prognosis and psychological state, patient’s view of her main problem.

COMMENTS

1. 
Management problems of SLE and its treatment.

2. 
Complicated history needs to be presented succinctly and logically – probably best given chronologically.

3. 
Some common management area for discussion, e.g. diabetes. This needs to be done smoothly – should be straightforward so a high standard would be expected.

4. 
Indication for and management of anticoagulation and management of initial or recurrent pericarditis are very likely areas for discussion depending on time available. Much detail about patient’s management and understanding of warfarin will be expected. You would need to know where and how often INR readings are taken, how result is communicated to patient and who makes dose adjustments. What happened after the last reading of 1.4?

5. 
Current management of stroke/TIA could be asked about and use of warfarin and aspirin.

6. 
Plenty of scope for effect of illness on family, income, work, self-esteem and so on.

7. 
Need to be able show how you would discuss the prognosis with the patient.

CASE 2

Mr BC is a 68-year-old accountant in full-time work. He has come in for the exam from home. He has a younger wife and his youngest child is only 5.

He has had a recent admission to hospital with a chest infection and was diagnosed with COPD.

In 1996 he was diagnosed with chronic kidney disease. He had a biopsy but the diagnosis was unclear, at least to him. He was treated with haemodialysis for 18 months. He still has a functioning fistula in the left arm.

In 1997 he had a cadaveric transplant. Immunosuppression was with prednisone and azathioprine.

In 1998 he developed gout and was treated with colchicine and allopurinol. There has been no recurrence.

Azathioprine led to bone marrow suppression, admission to hospital and he required blood transfusion. Azathioprine was stopped and cyclosporin started.

His current creatinine is 250. He doesn’t know his eGFR, but says his creatinine has been stable for many years, but had increased to 270 umol/L during his recent admission.

His cyclosporin dose was reduced last year and mycophenolate added to his treatment.

He is not worried about his current renal function.