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2002 FRACP paper two


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Question 1 top download pdf

A 45 year old man presents with 6/24 history of palpitations, sweating, dyspnoea and chest pain. His BP is 90/60 mmHg. His ECG is shown below:

The most appropriate treatment of his arrhythmia is:
A. IV amiodarone
B. IV digoxin
C. IV sotalol
D. Cardioversion
E. Overdrive cardiac pacing

Answer: D

Sustained, monomorphic ventricular tachycardia:
- Wide, regular QRS complexes (> 120ms)

Differential Diagnosis

1) SVT with aberrances (may be revealed with vagal manoeuvres)
2) Pacemaker or ICD
3) ECG artefact

If unsure, treat as VT because:

- 80% of wide complex tachycardias are caused by VT (up to 95% in those with previous AMI)
- VT treatment can terminate other arrhythmias
- SVT treatment (eg adenosine) may precipitate VF

VT is classified and managed according to:

1) Duration: sustained vs non-sustained (3-15 beats)
2) Morphology: monomorphic vs polymorphic
3) Symptoms: palpitations, dyspnoea, chest pain, syncope
4) Haemodynamic stability
5) ?Caused by AMI- if yes, treat as unstable because can deteriorate quickly and worsen ischaemia

Unstable patient
  • conscious but pulse and BP still present
    • Synchronised cardioversion
    • If not possible because cannot differentiate between QRS and T, defibrillate as per VF
    • Treat low K (commonest cause) and Mg
  • unconscious/ pulseless
    • Defibrillate as per VF
    • CPR +/- adrenalin
    • Treat low K and Mg
Stable patient
  • Urgent synchronised cardioversion
  • If refractory or prolonged, anti-arrythmics (class 1 or 3)
    • IV Lignocaine (especially effective if known cardiac ischaemia) or
    • IV amiodarone
    • Or if EF >40%, IV sotalol or IV procainamide
  • Treat low K and Mg, heart failure, ischaemia
  • If known VT syndrome with no structural abnormalities, consider using previous calcium channel blocker or beta-blocker

A. and C.
IV amiodarone and sotalol is appropriate and can be used, but is 2nd line to cardioversion (some studies suggest it is less useful in reversion compared to procainamide and sotalol (Marill KA et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med 2006 Mar)

Digoxin suppresses the AV node by increasing vagal tone, thus it precipitates ventricular arrythmias, not suppress it.

Overdrive cardiac pacing will not change the ventricular response.
Cardiac pacing eg in pacemakers work by providing electrical stimuli when they sense intrinsic cardiac potentials being too low or absent (eg in heart block).
For ventricular tachycardias, an ICD is required to cardiovert/defibrillate when it senses that ventricular rate exceeds a programmed cut-off rate.

Monomorphic VT
  • usually from heart disease (IHD)
  • or “idiopathic” (named after sites of origin, usually exercise induced)
Polymorphic VT
  • malignant form of VT that degenerates into VF
  • usually from QT prolongation (drugs or congenital) or electrolyte imbalance
  • classically Torsades de pointes


Cardiology - Arrhythmias


Question 2 top Download PDF

2) A couple comes to you because they want to start a family. There is a vague history of thalassaemia in both families. Which one of the following would cause the least concern to this couple?


The woman is carrier for

The man is carrier for


b thalassaemia

b thalassaemia


a0 thalassaemia

a0 thalassaemia


a+ thalassaemia

a0 thalassaemia


Haemoglobin E

b thalassaemia


a0 thalassaemia

b thalassaemia

b = beta
a= = decreased alpha chain production
a0 = absent alpha chain production



  • Disorders affecting structure, function or production of Hb
  • Common and selective advantage in endemic malaria areas
  • Different Hb are produced during embryonic, foetal and adult life
  • Each Hb is a tetramer comprising 4 globin chains
    • Major adult Hb (Hb A): a2b2
    • Minor adult Hb (HbA2): a2d2
    • Foetal Hb (Hb F): a2g2 (dominates from 10 weeks gestation to 6/12 old)
  • Each globin chain consists of protophyrin IX ring complexed with iron atom Fe2+
  • Each binds one oxygen molecule; every molecule of Hb binds 4 oxygen molecule


  • Oxygen binding to Hb increase in affinity with increase oxygen tension -> Oxygen dissociation curve
  • Hb has decrease affinity in decreasepH and increase2,3 bisphosphoglycerate -> oxygen transport to tissues
  • When one molecule of oxygen binds, it is easier for the next to bind -> Cooperativity
  • Inheritance: Autosomal co-dominant traits
    • Compound heterozygotes who inherit a different abnormal allele exhibit features of both


  • Detection: Electrophoresis
    • Some Hb variants are electrophoretically silent
      • High pressure liquid chromatography (HPLC)
      • Isoelectric focusing
      • PCR to identify globin chain mutation
    • Functional tests: sickling test; solubility, oxygen affinity tests
    • Antenatal dx: PCR amplification of foetal DNA (amniocentesis/ chorionic villus sampling)

Types of Haemaglobinopathies





Mutations affect amino acid sequence of globin chain

Sickle cell anaemia


Mutations that impair production or translation of globin mRNA -> deficient globin chain synthesis

decrease globin supply -> decrease Hb tetramers
Unbalanced chain synthesis
Hypochromia and microcytosis
Clincal phenotype depends on which globin affected, degree of impairment, altered synthesis of other globins + coninheritence of other abnormal globin alleles

b thalassaemia

Thalassaemia haemoglobin variants

Combined deficient globin chain synthesis with structural haemaglobinopathies

Importance is that compound heterozygotes with b thalassaemia can have intermedia or major, rather than the homozygotes who usually have mild disease

Hb Lepore
Hb E
Hb Constant Spring

Hereditary persistence of HbF

increase levels of HbF in adult life with no deletrious effect



Modification of Hb molecule by toxins and abnormal Hb synthesis

CO poisoning
increase HbF in preleukaemia


a Thalassaemia Syndromes

  • a thalassemias are symptomatic in utero and after birth because a globin needed for synthesis for foetal Hb too
  • Non deletion alleles are also common -> increase unstable a globin variants that are functionally useless




a thal 2
(a thal minima)

One allele of one chromosome deleted

Asymptomatic silent carrier

a thal 1
(a thal minor)

Both alleles on one chromosome deleted
- -/aa

Clinically resembles b thalassemia minor


Hb H disease
(Heterozygous a thal1 athal2)


HbA production only 25% normal
Accumulate unpaired b chains
Can form b4 tetramers (HbH)

Clinically b thalassaemia intermedia

  • Moderate haemolytic anaemia
  • Mildly ineffective erythropoiesis
  • Can survive into mid adulthood w/o transfusions

Hydrops fetalis
(Homozygous a thal 1)


Total absence of a globin synthesis

Excess g chains form Hb Barts (g4 tetramers): increaseincrease oxygen affinity thus delivers almost no oxygen to foetus

  • death in utero (increase output cardiac failure)
  1. Risks b thalassaemia major


  1. Disaster – risks complete absence of a globin synthesis ie hydrops fetalis
  1. Risks Hb H


  1. Hb E (a2b2 26Glu->Lys) mildly unstable Hb variant. Interaction of HbE and b thalassaemia can lead to compound heterozygotes with b thal intermedia/ major
  1. Correct. In fact may lead to comparatively less excess a globin chains. a globin chains are highly insoluble and tend to accumulate -> form toxic inclusion bodies -> kill developing erythroblasts in marrow.


Haematology: Haemoglobinopathies Repeat question2001 paper two question 65


Question 3 top

Question 4 top

Question 5 top top Download PDF

5) A 90 year old man with dementia is about to commence donepezil. Which one of the following is least likely to change with treatment?

  1. Visuospatial function
  2. Memory
  3. Social engagement
  4. Completion of activities of daily living
  5. Rate of cognitive decline after 3 months




  • Acquired, progressive deterioration in cognition that impairs ADLs
  • Not just memory loss – loss of executive function
  • Neuropsychiatric and social deficits +/- mood disturbances
  • Many forms but Alzheimer’s most common
    • Then vascular, Parkinson’s related dementia (DLB) and alcohol

Alzheimer’s Disease

  • Usually subtle memory loss -> progress
  • 20%: non-memory – word finding, organisational
  • Evolves over years
  • Pathology:
    • Diffuse atrophy of cortex
    • Secondary ventricular enlargement
    • Plaques with Abamyloid
    • Neurofibrillary tangles (silver stain) in cytoplasm
    • Hyperphosphorylated tau protein
    • Abamyloid in arteriolar walls -> amyloid angiopathy (may cause lobar bleeds)


  • Imaging:
    • CTB: often normal early on -> diffuse atrophy
    • MRI: hippocampal atrophy
    • PET (functional): hypometabolism of posterior temporal parietal cortex
    • EEG: normal/ non-specific slowing

Pharmacological Treatment:

Cholinesterase inhibitors
Tacrine (rarely used due to hepatotoxicity), Donepezil, Rivastigmine, Galantamine

  • Theory: decrease cerebral production of choline acetyl transferase -> decrease acetylcholine -> decrease cholinergic function
  • Cholinesterase inhibitors decrease degradation of acetylcholine -> increase levels
  • Does not modify disease


  • Generally: increase carer ratings of patient’s function, decrease rate of cognitive decline over 3 years
  • AD 2OOO study (only one not funded by pharmaceutical companies)
    • Donepezil vs placebo: NO DIFFERENCE in endpoints: progression of disease and entry into institutionalised care


Australian Guidelines:
(Donepezil and rivastigmine PBS listed)

  • Need to be diagnosed and prescribed by consultant geriatrician
  • MMSE Score 10-24
  • If MMSE > 25 + clinical features: need ADAS-Cog score
  • Only 6 month prescription
    • To renew: increase MMSE by > 2 points (or) decrease ADAS Cog by > 4


  • Oestrogen: useless
  • Anti-oxidants (selegiline/ vitamin E): small benefit to decrease institutionalisation and death
  • Gingko biloba: little evidence
  • Memantine (NMDA antagonist): small study showed decrease progression over 28 weeks
  • NSAIDS: small study showing indomethacin slowed progression
  • Statins: watch this space
  • Vaccine against Ab protein: great in mouse but bad in humans (meningioencephalitis)


Other possible dementia-related questions:
1. Which of the following is not a risk factor for developing dementia?

  1. A positive family history
  2. Increasing age
  3. Low level of education
  4. Chronic alcohol abuse
  5. Parkinson’s disease

Answer: C. The strongest risk factor is age, followed by family history. Another risk factor is vascular disease.

2. Which of the following genes have not been found to be associated with Alzheimer’s disease?

  1. Presenilin-1 (PS-1) gene
  2. Presenilin-2 (PS-2) gene
  3. APP gene
  4. Apo E gene
  5. APC gene

Answer: E – APC gene germline mutation (chromosome 5) is autosomal dominant and associated with familial adenopolyposis coli (FAP)/ colorectal cancer.

PS-1, PS-2 and APP are all autosomal dominant and associated with familial, early onset dementia.

APO E on chromosome 19 – strongly implicated in familial late-onset and sporadic forms of Alzheimer’s. May be associated with poor clearance of amyloid. APO E4 worst, APO E2 possibly protective. Testing not indicated even though available.



Pharmacology: Drug treatment in the elderly


Question 6 top Download PDF

A 35 year old man is found to be hypertensive with a blood pressure of 180/110 mmHg. At presentation, on no treatment, the following results are obtained.

Serum potassium          3.3 mmol/L        (3.5 – 5.0)
Urinary potassium         40 mmol/L         (<30)
Plasma aldosterone       620 pmol/L        (supine 50-450)
Plasma renin                 4mU/L               (ambulatory 5 -75)

The most appropriate next investigation is measurement of:

  1. 24 hour urinary aldosterone
  2. Plasma aldosterone after 4 hours of saline infusion
  3. Plasma aldosterone after 5 days of dexamethasone administration
  4. Plasma aldosterone after synthetic ACTH administration
  5. Adrenal venous aldosterone concentration during bilateral venous catheterisation


Important facts provided:

  • Severe hypertension in a young person - look for secondary causes
  • Hypokalaemia with increased urinary potassium losses
  • Inappropriately high plasma aldosterone: renin ratio, suggesting autonomous aldosterone secretion

Secondary causes of Hypertension

  • Check: if young (<50), severe or refractory hypertension, no family history of hypertension, acute rise over previously stable blood pressure values
  • Also check for end organ damage (retinopathy and papilloedema, nephropathy and cardiomyopathy) and other cardiovascular risk factors






increased steroids (Cushing’s)

  • Primary eg adrenal tumour
  • Secondary eg increased ACTH
  • Exogenous steroids

increased renin

  • Primary eg renin secreting tumour (rare)
  • Secondary eg renal artery stenosis

increased mineralocorticoid (aldosterone)

  • Primary eg adrenal tumour/ hyperplasia
  • Secondary eg high renin or high ACTH (glucocorticoid remediable aldosteronism GRA)


Hypercalcaemia eg primary parathyroidism


Renal failure


Renal artery stenosis

Coarctation of the aorta
- suspect if bilateral upper limb hypertension and faint femoral pulses

Sleep apnoea


When triad of hypertension, hypokalaemia and metabolic alkalosis present

  • Suggests increased mineralocorticoid levels (mainly hyperaldosteronism and to lesser extent, deoxycortisone)
  • Leads to sodium and water retention, urinary potassium loss and thus hypokalaemia, loss of urinary hydrogen ions thus alkalosis
  • Note: normokalaemia often more common in primary hyperaldosteronism (>50%) and always the case in GRA


  1. Primary hyperaldosteronism (increased plasma aldosterone, decreased plasma renin)
    • Aldosterone secreting adrenal adenoma (unilateral/ bilateral)
    • Ectopic adrenal adenoma
    • Adrenal hyperplasia (idiopathic ?increased sensitivity to angiotensin)
    • Familial hyperaldosteronism (autosomal dominant)
        • Type 1: GRA
        • Type 2: Non- GRA
  2. Apparent mineralocorticoid excess (decreased plasma aldosterone, decreased plasma renin)
    • Genetic disorder: mutation in 11-beta-hydroxysteroid dehydrogenase Type 2 enzyme
    • Chronic liquorice ingestion: deactivation of this enzyme
  3. Renovascular disease (increased plasma aldosterone,inceased plasma renin)
  4. Diuretics
    • Pre-existent hypertension, diuretics cause urinary potassium losses eg frusemide
  5. Cushing’s (decreased or normal aldosterone, decreased or normal renin)
    • Aldosterone and cortisol bind to mineralocorticoid receptors with equal affinity
    • Normally, even though plasma glucocorticoid levels are >100x than aldosterone, enzyme 11B- HSD Type 2 inactivates cortisol
    • In Cushing’s, this mechanism is overwhelmed by the vast excess of cortisol
  6. Liddle’s syndrome (decreased plasma aldosterone, decreased plasma renin)
    • Rare autosomal dominant disease: primary increased sodium reabsorption and potassium loss in proximal tubules
  7. Renin secreting tumours (increaed plasma aldosterone, increased plasma renin)

Approach to this patient

  • Plasma aldosterone: renin ratio
  • Urinary potassium (spot value also acceptable)
  • To confirm primary hyperaldosteronism either:
  • 3 days oral sodium chloride then retesting of plasma aldosterone
  • 4 hour 2L saline infusion IV then retesting of plasma aldosterone

(Principle is that in normal subject, aldosterone will be suppressed)

  • To confirm source
  • Imaging (either CT or MRI are reasonable)
  • Bilateral adrenal vein testing (gold standard) if no adrenal masses seen on imaging, or if both adrenals are asymmetrical/abnormal

Back to the question

  1. Not helpful
  2. Correct
  3. This is assuming the hyperaldosteronism is GRA, so that when dexamethasone is administered -> suppresses ACTH which is stimulating aldosterone secretion. In any case there is hypokalaemia in this patient, which is unusual for GRA
  4. Synthetic ACTH (or Synacthen test) usually used to test for cortisol deficiency. Under normal circumstances, aldosterone secretion is NOT ACTH-dependant.
  5. As above


Endocrinology: Endocrine causes of hypertension

Question 7 top Download PDF

7) Which one of the following is least characteristic of cyclosporin toxicity?

  1. Interstitial fibrosis
  2. Arterial endothelial injury
  3. Reduced uric acid secretion
  4. Impaired potassium secretion
  5. Glomerulopathy



Another either you-know-it-or-you-don’t question!

Cyclosporin/ Tacrolimus (FK 506): Calcineurin inhibitors

  • Isolated from fungi
  • Main indications: organ transplantation, immune-mediated/ rheumatological disorders
  • Main action on T helper cells


  • Bind with increase affinity to cytoplasmic proteins
    • Cyclophilins for cyclosporin
    • FK proteins for tacrolimus
  • Drug/protein complex selectively and competitively inhibits calcineurin
    • Calcium and calmodulin dependant phosphatase
    • Thus inhibits transcription of IL 2 and other cytokines
    • However cyclosporin upregulates IL-10 production (anti-inflammatory which may explain effects in RA)
  • Also potent inhibitors of prolactin gene
  • Does NOT have myelosuppressive effects
  • Oral absorption very variable
  • Lipophilic and distributes widely
  • Metabolised by cytochrome p450 and excreted into bile
  • Not removed by HDx
  • Can monitor levels


Side effects:

  • Nephrotoxicity (commonest)
  • Acute renal failure: reversible after dose reduction/ cessation
    • Vasoconstriction in afferent/efferent arterioles
    • Can try treating with calcium channel blockers
  • Chronic renal failure: irreversible and progressive
    • Obliterative arteriopathy
    • Tubular atrophy and interstitial fibrosis (“striped” fibrosis)
    • Ischaemia and scarring of glomerulus


  • Other renal effects:
    • Hyperkalemia: ß renal excretion of potassium by impairing action of cortical collecting tubules
    • Hyperuricaemia and gout
    • Hypophosphataemia
    • Hypomagnesaemia
    • Metabolic alkalosis (increase H+ losses)
    • HUS (rarely)



  • Neurotoxicity
  • Headache, visual changes, seizures resembling HT encephalopathy
  • Mild tremor
  • Akinetic mutism (rare)


  • Hypertension
  • Renal constriction and sodium retention
  • Usually weeks post treatment
  • Responds to dose reduction
  • May need antihypertensives (calcium channel blockers)
  • Metabolic disturbances
  • Hyperglyceamia and frank diabetes (unknown aetiology)
  • Accelerated bone loss (increase turn over)


  • Risk of malignancy
  • Related to immunosuppression
  • Mainly SCC and lymphoproliferative disease
  • Infections
  • Also related to immunosuppression
  • Bacterial, viral (mostly CMV) and fungal


  • Miscellaneous
  • Cyclosporin: gingival hyperplasia, hirsutism (increaseer risk with use of nifedipine)
  • Tacrolimus: alopecia (up to 30% affected in case series)


Renal: Renal Transplantation

Pharmacology: Renal

Question 8 top

Question 9 top Download PDF

 A 37 year old man with known human immunodeficiency virus (HIV) infection for 10 years presents with severe renal colic for which he has no prior history. Tests performed 2 weeks before have shown a normal full blood count and biochemistry screen (including serum calcium), CD 4+ T cell lymphocyte count of 36 cells/mm3, HIV RNA concentration (viral load) of 83,000 copies/mL. His medications include zidovudine (AZT) , lamivudine (3TC), indinavir, azithromycin and dapsone.

The most likely cause for his renal colic is:

A. HIV associated opportunistic infection

B. HIV associated malignancy

C. HIV associated hypercalciuria

D. Adverse drug reaction

E. Unrelated to HIV infection or therapy


Learning issues

  1. Natural history of HIV
  2. Renal disease in HIV patient
  3. Anti retrovirals, drug classes and common side effects
  4. Prophylaxis

Natural history of HIV

  1. Primary infection: 50% asymptomatic, 50% develop “acute HIV syndrome” with flu-like symptoms and lymphadenopathy
  2. Initial viral load does not appear to be related to degree of disease progression
  3. Set point of steady state plasma viremia after 1 year correlates well with degree of disease progression
  4. Chronic infection persists in untreated patient for a median of 10 years before clinical illness
  5. CDC case definition of AIDS: any HIV infected person with CD4 < 200/microL, regardless of symptoms
  6. Long term survivor: if remain alive > 20 years after initial infection, in most there would be disease progression
  7. Long term non-progressor: infected for > 20 years with normal CD4 counts and plasma HIV RNA < 50 copies/mL without anti-viral therapy (noted strong associations with HLA B57 and HLA B27)

Renal disease in HIV patient

  1. HIV associated nephropathy
  2. 90% cases in African American and Hispanics (also more severe)
  3. Seen in children, first described in IVDU
  4. Leading cause of ESRF in HIV population
  5. Proteinuria
  6. HT and oedema rare
  7. Renal biopsy: 80% FSGS, 50% mesangial proliferation
  8. Some responsive to high dose steroids
  1. Drug toxicity
  2. Directly nephrotoxic: amphotericin,pentamidine, adefovir, tenofovir
  3. Most common: indinavir associated renal calculi (10% of patients receiving indinavir), ranges from asymptomatic haematuria to renal colic, treat with hydration


  1. Urinary tract infections (opportunistic or otherwise)
  1. Urinary tract malignancies
  2. increased risk of malignancies in HIV population
  3. mainly KS and NHL
  4. no particular mention of increased risk of urological cancers
  5. KS can affect any organ but not particularly the urinary tract

Goals of treatment

  1. Maximal viral suppression
  2. Sustain rise in CD4 counts
  3. Improve morbidity and mortality
  4. Prevention of resistance + compliance
  5. Minimisation of side effects

Indications for treatment

  1. Acute HIV syndrome (primary infection)
  1. Chronic infection
  2. Symptomatic (regardless of CD4 count and viral load)
  3. Asymptomatic (CD4 count < 350 and decreasing or viral load > 50 000 copies/mL)


  1. Post-exposure prophylaxis
  2. Percutaneous risk 0.3%
  3. Mucous membrane exposure 0.09%
  4. Through intact skin/ other body fluids eg urine: cases documented but risk < 0.09%


Drug Class

Mechanism of Action

Examples and side effects

Reverse transcriptase inhibitors


  1. Nucleoside analogue (NRTI)

(-udines and osines)










  1. Nucleotide analogue





  1. Non-nucleoside analogue (NNRTI)

Block HIV replication at point of RNA dependant DNA synthesis


1) and 2) inhibit a variety of DNA polymerases including that of human mitochondria















Generally 3) are more selective for HIV 1 reverse transcritptase thus less side effects, often used in salvage regimens


Drug interactions as involved with cytochrome p4503A4

  1. NRTI

eg zidovudine (AZT)

  1. mitochondrial toxicity with lactic acidosis, fatty liver, myopathy, pancreatitis
  2. initial fatigue/ N+V and headache tends to subside

eg didanosine

  1. painful sensory neuropathy in 30% (resolves with durg cessation)
  2. pancreatitis at higher doses 10%

eg stavudine

  1. antagonistic with zidovudine
  2. fatty liver and neuropathy

eg lamivudine

  1. best tolerated, often used with AZT
  2. strains resistant to lamivudine have enhanced sensitivity to other nucleosides

eg abacavir

  1. hypersensitivity reaction in 4%
  2. stop drug as rechallenge can be fatal


  1. Nucleotide analogue

eg tenofovir

  1. renal impairment with hyperphosphataemia
  2. increases in vivo levels of didanosine (needs dose reduction)



  1. NNRTI
  2. eg neviparine, delavirdine, efavirenz
  3. no activity against HIV 2
  4. maculopapular rash in 1st few weeks
  5. fatal hepatotoxicity
  6. vivid dreams and light-headedness with efavirenz (take nocte)
  1. nevirapine induces p450
  2. delavirdine inhibits p450
  3. efavirenz unpredictable


Protease inhibitors
(-avirs) except abacavir which is a NRTI

Used together with reverse transcriptase inhibitors

  1. can suppress viral load to <50/mL > 5 years



Many drug interactions


Absolute contraindications

  1. benzodiazepines (prolonged sedation), use propafol
  2. lovastatin (rhabdomyolosis), use pravastatin
  3. ciscapride (prolong QT, torsades)
  4. most antihistamines except loratidine

Hepatic cytochrome p450 3A4

  1. Ritonavir potent competitive inhibitor of these enzymes
  2. Saquinar, indavinar etc metabolised by these enzymes
  3. Thus baby dose ritonavir used as pharmacological boosting
  4. Ritonavir seldom used alone in full doses as poorly tolerated (GIT and neuropathy)


  1. 1st PI used in triple therapy
  2. Nephrolithiasis in 4%
  3. Asymptomatic indirect hyperbilirubinaemia 10%
  4. Dose reduce in liver cirrhosis

Nelfinavir and amprenavir

  1. unique reistance profiles and GIT side effects
  2. nelfinavir resistance with D30N substitution as viruses with this mutation are more sensitive to other PIs (so good initial PI
  3. Amprenavir resistance with single amino acid substitution (good salvage drug): fatal skin reaction in 1%


  1. may not be associated with as severe lipid effects as other PI


Entry inhibitors

Trials on going

  1. CCR5 inhibitors
  2. Integrase inhibitors

Interferes with virus binding to target cell CD4 receptor/ co-receptor (CCR5 or CXR4), or affects viral fusion

Fusion inhibitor

  1. enfuvirtide T20
  2. binds to viral envelope and prevents fusion of viral and host membrane
  3. twice daily C/S injection
  4. 98% injection site reactions
  5. increased risk of bacterial pneumonia


Lipodystrophy syndrome

  1. fat wasting/ accumulation, high lipids, glucose intolerance +/- insulin resistance




Hepatitis B vaccine (3 doses)

Anti HBc and antiHBs negative

Hepatitis A vaccine (2 doses)

Anti HAV negative

Chronic HBV
Chronic HCV

Influenza virus (annual)


Pneumococcal vaccine
(Strep pneumoniae)

All when CD4 > 200


For prevention of severe/ frequent occurrences


What to use

Herpes simplex

Acyclovir 200mg TDS


Fluconazole 200mg BD

Other prophylaxis





  1. when CD4 < 200
  2. can stop when CD4 > 200 for 6/12

Bactrim DS

Pentamidine neb


  1. high exposure
  2. skin test >5mm

Isoniazid + Pyridoxine

If isoniazid resistant, use
Rifampicin or rifambutin



  1. when CD4 < 50
  2. prior disemminated disease
  3. can stop when CD4 > 100 for 6/12

Azithromycin or clarithromycin


Toxoplasmosis gondii

  1. Ig G positive
  2. CD4 < 100

Bactrim DS

If prior encephalitis, use
Sulfadiazine + pyrimethamine + leucovorin

Dapsone + leucovorin + pyrimethamine



Varicella zoster (exposed)

  1. no previous disease
  2. no immunisation

Varicella zoster immunoglobulin IM within 96 hours


Cryptococcus neoformans

Fluconazole oral

Amphotericin IV 3x/week

Itraconazole oral


  1. prior end organ disease
  2. can stop when CD4 >100 for 6/12

Ganciclovir oral/IV


Doses and duration vary dependant on what end organ affected



Amphoterecin weekly IV

Coccidiodes immitis


Amphotericin weekly IV

Itraconazole oral


  1. prior bacteraemia

Cirpofloxacin oral



Infectious Diseases: HIV

Reapeated Question 2003 paper two question 66

Question 10 top Download PDF

10) The need for informed consent as a prerequisite for the enrolment of a patient in clinical trial investigating a novel cancer treatment is primarily based on the principle of:

  1. Non maleficence
  2. Autonomy
  3. Beneficience
  4. Risk management
  5. Justice



5 core values of Medical Ethics:

Non maleficience

Primum non nocere

First, do no harm


Salus aegroti suprema lex

Doctors should act in the best interests of the patient


Voluntas aegroti suprema lex

Patients have the right to choose/ refuse their treatment, ideally after informed consent, which in turn is dependant on competence


Aiming distribution of scarce resources


Both patient and the doctor has the right to dignity

The answer is B.


Oncology: Study Design

Statistics: Study Design