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2004 FRACP paper one


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Question 3 top Download PDF

A 68yo man scheduled for hemiorrhaphy presents for pre-anaesthetic assessment and is found to have non-tender cervical lymphadenopathy.

Full blood examination shows:

                Haemoglobin          125 g/L                                                  [128-175]
                MCV                         96 fL                                                       [80-97]
                White cell count      19.5 x 109/L                                         [3.9-12.7]
                                                Neutrophils           2.5 x 109/L          [1.9-8.0]
                                                Lymphocytes        16.2 x 109/L        [0.9-3.3]
                                                Monocytes            0.3 x 109/L           [0.3-1.1]
                                                Eosinophils            0.4 x 109/L          [0-0.5]
                                                Basophils               0.1 x 109/L          [0-0.1]
                Platelet count                                       213 x 109/L         [150-396]

The blood film is shown below.


With respect to the peripheral blood lymphoid cell immunophenotype, which of the following surface antigens is most likely to be co-expressed with CD19 (cluster of differentiation 19)?

  1. CD3
  2. CD5
  3. CD8
  4. CD10
  5. CD34





The blood film shows smear cells and mature-looking lymphocytes.
This, along with the elevated lymphocyte count indicates a diagnosis of CLL.


  1. B-cell CLL is considered to be identical to the mature B-cell small lymphocytic lymphoma
  2. Characterised by progressive accumulation of functionally incompetent lymphocytes which are monoclonal in origin


Clinical Presentation

  1. B symptoms – weight loss, fever, night sweats, fatigue
  2. Lymphadenopathy
  3. Splenomegaly
  4. Hepatomegaly
  5. Elevated WCC
  6. Anaemia
  7. Thrombocytopaenia
  8. Many people asymptomatic


Laboratory Findings

  1. Lymphocytosis in peripheral blood and bone marrow
  2. Smudge cells on blood smear – reflects fragility of B-CLL cells – characteristic of CLL
  3. Mature-appearing small lymphocytes with large nucleoli and only a thin rim of surrounding cytoplasm
  4. Mature-appearing but functionally and developmentally immature
  5. 3 major sets of phenotypic findings of B-CLL lymphocytes:
    1. Extremely low levels of surface Ig
    2. Expression of one or more B-cell associated antigens – CD19, CD20 (weak), CD21, CD23 and CD24 monoclonal antibodies
    3. Expression of CD5, a T-cell associated antigen
  6. In addition, CLL cells are usually negative for cyclin D1 and CD10. FMC7, CD22 and CD79b are usually negative or weakly expressed
  7. Scoring system – one point for each cellular characteristic:
    1. Staining for surface Ig weakly positive
    2. CD5 positive
    3. CD23 positive
    4. CD79b or CD22 weakly positive
    5. FMC7 negative
  8. 4-5 points = 97% accuracy for Dx of CLL
  9. Most non-CLL B-cell lymphoproliferative diseases had scores 0-2
  10. Higher risk of autoimmune haemolytic anaemia and thrombocytopaenia and hypogammaglobulinaemia



    • Increased percentage of mature-appearing lymphocytes
    • Nodular, interstitial or diffuse infiltrative patterns


    From UTD – bone marrow aspirate
    Note lymphocytosis

    Lymph Node Biopsy

    1. Diffusely effaced nodal architecture with occasional residual naked germinal centres
    2. Infiltrate of mature-appearing small lymphocytes
    3. Low mitotic activity


    Chromosomal Changes

    1. No changes that are specifc for CLL but certain patterns are common:
      1. Trisomy of chromosome 12, 3, 16
      2. Del (13q14)
      3. Del (11q)
      4. Del (17p)


    Minimum Diagnostic Requirements

    1. Absolute lymphocyte count in peripheral blood >10 with predominantly mature-appearing small lymphocytes
    2. Normocellular to hypercellular bone marrow with lymphocytes accounting for >30% of all nucleated cells
    3. If lymphocyte count 5-10 then need to do lymphocyte phenotyping to show low surface Ig, one or more B cell associated antigens (CD19, CD20, CD21, CD23, CD24) and T cell associated antigen CD5


    Differential Diagnosis

    1. Lymphoma (generally has abundant surface Ig)
    2. Other forms of leukaemia – can differentiate on film/BMAT/ immunohistochemistry
    3. Infectious mononucleosis, pertussis, toxoplasmosis – transiently elevated lymphocyte count


    Answer: B


    1. Usually an initial asymptomatic phase which can last a few months to many years
    2. Survival 2 to 20 years
    3. Often transforms into another lymphoproliferative disorder which can be related to the original B-CLL cells or derived from a separate cell of origin
    4. Most common transformations are:
      1. Prolymphocytic leukaemia
      2. Aggressive lymphoma (Richter’s transformation)
      3. Hodgkin’s disease
      4. Multiple myeloma
    5. Higher risk of second malignancy (lung, GIT, skin)
    6. Prognosis based on staging (Rai):
      1. Lymphocytosis only – 150 month survival
      2. Lymphadenopathy, organomegaly – 70-100 month survival
      3. Anaemia, thrombocytopaenia – 9 month survival



      • Not felt to be a curable disease
      • Best treatment regime not known
      • Chlorambucil or cyclophosphamide with or without corticosteroids
      • Second line are nucleoside analogs (eg: fludarabine)
      • Rituximab has also be used as first line
      • Autologous haematopoietic cell transplantation



      Haematology: Leukaemia

      Question 4 top Download PDF

      A hospitalised patient with a rash on her face and a lace-like rash on her extremities has a confirmed diagnosis of erythema infectiosum (parvovirus B19).

      Which of the following infection controls would be the most appropriate?
      A. Standard.
      B. Contact.
      C. Respiratory.
      D. Single room.
      E. Negative pressure room.

      Infection with parvovirus B19 can lead to a variety of clinical manifestations depending on the patient infected.

      Most commonly affects children causing erythema infectiosum, a mild febrile illness with a rash.

      In adults 25% will be asymptomatic, 50% will have a flu-like illness and 25% will develop rash or arthralgia.

      Parvovirus infects erythroid cells.

      Infection with parvovirus leads to a Th-1-mediated cellular immune response with production of IgM antibodies and subsequent formation of immune complexes.

      Can occur at any age but primarily affects children aged 3 to 15yrs.

      Incubation period is to 14 days. Spread primarily via aerosol respiratory droplets. In hosts who are immunocompetent, the patient is viraemic and capable of spreading the infection only during the incubation period. Once the patient has developed clinical signs such as a rash or arthralgias they are no longer infective.
      Tends to spread easily among families (but less so in schools).

      Physical Findings:
      • Slapped-cheek appearance (2-4 days)
      • Macular rash mainly on extremities then develops (1-4 days)
      • Followed by lacy, reticular pattern on proximal extremities (3 days-3 weeks)
      • Polyarthropathy (more common than skin findings in adults) – symmetrical, worsens over the day, hands, wrists, knees, ankles


      • Aplastic crisis - high risk in patients with underlying haematological disorders (eg: sickle cell, thalassaemia, G6PD deficiency)
      • Chronic bone marrow failure - immunocompromised hosts are at risk
      • Congenital infection - PV-B19 crosses placenta and can lead to:
        • Severe fetal anaemia
        • Congestive heart failure
        • Hydrops fetalis
        • Intrauterine death (in 3 to 10% of mothers who are infected)
      • Variety of other disorders that may be linked to or triggered by PV-B19:
        • Hepatitis
        • Myocarditis
        • Viral-associated haemocytophagia
        • Vasculitis
        • Nephrotic syndrome
      So the correct answer is A - no precautions required as the patient has already developed the rash so is no longer infective.

      If the patient was known to be infected but had not yet developed any signs or symptoms (even though very unlikely to ever know this) then respiratory precautions would be advisable to prevent spread.


      Infectious Diseases - Simple principles of infection control in hospital and notification of infectious diseases.


      Question 5 top

      Question 6 top Download PDF

      During pregnancy, many cardiovascular conditions are associated with an increased risk of maternal mortality.

      Which one of the following cardiovascular conditions is associated with the highest rate of maternal mortality?

      Moderate to severe:

      A. Pulmonary hypertension
      B. Hypertrophic cardiomyopathy
      C. Coarctation
      D. Aortic regurgitation
      E. Peripartum cardiomyopathy

      While all the conditions are associated with an increased risk pulmonary HT carries the greatest risk to the mother so answer is A.

      Cardiac Output
      • rise 30 – 50%
      • influenced by posture (increased in L lateral, decreased when supine)
      • preload increased due to increased blood volume
      • afterload reduced due to decreased systemic resistance
      • increased HR
      • Can cause decompensation in pts with previously asymptomatic heart disease
      Blood Pressure
      • Lower due to reduced systemic vascular resistance
      • Resistance reduced due to vasodilation and low-resistance circuit of uteroplacental circulation
      Physical Examination
      • Distended neck veins, basal creps, left and right ventricular heaves, exaggerated heart sounds and flow murmur are all normal in pregnancy
      • Physiological S3 gallop
      • Peripheral oedema in 3rd trimester
      • Shortened PR and QT intervals, increased HR
      • Non-specific ST and T wave changes in 4-14% of pregnancies
      Labor and Delivery
      • Increased cardiac output due to increased blood volume from intramyometrial blood and increased BP and HR associated with uterine contractions

      Predictors of cardiac events during pregnancy
      • NYHA class II to IV or cyanosis
      • Previous cardiac event
      • Left heart obstruction (MV area < 2cm2, AV area <1.5cm2, peak LV outflow gradient >30mmHg)
      • Left ventricular systolic dysfunction (LVEF <40%)
      • 0 points: 5% risk of event
      • 1 point: 27% risk of event
      • 2 or more points: 75% risk of events
      • Correlates with neonatal risk


      High risk:
      • Severe AS with or without symptoms

      Severity of aortic stenosis in adults

        Aortic jet velocity, m/sec Mean gradient, mmHg Valve area, cm2

      1.5 less than 5 3.0-4.0
      Mild 1.5 - 3.0 5 - 25 1.5 - 3.0
      Moderate 3.0-4.0 25-40 1.0-1.5
      Severe* greater than 4.0 greater than 40 less than 1.0
      • Symptomatic MS (NYHA class II to IV)
      • Aortic or mitral regurgitation with NYHA class III to IV
      • Aortic or mitral valve disease with severe LV dysfunction (EF <40%) or severe pulmonary HT (PAP >75% of systemic pressure)
      • Marfan syndrome with or without AR
      • Mechanical prosthetic valve requiring anticoagulation
      Low risk:
      • Asymptomatic AS with LVEF >50% and mean gradient less than 25mmHg
      • AR or MR with no or mild symptoms (NYHA class I to II)
      • MV prolapse with either no MR or mild-mod MR with LVEF >50%
      • Mild MS (valve area >1.5cm2, mean gradient less than 5mmHg) without severe pulmonary HT
      • Mild to mod pulmonary valve stenosis


      • Heart failure, arrhythmia and stroke more common in women whose LVEF <40%
      • Pregnancy not recommended if LVEF <40%
      • Pregnancy generally well tolerated in HCM (low mortality)
      Major risk factors for complications
      • Pulmonary HT
      • Maternal cyanosis
      • Poor maternal functional class
      • History of arrhythmia
      • Maternal anticoagulants
      Pulmonary HT
      • Pulmonary HT is the most serious risk to the mother, especially Eisenmenger syndrome
      • Limits appropriate adaptive responses to circulatory changes
      • Maternal mortality with Eisenmenger syndrome is 30 – 50%
      • Reversed right to left shunt is worsened with decreased systemic vascular resistance ? cyanosis
      • During labor increased systemic resistance can cause abrupt reduction in CO and fatal syncope
      • Arterial oxygen saturation prior to pregnancy is one of the most important predictors of poor fetal and maternal outcomes
      • Likelihood of live birth significantly reduced when sats < 85%
      • Increased risk of rupture or dissection
      • Independent predictor of preeclampsia
      Left to Right Shunts
      • ASD generally not a problem in young, otherwise well women
      • ASDs associated with increased risk of AF, flutter in pts >30yrs
      • Risk of paradoxical embolisation
      • VSD ok if mild-mod
      • Large VSD (>1cm2) usually have Eisenmenger syndrome and are at high risk
      • PDA usually ok, most often repaired

      So while all the conditions are associated with an increased risk pulmonary HT carries the greatest risk to the mother so answer is A.


      Cardiology - Cardiac changes and problems in pregnancy

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      Question 10 top Download PDF

      A patient presents 12 hours after a thunderclap headache. A contrast cranial CT scan is normal.

      To determine if there is aneurysmal bleeding, the most appropriate next investigation is:

      1. Cranial MRI with diffusion weighted imaging
      2. CSF spectroscopy for bilirubin
      3. CSF spectroscopy for crenated red blood cells
      4. Four vessel cerebral angiogram
      5. Cranial magnetic resonance imaging/angiography (MRI/MRA)



      • 80% causes by ruptured aneurysms
      • Other causes include trauma, AV malformations, vasculitis, dissection, amyloid, bleeding diathesis and illicit drug use (especially cocaine and amphetamines)


      Risk Factors:

      • Smoking
      • HT
      • Alcohol
      • Family history
      • Oestrogen deficiency
      • ?Antithrombotic therapy



      • Ruptured aneurysm --> blood in CSF --> increased intracranial pressure --> thunderclap headache (97%)
      • May be brief LOC, SZ, nausea or vomiting
      • Meningism and lower back pain can occur after several hours
      • Warning leak (sentinel headache) in 30 to 50%
      • Physical exertion may be trigger
      • Lack of lateralising signs
      • Terson’s syndrome = vitreous haemorrhages
      • Retinal subhyaloid haemorrhages


      Hunt and Hess grading system for patients with subarachnoid haemorrhage




      Asymptomatic or mild headache and slight nuchal rigidity


      Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy


      Drowsy or confused, mild focal neurologic deficit


      Stuporous, moderate or severe hemiparesis


      Coma, decerebrate posturing

      Based upon initial neurologic examination; adapted from Hunt, W, Hess, R, J Neurosurg 1968; 28:14.
      From UTD


      • Death (average 51%)
      • Vasospasm
        • Due to release of vasoactive substances from clot lysis
        • Uncommon prior to day 3, peaks day 7-8
        • More likely with large clot, GCS < 14
        • Can lead to infarction
        • Early vasospasm is rare but can occur (likely different mechanism)
      • Hydrocephalus (acute or chronic)
      • Increased ICP
      • Seizures
      • Hyponatraemia
        • Hypothalamic injury --> ADH secretion --> water retention
        • Or could be due to cerebral salt wasting
      • Cardiac abnormalities
        • STD, TWI, prolonged QT, arrhythmias
        • Hypoperfusion of posterior hypothalamus --> centrally mediated release of catecholamines within myocardium --> LV ischaemia
        • Other factors likely involved
      • Rebleeding (highest risk in first 24/24)
          • Higher risk if large aneurysm, high Hunt-Hess grade, sentinel headache



      • CT and LP
      • CT within 12 hours has high sensitivity (close to 100%)
      • LP should always be performed if high clinical suspicion but CT normal
      • Classic findings are elevated opening pressure and RBCs in all tubes
      • Xanthrochromia represents haemoglobin degradation products (means blood in CSF for > 2hours)
      • Spectrophotometry detects blood breakdown products (oxyHb --> metHb --> bilirubin)
      • Highly sensitive when done after 12 hours
      • Negative CT and CSF effectively eliminates the diagnosis of SAH
      • Could consider angiography/MRA if diagnosis still in doubt
      • FLAIR and T2 sequences on MRI have high sensitivity for subacute SAH (ie. Few days after bleed)

      Identifying Aetiology:

      • Cerebral angiography
      • CTA and MRA are useful for screening and presurgical planning but not as good resolution as angiogram – miss aneurysms < 3mm

      Answer is B



      • SAH
      • Sentinel headache
      • Cerebral venous thrombosis
        • Usually also have papilloedema, SZ, bilateral focal deficits and/or decreased GCS
        • Usually gradual onset of headache
        • Usually history of thromboembolic disease
        • CT can be normal
        • LP will have elevated opening pressure, can be elevated lymphocytes, RBCs and protein in 30-50%
        • MRV for diagnosis
      • Cervical artery dissection
        • Headache common presentation
        • Usually gradual and unilateral +/- neck pain
        • Neurological signs
        • CT, LP normal – need U/S or angiography or MRA or CTA
      • Spontaneous intracranial hypotension
        • Orthostatic headaches
        • Nausea/vomiting, dizziness, auditory changes, visual blurring, interscapular pain, radicular pain of ULs
        • Most common cause is CSF leak
        • Thunderclap headache uncommon presentation
        • Dx with MRI (CT, LP normal)
      • Pituitary apoplexy
        • TCH may be predominant feature
        • Other features include ophthalmoplegia, decreased visual acuity, change in mental status
        • Adrenal crisis can occur
        • CT, LP normal
        • Need MRI to diagnose
      • Retroclival haematoma
        • Rare manifestation of severe head and neck injuries where there is atlantoaxial dislocation
        • Spontaneous haemorrhage can also occur
      • Ischaemic stroke
        • Rarely
      • Acute hypertensive crisis
        • Headaches more commonly throbbing and indistinct
        • MRI more sensitive than CT at showing white matter changes consistent with reversible posterior leukoencephalopathy syndrome
      • Colloid cyst of third ventricle
        • Cyst can suddenly impede flow of CSF results in obstructive hydrocephalus
        • Headaches usually of sudden onset and resolution lasting seconds to 1 day
        • Associated nausea, vomiting, changes in mental state, SZ, coma and death can occur
        • Dx by CT or MRI
      • Infections
        • Usually gradual onset, rarely TCH with meningitis
        • Acute sinusitis can rarely cause TCH
      • Reversible cerebral vasoconstriction syndrome
        • Group of disorders characterised by reversible vasospasm of cerebral arteries
        • Dx by angiography/MRA
        • Usually self-limiting
      • Primary TCH
        • Benign, potentially recurrent headache disorder
        • No organic pathology
        • Diagnosis of exclusion


      Neurology: subarachnoid haemorrhage | headache


      Question 11 top

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      Question 15 top Download PDF

      In patients with untreated post-transfusion hepatitis C, the lifetime risk of progression to cirrhosis best approximates:

      1. 1%
      2. 5%
      3. 20%
      4. 50%
      5. 80%



      1. Acute and chronic hepatitis
      2. Acute usually asymptomatic or mild symptoms for few weeks
      3. 60 – 80% develop chronic hepatitis
      4. 30% of those with chronic hepatitis will progress to cirrhosis over 20 to 30 years
      5. Therefore 30% of the 80% of patients with hepatitis C develop cirrhosis = 24%


      Answer = C


      1. Most asymptomatic
      2. Jaundice in < 25%
      3. Malaise, nausea, RUQ pain
      4. Symptoms (if present) can last 2 to 12 weeks
      5. Fulminant hepatic failure rare but more likely if also infected with hepatitis B



      1. Spontaneous clearance of virus after it has persisted for 6/12 is uncommon
      2. Children more likely to clear virus
      3. Most patients asymptomatic or mild non-specific symptoms – fatigue, nausea, anorexia, myalgia, arthralgia, weakness, weight loss
      4. Severity of symptoms do not correlate with disease activity
      5. ALT and AST levels are variable, may be normal, usually only mildly elevated
      6. Cirrhosis suggested by elevated bilirubin, hypoalbuminaemia, low platelets


      Hepatic Complications

      1. Hepatic decompensation (risk is 4% per yr in pts w cirrhosis)
        1. Ascites
        2. Variceal bleeding
        3. Encephalopathy
        4. Jaundice
      2. Survival after diagnosis of decompensated liver disease estimated at 50% at five years
      3. Hepatocellular carcinoma (up to 3% per year in pts with cirrhosis)
        1. Cirrhosis is major risk factor
        2. Uncommon in hep C pts without cirrhosis (cf. hepatitis B)
        3. Most deaths due to decompensation rather than HCC



      Factors Predictive of Progression

      1. Younger age of HCV infection results in increased risk
      2. Children results in decreased risk
      3. Host immune response
      4. HIV co-infection
      5. Infection from blood transfusion results in ?increased risk
      6. Marijuana use results in increased risk
      7. Higher BMI results in steatosis/fibrosis results in increased risk
      8. Alcohol results in increased risk
      9. Ethnic background
      10. Viral diversity


        • Best clinical predictor of disease progression is liver biopsy – amount of inflammation and fibrosis
        • Mild inflammation, no fibrosis = 1.2% annual risk of progression to cirrhosis
        • Moderate inflammation = 4.6% annual risk, 90% cirrhosis by 20 years
        • Severe inflammation and fibrosis = nearly all develop cirrhosis by 10 years

        Extrahepatic Manifestations of Chronic Hepatitis C

          • Haematological diseases (eg: essential mixed cryoglobulinaemia, lymphoma)
          • Renal disease (eg: membranoproliferative GN)
          • Autoimmune disoriders (eg: thyroiditis, autoantibodies)
          • Dermatological conditions (eg: porphyria, lichen planus)
          • Diabetes mellitus


          Gastroenterology: viral hepatitis Question repeated 2003 paper one question 19


          Question 16 top

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          Question 19 top Download PDF

          Multiple sclerosis is a disease primarily of the:

          1. Oligodendrocyte
          2. Schwann cell
          3. Astrocyte
          4. Axon
          5. Neural cell body


          Oligodendrocytes are a variety of neuroglia. Their main function is the myelination of axons exclusively in the central nervous system of the higher vertebrates, a function performed by Schwann cells in the peripheral nervous system. A single oligodendrocyte can extend to up to 50 axons, wrapping around approximately 1 mm of each and forming the myelin sheath.
          Glial cells, commonly called neuroglia or simply glia, are non-neuronal cells that provide support and nutrition, maintain homeostasis, form myelin, and participate in signal transmission in the nervous system. In the human brain, glia are estimated to outnumber neurons by about 10 to 1.[
          Astrocytes are sub-type of the glial cells in the brain. They are also known as astrocytic glial cells. Star-shaped, their many arms span all around neurons. Astrocytes are classically identified histologically by their expression of glial fibrillary acidic protein (GFAP). Previously in medical science, the neuronal network was considered the only important one, and astrocytes were looked upon as gap fillers. But recently they have been reconsidered and are now thought to play a number of active roles in the brain.


          • Structural: involved in the physical structuring of the brain.
          • Metabolic support: they provide neurons with nutrients such as glucose.
          • Blood-brain barrier: the astrocyte end-feet encircling endothelial cells form part of the blood-brain barrier.
          • Transmitter reuptake and release: astrocytes express plasma membrane transporters such as glutamate transporters for several neurotransmitters, including glutamate, ATP and GABA. More recently, astrocytes were shown to release glutamate or ATP in a vesicular, Ca2+-dependent manner.
          • Regulation of ion concentration in the extracellular space: astrocytes express potassium channels at a high density. When neurons are active, they release potassium, increasing the local extracellular concentration. Because astrocytes are highly permeable to potassium, they rapidly clear the excess accumulation in the extracellular space. If this function is interfered with, the extracellular concentration of potassium will rise, leading to neuronal depolarization by the Goldman equation. Abnormal accumulation of extracellular potassium is well known to result in epileptic neuronal activity.
          • Modulation of synaptic transmission: in the supraoptic nucleus of the hypothalamus, rapid changes in astrocyte morphology have been shown to affect heterosynaptic transmission between neurons.
          • Vasomodulation: astrocytes may serve as intermediaries in neuronal regulation of blood flow.
          • Promotion of the myelinating activity of oligodendrocytes: electrical activity in neurons causes them to release ATP, which serves as an important stimulus for myelin to form. Surprisingly, the ATP does not act directly on oligodendrocytes. Instead it causes astrocytes to secrete LIM, a regulatory protein that promotes the myelinating activity of oligodendrocytes. This suggest that astrocytes have an executive-coordinating role in the brain.

          Neurons (also known as neurones and nerve cells) are electrically excitable cells in the nervous system that process and transmit information. In vertebrate animals, neurons are the core components of the brain, spinal cord and peripheral nerves.
          Neurons are typically composed of a soma, or cell body, a dendritic tree and an axon. The majority of vertebrate neurons receive input on the cell body and dendritic tree, and transmit output via the axon. However, there is great heterogeneity throughout the nervous system and the animal kingdom, in the size, shape and function of neurons.
          An axon or nerve fiber, is a long, slender projection of a nerve cell, or neuron, that conducts electrical impulses away from the neuron's cell body or soma.
          Neurons communicate via chemical and electrical synapses, in a process known as synaptic transmission. The fundamental process that triggers synaptic transmission is the action potential, a propagating electrical signal that is generated by exploiting the electrically excitable membrane of the neuron. This is also known as a wave of depolarization.

          Answer: A


          Neurology: multiple sclerosis


          Question 20 top

          Question 21 top Download PDF

          Which one of the following is least likely to be associated with a reduced risk of mother-to-child transmission of human immunodeficiency virus (HIV)?
          A. Maternal plasma HIV RNA concentration (viral load) <1000 copies/mL.
          B. Maternal CD4+ T cell count >500 cells/mm3.
          C. Maternal antiretroviral therapy.
          D. Avoidance of breastfeeding.
          E. Elective Caesarean delivery

          Transmission can occur during 3 periods: prenatal or in utero, perinatal and delivery, and postnatal.

          • Prenatal transmission appears to occur in 15-38% of vertically acquired HIV infections.
          • Most vertical infections occur during delivery.
          • Although the concentration of HIV in the cervicovaginal secretions is lower in women with lower viral loads, HIV particles exist in the cervicovaginal secretions of women with undetectable viral loads.
          • Any factor that reduces contact between the neonate and maternal blood or cervicovaginal secretions reduces vertical transmission. This observation is supported by the decreased transmission rates with elective cesarean delivery. However, this protective effect occurs only when women were treated with zidovudine during pregnancy. Because the postpartum complication rate is higher for elective cesarean delivery, whether regimens that use highly active antiretroviral therapy can substantially reduce vertical transmission during vaginal delivery, thereby improving both child and mother morbidity and mortality rates, remains to be determined.
          • Postnatal vertical transmission occurs with breastfeeding and has a transmission incidence of 0.7% per month.
          • Although recommendations state that women infected with HIV should not breastfeed, the World Health Organization advises women in developing countries to breastfeed because death rates from infectious diarrhea and dehydration are higher than death rates from AIDS.

          The CDC has approved the following regimen to reduce vertical HIV transmission:

          • Antepartum women - Zidovudine 300 mg by mouth twice a day (In women who present during the prenatal period, zidovudine treatment should be started regardless of the use of other antiretroviral agents and the history of zidovudine resistance.)
          • Intrapartum women - Continuous IV zidovudine at a rate of 1 mg/kg/h (In women who present in labor, the intrapartum regimen should be started.)
          • Neonates - Zidovudine within their first 6-12 hours of life until aged 6 weeks
          Period Factors That Increase Risk Factors That Decrease Risk

          Acute HIV infection
          Viral load greater than 10,000
          Cigarette smoking
          Illicit injection drug use

          Viral load less than 1,000
          Zidovudine treatment
          Neutralizing antibodies
          Perinatal 4 h
          Emergency cesarean section
          Surgical delivery
          Scalp electrodes
          Elective cesarean delivery with zidovudine treatment
          Neonatal Prematurity
          Low birth weight
          First-born twins
          Full term-term
          Second-born twin
          Postdelivery Breastfeeding None
          So A, C, D and E all reduce the incidence of vertical transmission of HIV. The correct answer is therefore B - no evidence that CD4 count greater than 500 reduces transmission.


          Infectious Diseases- HIV


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          Question 26 top Download PDF

          QUESTION 26

          In the acute management of oesophageal variceal bleeding, which of the following is least likely to control bleeding?

          1. Intravenous omeprazole
          2. Intravenous octreotide
          3. Endoscopic band ligation
          4. Endoscopic injection therapy
          5. Intravenous vasopressin



          1. Accounts for about 1/3 deaths related to cirrhosis
          2. Need to:
            1.  Identify patients at risk and treat prophylactically
            2.  Treat active bleeding
            3. Prevent re-bleeding



          1. A number of treatment options, none of which are ideal



          1. Constricts mesenteric arterioles and decreases portal venous inflow à reduced portal pressures
          2. Achieves initial haemostasis in 60-80% but little effect on early re-bleeding
          3. Does not improve survival
          4. Risk of myocardial, cerebral, bowel and limb ischaemia
          5. Combining with nitroglycerin may reduce side effects and further reduces portal pressures


          Somatostatin (Octreotide)

          1. Inhibits release of vasodilator hormones (such as glucagon) à indirectly causes splanchnic vasoconstriction and decreased portal inflow
          2. Superior to vasopressin and balloon tamponade
          3. Few side effects
          4. No proven benefit on mortality


          Endoscopic Treatment

          1. Definitive treatment of choice
          2. Sclerotherapy (injection)
          3. Variceal band ligation
          4. Both as good as octreotide and used in combination with octreotide are better
          5. Band ligation may have long-term benefits over sclerotherapy but can be more difficult to do during acute bleed
          6. Less complications with band ligation (eg: ulceration, bleeding, strictures, portal hypertensive gastropathy, perforation, sepsis, aspiration)


          Balloon Tamponade

          1. Good for short-term haemostasis when endoscopic therapies fail
          2. High risk of re-bleeding when deflated



          1. Portosystemic shunts can be used in emergency cases where bleeding cannot be controlled
          2. Surgical shunts or TIPS (latter generally for pts not fit for surgery)



          1. Recommended for all patients with upper GI bleeding and cirrhosis prior to endoscopy
          2. Most common infections are UTIs, SBP, LRTIs and bacteraemia
          3. Not clear which is best antibiotic – most use norfloxacin/ciprofloxacin +/- augmentin DF and ceftriaxone


          Other Complications

          1. Aspiration – NGT
          2. Renal Failure – volume replacement
          3. Encephalopathy – lactulose
          4. Alcohol withdrawal/nutritional deficiencies


          Answer: A – omeprazole is not an effective treatment for acute variceal bleeding


          Gastroenterology: CLD complications


          Question 27 top Download PDF

          Which of the following antibiotics would be the most appropriate oral medication for the outpatient treatment of a wound infection caused by E.coli and Pseudomonas aeruginosa?

          1. Moxifloxacin
          2. Gatifloxacin
          3. Ciprofloxacin
          4. Linezolid
          5. Amoxycillin/clavulanate



          Linezolid is an oxazolidinone which inhibits protein synthesis by binding to the 50S ribosomal subunit of the bacteria and preventing formation of a functional 70S complex.
          It is active against gram positive organisms but not against gram negatives so would be ineffective against E.coli or P.aeruginosa. Note that linezolid is a weak MOAI – has potential to cause serotonin syndrome.


          Amoxycillin/clavulanate is effective against some gram negative organisms such as E.coli, H.influenzae, Proteus, Klebsiella, Moraxella and N. meningitides but not against Pseudomonas.


          Moxifloxacin, ciprofloxacin and gatifloxacin (along with norfloxacin and orfloxacin) are the quinolones which can effectively treat most gram negative organisms including Pseudomonas. They inhibit bacterial DNA synthesis by blocking DNA gyrase and topoisomerase IV – bactericidal.

          Gatifloxacin is not covered by the PBS and costs about $120 for 7 tablets.

          Ciprofloxacin and moxifloxacin both require PBS approval.

          Moxifloxacin is approved for CAP, acute bacterial exacerbations of chronic bronchitis or acute bacterial sinusitis where other treatments have failed or are inappropriate. The cost is $45 for 5 tablets (PBS).

          Ciprofloxacin is approved for any infection proven to be due to pseudomonas or another gram negative organism which is resistant to all other antimicrobials. The cost is $50 for 14 tablets (PBS).

          Ciprofloxacin is particularly active against gram negative organisms including pseudomonas (but N.gonorrhoea is now resistant). Moxifloxacin has more activity against gram positive organisms but is less effective against pseudomonas.

          Norfloxacin has poor systemic availability and is reserved for UTIs or traveller’s diarrhea.

          Ciprofloxacin is therefore the only quinolones approved for treatment of pseudomonas infections and is the most effective in treating this organism – answer C.


          References: Therapeutic Guidelines, Australian Medicines Handbook – Anti-infectives – Organism susceptibility to antimicrobials


          Infectious Disease : skin and soft tissue infection

          Pharmacology: Infections

          Question 28 top

          Question 29 top Download PDF

          A patient with aortic regurgitation has the following haemodynamic measurements:

          Cardiac output (CO) 7.5L/min
          Heart rate (HR) 75/minute
          Left ventricular end-diastolic volume (LVEDV) 200mL
          Left ventricular end-systolic volume (LVESV) 50mL

          The regurgitant fraction is defined as the ratio of the regurgitant volume to the total volume flowing through the valve with each beat.

          The regurgitant fraction in this patient is:

          A. 25%
          B. 33%
          C. 50%
          D. 67%
          E. 75%

          Cardiac output per beat = cardiac output per minute / heart rate
          = 7500mL / 75
          = 100mL/beat

          LVEDV - LVESV = 150mL which is the amount of blood pumped out with each systole.

          But 50mL of this must be regurgitated as CO = 100mL (150mL – 100mL = 50mL regurgitant volume)

          So regurgitant fraction = 50mL / 150mL = 33%

          Answer is B.


          Cardiolgy - Aortic Regurgitation


          Question 30 top

          Question 31 top

          Question 32 top Download PDF

          A 55yo man has the following lung function test results:

          FEV1 2.0L (61% predicted)
          FVC 2.6L (68% predicted)
          FEV1/FVC 77% (85% predicted)
          Total lung capacity 72% predicted
          Residual volume 75% predicted
          DLCO 64% predicted
          KCO 110% predicted

          His BMI is 31kg/m2.
          Which of the following is the best explanation for these results?

          A. Previous lobectomy
          B. Obesity
          C. Pulmonary fibrosis
          D. Asthma
          E. Pulmonary haemorrhage

          The key to this question is the DLCO and KCO. Without this the results would look like a standard restrictive deficit (FVC less than 80%, FEV1/FVC greater than 70%).
          DLCO measures the ability of CO to diffuse across the alveolar-capillary membrane.
          KCO is the DLCO corrected for alveolar volume, or the DLCO per unit lung volume.

          decreased DLCO, Normal or increased KCO
          • Decreased lung volume
            eg: muscle weakness/chest wall disease
            lung resection
          decreased DLCO, decreased KCO
          • Due to parenchymal lung or pulmonary vascular disease
            eg: ILD, intrapulmonary shunt, anaemia, significant cardiac failure

          Measures of gas exchange can be unreliable in obstructive disease due to gas trapping, but would expect a reduction in both DLCO and KCO with conditions such as emphysema, CF and BOOP.
          Note DLCO is usually preserved in chronic bronchitis and asthma.

          Increased DLCO
          • Alveolar haemorrhage
          • Polycythaemia
          • Left-right cardiac shunt
          • Supine position (change in distribution of pulmonary blood flow)
          • Mild cardiac failure (increased pulmonary blood flow
          Answer A. Previous lobectomy


          Respiratory - Essential respiratory investigations

          Question 33 top Download PDF

          In patients dying of Sudden Unexpected Death in Epilepsy (SUDEP), the most likely mechanism of death is:

          1. Aneurysmal rupture
          2. Central hypoventilation
          3. Ventricular fibrillation
          4. Neurogenic pulmonary oedema
          5. Laryngospasm


          • Sudden unexpected death in epilepsy
          • Unexpected, non-traumatic, non-drowning death in an individual with epilepsy in which the post-mortem does not reveal an anatomical or toxicological cause of death; death not a direct result of seizure or status
          • Evidence of recent SZ does not exclude diagnosis of SUDEP
          • Causes 2 to 18% of deaths in patients with epilepsy
          • Incidence increases with severity of epilepsy
          • Patients with epilepsy have 2-3x increased mortality rate than general population

          Risk Factors:

          • Young age at onset of epilepsy
          • Male > Female
          • Frequent GTCS
          • Intractable epilepsy
          • Right-sided mesial temporal SZ greater risk than left-sided
          • Low IQ
          • Excess alcohol
          • ?Poor compliance with AEDs
          • Multiple AEDs


          • Likely multifactorial
          • Respiratory events (airway obstruction, central apnoea and neurogenic pulmonary oedema) are probable terminal events
          • Possible causes include:
            • Cardiac arrhythmia
            • Central apnoea
            • Neurogenic pulmonary odema


          • Education, compliance
          • Aggressive treatment of refractory epilepsy
          • Supervision at night (ie. Someone sleeping in same room) may reduce risk

          Answer: B


          Neurology: epilepsy


          Question 34 top

          Question 35 top

          Question 36 top Download PDF

          The most likely cause of thyrotoxicosis producing the appearance shown in this thyroid scintiscan is:

          1. Activating mutation of the TSH receptor
          2. Abnormal Gs-alpha protein
          3. Thyroid-stimulating immunoglobulin
          4. ret prot-oncogene mutation
          5. Coxsackievirus infection


          This patient has a hot nodule ie. an autonomously-functioning (toxic) adenoma.

          Hyperfunctioning Solitary Nodule
          • Due to mutations that stimulate the TSH-R signaling pathway
          • Most patients have acquired somatic, activating mutations in the TSH-R
          • Mutations induce receptor coupling to Gs, increasing cyclic AMP levels and leading to enhanced thyroid follicular cell proliferation and function
          • Less commonly, somatic mutations are identified in Gs
          • These mutations impair GTP hydrolysis, also causing constitutive activation of the cyclic AMP signaling pathway
          • Similar to mutations seen in McCune-Albright syndrome or in a subset of somatotrope adenomas
          • Activating mutations in either the TSH-R or the Gs subunit genes are identified in >90% of patients with solitary hyperfunctioning nodules
          • Thyrotoxicosis is usually mild
          • Disorder is suggested by the presence of the thyroid nodule and by the absence of clinical features suggestive of Graves' disease or other causes of thyrotoxicosis
          • A thyroid scan provides a definitive diagnostic test, demonstrating focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of the gland, as activity of the normal thyroid is suppressed
          • Radioiodine ablation is usually the treatment of choice
          • Because normal thyroid function is suppressed, 131I is concentrated in the hyperfunctioning nodule with minimal uptake and damage to normal thyroid tissue
          • Relatively large radioiodine doses have been shown to correct thyrotoxicosis in about 75% of patients within 3 months
          • Hypothyroidism occurs in <10% of patients over the next 5 years
          • Surgical resection is also effective (usually lumpectomy or lobectomy only)
          • Medical therapy using antithyroid drugs and beta blockers can normalize thyroid function but is not an optimal long-term treatment
          • Ethanol injection under ultrasound guidance has been used successfully in some centres to ablate hyperfunctioning nodules

          So the answer is A – activating mutation of the TSH-R
          B is a possible cause but is less common than A
          C and D are associated with malignancies, which are rarely hot on thyroid scans
          E – don’t really know why they put this one in there. Couldn’t find any association between Coxsackie and thyroid

          • More common in women
          • More common in iodine-deficient regions
          • Most are polyclonal (ie. arising from all or most cells in a tissue)
          • Most patients asymptomatic and by definition euthyroid
          • Can develop compressive symptoms if very large
          • Usually conservative management
          • Can use radioiodine to decrease goitre size
          • Surgery if compressive symptoms
          • Molecular basis for autonomy unknown
          • Some polyclonal, some monoclonal
          • TSH-R or Gs-alpha mutations not normally seen
          • Subclinical hyperthyroidism or mild thyrotoxicosis
          • TSH low, T4 normal or mildly increased, T3 increased
          • Thyroid scan – heterogeneous uptake
          • Surgery is definitive treatment
          • Antithyroid drugs can normalise thyroid function but goitres enlarge
          • Radioiodine can treat areas of autonomy and decrease goitre mass but some autonomy remains
          • Follicular adenomas
            • Marcrofollicular (colloid)
            • Normofollicular (simple)
            • Microfollicular (fetal)
            • Trabecular (embryonal)
            • Hurthle cell variant (oncocytic)
          • Risk of malignancy low for macrofollicular and normofollicular adenomas
          • Higher with microfollicular, trabecular and Hurthle cell adenomas
          • Treatment with TSH suppression (levothyroxine) should reduce size
          • Increasing incidence with age up to about 50yrs
          • Worse prognosis if <20yrs or >65yrs
          • Papillary and follicular carcinomas have good prognosis in early stage
          • Undifferentiated carcinomas (such as anaplastic) have poor prognosis


          Follicular epithelial cell
          • Well-differentiated carcinomas
            • Papillary carcinomas (80-90%)
              • Pure papillary
              • Follicular variant
              • Diffuse sclerosing variant
              • Tall cell, columnar cell variants
            • Follicular carcinomas  (5-10%)
              • Minimally invasive
              • Widely invasive
              • Hurthle cell
              • Insular carcinoma
          • Undifferentiated (anaplastic) carcinomas
          C cell (calcitonin-producing)
          • Medullary thyroid cancer   (10%)
            • Sporadic
            • Familial
            • MEN 2
          Other malignancies  (1-2%)
          • Lymphomas
          • Sarcomas
          • Metastases
          • Others
          Oncogenes and Tumour Suppressor Genes
          • Mutations of the RET oncogene (chromosome 10) lead to overexpression of the tyrosine kinase receptor
          • RET mutations in 20-40% of papillary carcinomas
          • TRK1 is another gene for tyrosine kinase
          • Mutations in TRK1 are also associated with papillary carcinoma
          • Identifying these mutations does not help with prognosis or treatment
          • RAS oncogene mutations have been found in 20-30% of thyroid neoplasms including adenomas
          • RET point mutations associated with medullary carcinoma/MEN2 leading to constitutive activity of tyrosine kinase
          Papillary Carcinoma
          • Most common
          • Tends to be multifocal and to invade locally and into adjacent structures
          • Mets via lymphatic system (commonly lung)
          • Excellent prognosis if identified early
          • Most cases are identified early
          Follicular Carcinoma
          • More common in iodine-deficient regions
          • Difficult to diagnose by FNA as hard to distinguish between benign and malignant
          • Haematogenous spread (bone, lung, CNS)
          • Tends to present later
          • Worse prognosis = age >50, nodule >4cm, Hurthle cell, marked vascular invasion, metastases
          Staging of Papillary or Follicular Carcinomas


          <45 years

          >45 years

          Stage I

          Any T, any N, M0

          T1, N0, M0

          Stage II

          Any T, any N, M1

          T2 or T3, N0, M0

          Stage III


          T4, N0, M0
          Any T, N1, M0

          Stage IV


          Any T, any N, M1

          T1≤1cm; 1cm<T2≤4cm; T3>4cm; T4 direct invasion through thyroid capsule
          N0 = no lymph node involvement; N1 = lymph node involvement
          M0 = no mets; M1 = mets

          Treatment of Well-Differentiated Carcinomas
          • Surgery
          • TSH suppression therapy
          • Radioiodine treatment (usually for higher risk patients)
          • Most have TSH receptors so that is why TSH suppression and radioiodine treatments are effective
          Anaplastic Cancer
          • Poor prognosis
          • Most patients die within 6 months
          • Usually poor uptake of radioiodine
          • Chemotherapy generally ineffective
          • XRT can be attempted
          • All anaplastic cancers are stage IV
          Thyroid Lymphoma
          • Often arises on background of Hashimoto’s thyroiditis
          • Rapidly expanding thyroid mass suggests this diagnosis
          • Often highly sensitive to radiation
          • Surgical resection is not advised as initial therapy as it may allow spread of lymphoma to other areas
          Medullary Thyroid Carcinoma
          • Sporadic or familial
          • Elevated serum calcitonin provides evidence of residual or recurrent disease
          • Should consider testing all patients for RET mutations - family screening
          • Surgical management
          • Chemo and XRT as palliative measures
          • Stage I = T1, N0, M0
          • Stage II = T2-T4, N0, M0
          • Stage III = Any T, N1, M0
          • Stage IV = Any T, any N, M1



          Endocrinology:thyroid nodule and goitre


          Question 37 top

          Question 39 top

          Question 40 top

          Question 41 top Download PDF

          An athlete has the following physiological measurements performed at rest and at maximal exercise. Which of these is most likely to remain unchanged from rest to maximal exercise?

          A. Coronary sinus oxygen concentration
          B. Ration of VO2 (rate of oxygen consumption) to VCO2 (rate of production of CO2)
          C. Coronary sinus lactate concentration
          D. Mixed venous oxygen concentration
          E. Systolic blood pressure

          answer is A


          Exercise Capacity

          • VO2 max is symptom-limiting maximum oxygen uptake
          • Increases linearly with work rate
          • Slope not effected by age/fitness etc
          • True max VO2 only occurs in a few people and is predicted by age, gender, height and lean body weight
          • VO2 increases with training

          Fick equation - reference uptodate

          Skeletal Muscle

          • Motor unit = single motor neuron and all the muscle fibres it innervates (1000 to 2000)
          • Each neuron will innervate only one type of muscle fibre (type I or II)
          • Type I fibres are slow twitch and have high oxidative capacity, are fatigue-resistant and are recruited for endurance exercise
          • Type II fibres are fast twitch and have a high glycolytic capacity, recruited for short bursts of rapid heavy exercise
          • Fibre type mix is genetically determined

          Energy Sources

          • ATP hydrolysed to ADP to allow cross bridging of actin and myosin ? muscle contraction
          • Enzyme that catalyses this reaction is actomyosin-ATPase
          • Intracellular stores of ATP are small and must be continually replenished
          • Three energy sources utilised:
            • Phosphocreatine shuttle
            • Anaerobic sources
            • Oxidative phosphorylation
          • Phosphocreatine is split by creatine kinase to make creatine and ATP
          • Training and oral loading of carbohydrates can improve PCr kinetics and exercise performance
          • Anaerobic Embden-Meyerhoff glycolysis
            • Glucose and ADP converted to lactate and ATP by adenylate kinase
          • Occurs when there is an imbalance between oxygen demand and production
          • Oxidative phosphorylation of glycogen and free fatty acids, improved by training


          Peripherally due to

          • Accumulation of byproducts
          • Depletion of high energy phosphates
          • Depletion of glycogen substrate


          • Lactate threshold is the metabolic rate at which a sustained rise in blood lactate detected
          • Lactate threshold is the VO2 at which pyruvate (and therefore lactate) production exceeds the ability of the Kreb’s cycle to metabolise them
          • LT varies with cardiovascular fitness


          VO2 = CO x (paO2 - pvO2)

          CO = HR x SV

          • Max HR = 220 - age
          • HR increases linearly versus VO2
          • SV increases in a hyperbolic fashion versus VO2
          • Can be increased with training

          SV = CC x VR

          • Rise in SV due to increased CC and increased LVEDV (as per Frank-Starling mechanism)
          • Venous return enhanced by venoconstriction, greater negative intrathoracic pressures and the pumping action of limbs
          • Diastolic filling limited by the constraints of the pericardium


          • CO generally limits VO2 max in healthy adults
          • Systolic BP increases due to muscle chemoreflex but is attenuated by arterial baroreceptor function
          • DBP usually remains near normal resting values

          BP = HR x TPR

          • Decreased TPR means SBP does not increase as much as CO
          • Rightward shift of oxygaemoglobin dissociation curve with acidosis and peripheral vasoregulation means oxygen released more easily to skeletal muscles
          • As such femoral venous pO2 is lowered and the systemic oxygen extraction ratio is high ([PaO2 – PvO2] / PaO2)

          Pulmonary Circulation

          • With exercise the pulmonary vascular resistance falls due to passive distension and vasodilatation (mediated by NO)
          • This means that pressure gradient across pulmonary circulation does not increase much


          • Minute ventilation increases due to increased RR and increased tidal volume
          • Ventilatory threshold is the point where minute ventilation increases out of proportion to VO2 due to accumulation of lactate (lactate threshold) and metabolic acidosis
          • VO2 max usually limited by cardiac factors, not ventilation
          • Minute ventilation requirement during exercise is determined by:
            • CO2 output
            • PaCO2 “set point”
            • Physiological dead space:tidal volume ratio
          • PaCO2 usually regulated to normal levels until late in exercise when metabolic acidosis occurs and RR increases to compensate ? fall in CO2
          • PaO2 remains near normal but PvO2 is reduced
          • Oxygenation increases due to:
            • Increased alveolar PO2
            • Decreased number of low V/Q units
            • Increased surface area for O2 diffusion
            • Smaller right-to-left shunt fraction
            • Hyperventilation


          • 15-fold increase in O2 uptake with intense exercise
          • 10-fold increase in minute ventilation
          • 5-fold increase in CO
          • 3-fold increase in systemic O2 extraction

          A. Coronary sinus oxygen concentration remains much the same
          B. VO2 increases more than VCO2 increases (??)
          C. Lactate concentration increases
          D. Venous oxygen concentration decreases
          E. Systolic blood pressure increases

          So answer is A


          Cardiology - Normal cardiac anatomy and physiology

          Respiratory - Basic respiratory and sleep physiology


          Question 42 top

          Question 43 top Download PDF

          QUESTION 43

          Which one of the following colonic polyps has the highest potential for malignant transformation?

          1. Hyperplastic
          2. Tubular
          3. Villous
          4. Hamartomatous
          5. Peutz-Jegher




          1. Neoplastic
            1. Adenomas
            2. Carcinomas
          2. Hamartomatous
          3. Non-neoplastic
            1. Hyperplastic
            2. Mucosal
            3. Inflammatory pseudopolyps
          4. Submucosal (neoplastic or non-neoplastic)



          1. Typically left colon
          2. <5mm
          3. Rarely develop into colorectal cancers


          Hyperplastic Polyposis Syndrome

          1. Characterised by multiple large and/or proximal hyperplastic polyps
          2. Increased risk of CRCa
          3. Molecular basic not clear


          Mucosal Polyps

          1. Usually small (<5mm)
          2. Histologically resemble normal mucosa
          3. No clinical significance


          Inflammatory Pseudopolyps

          1. Result of mucosal ulceration and regeneration that occurs in IBD
          2. Usually multiple
          3. Not dysplastic
          4. Not an independent risk factor for CRCa


          Submucosal Polyps

          1. A variety of submucosal lesions including lymphoid aggregates, lipomas, leiomyomas, pneumatosis cystoids intestinalis, haemangiomas, fibromas, carcinouds and metastatic lesions can give a polypoid appearance to the overlying mucosa


          Hamartomatous Polyps

          1. Juvenile polyps and Peutz-Jeghers polyps are both hamartomatous lesions
          2. Juvenile polyps consist of lamina propria and dilated cystic glands rather than increased numbers of epithelial cells
          3. High likelihood of bleeding
          4. Familial juvenile polyposis is a rare condition with multiple juvenile polyps with an increased risk for CRCa
          5. Peutz-Jeghers polyps are lesions of glandular epithelium supported by smooth muscle cells that is contiguous with the muscularis mucosa
          6. Almost always associated with the Peutz-Jeghers syndrome
          7. Usually benign but can undergo malignant transformation


          Adenomatous Polyps

          1. 2/3 colonic polyps are adenomas
          2. Dysplastic by definition à potential for malignant transformation
          3. Nearly all CRCas arise from adenomas
          4. Only a small minority of adenomas progress to Ca
          5. Age is major risk factor for adenomas
          6. Tubular adenomas (80%)
            1. Must be at least 75% tubular
          7. Villous adenomas (5-15%)
            1. Must be at least 75% villous
          8. Tubulovillous adenomas (5-15%)
          9. Sessile or pedunculated


          Risk Factors for Colorectal Cancer

          1. Adenomatous polyps >1cm
          2. Adenomatous polyps with high grade dysplasia
          3. Adenomatous polyps with >35% villous histology
          4. Adenomatous polyps with invasive cancer


          Serrated Adenomas

          1. Mixed features of both hyperplastic and adenomatous polyps
          2. Malignant potential
          3. Managed like adenomatous polyps


          Management of Colonic Adenomas

          1. If adenomas >1cm or villous adenomas are found during sigmoidoscopy, full colonoscopy should be performed
          2. Probably should also do colonoscopy for tubular adenomas unless multiple comorbidities
          3. If polyps >2cm removed, follow up colonoscopy in 3-4 months to ensure full removal
          4. 3-5 year surveillance with colonoscopy is reasonable for pts with adenomas completely removed


          Answer: C


          Gastroenterology: colorectal ca


          Question 44 top Download PDF

          A previously well 32yo man presents with progressive lethargy and no other symptoms. Physical examination shows him to have an enlarged spleen 6cm below the left costal margin. There is no jaundice or lymphadenopathy and he is not clinically anaemic.

          The full blood examination shows:

                          Haemoglobin                        125 g/L                                  [128-175]
                          Mean cell volume                95 fL                                       [80-97]
                          White cell count                  85.5 x 109/L                          [3.9-12.7]
                          Platelet count                       525 x 109/L                           [150-396]

          The blood film is shown below.

          The most likely marrow cytogenetic abnormality is:

          1. Hyperdiploidy
          2. t(9;22)
          3. t(15;17)
          4. 5q minus
          5. Trisomy 21


          The blood film shows lots of myeloid cells at different stages of development. This indicates CML. The cytogenetic change diagnostic of CML is translocation of chm 9 and 22 to produce the Philadelphia chromosome.


          Haematology: Leukaemia


          Question 45 top Download PDF

          QUESTION 45

          A 37yo man presents to the emergency department with symptoms of meningitis. Gram stain of the CSF reveals the presence of gram-negative diplococci.

          His 12-week pregnant partner should receive which one of the following as prophylaxis?

          1. Ciprofloxacin
          2. Ceftriaxone
          3. Penicillin
          4. Meningococcal vaccine
          5. Erythromycin


          Chemoprophylaxis is used for N.meningitidis and H.influenzae meningitis. Haemophilus is a gram negative rod, not a diplococcus. N.meningitidis is a gram negative diplococci, however.

          Chemoprophylaxis for meningococcal is:

          CEFTRIAXONE 250mg IM                      Preferred during pregnancy
          Single dose


          CIPROFLOXACIN 500mg PO                 Preferred for women on OCP
          Single dose


          RIFAMPICIN 600mg bd for 2 days          Preferred in children

          For H.influenzae the preferred antibiotic is rifampicin 600mg daily for 4 days (Ceftriaxone 1g IM daily for 2 days is the alternative but data is limited on efficacy).

          Answer: B

          Reference: Therapeutic guidelines


          Infectious Disease: Meningitis

          Question repeated2003 paper one question 60


          Question 46 top Download PDF

          A 66yo man with a 40 pack year smoking history has the following spirometry:

          FEV1 0.65L 24% predicted
          FVC 2.10L 60% predicted
          FEV1/FVC 31%

          His BMI is 30kg/m2.
          Which of the following is the most likely explanation for the observed reduction in FVC?

          A. Extrapulmonary restriction due to obesity
          B. Extrapulmonary restriction due to altered operating length of the diaphragm
          C. Intapulmonary restriction due to reduced lung compliance
          D. Gas trapping due to increased airway closure
          E. Gas trapping due to reduced expiratory time

          The spirometry shows an obstructive defect ( FEV1/FVC is < 70%) with a restrictive component (FVC < 80%).

          The obstructive defect is enough to diagnose this patient with COPD (assuming no reversibility which would give a diagnosis of asthma).

          Gas trapping is common in COPD and will produce a restrictive defect in lung function tests.

          Given that this patient has severe COPD with only a mild restrictive component the most likely cause is gas trapping.

          This is due to increased airway closure (obstruction).

          It is not possible with these test results to exclude an underlying restrictive defect due to one of the other options but it is much less likely.

          To confirm gas trapping as the cause would need to do static lung volumes:
          • Reduced FVC
          • Proportional increase in residual volume (due to trapped gas)
          • Therefore total lung capacity and functional residual capacity remain normal
          In restrictive lung disease:
          • Reduced FVC
          • Reduced TLC
          • Reduced residual volume
          • Reduced functional residual capacity

          Answer D. Gas trapping due to increased airway closure


          Respiratory - Essential respiratory investigations | Smoking-related chronic lung disease


          Question 47 top Download PDF

          A 58yo man is noted to have a right foot drop three days following a right total hip replacement. On examination there is weakness of right ankle dorsiflexion and toe extension (grade 4/5). Other muscle groups are normal. The knee jerks are symmetrical with an absent right ankle jerk. Sensation is reduced on the sole and dorsum of the right foot.

          The most likely diagnosis is:

          A. Femoral neuropathy

          B. Sciatic neuropathy

          C. L5 radiculopathy

          D. Tibial neuropathy

          E. Peroneal neuropathy



          1. Common peroneal nerve palsy
          2. Sciatic nerve palsy
          3. L4,L5 root lesion
          4. Peripheral motor neuropathy
          5. Distal myopathy
          6. Motor neuron disease
          7. Stroke



          Femoral Nerve:

          • Largest branch of the lumbar plexus
          • L2, L3, L4
          • Forms in the abdomen and runs through the pelvis and under the inguinal ligament
          • Runs lateral to the femoral vessels in the femoral triangle and outside the femoral sheath
          • Breaks up into several terminal branches
          • Supplies the anterior femoral muscles
          • Sends articular branches to the hip and knee joints
          • Gives several branches to the skin on the anteromedial side of the lower limb
          • Saphenous nerve (L2, L3, L4) is a cutaneous branch of femoral nerve
          • It descends through femoral triangle lateral to the femoral sheath
          • Then accompanies the femoral artery in the adductor canal and passes anteriorly to supply the skin and fascia of the anterior and medial aspects of the knee, leg and foot
          • Knee reflex (L2, L3, L4)


          Sciatic Nerve:

          • L4, L5, S1, S2, S3
          • Largest nerve in the body
          • Leaves the pelvis through the greater sciatic foramen
          • Runs deep to gluteus maximus but usually supplies no structures in gluteal region
          • Supplies all the hamstring muscles (mainly via tibial division but short head of biceps via common peroneal division)
          • Tibial and common peroneal nerves usually separate in inferior part of thigh
          • Tibial nerve (L4, L5, S1, S2, S3) runs behind the knee in the popliteal fossa
          • Gives branches to the knee
          • Supplies gastrocnemius, plantaris, popliteus and soleus muscles (posterior compartment muscles)
          • Divides into medial and lateral plantar nerves which supply the skin on the sole of the foot
          • Uncommonly injured but can occur with lacerations or posterior dislocations of the knee
          • Results in loss of plantarflexion and flexion of toes and loss of sensation over sole of foot
          • In the foot, all intrinsic muscles are supplied by branches of the tibial nerve except for flexor extensor digitorum brevis which is supplies by the deep peroneal nerve
          • Ankle reflex S1, S2
          • Tibial nerve gives the medial sural cutaneous nerve which usually joins the communicating branch of the peroneal nerve to form the sural nerve
          • Sural nerve (S1, S2) supplies the lateral aspect of the ankle and foot
          • Common peroneal nerve (L4, L5, S1, S2) runs down the medial border of the popliteal fossa
          • Gives branches to the knee
          • Gives off lateral sural cutaneous nerve which supplies the skin on the lateral aspect of the leg (L5, S1, S2)
          • Also gives off the peroneal communicating branch which joins the medial sural cutaneous nerve to form the sural nerve
          • Winds around the neck of fibula and runs down behind the peroneus longus muscle
          • Divides into superficial and deep branches
          • Deep peroneal nerve supplies the muscles of the anterior crural compartment, the ankle joint and the skin between the big and 2nd toes (L4, L5)
          • The anterior compartment muscles are mainly involved in dorsiflexion of the foot and extension of the toes
          • Superficial peroneal nerve (L5, S1, S2) supplies the lateral crural compartment muscles
          • These muscles (peroneal muscles) plantarflex and evert the foot
          • Superficial peroneal nerve also supplies an area of skin over the anterior aspect of the ankle, the dorsum of the foot and most of the toes


          • Injury to the femoral nerve would result in weakness of knee extension and reduced knee jerk. Would also lead to loss of sensation over anteromedial aspect of thigh and leg.
          • Sciatic neuropathy would results in weakness of knee flexion and all movements of the ankle/foot. Also there would be loss of sensation of the posterior, lateral and medial areas of the leg and all of the foot (ie. all areas below the knee except for that supplied by the saphenous nerve). Note sciatic nerve is most likely to be injured with hip surgery.
          • L5 radiculopathy would result in loss of sensation over the dorsum of the foot and the anterolateral portion of the leg. There may be some weakness of all the movements of the ankle as L5 is involved in the supply to all 3 compartments and also to the feet.
          • Tibial neuropathy would lead to weakness of plantarflexion as it supplies the muscles of the posterior crural compartment. Also loss of flexion of the toes and loss of sensation over the sole of the foot.
          • Peroneal neuropathy results in weakness of dorsiflexion and extension of the toes. Loss of sensation of the skin over dorsum of foot and toes and anterior aspect of lower leg. May also be weakness of eversion due to involvement of superficial peroneal nerve.


          This man has weakness of dorsiflexion and toe extension (deep peroneal nerve) but also has reduced sensation on the sole (tibial nerve) and dorsum (peroneal nerve) of the foot. Absent ankle jerk indicates the tibial nerve or S1, S2. Only the sciatic nerve is involved in all these processes so there must be a partial lesion of this nerve.

          Answer: B

          Table 363–1. Common Mononeuropathies (from Harrisons)



          Muscles Innervated

          Usual Site of Lesion

          Clinical Features




          C5, C6


          Suprascapular notch of scapula

          Weakness of lateral rotation of the humerus

          No sensory deficit

          Long thoracic


          Serratus anterior


          Winging of scapula

          No sensory deficit


          C5, C6

          Deltoid, teres minor

          Near shoulder joint

          Weakness of shoulder abduction; atrophy of shoulder

          Sensory deficit similar to C5 dorsal root lesion (See Figs. 22-2 and 22-3)



          Triceps, brachioradialis, wrist, finger, and thumb extensors

          Spiral groove of humerus

          Wrist drop most obvious, also finger and thumb extensors paralyzed

          Saturday night palsy (acute compression) is frequent cause

          Posterior interosseous branch

          C7, C8

          Finger and thumb extensors

          Edge of supinator muscle below elbow

          Finger drop; wrist relatively spared

          No sensory deficit


          C8, T1

          Ulnar flexor of the wrist, long flexors of 4th and 5th digits, and most intrinsic hand muscles

          Ulnar groove at the elbow

          Weakness of finger adduction and abduction and thumb adduction (see text); interosseous atrophy, claw-hand

          May be acute or insidious; sensory symptoms/signs are distinctive (Figs. 22-2 and 22-3); see also text




          Cubital tunnel

          Same as above

          Often pain over medial proximal forearm (cubital tunnel)




          Medial base of palm

          Intrinsic hand muscles only, interosseous atrophy

          No sensory deficit



          Abductor pollicis brevis; more proximal muscles include forearm pronator, long finger and thumb flexors

          Carpal tunnel

          Characteristic sensory symptoms and deficit and inability to make a circle with thumb and index finger

          Sensory deficit as per Figs. 22-2 and 22-3 (see text); known as carpal tunnel syndrome

          Anterior interosseous branch


          Long flexors of thumb and index and middle fingers

          Anterior interosseus branch below the elbow

          Weakness of pinch; pain in volar forearm

          No sensory deficit




          Iliopsoas (hip flexor) and quadriceps femoris (knee extensor)

          Proximal to inguinal ligament

          Knee buckling; absent knee jerk; weak anterior thigh muscles with atrophy

          Association with diabetes mellitus; sensory disturbance as per Fig. 22-2

          Lateral femoral cutaneous branch

          L2, L3


          Inguinal ligament

          Dysesthetic hyperpathia of lateral thigh

          Known as meralgia paresthetica


          L3, L4

          Thigh adductors

          Intrapelvic or at pubis

          Weakness of hip adduction

          Sensory deficit on medial thigh



          Hamstring muscles, hip abductor, and all muscles below the knee

          Near sciatic notch

          Severe lower leg and hamstring weakness; flail foot; severe disability

          Uncommon except from war wounds; sometimes after a misdirected injection

          Posterior tibial


          Calf muscles (proximally), toe flexors, and other intrinsic foot muscles

          Tarsal tunnel, near medial malleolus

          Pain and numbness of sole, weak toe flexors

          Known as tarsal tunnel syndrome (see text)



          Dorsiflexors of toes and foot, evertors of foot

          At neck of fibula

          Foot drop and weakness of foot eversion

          Sensory deficit is similar in distribution to L5, S1 sensory roots

          Spinal segments.


          Neurology: peripheral neuropathy

          Question 48 top

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          Question 52 top Download PDF

          A 55yo woman presents with right shoulder pain and a cough. Her CXR is shown below. Bronchoscopy confirms a malignant process.

          The most likely neurological complication of a tumour in this location would be involvement of the:

          A. Axillary nerve

          B. Stellate ganglion

          C. Parasympathetic chain

          D. Recurrent laryngeal nerve

          E. Coeliac plexus


          The CXR shows a mass in the apex of the R lung. Immediately we can exclude the coeliac plexus as this is located around the stomach.
          The axillary nerve is formed in the axilla from branches of the brachial plexus. It is not closely related to the lung apices. The brachial plexus, however, can be involved if the tumour is in the superior sucus of the lung results in Horner’s syndrome, rib destruction, atrophy of hand muscles and pain in the distribution of C8, T1 and T2 nerve roots (Pancoast’s syndrome).
          There is no parasympathetic chain. There is a sympathetic chain with paravertebral and prevertebral ganglia. The parasympathetic fibres run in a number of cranial nerves and from the sacral plexus.
          We are then left with 2 possibilities... stellate ganglion or recurrent laryngeal nerve.

          The recurrent laryngeal nerves can be affected in patients with apical lung masses causing hoarseness by paralysing the vocal cords. More common with left sided tumours (2-18%).
          The left recurrent laryngeal nerve passes around the arch of the aorta. The right recurrent laryngeal nerve passes around the right subclavian artery.

          The stellate ganglion (or cervicothoracic ganglion) is a ganglion formed by the fusion of the inferior cervical ganglion and the first thoracic ganglion. These form part of the sympathetic trunk. Local invasion of an apical tumour can cause Horner’s syndrome as well as pain in the shoulder and axilla.

          So the 2 possible answers are B and D. I wasn’t able to find which is more common though the history of shoulder pain is suggestive of involvement of the stellate ganglion.

          The correct answer is B.


          Neurology: peripheral neuropathy


          Question 53 top

          Question 54 top Download PDF

          The cell population responsible for driving the pathogenesis of sarcoidosis is:

          a) macrophage
          b) fibroblast
          c) B lymphocyte
          d) Type 1 helper T lymphocyte
          e) Type 2 helper T lymphocyte

          Answer D


          • Chronic, multi-system disease
          • Unknown aetiology
          • Characterised by accumulation of leukocytes, macrophages and non-caseating granulomas
          • Initial lesion in lungs is CD4 T cell alveolitis with accumulation of macrophages and T helper 1 cells
          • Followed by the development of granulomas
            • macrophages, epithelioid cells and multinucleated giant cells centrally
            • surrounded by lymphocytes, monocytes, mast cells and fibroblasts
          • Majority of lymphocytes are CD4 T cells (ie. T helper 1 cells)
          • Thought that a particular antigen triggers the activation of T lymphocytes. The proliferation and activation is greatly skewed towards T helper 1 lymphocytes
          • TH1 cells release mediators (cytokines) which attract and activate macrophages
          • T cell proliferation is maintained by the spontaneous release of IL-2 from the activated TH1 lymphocytes.
          • Thus the evidence suggests that the disease results from the exaggerated cellular immune response (mainly TH1) to a limited class of persistent or self-antigens.
          • Not sure what the antigen is that causes this reaction
            • Self antigen?
            • Infectious?
            • Genetic component (perhaps to do with MHC)?: can occur in multiple family members
            • Environmental component: have been reports of spouses both developing sarcoid
          • Can affect any organ (approximately in order of most commonly affected):
            • Lungs (95%)
            • Skin (15%)
            • Lymph nodes (15%)
            • Eyes (12%)
            • Liver
            • Spleen (7%)
            • Neurological
            • Parotids (4%)
            • Bone marrow
            • ENT
            • Cardiac (2%)
            • Renal
            • Bones/joints
            • Muscles (<1%)


          Immunology - Sarcoidosis


          Question 55 top

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          Question 58 top Download PDF

          In patients presenting with subacute lower extremity symptoms, the presence of pyramidal lower extremity weakness, a mid-thoracic sensory level to pin-prick but relatively preserved posterior columns is most consistent with:

            A. Subacute combined degeneration of the cord

            B. Brown-Sequard syndrome

            C. Syringomyelia

            D. A central cord syndrome

            E. An anterior spinal artery syndrome


            1. First order neuron enters the spinal cord through the dorsal root of the spinal nerve and its cell body lies in the dorsal root ganglion
            2. Synapses with a second order neuron on the same side, either in the spinal cord or in the medulla
            3. The second order neuron crosses to the other side and ascends to the thalamus where it synapses with the 3rd order neuron
            4. 3rd order neuron passes to the somatosensory cortex of the parietal lobe


            DORSAL COLUMNS

            1. Carry proprioceptive and discriminative touch fibres
            2. Located posteriorly in the spinal cord
            3. 2 tracts – fasciculus gracilis (medially) and fasciculus cuneatus (laterally)
            4. Fasciculus gracilis contains fibres from sacral, lumbar and thoracic regions
            5. Fasciculus cuneatus contains fibres from upper thoracic and cervical regions
            6. Ascend ipsilaterally to medulla and synapse with 2nd order neurons which then cross to other side
            7. 2nd order neurons ascend in medial lemniscus to the thalamus and then on to the cortex



            1. Tabes dorsalis is a late manifestation of syphilis
            2. Mainly affects the dorsal columns and lumbosarcral dorsal spinal roots
            3. Loss of proprioception leads to high steppage and unsteady gait with a positive Romberg’s sign
            4. Subacute combined degeneration of the spinal cord results from B12 deficiency
            5. Causes degeneration of the dorsal columns, producing sensory ataxia, and lateral columns, producing spasticity of the limbs



            1. Carry pain and temperature fibres
            2. Located anterolateral to the ventral horn
            3. 1st order neurons synapse in the spinal cord with the 2nd order neurons
            4. 2nd order neurons cross over at or near the level at which they begin
            5. Run to thalamus in tract called spinal lemniscus



            1. Syringomyelia selectively damages the spinothalamic tract
            2. Central canal becomes enlarged and compresses adjacent fibres results in central cord syndrome
            3. Second order neurons are damaged as the decussate close to the central canal
            4. Causes selective loss of pain and temperature – dissociated sensory loss – of the upper limbs
            5. May also be upper limb flaccid weakness due to damage of cell bodies in anterior horn
            6. As lesion enlarges, spastic weakness of lower limbs may occur +/- Horner’s syndrome




            1. Carry information from muscles, tendons and skin to cerebellum for control of posture and coordination of movement
            2. Dorsal and ventral tracts run laterally in spinal cord
            3. 1st order neurons synapse in spinal cord and 2nd order neurons ascend ipsilaterally (dorsal fibres) or contralaterally (ventral fibres) to cerebellum



            1. Friedreich’s ataxia is an inherited degenerative disease in which the spinocerebellar tracts are particularly disordered
            2. Leads to profound incoordination of the arms and ataxia
            3. Begins in childhood




            1. Control of voluntary movement
            2. Arise from cell bodies in cerebral cortex
            3. Pass through corona radiata and internal capsule to medulla where they for the pyramidal tracts
            4. Most fibres decussate in medulla, some cross near their termination



            1. Hereditary spastic paraparesis is an inherited degenerative disorder
            2. Degeneration of the lateral columns causes spastic paraparesis but sensation and bladder function are preserved



            1. From red nucleus of midbrain
            2. Controls tone of limb flexors
            3. Crosses in midbrain
            4. Receives input from motor cortex and medulla



            1. From midbrain
            2. Cross in midbrain
            3. Mediates reflex movements in response to visual stimuli



            1. Arise from vestibular nuclei in pons and medulla
            2. Lateral fibres descend ipsilaterally and control extensor muscle tone




            1. From pons and medulla
            2. Descend ipsilaterally
            3. Influence voluntary movement, reflex activity and muscle tone



            1. Hemisection of the spinal cord
            2. Ipsilateral loss of proprioception and upper motor neuron weakness
            3. Contralateral loss of pain and temperature



              • Results from damage to the grey matter nerve cells and crossing spinothalamic tracts
              • Results in lower motor neuron weakness as the cell bodies are affected rather than the descending tracts
              • In cervical cord, produces arm weakness out of proportion to leg weakness and dissociated sensory loss (loss of pain and temperature with preservation of dorsal columns) in the cape distribution
              • Trauma and syringomyelia are main causes

              In these figures, the blue shading indicates hypalgesia (loss of pain and temperature sensation) and the arrows indicate limbs with significant accompanying weakness. In the Brown-Sequard syndrome (hemisection of the cord, top row, right) there is often diminished tactile sensation on the side of weakness and opposite the side with hypalgesia. Reproduced with permission from McGee, S, Evidence-based Physical Diagnosis, WB Saunders, Philadelphia, 2001. Copyright © 2001 Elsevier.
              From Up To Date


              1. There are 2 posterior spinal arteries and a single anterior spinal artery
              2. The anterior spinal artery arises in a Y-shaped configuration from the 2 vertebral arteries
              3. The posterior spinal arteries arise from either the vertebral arteries or the posterior inferior cerebellar arteries
              4. All 3 arteries run inferiorly along the spinal cord
              5. The anterior spinal artery supplies the anterior 2/3 of the spinal cord
              6. Spinal cord also gets some supply from radicular arteries
              7. Blood supply is most vulnerable in the thoracic region (watershed area) and in the anterior portion of the spinal cord



              1. Bilateral tissue destruction that spares the dorsal columns
              2. All spinal cord functions – motor, sensory and autonomic – are lost below the level of the lesion with the exception of retained vibration and position sense
              3. Leads to spastic weakness of the lower limbs, incontinence and loss of pain and temperature sensation below the level of the lesion
              4. Dorsal columns preserved
              5. Lesions usually in the thoracic region as this is where the blood supply is most vulnerable


              Back to the question...

                A. Subacute combined degeneration (due to B12 deficiency) causes degeneration of the lateral and dorsal columns so this is incorrect

                B. Brown Sequard (due to hemisection of the spinal cord) produces loss of pain and temperature on the contralateral side and loss of proprioception and light touch on the ipsilateral side – dorsal columns involved so this is also incorrect

                C. Syringomyelia causes loss of pain and temperature of the upper limbs. Weakness of the upper limb can occurs but lower limb weakness is a late sign

                D. Central cord syndrome – syringomyelia is an example – would cause primarily loss of pain and temperature perhaps with some LMN weakness

                E. Occlusion of the anterior spinal artery leads to spastic paraplegia and loss of pain/temp with relative preservation of the dorsal columns – correct answer


                Neurology: peripheral neuropathy


                Question 59 top

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                Question 64 top Download PDF

                Inhaled beta-agonists reduce breathlessness and increase exercise tolerance in patients with COPD.
                Which of the following is the most likely mechanism for these effects?

                A. Increased FEV1
                B. Improved VQ matching
                C. Reduced dynamic hyperinflation
                D. Increased cardiac output
                E. Decreased pulmonary artery pressure


                Airflow Obstruction

                • Airflow during forced expiration is the result of a balance between the elastic recoil of the lungs promoting flow and the resistance of the airways limiting flow


                • In COPD there is often air trapping – increased RV to TLC
                • Progressive hyperinflation – increased TLC in late disease
                • As lung volume increases, elastic recoil pressure increases and airways enlarge so this reduces airway resistance
                • As such, hyperinflation helps compensate for airway obstruction
                • Leads to reduced effectiveness of abdominal muscles, reduced inspiratory pressures of the diaphragm and increased work of other inspiratory muscles to produce normal tidal volume

                Gas Exchange

                • PaO2 usually remains near normal until the FEV1 is decreased to about 50% predicted
                • PaCO2 is usually close to normal until the FEV1 is = 25% predicted
                • VQ mismatching is characteristic of COPD
                • Accounts for essentially all of the reduction in PaO2 (shunting is minimal)
                • Thus hypoxaemia can be easily corrected with supplemental oxygen
                • Pulmonary hypertension/cor pulmonale is usually only present in patients with an FEV1 = 25% and chronic hypoxaemia (although can have some elevation in PAP earlier in course of disease, especially with exercise)

                In general, patients with COPD have little or no improvement in FEV1 with bronchodilators, so A cannot be correct.

                Beta-agonists are not a treatment option for pulmonary hypertension.

                Increased cardiac output will not provide symptom relief in COPD.

                While VQ mismatches exist in COPD, beta-agonists are unlikely to significantly improve this.

                The answer is therefore C – reduced airways resistance means reduced hyperinflation.


                Respiratory - Smoking-related chronic lung disease

                Clinical Pharmacology - Respiratory

                Question 65 top Download PDF

                Maximal oxygen consumption (VO2 max) is the best measure of aerobic capacity or cardiovascular fitness and declines with age. In healthy ageing, the most important physiological change which contributes to this decline is a reduction in:

                A. Maximum heart rate
                B. Stroke volume
                C. Arterial PO2
                D. Forced expiratory volume in 1 second (FEV1)
                E. Total lung capacity

                Answer A

                Fick’s Equation – Uptodate


                Cardiology - Normal cardiac anatomy and physiology

                Respiratory - Basic respiratory and sleep physiology


                Question 66 top Download PDF

                The most common cause of diarrhea in an adult traveler to a developing country is:

                1. Shigella species
                2. Salmonella species
                3. Campylobacter species
                4. Enterotoxigenic Escherichia coli
                5. Giardia lamblia




                (most common cause)


                Malaise, anorexia, cramps, sudden onset of watery diarrhoea
                Can have nausea and vomiting
                No symptoms of colitis

                Campylobacter jejuni


                Similar to above initially (without vomiting)
                Followed by symptoms of colitis such as tenesmus, urgency, blood or pus in stool



                Upper GI symptoms, bloating, belching


                Africa, Asia and South America

                Severe watery diarrhoea without blood or pus (rice water stool)
                Usually no cramps or fever, vomiting not a prominent feature


                Western countries, Mexico

                Diarrhoea and abdominal cramps, can sometimes have fever
                Can last 1-2 weeks


                India, South America

                Vary from asymptomatic to severe dysentery with blood and pus in stool
                Can lead to perforation/peritonitis or abscess formation

                Clostridium species

                New Guinea

                Diarrhoea and abdominal cramps without vomiting or fever



                Clinically indistinguishable from campylobacter



                Symptoms range from mild to severe – usually watery diarrhoea first followed by mucus and blood

                More than 90% of illnesses are caused by bacteria. The most common organism is enterotoxigenic E.coli.

                Other causes to consider are viral (eg: rotavirus) as well as some of the more uncommon parasites (eg: cryptosporidium, entamoeba, microsporidia)

                There are four different groups of E. coli with different pathogenic mechanisms.

                ETEC (enterotoxigenic)

                1. has colonization factors which bind the bacteria to specific receptors on the intestinal cell membrane
                2. then produce powerful enterotoxins


                EHEC (verotoxin-producing)

                1. is a verotoxin-producing E. coli
                2. can cause haemorrhagic colitis and HUS by destroying the mucosa

                EPEC (enteropathogenic)

                1. has an unclear mechanism of pathogenicity
                2. do not appear to produce toxins
                3. have a particular mechanism of adhering to the enterocytes which destroys the microvilli

                EIEC (enteroinvasive)

                1. attaches specifically to the mucosa of the large intestine
                2. invades the cell by endocytosis
                3. inside the cell they lyse the endocytic vacuole, multiply and spread to adjacent cells causing tissue destruction and inflammation

                References: Medical Microbology


                Infectious Diseases: Returned Traveller

                Question 67 top

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                Question 69 top Download the PDF

                Which one of the following most differentiates between antigen-dependent and antigen-independent B cell development?

                a) B cell surface expression of surrogate light chain
                b) B cell surface expression of µ heavy chain
                c) B cell surface expression of CD79a (immunoglobulin a)
                d) Immunoglobulin gene rearrangement
                e) Somatic hypermutation

                B CELL DEVELOPMENT

                • Mature B cells constitute 10-15% of blood lymphocytes, 50% of spleen lymphocytes and 10% of bone marrow lymphocytes
                • Have surface immunoglobulins which act as antigen receptors
                • Capable of recognising and proliferating in response to whole native antigens (as opposed to T cells which require antigen-presenting cells to modify antigen)
                • Primary function is to produce antibodies but can also act as antigen-presenting cells


                • Occurs in bone marrow (or in liver during gestation)
                • Includes up to mature B cells
                Stem cell becomes B cell precursor (pro-B cell)
                • First committed cell (ie. Committed to B cell lineage)
                • No immunoglobulin (cytoplasmic or surface)
                • Early pro-B cells express CD 34 as well as CD10, CD19 and CD38
                • Late pro-B cells express CD20 and CD40 as well as CD10, CD19 and CD38
                Pre-B cell
                • Ig heavy chains with surrogate light chains are expressed on surface (not true immunoglobulin as not proper light chains)
                • CD19, CD20, CD38 and CD40 expressed
                Immature B cell
                • Has surface IgM (with real light chains) and has receptors for Fc portion of IgG
                • CD19, CD20, CD40
                Mature B cell
                • Has surface IgM and IgD
                • CD19, CD20, CD21, CD40
                • Exit the bone marrow to the peripheral circulation

                Gene rearrangement occurs multiple times during B cell development resulting in a large diversity of antigen binding sites (immunoglobulins).


                • Driven by interaction of antigen with mature B cell immunoglobulins leading to:
                  1. Memory B cell induction
                  2. Plasma cell formation
                • Occurs in secondary lymphoid organs such as lymph nodes, spleen and Peyer’s patches in gut
                • The mature B cell enlarges and divides. Forms plasma cells which secrete antibodies and memory B cells which are identical in appearance to mature B cells but are much more sensitive to antigen stimulation: proliferate and generate plasma cells more rapidly, responsible for the rapid production of antibodies in the secondary immune response.
                • Antigen-reactive sites are modified by further alteration of Ig genes after stimulation by the antigen. This is called somatic mutation.
                • Somatic hypermutation is the process in which point mutations occur in Ig genes on antigen activation of B cells. Gives rise to mutant immunoglobulins, some of which bind better than the original Ig. This therefore creates memory B cells with the highest affinity antibodies.
                • The overall process is called affinity maturation of antibodies.
                • Ig class switching occurs when the CD40 ligand of T cells binds to the CD40 receptor on B cells. Cytokines from the T cell mediate gene recombination which results in a change of Ig class (eg: IgM to IgA)

                So, b) and c) are not correct. Heavy chains are present in both the Ag-dependent and Ag-independent phase. No reference was made to CD79a.

                Gene rearrangement seems to occur to some degree throughout the whole of B cell development, not confined to one phase.

                Although there are surrogate light chains only in the Ag-independent phase of development, this is only in pre-B cells and does not play any major part.

                Somatic hypermutation, however, is responsible for the greater affinity of antibodies to specific antigens and only occurs in the Ag-dependent phase.

                I suppose somatic hypermutation is a reasonably important point but the only reference I found to it specifically was in Harrison’s!


                Immunology - Structure and function of the cellular and humoral components of the immune system.


                Question 70 top