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					Paper 1; Question 1

Retinopat hy of Prematurity

    (a) Risk Factors
               Prematurity as the major factor
               BW and GA – highest under 28 weeks and <1500 gms
               Incidence inversely proportional to this
               Hyperoxia and hypoxia + fluctuations
               <1500gms AGA 16-34% have disease 5-11% blindness (estimate acceptable or
               statement to that effect)
               Blood transfusion
               VEGF levels
               Genetics

        Aggravating factors
               Pregnancy complications
               Apnoea/bradycardia
               Asphyxia
               Sepsis
               IVH, BPD, PDA
               Ventilatory support
               Bright lights

    (b) Medico-legal
                Guidelines for screening
                <1500 gms and <28 weeks
                Any baby with difficult clinical course
                Two examinations – first 4-6 weeks after birth or 31-33 weeks
                Written guidelines for PaO2 55-88mmHg and Sats 88-92%
                Antenatal steroids stabilising effect on retina
                Discussion with parents – often
                Inform them of modes of therapy –
                        cryotherapy + complications of periorbit al oedema, retinal scarring and
                        detachment
                       Laser therapy + complications of choroidal Hx scarring


                Marked liberally and accepted points if they were in section (a) or (b)



Paper 1; Question 2

Write short notes on

    a) The causative organisms, clinical presentation and diagnosis on non -tuberculous mycobacterial
       infection.

Introduction The term non-tuberculous mycobacteria (NTM) is the favoured term for a large group of
mostly saprophytic mycobacteria that are responsible for infections in people with impaired local or
systemic immunity. The term NTM is used synonymously with atypical mycobacteria, opport unistic
mycobacteria and mycobacteria ot her than tubercle bacilli (MOTT). M leprae and M bovis are obviously
also examples of NTMs but are not included in the discussion. Similarly a discussion of infection with
BCG is not required. If candidat es discuss M.leprae, M bovis or BCG they will be given marks for this
but those who do not mention it will not be penalized.
Caus ative Organisms. The list of species of mycobacteria is long (95) with about 1/3 of them
associated with human disease. The most import ant NTMs are:
M. avium, M. intracellulare, M. kansasii, M. paratuberculosis and M. Scrofulaceum.
Clinical Pres entation.
Localised Disease – pulmonary, adenitis, soft tissue infections joints and bones.
Systemmic Disease – symptoms include high grade fevers, night sweats, anaemia, weight loss,
malaise, anorexia, diarrhoea, myalgia, and painful adenopathy.
MAC. Frequently reported in AIDS patients. Usually associated with very low CD4 counts. The portal of
entry is thought to be the GUT. The symptoms are fever, night sweats anaemia, wei ght loss, anorexia,
diarrhoea, myalgia and adenopathy.
Diagnosis. The differential diagnosis is that of MTB or lymphoma. The clinical picture of wasting,
lymphadenopathy and fever is often suggestive. Radiology including scans may show marked
adenopathy often wit h liquefaction of glands with fistulae. Tuberculin skin tests generally cross react
with NTBs although many patients are anergic bec ause of their depressed immune state. Specific PPD
has proved useful for diagnosing MAC. The definitive diagnosis depends on culturing the NTB.
Because NTBs are ubiquitous in nature, careful attempts to exclude contamination are necessary. The
organism is fastidious but is usually obtained from infected glands, bone marrow, bronchial lavage or
especially blood culture. BACTEC, Gene probes and PCR have speeded up laborat ory identification
The finding of NTB in sputum must be considered in the light of clinical findings.


Write short notes on

    b) Use and abuse of intravenous immunoglobulins (IV IG)

Introduction Intravenous immunoglobulin was licensed 20 years ago for replacement therapy of patients
with primary antibody deficiency. This remains the most legitimate indication. The observation was
serendipitously made that thrombocytopenia from ITP improved in a patient wit h common variable
immune deficiency. This led to the use of IV IG in a variety of immune mediated and infectious
conditions. There is no doubt that IVIG is not indicated in many of the conditions for which it is
prescribed. Numerous systematic reviews have been performed in an attempt to encourage an
evidence based approach. These reviews have largely been included in the Cochrane Database.

Clear Indications supported by RCTs

Primary Humeral Immunodeficiencies
IVIG is useful in X-linked agammaglobulinemia, Hyper IgM syndrome, Transient
hypogammaglobulinemia of infancy, IgG subclass deficiency. It is also indicated in Combined
immunodeficiencies such as SCIDS, Common variable immunodeficiency,
Wiskott-Aldrich Syndrome, Ataxia-t elangiectasia,etc.
The rationale for use in the immunodeficiencies is the “passive” provision of antibodies from a large
pool of thousands of donors

Kawasaki Disea se
IVIG and aspirin in combination are the standard treatment of KD. This treatment results in rapid
resolution of fever and in a decrease risk for developing coronary artery aneurysms. The rationale of
action is not completely understood.

Guillian-Barre Syndrome
If given early in the course of the disease IVIG is as effective as plasmapheresis in the management of
adults with GBS. Adequate data is not available foe assessing the use in children but it appears likely
that IVIG is highly efficacious.

Myasthenia Gravis
IVIG is as effective as plasms exchange in MG. It is usually reserved for refractory cases.

ITP in Adults

Indications not supported by RCTs

Neut ropenia, haemolytic anemia, red cell aplasia, intractable seizures, burns, SLE, recurrent
miscarriage, rheumatoid arthritis, inflammatory bowel diseas e, prevention or management of infections
in prematures etc., etc.

Cont ra-indication to IV IG

Selective IgA deficiency
Write short notes on

    c) Management of primary enuresis in a seven-year old male child

Introduction Primary enuresis means bet-wetting in a child who has never been dry. The age at which
enuresis is considered problematic and appropriat e to investigate is over the age of 5 years (or six
years in the Sout h African guidelines). Nocturnal enuresis should be defined at this age as bet wetting>
3times /week.. History and examination should exclude pathological causes such as urinary tract
infections, constipation and enc opresis, spinal dysraphism etc. Major psychopat hology and mental
retardation should be excluded.
Management

    i)         Natural History About 15% of children over 5 years suffer from primary nocturnal enuresis.
               If no therapy is instituted at least 15% will be dry per year. This gives testimony to the fact
               that enuresis is often no more than a maturational delay. The parents may opt for no
               intervention after education and reassurance.
    ii)        Enuresis Alarms These are highly effective resulting in nearly 4 fewer wet nights per week
               than no treatment or placebo. Alarms that wake the child are more effective than those that
               wake the parent. .Response to treatment may take up to 8 weeks. There is a permanent
               cure rate of nearly 50%. Family motivation is essential if this mode is to be prescribed.
    iii)       Desmopressin (DDAVP ) Administered as a nasal spray of 10mcg at night. Fluid restriction
               is necessary to avoid water intoxication. The drug is usually well tolerat ed. Success is
               immediat e but relapse rates are very high. The drug can be used in combination with other
               modes of therapy when sleeping out,camps etc.
    iv)        Anticholinergics These may be useful where “bladder overactivity”or poor bladder capacity
               seems likely on history.
    v)         Tricyclics (imipramine) These drugs are moderat ely successful but relapse rat es are
               common. Side effects especially in overdosage have resulted in tricyclics falling from
               favour.
    vi)        Positive & negative re-inforc ements There is no good evidence that rewards or
               punishments have any effects.
    vii)       Other approaches “Bladder training”, fluid restriction, lifting the child at night are all
               commonly tried but there is little evidence that these interventions work.


Paper 1; Question 3

Five year old boy diagnosed with Diabetes mellitus
(Topics could have been discussed under different headings)
    1. Parental education (I n no particular order)
     Discuss causes (genetic)
     Pathophysiology
     Deal with guilt
     Get co-operation
     Full vaccination
     Medic alert bracelet
     Dietary management – regular eating pattern
     Encourage physical activity and precautions
     Glucose and ketone monitoring
     Keeping a diary
     Administration of ins ulin
     Recognize signs of hypo- and hyperglycaemia
     When to ask for help
     Whom to contact
     Join parent associations
     Give literature, internet sites
     Conditions that require more/less insulin (eg infections, vomiting etc)

    2.     Monitoring and cont rol
          Yearly extensive check-up for general health status
          Periodic visits for glycaemic control
        Quarterly HbA1c/fructosamine
        Monitor growth/sexual maturity
        Monitor school performance
        Fasting lipid profile
        Thyroid function test
        Check diary and adjust medication

    3.   Prevention and treatment of complications
        Good glucose control
        Keep Hb1Ac <7-8
        Screen for complications yearly (after 5years of disease)
        Fundus examination and treatment follow-up
        Screening fro micro-albuminuria
        Monitor blood pressure
        Check sensation
        Monitor skin, injection sites etc.
        Treat any infections.



Paper 1; Question 4

a) The indic ations for a pilocarpine sweat test and the int erpretation of the results obtained. (10)

Indications:
Pulmonary – Chronic/Recurrent Right upper lobe pneumonia
             - Bronchiectasis
             - Digital clubbing
             - Nasal polyps
             - Chronic recurrent bronc hiolitis
             - Pansinusitis etc.

Gastroint estinal: Cirrhosis, port al hypertension.
             -    Meconium plug/ ileus/ rectal prolapse
             -    Recurrent intusseption
             -    Steatorrhoea
             -    Malabsorption

Metabolic: Acrodermatitis enteropathica
            -   Failure to thrive
            -   Metabolic alkalosis
            -   Family history of cystic fibrosis
            -   Salty taste
            -   Salt depletion syndromes

Interpretation:

Sweat chloride > 60 Meq/l abnormal
              40-60 Meq/l borderline
                <40 Meq/l normal

Child must be off sodium containing antibiotics 10 to 14 day prior to sweat test e.g. oral penicillin,
rifampicin etc.

The test pad must have a minimum of 100mg of s weat for the result to be valid.


b) The differential diagnosis for an eight year old child with metabolic alkalosis on a blood gas. What
are the principles of investigation and management of this condition?(15)

Most candidates did not heed the age category! It was an eight year old child so it ruled out most of the
causes of vomiting in the newborn period e.g. pyloric stenosis!
Metabolic alkalosis is a net gain alkali or loss of acid whic h leads to a change in serum bicarbonat e
concentration and pH. The respiratory res pons e is alveolar hypoventilation to ret ain CO 2.
                                               -
Two major categories based on the urinary Cl concentration and the response to volume expansion
with saline infusion.
                                      -
Saline   Responsive: usually have Cl concent ration <10 Meq/l and significant volume depletion e.g.
    1.   Severe vomiting
    2.   Excessive upper GI suctioning
    3.   Laxative abuse
    4.   Diuretic abuse
    5.   Cystic fibrosis
    6.   Post hypercapnia syndromes
    7.   Poorly reabsorbable anion administration
                                                         -
Saline   Resi stant: usually associated with high urine Cl concentration and often hypertensive e.g.
    2.   Primary hyperaldosteronism
    3.   Hyper-reninaemic hypertension
    4.   CAH - 17 α OH deficiency
                - 11 β OH deficiency
    5.   Liquorice ingestion
    6.   Liddle syndrome
    7.   Barters or Gittelman syndrome
    8.   Severe Potassium deficiency

Investigations:

    1.   A good history
    2.   Venous gas
    3.   Urea, electrolytes, creatinine and osmolality in serum an d urine
    4.   Aldosterone, Rennin & 17 OH progesterone
    5.   Sweat Test
    6.   Stool chloride
    7.   ?Barium studies

Management:
Treat the cause.
Make sure give alkali free fluid! No Ringer’s lactate or Half Darrow’s.




Paper 2; Question 2

a) Perinatal group B streptococcal infections : Prevention

Detection of mat ernal colonization offers an opport unity for treatment before delivery. Genital and
rectal cultures taken 1-5 weeks before delivery.

CDC consensus strategies

Antepartum culture based screening of pregnant women at 35-37 weeks of gestation using combined
vaginal - rectal swabs and antepartum treatment of the following groups of women:

    -    previous infant invasive disease
    -    GBS bacteruria during pregnancy
    -    Positive GBS screening culture res ults during pregnancy
    -    Unknown GBS status with any of the following:
         i.       Delivery before 37 weeks gestation
         ii.      Prolonged rupture of membrane >24hrs
                                       0
         iii.     Intrapartum fever >38 C
     Intrapartum management

     Pen G 5million units loading dose then 2, 5 million units 4 hourly until delivery, or Ampicillin 2g
     loading dose then 1g 4 hourly until delivery

     Alternative drugs include Erythromycin, Clindamycin & Cefazolin

     Baby: at birth

     Symptomatic babies – must have a full septic screen and empiric antibiotics. The duration of the
     treatment will depend on the clinical course and culture results

     Asymptomatic - Before 35 weeks gestation – screen + antibiotics
                     After 35 weeks gestation - observe


b)        Prevention of Ophthalmia Neonatorum

     Caus ative organisms are most likely to be:

                       -       Neiserria gonorrhea
                       -       Chlamydia trachomatis
                       -       Haemophilus influenzae
                       -       Streptococcus pneumoniae
                       -       Staph aureus



General measures:

     Screen patients for genitourinary infections at antenatal clinic
     Prevent and treat STI’s in pregnancy

     Topical:      All babies should have their eyes treated soon after delivery with 1% silver nitrate drops
                   (expensive, tends to cause chemical conjunctivitis)

     OR            0,5% erythromycin ointment
     OR            1% tetramycin ointment
     OR            2,5% povidone-iodine solution (not approved for general use but may be cheaper and
                   effective)


Antibiotics:

     Penicillin 50 000 IVI/imi given to babies whose mothers have proven gonococcal infection has not
     been accepted as routine practice.
     * Ceft riaxone imi (also not routine practice)

c)   Prevention of Meningoc occal Disease.

     Who should get:
     All close contacts only e.g: household members of index patient, day care cent re contacts and all
     those exposed to the oral secretions from the patient.

     When:
     Ideally prophylaxis should be given within 24 hrs of contact

     Modalities:

Vaccinations (not in general use)

                       -       Has been used in outbreaks to limit spread of disease
                       -       Used in Asplenic individuals
                     -        Used in travelers to endemic areas

Chemoprophylaxis:

Children         -        < 1 month – Rifampicin 5mg/kg bd x 2 days
                          > 1 month – Rifampicin 10m g/kg bd x 2 days

Adults           -        Ciprofloxacin 500mg stat or Rifampicin 600mg bd for 2 days

Alternatives :            Ceftriaxone <12yrs 125mg imi stat
                                       >12yrs 250mg imi stat
                          Azithromycin 500mg orally stat (not in CDC guidelines)



d) Prevention of bacterial endocarditis in a child with a congenital heart lesion (see
   recommendations of the AHA 1997)

General: Maint ain good oral hy giene

Antibiotic Prophylaxis:

Standard general prophylaxis
Amoxil 50mg/kg orally one hour before procedure, O R
Ampicillin 50mg/kg IV/imi within 30 minutes before procedure if unable to us e oral rout e

Alternative:
In Penicillin allergy use Erythromycin or Clindamycin.

Prophylaxis for genitourinary and GIT procedures, depending on the risk category of the patient .

High risk:
Ampicillin (50mg/kg IV I or imi)
Gentamycin (1,5mg/kg) within 30 minutes of starting procedure then 6 hours after procedure.
Ampicillin 25mg/kg IVI/imi, or Amoxil 25mg/kg

Alternative:
In Penicillin allergy use Vancomycin 20mg/kg

Moderate risk:
Amoxil 50mg/kg orally, or ampicillin 50mg/kg IVI/imi 1 hour before procedure.

In Penicillin allergy used Vancomycin


e) PCP Prophylaxis

Who should get it:
               -          Any HIV exposed baby
               -          Any child below 12 months diagnos ed HIV
               -          Any child above 12 mont hs with a proven PCP infection or 2 or > episodes of
                          pneumonia
                 -        Any child with CD4 below 15%

When:
It should be started at 4-6 weeks
Any time the above criteria are fulfilled

Drugs:
Cotrimoxazole (B actrim) at 5mg/kg trimethoprim
                             20mg/kg sulphamethoxazole
Alternatives:
Daps one daily
Aerosolized pentamidine monthly (expensive)

When to stop:
    In babies <12 months
    When they are proven to be HIV negative
    Consider stopping in children on ARV’s when CD4 consistently above 20%
    Otherwise continue for life



Paper 2; Question 3

a.    Describe the clinical features of eczema in childhood [10
marks]

b.   Give an approach to the management of eczema in childhood [15
marks]

Framework for marking questions

a.    Describe the clinical features of eczema in childhood

      - Age of onset
      - Acute features e.g. erythema scaling, itching irritablity
      - Secondary infection
      - Distribution - (age variablility)
      - Trigger factors
      - Family history
      - Course + prognosis

b.    Give an approach to the management of eczema in childhood

      - Prevention
      - Avoiding trigger factors (foods, irritants etc)
      - Emollients
      - Steroids
      - Immunomodulatores (e.g Topical Tacrolimus and Pimecrolimus)
      - Treatment of secondary infection


Paper 2; Question 4

Discuss the public health problem of anaemia in children on the continent of Africa. Discuss the
strategies that you will develop for the WHO t o address the problem if asked as a paediatric expert on
child health.

Memorandum: Rubric

       Levels of                        3                           2                   1
     achievement →
                                   Excellent                  Satisfactory    Needs improvement
 Asse ssment criteria

            ↓
      Organization         Answer is clear,           The answer is             The answer is read
                           understandable, and        generally clear and       with effort and the
                           logical. It is easy to     understandable. There     answer is not clear.
                           determine the              are a couple of minor     There is no systematic
                           reasoning of the           confusing points.         organization.
                           author.

Accuracy of content        All the facts present ed   There are no              There are incorrect
                           are accurate. The          significant incorrect     facts. The author is
                           author has in-depth        facts. The author has     unsure of how to
                           knowledge of anaemia       an approach to            manage anaemia in
                           in African children and    anaemia in children,      children in Africa.
                           can pres ent the           but there are minor       There is no or little
                           relevant interventions     mistakes or lack of       knowledge of the
                           needed to address the      some facts.               public health issues or
                           problem.                                             long term
                                                                                complications of
                                                                                childhood anaemia.

     Profe ssionalism      The author illustrates a   The author illustrates    The author is not able
                           professional approach      an acceptable level of    to prepare a guideline
                           to provide WHO with a      professionalism with      for the WHO regarding
                           guideline for the          regards to the WHO        childhood anaemia in
                           management of              guideline, but the        Africa.
                           childhood anaemia in       guideline is not fully
                           Africa.                    comprehensive or
                                                      clear.


       Conclusion          The author                 The author                The author is not able
                           summarises the             summarises the            to discuss the
                           importance of effective    importance of effective   importance of anaemia
                           management of              management of             management in
                           anaemia in children in     anaemia in children,      children.
                           a concise and accurate     but is inaccurate.
                           manner.

Referenc e as part of the memorandum:

1.       Hall A, Bobrow E, Brook er S, et al. Anaemia in schoolchildren in eight countries in Africa and
        Asia. Public Health Nutrition, Volume 4, Number 3, June 2001, 749-756(8).

2.        Crawley J. Reducing the burden of anemia in infants and young children in Malaria -endemic
        countries of Africa: from evidence to action. Am. J. Trop. Med. Hyg., 71(S uppl 2), 2004; 25–34.

				
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