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Phase 3A Medicine > Paediatrics - Infection, immunity and allergy (1) > Flashcards

Paediatrics - Infection, immunity and allergy (1) Flashcards

1
Q

Red flag symptoms for serious illness and urgent investigation

A 
Fever of over 38 in <3 months
Fever of over 39 if 3-6 months
Colour - pale, mottled, blue
Reduced consciousness, bulging fontanelle, neck stiffness, focal  neurological signs, seizures 
Respiratory distress
Bile-stained vomiting
Severe dehydration/ shock
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2
Q

What form of antibody are transferred from mother to baby and for how long does this protection last?

A 
IgG
6 months (but starts to reduce immediately)
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3
Q

4 investigations essential in a septic screen

and others that may be indicated (5)

A
  1. Blood culture
  2. FBC (inc. white cell count)
  3. CRP (acute phase reactant)
  4. Urine sample

Others: CXR, LP, Rapid antigen screen (blood/CSF/urine), meningococcal and pneumococcal PCR on CSF/blood, PCR for viruses in CSF (HSV/enterovirus)

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4
Q

Seriously unwell child presents to A&E, what antibiotic would be prescribed?

a) Child >3 months
b) Child<3months

A

a) Parenteral - 3rd generation cephalosporin (cefotaxime, ceftriaxone)
b) Parenteral Cefotaxime and ampicillin (if listeria infection suspected)

Can also give aciclovir if HS encephalitis suspected.

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5
Q

Common causes of a febrile child

A
  1. URTI
  2. Otitis media
  3. Serious bacterial infection if no focus (septicaemia, UTI)
  4. Tonsillitis
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6
Q

Most common cause of meningitis?

A

Viral infection

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7
Q

Two causes of non-infectious meningitis?

A
  1. Malignancy

2. Autoimmune disease

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8
Q

Percentage of patients in UK with bacterial meningitis that are under 16

A

80%

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9
Q

Pathophysiology of bacterial meningitis

A

Damage is due to host response to bacteraemia

  1. Release of inflam mediators and activated leucocytes with endothelial damage leads to cerebral oedema, ^ICP, decreased cerebral blood flow
  2. Inflammatory response below the meninges causes a vasculopathy resulting in a cerebral cortical infarction, fibrin deposits and resorption of CSF by arachnoid villi –> hydrocephalus
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10
Q

Most common bacteria causing meningitis in neonate - 3 months? (3)

A
  1. Group B strep
  2. Ecoli/other coliforms
  3. Listeria monocytogenes
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11
Q

Most common bacteria causing meningitis in 1 month - 6 years? (3)

A
  1. Neisseria meningitides
  2. Strep pneumoniae
  3. Haemophilus influenzae
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12
Q

Most common bacteria causing meningitis in >6 years?

A
  1. Neisseria meningitidis

2. Strep pneumonaie

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13
Q

Differentials for neck stiffness?

A
  1. Meningitis
  2. Tonsillitis
  3. Cervical lymphadenopathy
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14
Q

Signs of shock?

A
  1. Tachycardia
  2. Tachypnoea
  3. Prolonged cap refill
  4. Hypotension
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15
Q

If lumbar puncture contraindicated in child with suspected meningitis what is the management?

A
  1. Postpone LP until child stabilises
  2. Prescribe 3rd generation cephalosporin (cefotaxime/ceftriaxone)
  3. Bacteriological diagnosis with blood PCR or culture OR rapid antigen screen on blood and urine
  4. Obtain throat swab for viral and bacterial cultures
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16
Q

In suspected bacterial meningitis what would you prescribe alongside 3rd generation cef to minimise the risk of long-term complications?

A

Dexamethasone

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17
Q

Give 3 cerebral complications of meningitis?

A
  1. Hearing loss - inflammatory damage to cochlear hair cells
  2. Local vasculitis - cranial nerve palsies
  3. Local cerebral infarction - focal or multifocal seizures
  4. Subdural effusion - H.influenzae and pneumococcal menigitis associated
  5. Hydrocephalus - impaired resorption of CSF
  6. Cerebral abscess - confirmed by CT
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18
Q

All household contacts of a patient with meningococcal meningitis and H.influenzae meningitis are given what prophylaxis?

A

Rifampicin + meningococcal vaccine

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19
Q

What is the disadvantage of giving children antibiotics for a non-specific febrile illness?

A

If have early meningitis it may cause diagnostic problems
CSF will show increased white cells but culture may be negative
Rapid antigen screen (RAS) and PCR helpful

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20
Q

Causes of viral meningitis?

A
  1. Enteroviruses
  2. EBV
  3. Adenoviruses
  4. Mumps
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21
Q

Describe the two signs associated with neck stiffness in meningitis?

A
  1. Brudzinski sign - Flexion of neck with child supine causes flexion of knees and hips
  2. Kernig sign - Child lying supine and with hips and knees flexed, there is back pain on extension of the knee
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22
Q

Clinical features of meningitis in a child under 18 months?

A
  1. Fever
  2. Poor feeding
  3. Vomiting
  4. Irritability/lethargy/drowsiness/reduced consciousness
  5. Hypotonia

Late signs: Bulging fontanelle, neck stiffness, arched back (opisthotonus)

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23
Q

What should any child with a purpuric rash be given pre-hospital before being transferred?

A

IM benzylpenicillin

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24
Q

Clinical features of meningitis in a child over 18 months?

A
  1. Fever
  2. Photophobia
  3. Neck stiffness
  4. Brudzinski’s/Kernig’s
  5. Headache
  6. LOC
  7. Seizures
    Can get papilloedema but rarely
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25
Q

Contraindications to LP in suspected meningitis

A
  1. Raised ICP (coma, high BP, low heart rate, pappiloedema)
  2. Cardiorespiratory instability
  3. Focal neurological signs
  4. Coagulopathy or thrombocytopenia
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26
Q

Investigations in suspected meningitis/encephalitis?

A
  1. FBC
  2. Blood glucose
  3. Coagulation screen/ CRP
  4. Culture of blood, throat swab, urine, stool for bacteria and viruses
  5. Rapid antigen test on CSF, urine or blood
  6. LP unless contraindicated
  7. PCR of blood and CSF
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27
Q

How would you confirm a diagnosis of viral meningitis?

A

Culture or PCR of CSF, stool, urine, throat swab and serology

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28
Q

Most common 3 clinical features in a child presenting with encephalitis?

A
  1. Fever
  2. Altered consciousness
  3. Seizures
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29
Q

Causes of encephalitis?

A
  1. Invasion of cerebrum by virus e.g. HSV
  2. Post-infectious encephalopathy (e.g. after chickenpox)
  3. Slow virus infection e.g. HIV/SSPE following measles
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30
Q

Most common organisms causing encephalitis in UK?

A

Enteroviruses, respiratory viruses or herpes viruses (HSV, varicella, HHV6)

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31
Q

Treatment of encephalitis?

A

High dose IV acyclovir

if HSV then prescribe for 3 weeks

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32
Q

Give the 3 signs of toxic shock syndrome?

A
  1. Fever >39
  2. Hypotension
  3. Diffuse erythematous, macular rash
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33
Q

Give other symptoms of TSS other than the 3 main signs of the syndrome (5)

A
  1. Mucositis (conjunctivitis, oral mucosa, genital mucosa)
  2. Vomiting/diarrhoea
  3. Liver impairment
  4. Clotting abnormalities e.g. thrombocytopenia
  5. Altered consciousness
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34
Q

Management of TSS

A
  1. Surgical debridement

2. 3rd generation cef + clindamycin

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35
Q

Two most common organisms causing necrotising fasciitis?

A
  1. Staphylococcus Aureus

2. Group A strep

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36
Q

Main form of meningococcal infection seen in UK?

A

Group B

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37
Q

What increases susceptibility to pneumococcal disease?

A

Hyposplenism (e.g. in sickle cell disease and nephrotic syndrome)

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38
Q

Main risk factor for impetigo?

A

Infants and young children with existing skin disease e.g. atopic eczema

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39
Q

Most common organisms causing impetigo?

A

Staph or strep

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40
Q

Where do impetigo lesions usually present?

A

Face, neck and hands

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41
Q

Describe the lesions in impetigo

A

Honey-coloured crusted lesions which emerge from erythematous macules.

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42
Q

Treatment for a) mild and b) severe impetigo

A

a) Topical antibiotic (mupirocin)

b) Flucloxacillin (narrow spectrum systemic)

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43
Q

Advice to parent of child with impetigo?

A

Shouldn’t be at school until lesions dry

Don’t touch as it will spread

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44
Q

Clinical features of periorbital cellulitis? (2)

A
  1. Fever

2. Erythema, tenderness and oedema of the eyelid (unilateral)

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45
Q

Causes of periorbital cellulitis?

A

a) H.influenzae in young, unimmunised children following trauma to the skin
b) Spread from paranasal sinus infection
c) Spread from dental abscess

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46
Q

What is the risk of periorbital cellulitis developing into?

A

Orbital cellulitis

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47
Q

Treatment of periorbital cellulitis?

A

IV antibiotics

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48
Q

Clinical features of orbital cellulitis?

A
  1. Proptosis
  2. Painful or limited ocular movement
  3. Reduced visual acuity
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49
Q

Investigations in suspected orbital cellulitis?

A
  1. CT to assess posterior spread of infection

2. LP to exclude meningitis

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50
Q

Organism commonly causing periorbital cellulitis?

A

Group A strep or staph aureus

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51
Q

What is scalded skin syndrome?

A

Staphylococcal toxin causes separation of the epidermal skin on gentle pressure. Seen in infants and young children
Also have fever, malaise, and purulent, crusting infection around eyes, nose, and mouth. Widespread erythema and tenderness of the skin.

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52
Q

Management of scalded skin syndrome? (3)

A

IV anti-staph antibiotic
Analgesia
Fluid monitoring

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53
Q

Treatment for HSV1 and 2

A

Aciclovir - DNA polymerase inhibitor

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54
Q

What is the most common for of primary HSV illness in children?

A

Gingivostomatitis

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55
Q

What is the cause of eczema herpeticum?

A

HSV - widespread vesicular lesions develop on eczematious skin and this can be complicated by secondary bacterial infection –> septicaemia

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56
Q

What virus causes chickenpox?

A

Varicella zoster

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57
Q

How is chickenpox spread?

A

Droplet

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58
Q

Normal incubation period of chicken pox?

A

10-23 days. Median 14

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59
Q

When is chickenpox infectious?

A

2 days before and up to 6 days after start of illness

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60
Q

Describe the symptoms of chickenpox?

A

Fever and itchy rash

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61
Q

Describe the rash in chickenpox

A

200-500 lesions
Start on the head and trunk
Progress to peripheries
Appear as crops of papules, vesicles, pustules and crusts with surrounding erythema
Appear at different times for up to 1 week

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62
Q

Complications of chickenpox?

A

Bacterial superinfection–>TSS/Nec fas
Aseptic meningitis or encephalitis (cerebellitis)
Pneumonitis/ DIC in immunocompromised

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63
Q

Which has a better prognosis, encephalitis due to varicella zoster virus or encephalitis as a result of HSV?

A

Varicella zoster.

Encephalitis as a result of HSV has a poor prognosis.

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64
Q

Treatment of chickenpox in an immunocompromised child?

What are you trying to prevent from happening?

A

Intravenous aciclovir/ valaciclovir

Attempting to prevent severe progressive disseminated disease which has a mortality of 20%

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65
Q

Treatment of chickenpox (primary varicella zoster infection) in adolescents/adults?

A

Oral valaciclovir

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66
Q

What would you prescribe in an immunocompromised child with deficient T-lymphocyte function following contact with chickenpox?

A

Human varicella zoster immunoglobulin (VZIG)

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67
Q

What virus causes shingles?

A

Herpes zoster

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68
Q

What causes shingles?

A

Reactivation of latent varicella zoster virus causing a vesicular eruption in the dermatomal distrubution of sensory nerves

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69
Q

Where is shingles most commonly seen on the body?

A

Thorax

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70
Q

Do children get neuralgic pain with shingles?

A

Generally no

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71
Q

Recurrent or multidermatomal shingles is generally associated with what?

A

Immunosuppression (e.g. HIV infection)

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72
Q

Maternal chickenpox shortly before or after delivery what would you give the fetus?

A

Human varicella zoster immunoglobulin (VZIG)

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73
Q

What virus causes glandular fever (infectious mononucleosis)?

A

Epstein-Barr virus

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74
Q

Which virus is associated with Burkitt’s lymphoma?

A

Epstein-Barr virus

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75
Q

What is Burkitt’s lymphoma?

A

High grade B-cell lymphoma (NHL) that is rapidly growing and aggressive. It is associated with EBV and chronic malaria or immunodeficiency.

Significantly more common in sub-saharan Africa

Often presents with swelling in maxilla or mandible, or rapidly enlarging non-tender lymph nodes in neck.

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76
Q

Transmission of EBV?

A

Oral contact

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77
Q

Syndrome seen in EBV

A
  1. Fever
  2. Malaise
  3. Tonsillopharyngitis - often severe, limiting oral ingestion of fluids and food and rarely, breathing
  4. Lymphadenopathy - cervical lymph nodes

Can also see: Petechaie on soft palate, splenomegaly (50%) hepatomegaly (10%) maculopapular rash (5%) and jaundice.

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78
Q

How do you diagnose glandular fever?

A 
Atypical lymphocytes (numerous large T cells seen on blood film) 
Positive monospot test (heterophile antibody positive)
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79
Q

How long do glandular fever symptoms persist?

A

1-3 months

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80
Q

Which antibiotics should be avoided in children with glandular fever and why?

A

Amoxicillin and ampicillin can cause a florid maculopapular rash in children infected with EBV and should be avoided

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81
Q

Treatment of glandular fever?

A

Symptomatic
If airway compromised give corticosteroids
Penicillin if Group A strep on tonsils

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82
Q

Methods of transmission of CMV?

A

Saliva, genital secretions, breast milk

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83
Q

What syndrome is seen in CMV?

A

Mononucleosis syndrome (pharyngitis and lymphadenopathy) but not as prominent as EBV

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84
Q

How do you diagnose CMV?

A

Atypical lympthocytes on blood film (numerous large T-cells seen)
Negative monospot test (heterophile antibody-negative)

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85
Q

CMV infection is commonly seen in which 2 types of patients?

A
  1. Immunocompromised

2. Recipients of organ transplant (test by PCR)

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86
Q

Consequences of CMV infection (in immunocompromised patient)

A
  1. Retinitis
  2. Pneumonitis
  3. Bone marrow failure
  4. Encephalitis
  5. Hepatits
  6. Colitis
  7. Oesophagitis
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87
Q

Treatment of CMV?

A

Ganciclovir/ foscarnet

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88
Q

HHV-6 and 7 classically cause what?

A

Roseola infantum (exanthem subitum)

  • high fever with malaise
  • followed by a generalised macular rash
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89
Q

Erythema infectiosum or fifth disease is caused by what virus?

A

Parvovirus B19 (called slapped cheek syndrome)

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90
Q

When is erythema infectiosum/fifth disease most prevalent?

A

In the spring

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91
Q

Parvovirus B19 transmission route?

A

Respiratory secretions
Vertical transmission
Transfusion of contaminated blood products

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92
Q

What cells does parvovirus B19 invade?

A

Erythroblastoid red cell precursors of the bone marrow

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93
Q

Most common presentation of parvovirus B19?

A

Asymptomatic or erythema infectiosum

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94
Q

Describe symptoms of erythema infectiosum

A
  1. Fever, malaise, headache and myalgia
  2. Followed by a rash a week later on the face ‘slapped cheek’
  3. Progressing to a maculopapular rash on the trunk and limbs
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95
Q

What is an aplastic crisis?

A

The most serious consequence of Parvovirus B19 infection
- Occurs in children with chronic haemolytic anaemias where there is an increased rate of red cell turnover e.g. sickle cell/thalassemia and in immunodeficient children e.g. malignancy

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96
Q

The worst outcome of fetal parvovirus B19 infection?

A

Fetal hydrops and death

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97
Q

Give three examples of an enterovirus infection

A
  1. Coxsackie virus
  2. Echovirus
  3. Poliovirus
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98
Q

Transmission route of enterovirus?

A

Faecal-oral

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99
Q

Give three examples of diseases that are more severe in older children and adults than in younger children

A
  1. Chickenpox
  2. Parvovirus
  3. Measles
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100
Q

Clinical features of measles?

A
  1. Fever
  2. Maculopapular rash (spreads from behind the ears to the whole of the body) Maculopapular initially and then becomes blotchy)
  3. Koplik’s spots
  4. Conjunctivitis and coryza
  5. Cough
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101
Q

What are Koplik’s spots, when are they seen and at what stage in the disease?

A

White spots of the buccal mucosa seen in measles (pathognomonic)
Manifest two to three days before the rash

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102
Q

Give two serious complications of measles

A
  1. Encephalitis
  2. Subacute sclerosing panencephalitis (SSPE) - very rare appears 7 years after illness in 1/100,000 due to virus persisting in CNS
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103
Q

Treatment of measles?

A
  1. Symptomatic
  2. Isolate children who are admitted
  3. Antivirals (ribavirin)
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104
Q

Transmission of mumps?

A

Droplet spread

105
Q

What cells does the mumps virus replicate within in the respiratory tract?

A

Epithelial

106
Q

Which glands tend to be affected in mumps?

107
Q

Incubation period of mumps?

A

15-24 days

108
Q

Clinical features of mumps (give 3)

A
  1. Fever
  2. Malaise
  3. Parotitis (initially only one side may be swollen) - generally uncomfortable and children complain of eating or drinking and of earache.
  4. Can also get hearing loss but often unilateral and transient
109
Q

What blood levels can be raised in mumps?

A

Plasma amylase

110
Q

Pancreatic involvement in mumps can be determined by what two symptom and signs?

A
  1. Abdominal pain

2. Increased plasma amylase

111
Q

Infectivity period in mumps?

A

Up to 7 days after onset of parotitis

112
Q

Give 3 potential complications of mumps

A
  1. Viral encephalitis
  2. Viral meningitis
  3. Orchitis
113
Q

Give 4 symptoms and 1 sign of viral meningitis following mumps

A
  1. Neck stiffness
  2. Headache
  3. Photophobia
  4. Vomiting

Sign - lymphocytes in CSF

114
Q

What type of rash is seen in rubella and where does it occur?

A

Maculopapular rash appearing initially on the face and spreading to the whole of the body

115
Q

Incubation period of rubella

A

15-20 days

116
Q

How long does a rash in rubella last for?

117
Q

Clinical features of rubella?

A
  1. Maculopapular rash
  2. Low grade fever
  3. Lymphadenopathy (suboccipital and postauricular)
118
Q

What is the treatment for rubella?

A

There isn’t one, lies in immunisation

119
Q

How is rubella diagnosed?

120
Q

Implications of rubella in 13-16 week fetus?

A

Impaired hearing in 30%

121
Q

At what week gestation does foetal risk due to maternal rubella infection become minimal?

122
Q

Give 5 non-infective causes of a fever in children?

A
  1. Systemic juvenile idiopathic arthritis (SJIA)
  2. Systemic lupus erythematosus (SLE)
  3. Vasculitis (including Kawasaki)
  4. IBD
  5. Sarcoidosis
  6. Malignancy (leukaemia, lymphoma, neuroblastoma)
  7. Macrophage activation syndromes (HLH)
  8. Drug fever
  9. Induced illness
123
Q

Give 5 infective causes of a fever in children?

A
  1. Localised infection
  2. Bacterial infection e.g. typhoid
  3. Deep absess
  4. Infective endocarditis
  5. TB
  6. Viral infection
  7. Parasitic infection e.g. malaria
124
Q

What is Kawasaki disease?

A

Idiopathic, systemic self-limiting vasculitis

125
Q

What is the classic devastating complication of Kawasaki disease?

A

Aneurysms of the coronary arteries

126
Q

What is the classic devastating complication of Kawasaki disease?

A 
Aneurysms of the coronary arteries 
Sudden death (due to narrowing of vessels from scar formation of aneurysms --> myocardial ischaemia and sudden death)
127
Q

Which ethnicities are generally more affected by Kawasaki disease?

A
  1. Japanese

2. Afro-Caribbean

128
Q

What is the cause of Kawasaki disease?

A

Specific cause unknown
Likely to be due to immune hyperreactivity to a variety of triggers in a genetically susceptible host (polymorphism of ITPKC gene ch.19)

129
Q

What is the cause of Kawasaki disease?

A

Specific cause unknown
Likely to be due to immune hyperreactivity to a variety of triggers in a genetically susceptible host (polymorphism of ITPKC gene ch.19)

130
Q

How is Kawasaki disease diagnosed?

A

There is no diagnostic test

Clinical diagnosis

131
Q

What are the clinical features of Kawasaki disease?

A 
1. Fever >5 days
\+ four other features from:
1. Conjunctivitis (non-purulent)
2. Red mucous membranes
3. Cervical lymphadenopathy 
4. Rash
5. Red and oedematous palms and soles
6. Peeling fingers and toes
132
Q

The coronary arteries are affected in what percentage of patients within the first 6 weeks of Kawasaki disease?

133
Q

How are aneurysms from Kawasaki disease best visualised?

A

Echocardiography

134
Q

How is Kawasaki disease managed?

A
  1. IVIG (reduces risk of aneurysms)
  2. Aspirin (reduces risk of thrombosis)
  3. Antiplatelet medication if platelet count high
135
Q

What is the treatment of persistent inflammation and fever in Kawasaki disease?

A

Infliximab (monoclonal antibody against TNF-a), steroids or ciclosporin

136
Q

Age of child typically affected by Kawasaki disease?

A

6 months to 4 years with peak at end of the first year

137
Q

What would the blood results of a patient with Kawasaki disease show?

A

Raised inflammatory markers (ESR/CRP/WCC)

Platelet count rises in second week

138
Q

Clinical features of TB in children?

A
  1. Prolonged fever
  2. Malaise
  3. Anorexia
  4. Weight loss
  5. Focal signs of infection
  6. Cough
139
Q

Investigation of suspected TB in a child?

A

Collect sputum through 3 consecutive mornings of gastric washings are collected through a NG tube to visualise or culture acid-fast bacilli as generally will struggle to get a sputum sample from a child under 8 years.

Mantoux test. Remember that history of BCG vaccination needs to be accounted for as this can mean that the test is positive. Induration of >10mm in child with no vaccine or greater than 15mm in child with vaccine is indicative of TB infection.

IGRA is also increasingly being used.

X ray

140
Q

Are the Mantoux test or IGRA tests for TB specific or sensitive?

A

No - the tests cannot distinguish well between TB infection and TB disease, therefore clinical signs and symptoms must also be considered.

141
Q

Why is diagnosing TB in children with HIV difficult?

A
  1. With advanced immune suppression both skin tests and IGRA are unreactive
  2. Lymphoid interstitial pneumonitis looks like TB and is present in 20% of children with HIV
142
Q

Treatment for TB

A

Rifampicin, isoniazid, pyrazinamide, ethambutol
Rifampicin and isoniazid after 2 months

Total treatment is generally 6 months

143
Q

What is the conjugate therapy given to post-pubertal children who are receiving isoniazid as part of a TB treatment regime and why?

A

Pyridoxine - to prevent peripheral neuropathy

144
Q

What is the treatment of latent TB in children?

A

Rifampicin and isoniazid for 3 months

145
Q

What groups of children are vaccinated with the BCG in the UK?

A

Babies of high risk groups e.g. Asian or African origin or TB in family member in the last 5 years or high local prevalence.

146
Q

Which children should not receive the BCG?

A

HIV positive or immunosuppressed as they are at risk of dissemination.

147
Q

What is the most common form of transmission of HIV to a child?

148
Q

What are the three potential routes of transmission of HIV from mother to child?

A
  1. Intrauterine
  2. Intrapartum
  3. Breast-feeding
149
Q

How is HIV diagnosed in children

a) Over 18 months of age
b) Under 18 months of age

A

a) Detecting antibodies to the virus

b) HIV DNA PCR ( 2 negative within the first 3 months of life at least 2 weeks after postnatal ART)

150
Q

Why can’t HIV antibodies be used to diagnose HIV in infants under 18 months?

A

Because transplacental IgG HIV antibodies will still be present in the child if mother has HIV, so this demonstrates exposure but not necessarily infection

151
Q

Give some symptoms of children with

a) mild immunosuppression from HIV (2)
b) moderate immunosuppression (4)

A

a) MILD - lymphadenopathy, parotitis
b) MODERATE - recurrent bacterial infection, candidiasis, chronic diarrhoea and lymphocytic interstitial pneumonitis (LIP)

152
Q

What is lymphocytic interstitial pneumonitis (LIP) a sign of in children?

A

HIV infection/ EBV

153
Q

Give some symptoms of severe AIDS in children? (4)

A
  1. Opportunistic infections such as pneumocystis jiroveci pneumonia (PCP)
  2. Severe failure to thrive
  3. Encephalopathy
  4. Malignancy
154
Q

Give 6 symptoms that would alert you to test for HIV in children.

A
  1. Persistent lymphadenopathy
  2. Hepatosplenomegaly
  3. Recurrent fever
  4. Parotid swelling
  5. Thrombocytopenia
  6. SPUR infections (serious, persistent, unusual, recurrent)
155
Q

Management of child with HIV infection.

A
  1. ART therapy
  2. Prophylaxis against PCP - co-trimoxazole
  3. Immunisation (not BCG as live)
156
Q

Give two features of lymphocytic interstitial pneumonitis on a chest x-ray

A
  1. Reticulonodular shadowing

2. Hilar lymphadenopathy

157
Q

Give 4 methods of reducing MTCT of HIV?

A
  1. Use of maternal antenatal, perinatal and postnatal antiretroviral drugs
  2. Avoiding breast-feeding
  3. Active management of labour to prevent prolonged rupture of membranes.
  4. Pre-labour C-section if viral load detectable.
158
Q

What pathogen causes Lyme disease?

A

Borrelia burgdorferi

159
Q

How is lyme idease transmitted?

A

The hard tick

160
Q

How does lyme disease present?

A

Erythematous macule emerges after incubation period of 4-20 days.
Fever, headache, myalgia, arthralgia, lymphadenopathy. Usually resolves after a number of weeks.

The late stage occurs over weeks to months and neurological, cardiac and joint manifestations occur.

161
Q

How is lyme disease diagnosed?

A

Clinical and epidemiological features

Serology (repeat titres after 2-4 weeks)

162
Q

How is lyme disease treated?

A

Doxycicline (over 12 years)

Amoxicillin for under.

163
Q

What vaccines are given to a newborn?

A

BCG if child at high risk.

164
Q

What vaccine is given to children at 2,3 and 4 months of age?

A

5 in 1 vaccine - diptheria, tetanus, pertussis, Hib, polio

165
Q

What vaccine is given to children at 2, 4 and 13 months?

A

Pneumococcal conjugate vaccine (PCV-13)

166
Q

What vaccine is given to children at 3 and 4 months?

A

Group C meningococcus

167
Q

What vaccines are administered to children at between 12-13 months

A
  1. Booster Hib
  2. MenC
  3. MMR
168
Q

What vaccine is given at between 12-13 years to females?

169
Q

What two strains of the human papillomavirus are protected against by the HPV vaccine and what percentage of cervical cancer do they cause?

A

HPV 16 and 18

70%

170
Q

What is primary immune deficiency?

A

An intrinsic defect in the immune system

171
Q

What is secondary immune deficiency and give 5 examples of causes.

A

Caused by another disease or treatment e.g.

  1. Malignancy
  2. HIV infection
  3. Immunosuppressive therapy
  4. Splenectomy
  5. Nephrotic syndrome
172
Q

Give 5 presentations of immune deficiency

A
  1. Recurrent or severe bacterial infection (e.g. meningitis, pneumonia, osteomyelitis)
  2. Atypical infections/ opportunistic pathogen
  3. Extensive candidiasis
  4. Severe or long lasting warts - molluscum contagiosum
  5. Recurrent or prolonged diarrhoea
173
Q

ALLERGY: Define hypersensitivity

A

Objectively reproducible signs and symptoms following exposure to a stimulus at a dose that would normally be tolerated by most people

174
Q

Define allergy

A

A hypersensitivity reaction inititated by specific immunological mechanisms. Can be either IgE or non-IgE mediated

175
Q

Define atopy

A

A familial or personal tendency to produce IgE antibodies in response to ordinary exposures to potential allergens . Strongly associated with asthma, allergic rhinitis, conjunctivitis, eczema and food allergy

176
Q

Define anaphylaxis

A

A serious allergic reaction with bronchial, laryngeal or cardiovascular involvement that is rapid in onset and may cause death

177
Q

Describe some of the symptoms in an early and late phase of IgE mediated reaction

A

Early - within 10 ish minutes caused by release of histamine from mast cells, urticaria, angioedema, sneezing, vomiting, bronchospasm and/or cardiovascular shock

Late- 4-6 hours later in reactions to inhalant allergens in particular. Nasal congestion in upper airway, cough and bronchospasm in lower airways

178
Q

A non-immunological hypersensitivity reaction to a specific food is called what?

A

Food intolerance

179
Q

Most common food allergens in infants?

A

Milk, egg, peanut

180
Q

Most common food allergens in older children?

A

Peanut, treenut, shellfish, fish

181
Q

What is primary and secondary food allergy

A 
Primary = children react on first exposure
Secondary = cross reactivity between proteins present in fresh fruit/veg/nuts and those present in pollens as they share similar proteins
182
Q

How does Non-IgE mediated reaction typically present?

A
  1. Diarrhoea
  2. Vomiting
  3. Abdo pain
  4. Faltering growth

Can get colic or eczema

183
Q

How is IgE mediated food allergy diagnosed?

A

Skin prick test

Measurement of IgE antibodies in blood

184
Q

How is Non-IgE mediated food allergy diagnosed?

A

Clinical history and examination

Endoscopy and intestinal biopsy if indicated - eosinophilic infiltrates confirms

185
Q

If in doubt about IgE and non-IgE allergies what is the gold standard investigation

A

Exclusion of relevant food under dietician supervision

186
Q

Wheals of what size are considered positive for IgE mediated allergy?

187
Q

What percentage of children with atopic eczema also develop other allergic diseases

188
Q

What is the key genetic risk factor for eczema development

A

Filaggrin gene mutations as impair the skin barrier function which leads to cutaneous sensitization to inhalant and food allergens

189
Q

Filaggrin gene mutations predispose to what?

A

Food allergy, asthma, hay fever and eczema

190
Q

Management of allergic rhinoconjunctivitis?

A
  1. Non-sedating antihistamines
  2. Topical corticosteroids (nasal or eye)
  3. Cromoglycate eye drops
  4. Leukotriene receptor antagonists (montelukast)
  5. Nasal decongestants
191
Q

What are the two main causes of acute urticaria?

A
  1. Viral infection (rash for days)

2. Allergen exposure (rash for hours)

192
Q

Treatment of urticaria?

A
  1. Second generation non-sedating antihistamines
  2. If resistant; leukotriene receptor antagonist
  3. anti-IgE antibody (omalizumab)
193
Q

Definition of acute urticaria?

A

Resolves within 6 weeks

194
Q

What is the main risk you worry about if an allergy (specifically food allergy) causes urticaria?

A

Risk of anaphylaxis

195
Q

HAEM: What are the three causative mechanisms of anaemia

A
  • Reduced production
  • Increased destruction
  • Blood loss
196
Q

What are the two causes of reduced RBC production and give 2 examples of each

A
  1. Ineffective erythropoeisis - iron deficiency, folic acid deficiency, chronic inflammation
  2. Red cell aplasia - parvovirus b19, diamond blackfan anaemia, transient erythroblasteamia of childhood, aplastic anaemia
197
Q

What are the blood findings of a child with ineffective erythropoiesis?

A
  1. Normal reticulocyte count

2. Abnormal MCV (low in ID, high in FAD, B12)

198
Q

What are the blood findings of a child with red cell aplasia?

A
  1. Low reticulocyte count despite low Hb
  2. Normal bilirubin
  3. Negative coombs test
  4. Absent red cell precursors on BM exam
199
Q

What is the definition of anaemia

A

Hb level below normal

200
Q

3 causes of iron deficiency anaemia

A
  1. Inadequate intake
  2. Malabsorption
  3. Bleeding
201
Q

Signs of iron deficiency anaemia

A
  1. Tire easily
  2. Poor cognition, reduced psychomotor development
  3. Pallor (conjunctiva, tongue, palmar creases)
  4. Pica
202
Q

How do RBC’s appear on blood film in iron deficiency anaemia
Ferritin level?

A

Microcytic
Hypochromic

Ferritin low

203
Q

Give three causes of microcytic anaemia

A
  1. Iron deficiency anaemia
  2. B-thalassemia
  3. Anaemia of chronic disease
204
Q

Management of iron deficiency anaemia

A

Ferrous fumarate until Hb normal + 3 months

205
Q

Give two causes of red cell aplasia

A

Diamond-Blackfan anaemia

Transient erythroblastopenia of childhood

206
Q

Give the four classes of increased destruction of RBC and give an example of each

A
  1. Haemoglobinopathy e.g. thalassemia, sickle cell
  2. Membranopathy e.g. spherocytosis
  3. Immune e.g. haemolytic disease of newborn
  4. Enzyme disorder G6PD deficiency
207
Q

Give 5 signs of increased destruction of RBC’s causing anaemia

A
  1. Hepatomegaly/splenomegaly
  2. Increased unconjugated bilirubin in blood
  3. Excess urinary urobilinogen
  4. Raised reticulocyte count
  5. Abnormal appearance on blood film
  6. Increased precursers in BM
208
Q

Hereditary spherocytosis?

A

AD
25% new mutations

Jaundice, anaemia, splenomegaly, aplastic crisis caused by parvovirus B19, gallstones

Caused by mutations in genes for membrane. Loses part of membrane through spleen, becomes spheroidal and destroyed in microvasculature

Rx: Oral folic acid to increase RBC production, splenectomy after 7y

209
Q

If child with hereditary spherocytosis has aplastic crisis what is management?

A

1/2 blood transfusions

210
Q

What must be done prior to splenectomy?

And after?

A

Vaccinate with Hib, Men C, strep pneumonaie

Lifelong oral penicillin daily

211
Q

G6PD deficiency?

A

Enzyme disorder causing anaemia

X-linked.
It is the rate limiting enzyme in pentose phosphate pathway and is essential for preventing oxidative damage to red cells

Presents with neonatal jaundice, acute haemolysis.

  • Fever
  • Malaise
  • Abdo pain
  • Dark urine

Manage by giving parent a list of things to avoid precipitation of haemolysis (infection, drugs, favabeans)
Drugs - antimalarials, antibiotics, aspirin
Tell them to look out for signs of haemolysis (jaundice, pallor, dark urine)

212
Q

Signs of acute haemolysis

A

Jaundice
Pallor
Dark urine

213
Q

Inheritance of sickle cell?

214
Q

Inheritance of G6PD

215
Q

HbS is a point mutation of which globin gene?

216
Q

What are the complications of HbSC disease?

A

Nearly normal Hb but proliferative retinopathy

Osteonecrosis of hips and shoulders

217
Q

What exacerbates HbS polymerisation?

A
  1. Low o2
  2. Dehydration
  3. Cold

be aware of strenuous exercise and stress

218
Q

Management of a patient with sickle cell?

A
  1. Immunize (pneumococcal, Hib, meningococcus)
  2. Daily oral penicillin
  3. OD folic acid
219
Q

Treatment of an acute crisis?

A 
Analgesia
Hydrate
O2 CPAP
Broad spec antibiotic
Exchange transfuse if acute chest syndrome, stroke, priapism
220
Q

3 scenarious you’d exchange transfuse in sickle cell?

A
  1. Acute Chest Syndrome
  2. Priapism
  3. Stroke
221
Q

If acute crises become chronic?

A
  1. Hydroxycarbamide

2. BMT

222
Q

What is the neonatal screening test for sickle cell?

A

Guthrie test

223
Q

Symptoms of Sickle cell?

A
  1. Anaemia
  2. Clinically jaundiced
  3. Infection from encapsulated organisms (functional asplenia)
  4. Splenomegaly
  5. Painful crises (ACC, avascular necrosis of femoral head, dactylitis)
224
Q

Long term sequelae of SCD?

A
  • Short stature and delayed puberty
  • Stroke/neuro damage
  • Adenotonsillar hypertrophy –> OSA
  • Cardiac enlargement/ HF due to uncorrected anaemia
  • Gallstones
225
Q

Inheritance of B thalassemia

226
Q

When does B thalassemia typically present?

A

3-6 months of life

227
Q

Symptoms of B thalassemia?

A
  1. Anaemia
  2. Faltering growth
  3. Jaundice
  4. Hepatosplenomegaly –> bone marrow expansion –> classical facies (maxillary overgrowth and skull bossing)
  5. Secondary haemochromatosis
228
Q

Signs of haemochromatosis?

A
  1. Pericarditis
  2. Arrhythmia
  3. DM
  4. Cirrhosis
  5. Hypothyroidism
229
Q

Management of B thalassemia major

A
  1. Regular transfusion (monthly)
  2. Desferrioxamine (iron chelate)

Or BMT

230
Q

B thalassemia trait can be confused with what and why?

A

Iron deficiency because both have microcytic hypochromic anaemias

Difference is SERUM FERRITIN

231
Q

How do you differentiate between iron deficiency anaemia and B thalassemia trait?

A

Serum ferritin

232
Q

How is B thalassemia diagnosed?

A

Haemoglobin electrophoresis

233
Q

Pathogenesis of haemolytic disease of the newborn?

A

Baby has blood group antigen e.g. rhesus D, A,B,O
Mother is negative for this antigen and baby is positive
Mother produces antibodies against blood group eg. Anti D. These cross placenta = haemolytic anaemia

234
Q

How is haemolytic disease of newborn diagnosed?

A

Coombs test

235
Q

Inheritance of haemophilia?

A

X linked

2/3 have family history

236
Q

What factor deficiencies are seen in Haemophilia A and B

A 
A = FVIII
B= FIX
237
Q

Symptoms of haemophilia

A

Recurrent bleeding into joints and muscles (arthritis)
Presents around 1 year when falling
40% in neonatal period with intracranial haemorrhage, prolonged heel prick bleed

238
Q

Rx of haemophilia

A

Recombinant FVIII/FIX concentrate by IV infusion when bleeding or constantly.

Desmopressin if mild

239
Q

What must be avoided in children with haemophilia?

A

IM injections, aspirin and NSAIDS

240
Q

What is the function of vWF?

A
  • Adheres platelets to damaged endothelium

- Acts as a carrier protein for FVIII

241
Q

Inheritance of vWD?

242
Q

When does vWD present?

A

Generally mild so not picked up until adulthood or puberty

243
Q

Symptoms of vWD?

A
  • Bruising
  • Prolonged bleeding after surgery
  • Mucosal bleeding - menorrhagia or epistaxis
244
Q

Differences between haemophilia and vWD in symptoms?

A

Soft tissue bleeding rare in vWD

245
Q

Rx of vWD?

A

Desmopressin and if severe plasma derived FVIII

246
Q

What is the cause of ITP?

A

Destruction of circulating platelets by antiplatelet IgG autoantibodies

247
Q

Typical presentation of ITP?

A

2-10 yr old child
1-2 weeks post viral infection
Petechiae, purpura, superficial bruising
Mucosal bleeding

248
Q

Thrombocytopenia?

A

<150 x 10^9 platelets/L

249
Q

Appearance of BM in ITP?

A

Increased megakaryocytes

250
Q

Atypical features of ITP?

What would you do?

A

Anaemia, neutropenia, hepatosplenomegaly, lymphadenopathy

Bone marrow investigation

251
Q

Differentials of ITP with atypical features?

252
Q

Management of ITP?

A

Majority at home as 80% acute and self limiting

If major bleeding or minor bleeding that is persistent can treat with oral prednisolone
anti-D and IV Ig

253
Q

Treatment of chronic ITP?

254
Q

What is DIC?

A

Coagulation pathway activation
Fibrin deposition in microvasculature
Consumption of coagulation factors and platelets

255
Q

Causes of DIC?

A

Sepsis, shock due to circulatory collapse e.g. tissue damage from trauma or burns

256
Q

Clinical features of DIC?

A

Bruising, purpura, harmorrhage, purpura fulminans

257
Q

Rx of DIC?

A

Treat underlying cause
FFP
Cryprecipitate
Platelets

258
Q

Give 3 causes of non-thrombocytopenic and thrombocytopenic purpura/petechiae

A

Non-thrombocytopenic - HSP, sepsis

Thrombocytopenic - ITP, Leukaemia, DIC

Phase 3A Medicine (12 decks)

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