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Phase 3a > Paediatrics (1) > Flashcards

Paediatrics (1) Flashcards

1
Q

Aetiology of pneumonia in children

A

<5YO = viruses (most common = RSV)
>5YO = Mycoplasma pneumoniae/ Strep. pneumoniae/ Chlamydia pneumoniae

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2
Q

Clinical presentation on pneumonia in children

A

Fever, cough, rapid breathing (usually preceded by URTI)

Other: nasal flaring, chest indrawing, poor feeding, ‘unwell’ child

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3
Q

Management of pneumonia children

A

Supportive - oxygen, analgesia, IV fluids
Admission criteria: O2<92%, recurrent apnoea, inability to maintain to adequate fluid/ feed

Medical - oral amoxicillin (consider erythromycin if >5YO)

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4
Q

Why might you admit a child with pneumonia to hospital?

A

Admission criteria: O2<92%, recurrent apnoea, inability to maintain to adequate fluid/ feed

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5
Q

What is croup?

A

viral laryngotracheal infection characterised by barking cough + acute stridor, most common in infants (6 months - 3YO) in winter

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6
Q

Most common age for croup in children

A

6 months to 3YO

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7
Q

Most common aetiology of croup

A

Parainfluenzae = most common

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8
Q

Clinical presentation of croup

A

Upper resp symptoms (e.g. runny nose), fever, hoarseness, barking cough, inspiratory stridor

Mild = no stridor at rest, barking cough, mild work of breathing
Moderate = stridor at rest, mild work of breathing, no agitation
Severe = significant stridor at rest, severe respiratory distress, child = anxious/ pale/ tired

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9
Q

Investigations of suspected croup

A

Clinical Dx - Upper resp symptoms (e.g. runny nose), fever, hoarseness, barking cough, inspiratory stridor

CXR if unclear (steeple sign = indicative, subglottic tracheal narrowing)

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10
Q

What does the steeple sign on a CXR indicate?

A

Croup

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11
Q

Management of croup

A

Mild: oral dexamethasone (0.15mg/kg) + discharge with advice

Moderate: oral dexamethasone (0.15-0.3mg/kg) + observe for improvement/ discharge when stable

Severe: nebulised adrenaline, oxygen, oral OR IV/IM dexamethasone (0.3-0.6mg/kg) + monitoring

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12
Q

Assessing the severity of croup

A

Mild = no stridor at rest, barking cough, mild work of breathing
Moderate = stridor at rest, mild work of breathing, no agitation
Severe = significant stridor at rest, severe respiratory distress, child = anxious/ pale/ tired

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13
Q

Define asthma

A

chronic respiratory condition associated with airway inflammation + hyperresponsiveness, presents with multiple trigger wheeze

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14
Q

List potential triggers for asthma

A

Dust, excercise, cold, emotional upset, animal dander

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15
Q

Pathophysiology of asthma

A

Environmental triggers (e.g. cold air, dust, exercise, animal dander, emotional upset) + genetic predisposition + atopy → bronchial inflammation → bronchial hyperresponsiveness to inhaled stimuli → airway narrowing (reversible airflow obstruction) → symptoms

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16
Q

Clinical presentation of asthma

A

Multiple episodic wheeze associated with cough/ SOB/ chest tightness

Personal/ family Hx of atopic diseases
Diurnal variation (worse at night/ early in morning)
Positive response to asthma therapy

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17
Q

Diagnosis of asthma

A

Usually clinical.
Spirometry - reversible obstructive pattern (FEV1:FVC <70%)
Improvement of FEV1 by 12% or 200ml w/ bronchodilator
Improvement of FEV1 by 400ml w/ bronchodilator
PEFR - diurnal variation + reversible airflow obstruction
Other - skin prick test (suggest atopy), FeNo (>= 35ppb eosinophilic inflammation

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18
Q

Spirometry findings that are indicative of asthma

A

reversible obstructive pattern (FEV1:FVC <70%)
Improvement of FEV1 by 12% or 200ml w/ bronchodilator
Improvement of FEV1 by 400ml w/ bronchodilator

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19
Q

Management of chronic asthma

A

PRN SABA (salbutamol OR ipratropium bromide) → + ICS (e.g. beclomethasone/ budesonide) → + LABA (salmeterol)/ LTRA (Montelukast)

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20
Q

Severity of asthma attacks

A

Moderate - able to talk, O2 sat>92%, peak flow >50% [best]
Severe - too SOB to talk, O2 sat <92% (if <12YO), peak flow 33-50% [best]
Life-threatening - silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, peak flow <33% [best], O2 sat <92% (all ages)

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21
Q

Features of a life-threatening asthma attack

A

silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, peak flow <33% [best], O2 sat <92% (all ages)

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22
Q

Management of a life-threatening asthma attack

A

high flow oxygen + SABA nebulised + oral prednisolone/ IV hydrocortisone + nebulised ipratropium

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23
Q

Management of a moderate asthma attack

A

Moderate: SABA via spacer (2-4 puffs, increase by 2 puffs every 2 mins until 10 puffs) +/- oral prednisolone (1-2mg/kg, max 40mg)

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24
Q

Define bronchiolitis

A

mucosal inflammation + swelling of bronchioles, usually caused by an acute viral illness (RSV = 80%), peak incidence at 3-6 months in winter

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25
Q

Most common cause of bronchiolitis

A

Acute viral illness - RSV = 80%

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26
Q

Risk factors for bronchiolitis

A

Chronic lung disease, congenital heart disease, prematurity, Down’s syndrome, CF, neuromuscular disease

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27
Q

Clinical presentation of Bronchiolitis

A

Coryzal symptoms → dry wheezy cough + increased SOB (often associated with feeding)

Clinical signs: hyperinflation of the chest, subcostal + intercostal recession, fine-end inspiratory crackles, prolonged expiratory/ wheeze (expiratory&raquo_space; inspiratory)

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28
Q

Diagnoses of bronchiolitis

A

Clinical. Coryzal symptoms for 3 days followed by cough/ tachypnoea/ wheeze/ crackles.

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29
Q

Management of bronchiolitis

A

Supportive (majority): monitor for apnoea, fluid support (oral/ NG/ IV), high flow oxygen/ CPAP

Admission criteria: O2<92%, poor feeding, persistent respiratory distress, social concern

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30
Q

Why might a child with bronchiolitis be admitted to hospital?

A

Admission criteria: O2<92%, poor feeding, persistent respiratory distress, social concern

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31
Q

What is cystic fibrosis?

A

autosomal recessive condition caused by a defective protein (CFTR) leading to a multisystem disorder characterised by thickened secretion + recurrent respiratory infections

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32
Q

Clinical presentation of CF

A

Neonatal screening - heel prick test + confirm w/ sweat test

Neonate w/ meconium ileus - in utero bowel obstruction (CP = vomiting, distent Abdomen, failure to pass meconium

Child w/ persistent ‘wet’ cough + recurrent respiratory infections
Other: pancreatic insufficiency (malabsorption, faltering growth, steatorrhoea, DM), nasal polyps, sinusitis, rectal prolapse, finger clubbing

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33
Q

Abnormal sweat test results

A

Cl concentration = 60-125mmol/L

Indicative of CF

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34
Q

Diagnoses of CF

A

2 +ve sweat tests + suggestive clinical assessment

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35
Q

How does heel prick screening test identify CF?

A

detects raised immunoreactive trypsinogen in neonates, +ve screening → screened for common CF gene mutations, 2 mutation → sweat test to confirm Dx

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36
Q

Management of CF

A

Rep: physiotherapy, mucolytics (hypertonic saline/ dornase alfa), prophylactic abx/ abx for for acute exacerbations

Nutrition: pancreatic enzyme supplementation (Creon)

Lung/ liver transplant: end stage organ failure

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37
Q

What is acute epiglottitis?

A

intense swelling of the epiglottis and surrounding tissues associated with septicaemia, life-threatening due to the risk of respiratory obstruction

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38
Q

Most common causative organism of acute epiglottitis

A

Haemophilus influenzae type b (Hib)

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39
Q

Clinical presentation of acute epiglottitis

A

Acute onset: high-grade fever, very ill child, drooling, muffled voice, inspiratory stridor, respiratory distress
TRIPOD POSITION
Cough minimal/ absent

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40
Q

Caution for investigating epiglottitis

A

Avoid assessment unless the airway is stable
First-line = laryngoscopy in controlled setting (second line = lateral neck radiograph)

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41
Q

Management of acute epiglottitis

A

Priority = secure airway
Other: nebulised adrenaline, high-flow oxygen, IV antibiotics (ceftriaxone), corticosteroids (dexamethasone), fluid replacement, analgesia

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42
Q

What is acute otitis media (AOM)?

A

infection of the middle ear that presents over days to weeks and is characterised by severe ear pain + visible inflammation of the tympanic membrane, peak incidence at 6-15 months

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43
Q

Aetiology of acute otitis media

A

S. pneumoniae = most common. Other bacterial = H. influenzae. Other viral = RSV.

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43
Q

Clinical presentation of otitis media

A

Ear pain, malaise, fever, coryzal symptoms lasting a few days

Otoscopy: erythematous tympanic membrane, potentially bulging/ perforated (small tear w/ purulent discharge in auditory canal)

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43
Q

Otoscopy findings for acute otitis media

A

Otoscopy: erythematous tympanic membrane, potentially bulging/ perforated (small tear w/ purulent discharge in auditory canal)

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44
Q

Management of acute otitis media

A

Majority resolve spontaneously within 24hrs - simple analgesia
Abx = systemically unwell, unwell for 4 days, discharge from ear, <2YO w/ bilateral infection

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45
Q

Complication of acute otitis media

A

Mastoiditis - infection spreads from middle ear to mastoid air cells → sub-periostal abscess behind ear → tenderness/ swelling behind + pushing forward of pinna AND neurological complications

Mx - IV abx (high-dose co-amoxiclav/ ceftriaxone)

Can lead to facial nerve palsy/ hearing loss

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46
Q

What is glue ear?

A

Otitis Media Effusion (OME) - build up of viscous inflammatory fluid within the middle ear → conductive hearing loss

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47
Q

Risk factors for glue ear

A

Bottle fed, paternal smoking, atopy, genetic disorders (Down’s syndrome, CF)

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48
Q

Clinical presentation + examination findings of glue ear

A

Difficulty hearing, pressure sensation, popping/ crackling in era

O/E: dull tympanic membrane, lost light reflexes

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49
Q

Management of glue ear

A

Monitoring (50% resolve within 3 months)
Non-surgical: hearing aids
Surgical: myringotomy + grommet insertion

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50
Q

What is a grommet?

A

tiny tubes inserted into tympanic membrane to allow fluid from the middle ear to drain out through membrane into ear canal, fall out within a year, ⅓ of patients require further grommet insertion

Insert if (NICE guidelines): > 3 months bilateral OME + hearing level in better ear <25-30dB

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51
Q

Criteria for inserting a grommet (NICE guidelines)

A

> 3 months bilateral OME + hearing level in better ear <25-30dB

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52
Q

Types of hearing loss

A

Sensorineural: caused by lesion on cochlear/ auditory nerve, usually present at birth and doesn’t improve, Mx: amplification/ cochlear implant

Conductive: caused by abnormalities in ear canal/ middle ear, intermittent/ may resolve, Mx: conservative/ amplification/ surgery

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53
Q

Aetiology of sensorineural hearing loss

A

genetic (majority), congenital infection, preterm baby, postnatal meningitis/ encephalitis

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54
Q

Aetiology of conductive hearing loss

A

OME (60%), eustachian tube defect (Down’s syndrome, cleft palate), wax (rare)

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55
Q

Investigating hearing loss

A

Objective (neonates/ infants) - e.g. otoacoustic emission (OAE) - part of newborn screening programme, identify moderate-profound deafness at birth (>40dB), misses mild losses

Subjective (behavioural) - e.g. Distraction Test - performed at 6-18 months, tests whether infant tries to turn/ find sound

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56
Q

What is moderate hearing loss?

A

Mild (20-40-dB) - may use hearing aids, struggle with background noise/ whispered conversation

Moderate (41-70-dB) - hearing aids, difficulty in a group/ background noise even with hearing aids

Severe (71-95-dB) - hearing aids w/ communication aids, without unable to hear speech

Profound (>95-dB) - hearing aids/ cochlear implant, without unable to hear speech/ most environmental sound

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57
Q

What is profound hearing loss?

A

Mild (20-40-dB) - may use hearing aids, struggle with background noise/ whispered conversation

Moderate (41-70-dB) - hearing aids, difficulty in a group/ background noise even with hearing aids

Severe (71-95-dB) - hearing aids w/ communication aids, without unable to hear speech

Profound (>95-dB) - hearing aids/ cochlear implant, without unable to hear speech/ most environmental sound

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58
Q

What is periorbital cellulitis?

A

infection of the periorbital soft tissue characterised by erythema + oedema, can lead to vision loss + life-threatening consequences

Staphylococcus aureus = most common (prev. Hib before immunisation)

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59
Q

Clinical presentation of periorbital cellulitis

A

Acute onset pain + swelling in the periorbital region +/- Hx of recent URTI/ trauma

Features of meningism on examination indicates intracranial spread of infection

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60
Q

Imaging for periorbital cellulitis

A

CT head - assess complications (e.g. abscess formation/ cavernous sinus thrombosis)

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61
Q

Management of periorbital cellulitis

A

IV abx + appropriate analgesia
Surgical drainage of subperiosteal + orbital abscesses

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62
Q

What is Starbismus?

A

Squint. When the eyes misaligned when focusing on an object can be occasional (phoria) or constant (tropia), often onset in childhood

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63
Q

Aetiology of squint

A

Primary - idiopathic/ congenital

Secondary - cranial nerve palsies, intracranial infection, intracranial/ intraorbital/ intraocular masses

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64
Q

Sequelae of squint

A

amblyopia (lazy eye) - brain unable to process input from one eye so favours the other leading to structural changes in visual pathway and cortex → decreased vision in an eye that’s otherwise normal

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65
Q

What is amblyopia?

A

Lazy eye.

brain unable to process input from one eye so favours the other leading to structural changes in visual pathway and cortex → decreased vision in an eye that’s otherwise normal

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66
Q

Why is it important to assess and treat squints early in life?

A

Need to start treatment <8YO (visual fields still developing). Delay = increased risk of permanent squint.

Occlusive patch - cover good eye and force weaker eye to develop

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67
Q

Types of squint

A

Esotropia/ phoria - inward deviation
Exotropia/ phoria - outward deviation
Hypertropia/ phoria - upward deviation
Hypotropia/ phoria - downward deviation

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68
Q

Clinical examination of potential squint

A

light reflex test (Hirschberg test), Bruckner test, cover test, cover-uncover test

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69
Q

What is Kawasaki’s disease?

A

Small/ medium vessel vasculitis, most common in children < 5YO, characterised by fever > 5 days + CREAM presentation

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70
Q

Clinical presentation of Kawasaki’s

A

Fever > 5 days + CREAM: conjunctivitis, rash (erythematous, maculopapular), edema (hands/ feet), adenopathy (cervical lymphadenopathy), mucous membrane changes (strawberry tongue, cracked/ red lips)

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71
Q

Investigations for Kawasaki’s

A

Echocardiogram/ ECG - identify/ monitor cardiovascular complications that often arise from 3rd week to 2nd month post-infection

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72
Q

Complications of Kawasaki disease

A

Gallop rhythm, myocarditis/ pericarditis, coronary artery aneurysms

73
Q

Management of Kawasaki disease

A

IV immunoglobulins
High-dose aspirin

74
Q

Why is aspirin usually avoided in children?

A

Reye’s syndrome - severe progressive encephalopathy affecting children that is accompanied by fatty infiltration of liver/ kidneys/ pancreas. Mx = supportive.

75
Q

Causative organism of measles

A

RNA paramyxovirus

76
Q

Clinical presentation of measles

A

Fever, cough, runny nose, conjunctivitis, marked malaise with specific features:

Koplik’s spots (white spots on buccal mucosa)
Rash (spreads downwards from behind ears to whole of body, initially maculopapular → blotchy + confluent)

77
Q

What are Koplik spots?

A

White spots on buccal mucosa that are associated with measles.

78
Q

Epidemiology of Kawasaki’s disease

A

Children (<5YO) of Japanese or black-Caribbean ethnicity

79
Q

Management of measles

A

Advice (drink water, rest, simple analgesia) - usually self-limiting within a week

Stay away from at risk groups for 4 days after initially developing rash (at risk = pregnant women, immunocompromised, infants, un-vaccinated)I

80
Q

Isolation of children with measles

A

4 days after onset of rash

81
Q

Isolation of children with chicken pox

A

Until all lesions have crusted over (usually 5 days from onset of rash)

82
Q

Isolation of children with Rubella

A

5 days from onset of rash

83
Q

Complications of Measles

A

Resp - pneumonia 2ry bacterial infection/ otitis media, tracheitis

Neuro - febrile convulsions, EEG abnormalities, encephalitis

Other - diarrhoea, hepatitis, appendicitis, corneal ulceration, myocarditis

84
Q

Chicken pox vs. shingles

A

Chicken pox = primary infection caused by varicella zoster virus + characterised by a very itch vesicular rash

Shingles = reactivation of dormant virus in dorsal root ganglia

85
Q

Causative organism of chickenpox

A

Varicella zoster virus

86
Q

Clinical presentation of chicken pox

A

Advice (fluid intake, smooth/ cotton fabrics)

Symptomatic Mx - paracetamol, topical calamine lotion (alleviate itch), chlorphenamine (avoid in pregnant/ breastfeeding women)

87
Q

Complications of chicken pox

A

Secondary bacterial infection of the lesions

Disseminated disease in immunocompromised: give high-risk individuals Human varicella zoster immunoglobulin (VZIG) following contact
(If chickenpox develops, consider IV acyclovir)

88
Q

Why might human varicella zoster immunoglobulins (VZIGs) be given to someone?

A

High-risk immunosuppressed individual following contact with chickenpox.

89
Q

When is chickenpox the most infective?

A

1-2 days before onset of rash

90
Q

Chickenpox rash description

A

Very itchy vesicular rash

Starts on head (check scalp) + trunk, progress to peripheries

91
Q

What is rubella?

A

Viral infection caused by togavirus + spread via direct contact, maternal infection in non-immune women can cause some serious complications

92
Q

Clinical presentation of rubella

A

Mild - fever, maculopapular rash initially on face then spread to whole of body (fades in 3-5 days)

Suboccipital and postauricular lymphadenopathy

NOT ITCHY

93
Q

Complications of rubella

A

Arthritis, thrombocytopenia, encephalitis, myocarditis

94
Q

What is congenital rubella syndrome?

A

Complications of rubella caused when a non-immune women is infected during her 1st trimester

Teratogenesis, sensorineural deafness, congenital cataracts, congenital heart disease, cerebral palsy, microcephaly

95
Q

Features of congenital rubella syndrome

A

Teratogenesis, sensorineural deafness, congenital cataracts, congenital heart disease, cerebral palsy, microcephaly

96
Q

Is Rubella a notifiable disease?

A

Yes. Alter local health protection unit

97
Q

Why should pregnant women not be offered the MMR vaccine?

A

Risk of congenital rubella syndrome

Wait until they are post natal

98
Q

Management of rubella

A

Supportive. Notifiable disease (alert local health protection team, HPT)

99
Q

5YO boy. Unsure about immunisations. 2wks ago had cough, coryza, conjunctivitis and fever. Now developed a maculopapular rash that’s started down from his hairline and spread downwards. What’s your top differential?

A

Measles

100
Q

6YO boy. Unsure of immunisation Hx. Come to paeds A&E in winter time. Had mild fever 1wk ago. Now has maculopapular rash, starting on face and spread down whole body. You spot Forchheimer spots + posauricular lymphadenopathy. Top differential?

A

Rubella

101
Q

A 3-year-old girl is brought into A&E following a 1 week history of fever, lethargy and irritability. Her symptoms came on suddenly and despite being given paracetamol and ibuprofen she remains pyrexic. She has a reduced appetite and earlier this morning a widespread red rash appeared on her trunk. Examination reveals a widespread maculopapular rash, cervical lymph node enlargement, a swollen, bright red tongue and conjunctivitis. She is tachycardic and has a temperature of 39.2ºC.

Given the likely diagnosis, what is the most important investigation in this child?

A

Echocardiogram - coronary artery aneurysms are a complication of Kawasaki disease. This should be screened for with an echocardiogram.

102
Q

A 6-year-old boy presents with a 3-day history of fever, sore throat, rash and enlarged lymph nodes behind his ears and back of his neck. He has an red, maculopapular rash on his face and neck that has started spreading down his body. He has not received any routine childhood immunisations.

Given the most likely diagnosis, what is the most appropriate school exclusion criteria?

A

Top differential = rubella - fever, mild coryzal, characteristic rash + lymphadenopathy

Exclusion criteria = children do not return to school for 5 days from the onset of the rash.

103
Q

What is diptheria?

A

Infection caused by Corynebacterium. Part of 1 in 5 vaccine giiven at 2, 3, 4 months.

Eradicated in the UK

104
Q

Clinical presentation of Diptheria

A

CP: thick white membrane over posterior pharynx in an unvaccinated child

Causes local disease (membrane formation affecting nose/ pharynx/ larynx) OR systemic disease (e.g. myocarditis/ neurological manifestations)

105
Q

What is scalded skin syndrome

A

staphylococcal toxin causes areas of epidermis to separate on gentle pressure (Nikolsky sign) leaving denuded areas of skin, rare but serious

106
Q

Clinical presentation of Scalded skin syndrome

A

Fever, malaise followed by… generalised patches of erythema → bullae (fluid-filled blisters) → bullae burst leaving tender erythematous skin similar to burn

Most fully recover with no scarring

107
Q

Management of scalded skin syndrome

A

IV anti-staphylococcal antibiotics + analgesia + monitor fluid balance (prone to dehydration)

107
Q

Causative organism of whooping cough

A

bordatella pertussis (gram -ve bacteria)

108
Q

What is whooping cough

A

respiratory infection caused by bordatella pertussis (gram -ve bacteria), characterised by paroxysmal cough followed by inspiratory whoop + vomiting, notifiable disease

109
Q

Clinical presentation of whooping cough

A

Catarrhal phase: wk of coryza (runny dose, sore throat, conjunctivitis, malaise)

Paroxysmal phase: severe dry cough followed by an inspiratory whoop, often culminates in vomiting

110
Q

Management of whooping cough

A

Vaccination @ 8,12,16wks

Low threshold for hospital admission + macrolide abx (erythromycin/ azithromycin/ clarithromycin) if cough onset < 21 days + supportive care (rest, hydration, analgesics, antipyretics)

Stay at home until 48hrs after abxs started (or 21 days after symptoms started)

111
Q

Diagnosis of whooping cough

A

Culture of per-nasal swab

Marked lymphocytosis on blood film

112
Q

Exclusion period for whooping cough

A

Stay at home until 48hrs after abxs started (or 21 days after symptoms started)

113
Q

Complications of whooping cough

A

Secondary pneumonia, apnoea, cerebral hypoxia, dehydration, weight loss, rectal prolapse, hernias, rib #s, pneumonthorax

Less serious: epistaxis, subconjunctival haemorrhage, otitis media

114
Q

What is polio?

A

vaccination given as part of ‘5 in 1’ vaccine at 2,3, and 4 months of age, almost eradicated worldwide, complication = paralytic polio

115
Q

Clinical presentation of polio

A

Children <5YO, most cases asymptomatic/ mild

Paralytic polio - CP: headache, vomiting, stiffness of neck, pain in limbs, paralysis within hrs, fatal when respiratory muscles become immobilised

116
Q

CXR changes seen in tuberculosis

A

Ghon complex

Lung collapse

Pleural effusion

117
Q

Investigations for diagnosing TB

A

Sputum culture = gold-standard

Sputum smear

Mantoux test - 0.1 ml of 1:1,000 purified protein derivative (PPD) injected intradermally, result read 2-3 days later

CXR

Clinical features

118
Q

Why might you not use Mantoux testing for suspected TB in children < 6 months?

A

Young age (< 6 months) can cause false negatives

119
Q

Clinical presentation of TB

A

Primary infection (fever, anorexia, weight loss, CXR changes) → Dormancy → Reactivation (most commonly = tuberculosis meningitis)

120
Q

Management of TB

A

RIPE - rifampicin, isoniazid, pyrazinamide, ethambutol

121
Q

What is the main route of HIV infection for children?

A

Mother-to-child transmission during pregnancy/ breastfeeding

(<1% MTCT w/ antenatal + labour/ delivery management)

122
Q

Clinical presentation of HIV in children

A

Child asymptomatic for years before progressing to clinical disease:
persistent lymphadenopathy
Hepatosplenomegaly
recurrent fever
parotid swelling
SPUR infections

123
Q

Diagnosis of HIV in children

A

<18 months - transplacental maternal IgG HIV antibodies (confirm exposure not infection)/ HIV DNA PCR (evidence of infection)

> 18 months - antibody tests

124
Q

Management of HIV

A

Antiretroviral therapy (ART) + prophylaxis against Pneumocystis jiroveci pneumonia (PCP)

125
Q

What is meningitis?

A

inflammation of the meninges covering the brain, confirm by finding WBCs in CSF, viral causes = most common (self-resolving)

126
Q

Bacterial aetiology of meningitis in neonates/ up to 3 months

A

Group B Strep. = most common

Other = E. coli, Listeria monocytogenes

127
Q

Bacterial aetiology of meningitis in children 1 month = 6YO

A

Neisseria meningitidis, Strep. pneumoniae, Haemophilus influenzae

128
Q

Bacterial aetiology of meningitis in children > 6YO

A

Neisseria meningitidis, Strep. pneumoniae

129
Q

Clinical presentation of Meningitis

A

Febrile children w/ non-blanching purpuric rash + features:
Brudzinski sign (flexion of neck w/ child supine causes flexion of knees + hips)
Kernig sign (child supine with knees + hips flexed. Back pain on extension of the knee)
Altered mental state

< 12 months: non-specific (fever, poor feeding, vomiting, irritability, lethargy, drowsiness, seizures, reduced consciousness)
later signs: bulging fontanelle, neck stiffness, arched back

130
Q

What is the Brudzinski sign? What disease is it associated with?

A

Seen in meningitis

(flexion of neck w/ child supine causes flexion of knees + hips)

131
Q

What is the Kernig sign? What disease is it associated with?

A

Seen in meningitis

(child supine with knees + hips flexed. Back pain on extension of the knee)

132
Q

Later signs of meningitis in children < 12 months

A

Bulging fontanelle, neck stiffness, arched back

133
Q

Management of viral meningitis

A

mostly self-limiting + improve over 7-14 days, consider acyclovir if meningitis secondary to HSV

134
Q

Changes in CSF in meningitis

A

Bacterial: turbid appearance, raised polymorphs/ protein, low glucocse

Viral: clear appearance, raised lymphocytes, normal/ raised protein, normal/ low glucose

Tuberculosis: turbid/ clear/ viscous, raised lymphocytes, raised protein, low glucose

135
Q

Management of meningitis

A

Abx + steroids if > 3 months (dexamethasone) + fluids + cerebral monitoring + public health notification
< 3 months = IV amoxicillin + IV cefotaxime
> 3 months = IV cefotaxime

Abx prophylaxis for contacts (ciprofloxacin/ rifampicin)

136
Q

Abx for bacterial meningitis in children < 3 months

A

IV amoxicillin + IV cefotaxime

137
Q

Abx for bacterial meningitis in children > 3 months

A

IV cefotaxime

138
Q

Abx for meningitis prophylaxis in contact

A

Ciprofloxacin + rifampicin

139
Q

What is encephalitis

A

Inflammation of the brain substance, most commonly caused by invasion by neurotoxic virus e.g. HSV/ enteroviruses/ resp viruses (e.g. influenza)

140
Q

Aetiologies of encephalitis

A

Direct invasion of the brain by a neurotoxic virus (e.g. HSV)

Delayed brain swelling following a dysregulated neuroimmunology response to an antigen, usually a virus (e.g. Post-chickenpox)

Slow virus infection e.g. HIV/ SSPE

Most common causes: enteroviruses, respiratory viruses (e.g. Influenza), and herpesviruses (e.g. HSV/ VSV)

141
Q

Clinical presentation of encephalitis

A

fever, altered consciousness, seizures

((HSV encephalitis = headache, psychiatric symptoms, vomiting, focal features e.g. aphasia))

142
Q

Management of encephalitis

A

High-dose IV acyclovir until HSV encephalitis can be ruled out

143
Q

What is HSV encephalitis?

A

Encephalitis caused by HSV characteristically affects the temporal lobes, high mortality rate if untreated (80%)
CP = fever, headache, psychiatric symptoms, seizures, vomiting, focal features (e.g. aphasia)
Ix = CT (medial temporal + inferior frontal changes, normal in ⅓ of cases)
Mx = IV acyclovir

144
Q

Management of HSV encephalitis

A

IV acyclovir

145
Q

CT findings in HSV encephalitis

A

medial temporal + inferior frontal changes

normal in 1/3 of changes

146
Q

7 YO boy presents to A&E and is feeling unwell + lethargic, non-blanching rash on torso, responsive to pain. Chest clear, HS normal, abdo SNT. Temp 39, RR 38, HR 142, Sp02 88% OA, CRT 5s.

What is the most likely diagnosis?

A

Child in a febrile state w/ purpric rash = meningococcal septicaemia

147
Q

Meningococcal septicaemia clinical presentation

A

Child in a febrile state (inadequacy of circulation to meet tissue demands leading to end-organ damage)

W/ purpuric rash

148
Q

What is slapped cheek syndrome?

A

most common presentation of Parvovirus B18 infection, characteristic erythematous rash on cheek, can cause aplastic crisis in high-risk groups

149
Q

What causes slapped cheek syndrome?

A

Parvovirus B18 infection

150
Q

Clinical presentation of Parvovirus B18 infections

A

Viraemic phase of fever, malaise, headache → rash 1wk later (maculopapular, lace-like, trunk/ limbs/ cheek) - Slapped cheek syndrome

Other presentations: asymptomatic, aplastic crisis (in immunocompromised/ ppl with thalassemias + sickle cell), foetal hydrops

151
Q

What infection can cause an aplastic crisis in immunocompromised people/ people with haemolytic anaemias + sickle cell disease?

A

Parvovirus B18

152
Q

Management of slapped cheek syndrome

A

Supportive (fluid/ analgesia) as symptoms fade over 1-2wks

Further investigations in high-risk groups

153
Q

What is impetigo?

A

localised + highly contagious staph/ strep infections, most common in infants/ young children (associated w/ pre-existing eczema)

154
Q

Aetiology of impetigo

A

Staph/ strep infection

155
Q

Clinical presentation of impetigo

A

Erythematous macules (face/neck/hands) → rupture → honey coloured crusting.
Rapidly spread to other parts of body (auto-inoculate, nasal carriage common)

Itching/ mild discomfort. No systemic features.

156
Q

Management of impetigo

A

Systemically well = hydrogen peroxide 1% cream
Topical abx = fusidic acid 2% cream (Mupirocin if MRSA/ resistance to fusidic acid)
Widespread = oral flucloxacillin (clarithromycin/ azithromycin if penicillin allergy)

Exclude from school until lesions crusted OR 48hrs after commencing abx

157
Q

Exclusion criteria for impetigo

A

Exclude from school until lesions crusted OR 48hrs after commencing abx

158
Q

What is toxic shock syndrome?

A

triad = high fever/ hypotension/ diffuse erythematous maculopapular rash caused by toxins from Staph. aureus/ group A strep, medical emergency

159
Q

Aetiology of Toxic Shock Syndrome

A

toxins from Staph. aureus/ group A strep

160
Q

Clinical presentation of toxic shock syndrome

A

Triad = high fever, hypotension, diffuse erythematous maculopapular rash (desquamation after 1-2wks)

Organ dysfunction = liver/ renal impairment, vomiting + diarrhoea, mucositis, altered consciousness

161
Q

Management of toxic shock syndrome

A

IV fluids + IV abx (ceftriaxone + clindamycin for 10 days)

162
Q

What is scarlet fever?

A

notifiable disease, caused by a reaction to erythrogenic toxins produced by Group A haemolytic streptococci, peak incidence 2-6YO

163
Q

Aetiology of scarlet fever

A

Reaction to erythrogenic toxins produced by Group A haemolytic streptococci

164
Q

Clinical presentation of scarlet fever

A

Distinct ‘sandpaper’ like rash, fever, vomiting, abdo pain, strawberry tongue.
Appears on torso, spreads onto palms/ soles

165
Q

Management of scarlet fever

A

Oral penicillin V for 10 days (azithromycin if allergic)

Return to school 24hrs after abx

166
Q

Exclusion policy for scarlet fever

A

Return to school 24hrs after abx

167
Q

Complications of scarlet fever

A

Otitis media = most common, rheumatic fever, acute glomerulonephritis

168
Q

4YO girl presents with 3 days Hx of fever, vomiting, abdominal pain. Diffuse rash in neck/ chest areas with pallor around the lips. Rash has spread to flexor creases. Mum notes its very rough to touch. Exudate on tonsils. Strawberry tongue.

What is the most likely diagnosis?

A

Scarlet fever

169
Q

Clinical presentation of candida infection

A

Skin - erythematous w/ large macules, ooze clear fluid, itching/ burning in skin folds

Oral - white coating on tongue/ top of mouth

170
Q

Management of candida infection

A

Skin - topical clotrimazole/ miconazole (+ hydrocortisone cream for inflammation/ itch)

Oral - topical miconazole gel = first-line, oral nystatin = alternative

171
Q

Difference between candida infection + nappy rash

A

Candida infection: large red macules + rash extending beyond areas of exposure to skin creases + groin

172
Q

What is Coxsackie’s?

A

acute viral infection caused by Coxsackie A16 or Enterovirus 71 viruses, characterised by blister-like vesicular eruptions on hands/ feet/ mouth, usually mild + self-limiting

173
Q

Clinical presentation of Coxsackie’s

A

Mild systemic upset (sore throat, fever, malaise, cough, abdo pain)

Oral ulcers

Macules/ papules of hands + feet develop soon after oral lesions

174
Q

Management of Coxsackie’s

A

Symptomatic (advice RE: hydration analgesia), no exclusion from school

175
Q

Exclusion of policy for Coxsackies’

A

no exclusion from school

176
Q

When should immunodeficiency be considered in children?

A

SPUR infections - extensive candidiasis, severe/ long-lasting warts, atypical infections (opportunistic pathogens, unusually severe/ chronic, fail regular Tx)

177
Q

Most common cause of primary immunodeficiency in children

A

selective IgA deficiency

CP = asymptomatic w/ recurrent ear/ sinus/ pulmonary infections, Mx = immunoglobulin therapy, long-term = stem cell transplant

178
Q

What is selective IgA deficiency?

A

most common cause of primary immunodeficiency in children

CP = asymptomatic w/ recurrent ear/ sinus/ pulmonary infections

Mx = immunoglobulin therapy, long-term = stem cell transplant

179
Q

Secondary causes of immunodeficiency

A

malignancy, malnutrition, HIV infection, immunosuppressive therapy, splenectomy

180
Q
A

Phase 3a (5 decks)

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