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Phase 3A Revision > Paediatrics II > Flashcards

Paediatrics II Flashcards

1
Q

Biochemical features of DKA

A

Hyperglycaemia (or history of diabetes)
Ketonaemia
Metabolic acidosis

Dehydration

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2
Q

Presentation of DKA

A

Polyuria
Polydipsia
Nausea + vomiting
Weight loss
Acetone smell to breath
Dehydration –> hypotension
Altered consciousness
Symptoms of underlying trigger e.g. sepsis

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3
Q

Diagnosis of DKA

A

Hyperglycaemia (>11mmol/L)
Ketosis (>3mmol/L, or >2+ on dipstick)
Acidosis (Venous pH <7.3, bicarbonate <15.0mmol/L)

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4
Q

Electrochemical imbalances in DKA

A

Mildly raised creatinine - sign of dehydration
Low bicarbonate - metabolic acidosis

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5
Q

Fluid management of DKA

A

0.9% NaCl (not dextrose) - give fluid bolus of 20ml/kg if in shock, 10ml/kg if not in shock
Given IV if N+V, or if clinically dehydrated
Correct dehydration over 48 hours

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6
Q

Further management of DKA

A

Give insulin after 1 hour of IV fluids: 0.1unit/kg/hour
Treat underlying triggers
Give IV dextrose once blood glucose <14mmol/L
Add potassium to IV fluids + monitor closely (40mmol/L)

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7
Q

How to calculate maintenance fluids in a child

A

First 10kg: 100ml/kg/day
10-20kg: 50ml/kg/day
>20kg: 20ml/kg/day

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8
Q

How to calculate fluid deficit in children

A

% dehydration x weight (kg) x 10

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9
Q

How to calculate hourly fluid requirements in children

A

= (fluid deficit-bolus given)/48 + maintenance hourly rate
NB: do not substract bolus given if given for shock

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10
Q

Fluid bolus use in children

A

20ml/kg of normal saline
In ?DKA, and HF, use 10ml/kg ue to fluid overload complications

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11
Q

Turner syndrome

A

Single X chromosome –> 45XO

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12
Q

Features of Turner syndrome

A

Short stature
Webbed neck
High arching palate
Downward sloping eyes with ptosis
Broad chest + widely spaced nipples
Cubital valgus
Multiple pigmented naevi
Underdeveloped ovaries with reduced function
Late or incomplete puberty
Most women are infertile

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13
Q

Conditions associated with Turner syndrome

A

Otitis media
UTIs
Coarctation of the aorta
Hypothyroidism
Hypertension
Obesity
Diabetes
Osteoporosis
LDs

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14
Q

Management of Turner syndrome

A

Growth hormone therapy - used to prevent short stature
Oestrogen + progesterone to help establish female secondary sex characteristics, regulate menstrual cycle and prevent osteoporosis
Fertility treatment

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15
Q

Definition of juvenile idiopathic arthritis

A

Group of chronic inflammatory arthritis diseases beginning before age of 16
Joint arthritis >6 weeks
Arthritis - swelling or effusion, increased warmth and/or painful limited movement +/- tenderness

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16
Q

Risk factors for JIA

A

Female
<6 years old
HLA polymorphisms
FHx autoimmunity

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17
Q

Presentation of JIA

A

Joint pain/swelling
May have fever - commonly observed in systemic-onset JIA
Morning stiffness
Limp
Limited movement
Rash - common in SoJIA, salmon-coloured on trunk + proximal ectremities. Or psoriatic rash if psoriatic arthritis
Enthesitis
Uveitis
Rheumatoid nodules

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18
Q

Imaging for JIA

A

Ultrasound - often abnormal early in disease. Can be used to identify joints for corticosteroid injection
MRI - may be required if monoarticular disease, useful to view synovial fluid

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19
Q

Phenotypic groups in JIA

A

Oligoarticular arthritis (arthritis of 4 or fewer joints)
Polyarticular arthritis (arthritis of 5 or more joints)
Active sacroilitis
Active enthesitis
Systemic-onset JIA

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20
Q

Management of polyarticular JIA

A

1st line = DMARD e.g. methotrexate (+ folic acid), or sulfasalazine
Consider biological therapy alongside DMARD e.g. TNF-alpha inhibitor (etanercept, adalimumab)
Consider NSAIDs
Consider intra-articular steroid injection (done under USS), or oral corticosteroids

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21
Q

Key information for oligoarticular JIA

A

4 joints or fewer
Most common form of JIA
Affects medium-sized joints e.g. knees + elbows
Most common in girls <6
Associated with anterior uveitis
Highest association with antinuclear antibody

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22
Q

Management of oligoarticular JIA

A

1st line = intra-articular corticosteroid
Consider: NSAIDs, methotrexate, TNF-alpha factor, oral corticosteroids

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23
Q

Management of active sacrolitis/active enthesitis JIA

A

1st line = NSAIDs
Consider: oral corticosteroids, sulfasalazine or TNF-alpha (methotrexate also in enthesitis)

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24
Q

Management of systemic-onset JIA

A

1st line: Oral or IV corticosteroid
Consider: NSAIDs, biological therapy e.g. tocilizumab

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25
Q

Eye condition associated with JIA

A

Chronic anterior uveitis
Can be seen prior to, or after JIA
Children with JIA screened on a 3 monthly basis

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26
Q

What is Stevens-Johnson syndrome/toxic epidermal necrolysis

A

Skin disorder
Immune-complex mediated hypersensitivity reaction
Typically a reaction to drugs
Less severe version of toxic epidermal necrolysis (>10% body coverage)

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27
Q

Causative agents of SJS

A

Medications:
- Anti-epileptics
- Antibiotics
- Allopurinol
- NSAIDs
Infections:
- HSV
- Mycoplasma pneumonia
- Cytomegalovirus
- HIV

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28
Q

Presentation of SJS/TEN

A

Start with non-specific symptoms: fever, cough, sore throat, mouth + eyes, and itchy skin
Develop a purple/red rash –> spreads + blisters
Skin then starts to break away + shed
Pain, erythema, blistering + shedding can also happen to lips + mucous membranes
Eyes can become inflamed and ulcerated
Can affect urinary tract, lungs +- internal organs

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29
Q

Management of SJS/TEN

A

Emergency –> admit to dermatology or burns unit
Supportive care - nutrition, antiseptics, analgesia, ophthalmology input
Treatment options: steroids, immunoglobulins, immunosuppressant medication

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30
Q

Complications of SJS/TEN

A

Secondary infection
Permanent skin damage
Visual complications –> scarring + blindness

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31
Q

Characteristics of juvenile myoclonic epilepsy

A

Myoclonic seizures = sudden brief muscle contractions, patient usually awake during episode
Common triggers include sleep deprivation + alcohol withdrawal (often have jerks in the hours after waking up)
10-20 years at onset
Can have periods of absence which disrupt schooling

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32
Q

Management of juvenile myoclonic epilepsy

A

1st line = sodium valproate
1st line in girls = levetiracetam

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33
Q

Management of absence seizures

A

1st line = ethosuximide (or sodium valproate)
Most stop having them as they get older

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34
Q

Investigation of seizures/epilepsy in children

A

Request an EEG - helps categorise type + severity
Head MRI/CT - if unclear history, or atypical features

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35
Q

Causative agent of chickenpox

A

Varicella zoster virus

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36
Q

Presentation of chickenpox

A

Widespread, erythematous raised, vesicular, blistering lesions
Starts on trunk or face –> spreads outwards –> affects whole body over 2-5 days
Eventually lesions scab over –> no longer contagious
Fever = often first symptom
Itch
General fatigue + malaise

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37
Q

Complications of chickenpox

A

Bacterial superinfection - avoid NSAIDs
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presents as ataxia)
DIC
Progressive disseminated disease

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38
Q

Management of chickenpox

A

Keep cool, trim nails
Calamine lotion
School exclusion

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39
Q

Infectivity of chickenpox

A

Spread through direct contact with lesions, or through infected droplets from cough/sneeze
Become symptomatic 10 days-3 weeks after exposure
Stop being contagious once lesions have crusted over

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40
Q

Bacterial superinfection of chickenpox

A

NSAIDs may increase risk
Most commonly caused by invasive group A streptococcal species –> soft tissue infections –> necrotising fasciitis

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41
Q

Presentation of Wilms tumour

A

Consider in child <5 presenting with mass in abdomen (occurs 2-5 years old)
Unilateral, painless, abdominal/flank mass
Abdominal pain/distension
Haematuria
Lethargy
Fever
Hypertension
Weight loss

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42
Q

Investigation of Wilms tumour

A

USS abdomen with doppler - visualise kidney
CT/MRI - staging of tumour
Biopsy to identify histology required for definitive diagnosis

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43
Q

Management of Wilms tumour

A

Surgical excision of tumour + nephrectomy
Adjuvant treatment depends on staging + histology: chemotherapy, or radiotherapy

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44
Q

Inheritance of Noonan syndrome

A

Majority are autosomal dominant

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45
Q

Features of Noonan syndrome

A

Short stature
Broad forehead
Downward sloping eyes with ptosis
Hypertelorism (wide space between eyes)
Prominent nasolabial folds
Low set ears
Webbed neck
Widely spaced nipples

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46
Q

Conditions associated with Noonan syndrome

A

Congenital heart disease - especially pulmonary valve stenosis, hypertrophic cardiomyopathy + ASD
Cryptoorchidism (normal fertility in women)
LD
Bleeding disorders
Lymphoedema
increased risk of leukaemia + neuroblastoma

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47
Q

Features of Kallman syndrome

A

Delayed onset of puberty is main presenting features e.g. small penis, reduced testicle size, no facial or body hair in males
Anosmia
Poor balance
Learning difficulties

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48
Q

Kleinefelter syndrome genetics

A

Male with additional X chromosome –> 47XXY
Can have even more X chromosomes –> more severe features

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49
Q

Features of Kleinfelter syndrome

A

Appear as normal males until puberty
At puberty –>
Taller height
Wider hips
Gynaecomastia
Weaker muscles
Small testicles
Reduced libido
Shyness
Infertility
Subtle LD (speech + language in particular)

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50
Q

Management of Kleinfelter syndrome

A

Testosterone injections
Advanced IVF may allow fertility
Breast reduction surgery
MDT e.g. SALT, OT, Physio for muscle weakness, educational support

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51
Q

Risk factors for GBS infection in neonates

A

Premature rupture of membranes
Preterm delivery
Maternal fever during labour
Chorioamnionitis
Siblings had previous GBS infection
Maternal age <20 years
hHeavy maternal colonisation (bacteriuria)

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52
Q

Management of GBS infection in neonates

A

Benzylpenicillin/ampicillin + gentamicin
If >1 month old –> cefotaxime or ceftriaxone instead
14-21 days of treatment if meningitis, 10 days otherwise
Vancomycin + gentamicin if penicillin allergy

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53
Q

Triad of features in shaken baby syndrome

A

Retinal haemorrhages
Subdural haematoma
Encephalopathy

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54
Q

Red features in child with fever - colour

A

Pale, mottled, ashen or blue

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55
Q

Red features in child with fever - activity

A

No response to social cues
Appears ill to professional
Does not wake, or, if roused, des not stay awae
Weak, high-pitched or continuous cry

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56
Q

Red features in child with fever - respiratory

A

Grunting
Tachypnoea: RR >60 in any age
Moderate or severe chest indrawing

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57
Q

Red features in child with fever - circulation + hydration

A

Reduced skin turgor

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58
Q

Red features in child with fever - other

A

Age <3 months, with temperature >/= 38
Non-blanching rash
Bulging fonatanelle
Neck stiffness
Status epilepticus
Focal neurological signs/seizures

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59
Q

Amber tachypnoea in a child with fever

A

6-12 months >50 breaths per minute
>12 months >40 breaths per minute

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60
Q

Amber tachycardia in a child with fever

A

<12 months >160bpm
12-24 months >150bpm
2-5 years >140 bpm

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61
Q

What is idiopathic thrombocytopenic purpura

A

Type II hypersensitivity reaction
Antibodies target + destroy platelets
Key differential of a non-blanching rash

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62
Q

Presentation of idiopathic thrombocytopenic purpura

A

Usually presents in children <10
History of recent viral ilness common
24-48 hour onset of symptoms
Bleeding e.g. gums, epistaxis, menorrhagia
Bruising
Petechial or purpuric rash

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63
Q

Investigation in idopathic thrombocytopenic purpura

A

FBC –> low plately count, other values should be normmal
Blood film
Bone marrow examination if there are atypical features

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64
Q

Management of idiopathic thrombocytopenic purpura

A

Usually no treatment required - tends to resolve within 6 months
Avoid activites that may result in trauma

If platelets <10, or active bleeding –>
- Prednisolone (commenced by a specialist)
- IVIG
- Blood transfusion if required
- Platelet transfusion (only works temporarily)

Avoid NSAIDs, aspirin and contact sports
Splenectomy required if life-threatening bleeding, or ITP with severe symptoms for 12-24 months

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65
Q

What is biliary atresia

A

Congenital condition of narrowing/absence of section of bile duct –> cholestasis

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66
Q

Presentation of biliary atresia

A

Typically presents in first few weeks of life
Significant jaundice (high conjugated bilirubin)
Growth + feeding disturbance
Hepatomegaly with raised liver transaminases (GGT>others)
Dark urine + pale stools

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67
Q

Management of biliary atresia

A

Surgery
May require full liver transplantation
Antibiotic coverage + bile acid enhancers following surgery

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68
Q

Pathophysiology of vesicoureteric reflux

A

Ureters displaced laterally –> enter bladder more perpendicular
Shortened intramural course of the ureter
Vesicoureteric junction cannot therefore function adequately

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69
Q

Presentation of vesicoureteric reflux

A

Antenatally: hydronephrosis on USS
Recurrent childhood UTIs
Reflux nephropathy
- Chronic pyelonephritis secondary to VUR (commonest cause)
- May have hypertension (increased renin due to renal scarring)

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70
Q

Investigation of vesicoureteric reflux

A

Micturating cystourethrogram
DMSA scan may be used to look for renal scarring

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71
Q

Triad of nephrotic syndrome

A

Hypoalbuminaemia
High urinary protein
Oedema

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72
Q

Presentation of nephrotic syndrome

A

Commonly aged 2-5 years old
Frothy urine
Generalised oedema
Pallor
High blood pressure
Deranged lipid profile: high cholesterol, triglycerides + LDLs
Hypercoagulability

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73
Q

Causes of nephrotic syndrome

A

Most common in children = minimal change disease
Intrinsic kidney disease
- Focal segmental glomerulosclerosis
- Membranoproliferative glomerulonephritis
Systemic illness
- Henoch schonlein purpura
- Diabetes
- Infection e.g. HIV, hepatitis, and malaria

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74
Q

Investigations in minimal change disease

A

Renal biopsy + microscopy –> usually shows no change
Urinalysis: small molecular weight proteins, hyaline casts

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75
Q

Management of nephrotic syndrome

A

High dose steroids (80% steroid sensitive)
If steroid resistant: ACEi and immunosuppressants
Low salt diet
Diuretics may be used for oedema
Albumin infusions may be required
Antibiotic prophylaxis in severe cases

76
Q

Complications of nephrotic syndrome

A

Hypovolaemia
Thrombosis
Infection
Acute/chronic renal failure
Relapse
Hypercholesterolaemia

77
Q

Risks associated with undescended testicles

A

Infertility
Testicular torsion
Testicular cancer

78
Q

Risk factors for undescended testes

A

FHx of undescended testes
Low birth weight
Small for gestational age
Prematurity
Maternal smoking during pregnancy

79
Q

Management of unilateral undescended testis

A

Referral considered around 3 months of age
Baby should see urological surgeon by 6 months
Orchidopexy carried out 6-12 months of age

80
Q

What is gastrochisis

A

Congenital defect in the anterior abdominal wall, just lateral to the umbilical cord
No peritoneal covering of the abdominal contents exists

81
Q

Management of gastrochisis

A

Operate on as soon as possible
In the meantime, cover the bowel with cling-film
TPN may be required whilst intestinal function recovers

82
Q

What is exomphalos/omphalocoele

A

Abdominal contents protrude through the anterior abdominal wall, however, they are covered in an amniotic sac formed by amniotic membrane and peritoneum

83
Q

Conditions associated with exomphalos

A

Beckwith-Wiedemann syndrome
Down’s syndrome
Cardiac + Kidney malformations

84
Q

Management of exomphalos

A

C-section indicated to reduce risk of sac rupture
Maybe repaired quickly, but a staged repair is generally preferred - gradual closure allows pulmonary system to adapt to increased abdominal contents over 6-12 months

85
Q

Inheritance of fragile X syndrome

A

X-linked (unclear dominant or recessive)
Caused by mutation in the fragile X mental retardation 1 gene (FMR1) on the X chromosome
Trinucleotide repeat disorder
Males always affected
Females can vary in how much they are affected

86
Q

Features of fragile X syndrome

A

Usually presents with delay in speech + language development
Intellectual disability
Long, narrow face
Large ears
Large testicles after puberty
Hypermobile joint (esp. hands)
ADHD
Autism
Seizures

87
Q

Cardiac complication of fragile X syndrome

A

Mitral valve prolapse

88
Q

Diagnosis of intestinal malrotation

A

Upper GI contrast study
USS

89
Q

Management of episodic viral wheeze

A

1st line = SABA e.g. salbutamol, or anticholinergic via a spacer
Next step = intermittemt LTRA (montelukast), intermittent inhaled corticosteroids, or both

90
Q

Irritant dermatitis

A

Most common cause of nappy rash
Due to irritant effect of urinary ammonia + faeces
Creases spared
Erythematous rash

91
Q

Features of candida dermatitis nappy rash

A

Erythematous rash
Involves flexures
Characteristic satellite lesions

92
Q

Features of seborrhoeic nappy rash

A

Erythematous rash
With flakes
May have coexistent scalp rash

93
Q

General management of nappy rash

A

Disposable nappies > towel nappies
Expose napkin area to air when possible
Barrier cream e.g. zinc + castor oil
Mild steroid cream in severe cases
Topical imidazole if candidal nappy rash (apply barrier cream until candida has settled)

94
Q

Presentation of constipation in children

A

<3 stools per week (but can vary with what is normal for the child)
Hard, difficult to pass stools
Rabbit dropping stools
Straining + painful passage
Abdominal pain
Retentive posutring
Rectal bleeding (hard stools)
Faecal impaction –> overflow soiling
Hard stools may be palpable
Loss of sensation of need to open bowels

95
Q

Lifestyle factors that may contribute to constipation in children

A

Habitually not opening bowels
Low fibre diet
Poor fluid intake + dehydration
Sedentary lifestyle
Psychsocial probelms at home or school etc

96
Q

Secondary causes of constipation in children

A

Hirschsprung’s disease
Cystic fibrosis
Hypothryoidism
Spinal cord lesions
Sexual abuse
Intestinal obstruction
Anal stenosis
Cow’s milk intolerance

97
Q

Red flags in constipation in children

A

Not passing meconium within 48 hours of birth –> cystic fibrosis, or Hirschsprung’s disease
Neurological signs or symptoms, esp in lower limbs –> cerebral palsy, spinal cord lesion
Vomiting –> obstruction, or Hirschsprung’s
Ribbon stool –> anal stenosis
Abnormal anus –> anal stenosis, IBD, sexual abuse
Failure to thrive –> coeliac disease, hypothyroidism or safeguarding
Acute severe abdo pain + bloating –> obstruction, intussusception

98
Q

Management of idiopathic constipation in children

A

Lifestyle + reversal of contributing factors - high fibre diet + good hydration
Laxatives
- Movicol on increasing dose first
- Add stimulant laxative e.g. senna, if no response
- Substitute stimulant if Movicol is not tolerated. Add another laxative e.g. lactulose or docusate if stools are hard
- Continue medication at maintenance dose for several weeks after regular bowel habit established, then reduce dose gradually

99
Q

Skin features of tuberous sclerosis

A

Depigmented ‘ash-leaf’ spots - fluoresce under UV light
Roughened patches of skin over lumbar spine (Shagreen patches)
Adenoma sebaceum (angiofibromas): butterfly distribution over nose
Fibromata beneath nails
Cafe-au-lait spots may be seen

100
Q

Neuro features of tuberous sclerosis

A

Developmental delay
Epilepsy
Intellectual impairment

101
Q

Other features of tuberous sclerosis

A

Retinal hamartomas
Rhabdomyomas of the heart
Gliomatous changes can occur in brain lesions
Polycystic kidneys, renal angiomyolipomata
Lymphangioleiomyomatosis

102
Q

Management of threadworm infection

A

1st line for children >6 months = mebendazole
Single dose given, alongside hygiene advice
Recommended to treat whole houshold

103
Q

What is transient tachypnoea of the newborn

A

Commonest cause of respiratory distress in term infants
Caused by delay in resorption of lung liquid
More common after birth by Caesarean section

104
Q

Appearance of transient tachypnoea of the newborn on CXR

A

Fluid in horizontal fissure
Hyperinflated lung fields

105
Q

Management of transient tachypnoea of the newborn

A

Usually settles within the first day of life
Supportive care - additional oxygen may be needed

106
Q

Causes of hypoxic ischaemic encephalopathy

A

Anything leading to asphyxia to the brain:
- Maternal shock
- Intrapartum haemorrhage
- Prolapsed cord –> cord compression
- Nuchal cord (wrappe around neck of the baby)

107
Q

When to suspect HIE in neonates

A

When there are events that could lead to hypoxia during perinatal or intrapartum period
Acidosis (pH <7) on umbilical artery blood gas
Poor Apgar scores
Features of HIE or evidence of multi organ failure

108
Q

Mild HIE (Sarnat Staging)

A

Poor feeding, general irritability + hyper-alert
Resolves within 24 hours
Normal prognosis

109
Q

Moderate HIE (Sarnat Staging)

A

Poor feeding, lethargic, hypotonic + seizures
Can take weeks to resole
Up to 40% develop cerebral palsy

110
Q

Severe HIE (Sarnat Staging)

A

Reduced consciousness, apnoeas, flaccid + reduced or absent reflexes
Up to 50% mortality
Up to 90% develop cerebral palsy

111
Q

Management of HIE

A

Supportive care
Therapeutic hypothermia - in certain circumstances, may protect brain from hypoxic injury

112
Q

Genetics of Patau syndrome

A

Trisomy 13

113
Q

Features of Patau syndrome

A

Dysmorphic features
Rocker bottom feet (convex soles of feet)
Learning disability
Microcephaly
Small eyes
Cleft lip/palate
Polydactyly

114
Q

Congenital causes of hydrocephalus

A

Aqueductal stenosis –> insufficient drainage of CSF
Arachnoid cysts (block outflow)
Arnold-Chiari malformation: cerebellum herniates downards through foramen magnum –> prevents outflow
Chromosomal abnormalities + congenital malformations

115
Q

Presentation of hydrocephalus (paediatrics)

A

Enlarged + rapidly increased head circumference (as skull expands)
Bulging anterior fontanelle
Poor feeding + vomiting
Poor tone
Sleepiness

116
Q

Management of hydrocephalus

A

Ventriculoperitoneal shunt
Complications include:
- Infection
- Blockage
- Excessive drainage
- Intraventricular haemorrhage
- Outgrowing them (typically need replacing every 2 years as the child grows)

117
Q

When should APGAR scores be assessed

A

Routinely at 1 and 5 minutes of age
If score <5 at 5 minutes –> repeat at 10, 15 and 30 minutes and consider umbilical cord blood gas sampling

118
Q

APGAR scores indicators

A

0-3 = very low
4-6 = moderately low
7-10 = suggests baby is in a good state

119
Q

Features assessed in APGAR scores

A

A-ppearance –> colour
P-ulse –> heart rate
G-rimace –> reflex irritability
A-ctivity –> muscle tone
R-espiration –> respiratory function

120
Q

Features of hemangiomas

A

Appear during first few weeks of life
Blue or pink macules or patches
Then enter proliferative phase –> may become elevated above surrounding skin surfaces

121
Q

What areas of the body are hemangiomas particularly bad covering?

A

Nose
Mouth
Eyes
Airway
Places they may easily get knocked and bleed

122
Q

Management of hemangiomas

A

Beta-blockers –> regression/prevents further growth
Tend to involute by around 18 months of age (may leave tissue paper scar)

123
Q

Risk factors for hemangiomas

A

Female
Premature
Low birth weight
Multiple birth e.g. twins, triplets, quadruplets
White ethnicity
Advanced maternal age

124
Q

Features of port wine stain/naevus flammeus

A

Present from birth
Persistent purple or dark red birth mark
Generally appears on face and neck
Grows with the infant
Due to vascular malformation of capillaries in the dermis

125
Q

Management of port wine stain

A

No treatment required (unless on the eye)
Can have laser therapy

126
Q

Features of Mongolian blue spots

A

Occur mainly in Asian/African chilldren
Blue-grey macules
Usually lumbrosacral
Asymptomatic

127
Q

Fever PAIN score

A

FEVER in past 24 hours = 1
Purulent tonsils = 1
Attend rapidly (<3 days) = 1
Inflamed tonsils = 1
No cough or coryza = 1

128
Q

Interpretation of Fever PAIN score

A

Likelihood of streptococcal pharyngitis
Score 4-5 –> consider immediate antibiotics (phenoxymethylpenicillin) if severe, or 48 hour short back-up prescription
2-3 –> delayed antibiotic prescription (3-5 days or worsening symptoms)
0-1 –> no antibitics

129
Q

Commonest causes of otitis media

A

Streptococcus pneumoniae (commonest for rhino-sinusitis and tonsillitis as well)
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus

130
Q

Presentation of otitis media

A

Ear pain
Reduced hearing in affect ear
Symptoms of upper airway infection e.g. fever, cough, coryzal symptoms, sore throat, malaise
Can cause balance issues/vertigo
Discharge from ear if membrane is perforated

131
Q

Examination findings in otitis media

A

Bulging, red, inflamed looking tympanic membrane
Discharge may be visible if there is a perforation

132
Q

Management of otitis media

A

Referral to specialist + consder admission if temperature >38 (0-3 months) or 39 (3-6 months)
Most cases resolve without antibiotics
- Consider if significant co-morbidities, systemically unwell or immunocompromised
- Give if <2 years with bilateral otitis media, or if have discharge
- Delayed prescriptions
- Amoxicillin for 5 days
Analgesia

133
Q

Risk factors for mastoiditis

A

Recurrent acute otitis media
Age
Learning difficulties
Immunocompromised
Anatomical abnormalities e.g. incomplete pneumatisation of the mastoid process, cholesteatoma

134
Q

Risk factors for otitis media

A

Parental smoking
Atopy
Formula-fed
Nursery/day-care
Socio-economic deprivation
Family history

135
Q

Features of mastoiditis

A

Recent episode of acute/recurrent otitis media
Proptosed auricle
Post-auricular swelling
Post-auricular erythema
Post-auricular tenderness

In young children, may have ear-pulling and non-specific symptoms of systemic upset

136
Q

Investigation of mastoiditis

A

Ear swab if discharging ear or oozing abscess –> MC+S
Blood tests: raised inflammatory markers incl WCC + CRP
CT head and mastoid with contrast
MRI head - helpful in suspected complicated mastoiditis

137
Q

Management of mastoiditis

A

Admit
Intravenous antibiotics - most likely co-amoxiclav + ceftriaxone (oral switch if recovering + pyrexia settled)
Surgical intervention
- Failing to improve clinically after 48 hours
- Continuing pyrexia, malaise
- Persistent erythema or soft tissue swelling
- Complications of mastoiditis

138
Q

Complications of mastoiditis

A

Extracranial
- Facial nerve palsy
- Hearing loss
- Labyrinthitis
- Subperiosteal abscess
- Cranial osteomyelitis
Intracranial
- Intracranial infections
- Dural sinus thrombosis

139
Q

Genetics of Edwards syndrome

A

Trisomy 18

140
Q

Antenatal features of Edwards syndrome

A

Unusually large uterus
Unusually small placenta
Polyhydramnios (likely secondary to renal dysfunction in the child)

141
Q

Comorbidities associated with Edwards syndrome

A

Congenital heart disease - VSD, PDA, ASV
Horseshoe kidneys

142
Q

Features of Edwards syndrome

A

Small jaw (micrognathia)
Low ears
Rocker-bottom feet
Overlapping fingers
Prominent occiput
Severe mental retardation

143
Q

Fractures associated with child abuse

A

Radial
Humeral
Femoral

144
Q

Common fractures in paediatrics not associated with NAI

A

Distal radial
Elbow
Clavicular
Tibial

145
Q

Risk factors for inguinal hernia

A

Prematurity
Male sex
Family history

146
Q

Presentation of inguinal hernia

A

Groin swelling
Inguinal/inguino-scrotal mass that you cannot ‘get above’
Reducible mass when lying flat
Does not transilluminate
Positive cough reflex
70% are right-sided, 10% bilateral

Nausea, vomiting, constipation, abdo pain/discomfort –> indicate obstruction or strangulation
Irreducible + tender if strangulated

147
Q

Differential diagnosis of inguinal hernia

A

Hydrocele - can get above, transilluminates, non-tender
Varicocele - scrotal heaviness, non-tender, ‘bag-of-worms’ on palpation

148
Q

Management of inguinal hernias

A

Surgical repair - performed on all full-term male infants
Emergency surgery if irreducible –> prevent bowel + testicular ischaemia
<6 weeks old = correct within 2 days
<6 months = within 2 weeks
<6 years = within 2 months

149
Q

Epidemiology of acute lymphoblastic leukaemia

A

Accounts for 80% of childhood leukaemias
Peak incidence 1-5 years
Boys>girls (slightly)
Most common malignancy affecting children
No strong family correlation, but some genetic disorders (Down’s syndrome) increase the likelihood

150
Q

Features of ALL

A

Bone marrow failure –>
- Anaemi: lethargy + pallor
- Neutropenia: frequent/severe infections
- Thrombocytopenia: easy bruising, petechiae

Bone pain (bone marrow infiltration)
Splenomegaly
Hepatomegaly
Lymphadenopathy
Fever present in upt o 50% of new cases
Testicular swelling

151
Q

Types of ALL

A

B-cell lineage (85% cases)
T-cell lineage (10-15%)
Rare cases of NK cell lineage

152
Q

Causes of Jaundice in the first 24 hours of life

A

Rhesus haemolytic disease
ABO haemolytic disease
Hereditary spherocytosis
Glucose-6-phosphodehydrogenase

153
Q

Causes of prolonged jaundice (i.e. 14 days or 21 days if premature)

A

Biliary atresia
Hypothyroidism
Galactosaemia
Urinary tract infection
Breast milk jaundice
Prematurity
Congenital infections e.g. CMV, toxoplasmosis

154
Q

Risk factors for surfactant deficient lung disease/respiratory distress syndrome

A

Prematurity
Male sex
Diabetic mother
Caesarean section
Second born of premature twins

155
Q

What is cerebral palsy

A

Non-progressive, permanent neurological disorder of abnormal movement and posture

156
Q

Antenatal causes/risk factors of cerebral palsy

A

80% antenatal causes
Gene deletions
Antenatal infecton
Vascular occlusion - may need to screen for haematological disorders to exclude an antenatal/post-natal stroke
Failure of cortical migration
Trauma during pregnancy

Multiple gestation
Chorioamnionitis
Maternal TORCH infections (toxoplasmosis, rubella, CMV, heres simplex)

157
Q

Perinatal causes/risk factors of cerebral palsy

A

Pre-term birth (periventricular leukomalacia)
Low birth weight
Birth asphyxia (hypoxic-ischaemic birth injury)
Neonatal sepsis

158
Q

Postnatal causes/risk factors of cerebral palsy

A

Meningitis
Severe hyperbilirubinaemi (neonatal jaundice)
Head injury
Encephalitis/encephalopathy
Hypoglycaemia

159
Q

Spastic cerebral palsy

A

Hypertonia
Reduced function
Resulting from damage to upper motor neurones
Can be hemiplegic, diplegic or quadriplegic

Also known as pyramidal CP

160
Q

Dyskinetic cerebral palsy

A

Athetoid movements
Oro-motor problems
Caused by damage to basal ganglia and substantia nigra
Hypertonia + hypotonia

Also known as athetoid or extrapyramidal CP

161
Q

Ataxic cerebral palsy

A

Caused by damage to the cerebellum with typical cerebellar signs –> problems with coordinated movement

162
Q

Mixed cerebral palsy

A

Mix of spastic, dysinetic and/or ataxic features

163
Q

General presentation/features of cerebral palsy

A

Failure to meet milestones - especially motor
Increased or decreased tone - can be general, or in specific limbs
Hand preference <18 months
Problems with coordination, speech or walking
Feeding or swallowing problems
Abnormal gait

164
Q

Common associated problems in cerebral palsy

A

Learning difficulties
Epilepsy
Squints
Hearing impairment
Visual impairment
Gastro-oesophageal reflux

Kyphoscoliosis
Muscle contractures

165
Q

Management of cerebral palsy

A

MDT approach
Treatment for spasticity e.g. oral diazepam, oral + intrathecal baclofen, botulinum toxin type A, orthopaedic surgery, selective dorsal rhizotomy
Anticonvulsants + analgesia as required
Glycopyrronium bromide for excessive drooling

166
Q

Distinguishing between true and pseudo precocious puberty

A

In true precocious puberty, the course of puberty sill occurs in a normal synchronous manner –> suggests hypothalamic-pituitary axis intact
In pseudo precocious puberty, puberty occurs in abnormal manner e.g. axillary + pubic hair in girls, with growth spurt but no breast budding, or prepubertal sized testicles with other signs of puberty in boys

167
Q

Causes of true precocious puberty

A

Idiopathic = 80-90%
Intracranial pathology e.g. tumours, haemorrhage, hydrocephalus, neurofibromatosis, cerebral palsy, primary hypothyroidism
Less common in boys –> more likely to be central cause

168
Q

Causes of pseudo precocious puberty

A

Gonadotrophin-independent, and usually extra-cranial
Adrenal virilising tumours
Congenital adrenal hyperplasia
Cushing syndrome
Testicular or ovarian malignancy
Gonadotrophin-secreting tumours e.g. hepatoblastoma

169
Q

Diagnostic adjunct tools used in ADHD

A

Conners’ rating scale
Strengths + Difficulties Questionnaire

170
Q

Diagnostic criteria of ADHD

A

At least 6 months
Persistent pattern of inattention and/or hyperactivity-impulsivity
Has a direct negative imapct on academic, occupational or social functioning

171
Q

DSM-5 criteria for Inattention in ADHD

A

6+ symptoms for children up to 16, 5+ for adolescents/adults aged 17+
Present for at least 6 months, and inappropriatre for developmental level

Fails to give close attention to details/makes careless mistakes
Trouble holding attention on activities
Does not seem to listen when spoken to directly
Does not follow through on instructions + fails to finish tasks e.g. loses focus/side-tracked
Trouble organising tasks and activities
Avoids/dislikes/reluctant to do tasks requiring mental effort over a long period of time
Loses things necessary for tasks + activities
Easily distracted
Forgetful in daily activities

172
Q

DSM-5 criteria for hyperactivity + impulsivity in ADHD

A

6+ symptoms for children up to 16, 5+ for adolescents/adults aged 17+
Present for at least 6 months, and inappropriatre for developmental level

Fidgets with/taps hands or feet, squirms in seat
Leaves seat in situations when remaining seated is expected
Runs about or climbs where it is not appropriate (or feels restless)
Unable to take part in activities quietly
Often ‘on the go’ acting as if ‘driven by a motor’
Talks excessively
Blurts out an answer before a question has been completed
Trouble waiting their turn
Interrupts or intrudes on others

173
Q

Additional DSM-5 criteria for ADHD

A

Several inattentive or hyperactive-impulsive symptoms present <12 years of age
Present in two or more settings
Clear evidence of interfering with functioning
Symptoms not explained by another mental disorder/do not happen only during course of another disorder

174
Q

General principles of management of ADHD

A

Healthy diet + exercise (find links between certain foods and behaviour using food diary)
Environmental modifications
Training programmes for person/their parents/carers
Consider medication in certain groups (not in children <5 without a second specialist opinion)

175
Q

Medication for management of ADHD in children 5+ young people

A

1st line = Methylphenidate
2nd line = lisdexamfetamine (used if 6-week trial of methylphenidate at adequate dose has not led to enough benefi)
3rd line = dexamfetamine (used if symptoms responding to lisdexamfetamine but unable to tolerate the longer effect profile)

Atomeoxetine or guanfacine given if cannot tolerate 1st/2nd line, or symptoms not responding to separate 6 week trials

176
Q

Early shock –> late shock

A

BP: normal –> hypotension
HR: tachycardia –> bradycardia
Respiration: tachypnoea –> acidotic (Kussmaul)
Extremities: pale/mottled –> blue
Urine output: reduced –> absent

177
Q

Signs indicating shock instead of clinical dehydration

A

Pale + cold extremities
Prolonged capillary refill time

178
Q

Definition of neonatal period

A

First 28 days of life
Early neonate = first week of life (relevant for death classification)

179
Q

Features of juvenile dermatomyositis

A

Fatigue
Joint pain
Weakness of proximal muscles
Malar rash
Heliotrope rash over eyelids

180
Q

Diagnosis of juvenile dermatomyositis

A

Raised ESR
Raised CK
MRI scans –> muscle oedema
Muscle biopsies
Nailfold capillaroscopy –> microangiopathy

181
Q

Management of juvenile dermatomyositis

A

Steroids during acute flares
Steroid-sparing immunosuppression for maintenance

182
Q

Genetics of Duchenne muscular dystrophy

A

X-linked recessive inherited disorder in the dystrophin genes

183
Q

Features of Duchenne muscular dystrophy

A

Progressive proximal muscle weakness
Calf pseudohypertrophy
Gower’s sign = child uses arms to stand up from squatted position
May have intellectual impairment

184
Q

Investigation of DMD

A

Raised creatinine kinas
Genetic testing used for diagnosis (previously muscle biopsy)

185
Q

Prognosis of DMD

A

Most children cannot walk by 12 years old
Typical survival is to 25-30 years old
Associated with dilated cardiomyopathy

186
Q

Kocher’s criteria for septic arthritis

A

Non-weight bearing = 1
Fever >38.5 = 1
WCC >12 = 1
ESR >40mm/hr = 1

0 = very low risk
1 = 3% chance
2 = 40% chance
3 = 93% chance
4 = 99% chance

Phase 3A Revision (12 decks)

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