Paediatrics II Flashcards

(186 cards)

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
Eye condition associated with JIA
Chronic anterior uveitis Can be seen prior to, or after JIA Children with JIA screened on a 3 monthly basis
26
What is Stevens-Johnson syndrome/toxic epidermal necrolysis
Skin disorder Immune-complex mediated hypersensitivity reaction Typically a reaction to drugs Less severe version of toxic epidermal necrolysis (>10% body coverage)
27
Causative agents of SJS
Medications: - Anti-epileptics - Antibiotics - Allopurinol - NSAIDs Infections: - HSV - Mycoplasma pneumonia - Cytomegalovirus - HIV
28
Presentation of SJS/TEN
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
29
Management of SJS/TEN
Emergency --> admit to dermatology or burns unit Supportive care - nutrition, antiseptics, analgesia, ophthalmology input Treatment options: steroids, immunoglobulins, immunosuppressant medication
30
Complications of SJS/TEN
Secondary infection Permanent skin damage Visual complications --> scarring + blindness
31
Characteristics of juvenile myoclonic epilepsy
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
32
Management of juvenile myoclonic epilepsy
1st line = sodium valproate 1st line in girls = levetiracetam
33
Management of absence seizures
1st line = ethosuximide (or sodium valproate) Most stop having them as they get older
34
Investigation of seizures/epilepsy in children
Request an EEG - helps categorise type + severity Head MRI/CT - if unclear history, or atypical features
35
Causative agent of chickenpox
Varicella zoster virus
36
Presentation of chickenpox
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
37
Complications of chickenpox
Bacterial superinfection - avoid NSAIDs Dehydration Conjunctival lesions Pneumonia Encephalitis (presents as ataxia) DIC Progressive disseminated disease
38
Management of chickenpox
Keep cool, trim nails Calamine lotion School exclusion
39
Infectivity of chickenpox
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
40
Bacterial superinfection of chickenpox
NSAIDs may increase risk Most commonly caused by invasive group A streptococcal species --> soft tissue infections --> necrotising fasciitis
41
Presentation of Wilms tumour
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
42
Investigation of Wilms tumour
USS abdomen with doppler - visualise kidney CT/MRI - staging of tumour Biopsy to identify histology required for definitive diagnosis
43
Management of Wilms tumour
Surgical excision of tumour + nephrectomy Adjuvant treatment depends on staging + histology: chemotherapy, or radiotherapy
44
Inheritance of Noonan syndrome
Majority are autosomal dominant
45
Features of Noonan syndrome
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
46
Conditions associated with Noonan syndrome
Congenital heart disease - especially pulmonary valve stenosis, hypertrophic cardiomyopathy + ASD Cryptoorchidism (normal fertility in women) LD Bleeding disorders Lymphoedema increased risk of leukaemia + neuroblastoma
47
Features of Kallman syndrome
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
48
Kleinefelter syndrome genetics
Male with additional X chromosome --> 47XXY Can have even more X chromosomes --> more severe features
49
Features of Kleinfelter syndrome
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)
50
Management of Kleinfelter syndrome
Testosterone injections Advanced IVF may allow fertility Breast reduction surgery MDT e.g. SALT, OT, Physio for muscle weakness, educational support
51
Risk factors for GBS infection in neonates
Premature rupture of membranes Preterm delivery Maternal fever during labour Chorioamnionitis Siblings had previous GBS infection Maternal age <20 years hHeavy maternal colonisation (bacteriuria)
52
Management of GBS infection in neonates
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
53
Triad of features in shaken baby syndrome
Retinal haemorrhages Subdural haematoma Encephalopathy
54
Red features in child with fever - colour
Pale, mottled, ashen or blue
55
Red features in child with fever - activity
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
56
Red features in child with fever - respiratory
Grunting Tachypnoea: RR >60 in any age Moderate or severe chest indrawing
57
Red features in child with fever - circulation + hydration
Reduced skin turgor
58
Red features in child with fever - other
Age <3 months, with temperature >/= 38 Non-blanching rash Bulging fonatanelle Neck stiffness Status epilepticus Focal neurological signs/seizures
59
Amber tachypnoea in a child with fever
6-12 months >50 breaths per minute >12 months >40 breaths per minute
60
Amber tachycardia in a child with fever
<12 months >160bpm 12-24 months >150bpm 2-5 years >140 bpm
61
What is idiopathic thrombocytopenic purpura
Type II hypersensitivity reaction Antibodies target + destroy platelets Key differential of a non-blanching rash
62
Presentation of idiopathic thrombocytopenic purpura
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
63
Investigation in idopathic thrombocytopenic purpura
FBC --> low plately count, other values should be normmal Blood film Bone marrow examination if there are atypical features
64
Management of idiopathic thrombocytopenic purpura
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
65
What is biliary atresia
Congenital condition of narrowing/absence of section of bile duct --> cholestasis
66
Presentation of biliary atresia
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
67
Management of biliary atresia
Surgery May require full liver transplantation Antibiotic coverage + bile acid enhancers following surgery
68
Pathophysiology of vesicoureteric reflux
Ureters displaced laterally --> enter bladder more perpendicular Shortened intramural course of the ureter Vesicoureteric junction cannot therefore function adequately
69
Presentation of vesicoureteric reflux
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)
70
Investigation of vesicoureteric reflux
Micturating cystourethrogram DMSA scan may be used to look for renal scarring
71
Triad of nephrotic syndrome
Hypoalbuminaemia High urinary protein Oedema
72
Presentation of nephrotic syndrome
Commonly aged 2-5 years old Frothy urine Generalised oedema Pallor High blood pressure Deranged lipid profile: high cholesterol, triglycerides + LDLs Hypercoagulability
73
Causes of nephrotic syndrome
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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Investigations in minimal change disease
Renal biopsy + microscopy --> usually shows no change Urinalysis: small molecular weight proteins, hyaline casts
75
Management of nephrotic syndrome
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
Complications of nephrotic syndrome
Hypovolaemia Thrombosis Infection Acute/chronic renal failure Relapse Hypercholesterolaemia
77
Risks associated with undescended testicles
Infertility Testicular torsion Testicular cancer
78
Risk factors for undescended testes
FHx of undescended testes Low birth weight Small for gestational age Prematurity Maternal smoking during pregnancy
79
Management of unilateral undescended testis
Referral considered around 3 months of age Baby should see urological surgeon by 6 months Orchidopexy carried out 6-12 months of age
80
What is gastrochisis
Congenital defect in the anterior abdominal wall, just lateral to the umbilical cord No peritoneal covering of the abdominal contents exists
81
Management of gastrochisis
Operate on as soon as possible In the meantime, cover the bowel with cling-film TPN may be required whilst intestinal function recovers
82
What is exomphalos/omphalocoele
Abdominal contents protrude through the anterior abdominal wall, however, they are covered in an amniotic sac formed by amniotic membrane and peritoneum
83
Conditions associated with exomphalos
Beckwith-Wiedemann syndrome Down's syndrome Cardiac + Kidney malformations
84
Management of exomphalos
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
Inheritance of fragile X syndrome
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
Features of fragile X syndrome
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
Cardiac complication of fragile X syndrome
Mitral valve prolapse
88
Diagnosis of intestinal malrotation
Upper GI contrast study USS
89
Management of episodic viral wheeze
1st line = SABA e.g. salbutamol, or anticholinergic via a spacer Next step = intermittemt LTRA (montelukast), intermittent inhaled corticosteroids, or both
90
Irritant dermatitis
Most common cause of nappy rash Due to irritant effect of urinary ammonia + faeces Creases spared Erythematous rash
91
Features of candida dermatitis nappy rash
Erythematous rash Involves flexures Characteristic satellite lesions
92
Features of seborrhoeic nappy rash
Erythematous rash With flakes May have coexistent scalp rash
93
General management of nappy rash
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
Presentation of constipation in children
<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
Lifestyle factors that may contribute to constipation in children
Habitually not opening bowels Low fibre diet Poor fluid intake + dehydration Sedentary lifestyle Psychsocial probelms at home or school etc
96
Secondary causes of constipation in children
Hirschsprung's disease Cystic fibrosis Hypothryoidism Spinal cord lesions Sexual abuse Intestinal obstruction Anal stenosis Cow's milk intolerance
97
Red flags in constipation in children
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
Management of idiopathic constipation in children
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
Skin features of tuberous sclerosis
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
Neuro features of tuberous sclerosis
Developmental delay Epilepsy Intellectual impairment
101
Other features of tuberous sclerosis
Retinal hamartomas Rhabdomyomas of the heart Gliomatous changes can occur in brain lesions Polycystic kidneys, renal angiomyolipomata Lymphangioleiomyomatosis
102
Management of threadworm infection
1st line for children >6 months = mebendazole Single dose given, alongside hygiene advice Recommended to treat whole houshold
103
What is transient tachypnoea of the newborn
Commonest cause of respiratory distress in term infants Caused by delay in resorption of lung liquid More common after birth by Caesarean section
104
Appearance of transient tachypnoea of the newborn on CXR
Fluid in horizontal fissure Hyperinflated lung fields
105
Management of transient tachypnoea of the newborn
Usually settles within the first day of life Supportive care - additional oxygen may be needed
106
Causes of hypoxic ischaemic encephalopathy
Anything leading to asphyxia to the brain: - Maternal shock - Intrapartum haemorrhage - Prolapsed cord --> cord compression - Nuchal cord (wrappe around neck of the baby)
107
When to suspect HIE in neonates
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
Mild HIE (Sarnat Staging)
Poor feeding, general irritability + hyper-alert Resolves within 24 hours Normal prognosis
109
Moderate HIE (Sarnat Staging)
Poor feeding, lethargic, hypotonic + seizures Can take weeks to resole Up to 40% develop cerebral palsy
110
Severe HIE (Sarnat Staging)
Reduced consciousness, apnoeas, flaccid + reduced or absent reflexes Up to 50% mortality Up to 90% develop cerebral palsy
111
Management of HIE
Supportive care Therapeutic hypothermia - in certain circumstances, may protect brain from hypoxic injury
112
Genetics of Patau syndrome
Trisomy 13
113
Features of Patau syndrome
Dysmorphic features Rocker bottom feet (convex soles of feet) Learning disability Microcephaly Small eyes Cleft lip/palate Polydactyly
114
Congenital causes of hydrocephalus
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
Presentation of hydrocephalus (paediatrics)
Enlarged + rapidly increased head circumference (as skull expands) Bulging anterior fontanelle Poor feeding + vomiting Poor tone Sleepiness
116
Management of hydrocephalus
Ventriculoperitoneal shunt Complications include: - Infection - Blockage - Excessive drainage - Intraventricular haemorrhage - Outgrowing them (typically need replacing every 2 years as the child grows)
117
When should APGAR scores be assessed
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
APGAR scores indicators
0-3 = very low 4-6 = moderately low 7-10 = suggests baby is in a good state
119
Features assessed in APGAR scores
A-ppearance --> colour P-ulse --> heart rate G-rimace --> reflex irritability A-ctivity --> muscle tone R-espiration --> respiratory function
120
Features of hemangiomas
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
What areas of the body are hemangiomas particularly bad covering?
Nose Mouth Eyes Airway Places they may easily get knocked and bleed
122
Management of hemangiomas
Beta-blockers --> regression/prevents further growth Tend to involute by around 18 months of age (may leave tissue paper scar)
123
Risk factors for hemangiomas
Female Premature Low birth weight Multiple birth e.g. twins, triplets, quadruplets White ethnicity Advanced maternal age
124
Features of port wine stain/naevus flammeus
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
Management of port wine stain
No treatment required (unless on the eye) Can have laser therapy
126
Features of Mongolian blue spots
Occur mainly in Asian/African chilldren Blue-grey macules Usually lumbrosacral Asymptomatic
127
Fever PAIN score
FEVER in past 24 hours = 1 Purulent tonsils = 1 Attend rapidly (<3 days) = 1 Inflamed tonsils = 1 No cough or coryza = 1
128
Interpretation of Fever PAIN score
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
Commonest causes of otitis media
Streptococcus pneumoniae (commonest for rhino-sinusitis and tonsillitis as well) Haemophilus influenzae Moraxella catarrhalis Staphylococcus aureus
130
Presentation of otitis media
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
Examination findings in otitis media
Bulging, red, inflamed looking tympanic membrane Discharge may be visible if there is a perforation
132
Management of otitis media
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
Risk factors for mastoiditis
Recurrent acute otitis media Age Learning difficulties Immunocompromised Anatomical abnormalities e.g. incomplete pneumatisation of the mastoid process, cholesteatoma
134
Risk factors for otitis media
Parental smoking Atopy Formula-fed Nursery/day-care Socio-economic deprivation Family history
135
Features of mastoiditis
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
Investigation of mastoiditis
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
Management of mastoiditis
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
Complications of mastoiditis
Extracranial - Facial nerve palsy - Hearing loss - Labyrinthitis - Subperiosteal abscess - Cranial osteomyelitis Intracranial - Intracranial infections - Dural sinus thrombosis
139
Genetics of Edwards syndrome
Trisomy 18
140
Antenatal features of Edwards syndrome
Unusually large uterus Unusually small placenta Polyhydramnios (likely secondary to renal dysfunction in the child)
141
Comorbidities associated with Edwards syndrome
Congenital heart disease - VSD, PDA, ASV Horseshoe kidneys
142
Features of Edwards syndrome
Small jaw (micrognathia) Low ears Rocker-bottom feet Overlapping fingers Prominent occiput Severe mental retardation
143
Fractures associated with child abuse
Radial Humeral Femoral
144
Common fractures in paediatrics not associated with NAI
Distal radial Elbow Clavicular Tibial
145
Risk factors for inguinal hernia
Prematurity Male sex Family history
146
Presentation of inguinal hernia
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
Differential diagnosis of inguinal hernia
Hydrocele - can get above, transilluminates, non-tender Varicocele - scrotal heaviness, non-tender, 'bag-of-worms' on palpation
148
Management of inguinal hernias
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
Epidemiology of acute lymphoblastic leukaemia
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
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Features of ALL
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
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Types of ALL
B-cell lineage (85% cases) T-cell lineage (10-15%) Rare cases of NK cell lineage
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Causes of Jaundice in the first 24 hours of life
Rhesus haemolytic disease ABO haemolytic disease Hereditary spherocytosis Glucose-6-phosphodehydrogenase
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Causes of prolonged jaundice (i.e. 14 days or 21 days if premature)
Biliary atresia Hypothyroidism Galactosaemia Urinary tract infection Breast milk jaundice Prematurity Congenital infections e.g. CMV, toxoplasmosis
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Risk factors for surfactant deficient lung disease/respiratory distress syndrome
Prematurity Male sex Diabetic mother Caesarean section Second born of premature twins
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What is cerebral palsy
Non-progressive, permanent neurological disorder of abnormal movement and posture
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Antenatal causes/risk factors of cerebral palsy
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)
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Perinatal causes/risk factors of cerebral palsy
Pre-term birth (periventricular leukomalacia) Low birth weight Birth asphyxia (hypoxic-ischaemic birth injury) Neonatal sepsis
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Postnatal causes/risk factors of cerebral palsy
Meningitis Severe hyperbilirubinaemi (neonatal jaundice) Head injury Encephalitis/encephalopathy Hypoglycaemia
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Spastic cerebral palsy
Hypertonia Reduced function Resulting from damage to upper motor neurones Can be hemiplegic, diplegic or quadriplegic Also known as pyramidal CP
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Dyskinetic cerebral palsy
Athetoid movements Oro-motor problems Caused by damage to basal ganglia and substantia nigra Hypertonia + hypotonia Also known as athetoid or extrapyramidal CP
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Ataxic cerebral palsy
Caused by damage to the cerebellum with typical cerebellar signs --> problems with coordinated movement
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Mixed cerebral palsy
Mix of spastic, dysinetic and/or ataxic features
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General presentation/features of cerebral palsy
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
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Common associated problems in cerebral palsy
Learning difficulties Epilepsy Squints Hearing impairment Visual impairment Gastro-oesophageal reflux Kyphoscoliosis Muscle contractures
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Management of cerebral palsy
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
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Distinguishing between true and pseudo precocious puberty
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
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Causes of true precocious puberty
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
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Causes of pseudo precocious puberty
Gonadotrophin-independent, and usually extra-cranial Adrenal virilising tumours Congenital adrenal hyperplasia Cushing syndrome Testicular or ovarian malignancy Gonadotrophin-secreting tumours e.g. hepatoblastoma
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Diagnostic adjunct tools used in ADHD
Conners' rating scale Strengths + Difficulties Questionnaire
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Diagnostic criteria of ADHD
At least 6 months Persistent pattern of inattention and/or hyperactivity-impulsivity Has a direct negative imapct on academic, occupational or social functioning
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DSM-5 criteria for Inattention in ADHD
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
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DSM-5 criteria for hyperactivity + impulsivity in ADHD
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
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Additional DSM-5 criteria for ADHD
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
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General principles of management of ADHD
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)
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Medication for management of ADHD in children 5+ young people
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
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Early shock --> late shock
BP: normal --> hypotension HR: tachycardia --> bradycardia Respiration: tachypnoea --> acidotic (Kussmaul) Extremities: pale/mottled --> blue Urine output: reduced --> absent
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Signs indicating shock instead of clinical dehydration
Pale + cold extremities Prolonged capillary refill time
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Definition of neonatal period
First 28 days of life Early neonate = first week of life (relevant for death classification)
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Features of juvenile dermatomyositis
Fatigue Joint pain Weakness of proximal muscles Malar rash Heliotrope rash over eyelids
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Diagnosis of juvenile dermatomyositis
Raised ESR Raised CK MRI scans --> muscle oedema Muscle biopsies Nailfold capillaroscopy --> microangiopathy
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Management of juvenile dermatomyositis
Steroids during acute flares Steroid-sparing immunosuppression for maintenance
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Genetics of Duchenne muscular dystrophy
X-linked recessive inherited disorder in the dystrophin genes
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Features of Duchenne muscular dystrophy
Progressive proximal muscle weakness Calf pseudohypertrophy Gower's sign = child uses arms to stand up from squatted position May have intellectual impairment
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Investigation of DMD
Raised creatinine kinas Genetic testing used for diagnosis (previously muscle biopsy)
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Prognosis of DMD
Most children cannot walk by 12 years old Typical survival is to 25-30 years old Associated with dilated cardiomyopathy
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Kocher's criteria for septic arthritis
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