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Year 4 > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Who can complete then routine examination of the newborn

A

Hospital paediatrician
Advanced neonatal nurse Practitioner
GP
Specially trained nurse/midwife

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2
Q

Routine examination of newborn

A

Head to toe
Completely undressed

  • Skull shape, maximum circumference, fontanelles
  • Face: any dysmorphisms, examine for cleft palate
  • Ears: position, size, shape, patency
  • Neck
  • Chest: shape, symmetry, nipple position. RR 40-60, palpate precordium
  • Abdomen: look at umbilical stump, inguinal hernias, palpate organs
  • Genital: female inspect. male - urinary meatus, descended testes
  • Femoral pulses
  • Anus: patency
  • Spine: deformity, dimple, naevi, hair
  • Limbs: tone. Digit number. Clubbed foot, palmar creases
  • DDH
  • CNS: tone (should be flexed at hip and knee), pull baby to sitting by holding wrists. Ventral suspension
    Moro reflex
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3
Q

Moro reflex

A

Act as if to drop the baby
Arms should extend and then flex

If bilateral absence then CNS damage
If unilateral then birth trauma e.g. Erb’s palsy

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4
Q

Define vernix

A

Normal cheesy white substance on the skin of baby at birth

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5
Q

Skull molding

A

Over riding skull bones
Palpable ridges
Normal
Resolves in 2-3 days

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6
Q

Caput succedaneum

A

Swelling or oedema on new born scalp
From prolonged pressure during delivery
Resolves in a few days

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7
Q

Chignon

A

Temporary swelling of infants head after ventouse suction cap
Increases rate of jaundice

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8
Q

Cephalhaematoma

A

Bruise on neonates head from prolonged stage 2 of labour or instrumental delivery
Subperisoteal
Boundaries are limited by bone margins

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9
Q

Subconjuctival haemorrhage in newborn

A

Can happen in precipitate delivery (<2 hours) or if cord around neck
Harmless
Will resolve in a few weeks

Be careful if later than newborn as can indicate abuse

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10
Q

Epstein’s peals

A

Self resolving white inclusion cysts on palate

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11
Q

Tongue tie

A

Shortened tongue frenulum

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12
Q

Ranula

A

Self resolving bluish mouth floor swelling

mucus retention cyst

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13
Q

Retracted testes

A

Due to exaggerated cremastus muscle

Palpate along to determine location of testes

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14
Q

Mongolian blue spot

A

Normal birth mark

Increased in Asian and Africans

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15
Q

Erythema toxicum

A

Normal neonatal rash
Erythematous base with small pustules
Unknown cause

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16
Q

Primitive reflexes

A 
Rooting
Grasping
Moro
Walking
Sucking
Asymmetrical tonic neck reflex - fencing posture
Galant reflex
Swimming reflex
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17
Q

Describe grasping reflex

A

Baby will grasp anything in palms

Disappears at 5-6 months

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18
Q

Describe asymmetrical tonic neck reflex

A

Fencing posture
Present from 1-4 months
When head is turned to the side, the arm on that side will straighten , opposite will bend
If >6months then UMN disorder

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19
Q

Characteristics of pathological heart murmur

A 
All Diastolic
All Pansystolic
Late systolic murmurs
Loud murmurs > 3/6
Continuous murmur
Associated cardiac abnormalities
Heard over upper L sternal border

Symptomatic:
SOB, easy fatigue, cyanosis, FTT, clubbing, hepatomegaly

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20
Q

Characteristic of innocent heart murmur

A 
Always systolic
Short duration
Low intensity
Increases with increased cardiac output
Intensity can change with posture
no thrill or heave
No radiation
No symptoms
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21
Q

Predisposing conditions for heart murmurs

A 
Down's
Noonan's
Turner's
Marfan's
Foetal alcohol syndrome
Foetal rubella infection
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22
Q

Still’s murmur

A 
Innocent murmur
Mid L sternal border
Mid-systolic
Grad 2-3
Twanging, musical, vibrating sound
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23
Q

Pulmonary flow murmur

A 
Innocent murmur
Upper L sternal border
Mid systolic
Grade 1-3
Grating
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24
Q

Acyanotic causes of congenital heart disease

A 
Ventricular septal defect
Atrial septal defect
Patent Ductus Arteriosus
Pulmonary valve stenosis
Coarctation of the aorta
Hypoplastic left heart syndrome
Hypertrophic obstructive cardiomyopathy 
Dextrocardia
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25
Q

Cyanotic causes of congenital heart disease

A 
Tetralogy of fallot
Transposition of great arteries
Tricuspid atresia
Total anomalous pulmonary drainage
Persistent truncus arteriosus
Ebstein's abnormality
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26
Q

Epidemiology of congenital heart disease

A 
8 per 1000 live births
1/3 of congenital abnormalities
Increased if FHx
Increased if parents are relatives
Intrauterine - drugs, alcohol, rubella infection
Down's syndrome
DiGeorge's syndrome
Williams syndrome
Noonan's syndrome
Turner's syndrome
Maternal diabetes
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27
Q

Atrial septal defect

A

Left to Right shunt
Can be ostium secundum defect (foramen ovale) with normal valves or partial AVSD affecting valves
Usually asymptomatic
Tx - close ASD in early childhood

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28
Q

Ventricular septal defect

A 
25% of all congenital heart disease
Typically asymptomatic
Pansystolic murmur at left lower sternal edge
Most close spontaneously 
Can have heart failure
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29
Q

Patent ductus arteriosus

A

Common
Defined as patent ductus arteriosus if patent at 1 month
Connects pulmonary artery to aorta
Low diastolic pressure due to back flow through pulmonary artery
Wide pulse pressure
Bounding peripheral pulses
Continuous or machinery murmur in left infraclavicular area
Most close spontaneously

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30
Q

Tetralogy of Fallot

A

4 cardinal anatomical abnormalities

  1. VSD
  2. Over-riding aorta
  3. R ventricular outflow obstruction
  4. R ventricular hypertrophy

Cyanosis
Paroxysmal hypercyanotic spells - Tachypnoea, restlessness. Become white or floppy for minute-hours

Treated with prostaglandin E infusion
R to L shunt

Increased risk of cerebral ischaemia, endocarditis, HF, brain abscess, polycythaemia

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31
Q

Transposition of the great arteries

A

2 separate parallel circuits
Systemic venous blood returns to R heart and back to systemic flow
Not compatible with life unless mixing ASD or PDA
Severe hypoxia
No heart failure

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32
Q

Heart defect associated with Noonan’s syndrome

A

Pulmonary stenosis

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33
Q

Heart defect associated with Turner’s syndrome

A

Coarctation of aorta

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34
Q

Neonatal history

A

PREGNANCY

  • parity
  • any extra scans
  • maternal problems in pregnancy
  • medications

BIRTH

  • gestation
  • induced or spontaneous labour
  • PROM?
  • RF for infection
  • Vaginal or C-section

SINCE BIRTH

  • Feeeding, meconium, urine, vomiting
  • Receive Vit K
  • Any problems or concerns

Fhx and social

  • genetic conditions
  • RF for DDH
  • SIDS
  • Social set up
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35
Q

Causes of sick newborn

A 
Sepsis
Hypoxic Ischaemia Encephalopathy
Transient Tachypnoea of newborn
RDS
Hypoglycaemia
Jaundice
Necrotising enterocolitis
Cardiac murmur
Neonatal abstinence syndrome
Seizures
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36
Q

Changes in foetal circulation at birth

A

In utero - blood vessels that supply and drain lungs are constricted
Increased pulmonary vascular resistance
Blood bypasses lungs through ductus arteriosus

Pulmonary vessels dilate due to increased O2
Encourages blood flow to lungs
Closure of ductus arteriosus

Pulmonary expansion
Increased O2 tension
Decreased pulmonary vascular resistance
Increased pulmonary blood flow
Increased LA filling
Closure of foramen ovale
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37
Q

Apgar score

A

HR - 0-absent, 1-<100, 2>100

Respiration - 0-absent, 1-gasping, 2-regular

Muscle tone - 0-flaccid, 1=some flexion, 2=well flexed

Reflex irritability 0-none, 1-grimace, 2-cry/cough

Colour - 0-pale/blue, 1-body pink, blue limbs, 2-pink

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38
Q

Cleft palate/lip

A

1 in 1000 children
Tends to run in families

Problems

  • Difficulty feeding
  • Milk aspiration
  • Speech difficulties
  • Conductive hearing loss due to Eustacian tube dysfunction
  • Dental problems

Surgically corrected at 9 months
Give specialist advice on managing baby

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39
Q

Neural tube defects

A

Failure of neural tube to close in early pregnancy - incidence decreased with folic acid supplements

Screening with US and alpha fetoprotein

Anencephaly - most severe. complete failure of development of cranial nerve tube

Myelomeningocoele - open lesion with malformed and exposed spinal cord covered by meninges. Severe neurological abnormality of lower limbs

Meningocoele - spinal cord intact, exposed meninges. High risk of meningitis and hydrocephalus

Spina bifida occulta - hidden abnormality. Develop bladder dysfunction and pyramidal tract signs in legs as child grows
- Deep pit, tuft of hair, naevus, lipoma in midline

US offers diagnosis

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40
Q

Hypospadias

A

Urethra abnormally placed
1 in 500 boys
Most commonly ventrally on glans up to perineum
Increased severity with increased penile curve
Severe cases require repair before 2 years
DO NOT CIRCUMCISE as foreskin used in reconstruction

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41
Q

Bowel obstruction

A

1 in 1000 babies
Can be anatomical or functional

Clinical features:

  • Bile stained vomiting
  • Failure to pass meconium
  • Abdominal distension
  • Visible peristalsis

Oesophageal atresia: mucus, chokes on first feed
Duodenal atresia - bile stained vomit, double bubble on AXR
Jejunal atresia = most common. distension. bile stained vomit

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42
Q

Hirschsprung’s disease

A

Absence of myenteric nerve plexus in the rectum
may extend along the colon
abdomen distends
15% present with acute enterocolitis

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43
Q

Exomphalos

A

Often diagnosed Antenatally
Also called omphalocele
Abdominal contents protrude through umbilical ring, covered by transparent sac.

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44
Q

Gastroschsis

A

Bowel protrudes through defect in anterior abdominal wall adjacent to umbilicus
no sac covering
Cover with cling film
Increased risk of dehydration

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45
Q

Hypoxic ischaemic encephalopathy

A

Hypoxia. Hypercapnia. Metabolic acidosis.
Decrease tissue perfusion.
Brain damage, disability or death

Causes:

  • prolonged uterine contractions
  • placental abruption
  • ruptured uterus
  • cord compression
  • shoulder dystocia
  • cord prolapse
  • maternal hypotension
  • anaemia
  • IUGR

MILD - infant irritable, responds excessively to stimulation

MODERATE - marked abnormalities in tone and movement

SEVERE - no normal spontaneous movements or response to pain. prolonged seizures. 30-40% mortality

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46
Q

Brachial nerve palsies

A

Occurs if breech birth or shoulder dystocia
Upper nerve root C5-6 = ERB’s palsy

Lower nerve root = KLUMPKEYS palsy

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47
Q

Facial nerve palsy

A 
Via compression of facial nerve on ischial spine
Unilateral
Facial weakness on crying
Eye remains open
Usually transient
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48
Q

Define pre-term infant

A

Under 34 weeks

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49
Q

Medical problems in pre-term infants

A 
Resuscitation at birth 
RDS
Hypotension
PDA
Temperature control issues
Hypoglycaemia, hypocalcaemia, electrolyte imbalance
Nutrition
Infection
Jaundice
Necrotising entercolitis
Retinopathy of prematurity 
Anaemia of prematurity
Brocnhopulmonary dysplasia
Inguinal hernias
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50
Q

Respiratory distress syndrome

A

Deficiency of surfactant from type II pneumocytes
Widespread alveolar collapse and inadequate gas exchange
Steroids given Antenatally stimulate surfactant production

Tachypnoea >60
Laboured breathing, chest wall recession, nasal flaring
Expiratory grunting
Cyanosis if severe

CXR - diffuse granular or ground glass appearance

Treat with CPAP and O2

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51
Q

Necrotising enterocolitis

A

Affects pre-term babies in first few weeks
Bacterial invasion of ischaemia bowel wall
increased if cows milk fed
Infant stops tolerating feeds, milk aspirated from stomach
Vomiting +/- bile staining
Distended abdomen
Fresh blood in stools
Distended loops of bowel
Thickening of bowel wall

Can cause perforation
Stop feeding
Start broad spec Abx

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52
Q

Retinopathy of prematurity

A

Affects developing blood vessels at the junction of vascular and non-vascularised retina

Vascular proliferation
Retinal detachment
Fibrosis
Blindness

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53
Q

Bronchopulmonary dysplasia

A

Infants who still require O2 at 36 weeks
Lung damage from pressure and volume trauma from ventilation

CXR - widespread opacification and cystic changes

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54
Q

Jaundice in neonates

A

Over 50% of newborns are visibly jaundiced

  • Marked physiological release of Hb from breakdown of Hb at birth
  • RBC lifespan is only 70 days
  • Hepatic bilirubin metabolism if less efficient in first few days

May be a sign of:

  • Haemolytic anaemia
  • Infection
  • metabolic or liver disease
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55
Q

Kernicterus

A

Encephalopathy resulting from deposition of unconjugated bilirubin in basal ganglia and brainstem nuclei

  • lethargy and poor feeding
  • irritability
  • Increased muscle tone
  • Seizures, coma
  • Survivors can develop choreoathetoid CP - learning disability and sensorineural deafness
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56
Q

Causes of jaundice in neonate

A

Haemolytic disorders: Rhesus/ABO incompatability. G6PD deficiency. Spherocytosis.

Physiological.
Breast milk jaundice
Infection
Haemolysis
Bruising
Polycythaemia
Hypothyroid
High GI obstruction
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57
Q

Management of jaundice

A

Phototherapy
- blue/green band converts unconjugated bilirubin to water soluble pigment

Exchange transfusion
- if dangerously high levels. Remove baby blood and replace with donor blood

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58
Q

Causes of infection in neonate

A

Group B Strep

  • Pneumonia or meningitis
  • Give prophylactic Abc intrapartum

Listeria monocytogenes

  • from unpasteurised milk, soft cheese, undercooked poultry
  • Bacteraemia with mild flu like illness
  • Meconium staining of licquor
  • Widespread rash, septicaemia

Conjunctivitis

  • sticky eye on day 3 or 4
  • Chlamydia, gonorrhoea,
  • Can be staph or strep
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59
Q

Epidemiology of sudden infant death syndrome

A

Most common aged 2-4 months
Incidence is decreasing with Back to Sleep campaign

RFs

  • Low birth weight and pre-term
  • Increased in males
  • Multiple births
  • Increasing maternal parity
  • Parental low income
  • Poor or overcrowded housing
  • Maternal age under 20
  • Single unsupported mother
  • Maternal smoking during pregnancy or in the same room post birth
  • Sleeping prone
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60
Q

Prevention of SIDS

A

Back to Sleep Campaign
Lie infant on back
Feet to foot position
Do not smoke in same room
Avoid overheating
Baby should sleep in same room for first 6 months
Avoid sleeping with the infant e.g. sofa, chair

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61
Q

Investigations and management for SIDS

A

Detailed clinical exam
Remove any ET tubes and needles but retain venous lines
Retain child clothes, bedding and nappy for police

Nasopharyngeal aspirate
Blood for toxicology, metabolic screen
Chromosomal anomalies
Blood cultures
Urine 
LP for virology and culture
PM and coroners review
Give parents opportunity to see and hold child
Social review
Case discussion
Bereavement counselling
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62
Q

Causes of shock in child

A

Hypovolaemia

  • Dehydration from gastroenteritis
  • DKA
  • Blood loss from trauma

Maldistribution of fluid

  • anaphylaxis
  • Septicaemia

Cardiogenic

  • Arrhythmia
  • Heart failure
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63
Q

Causes of respiratory distress in children

A 
Croup
Epiglottitis
Foreign body
Congenital malformations
Trauma
Asthma
Bronchiolitis
Pneumonia
pneumothorax
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64
Q

Causes of drowsiness in children

A 
Post-ictal
Status epilepticus
Meningitis
Encephalitis
DKA
Hypoglycaemia
Electrolyte disturbance
Inborn metabolism error
Head injury
Drug/ poison ingestion
Intracranial haemorrhage
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65
Q

Paediatric BLS

A

Open airway

  • Infants: neutral position
  • Children: sniffing position

5 rescue breaths
Check pulses
- < 1 year = brachial and femoral
- > 1 year = carotid and femoral

If no pulse or pulse <60 then chest compressions
15:1

Adrenaline every 3-5 minutes
10 micrograms per kg IV

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66
Q

Apparent life-threatening events

A

Combination of apnoea, colour change, alteration in muscle tone, choking
Most common in under 10 weeks
Most are brief with rapid recovery

Causes

  • Infections (RSV, pertussis)
  • Seizures
  • Upper airway obstruction
  • GORD
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67
Q

Clinical manifestations of Down’s syndrome

A 
Round face, flat nasal bridge
Upslanted palpebral fissures
Epicanthic folds
Brushfield spots in iris
Small mouth, protruding tongue
Small low set ears
Short neck
Flat occiput
Single palmar crease
Incurved 5th finger
Hypotonia
Congenital heart defects
Duodenal atresia
Hirschsprung's disease
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68
Q

Later medical problems in Down’s syndromes

A

Delayed motor milestones
Moderate-severe LD
Small stature
Increased susceptibility to infection
hearing impairment from secretory otitis media
Visual impairment - cataracts, squint, myopia
Increased risk of leukaemia and solid tumour
Hypothyroidism
Coeliac disease
Epilepsy
Alzheimer’s disease

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69
Q

Genetics of Down’s

A

TRISOMY 21

94% meiotic non-disjunction (increases with maternal edge)

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70
Q

Edward’s syndrome

A 
TRISOMY 18
1 in 8000
Multiple severe abnormality
Low birth weight
Prominent occiput
Small mouth and chin
Short sternum
Fixed overlapping fingers
Rocker bottom feet
Cardiac and renal malformations
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71
Q

Patau’s syndrome

A 
TRIMSOMY 13
1 in 14,000
Structural defect in the brain
Scalp defects
Small eyes (microphthalmia)
Cleft palate and lip
Polydactyly
Cardiac and renal malformations
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72
Q

Turner’s syndrome

A 
45 XO
95% are spontaneously miscarried
Often diagnosed on US - cystic hygroma and foetal neck oedema
Lymphoedema of hands and feet 
Spoon shaped nails
Short stature
Neck webbing
Wide carrying angle
Widely spaced nipples
Congenital heart defects
Delayed puberty
Infertile
Hypothyroidism
Renal anomalies
Pigmented moles
Recurrent otitis media
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73
Q

Klienfelter’s syndrome

A 
47 XXY
1-2 per 1000 males
Infertility
Hypogonadism
Small testes
Pubertal development, may appear normal
Gynaecomastia
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74
Q

Autosomal dominant conditions

A 
Achondroplasia
Ehler's Danlos syndrome
Familial hypercholesterolaemia
Huntington's disease
Noonan's syndrome
Otosclerosis
Tuberous Sclerosis
Marfan's syndrome
Myotonic dystrophy
Neurofibromatosis
Osteogenesis imperfect
Polyposis coli
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75
Q

Describe autosomal dominant inheritance

A

Chromosomes 1-22
Children of someone affected
50% affected
50% normal

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76
Q

Autosomal recessive conditions

A 
Cystic fibrosis
Congenital adrenal hyperplasia
Galactosaemia
Freidreich ataxia
Glycogen storage disease
Phenylketonuria
Hurler syndrome
Tay-Sachs disease
Sickle cell disease
Thalassaemia
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77
Q

X linked inheritance & diseases

A

Can be dominant or recessive
males affected, females usually healthy but carriers

  • Colour blindness
  • Duchenne’s and Becker’s muscular dystrophy
  • Fragile X syndrome
  • G6PD
  • Haemophilia A and B
  • Hunter’s syndrome
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78
Q

Fragile X syndrome

A 
Moderate-severe LD
Macrocephaly
Macro-orchidism
Long face
Large everted ears
Prominent mandible
Broad forehead
mitral valve prolapse
Joint laxity and scoliosis
Autism
Hyperactivity
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79
Q

Imprinting

A

Normally in a gene - mothers and fathers acts equally

In imprinting, one is more functional that the other

Chromosome 15

  • If mothers unfunctional: Angelman’s syndrome
  • If fathers unfunctional: Prader-Willi syndrome
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80
Q

Prader-Willi Syndrome

A

Chromosome 15 - parental gene unfunctional

Hypotonia
Neonatal feeding difficulties
Failure to thrive
Obesity in later childhood with hyperphagia
Hypogonadism
Developmental delay and LD
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81
Q

Angelman’s syndrome

A

Chromosome 15 - maternal gene non-functional

Severe intellectual and developmental disability
Sleep disturbance
Seizures and jerky movements (hand flapping)
Frequent laughter and smiling

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82
Q

William’s syndrome

A

Short stature
Transient neonatal hypercalcaemia
Congenital heart disease - aortic stenosis
Mild-moderate LD

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83
Q

Newborn screening

A

Hearing

Blood spot test

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84
Q

Newborn hearing screening

A

Within 4-5 weeks usually prior to discharge

1st test: Automated Oto-Acoustic Emission (AOAE)
- play sound in ear, try to detect echo response from baby’s cochlea

2nd test: Automated Auditory Brainstem Response (AABR)
- play sound, detect response from brain stem via electrodes. assesses integrity from inner ear

AABR if no clear response on AOAE or >48 hours in SCBU or NICU

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85
Q

Newborn Blood Spot Test

A

Blood spot/heel prick/Guthrie test
Ideally on day 5 (day 5-8)

Tests for:

  • Phenylketonuria
  • Cystic fibrosis
  • Congenital hypothyroidism
  • Maple syrup urine disease
  • Sickle cell disease
  • MCAD deficiency
  • Homocysteinuria
  • Glutaric aciduria type 1
  • Isoraleric acidaemia
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86
Q

Phenylketonuria

A

Testing looks for total biopterin and dihydropteridine reducates
allows for early implementation of phenylalanine restricted diet

Early diagnosis and treatment decreases handicap
Inborn error of amino acid metabolism
Absent phenylalanine hydroxylase - important in formation of catecholamine’s, neurotransmitters and melanine

Musty or mousey odour
Developmental delay
Recurrent vomiting

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87
Q

Homocysteinuria

A 
Rare inherited metabolic disorder
Raised blood and urine concentration of homocysteine
Autosomal recessive
Normal at birth
Complications in childhood
Tall stature (Marfanoid habitus)
Fine brittle hair
High arched palate
Pectus excavatum
Limited joint mobility
Dislocation of lens
Increased risk of VTE,MI, osteoporosis, mitral valve prolapse
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88
Q

Maple syrup urine disease

A 
1 in 185,000
Autosomal recessive
Maple syrup odour in cerumen
Poor feeding
Vomiting
Poor weight gain
Lethargy 
Dystonia
Seizures
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89
Q

Clinical features of foetal alcohol syndrome

A

Failure of growth
- Never catch up

Facial abnormalities

  • Microcephaly
  • Flat philtrum
  • Thin upper lip
  • Retrognathia, micrognathia
  • Microphalamia
  • Cleft palate/lip
  • posterior rotation of ears

Neurodevelopement

  • Low IQ, memory problems
  • Hyperactivity, attention deficits
  • Poor judgement
  • Immature behaviour
  • Speech and language delay
  • Sucking and feeding problems

Also

  • Congenital heart disease (ASD and VSD)
  • Partial deafness
  • Significant visual disability
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90
Q

Stages of growth

A

FOETAL

  • fastest period of growth, accounting for 30% of eventual height
  • Size at birth depends on size of mother and placental nutrient supply
  • IGF-2, insulin and human placental lactogen control growth

INFANTILE

  • growth dependent on adequate nutrition
  • good health and normal thyroid function necessary
  • rapid but decelerating growth rate
  • inadequate weight gain = FTT

CHILDHOOD

  • slow and steady
  • role of pituitary growth hormone. GH is secreted to produce insulin life growth factor 1 - IGF-1
  • profound unhappiness can decrease GH and causes psychological short stature

PUBERTY

  • sex hormones (testosterone and estradiol) causes back lengthening and increased GH secretion
  • Adds 15% to final height
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91
Q

Define short stature

A

Height below the 2nd centile (2SD below the mean)
Many will be normal, just short with short parents

The further under the centile, the high risk of pathological cause
Height will fall through centile lines
Can be plotted on height velocity chart

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92
Q

Calculating genetic height

A

Mothers height + fathers height /2
If female -7cm
If male +7cm

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93
Q

Aetiology of short stature

A
  • Familial
  • IUGR and extreme prematurity
  • Constitutional delay of growth and puberty
  • Hypothyroidism
  • Growth hormone deficiency
  • Corticosteroid excess, Cushing’s
  • Nutritional / chronic illness
  • Psychosocial deprivation
  • Chromosomal disorders/syndromes
  • Achondroplasia

Extreme short stature

  • Laron syndrome
  • Primordial dwarfism
  • idiopathic
  • SHOX gene abnormality
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94
Q

Constitutional delay of growth and puberty

A

Increased in males
Variation in normal puberty timings
Not pathological
Can be induced by dieting or excessive physical training
Long legs in comparison to back
Onset of puberty can be induced with androgens/oestrogens

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95
Q

Hypothyroidism causing short stature

A

Usually caused by autoimmune thyroiditis in childhood
Growth failure
Excessive weight gain
When treated = catch up, can limit final height
Congenital hypothyroidism is often diagnosed at birth and therefore does not cause short stature

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96
Q

Causes of growth hormone deficiency

A

Craniopharyngioma - bitemporal hemianopia, papilloedema, optic atrophy

  • hypothalamic tumour
  • head injury
  • meningitis
  • cranial irradiation
  • Laron syndrome
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97
Q

Chromosomal syndromes causing short stature

A 
Laron's syndrome
Down's syndrome
Noonan's syndrome
Russell-Silver syndrome
Turner's syndrome
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98
Q

Investigations for short stature

A 
FBC
U&amp;Es
LFTs
TFTs
ESR and CRP
Urinalysis
Karyotyping
Bone age - radiograph of L hand and wrist
If pathological short stature then delay in bone age

Growth hormone provocation tests
MRI scan if neurological symptoms

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99
Q

Management of short stature

A

Somatotropin
used in growth hormone deficiency
Stop when final height attained or adherence poor

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100
Q

Noonan’s syndrome

A 
Autosomal dominant
Congenital heart defects - pulmonary vascular stenosis
Short stature
Learning problems
Pectus excavatum
Impaired blood clotting
Webbed neck
Flat nose
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101
Q

Silver Russell Syndrome

A 
Primordial dwarfism
SGA
Feeding problems
Hypoglycaemia
Excessive sweating 
Blue tinge to sclera
Triangular face, small jaw, pointed chin
Wide and late closing fontanelle
Decreased subcut fat
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102
Q

Laron syndrome

A 
Autosomal recessive
Insensitivity to growth hormone
Abnormally short stature
Prominent forehead, depressed nasal bride, underdeveloped mandible
Truncal obesity
Micropenis in males
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103
Q

William’s syndrome

A 
Deletion of sections of chromosome 7
Developmental disorder
Broad forehead, short nose, full cheeks
Elfin face
Intellectual disability
Short stature
Aortic stenosis
Hypercalcaemia
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104
Q

Advantages of breast feeding

A

Ideal nutrition for infants during first 6 months
Life saving in developing countries
Decreases GI infection risk
Decreased necrotising enterocolitis
Increased mother child bond
Decreased diabetes, HTN and obesity in later life

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105
Q

Disadvantages of breast feeding

A

Unknown volume intake
Transmission of infection
Transmission of drugs
Vit K deficiency as not in breast milk (but in formula)
Less flexibility - other family can’t help

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106
Q

Colostrum

A

Produced for first few days
Increased protein and immunoglobulin component
Decreased volume
First breast feed should take place as soon as possible after birth

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107
Q

Physiology of breast feeding

A

Baby roots and sucks
Tactile receptors in nipple activated
Hypothalamus sends efferent impulses to pituitary
Anterior pituitary produces PROLACTIN which stimulates milk production by cuboidal cells in acini of breast
Posterior pituitary produces OXYTOCIN to contract myoepithelial cells in alveoli into large ducts (let down reflex)

Prolactin = increased milk production
Oxytoxin = contraction of breast
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108
Q

Describe nutritional requirements of the baby

A

Breast of formula feeding for first 12 months
Cow’s milk may be given from 1 year
Introduce solid foods after 6 months
Done gradually
If starting food before 6 months - avoid wheat, eggs and fish

No honey in under 1s due to infantile botulinism

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109
Q

Define failure to thrive

A

Suboptimal weight gain in children (infants and toddlers)
Below 5th percentile or fall across centiles
- Mild: fall across 2 centile lines
- Severe: fall across 3 centile lines

Hard to distinguish TT from a normal but small baby
They will be asymptomatic

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110
Q

Aetiology of failure to thrive

A

70% inorganic (under feeding/psychosocial)
30% organic (secondary to disease)

  • Decreased intake (social/economic/education)
  • Decreased ability
    CNS: CP, tumour, suck/swallow reflex
    GI; GORD, pyloric stenosis
    Cleft palate
    Micrognathia
  • Decreased absorption:
    Lactose allergy, CF, IBD, Coeliac
    Biliary atresia, cirrhosis
    Obstruction: hernia, malrotation, intussusception
    Neonatal: NEC, short bowel syndrome
  • Increased requirement
    Storage disease, inborn error
    CHD
    CF, bronchopulmonary dysplasia
    Hypo/hyperthyroid disease
    Malignancy
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111
Q

Investigations in failure to thrive

A 
FBC, ESR, CRP, U&amp;Es
Glucose
TFTs
Sweat chloride
Coeliac - tissue transglutaminase

2nd line

  • Lead levels
  • Abdominal US
  • CXR
  • Head US
  • ECG/ echo
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112
Q

Management of failure to thrive

A 
Health visitor involvement
3 meals a day + snacks
Increased energy density foods
Regular meal times
Praise when food eaten
Never force feed a child

MDT: health visitor, paediatrician, dietician, social worker

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113
Q

Marasmus

A

Weight for height > 3SD
Wasted, wizened appearance
No oedema
Withdrawn and apathetic

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114
Q

Kwashorkor

A 
Generalised oedema and severe wasting
Flaky pain skin
Hyperkeratosis
Distended abdomen
Hepatomegaly
angular stomitis
Diarrhoea, hypothermia, bradycardia, hypotension
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115
Q

Types of abuse

A 
Physical
Emotional
Neglect
Sexual
Fabricated or induced illness
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116
Q

Risk factors for abuse

A

Child

  • Failure to meet parental expectation e.g. wrong gender or disabled
  • Resulted from forced, coercive or commercial sex

Parent

  • Mental health problems
  • Parental indifference, intolerance or over anxious
  • Alcohol or drug use

Family

  • Step parents
  • Domestic violence
  • Social isolation
  • Young parental age

Environment
- Poverty, poor housing

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117
Q

Injuries more likely to indicate physical abuse

A

Fractures: in non-mobile child, rib fractures, multiple fractures, fractures of different ages, skull fractures

Bruises: shape of hand or object, on the neck (e.g. strangulation), Wrists and ankles, buttocks in under 2s

Burns: in non-mobile child, in shape of implement e.g. iron or cigarette, glove and stocking from forced immersion

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118
Q

Emotional abuse

A

Persistent emotional maltreatment resulting in severe adverse effects on child’s emotional development

Inappropriate expectations / over protection / made to feel worthless, unloved or inadequate

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119
Q

Presentation of emotional abuse

A

Hardest to identify

Babies – apathetic, delayed development

Toddlers: violent, apathetic, fearful

School age: wetting, soiling, non-attendance

Adolescents: self-harm, depression, aggressive

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120
Q

Neglect

A

Persistent failure to meet a child’s physical or psychological needs. Failure of:
Adequate food and clothing
Shelter
Protection from physical and emotional harm or danger
Inadequate supervision

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121
Q

Presentation of neglect

A 
Consistently misses important medical appointment
Lacks needed medical and dental care
Dirty
Inadequate clothing in cold weather
Using alcohol or drugs
Child mentions no one at home
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122
Q

Sexual abuse

A

Forcing or enticing a child to take part in sexual activity
Includes: physical contact (rape, oral sex), non-contact (watching sexual activities, looking at pornographic material, encouraging them to behave inappropriately

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123
Q

Presentation of sexual abuse

A 
Child may tell someone
STI with no cause
Vaginal bleeding, discharge, itching
Rectal bleeding
Self harm, aggressive or sexualised behaviours
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124
Q

Fabricated or induced illness

A

Behaviour of parents (usually mother >80%) which causes harm to children
Verbal fabrication: parents invent signs and symptoms. Abuse is done through tests and treatments

Induction of illness:

  • Suffocation of child presenting as acute life threatening event
  • Administration of noxious substance or poison
  • Excessive administration of normal substance e.g. salt
  • Excessive or unnecessary use of medication

Only happens when a parent/guardian around

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125
Q

Effects of alcohol abuse on the child

A

Severe congential abnormalities
Imapired growth and leaning and behavioural impairment
Foetal alcohol syndrome

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126
Q

Effects of heroin abuse on the child

A

Withdrawal syndrome
Advise methadone
Decreased birth weight

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127
Q

Effects of cocaine abuse in the child

A 
Powerful vasoconstrictor
Increased miscarriage
Increased placental abruption
Premature labour
Foetal death in utero
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128
Q

Effects of alcohol/drug misuse on child

A

Physical harm

  • access to drugs or paraphernalia
  • increased violence due to decreased inhibition
  • Increased strangers in home
  • Chemical dependence
Not meeting child's physical needs
Inadequate supervision
Disruption to education or poor school attendance
Child assuming parental role
Decreased boundaries and routine
Frightening
Emotional stresses - fear of abandonment/parents dying/not loving child
Feeling responsible for parents drug use
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129
Q

Describe meconium

A 
Black colour
First stool
GI cells
Filled with bilirubin
If not expelled quickly, increased risk of jaundice
Should be expelled in <24 hours
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130
Q

Palpable posterior fontanelle indicates what?

A

hypothyroidism or Down’s syndrome

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131
Q

Describe presentation of metabolic conditions

A

If problem with fat/protein/carbohydrate metabolism
Presents after first 1-2 days
Have a good first feed
Then start to get unwell, minimal further feeds
Ill due to build up of toxic metabolites from failed metabolism

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132
Q

Fields of development

A

Gross motor
Vision and fine motor
Hearing, speech and language
Social, emotional and behavioural

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133
Q

How are developmental milestones judged?

A

Median age - when half of the population at that level

Limit age - 2SD above mean. Age at which it should have been achieved

If a baby is pre-term should be calculated from expected date of delivery to allow to catch up. Only up to 2 year.

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134
Q

Gross Motor Developmental milestones

A

6-8 weeks: raises head to 45 degrees when prone

6-8 months: sits without support. At 6m = round back, 8m = straight back (limit 9 months)

8-9 months: crawling

10 months: cruising around furniture

12 months: walking unsteady (limit 18m)

15 months: walks steadily

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135
Q

Vision and fine motor milestones

A

6 weeks: follows object by moving head (limit 3 months)

4 months: reaches for toys

4-6 months: palmar grasp

7 months: Transfers objects between hands

10 months: pincer grip (limit 12 months)

16-18 months: makes marks with crayons

18 months: 3 blocks
2 years: 6 blocks
2.5 years: 8 blocks
3 years: 3 block bridge
4 years: steps
2 years - line
3 years - circle
3.5 years - cross
4 years - square
5 years - triangle
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136
Q

Hearing, speech and language milestones

A

Newborn - startles to loud noise

3-4 months: vocalises alone or when spoken too. Coos and laughs

7 months: turns to soft sounds out of sight. Uses should indiscriminately

10 months: sounds used discriminately to parents

12 months: 2-3 words (other than mama and dada)

18 months: 6-10 words. Shows 2 parts of body.

20-24 months: uses 2+ words to make simple phrases

2.5-3 years: talks constantly in 3-4 word sentences

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137
Q

Social, emotional and behavioural normal milestones

A

6 weeks: smile

6-8 months: puts food in mouth

10-12 months: waves bye. peek a boo.

12 months: drinks from a cup 2 handed

18 months: self feeds with spoon

18-24 months: symbolic play

2 years: dry by day. pulls off some clothing

2.5-3 years: parallel play, starting interactive play. taking turns

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138
Q

Standardised testing of milestones

A

Screening

  • schedule of growing skills
  • Denver development screening test

Assessment
- Griffith’s/ Bailey Infant Development scales

Formal IQ testing

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139
Q

Define developmental delay

A

Slow acquisition of all skills (global delay) or one of specific delay particularly in relation to developmental problems in 0-5 years

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140
Q

Define learning difficulty

A

Used in relation to children of school age and may be cognitive, physical or both

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141
Q

Define impairment

A

Loss or abnormality of physiological function or anatomical structure

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142
Q

Define disability

A

Restriction or lack of ability due to impairment

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143
Q

Features suggestive of neurodevelopmental concerns

A 
Positive FHx
Antenatal screening positive
Neonatal encephalopathy
Birth asphyxia
Dysmorphic features
Pre-term infants
Abnormal neurological behaviour
Global delay
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144
Q

Conditions that cause abnormal development and learning difficulty
PRE NATAL

A

PRE-NATAL

  • Genetic: Down’s, Fragile X
  • Cerebral dysgenesis: microcephaly, absent corpus collosum, hydrocephalus
  • Vascular: occlusions, haemorrhage
  • Metabolic: hypothyroid, phenylketonuria
  • Teratogens: alcohol, drugs
  • Infection: rubella, CMV, toxoplasmosis, HIV
  • Tuberosclerosis, neurofibromatosis
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145
Q

Conditions that cause abnormal development and learning difficulty
PERINATAL

A

Extreme prematurity
Birth asphyxia - hypoxic ischaemic encephalopathy
Metabolic - hypoglycaemia, hyperbilirubinaemia

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146
Q

Conditions that cause abnormal development and learning difficulty
POSTNATAL

A

Infection: meningitis, encephalitis
Anoxia: suffocation, near drowning, seizures
Trauma: head injury
Vascular: stroke

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147
Q

Investigations for developmental delay

A

Cytogenic

  • chromosome karyotyping
  • Fragile X analysis

Metabolic: TFTs, LFTs, U&Es, plasma amino acids
CK, blood lactate, ammonia
ABG
Urate, ferritin

Congenital infection screen
Cranial US in newborn
CT/MRI
Skeletal survey - bone age
EEG
Nerve conduction studies
hearing. vision.
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148
Q

Global developmental delay

A

All fields
Usually apparent in the first 2 years
Always investigate for cause
Gets clearer to define as child gets older

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149
Q

Abnormal motor development symptoms

A 
Delay in acquisition of motor skills
Balance problems
Abnormal gait
Asymmetry of hand use - hand dominance not acquired until 1-2 years
Involuntary movements
Loss of motor skills (rare)

usually presents between 3months-2years

150
Q

Causes of abnormal motor development

A 
Central motor deficit - cerebral palsy
Congenital myopathy
Primary muscle disease
Spinal cord lesions - spina bifida
Global developmental delay
151
Q

Define cerebral palsy

A

Abnormality of movement and posture causing activity limitation attributed to non-progressive disturbances that occurred in developing foetal or infant brain

Often accompanied by distrubances in cognition, communication, perception, sensation or behavioural problems.

152
Q

Causes of cerebral palsy

A

80% antenatal

  • Vascular occlusion
  • cortical migration disorders
  • structural maldevelopment
  • genetic syndromes
  • congenital infections

10% hypoxic ischaemic injury during delivery

10% post natal

  • meningitis/encephalitis
  • encephalopathy
  • head trauma
  • hypoglycaemia
  • hydrocephalus
  • hyperbilirubinaemia
153
Q

Presentation of cerebral plasy

A 
Abnormal limb and/or trunk posture
Abnormal tone in infancy
Delayed motor milestones
Feeding difficulties - slow feeding, gagging, vomiting
Abnormal gait once walking
Asymmetric hand function <12 months
Primitive reflexes may persist
154
Q

Types of cerebral palsy

A

Spastic - can be split into hemiplegia, quadriplegia or diplegia

Dyskinetic

Ataxic

155
Q

Spastic CP

A 
Damage to upper motor neurone
limb tone increases (spasticity)
Brisk reflexes, extensor plantars
Tone is velocity dependent (faster movement = increased tone)
Presents early
156
Q

Spastic CP - hemiplegia

A

Arms > Legs
Unilateral
Face spared
presents at 4-12 months
Fisting of hand, flexed arm, pronated forearm
Then tiptoe walking
If large brain lesion may have hemianopia

157
Q

Spastic CP - quadriplegia

A

All 4 limbs
Severe
Extensor posturing
Poro head control
Low central tone
Seizures, microcephaly, moderate-severe LD
May have history of hypoxic ischaemic injury

158
Q

Spastic CP - diplegia

A 
Legs >> arms
All 4 limbs
Walking abnormal
Can appear normal arm movements
Assocaited with pre-term births due to periventricular haemorrhage
159
Q

Dyskinetic CP

A 
Movements which are involuntary, uncontrolled, occasionally stereotypes
Often more evident on movement
- Muscle tone variable
- primitive reflexes predominate
- Can have: chorea, athetosis, dystonia
- Intellect usually intact
- Usually presents with floppiness and poor trunk control
Movements appear ~ 1 year

Most commonly caused by hypoxic ischaemic brain injury

160
Q

Ataxic CP

A 
Hypotonic
Most are genetic
Early trunk and limb hypotonia 
Poor balance
Delayed motor development
Inco-ordinate movements
Intention tremor 
Ataxic gait
161
Q

Causes of speech and language delay

A

Hearing loss
Global developmental delay
Difficulty in speech production - cleft palate, CP
Environmental deprivation - lack of opportunity for social interaction
Normal variant / familial pattern

162
Q

Speech and language disorders

A

Disorders in

  • Language comprehension
  • Language expression
  • Phonation and speech production e.g. stammer (dysfluency), dysarthria, dyspraxia
  • Pragmatics
  • Social and communication disorders
163
Q

Testing language development

A

Symbolic Toy Test - for early language development

Reynell test - for expressive/receptive language in pre-school children

164
Q

Dyspraxia

A

Disorder of motor planning or execution
No findings in neurological exam
Disorder of higher cortical function

Problems with:
- Hand writing
- Dressing
- Cutting up food
- Poorly established laterality
- Copying and drawing
- Difficulty co-ordinating biting and chewing. Drooling common.
Achieves normal gross motor milestones
165
Q

Dyslexia

A

Disorder of reading skills disproportionate to IQ

Reading age > 2 years behind chronological age

166
Q

Causes of sensorineural hearing impairment

A

Antenatal: congenital infection, pre-term, hyperbilirubinaemia, hypoxic ischaemic brain injury

Post-natal: meningitis, encephalitis, trauma, drugs, neurodegenerative disease

167
Q

Sensorineural hearing loss in child

A 
1 in 1000
May be profound
Does not improve
May progress
Manage with amplification and cochlear implant if required
168
Q

Conductive hearing loss

A

Causes: otitis media + effusion, Eustachian tube dysfunction (Down’s, cleft palate, mid facial hypoplasia), wax
Intermittent or resolves
Max 60dB hearing loss

169
Q

Stabismus

A

Squint - misalignment of visual axes

  • Refer after 3m to ophthalmology
  • Usually caused by failure to develop binocular vision due to refractive errors
  • Concomitant: common, refractive error. generally convergent squint eye
  • paralytic: varies with gaze direction due to paralysis of motor nerves: SINISTER ? space occ lesion
170
Q

Aetiology of visual impairment in child

A

Genetic - cataracts, albinism, retinal dystrophy, retinoblastoma

Antenatal: congenital infection, retinopathy of immaturity, hypoxic ischaemic encephalopathy, trauma, optic nerve hypoplasia

Postnatal - trauma, infection, juvenile idiopathic arthritis

171
Q

Gross motor function classification

A

Level 1 - walks without limitations
Level 2 - walks with limitations
Level 3 - walks with handheld mobility device
Level 4 - self-mobility without limitations (can be powered mobility)
Level 5 - transported in manual wheelchair

172
Q

Common medical problems in those with developmental delay

A

Hearing
Vision
Orthopaedic (fixed contractures, spasms, spinal deformity, osteoporosis, fractures)
GI - GORD, constipation, aspiration
GU - UTI, delay in continence, neuropathic bladder
Resp - infections, aspiration, chronic lung disease, sleep apnoea
Neuro - epilepsy, CP, microcephaly, hydrocephalus
Failure to thrive
Poor weight gain

173
Q

Causes of vomiting in infants

A 
GORD
Feeding problems
Infection (gastroenteritis, meningitis, UTI, pertussis, Otitis media)
Dietary protein intolerances
Obstruction 
- Pyloric stenosis
- Atresia
- Intussusception
- Malrotation
- Volvulus
- Strangulated inguinal hernia
- Hirschsprung's disease
Inborn errors of metabolism
Congenital adrenal hyperplasia
Renal failure
174
Q

Causes of vomiting in Pre-school children

A 
Gastroenteritis
infection
Appendicitis
Obstruction
- Intussusception 
- Malrotation
- Volvulus
- Adhesions
Raised ICP
Coeliac disease
Renal failure
Testicular torsion
Metabolism errors
175
Q

Causes of vomiting in school age+ adolescents

A 
Gastroenteritis
Infection (sepsis, meningitis, pyelonephritis)
Peptic ulcers
H. pylori infection
Appendicitis
Migraine
Raised ICP
DKA
Coeliac
Alcohol/drugs
Cyclical vomiting syndrome
Bulimia, anorexia
Pregnancy
Testicular torsion
176
Q

Red flags for vomiting

A 
Bile stained
Haematemesis
Projectile vomiting in first few weeks
Abdominal tenderness
Abdominal distension
hepatosplenomegaly
Blood in stool
Severe dehydration
Bulging fontanelle
FTT
177
Q

What does bile stained vomit indicate?

A

Intestinal obstruction

Surgical emergency until proven otherwise

178
Q

What does bulging fontanelle indicate?

A

Raised ICP

179
Q

Define posseting

A

Small amounts of milk which accompany the return of swallowed air

180
Q

GORD

A

Involuntary passage of gastric contents into oesophagus
Extremely common in infancy
Due to inappropriate relaxtion of LOS due to functional immaturity
Usually resolves by 1 year

More common in

  • CP
  • Pre-term infnats
  • Post-op oesophageal atresia
181
Q

Investigations for GORD

A

Usually just a clinical diagnosis

  • 24 hour oesophageal pH monitoring to quantify degree of reflux
  • 24 hour impedance monitoring
  • Endoscopy and biopsy
182
Q

Management of GORD

A 
Parental reassurance
Adding inert thickening agents to feed
Position in 30 degrees prone after feeds
Ranitidine/Omeprazole
Consider cow's milk allergy
Surgery only if unresponsive (Nissen fundoplication)
183
Q

Pyloric stenosis

  • Define
  • Presentation
  • Epidemiology
A

Hypertrophy of pyloric muscle causing gastric outlet obstruction.
Presents at 2-7 weeks
Increase in boys (4:1), first borns, maternal FHx
Vomiting increases in frequency and forcefulness, becomes projectile
Weight loss if delayed presentation
Hypochloraemic metabolic alkalosis

184
Q

Diagnosis of pyloric stenosis

A

Give feed to calm the baby and then examine

  • Gastric peristalsis may be seen as wave from L to R
  • Palpable pyloric mass in RUQ
  • US useful if diagnosis in doubt
185
Q

Management of pyloric stenosis

A

Correct fluids and electrolytes
Pyloromyotomy - division of hypertrophied muscle
Can feed within 6 hours of Op
Discharged after 2 days

186
Q

Infant colic

A

Paroxysmal, inconsolable crying or screaming
Drawing up of knees and passage of excessive flatus
40% of all babies in first few weeks, resolves by 4 months
Benign but frustrating
Give support and reassurance
May be due to milk protein allergy or GORD

187
Q

Appendicitis

A

Most common cause of abdo pain requiring surgery
Uncommon in under 3s
Symptoms: anorexia, vomiting, central colicky abdominal pain
Signs: flushed face, low grade fever, abdo pain, increased on movement, tenderness at McBurneys point
Perforation is rapid as omentum less well developed
Appendectomy or IV ABx

188
Q

Non-specific abdo pain and mesenteric adenitis

A

Abdo pain resolves in 24-48 hours
Pain less severe than appendicitis
Often accompanied by URTI and cervical lymphadenopathy
Can only be diagnosed if large mesenteric nodes notes on laparatomy

189
Q

Intussusception

A

Invagination of proximal bowel into a distal segment
Most commonly ileum into caecum
Most common cause of obstruction after the neonatal period
Peaks at 3 months-2 years

190
Q

Presentation of intussusception

A

Paroxysmal severe colicky pain and pallor
Draws up legs
Initially recovers between painful episodes then lethargic
May refuse feeds
May vomit, becomes bile stained
Sausage shaped mass in abdomen
Redcurrant jelly stool (blood stained mucus)
Abdominal` distension or shock

191
Q

Investigations and management of intussusception

A

X-ray: distended small bowel, absence of gas pattern in distal colon
US can confirm diagnosis

Management

  • Rectal air insufflation unless peritonitis present
  • Surgery if that fails or peritonitis
192
Q

Meckel diverticulum

A

Ileal remnant of vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue
Present in 2%
Asymptomatic in most

Severe rectal bleeding, neither fresh or melena
Can present as intussusception, volvulus or appendicitis.
Treat with surgical resection

193
Q

Malrotation

A

During rotation of the small bowel in foetal life the mesentery is not fixed at the duodenojejunal flexure or ileocecal region.
Predisposed to volvulus
Ladd bands may cross the duodenum, contributing to bowel obstruction

Presents

  • Obstruction with bilious vomiting
  • obstruction with compromised blood supply

Surgery untwists the volvulus. Does not correct the Malrotation.

Remove appendix to avoid later confusion.

194
Q

Define recurrent abdominal pain

A

Pain sufficient to interrupt normal activities
Lasts >3 months
10% of school age children

195
Q

Causes of recurrent abdominal pain

A

Cause only found in 10%

  • IBS. Constipation. Dyspepsia. Abdominal migraine. Gastritis. Peptic ulcer. IBD. Malrotation
  • Dysmenorrhoea. Ovvairan cysts. PID
  • Hepatitis, gallstones, pancreatitis
  • UTI
  • Bullying, abuse, stress
196
Q

Abdominal migraine

A

Associated with abdominal pain and headaches.
In some abdominal symptoms predominate
Midline pain with vomiting

197
Q

IBS

A

Altered GI motility and abnormal sensation of intra-abdominal events
Symptoms can occur post GI infection
Abdominal pain, often worse before or relieved by defaecation
Loose stools/constipation
Bloating
Tenesmus

198
Q

Causes of gastroenteritis

A 
Most commonly ROTAVIRUS (60% of <2s)
Increased in early spring and winter
- Adenovirus
- Norovirus
- Calcivirus
- Coronavirus
- Campylobacter
- E.coli
199
Q

Degrees of dehydration

A

No clinically detectable dehydration (<5% body weight)
Clinical dehydration (5-10%)
Shock (>10%)

200
Q

Signs and symptoms of dehydration

A 
Appears unwell or deteriorating
Altered responsiveness, irritable, lethargic
Decreased consciousness (shock)
Pale or mottled skin (shock)
Cold peripheries
Sunken eyes
Dry mucus membranes
Tachycardia
Tachypnoea
Weak pulse
Increased cap refill (shock)
Decreased skin turgor
Hypotension (shock)
201
Q

Management of dehydration

A 
CLINICAL DEHYDRATION
Oral Rehydration Solution 
Often and small volumes
Consider NG
- If deteriorating  step 2

SHOCK

  • IV therapy
  • Rapid 0.9% NaCl
  • Consider ICU
  • Then step 2
  1. IV therapy for rehydration. Replace deficit + maintenance
    Monitor U&Es, creatinine, glucose

After: full strength milk. Reintroduce solid food. Diligent hand washing. No school for 48 hours.

202
Q

Post-gastroenteritis syndrome

A

Introduction of normal diet can cause watery diarrhoea

Normally ORS for further 24 hours then reintroduce solids again.

203
Q

Presentation of malabsorption

A

Abnormal stools
Failure to thrive
Specific nutrient deficiencies

204
Q

Coeliac disease

A

Gliadin provokes immunological response in proximal small bowel.
1 in 3000
Presents as profound malabsorption aged 8 months - 2 years after introduction of gluten.
FTT and abdominal distension
Buttock wasting
Abnormal stools

Positive IgA tissue transglutaminase
Diagnosis on small bowel biopsy

205
Q

Causes of nutrient malabsorption

A

Cholestatic liver disease or biliary atresia

Lymphatic leakage or obstruction

Short bowel syndrome

Loss of terminal ileum function (Crohn’s, resection)

Exocrine pancreatic dysfunction
- CF. Absent lipase, protease, amylase

Small intestine mucosal disease (Coeliac, lactase deficiency)

206
Q

Acrodermatitis enteropathica

A

Due to zinc malabsorption

Erythematous rash and mouth and anus.

207
Q

Red flags of constipation

A

Failure to pass meconium in first 24 hours (HIRSCHSPRUNG’S)
FTT/growth failure
Gross abdominal distension (Hirschprung’s)
Abnormal lower limb neurology
Spina bifida signs
Abnormal anorectal anatomy
Perianal bruising, fissures = sexual abuse

208
Q

Long standing constipation

A

Rectum becomes over distended
Loss of sensation to poo
Involuntary soiling
Requiring long term laxative use

209
Q

Hirschsprung’s disease

A

Absence of ganglion cells from myenteric and submucosal plexus of large bowel results in narrow contracted segment.

Abnormal bowel extends from rectum ending in normally innervated dilated colon

75% only affects rectum/sigmoid
10% whole colon

failure to pass meconium in first 24 hours
Later abdominal distension and bile stained vomiting

On DRE narrow segment and gush of fluid/stool/flatus on removal

Diagnosed by absence of ganglion cells and presence of ACHE + nerve trunks on suction rectal biopsy

Management: colostomy with later anastomoses.

210
Q

Management of constipation

A

If faeces not palpable - encouragement and close supervision

If palpable

  • Macrogol e.g. Movicol for 2 weeks
  • If stools passed done
  • If not then add stimulant laxative e.g. senna with or without lactulose
  • If no success then consider enema or manual evacuation under GA

After - balanced diet, sufficient fluids, maintenance laxatives

211
Q

Epidemiology of UTI

A

3-7% of girls <6
1-2 % of boys <6

12-30% have recurrence within 1 year

Up to 50% have structural abnormality

212
Q

Presentation of UTI in infant

A 
Fever
Vomiting
Lethargy
FTT/ poor feeding
Jaundice
Septicaemia
Offensive urine
Febrile convulsion
213
Q

Presentation of UTI in children

A 
Dysuria
Frequency
Abdo/loin pain
Fever/rigors
Lethargy
Anorexia
D&amp;V
Haematuria
Offensive cloudy urine
Febrile convulsions
Recurrence of enuresis
214
Q

Collecting urine in children

A 
Clean catch - waiting clean pot when nappy removed *recommended*
Adhesive plastic bag on cleaned perineum
Urethral catheter if urgent
Suprapubic aspiration - rarely done
In older children MSU
215
Q

In UTI - dipstick findings and when to treat

A

Positive leukocytes and nitrites = regard as UTI and treat
Negative leukocytes, positive nitrites = start Abx, diagnosis depends on urine culture
Positive leukocyte, negative nitrites = only Abx if clinical UTI
If both negative - UTI unlikely.

216
Q

Aetiology of UTI

A
  1. E.coli
  2. Klebsiella
  3. Proteus (increased in boys)
  4. Pseudomonas
  5. Strep faecalis
217
Q

Factors contributing to UTI

A

Incomplete bladder emptying

  • Infrequent voiding
  • Vulvitis
  • Obstruction from constipation
  • Neuropathic bladder
  • Vesicoureteral reflex
218
Q

Vesicoureteric reflux

A

Developmental abnormality of vesicoureteric junctions.

Ureters are displaced laterally and enter the bladder directly rather than at an angle

219
Q

Investigations for UTI

A

Some debate over benefit of investigating
Investigate atypical or recurrent UTI

Atypical:

  • Seriously ill/ sepsis
  • Poor urine flow
  • Abdominal or bladder mass
  • Raised CK
  • Failure to respond to Abx in 48 hours

US to detect structural abnormalities
Further investigations depends on US findings

220
Q

Management of UTI

A

If under 3 months - refer to hospital for IV Abx
If over 3 months - oral Abx for 7-10 days
If only LUTS then 3 days oral

High fluid intake
Regular voiding
Ensure complete emptying
Prevent or treat constipation
Good perineal hygiene
Consider circumcision
221
Q

Define enuresis

A

Lack of bladder control

Primary - lack of control to be continent
Secondary - loss of previously achieved enuresis

222
Q

Aetiology of primary daytime enuresis

A 
Lack of attention to bladder sensation - developmental or psychogenic
Too preoccupied to respond
Detrusor instability
Bladder neck weakness
Neuropathic bladder
UTI
Constipation
Ectopic ureter
223
Q

Examination/investigation in enuresis

A 
Test perineal sensation - S4/5
Urine sample - dip, microscopy and culture 
US may show bladder pathology
Urodynamic studies may be required
Spine X-ray or MRI for defects
224
Q

Management of enuresis

A

Once neurological cause excluded - star charts, bladder training, pelvic floor exercises
Treat constipation
Last resort - anticholinergic drugs (oxybutynin)

225
Q

Causes of secondary enuresis

A

Emotional upset most common
UTI
Polyuria from osmotic diuresis (diabetes, CKD)

Test osmolality of urine

226
Q

Management of nocturnal enuresis

A

Straightforward but pain staking
Treatment is rare in under 6s
Explain to parent and child than problem is beyond conscious control
Stop punishment
Star chart for each dry night
Enuresis alarm - ideally child should get up when alarm indicates wet pants
Desmopressin - short term relief (sleepovers, holidays) - synthetic analogue of ADH

227
Q

Epidemiology of nocturnal enuresis

A

6% of 5 years olds 3% of 10year olds
Increased in boys (2:1)

Most are psychologically normal - child needs to be free from stress

228
Q

Define encopresis

A

Voluntary or involuntary passage of faeces, usually into clothing, after the age at which bowel control is usually achieved (any defaecation not in toilet)
No known cause

Bowel control normally achived by age of 3
Soiling at 4 or older is abnormal

229
Q

Epidemiology of encopresis

A

1% of 5 year olds

Increased in boys

230
Q

Causes of encopresis

A

Bowel control never established - disorganised family, understaffed institution, mental retardation

Emotion causes -

  • Regressive soiling due to upsetting event
  • Aggressive soiling - poor relationships between sibling. Rebellious act.

Physical causes

  • Faecal impaction
  • Hirschsprung’s disease
231
Q

management of encopresis

A

Assess possible cause
Treat faecal retention
Give adequate toilet training
Emotional support

Regressive usually settles with emotional problems. Aggressive more troublesome.

232
Q

Causes of proteinuria

A 
Orthostatic proteinuria (only proteinuria when child upright)
Glomerular abnormalities
- Minimal change disease
- Glomerulonephritis
- Abnormal GBM
Raised glomerular filtration pressure
Decreased renal mass
Hypertension
Tubular proteinuria
233
Q

Nephrotic syndrome

A

Heavy proteinuria
Hypoalbuminaemia
Oedema

234
Q

Investigations in nephrotic syndrome

A 
Urine protein on dipstick
FBC and ESR
U&amp;Es and creatinine
Complement leves C3 and C4
Antistreptolysin O or anti-DNAase B titres 
Urine microscopy and culture
Urine sodium concentration
Hep B and C screen
235
Q

Steroid sensitive nephrotic syndrome

A 
85-90% of nephrotic syndrome
Do not progress to renal failure
Increased in boys
Increased in Asians
Often precipitated by respiratory infections

No macroscopic haematuria, normal BP, complement levels and renal function,

Most commonly minimal change disease

236
Q

Management of nephrotic syndrome

A

Oral corticosteroids 60mg/m2
After 4 weeks decrease dose to 40mg/m2 on alternate days for 4 weeks
If not responding - renal biopsy

237
Q

Biopsy of minimal change disease

A

Normal light microscopy

Fusion of podocytes on electron microscopy

238
Q

Complications of nephrotic syndrome

A

Hypovolaemia - treat with IV albumin

Thrombosis - hypercoagulable state

Infection

1/3 resolve. 1/3 frequent relapses (steroid dependent). 1/3 infrequent relapses

239
Q

Steroids resistant nephrotic syndrome

CAUSES

A

Refer to paeds nephrologist

  • Focal segmental glomerulosclerosis
  • Membranoproliferative GN (mesangiocapillary GN)
  • Membranous nephropathy
240
Q

Focal segmental glomerulosclerosis

A

Most common steroid resisntat nephrotic syndrome
Familial or idiopathic
30% cause end stage renal failure in 5 years
20% respond to cyclophosphamide/ciclolsporin/tacrolimus
Recurrence post transplant is common

241
Q

Membranoproliferative glomerulonephritis

A

Also called mesangiocapillary GN
Increased in older children
Haematuria and low complement present
Decreasing renal function over many years

242
Q

Membranous nephropathy

A

Associated with Hep B
May precede SLE
Most remit spontaneously in 5 years

243
Q

Congenital nephrotic syndrome

A 
Presents in first 3 months
Rare
Autosomal recessive
Increased in Finnish
High mortality
Albuminuria is so severe that unilateral nephrectomy may be required to control it.
244
Q

Appearances of haematuria

A

Glomerular haematuria - brown urine, deformed red cells and casts +/- proteinuria

LUT haematuria = red urine, beginning or end of urinary stream. No proteinuria

245
Q

Causes of Haematuria

A

Non glomerular

  • Infection
  • Trauma
  • Stones
  • Tumours
  • Sickle cell disease
  • Bleeding disorders
  • Renal vein thrombosis
  • Hypercalciuria

Glomerular

  • Acute glomeruloneprhtisi (usually with proteinuria)
  • Chronic glomerulonephritis (usually with proteinuria)
  • IgA nephropathy
  • Familial nephritis (Alport’s)
  • Thin basement membrane
246
Q

Investigations in haematuria

A

Urine microscopy and culture
Protein and calcium excretion
Kidney and urinary tract US
U&Es, creatinine, calcium, phosphate, albumin
FBC, platelets, clotting screen, sickle cell screen

If suggestive of glomerular haematuria

  • ESR. Complement levels. Anti-DNA antibodies
  • Throat swab.
  • Abtistreptolysin O / anti-DNAase B titres
  • Hep B and C screen
  • Renal biopsy if indicated
247
Q

Acute nephritis

A

Hypertension
Haematuria
Oedema
Decreased urine output and volume overload

248
Q

Causes of nephritic syndrome

A 
Post infections (streptococcal)
Vasculitis
- Henoch-Schonlein putpura
- SLE
- Wegner's granulomatosis
- Polyarteritis nodosa
IgA nephropathy
Mesangiocapillary GN
Goodpasture's syndrome
249
Q

Post-streptococcal glomerulonephritis

A 
Following strep sore throat or skin infection
Raised anti-DNAase B titres
Low C3 complement
Long term prognosis good
ASO positive
250
Q

Features of Henoch-Schonlein purpura

A

Characteristic skin rash
- Symmetrical, over buttocks and extensor limb surfaces
- Trunk spared
- Urticarial, rapidly becoming maculopapular and purpuric
- palpable
Arthralgia
Periarticular oedema
Adnominal pain - colicky. Haematemesis or malena
Glomerulonephritis

Increased in boys aged 3-10 years
Often preceded by URTI

251
Q

Alport’s disease

A

X linked recessive
Haematuria
Progresses to end stage renal failure by early adult life
Associated with deafness and ocular defects

252
Q

Pathophysiology of meningitis

A

Infection of meninges usually follows bacteraemia
Much of the damage is caused by the host response
Release of inflammatory mediators and leukocytes causes endothelial damage
Causes cerebral oedema. Raised ICP, decreased cerebral blood flow
Inflammation causes vasculopathy and cerebral cortical infarction
Fibrin deposits can block resorption of CSF causing hydrocephalus

253
Q

Organisms causing meningitis in newborns

A

Group B streptococcus
E. Coli and other coliforms
Listeria monocytogenes

254
Q

Organisms causing meningitis in 1 months - 6 years

A

Neisseria meningitides
Streptococcus pneumonia
Haemophilus influenza (not common beyond 6 years)

255
Q

Presentation of meningitis (symptoms)

A 
Fever
Headache
Photophobia
Neck stiffness
Irritable
Reduced consciousness
Lethartgy
Poor feeding
Seizures
Vomiting
Hypotonia
256
Q

Signs of meningitis

A 
Fever
Purpuric rash
neck stiffness (not always in infants)
Bulging fontanelle
Opistghotonus - arching back
\+ Brudzinski's and Kernig's sign
Signs of shock
Focal neurology
Papilloedema (rare)
257
Q

Investigations for meningitis

A

FBC (raised WCC and platelets)
U&Es
LFTs
Raised CRP

Blood cultures

LP for red cells, white cells, glucose, culture and microscopy

Blood/urine/CSF for rapid antigen testing and PCR

MRI

258
Q

Brudzinski’s sign

A

Lay supine

Flexion of neck causes flexion of the legs

259
Q

Kernig’s sign

A

Lay supine with hips and knees flexed

On straightening of legs - pain

260
Q

CSF changes in bacterial meningitis

A

Purulent CSF
Raised protein
Low glucose
Raised WCC

261
Q

CSF changes in viral meningitis

A

Clear CSF
Normal or raised protein
Normal or low glucose
Raised lymphocytes

262
Q

CSF changes in TB meningitis

A

Turbid/Clear or viscous CSF
Mildly raised lymphocytes
Very raised protein
Very low glucose

263
Q

CSF changes in encephalitis

A

Clear CSF
Normal or raised protein
Normal or low glucose
Raised lymphocytes

264
Q

Management of meningitis

A

No delay in IV ABx and supportive therapy
ABx depend on pathogen found
Start with 3rd gen cephalosporin - cefotaxime or ceftriaxone
Dexamethasone to decrease complications

265
Q

Complications of meningitis

A

Hearing loss
Local vasculitis - CN palsies or other focal lesions
Local cerebral infection - epilepsy
Subdural effusion - particularly in H. influenzae or pneumococcal. Most resolve spontaneously
Hydrocephalus
Cerebral abscess

266
Q

Causes of viral meningitis

A 
2/3 are viral
Enteroviruses
EBV
Adenovirus
Mumps

Less severe, makes full recovery

If fail to respond to treatment or supportive therapy consider atypical pathogens
- Mycoplasma or Borelia burgdorferi (lyme disease)

267
Q

Encephalitis

A

Inflammation of brain substance
Meninges can also be affected

Can be caused by

  • Direct invasion of cerebrum by neurotoxic virus e.g. herpes simplex
  • Delayed brain swelling following disordered immunological response (post-infectious encephalopathy from chicken pox)
  • Slow virus infection (HIV)
268
Q

Causes of encephalitis

A 
Enteroviruses
Respiratory viruses
Herpes viruses (HSV, varicella, HHV6)
Mycoplasma
Boreglia burgdorferi
Rocky mountain spotted fver

Herpes simplex virus is rare but has devastating consequences

269
Q

Presentation of encephalitis

A

As meningitis - manage as meningitis until proven otherwise

Fever
Headache
Photophobia
Neck stiffness
Irritable
Reduced consciousness
Lethartgy
Poor feeding
Seizures
Vomiting
Hypotonia
270
Q

Management of encephalitis

A

High dose IV aciclovir

271
Q

HSV encephalitis

A

Destructive infection
EEG and CT/MRI may show focal changes particularly in temporal lobes
3 weeks of acyclovir required
Untreated mortality rate = 70%
Survivors often have severe neurological problems

272
Q

Define fever

A

Temperature over 37.5 degrees

273
Q

How to measure fever

A

In under 4 weeks - electronic thermometer in axilla

Over 4 weeks as above or tympanic infrared thermometer

274
Q

Fever & age of child

A

Under 3 months - often bacterial

Over 3 months - more likely to be viral

275
Q

RFs for infection

A 
Illness of other family members
Prevalent illnesses in community
Unimmunised
recent travel abroad
Contact with animals - brucellosis
Immunodeficient
276
Q

Red flags for child with fever

A 
Maculopapular non blanching rash
Irritable/reduced consciousness
Over 38 degrees if <3m, over 39 if >3m
Bulging fontanelle, neck stiffness, seizures, focal neurology
Bile stained vomiting
Significant respiratory distress
Severe dehydration or shock
277
Q

Septic screen

A

Blood cultures
FBC
CRP
Urine sample

Consider

  • CXR
  • LP
  • Rapid antigen screen on blood/urine/CSF
  • Meneningococcal and pneumococcal PCR on blood/CSF
278
Q

Causes of fever & presentation

A 
Meningitis
Seizures - meningitis, encephalitis
Otitis media
Tonsillitis
Epiglottitis, viral croup - stridor
URTI
Appendicitis, pyelonephritis, hepatitis - abdo pain
Gastroenteritis - diarrhoea
Septicaemia - shock
Septic arthritis
279
Q

Causes of prolonged fever

A 
Bacterial infection - endocarditis
Kawasaki disease
Drug reaction
Malignant disease
Connective tissue disorder
280
Q

Toxic shock syndrome

A 
Caused by toxin producing Staph aureus and Group A strep
Characterised by:
- Fever > 39
- Hypotension
- Diffuse erythematous macular rash

1-2 weeks later - desquamation of fingers and toes.

Toxin causes organ dysfunction: mucositis, D&V, renal and liver impairment, altered consciousness

need to surgical debride areas of infection + 3rd cephalosporin + clindamycin

281
Q

Necrotising fascitis

A

Severe subcut infection involving skin, fascia and muscle
Enlarges rapidly, leaving poorly perfused areas of necrotic tissue
Severe pain and systemic illness requiring ITU
Surgical debridement necessary + IV abx`
Caused by Staph Aureus or group A strep

282
Q

Impetigo

A

High contagious skin infection with staph or strep
No school until resolved
Weepy red honey coloured crush
Increased if pre-existing skin disease
Start as erythematous macules then vesicular/pustular then secretes the honey coloured exudate.
Lesions common on hands, face and neck
Topical antibiotics

283
Q

Cuases of maculopapular rash + fever

A 
Human herpes virus 6&amp;7
Enteroviral rash
Parovirus (slapped cheek)
measles
rubella
scarlet fever (group A strep)
erythema marginatum (rheumatic fever)
Salmonella typhi (rose coloured spots_
Lyme disease
Kawasaki disease
Juvenile idiopathic arthritis
284
Q

Causes of vescicular/pustular rash + fever

A 
Varicella zoster
Herpes simplex
Coxsackie (hand foot and mouth)
Impetigo
Boils
Toxic epidermal necrolysis
Erythema multiforme
Steven-Johnson's syndrome
285
Q

Causes of petechial purpuric rash + fever

A 
Meningitis
Infective endocarditis
Enterovirus
Henoch-Schonlein purpura
Vasculitis
Malaria
Thrombocytopaenia
286
Q

Herpes viruses

A 
HSV 1
HSV 2 - Herpes simplex 1 and 2. Responsible for cold sores and genital 
Varicella Zoster
CMV
EBV
Human herpes virus 6, 7 and 8 
HHV8 is associated with Kaposi's sarcoma

Hallmark
1. Primary infection
2, Latency and long term persistence
3. Reactivation

287
Q

Herpes simplex 1 & 2

A

Wide variety of presentations
Treat with acyclovir
Can by asymptomatic
Can cause:
- Gingivostomatitis - most common in children, 10mont-3years. vesicular lesions on lips, gums, tongue and soft palate. Painful ulceration
- Eczema herpeticum - herpes infection + eczema
- Herpetic whitlow

288
Q

Chicken pox

A

Primary infection with varicella zoster
200-500 lesions on head and trunk then progresses to limbs
Appears as crops of papules, vesicles with surrounding erythema and pustules for up to 1 week
lesions may occur on palate.
Can causes permanent depigmentation from scratching
If new lesions after 10 days = defective immunity

Complications:

  • Staph/strep infection
  • Encephalitis
  • Purpura fulminans - large areas of skin necrosis

Supportive treatment unless immunocompromised then IV acyclovir

289
Q

EBV infection

A 
Causes infectious mononucleosis, Burkitt's lymphoma or associated with nasopharyngeal carcinoma
- Fever
- Malaise
- Tonsillopharyngitis
- Lymphadenopathy
- Splenomegaly (50%) hepatomegaly (10%)
- Maculopapular rash
Symptoms persist for 1-3 months
`
Diagnosed with atypical lymphocytes, Positive monospot and IgM and IgG to EBV
290
Q

CMV infection

A 
Transmitted in saliva, genital secretions or breast milk
Can cause infectious mononucleosis symptoms
can cause
- retinitis
- pneumonitis
- bone marrow failure
- encephalitis
- hepatitis
- colitis
- oesophagitis
291
Q

Human Herepes virus 6 and 7

A

Most children are infected by age of 2 from family members
Can cause exanthem subitum - roseola infantum
High fever and malaise for few days followed by macular rash as fever wains

292
Q

Parvovirus B19

A

Slapped cheek
Causes erythema infectiosum or 5th disease
- most common
- fever, malaise, headache, myalgia
- followed by slapped cheek rash on face
- then maculopapular rash “lace like rash” on trunk and limbs

outbreaks in spring
Infects erythroblastoid red cell precursors in bone marrow
Can cause aplastic crisis - in children with chronic haemolytic anaemias

Maternal transmission can cause foetal hydrops

293
Q

Enteroviruses

A

Includes coxsackie, echovirus, poliovirus
Transmission if faecal oral
90% are asymptomatic

Hand, foot and mouth disease - painful vesicular lesions on hands, feet or mouth. Self resolving

Herpangia - vesicular and ulcerated lesions on soft palate and uvula.

Meningitis/encephalitis

Bornholme disease/ Pleurodynia = fever, pleuritic chest pain and muscle tenderness

294
Q

Measles

A

Rash

  • Spreads downwards from behind ears to whole body
  • From discrete maculopapular to confluent and blotchy
  • May desquamate in 2nd week

Cough
Conjunctivitis and cold symptoms

Koplik’s pots - white spots on buccal mucosa

Complications

  • Encephalitis (mortality 15%0
  • Subacute sclerosing panencephalitis - 7 years post infection

Treatment symptomatic

295
Q

Mumps

A

Spread via droplet infection.
Infection from parotid gland before dissemination
Fever, malaise, parotitis (earache and pain on eating)
Fever settles in 3-4 days
Raised amylase
Mild and self-limiting
Hearing loss can occur (transient)

296
Q

Rubella

A

German measles

  • Causes damage to foetus
  • Prodrome with mild low grade fever
  • Maculopapular rash from face down
  • Fades in 3-5 days
  • Not itchy (in children)
  • Prominent lymphadenopathy (particular post-auricular)

No treatment

297
Q

Kawasaki disease

A

Systemic vasculitis
6 months - 4 years
Increased in Japanese and Blacks
High fever, difficult to control for > 5 days

Need 4 of 5 other features

  • Conjunctival infection
  • Mucus membrane changes
  • cervical lymphadenopathy
  • polymorphous rash
  • peeling of skin on fingers and toes

Can cause coronary aneurysms
Mortality 1-2%

298
Q

Pathogens causing respiratory infections

A

80-90% are VIRAL

  • Respiratory syncytial virus
  • Rhinovirus
  • Parainfluenza
  • Influenza
  • Metapneumovirus
  • Adenovirus

Bacterial

  • Streptococcus pneumoniae
  • H. influenzae
  • morexella catarrhalis
  • Bordetella pertussis
  • mycoplasma pneumoniae
299
Q

RF for respiratory infection

A 
Parental smoking
Low socioeconomic status
Decreased nutrition
Underlying lung disease
Congenital heart disease
Boys
Immunodeficiency
300
Q

Classification of respiraotyr infections

A 
URTI
laryngeal/tracheal infection
Bronchitis
Bronchiliolitis
Pneumonia
301
Q

URTI

A

Includes

  • Common cold (coryza)
  • Sore throat (pharyngitis, tonsillitis)
  • Acute otitis media
  • Sinusitis
302
Q

presentation of URTI

A 
Nasal discharge and blockage
Fever
Painful throat
Earache
Cough
Difficulty feeding
febrile convulsions
Acute exacerbation of asthma
303
Q

Causes of coryza

A

Most common infection

  • rhinovirus
    Coronavirus
    Respiratory syncytial virus
304
Q

Causes of pharyngitis

A 
Sore throat 
Adenovirus
Enterovirus
Rhinovirus
In older child Group A beta haemolytic strep
305
Q

Causes of tonsillitis

A

Group A haemolytic strep

EBV

306
Q

Symptoms and management of tonsillitis

A 
Sore throat
Headache
Apathy
Abdo pain
Cervical lymphadenopathy
White exudate

Treat with penicillin (erythromycin)
Avoid amoxicillin as maculopapular rash if EBV infection

307
Q

Otitis media

A

Increased at 6-12 months
Tympanic membrane = red and bulging and loss of light reflection
Caused by RSV and rhinovirus
OR pneumococcus, H.influenzae or M. catharalis
Regualr analgesia
If ABx = amoxicillin

308
Q

When is tonsillectomy indicated

A

Recurrent severe tonsillitis
Peritonsilar abscess
Obstructive sleep apnoea

309
Q

Causes of upper airways obstruction / STRIDOR

A 
* viral laryngotracheobronchitis * - "Croup"
Epiglottiits
Bacterial tracheitis
Inhalation of smoke and hot air
Trauma to throat
Foreign body
Hypocalcaemia
Measles
Infectious mononucleosis
Diphtheria
310
Q

Characteristic features of laryngeal and tracheal infections

A

Stridor
Hoarseness
Barking cough
Dyspnoea

Can rapidly be life threatening in young chgildren

311
Q

Croup

A

Laryngotracheobronchitis
Mucosal infections & increased secretion
Can cause critical narrowing if subglottic

95% viral - parainfluenza, RSV, influenza

6 months - 6 years

Barking cough, hoarseness, stridor, fever
Symptoms worse at night

Low threshold for admission in < 1 year due to narrow airway
If severe mange with nebulised adrenaline and ITU

312
Q

Acute epiglottitis

A 
Life threatening emergency
Caused by H. influenza B
Intense swelling of epiglottis
1-6 years 
Acute onset
Toxic looking child
Saliva drooling
Soft inspiratory stridoe
Child sitting immobile, upright with mouth open
Admit to ICU ASAP, RSI under GA
IV abx
313
Q

Whooping cough

A

Bordetella pertussis
Bronchitis
highly contagious
Catarrhal phase - week of coryza (cold symptoms)
Characteristic - INSPIRATORY WHOOP
Paroxysmal cough
Spasms of cough - worse a night
Can cause vomiting, conjunctival haemorrhages, epistaxis
3-6 weeks
Symptoms decrease slowly
Complications - pneumonia, bronchiectasis

314
Q

Bronchiolitis

A

Rare after age of 1
90% aged 1-9 months
80% due to RSV (respiratory syncytial virus)
Others: metapneumovirus, parainfluenza, rhinovirus, adenovirus, influenza
Coryzal symptoms precede a dry cough and SOB
Feeding difficulty due to SOB

315
Q

Signs and symptoms of bronchiolitis

A 
Sharp dry cough
Tachypnoea
Subcoastal and intercostal recession
Hyperinflation of chest - prominent sternum, downwards displaced liver
high pitched wheeze exp>ins
Tachycardia
Fine end expiratory crackles
Cyanosis
Pallor
316
Q

Features of croup

A 
Onset over days
Preceding coryza
Cough severe and barking
Able to drink
No drooling of saliva
Appears unwell
Fever <38.5
Harsh rasping stridor
Hoarse voice
317
Q

Features of epiglottiits

A 
Onset over hours
No preceding coryza
Absent or slight cough
Not able to drink
Drooling saliva
Toxic looking child 
Fever > 38.5
Soft whispering stridor
Reluctant to speak
318
Q

Investigations in URTI

A

PCR of nasopharyngeal secretions
CXR unnecessary if straightforward
CXR - hyperinflation of lungs and focal atelectasis

319
Q

Causes of pneumonia in childhood

A

Newborn - group B strep. gram negative enterococci

Infants - RSV, Step pneumoniae, H. influenza, Bordella pertussis, chlamydia trachomatis

Over 5s - mycoplasma pneumoniae, strep pneumoniae, chlamydia pneumoniae

320
Q

Symptoms and signs of pneumonia

A 
Fever
SOB
Usually preceded by URTI
Cough
Lethargy
Unwell
Tachypnoea
Nasal flaring 
Chest in drawing
End expiratory crackles
321
Q

Management of pneumonia

A 
Most managed at home
Admit if sats < 93%, severe raised RR, SOB, grunting, apnoea, not feeding
Oxygen for hypoxia
Analgesia if required
ABx
IV fluids for dehydration
322
Q

Malaris

A

From female anopheles mosquito - plasmodium falciparum
700,000 deaths per year
Fever, diarrhoea, vomiting, flu like symptoms, jaundice, anaemia, thrombocytopaenia

Typical onset 7-10 days after inoculation

Children are susceptible to severe anaemia and cerebral malaria
Quinine required in most cases

323
Q

Typhoid

A

Worsening fever, headaches, cough, abdominal pain, anorexia, malaise and myalgia
Salmonella typhi
GI symptoms may not appear until 2nd week
Rose colour spots on trunk

Complications: GI perforation, myocarditis, hepatitis, nephritis

324
Q

Dengue fever

A

Viral infection transmitted by mosquitos
Fine erythematous rash, myalgia, arthralgia, high fever
2y rash with desquamation after

Dengue haemorrhagic fever when previously infected child reinfected with different strain: severe capillary leak, hypotension
most recover

325
Q

Common allergies in children

A 
Food allergy
Eczema
Allergic rhinitis and conjunctivitis
Asthma
Urticaria
Insect sting hypersensitivity
Anaphylaxis
326
Q

Define hypersensitivity

A

Objectively reproducible symptoms or signs following exposure to defined stimulus at a dose which is tolerated in normal people

327
Q

Define allergy

A

Hypersensitivity reaction initiated by specific immunological mechanism. Can be IgE mediated (peanut allergy) or non IgE mediated (Coeliac)

328
Q

Define atopy

A

Personal or familial tendency to produce IgE antibodies to potential allergens, usually proteins. Strongly associated with asthma, allergic rhinitis and conjunctivitis, eczema and food allergy

329
Q

Pathophysiology of atopy

A

Allergens bind to IgE sensitised mast cells and basophils
Histamine is released from intracellular granules
mast cells are concentrated in skin, lungs and GI
Histamine causes:
- Local vasodilation (erythema)
- Increased capillary permeability (wheal)
- Vasodilation of surrounding arterioles (flare)
- Stimulation of sensory nerves (itching)
- Smooth muscle contraction (bronchoconstriction and increased GI motility)
- Increased nasal, salivary and gland secretions

As histamine is a potent vasodilator, can cause peripheral blood pooling, hypotension and circulatory shock

330
Q

Allergic march

A

Children develop allergic disorders at different ages

  • Eczema and food allergy in infancy
  • Allergic rhinitis and conjunctivitis in preschool/primary school
  • hayfever often precedes asthma
331
Q

Epidemiology of food allergies

A

5% of children
3% of adults
Increasing incidence ? processed diet ? hygiene hypothesis
2% of infants have cow’s milk protein allergy

332
Q

Symptoms of IgE mediated food allergy

A 
Pruritus
Erythema
Diarrhoea
Abdominal pain
Acute urticaria
Acute angio-oedema (usually facial)
Oral itching
Nausea and vomiting
Nasal itching, rhinorrhoea, sneeze
Allergic conjunctivitis
Cough, SOB, wheeze, asthma
Feeling of impending doom
CV collapse
333
Q

Symptoms of non-IgE mediated food allergy

A 
Pruritus
Erythema
Diarrhoea
Abdominal pain
Atopic eczema
GORD
Infantile colic
Stools loose/frequent/blood/mucus
Constipation
Perianal redness
Pallor and tiredness
FTT
Food aversion or avoidance
334
Q

Investigations for food allergy

A

Food diary

Physician supervised oral food challenge, skin prick, food specific IgE tests

335
Q

Describe skin prick testing

A

Drop of food placed on forearm
Needle pricks skin through food
Saline for comparison
Reaction read after 15-20 minutes

336
Q

Common food allergen

A 
Milk
Eggs
Fish and seafood
peanuts
Sesame
Tree nuts
Soybeans
Wheat
Kiwi
337
Q

Investigations for non-IgE mediated food allergy

A

2-6 weeks trial elimination and reintroduce after to determine symptoms

338
Q

Food protein induced enterocolitis

A

Presents with projectile vomiting, diarrhoea and FTT for first few months.
Usually due to Cow’s milk and soy protein formulas

non-IgE mediated

339
Q

Eosinophilic oesophagitis and gastroenteritis

A

Nausea, abdominal pain, reflux, FTT
Does not respond to antacids.
Non-IgE mediated food allergy

340
Q

Management of food allergies

A

Food avoidance - particularly if anaphylactic
Dietician referral - reading food labels, preventing deficiencies
Antihistamines - for mild symptoms e.g. urticaria, itching
Adrenaline - if resp symptoms or anaphylaxis
Medical emergency bracelets
Injection immunotherapy (desensitisation) only used for pollen and venom

341
Q

Non-immunologically mediated food intolerance causes

A

Metabolic: lactase deficiency
Pharmacological: preservatives, artificial food colours, sweeteners, alcohol, caffeine
Toxic - contaminated foods
Psychological: food aversion

Avoid trigger foods

342
Q

Non-immunologically mediated food intolerance symptoms

A 
Headache
Fatigue
GI upset
Urticaria
Behavioural problems
343
Q

Define anaphylaxis

A

Severe life threatening generalised or systemic hypersensitivity reaction

  • Sudden onset and rapid progression of symptoms AND
  • life threatening A/B/C problem
344
Q

Aetiology of anaphylaxis

A

Occurs when allergen reacts with IgE antibodies on mast cells in type 1 hypersensitivity reaction
Rapid release of histamine

  • Peanuts, pulses, tree nuts (brazil, almond, hazelnut), fish, shellfish, eggs, sesame, milk
  • bee/wasp sting
  • antibiotics, NSAIDs, contrast media, anaesthetic drugs
345
Q

presentation of anaphylaxis

A 
Initially skin symptoms: generalised itching, urticaria, erythema, rhinitis, conjunctivitis, angio-oedema
Dyspnoea
Stridor
Wheeze
Palpitations
Tachycardia
nausea and vomiting
Abdominal pain
LOC
346
Q

Management of anaphylaxis

A

ABCDE
High flow O2 through non-rebreathe
Lie flat
Raise legs
Adrenaline IM 0.5ml of 1:1000 (500 micrograms)
Repeat after 5 minutes if no improvement
May benefit from IV adrenaline (anaesthetist only)
Establish airway (often intubation)
IV fluid challenge - 1L in 10 minutes if hypotensive

If further deterioration: salbutamol, ipratropium, aminophylline, mag sulphate)

After initial resus

  • Chlorphenamine 10mg
  • Hydrocortisone 200mg

Lower doses for children - age appropriate

347
Q

Investigations for anaphylaxis

A

Serum mast cell tryptase can be measured for diagnosis if required.
Peak at 1 hour, Do at emergency and then 1-2 hours later

348
Q

Follow up management of anaphylaxis

A 
Observe for 6-12 hours
If under 16 admit to paediatric ward
- Organise allergen testing
- Organise epi pen and training
- Written management plan
- Encourage emergency medical bracelet
349
Q

Types of allergic rhinitis

A

Seasonal allergic rhinitis (hayfever): occurs at certain times of year. Tress grass or pollen

Perennial rhinitis - persistent, occurs year round. dust mites, domestic pets

Occupational: flour, wood dust, latex gloves

350
Q

Pathogenesis of allergic rhinitis

A

IgE mediated inflammation of nasal mucosa due to histamine release

  • Acute phase (mins) - sneezing, increased nasal secretion
  • Late phase (6-12hours) - nasal obstruction
351
Q

Epidemiology of allergic rhinitis

A

20% of UK population
Children and adolescents tend to have seasonal, adults = perennial
Peak onset is in children, 80% diagnosed under 20
10% of 6 year olds, 15% adolescents
Often persists into adult hood

RFs

  • History or FH of atopy
  • Exposure to common allergens
  • Air pollution
  • Decreased exposure to infection
  • Exposure to cigarette smoke
352
Q

Conditions associated with allergic rhinitis

A

Asthma
Eczema
Conjunctivitis

353
Q

Presentation of allergic rhinitis

A

If seasonal. Spring = tree pollen, summer = grass pollen
If house or dust mites = worse on waking and worse in winter

Sneezing
Rhinorrhoea and nasal congestion
- usually bilateral
- Normal = clear
- Infection: yellow/green
- If blood and unilateral: tumour, foreign body, nose picking
- Blood and bilateral: nose picking, bleeding points, granulomatous disorder
Itchy nose and/or palate
Eyes: watering, itchy, red, swollen

Controlled by antihistamines or topical steroids

Nasal mucosa appears swollen and greyish

354
Q

Investigations for allergic rhinitis

A

usually a clinical diagnosis

RAST testing
Skin prick testing

355
Q

Management of allergic rhinitis

A

Education, allergy avoidance, antihistamines, topical steroids

  • Avoid open grassy spaces, keep windows closed, no animals in the house
  • Topical nasal antihistamines AS REQUIRED
  • Oral antihistamines REGULAR THERAPY (cetirizine)
  • Topical nasal steroids - in obstruction. Slower onset than antihistamines

Other

  • nasal saline washouts
  • sodium cromoglicate (less effective)
  • intranasal ipratropium

Surgery - reduction of inferior turbinates or to correct a deviated septum

356
Q

Define wheeze

A 
High pitched whistling sounds that occurs when smaller airways are narrowed
Occurs in
- bronchospasm
- swelling of mucosal lining
- excessive secretions
- foreign body
357
Q

Causes of wheeze in the child

A 
Asthma
Bronchiolitis
URTI
Transient wheezing in infancy
Croup
Pneumonia
Cardiac failure
Recurrent feed aspiration
GORD
Foreign body inhalation
CF
Congenital abnormality of lung, airway or heart
Idiopathic
358
Q

Key features of bronchiolitis

A

Aged 1-9 months
Poor feeding, apnoea, dry cough
Laboured breathing
Apnoea, cyanosis, resp failure

359
Q

Transient wheezing in infancy

A

Often after viral infection (RSV)
Disappears by 3 years
Increased in pre term babies or maternal smokers

360
Q

How long do maternal antibodies circulate in the neonate

A

First 3 months

361
Q

Causes of prolonged fever

A 
Atypical infections
Connective tissue disease
Kawasaki's disease
Systemic JIA (juvenile idiopathic arthritis)
SLE
Malignancy (lymphoma or leukaemia)
362
Q

Kawaski’s disease

A 
Fever > 5 days
Rash
Conjunctivitis
Cervical lymphadenopathy
Peeling of hands and feet
Strawberry tongue

Untreated causes coronary aneurysms

Treat with aspirin and steroids (serial echoes)

363
Q

Systemic juvenile idiopathic arthritis

A

Extraarticular manifestations apart from arthritis

Splenomegaly
Fever (high grade)
Anaemia
Salmon pink rash - seen on trunk or pressure areas

Fever and rash can come and go - often at the same time every day or twice a day

Anaemia of chronic disease
Neutrophilia
Thrombocytosis
Raised ESR and CRP

364
Q

Investigations for fever in under 1 month old

A 
FBC
CRP
Blood culture
Urine culture
LP ALWAYS
Treat ABx empirically
365
Q

Measles

A

Caused by measles virus

Fever > 40
Cough
Runny nose
Coryza
Inflamed eyes
Kolpik's spots (white spots in the mouth) / Enanthem
Red flat rash starts on face and spreads
- Cephalocaudal progression

No treatment!

366
Q

Complications of measles

A

Occur in 30%

Diarrhoea
Blindness
Inflammation of the brain
Pneumonia

Subactue sclerosing panencephalitis

367
Q

Subacute sclerosing panencephalitis

A

Inflammation of the entire brain
Can occur 7-10 years after measles virus

Symptoms initially subtle
- Mood changes
Then severe
- Seizures
- Coma
- Death
368
Q

Mumps

A

Also known as epidemic parotitis

Caused by the mumps virus

Fever
Muscle pain
Headache
Fatigue
Trismus - spasm of muscles of mastication

Followed by painful swelling of one or both parotid salivary glands
Can be associated with ear ache

No treatment

369
Q

Complications of mumps

A 
Meningitis
Encephalitis
Orchiditis (usually unilateral)
Epididymitis (usually unilateral)
Rarely causes infertility

Glomerulonephritis
Arthritis of large joints
Myocarditis
Pancreatitis

No increased risk of congenital malformation in pregnant women

370
Q

Rubella

A

Also known as German measles or 3 day measles
Caused by rubella virus

Rash starts 2 weeks after exposure and lasts 3 days - pink or light red
Starts on face and spreads
Rash is not as bright as measles

Lymphadenopathy
Flu like symptoms
Exanthem (rash on face)
Joint pains
Headache
Conjunctivitis
371
Q

Which of the MMR can cause congenital malformations?

Year 4 (7 decks)

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