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Clinical > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Define acute epiglottitis

A

Rapidly progressing infection causing inflammation to epiglottis. Paediatric emergency as epiglottis can block upper airway

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2
Q

What are the causes of acute epiglottis?

A

Haemophilus influenza B virus
Rare now as many children are vaccinated, but always check

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3
Q

What is the presentation of acute epiglottitis in a child?

A

High fever, ill, toxic looking, intensely painful throat, difficulty swallowing or speaking, drooling down chin, soft inspiratory stridor, rapidly increasing resp rate, child sat immobile upright with open mouth

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4
Q

What is the management of acute epiglottitis?

A
  1. Secure airway, endotracheal intubation may be necessary
  2. Once airway secure, take cultures and examine throat
  3. Treat with IV antibiotics: cefuroxime
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5
Q

Aetiology of acute lymphocytic leukaemia (ALL)?

A

Malignant clonal disease that develops when a lymphoid progenitor cell becomes genetically altered through somatic changes and undergoes proliferation.
Leads to ALL, early lymphoid precursors replace normal haematopoietic cells of bone marrow

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6
Q

Who is affected by acute lymphocytic leukaemia (ALL)?

A

Children under 6 and adults over 80

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7
Q

What is the presentation of acute lymphocytic leukaemia (ALL) in children?

A

Any child presenting to GP with bruising, enlarged lymph nodes, and systemic illness should be referred.
- Lymphadenopathy most common sign
- hepatosplenomegaly, pallor/petechiae, fever, fatigue, dizziness, weakness, epistaxis

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8
Q

How is acute lymphocytic leukaemia (ALL) diagnosed?

A

Through bone marrow biopsy

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9
Q

What are some triggers for an acute asthma exacerbation?
(paeds)

A

Exposure to allergens such as dust, pollution, animal hair or smoke

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10
Q

What is the pathophysiology behind an acute asthma exacerbation?
(paeds)

A

Exposure to allergen triggers an IgE type 1 hypersensitivity reaction, leading to smooth muscle contraction, bronchial oedema and mucus plugging

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11
Q

Presentation of an acute asthma attack?
(paeds)

A
  • fast onset breathlessness
  • wheeze; may be audible bedside or if not should be bilaterally on auscultation
  • possible subjective chest tightness
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12
Q

What are some signs of an acute severe asthma attack?
(paeds)

A
  • Respiratory distress (resp rate >30/min in children over 5, unable to complete sentence)
  • Tachycardia (>125bpm in children over 5)
  • peak expiratory flow rte 33-50% of predicted
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13
Q

What are some lifethreatening features of a severe asthma attack in a child?

A
  • peak expiratory flow rate <33% of predicted
  • oxygen sats <92%
  • silent chest on auscultation
  • weak or no respiratory effort
  • hypotension
  • exhaustion
  • confusion
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14
Q

What are the differentials for an asthma attack in children?

A
  • pneumothorax
  • anaphylaxis
  • inhalation of foreign body
  • cardiac arrhythmia
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15
Q

Management of an acute exacerbation of asthma in a child

A

Stepwise approach:
1. Inhaled slabutamol
2. nebulised salbutamol
3. add nebulised ipratropium bromide
4. if O2 sats<92% add magnesium sulfate
5. oral or intravenous steroids
6. add intravenous salbutamol if no response to inhaled therapy
7. if severe or life threatening not responsive to inhaled therapy add aminophylline

O2 sats should be maintained between 94-98% with high flow oxygen if necessary

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16
Q

What is the definition of an atrial septal defect?

A

Relatively common cardiac malformation where there is a hole between the left and right atria (caused by a defect in the septum secundum during development)

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17
Q

Pathophysiology of atrial septal defect

A

hole - causes flow from higher pressured left atrium into lower pressured right atrium.
low pitched diastolic rumble in tricuspid area (lower left sternal border), flow murmur over pulmonary valve.
ejection murmur sternal edge

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18
Q

Presentation of an atrial septal defect

A

May be aysymptomatic or present with late onset cyanosis or even heart failure

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19
Q

How is an atrial septal defect diagnosed?

A

Echocardiogram

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20
Q

Management of an atrial septal defect

A

depends on severity
most managed conservatively
some require surgery
routine echocardiograms

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21
Q

Complications of an atrial septal defect

A

Heart failure - later on in life (20’s+30’s)
paradoxical embolisms

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22
Q

What is the aeitiology of ADHD?

A

associated with reduced activity in the frontal lobe causing in problems in executive functioning
impairs ability to focus on different tasks and inhibit impulsive behaviours

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23
Q

Management of ADHD

A

Conservative: behavioural techniques, extra support in school
Medical: stimulant medication (methylphenidate)

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24
Q

What is autistic spectrum disorders?

A

characterised by a spectrum of social, language and behavioural deficits
Socially, children with autism don’t enjoy or seek comfort from company with other people and aren’t able to imagine the persepctive of other people

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25
Q

Presentation of autistic spectrum disorders (most severe cases)

A
  • not able to understand that other people have thoughts and feelings, prefer to play alone and avoids eye contact
  • speech and language delay, monotonous tones of voice, limited expression and problems. Intepret speech literally
  • narrow interests, ritualistic behaviours that rely heavily on routine and sterotyped movements
  • commonly associated with learning difficulties
  • about 25% children with autism may also have seizures
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26
Q

Management of autistic spectrum disorders

A

MDT approach
Applied behavioural analysis, positive behaviours encouraged, negative behaviours ignored

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27
Q

What is bacterial tracheitis

A

Rare, but dangerous
Presents similar to croup
Presents: high fever and rapidly progressive airway obstruction with copious thick airway secretions

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28
Q

Cause of bacterial tracheitis

A

Most common: staphylococcus aureus typically following upper resp tract infection

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29
Q

Management of bacterial tracheitis

A

IV antibiotics
some cases require intubation

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30
Q

Causes of constipation in children?

A
  • low fibre diet
  • dislike of using toilet
  • pain on passing stool; secondary to anal fissure or very hard stool
  • not regonising sensation of needing to pass stool
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31
Q

How is chronic constipation diagnosis made in children?

A

history and palpation of impacted faeces (hard, depressible masses) on abdo exam

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32
Q

Management of constipation in children

A

1st; movicol disimpaction regimen
followed by maintainence movicol, alongside high fibre diet and advice about encouraging good toilet habits

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33
Q

Presentation of Hirchsprung’s disease?

A

delay in passing meconium (>48hrs)
distended abdomen
forceful evacuation of meconium after digital rectal examination

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34
Q

How is Hirchsprung’s disease diagnosed?

A

confirmed by rectal suction biopsy

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35
Q

Management of Hirchsprung’s disease?

A

through removal of section of aganglionic colon and health bowel is pulled through

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36
Q

Definition of ventricular septal defect

A

birth defect of heart - hole in wall (septum) that separates ventricles of the heart

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37
Q

Presentation of a ventricular septal defect

A

pan-systolic murmur heard on auscultation
large - sob on exertion, maybe poor weight gain

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38
Q

Diagnosis of ventricular septal defect

A

Echocardiogram
chest xrays and ecg useful too but not diagnostic

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39
Q

management of ventricular septal defect

A

many self resolve, managed conservatively with increased calorie intake and observation
those which don’t resolve or cause heart failure - catheter intervention

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40
Q

Definition of jaundice

A

eyes and skin turn yellow due to build up of bilirubin.

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41
Q

Causes of neonatal jaundice <24hrs

A

ALWAYS PATHOLOGICAL <24hrs!
- haemolytic disorders; rhesus incompatibity, ABO incompatibility, G6PD, spherocytosis
- congenital infection (TORCH screen indicated)
- sepsis

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42
Q

causes of neonatal jaundice 24hrs - 14 days

A
  • physiological jaundice
  • breast milk jaundice
  • dehydration
  • infection, including sepsis
  • haemolysis
  • bruising
  • polycythaemia
  • crigler-najjar syndrome
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43
Q

Causes of neonatal jaundice >14days (>21 if preterm)

A
  • physiological
  • breast milk
  • infection
  • hypothyroidism
  • biliary obstruction (incl biliary atresia)
  • neonatal hepatitis
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44
Q

What causes physiological neonatal jaundice?

A

elevated bilirubin due to:
- babies being relatively polycythaemic at birth
- red cell life span of newborns shorter than adults
- hepatic bilirubin metabolism less efficient in 1st few days of life

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45
Q

Management of neonatal jaundice

A

bilirubin levels should be measured and plotted on nomograms
pts may need phototherapy or an exchange transfusion

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46
Q

Complications of jaundice

A

kernicterus is rare but serious; caused by excess bilirubin damaging the brain (esp basal ganglia)

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47
Q

What is cystic fibrosis (CF)?

A

progressive, autosomal recessive disorder that causes persistent lung infections and limits ability to breathe over time

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48
Q

Causes of CF?

A

mutations of CFTR protein
Most common mutation affecting delta-F508 results in abnormal glycosylation and subsequent degradation of CFTR protein
defects of chloride transport across cell membranes cause mucous secretions to be very thick

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49
Q

Respiratory complications of CF

A

thick mucus in lungs; cough, recurrent infections, bronchiectasis
sinusitis and nasal polys common. Pts usually colonised with pseudomonas in lung by age of 20

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50
Q

Digestive system complications for CF

A

reduced pancreatic lipase enzyme secretion inhibits fat absorption, causing steatorrhoea
poor fat absorption consequently contributes deficiency of fat soluble vits (ADEK)
poor weight gain
damage to pancreas - diabetes

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51
Q

reproductive complications of CF

A

seminiferous tubes blocked; men with CF unable conceive naturally
fertility in women lower than average; thicker cervical mucus

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52
Q

Presentation of CF in neonate

A

meconium ileus
delay passing meconium and GI obstruction
meconium ileus dx and treated with a gastrograffin enema

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53
Q

presentation of CF in infants

A

baby’s sweat very salty - parents describe
faltering growth
recurrent chest infections

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54
Q

presentation of CF in toddlers

A

faltering growth
recurrent chest infections
malabsorption syndromes

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55
Q

presentation of CF in older children

A

faltering growth
recurrent chest infections
malabsorption syndromes
delayed onset puberty

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56
Q

Diagnosis of CF

A

sweat test
- also screen for on neonatal blood spot test in 1st few days of life; raised blood immunoreactive trypsinogen.

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57
Q

management of CF

A

MDT management
daily chest phsyiotherapy techniques to help clear mucus and prevent pneumonias
prophylactic antibiotics, bronchidilators, medicines to thin secretions (dornase alfa)
pancreatic enzymes replacement (creon) and fat soluble vits (ADEK) also useful
vaccines; influenza, pneumococcal
end stage; bilateral lung transplant

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58
Q

Definition of meconium ileus

A

baby’s first stool (meconium) is so thick and sticky that is causes intestinal obstruction

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59
Q

90% of meconium ileus is associated with CF. T/F?

A

True

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60
Q

Presentation of meconium ileus

A

no meconium passed within 48hrs from birth
signs of intestinal obstruction

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61
Q

diagnosis of meconium ileus

A

abdo xray - shows ‘bubbly’ appearance of intestine with lack of air fluid levels

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62
Q

management of meconium ileus

A

IV fluids and stomach drainage with an Ryles tube
enemas
surgery in severe cases

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63
Q

aetiology of neonatal resp distress syndrome (NRDS)

A

lack of surfactant (phospholipid containing fluid produced by type 2 pneumocytes)
lack of surfactant increases surface tension and causes alveoli to collapse, triggering resp distress
prem babies are more at risk of NRDS

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64
Q

diagnose of Neonatal respiratory distress syndrome (NRDS)

A

clinical evaluation
‘ground glass’ appearance seen on chest xray

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65
Q

management of Neonatal respiratory distress syndrome (NRDS)

A

intratracheal instillation of artificial surfactant
premterm delivery expected - give mother glucocorticoids before delivery increases surfactant production in baby

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66
Q

complications of Neonatal respiratory distress syndrome (NRDS)

A

preterm mortality

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67
Q

What is pyloric stenosis?

A

hypertrophy of pyloric sphincter

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68
Q

What age does pyloric stenosis usually occur?

A

babies aged 6-8 weeks old

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69
Q

presentation of pyloric stenosis

A

vomiting after feeds (can be projectile - hitting walls)
may increase with intensity as obstruction becomes more severe
o/e palpable as smooth olive size mass

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70
Q

complications of pyloric stenosis

A

acid base abnormality due to vomiting of hypocholoremic hypokalaemia metabolic acidosis
dehydration

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71
Q

diagnosis of pyloric stenosis

A

abdo ultrasound

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72
Q

management of pyloric stenosis

A

surgical - pyloromyotomy
until surgery, baby should be nil by mouth and kept on IV fluids
severely dehydrated babies may require acute fluid resus

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73
Q

Whats hydrocephalus in paeds?

A

result of excess cerebrospinal fluid (CSF) accumulating in brains ventricular system
puts pressure on brain parenchyma

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74
Q

causes of non-communicating hydrocephalus (paeds)

A

something obstructs flow through ventricular system: congenital malformation (stenosis of aqueduct or a chiari malformation), tumour or vascular malformation in posterior fossa, intraventricular haemorrhage (prem babies at risk)

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75
Q

causes of communicating hydrocephalus (paeds)

A

failure to reabsorb CSF occurs from an insult to arachnoid villi
meningitis, subarachnoid haemorrhage

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76
Q

presentation of hydrocephalus (paeds)

A

enlarged head circumference
bulging of anterior fontanelle, distension of veins across scalp
late sign - sunsetting of eyes, upwards gaze limited

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77
Q

diagnosis of hydrocephalus (paeds)

A

cranial ultrasound or by MRI/CT

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78
Q

management of hydrocephalus (paeds)

A

insertion of ventriculoperitoneal shunt

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79
Q

complications of hydrocephalus (paeds)

A

raised intracranial pressure - lead to long term neurological deficits

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80
Q

Which bacteria is meningococcal infection caused by

A

caused by Neiseria meningitidis (gram neg intracellular diplococcus)

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81
Q

Causes of meningococcal infection

A

transmission by resp droplet spread
bacteria enters circulation, initiating inflammatory process leading to capillary leakage and intravascular thrombosis

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82
Q

presentation of meningococcal infection

A

meningococcaemia (septicaemia)
meningitis (lethargy, headache, fever, rigors, vomiting)
mixture of both, developing purpuric skin rash
hypovolaemic shock presents as; cold peripheries, poor cap refill, tachycardia, decreased urine output
Waterhouse-Friderichsen sydrome (rare): massive adrenal haemorrhage, septic shock

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83
Q

diagnosis of meningococcal infection

A

confirmed by blood or CSF cultures
PCR for Neisseria meningitidis highly sensitive

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84
Q

management of meningococcal infection

A

ealry abx - broad spectrum IV until pathogen confirmed
PICU admission if septic
notifiable diseases

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85
Q

Prevention of meningococcal infection

A

all household or close contacts should receive ciprofloxcin or rifampicin as post exposure prophylaxis

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86
Q

Other names of parvovirus B19

A
  • fifth disease
  • slapped cheek syndrome
  • erythema infectiosum
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87
Q

Presentation of parvovirus B19

A

prodrome of fever, coryza, diarrhoea
diffuse ‘lace like’ rash across body with characteristic bright red rash on cheeks

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88
Q

complications of parvovirus B19

A

red cell aplasia
severe foetal anaemia
cardiomyopathy

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89
Q

What is DKA?

A

diabetic ketoacidosis. Medical emergency. Hyperglycaemia, acidosis, and ketonaemia,

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90
Q

What are the specific values in DKA to make tbe diagnosis?

A

ketonaemia: 3mmol/L and over
Blood glucose: >11mmol/L
Bicarbonate: <15mmol/L or venous pH <7.3

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91
Q

Causes of DKA?

A

infection, dehydration, fasting, or 1st presentation of T1DM

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92
Q

Presentation of DKA

A

smell of acetone on breath (fruity breath)
vomiting
dehydration
abdopain
hyperventiliation
hypovalaemic shock
drowsiness
coma

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93
Q

Investigations for DKA

A

blood glucose (>11.1mmol/L)
Blood ketones (>3mmol/L)
urea and electrolytes
blood gas analysis
urinary glucose and ketones
blood cultures (if evidence of infection)
cardiac monitoring/ECG

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94
Q

Management of DKA

A

if pt alert, not sig dehydrated and able to tolerate oral intake without vomiting - encourage oral intake and give subcut insulin

if pt vomiting, confused, sig dehydrated - IV fluids (10ml/kg 0.9% NaCl, insulin infusion 0.1 units/kg). if evidence of shock, initial bolus should be 20ml/kg.

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95
Q

What is the major complication of DKA?

A

cerebral oedema

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96
Q

Where is best place on a neonate to check pulse?

A

femoral and bracheal

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97
Q

Neonate: baby is blue, not crying, floppy, some felxing of four limbs, HR 140bpm. What is APGAR?

A

3

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98
Q

What is whooping cough/pertussis?

A

Severe URTI characterised by severe bouts of spasmodic coughin, which may lead to apnoea in infants

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99
Q

What’s causes for whooping cough/pertussis?

A

Bordetella pertussis (gram neg coccobaciliis)

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100
Q

Presentation of whooping cough/pertussis

A
  • cough with prolonged period of coughing per episode
  • inspiratory whooping
  • rhinorrhoea
  • post-tussive vomiting
  • apnoeas
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101
Q

Management of whooping cough/pertussis

A

macrolides 1st line ( erythromycin, azithromycin or clarithromycin)
notifiable disease

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102
Q

Investigation for whooping cough?

A

PCR is most sensitive

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103
Q

When would you suspect whooping cough?

A

In child who didn’t receive all vaccinations as a baby, and presents with coughing episodes followed by gasping for air

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104
Q

What is rubella caused by?

A

rubella togavirus

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105
Q

When are children normally vaccinated for Rubella?

A

As part of MMR vaccine which starts at 12months old

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106
Q

Presentation of rubella

A

non-specific symptoms: fever, coryza, arthralgia, rash (typically starts on face then moves down trunk, sparing arms and legs). and Lymphadenopathy (post-auricular).

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107
Q

Dx of rubella

A

serological testing

108
Q

Complications of rubella infection in unvaccinated pregnant women?

A

cataracts, deafness, patent ductus arteriosus, brain damage

109
Q

What is encephalitis?

A

inflammation of encephalon or brain parenchyma

110
Q

Clinical features of encephalitis

A

altered mental state, fever, flu-like prodromal illness, early seizures

111
Q

Most common cause of encephalitis

A

herpes simplex virus type 1

112
Q

Investigations for encephalitis

A

suspected in any pt with sudden onset behavioural change, new seizures, unexplained acute headache.
Routine blood tests, blood cultures, viral PCR.

113
Q

Treatment for encephalitis

A

broad spectrum abx with 2g IV ceftriaxone BD and 10mg/kg acyclovir TDS for 2 weeks

114
Q

Side effects of acyclovir

A

generalised fatigue/malaise
GI disturbance
photosensitvity and utricarial rash
acute renal failure, haem abnormalities, hepatitis, neurological reactions

115
Q

What is impetigo and what is it caused by?

A

skin infection caused by staphylococcal and streoptococcal bacteria

116
Q

Clinical features of impetigo

A

pruritic rash with discrete patches that have golden crusting
pts may be febrile
common in infants and school aged children

117
Q

Management of impetigo

A

fusidic acid oral flucloxacillin
highly infectious, dont go school

118
Q

What causes Scarlet fever?

A

streptooccus species

119
Q

Presentation of scarlet fever

A

coarse red rash on cheeks, sore throat, fever, headache, ‘sandpaper’ texture rash, tongue appears bright red

120
Q

Treatment for scarlet fever

A

abx - phenoxymethylpenicilin 10 days

121
Q

Presentation of hand, foot and mouth disease

A

blisters on hands and feet, grey ulcerations in buccal cavity. usually preceded by 1 day hx of fever and lethargy.

122
Q

common cause of hand, foot, mouth disease

A

coxsackie virus A16

123
Q

Presentation of slapped cheek syndroem/ fifth disease/ Parvovirus B19

A

rash on both cheeks, fever

124
Q

Presentation of measles

A

erythematous, blanching maculopapular rash all over body preceded by fever, cough, runny nose or conjunctivitis. Koplik spots

125
Q

Complications of measels

A

pneumonia, encephalitis, immunosuppression and subacute scleorising panencephalitis

126
Q

Presentaion of urticaria (hives)

A

raised, red itchy red rashes, associated with allergies or idiopathi.c. No fever

127
Q

Urticaria (hives) management

A

antihistamines +/- steroids

128
Q

Presentation of chicken pox

A

maculopapular vesicular rash that crust over and form blisters, itchy

129
Q

Cause of chickenpox

A

varicella zoster virus (human herpes virus 3)

130
Q

Tx of chickenpox

A

kept from school.

131
Q

Features of roseola

A

lace-like rash across whole body with high fever

132
Q

What causes roseola

A

human herpes virus 6

133
Q

Presentation of septicaemia

A

rapidly developing non-blanching purpuric rash + lethargy, headache, fever, rigors, vomiting

134
Q

Management of septicaemia

A

cultures taken, broad spectrum IV abx
senior paediatrician notified to review pt

135
Q

Differentials of purpuric rash (other than septicaemia)

A

trauma
liver disease
drugs (anticoagulants)
vasculitis
thrombocytopenia
coagulopathy
malignancy
disseminated intravscualr coagulation (DIC)

136
Q

if pt is seen in community and meningitis is suspected along side septicaemia, what should you do?

A

Give immediate intramuscular benzylpenicillin and send to hospital

137
Q

14yr girl, developed erythematous maculopapular rash on chest, and has excoriatrions. Saw GP last week for sore throat, abdo pain and fever. was treated with bacterial tonsilitis with amoxicillin. What’s most likely cause of rash?

A

Morbiliform eruption
- characteristed by generalised maculopapular rash. Presented with symptoms of infectious mononucleosis before (not tonsilitis). Morbiliform reactions common in pts with infectious mononucleosis taking amoxicillin

138
Q

Perianal/vulval itching, worse at night, no abnormalities on examination. Disease and treatment?

A

Threadworm, 1st line: oral mebendazole

139
Q

What is acute otitis media?

A

common infection causing inflammation of the middle ear

139
Q

What is acute otitis media?

A

common infection causing inflammation of the middle ear

140
Q

Clinical features of otitis media

A

pain, fever, irritability, anorexia, vomiting
often occurs after a viral upper resp infection

141
Q

Features of acute otitis media

A

deep seated pain, impaired hearing with systemic illness and fever
onset usually rapid, feeling of aural fullness followed by discharge when tympanic membrane perforates with relief of pain

142
Q

features of crhonic secretory otitis media (glue ear)

A

presents as persistant pain lasting a couple of weeks after initial episode
drum looks abnormal and will show reduced mobility of membrane

143
Q

Management of otitis media

A
  • admit any children under 3 months with temp of 38 or more, or children with suspected complications (meningitis, mastoiditis, facial nerve palsy)
  • consider admitting any child who is very systemically unwell
  • otherwise treat pain and fever with paracetamol or ibuprofen
  • most children will not require abx
    offer immediate abx prescription to children systemically unwell who dont require admission or those at high risk of complications (immunocompromised pts)
144
Q

what to do if suspected Complications of otitis media

A

important to assess and resus the pt and discuss with ent registrar

145
Q

What are extra-cranial complications of otitis media?

A

facial nerve palsy - lower motor neuron lesion of VII cranial nerve (facial nerve)
Mastoiditis - inflammation spread to form abscess in mastoid air spaces of temporal lobe
Petrositis - infection spread to apex of petrous temporal bone, triad of sx: otorrhoea, pain deep inside ear and eye, ipsilateral VI nerve palsy
Labyrinthitis - inflammation of semicircular canals leading to sx of vertigo, nausea, vomiting and imbalance.

146
Q

Intra-cranial complications of otitis media

A

meningitis - present with sepsis, headache, vomiting, photophobia, phonophobia
sigmoid sinus thrombosis - present with sepsis, swinging pyrexia and meningitis
brain abscess - sepsis, neurological signs due to compression of cranial nerves

147
Q

Definition of intussusception

A

invagination of proximal bowel into a digital segment (commonly ileum) passing into caecum through ileocaecal valve

148
Q

peak ages for intussusception

A

3 months - 2yrs old

149
Q

Complications of intussusception

A

bowel perforation
peritonitis
gut necrosis

150
Q

Presentation of intussusception

A

paroxysmal, severe colicky pain and the child characteristically draws up legs
lethargic
may refuse feeds
vomiting; bile stained
passage of red-jelly stool component of blood stained mucus
abdo distension
sausage-shape mass may be palpated

151
Q

Abdominal USS findings for intussusception

A

target sign (cocentric echogenic and hypoechogenic bands
complications; free-abdominal air or presence of gangrene

152
Q

mx of intussusception

A

1st line once stable: air enema (rectal air insufflation or contrast enema (only to be performed if child stable))
operative reduction indicated if:
- failure of non-operative management
- peritonitis or perforation present
- haemodynamically unstable

153
Q

presentation of juvenile idiopathic arthritis (JIA)

A

systemic signs followed by joint pain
- fevers
- malaise
- salmon pink rash
- joint involvment

154
Q

dx of juvenile idiopathic arthritis (JIA)

A

clinical once other differentials have been excluded; infections, malignancy, lupus

155
Q

mx of juvenile idiopathic arthritis (JIA)

A

MDT input - chronic condition
psychological help aswell
NSAIDs
Steroids
Steroid sparing e.g methotrexate or biologicals such as TNF-a inhibitors

156
Q

Complications of juvenile idiopathic arthritis (JIA)

A

flexion contractures
joint destruction
growth failure
anterior uvetitis

157
Q

most appropiate 1st line mx for juvenile idiopathic arthritis (JIA) where 4 or fewer joints affected? (oligoarticular)

A

intra-auricular steroid injections; methlyprednisolone acetate

158
Q

what is GORD children

A

passage of gastric contents into oesophagus

159
Q

Presentation of GORD children

A

babies commonly present with:
- milky vomits after feed
- crying/irritability
- arching of back
- drawing up knees to chest

160
Q

Mx of GORD children

A

keep baby upright post-feeds and burp after feeds
keep cot on slight incline
reassure parents that most cases will resolve as baby grows and the cardiac sphincter matures

161
Q

medical mx for GORD children

A

gaviscon (infant formulation)
omeprazole

162
Q

surgical mx ofGORD children

A

fundoplication

163
Q

A 2 month old baby boy with DiGeorge syndrome is brought in to PAU by his worried mother due to his recent episodes of non-bloody and non-bilious vomiting which have been occurring regularly after most of his feeds. He is predominantly formula fed having been weaned at 6 weeks. The pregnancy and delivery were both uncomplicated and he was born at term. He has continued to feed as normal and no change has been noted in his bowel movements. He was born weighing 3.5 kg and now weighs 4.8 kg. Given the presenting history what is the most likely diagnosis?

A

gastro-oesophageal reflux

164
Q

A 4 week old baby attends the GP with an upset mother. She reports that her breastfed baby is struggling to put weight on and is often distressed throughout the day. Her cry sounds hoarse and she occasionally coughs and vomits feeds. She often cries and arches her back during the day.

What initial step might help identify the cause for this child’s symptoms?

A

Probably GORD -
trial of alginate

165
Q

What is nephrotic syndrome

A

clinical syndrome arises secondary to increased permeability of serum protein through a damaged basement membrane in renal glomerulus

166
Q

Clinical features of nephrotic syndrome

A

proteinuria
oedema
hypoalbuminaemia
hyperlipidaemia
lipiduria

167
Q

Pathophysiology of nephrotic syndrome

A

cytokines damage podocytes causing them to fuse together and destroy charge of the glomerular basement membrane
allows increased permeability to plasma proteins - causing massive protein loss in urine
serum albumin levels reduced
pts experience oedema because of less oncotic pressure
lets fluid leak into interstitium
liver tries to compensate by increased synthesis of lipoproteins - causing hyperlipidaemia

168
Q

The most common cause of nephrotic syndrome in children

A

minimal change disease
- treat with steroids

169
Q

Clinical presentation of nephrotic syndrome

A

periorbital and peripheral oedema

170
Q

Investigations for nephrotic syndrome

A

bedside: urine dipstick (proteinuria) Raised albumin creatinine ratio

171
Q

mx of nephrotic syndrome

A

high dose steroids

172
Q

Complications of nephrotic syndrome

A

infection
venous thromboembolism
hyperlipidaemia
hypercholesteraemia
relapse

173
Q

What is Henoch Schonlein purpura (HSP)

A

most common small vessel vasculitis in children
commonly affects 3-5yrs old

174
Q

Presentation of Henoch Schonlein purpura (HSP)

A

Purpura or petechiae on buttocks and lower limbs (usually starts off urticarial, then becomes maculopapular and purpuric, Trunk is spared)
abdo pain
arthralgia
fever
nephritis (haematuria +/- proteinuria)
may be pyrexial
Commonly preceded by viral upper resp tract infection

175
Q

Mx of Henoch Schonlein purpura (HSP)

A

NSAIDs analgesia
Antihypertensives for BP
Childen should have regular urine dips for 12 months to check renal impairment

176
Q

How does ranitidine work?

A

H2 receptor antagonist
suppresses acid production and can reduce the volume of gastric contents

177
Q

if a FeverPAIN score for tonsilitis is a 2, should you prescribe abx or prescribe delayed treatment abx?

A

delayed treatment - advise to use prescription if no improvement in symptoms in 3 to 5 days or if symptoms worsen

feverPAIN score of 4 or 5, would prescribe immediate abx prescription

178
Q

Presentation of acute otitis media

A

pain, fever, irritability, anorexia, vomiting
Otoscope: red, bulging, tender tympanic membrane. No discharge/

179
Q

What is naevus flammeus

A

port-wine stain
present from birth and grows with the infant
caused due to a vascular malformation of capillaries in dermis
laser therapy can be used as treatment

180
Q

What is Hirchsprung’s disease

A

disease causing chronic constipation.
Back pressure of stool trapped in more proximal colon

181
Q

Presentation of Hirchsprung’s disease

A

delay in passing meconium (>48hrs)
distended abdomen
forceful evacuation of meconium after digital rectal examination

182
Q

How is Hirchsprung’s disease diagnosed?

A

Rectal suction biopsy

183
Q

mx of Hirchsprung’s disease

A

removal of section of aganglionic colon and health bowel pulled through (Swenson procedure)

184
Q

Define constipation in children

A

defecation less than 3 times a week or significant difficulty passing stool

185
Q

Causes of constipation in children

A

pts diet - low fibre
dislike of using toilet
pain on passing e.g hard stool or anal fissure
no recognising sensation to pass stool

186
Q

Mx of constipation in children

A

1st, movicol disimpaction regimen
followed by maitainence of movicol alongside high fibre diet and encouraging good toileting habits

187
Q

What is immune thrombocytopenic purpura in children

A

ITP
autoimmune disease of unknown cause where number of circulating platelets reduced

188
Q

Mx of immune thrombocytopenic purpura in children

A

watch and wait
most cases resolve in 3-6 months

189
Q

Presentation and inx of immune thrombocytopenic purpura in children

A

follows viral infections
petechiae, and low platelets following viral infection, otherwise well

inx:
FBC, blood film, bone marrow (if atypical), further tests to exclude differentials (aplastic anaemia, leukaemia, thrombocytic thrombocytopenic purpura)

190
Q

1yr old, 2/7 hx of irritability and fever, change in behaviour and reduced eating. Bilateral acute otitis media. Management?

A

1st line of bilateral acute otitis media under 2yrs - 5 day course of amoxicillin

2nd line - clarithromycin if penicilliin allergy

191
Q

What is tetraology of fallot

A

rare congenital cardiac disease
cyanotic
comprises of:
1. ventricular septal defect (VSD)
2. Overriding aorta
3. right ventricular outflow tract obstruction
4. right ventricular hypertrophy

192
Q

Presentation of tetraology of fallot

A

detection of murmur antenatally
cyanosis
babies: tet spells (acute episodes of cyanosis)

193
Q

mx of tet spells (babies in tetraology of fallot)

A

emergency, can be fatal
acutely: lie baby on back and bend knee
O2 should be provided if in hospital
prophylaxis: propanalol

194
Q

mx of tetraology of fallot

A

surgery

195
Q

What are the features of Patau’s syndrome

A

caused by trisomy 13
holoprosencephaly
cleft lip and palate
microcephaly
polydactyly
congential heart disease

196
Q

What is Turner’s syndrome

A

condition that affects only females
results when one of X chromosomes is missing or partially missing

197
Q

Cause of Turner’s syndrome

A

XO karotype
45 XO

198
Q

Presentation of Turner’s syndrome

A

short stature
lymphoedema of hands and feet in neonate
spoon shaped nails
webbed neck
widely spaced nipples
wide carrying angle
congenital heart defects - bicuspid aortic valve most common
delayed puberty
ovarian dysgenesis causing infertility
hypothyroidism
recurrent otitis media
normal intellect

199
Q

Mx of Turner’s syndrome

A

growth hormone therapy
oestrogen replacement

200
Q

complications of Turner’s syndrome

A

increased risk of cardiovascular disease specifically aortic stenosis and aortic dissection

201
Q

What is sickle cell disease

A

red blood cells, autosomal recessive single gene defect in beta chain haemoglobin

sickled red blood cells clump together and obstruct blood flow and break down prematurely.
associated with anaemia

202
Q

What are vaso-occlusive crisis

A

common in those with sickle cell
sickled red blood cells occlued vessels resulting in ischaemia
pain, recurrent episodes
acute chest syndrome - infarct of lung parenchyma

203
Q

mx of vaso-occlusive crisis

A

strong pain relief (IV opiates)
O2 as required and IV fluids
treat any suspected infectionstop-up infusions may be needed
haem input

204
Q

long term mx of sickle cell disease

A

top up infusions, folic acid, iron chelation
immunisations: flu, pneumococcal
prophylactic penicillin if asplenic
genetic counselling

205
Q

Clinical features of Fanconi anaemia

A

pigmentation abnormablities, hearing defectsm renal abnormalities, solid tumours, short stature

206
Q

What is haemophillia A

A

x linked recessive bleeding disorder caused be defiency in clotting factor VIII

207
Q

Clinical features of haemophilia A and dx

A

deep, severe bleeding into soft tissues and joints and muscles
factor VIII assay

(bruising) ‘large, deep ecchymosis along the patient’s right thigh’

208
Q

Mx of haemophillia A

A

desmopressin
major bleeds - recombinant factor VIII

209
Q

What is haemophilia B

A

X linked recessive inherited bleeding disorder caused by defiency in clotting factor IX

210
Q

What is Von Willebrand disease

A

most common inherited bleeding disorder
reduced quantity or function of von willebrand factor (VWF) leads to increased risk of bleeding

211
Q

What does von willebrand factor normally do?

A

links platelets to exposed endothelium and stabalises clotting factor VIII

212
Q

Clinical features of Von Willebrand disease

A

excess or prolonged bleeding from minor wounds
excess or prolonged bleeding post operatively
easy bruising
menorrhagia
epistaxis
GI bleeding

213
Q

Investigations for Von Willebrand disease

A

decreased factor VIII activity
PT normal
APTT prolonged
Bleeding time prolonged

214
Q

What is Immune thrombocytopenia

A

autoimmune disease of unknown cause
number of circulating platelets is reduced

215
Q

investigations for Immune thrombocytopenia

A

FBC
blood film
bone marrow (only if atypical)

216
Q

mx of Immune thrombocytopenia

A

steroids used in persistent cases
splenectomy may be considered in refractory cases
platelet transfusions should be avoided
watch and wait normally self resolves

217
Q

What is wilms tumour

A

nephroblastoma
embryonic tumour from developing kindey
most common abdominal tumour in children

218
Q

Presentation of Wilm’s tumour

A

abdo mass that doesn’t cross midline
abdo distension
haematuria
hypertension

219
Q

dx of Wilm’s tumour

A

CT chest, abdoment and pelvis

renal biopsy diagnostic

220
Q

mx of Wilm’s tumour

A

depends on staging
surgical options - nephroectomy, chemo, radio-therapy

221
Q

Presentation of brain tumours in children

A

persistent headache, worse in morning
signs of raised intracranial pressure
seizure in older children with no fever and no previous hx of seizures

222
Q

dx of suspect brain tumours in children

A

MRI / CT head

223
Q

Presentation of retinoblastoma in children

A

white eye reflex (loss or normal red reflex)

224
Q

features of patau’s syndrome

A

trisomy 13
holoprosencephal : failure of 2 cerebral hemispheres to divide; only one eye, a nose with single nostril
celft lip and palate
microcephaly
polydactyl
congenital heart disease
rare for these children to survive more than a few weeks

225
Q

Features of Edward’s syndrome

A

trisomy 18
low set ears
micrognathia
microcephaly
overlappy 4th and 5th fingers
rocked bottom feet
congential heart disease
rare for these children to survive more than a few months

226
Q

What is fragile X syndrome

A

CGG trinucleotide repeat in FMR1 gene on X chromosome

227
Q

features of Fragile X syndrome

A

long face
large, protruding ears
intellectual impairment
macroorchidism (large testes)
social anxiety
autistic spectrum features

228
Q

features of Fragile X syndrome

A

long face
large, protruding ears
intellectual impairment
macroorchidism (large testes)
social anxiety
autistic spectrum features

229
Q

what is Prader Willi syndrome

A

genetic condition inherited by genomic imprinting
- deletion of either maternal or paternal copy
- inheritance of 2 copies from one parent and non from the other parent

230
Q

Clinical features of Prader Willi syndrome

A

hypotonia and poor feeding in infancy
developmental delay in early childhood
learning disabilities
short stature
hyperphagia and obesity in older childhood

231
Q

What defect is associated with Noonan syndrome

A

pulmonary stenosis

232
Q

What defect is associated with down syndrome

A

atrioventricular septal defects (AVSD)

233
Q

What defect is associated with foetal alcohol syndrome

A

ventricular septal defect

234
Q

What defect is associated with DiGeorge syndrome

A

aortic arch defects

235
Q

What defect is associated with Turner syndrome

A

bicuspid aortic valves and coarction of aorta

236
Q

What defect is associated with Edwards syndrome

A

septal defects

237
Q

What defect is associated with Patau syndrome

A

dextrocardia

238
Q

What is Osteogenesis imperfecta

A

genetic disorder characterised by inadequate collgen formation in bones leading to fragile bones prone to fractures

239
Q

Features of Osteogenesis imperfecta

A

BITE
bones
I - eyes
T - teeth
E- ears

240
Q

What is Rickets

A

clinical manifestation of vit D defiency in children

241
Q

presentation of Rickets

A

aching bones and joints
poor growth and development
delayed dentition
weakness
constipation

242
Q

dx and mx of Rickets

A

low blood level of vit D

Vit D oral supplementation

243
Q

what is Transient synovitis

A

benign cause of limp in children from inflammation of synovial lining of hip joint

244
Q

Cause of Transient synovitis

A

viral infection (URTI) 1-2 weeks before pain and limp

245
Q

Presentation of Transient synovitis

A

inflammtory reaction following viral infection
sx milder than those of septic arthritis

246
Q

What causes septic arthritis and osteomyelitis in children

A

staphylococcus aureus, coagulase negative taphylococci

246
Q

What causes septic arthritis and osteomyelitis in children

A

staphylococcus aureus, coagulase negative taphylococci

247
Q

Risk factors for septic arthritis and osteomyelitis in children

A

diabetes
peripheral vascular disease
malnutrition
immunosuppression
maliganancy

248
Q

Clinical features of septic arthritis and osteomyelitis in children

A

fever
pain
swelling
erythema of affected site
unable to weight bear

249
Q

investigations for septic arthritis and osteomyelitis in children

A

bone biopsy/aspiration diagnostic
blood inflammatory markers
xray
blood cultures

250
Q

mx for septic arthritis and osteomyelitis in children

A

ab min 4-6 weeks
flucloacillin plus fusidic acid/rifampcin
if allergic to penicillin give clindamycin

251
Q

What is Perthes disease

A

avascular necrosis of femoral head in children aged 4-8
causes ischaemia

252
Q

Presentation of Perthes disease

A

gradual onset of limp and hip pain
pain persisting over 4 weeks

253
Q

dx of Perthes disease

A

xray hip - sclerosis and fragmentation of epiphysis

254
Q

what is Slipped upper femoral epiphysis (SUFE)

A

most common hip disorder in adolescents

255
Q

presentation of Slipped upper femoral epiphysis (SUFE)

A

hip pain and limp - acute or chronic adolescents
pain may be referred to knee
Reduced ROM on hip flexion
positive Trendelenburg gait

256
Q

dx of Slipped upper femoral epiphysis (SUFE)

A

anterolateral and frog legs xray

257
Q

mx of Slipped upper femoral epiphysis (SUFE)

A

surgical

258
Q

what is Meconium aspiration

A

meconium in amniotic fluid (sign of foetal distress and hypoxia) travels into foetal lungs

259
Q

What is meconium ileus

A

meconium thickens and causes obstruction of bowel in noenate
early sign of CF

presents as bilious vomiting, distended abdomen, failure to pass meconium in 12-24hrs life

bubbly appearance on xray

260
Q

What is meconium ileus

A

meconium thickens and causes obstruction of bowel in noenate
early sign of CF

presents as bilious vomiting, distended abdomen, failure to pass meconium in 12-24hrs life

bubbly appearance on xray

mx: drip and suck

261
Q

sx of Coeliac disease (paediatrics)

A

steatorrhoea
weight loss or failure to thirve
short stature and wasted buttocks
dermatitis herpetiformis

262
Q

dx of Coeliac disease (paediatrics)

A

1st line: anti- TTG IgA antibody (blood test)

gold standard: OGD and duodenal/jejunal biopsy - sub-total villous atrophy, crypt hyperplasia, and intra-epithelial lymphocytes

263
Q

mx of UTIs in children

A

Lower UTIs; nitrofurantoin
Upper UTIs: cephalosporin

264
Q

A 6 month old boy presents to the GP with his mother. She is concerned because her son has developed a pruritic rash. On examination he has a dry, erythematous rash on his cheeks and the extensor aspects of both his elbows. He has previously been well and there are no concerns about his development. His mother reports also having pruritic rashes when she was young. Which of the following is the most likely diagnosis?

A

atopic eczema

  • common in children to get on cheeks and extensor limbs

Clinical (12 decks)

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