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Year 4 revision > Paeds revision > Flashcards

Paeds revision Flashcards

1
Q

what can cause physiological jaundice

A

Increased RBC breakdown:

  • Increased RBC in uterus to increase oxygen delivery to fetus
  • RBC no longer needed so breaks down

Immature liver

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2
Q

causes of pathological jaundice (if <24 hours - always pathological)

A

Haemolytic disease:

  • ABO incompatibility
  • Rhesus disease of newborn
  • G6PD deficiency
  • Spherycytosis
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3
Q

how can ABO incompatibility cause jaundice

A

Mom is O and fetus is A,B, or AB
Blood type A,B, or AB all carry antigens not present in O
Unlike antibodies formed against Rh factor, these antibodies are IgM and do not cross the placenta
Infant is not born anemic, as in Rh sensitized infant
Blood and antibodies are exchanged during delivery of placenta
Destruction of RBCs may occur after delivery for up to 2 weeks of age
Less severe

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4
Q

4 causes of prolonged jaundice (>14 days)

A

Jaundice >14 days

  • Infection
  • Metabolic: Hypothyroid, hypopituitarism, galactosaemia
  • Breast milk jaundice (resolves by 1.5-4 months)
  • Biliary atresia
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5
Q

what does a diabetic mother increase the risk of

A

neonatal jaundice

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6
Q

when can a transcutaneous bilirinometer be used

A

in neonates >35 weeks gestation and >24 hours old

if level under 250umol/L and not had treatment

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7
Q

investigations for neonatal jaundice

A
  • serum bilirubin
  • total and conjugated bilirubin
    • Blood group of mother and baby + direct coombes test
  • U&E’s
  • Infection screen
  • G6PD
  • LFT’s
  • TFT’s
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8
Q

how often should bilirubin levels be measured during phototherapy

A
  • Repeat 4-6 hours after starting to make sure not still rising
  • 6-12 hourly once level is stable or reducing
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9
Q

when his exchange transfusion indicated

A

Signs of acute bilirubin encephalopathy or threshold graphs

e.g. kernicterus

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10
Q

at what level of serum bilirubin does neonatal jaundice occur from

A

> 100umol/L

50% neonates

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11
Q

what is Kramer’s index

A

level of bilirubin needed for baby to appear jaundiced in that area

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12
Q

what can kernicterus lead to

A

coreoathetoid palsy (type of cerebral palsy)

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13
Q

what can cause conjugated jaundice in the first 24 hours of life

A
  • neonatal hepatitis

- congenital infections: CMV, rubella, syphilis

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14
Q

symptoms of mild HIE

A
  • poor sucking
  • irritability
  • hyperalert
  • mild hypotonia
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15
Q

4 features of moderate HIE

A
  • lethargy
  • seizures
  • abnormalities of tone
  • need for NG feeding
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16
Q

4 features of severe HIE

A
  • coma
  • prolonged seizures
  • severe hypotonia
  • failure to maintain spontaneous respiration
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17
Q

management of HIE and when can it not be done

A

active cooling (33-35)

not if premature (36 weeks or below)

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18
Q

criteria used for active cooling in HIE

A 
TOBY criteria: 
Criteria A: 
- Apgar <5 at 10 mins
- Cord blood pH <7
- Base deficit =16

Criteria B:

  • Altered consciousness
  • Abnormal tone
  • Abnormal primitive reflexes

Need criteria from A and B

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19
Q

what is a stalk mark/ salmon patch also called

A

naevus simplex - most common form of birth mark

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20
Q

what is port wine stain also called

A

naevus flammus - doesn’t go away, more noticeable with hormones

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21
Q

what can port wine stain also be part of

A

webber’s syndrome - seizures, learning disorder, glaucoma

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22
Q

how can strawberry naevi be treated if problematic

A

propanolol

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23
Q

why must Mongolian spots be documented

A

look like bruises - come up in safe guarding

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24
Q

what is acrocyanosis

A

bluish colour of hands and feet of the newborn - caused by poor peripheral circulation

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25
Q

common non-toxic rash in neonates

A

erythema toxicum:

  • widespread pustular rash
  • tends to get worse then improves
  • appears within 72 hours
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26
Q

features of transient neonatal pustular melanosis

A
  • Widespread pustules
  • Presence of pigmented macules
  • Present from birth
  • Benign and idiopathic
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27
Q

where is cephalohaematoma located

A

beneath periosteum - does NOT cross suture lines

unlike subglial haematoma - does cross suture lines

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28
Q

what is G6PD deficiency

A

x-linked recessive disease that increases RBC sensitivity to oxidative stress- so increased breakdown leading to jaundice

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29
Q

what is hereditary spherocytosis

A

abnormality of RBC membrane = more likely to haemolyse = jaundice

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30
Q

when does respiratory distress syndrome usually occur (ground glass appearance on CXR)

A

those born before 28 weeks due to absence of lung surfactant

begins being produced around 24 weeks (from type II pneumocytes)

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31
Q

2 things making RDS more likely to occur at any gestation

A
  • meconium liquor

- diabetic mothers

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32
Q

3 complications of RDS

A
  • pneumothorax
  • bronchopulmonary dysplasia
  • chronic lung disease
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33
Q

how is RDS managed

A

antenatal and neonatal steroids

respiratory support + administering surfactant

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34
Q

causes of symmetrical SGA

A

intrinsic cause: often in first trimester - either normal small or congenital infection/genetic condition

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35
Q

causes of asymmetrical SGA

A

extrinsic cause: placental, maternal HTN/ renal/cardiac disease, pre-eclampsia, maternal substance abuse

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36
Q

when does GORD tend to resolve

A

12 months

usually more severe in children with neurological disorders e.g. cerebral palsy

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37
Q

how is GORD managed in uncomplicated cases

A
  • education and reassurance
  • feed thickeners
  • positioning 30 degrees after feeds
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38
Q

how is more severe GORD managed

A
  • PPI or H2RA (Ranitidine)
  • antacids or alginates
  • reserved use of pro kinetics
  • surgery: Nissen’s
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39
Q

when does pyloric stenosis present

A

2-5th week of life - very rare after 12 weeks

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40
Q

definition of diarrhoea in infants and toddlers

A

> 10kg/day of stool in an infant or toddler

persistent loose or watery stools 3+ times a day

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41
Q

definition of diarrhoea in an older child

A

> 200g/kg/day

3+ times a day

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42
Q

how long must diarrhoea be present for it to be chronic

A

> 4 weeks

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43
Q

investigations for persistent diarrhoea

A
  • Stool sample and culture
  • Faecal calprotectin
  • Faecal elastase
  • Bloods: U&E’s, TFT’s, LFT’s, CRP, immunoglobulins, coeliac antibodies
  • Faecal alpha 1 antitrypsin for protein losing enteropathy
  • USS abdomen
  • Endoscopy and biopsies
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44
Q

what is acute gastroenteritis

A

a clinical syndrome often defined by increased stool frequency (eg, ≥3 loose or watery stools in 24 hours or a number of loose/watery bowel movements that exceeds the child’s usual number of daily bowel movements by two or more), with or without vomiting, fever, or abdominal pain

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45
Q

how is gastroenteritis managed

A
  1. Fluid replacement to prevent dehydration
  2. Zinc supplementation
  3. Rota virus and measles vaccinations
  4. Promotion of only breastfeeding and vitamin A supplementation
  5. Encourage handwashing
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46
Q

how long do D&V usually last in gastroenteritis

A
  1. Vomiting: usually lasts 1-2 days and stops within 4 days

2. Diarrhoea: usually lasts for 5-7 days and stops within 2 weeks

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47
Q

how would suspected coeliac disease be investigated

A
  1. FBC, LFT’s, TFT’s, Ferritin
  2. Immunoglobulins, coeliac’s antibodies- tGA, EMA
  3. Endoscopy & duodenal biopsy - if antibodies high and high suspicion
  4. HLA DQ2/8 if trying to avoid biopsy
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48
Q

some rogue things to ask about in a paeds abdo history

A
  • lightheadedness, fatigue, dizziness
  • anxiety/depression in family
  • separation anxiety
  • social phobia
  • bullying
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49
Q

what should be examined in an abdo pain exam

A
  • abdo exam
  • plot height and weight on growth chart
  • clubbing
  • anal signs
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50
Q

investigations into abdo pain

A
  • urine dip
  • bloods: FBC, glucose (DKA, diabetes), CRP, LFTs, TFTs
  • coeliac antibodies
  • abdo USS
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51
Q

how does UC tend to present (3)

A
  • diarrhoea/ increased frequency
  • colicky abdo pain
  • bloody stool
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52
Q

4 extra-intestinal manifestations of UC

A
  • uveitis
  • pyoderma gangrenous
  • erythema nodosum
  • ankylosing spondylitis
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53
Q

4 main complications of UC

A
  • fulminant colitis
  • haemorrhage
  • toxic megacolon
  • colorectal cancer
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54
Q

5 main presentations of Crohn’s disease

A
  • pubertal delay
  • abdo pain
  • diarrhoea
  • weight loss
  • growth failure
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55
Q

extra-intestinal manifestations of Crohn’s

A
  • uveitis
  • Erythema nodosum
  • Perianal tags
  • Arthralgia
  • Fever, weight loss, lethargy
  • Strictures
  • Anal fistulas
  • Cobblestone, patchy appearance
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56
Q

how can crohn’s lead to masses

A

fibrotic thickenings of bowel wall + non-caseating granulomas

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57
Q

investigations for IBD

A
  1. Blood tests (Anaemia), CRP, ESR
  2. Stool tests: Faecal calprotectin + Faecal pathogens
  3. Endoscopies, colonoscopy
  4. Ultrasound, MRI, barium X-ray
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58
Q

how is crohn’s managed

A
  1. Nutritional therapy:
    - Whole protein feed replacement
    - Exclusion diets
  2. 5-ASA and sulphalazine
  3. Corticosteroids
  4. Methotrexate
  5. Infliximab
  6. Surgery commonly needed
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59
Q

how is UC managed

A

depends on severity of the disease - Sulphasalzine - Corticosteroids - Antibiotics - Surgery - Azathioprine - Infliximab

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60
Q

associated symptoms to ask about in paeds MSK history

A
  • rash
  • fever
  • weight loss
  • night sweats
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61
Q

VITAMIN CD causes of MSK problems

A
  • Vascular - haemophilia, haemangioma
  • Infection - septic arthritis, osteomyelitis, reactive arthritis
  • Trauma
  • Autoimmune - JIA, IBD, lupus, HSP
  • Metabolic
  • Iatrogenic
  • Neoplasia - leukaemia
  • Congenital - CDH
  • Degenerative - Perthes, SUFE
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62
Q

how is transient synovitis managed

A
  • reassurance - improves within a week
  • NSAIDs for pain
  • safety net (SA) - i.e. come back if high temp, increasing pain, night pain, no weight bearing, other joints, goes on for 2+ weeks
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63
Q

when does Perthe’s disease most commonly occur

A

avascular necrosis of femoral hear due to interruption of blood supply - M>F, ages 5-10

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64
Q

how is Perthe’s disease investigated

A
  • blood tests usually normal
  • bilateral hip XR including frog position
  • if still suspected MRI or bone scan
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65
Q

how is Perthe’s disease managed

A
  1. early disease with <50% of femoral head:
    - Bed rest + traction
  2. Late disease:
    - Femoral head needs to be covered by acetabulum to reossify epiphysis
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66
Q

when do growing pains occur

A

at NIGHT (pain free in the day)

usually 3-5 year olds and 8-12 year old

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67
Q

management of growing pains

A

reassurance
massage and analgesia
stretching
safety netting

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68
Q

ARTHRITIS mnemonic for swollen joint differentials

A 
A: acute septic arthritis
R: Reactive: to infection 
T: Trauma + safeguarding
H: Haematological- Haemophilia, leukaemia
R: Rheumatological: juvenille idiopathic, Juvenille dermatomyositis, lupus
T: TB
I: Immunological: HSP
S: Sarcoidosis
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69
Q

when does JIA occur

A

> 6 weeks in under 16 year olds

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70
Q

3 main types of JIA

A
  1. Polyarthritis: affecting >4 joints
  2. Oligoarthritis: affecting = 4 joints
  3. Systemic: arthritis with fever and rash
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71
Q

extra-articular complication of JIA

A

anterior uveitis

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72
Q

investigations for JIA

A
  1. Hb: anaemia of chronic disease possible
  2. WCC: leucocytosis
  3. Platelets: thrombocytosis
  4. ESR: RAISED
  5. CRP: normal or raised
    ANA: negative or positive
  6. RF: can be positive or negative
  7. X-ray
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73
Q

1st and 2nd line medical managements of JIA

A
  • 1st line = NSAIDs and intra-articular steroids

- 2nd line = methotrexate

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74
Q

2 things to monitor in methotrexate use

A
  • LFTs

- FBC (for BM suppression)

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75
Q

what is benign joint hyper mobility syndrome also known as

A

EDS type 3

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76
Q

how can systemic juvenile arthritis present

A
  • daily fever spikes (QUOTIDIAN)
  • transient pink rash
  • decreased appetite
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77
Q

how is systemic JIA managed

A
  1. Systemic steroids- oral if possible, IV if severe
  2. Steroid sparing meds: methotrexate
  3. Biologics
  4. Physiotherapy and OT input
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78
Q

CREAM for Kawasaki disease symptoms

A
  • Conjunctivitis (bilateral, non-exudative)
  • Rash (polymorphous non-vesicular)
  • Edema (or erythema of hands and feet)
  • Adenopathy (cervical, unilateral?)
  • Mucosal involvement (erythema or fissures, strawberry tongue)
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79
Q

how is Kawasaki disease managed

A
  • high dose IV immunoglobulin
  • aspirin
  • steroids???
  • echo
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80
Q

pathophysiology of bronchiolitis

A
  • IgE mediated reaction to virus (RSV)
  • Increased mucus production and bronchiole oedema
  • Leading to bronchiole constriction and hyperinflation of the chest + atelectasis
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81
Q

what can increase the risk of bronchiolitis

A
  • preterm
  • smoke exposure
  • breast feeding <2 months (NB: bronchiolitis presents with problems feeding!)
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82
Q

when should urgent hospital admission for bronchiolitis be carried out

A
  • Apnoea
  • Child looks seriously unwell
  • Severe respiratory distress: grunting, cyanosis, intercostal recession
  • RR >70
  • Oral intake <50%
  • Oxygen sats below 92%
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83
Q

main causes of croup

A

parainfluenza

RSF

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84
Q

how is a child with croup managed at home

A
  1. Dexamethasone: 0.15mg/kg PO
  2. Keep well hydrated
  3. No need for antibiotics- viral infection, so reassure
  4. symptoms resolve within 48 hours
  5. Safety net: drowsy, off food and drink, lethargy, stridor, wheeze, getting very ill
  6. Paracetamol and ibruprofen for symptom relief
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85
Q

treatment for croup in hospital

A
  1. Dexamethasone 0.15mg/kg
  2. Nebulised adrenaline
  3. Keeping child calm
  4. IV fluids +/- NG tube and feeding
  5. Oxygen therapy
  6. ENT and anaesthetist input
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86
Q

scoring system for croup

A

Westley scoring

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87
Q

first line antibiotic for bacterial pneumonia in 1-17 years

A

amoxicillin (clarithromycin if penicillin allergic)

doxycycline can be used from 12-17 years

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88
Q

1st choice Abx in severe pneumonia

A

co-amoxiclav

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89
Q

important risk factors to ask about in asthma history

A
  • neonatal (pre-term birth)
  • family history of atopy
  • smoking in family
  • pets
  • poor housing
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90
Q

first 2 steps in asthma management in children under 5

A
  1. Start PRN salbutamol with spacer
  2. Add in ICS of 200-400mcg daily OR leukotriene receptor antagonist if cannot use corticosteroid
    - Start at a low dose if possible of ICS
91
Q

3rd step in asthma management in children under 5

A
  1. Medications review
  2. If taking ICS- add in LRA
  3. If taking LRA- add in ICS 200-400mcg

step 4 = REFER

92
Q

first 2 steps in asthma management in children aged 5-12

A
  1. SABA as required with spacer
  2. Add in ICS: 200-400mcg daily
    - 200mcg is good starting dose
93
Q

3rd step in asthma management in children aged 5-12

A
  1. Add in a LABA
  2. Assess response of LABA:
    - If good response then continue
    - If benefit but still not enough increased ICS to 400mcg
  3. If no response to LABA:
    - Stop and increase ICS to 400mcg daily
  4. If control still not good:
    - LRA or Theophylline
94
Q

4th step in asthma management children aged 5-12

A

increase ICS to 800mcg per day

95
Q

5th step in asthma management children aged 5-12

A
  • daily steroid tablet at lowest dose
  • keep ICS at 800mcg
  • referral
96
Q

things to counsel parents on in asthma management

A
  • information and education
  • avoiding triggers
  • up to date with immunisations
  • inhaler technique
97
Q

what is red and amber flag pyrexia

A

red flag = 38 degrees in child <3 months

amber flag = 39 degrees in child 3-6 months

98
Q

features of febrile convulsions

A
  • can’t prevent even with paracetamol
  • generalised TC seizures
  • unconscious and post-ictal
  • 6 months - 6 eyars
99
Q

3 risk factors for developing epilepsy relating to febrile convulsions

A
  • atypical (still only 1%)
  • abnormal neurology prior to event
  • Fix of epilepsy
100
Q

main criteria for Kawasaki’s + 5 extra (must have 4/5)

A
  1. Fever lasting >5 days
    Presence of 4/5:
    - Changes in extremitites: desquamation, erythema, oedema
    - Rash
    - Bilateral, non-purulent conjunctivitis
    - Cervical lymphadenopathy
    - Changes in lips/oropharnyx: cracked lips or red tongue
101
Q

difference between petechiae, purpura and ecchymosis

A 
petechiae = <2mm
purpura = 2-10mm
ecchymosis = >10mm
102
Q

what is done in a neonatal/child sepsis screen

A

BUFALO:

  • Blood cultures
  • Urine sample
  • CXR
  • Lumbar puncture
  • Viral nose swab
  • FBC, CRP, U&E’s, LFT’s
  • GLUCOSE
103
Q

when should a lumbar puncture be considered

A

febrile under 1 and almost always under 6 months

104
Q

3 main causes of meningitis in neonates

A

GBS
E. coli
Listeria

105
Q

4 long term consequences of meningitis

A
  • cerebral palsy
  • deafness
  • epilepsy
  • coning and death
106
Q

how much weight is a child expected to gain daily from 10 days - 6 months

107
Q

how to calculate expected weight of children from 1-10 years

A

2 x (age + 4)

108
Q

normal head circumference at birth, 1 year and 2 years

A

birth = 35cm
1 year = 47cm
2 years = 49cm

109
Q

how to work out milk requirement

A

after 5-7 days from birth:
- 150ml/kg daily

so if 5kg = 750ml daily

110
Q

how is calorie needs daily worked out in <1 years

A

110kcal/kg day

so if 5kg = 550 calories

111
Q

how is calorie needs daily worked out in >1 years

A

1000 + (100 x age)

so 8 years old 1800 calories

112
Q

what is overweight and obesity classed

A

overweight >91st centile

obese >98th centile

113
Q

which screening procedures are done at birth, 1 week and 8 weeks

A
  • birth = eyes, heart, hips, hearing
  • 1 week = Guthrie - PKu, hypothyroidism, CF, haemoglobinopathies, acylcarnitine
  • 8 weeks = general exam by GP
114
Q

at what age are children dry by day and dry at night

A
  • day = 2-3 years

- night = 4-5 years

115
Q

at what age is encopresis abnormal

A

over 4 years

116
Q

when should a newborn micturate, pass meconium and regain any lost birthweight

A
  • micturition and meconium in first 48 hours

- regain any lost birthweight by day 10 (more than 10% is abnormal)

117
Q

Which airway position is used for:

a) . Infants (<1 year)
b) . Children 1-6
c) . Children 6-12 upwards

A

a) . Neonates/infants: neutral
b) . Children: sniffing morning air
c) . Older children: Head-tilt-chin-lift

118
Q

3 Es of assessing breathing

A
  • Effort: signs of respiratory distress
  • Efficacy: sats, chest expansion, CO2 levels
  • Effects: HR, RR, consciousness, skin mottling, cyanosis
119
Q

3 pre-terminal breathing signs

A
  • silent chest
  • cyanosis
  • O2 <85% on air
120
Q

fluid bolus in children

A

20ml/kg of 0.9% saline and assess response

121
Q

how is disability responded to

A
  1. Protect airway
  2. GCS <8 then ET tube- call anaesthetist
  3. Recovery position if vomiting
  4. Give IM glucose if is less than 4mmol/L
  5. Seizures = benzo’s
122
Q

what is assessed in exposure

A
  1. Temperature
  2. Expose with dignity:
    - Rashes
    - Cuts, bruises, trauma
    - Signs of seizure activity
  3. Full hx and exam
  4. PMH and drug chart
  5. Investigation results
123
Q

when would a child need to be referred for a murmur

A
  • symptomatic: SOB, cyanosis, failure to thrive, problems feeding, chest pain
  • diastolic murmur
  • louder when standing
  • louder than grade 2
124
Q

3 pan systolic murmurs

A
  1. Mitral regurgitation
    - Loudest at 5th intercostal, mid-clavicular
  2. Tricuspid regurgitation:
    - Loudest at 5th intercostal, left sternal edge
  3. Ventricular septal defect
125
Q

3 ejection systolic murmurs

A
  1. Aortic stenosis:
    - Loudest at 2nd intercostal, right sternal edge
  2. Pulmonary stenosis:
    - Loudest at 2nd intercostal, left sternal edge
  3. Hypertrophic, obstructive cardiomyopathy
126
Q

3 causes of mid diastolic murmurs

A
  • mitral stenosis
  • ASD
  • tricuspid stenosis
127
Q

cause of early diastolic murmur

A

aortic regurgitation

128
Q

what causes a constant murmur

129
Q

what is Still’s murmur

A

early systolic grade 1-3 murmur best heard supine at the apex of the heart and has a vibratory musical quality

130
Q

what is examined in the NIPE

A
  1. Weight, length, HC
  2. Hips: Barlow’s + Ortoloni’s
  3. Testes
  4. Eyes
  5. Heart + pulses & color
  6. everything else: fontanelle, spine, abdomen, urinary, meconium passage
131
Q

when to refer for bilateral vs unilateral undescended testes

A
  • bilateral = more concerning so refer early

- unilateral = refer in 4-6 weeks

132
Q

which 9 conditions are screened for via heel prick

A
  1. Hypothyroidism
  2. CF
  3. Sickle cell
  4. Phenylketonuria
  5. Homocysteinuria
  6. Maple syrup urine disease
  7. Medium chain acyl- coA
  8. Isovaleric acidaemia
  9. Gltaric aciduria type 1
133
Q

how are inguinal hernias treated

A
  • reduction with opiates

- if doesn’t work/risk of strangulation = surgery

134
Q

where is a hydrocele located

A

within the tunica vaginalis

135
Q

what causes a hydrocele

A

incomplete closure of processus vaginalis = too small for bowel contents but peritoneal fluid enters

136
Q

management of hydrocele

A

usually resolve by 18-24 months after this consider surgery

137
Q

management of umbilical hernia

A
  • 96% close spontaneously by 3 months
  • if not closed by 3-5 months = unlikely to close by themselves
  • repaired before school for cosmetic reasons
138
Q

3 investigations for undescended testes

A
  • USS
  • hCG injection to check to see if they’re testes - should release testosterone
  • laparoscopy if unsure
139
Q

3 risks of undescended testes

A
  • infertility
  • testicular cancer
  • torsion
140
Q

what is phimosis

A

inability to retract foreskin - physiological at birth

pathological - white scarring of foreskin, often over 5 years

141
Q

when is it uncommon to have appendicitis

A

under age of 3 - think of something else

142
Q

how is appendicitis treated

A

NPO + IV hydration, analgesia, antiemetics, and antibiotics with anaerobic and gram (-) coverage

Laproscopic appendectomy is definitive. Exploratory surgery if no appendix found.

In perforation, antibiotics until afebrile with a normalized WBC count. Should be closed by delayed primary closure.

In abscess formation, broad spec antibiotics and percutaneous drainage. Appendectomy 6-8 weeks later

Trials of just abx

143
Q

where is intussusception most common

A

near ileo-caecal valve

144
Q

2 causes of intussusception

A
  • viruses: enlarged peers patches

- polyps

145
Q

intussusception presentation

A
  • bilious vomiting
  • paroxysmal colicky pain - may bring knees to chest and arch back
  • pallor
  • refusal to feed
  • sausage shaped mass
  • redcurrant jelly stool (late)
  • shock (perforation?)
146
Q

how is intussusception managed

A
  • no peritonitis = gas inflation reduction by radiologist

- peritonitis = operative reduction

147
Q

what to ask in an obstruction history

A

past history of surgery (adhesions causing obstruction?)

148
Q

what is bell-clapper deformity

A

testes not anchored to scrotum - increases risk torsion

149
Q

how is pyloric stenosis diagnosed

A
  • test feed

- abdominal USS

150
Q

biggest risk factor for NEC

A

prematurity

151
Q

AXR finding for NEC

A

pneumatosis intestinalis (intramural bowel gas)

152
Q

how is NEC managed

A
  • NBM and TPN
  • broad spec antibiotics
  • artificial ventilation and cardiac support
  • perforation needs laparotomy
153
Q

what is oesophageal atresia associated with in 80% of cases

A

tracheo-oesophageal fistula

154
Q

what is TOF and OA associated with (VATERL)

A

Vertebral
Anorectal
Tracheo-oEsophageal
Radial Limb deformities

155
Q

what is malrotation

A

abnormal rotation around superior mesenteric artery during embryonic development - often causes volvulus (usually 1st month of life)

156
Q

difference between exomphalos and gastroschisis

A
  • exomphalos = umbilical hernia at birth where some abdo organs are pushed into umbilical cord - detected via USS at 18 weeks, 50% risk chromosomal abnormality
  • gastroschisis = extrusion of abdo contents through abdo folds not covered by peritoneum - lateral to umbilicus
157
Q

signs of CDH

A
  • Problems with resuscitation/early breathing
  • Displaced apex beat
  • Lack of bowel sounds in abdomen
  • Poor air entry in chest
158
Q

main problem with CDH

A

pulmonary hypoplasia in utero = high mortality

159
Q

2 main types of CDH

A
  1. Bochadlek hernia: postero-lateral- most common

2. Morgagni: anteromedial

160
Q

management of CDH

A

do NOT BVM

intubation and ventilation, correction of acidosis and hypercapnia and surgery

161
Q

growth plate - what is it stimulated and inhibited by

A

the area just below the head of a long bone in which growth in bone length occurs; the epiphyseal plate

Stimulated by: Growth hormones, IGF-I, thyroid hormones, Oestrogen, PTH

Inhibited by: Cytokine, certain drugs, high dose steroids/oestrogen

162
Q

how much growth per year is there in pre-pubescent children

163
Q

how accurate is mid parental centile

A

4/5 have adult height within +/- 6cm of predicted adult height

164
Q

how is bone age measured

A

X ray of left hand

  • gaps seen where there is no epiphysis
  • age 5 = start to see epiphysis
  • age 15 = epiphysis seals (growth stops)
165
Q

stature in Turner’s syndrome (45XO)

166
Q

endocrine causes of short stature

A
  • Hypothyroidism
  • Pseudohypoparathyroidism
  • Growth hormone deficiency
  • Delayed/precocious puberty
  • Cushing’s disease: ACTH secreting pituitary adenoma
  • Cushing’s syndrome- often iatrogenic, such as steroids
  • Anything which affects puberty
167
Q

when does growth hormone deficiency present

A

1-2 years - often becomes evident only after age 3

168
Q

pathological vs nutritional obesity

A 
pathological = short and fat
nutritional = tall and fat
169
Q

pathological cause of obesity

A

Cushing’s disease - increased cortisol = weight gain

but higher steroids = growth inhibition of epiphyses

170
Q

where are androgens produced

A

adrenal gland

171
Q

Tanner staging of puberty in girls

A

Tanner stages:

  1. Stage 1:
    - No signs of puberty
  2. Stages 2-3:
    - Any breast enlargement/pubic or axilla hair
  3. Stages 4-5:
    - Started periods with signs of pubertal features
172
Q

Tanner staging of puberty in boys

A
  1. Stage 1:
    - High voice only + no signs
  2. Stages 2-3
    - Any of deepening of voice, Early pubic/axilla hair, Testicular/penile enlargment
  3. Stages 4-5:
    - Any of: voice broken, facial hair, adult size penis, pubic and axilla hair
173
Q

what is used to assess testicular volume

A

prader orchidometer

174
Q

what is central precocious puberty

A

Concordant:
Premature activation of puberty axis:
- Puberty happening in the right order, often idiopathic or CNS disorder
- In boys is often pathological: brain tumour
- In girls: idiopathic, non pathological

175
Q

what is peripheral precocious puberty

A

Pseudo pre puberty where the release of sex hormones is independent of GnRH release

  • Not happening in the right order
  • Discordant
  • Such as hair but no testicular enlargment
176
Q

what is virilization

A

the development of male physical characteristics (such as muscle bulk, body hair, and deep voice) in a female or precociously in a boy, typically as a result of excess androgen production.
- Due to increased adrenal androgen secretion

177
Q

investigations for precocious puberty

A
  • Bone age (would usually be increased)
  • TFT’s (overactive can cause early puberty)
  • Oestridiol, testosterone
  • Pituitary function tests
  • Scan of adrenals and pelvis
  • MRI
178
Q

delayed puberty in girls vs boys

A

girls = no signs by age 13, no menarche after 15

boys = no signs by age 14 (v common)

179
Q

5 causes of hypogonadotrophin hypogonadism (pituitary)

A
  • Constitutional delay
  • Kalman’s syndrome
  • BMI <17
  • Chronic disease
  • Tumours
180
Q

3 causes of hypergonadotrophin hypogonadism - problem with testes or ovaries/adrenals = GnRH/LH or FSH v high

A
  • Turner’s syndrome
  • Kleinfelter’s syndrome
  • cryptorchidism
181
Q

signs and symptoms of Turner’s syndrome

A
  • Can have differing BP’s in each arm + absent radial pulses (coarctation of aorta)
  • Horseshoe kidney
  • Webbing of neck
  • Low hair line
  • Short stature
182
Q

how is Turner’s managed

A

oestrogen - maintain bone health

183
Q

primary vs secondary bed wetting (nocturnal enuresis = 2+ times a week)

A

primary = no period of dry nights for at least 6 months

secondary = bedwetting after prior dryness for at least 6 months

184
Q

4 differentials for nocturnal enuresis

A
  • UTI
  • constipation
  • neurological, spina bifida
  • diabetes
185
Q

short term treatment for nocturnal enuresis (e.g. for sleepovers, school trips)

A

desmopressin - take 1-2 hours before bed

186
Q

1st and 2nd line long term managements for nocturnal enuresis

A
  1. enuresis alarm (buzzer goes off when wet)

2. antimuscarinic - oxybutanin OR TCA - imipipramine

187
Q

which laxatives are used for constipation

A

firstly- Osmotic softeners:

  1. Laxido/MOvical 1-4 daily
  2. Lactulose: 5-10ml BD

secondly:
1. Senokot for 6-12 years
2. Sodium picosulphate for 4-10 years

188
Q

5 gross motor red flags

A
  • asymmetrical neonatal reflexes
  • persistent neonatal reflexes
  • not weight bearing by 12 months
  • exclusive toe walking
  • not walking by 18 months
189
Q

3 fine motor red flags

A
  • fixed squint
  • not fixing and following by 6 weeks
  • hand preference before 18 months
190
Q

4 social/speech and language red flags

A
  • no smile by 6 weeks
  • no babbling by 12 months
  • no words or doesn’t understand commands by 18 months
  • unintelligible speech by 2.5 years
191
Q

pathognomonic sign of DMD

A

Gower’s sign - compensating for weak pelvic muscles = uses hands and knees to stand then pushes down on thighs

toe walking also common

might also have calf muscle hypertrophy

192
Q

some differentials for speech delay

A
  • Bilingual household
  • Hearing problem
  • Tongue tie, cleft palate
  • ASD
  • NEGLECT
193
Q

4 motor cerebral palsy’s

A
  1. Spastic: most common, with increased tone
    - Motor cortex damaged
  2. Athetoid: writhing, uncontrolled movements
    - Basal ganglia damaged
  3. Ataxic: cerebellar signs- balance, shaking and positioning
    - Cerebellar damage
  4. Mixed
194
Q

GMFCS 1

A

Child very mildly affected:

  • Can walk
  • Up stairs with railing
  • Balance, speed and coordination reduced
195
Q

GMFCS 2

A
  • Walk in most settings, difficulty with long distances and uneven terrain
  • Use of railings on stairs
  • May use mobility aids, wheels over long distance
  • Difficulty walking and running
196
Q

GMFCS 3

A
  • Hand-held mobility aid indoors
  • Wheelchair long distance
  • Stairs with assistance and supervision
197
Q

GMFCS 4

A
  • Powered motor assistance or physical assistance from others (pushed on wheelchair)
  • May walk supported shortly at home
198
Q

GMFCS 5

A
  • Wheelchair in all situations- powered

- May need straps due to lack of posture

199
Q

prenatal causes of CP

A
  • Abnormal cerebral development: chromosomal, maternal infection
  • Periventricular leukomalacia: prematurity, maternal infection:
  • Intraventricular haemorrhage
  • Stroke
200
Q

intra-partum / postnatal causes of cerebral palsy

A
  • Birth asphyxia
  • CNS infection
  • hypoglycaemia
  • Head injury
  • Stroke
  • Hyperbilirubinaemia
201
Q

how does CP present

A
  • Motor delay
  • Abnormal posture
  • Abnormal movements
  • Spascity
  • Epilepsy
  • Feeding and nutritional problems
  • Bladder infections & incontinence
  • Constipation
202
Q

nutritional and feeding problems in CP

A
  • coordination of suck and swallow

- spasticity: uses more energy so tend to need more calories per day

203
Q

what can be used to manage spasticity with CP

A
  • baclofen
  • selective botox injection s
  • orthopaedics
204
Q

shaken baby triad

A
  • retinal haemorrhage
  • subdural haematoma
  • encephalopathy
205
Q

4 signs of TOF

A
  • cyanosis
  • right to left shunt
  • ejection systolic murmur - pulmonary stenosis
  • boot shaped heart
206
Q

how is Perthe’s disease managed before age 6

A

conservatively - most resolve on their own

if over 6 or severe deformity then do surgical reduction

207
Q

how common is GORD

A

40% infants often in first 2 weeks of life

208
Q

why does GOR/GORD happen

A

Baby’s have an immature LOS so can easily reflux up feed

  • Also have a shorter oesophagus under diaphragm (more in thorax) so reflux more common
  • Stomach is also very small
209
Q

most common cause of GORD

A

over feeding >150ml/kg/day - therefore first line management is to reduce feed quantity and position at 30 degrees during feeding

210
Q

what does cerebral palsy increase the risk of

211
Q

when does GORD usually resolve by

212
Q

2nd and 3rd line and 4th line managements for GORD

A

2nd line = feed thickener
3rd line = 2 weeks of alginates (e.g. Gaviscon)
4th line = PPI or H2RA - referral to paediatrics

213
Q

when is there an exception to the 20ml/kg fluid bolus in paediatrics

A

10ml/kg in:

  • DKA
  • cardiac pathology
  • trauma
214
Q

estimated weight calculated in 0-12 month olds

A

(0.5 x age in months) + 4

215
Q

estimated weight calculated in 1-5 year olds

A

(2 x age) + 8

216
Q

estimated weight calculated in 6-12 year olds

A

(3 x age) + 7

217
Q

what imaging technique for pyloric stenosis

A

USS - shows thickened pylorus

218
Q

what investigation for GORD

219
Q

what is double bubble sign for

A

duodenal atresia

220
Q

how is intussusception treated

A

air enema reduction

221
Q

2 investigations for appendicitis

A
  • AXR: showing appendicolith

- USS: non-compressive blind ending structure >6mm

222
Q

what’s used for ovarian cyst imaging

A

USSL then repeat at 6 weeks to see if it has resolved

whirlpool sign on USS

223
Q

what is round pneumonia

A

type of pneumonia only seen in children

224
Q

what is seen on CXR of foreign body

A
  • hyperinflated lung in partial obstruction - radiolucent

- OR in complete obstruction = lung collapse

Year 4 revision (5 decks)

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