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Danny's Phase 3A Medicine > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Name some common viral causes of RESPIRATORY infections (80-90% of infections are viral)

A
  • Respiratory syncytial virus (RSV)
  • Rhinovirus
  • Influenza
  • Metapneumovirus
  • Adenoviruses
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2
Q

Name some common bacterial causes of RESPIRATORY infections

A
  • Strep penumoniae
  • haemophilus influenza
  • Moraxella catarrhalis
  • Bordetella pertussis
  • Mycoplasma pneumoniae
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3
Q

Risk factors of RESPIRATORY infections?

A
  • Parental smoking
  • Poor socioeconomic status (damp/ overcrowded)
  • Poor nutrition
  • Male gender
  • Immunodeficiency

Underlying condition

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4
Q

Give some examples of URTIs and what they can cause

A
  • Coryza (cold)
  • Sore throat (pharyngitis, tonsillitis)
  • Acute otitis media
  • Sinusitis

Cause:
Difficulty feeding
Febrile convulsions
- Asthma exacerbations

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5
Q

Describe symptoms of the common cold

Common pathogens

and the treatment

A
  • Clear/ mucopurulent nasal discharge and nasal blockage

Common pathogens:
Rhinovirus
coronaviruses
RSV

Paracetamol
Ibruprofen

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6
Q

Common pathogens and symptoms of Pharyngitis

A

Viral

  • Common cold viruses
  • Adenoviruses
  • EBV

Bacterial (older children)
- Group A beta-haemolytic strep

Pharynx and soft palate inflamed

Local lymph nodes enlarged and tender

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7
Q

What is Tonsillitis?

A

Form of pharyngitis where there is intense inflammation of the tonsils often with purulent exudate

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8
Q

What is the CENTOR criteria?

A
  • Tonsillar exudate
  • Tender anterior cervical lymphadenopathy
  • Fever
  • Absence of cough

3+ of these criteria = Strep infection- Abx

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9
Q

What is Quinsy?

A

Peritonsillar abscess (complication of tonsillitis)

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10
Q

Give some symptoms of Quinsy

A
  • Sore throat, dysphagia, uvula deviation, trismus (lockjaw)
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11
Q

Management of tonsillitis?

A

Symptomatic relief : Para and Ibruprofen

Penicillin V or Erythromycin

Tonsillectomy in recurring cases

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12
Q

What is Acute Otitis media and why is it common in children?

A

Infection of the middle ear due to short, horizontal eustachian tubes and mucal discharge almost always the middle ear

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13
Q

Presenting complaint of Acute Otitis media?

A
  • Rapid onset ear pain (due to bulging of tympanic membrane)

Pyrexia/fever

Otorrhoea

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14
Q

Management of Otitis media?

A

> 4 days of no symptoms: Amoxicillin / Erythromycin

Grommet insertion if recurrent

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15
Q

What is the leading cause of hearing loss in children?

A

Otitis media with effusion or glue ear

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16
Q

management of sinusitis?

A

Amoxicillin/ doxycycline

Avoid antihistamines as it may thicken secretions

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17
Q

Signs of upper airway obstruction?

A
  • Stridor
  • Hoarseness
  • Barking cough (sea lion)
  • Dyspnoea
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18
Q

How is the severity of upper airway obstruction assessed?

A

Degree of chest retraction and degree of stridor

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19
Q

What should you avoid in a suspected upper airway obstruction?

A

Avoid examination using a spatula as this may precipitate total obstruction

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20
Q

Describe why hoarseness occurs

A

Inflammation of the vocal cords

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21
Q

What is stridor?

A

Rasping sound heard predominantly on inspiration

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22
Q

CROUP

What is it otherwise known as?

A

Laryngotracheobronchitis

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23
Q

CROUP

What is it?

A

Mucosal inflammation and increased secretions that affect the airway

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24
Q

CROUP

Where is oedema dangerous?

A

Subglottic area as this may result in critical narrowing of the trachea

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25
Q

CROUP

Viral causes?

A

Parainfluenza 1, 2, 3 (most common)

Metapneumovirus
RSV
Influenza

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26
Q

CROUP

When is it most common?

A

Autumn time, between the ages of 6 months to 6 years with a peak incidence around 2 years old

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27
Q

CROUP

Clinical presentation?

A
  • Barking cough (worse at night)
  • Harsh stridor
  • Hoarseness
  • Preceding non specific viral URTI

(coryza, fever, cough)

WORSE AT NIGHT

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28
Q

CROUP

Signs of severe disease?

A

Cyanosis

Altered consciousness

Rising HR/RR

Restlessness

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29
Q

What is Bacterial Tracheitis?

A

Pseudomembranous croup is an uncommon but dangerous disease very similar to severe croup but with:

  • High fever
  • Appears toxic
  • Tracheal tenderness
  • Rapidly progressive airways obstruction (thick exudate cant be cleared by coughing)
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30
Q

What is bacterial tracheitis caused by and what is the management?

A

S.aureus, Strep A, haemophilus

IV Abx

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31
Q

What is Acute Epiglottitis and what is it caused by?

A

Life threatening emergency due to high risk of respiratory obstruction caused by:

Haemophilus influenza type B

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32
Q

What affect has the Hib immunisation had an the incidence of epiglottitis?

A

> 99% reduction in cases, most common in ages 2-7 years

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33
Q

Clinical presentation of Acute Epiglottitis?

A
  • Intense swelling of epiglottis
  • Onset very acute
  • High fever
  • Dysphagia and speech difficulty due to pain
  • Drooling
  • Stridor
  • Minimal cough
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34
Q

In what position would you expect a child with trachea obstruction to be in?

A

Immobile, upright, with an open mouth to optimise the airway

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35
Q

What should you never do when suspecting obstruction of the respiratory tract/ acute epiglottitis?

A

Do not examine throat with spatula or lie the child down

Do not upset or cannulate

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36
Q

Management of Acute Epiglottitis?

A

IV Abx- Cefotaxime

Intubate

Tracheostomy may be required if complete obstruction

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37
Q

What is the difference between Croup and Acute Epiglottitis in terms of:

1) Onset
2) Cough
3) Preceding coryza
4) Able to drink

A

Croup

1) onset: days
2) Severe barking cough
3) preceding coryza
4) can drink

Acute Epiglottitis

1) onset: hours
2) absent/ minor cough
3) no preceding coryza
4) cant drink

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38
Q

What is the difference between Croup and Acute Epiglottitis in terms of:

1) Drooling?
2) Appearance of child
3) Fever
4) Stridor and voice/cry?

A

Croup

1) no drooling
2) unwell appearance
3) fever <38.5
4) harsh stridor with hoarse cry

Acute Epiglottitis

1) drooling
2) toxic, very unwell
3) fever >38.5
4) soft whsipering stridor, muffled cry/ reluctant to speak

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39
Q

WHOOPING COUGH (PERTUSSIS)

What is it?

A

NOTIFIABLE DISEASE

Acute, highly contagious resp infection transmitted by respiratory droplets

Co- infection with RSV (Bronchiolitis) common

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40
Q

WHOOPING COUGH (PERTUSSIS)

Causing agent?

A

Bordetella pertussis, gram negative coccobacillus

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41
Q

WHOOPING COUGH (PERTUSSIS)

How long do symptoms last and what is the first stage?

A

6-8 weeks and the first stage is the

Catarrhal Stage

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42
Q

WHOOPING COUGH (PERTUSSIS)

Clinical presentation of the Catarrhal stage?

(1st stage)

A
  • Malaise
  • Conjunctivitis
  • Nasal discharge
  • Sore throat
  • Dry cough
  • Mild fever
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43
Q

WHOOPING COUGH (PERTUSSIS)

What is the second stage?

A

After two weeks of the catarrhal phase it becomes the

Paroxysmal coughing stage

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44
Q

WHOOPING COUGH (PERTUSSIS)

Describe the Paroxysmal coughing stage

A

Dry hacking cough that is worse at night and after feeds

coughing episodes folllowed by characteristic ‘whoop’

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45
Q

WHOOPING COUGH (PERTUSSIS)

What is the characteristic ‘whoop’?

A

Inspiration against a closed glottis,

Child chokes, gasps and face reddens

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46
Q

WHOOPING COUGH (PERTUSSIS)

What can happen post cough?

A

Vomiting,
Apnoea
Cyanosis

subconjunctival haemorrhage/ anoxia can be brought on by coughing fits, leading to seizures/syncope

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47
Q

WHOOPING COUGH (PERTUSSIS)

Diagnostic tests?

A
  • Notifiable disease
  • PCR via nasal swab
  • Nasopharyngeal swabs
  • test for anti- pertussis IgG
  • Marked lymphacytosis= COMMON
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48
Q

WHOOPING COUGH (PERTUSSIS)

treatment?

A
  • Hospitalised 1%- if <6 months (risk of apnoea)

10-14 days incubation

Macrolides 1st Line:
Azithromycin or Clarithromycin or
Erythromycin

Erythromycin for pregnant women

Off school for 48 hours after Abx commencement

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49
Q

BRONCHIOLITIS

What is it?

A

commonest lung infection in infants

rare after 1 years of age and peak 3-6 months

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50
Q

BRONCHIOLITIS

what makes this more severe?

A

Congenital heart defects

Cystic Fibrosis

Down’s

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51
Q

BRONCHIOLITIS

Cause?

A

RSV in 80%of cases
( Respiratory syncytial virus)

Metapneumovirus

Parainfluenza
Rhinovirus
Adenovirus

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52
Q

BRONCHIOLITIS

Cause of severe bronchiolitis?

A

RSV and Metapneumovirus dual infection is associated with severe bronchiolitis

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53
Q

BRONCHIOLITIS

Risk factors?

A
  • Premature/ low birth weight
  • Cystic Fibrosis
  • Congenital heart disease
  • Down’s
  • Immunocompromised
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54
Q

BRONCHIOLITIS

Clinical presentation?

A
  • Coryza precedes dry cough
  • Increasing breathlessness
  • feeding difficulties
  • fever
  • tachycardia
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55
Q

BRONCHIOLITIS

When should a child be admitted?

A
  • Infrequent feeding
  • Respiratory distress
  • hypoxia
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56
Q

BRONCHIOLITIS

Diagnostic tests and results?

A
  • Pulse oximetry
  • viral throat swab

Not routine:
CXR- exclude pneumothorax

blood gas analysis, FBC

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57
Q

BRONCHIOLITIS

Treatment?

A

Oxygen therapy

Supportive (NG nutrition, fluids, temp control)

ventilation (CPAP)

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58
Q

BRONCHIOLITIS

What is Ribavirin?

A

Antiviral meds against RSV,

Used for Hep C with (interferons/ simeprevir, sofosbuvir)

and some haemorrhagic fevers

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59
Q

BRONCHIOLITIS

What is Ribavirin?

A

Antiviral meds against RSV,

Used for Hep C with (interferons/ simeprevir, sofosbuvir)

and some haemorrhagic fevers

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60
Q

BRONCHIOLITIS

Signs on examination

A

wheeze and end inspiratory crackles

Cyanosis

Sub/ intercostal recession

Hyperinflation of chest

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61
Q

BRONCHIOLITIS

Associated signs with hyperinflation of the chest

A

Prominent sternum

Liver displaced downwards

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62
Q

What should be given if SpO2 <92%?

A

High flow humidified oxygen via nasal cannulae

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63
Q

PNEUMONIA

Cause in:

Newborns?

A

Group B strep- maternal

Gram negative enterococci

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64
Q

PNEUMONIA

Cause in:

Infants and young children?

A

Strep pneumoniae

haemophilus influenza B

Staph A (infrequent but serious)

Mycobacterium tuberculosis

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65
Q

PNEUMONIA

Cause in:

Viral cases?

A

RSV
Influenza A/B
Parainfluenza
Adenovirus

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66
Q

PNEUMONIA

Cause in:

Atypical?

A

Mycoplasma pneumoniae

Chlamydia pneumoniae

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67
Q

PNEUMONIA

Diagnostic tests?

A
  • Cough
  • fever
  • lethargy
  • poor feeding
  • respiratory distress
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68
Q

PNEUMONIA

Symptoms of respiratory distress?

A 
tachypnoea
cyanosis
grunting
intercostal recession
use of accesory muscles
nasal flaring
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69
Q

PNEUMONIA

Tests for severe?

A

blood cultures
sputum culture
FBC, CRP
CXR

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70
Q

PNEUMONIA

Signs in older children?

A

end inspiratory crackles
bronchial breathing
pleuritic pain

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71
Q

PNEUMONIA

Treatment?

A

If resp distress/ O2 <92%- admit to hospital

  • Oxygen
  • IV fluids
  • IV Abx for newborns
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72
Q

PNEUMONIA

What Abx are 1st line?

A

Amoxicillin

Alternatives:
Clarithromycin
Co-amoxiclav
Azithromycin

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73
Q

ASTHMA

What are the two types of wheeze?

A

transient early wheeze

persistent and recurrent wheezing

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74
Q

ASTHMA

What is transient early wheeze?

A

viral associated wheeze- RSV

small airways obstructed due to inflammation

more common in males and resolves by 5 years of age

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75
Q

ASTHMA

What is persistent and recurrent wheeze?

A

Presence of IgE to common inhalant allergens (Atopic Asthma)

Common in family Hx and associated with eczema, hayfever, food allergies

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76
Q

ASTHMA

Pathophysiology?

A

Bronchial inflammation leads to:

1) Oedema
2) Excessive mucous production
3) Infiltration of cells

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77
Q

ASTHMA

What does bronchial inflammation lead to?

A

Airway narrowing and reversible airflow obstruction

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78
Q

ASTHMA

What cells infiltrate the bronchials

A

Eosinophils
Neutrophils
Mast cells
Lymphocytes

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79
Q

ASTHMA

Risk factors?

A 
Low BW
Family Hx
Bottle fed
Atopy
Male
Pollution

ADAM33 Gene

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80
Q

ASTHMA

Triggers?

A 
Pollen 
Dust
Feathers
Exercise
Pollution
Cold air
Illness (viruses)
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81
Q

ASTHMA

Diagnostic tests?

A

CXR to rule out other causes

Spirometry

Peak flow shows diurnal variation

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82
Q

ASTHMA

Clinical presentation?

A

Polyphonic wheeze (expiratory- obstruction)

Coughing
SOB
Symptoms worse at night and morning

SILENT CHEST RED FLAG- exacerbation

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83
Q

ASTHMA

treatment for ages 5-16

A

Step 1: SABA (salbutamol)

Step 2: SABA + low dose ICS (beclomethasone)

Step 3: SABA+ ICS + LTRA (Montelukast)

Step 4: SABA+ ICS + LABA (salmeterol)

Step 5:
SABA + low dose MART
(ICS and fast acing LABA- formoterol)

Step 6: SABA + moderate dose MART

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84
Q

ASTHMA

Treatment to under 5

A

1) SABA
2) 8 week moderate dose ICS trial
3) Add LTRA

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85
Q

ASTHMA

Treatment to severe asthma attack?

A

O SHIT ME

Oxygen

Salbutamol (nebulised)

Hydrocortisone IV/ oral prednisolone

Ipratropium bromide (nebulised)

Theophylline IV

Magnesium sulphate IV
Escalate

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86
Q

What is Kartagener syndrome?

A

rare, autosomal recessive genetic ciliary disorder comprising the triad of situs inversus, chronic sinusitis, and bronchiectasis.

This leads to recurrent chest infections

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87
Q

CYSTIC FIBROSIS

What is it?

A

Alteration of the viscosity and tenacity of mucous produced at epithelial surfaces

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88
Q

CYSTIC FIBROSIS

What is the classic form of CF?

A

Bronchiopulmonary infection and pancreatic insuffieciency with a high sweat sodium and chloride concentration

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89
Q

CYSTIC FIBROSIS

Defective gene?

A

Mutations with cystic fibrosis transmembrane conductance regulator gene on chromosome 7

(CFTR)

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90
Q

CYSTIC FIBROSIS

How is it caused?

A

CFTR gene is for a critical chloride channel,

1) Decreased excretion of chloride into the airway lumen and an increased reabsorption of sodium into the epithelial cells
2) With less excretion of salt there is less excretion of water and increased viscosity/ tenacity of airway secretion

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91
Q

CYSTIC FIBROSIS

Cause?

A

Autosomal recessive

Commonest is a deletion at position 508 in amino acid sequence which results in a defect to the CFTR gene

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92
Q

CYSTIC FIBROSIS

Respiratory Clinical presentation?

A

Recurrent infections

Sinusitis

Nasal polyps

SOB and haemoptysis

Airflow limitation and
bronchiectasis

Respiratory failure

cor pulmonale (RVH - late sign)

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93
Q

CYSTIC FIBROSIS

GI Clinical presentation?

A

Steatorrhoea due to pancreatic dysfunction

10% meconium ileus

cholesterol gallstones

Increased incidence of peptic ulceration and GI malignancy

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94
Q

CYSTIC FIBROSIS

Nutritional effects?

A
  • Malnutrition due to malabsorption

- Failure to thrive and slow growth

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95
Q

CYSTIC FIBROSIS

Other Clinical signs?

signs in a male/female?

A

Puberty and skeletal maturity delay

  • Male almost always infertile
  • Secondary amenorrhoea in females

Arthropathy and DM in 11% of adults with CF

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96
Q

CYSTIC FIBROSIS

Diagnostic tests?

A

All UK newborns screened

SWEAT TEST:
- sodium conc >60mmol/L

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97
Q

CYSTIC FIBROSIS

Antibiotic Treatment?

A

younger: s.aureus, strep. pneumoniae

EVENTUALLY >90%:

Pseudomonas aeruginosa,

(nebulised anti-pseudomonal Ab therapy helps improve lung function)

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98
Q

CYSTIC FIBROSIS

Drug therapy?

A

B2- agonists
ICS
Symptomatic relief

Lung transplant if FEV1 <30% expected

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99
Q

CYSTIC FIBROSIS

method of airway clearance?

A

inhalation of recombinant human deoxyribonuclease (rhDNAse)

hypertonic saline by inhalation

Amiloride (inhibits sodium transport)

Acetylcysteine

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100
Q

CYSTIC FIBROSIS

Pancreatic insufficiency treatment?

A

PERT

pancreatic enzyme replacement therapy

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101
Q

CYSTIC FIBROSIS

Complications?

A
  • Cirrhosis
  • DM
  • Haemoptysis
  • Male infertility
  • Pneumonia
  • Pneumothorax
  • Pulmonary osteoarthropathy
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102
Q

What are the 3 categories of Congenital Heart Disease?

A

1) Holes / connections
2) Narrowing / stenosis
3) Complex (right to left shunt)

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103
Q

Give some examples of ‘holes/ connections of CHD?

A

ASD

PDA

VSD

AVSD

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104
Q

Give some examples of ‘narrowing/ stenosis’ of CHD?

A

Coarctation of the aorta (collapse with shock)

AS

PS

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105
Q

Give some examples of complex CHDs?

A

Tetralogy of Fallot

Transposition of the great arteries

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106
Q

What does right to left shunts cause?

A

Cyanosis

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107
Q

Signs of a possible CHD?

A
  • Poor feeding
  • Dyspnoea
  • Tachycardia
  • Cool peripheries
  • Acidosis on ABG
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108
Q

Investigations of CHD

A

FBC. CXR, PaO2, Echo +/- cardiac catheterisation

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109
Q

ATRIAL SEPTAL DEFECT

Causes?

A

Foetal alcohol syndrome,

common in trisomy 21

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110
Q

ATRIAL SEPTAL DEFECT

Types?

A
  • Ostium Primum 10%
  • Ostium Secondum 90%
    (10-15% of all CHDs)
  • AVSD
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111
Q

Listening to S2:

If it is split (double) during inspiration and single during expiration what does it mean?

A

Normal!

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112
Q

Listening to S2:

If it is split (double) all the time what does it mean?

A

ASD

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113
Q

Listening to S2:

If it is never split (double) what does it mean?

A

All other CHDs

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114
Q

ATRIAL SEPTAL DEFECT

Clinical features?

A

Fixed and widely split S2

ejection systolic murmur in pulmonary area

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115
Q

ATRIAL SEPTAL DEFECT

Investigations and management?

A

CXR

ECG

Surgical correction

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116
Q

PATENT DUCTUS ARTERIOSIS

What is it?

A

tube between the aorta and pulmonary artery that fails to close after birth

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117
Q

PATENT DUCTUS ARTERIOSIS

Clinical features?

A
  • poor feeding
  • Tachypnoea
  • Hepatomegaly
  • Oedema
  • Pneumonias
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118
Q

PATENT DUCTUS ARTERIOSIS

Severe clinical features?

A

CCF + pulmonary hypertension

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119
Q

PATENT DUCTUS ARTERIOSIS

Features on examination?

A

Large, bounding collapsing pulse

Heaving apex beat

Left subclavicular thrill

LOUD S2

gallop rhythm

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120
Q

PATENT DUCTUS ARTERIOSIS

murmur heard?

A

Classical continuous machinery murmur pulmonary area

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121
Q

PATENT DUCTUS ARTERIOSIS

Investigations?

A

ECG and CXR often normal

Echo- ensure no duct dependant circulation (e.g in pulmonary atresia)

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122
Q

PATENT DUCTUS ARTERIOSIS

management?

A

Ibuprofen/ Indomethacin (prostaglandin inhibitor) to close

Abolish lifelong bacterial endocarditis risk by SURGERY

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123
Q

VENTRICULAR SEPTAL DEFECT

what is there risk of?

A

HIGH risk of bacterial endocarditis

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124
Q

VENTRICULAR SEPTAL DEFECT

Clinical features?

A

Usually mild

  • poor feeding
  • Tachypnoea
  • Hepatomegaly
  • Oedema
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125
Q

VENTRICULAR SEPTAL DEFECT

Examination findings?

A

Thrill
Gallop rhythm
Active pre-cordium

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126
Q

VENTRICULAR SEPTAL DEFECT

What murmur is heard?

A

Harsh loud pansystolic mumur best heard in LLSE +/- thrill

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127
Q

VENTRICULAR SEPTAL DEFECT

Investigations?

A

Echo - precise defect

ECG - hypertrophy

CXR- cardiomegaly and enlarged PA + pulmonary oedema

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128
Q

VENTRICULAR SEPTAL DEFECT

Management?

A

Muscular VSDs 30% close spontaneously

Heart failure: Diuretics
additional calorie input

SURGERY to prevent damage to pulmonary capillary bed due to pulmonary HTN and high blood flow

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129
Q

ATRIOVENTRICULAR SEPTAL DEFECT

What is it common in?

A

Trisomy 21

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130
Q

ATRIOVENTRICULAR SEPTAL DEFECT

Clinical features?

A
  • poor feeding
  • Tachypnoea
  • Hepatomegaly
  • Oedema
  • Failure to thrive

EXAM

  • Thrill
  • Gallop rhythm
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131
Q

ATRIOVENTRICULAR SEPTAL DEFECT

Examination findings?

A

Present at antenatal US scan

Cyanosis at birth/ heart failure at 2-3 weeks

No murmur

Often detected by echo check up in Down’s

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132
Q

ATRIOVENTRICULAR SEPTAL DEFECT

Management?

A

Treat heart failure

Surgical repair at 3-6 months

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133
Q

COARCTATION OF THE AORTA

What is it?

A

Arterial duct tissue encirculing the aorta at the point it inserts into the duct:

1) Constricts aorta when duct closes
2) Obstruction to LV outflow

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134
Q

COARCTATION OF THE AORTA

Clinical features?

A

When ductus arteriosus closes; acute circulatory collapse

Weak femoral pulses

Radio-femoral delay

Heart failure

Metabolic acidosis

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135
Q

COARCTATION OF THE AORTA

Investigations and examination findings?

A

4 limb BP

Ejection systolic murmur

CXR- cardiomegaly

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136
Q

COARCTATION OF THE AORTA

Management?

A

Surgical repair by 5 years old

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137
Q

AORTIC STENOSIS

What is it?

A

Aortic valve leaflets partly fused together- restricted exit from LV

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138
Q

AORTIC STENOSIS

Clinical features?

A
  • Ejection systolic murmur - URSE!
  • Carotid thrill in suprasternal region
  • Critical AS- severe heart failure
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139
Q

AORTIC STENOSIS

Investigations, findings and management?

A

Radiograph- prominent LV

ECG

  • Regular echos
  • balloon valvotomy/ dilation

Valve replacement

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140
Q

PULMONARY STENOSIS

What is it?

A

pulmonary valve leaflets partly fused together which restricts exit from the RV

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141
Q

PULMONARY STENOSIS

Clinical features?

A

Systolic ejection murmur in ULSE

right ventricular heave

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142
Q

PULMONARY STENOSIS

Investigations and management?

A
  • ECG- upright T wave/ RV hypertrophy

CXR

Transcathether balloon dilation

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143
Q

TRANSPOSITION OF THE GREAT ARTERIES

What is the underpinning basic science?

A

1) Aorta connected to RV, pulmonary artery connected to LV (deoxygenated blood to body)
2) Incompatible with life (often have naturally occurring ASD,VSD, PDA)

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144
Q

TRANSPOSITION OF THE GREAT ARTERIES

Clinical features?

A
  • Cyanosis
  • S2 usually loud and singular
  • Reduced sats
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145
Q

TRANSPOSITION OF THE GREAT ARTERIES

Investigation?

A

Check for 22q deletion

CXR- narrow upper mediastinum ‘egg on side’ appearance of cardiac shadow

Echo- abnormal arterial connections

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146
Q

TRANSPOSITION OF THE GREAT ARTERIES

Management?

A

Maintaining patency of ductus arteriosus is key- prostaglandin infusion

Balloon atrial septostomy

Surgery- arterial switch procedure in first few days of life

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147
Q

TETRALOGY OF FALLOT

What are the 4 clinical features?

A
  • Large VSD
  • Overriding aorta
  • Sub pulmonary stenosis
  • RVH
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148
Q

TETRALOGY OF FALLOT

Signs and symptoms

A
  • Cyanotic
  • Breathlessness
  • Easy tiring
  • Low sats

Associated with Down’s and 22q deletions

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149
Q

TETRALOGY OF FALLOT

Investigations?

A

echo
CXR- small, up tilted, boot shaped apex

Harsh systolic murmur in LLSE

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150
Q

TETRALOGY OF FALLOT

Management?

A

Close VSD and relieve right ventricular outflow tract obstruction

  • Shunt to increase pulmonary blood flow
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151
Q

What is Ebstein’s Anomaly

A

Posterior leaflets of tricuspid valve displaced anteriorly

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152
Q

Cause of Ebsteins Anomaly?

A

Lithium in pregnancy (.eg.g bipolar mum)

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153
Q

What heart problems can develop due to Ebstein’s Anomaly

A

Tricuspid regurg
Tricuspid Stenosis
RA enlargement

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154
Q

Murmur heard in tricuspid regurg?

A

Pan-systolic

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155
Q

Murmur heard in tricuspid stenosis?

A

Mid-diastolic

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156
Q

KAWASAKI’S DISEASE

What is it?

A

Idiopathic systemic vasculitis that most commonly effects children 6 months- 5 years

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157
Q

KAWASAKI’S DISEASE

Major complication?

A

Coronary artery aneurysm formation

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158
Q

KAWASAKI’S DISEASE

Clinical presentation?

A

MyHEART

Mucosal Involvement:-inflamed dry lips/ strawberry tongue

Hand and feet swelling

Eyes- bilateral conjunctivitis

lymphAdenopathy (cervical)

Rash

Temperature- >5 days of fever

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159
Q

KAWASAKI’S DISEASE

3 Phases?

A 
Acute febrile (1-2 weeks)
Fever + 4 of criteria (MyHEART)

Subacute- remission of fever (4-6 weeks)
development of coronary artery aneurysms

Convalescent (6-12 weeks)
resolution of clinical signs + normalisation of inflammatory markers

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160
Q

KAWASAKI’S DISEASE

Ddx?

A
  • Measles
  • Rubella
  • Parvovirus B19 infx
  • Infectious Mononucleosis / Glandular Fever
  • Scarlet fever
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161
Q

KAWASAKI’S DISEASE

Investigations?

A 
Increased:
ESR&amp;CRP
WCC
Platelets
AST
a1-antitrypsin 
bilirubin

Echo is essential as it can reveal dilation and aneurysms of coronary arteries

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162
Q

KAWASAKI’S DISEASE

Treatment?

A
  • Aspirin
  • IV Immunoglobulins

(reduce the risk of aneurysms and thrombosis)

Echo 6 weeks later to check for aneurysms

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163
Q

KAWASAKI’S DISEASE

Tx for permanent inflammation?

A

Infliximab (anti-TNF)

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164
Q

HENOCH-SCHONLEIN PURPURA

What is it?

A

HSP is an IgA mediated, autoimmune hypersensitivity vasculitis of childhood

(Skin, joint, gut, kidneys)

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165
Q

HENOCH-SCHONLEIN PURPURA

Risk factors?

A

Infections ( group A strep, mycoplasma, EBV)

Vaccinations

Exposure to allergens, cold, pesticides

insect bite

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166
Q

HENOCH-SCHONLEIN PURPURA

Clinical presentation?

A
  • Fever
  • Rash
  • Abdo pain/symptoms
  • Renal involvement
  • Arthritis
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167
Q

HENOCH-SCHONLEIN PURPURA

Diagnostic tests?

A

urinanalysis- protein/ haematuria

Raised ESR

raised serum IgA

Raised WCC

Anti-streptolysin O titrates increased (36%)- detect group A strep

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168
Q

HENOCH-SCHONLEIN PURPURA

Treatment?

A

NSAIDs for joint pain

Corticosteroids for arthralgia

Most recover in 2 months

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169
Q

INFECTIVE ENDOCARDITIS

risk factors?

A

IV drug users
prosthetics
structural heart defects

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170
Q

INFECTIVE ENDOCARDITIS

What is it?

A

Infection of valves/ endocardium, causing destruction due to infective organisms forming vegetation.

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171
Q

INFECTIVE ENDOCARDITIS

Symptoms?

A
  • Fever
  • Weight loss
  • Night sweats
  • Anaemia
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172
Q

INFECTIVE ENDOCARDITIS

Symptoms?

A
  • Fever
  • Weight loss
  • Night sweats
  • Anaemia
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173
Q

HENOCH-SCHONLEIN PURPURA

Complications?

A

massive GI bleeds
ileus
Haemoptysis (rare)
AKI (rare)

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174
Q

HENOCH-SCHONLEIN PURPURA

Classic Triad?

A

1) Purpura (purple spots/nodules not dissapearing on palpation)
2) Arthritis/ arthralgia (74%)
3) Abdominal pain (51%)

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175
Q

HENOCH-SCHONLEIN PURPURA

worries if purpura is non blanching?

A

Meningococcal disease

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176
Q

HENOCH-SCHONLEIN PURPURA

worries if purpura is non blanching?

A

Meningococcal disease

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177
Q

RHEUMATIC FEVER

What is it?

A

x

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178
Q

RHEUMATIC FEVER

What is it?

A

Systemic febrile ilness- reaction to group A B-haemolytic strep

+ Pharyngitis

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179
Q

RHEUMATIC FEVER

What is the Jones diagnostic criteria?

A

1/2 major + 2 minor plus evidence of preceding strep infection (scarlet fever/ throat swab/ high serum ASO titre)

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180
Q

RHEUMATIC FEVER

Major signs?

A
  • Carditis(+ve echo, changed murmur, CCF, cardiomegaly)
  • Polyarthritis
  • Erythema marginatum
  • Subcutaneous nodules
  • Sydenham’s chorea- neurological manifestation
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181
Q

RHEUMATIC FEVER

Minor signs?

A
  • Fever
  • ^ ESR/ CRP
  • Arthralgia pain
  • ECG PR interval <0.2s
  • Previous rheumatic fever/ rheumatic heat disease
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182
Q

RHEUMATIC FEVER

Treatment?

A

Aspirin- careful of Reye’s

Benzylpenicillin then Phenoxymethylpenicillin for Pharyngitis (sore throat)

Prednisolone may help

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183
Q

RHEUMATIC FEVER

What is given for Synderham’s Chorea?

A

Prednisolone

consider haloperidol, carbemazepine, valproic acid

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184
Q

What is Haloperidol?

A

Anti-psychotic- used to treat psychotic disorders like Schizophrenia, Tourettes, severe behavioural problems in children

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185
Q

CHICKEN POX

What is it?

A

Highly infectious disease caused by varicella zoster virus (VZV)

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186
Q

CHICKEN POX

What does reactivation of VZV lead to?

A

Reactivation of dormant virus after a bout of chicken pox leads to herpes zoster (shingles) in posterior root ganglia

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187
Q

CHICKEN POX

Risk factors?

A
  • Immunocompromised
  • Older age
  • Steroid use
  • Malignancy
  • Dangerous in neonates and to the foetus if contracted in pregnancy
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188
Q

CHICKEN POX

How long are you infectious for?

A

Infective from 4 days prior to rash until all lesions have scabbed. (day 5)

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189
Q

CHICKEN POX

Clinical presentation?

A
  • temp 38-39
  • Headache, malaise
  • Crops of vesicles (itchy)
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190
Q

CHICKEN POX

Where are the vesicles normally found?

A

Mostly on the head, neck and trunk, very sparse on the limbs

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191
Q

CHICKEN POX

Cycle of a vesicle?

A

1) Macule
2) Papule
3) Vesicle (red surround)
4) Ulcers
5) Crust

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192
Q

CHICKEN POX

What does redness around the lesion suggest?

A

Bacterial superinfection

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193
Q

CHICKEN POX

Ddx?

A

Shingles- only one dermatome

(patient with vesicles at different stages of evolution in a one dermatome distribution)

  • Generalised herpes zoster/ simplex
  • Dermatitis herpetiformis
  • Impetigo
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194
Q

CHICKEN POX

Diagnostic tests?

A

Clinical

- Fluorescent antibody tests- test for IgM and IgG

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195
Q

CHICKEN POX

Complications?

A

Secondary bacterial infection of lesions

Pneumonia
Encephalitis
Disseminated haemorrhage chickenpox
Arthritis, nephritis, pancreatitis

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196
Q

CHICKEN POX

Treatment?

A

Calamine lotion

Antivaricella- zoister immunoglobulin &

Acyclovir (if severe) / at risk

Flucloxacillin in bacterial superinfection

  • 5 days off school for kids
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197
Q

CHICKEN POX

Treatment?

A

Calamine lotion

Antivaricella- zoister immunoglobulin &

Acyclovir (if severe) / at risk

Flucloxacillin in bacterial superinfection

  • 5 days off school for kids
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198
Q

MEASLES

How is it transmitted?

A

Respiratory droplets

incubation 7-12 days

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199
Q

MEASLES

What is it?

A

Acute viral infection caused by single stranded RNA morbillivirus from the paramyxovirus family

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200
Q

MEASLES

How long are you infectious for?

A

From prodrome until 4 days after the rash of measles appear

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201
Q

MEASLES

What is it?

A

NOTIFIABLE DISEASE

Acute viral infection caused by single stranded RNA morbillivirus from the paramyxovirus family

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202
Q

MEASLES

How long are you infectious for?

A

From prodrome until 4 days after the rash of measles appear

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203
Q

MEASLES

Cause?

A

RNA Morbillivirus from the paramyxovirus

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204
Q

MEASLES

Clinical presentation?

A
  • Rash for at least 3 days

Fever for at least one day (often >40) and at least one of:

Cough
Coryza
Conjunctivitis

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205
Q

MEASLES

What is the prodrome made up of?

A

3-5 days of the 4 C’s

  • Cough
  • Coryza
  • Conjunctivitis
  • Cranky

+ koplik’s spots on palate - small, red spots each with a bluish- white speck in the centre

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206
Q

MEASLES

Describe the measles rash

A

First seen on forehead, neck and behind the ears and spreads to limb/trnk over 3-4 days

Fades after 3-4 days

Leaves behind brown discolouration

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207
Q

MEASLES

Ddx?

A

Rubella
Parvovirus B19
Enterovirus
- Scarlet fever

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208
Q

MEASLES

Diagnostic tests?

A

Lab diagnosis:

IgM & IgG positive

Salivary swab or serum sample for measles specific immunoglobulin taken within 6 weeks of onset

RNA detection in salivary swabs

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209
Q

MEASLES

Treatment?

A

Paracetamol/ Ibuprofen + fluids

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210
Q

MEASLES

Complications?

A

more common if <5 years or >20 years

  • Otitis media
  • Croup/ tracheitis
  • Pneumonia
  • Encephalitis
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211
Q

MEASLES

Complication of vitamin A deficiency?

A

Blindness

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212
Q

MEASLES

What is the most common cause of death in measles?

A

Pneumonia

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213
Q

MEASLES

What may be a complication in older patients?

A

Encephalitis

Pneumonia

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214
Q

What is subacute sclerosing panencephalitis?

A

7-13 years post measles: chronic complication

Progressive changes in behaviour, myoclonus, dystonia, dementia > death

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215
Q

MEASLES

Risks in pregnancy?

A

Increased risk of miscarriage, prematurity and low birthweight

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216
Q

SCARLET FEVER

What is it?

A

NOTIFIABLE DISEASE

  • Endotoxin mediated disease arising from a specific bacterial infection by an erythrogenic toxin- producing strain of:
    strep. pyogenes- Group A haemolytic streptococci
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217
Q

SCARLET FEVER

Epidemiology?

A

87% under 10 years old

Unusual under 2 years

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218
Q

SCARLET FEVER

Clinical presentation?

A
  • Acute onset sore throat and fever then rash 24-48 hours after
  • Strawberry tongue
  • Scarletiniform rash:
    Typically appears first on chest, axilla, behind ears

then trunk and legs after

Around mouth (circumoral)

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219
Q

SCARLET FEVER

Describe the rash?

A

Red, ‘pin prick’ blanching rash

sandpaper/ rough- like

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220
Q

SCARLET FEVER

Describe the prodrome?

A
  • Sore throat + Tonsillitis
  • Fever
  • Headache
  • Vomiting and abdo pain
  • Myalgia
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221
Q

SCARLET FEVER

Complications?

A
  • Syndenhams Chorea
  • Otitis media
  • Rheumatic fever
  • Glomerulonephritis
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222
Q

SCARLET FEVER

Ddx?

A

other viral exanthema

  • Infectious mononucleosis (cause EBV)
  • Toxic shock syndrome
  • Kawasaki’s
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223
Q

SCARLET FEVER

Diagnosis?

A

Clinical
Throat swab
Antigen detection kits
- Strep antibody tests

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224
Q

SCARLET FEVER

Treatment?

A

Penicillin/ Azithromycin for 10 days

Rest, fluids, para/ ibuprofen

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225
Q

RUBELLA

What is it?

Causative organism?

A

NOTIFIABLE DISEASE

An RNA virus (Rubivirus Togaviridae), transmitted as droplets, with an incubation period of 14-21 days

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226
Q

RUBELLA

How long are you infectious for?

A

Infectious for up to 5 days before and 5 days after start of rash

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227
Q

RUBELLA

Describe the prodrome?

A
  • Lethargy
  • Low grade fever
  • Headache
  • Mild conjunctivitis
  • Anorexia
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228
Q

RUBELLA

Describe the rash?

A

Initially pink discrete macular rash that coalesce starting behind the ear and face, spreading the entire body

  • Suboccipital lymphadenopathy
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229
Q

RUBELLA

Ddx?

A
  • Contact dermatitis
  • Erythema multiforme/drug allergy
  • Measles
  • Scarlet fever
  • Kawasaki disease
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230
Q

RUBELLA

Diagnostic tests?

A

PCR testing

FBC shows low WBC with increased proportion of lymphocytes and thrombocytopenia

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231
Q

RUBELLA

Treatment?

A

Vaccine

Antipyretics for fever

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232
Q

RUBELLA

What can infections during fetal development cause?

A

wks 1-4 = eye anomaly (70%)

wks 4-8 = cardiac abnormalities (40%)

wks 8-12 = deafness (30%)

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233
Q

SLAPPED CHEEK SYNDROME (Erythrovirus)

What is it?

A

Parvovirus B19 transmitted through droplets

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234
Q

SLAPPED CHEEK SYNDROME (Erythrovirus)

Prodrome symptoms?

A

(around 1 week)

  • Mild
  • Headache, rhinitis, sore throat, fever, malaise

THEN- 1 week of symptom free

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235
Q

SLAPPED CHEEK SYNDROME (Erythrovirus)

What happens after the 7-10 days of no symptoms after the prodrome?

A

Classic ‘slapped cheek’ rash

1-4 days after the facial rash, erythematous macular morbilliform rash develops on the limbs

  • Arthralgia
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236
Q

SLAPPED CHEEK SYNDROME (Erythrovirus)

Ddx?

A

Rubella
Measles
Scarlet fever
EBV

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237
Q

SLAPPED CHEEK SYNDROME (Erythrovirus)

Diagnostic tests?

A

B19 specific IgM indicates current or recent infection

B19 specific IgG indicates immunity

PCR

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238
Q

cause of Impetigo?

A

staph aureus +/- strep pyogenes

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239
Q

What does Impetigo look like?

A

Well defined lesions starting around nose and face with honey/golden coloured crusts on erythematous base

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240
Q

Treatment to Impetigo?

A

Topical fusidic acid or oral flucloxacillin if severe

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241
Q

MENINGITIS

What is it?

A

When Micro-organisms reach the meninges by direct extension or by the bloodstream

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242
Q

MENINGITIS

Bacterial cause?

A
  • Neisseria meningitidis
  • Strep pnuemoniae
  • Haemophilus influenza

GREAT KILLERS = give benzylpenicillin immediately

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243
Q

MENINGITIS

Viral cause?

A 
Enterovirus
Mumps
HSV
HIV
EBV
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244
Q

MENINGITIS

Fungal cause?

A

Cryptococcus neoformans

Candida albicans

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245
Q

MENINGITIS

Risk factors?

A
  • Immunocompromised
  • Endocarditis
  • DM
  • Alcoholism and cirrhosis
  • IV drug abuse
  • Renal/adrenal insufficiency
  • Malignancy
  • SIckle cell disease

CROWDING

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246
Q

MENINGITIS

Pathophysiology?

Bacterial?

Viral?

A

BACTERIAL:
1) The pia-arachnoid is congested with polymorphs causing a layer of pus to form

VIRAL:
1) Lymphocytic inflammatory CSF without pus formation

2) No polymorphs/ adhesions
3) Little or no cerebral oedema unless encephalitis develops

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247
Q

MENINGITIS

Epidemilogy?

A

Common in infants, children or elderly

Viral meningitis> Bacterial

3,200 cases of bacterial per year

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248
Q

MENINGITIS

Septic signs?

(often before meningeal signs)

A
  • Malaise, fever, headache, temperature, rigor, vomiting
  • ^ HR/RR, reduced BP
  • Poor feeding
  • Abnormal cry
  • PETECHIAL PURPURIC RASH (NON-BLANCHING)- dont expect this
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249
Q

MENINGITIS

Meningeal signs?

(comparatively late, less common in young children)

A

Neck stiffness
Photophobia
Bulging fontanelle

+ve Kernigs (resistance to extending knee when hip is flexed)

+ve Brudzinki’s (neck flexion = hip flexion)

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250
Q

MENINGITIS

Ddx?

A
  • Subarachnoid haemorrhage
  • Migraine
  • Intracranial mass lesion
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251
Q

MENINGITIS

Diagnostic tests?

A
  • Lactate
  • FBC
  • Glucose
  • U&Es
  • Blood cultures
  • Throat swabs
  • Immediate lumbar puncture
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252
Q

MENINGITIS

Treatment?

A

Immediate IV Abx and blood/CSF cultures!
(Cefotaxime)

High flow O2

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253
Q

MENINGITIS

Treatment?

A

Immediate IV Abx and blood/CSF cultures!
(Cefotaxime)

High flow O2
Fluids if in shock

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254
Q

MENINGITIS

If this is suspected what must be given immediately to:

<3 months old?

> 3 months old - 18years?

In GP before hospital?

A

<3 months= Cefotaxime + Amoxicillin

> 3 months= Ceftriaxone + Dexamethasone

In GP = Benzylpenicillin (Cefotaxime if allergic)

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255
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

What is it?

A

Viral illness commonly causing lesions involving mouth hands and feet;

Transmitted by faecal-oral route

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256
Q

MENINGITIS

If this is suspected what must be given immediately to:

<3 months old?

> 3 months old - 18years?

In GP before hospital?

A

<3 months= Cefotaxime + Amoxicillin

> 3 months= Ceftriaxone + Dexamethasone

In GP = Benzylpenicillin (Cefotaxime if allergic)

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257
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Aetiology?

A

Coxsackievirus A16

Enterovirus 71

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258
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Epidemiology?

A

Common among infants younger than 10

outbreaks common in nurseries, schools and childcare centres

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259
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Epidemiology?

A

Common among infants younger than 10

outbreaks common in nurseries, schools and childcare centres

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260
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Prodrome?

A
  • Fever
  • Malaise
  • Loss of appetite
  • Sore mouth/throat
  • Cough
  • Abdo pain
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261
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Describe the mouth lesions?

A

On buccal mucosa, tongue or hard palate

Begin as macular lesions that progress to vesicles which then erode

YELLOW ULCERS SURROUNDED BY RED HALOES

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262
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Describe the skin lesions?

A

Palms, soles and between fingers/ toes

Erythematous macules but rapidly progress to grey vesicles with an erythematous base

Can also appear on trunk, thighs, buttocks, genitalia

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263
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Ddx?

A

Herpes simplex/ zoster virus

Chicken pox

kawasakis disease

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264
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Diagnostic tests?

A

Clinical diagnosis

swab of lesions

PCR

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265
Q

COXSACKIE’S DISEASE (HAND FOOT AND MOUTH)

Treatment?

A

Fluid intake
Soft diet
Para/ Ibuprofen

If mouth is very painful, use topical agents e,g, lidocaine oral gel

Stay off school until better

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266
Q

ENCEPHALITIS

Infective Causes?

A
  • HSV
  • Mumps
  • Varicella zoster
  • Rabies
  • Parvovirus
  • Immunocompromised
  • Influenza
  • TB
  • Toxoplasmosis
  • Malaria
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267
Q

ENCEPHALITIS

Clinical signs?

A
  • Flu like prodrome
  • Reduced consciousness
  • Odd behaviour
  • vomiting
  • Fits/ seizures
  • Raised temp
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268
Q

ENCEPHALITIS

Ix?

A
  • CSF, MC&S, PCR
  • Bloods
  • Stool (enteroviruses)
  • Urine
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269
Q

ENCEPHALITIS

Management?

A

HSE- Herpes simplex encephalitis= most treatable = Acyclovir

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270
Q

TUBERCULOSIS

When should you suspect?

A

IF:

Overseas contact
HIV +ve
Odd CXR

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271
Q

TUBERCULOSIS

Clinical signs

A 
Anorexia
Low fever
failure to thrive
cough 
malaise
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272
Q

TUBERCULOSIS

Diagnosis?

A

Tuberculin tests

Interferon gamma release assays/ Mantoux

Sputum culture + ziehl-neelson stain x3

CXR- consolidation, military spots (fine white dots on CXR- rare)

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273
Q

TUBERCULOSIS

Management?

A

Expert help;

Isoniazid (6 months)
Rifampicin (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)

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274
Q

TUBERCULOSIS

Tests?

A

Zeihl-Neeson Test with a Lowenstein Jenson culture medium

Mantoux test
Interferon gamma testing

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275
Q

TUBERCULOSIS

Complications?

A

1) Pleural effusion
2) Pericardial effusion
3) Lung collapse
4) Lung consolidation (becomes solid)

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276
Q

TUBERCULOSIS

Side effects of Isoniazid?
Rifampicin?

A

Isoniazid: neuropathy, low WCC, inhibits CYP450

Rifampicin: pink urine, low platelets, induces CYP450, Flu symptoms

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277
Q

TUBERCULOSIS

Side effects of Pyrazinamide?
Ethambutol?

A

Pyrazinamide: Rash/ arthralgia

Ethambutol: Optic Neuritis

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278
Q

TUBERCULOSIS

Tx of latent TB?

A

Isoniazid for 6 months

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279
Q

HIV

When should this be diagnosed in childhood?

A

AIM: Before 1st birthday

tests at 3&6 months:
HIV viral PCR
p24 antigen
Specific IgA

  • Monitor CD4 count
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280
Q

HIV

When should you consider HIV in children?

A
  • Unknown pyrexia (PUO)
  • Parotid enlargement
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Slow to clear infections
  • Persistent diarrhoea
  • Shingles
  • Reduced platelets
  • with TB/ pneumocytosis
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281
Q

HIV

When should HAART begin

A

Those with AIDs defining conditions / CD4 <15%

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282
Q

TOXIC SHOCK SYNDROME

Characteristics?

A
  • Fever >39 degrees
  • Hypotension
  • Diffuse erythematous, macular rash
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283
Q

TOXIC SHOCK SYNDROME

How is the toxin produced?

A

by s.aureus + group A strep

Toxin acts as a super antigen that can cause organ dysfunction, it can be released from infection at any site

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284
Q

TOXIC SHOCK SYNDROME

Management?

A

Intensive care

Infection areas- surgically debrided

Abx- Ceftriaxone + Clindamycin

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285
Q

BIRTH MARKS AND RASHES

What are strawberry marks?

A

Cavernous haemangioma

normally self limiting but beware over eye and in airway

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286
Q

BIRTH MARKS AND RASHES

What is a Port Wine Stain?

A

permanent capillary haemangioma

seen in Sturge-Weber Syndrome

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287
Q

BIRTH MARKS AND RASHES

What syndrome are moles common in? (Naevi)

A

Turner’s

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288
Q

BIRTH MARKS AND RASHES

What are mongolian blue spots?

A

non- caucasian ancestry

Congential dermal melanocytosis

Commonly seen on lower back/ buttocks

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289
Q

BIRTH MARKS AND RASHES

What are cafe au lait spots?

A

flat light brown patches on the skin.

Over 5 = Neurofibromatosis

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290
Q

BIRTH MARKS AND RASHES

What are Milia (milk spots)?

A

sebaceous plugs from sweat glands

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291
Q

BIRTH MARKS AND RASHES

What are infantile urticaria?

A

erythema toxicum neonatorum-

Histamine reaction

Harmless red blotches- come and go in crops

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292
Q

Key points to remember in chickenpox?

A

beware in immunocompromised

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293
Q

Key points to remember in Measles?

A

Prodromal CCCK

  • Cough
  • Coryza
  • Conjunctivitis
  • Koplik spots (inside mouth)
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294
Q

Key points to remember in Parvovirus?

A

slapped cheek

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295
Q

Key points to remember in Coxsackie?

A

Hand, foot and mouth

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296
Q

Key points to remember in Mumps?

A

prodromal malaise

Parotids

can cause orchitis and infertility

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297
Q

What is Molluscum contagiosum?

A

pox like nodules that last for months, generally in axilla

298
Q

What do you call a rash that accompanies a disease/ fever?

A

Exanthema

299
Q

What rash is diabetes associated with

A

Acanthosis nigricans

300
Q

Cause of Toxoplasmosis?

A

Infected cat faeces-

  • Microcephaly
  • Fits
  • Sensorineural deafness
301
Q

What infections are associated with Cat/Dog faeces?

A

Cat- Toxoplasmosis (fits, deafness)

Dog- Toxocara (acquired blindness)

302
Q

What is Toxocara?

A

Infected associated with eating dog faeces

303
Q

What is Urticaria?

A

‘nettle-like’ rashes, raised and itchy patches

allergen exposure,

linked to child abuse if late presentation, symmetry, odd history

304
Q

TORCH

What is a TORCH infection and what does it stand for?

A

Infection to the developing foetus/ newborn by any of:

Toxoplasmosis
Other agents
Rubella (german measles)
Cytomegalovirus
Herpes simplex
305
Q

TORCH

Signs of CMV?

A
  • Growth retardation
  • Microcephaly
  • Hepatosplenomegaly
  • Hepatitis
  • Anemia/jaundice/ thrombocytopenia
306
Q

TORCH

What is the most common congenital infection in the U.K?

A

Cytomegalovirus

CMV

307
Q

TORCH

Signs of Rubella?

A

Sensorineural deafness

congenital cataracts + glaucoma

heart disease (PDA)

308
Q

TORCH

Signs of Toxoplasmosis?

A
  • Cerebral calcification
  • Microcephaly/ hydrocephalus
  • Chorioretinitis
  • Cerebral palsy
309
Q

How is Toxoplasmosis diagnosed, what is the cause and what is the treatment?

A

Diagnosed by serology >95% asymptomatic

Caused by raw meat/ cat faeces

Tx= Pyrimethamine + Sulphadiazine + Spiramycin

310
Q

TORCH

GIve examples of ‘other’ infections?

A
  • Syphillis
  • Varicella- zoster
  • Parvovirus B19
311
Q

TORCH

Treatment of Syphillis?

Treatment of Herpes Simplex?

A

Benzylpenicillin

Acyclovir

312
Q

TORCH

Signs of Herpes Simplex?

A 
Blindness
Low IQ
epilepsy
Jaundice
Resp distress
30% die even when treated
313
Q

ECZEMA

How common is it?

A

15-20% of children and is becoming more common

314
Q

What is Eczema Herpeticum?

A

Severe infection of skin (HSV 1+2)

more commonly seen in kids with eczema, potentially life threatening = treat with Acyclovir

315
Q

Causative drugs of Stevens- Johnson Syndrome?

Presentation?

A
  • Sulfonamides
  • Anti- epileptics
  • Penicillin
  • NSAIDs

Painful erythematous macules, severe mucosal ulceration

316
Q

ANAPHYLAXIS

What is it and how is it diagnosed?

A

severe life threatening hypersensitivity reaction of sudden onset

ABC

317
Q

ANAPHYLAXIS

What may bring on the IgE mediated reaction?

A 
foods
insect sting
drugs
latex
exercise
inhaled allergens
318
Q

ANAPHYLAXIS

Cause of fatal anaphylaxis’ in adults?

A

Mainly nuts

319
Q

ANAPHYLAXIS

Management?

A

ABCDE

IM Adrenaline
Under 6 months: 0.01mg
6 months to 6 years: 0.15mg
6-12 years: 0.3mg
Over 12 years: 0.5mg

Antihistamine
Hydrocortisone
Salbutamol if wheeze

high flow O2
IV fluids

Monitor pulse oximetry, ECG, BP

320
Q

What is classed as low birth weight?

Extremely low?

Incredibly low?

A

<1500g

<1000g

<750g

ensure adequate resus once born

321
Q

FAILURE TO THRIVE

Definition?

A

Failure to gain adequate weight or achieve adequate growth at the normal rate for age

322
Q

What is the key determinant in questioning health of child?

A

Growth

323
Q

FAILURE TO THRIVE

Most common cause?

A

Inadequate calorie intake:

Poor breastfeed technique

Poverty

Unsuitable food offered

Neglect

324
Q

CHILDHOOD DEVELOPMENT

4 Domains of development?

A
  • Gross motor
  • Fine motor and vision
  • Language and hearing
  • Social
325
Q

CHILDHOOD DEVELOPMENT

What is developmental surveillance?

A

Ongoing process of following child over time- can be incorporated into well-child checks, general physical examination, routine immunisation visits

326
Q

CHILDHOOD DEVELOPMENT

Definition of Dev Delay?

Definition of Dev Disorder?

A

Dev. Delay- along normal route but takes longer to reach milestones

Dev. Disorder- does not follow normal pattern, impairment

327
Q

CHILDHOOD DEVELOPMENT

Risk factors?

A

Biological:

  • Prematurity
  • Low birth weight
  • birth asphyxia
  • hearing/vision impairment

Environmental:

  • poverty
  • poor parental education
  • maternal alcohol/drugs
328
Q

CHILDHOOD DEVELOPMENT

What is the ‘stepping’ reflex and when should it be seen?

A

1) hold baby upright with one sole on table top
2) Hip and knee will flex and other foot step forward

(birth - variable [6 weeks])

329
Q

CHILDHOOD DEVELOPMENT

What are the ‘Palmar’ and ‘plantar’ grasp reflexes and when should it be seen?

A

touch hand/ soles and baby will grasp / curl toes

palmar = until 6 months

plantar = until 9-12 months

330
Q

CHILDHOOD DEVELOPMENT

What is the ‘moro’ reflex and when should it be seen?

A

1) hold baby supine and abruptly lower the body about 2 feet.
2) Arms will abduct/extend and legs flex

(until 2 months)

331
Q

CHILDHOOD DEVELOPMENT

What is the ‘tonic neck’ reflex and when should it be seen?

A

1) baby supine, turn head to one side and hold jaw on shoulder
2) Arms/ legs the heads turned to will extend and opposite will flex

(until 6 months)

332
Q

CHILDHOOD DEVELOPMENT

What is the ‘sucking and rooting’ reflex and when should it be seen?

A

1) stroke perioral skin at corner of the mouth
2) mouth will open and baby will turn head toward stimulus and suck

(until 4 months)

333
Q

Name the primitive reflexes

A

Atonic neck reflex

Moro reflex

Landau reflex

Plantar grasp reflex

Palmar grasp reflex

Parachute reflex

Positive support reflex

Rooting reflex

Stepping reflex

Trunk incurvation

A M L PPPP R S T

334
Q

CHILDHOOD DEVELOPMENT

What is the ‘trunk incurvation’/ Galant’s reflex and when should it be seen?

A

1) support baby prone and stroke one side of the back
2) spine will curve towards stimulated side

(0-2 months)

335
Q

CHILDHOOD DEVELOPMENT

What is the ‘Landau’ reflex and when should it be seen?

A

1) suspend baby prone
2) head will lift up and the spine will straighten

(0-6 months)

336
Q

CHILDHOOD DEVELOPMENT

What is the ‘Parachute’ reflex and when should it be seen?

A

1) suspend baby prone and slowly lower the head towards a surface
2) arms and legs will extend in a protective fashion

(8 months onwards)

337
Q

CHILDHOOD DEVELOPMENT

What is the ‘Positive support’ reflex and when should it be seen?

A

1) hold baby upright until feet touch a surface
2) hips, knees and ankles will extend and partially bear weight for 20/30 seconds

(0-6 months)

338
Q

What are the postural reflexes?

A
  • Parachute
  • Positive support
  • Landau
  • Neck/ head righting reflexes
  • Lateral propping
339
Q

What does persistence of primitive reflexes and lack of development of postural reflexes show?

A

Hallmark of motor neuron abnormality in the infant

340
Q

Definition of childhood disability and 2 examples?

A

Physical or mental impairment preventing them going about their daily life

1) Down’s
2) Cerebral Palsy

341
Q

CEREBRAL PALSY

What is it?

A

Chronic disorder of movement and posture attributed to non-progressive disturbances that occurred in the fetal brain.

342
Q

CEREBRAL PALSY

other problems as well as movement/posture?

A
  • Cognition
  • Communication
  • Perception
  • Sensation
  • Behaviour
  • Seizures
343
Q

CEREBRAL PALSY

Antenatal causes?

A

80% antenatal e.g vascular occlusion/ congenital infection (CMV, toxo, rubella)

10% birth asphyxia/trauma

344
Q

CEREBRAL PALSY

Postnatal causes?

A
  • Meningitis/ encephalitis/ encephalopathy
  • Head trauma
  • Intraventricular haemorrhage
345
Q

CEREBRAL PALSY

Clinical presentation?

(motor)

A
  • Abnormal limb/trunk posture and tone
  • Delayed motor milestones
  • Abnormal gait
346
Q

CEREBRAL PALSY

Clinical presentation?

(non-motor)

A
  • feeding difficulties
  • learning difficulties
  • epilepsy
  • language/speech difficulties
  • persistent primitive reflexes
347
Q

CEREBRAL PALSY

How is functional ability described/assessed?

A

Gross Motor Function Classification System (GMFCS)

348
Q

CEREBRAL PALSY

What are the 5 levels of the GMFCS?

A

Level 1- walks without limitation

Level 2- walks with limitations

Level 3- walks using handheld mobility device

Level 4- self mobility with limitations may use powered mobility

Level 5- manual wheelchair transportation

349
Q

CEREBRAL PALSY

Diagnosis?

A

Made on clinical presentation

MRI can identify cause but not routinely used for diagnosis

350
Q

CEREBRAL PALSY

What are the 4 clinical subtypes?

A
  • Spastic
  • Dyskinetic
  • Ataxic
  • Mixed
351
Q

CEREBRAL PALSY

Describe Spastic (90%)

A
  • Damage to UMN pathway
  • Limb tone persistently increased (spastic)
  • Brisk deep tendon reflexes
  • Clasp knife reflexes
352
Q

CEREBRAL PALSY

Types of spastic?

A

Hemiplegia
Diplegia
Quadriplegia

353
Q

CEREBRAL PALSY

What is quadriplegia associated with?

A
  • Seizures
  • Low IQ
  • Swallowing difficulties
354
Q

CEREBRAL PALSY

Decribe Dyskinetic

A
  • Movements of involuntary control
  • Muscle tone variable

Chorea

Athetosis

Dystonia

355
Q

what is Chorea?

A

Jerky movements

356
Q

what is Athetosis?

A

slow writhing movements distally eg fanning fingers

357
Q

what is Dystonia?

A

twisting appearance from simultaneous contraction of agonist and antagonist muscle groups

358
Q

CEREBRAL PALSY

What damage is associated with Ataxic CP

A

cerebellum damage

359
Q

CEREBRAL PALSY

What damage is associated with Dyskinetic CP

A

basal ganglia damage

360
Q

CEREBRAL PALSY

Describe Ataxic

A
  • poor balance
  • delayed motor development
  • can be hypo/ hypertonia
  • uncoordinated , intention tremor and ataxic gait (evident later on)
361
Q

What is Ataxia?

A

Lack of voluntary co-ordination of muscle movements that can include ataxic gait, speech and abnormal eye movements

362
Q

CEREBRAL PALSY

Tx for spasticity?

A

Oral Diazepam

Baclofen

Botulinum toxin (botox) for relaxing muscles

363
Q

CEREBRAL PALSY

Professionals involved?

A
  • Physiotherapist
  • Speech Therapist
  • Occupational Therapist
  • Orthoptist/ Audiologist
  • Dietitian
  • Social worker
364
Q

DOWN’S SYNDROME

What is it?

A

Trisomy 21

Cognitive impairment can be variable

365
Q

DOWN’S SYNDROME

Risk factors?

A

Family Hx
Old maternal age

.40 increases risk of non-dysjunction

366
Q

DOWN’S SYNDROME

Clinical presentation?

Cardio
GI
Eyes
Ears

A

Cardio Disorders (VSDs, Tetralogy of Fallot)

90% have hearing loss (sensorineural&conductive)

Eyes - Brushfield spots, cataracts, nystagmus, stabismus

GI- Atresias, Hirschsprungs, pyloric stenosis, Meckel’s diverticulum

367
Q

DOWN’S SYNDROME

Facial features?

A
  • Epicanthic folds
  • Protruding tongue
  • Small low set ears
  • Flat occiput + facial profile
  • High arched palate
368
Q

DOWN’S SYNDROME

Clinical features?

Orthopaedic
Endocrine
Neuro
Haemotological

A

Ortho- Hypotonia, short stature, single palmar crease, sandal gap deformity

Endo- hypothyroid

Neuro- learning difficulties, low IQ, Seizures, Dementia

Haem- 12x greater risk of infections due to impaired cellular immunity, increased risk of AML, ALL
Polycythaemia

369
Q

EDWARD’S SYNDROME

What is it?

A

Trisomy 18

80% female

Severe psychomotor + growth retardation in those that survive 1st year of life

370
Q

EDWARD’S SYNDROME

Skeletal abnormalities?

A

Typical hand feature

Radial/ Thumb aplasia

Short sternum- nipples look widely spread

Rocker bottom feet (flat)

Microcephaly/ microstomia

371
Q

EDWARD’S SYNDROME

Craniofacial abnormalities?

A
  • Odd low set ears
  • Micrognathia (small jaw)
  • Prominent occiput
372
Q

EDWARD’S SYNDROME

What is the typical hand posture?

A

Fingers cannot be extended:

Index overriding middle finger

5th finger overriding 4th finger

373
Q

PATAU’S SYNDROME

What is it?

A

Severe physical and mental congenital abnormalities due to

Trisomy 13

374
Q

PATAU’S SYNDROME

Clinical presentation?

A

Congenital heart defects

IUGR and low BW

polydactyly and rocker bottom feet

Severe learning difficulties

Cleft lip palate

375
Q

PATAU’S SYNDROME

What is Holoprosencephaly?

A

the brain doesnt divide into two halves

376
Q

PATAU’S SYNDROME

Facial features?

A

Cleft lip and palate

Microphthalmia

Hypotelorism (reduced distance between eyes)

377
Q

PATAU’S SYNDROME

Treatment?

A

Prognosis is BAD- average survival is 2.5 days.

50% live longer than one week

5-10% live longer than one year

378
Q

Give examples of Genomic imprinting?

pair of genes come from one parent

A

Angelmans

Prader Willi

379
Q

Give an example of a Minosomy disorder?

A

Turner’s syndrome

380
Q

Give 5 examples of Trisomy disorders

A

Downs
Edwards
Pataus

XXX syndrome

Klinefelter’s

381
Q

Give examples of Autosomal Dominant conditions

A

Huntingtons

Neurofibromatosis

Hereditary spherocytosis

Marfans

382
Q

Give examples of Autosomal recessive conditions

A

CF

Albinism

PKU (phenylketouria)

383
Q

Give examples of X linked inheritance conditions

A

Duchenne’s muscular dystrophy

Red-green colour blindness

G6PD deficiency

Haemophilia A/B

384
Q

PRADER-WILLI SYNDROME

What is it?

A

First human disorder attributed to genomic imprinting

Characteristics

Infant: Hypotonia and development delay

Adolescence: Obesity, learning and behavioural difficulties (especially food)

385
Q

PRADER-WILLI SYNDROME

Cause?

A

Deletion in the paternally inherited chromosome 15 or maternal uniparental disomy 15

OPPOSITE TO ANGELMAN’S

386
Q

PRADER-WILLI SYNDROME

Clinical presentation?

(Infant)

A
  • Hypotonia at birth
  • Failure to thrive/ poor feeding
  • Genital hypoplasia
  • Delayed motor milestones

USUALLY blue eyes blonde hair

387
Q

PRADER-WILLI SYNDROME

Clinical presentation?

(Childhood)

A
  • Hyperphagia (always hungry)

Obesity (due to ^)

Short stature

Behavioural problems

Low IQ

388
Q

PRADER-WILLI SYNDROME

Treatment?

A

Growth Hormone

Anti-psychotics- Olanzapine, haloperidol

Fluoxetine and SSRI’s are sometimes efftective

389
Q

ANGELMAN’S SYNDROME

What is it?

A

Genetic imprinting disorder due to maternal deletion of chromosome 15

OPPOSITE OF PRADER WILLI

390
Q

PRADER-WILLI SYNDROME

Why do patients have hyperphagia?

A

Markedly elevated levels of ghrelin, hormone associated with hunger

391
Q

ANGELMAN’S SYNDROME

Clinical presentation?

A

developmental delay

Motor milestones delayed

Speech impairment

behavioural signs

Ataxia (broad based gait)

Strabismus

Drooling

Fascination with water

Epilepsy 90%

Microcephaly

392
Q

ANGELMAN’S SYNDROME

behavioural signs?

A
  • Short attention span
  • Laughter and happiness/ excited
  • Laughs at most stimuli
  • Hand flapping common
  • Tendency to pinch/grab/bite
  • Fascination with water
393
Q

ANGELMAN’S SYNDROME

Facial features?

A 
Microcephaly
flat occiput
Prominent mandible
wide mouth
wide spaced teeth
drooling/ tongue thrusting
394
Q

ANGELMAN’S SYNDROME

Diagnosis?

A

Chromosomal analysis

v similar to autism

Fluorescence in situ hybridisation (FISH) is able to detect 80-85% of all deletions.

395
Q

ANGELMAN’S SYNDROME

Treatment?

A

Behavioural modification programmes

speech therapy

physio therapy

Parental education

Anti-convulsants for Epilepsy- valproate/ clonazepam

396
Q

TURNER’S SYNDROME

What is it?

A

Loss or abnormality of the second X chromosome

almost all affected infertile and many girls experience only short stature and ovarian failure

397
Q

TURNER’S SYNDROME

What is there increased risk of?

A

Increased risk of CHD

Renal malformations

Hearing loss

osteoporosis

Obesity

Diabetes

Atherogenic lipid profile

398
Q

TURNER’S SYNDROME

Clinical presentation of a Newborn?

A

Lymphoedema

  • Cardiac/renal abnormalities

(coarctation, asbence of kidney)

399
Q

TURNER’S SYNDROME

Clinical presentation of an infant?

A
  • Short stature
  • Webbed neck
  • Broad chest/ widely spaced nipples
  • Bicuspid aortic valve (15%)
  • Coarctation of the aorta (10%)
  • high arched palate
  • Behavioural problems
  • Recurrent otitis media/ hearing loss
400
Q

TURNER’S SYNDROME

Clinical presentation of adolescence?

A

Gonodal dysgenisis:

Absent/incomplete puberty

Amenorrhoea

Impaired growth

401
Q

NOONAN’S SYNDROME

What is it?

A

Autosomal dominant condition characterised by:
- CHD,

short stature,

broad/webbed neck,

sternal deformity,

developmental delay,

cryptochidism (1 testes drops)

increased bleeding tendency

characteristic facial features.

402
Q

TURNER’S SYNDROME

Associated with what?

A

Autoimmune conditions:

Thyroid
Diabetes
Coeliac
Crohn’s

403
Q

TURNER’S SYNDROME

Diagnostic tests?

A
  • Can be diagnosed by amniocentesis or chorionic villous sampling
  • Chromosomal analysis
404
Q

TURNER’S SYNDROME

Treatment?

A

treat complications and monitor autoimmune associations

SHORT STATURE: recombinant human growth hormone

Oestrogen (12 years) to initiate puberty and prevent osteoporosis

405
Q

NOONAN’S SYNDROME

Cause?

A

Caused by mutations in the RAS/ MAPK pathway

406
Q

NOONAN’S SYNDROME

Epidemiology?

A

Autosomal dominant

60% are new spontaneous mutations

407
Q

NOONAN’S SYNDROME

Facial appearance?

A

wide, tall forehead

Hypertelorism

Ptosis/ down slanting eyes

Low set ears

408
Q

NOONAN’S SYNDROME

MSK presentation?

A

short webbed neck
broad chest with widely spaced nipples

Pectus carinatum superiorly

Pectus excavatum inferiorly

short fingers and short stature

409
Q

NOONAN’S SYNDROME

Appearance in general?

A

striking blue/green irises

curly or wooly hair

410
Q

NOONAN’S SYNDROME

neuro/ haem/ cardiac/ feeding problems?

A

feeding and growth problems

Neuro: Learning disaility/ developmental delay

bleeding disorders with easy bruising/ bleeding

Cardiac: Pulmonary stenosis/ hypertrophic cardiomyopathy

411
Q

NEUROFIBROMATOSIS

What is it?

A

Autosomal dominant disorder that encompass the rare diseases NF1, NF2 and Schwannomatosis

412
Q

NEUROFIBROMATOSIS

What is NF1?

A

More common and caused by a defect to the NF1 gene- Skin lesions

413
Q

NEUROFIBROMATOSIS

What is NF2?

A

Central form with CNS tumours rather than skin lesisons.

Inherited schwannomas, typically bilaterally, also meningiomas and ependymonas

414
Q

NEUROFIBROMATOSIS

What is Schwannomatosis?

A

recently recognised form, characterised by multiple non cutaneous schwannomas which is a histologically benign nerve sheath tumour

415
Q

NEUROFIBROMATOSIS

Epidemiology?

A

50% have no family Hx

416
Q

NEUROFIBROMATOSIS

Clinical presentation of NF1?

A

Cafe-au-lait spots

Freckling in skin folds

Neurofibromas

Lisch nodules

Short stature and macrocephaly

417
Q

NEUROFIBROMATOSIS

Complications of NF1?

A

Mild learning difficulties

Nerve root compression from neurofibromas

Increased risk of malignancy e.g. optic glioma

418
Q

NEUROFIBROMATOSIS

Presentation of NF2?

A

45% have hearing problems

Schwannomas bilaterally, especially vestibular nerve (cranial/spinal)

Meningiomas/ ependymomas

presents generally in 20s

419
Q

NEUROFIBROMATOSIS

Difference between NF1&NF2?

A

Rarely more than 6 cafe-au-lait spots in NF2, not as many as NF1.

420
Q

NEUROFIBROMATOSIS

diagnostic criteria?

(NF1)

A

2 OR MORE OF:

1) 6+ cafe au lait spots (>5mm kids, >15mm older)
2) 2 or more neurofibromas
3) Freckling (skin folds)
4) Optic glioma
5) Lisch nodules (clumps of pigment in eyes)
6) Bone abnormalities ( sphenoid dysplasia- absence of bone around eyes)
7) Parent/sibling/child with NF1

421
Q

NEUROFIBROMATOSIS

Treatment?

A

Intervene appropriately where tumours produce pressure symptoms or suggestive of malignant change

Possible surgery

422
Q

FRAGILE X SYNDROME (MARTIN-BELL)

Cause?

A

FMR1 gene includes a CCG repeat.

As its passed from each generation it lengthens.

Once it reaches >200 no fragile X protein is made.

TRINUCLEOTIDE REPEAT DISORDER

423
Q

FRAGILE X SYNDROME (MARTIN-BELL)

Clinical Signs?

A

Delayed speech + language

Delayed motor milestones secondary to hypotonia

Low IQ/ learning difficulties

hyperactivity/ emotional & behavioural problems

Autism

424
Q

FRAGILE X SYNDROME (MARTIN-BELL)

Physical symptoms?

A

Long, narrow face

Large ears

Prominent jaw

Big testes

425
Q

FRAGILE X SYNDROME (MARTIN-BELL)

Ix and Tx?

A

Molecular genetic testing of FMR1 gene

Minocycline = shows improvement in behaviour

426
Q

KLINEFELTER SYNDROME

What is it?

A

47XXY

chief genetic cause of hypogonadism

427
Q

KLINEFELTER SYNDROME

Clinical presentation?

A

Gyaecomastia

Infertility

taller than average

small testes/penis

Delayed/ absent puberty

less body hair, broader hips, longer legs

428
Q

KLINEFELTER SYNDROME

Associations?

A

Psychosocial issues

Learning disability

Autoimmune disease

Osteoporosis

Decreased Sexual Maturation

429
Q

KLINEFELTER SYNDROME

Management

A

Androgen therapy

mastectomy (gynaecomastia)

lifespan normal
Arm span may be longer than body length

430
Q

Key Features of:

Patau Syndrome?

A

Microcephalic
small eyes
cleft lip/palate
scalp lesions

431
Q

Key Features of:

Edward’s Syndrome?

A

Micrognathia
Low set ears
Rocker bottom feet
Overlapping of fingers

432
Q

Key Features of:

Fragile X Syndrome?

A 
learning difficulties
macrocephaly
long face
large ears
Macro-orchidism
433
Q

Key Features of:

Noonan Syndrome?

A

webbed neck
pectus excavatum
short stature
pulmonary stenosis

434
Q

Key Features of:

Pierre- Robin Syndrome?

A

micrognathia
posterior displacement of the tongue (UAO)
cleft palate

435
Q

Key Features of:

Prader- Willi Syndrome?

A

Hypotonia
Hypogonadism
Obesity/ Hyperphagia

436
Q

Key Features of:

William’s Syndrome?

A

short stature

learning difficulties

friendly, extrovert personality

transient neonatal hypercalcaemia

Supravalvular aortic stenosis

437
Q

AUTISM

What is it?

A

neurodevelopmental disorder that includes a range of possible impairments in social interaction, repetitive behaviour and communication.

438
Q

AUTISM

Definition?

A

the presence of abnormal or impaired development that is manifest before the age of 3.

439
Q

AUTISM

Three characteristics of abnormal functioning?

A

1) Reciprocal social interaction
2) Impairment of language and communication
3) Restricted, repetitive behaviour

440
Q

AUTISM

Male to female ratio?

A

3/4:1

75% male

441
Q

AUTISM

Clinical presentation?

A
  • Communication difficulties
  • Social interaction
  • Difficulties with imagination/ rigidity of thought
442
Q

AUTISM

Examples of social interaction difficulties?

A
  • no desire to interact with others
  • oblivious to others feelings
  • no understanding of unspoken social rules
  • lack of empathy
  • poor eye contact
443
Q

AUTISM

Examples of imagination difficulties?

A

restrictive/ repetitive behaviours

obsessive fixations

inability to play/write imaginatively

same questions

444
Q

AUTISM

Examples of communication difficulties?

A

repeats speech

disordered language

poor non-verbal communication

no social awareness, unable to start up or keep a conversation

445
Q

AUTISM

Associated medical problems?

A

epilepsy 25-30%

visual and hearing impairment

mental health (ADHD, depression, anxiety)

446
Q

AUTISM

Treatment?

A

Early behavioural intervention

education for parents

Support in schools

447
Q

AUTISM

Treatment for Aggression/irritability?

A

Risperidone

448
Q

AUTISM

Treatment for sleep difficulties?

A

Melatonin

449
Q

AUTISM

Treatment for repetitive behaviours?

A

SSRI’s

450
Q

ASPERGER’S SYNDROME

What is it?

A

Pervasive development disorder which lies within the autistic spectrum.

451
Q

ASPERGER’S SYNDROME

Ratio of boys to girls?

A

Boys 8:1 Girls

452
Q

ASPERGER’S SYNDROME

Difference to autism?

A
  • lack of delayed cognition and language,
  • aspergers are above average intelligent
  • Aspergers are more likely to seek social interaction and share activities/ friendships
453
Q

ASPERGER’S SYNDROME

Clinical presentation?

A
  • Obsessed with complex subjects
  • concrete thinking
  • Pedantic
  • Normal speech
  • Clumsiness
  • Solitary but socially aware
  • Poor sleep patterns
454
Q

ADHD

What is the criteria?

A

1) Present before 12
2) developmentally inappropriate
3) Severel symptoms in multiple settings
4) clear effect on social/academic/ occupational functioning

455
Q

ADHD

How many inattentive and hyperactive symptoms must be evident?

A

6/9 inattentive

6/9 hyperactive/impulsive symptoms

456
Q

ADHD

Cause?

A

Prematurity

Fetal alcohol syndrome

457
Q

ADHD

3 core symptoms?

A
  • Hyperactivity
  • Inattention
  • Impulsivity
458
Q

ADHD

inattentive symptoms?

(9)

A

1) easily distracted
2) does not appear to be listening when spoken to
3) has difficulty sustaining attention
4) avoids/ dislikes sustained mental effort
5) forgetful in daily activities
6) difficulty following instructions/ fails to complete tasks
7) difficulty organising tasks
8) careless mistakes/ lack of attention to detail
9) loses important items

459
Q

ADHD

Hyperactive/ impulsive symptoms?

(9)

A

Hyperactive:

1) squirms/ fidgets
2) cannot remain seated
3) runs/ climbs in inappropriate situations
4) often ‘on the go’
5) talks excessively
6) cannot perform leisure activities quietly

Impulsive:

7) blurts out answers
8) has difficulty awaiting turn
9) interrupts / intrudes others

460
Q

ADHD

Primary school child clinical picture?

A
  • Distractibility
  • restlessness
  • disruptive behaviour
  • low self esteem
  • rejection by peers
  • impaired family relations
461
Q

ADHD

Adolescence clinical picture?

A
  • difficulty in organisation
  • persistent inattention
  • aggressive anti-social behaviour
  • alcohol and drug problems
  • sexually inappropriate
  • lack of achievement
462
Q

ADHD

treatment?

A

1st: Methylphenidate (ritalin)- 6 week trial, monitor growth during tx

2nd- Atomoxetine

3rd- Lisdexamfetamine

(when unresponsive to maximum doses of other two treatments)

463
Q

OCD

What are obsessions?

What are compulsions?

A

Obsessions are unwanted intrusive thoughts, images or urges that repeatedly enter the person’s mind

Compulsions are repetitive behaviours or mental acts that the person feels drive to perform

464
Q

OCD

Causes?

A

Neuro conditions

developmental factos (abuse)

Stressors/triggers (pregnancy)

465
Q

OCD

Associated conditions?

A
  • Depression
  • Social and other phobias
  • Alcohol misuse
  • Generalised anxiety disorder
  • Body dysmorphic disorder (BDD)
  • Eating disorders - Schizophrenia
  • Bipolar disorder
  • Tourette’s
  • Autism
466
Q

OCD

clinical presentation?

A

Must be present on most days for at least two weeks

  • not imposed by outside influences
  • repetitive and unpleasant/ excessive
  • interfere with individual functioning e.g. wasting time
467
Q

OCD

Tx?

A

CBT

Exposure and repsonse prevention

SSRI’s

468
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

Triggers?

A

Seizure:
Flashing lights/ hyperventilation

Syncope:
upright, exertion, blood, needles

469
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

Prodrome?

A

Seizure: Typical aura

Syncope:
nausea, sweating, palpitations

470
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

Duration?

A

Seizure: variable

Syncope: 1-30s

471
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

Convulsive jerks?

A

Seizure: Common prolonged

Syncope: less common and brief

472
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

incontinence?

A

Seizure: Common

Syncope: Uncommon

473
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

tongue bite?

A

Seizure: Common

Syncope: rare

474
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

colour?

A

Seizure:
Partial- pale
tonic clonic- red,blue

Syncope: very pale

475
Q

DIFFERENCE BETWEEN SYNCOPE AND SEIZURE

post-ictal phase?

A

Seizure: yes, slow and confused

Syncope: no, rapid orientation

476
Q

What is a seizure?

A

Transient occurence of signs/ symptoms due to abnormal excessive neuronal activity in the brain

477
Q

what is syncope?

A

sudden reduction in cerebral perfusion with oxygenated blood

478
Q

FEBRILE SEIZURES

What are they?

A

seizures occuring in children aged 6 months to 6 years with fever and raised temperature (>37.8)

479
Q

FEBRILE SEIZURES

what is a simple febrile seizure?

A
  • generalised tonic-clonic
  • less than 15 mins
  • typically do not recur within 24 hrs
  • should be recovered/ drowsy within 1 hr
480
Q

FEBRILE SEIZURES

what is a complex febrile seizure?

A

Focal features

may be recurrence within 24 hours

duration of more than 15 mins

481
Q

How long is a febrile status epilepticus seizure?

A

longer than 30 mins

482
Q

FEBRILE SEIZURES

Causes?

A
  • metabolic (electrolytes/glucose)
  • Viral (meningo)
  • CNS lesion
  • epilepsy
  • trauma
483
Q

FEBRILE SEIZURES

When should you urgently refer?

A

1) First febrile seizure
2) >5 min duration
3) Drowsy >1 hour after seizure

4) Previous history of:

  • <18 months
  • Complex seizure
  • On Antibiotics
484
Q

FEBRILE SEIZURES

when should a LP be considered?

A

In children up to 18 months

485
Q

Contra- indications of LP?

A
  • reduced consciousness
  • septicaemic shock
  • likely invasie meningococcal
  • signs of raised ICP
  • focal neurology
  • bleeding tendency
486
Q

REFLEX ANOXIC SEIZURE

What is it?

A

Paroxysmal, self limiting brief asystole (<15s) that occurs in infants (6 months- 2 yrs) due to common triggers such as:

  • Pain
  • cold foods
  • Fright
  • Fever
487
Q

treatment of seizures?

A

Diazepam/ Midazolam, Lorazepam

if lasting >5 min

488
Q

REFLEX ANOXIC SEIZURE

Clinical presentation?

A

stops breathing
stiff/rigidity
incontinence
pale/blue

  • NO tongue bite
489
Q

REFLEX ANOXIC SEIZURE

Pathophysiology?

A

Cardiac asystole from vagal inhibition, diagnosis through vagal excitation tests

490
Q

REFLEX ANOXIC SEIZURE

Tx?

A

Check ferritin
No drugs needed

pacemaker might be a option, child usually grows out of it

491
Q

EPILEPSY

What is it?

A

Chronic neurological disorder characterised by recurrent unprovoked seizures

492
Q

EPILEPSY

2 broad classifications?

A

Generalised (both hemispheres)

Focal/Partial

493
Q

EPILEPSY

Describe absent epilepsy?

A

1) transient LoC for no more than 30s
2) Abrupt onset and no motor phenomena apart from eyelid flickering
3) Often precipitated by hyperventilation
4) Stare momentarily and stop moving
5) No recall but knows theyve missed something
6) 2/3rds female
7) 4-12 yrs old

494
Q

EPILEPSY

types of generalised seizures?

A 
Absent
Myoclonic
Tonic
Tonic-clonic
Atonic
495
Q

EPILEPSY

Types of partial/focal seizures?

A

Frontal
Temporal
Parietal
Occipital

496
Q

EPILEPSY

Describe myoclonic seizure?

A

Brief, repetitive jerking movements of limbs, neck or trunk

497
Q

What is a hiccough/ hiccups?

A

non epileptic myoclonic seizure of diaphragm

498
Q

EPILEPSY

Describe a tonic seizure?

A

Generalised increase in tone

499
Q

EPILEPSY

Describe Tonic- clonic seizures?

(tonic phase)

A
  • Rigid
  • Fall to ground
  • Stop breathing/ cyanosis
500
Q

EPILEPSY

Describe Tonic- clonic seizures?

(clonic phase)

A
  • Rhythmic contractions
  • Limb jerking
  • irregular breathing
  • Saliva/ cyanosis
  • tongue bite/incontinence
501
Q

EPILEPSY

what follows a tonic-clonic seizure and how long do they last?

A

Followed by deep sleep/ unconsciousness for up to several hours

Seizure lasts seconds to minutes

502
Q

EPILEPSY

Describe an atonic seizure

A

Transient loss of muscle tone causing drop to the floor or drop of head

503
Q

EPILEPSY

Describe a frontal seizure

A

motor phenomena (clonic)

Assymetrical

504
Q

EPILEPSY

Describe a parietal seizure

A

Contralateral altered sensation

505
Q

EPILEPSY

Describe a temporal seizure

A
  • Auditory/ smell/ taste phenomena
  • Lip smacking/ plucking clothes
  • Longer seizures
  • Deja vu
506
Q

EPILEPSY

Describe a occipital seizure

A

Vision distortion

507
Q

EPILEPSY

Causes?

A

Usually none found

Infection

Hypo (glucose, Na, Ca, Mg)

Trauma

Metabolic defects

CNS tumour

Lights/ exercise

508
Q

EPILEPSY

Ix?

A

EEG

History diagnosis

CT/MRI

509
Q

EPILEPSY

Management of generalised?

A

Trigger education

1st line- Valoproate/ carbamazepine

2nd line- Lamotrigine

510
Q

EPILEPSY

Management of focal?

A

1st line- Valproate/ carbamazepine/ lamotrigine

2nd line- Topiramate, gabepentin, tigabine, bigatrin

511
Q

EPILEPSY

Management of prolonged seizures?

A

Rectal diazepam

512
Q

STATUS EPILEPTICUS

Management?

A

ABC

Supportive therapy:

Secure airway
IV access
check temp
Check glucose

Drugs:

Lorazepam IV (5 min)

Lorazepam IV (15 min)

Phenytoin IV (20 min)

Refer to PICU

513
Q

INFANTILE SPASMS/ WEST SYNDROME

3 components?

A

1) infantile spasms
2) hypsarrhythmia
3) General learning disability

514
Q

INFANTILE SPASMS/ WEST SYNDROME

Epidemiology?

A

Peak incidence around 4-7 months

Confined to infants and v small children

515
Q

INFANTILE SPASMS/ WEST SYNDROME

Clinical presentation?

Describe the spasms?

A

Spasms
Learning disability (70-90%)
Hypopigmented skin lesions
Mild/Moderate growth restriction

516
Q

INFANTILE SPASMS/ WEST SYNDROME

Describe the spasms?

A
  • Clusters of head nodding/jerks

Sudden rapid tonic contraction of the trunk and limb muscles

  • last between 5-10 seconds

Occur just before/ after sleep

517
Q

INFANTILE SPASMS/ WEST SYNDROME

Diagnosis?

A

EEG shows hypsarrhythmia which is crucial to diagnosis

518
Q

INFANTILE SPASMS/ WEST SYNDROME

treatment?

A

Vigabatrin (50% success)

ACTH (50-65% success) {daily IM injections}

Prednisolone

PROGNOSIS IS POOR

519
Q

TUBEROUS SCLEROSIS

What is it?

A

Multi-system

Formation of hamartomas in many organs, commonly the brain, skin and kidneys, which account for many of the clinical symptoms

520
Q

TUBEROUS SCLEROSIS

Cause?

A

Mutation of TSC1 or TSC2 gene on chromosome 9 or 16

521
Q

TUBEROUS SCLEROSIS

How does the affected gene cause the defect?

A

Hamartin and tuberin which form a regulatory complex responsible for limiting the activity of an important intracellular regulator of cell growth and metabolism

522
Q

TUBEROUS SCLEROSIS

Epidemiology?

A

1 in 5,800

Autosomal dominant

TSC2 mutations are associated with more severe disease

523
Q

TUBEROUS SCLEROSIS

Clinical presentation?

A

Epilepsy/ neuro

Behavioural problems

Skin/teeth involvement

CKD

524
Q

TUBEROUS SCLEROSIS

Epilepsy seen?

A

Focal seizures and infantile spasms occur in infancy secondary to tuber formation in the brain

525
Q

TUBEROUS SCLEROSIS

Cutaneous Features?

A

depigmented ‘ash-leaf’ spots which fluoresce under UV light

roughened patches of skin over lumbar spine (Shagreen patches)

adenoma sebaceum (angiofibromas): butterfly distribution over nose

fibromata beneath nails (subungual fibromata)

526
Q

TUBEROUS SCLEROSIS

Behavioural problems?

A

Learning difficulties

Social deficits

Receptive/ expressive language deficits

Attention deficit

527
Q

TUBEROUS SCLEROSIS

Diagnosis?

A

Clinical

EEG- epilepsy

MRI head- cortical tubers

528
Q

TUBEROUS SCLEROSIS

Tx?

A

Treat complications

Vigabatrin is 1st

529
Q

MUSCULAR DYSTROPHY

What type of genetic defect is it?

A

X-linked recessive

Mutation to gene encoding dystrophin

530
Q

what is dystrophin?

A

Part of a large membrane associated protein in muscle which connects the muscle membrane to actin

531
Q

MUSCULAR DYSTROPHY

Types?

which is more severe?

A

Duchenne- loss of Dystrophin

Becker - misshapen dystrophin

  • Duchenne is more severe as 1 or both of the binding sites are lost (frameshift mutation) (No dystrophin)
532
Q

MUSCULAR DYSTROPHY

Clinical presentation?

A
  • Waddling clumsy gait
  • Calf pseudohypertrophy
  • Boys aged 1-6 for Duchenne and 10-20 for Becker
  • Classic gower manoeuvre
  • resp impairment
  • Wheelchair needed 9-12 years
  • Scoliosis
  • osteoporosis
533
Q

MUSCULAR DYSTROPHY

Diagnostic tests?

A

Creatinine kinase RAISED

Muscle biopsy

Abnormal fibres surrounded fat/fibrous tissue

534
Q

MUSCULAR DYSTROPHY

Treatment?

A

Appropriate exercise helps to maintain muscle power and mobility and delays the onset of scoliosis

PREDNISOLONE- slows the decline in muscle strength and function in the short term

535
Q

MUSCULAR DYSTROPHY

What is the Gower Manoeuvre?

A

Using hands to crawl up from a sitting position to a standing position

536
Q

GASTROENTERITIS

Common cause in children and adults?

A

Children= Rotavirus

Adults = Noravirus

537
Q

GASTROENTERITIS

how many deaths of children per year due to rotavirus?

A

600k

Vaccine is part of the schedule

538
Q

GASTROENTERITIS

Risk factors?

A

Poor hygiene

Immunocompromised

Poorly cooked food

539
Q

GASTROENTERITIS

Clinical presentation?

tests?

A

Sudden onset D+V

Pain

Stool sample test

540
Q

GASTROENTERITIS

complications?

A
  • Dehydration
  • Malnutrition
  • RARE temporary intolerance to sugar following D+V
541
Q

GASTROENTERITIS

management?

A

Correct dehydration

Start Oral Rehydration therapy (Dioralyte)

IV for those in shock

542
Q

GASTROENTERITIS

Common complication?

A

transient lactose intolerance

remove lactose from diet and then slowly reintroduce after a few months

543
Q

what is colic?

A

when an infant who isn’t sick or hungry cries for more than 3 hours a day, more than 3 days a week, for more than 3 weeks

544
Q

COWS MILK ALLERGY (CMPI)

What immunoglobulin is it associated to

A

IgG & IgE

545
Q

COWS MILK ALLERGY (CMPI)

How is it confirmed?

A

RAST test- skin prick blood test to measure IgE specific antibodies in the blood

546
Q

COWS MILK ALLERGY (CMPI)

management?

When is it normally resolved by?

What to do in severe/ allergic reactions?

A

Avoid Cows milk

Normally resolved by 5 years old

Adrenaline in severe reactions

Antihistamines for allergic

547
Q

Signs of Post Infective lactose Intolerance and how is it confirmed?

A
  • weight loss
  • stools green and frothy
  • Increased frequency

Confirmed by presence of non-absorbed sugars in the stool

548
Q

How to reduce toddlers diarrhoea and what may be the underlying cause?

A

Potential intestinal motility delay

reduced by adequate fat/fibre to slow motility

Presence of mucous and undigested vegetables common

549
Q

COELIAC DISEASE

What is it?

A

Gluten sensitive enteropathy- damaging immunological response to proximal small intestine mucosa

550
Q

COELIAC DISEASE

genetic association?

A

Linked to HLA DQ2 and less so to DQ8

551
Q

COELIAC DISEASE

Risks?

A

Downs

T1DM

Autoimmune thyroid disease

552
Q

COELIAC DISEASE

gastro clinical presentation?

A

Profound malabsorption

foul smelling diarrhoea

Abdo distension

weight loss

failure to thrive/ anaemia/low folate and ferritin

553
Q

COELIAC DISEASE

Non- GI manisfestations?

A

Dermatitis herpetiformis

Severe pruritis

osteoporosis

Dental enamel defects

macules/ papules/ vesicles

554
Q

COELIAC DISEASE

diagnosis?

A

IgA TTG antibodies and endomysial antibodies

small intestinal biopsy

555
Q

COELIAC DISEASE

What does small biopsy show?

A

1) Villous atrophy
2) Intraepithelial lymphocytes
3) Crypt hypertrophy

556
Q

CROHN’S

what is it?

A

Transmural chronic inflammatory disease affecting distal ileum and proximal colon (ileocaecal)

  • Fistulae may develop between loops of bowel, skin, or other organs
557
Q

CROHN’S

Presentation?

A

Triad:

Weight loss
Bad smell diarrhoea
Abdominal pain
Nausea/vomiting

Fever
Urgency
growth delay

558
Q

CROHN’S

Non-intestinal manifestations?

A

Oral lesions

Clubbing

Uveitis (middle layer of eye)

Arthralgia (UC too)

Erythema nodosum (UC too)

559
Q

CROHN’S

What is Erythema Nodosum

A

Erythema nodosum is a type of skin inflammation that is located in a part of the fatty layer of skin.

Erythema nodosum results in reddish, painful, tender lumps most commonly located in the front of the legs below the knees

560
Q

CROHN’S

Diagnosis?

A

Exclude infection with stool MC&S

Colonoscopy with biopsy

561
Q

CROHN’S

histological findings?

A
  • non caseating, epithelioid cell granulomata
562
Q

CROHN’S

Endoscopic findings?

A

small bowel narrowing, fissuring, and bowel wall thickened

Skip lesions

563
Q

Management?

A

Flare ups- Steroids

Immunosuppression- Methotrexate/ Azathioprine

Anti- TNF biologics

564
Q

ULCERATIVE COLITIS

What is it?

A

Recurrent ulcerating disease involving mucosa of the colon (mainly distal colon)

565
Q

ULCERATIVE COLITIS

Presentation?

A

Rectal bleeding

bloody diarrhoea

Colicky pain

weight loss

growth failure

566
Q

ULCERATIVE COLITIS

Diagnosis?

A

Upper and ileocolonscopy

Barium swallow to rule out Crohn’s

never further than ileocaecal valve

goblet cell depletion

crypt abscesses

567
Q

ULCERATIVE COLITIS

histology?

A

ulceration

Crypt damage

mucosal inflammation

568
Q

ULCERATIVE COLITIS

management?

A

5-ASA’s

sulfasalazine/ Mesalazine/ Balsalazide

steroids for widespread exacerbations

Azathioprine for induction of remission + low dose corticosteroid

569
Q

Difference between Crohn’s and UC?

A

Crohn’s vs UC

Transmural vs Mucosal

Granulomas vs polymorphonuclear aggregation

Skip lesions vs continuous

Whole gut vs colon

goblet cells vs reduced goblet cells

Strictures/fistula/abscess vs presence of crypts (pseudopolyps as cells try to regenerate)

570
Q

What is Kwashiorkor malnutrition?

A

Due to low intake of protein + essential amino acids but has enough energy from other sources

  • Oedema
  • Hair changes
  • Mental changes
571
Q

What is Marasmus?

A

Malnutrition due to lack of calories from all energy sources

572
Q

What is Intussusception?

A

Most common cause of intestinal obstruction, one segment of the bowel invaginate the other.

573
Q

where is Intussusception likely to occur?

A

Ileocaecal

574
Q

Clinical presentation of Intussusception?

A

Sudden onset

paroxysms of colicky abdominal pain

Early bile stained vomit

RUQ mass (sausage shape)

RED CURRENT JELLY stools

575
Q

PYLORIC STENOSIS

Presentation?

A
  • Projectile vomiting
  • No bile
  • Constipation
576
Q

PYLORIC STENOSIS

Metabolic signs?

A

Metabolic alkalosis

  • Hyponatraemia
  • Hypochloraemia
  • Hypokalaemia
577
Q

PYLORIC STENOSIS

Signs on examination?

A

Olive sized pyloric mass

Clearly visible LUQ peristalsis

578
Q

PYLORIC STENOSIS

Management?

A

Ramstedt’s Pyloromyotomy

579
Q

NECROTISING ENTEROCOLITIS (NEC)

What is it?

A

Inflammatory bowel necrosis, most common GI emergency in neonates

(tends to affect premature)

580
Q

NECROTISING ENTEROCOLITIS (NEC)

Risk factors?

A
  • Prematurity
  • Low BW
  • PDA
581
Q

NECROTISING ENTEROCOLITIS (NEC)

Clinical presentation?

A
  • Feeding problems with abdominal distension and vomiting

Bloody mucoid stool and bilious vomiting

582
Q

NECROTISING ENTEROCOLITIS (NEC)

Diagnosis?

A

Abdo X-ray

  • Pneumatosis intestinalis (gas in gut wall)

Portal venous gas

583
Q

NECROTISING ENTEROCOLITIS (NEC)

Tx/

A

Nil by mouth

IV Cefotaxime/ Vancomycin
for 10-14 days

584
Q

HIRSCHPRUNG’S DISEASE

What is it?

A

No bowel movements due to missing nerve cells (ganglia) in segment of
baby’s colon

585
Q

HIRSCHPRUNG’S DISEASE

Presentation?

A
  • No bowel movements in 1st 48hrs = Meconium Ileus
  • Vomiting bilious green
  • Constipation
586
Q

HIRSCHPRUNG’S DISEASE

Complications?

A

GI perforation

Short gut syndrome after surgery

587
Q

HIRSCHPRUNG’S DISEASE

Diagnosis?

A

X ray with barium contrast

Rectal biopsy

588
Q

HIRSCHPRUNG’S DISEASE

Management?

A

Bowel washouts/irrigation

Bypass surgery/ ileostomy//colostomy

589
Q

JAUNDICE

Why do neonates have higher bilirubin levels than adults?

A

1) higher concentration of RBCs with short lifespan
2) RBCs breakdown = unconjugated bilirubin
3) unconjugated bilirubin becomes conjugated in liver = liver immaturity = slower conjugation

590
Q

JAUNDICE

What may be the possible cause of jaundice in neonates at:

<24 hours?

> 14 days?

A

<24hrs = Rhesus haemolytic disease (+ve Coombs test)

> 14 days = Biliary atresia (pale stools)

591
Q

JAUNDICE

Risk factors?

A
  • Low BW
  • Prematurity
  • Breast fed babies
  • Maternal diabetes
  • Family Hx
592
Q

JAUNDICE

Clinical presentation?

A

First seen normally on forehead and face

Neuro signs:
- change in muscle tone, altered crying

  • Pale stools and dark urine
593
Q

JAUNDICE

What is the name of continued high levels of jaundice?

A

Kernicterus

594
Q

JAUNDICE

Treatment of jaundice?

A

Phototherapy

Exchange transfusion

595
Q

JAUNDICE

What is Kernicterus?

A

Acute bilirubin encephalopathy that can cause:

Athetoid movements
Deafness
Low IQ
(brain damage)

prevented by jaundice treatments

596
Q

GORD

Signs?

How is it diagnosed?

A

Regurgitation

Distress after feeds / failure to feed & thrive

Apnoea

Diagnosed by endoscopy if required

597
Q

GORD

Management?

A

1) Avoid over-feeding
2) Thicken feeds
3) Antacid + Na/Mg alginate (Gaviscon)
4) Introduce PPI

598
Q

GORD

If GORD does not resolve in 6-9 months what can be done?

A

Fundoplication if still failure to thrive / severe oesophagitis

599
Q

What is Meckel’s Diverticulum?

What is the Rule of 2’s?

A

most frequent malformation of GI tract

2% of population
2 feet from ileocaecal valve 
2 different mucosa 
common in less than 2 years old
Males 2x than females
2 inches long or less

Meckel diverticulum occurs in 2% of the population, 2% are symptomatic, children are usually less than 2 years, affects males twice as often as females, is located 2 feet proximal to the ileocecal valve, is 2 inches long or less, and can have 2 types of the mucosal lining.

600
Q

How is Meckel’s Diverticulum diagnosed?

A

Always considered when patients have haemorrhage or obstruction

CT scan if volvulus/intusseception

601
Q

When should a Diverticula be resected?

A

> 2cm
narrow neck
fibrous band to abdominal wall
inflamed/ thickened

602
Q

what can congenital diaphragmatic hernia lead to?

A

Impaired lung development

  • Pulmonary hypoplasia
  • Pulmonary hypertension
603
Q

What is Gastroschisis?

A

Evisceration of abdominal contents, opening usually >5cm

604
Q

Signs of biliary atresia?

Treatment?

A

Elevated unconjugated/conjugated bilrubin = Jaundice

Pale stools/ dark urine

kasai procedure

605
Q

Causes of increased interstitial fluid?

A

o Lymph drainage – lymphoedema (eg congenital, blockade)

o Venous pressure and drainage – venous obstruction eg
thrombosis

o Lowered oncotic pressure (low albumin / protein)
▪ Malnutrition
▪ Decreased production from liver
▪ Increased loss eg gut, Kidney (nephrotic syndrome)

o Salt and Water retention
▪ Heart failure
▪ Kidney – impaired GFR

606
Q

Causes of Oedema (renal)

A

o Glomerulonephritis (Nephrotic syndrome, diabetes, HSP, SLE, infection, malignancy, Alports)

o orthostatic proteinuria, reduced renal mass, hypertension

o tubular proteinuria (ATN, PKD)

607
Q

NEPHROTIC SYNDROME

most common cause?

A

minimal change disease

608
Q

NEPHROTIC SYNDROME

Triad?

A

o Heavy proteinuria
▪ First morning urine (protein:creatinine)
• >1g/m2/24 hrs

o Hypoalbuminaemia
▪ Normal range 35-45g/l
▪ Fluid retention and oedema normally <25-30 but not cut
off

o Oedema
▪ Pitting oedema and gravitational

o Can also have Hyperlipidaemia

609
Q

NEPHROTIC SYNDROME

Investigations?

A

Urinalysis (dipstick = UTI, MC&S = protein)

BP

Low serum albumin
Low Anti- T III = prone to renal vein thrombosis/ DVT/ PE
- Antistreptolysin O and anti-DNAse B titres and throat swab

610
Q

NEPHROTIC SYNDROME

3 types?

A

Congenital (<1 year)

Steroid sensitive

steroid resistant

611
Q

NEPHROTIC SYNDROME

Signs of Steroid sensitive NS?

A

1) Normal BP, renal function
2) no macroscopic haematuria
3) no features to suggest nephritis
4) Normally minimal change histologically

612
Q

NEPHROTIC SYNDROME

Signs of Steroid resistant NS?

A

1) Elevated BP, impaired renal function
2) haematuria
3) features to suggest nephritis
4) underlying glomerulopathy/ basement membrane abnormality histologically

613
Q

NEPHROTIC SYNDROME

Tx of Steroid sensitive NS?

A

1st - Prednisolone

2nd - renal biopsy if unresponsive

614
Q

NEPHROTIC SYNDROME

Tx of Steroid resistant NS?

A

Diuretics/ACE-I = To treat oedema

NSAIDs may reduce proteinuria

615
Q

NEPHRITIC SYNDROME

Causes?

A

Post infection - Grp A b-haemolytic strep

HSP vasculitis

IgA nephropathy

616
Q

Clinical features of Acute Glomerulonephritis?

A

Haematuria
Proteinuria
Decreased urine output (salt and water retention = HTN)

Impaired GFR (Increased Creatinine)

617
Q

Investigations of Acute Glomerulonephritis?

A

o FBC – mild normochromic, normocytic anaemia

o U&Es – increased urea and creatinine (hyperkalaemia, acidosis)

o Low C3 + normal C4 complement

o Urinalysis
▪ Macroscopic haematuria
▪ Dipstick – protein (albumin): creatinine ratio showing proteinuria
▪ Microscopy – RBC casts

618
Q

Management of Acute Glomerulonephritis?

A

o Fluid balance (salt restriction + diuretics)

o Treat HTN

o Correct electrolyte imbalance (potassium/ acidosis)

o Penicillin if infection

619
Q

What is Alport Syndrome?

A

X linked recessive disorder associated with hearing loss, ocular defects and progressive kidney disease

Almost always have haematuria

620
Q

UTI

give an example of an upper and lower

A

Upper = Pyelonephritis

Lower = Cystitis

621
Q

UTI

Most common organisms?

A

E.coli

Klebsiella

622
Q

UTI

Presentation of Upper/Lower UTI?

A

Upper:

  • Fever
  • Loin pain
  • failure to thrive, jaundice

Lower:

  • Dysuria
  • Urinary frequency
  • Incontinence
  • Lower abdominal pain
  • Haematuria
623
Q

UTI

What could dysuria alone mean?

A

Vulvitis in girls

Balanitis in boys

624
Q

UTI

Diagnosis and Investigations?

A

Urinalysis:
MC&S
Dipstick (leucocytes and nitrites)

625
Q

UTI

Management?

A

<3months - IV Amoxicillin and Gentamycin

> 3 months - Trimethoprim/ Nitrofurantoin/ Amoxicillin

626
Q

What is Vesicoureteric reflux?

A

Anomaly of vesicoureteric junction where the ureters are displaced laterally and enter bladder directly = not at an angle means back flow

627
Q

What can VUR cause?

How is VUR diagnosed?

A

incomplete emptying = increase risk of UTI (cystitis)

Renal damage if high pressure / infrarenal reflux

Dx = micturating cystourethrogram

628
Q

AKI

Pre renal Causes?

A
  • Hypovolaemia (nephrotic syndrome, gastroenteritis, haemorrhage)
  • circulatory failure
629
Q

AKI

Renal causes?

A

Vascular- haemolytic uraemia syndrome/ vasculitis

tubular - Acute tubular necrosis

Glomerular - glomerulonephritis

Interstital - pyelonephritis

630
Q

AKI

Post renal causes?

A

Obstruction

congenital- posterior urethral valves

acquired- blocked urinary catheter

631
Q

What is AKI?

A

Acute kidney injury characterised by rapid rise in creatinine and development of oliguria/anuria.

632
Q

Secondary causes of AKI?

A

Cardiac surgery

Bone marrow transplant

Toxicity - DRUGS (NSAIDs, vancomycin, acyclovir, aminoglycosides)

633
Q

AKI

Signs on bloods?

A 
High:
K
Creatinine
Urea
maybe phosphate

Low:
Ca
Na
Cl

634
Q

AKI

management?

A
  • Fluids
  • If urine osmolality low = furosemide

Renal replacement therapy = pulmonary oedema/HTN/ not responding to tx

635
Q

Management of Hyperkalaemia?

A

IV calcium gluconate (protect cardiac membrane)

Nebulised salbutamol

Diuretics/Dialysis to remove K from body

636
Q

CKD

Causes?

A
  • Congenital dysplastic kidney
  • pyelonephritis
  • glomerulonephritis
  • recurrent infection
  • reflux nephropathy
  • AKI - leading to necrosis
637
Q

CKD

Investigations?

A
  • Monitor growth
  • BP-
  • U+E
  • Ca2+ (often low), Phosphate (often high)
638
Q

CKD

Presentation?

A
  • Anorexia/lethargy
  • Polydipsia/polyuria
  • ^BP, hypertensive, retinopathy
  • anaemia
  • Failure to thrive
  • seizures
  • renal Ricketts
639
Q

Management of CKD?

A

Treat Anaemia, acidosis

Manage diet

Prevent renal osteodystrophy

Dialysis + transplant

640
Q

Ddx of Proteinuria?

A
  • Orthostatic proteinuria
  • Glomerular abnormalities

o Minimal change disease - nephrotic syndrome

o Glomerulonephritis (nephrotic syndrome)

o DM
- Increased glomerular filtration pressure 
- Reduced renal mass
- Hypertension
- Tubular proteinuria
o ATN
o PKD
o Pyelonephritis
641
Q

Ddx of Haematuria?

A

Non glomerular:

  • Infection
  • Trauma to genitalia/ kidney
  • stones
  • tumour
  • sickle cell
  • renal vein thrombosis
Glomerular:
- Vasculitis 
- SLE
- Post infectious
- Glomerulonephritis 
IgA nephropathy

Alports syndrome

Goodpastures

642
Q

DIABETES

Cause of T1 DM?

A

T-cell mediated B-cell destruction in the Islets of Langerhan causing no insulin production

643
Q

DIABETES

What % of childhood diabetes is type 1?

A

97%

644
Q

DIABETES

Insulin actions?

A

1) Stimulates formation of glycogen from glucose in the liver
2) Stimulates glucose uptake form blood into cells
3) Lowers blood sugar

645
Q

DIABETES

What is the threshold for:

Fasting glucose

OGTT

HbA1c

A

Fasting = >7mmol/L

OGTT = >11.1mmol/L

HbA1c = >6.5%

646
Q

DIABETES

How does the body respond when insulin is not working efficiently?

A

Gluconeogenesis = produce glucose from amino acids / muscle breakdown

Ketogenesis = fatty acids converted to ketones

647
Q

DIABETES

Clinical presentation?

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Lethargy
  • Poor growth
648
Q

Signs of DKA?

A
  • Vomiting
  • Acidosis
  • Reduced consciousness
  • Ketonuria
649
Q

DKA on investigation?

A

Hyperglycaemia = >7mmol/L

Acidosis pH <7.3

Ketones in urine

650
Q

DKA management?

A

1) Resus ABC
2) Correct dehydration
3) Give insulin 1hr after giving fluids
4) Monitor - hourly blood glucose

Avoid bicarbonate as increases risk of cerebral oedema

651
Q

Hypoglycaemia features?

A
  • Irritable
  • Sweaty
  • Headache
  • Pallor
  • Drowsy
  • Slurred speech
  • Convulsions
652
Q

HYPOTHYROIDISM

Congenital and acquired causes?

A

Congenital:

  • iodine deficiency
  • pituitary dysfunction
  • maldescent of thyroid

Acquired:

  • Prematurity
  • Hashimoto’s
  • Trisomy 21
653
Q

HYPOTHYROIDISM

Clinical features?

(Congenital normally picked up on screening and asymptomatic)

A 
Bradycardia
Cold intolerance
Dry skin 
Thin,dry hair
Constipation
Delayed puberty 
Obesity
Learning difficulties

§

654
Q

Treatment of Thyroid storm/crisis?

A
  • IV hydrocortisone
  • IV Fluids
  • Propanolol
655
Q

CONGENITAL ADRENAL HYPERPLASIA

How is it diagnosed?

A

Virilisation of external female genitalia

SALT-LOSERS:- (no aldosterone production)

  • Low Na
  • High K
  • Metabolic acidosis
  • Hypoglycaemia
656
Q

Treatment of a salt-losing crisis?

A

Sodium chloride
Glucose
IV Hydrocortisone

657
Q

What is Kallmann’s?

A

Hypogonadotrophic hypogonadism causing:

  • Delayed puberty
  • Anosmia
658
Q

Definition of Precocious puberty?

A

‘development of secondary sexual characteristics before 8 years
in females and 9 years in males’

659
Q

What is Thelarche?

A

First stage of breast development

660
Q

What is Adrenarche?

A

First stage of pubic hair development

661
Q

What is the Gonadotrophin pathway?

A

GnRH (from hypothalamus) —> ^FSH+LH —>
testes/ovaries —>
^testosterone & oestrogen/progesterone —> inhibits FSH/LH secretion

662
Q

Ddx of pain with swelling?

A
  • Trauma
  • Infection (septic arthritis/osteomyelitis)
  • JIA
  • Arthritis (IBD)
  • Vasculitis (HSP/Kawasaki’s)
  • CTD
  • CF
  • Sarcoidosis
  • Developmental/congenital
663
Q

JIA

Definiton?

A

Joint inflammation presenting in children and persisting for at least 6 weeks with other causes excluded

664
Q

JIA

Classification?

A

Oligoarticular = 1-4 joints in first 6 months

Polyarticular RF -ve = 5+ joints in first 6 months

Polyarticular RF +ve = 5+ joints in first 6 months / +ve RF seen on two occasions

Systemic onset JIA = Arthritis + 2 weeks fever

Psoriatic = arthritis + psoriasis

665
Q

JIA

Complications?

A

Chronic anterior uveitis

Growth failure

Osteoporosis

666
Q

JIA

Investigations?

A

Normocytic anaemia

Raised: WCC, CRP, Platelets

RF / HLA-B27

MSK examination

X-rays

667
Q

JIA

Treatment?

A

NSAIDs + Analgesics

Steroids

DMARDs (metho/sulfa)

Biologics

668
Q

What is juvenile SLE?

A

Chronic autoimmune disease affecting every organ of the body

relapsing and remitting

669
Q

Diagnostic criteria for Juvenile SLE?

A

SOAP BRAIN MD

Serositis (pleuritis/pericarditis)
Oral ulcers
Arthritis
Photosensitivity

Blood (pancytopenia) 
Renal (proteinuria)
ANA +ve (anti-nuclear antibody)
Immunological 
Neurological (psych/seizures)

Macular rash
Discoid rash

670
Q

OSTEOMYELITIS

Where are the most common sites?

A

Distal femur

Proximal tibia

671
Q

OSTEOMYELITIS

most common bacterial causes?

A

Staph Aureus

h.influenza

Group A beta haemolytic strep

672
Q

OSTEOMYELITIS

Classic signs?

A

Severe pain

Immobile limb (pseudo paresis)

Swollen over area

Acute febrile illness (lethargy/high temp)

673
Q

OSTEOMYELITIS

Investigations?

A

x-ray

MRI

blood cultures

FBC (^WCC/CRP)

674
Q

OSTEOMYELITIS

Treatment?

A

(over 3 months old)
= IV Cefuroxime

SWITCH TO ORAL AFTER 1 WEEK IF CAN TOLERATE AND CRP <10:

Flucloxacillin if s.aureus

Co-amoxiclav if unsure

675
Q

SEPTIC ARTHRITIS

What is it?

A

Serious infection of the joint space - can lead to bone destruction

676
Q

What should you assume in a limping child?

A

Septic arthritis until proven otherwise

677
Q

SEPTIC ARTHRITIS

Common organism causes?

A

1) S.aureus

2) h.influenza

678
Q

SEPTIC ARTHRITIS

clinical presentation?

A

Red, hot, acutely tender joint

reduced ROM

Acutely febrile child

679
Q

SEPTIC ARTHRITIS

Investigations?

A

Joint aspiration under USS = definitive

blood cultures

^WCC, CRP/ESR

680
Q

SEPTIC ARTHRITIS

Treatment?

A

early treatment is vital to prevent destruction of articular cartilage + bone

IV Abx / possible surgical drainage

681
Q

DDH

Risk factors?

A
  • Female 6x more likely
  • breech presentation
  • Family Hx
  • Firstborn child
  • Oligohydramnios
682
Q

DDH

Clinical presentation?

A

Screened in examination

BARLOW TEST = attempt to dislocate femoral head posteriorly

ORTOLANI TEST = attempt to relocate a dislocated femoral head

Observe for asymmetry

683
Q

DDH

investigations?

A

Dynamic USS

early diagnosis important as if appropriately aligned in first few months = dysplastic hip can resolve spontaneously

684
Q

DDH

Treatment?

A

Most will spontaneously stabilise in 3-6 weeks

Pavlik harness (flexion-abduction orthosis) in children under 4-5 months

685
Q

PERTHE’S DISEASE

what is it?

How is it diagnosed?

A

Temporarily disrupted blood flow to femoral head causing avascular necrosis in children aged 4-8 years old

Limited abduction and internal rotation - abnormal ossification on x-ray

686
Q

What is Achondroplasia?

A

Autosomal dominant condition that is the most common form of short-limb dwarfism due to REDUCED growth of cartilaginous bone

687
Q

Clinical presentation of Achondroplasia?

A
  • Large skull, normal trunk, short arms and legs
  • Short stature
  • Frontal bossing
  • Marked lumbar lordosis
688
Q

OSTEOPOROSIS

Definition?

A

Low bone mass and deterioration of bone tissue, leading to bone fragility and increased fracture risk

689
Q

OSTEOPOROSIS

Possible causes?

A

Inherited - Osteogenesis Imperfecta

Acquired - Drug induced, malabsorption

690
Q

OSTEOGENESIS IMPERFECTA

What is it?

A

Autosomal dominant condition causing increased fragility of bone

(collagen type 1 = bone/teeth)

691
Q

OSTEOGENESIS IMPERFECTA

There is 4 types

Name some associated symptoms and treatment

A

Blue sclerae

Hearing loss

Bisphosphonates

692
Q

Give examples of bisphosphonates?

A

Alendronate

Zoledronate

Pamidronate

693
Q

ANAEMIA

What Hb figures show anaemia in

neonates?

1-12 months?

1-12 years?

A

o Neonate: Hb <140g/L

o 1month-12months: Hb<100g/L

o 1year-12years: Hb<110g/L

694
Q

ANAEMIA

Causes?

A
  • Impaired red cell production
    (Iron deficiency,
  • Increased red cell destruction (haemolytic disease of newborn, thalassaemias, sickle cell, G6PD deficiency)
  • blood loss (meckel’s diverticulum, von willebrand disease)
695
Q

Signs of Anaemia?

A

jaundice -> kernicterus

Oedema

hepatosplenomegaly

696
Q

Pathophysiology and treatment of haemolytic disease of a newborn?

A

1) negative rhesus mother and positive baby
2) baby has D antigen and mother does not
3) Mother produces antibody against D antigen and haemolysis of newborns RBCs

treatment?

give mother purified anti-D so she does not sensitise to babies antigen = not exposed to immune system = no haemolysis

697
Q

Cause of iron-deficiency?

A

1) Inadequate intake (poor feeding)
2) Malabsorption (CMPI)
3) blood loss

698
Q

Investigations of IDA?

A
  • Microcytic hypo chromic reticulocytes

- low ferritin and serum Fe

699
Q

treatment of IDA?

A

Ferrous fumigate (oral iron therapy)

700
Q

What is G6PD?

A

enzyme essential for preventing oxidative damage to red cells.

RBCs lacking G6PD = exposed to oxidant induced haemolysis

701
Q

How is G6PD transmitted?

A

X-linked

702
Q

G6PD

Presentation?

A

Neonatal jaundice

Acute intravascular haemolysis (triad signs below)

  • Dark urine
  • Fever
  • Flank pain
703
Q

What is sickle cell?

A

HbS forming due to mutation on chromosome 11.

the cells cannot flex through capillaries which leads to:

1) Blockage
2) Vessel occlusion
3) Ischaemia
4) Low O2 tension

(autosomal recessive)

704
Q

How does HbS form?

A

Mutation on codon 6 of B-globulin gene - change in AA sequence from:

Glutamine to Valine

705
Q

What is B-Thalassemia?

A

Excess of alpha chains

Autosomal recessive HBB gene on chromosome 11

HbA2 RAISED = ANAEMIA

706
Q

Treatment of B-Thalassemia?

A

Long term folic acid

BM transplant

Regular transfusions

707
Q

What is ITP?

A

Immune Thrombocyotpenic Purpura =

Destruction of platelets by IgG autoantibodies

708
Q

Acute signs of ITP?

A

Petachie on extremities

Purpura/ bruising

709
Q

Diagnosis?

A

Dx of exclusion, low platelets!

710
Q

What is Von Willebrand Haemophilia?

A

Abnormality to vWF = no longer adhesive between platelets and damaged endothelium =

Excessive bleeding

711
Q

Tx of vWF disorder?

A

Tranexamic acid (stop excessive bleeding post surgery)

712
Q

ACUTE LYMPHOBLASTIC LEUKAEMIA (ALL)

What is it?

A

Disorder of lymphoid progenitor cells

Lymphoid precursors proliferate and replace normal cells of the bone marrow

713
Q

What is the most common cancer in children?

A

Acute Lymphoblastic Leukaemia

714
Q

Symptoms of ALL?

A
  • Pancytopenia:
  • Fatigue (anaemia)
  • Increased infections (leukopenia)
  • bleeding (thrombocytopenia)
  • bone and joint pain
715
Q

Cause of ALL?

A

abnormal chromosome number OR

chromosomal translocation of

[t(12;21] or

[t(9;22)] which is Philadelphia chromosome

716
Q

Signs of ALL?

what is seen on examination

A
  • Hepatosplenomegaly (blast cells settle here so enlarge - abdominal distension)
  • Lymphodenopathy (^ settle in lymph nodes)
  • Petechiae
  • Pallor
717
Q

Diagnosis of ALL?

A

FBC - pancytopenia

Blood film - show blast cells

Bone marrow biopsy (CONFIRMS)

718
Q

Treatment of ALL?

A
  • Chemo/ Radio

- BM/stem cell transplant

719
Q

5 stages of Chemo?

A

1) Induction
2) Consolidation
3) Interim maintenance
4) Delayed intensification
5) Maintenance

720
Q

Most common presentation of a Neuroblastoma?

A

Abdo mass (can be anywhere on sympathetic chain)

721
Q

What is Wilm’s tumour?

A

Most common renal tumour in childhood that is:

95% unilaterally

Presents as asymptomatic abdominal mass

722
Q

Signs of raised ICP?

A

Headache

Change in behaviour

Nausea/vomiting

Over-sleepy

Papilloedema (may be decreased visual acuity)

723
Q

Features of Retinoblastoma?

A
  • Loss of red-reflex = replaced by white pupil (leukocoria)
724
Q

Name the components of the traffic light system for an unwell child

A

1) Colour (skin, lips, tongue)
2) Activity
3) Respiratory
4) Circulation / Hydration
5) Other

725
Q

Name high risk signs of an unwell child (Traffic light)

A

Colour :
Pallor, blue

Activity :
not responding to social cues, does not stay awake, high pitched cry

Respiratory :
grunting, tachypnoea, chest indrawing, RR >60

Circulation / Hydration :
reduced skin turgor
tachycardia

Other :
temperature 
non-blanching rash 
bulging fontanelle
neck stiffness
status epilepticus 
focal signs/seizures
726
Q

What heart rate is a high risk sign for the following ages:

<12 months

12-24 months

2-5 years

A

<12 months : >160 bpm

12-24 months : >150bpm

2-5 years : >140bpm

727
Q

what temperature is a high risk sign for the following ages:

<3 months

3-6 months

A

<3 months : >38

3-6 months : >39

728
Q

What breathing rate is a high risk sign for the following ages:

6-12 months

> 12 months

A

6-12 months: >50

> 12 months : >40

729
Q

What is Respiratory Distress Syndrome?

A

Insufficient surfactant production seen in immature lungs

730
Q

Risk factors of RDS?

A

Prematurity

C-section

731
Q

Clinical presentation of RDS?

A 
Tachypnoea >60 min 
Grunting
Nasal flaring 
Intercostal recession 
Cyanosis
732
Q

Treatment of Respiratory Distress Syndrome?

A

give maternal corticosteroids (Betamethasone/dexomethasone)
= induce foetal lung maturation

Oxygen (CPAP)

exogenous surfactant by endotracheal tube

733
Q

What is Bronchopulmonary Dysplasia?

A

Still needing O2 requirements after 36 weeks

complication of RDS

734
Q

What is MSAF?

A

meconium stained amniotic fluid.

This can lead to meconium aspiration syndrome when the baby inhales the meconium leading to Respiratory Distress

Treated with: Surfactant / inhaled nitric oxide

735
Q

what is Chorioamnionitis?

A

Chorioamnionitis is a bacterial infection that occurs before or during labor. The name refers to the membranes surrounding the fetus: the “chorion” (outer membrane) and the “amnion” (fluid-filled sac). The condition occurs when bacteria infect the chorion, amnion, and amniotic fluid around the fetus

736
Q

who is most likely to get Intussusception?

A

Male

between 6-18 months

737
Q

Diagnostic investigation for Intussusception?

A

Ultrasound

738
Q

Treatment for Croup?

A

Single dose Dexamethsone/ prednisolone to reduce throat swelling

739
Q

What is a Dermoid cyst?

A

Dermoid cysts are usually multiloculated and heterogeneous. Most are located above the hyoid

740
Q

What are Cystic Hygromas?

A

Cystic hygromas are soft and transilluminate. Most are located in the posterior triangle.

741
Q

Where will you find a Branchial cyst

A

smooth mass located on the lateral aspect of his anterior triangle, near to the angle of the mandible. On ultrasound; it has a fluid filled, anechoic, appearance

Danny's Phase 3A Medicine (10 decks)

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