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Phase 3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

At what age should a child be able to hop on one leg?

A

From the age of 4

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2
Q

What is the normal gross motor developmental progress be of a newborn?

A

Limbs flexed, symmetrical pattern
Marked head lag on pulling up

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3
Q

What is the normal gross motor developmental progress be of a 6-8week old?

A

Raises head to 45 degrees in prone (tummy-time)

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4
Q

What is the normal gross motor developmental progress be of a 6-8month old?

A

Sits without support (initially with a round back, then eventually with a straight back by 8 months)
Limit age: 9 months

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5
Q

What is the normal gross motor developmental progress be of a 8-9month old?

A

Crawling

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6
Q

What is the normal gross motor developmental progress be of a 10month old?

A

Standing independently
Cruising around furniture

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7
Q

What is the normal gross motor developmental progress be of a 12month old?

A

Unsteady walking - broad gait, hands apart

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8
Q

What is the age limit of early unsteady walking?

A

18 months

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9
Q

What is the normal gross motor developmental progress be of a 15month old?

A

Walking steadily

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10
Q

What is the normal gross motor developmental progress be of a 2.5 year old?

A

Running and jumping

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11
Q

What is the normal respiratory rate of a child aged 2-5years old?

A

20-30 breaths per minute

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12
Q

What is the normal respiratory rate for a child under 1 years old?

A

30-40breaths per minute

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13
Q

At what age would a child develop a palmar grasp?

A

4-6 months

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14
Q

At what age would a child develop a mature pincer grip?

A

10 months
Limit age of 12 months

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15
Q

What is urticaria?

A

An itchy blotchy red rash resulting from swelling of the superficial part of the skin

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16
Q

What is the typical presentation of urticaria?

A
  • Central itchy white papule or plaque due to swelling of the surface of the skin (wheal).
  • Surrounded by an erythematous flare
  • Lesions variable in size and shape and may be associated with swelling of soft tissues of eyelids, lips and tongue
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17
Q

What are the possible triggers of acute urticaria?

A

Allergies: foods, bites, stings, medication
Viral infections
Skin contact with chemicals, nettles, latex, etc
Physical stimuli: firm rubbing (dermatographism), pressure, cold, heat

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18
Q

What is psoriasis?

A
  • Chronic, relapsing inflammatory skin disorder
  • Can start at any age including childhood
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19
Q

How is urticaria diagnosed?

A

Usually from history and clinical findings alone

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20
Q

How is urticaria managed?

A
  • Avoiding triggers
  • Antihistamines, emollients
  • In severe cases, prednisolone for a short duration
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21
Q

What is chronic plaque psoriasis characterised by?

A
  • Itchy, well-demarcated circular-to-oval bright red/pink elevated lesions (plaques) with overlying white or silvery scale
  • Distributed symmetrically over extensor body surfaces
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22
Q

How might plaque psoriasis present in children?

A

With the plaques being less thick and the lesions are being less scaly.

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23
Q

Where may psoriasis appear in infancy?

A

In the nappy region as well as the extensors

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24
Q

What does atopic eczema present as?

A

Dry, red, itchy, inflamed skin over flexural regions (e.g. popliteal fossa/antecubital fossa)

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25
Q

What is Eisenmenger’s Syndrome?

A

An initial left to right shunt becomes a right to left shunt due to increased pulmonary blood flow and eventual right ventricular hypertrophy

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26
Q

What is epiglottitis?

A

Inflammation and swelling of the epiglottis, usually secondary to infection

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27
Q

What are the symptoms of epiglottitis and how does it progress?

A

Sore throat
Difficulty and pain on swallowing
Respiratory distress (may improve leaning forward)
Stridor
Fever
Irritability/restlessness
Muffled/hoarse ‘hot potato’ voice
Drooling

Symptoms progress quickly, but may be slower and take a few days in older children

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28
Q

How is epiglottitis treated?

A
  1. Admission to hospital - airway secured and supplemental oxygen administration immediately
  2. IV fluids and antibiotics
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29
Q

What are the features of bronchiolitis?

A
  • Coryzal symptoms
  • Increased work of breathing (Subcostal recession, head bobbing)
    Difficulty in feeding
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30
Q

What is bronchiolitis most commonly caused by?

A

Respiratory synctial virus (RSV)

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31
Q

What is the primary cause of croup?

A

Parainfluenza

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32
Q

What is primary age group affected by bronchiolitis?

A

3-6 months

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33
Q

What is cryptochidism?

A

An undescended testicle, seen in 2-5% of term males

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34
Q

What are the risk factors for cryptorchidism?

A

Prematurity
Small for gestational age

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35
Q

What are the complications of cryptorchidism?

A

Testicular torsion
Increased infertility
Increased rates of testicular cancer

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36
Q

What would the treatment for cryptorchidism be?

A

Orchipexy by the age of 12 months if the testicles have not spontaneously descended by 6 months of age

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37
Q

What is meconium?

A

The first stool passed by a child

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38
Q

What is Bartter Syndrome?

A

An inherited defect in the thick ascending limb of the loop of Henle
- Characterised by hypokalaemia, alkalosis and normal to low BP

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39
Q

What would GORD present as in children?

A

Vomiting
Effortless regurgitation of milk
Cough

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40
Q

What would pyloric stenosis present with in children?

A

Progressively worsening non-bilious vomiting
Hypokalaemia, metabolic alkalosis
Dehydration

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41
Q

What features in an ill child would prompt consideration of meningococcal disease?

A

Petechial rash
Altered mental state
Cold hands and feet
Extremity pain
Fever
Headache
Neck stiffness
Skin mottling

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42
Q

What would initial management of suspected meningococcal septicaemia be in primary care?

A

IM or IV benzylpenicillin
Urgent ambulance transfer to hospital

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43
Q

Which diseases does the 4 in 1 pre-school booster vaccine protect against?

A

Diphtheria
Tetanus
Whooping cough
Polio

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44
Q

What is orbital cellulitis?

A

Infection behind the orbital septum
A medical emergency requiring hospital admission and IV antibiotics

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45
Q

What are the symptoms of orbital cellulitis?

A

Pain on eye movement
Reduced eye movements
Changes in vision
Abnormal pupil reactions
Forward movement of the eyeball (Proptosis)

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46
Q

What is periorbital cellulitis, and what are its symptoms?

A
  • Eyelid and skin infection in front of the orbital septum
  • Presents with:
    Swelling
    Redness
    Hot skin around eyelids and eye
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47
Q

How would you differentiate between orbital and periorbital cellulitis?

A

CT Scan
Clinical presentation:
- Pain on eye movement, changes in vision, pupil reactions and proptosis not present in periorbital cellulitis

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48
Q

How would you treat periorbital cellulitis?

A

Systemic antibiotics (Oral or IV)
Admission in children or in severe cases

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49
Q

How would you manage orbital cellulitis?

A

Admission and IV antibiotics
Surgical drainage in case of abscess formation

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50
Q

What is Brachydactyly?

A

Shortening of the fingers and toes due to unusually short bones.

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51
Q

What are the clinical features of septic arthritis?

A
  • Refusal to bear weight
  • Reduced passive range of motion
  • Pain on palpation of the affected joint
  • Leukocytosis
  • Elevated inflammatory markers (ESR, CRP)
  • Fever
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52
Q

What are the common pathogens causing septic arthritis?

A

Staphylococcus aureus
N Gonorrhoea
Streptococcus (Group A and B)

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53
Q

How is septic arthritis diagnosed?

A

Immediate joint aspiration with synovial fluid analysis

Results:
Appearance: yellow/green on aspiration (as opposed to clear and colourless when uninfected)
White cell count: raised (particularly neutrophil count), though this is not 100% sensitive or specific and can be raised in other arthropathies
Culture: identification of the causative bacterium and its sensitivities

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54
Q

What is transient synovitis and what are its symptoms?

A
  • A benign, self-limiting condition following an upper respiratory infection, acute otitis media or pharyngitis
  • Symptoms:
    Mild fever
    Full range of motion of affected joint
    Mild pain
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55
Q

How would transient synovitis be diagnosed?

A

Through exclusion after septic arthritis has been ruled out

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56
Q

What is the most common cause of vasculitis in childhood?

A

Henoch-Schonlein Purpura (HSP)

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57
Q

What are the clinical features of HSP?

A
  • Palpable purpura usually on buttocks and lower extremities
  • Abdominal pain
  • Arthritis - usually large joints
    Usually occurs after previous history of upper respiratory tract infection several weeks prior
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58
Q

What is pyloric stenosis caused by?

A

Hypertrophy of the pylorus resulting in functional gastric outlet obstruction

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59
Q

How do patients with pyloric stenosis present?

A

Projectile vomiting that is usually non-bilious and non-bloody

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60
Q

What clinical findings would be present upon examination in pyloric stenosis?

A
  • An enlarged pylorus, classically described as an “olive,” can be palpated in the right upper quadrant or epigastrium of the abdomen
  • ## Visible peristalsis due to the obstruction
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61
Q

How would pyloric stenosis be definitively treated?

A

Pyloromyotomy - relieve the obstruction
- Involves an incision being made in the longitudinal and circular muscles of the pylorus.

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62
Q

What may Meckel’s Diverticulum present with?

A
  • Abdominal pain
  • GI bleeding and/or bowel obstruction
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63
Q

What would duodenal atresia present with?

A
  • Abdominal distension
  • Non-bilious vomiting
  • Absent bowel movements
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64
Q

What would complete atresia present as?

A
  • The atretic segment is usually just distal to the ampulla of Vater
  • Bilious vomiting
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65
Q

What does double syllable babble involve?

A

Repetition of the same syllable
- Typically displayed by infants between 9-12 months

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66
Q

What is the most important step in treatment for measles?

A

Isolation - VERY CONTAGIOUS

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67
Q

Which presenting features would be strongly indicative of measles?

A
  • Rash for at least three days - first seen on the neck and spreads to involve trunk and limbs
  • Fever for at least one day and at least one of:
    Cough
    Coryza
    Conjunctivitis
  • Koplik spots - pathognomonic for measles
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68
Q

What are the diagnostic criteria for Kawasaki disease be?

A

Fever persisting for at least 5 days and 4 or more of:
1. Changes in extremities (erythema or oedema of hands or feet)
2. Polymorphous exanthema (widespread rash)
3. Bilateral, painless bulbar conjunctival injection without exudate
4. Changes in lips and oral cavity
5. Cervical lymphadenopathy.

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69
Q

What would the immediate management of Kawasaki disease be?

A

IVIg 2g/kg over 12 hours and aspirin 30-50mg/kg in four divided doses

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70
Q

What investigations are necessary in Kawasaki disease?

A

ECG and Echocardiogram - look for coronary artery aneurysms or damage to the heart muscle/valve

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71
Q

What does Williams Syndrome present as?

A
  • Typical facial features - elfin facies - broad forehead, short nose, wide mouth, full lips
  • Behavioural abnormalities
  • Supravalvular aortic stenosis
  • Hypercalcaemia
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72
Q

What does Noonan syndrome present with?

A
  • Webbed neck, low set ears and short neck
    +/- Pulmonary valve stenosis
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73
Q

What does Down’s syndrome present with?

A
  • Facial features - upward slanting of eyes
  • Epicanthal folds
  • Hypotonia
  • Single palmar crease
  • Protruding tongue
  • Half of patients will have cardiac defect, commonly AVSD
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74
Q

What is Von Willebrand’s disease?

A

Most common genetic bleeding disorder - inherited in an autosomal dominant manner

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75
Q

What is Von Willebrand Factor (vWF)?

A

Large glycoprotein which:
- Promotes platelet adhesion to a damaged endothelium (which helps form the platelet plug)
- Acts as a carrier molecule/stabiliser for factor VIII
- Stabilises factor VIII - lack of vWF will prolong APTT time

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76
Q

What investigations would be completed if Von Willebrand’s disease was suspected?

A
  • Baseline blood tests (FBC): patients with profuse bleeding should have two wide-bore cannulae inserted with blood taken for a full blood count. APTT time will be increased.
  • Group and save: important to perform as the patient may require a blood transfusion.
  • Coagulation studies: should be performed if there is clinical evidence of coagulopathy, or the patient is taking an anticoagulant
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77
Q

What does APTT measure?

A

Factors 9-12, 5 and 2
(The intrinsic and common pathways)

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78
Q

What does Prothrombin time measure?

A

Factors 7, 10, 5 and 2
(Extrinsic and common pathways)

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79
Q

What is Potter’s Syndrome?

A

Characteristic appearance and pulmonary hypoplasia of a neonate due to oligohydramnios and thus compression in utero

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80
Q

What are the causes of Potter’s syndrome?

A

Renal agenesis
Obstructive uropathy
Cystic kidney disease (eg autosomal dominant polycystic kidney disease)
Early rupture of membranes

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81
Q

What are the features of Potter’s syndrome?

A

Flattened nose, recessed chin, prominent epicanthic folds and low set abnormal ears
Skeletal: hemivertebrae, sacral agenesis, limb anomalies
Ophthalmology: cataract, lens prolapse, haemorrhage
Cardiovascular: tetralogy of Fallot, VSD, patent ductus arteriosus

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82
Q

How would oligohydramnios be analysed?

(Not sure if relevant to 3a exam?)

A
  1. Ferning test - dried cervical secretions crystals viewed under microscope
  2. Amnisure - vaginal swav to screen for PAMG-1 (Placental microglobulin-1)
  3. Actim-PROM - swab screening for insulin-like growth factor binding protein-1 (IGFBP-1)
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83
Q

How would fluid volume be assessed?

A

Ultrasonography using one of:
1. Maximum vertical pocket (MVP) identified and measured - normally 2cm-8cm
2. Amniotic fluid index (AFI) - dividing uterus into 4 quadrants, adding together MVP from each quadrant - normal AFI 5cm to 25cm

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84
Q

How is oligohydramnios defined?

A

On ultrasound:
AFI <5cm OR
MVP <2cm

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85
Q

What are the clinical pathologies of the Tetralogy of Fallot?

A
  1. Overriding aorta
  2. Right ventricular hypertrophy
  3. Right ventricular outflow obstruction (pulmonary stenosis)
  4. Ventricular septal defect
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86
Q

What is Perthes’s disease?

A
  • Caused by idiopathic avascular necrosis of the femoral head
  • Lack of blood supply causes it to soften and break apart
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87
Q

What is the characteristic progression of Perthes disease?

A
  1. The essential lesion is loss of blood supply (avascular necrosis) of the nucleus of the proximal femoral epiphysis.
  2. Abnormal growth of the epiphysis results.
  3. Eventual remodelling of regenerated bone.
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88
Q

What are the features of Perthes disease?

A
  • Onset over weeks, no hx of trauma
  • Limitation of hip rotation and a subacute limp, sometimes with pain referred to groin thigh or knee
  • Typically unilateral (10% bilateral)
  • Antalgic gait
  • Roll test invokes guarding or spasm
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89
Q

What are the investigations of Perthes disease?

A
  • FBC and ESR
  • X-Ray - Progressive loss of joint space and bone loss around the femoral head and neck
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90
Q

What would the non-operative treatment for Perthes disease be?

A

Restriction of activities and weight-bearing until ossification is complete.
Physiotherapy
NSAIDs

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91
Q

What would the operative treatment for Perthes disease be?

A

Femoral or pelvic osteotomy.
Valgus or shelf osteotomies.
Hip arthroscopy.
Hip arthrodiastasis (controversial).

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92
Q

What are febrile seizures?

A

Seizures generally occurring between 6 months and 5 years, triggered by fever often due to infection
- Other causes e.g. hypoglycaemia, hypomagnesemia are absent

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93
Q

What would positive Kernig’s sign indicate?

A

CNS infection:
Meningitis
Encephalitis

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94
Q

What causes Henoch-Schonlein purpura?

A

IgA mediated vasculitis often post-infection

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95
Q

What would be the management for HSP be?

A

Admission to monitor for development of nephrotic syndrome and intussusception

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96
Q

Before causative organism is know, how would suspected causes of sepsis be treated?

A
  • IV 3rd generation cephalosporin - cefotaxime
  • IV amoxicillin
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97
Q

What causes measles?

A

A paramyxovirus

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98
Q

What are koplik spots?

A
  • Pathognomonic spots in measles
  • Small bright red spots with white centre on the buccal mucosa
  • Precede the measles rash by 1-2 days
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99
Q

What would scarlet fever typically present with?

A
  • Maculopapular “sandpaper rash” that feels rough on palpation
  • Rash classically spares the area around the mouth - perioral pallor
  • Bright red “strawberry tongue”
  • Sore throat
  • Fever
  • Headache, nausea, fatigue, vomiting
  • Cervical lymphadenopathy
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100
Q

What are the features of Rickets?

A

Condition caused by vitamin D deficiency
- Delayed motor development due to hypotonia and poor bone growth
- Often associated with predominant milk
- Delayed closure of anterior fontanelle
- Craniotabes
- Rachitic rosary
- Widening of wrist joint and sometimes ankle joint
- Severe cases - bowing of legs and short stature

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101
Q

What would investigations of Rickets show?

A
  • Low Vitamin D levels
  • Low serum calcium and phosphorus
  • High Alkaline Phosphatase
    X-Ray:
  • Cupping and fraying of ends of long bones (radius and ulna)
  • Osteopenia
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102
Q

What would treatment of Rickets be?

A
  • Sun exposure
  • Calcium and Vitamin D rich diet
  • Supplementation of vitamin D and calcium
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103
Q

What criteria is used to diagnose functional constipation?

A

ROME III

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104
Q

What would be seen in functional constipation

A
  • Passage of stool twice or fewer times per week or passage of hard stool
  • Associated abdominal pain
  • No abdominal distension and no impact on growth
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105
Q

What would hypothyroidism present with in children?

A
  • Constipation
  • Short height
  • Developmental delay
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106
Q

How would anal fissures present in children?

A
  • Painful defecation
  • Worse on hard stool
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107
Q

What would Hirschsprung’s disease present with?

A
  • Constipation with associated abdominal distension
  • Abdominal pain
  • Vomiting
  • May be history of delayed passage of meconium during the neonatal period
108
Q

What is the most common cause of haematemesis in children?

A

Extrahepatic portal vein obstruction (EHPVO)

109
Q

What would extrahepatic portal vein obstruction present with?

A

Haematemesis
- Child is typically well

110
Q

What is b thalassaemia?

A

An inherited disorder affecting the production of Hb chains in the red blood cell
Results in microcytic and hypochromic anaemia

111
Q

What anaemia is found in b thalassaemia?

A

Microcytic hypochromic anaemia
(Low mean corpuscular/cell volume)
(Low mean cell haematocrit

112
Q

What anaemia is found in cobalamin (B12) deficiency

A

Megaloblastic, macrocytic anaemia

113
Q

Which 9 conditions are screened in newborns using heel-prick test?

A
  1. Congenital hypothyroidism
  2. Sickle cell disorder
  3. Cystic fibrosis
  4. Phenylketonuria
  5. Medium-chain-acyl-CoA dehydrogenase deficiency
  6. Maple syrup urine disease
  7. Isovaleric acidaemia
  8. Glutaric aciduria type 1
  9. Homocystinuria
114
Q

What are the respective signs of puberty in each sex?

A

Breast budding is the first pubertal sign in females.

Testicular enlargement is the parallel sign in males.

115
Q

What is Turner’s Syndrome?

A
  • A sex chromosome disorder of female sexual development (45, XO).
116
Q

What are the symptoms of Turner’s syndrome?

A
  • Short stature
  • Ovarian dysgenesis
  • Lymphatic defects
  • Cystic hygroma
  • Webbed neck
  • Lymphoedema
  • Preductal coarctation of the aorta (Hypertension in upper extremities and weak pulses in the lower extremities)
117
Q

What is minimal change disease?

A
  • Most common cause of nephrotic syndrome in children
  • Characterised by peripheral oedema associated with heavy proteinuria, hypoalbuminaemia and hyperlipidaemia
  • Nephrons appear normal under optical microscope
118
Q

How is nephrotic syndrome defined?

A

Heavy proteinuria (≥3.5 g/day); and
Hypoalbuminaemia (serum albumin ≤30* g/L)
Peripheral oedema.

119
Q

What are the signs and symptoms of nephrotic syndrome?

A

Oedema
Hypovolaemia
Symptoms of infection
Breathlessness

120
Q

How is patent ductus arteriosus treated?

A

IV Indomethacin
Prostacyclin synthetase inhibitors

121
Q

How would a patent ductus arteriosus be kept open?

A

Prostaglandin infusion

122
Q

What is tinea corporis?

A

Infection of the trunk, legs or arms with a dermatophyte fungus

(Also known as ringworm)

123
Q

What are the symptoms of tinea corporis?

A
  • Rash presenting as enlarging raised red rings with central area of clearing
  • Edge of the rash is elevated and scaly to touch
  • Sometimes skin surrounding rash may be dry and flaky
124
Q

How is tinea corporis diagnosed?

A

Clinically
Skin scrapings may be sent for microscopy - showing hyphae and spores

125
Q

What is the management for tinea corporis?

A

Topical antifungal continued for 2 weeks after lesions disappear:
- Clotrimazole
- Ketoconazole
- Miconazole
Steroids may be used with intense inflammation for maximum of 1 week

126
Q

What would immediate management of epiglottitis be?

A
  • Avoid stressing the child, as airway can quickly become compromised
  • Avoid examination of throat and invasive procedures
  • Call for a senior paediatrician and anaesthetics/ENT support
127
Q

What are the clinical features of pityriasis rosea?

A
  • Rash starting as singular patch and then spreading to involve trunk
  • Initial patch typically measures 2-5cm in diameter - oval or round with a central wrinkled salmon coloured area, separated from a dark-red peripheral zone by fine scales
128
Q

What does impetigo present with?

A

Honey-coloured crusted plaques that tend to be under 2cm in diameter
- Usually on face but also may be on extremities
- Regional lymph node involvement

129
Q

What causes impetigo?

A

Most commonly Staphylococcus aureus or Streptococcus pyogenes

130
Q

What causes erythema infectiosum?

A

Parvovirus B19

131
Q

What would the prodromal phase of erythema infectiosum be?

A
  • Approximately 1 week after exposure
  • Headache, rhinitis, sore throat, low-grade fever and malaise
132
Q

What would be present in the main phase of erythema infectiosum?

A
  • After 7-10 days from the prodromal phase a “slapped cheek” rash appears as erythema on the cheeks, sparing the nose, perioral and periorbital regions
  • After a few days an erythematous macular rash develops on extremities, mainly on extensor surfaces
133
Q

What causes Molluscum contagiosum?

A

Pox virus
Transmitted through direct skin contact - infectious so long as lesions are present

134
Q

What lesions are present in molluscum contagiosum?

A
  • Firm, smooth, umbilicated papules, usually 2-5mm in diameter
  • May be the colour of skin, white, translucent or slightly yellow
135
Q

What is the usual developmental order of drawing shapes?

A
  1. Line
  2. Circle
  3. Cross
  4. Square
  5. Triangle
136
Q

How soon before being able to draw a shape can a child copy it?

A

6 months

137
Q

What could the presentation of meningitis/meningococcal sepsis be in neonates?

A

Seizures
Bulging fontenelle
Tachycardia, cyanosis, increased temperature

138
Q

What are the risk factors for neonatal sepsis?

A
  • Preterm
  • Low birth weight
139
Q

When would early-onset neonatal sepsis present?

A

Within the first 48-72 hours of life

140
Q

When would late-onset neonatal sepsis present?

A

After the first 72 hours of life

141
Q

What is the treatment for meningitis ages <3 months?

A

IV Amoxicillin and IV cefotaxime

142
Q

What is Haemophilia A?

A

An X-Linked recessive disease
Occurs due to deficiency of factor VIII

143
Q

What are the symptoms of Haemophilia A?

A
  1. Severe epistaxis
  2. Bleeding gums
  3. Haematuria: gross or microscopic (i.e. detected on dipstick).
  4. Intra-articular or intramuscular bleeds: commonly affected joints include the knees, ankles and elbows.
  5. Excessive bruising/ecchymoses, contusions or spontaneous haemorrhage during childhood play.
  6. Prolonged bleeding after a surgical or dental procedure, or post-venepuncture.
144
Q

What would investigations of Haemophilia A show?

A
  • Prolonged APTT
  • Normal PT
145
Q

What would acute leukaemia present with?

A

Fever
Lethargy
Pallor
Petechiae

146
Q

How would symptoms of acute leukaemia be investigates?

A
  • FBC - High white cell counts, anaemia, thrombocytopenia
  • Bone marrow aspirate/biopsy - required for diagnosis
147
Q

Why do petechiae occur in idiopathic thrombocytopenic purpura?

A

Due to low platelet counts

148
Q

What may clinical examination in a patient with haemophilia show?

A

Bruising
Haematoma
Active bleeding
Joint swelling (Haemarthrosis)

149
Q

What is intussusception?

A

Commonest cause of childhood intestinal obstruction
- Caused by ‘telescoping’ of the small bowel in on itself
- Typically occurs at 3-12 months

150
Q

What are the signs and symptoms of intussusception?

A
  • Inconsolable crying
  • Drawing up of the legs (Indicative of colic)
  • Vomiting
  • PR blood (Like redcurrant jelly, or just flecks)
151
Q

What may be seen on examination in intussusception?

A

‘Sausage-shaped’ abdominal mass in the right upper quadrant of the

152
Q

How is intussusception investigated?

A

Ultrasound scan
(Also used to guide reduction by air enema)

153
Q

What is Hirschsprung’s disease?

A

Absence of myenteric plexus at the rectum - results in constipation, loading and dilatation of the normally innervated bowel immediately before affected section

154
Q

What are the risk factors for SIDS (Sudden Infant Death Syndrome) relating to baby?

A

Sleeping position (prone sleeping, use of blankets)
Male gender
Age 2-4 months
Prematurity/low birth weight
Formula feeding

155
Q

What are the risk factors for SIDS (Sudden Infant Death Syndrome) relating to mum?

A

Smoking in pregnancy
Alcohol or substance abuse
Age less than 20 at first pregnancy

156
Q

When can a child turn one page of a book at a time?

A

At 3 years

157
Q

When will a child develop mature pincer grip?

A

1 year

158
Q

When will a child be able to turn several pages of a book at a time?

A

2 years

159
Q

When will a child be able to draw a cross?

A

4 years

160
Q

What causes chickenpox?

A

Varicella-zoster virus

161
Q

What is the incubation period of chickenpox?

A

10-14 days between exposure and first skin lesions

162
Q

What are the initial presenting features of chickenpox?

A

Pyrexia
Headache
Malaise
Abdominal pain

163
Q

What do skin lesions present with in chickenpox?

A

Crops of vesicles present over 3-5 days
- Typically on the head, neck and trunk - less on the limbs
- Lesions are intensely itchy
- Pass through stages of papule, vesicle, pustule and crust

164
Q

When are the skin lesions infectious from in chickenpox?

A

From a few days before the onset of lesions until crusts fall off

165
Q

How is chickenpox diagnosed?

A

Diagnosed clinically

166
Q

What causes measles?

A

A single-stranded RNA Morbillivirus

167
Q

Between the ages of 1 to 5, what clinical signs would indicate an acute severe exacerbation of asthma?

A
  1. Heart rate >=145bpm
  2. Oxygen saturations <92%
168
Q

What is necrotising enterocolitis?

A

Condition in which the bowel becomes ischaemic
- Typically occurs in newborns that are either premature or otherwise unwell

169
Q

What are the symptoms of necrotising enterocolitis?

A

Typical symptoms:
- A new feed intolerance
- Vomiting (which may be bilious)
- Haematochezia (fresh blood in the stools)

  • Bloating, decreased activity
170
Q

What are the risk factors for necrotising enterocolitis?

A

Congenital heart disease
Birth asphyxia
Exchange transfusion
Prematurity
Prolonged rupture of membranes

171
Q

What are the typical examination findings in necrotising enterocolitis?

A

Abdominal distension
Reduced bowel sounds
Palpable abdominal mass
Visible intestinal loops
Signs of sepsis

172
Q

What are the typical presenting features of Duchenne’s muscular dystrophy?

A

Progressive weakness: starting proximally and moving distally with the lower limbs being affected before the upper limbs.
Delayed motor milestones: typically the ability to walk independently.
Waddling gait

173
Q

What are the clinical findings in muscular dystrophy?

A

Weakness: typically the proximal and distal leg muscles in the earlier phases of the disease.
Calf pseudohypertrophy: due to the accumulation of connective tissue and fat replacing muscle tissue.
Waddling gait: typically exacerbated when attempting to run.
Tip-toe walking: occurs due to shortening of the Achilles tendon.
Gower’s sign: the child climbs up their legs when rising from the floor.
Hyporeflexia or areflexia
Loss of the arches of the feet (i.e. flat feet)
Difficulty or inability to squat

174
Q

What is the classical triad of haemolytic-uraemic syndrome?

A
  1. Microangiopathy haemolytic anaemia
  2. Thrombocytopenia
  3. Acute kidney injury
175
Q

How can haemolytic-uraemic syndrome be investigated?

A

FBC
Peripheral blood smear
Renal function studies
Urinalysis

176
Q

What can cause haemolytic-uraemic syndrome?

A

Primary causes:
- Complement dysregulation disorders
- Mutations of proteins in coagulation pathway and cobalamin metabolism
Secondary causes (More common):
- Infectious disease - Shiga toxin-producing Escherichia coli, pneumococcus

177
Q

What commonly causes epiglottitis?

A

Haemophilus influenzae type B (HiB)

178
Q

How does coeliac present in children?

A

Failure to thrive (stunted growth, growth chart faltering)
Chronic diarrhoea
Constipation (coeliac disease should be considered whenever diagnosing idiopathic constipation)
Abdominal bloating
Irritability
Features of anaemia (adolescents)

179
Q

What is important to cover in a coeliac history?

A

Family history: coeliac disease often runs in families and those with an affected first-degree family member have around a 10% chance of developing it.
Associated conditions: there are a range of conditions that, if present, would increase the risk of coeliac disease.

180
Q

What can be identified in clinical examination in children with coeliac disease?

A

Failure to thrive (although less common due to increased calorific diets in modern western diet)
Abdominal distension
Abdominal pain
Muscle wasting (usually the buttocks are predominantly affected)
Features of anaemia (adolescents) e.g. angular cheilitis, fatigue and pallor

181
Q

What causes Coeliac disease

A

Immune-mediated, inflammatory systemic disorder to a protein in gluten
Gluten is found in wheat, rye and barley

182
Q

In the first 12 months of life, what are the relevant speech and hearing developmental milestones?

A

Birth: Quiets to voice
6-8 weeks: Vocalises
3 months: Turns to sound
4-5 months: Squeals
6-9 months: Babbles - turns to voice
10-12 months - double syllable babble - Da-Da

183
Q

From 12 months to 5 years what are the relevant speech and hearing developmental milestones?

A

13 months: Single words
18 months: Knows 1 body part
2 years: Speaks 2-word sentences ~50 words, names 2 body parts
3 years: Can say name, age, sex, Asks “What’s that”, counts to 10, can name 5 body parts
4 years: Uses past tense, can count to 20
5 years: Knows colours, age, address

184
Q

What is syndactyly?

A

Being born with toes or fingers joined together

185
Q

What is polydactyly?

A

Being born with extra toes or fingers

186
Q

What is polysyndactyly?

A

Being born with extra fingers, some of which are fused together
- Results as a failure of apoptosis

187
Q

What is Osgood-Schlatter disease?

A

Disease occurring as a result of the strength of the quadriceps muscle exceeding ability of the tibial tuberosity to resist its pull

188
Q

How would Osgood-Schlatter disease present?

A

Gradual onset pain and swelling over the tibial tuberosity exacerbated with exercise
- Presenting most commonly between 12 and 15 years

189
Q

How would Osgood-Schlatter disease be investigated?

A

X-Ray
- Shows irregularity of apophysis, separation from the tibial tuberosity in early stages and fragmentation in later stages

190
Q

What is the management for Osgood-Schlatter disease?

A

Rest, reduced exercise intensity
Physiotherapy
- Most cases resolve as the growth plates ossify

191
Q

What is a barky, seal-like cough characteristic of?

A

Croup

192
Q

What is the management of bronchiolitis?

A

Mainly supportive
- Oxygen supplementation when sats <92%
- CPAP or High flow oxygen if respiratory distress
- NG Tube if child does not have adequate feeding/fluid intake

193
Q

When is hospital admission indicated in bronchiolitis?

A

Apnoeas
Reduced oxygen saturation: <92%
Reduced oral intake: <50-75% of normal
Persistent respiratory distress: significant chest recessions, grunting
Presence of risk factors for severe disease
Difficult social factors: living very far from the hospital, lack of parental confidence

194
Q

What is the management of psoriasis

A

Emollients to moisturise dry skin, reduce scale and relieve itching
Topical steroids to reduce skin inflammation
Tar preparations to reduce scaling and slow skin overgrowth
Dithranol for stubborn plaques of psoriasis on ‘non-delicate’ skin such as elbows and knees
Vitamin D analogues (calcipotriol, tacalcitol, and calcitriol) help regulate the immune system in the skin and slow the overgrowth of skin

195
Q

What are the characteristics of guttate psoriasis?

A

Multiple small, scaly plaques distributed across the trunk and limbs
- Resemblance of raindrops

196
Q

When should solid foods be introduced into an infant’s diet?

A

6 months

197
Q

What is post-infectious glomerulonephritis?

A

Inflammatory reaction within glomeruli, typically occurring 1-4 weeks after a pharyngeal infection with a bacterium

198
Q

Infection with what bacteria classically precedes post-infectious glomerulonephritis?

A

Streptococcus pyogenes

199
Q

How does post-infectious glomerulonephritis present?

A

Malaise
Slight fever
Nausea
Mild nephritic syndrome:
- Increased BP
- Gross haematuria
- Smoky-brown urine

200
Q

How is post-infectious glomerulonephritis diagnosed?

A

Antistreptolysin-O antibodies
- Levels begin to rise after 1-3 weeks of Strep infection, peak at 3-5 weeks and fall back to insignificant levels within 6 months

201
Q

How does pyelonephritis present?

A

Renal angle pain
Vomiting
Rigors
Sepsis

202
Q

Which factor is affected in Haemophilia A?

A

Factor VIII

203
Q

Which factor is affected in Haemophilia B?

A

Factor IX

204
Q

What is the inheritance pattern of phenylketonuria?

A

Autosomal recessive

205
Q

What are febrile convulsions?

A

Seizures occurring at the beginning of a febrile illness
- Usually tonic-clonic seizures and last for less than 5 minutes

206
Q

What are the relevant investigations needed to rule out other forms of seizures in febrile convulsions?

A
  1. Blood glucose
  2. Electrolytes - to check for electrolyte imbalances
  3. Full blood count, CRP, blood culture - to screen for infection
  4. EEG
  5. MRI - to look for mass lesions
207
Q

How are febrile convulsions treated?

A

Treating fever
IV/Rectal diazepam if necessary

208
Q

What ages are most likely to have febrile convulsions?

A

Ages 6months to 6years of age

209
Q

What is the typical presentation of diphtheria?

A
  1. Nasal discharge, initially watery but becomes purulent and blood-stained
  2. Membranous pharyngitis - fever, enlarged anterior cervical lymph nodes, oedema of soft tissues giving a bull-neck appearance
  3. Respiratory obstruction
210
Q

What are the long-term effects of diphtheria toxins?

A
  • Cardiomyopathy and myocarditis, usually evident by 10th to 14th day
  • Neuritis affecting motor nerves, paralysis of soft palate, ocular nerves, peripheral nerves and diaphragm
  • Nephritis
    Thrombocytopenia
211
Q

What is the characteristic cutaneous infection of diphtheria?

A

Mild, but chronic:
1. Vesicles or pustules that quickly rupture to form a punched-out ulcer ~several cm in diameter
2. Often appears on lower legs, feet and hands
3. Painful in first week or two, covered with dark pseudomembrane which separates to show haemorrhagic base

212
Q

How is diphtheria definitively diagnosed?

A

Through a positive culture from respiratory tract secretions or cutaneous lesions
Positive toxin assay

213
Q

How is diphtheria managed?

A
  1. Abx - erythromycin, azithromycin, clarithromycin or penicillin
  2. Immunisation in the convalescent stage
  3. Management of contacts - given antibiotic prophylaxis
214
Q

Which bacterium is responsible for diphtheria?

A

Corynebacterium diphtheriae
- Gram-positive, aerobic, non-motile, rod-shaped bacterium

215
Q

What is biliary atresia?

A

Condition of uncertain cause in which all or part of the extrahepatic bile ducts are obliterated by inflammation and subsequent fibrosis
- Leads to biliary obstruction and jaundice

216
Q

How does biliary atresia present?

A

Persistent jaundice
Pale stools
Dark urine
Splenomegaly after 3 months - sign of portal hypertension
Failure to thrive - result of poor absorption of long-chain fats and catabolic state

217
Q

How is biliary atresia investigated?

A

LFTs - conjugated hyperbilirubinaemia, high GGT
Ultrasound and hepatobiliary scintigraphy - differentiate atresia from neonatal hepatitis

218
Q

How is biliary atresia managed?

A

Surgery - Kasai portoenterostomy and liver transplantation
Medical - abx to prevent cholangitis, ursodeoxycholic acid to encourage bile flow, fat soluble supplementation and nutritional support

219
Q

What is Barlow’s test?

A

Physical examination performed on infants to screen for developmental dysplasia of the hip
- Adduction of the hip (bringing the thigh towards the midline) while applying light pressure on the knee, directing the force posteriorly
- Positive if hip can be dislocated

220
Q

What is the Ortolani manoeuvre?

A

Flexing the hips and knees of a supine infant to 90 degrees, then placing anterior pressure on the greater trochanters
Then smooth and gentle abduction of the legs - positive sign is a distinctive clunk

221
Q

What is slipped femoral epiphysis?

A

Fracture in the growth plate, resulting in slippage of the metaphysis

222
Q

What is Osteogenesis imperfecta?

A

Genetic disorder that results in bones which break easily - disorder of collagen type I

223
Q

How do patients with slipped femoral epiphysis present?

A

Groin pain
Pain extending along distribution of the obturator nerve
Reduced range of motion in flexion and abduction
Antalgic gait

224
Q

How do patients with Osteogenesis imperfecta present?

A

Blue sclera
Short height
Loose joints

225
Q

What is developemental dysplasia of the hip?

A

A condition in which the femoral head has an abnormal anatomical relationship with the acetabulum
- Leads to abnormal bony development which often results in premature arthritis and significant disability

226
Q

What is transposition of the great arteries?

A

Anatomical reversal of the aorta and pulmonary artery
- Not typically picked up on routine antenatal scans

227
Q

What is scarlet fever caused by?

A

Streptococcal infection

228
Q

What does Juvenile idiopathic arthritis present with?

A

Non-specific presentation involving extended period of:
- Fever
- Arthritis
- Rash

229
Q

What is Reye’s Syndrome?

A

Rapidly progressive encephalopathy
- Caused by high-dose aspirin
- Damage to mitochondria in the liver, leading to ammonia buildup

230
Q

What is retinoblastoma?

A

Embryonal tumour of the retina
Most common malignancy of the eye in children
- 40% caused by a hereditary mutation on chromosome 13 - retinoblastoma 1 gene

231
Q

What are the presenting features of retinoblastoma?

A

Leukocoria - abnormal appearance of the eye
Deterioration of vision
Red, irritated eye
Squint
Strabismus
Buphthalmos, pain, glaucoma

232
Q

How is retinoblastoma diagnosed?

A

Investigated under anaesthesia with a maximally dilated pupil
Imaging - bi-dimensional ocular ultrasound and MRI

233
Q

What is staphylococcal scalded skin syndrome?

A

Illness characterised by red blistering skin resembling scalds

234
Q

What causes staphylococcal scalded skin syndrome (SSSS)?

A

Two exotoxins - epidermolytic toxins A and B

235
Q

What are the initial features of SSSS?

A

Fever
Generalised erythema
Skin tenderness
Extremely tender flaccid bullae develop within 48 hours - commonly affect flexures

236
Q

What are the features of the SSSS rash?

A

Bullae develop, commonly affecting flexures
Bullae enlarge and rupture easily to reveal a moist erythematous base - gives rise to scalded appearance

237
Q

How are patients treated for SSSS?

A

Hospital admission
IV flucloxacillin
Manage fluid balance
(Most patients rapidly recover within a few days)

238
Q

What is Gillick competence?

A

Children <16 can consent to medical treatment (but not refuse it) if they have sufficient maturity and understanding of what is being proposed without parental consent

239
Q

What is laryngomalacia?

A

A self-limiting condition seen in infants, commonly causing stridor, but with no associated respiratory distress

240
Q

What would be the most sensitive investigation for cystic fibrosis?

A

Sweat test - 98% sensitive

241
Q

What is cystic fibrosis (CF)?

A

An autosomal recessive disease affecting CFTR gene on chromosome 7
- Leads to thickened secretions, predisposing to recurrent respiratory infections

242
Q

What are the clinical features of CF?

A
  1. Respiratory - recurrent lower respiratory tract infections and bronchiectasis, nasal polyps
  2. GI - pancreatic insufficiency (exocrine and endocrine dysfunction), CF-related diabetes (CFRD), pancreatitis, gallstones
    - Intestinal obstruction in newborn (meconium ileus)
    - Diarrhoea (due to malabsorption)
  3. Infertility - congenital absence of vas deferens, irregular menstruation
243
Q

What is WAGR Syndrome?

A

Deletion in WIlm’s Tumour gene (WT1) on chromosome 11 - gene functioning as a factor of transcription in development of both gonadal and renal tissues

Quartet of:
- Wilm’s Tumour
- Aniridia
- Genitourinary abnormalities
- Intellectual disability

244
Q

What is the cut-off for acceptable weight loss in the first 7 days of life?

A

10%

245
Q

What ages does a slipped femoral epiphysis present?

A

Between 10-16

246
Q

What would first-line management option in a child wetting the bed frequently?

A

Over the age of 5, non-pharmacological treatments:
- Fluid intake, diet, toilet behavioural training, reward systems
Then, nocturnal enuresis alarms would be used - form new behaviours

247
Q

Which vitamin deficiency is associated with an increased risk of severe measles infection?

A

Vitamin A

248
Q

When should a child see a paediatrician if they are not walking by?

A

18 months

249
Q

What are the main complications of Kawasaki disease?

A

Coronary artery aneurysms

250
Q

What is patent ductus arteriosus (PDA)?

A

Acyanotic congenital heart disease
Unclosed connection between pulmonary trunk and descending aorta

251
Q

What are the features of a PDA?

A
  1. Left subclavian thrill
  2. Continuous machinery murmur
  3. Large volume, bounding, collapsing pulse
  4. Wide pulse pressure
  5. Heaving apex beat
252
Q

How is PDA managed?

A

Indomethacin or ibuprofen - inhibits prostaglandin synthesis

(If associated with another congenital heart defect treatable with surgery, then prostaglandin E1 useful to keep duct open until after surgical repair)

253
Q

What symptoms are seen in Kawasaki disease?

A
  1. Dry cracked lips
  2. Bilateral conjunctivitis
  3. Peeling of skin on fingers and toes
  4. Cervical lymphadenopathy
  5. Red rash over trunk
254
Q

When would a child be able to sit without support?

A

6-8 months

255
Q

When is puberty considered delayed in females?

A

When they have not begun thelarche by 13 or menarche by 15

256
Q

What is the most common cause of neonatal sepsis?

A

Group B streptococcus
Escherichia coli

257
Q

What will neonates usually present with in GBS sepsis?

A
  1. Respiratory distress - drunting, nasal flaring, use of accessory muscles, tachypnoea
  2. Tachycardia
  3. Apnoea
  4. Jaundice
  5. Seizures
258
Q

What is therapeutic cooling?

A

Deliberate lowering of patient’s body temperature to cool the brain and prevent brain damage

  • Used in neonates with moderate to severe hypoxic ischaemic encephalopathy
259
Q

What can Abdominal X-Rays show in necrotising enterocolitis?

A

Dilated bowel loops
Bowel wall oedema
Intramural gas
Portal venous gas
Pneumoperitoneum
Gas cysts

260
Q

What investigation is diagnostic for Hirschsprung’s disease?

A

Rectal biopsy

261
Q

What is Ebstein’s anomaly?

A

Congenital heart defect characterised by low insertion of the tricuspid valve
- Results in large atrium and small ventricle

262
Q

What is Ebstein’s anomaly associated with?

A

Patent foramen ovale or ASD
Wolff-Parkinson-White

263
Q

What are the clinical features of Ebstein’s anomaly?

A

Cyanosis
Prominent ‘a’ wave in the distended jugular venous pulse
Hepatomegaly
Triscuspid regurgitation - pansystolic murmur
Right bundle branch block

264
Q

What disease can raised Immunoreactive trypsinogen implicate on a heel prick test?

A

Cystic fibrosis

265
Q

What would be present upon sweat test in CF?

A

Abnormally high sweat chloride (Normal value < 40 mEq/l)
CF indicated by > 60 mEq/l

Phase 3a (6 decks)

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