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Child health > Pathology Part 1 > Flashcards

Pathology Part 1 Flashcards

1
Q

Achondroplasia

A

An autosomal dominant disorder associated with short stature. It is caused by a mutation in the fibroblast growth factor receptor 3 (FGFR-3) gene.

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2
Q

Features of Achondroplasia

A 
>   Short limbs with shortened fingers 
>   Large head with frontal bossing 
>   Narrow foramen magnum
>   Midface hypoplasia with a flattened nasal bridge
>   'Trident' hands
>   Lumbar lordosis
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3
Q

Rhizomelia

A

Short limbs

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4
Q

Brachydactyly

A

Shortened fingers

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5
Q

Risk factors for Achondroplasia

A

Advancing parental age at the time of conception

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6
Q

Treatment for Achondroplasia

A

No specific therapy
Some individuals benefit from limb lengthening procedures - involves application of Ilizarov frames and targeted bone fractures

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7
Q

Acute epiglottitis

A

Acute epiglottitis is rare but serious infection characterized by swelling and inflammation of the epiglottis.

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8
Q

What is the main cause of Acute epiglottitis?

A

Haemophilus influenzae type B

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9
Q

What vaccine has a caused a decrease in Acute epiglottitis?

A

Haemophilus influenzae type B vaccine (HiB vaccine)

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10
Q

Features of Acute epiglottitis

A
  1. rapid onset
  2. high temperature, generally unwell
  3. stridor
  4. drooling of saliva
  5. ‘tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
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11
Q

Stridor

A

A high-pitched sound that is heard best with inspiration. Caused by an obstruction or narrowing in upper airway.

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12
Q

Diagnosis of Acute epiglottitis

A

Direct visualization (only by senior/airway trained staff)

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13
Q

Why is acute epiglottitis only examined by senior/airway trained staff?

A

Due to the risk of acute airway obstruction

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14
Q

Treatment of Acute epiglottitis

A
  1. Immediate senior involvement
  2. endotracheal intubation to protect the airway
  3. Oxygen therapy
  4. Intravenous antibiotics
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15
Q

Acute lymphoblastic leukaemia

A

The most common malignancy affecting children and accounts for 80% of childhood leukaemias.

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16
Q

Features of Acute lymphoblastic leukaemia

A

Features of bone marrow failure:

  1. anaemia: lethargy and pallor
  2. neutropaenia: frequent or severe infections
  3. thrombocytopenia: easy bruising, petechiae
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17
Q

Additional features of Acute lymphoblastic leukaemia besides bone marrow failure

A 
>   bone pain 
>   splenomegaly
>   hepatomegaly
>   fever is present in up to 50% of new cases 
>   testicular swelling
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18
Q

Why is fever a presenting feature in up to 50% of new cases of Acute lymphoblastic leukaemia?

A

Represents infection or constitutional symptom

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19
Q

Poor prognostic factors for Acute lymphoblastic leukaemia

A
  1. age < 2 years or > 10 years
  2. WBC > 20 * 109/l at diagnosis
  3. T or B cell surface markers
  4. non-Caucasian
  5. male sex
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20
Q

What age does testicular torsion usually occur?

A

Most common around puberty

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21
Q

What age does irreducible inguinal hernia usually occur?

A

Most common in children < 2 years old

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22
Q

What age does epididymitis usually occur?

A

Rare in prepubescent children

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23
Q

Alpha-thalassaemia

A

Inherited condition which causes a deficiency of alpha chains in haemoglobin

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24
Q

What is the sex determining gene present on the Y chromosome?

A

SRY gene - which causes differentiation of the gonad into a testis

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25
Q

What happens if the SRY gene is absent on the Y chromosome?

A

If absent (i.e. in a female) then the gonads differentiate to become ovaries

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26
Q

What is the most common cause of Ambiguous genitalia in newborns?

A

Congenital adrenal hyperplasia

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27
Q

Apgar score

A

Used to assess the health of a newborn baby

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28
Q

What are the categories present in the APGAR score?

A 
Pulse
Respiratory effect
Colour
Muscle tone
Reflex irritability
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29
Q

Acute appendicitis features

A
  1. Central abdominal pain - radiates to the right iliac fossa
  2. Low-grade pyrexia
  3. Minimal vomiting
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30
Q

What age group is acute appendicitis uncommon?

A

Under 4 years old but in this group often presents with perforation

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31
Q

Features of severe asthma attack in children

A 
>   SpO2 < 92%
>   PEF 33-50% best or predicted
>   Too breathless to talk or feed
>   HR over 125 (>5 years) 
>   HR over 140 (1-5 years)
>   RR over 30 breaths/min (>5 years) 
>   RR over 40 (1-5 years)
>   Use of accessory neck muscles
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32
Q

Features of Life-threatening asthma attack in children

A 
>   SpO2 <92%
>   PEF <33% best or predicted
>   Silent chest
>   Poor respiratory effort
>   Agitation
>   Altered consciousness
>   Cyanosis
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33
Q

Features of Moderate asthma attack in children

A

> SpO2 > 92%
No clinical features of severe asthma
PEF > 50% best or predicted in children >5 years old

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34
Q

Management of severe/life-threatening asthma attack in children

A

Transferred immediately to hospital.

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35
Q

Management of mild/moderate asthma attacks in children

A
  1. Give a beta-2 agonist via a spacer (for a child < 3 years use a close-fitting mask)
  2. Give 1 puff every 30-60 seconds up to a maximum of 10 puffs
  3. If symptoms are not controlled repeat beta-2 agonist and refer to hospital
  4. Steroid therapy should be given to all children with an asthma exacerbation - should be given for 3-5 days
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36
Q

Asthma management of children 5 to 16 years old

A
  1. Short-acting beta agonist (SABA)
  2. SABA + paediatric low-dose ICS
  3. SABA + paediatric low-dose ICS + (LTRA)
  4. SABA + paediatric low-dose ICS + (LABA)
  5. SABA + switch ICS/LABA to a MART, that includes a paediatric low-dose ICS
  6. SABA + paediatric moderate-dose ICS + MART
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37
Q

Asthma management of children under 5 years old

A
  1. Short-acting beta agonist (SABA)
  2. SABA + an 8-week trial of paediatric MODERATE- (ICS)
  3. SABA + paediatric low-dose ICS + (LTRA)
  4. Stop the LTRA and refer to asthma specialist
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38
Q

What should be done after a child under 5 years old has been given a SABA + an 8-week trial of paediatric MODERATE-dose inhaled corticosteroid (ICS) for asthma management?

A

After 8-weeks stop the ICS and monitor the child’s symptoms:
if symptoms did not resolve during the trial period, review whether an alternative diagnosis is likely

if symptoms resolved then reoccurred within 4 weeks of stopping ICS treatment, restart the ICS at a paediatric low dose as first-line maintenance therapy

if symptoms resolved but reoccurred beyond 4 weeks after stopping ICS treatment, repeat the 8‑week trial of a paediatric moderate dose of ICS

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39
Q

Maintenance and reliever therapy (MART)

A

A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required

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40
Q

What is a low dose paediatric ICS?

A

<= 200 micrograms budesonide or equivalent = paediatric low dose

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41
Q

What is a paediatric moderate dose ICS?

A

200 micrograms - 400 micrograms budesonide or equivalent = paediatric moderate dose

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42
Q

What is a paediatric high dose ICS?

A

> 400 micrograms budesonide or equivalent= paediatric high dose.

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43
Q

ADHD

A

DSM-V defines ADHD as a condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent. Like many paediatric conditions, there has to be an element of developmental delay.

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44
Q

Diagnosis of ADHD by DSM-V criteria

A

For children up to the age of 16 years, six of these features have to be present; in those aged 17 or over, the threshold is five features.

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45
Q

What are the symptoms of Inattention in ADHD?

A

Does not follow through on instructions
Reluctant to engage in mentally-intense tasks
Easily distracted
Finds it difficult to sustain tasks
Finds it difficult to organise tasks or activities
Often forgetful in daily activities
Often loses things necessary for tasks or activities
Often does not seem to listen when spoken to directly

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46
Q

What are the symptoms of Hyperactivity/Impulsivity in ADHD?

A

Unable to play quietly
Talks excessively
Does not wait their turn easily
Will spontaneously leave seat when expected to sit
Is often ‘on the go’
Often interruptive or intrusive to others
Will answer before a question has been finished
WIll run & climb where not appropriate

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47
Q

When is drug therapy given in ADHD?

A

As a last resort and is only available to those aged 5 years or more.

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48
Q

Methylphenidate

A

Drug used in ADHD - A CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor.

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49
Q

Methylphenidate side effects

A

Abdominal pain, nausea and dyspepsia.

In children, weight and height should be monitored every 6 months

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50
Q

Drugs available for management of ADHD

A

Methylphenidate
Lisdexamfetamine
Dexamfetamine

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51
Q

What should be done before giving drug therapy in ADHD?

A

All of these drugs are potentially cardiotoxic.

Perform a baseline ECG before starting treatment, and refer to a cardiologist if there is any significant past medical history or family history, or any doubt or ambiguity.

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52
Q

Autism spectrum disorder (ASD)

A

A neurodevelopmental condition characterized by qualitative impairment in social interaction and communication as well as repetitive stereotyped behaviour, interests, and activities. Symptoms are usually present during early childhood, but may be manifested later.

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53
Q

Pharmacological interventions for Autism spectrum disorder

A

SSRIs: helpful to reduce symptoms like repetitive stereotyped behaviour, anxiety, and aggression

Antipsychotic drugs: useful to reduce symptoms like aggression, self-injury.

Methylphenidate: for attention deficit hyperactivity disorder (ADHD).

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54
Q

Biliary atresia

A

Involves either obliteration or discontinuity within the extrahepatic biliary system, which results in an obstruction in the flow of bile.

This results in a neonatal presentation of cholestasis in the first few weeks of life.

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55
Q

The three types of Biliary atresia

A

Type 1
Type 2
Type 3

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56
Q

Type 1 Biliary atresia

A

The proximal ducts are patent, however, the common duct is obliterated

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57
Q

Type 2 Biliary atresia

A

There is atresia of the cystic duct and cystic structures are found in the porta hepatis

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58
Q

Type 3 Biliary atresia

A

There is atresia of the left and right ducts to the level of the porta hepatis, this occurs in >90% of cases of biliary atresia

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59
Q

Symptoms of Biliary atresia

A

Patients typically present in the first few weeks of life with:
> Jaundice extending beyond the physiological two weeks
> Dark urine and pale stools
> Appetite and growth disturbance, however, may be normal in some cases

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60
Q

Complications of Biliary atresia

A

Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma

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61
Q

Definitive management of Biliary atresia

A

Surgical intervention is the only definitive treatment

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62
Q

Investigations for Biliary atresia

A 
Serum bilirubin 
Liver function tests (LFTs)
Serum alpha 1-antitrypsin
Sweat chloride test
Ultrasound of the biliary tree and liver
Percutaneous liver biopsy with intraoperative cholangioscopy
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63
Q

Diagnostic markers for Biliary atresia

A

Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high

Serum bile acids and aminotransferases are usually raised

Ultrasound of the biliary tree and liver: May show distension and tract abnormalities

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64
Q

Bronchiolitis

A

A condition characterised by acute bronchiolar inflammation. Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases.

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65
Q

Causative agent for Bronchiolitis

A

Respiratory syncytial virus (RSV)

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66
Q

Epidemiology of Bronchiolitis

A

> Most common cause of a serious LRT infection in < 1yr olds.

> Maternal IgG provides protection to newborns against RSV

> Higher incidence in winter

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67
Q

Symptoms of Bronchiolitis

A

> coryzal symptoms precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

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68
Q

Symptoms requiring immediate referral to hospital (emergency).

A
  1. apnoea (observed or reported)
  2. child looks seriously unwell to a professional
  3. severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
  4. central cyanosis
  5. persistent oxygen saturation of less than 92%
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69
Q

Investigation for Bronchiolitis

A

immunofluorescence of nasopharyngeal secretions may show RSV

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70
Q

Management of Bronchiolitis

A
  1. Humidified oxygen if the oxygen saturations are persistently < 92%
  2. Nasogastric feeding if children cannot take enough fluid/feed by mouth
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71
Q

Caput succedaneum

A

Describes oedema of the scalp at the presenting part of the head, typically the vertex.

This may be due to mechanical trauma of the initial portion of the scalp pushing through the cervix in a prolonged delivery or secondary to the use of ventouse (vacuum) delivery

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72
Q

Caput succedaneum features

A

> Soft, puffy swelling due to localised oedema
crosses suture lines
Resolves within days
Present at birth

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73
Q

Cephalohaematoma

A

Seen as a swelling on the newborns head. It typically develops several hours after delivery and is due to bleeding between the periosteum and skull.

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74
Q

How long does it take for a Cephalohaematoma to resolve?

A

Up to 3 months

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75
Q

Most common site for Cephalohaematoma

A

Parietal region

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76
Q

Difference in presentation of Cephalohaematoma and Caput succedaneum

A

Caput succedaneum - present at birth

Cephalohaematoma - develops 2-3 hours after birth

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77
Q

Features of Cephalohaematoma

A

> Does not cross suture lines
Takes months to resolve
Develops several hours after birth

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78
Q

Cerebral palsy

A

May be defined as a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain.

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79
Q

Causes of Cerebral palsy

A

Antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)

Intrapartum (10%): birth asphyxia/trauma

Postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma

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80
Q

Cerebral palsy features

A
  1. abnormal tone early infancy
  2. delayed motor milestones
  3. abnormal gait
  4. feeding difficulties
  5. learning difficulties (60%)
  6. epilepsy (30%)
  7. squints (30%)
  8. hearing impairment (20%)
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81
Q

Chickenpox and Shingles

A

Chickenpox is caused by primary infection with varicella zoster virus.

Shingles is a reactivation of the dormant virus in dorsal root ganglion

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82
Q

Common complications of chickenpox

A

Secondary bacterial infection of the lesions

Whilst this commonly may manifest as a single infected lesion/small area of cellulitis, in a small number of patients invasive group A streptococcal soft tissue infections may occur resulting in necrotizing fasciitis

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83
Q

Complications (rare) for chickenpox

A

pneumonia
encephalitis
disseminated haemorrhagic chickenpox
arthritis, nephritis and pancreatitis

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84
Q

Chickenpox route of transmission

A

Spread via the respiratory route
Can be caught from someone with shingles
incubation period = 10-21 days

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85
Q

Infectivity period for Chicken pox

A

= 4 days before rash, until 5 days after the rash first appeared*

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86
Q

Features of chickenpox

A
  1. fever initially
  2. itchy, rash starting on head/trunk before spreading.
  3. Initially macular then papular then vesicular
  4. systemic upset is usually mild
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87
Q

Mumps

A

Fever, malaise, muscular pain

Parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

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88
Q

Parotitis

A

Inflammation of parotid glands - earache and ‘pain on eating’

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89
Q

Rubella

A

Rash: pink maculopapular, initially on face before spreading to whole body,

usually fades by the 3-5 day

Lymphadenopathy: suboccipital and postauricular

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90
Q

Erythema infectiosum

A

Also known as fifth disease or ‘slapped-cheek syndrome’
Caused by parvovirus B19
Lethargy, fever, headache
‘Slapped-cheek’ rash spreading to proximal arms and extensor surfaces

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91
Q

Hand, foot and mouth disease

A

Caused by the coxsackie A16 virus

Mild systemic upset: sore throat, fever

Vesicles in the mouth and on the palms and soles of the feet

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92
Q

Patau syndrome (trisomy 13)

A

Microcephalic, small eyes
Cleft lip/palate
Polydactyly
Scalp lesions

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93
Q

Edward’s syndrome (trisomy 18)

A

Micrognathia
Low-set ears
Rocker bottom feet
Overlapping of fingers

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94
Q

Micrognathia

A

A term for a lower jaw that is smaller than normal.

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95
Q

Microcephalic

A

A condition where a baby’s head is much smaller than expected.

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96
Q

Macrocephaly

A

The measurement around the widest part of the head) that is greater than the 98th percentile on the growth chart.

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97
Q

Pierre-Robin syndrome

A

Micrognathia
Posterior displacement of the tongue (may result in upper airway obstruction)
Cleft palate

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98
Q

Prader-Willi syndrome

A

Hypotonia
Hypogonadism
Obesity

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99
Q

William’s syndrome

A 
Short stature
Learning difficulties
Friendly, extrovert personality
Transient neonatal hypercalcaemia
Supravalvular aortic stenosis
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100
Q

Cause of Cleft Lip

A

Results from failure of the fronto-nasal and maxillary processes to fuse

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101
Q

Cause of Cleft palate

A

Results from failure of the palatine processes and the nasal septum to fuse

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102
Q

Most common congenital deformity affecting the orofacial structures

A

Cleft lip and palate

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103
Q

Management of cleft lip and palate

A

Cleft lip is repaired earlier than cleft palate

Cleft palates are typically repaired between 6-12 months of age

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104
Q

Coeliac disease

A

Caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years, following the introduction of cereals into the diet

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105
Q

Coeliac disease

A

Caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years, following the introduction of cereals into the diet

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106
Q

Coeliac disease

A

Caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.

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107
Q

Features of Coeliac disease in children

A

> failure to thrive
diarrhoea
abdominal distension
older children may present with anaemia
many cases are not diagnosed to adulthood

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108
Q

Diagnosis of Coeliac disease

A

Jejunal biopsy showing subtotal villous atrophy

anti-endomysial and anti-gliadin antibodies are useful screening tests

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109
Q

Antibodies in Coeliac disease

A

anti-endomysial and anti-gliadin antibodies

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110
Q

Antibodies in Coeliac disease

A

Anti-endomysial and anti-gliadin antibodies

111
Q

Congenital diaphragmatic hernia

A

It is characterised by the herniation of abdominal viscera into the chest cavity due to incomplete formation of the diaphragm.

112
Q

Pathophysiology of Congenital diaphragmatic hernia

A

Usually represents a failure of the pleuroperitoneal canal to close completely

113
Q

The most common type of Congenital diaphragmatic hernia

A

Left-sided posterolateral Bochdalek hernia which accounts for around 85% of cases.

114
Q

Cyanotic congenital heart disease examples

A

tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia

115
Q

Acyanotic congenital heart disease examples

A 
ventricular septal defects (VSD) - most common, accounts for 30%
atrial septal defect (ASD)
patent ductus arteriosus (PDA)
coarctation of the aorta
aortic valve stenosis
116
Q

What are the causes of the three major types of congenital infections?

A

Rubella, toxoplasmosis and cytomegalovirus

117
Q

Cow’s milk protein intolerance/allergy

A

Both immediate (IgE mediated) and delayed (non-IgE mediated) reactions are seen. The term CMPA is usually used for immediate reactions and CMPI for mild-moderate delayed reactions.

118
Q

Features of Cow’s milk protein intolerance/allergy

A

> regurgitation and vomiting
diarrhoea
urticaria, atopic eczema
‘colic’ symptoms: irritability, crying
wheeze, chronic cough
rarely angioedema and anaphylaxis may occur

119
Q

Management of Cow’s milk protein intolerance/allergy if child is formula fed

A
  1. extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms
  2. amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF
120
Q

Management of Cow’s milk protein intolerance/allergy if child is breast fed

A
  1. continue breastfeeding
  2. eliminate cow’s milk protein from maternal diet.
  3. use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months
121
Q

Croup

A

Upper respiratory tract infection seen in infants and toddlers. It is characterised by stridor which is caused by a combination of laryngeal oedema and secretions.

122
Q

Causative agent for croup

A

Parainfluenza viruses account for the majority of cases.

123
Q

Features of croup

A
  1. stridor
  2. barking cough (worse at night)
  3. fever
  4. coryzal symptoms
124
Q

Management of Croup

A

Single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity

Prednisolone is an alternative if dexamethasone is not available

125
Q

Mild croup features

A

Occasional barking cough
No audible stridor at rest
No or mild suprasternal and/or intercostal recession
The child is happy and is prepared to eat, drink, and play

126
Q

Moderate croup features

A

Frequent barking cough
Easily audible stridor at rest
Suprasternal and sternal wall retraction at rest
No or little distress or agitation
The child can be placated and is interested in its surroundings

127
Q

Severe croup features

A

Frequent barking cough
Prominent inspiratory stridor at rest
Marked sternal wall retractions
Significant distress and agitation, or lethargy or restlessness (a sign of hypoxaemia)
Tachycardia occurs with more severe obstructive symptoms and hypoxaemia

128
Q

Criteria for immediate referral to hospital for croup

A
  1. < 6 months of age
  2. Known upper airway abnormalities (e.g. Laryngomalacia, Down’s syndrome)
  3. Uncertainty about diagnosis (important differentials include acute epiglottitis, bacterial tracheitis, peritonsillar abscess and foreign body inhalation)
129
Q

Cystic fibrosis (CF)

A

An autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

130
Q

Organisms which may colonise CF patients

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus

131
Q

Diagnosis of CF

A

Patient’s with CF have abnormally high sweat chloride

Normal value < 40 mEq/l, CF indicated by > 60 mEq/l

132
Q

Common features of CF

A
  1. Neonatal period (around 20%): meconium ileus,
  2. Prolonged jaundice
  3. Recurrent chest infections (40%)
  4. Malabsorption (30%): steatorrhoea, failure to thrive
  5. Other features (10%): liver disease
133
Q

Management of CF

A

> Chest physiotherapy and postural drainage.
High calorie diet, including high fat intake*
Minimise contact with other CF patients
Vitamin supplementation
Pancreatic enzyme supplements taken with meals
Lung transplantion

134
Q

Developmental referral points

A
  1. doesn’t smile at 10 weeks
  2. cannot sit unsupported at 12 months
  3. cannot walk at 18 months
135
Q

Risk factors for Developmental dysplasia of the hip

A 
female sex: 6 times greater risk
breech presentation
positive family history
firstborn children
oligohydramnios
birth weight > 5 kg
congenital calcaneovalgus foot deformity
136
Q

Screening for Developmental dysplasia of the hip

A

The following infants require a routine ultrasound examination

> first-degree family history of hip problems
breech presentation at or after 36 weeks gestation
multiple pregnancy

137
Q

Barlow test

A

attempts to dislocate an articulated femoral head

138
Q

Ortolani test

A

attempts to relocate a dislocated femoral head

139
Q

Clinical diagnosis of DDH

A

Barlow test
Ortolani test
Symmetry of leg length
Level of knees when hips and knees are bilaterally flexed
Restricted abduction of the hip in flexion

140
Q

Imaging of DDH

A

Ultrasound is generally used to confirm the diagnosis if clinically suspected

Infant is > 4.5 months then x-ray is the first line investigation

141
Q

Management of DDH

A

> Most spontaneously stabilise by 3-6 weeks of age
Pavlik harness in children younger than 4-5 months
older children may require surgery

142
Q

Developmental milestones: fine motor and vision at 3 months

A

Reaches for object
Holds rattle briefly if given to hand
Visually alert, particularly human faces
Fixes and follows to 180 degrees

143
Q

Developmental milestones: fine motor and vision at 6 months

A

Holds in palmar grasp
Pass objects from one hand to another
Visually insatiable, looking around in every direction

144
Q

Developmental milestones: fine motor and vision at 9 months

A

Points with finger

Early pincer

145
Q

Developmental milestones: fine motor and vision at 12 months

A

Good pincer grip

Bangs toys together

146
Q

Tower of 2

A

15 months

147
Q

Tower of 3

A

18 months

148
Q

Tower of 6

A

2 years

149
Q

Tower of 9

A

3 years

150
Q

Circular scribble

A

18 months

151
Q

Copies vertical line

A

2 years

152
Q

Copies circle

A

3 years

153
Q

Copies cross

A

4 years

154
Q

Copies triangle and square

A

5 years

155
Q

Looks at book, pats page

A

15 months

156
Q

Turns pages, several at time

A

18 months

157
Q

Turns pages, one at time

A

2 years

158
Q

Reaches for object
Holds rattle briefly if given to hand
Visually alert, particularly human faces
Fixes and follows to 180 degrees

A

3 months

159
Q

Holds in palmar grasp
Pass objects from one hand to another
Visually insatiable, looking around in every direction

A

6 months

160
Q

Points with finger

Early pincer

A

9 months

161
Q

Good pincer grip

Bangs toys together

A

12 months

162
Q

Little or no head lag on being pulled to sit
Lying on abdomen, good head control
Held sitting, lumbar curve

A

3 months

163
Q 
Lying on abdomen, arms extended
Lying on back, lifts and grasps feet
Pulls self to sitting
Held sitting, back straight
Rolls front to back
A

6 months

164
Q

Sits without support (Refer at 12 months)

A

7-8 months

165
Q

Pulls to standing

Crawls

A

9 months

166
Q

Cruises

Walks with one hand held

A

12 months

167
Q

Walks unsupported (Refer at 18 months)

A

13-15 months

168
Q

Squats to pick up a toy

A

18 months

169
Q

Runs

Walks upstairs and downstairs holding on to rail

A

2 years

170
Q

Rides a tricycle using pedals

Walks up stairs without holding on to rail

A

3 years

171
Q

Hops on one leg

A

4 years

172
Q

Smiles (Refer at 10 weeks)

A

6 weeks

173
Q

Laughs

Enjoys friendly handling

A

3 months

174
Q

Not shy

A

6 months

175
Q

Shy

Takes everything to mouth

A

9 months

176
Q

May put hand on bottle when being fed

A

6 months

177
Q

Drinks from cup + uses spoon, develops over 3 month period

A

12-15 months

178
Q

Competent with spoon, doesn’t spill with cup

A

2 years

179
Q

Uses knife and fork

A

5 years

180
Q

Helps getting dressed/undressed

A

12-15 months

181
Q

Takes off shoes, hat but unable to replace

A

18 months

182
Q

Puts on hat and shoes

A

2 years

183
Q

Can dress and undress independently except for laces and buttons

A

4 years

184
Q

Quietens to parents voice
Turns towards sound
Squeals

A

3 months

185
Q

Double syllables ‘adah’, ‘erleh’

A

6 months

186
Q

Says ‘mama’ and ‘dada’

Understands ‘no’

A

9 months

187
Q

Knows and responds to own name

A

12 months

188
Q

Knows about 2-6 words (Refer at 18 months)

Understands simple commands - ‘give it to mummy’

A

12-15 months

189
Q

Combine two words

Points to parts of the body

A

2 yeares

190
Q

Vocabulary of 200 words

A

2.5 years

191
Q

Talks in short sentences (e.g. 3-5 words)
Asks ‘what’ and ‘who’ questions
Identifies colours
Counts to 10 (little appreciation of numbers though)

A

3 years

192
Q

Asks ‘why’, ‘when’ and ‘how’ questions

A

4 years

193
Q

The most common cause of gastroenteritis in children in the UK

A

Rotavirus

194
Q

Clinical shock

A 
Decreased level of consciousness
Cold extremities
Pale or mottled skin
Tachycardia
Tachypnoea
Weak peripheral pulses
Prolonged capillary refill time
Hypotension
195
Q

Clinical dehydration management

A
  1. Give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts
  2. continue breastfeeding
  3. consider supplementing with usual fluids
196
Q

Gastroenteritis

A

> main risk is severe dehydration
most common cause is rotavirus
The diarrhoea may last up to a week
treatment is rehydration

197
Q

Most common cause for chronic diarrhoea

A

Cows’ milk intolerance

198
Q

Toddler diarrhoea:

A

Stools vary in consistency, often contain undigested food

199
Q

Causes for chronic diarrhoea in children

A

> Cows’ milk intolerance
Toddler diarrhoea
Coeliac disease
Post-gastroenteritis lactose intolerance

200
Q

Clinical features of Down’s syndrome

A 
Upslanting palpebral fissures, epicanthic folds, Brushfield spots in iris, protruding tongue, 
Small low-set ears, round/flat face
Flat occiput
Single palmar crease, 
Hypotonia
Congenital heart defects
Duodenal atresia
Hirschsprung's disease
201
Q

Duchenne muscular dystrophy

A

> progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign
associated with dilated cardiomyopathy
30% of patients have intellectual impairment

202
Q

Ebstein’s anomaly

A

A congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle. It is sometimes referred to as ‘atrialisation’ of the right ventricle.

203
Q

Cause of Ebstein’s anomaly

A

Exposure to lithium in-utero

204
Q

Ebstein’s anomaly features

A
  1. cyanosis
  2. prominent ‘a’ wave in the distended jugular venous
  3. hepatomegaly
  4. tricuspid regurgitation
  5. pansystolic murmur, worse on inspiration
  6. right bundle branch block → widely split S1 and S2
205
Q

Features of Eczema in children

A

> Infants the face and trunk often affected
Younger children - extensor surfaces
Older children - flexor surfaces, creases face/neck

206
Q

Epstein’s pearl

A

A congenital cyst found in the mouth commonly on hard palate, but may be seen on gums where mistaken it for a tooth. No treatment as they tend to spontaneously resolve over the course of a few weeks.

207
Q

Febrile convulsions

A

Seizures provoked by fever in otherwise normal children.

208
Q

What age does Febrile convulsions usually affect?

A

6 months and 5 years

209
Q

Features of Febrile convulsions

A
  1. Occur early in a viral infection as the temperature rises rapidly
  2. seizures are usually brief, lasting <5 minutes
  3. are most commonly tonic-clonic
210
Q

Management following a seizure

A

Children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics

211
Q

Simple seizure

A

< 15 minutes
Generalised seizure
Typically no recurrence within 24 hours
Should be complete recovery within an hour

212
Q

Complex seizure

A

15 - 30 minutes
Focal seizure
May have repeat seizures within 24 hours

213
Q

Febrile status epilepticus

A

> 30 minutes seizure

214
Q

Fraser guidelines

A

Used to assess if patient who has not yet reached 16 years of age is competent to consent to treatment, for example with respect to contraception

215
Q

Risk factors for GORD in children

A

preterm delivery

neurological disorders

216
Q

Features of GORD in children

A

typically develops before 8 weeks

vomiting/regurgitation following feeds

217
Q

Complications of GORD in children

A 
distress
failure to thrive
aspiration
frequent otitis media
in older children dental erosion may occur
218
Q

Examples of congenital visceral malformations.

A

Gastroschisis and exomphalos

219
Q

Gastroschisis

A

Describes a congenital defect in the anterior abdominal wall just lateral to the umbilical cord.

220
Q

Exomphalos

A

Also known as an omphalocoele - the abdominal contents protrude through the anterior abdominal wall but are covered in an amniotic sac formed by amniotic membrane and peritoneum.

221
Q

Management of Exomphalos

A

C section is indicated to reduce the risk of sac rupture

A staged repair may be undertaken as primary closure may be difficult due to lack of space/high intra-abdominal pressure

222
Q

Growing pains

A

Pain presentations, in the absence of any worrying features, are often attributed to ‘growing pains’

223
Q

Haemorrhagic disease of the newborn (HDN).

A

Newborn babies are relatively deficient in vitamin K. This may result in impaired production of clotting factors which in turn can lead to haemorrhagic disease of the newborn (HDN).

224
Q

What is a risk factor for developing Haemorrhagic disease of the newborn (HDN)?

A

Maternal use of antiepileptics

225
Q

What action is taken to reduce the incidence of Haemorrhagic disease of the newborn (HDN)?

A

All newborns in the UK are offered vitamin K, either intramuscularly or orally

226
Q

Hand, foot and mouth disease

A

A self-limiting condition affecting children. Caused by the intestinal viruses of the Picornaviridae family (most commonly coxsackie A16 and enterovirus 71).

227
Q

Clinical features of Hand, foot and mouth disease

A
  1. mild systemic upset: sore throat, fever
  2. oral ulcers
  3. followed later by vesicles on the palms and soles of the feet
228
Q

Management of Hand, foot and mouth disease

A

Symptomatic treatment only: hydration and analgesia

Children do not need to be excluded from school

229
Q

Head lice treatment

A

Treatment is only indicated if living lice are found

Choice of treatments - malathion, wet combing, dimeticone, isopropyl myristate and cyclomethicone

230
Q

Most common cause of primary headache in children

A

Migraine without aura

231
Q

Migraine management in children

A

Ibuprofen>paracetamol for pediatric migraine

Triptans in children >= 12 years but follow-up is required

232
Q

Second most common cause of headache in children

A

Tension-type headache

233
Q

Diagnosis of Migraine

A

A >= 5 attacks fulfilling features B to D
B Headache attack lasting 4-72 hours

C Headache has at least two of the following four features:
> bilateral or unilateral (frontal/temporal) location
> pulsating quality
> moderate to severe intensity
> aggravated by routine physical activity

D At least one of the following accompanies headache:
> nausea and/or vomiting
> photophobia and phonophobia

234
Q

Diagnosis of Tension-type headache

A

A At least 10 previous headache episodes fulfilling features B to D
B Headache lasting from 30 minutes to 7 days

C At least two of the following pain characteristics:
> pressing/tightening (non/pulsating) quality
> mild or moderate intensity
> bilateral location
> no aggravation by routine physical activity

D Both of the following:
> no nausea or vomiting
> photophobia and phonophobia, or one, but not the other is present

235
Q

Otoacoustic emission test

A

Hearing test for the newborn

236
Q

Hearing test for newborns

A

Otoacoustic emission test

237
Q

Newborn & infants hearing test

A

Auditory Brainstem Response test

238
Q

Auditory Brainstem Response test

A

Newborn & infants hearing test

239
Q

Distraction test

A

Hearing test in 6-9 month olds

240
Q

Hearing test in 6-9 month olds

A

Distraction test

241
Q

Hearing test in 18 months-2 years olds

A

Recognition of familiar objects

242
Q

Recognition of familiar objects

A

Hearing test in 18 months-2 years olds

243
Q

Pure tone audiometry

A

Hearing test for >3 year olds

244
Q

Hearing test for >3 year olds

A

Pure tone audiometry

245
Q

Pathophysiology of Hirschsprung’s disease

A

Parasympathetic neuroblasts fail to migrate from the neural crest to the distal colon → developmental failure of the parasympathetic Auerbach and Meissner plexuses → uncoordinated peristalsis → functional obstruction

246
Q

Hirschsprung’s disease

A

Caused by an aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses.

247
Q

What conditions are associated with Hirschsprung’s disease?

A

3 times more common in males

Down’s syndrome

248
Q

Features of Hirschsprung’s disease

A

neonatal period e.g. failure or delay to pass meconium

older children: constipation, abdominal distension

249
Q

Investigations in Hirschsprung’s disease

A

abdominal x-ray

rectal biopsy: gold standard for diagnosis

250
Q

Management of Hirschsprung’s disease

A

initially: rectal washouts/bowel irrigation

definitive management: surgery to affected segment of the colon

251
Q

Gold standard for diagnosis of Hirschsprung’s disease

A

Rectal biopsy

252
Q

Definitive management of Hirschsprung’s disease

A

Surgery to affected segment of the colon

253
Q

Hypospadias

A

A congenital abnormality of the penis where urethra is not present at tip of penis - which occurs in approximately 3/1,000 male infants.

254
Q

Hypospadias features

A

> a ventral urethral meatus
a hooded prepuce
chordee (ventral curvature of the penis) in more severe forms
the urethral meatus may open more proximally in the more severe variants.

255
Q

Hypospadias management

A

Corrective surgery around 12 months of age

256
Q

Most common cause of hypothyroidism in children

A

Autoimmune thyroiditis

257
Q

Immune (or idiopathic) thrombocytopenic purpura (ITP)

A

An immune-mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.

258
Q

Features of Immune (or idiopathic) thrombocytopenic purpura (ITP) in children

A

> Typically more acute than in adults
May follow an infection or vaccination
Self-limiting course over 1-2 weeks

259
Q

Contraindications to live vaccines

A

pregnancy

immunosuppression

260
Q

Situations where vaccines should be delayed

A

febrile illness/intercurrent infection

261
Q

General contraindications to immunisation

A

Confirmed anaphylactic reaction to a previous dose of a vaccine containing the same antigens

Confirmed anaphylactic reaction to another component contained in the relevant vaccine (e.g. egg protein)

262
Q

What vaccine is given at birth?

A

BCG should be given if the baby is deemed at risk of tuberculosis (e.g. Tuberculosis in the family in the past 6 months).

263
Q

What vaccines are given at 2 months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)

Oral rotavirus vaccine

Men B

264
Q

The 6-1 vaccine

A

Contains diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B

265
Q

What vaccines is given at 3 months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)

Oral rotavirus vaccine

PCV

266
Q

What vaccines is given at 4 months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Men B

267
Q

What vaccines is given at 12-13 months?

A

Hib/Men C
MMR
PCV
Men B

268
Q

What vaccines is given at 3-4 years?

A

‘4-in-1 pre-school booster’ (diphtheria, tetanus, whooping cough and polio)
MMR

269
Q

What vaccine is given at 12-13 years?

A

HPV vaccination

270
Q

What vaccines are given at 13-18 years?

A

3-in-1 teenage booster’ (tetanus, diphtheria and polio)

Men ACWY

271
Q

3-in-1 teenage booster

A

Contains tetanus, diphtheria and polio

272
Q

MMR

A

Measles, Mumps, Rubella vaccine

273
Q

Men ACWY

A

Meningococcal vaccine covering A, C, W and Y serotypes

Child health (2 decks)

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