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Paediatrics Flashcards

1
Q

Describe the process of immunisation.

A

Procedure generating immunity without complications of natural infection via administering a vaccine, generating immunity without harm.

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2
Q

What types of vaccines are there?

A

Whole organism

Isolated antigenic components (HPV; Shingles; HBV; Pertussis; HiB)

Live attenuated (MMR; BCG; Chickenpox; Nasal influenza; Rotavirus)

Inactivated toxins (DT)

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3
Q

Compare and contrast the benefits and drawbacks to vaccinations,

A

Protect from disease: Eradicate/Eliminate disease
Prevent spread of disease
Safe + effective
Time-effective + Cheaper cf hospital care

Parental autonomy
Side effects
Ethnoreligious beliefs?
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4
Q

A mother to a newborn is curious regarding the vaccines. Outline the vaccine schedule for children.

A

2 months:

  • 6-in-1 (DTP; Pertussis; HiB; HBV)
  • Men B
  • Rotavirus

3 months:

  • 6-in-1 (DTP; Pertussis; HiB; HBV)
  • Pneumococcal
  • Rotavirus

4 months:

  • 6-in-1 (DTP; Pertussis; HiB; HBV)
  • Men B
1 year: 
HiB/MenC
MMR
PCV
MenB

2-11 years:
- Nasal Flu

Teenage:

  • HPV
  • DTP
  • MenACWY
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5
Q

What vaccines will a child receive at 2 months?

A
  • 6-in-1
  • Men B
  • Rotavirus
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6
Q

What vaccines will a child receive at 3 months?

A

3 months:

  • 6-in-1 (DTP; Pertussis; HiB; HBV)
  • Pneumococcal
  • Rotavirus
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7
Q

What vaccines will a child receive at 4 months in the UK?

A

4 months:

  • 6-in-1 (DTP; Pertussis; HiB; HBV)
  • Men B
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8
Q

What vaccines will a child receive at 1 year?

A
  • 2-in-1 (Hib/MenC)
  • Men B
  • MMR
  • Pneumococcal
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9
Q

What strain of HPV is the vaccine against?

A

Strains 6, 11, 16 and 18

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10
Q

Which strains of HPV cause cervical cancer?

A

HPV-11 and HPV-16

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11
Q

How do you take a paediatric history?

A

PC

HPC

BFG-D:

  • Birth: pregnancy complications; scans; delivery; neonatal care
  • Feeding: Diet/Appetite/ Toileting
  • Growth: weights/milestones
  • Development: Milestones; Schooling and attendance; friends/social

DHx + Allergies

FHx

SHx

ICE

SE

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12
Q

How do you examine a child?

A

A-E assessment

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13
Q

State the commonly tested reflex tests for neonates.

A

Moro Reflex (Mor-Oh startle reflex)

Napier Reflex (fencing)

Stepping Reflex

Positive support Reflex (attempts to stand)

Babinski (elicits extension)

Galant (lateral flexion)

Landau Reflex (looking at the ‘Land’)

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14
Q

What is the mean age for a child to roll over?

A

3 months

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15
Q

What is the mean age for a child to reach out?

A

3 months

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16
Q

What is the mean age for a child to sit unsupported?

A

6 months

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17
Q

What is the mean age for a child to walk unsupported?

A

12 months

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18
Q

What is the mean age for a child to hop on one foot?

A

3.5 years

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19
Q

What is the mean age for a child to ride a tricycle?

A

3 years

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20
Q

What is the mean age for a child to have a pincer grip?

A

8 months

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21
Q

What is the mean age for a child to eat with a spoon?

A

12-21 months

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22
Q

What is the mean age for a child to tie their shoelaces?

A

5 years old

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23
Q

What is the mean age for a child to respond to a smile?

A

6 weeks

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24
Q

What is the mean age for a child to play in a group?

A

3 years

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25
Q

What are the vital ranges for HR and RR in a neonate?

A

120-160

30-60

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26
Q

What are the vital ranges for HR and RR in a child 1-2 years?

A

90-150

24-40

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27
Q

What are the vital ranges for HR and RR in a child 2-5 years old?

A

80-140

22-34

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28
Q

What are the vital ranges for HR and RR in a child 6-12 years old?

A

70-120

18-30

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29
Q

What are the clinical features in hypoxic ischaemic encephalopathy?

A

Irritable
Increased tone
Increased reflexes
Poor feeding

Lethargy
Seizure

Coma
Absent reflexes
Prolonges seizures
Multi-organ failure

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30
Q

What scoring system can be used for a neonate shortly after birth?

Outline it

A

APGAR Score (1 min and 5 mins)

Appearance: Pink/Blue extremities/ Pale or blue

Pulse: >100bpm; <100bpm; none

Grimace: Cries; weak cry; no response

Activity: Active; arms and legs flexed; none

Respiration: Strog cry; slow and irregular; no breathing

<7 is not normal

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31
Q

How do you manage hypoxic ischaemic encephalopathy?

A

Supportive: SCBU/ITU; Paeds involvement; Resuscitation; Therapeutic hypothermia (33-34C)
+
Anti-convulsants: Phenytoin

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32
Q

What is the cause of Respiratory Distress Syndrome in Neonates?

A

Inadequate levels of pulmonary surfactant leading to high surface tension alas atelectasis resulting in inadequate GE and hypoxia, hypercapnia and respiratory distress

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33
Q

How can you manage a neonate with respiratory distress syndrome?

A

Supportive: A-E; Oxygen; Endotracheal surfactant; CPAP (NIV) or Intubation
+
Steroids: Dexamethasone

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34
Q

Outline the complications of respiratory distress syndrome in the neonate?

A 
Short-term: 
Pneumothorax 
Infection
Intraventricular haemorrhage 
Pulmonary haemorrhage 
Necrotising enterocolitis

Long-term
Chronic lung disease of prematurity
Retinopathy of prematurity
Neurological, hearing and visual impairment

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35
Q

What are some of the potential causes of Respiratory Distress in the neonate?

A

Prematurity

Transient Tachypnoea of the newborn

Meconium aspiration

Pneumonia

Pneumothorax

Diaphragmatic hernia

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36
Q

Outline the clinical features of respiratory distress syndrome in a neonate?

A
  • RR>60
  • Grunting
  • Intercostal/subcostal recession
  • Nasal flaring
  • Cyanosis
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37
Q

What is a premature baby?

A

<36 weeks

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38
Q

A mother is worried about the potential complications of prematurity. What are these?

A

Respiratory distress syndrome

Patent Ductus Arterious

Necrotising enterocolitis

Retinopathy of prematurity

Intraventricular haemorrhage

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39
Q

Why does normal labour and delivery lead to hypoxia?

A

During contractions, the myometrium is squeezes which results in constriction of blood supply to the placenta thus hypoxia. However, extended hypoxia will result in bradycardia and potential reduction in respiratory effort which may progress to hypoxic ischaemic encephalopathy (HIE)

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40
Q

Outline the principles of neonatal resuscitation.

A

Warm the baby (dry them, keep under heat lamp)

Calculate Apgar score

Stimulate breathing

Supportive: reheat (dry, heat lamp, wrap); Apgar score; neutral position; A-E (inflation breaths 2-5; ventilation (NIV or intubation); therapeutic hypothermia (33-34C)

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41
Q

Describe the process of placental transfusion. What may the negatives be?

A

Delayed cord clamping allowing foetal blood to enter circulation

Negative effect is potential neonatal jaundice - Tx w/ Phototherapy.

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42
Q

What cells produce surfactant?

A

Type II alveolar cells

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43
Q

Explain how surfactant enables the first breath.

A

Pulmonary surfactant sits above water in the lungs with a hydrophilic side facing water and a hydrophobic side facing the air to reduce surface tension and facilitate lung expansion, reducing the force required to expand the alveoli thus increasing compliance

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44
Q

Outline the process of foetal heart shunt closure.

A

During the first breath which expands alveoli, pulmonary vascular resistance drops which causes a fall in RA thus LA > RA which results in a functional closure of the foramen ovale to become the fossa ovalis

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45
Q

Outline the process by which the ductus arteriosus closes.

Should it fail to close, what clinical sign is heard and how can you manage this?

A

Increased blood oxygenation results in a reduction in prostaglandins which causes closure of the ductus arteriosus and become the ligamentum arteriosum.

Should this not close, a continuous machinery murmur is heard at the upper left sternal border.

Treat with Indometacin (PGE inhibitor)

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46
Q

Outline the standard care after birth for a neonate.

A

Skin to skin contact (warm baby, interaction, calm, breast feeding)
Vitamin K IM
Blood spot screening (4 separate drops on day 5 via heel prick test)

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47
Q

What conditions are screened for on blood spot screening?

A 
Sickle cell disease
Cystic fibrosis
Congenital hypothyroidism
Phenylketonuria
Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
Maple syrup urine disease (MSUD)
Isovaleric acidaemia (IVA)
Glutaric aciduria type 1 (GA1)
Homocystin
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48
Q

When would you conduct a neonatal exam?

Describe how you would conduct a neonatal examination.

A

72 hours

6-8 weeks

Conducting a neonatal examination:

1) Introduction
2) Explain procedure
3) Gain consent

4) Screening questions:
- Feeding ok?
- Passed meconium?
- FHx of CHD; eye or hip problems?

5) General appearance
- Colour
- Tone
- Cry

6) Head:
- Inspect: shape; size; ears; eyes; mouth
- Palpate (OCP; Ant. and Post. fontanelles; Sutures; Suckle reflex
- Retinal reflex

7) Shoulders and arms
- Inspect: shoulder symmetry; arm movements; radial pulses; digits
- Palpate: Radial pulses; Pre-ductal reading (RH)

8) Chest
- Inspect: Chest expansion; Chest shape
- Palpate: breathing; SpO2
- Auscultate: Breath sounds; Heart sounds

9) Abdomen:
- Inspect: Shape
- Palpate: organomegaly; hernias; masses

10) Genitals
- Inspection: Genital presence; meconium

11) Legs:
- Inspect: shape; length; movement; digits
- Palpate: Barlow and Ortolani manoeuvres

12) Reflexes
- Moro
- Suckling
- Rooting
- Grasp
- Stepping

13) Document in notes on NIPE and in Red Book
14) Thank parent(s) and explain findings

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49
Q

The presence of a port wine stain, focal neurological deficits, seizures and visual impairments can make you suspicious of what condition?

A

Sturge-Weber Syndrome

Mnemonic: 
Seizure 
Tram track calcifications
U/L Port wine stain
Glaucoma 
Epilepsy
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50
Q

Explain the difference between caput succedaneum and cephalohaematoma.

A

Capu succedaneum is oedema outside the periosteum following trauma which may cross suture lines.

Cephalohaematoma is subperiosteal haematoma due to trauma which results in restriction of fluid to the suture lines.

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51
Q

Shoulder dystocia may result in which palsy? What clinical features are present?

A

Erb’s Palsy (C5/C6 damage) resulting in reduced shoulder abduction and external rotation and arm flexion and finger extension thus ‘waiters tip’ appearance.

Internally rotated shoulder
Extended elbow
Flexed wrist facing backwards (pronated)
Lack of movement in the affected arm

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52
Q

What are the clinical features of neonatal sepsis?

A
  • Signs associated with infection: Cx pain/ Surgical site/Wound/Catheter site/Abdominal pain/Fever/ Flank pain/Dysuria
  • Tachycardia
  • Tachypnoea
  • Fever
  • Low temperature
  • Oliguria
  • Poor capillary refill/mottling of skin
  • Cyanosis
  • Vasoplegia (pathological low TPR) -> flash capillary refill; warm peripheries
  • Hypotension
  • Malaise
  • Lethargy
  • Altered mental status
  • Non-blanching purpuric rash
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53
Q

What is the management for neonatal sepsis?

A

Sepsis 6 protocol

Give 3 and take 3

Blood cultures 
Urine output 
Fluids (IV) 
ABX: Amoxicillin + Gentamicin; Ceftriaxone
Lactate 
Oxygen

±
Vasopressor: NA

Inotropes: Dobutamine

Steroids: IV Hydrocortisone

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54
Q

What are the common organisms causing Neonatal Sepsis?

A 
GBS
E. coli
Listeria 
Klebsiella
S aureus
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55
Q

State 3 RFs for neonatal sepsis

A 
GBS +ve mother 
GBS PMHx 
Premature 
Early rupture of membrane 
PROM
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56
Q

What are the causes of neonatal jaundice?

A 
Haemolytic disease of the newborn
ABO incompatibility
Haemorrhage
Intraventricular haemorrhage
Cephalo-haematoma
Polycythaemia
Sepsis and disseminated intravascular coagulation
G6PD deficiency
Physiological jaundice 
Prematurity
Breast milk jaundice
Neonatal cholestasis
Extrahepatic biliary atresia
Endocrine disorders (hypothyroid and hypopituitary)
Gilbert syndrome
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57
Q

How would you manage neonatal jaundice?

A

Supportive: monitor sBr (treatment threshold charts); Phototherapy (measure rebound 12-18 hours later; Exchange transfusion (donor blood)
+
Tx cause

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58
Q

What are the clinical features of neonatal jaundice?

A
  • Yellow pigmentation of skin
  • Sleepy, lethargic, poor feeding, weight gain
  • Pale stool
  • Dark urine
  • Hyperbilirubinaemia
  • If liver disease- hepatomegaly

• Neurological: Seizures; floppy; unresponsive

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59
Q

Outline the pathophysiology behind retinopathy of the neonate.

A

Retinal vessel development finishes at 37-40 wks thus prematurity results in higher oxygen exposure which reverses/stagnates retinal neovascularisation thus scar tissue and subsequent retinal attachment may occur

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60
Q

How may you divide the retina when reporting on findings in Retinopathy of the newborn?

A

3 retinal zones:

1) Optic nerve and macula
2) Edge of zone 1 to ora serrata
3) Outside ora serrata

Describe using clock face analogy e.g. ‘disease from 3 o’clock to 5 o’clock’

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61
Q

When should you screen a neonate for retinopathy of the newborn?

A

Babies born before 32 weeks or under 1.5kg should be screened for ROP. Screening is performed by an ophthalmologist. Screening starts at:

30 – 31 weeks gestational age in babies born before 27 weeks
4 – 5 weeks of age in babies born after 27 weeks
Screening should happen at least every 2 weeks and can cease once the retinal vessels enter zone 3, usually at around 36 weeks gestation.

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62
Q

What is the management of a neonate with retinopathy?

A

1st line: Transpupillary laser photocoagulation
±
Intravitreal VEGFi: Sorafenib

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63
Q

How may necrotising enterocolitis present?

A 
Intolerance to feeds
Vomiting, particularly with green bile
Generally unwell
Distended, tender abdomen
Absent bowel sounds
Blood in stools

When perforation occurs there will be peritonitis and shock and the neonate will be severely unwell.

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64
Q

What is the gold-standard investigation for diagnosing necrotising enterocolitis?

What may the findings show?

A

Abdominal xray is the investigation of choice for diagnosis. This is done front on in the supine position (lying face up). Additional views can be helpful, such as lateral (from the side with the patient on their back) and lateral decubitus (from the side with the neonate on their side).

Dilated bowel loops
Bowel wall oedema
Pneumatosis intestinalis
Pneumoperitoneum

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65
Q

How do you manage a neonate with necrotising enterocolitis?

A

Supportive: NBM; IV Fluids; TPN; ABX; Surgical referral
+
Surgery: Laparotomy

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66
Q

What are the potential complications of necrotising enterocolitis?

A 
Perforation and peritonitis
Sepsis
Death
Strictures
Abscess formation
Recurrence
Long term stoma
Short bowel syndrome after surgery
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67
Q

Describe the process of Neonatal Abstinence Syndrome (NAS).

A

withdrawal symptoms that happens in neonates of mothers that used substances in pregnancy

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68
Q

Outline the clinical features of neonatal abstinence syndrome.

A 
Irritability
Increased tone
High pitched cry
Not settling
Tremors
Seizures

Yawning
Sweating
Unstable temperature and pyrexia
Tachypnoea (fast breathing)

Poor feeding
Regurgitation or vomiting
Hypoglycaemia
Loose stools with a sore nappy area

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69
Q

How do you manage Neonatal Abstinence Syndrome?

A

Supportive: Document in patient notes prior to delivery; document NAS chart for 3 days (2 for SSRIs); urinalysis
± Moderate/Severe Symptoms

Medical: Oral morphine sulphate (opiate); Oral phenobarbitone (non-opiate)

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70
Q

What medication is given to manage neonatal abstinence syndrome whereby the mother was a heroine user?

A

Oral morphine sulphate

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71
Q

What medication is given to manage neonatal abstinence syndrome whereby the mother was a cocaine user?

A

Oral phenobarbitone

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72
Q

Significant alcohol consumption during pregnancy may lead to which condition?

Outline the clinical features

A

Foetal Alcohol Syndrome

Microcephaly 
Smooth, flat philtrum
Short palpebral fissure 
Learning disability
Behavioural difficulties
Hearing and visual problems
Cerebral palsy
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73
Q

When is the risk of congenital rubella syndrome highest?

A

First 3 months of pregnancy

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74
Q

How do you mitigate the risk of congenital rubella syndrome in the neonate?

A

Supportive: Ensure maternal MMR vaccine history; Test for rubella immunity (Abs)
+
Medical: MMR vaccine (2 doses, 3 months apart)

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75
Q

What clinical features may occur in the neonate should a rubella positive mother give birth?

A

Congenital Rubella Syndrome

Congenital cataracts
Congenital heart disease (PDA and pulmonary stenosis)
Learning disability
Hearing loss

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76
Q

What is the normal range for weight-loss in a neonate?

A

<10%

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77
Q

What is normal feeding volume for a neonate?

How might these requirements change in a premature birth?

A

≈ 150mL/kg/day

Increase to 170-180mL/kg/day in premature (increased requirements)

  • ADEK (fat-soluble vitamins)
  • Fortification
  • Iron (day 28)
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78
Q

What decision-making tool can be used to decide on management strategies in neonatal jaundice?

How may you interpret the chart?

A

Bilirubin charts

Plot according to age and sBr and look at if the value is above the threshold for phototherapy or exchange transfusion.

Note: Increases of 8.5mmol/L per hour warrant consideration for intervention: phototherapy or exchange transfusion (if more severe)

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79
Q

In a neonate that is delivered at 33+3, who’s mother was pre-eclamptic treated with Labetalol, why would you monitor glucose?

A

Labetalol (ß-blocker) can cause hypoglycaemia

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80
Q

What is the target glucose in a neonate?

A

2.6mmol/L

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81
Q

What virus causes chickenpox?

A

VZV

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82
Q

A pregnant woman reports that she met with her friend 4 days ago and since then her friend has developed pruritic vesicles systemically - thought to be chickenpox.

What is your management of this?

A

Consider her immunity - has she had chickenpox?

If not, test VZV IgG

Give IV Varicella IgG within 10 days

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83
Q

A pregnant woman reports that she met with her friend 4 days ago and since then her friend has developed pruritic vesicles systemically - thought to be chickenpox.

The pregnant woman shows you itchy lesions across her abdomen and arms which you suspect are chickenpox.

What do you do?

A

Give Oral Aciclovir within 24 hours and if more than 20 weeks gestation

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84
Q

What may happen if a neonate is exposed to varicella zoster virus in utero?

A

Congenital Varicella Syndrome

Foetal growth restriction
Microcephaly, hydrocephalus, learning disability
Cataracts and eye inflammation (chorioretinitis)
Scars and skin changes (dermatomal)
Limb hypoplasia

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85
Q

What are the features of congenital cytomegalovirus syndrome?

A 
Fetal growth restriction
Microcephaly
Hearing loss
Vision loss
Learning disability
Seizures

Mnemonic:
Cataracts
Microcephaly
Vision loss

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86
Q

How is toxoplasmosis transmitted?

A

Transmitted faeco-orally via faeces from cat

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87
Q

What are the clinical features of congenital toxoplasmosis?

A

Intracranial calcification
Chorioretinitis
Hydrocephalus

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88
Q

How is Zika virus spread?

A

Aides mosquitous in endemic areas

Sexual transmission

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89
Q

What are the features of congenital Zika syndrome?

A

Microcephaly
Foetal growth restriction
Intracranial abnormalities: ventriculomegaly; cerebellar atrophy

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90
Q

What are the risk factors for Sudden Infant Death Syndrome?

A

Prematurity
Low birth weight
Smoking during pregnancy
Male baby (only slightly increased risk)

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91
Q

A worried parent asks you about SIDS following her reading a news report. Advise her on how you may minimise the risk of Sudden Infant Death Syndrome?

A

Put the baby on their back when not directly supervised
Keep their head uncovered
Place their feet at the foot of the bed to prevent them sliding down and under the blanket
Keep the cot clear of lots of toys and blankets
Maintain a comfortable room temperature (16 – 20 ºC)
Avoid smoking. Avoid handling the baby after smoking (smoke stays on clothes).
Avoid co-sleeping, particularly on a sofa or chair
If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers

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92
Q

A neonate is brought in by the mother who describes periods where the child stops breathing for half a minute or so.

What do you suspect this may be?

What clinical findings would aid confirmation of this suspicion.

How do you manage this?

A

Apnoea of the newborn

Bradycardia
Oxygen desaturation

Tx w/
Supportive: Apnoea monitors; Tactile stimulation
+
Medical: IV Caffeine citrate

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93
Q

Why is caffeine citrate given in apnoea of the newborn?

A

Stimulant thus increase diaphragmatic contractility, stimulate medulla respiratory centre

Neuroprotection

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94
Q

What is the infective period for chickenpox?

A

2 days pre-rash to crusting of lesion

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95
Q

A 32+3/40 pregnant woman presents with a rash beginning on her trunk spreading to her hand. The rash is red and flat with some raised bumps. She has had a fever for 2/7 and coryzal for 2/7.

O/E you see red spots with a blue dot on reddened mucosa in the mouth.

What is your clinical suspicion?

What are the clinical features this woman has?

What investigation can you run?

How would you manage this?

A

Measles

Maculopapular rash
Koplik spots

Serology (ELISA) or PCR

  • Supportive: Paracetamol/Ibuprofen
  • Vitamin A supplementation:
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96
Q

What are the clinical features of infection with Coxsackie Virus?

A

Sx + S:
• Fever
• Ulcers and spots - across the body
• Dry cough

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97
Q

How long is the infective period of measles?

A

4 days before to 4 days post-rash

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98
Q

What pathogen causes an erythematous rash on the cheeks, spreading to the trunk with muscle aches and coryza?

A

Parvovirus B19

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99
Q

A 33 week old child who was diagnosed and treated for neonatal sepsis 3/7 has deteriorated. It is reports that they have purpuric lesions on the legs with some blue/black discolouration of the skin.

They are haemodynamically unstable at 170bpm, 92% SpO2 RA; 40/30mmHg.

What is your diagnosis?

What is your management?

A

Neonatal purpura fulminans

Supportive: NICU; IV Fluids; Anticoagulation; Blood products (factors and platelets)
\+
Medical: ABX; Oxygen
\+
Surgery: Surgical debridement
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100
Q

What does the management of sepsis involve?

A

Give 3, take 3

BUFALO

Blood cultures
Urine output 
IV Fluids 
ABX 
Lactate
Oxygen
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101
Q

What are the common causes of Acute Otitis Media in a neonate?

A
  • S. pnumoniae
  • H. influenzae
  • M. catarrhalis
  • RSV
  • Rhinovirus
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102
Q

A 3 year old child presents with fever and ear pain for 5 days as reported by the mother.

O/E the child is guarding the ear, sat close to the mother. You see vesicles present on the tympanic membrane. Additionally, you see a swollen tympanic membrane.

What clinical signs are observed?

What is your diagnosis?

How may you manage this?

A

Fever
Otalgia
Myringitis
Bulging tympanic membrane

AOM

Tx
Supportive: Paracetamol
+
ABX: Amoxicillin

± Resistant to ABX
Surgery: Tympanocentesis

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103
Q

What pathogens can cause Sinusitis?

A
  • S. pneumoniae
  • H. influenzae
  • M. catarrhalis
  • S. milleri
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104
Q

A 5 year old child presents with excess mucous from the nose and facial pain at the cheekbones for 2/52. They say they cannot smell very well.

O/e they appear coryzal.

What is your clinical diagnosis?

How can you manage this?

A

Acute Sinusitis

• Supportive therapy: Rest/Hydration/Warm facial packs/Steam inhalation
±
• Analgesic: Paracetamol/Ibuprofen
±
• Decongestant: Oxymetazoline nasal/ Pseudoephedrine
±
• Intranasal corticosteroid: Mometasone nasal
±
• Intranasal saline: Saline nasal

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105
Q

A 7 year old presents with a rash on their abdomen. She says the rash has been present for 2/7. Additionally the mother says she has had a fever 2/7 and sore throat.

O/E you see a sandpaper appearance to the rash with a white coating on a swollen tongue. There is cervical lymphadenopathy.

What is your differential diagnosis?

What is the causative organism?

How can you confirm this?

How do you manage this patient?

A

Scarlett Fever/Strep Throat

S. pyogenes

ASO titres
CXR
ECG

Supportive: Ibuprofen; Fluids; Worsening advice; Bed rest
+
Medical: Benzylpenicillin STAT + Oral Penicillin V 10/7
+
High dose-aspirin

± Myocarditis signs
- Corticosteroids

± HF
- ACEi
+
- Diuretics

± Chorea
- Benzodiazepine: Diazepam

AND

IM BenPen every 4/52 for 5 years (if no carditis); 10 years (if carditis); life (carditis and valvular disease)

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106
Q

What criteria can be used to diagnose Rheumatic Fever?

Outline these.

A

Jones Criteria

Positive throat swab
Positive rapid streptococcal antigen test
Raised ASO
Recent episode of Pharyngitis

± 2 major or 1 major and 2 minor

Major:
Polyarthritis
Carditis
Syndenhams chorea
Erythema marginatum (pink erythematous rash which extends outwards giving geographical rash appearance)
Subcutaneous nodules (hard pea-sized nodules on extensor surfaces)

Minor:
Polyarthralgia
PR prolongation
Hx rheumatic fever 
Fever 
Raised inflammatory markers
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107
Q

What phenomenon explains why valvular damage occurs in Rheumatic Fever?

A

Antigen mimicry whereby the cell wall component of S. pyogenes mimics that of human heart valve tissue resulting in Abs attacking the valves resulting in valvulopathy - commonly mitral regurgitation.

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108
Q

What are some of the clinical features of Sydenham’s Chorea?

A

Spooning sign (wrist flex + finger extend)

Milkmaid’s grip (rhythmic squeezing when pt grasps examiner’s hand)

Dyskinesia (jerky movements)

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109
Q

A 3 year old patient presents with a fever for 6/7, blanching, maculopapular rash, strawberry tongue, cracked lips, cervical lymphadenopathy and erythema of the hands. Additionally, skin peeling of the volar surfaces is observed.

What is your differential diagnosis?

How do you manage this?

At what phase may vascular complications occur?

A

Kawasaki’s Disease

Medical: Aspirin
+
IVIG

Phases: Acute (1-2 weeks of fever, rash and lymphadenopathy); Subacute phase (2-4 weeks of desquamation, arthralgia and coronary aneurysms); Convalescent stages (2-4 weeks)

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110
Q

What is the management for Kawasaki’s Disease?

A

High dose aspirin to reduce the risk of thrombosis
+
IV immunoglobulins to reduce the risk of coronary artery aneurysms

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111
Q

A 9 month year old child presents with a cough, fever 2/7 and a wheeze as reported by the mother.

O/E they are tachypnoeic, increased WOB and SpO2 92% RA. On auscultation you hear a wheeze throughout and crackles.

What is your diagnosis?

What pathogen commonly causes this?

How do you manage this?

A

Bronchiolitis with some respiratory distress

RSV

Tx
Supportive: Admission; adequate fluid intake; supplementary Oxygen; Ventilatory support (PEEP; CPAP or Intubation)

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112
Q

Which babies receive Palivizumab as prophylaxis for?

A

Ex-premature

Congenital heart disease

Monoclonal antibody for RSV

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113
Q

Give 5 signs of respiratory distress.

A 
Raised respiratory rate
Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
Intercostal and subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis (due to low oxygen saturation)
Abnormal airway noises
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114
Q

What is the pathophysiology behind post-viral wheeze regarding airflow?

A

Children have a smaller, narrower airway thus a virus results in swelling, oedema and constriction of the airway which, according to Poiseuille’s Law results in a marked reduction in airflow.

Therefore, turbulent airflow results in a wheeze and potential respiratory distress.

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115
Q

How is acute post-viral wheeze managed?

A

Mnemonic: O SHIT MAN

Oxygen

Salbutamol 5mg (repeat after 15 mins if wheee still present)
Ipratropium 500mcg

Hydrocortisone: Pred or Hydrocortisone
Theophylline infusion
Magnesium sulphate

Anaesthetist/Urgent review

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116
Q

How may asthma present?

A

3 years and above…

Progressively worsening shortness of breath
Use of accessory muscles
Fast respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation with reduced air entry

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117
Q

How may Asthma be graded?

A

Moderate:
50-75% PEFR

Severe: 
33-50% PEFR
RR >25 
HR >110
Incomplete sentences
Life-threatening:
<33% PEFR 
SpO2 <92% 
Tiredness
Silent chest 
Haemodynamically unstable
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118
Q

What might an ABG in a patient with severe asthma show?

A

Metabolic alkalosis due to tachypnoea causing a drop in CO2 resulting in hypoxia

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119
Q

Outline the paediatric asthma ladder.

A 
SABA 
±
low-dose ICS
± 
Very-low dose ICS + LABA 
± 
Increase ICS or LTRA 
±
Biologics: Omalizumab

Under 5: Do not give LABA

SABA
±
ICS 
±
LTRA 
±
Specialist
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120
Q

What investigations can be used to diagnose Asthma?

A

There is no gold-standard investigation for asthma

PEF

Spirometry

Bloods: FBC; IgE; Culture

Bronchodilator-response spirometry

BPT (mannitol or metacholine)

FeNO

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121
Q

What are the typical triggers for asthma?

A 
Dust (house dust mites)
Animals
Cold air
Exercise
Smoke
Food allergens (e.g. peanuts, shellfish or eggs)
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122
Q

Talk a patient through inhaler technique.

A

Remove the cap
Shake the inhaler (depending on the type)
Sit or stand up straight
Lift the chin slightly
Fully exhale
Make a tight seal around the inhaler between the lips
Take a steady breath in whilst pressing the canister
Continue breathing for 3 – 4 seconds after pressing the canister
Hold the breath for 10 seconds or as long as comfortably possible
Wait 30 seconds before giving a further dose
Rinse the mouth after using a steroid inhaler

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123
Q

Talk a patient through MDI technique with a spacer.

A

Assemble the spacer
Shake the inhaler (depending on the type)
Attach the inhaler to the correct end
Sit or stand up straight
Lift the chin slightly
Make a seal around the spacer mouthpiece or place the mask over the face
Spray the dose into the spacer
Take steady breaths in and out 5 times until the mist is fully inhaled

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124
Q

What are the clinical features of Pneumonia?

A 
Cough (typically wet and productive)
High fever (> 38.5ºC)
Tachypnoea
Tachycardia
Increased work of breathing
Chest sounds: Bronchial breathing/Coarse crackles
Hyporesonant
Lethargy
Delirium (acute confusion associated with infection)

Hypotension (shock)
Fever
Confusion

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125
Q

What is the most common viral cause of Pneumonia?

A

RSV

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126
Q

How do you manage pneumonia?

A

Supportive: Admission (CRB65 score); Fluids; Monitoring; Worsening advice
+
Medical: Amoxicillin

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127
Q

Outline the common causes of Croup.

A

Parainfluenza
Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

Diptheria (leads to epiglottitis)

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127
Q

Outline the common causes of Croup.

A

Parainfluenza
Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

Diptheria (leads to epiglottitis)

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128
Q

Outline the key differences between croup and epiglottitis,

A

Croup:

  • Onset over days
  • Unwell
  • Severe barking cough
  • Able to drink
  • Low-grade <38.5C fever
  • Hoarse voice

Epiglottitis:

  • Onset over hours
  • Toxic appearance, tripod stance
  • No cough
  • Cannot drink
  • High-grade >38.5C fever
  • Muffled voice
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129
Q

How do you manage Croup?

A

Oral dexamethasone 150mcg/kg

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130
Q

How do you diagnose epiglottitis?

A

XR-Neck (lateral): Thumbprint sign due to oedematous epiglottis

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131
Q

How do you manage epiglottitis?

A

Supportive: do not distress patient; call senior; secure airway
+
Medical: IV Ceftriaxone + IV Dexamethasone

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132
Q

Explain the pathophysiology in laryngomalacia.

A

There are two aryepiglottic folds at the entrance of the larynx. They run between the epiglottis and the arytenoid cartilages. They are either side of the airway and their role is to constrict the opening of the airway to prevent food or fluids entering the larynx and trachea. In laryngomalacia the aryepiglottic folds are shortened, which pulls on the epiglottis and changes it shape to a characteristic “omega” shape.

The tissue surrounding the supraglottic larynx is softer and has less tone in laryngomalacia, meaning it can flop across the airway. This happens particularly during inspiration, as the air moving through the larynx to the lungs pulls the floppy tissue across the airway to partially occlude it. This partial obstruction of the airway generates the whistling sound.

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133
Q

What are the management options for laryngyomalacia?

A

Supportive: Self-resolves as larynx matures and grows

or

Surgical: Tracheostomy; Supraglottoplasty

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134
Q

What is the causative organism in Whooping Cough?

A

Bordatella pertussis

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135
Q

What are the clinical features of whooping cough?

A

Fever
Coryzal symptoms
Dry cough: Paroxysmal cough with severe recurring coughing attacks followed by large, audible inspiratory whoop when coughing ends

Apnoeas (newborn)

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136
Q

What investigations may secure a diagnosis of Whooping Cough?

A

NP Swab and PCR

Anti-pertussis toxin IgG

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137
Q

How do you manage Pertussis?

A

Supportive: Notifiable disease; Supportive care
+
ABX (macrolides): Erythromycin

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138
Q

Describe Chronic Lung Disease of Prematurity.

A

Chronic lung disease of prematurity (CLDP) is also known as bronchopulmonary dysplasia. It occurs in premature babies, typically those born before 28 weeks gestation. These babies suffer with respiratory distress syndrome and require oxygen therapy or intubation and ventilation at birth. Diagnosis is made based on chest xray changes and when the infant requires oxygen therapy after they reach 36 weeks gestational age.

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139
Q

What measures do physicians take to try to prevent Chronic Lung Disease of Prematurity?

A

Betamethasone in premature labour
Caffeine citrate
NIV (CPAP)

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140
Q

How is Chronic Lung Disease of Prematurity diagnosed?

A

CXR

Formal sleep study

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141
Q

What prophylaxis does a baby with chronic lung disease of the newborn require?

A

Monthly injections against RSV of Palivizumab (mAb to RSV)

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142
Q

What gene mutation is responsible for Cystic Fibrosis?

A

CFTR gene (delta-F508) on chromosome 7

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143
Q

How is Cystic Fibrosis inherited?

A

Autosomal recessive

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144
Q

How is cystic fibrosis diagnosed?

A

Clinical features: ileus; recurrent infections; failure to thrive; pancreatitis

Newborn blood spot test
Chloride sweat test
Genetic testing

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145
Q

What is the gold-standard test for cystic fibrosis?

Outline this.

A

Chloride sweat test

Patch of skin chosen, pilocarpine applied to skin on patch and electrodes placed either side, inducing diaphoresis. Sweat absorbed and sent to test for Cl- concentration - 60mmol/L

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146
Q

Which pathogens are patients with Cystic Fibrosis susceptible to?

How can they mitigate this?

A

P aeruginosa

S aureus

Prophylactic Flucloxacillin

If P. aeroginosa infection, inhaled tobramycin used

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147
Q

How is cystic fibrosis managed?

A

Supportive: Cx physiotherapy; Exercise; High calorie diet; Pancreatin; CREON tablets (digest fats); Prophylactic ABX; Dorase alfa; Hypertonic saline; Bronchodilators; Vaccinations (varicella; influenza; pneumococcal)

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148
Q

what is the eponymous term for primary ciliary dyskinesia?

How is it inherited?

A

Kartagner’s Syndrome

Autosomal recessive

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149
Q

What are the clinical features of Kartagner’s Syndrome?

A

Paranasal sinusitis
Bronchiectasis
Situs Inversus

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150
Q

What is the gold-standard investigation to diagnose Kartagner’s Syndrome?

A

Nasal brushing
or
Bronchoscopy

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151
Q

List 10 potential causes of abdominal pain in a child.

A

Non-organic (functional)

Abdominal migraine 
Constipation 
Coeliac disease
IBS
IBD
Mesenteric adenitis
Gastroenteritis 
Appendicitis 
DKA 
UTI
Pyelonephritis 
PCKD
HSP 
Infantile colic 
Ectopic pregnancy
Dysmenorrhoea 
PID
Pregnancy 
Mittelschmerz (Ovulation pain) 
Pyloric stenosis 
Intususseption 
Bowel obstruction
Testicular torsion
Ovarian torsion
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152
Q

What are the red flags for abdominal pain?

A 
Persistent or bilious vomiting
Severe chronic diarrhoea
Fever
Rectal bleeding
Weight loss or faltering growth
Dysphagia (difficulty swallowing)
Nighttime pain
Abdominal tenderness
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153
Q

What are the clinical features of abdominal migraine?

A 
Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura
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154
Q

How may you manage abdominal migraine?

A

Acute: Ibuprofen; Paracetamol; Sumitriptan

Prophylaxis: Pizotifen

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155
Q

What are some of the clinical features of constipation in children?

A

Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools
Abdominal pain
Holding an abnormal posture, referred to as retentive posturing
Rectal bleeding associated with hard stools
Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
Hard stools may be palpable in abdomen
Loss of the sensation of the need to open the bowels

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156
Q

How do you manage constipation?

A 
Supportive: high fibre; fluids; reverse contributing factors; Toiletting charts
\+
Medical: Movicol (PEG)
\+
Tx any cause (if an organic cause)
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157
Q

At what age is GORD considered pathological?

A

1 year, as cardiac sphincter should have formed by then

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158
Q

State 5 causes of vomiting

A 
Overfeeding 
GORD
Pyloric stenosis 
Gastritis 
Appendicitis
Infection
Intestinal obstruction 
Bulimia
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159
Q

How is GORD managed in the young child?

A

Supportive: smaller, frequent meals; burp regularly; keep upright
+
Medical: Gaviscon (alginate); Ranitidine

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160
Q

A young child with known GORD presents with forceful contraction of the neck muscles causing twisting of the neck and twisting movements of the neck/back, what condition is this?

A

Sandifer’s Syndrome

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161
Q

What are the clinical features of Sandifer’s Syndrome?

A

GORD

Torticolis

Dystonia

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162
Q

What is the pathophysiology involved in pyloric stenosis?

A

There is hypertrophy of the pyloric sphincter, palpable as the olive sized mass in the abdomen.

Following a feed, food is expelled retrograde which manifests as projectile vomiting

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163
Q

In pyloric stenosis, what will an ABG show?

A

Hypochloric metabolic alkalosis

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164
Q

What is the gold-standard diagnosis for pyloric stenosis?

A

US-Abdomen

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165
Q

How do you manage pyloric stenosis?

A

Laparoscopic pyloromyotomy (Ramstedt’s operation)

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166
Q

Outline the clinical features of allergic colitis.

What may the investigations show?

A

Presentation:
• Diarrhoea with blood and mucus
• Failure to thrive

Investigations
• Bloods- eosinophilia, raised IgE
• positive RAST/skin prick to specific foods

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167
Q

How do you manage allergic colitis secondary to cow’s milk allergy?

A

• Offer substitute e.g. hydrolysed milk

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168
Q

What is the most common cause of gastroenteritis?

A

Rotavirus (viral)

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169
Q

How would you manage a Gastroenteritis?

A

Supportive: Isolate (48 hours after symptoms stopped); Fluids; Dioralyte

± Bacterial gastroenteritis
- Empirical ABX

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170
Q

How long should a child isolate following Gastroenteritis?

A

48 hours after symptoms cleared

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171
Q

Give 5 differentials for diarrhoea in the child.

A 
Infection 
IBD
IBS
Lactose intolerance
Coeliac disease
Cystic fibrosis 
Toddler's diarrhoea 
Medications
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172
Q

What are the most common causes of viral gastroenteritis?

A

Rotavirus

Norovirus

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173
Q

Which strain of E.coli produces the Shiga toxin?

A

E.coli 0157

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174
Q

What condition can E.coli producing bloody diarrhoea and vomiting suggest?

A

Haemolytic Uraemic Syndrome

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175
Q

A 25 year old man returns from travelling around Indonesia for 2 weeks. He is having some bouts of diarrhoea without blood which he had towards the latter stage of his trip.

The culture shows a curved bacterium and gram stain is negative.

What is the pathogen?

A

Campylobacter jejuni

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176
Q

How is shigella transmitted?

A

Faeco-oral through contaminated water

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177
Q

What syndrome may Shigella infection cause?

How may severe cases be treated?

A

Haemolytic Uraemic Syndrome (HUS)

Ciprofloxacin

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178
Q

How’s salmonella transmitted?

A

Faeco-oral via food or raw eggs or poultry

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179
Q

A 18 year old uni student eats his leftover egg fried rice which was not refrigerated. He develops abdominal cramping, tenesmus and diarrhoea within 3 hours.

What is the cause?

A

Gastroenteritis secondary to Bacillus cereus

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180
Q

A 12 year old girl presents with bloody diarrhoea, abdominal pain and fever. She has not travelled anywhere or does not exhibit any risky behaviour. The last thing she ate was some pork.

O/E she is tender in the RIF.

A stool culture shows a gram negative bacillus.

What could be the cause?

A

Gastroenteritis
with features of mesenteric lymphadenitis

Rule out appendicitis

Yersinia enterocolitica (from the pork)

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181
Q

Which meat is a carrier of Yersinia enterocolitica?

A

Pork

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182
Q

How is Giardiasis transmitted?

A

Faeco-oral from SI of mammals

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183
Q

How do you manage a patient with Giardasis?

A

Metronidazole

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184
Q

What are the potential complications of gastroenteritis?

A

IBS
Reactive arthritis
Lactose intolerance
Guillain-Barré Syndrome

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185
Q

Which antibodies are seropositive in Coeliac disease?

A

anti-TTG

anti-EMA

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186
Q

What rash is associated with Coeliac Disease?

A

Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen

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187
Q

In all patients with Type 1 Diabetes Mellitus, what other autoimmune condition is tested for?

A

Coeliac disease

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188
Q

What is the strongest gene association in a patient with Coeliac Disease?

A

HLA-DQ2 (90%)

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189
Q

Why should you test for total immunoglobulin A levels when testing for Coeliac disease?

A

Anti-TTG and anti-EMA are IgA antibodies thus test for total IgA levels in case of a deficiency which will produce a false negative

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190
Q

What would intestinal biopsy show in a Coeliac disease patient?

A

“Crypt hypertrophy”

“Villous atrophy”

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191
Q

How do you manage a patient with Coeliac disease?

A

Gluten free diet

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192
Q

Give 3 potential complications of Untreated Coeliac Disease.

A 
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)
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193
Q

Outline the key differences between Crohn’s Disease and Ulcerative colitis.

A 
Crohn's Disease: 
No blood or mucous 
Entire GI tract
Skip lesions
Terminal ileum and transmural thickness
Smoking is a RF 
Ulcerative colitis: 
Continuous inflammation 
Limited to colon and rectum 
Only superficial mucosa affected
Smoking is protective 
Excrete blood and mucuous
Use aminosalicylates
Primary sclerosing cholangitis
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194
Q

What are the extra-intestinal manifestations of Inflammatory Bowel Disease?

A 
Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
Episcleritis and iritis
Inflammatory arthritis
Primary sclerosing cholangitis (ulcerative colitis)
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195
Q

What are the gold-standard investigations for Irritable Bowel Syndrome?

A

Faecal calprotectin

Endoscopy

Imaging (CT/MRI)

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196
Q

In biliary atresia, which form of bilirubin will be markedly raised?

A

Conjugated bilirubin

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197
Q

How is biliary atresia diagnosed?

A

Liver biopsy

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198
Q

How do you manage biliary atresia?

A

Kasai portoenterostomy - attaching SI to opening of liver

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199
Q

Give 5 causes of an Intestinal Obstruction in a child.

A 
Dehydration 
Medication 
Meconium ileus
Pyloric Stenosis 
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia
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200
Q

How is an intestinal obstruction diagnosed?

A

AXR - bowel loop dilation

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201
Q

How do you manage an intestinal bowel obstruction?

A

Supportive: PAU admission; NBM; NG tube (drip and suck); IV fluids; monitor
+
Tx cause

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202
Q

What is Hirschprung’s Disease?

A

Absence of parasympathetic ganglion cells in Auerbach’s plexus

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203
Q

What are the types of Hirschprung’s Disease?

A

Rectal
Rectosigmoid
Long segment
Total

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204
Q

How do you diagnose Hirschsprung’s disease?

A

AXR

Rectal biopsy

205
Q

How is Hirschsprung’s disease managed?

A

Surgical removal of ganglionic sections

206
Q

In what age range is Intussusception most common?

A

6mo - 2 years

207
Q

How may Intussusception present?

A 
Severe, colicky abdominal pain
Pale, lethargic and unwell child
“Redcurrant jelly stool”
Right upper quadrant mass on palpation. This is described as “sausage-shaped”
Vomiting
Intestinal obstruction
208
Q

How is Intussusception managed?

A

Therapeutic enema
Surgical reduction

± Gangrenous
Surgical resection

209
Q

Where is tender to palpation in appendicitis?

A

LIF (Rosving’s sign)

RIF (McBurney’s point)

General abdominal wall (rebound and percussion tenderness)

210
Q

How is appendicitis managed?

A

Supportive: Admission; IV Fluids; NBM;
+
Surgical: Lap appendicectomy; Laparotomy

211
Q

What are the most common anatomical positions of the appendix?

A

Retrocaecal

Pelvic

Subcaecal

Preileal

Postileal

212
Q

List some common signs associated with Appendicitis.

A

Cope’s Psoas Test (laying in L lateral decubitus app side of pain and extension of thigh causes pain)

Dunphy sign: Pain when coughing (increased IA pressure)

Markle Sign (stand on toes and drop down on heels with audible thump = localised abdominal pain)

Massouh Sign (sweeping motion from xiphisternum to LIF cf RIF)

McBurney’s Point (pain at 1/3 from umbilicus to ASIS)

Rosving’s sign (LIF pain on palpation)

213
Q

Give an example of two potential infective causes associated with Type 1 Diabetes Mellitus.

A

Coxsackie B virus

Enterovirus

214
Q

Which cells produce insulin?

A

beta cells in the Islets of Langerhans in the pancreas

215
Q

Which cells produce glucagon?

A

alpha cells in the Islets of Langerhans in the pancreas

216
Q

What are the clinical features of a DKA?

A 
Reduced consciousness 
Abdominal pain 
Polyuria 
Polydipsia 
Weight loss

Ketotic breath

Recurrent secondary infections

217
Q

What is the long-term management for Type 1 Diabetes Mellitus?

A

Supportive: Patient education; Annual review; Ophthalmology; Renal check up; Podiatry
+
Medical: Insulin regime (basal-bolus cf CSII)

218
Q

A newly diagnosed diabetic patient presents with hard, discrete, mobile lumps on her abdomen. She says that is where she usually injects her insulin.

What advice would you give this patient?

A

This is lipodystrophy where subcutaneous fat hardens at the injection site.

Rotate injetion site

219
Q

A patient asks you to explain the insulin pump. They are finding daily injections time-consuming and embarrassing.

Outline how it works, pros and cons.

A

An insulin pump is a small device which allows insulin to continuously infuse at a variable rate according to blood glucose levels.

Pump pushes insulin via a small cannula into the skin.

Child must be:

  • Over 12
  • Difficulty managing insulin

Pros:

  • Better control
  • Less injections
  • More control

Negatives:

  • Learning to use
  • Attached at all times
  • Risk of injection
220
Q

What are the long-term complications of Diabetes?

A

Macrovascular Complications:
Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

Microvascular Complications:
Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

Infection Related Complications:
Urinary tract infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis

221
Q

What ways can you monitor glucose in Diabetes?

A

HbA1c

Capillary blood glucose

Flash glucose monitoring

222
Q

Outline the pathophysiology of DKA. What derangements are noted?

A

Inadequate insulin due to pancreatic insufficiency and hypoinsulinaemia results in reduces intracellular uptake of glucose. The elevated glucose increases the osmolarity which results in osmotic diuresis (polyuria) and polydipsia. The prolonged post-prandial state results in ketogenesis and subsequent metabolic acidosis. Finally, hyperinsulinaemia results in reduced amount of potassium driven into cells resulting in hyperkalaemia and subsequent arrhythmia.

223
Q

What is the worrying complication of DKA in children? Outline the pathophysiology.

A

Cerebral oedema may occur due to fluid shifting from the intracellular space in brain to the extracellular space resulting in brain cell shrinking, dehydrating.

Rapid correction of dehydration and hyperglycaemia may result in rapid shift in water from EC to IC which results in brain swelling and cerebral oedema.

224
Q

What is the diagnostic criteria for DKA?

A

Hyperglycaemia >11mmol/L

Ketosis >3mmol/L

Acidosis pH <7.3

225
Q

Deficiency of what enzyme causes Congenital Adrenal Hyperplasia?

A

21-alpha hydroxylase

226
Q

What is the pathophysiology of Congenital Adrenal Hyperplasia?

A

21 alpha hydroxylase deficiency therefore no progesterone converted into aldosterone and cortisol thus reduction in mineralocorticoids and glucocorticoids however, excessive androgen production

227
Q

In a patient with Congenital Adrenal Hyperplasia, what clinical features would you expect?

A

Dehydration
Fatigue
Thirst
Arrhythmias
Tall
Skin pigmentation (elevated ACTH which binds at melanocytes)
Genitalia changes: virilised genitalia and clitoromegaly

Hyponatraemia + Hyperkalaemia (Aldosterone deficiency)

Hypoglycaemia (Cortisol deficiency)

High androgen levels

228
Q

How do you manage Congenital Adrenal Hyperplasia?

A

Medical: Hydrocortisone; Fludrocortisone
±
Surgery: Clitorectomy

229
Q

How do you diagnose growth hormone deficiency in a child?

A

GH stimulation test - measuring GH release in response to glucagon, insulin, arginine and clonidine for 2-4 hours after administering medication

230
Q

What effect does clonidine have on GH release?

A

Clonidine is an alpha 2 adrenoceptor agonist which also has weak effect in inhibiting SS release and increases release of GHRH

231
Q

How is growth hormone deficiency managed in children?

A 
Supportive: Paediatric endocrinology referral; annual review
\+
Medical: Insulin SC 
\+
Tx other problems
232
Q

Which antibodies are present in Hashimoto’s Thyroiditis?

A

anti-TPO

antithyroglobulin antibodies

233
Q

What can congenital hypothyroidism be the result of?

How may it be detected?

A

Dysgenesis

Dyshormonogenesis

Newborn blood spot screening tool

234
Q

How is hypothyroidism managed?

A

Levothyroxine 1.6mcg/kg - titrate on TFTs and symptoms

235
Q

How is a UTI managed in a child?

A

All children <3 months + fever

  • Initiate Sepsis 6
  • IV ABX (Ceftriaxone)

> 3 months

  • Nitrofurantoin
  • Trimethoprim
236
Q

How should recurrent UTIs be investigated in children?

A

Investigate for underlying cause and renal damage

Options:

  • US-Renal
  • DMSA Scan
  • MCUG scan
<6 months old 
- US-Abdomen (6 weeks)
- MCUG Scan 
±
DMSA scan (4-6 months after)

Recurrent UTIs

  • US-Abdomen (6 weeks)
  • DMSA Scan
237
Q

How do you broadly interpret a DMSA scan?

A

This involves injecting a radioactive material (DMSA) and using a gamma camera to assess how well the material is taken up by the kidneys. Where there are patches of kidney that have not taken up the material, this indicates scarring that may be the result of previous infection.

238
Q

How does a MCUG work?

A

It involves catheterising the child, injecting contrast into the bladder and taking a series of xray films to determine whether the contrast is refluxing into the ureters. Children are usually given prophylactic antibiotics for 3 days around the time of the investigation.

239
Q

What age is vulvovaginitis most common in children?

A

3-10 years

240
Q

Give 3 causes of vulvovaginitis?

A

Wet nappies
Use of chemicals or soaps in cleaning the area
Tight clothing that traps moisture or sweat in the area
Poor toilet hygiene
Constipation
Threadworms
Pressure on the area, for example horse riding
Heavily chlorinated pools

241
Q

How is vulvovaginitis managed?

A

Supportive:
Avoid washing with soap and chemicals
Avoid perfumed or antiseptic products
Good toilet hygiene, wipe from front to back
Keeping the area dry
Emollients, such as sudacrem can sooth the area
Loose cotton clothing
Treating constipation and worms where applicable
Avoiding activities that exacerbate the problem

242
Q

What are the features of nephrotic syndrome?

A

Low serum albumin
High urine protein content (>3+ protein on urine dipstick)
Oedema

may feature…
Deranged lipid profile, with high levels of cholesterol, triglycerides and low density lipoproteins
High blood pressure
Hyper-coagulability, with an increased tendency to form blood clots

243
Q

What is the most common cause of nephrotic syndrome in children?

A

Minial change disease

244
Q

What does light microscopy show in minimal change disease?

A

No abnormality

245
Q

What does light microscopy show in minimal change disease?

A

Loss of podocytes

246
Q

How is minimal change disease treated?

A

Prednisolone

247
Q

How do you manage a nephrotic syndrome?

A

Supportive: salt-restrict; fluid-restrict
+
Medical: Steroids; diuretics

± Resistant
ACEi/ Immunosuppressants

248
Q

What are the complications of nephrotic syndrome?

A 
Hypovolaemia 
Thrombosis 
Infection 
Acute or chronic renal failure 
Relapse
249
Q

What are the key clinical features of nephritic syndrome?

A

Reduced eGFR
Haematuria
Proteinuria

250
Q

What are the two most common causes of nephritic syndrome in children?

A

Berger’s Disease

Post-streptococcal Nephropathy

251
Q

What clinical features may suggest post-streptococcal glomerulonephritis?

A

Haematuria
Proteinuria
Oedema

PMHx sore throat (tonsilitis)

ASO titres elevated

252
Q

What would a kidney biopsy of a patient with Berger’s disease show?

A

IgA deposits in nephrons and glomerular mesangial proliferation

253
Q

What is the most common cause of Haemolytic Uraemic Syndrome?

A

E.coli 0157 bacteria which produce the shigella toxin

Shigella

254
Q

What clinical features may be suggestive of Haemolytic Uraemic Syndrome?

A

Gastroenteritis: diarrhoea; nausea

Haematuria
Oliguria/Anuria
Abdominal pain
Oedema
Hypertension
Bruising
255
Q

How do you manage Haemolytic Uraemic Syndrome?

A

Supportive: Admission; IV Fluids;
±
RRT; Antihypertensives

256
Q

How may enuresis be classified?

A

Nocturnal

Diurnal

Primary (never dry)

Secondary (>6 months)

257
Q

What are the causes of primary nocturnal enuresis?

A

Overactive bladder
Fluid intake
Failure to wake
Psychological stress

UTI
Chronic constipation
Cerebral palsy

258
Q

What are some causes of secondary enuresis?

A 
UTI
Constipation
T1DM
New psychosocial problems
Maltreatment
259
Q

How may enuresis be managed?

A

Supportive: bed wetting alarms; toilet training; reward systems; reduce fluid intakes; positive reinforcement
+
Medical: Oxybutinin; Desmopressin; Imipramine

260
Q

Which form of polycystic kidney disease presents earlier?

A

ARPKD (neonates) cf ADPKD (20-30)

261
Q

What are the complications or associated conditions with polycystic kidney disease?

A 
CKD 
Hypertension
CLD
Liver failure (fibrosis) 
Portal hypertension
262
Q

The presence of multiple cysts in one kidney with the other kidney remaining normal is termed?

When is it detected?

A

Multicystic Dysplastic Kidney

Antenatal ultrasound scan

263
Q

What are the clinical features of a Wilms tumour?

A 
Abdominal pain
Hypertension
Haematuria 
Lethargy
Fever
Weight loss
264
Q

What is the gold-standard investigation for a Wilms tumour?

A

US-Renal

265
Q

How is a Wilm’s tumour managed?

A

Surgery: Nephrectomy
±
Medical: chemotherapy + radiotherapy

266
Q

What is the gold-standard investigation for investigation of urinary retention and recurrent urinary tract infections in a child?

A

US-Abdomen

MCUG

267
Q

How are posterior urethral values onitored?

A

Surgery: Ablation/ Endoscopic incision

268
Q

Upon a newborn baby check, you cannot observe testicles in the scrotum. What is this called?

A

Cryptorchidism (undescended teste)

269
Q

What are the risks associated with undescended testes?

A

Testicular torsion
Infertility
Testicular cancer

270
Q

How are undescended testes managed?

A

If salvageable:
- Orchidopexy

If unsalvageable:
- Orchiectomy

271
Q

How is hypospadias managed?

A

Urethroplasty

272
Q

How is epispadias managed?

A

Urethroplasty

273
Q

What are the clinical features of a hydrocoele?

A

Soft, smooth swelling around the testes
Transilluminates

Negative Prehn’s test
Positive Cremasteric reflex

274
Q

Where does fluid collect in a hydrocoele?

A

Tunica vaginalis surrounding the testes

275
Q

Describe how a communicating hydrocoele works?

A

Tunica vaginalis has a conduit with the peritoneal cavity therefore a pathway created called the processus vaginalis, allowing fluid to drain into the scrotum to form a hydrocoele

276
Q

How is a hydrocoele managed?

A

Supportive: Self-dresolving

or

Surgery: Hydrolectomy

277
Q

How long is recommended to breast feed?

A

6/12

278
Q

How much milk should a baby be consuming?

What is the frequency?

A

150mL/kg

2-3 hours then 4 hours + between feeds

279
Q

What is an acceptable amount of weight loss for a baby?

Why may this occur?

A

<10%

SA:V ratio = high metabolic ratel dehydration; switch from nutrition, colostrum then milk

280
Q

If a child is in the 91st centile for height, what does this mean? Explain to the parent.

A

Child is taller than 91% of other children at that same age and gender

281
Q

what is childhood obesity defined as according to growth charts?

A

BMI > 95th percentile

282
Q

What is the criteria for faltering growth?

A

Have a higher index of suspicion if the child is underweight to begin

One or more centile spaces if their birthweight was below the 9th centile

Two or more centile spaces if their birthweight was between the 9th and 91st centile

Three or more centile spaces if their birthweight was above the 91st centile

283
Q

What investigation should be conducted in a suspected case of failure to thrive?

A 
Urine dipstick, for urinary tract infection
Coeliac screen (anti-TTG or anti-EMA antibodies)

Bloods
US-Abdomen (PS)
Chloride sweat tests

284
Q

How do you predict a child’s height based on parents?

A

(Maternal height + paternal height ± 14cm) / 2

M = +14cm

F = -14cm

285
Q

What is the key feature of Constitutional Delay in Growth and Puberty?

What is the gold-standard investigation for this?

A

Delayed bone age - delayed bone age cf children their age

XR

286
Q

At what age should a child support their head in the midline?

A

4 months

287
Q

At what age can a child sit upright?

A

6 months

288
Q

At what age does a child crawl?

A

9 months

289
Q

At what age does a child begin cruising?

A

12 months

290
Q

At what age can a child kick a ball?

A

2 years

291
Q

At what age can a child walk up stairs?

A

3 years

292
Q

At what age can a child grasp an object in their palm?

A

6 months

293
Q

At what age does a child demonstrate a pincer grasp?

A

12 months

294
Q

At what age can a child use a spoon to bring from the bowl to mouth?

A

18 months

295
Q

When can a child hold a crayon and scribble?

A

12 months

296
Q

When can a child draw a circle?

A

3 years

297
Q

When can demonstrate a a mature tripod pencil grasp?

A

5 years

298
Q

When can a child make cooing noises?

A

3 months

299
Q

When can a child make noises with consonants?

A

6 months

300
Q

When can a child say single monosyllabic words in context?

A

12 months

301
Q

When can a child combine words to make basic sentences?

A

3 years

302
Q

At what age can a child follow simple instructions?

A

12 months

302
Q

At what age can a child follow simple instructions?

A

12 months

303
Q

At what age can a child understand two key words?

A

2 years

304
Q

At what age can a child understand three key words?

A

3 years

305
Q

At what age does a child become engaged with people?

A

6 months

306
Q

At what age does a child begin pointing and handing objects?

A

12 months

307
Q

At what age does a child begin to imitate activities such as using a phone?

A

18 months

308
Q

At what age does a child become dry by night and have bowel control?

A

4 years

309
Q

What are the red flags of development?

A 
Lost developmental milestones
Not able to hold an object at 5 months
Not sitting unsupported at 12 months
Not standing independently at 18 months
Not walking independently at 2 years
Not running at 2.5 years
No words at 18 months
No interest in others at 18 months
310
Q

What are some common causes for Global Developmental Delay?

A 
Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders
311
Q

What are the reasons for Gross Motor Delay?

A 
Cerebral palsy
Ataxia
Myopathy
Spina bifida
Visual impairment
312
Q

What are the reasons for fine motor delay?

A 
Dyspraxia
Cerebral palsy
Muscular dystrophy
Visual impairment
Congenital ataxia (rare)
313
Q

What are the common reasons for language delay?

A 
Specific social circumstances, for example exposure to multiple languages or siblings that do all the talking
Hearing impairment
Learning disability
Neglect
Autism
Cerebral palsy
314
Q

What are the common causes for personal and social delay?

A

Emotional and social neglect
Parenting issues
Autism

315
Q

What is a normal IQ?

A

70-120

316
Q

What category of learning disability is an IQ of 58?

A

Mild (55-70)

317
Q

What category of learning disability is an IQ of 68?

A

Mild

318
Q

What category of learning disability is an IQ of 48?

A

Moderate

319
Q

What category of learning disability is an IQ of 35?

A

Severe

320
Q

What category of learning disability is an IQ of 18?

A

Profound

321
Q

How do you manage a learning disability?

A

Supportive: MDT approach

322
Q

How should you determine capacity broadly in a patient with a learning disability?

A

Capacity is decision specific, does not prevent the ability to make decisions

Require time, effort and decision aids

Check they can:

  • Understand
  • Retain
  • Weigh up
  • Communicate
323
Q

What staging criteria can used to determine the stage of puberty a child is at?

A

Tanner staging

324
Q

A child presents with short stature and at aged 16, has not began puberty.

His bloods show low LH and FSH.

What condition does he have?

A

Hypogonadotrophic hypogonadism

325
Q

A child presents with short stature and at aged 16, has not began puberty.

His bloods show elevated LH and FSH.

What condition does he have?

A

Hypergonadotrophic hypogonadism

326
Q

What are the potential causes of hypogonadotrophic hypogonadism?

A 
HP axis damage - radiotherapy/surgery 
GH deficiency 
Hypothyroidism
Hyperprolactinaemia 
Cystic fibrosis 
IBD 
Excessive exercise/dieting (eating disorders) 
Constitutional delay 
Kallman Syndrome
327
Q

How do you manage a suspected case of child abuse?

A

Refer to a specialist - safeguarding team/CAMHS/Police

327
Q

How do you manage a suspected case of child abuse?

A

Refer to a specialist - safeguarding team/CAMHS/Police

328
Q

At what age can a child consent to a treatment?

A

Recognised as an adult aged 16 (Scots Law) and 18 (England + Wales)

If younger, use Gillick competence on a decision-by-decision basis

329
Q

What chromosome abnormality gives rise to Down’s Syndrome?

A

Trisomy 21

330
Q

What are the clinical features of Down’s Syndrome?

A 
Hypotonia (reduced muscle tone)
Brachycephaly (small head with a flat back)
Short neck
Short stature
Flattened face and nose
Prominent epicanthic folds
Upward sloping palpable fissures
Single palmar crease
331
Q

What screening tests are offered in pregnancy for Down’s Syndrome?

A

Combined test (11-14 weeks)

1) US: ? Nuchal translucency (>6mm)
2) Bloods: elevated ßhCG and lower PAPPA

Quadruple test (14-20 weeks)
ßhCG = higher 
AFP = lower
Serum oestriol = lower
Inhibin: higher
332
Q

A woman tests at 16 weeks with deranged quadruple test. Her ßhCG is elevated, as with her inhibin-A. Whilst her PAPPA and oestriol is lower.

She asks what her risk of Down’s Syndrome in this pregnancy is?

What further testing is available?

A

5%

Amniocentesis

CVS <15 weeks thus not this option

Amniocentesis

333
Q

How do you manage Down’s Syndrome?

A

Supportive: MDT involvement; Regular review
±
Medical: Tx consequences

334
Q

What is the karyotype for Klinefelter’s Syndrome?

A

47 XXY

335
Q

What are the clinical features of Klinefelter Syndrome?

A 
Taller height
Wider hips
Gynaecomastia
Weaker muscles
Small testicles
Reduced libido
Shyness
Infertility
Subtle learning difficulties (particularly affecting speech and language
336
Q

How do you manage someone with Klinefelter Syndrome?

A 
Supportive: MDT
\+
Medical: Testosterone IM
\+
Surgery: Breast reduction surgery
337
Q

A patient presents with a short stature, webbed neck, cubitus valgus and late puberty. She is worried. She also says she has widely spaced nipples and a broad chest.

What is her genotype likely to be?

What condition does she have?

A

45XO

Turner Syndrome

338
Q

How is Turner Syndrome managed?

A

Supportive: MDT referral
+
Medical: GH therapy; Sex hormone replacement; Fertility Tx

339
Q

A patient presents with a short stature. O/E you see a broad forehead, wide spaces between the eye, low set ears and a webbed neck. Additionally, they have widely spaced nipples.

What condition do you think they have?

A

Noonan Syndrome

340
Q

A patient presents complaining that his knee feels like it will give way. with tall stature and a long neck. You observe long limbs and long fingers.

What might you observe when inspecting his mouth?

What might you observe when inspecting his chest?

What condition do you think this patient has?

What causes this condition?

A

High arching palate

Chest wall deformities

Marfan Syndrome

Fibrillin gene mutation -> ∆ECM

341
Q

What murmurs are associated with Marfan Syndrome?

A

Mitral valve prolapse (with regurgitation)

Aortic valve prolapse (with regurgitation)

342
Q

A child is brought in by their mother who is concerned about their development. The child is not social with other children at nursery and at the age of 8 months, cannot recognise the faces of their family/friends and appears unreceptive.

O/E you notice a long, narrow face. The child has large ears.

What condition is this?

What causes this condition?

A

Fragile X Syndrome

FMR1 gene ∆

343
Q

A 4 year old is brought in by their mother due to their constant hunger. The child eats everything they see. She is very distressed and worried it is not healthy.

O/E you identify skin that easily bruises, a narrow forehead, a squint and the child is morbidly obese in the 99th centile for weight.

What condition do you think this child has?

A

PWS

344
Q

A young girl presents with balance issues. She laughs at random times, is described to be fascinated with water. She is very happy and excitable.

O/E you see a small head and light hair with blue eyes. She has a wide mouth and widely spaced teeth.

What condition does she have?

A

Angelman Syndrome

345
Q

A child is brought in by his mother due to his wide mouth and widely spaced teeth. She says he is very sociable and trusting.

O/E he has a flattened nasal bridge, long philtre and small chin. You notice starburst eyes.

What condition do you think he has?

What associated conditions are there?

A

William Syndrome

Supravalvular aortic stenosis
ADHD
HTN
Hypercalcaemia

346
Q

Outline the process of a vasovagal episode.

A

A vasovagal episode (or attack) is caused by a problem with the autonomic nervous system regulating blood flow to the brain. When the vagus nerve receives a strong stimulus, such as an emotional event, painful sensation or change in temperature it can stimulate the parasympathetic nervous system. Parasympathetic activation counteracts the sympathetic nervous system, which keeps the smooth muscles in blood vessels constricted. As the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”.

347
Q

How may you categorise a syncopal episode?

A

Primary vs Secondary

348
Q

What investigations may you conduct in a patient with syncope?

A

Bloods

ECG

Echocardiogram

349
Q

What advice would you give to someone suffering from primary syncopal episodes?

A

Supportive: fluid intake; 3 meals; snacks; take breaks; try to prevent when experiencing prodromal symptoms

350
Q

Describe what occurs in a Generalised Tonic-Clonic seizure.

How are they managed?

A

There is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) movements. Typically the tonic phase comes before the clonic phase. There may be associated tongue biting, incontinence, groaning and irregular breathing.

Post-ictal period

Sodium valproate (if not pregnant/on contraception)

351
Q

How may a focal seizure present?

How are they managed?

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

Lamotrigine (reverse order of tonic-clonic)

352
Q

A child’s mother reports episodes of the child staring blankly into space and after a period of 30 seconds, will return to normal. They seem in a frozen state.

What form of epilepsy is being described?

How do you manage this?

A

Absence seizure

Sodium valproate

353
Q

In a child experiencing Atonic Seizures, what condition must you be suspicious of?

What are the key features of this condition?

How do you manage atonic seizures?

A

Lennox-Gastaut Syndrome

Intellectual impairment + EEG findings + Multiple types of seizures

Sodium valproate

354
Q

A mother brings in her 6 month year old child reporting full body spasms. She is worried.

What condition may this be?

How is this managed?

A

West Syndrome (infantile spasms)

Prednisolone

355
Q

A 2 year old child is brought in with a high temperature. The mother says recently she had her vaccines and has had a temperature spike. Also she is having some brief periods whereby she is tensing up and then has some muscle jerking.

What condition is this?

A

Febrile convulsions

356
Q

What is the management of seizures in children?

A

Supportive: showers; cautious swimming; avoid heights; do not drive; cautious with high powered equipment; annual review; referral to neurologist
+
Medical: Sodium valproate; Lamotrigine

357
Q

What are the side effects of carbamazepine?

A

Agranulocytosis
Aplastic anaemia
Induces the P450 system so there are many drug interactions

358
Q

What are the side effects of phenytoin?

A 
Folate and vitamin D deficiency
Megaloblastic anaemia (folate deficiency)
Osteomalacia (vitamin D deficiency)
359
Q

What are the side effects of ethosuximide?

A

Night terrors

Rashes

360
Q

A child presents with a seizure that has lasted 7 minutes. You have put them in a recovery position and moved obstacles which may cause injury.

What condition do you suspect?

How would you manage this?

A

Status Epilepticus

A-E

Call for help

A - secure airway; recovery position
B - Oxygen
C - monitor; access
D - Glucose; IV Lorazepam (secondary care) or Buccal midazolam (community)

If persists, give IV Phenytoin

361
Q

What is the risk of developing epilepsy following a febrile convulsion?

A

2-7.5% after a simple febrile convulsion

10-20% after a complex febrile convulsion

362
Q

What are the potential causes of febrile convulsions?

A

Immunisation
Epilepsy
Meningitis, encephalitis or another neurological infection such as cerebral malaria
Intracranial space occupying lesions, for example brain tumours or intracranial haemorrhage
Syncopal episode
Electrolyte abnormalities
Trauma (always think about non accidental injury)

363
Q

When are breath holding spells most common?

What two types are there? Explain the difference.

A

6-18 months

1) Cyanotic Breath Holding - v upset, crying, long cry; lethargic following cry
2) Reflex anoxic seizures - child v startled, heart stops beating; child goes pale and have some seizures - normal after 30 seconds

364
Q

What condition is associated with breath holding spells?

A

Breath holding spells have been linked with iron deficiency anaemia. Treating the child if they are iron deficiency anaemic can help minimise further episodes.

365
Q

A child presents with dull-pressure headache. He describes it coming on in a band-like pattern around the forehead.

There are no associated visual changes. Following 30 minutes, the pain is gone. It gets worse when they are stressed or skipped meals.

What is your DDx?

What is your Tx?

A

Tension headaches

Supportive: Reassurance; regular meals; fluid intake; reduce stress; analgesia

366
Q

A child presents with a unilateral headache located in the temporal region. Prior to it beginning, they have some visual changes. Additionally they feel sick.

What is your DDx?

What is your Tx?

A

Supportive: Rest; fluid intake; Analgesia

± Recurrent migraines
Medical: Propanolol; Pizotifen; Topiramate

367
Q

How may you categorise the causes of cerebral palsy?

A

Antenatal
Perinatal
Postnatal

368
Q

What are the types of cerebral palsy?

A

Spastic (hypertonia)

Dyskinetic (muscle tone + hypertonia + hypotonia + athetoid movements)

Ataxic (coordination and balance problems)

Mixed (elements of each)

369
Q

What are the different patterns of cerebral palsy?

A

Monoplegia: one limb affected

Hemiplegia: one side of the body affected

Diplegia: four limbs are affects, but mostly the legs

Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments

370
Q

What are the fundamental differences between upper and lower motor neurone lesions?

A

Upper:

  • Muscle bulk fine
  • Hypertonia
  • Hyperreflexia
  • Power fine

Lower:

  • Reduced muscle bulk
  • Hypotonia
  • Hyporeflexia
  • Reduced power
371
Q

How do you manage Cerebral Palsy?

A 
Supportive: MDT; feeding 
\+
Medical: Baclofen; Lamotrigine; Glycopyrronium bromide
±
Surgery: Tenotomy
372
Q

A child is brought in by the mother due to having one eye ‘less open than the other’.

O/E the child has an obvious strabismus.

Why should this be corrected?

How can you test for this?

How is this managed?

A

Prevent amblyopia.

Hirschberg’s test (shine light from 1m and should be equal and symmetrical)

Cover test (if eye moves inwards, it has drifted outside thus exotropia; if eye moves outwards, it has drifted inwards thus esotropia)

Supportive: Occlusive patch (cover good eye); Ophthalmologist referral
±
Medical: Atropine eye drops (in good eye)

373
Q

Outline the process of CSF fluid production and drainage in the brain.

A

Produced by the choroidal plexus by ependymal cells then drains from lateral to third to fourth ventricles and absorbed into venous system by arachnoid granulations

374
Q

What is the most common congenital cause of hydrocephalus?

A

The most common cause of hydrocephalus is aqueductal stenosis, leading to insufficiency drainage of CSF. The cerebral aqueduct that connects the third and fourth ventricle is stenosed (narrowed). This blocks the normal flow of CSF out of the third ventricle, causing CSF to build up in the lateral and third ventricles.

375
Q

What age do sutures fuse in a child?

A

2 years

376
Q

What are the clinical features of hydrocephalus in a child?

A

enlarged and rapidly increasing head circumference (occipito-frontal circumference)

Bulging anterior fontanelle
Poor feeding and vomiting
Poor tone
Sleepiness

377
Q

How do you manage a hydrocephalus?

A

Surgery: VP shunt

378
Q

What are the complications of a VP shunt?

A

Infection
Blockage
Excessive drainage
Intraventricular haemorrhage during shunt related surgery
Outgrowing them (they typically need replacing around every 2 years as the child grows)

379
Q

How may premature skull suture closure be classified?

A

Classified based on suture closure

Sagittal synostosis

Coronal synostosis

Metopic synostosis

Lambdoid synostosis

380
Q

What is the gold standard investigation to investigate a craniosynostosis?

How would you manage a cranyosynostosis?

A

XR-Skull

Surgery: Craniectomy

381
Q

A mother is worried that if she lets her child rest their head on a flat surface, it will change the shape of their head.

What is this condition caused?

A

Plagiocephaly - potential Brachycephaly if back of the head

382
Q

How is Plagiocephaly managed?

A

Supportive: XR-Skull (exclude Craniosynotosis); Physiotherapy; Plagiocephaly helmets; Positioning; use rolled towels to position head

383
Q

What is the name of the sign of a child using their hands and knees to get up in order to walk?

What condition does it suggest?

A

Gower’s Sign

DMD/BMD

384
Q

Mutation of what gene causes DMD?

A

Dystrophin gene

385
Q

What are the clinical features of myotonic dystrophy?

A

Progressive muscle weakness
Prolonged muscle contractions
Cataracts
Cardiac arrhythmias

386
Q

What are the clinical features of myotonic dystrophy?

A

Progressive muscle weakness
Prolonged muscle contractions
Cataracts
Cardiac arrhythmias

387
Q

A patient’s mother reports they sleep with their eyes slightly open. O/E they have a weakness when pursing their lips, unable to blow their cheeks out against resistance. Additionally, they have weakness on in the face, progressing to the shoulders and arms.

What is the DDx?

A

Facioscapulohumeral Muscular Dystrophy

388
Q

A 24 year old patient presents with weakness of eye movements and a weak swallow. O/E they have a bilateral ptosis, restricted eye movements and swallowing problems.

What is your DDx?

A

Oculopharyngeal Muscular Dystrophy

389
Q

What is Emery-Dreifuss Muscular Dystrophy?

A

Childhood presentation of contractures in the elbow and ankles with shortening of muscles and tendons which result in progressive weakness and muscle wasting - beginning in the upper arms and lower legs

390
Q

What are the clinical features of Spinal Muscular Atrophy?

A

LMN of spinal cord thus LMN signs

Atrophy
Fasciculations
Hypotonia 
Reduced power 
Hyporeflexia
391
Q

How is Spinal Muscular Atrophy managed?

A

Supportive: MDT management; Physiotherapy; NIV; Feeding

392
Q

What are the clinical features of depression in children?

A 
Low mood
Anhedonia, a lack of pleasure in activities
Low energy
Anxiety and worry
Clinginess
Irritability
Avoiding social situations (e.g. school)
Hopelessness about the future
Poor sleep, particularly early morning waking
Poor appetite or over eating
Poor concentration
393
Q

How is depression managed in children?

A

Supportive: Psych. referral; counselling
+
Medical: Fluoxetine 10mg

394
Q

How do you manage Anxiety in a child?

A

Supportive: Self-help; avoid caffeine; exercise; diet

± Moderate/Severe
Medical: Sertraline

395
Q

How is autism managed in children?

A

MDT
+
Tx comorbidities

396
Q

What is the management of ADHD in children?

A

Methylphenidate

397
Q

Lanugo hair is a pathognomonic sign of what condition?

A

Anorexia nervosa

398
Q

What clinical features typify Bulimia Nervosa?

A

Purging behaviours

Russel Sign

GORD

Dental erosion

Metabolic alkalosis

399
Q

How are eating disorders managed in children?

A

Supportive: Psych. referral; Counselling; CBT; gradual refeeding (specialist care)

±
Medical: Fluoxetine

400
Q

Outline the process of refeeding syndrome?

How is this managed?

A

Hypomagnesaemia
Hypokalaemia
Hypophosphataemia

Supportive: A-E; admission; Monitoring; Monitor fluid balance; ECG; electrolyte replacements

401
Q

How is Tourette’s managed in children?

A

Supportive: exposure with response prevention

± Tics
Medical: Guanfacine

402
Q

State 5 potential complications of prematurity.

A

Respiratory Distress Syndrome

Patent Ductus Arteriosus

Necrotising enterocolitis

Intraventricular haemorrhage

Retinopathy of prematurity

403
Q

Give 5 potential pathogenic causes of neonatal sepsis.

A

GBS

E. coli 
Chlamydia 
HSV 
Gonorrhoea 
Listeria

S. epidermidis

404
Q

What pathogen is most likely to cause sepsis in a neonate who has received a central line?

A. S aureus

B. S pyogenes

C. S epidermidis

D. E coli

A

C

405
Q

Outline the potential causes of neonatal jaundice.

A

<1 day: Rh incompatibility; ABO incompatibility; G6PD deficiency; hereditary spherocytosis; sepsis (GBS)

2days-2wks: Physiological jaundice

> 2 wks: Sepsis; UTI; hypothyroidism; galactosaemia; G6PD; Hereditary spherocytosis;
Biliary atresia; neonatal hepatitis

406
Q

What investigations would you wish to run in a neonate with jaundice?

A 
FBC, U+Es, LFTs, TFTs, CRP, 
Blood cultures
Haemolytic screen: Haptoglobin, Reticulocytes, LDH, DAT
Urine MC+S
Liver-US
407
Q

How does phototherapy work in jaundice?

A

Blue light helps conjugate unconjugated Br into conjugated Br

408
Q

What is the threshold for neonatal hypoglycaemia?

A

<2.6mmol/L

409
Q

What are the potential causes of Neonatal Hypoglycaemia?

A 
Prematurity
SGA
Macrosomia 
Diabetic mother 
Sepsis 
Hyperinsulinaemia
Galactosaemia 
BWS/CAH
410
Q

Outline the main difference between Omphalocoele and Gastroschisis.

A

Omphalocele is a herniation of IA contents through the umbilicus WITH a sac

Gastroschisis is a herniation of IA contents through the R of the abdomen WITHOUT a sac

411
Q

State 3 potential birthing injuries.

A

Ischaemic encephalopathy/Cerebral Palsy

Klumpke’s Palsy
Erb’s Palsy
Shoulder dystocia

DDH

Cephalohaematoma
Caput succadeum

Facial nerve injury

412
Q

Draw out the sutures and bones of a foetal skull.

A 
Include:
Metopic suture 
Coronal suture 
Sagittal suture 
Lambdoid suture

Frontal bone
Parietal bone
Occipital bone

413
Q

How can you determine the difference between type of infection in meningitis?

A

LP !!!

Bacterial: Cloudy; low glucose; high protein; high polymorphs

TB: Cloudy (fibrin web); low glucose; high protein; high lymphocytes

Viral: Clear; mildly reduced glucose; normal protein; high lymphocytes

414
Q

What is the management for Kawasaki disease?

A

High-dose aspirin
+
IVIG

415
Q

What is Reye’s syndrome?

A

Progressive encephalopathy resulting from Aspirin use in child with Viral illness resulting in impaired FA metabolisation and damage to areas of FA metabolism e.g. Brain, Liver and Pancreas.

The peak incidence is 2 years of age, features include:
there may be a history of preceding viral illness
encephalopathy: confusion, seizures, cerebral oedema, coma
fatty infiltration of the liver, kidneys and pancreas
hypoglycaemia

416
Q

What type of seizure is involved in Febrile Convulsions?

A

Brief generalised tonic-clonic seizure

417
Q

What is the age range at which children may experience febrile convulsions?

A

6mo - 6 years.

418
Q

What is the risk of developing epilepsy following a febrile convulsion?

A

1%

419
Q

What is the risk of developing a further febrile convulsion following the first?

A

30%

420
Q

What are the features of Epilepsy?

A

Generalised or Focal

Generalised: Absence; Tonic-Clonic (tightening and contractions); Myoclonic (groups of jerking); Atonic (drop attacks, with loss of muscle tone)

Focal: Frontal lobe (simple partial seizures); Temporal lobe (automatisms, deja vu, sensory phenomena); Parietal lobe (vertigo, distorted body image); Occipital lobe (visual symptoms)

421
Q

When do absence seizures occur?

A

3-12 years old

422
Q

What investigation proves an absence seizure?

A

Collateral history

3Hz spikes

423
Q

What may precipitate an absence seizure?

A

Hyperventilation

424
Q

When do infantile spasms occur most commonly?

A

4-6 months

425
Q

What is the management for West Syndrome?

A

Vigabatrin or ACTH analogue

426
Q

What are the characteristic findings of West Syndrome on EEG?

A

Hypsarrhythmia

High amplitude spikes + irregular spikes on EEG

427
Q

What is Lennox-Gastaut Syndrome?

A

Myoclonic jerks; absence seizures; atonic seizure

428
Q

What are the EEG findings of Lennox-Gastaut Syndrome?

A

1.25-2.5Hz spike + waves

429
Q

What diet may help a Lennox-Gastaut Syndrome?

A

Ketogenic diet

430
Q

What are the features of a Benign Rolandic Syndrome?

A

3-10 years

Tonic-clonic during sleep
Partial seizures affecting sensation thus paraesthesia

Rolandic spikes on EEG

431
Q

What is Juvenile myoclonic seizures?

A

Myoclonic seizures after waking; worse from sleep deprivation

EEG shows multi-spike with fragmentation

432
Q

What are the types of cerebral palsy?

A

Spastic - hypertonic; hyperreflexia, loss of power (hemiplegia, diplegia, quadriplegia)

Dyskinetic - chorea, athetosis

Ataxic - DANISH signs

433
Q

What are the types of neural tube defect?

A

Anencephaly: Abnormal brain development - dies

Encephalocoele: herniation of brain through midline of skull

Myelomeningocoele: Abnormal spinal cord and exposed defect

Meningocoele: Normal spinal cord, defect covered with skin

Spina bifida occulta: Cord covered with bone and skin with overlying lesion e.g. lipoma/sinus/hair

434
Q

What are the potential consequences of neural tube defects?

A

Depends on the type of neural tube defect

Lower limb paralysis 
Sensory loss
Neuropathic bladder/bowels and UTIs/gastroparesis/constipation 
Contractures 
Scoliosis
435
Q

What are the clinical features of Hydrocephalus in a child?

A 
Irritability 
Poor feeding 
Headaches
Vomiting 
Seizures

Enlarged head
Bulging fontanelles
Sunsetting eyes (downward deviation)
Papilloedema

436
Q

What type of cell is degenerating in Spinal Muscular Atrophy?

A. Dorsal Horn

B. Myocyte

C. Anterior Horn

D. Fibroblast

A

C

437
Q

What are the clinical features of Neurofibromatosis?

A

Cafe au Lait spots
Peripheral neurofibromas
Irish hamartomas (Lisch Nodules)
Scoliosis

Type 2: Bilateral acoustic neuromas

438
Q

What are the clinical features of Tuberous Sclerosis?

A

Ashleaf spots
Shagren’s nodules
Heart rhabdomyomas

Lymphangioleiomyomatosis
Epilepsy
Angiomyolipomata/Angiofibromas
Fibromas

439
Q

Which cancer is linked to ataxia telangiectasia?

A

ALL

440
Q

What are the clinical features of ataxia telangiectasia?

A

Telangiectasia

Ataxia

441
Q

Which of the following blood markers may be elevated in Ataxia telangiectasia?

A. ALP

B. WBCs

C. AFP

D. Ca-19

A

C

442
Q

How is Friedrich’s ataxia inherited?

A

Autosomal recessive

GAA triplet expansion

443
Q

Which of the following is not a clinical feature of Friedrich’s Ataxia?

A. Extensor plantars

B. Brisk ankle reflex

C. Cardiomyopathy

D. Sensory ataxia

A

B - absent ankle reflexes

444
Q

What is the inheritance of DMD?

A

X-linked recessive

445
Q

What are the clinical features of DMD?

A 
Global developmental delay 
Waddling gait 
Cardiomyopathy 
Gower's sign
Pseudohypertrophy 
Muscle wasting
446
Q

What biochemical abnormality is often noted in DMD?

A

CK raised

447
Q

Infants which are at risk of RSV can take which drug as prophylaxis?

A

Palivizumab

448
Q

What pathogen causes Croup?

A

Parainfluenza virus

449
Q

What are the clinical features of a severe asthma attack?

A

SpO2 <92%

Cannot finish full sentence
HR >140
RR >40
DIB

450
Q

What are the clinical features of a life-threatening asthma attack?

A 
SpO2 <92%
Silent chest
Poor respiratory effort 
Confusion
Cyanosis
451
Q

State 5 causes of a wheeze in a child

A 
Post-viral wheeze
Asthma
Bronchiolitis 
Foreign body inhalation 
Aspiration/GORD 
Mediastinal mass (e.g. Lymphoma)
452
Q

What are the features of Kartagener’s Syndrome?

A

Situs inversus
Chronic sinusitis
Bronchiectasis

453
Q

What is the most common cause of Pneumonia?

A

S pneumonia

454
Q

What is Sandifer syndrome?

A

Paroxysmal movement disorder featuring dystonic movements in association with GORD

455
Q

What type of metabolic disturbance is seen in Pyloric stenosis?

A

Hypochloraemic hypokalaemia metabolic alkalosis

456
Q

What are the potential causes of feeding difficulties in a baby? Give a defining feature for each.

A

Colic: Long cries, absence of other pathologies; resolves by 3 months

GORD: regurgitation, vomiting, uncomfortable during feeds

Allergic colitis: rash, raised IgE, Eosinophilia, failure to thrive

Pyloric stenosis: projectile, non-bilious vomiting, RUQ olive mass

Gastroenteritis: vomiting and diarrhoea; depleted fluid balance

Oesophageal atresia: choking and cyanotic spells

457
Q

Give 3 potential causes of recurrent abdominal pain in children.

A

Abdominal migraine

GORD

Mesenteric adenines

IBS

458
Q

How does DMSA scintigraphy work?

A

Dimercaptosuccinic acid (DMSA) localises to renal cortex thus helps see cortical defects such as scarring

459
Q

How does MAG3 scan work?

A

Mercaptoacetyle triglycine is protein bound thus secreted by tubular cells thus useful for imaging kidneys in a renally-impaired patient

460
Q

When should you refer for a single undescended testes?

What about both testes being undescended?

A

One = 3 months

Two = 24 hours

461
Q

When is the surgery for an undescended testes conducted?

A

Orchidopexy at 1 year

462
Q

What are the features of an innocent murmur?

A

Two types of murmur:

1) Still’s murmur: LSE
2) Venous hum: Turbulent flow in great veins - continuous blowing noise

Soft - grade 1 or 2
Systolic
No thrill, no heave, no radiation
Chid well, asymptomatic

463
Q

Give an example of cyanotic heart disease?

A

ToF

TGA

464
Q

Which inherited syndrome is CoA associated with?

A

Turner Syndrome

465
Q

What should NOT be given in CoA?

A

Do not give Indomethacin, give PGE2 to keep shunts open until angioplasty undertaken

466
Q

What are the clinical features of ToF?

A

Mnemonic: PROV

Pulmonary stenosis
RV hypertrophy
Overarching aorta
VSD

467
Q

What may exacerbate or relieve cyanosis?

A

Child squat to assist venous return

Cyanotic when crying

468
Q

What is TGA?

A

Aorta from RV and PA from LV with blood mixing via foetal shunts

469
Q

What are the clinical features of Rheumatic Fever?

A

Mnemonic: JONES

Joint involvement
O looks like heart - myocarditis 
Nodules 
Erythema marginatum
Sydenham chorea
470
Q

Where is a neuroblastoma derived from?

A

Neuroendocrine tumour from sympathetic chain - usually adrenal in origin

471
Q

Where is a rhabdomyosarcoma derived from?

A

Skeletal muscle tissue

472
Q

What is a clinical feature of a Retinoblastoma?

A

No retinal reflex
Squint
Visual symptoms

473
Q

What is an osteosarcoma? Where are they found?
What shows on X-Ray?
What is it linked to?

A

Cancer of the osteoblasts resulting in deposition of bone matrix which invade and destroy healthy tissue

Long bones prior to epiphyseal closure
Femur > Tibia > Humerus

XR shows Codman triangle (periosteal reaction) and sunburst pattern (fast growth with no new layer added down and Sharpey’s fibres stretch out perpendicular to bone)

∆Rb gene thus links with Retinoblastoma

474
Q

What is an Ewing’s Sarcoma? Where are they found?
What shows on X-Ray?
What is it linked to?

A

Solid tumour derived mesenchymal cells but unsure which

Seen in pelvis and long bones - cause a lot of pain

XR: Onion skin appearance

PAIN

475
Q

What are some of the potential complications of Down’s Syndrome?

A 
Hearing/visual impairment
CHDs
Hypothyroidism 
Duodenal atresia 
Coeliac disease
476
Q

What are the clinical features of Turner’s syndrome?

A 
Webbed neck
Wide spaced nipples
Short 
Normal IQ 
CoA 
Bicuspid aortic valve (aortic stenosis)
477
Q

What are the clinical features of Patau Syndrome?

A

Trisomy 13

Microcephaly
Cleft palate
Polydactyly
Scalp lesions

478
Q

What are the clinical features of Edward’s Syndrome?

A

Micrognathia
Low set ears
Rocker bottom feet
Overlapping fingers

479
Q

What are the clinical features of Fragile X syndrome?

A 
Macrocephaly
Long face
Large ears
Macro-orchidism 
Learning difficulties
480
Q

What are the clinical features of Noonan Syndrome?

A

Webbed neck
Pes excavatum
Short stature
Pulmonary stenosis

481
Q

What are the clinical features of William’s syndrome?

A

Short stature
Friendly, extroverted
Supravalvular aortic stenosis
Transient neonatal hypercalcaemia

482
Q

At what age should a child be able to pull self to sitting?

A

6 months

483
Q

When should a child be able to sit without support?

A

8 months

484
Q

When should a child be able to crawl?

A

9 months

485
Q

When should a child be walking without support?

A

13-15 months

486
Q

When should a child be cruising by?

A

12 months

487
Q

When should a child be cruising by?

A

12 months

488
Q

When should a child be able to run?

A

2 years

489
Q

When should a child be able to ride a tricycle?

A

3 years

490
Q

When should a child be able to hop on one leg?

A

4 years

491
Q

When should a child be able to smile?

A

6 weeks

492
Q

When should a child be laughing and enjoy friendly handling?

A

3 months

493
Q

When should a child be able to use a spoon?

A

2 years

494
Q

When should a child be able to use a spoon and fork?

A

3 years

495
Q

When should a child be able to take off their shoes?

A

18 months

496
Q

When should a child be able to dress and undress?

A

4 years

497
Q

When should a child be able to wave bye-bye?

A

12 months

498
Q

When should a child be able to play near others?

A

2 years

499
Q

When should a child be able to hold using palmar grasp?

A

6 months

500
Q

When should a child be able to point with their finger?

A

9 months

501
Q

When should a child be able to use a good pincer grip?

A

12 months

502
Q

When should a child be able to build a brick tower of 3?

A

18 months

503
Q

When should a child be able to build a brick tower of 6?

A

2 years

504
Q

When should a child be able to build a brick tower of 9?

A

3 years

505
Q

When should a child turn towards sound?

A

3 months

506
Q

When should a child be able to say mama and dada?

A

9 months

507
Q

When should a child recognise their own name?

A

12 months

508
Q

When should a child be able to combine 2 words?

A

2 years

509
Q

When should a child be able to use 3-5 words?

A

3 years old

Medicine (18 decks)

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