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AMC MCQ > Child & Adolescent Health > Flashcards

Child & Adolescent Health Flashcards

15%

1
Q

Classification by ages: Neonate

A

< 1 month

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2
Q

Classification by ages:
Infant

A

1 month - 1 yo

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3
Q

Classification by ages: Toddler

A

1 - 3 yo

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4
Q

Classification by ages:
Child

A

4-10 yo

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5
Q

Classification by ages: Adolescent

A
  • Girls: 10 - 15/17
  • Boys: 12 -16/18
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6
Q

Screening for children: Head

A

Recorded until 2 years.

Should increase by 1 cm per month in the first 3 months, then 0.5 cm per month from 3–6 months.

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7
Q

Screening for children: Hips

A

At birth, 6–8 weeks, 6–9 months and 12–24 months.

Ortolani: most likely to be positive at 3–6 weeks and usually negative after 8 weeks. Shortening or limited abduction is also abnormal.

Ultrasound examination is more sensitive between 3–4 months.

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8
Q

Screening for children: Visual acuity

A

At birth and 6-8 weeks: Cataracts and red reflexes.

At 9 months: Gross vision (ability to see common objects)

Formal assesment: School entry, using Sheridan Gardiner charts.

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9
Q

Visual acuity REFERRAL indications

A
  1. Nystagmus
  2. Wandering eye
  3. Lack of fixation, or lack of following movements
  4. Photophobia
  5. Opacities
  6. Visual delayed development

To rule out: Retinoblastoma, congenital cataract and glaucoma (all needs emergency surgery)

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10
Q

Strabismus physical exam

A
Differential of Pseudosquint: Light reflex will be in exactly the same position in both eyes in the pseudosquint but in different spots with the true squint.
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11
Q

Strabismus types (4)

A

Transient and latent (occurs under stress, e.g. fatigue) usually are not a problem.

Early referral: constant and alternating

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12
Q

Screening for children: Strabismus

A

AGE: Infants and toddlers

Examination:
1. Occlusion testing (not very sensitive)

  1. Examining light reflexes
  2. Questioning parents
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13
Q

Strabismus COMPLICATION

A

**Amblyopia **can be prevented and treatment of strabismus by occlusion (the good eye) OR surgery (Best at 1–2 yo). Early referral is essential.

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14
Q

Amblyopia Description

A

Same as ‘lazy eye’

Reduction in visual acuity due to abnormal visual experience in early childhood. It is the main reason for poor unilateral eyesight until middle age.

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15
Q

Amblyopia Causes (3)

A
  1. Strabismus
  2. Hypermetropia
  3. Congenital cataract
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16
Q

Blindness in children causes by order (5)

A
  1. Cortical blindness (bilateral lesions of the striate cortex in the occipital lobes)
  2. Optic atrophy
  3. Choroidoretinal degeneration
  4. Cataract
  5. Retinopathy of prematurity (abnormal blood vessels grow in the retina)
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17
Q

Screening for children: Hearing

A

9 months or earlier: Distraction.

4 years (preschool entry) and 12 years: Pure tone audiometry at 1000 and 4000 hertz

Formal audiological evaluation should be carried out at any time if there is clinical suspicion or parental concern. No simple screening test is very reliable for sensorineural or conductive deafness.

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18
Q

Screening for children: Testes

A

Screen at birth, and 6–8 weeks, 6–9 months and 3 years for absence or maldescent.

Those who have been treated for maldescent have a higher risk of neoplastic development in adolescence.

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19
Q

Screening for children: Speech and language

A

A child’s speech should be intelligible to strangers by 3 years.

It is related to hearing.

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20
Q

Screening for children: BMI Percentile > 95 indicates

A

Obese

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21
Q

Screening for children: BMI Percentile between 85-95 indicates

A

Overweight

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22
Q

Screening for children: BMI Percentile between 5 - 85 indicates

A

Normal

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23
Q

Screening for children: BMI Percentile < 5 indicates

A

Underweight

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24
Q

Correction in prematurity

A

Correct for prematurity but only until 24 months.

If an infant was born at 36w, then you add 4w to the normal milestone

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25
Q

Height Calculation (2 formulas)

A

1 FORMULA

Father + Mum / 2

*Boys + 6.5
*Girls - 6.5
—————————————–
#2 FORMULA

 Boys: [father’s height in cm + (mother’s height in cm + 13 cm)]/2

 Girls: [(father’s height in cm – 13 cm) + mother’s height in cm]/2

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26
Q

Normal development Milestones Chart (6 weeks - 4yo)

A
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27
Q

Areas of Development (4)

A

 Gross motor
 Vision and fine motor
 Hearing, speech, and language
 Social, emotional, and behavioral

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28
Q

Global Development Delay DEFINITION

A

2 or more development areas delayed

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29
Q

Normal development Milestones 4 weeks old

A

Gross motor: Lifts chin up

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30
Q

Normal development Milestones 2 months old

A

Social, emotional, and behavioral:
- Social smile

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31
Q

Normal development Milestones 3 months old

A

Social, emotional, and behavioral:
- Recognize the mother

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32
Q

Normal development Milestones 4 months old

A

Gross motor:
- Roll over (prone to supine)
- Lifts head up 90 degrees when lying prone

Vision and fine motor:
- Grasps and plays/shakes with an object

Hearing, speech, and language:
- Turns to voice

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33
Q

Normal development Milestones 5 months old

A

Gross motor:
- Rolls (supine to prone). So… Roll both directions

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34
Q

Normal development Milestones 6 months old

A

Gross motor:
- Begins to sit with support

Vision and fine motor:
- Palmar grasp

Hearing, speech, and language:
- Babbling well established
- Respond to own name

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35
Q

Normal development Milestones 6 months old

A

Vision and fine motor:
- Transfers objects from hand to hand

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36
Q

Normal development Milestones 9 months old

A

Gross motor:
- Sits without support
- Crawling

Vision and fine motor:
- Inferior / Crude pincer grip

Social, emotional, and behavioral:
- Anxious with strangers

Other: First tooth (review info)

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37
Q

Normal development Milestones 10 months old

A

Gross motor:
- Standing with support (holding on)

Hearing, speech, and language:
- Understands “NO”

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38
Q

Normal development Milestones 12 months old

A

Gross motor:
- Walk with support
- Cruises around furniture

Vision and fine motor:
- Finger feeds

Hearing, speech, and language:
- First word

Social, emotional, and behavioral:
- Waves “goodbye”
- Plays ‘peek-a-boo’
- Claps hands
- Possible separation anxiety (since 6 months)

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39
Q

Normal development Milestones 2 years old

A

4Gross motor:
- Walks up and down stairs holding on

Vision and fine motor:
- Turns pages
- Uses a spoon
- Build a 4 block tower
- Scribbling
- Pencil skills: LINE

Hearing, speech, and language:
- 2 to 4 words sentences

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40
Q

Normal development Milestones 3 years old

A

Gross motor:
- Climbs stairs alternating foot
- Rides a tricycle

Vision and fine motor:
- Build a nine-block tower
- Pencil skills: Circle

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41
Q

Normal development Milestones 4 years old

A

Gross motor:
Hops and stand on one foot > 2 sec

Vision and fine motor:
-Pencil skills (in order)
*Cross
*Square
*Triangle

Hearing, speech, and language:
- Give first and last name

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42
Q

Normal development Milestones 5 years old

A

Gross motor:
- Climb
- Somersault

Vision and fine motor:
- Self toilet
- Use a fork and spoon
- Can get dressed and undressed

Hearing, speech, and language:
- Speaks very clearly
- Name colors

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43
Q

Normal development Milestones 6 years old

A

Gross motor:
- Riding a bicycle
- Skipping

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44
Q

Normal development Milestones 15 months old

A

Gross motor:
Walk alone or with one hand held

Vision and fine motor:
Neat/mature pincer grip

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45
Q

Individual finger activities (9–18 months) ORDER (3):

A
  1. Pinching (pulp-to-pulp)
  2. Pincing (tip-to-tip with curled fingers)
  3. Pointing
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46
Q

Normal development Milestones 18 months old (1.5 yo)

A

Gross motor:
- Pointing
- Walks well
- Probably holding hand upstairs

Vision and fine motor:
- Drinks from a cup
- Builds a 2-3 block tower

Hearing, speech, and language:
-3 words
- Points to body parts

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47
Q

Pencil Grasp by ages

A
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48
Q

Corrected gestational age for premature babies

A

Corrected age = Chronological age (-) # weeks or months premature

weeks or months premature = 40 weeks (-) weeks at birth

NOTE: The corrected age is taken into consideration when looking at
milestones until the age of 2 years old.

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49
Q

NEWBORN SCREENING – Heel Prick Test – Guthrie (9)

A

Done at 2-4 days old

Include 9 conditions:
1. Congenital hypothyroidism (CHT)
2. Sickle cell disorders
3. Cystic fibrosis (CF)
4. Phenylketonuria (PKU)
5. Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
6. Maple syrup urine disease (MSUD)
7. Isovaleric acidaemia (IVA)
8. Glutaric aciduria type 1 (GA1)
9. Homocystinuria (pyridoxine unresponsive) (HCU)

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50
Q

Apnoea after birth MANAGEMENT (4 steps)

A
  1. Call for help
  2. Stimulate (rubbing of soles of feet
    or chest) and assess response
  3. Airway - opening manoeuvres
    - Head and neck positioned in a neutral position
    - Gently suction mouth and nostrils if necessary
  4. Positive pressure ventilation:
    BAG AND MASK.
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51
Q

Neonatal Respiratory Distress Clinical Features (6)

A

 RR > 60/ min

 HR > 160/min

 Grunting

 Intercostal space drawing

 Nasal flaring

 Central cyanosis

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52
Q

Neonatal Respiratory Distress CAUSES (3)

A
  1. Transient Tachypnoea of the Newborn (TTN)
  2. Meconium Aspiration Syndrome (MAS)
  3. Hyaline Membrane Disease (HMD)
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53
Q

Neonatal Respiratory Distress Comparison Table

A
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54
Q

Neonatal Respiratory Distress Initial investigation

A
  1. Pulse oximetry (Continuous monitor)
  2. Arterial blood gas (ABG): not indicated initially, unless an underlying condition is suspected or ongoing respiratory
    difficulty exists.
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55
Q

Neonatal Respiratory Distress Best Investigation

A

Chest X-Ray

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56
Q

Transient Tachypnoea of the Newborn FOLLOW-UP TREATMENT

A
  • Medical care is supportive: Supplemental oxygen to maintain adequate arterial
    oxygen saturation.
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57
Q

Transient Tachypnoea of the Newborn IMAGING

A

CHEST X-RAY (diagnostic standard)

  • Prominent perihilar streaking, which correlates with the engorgement of the lymphatic system with retained lung fluid, and fluid in the fissures.
  • Small pleural effusions.
  • Patchy infiltrates.
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58
Q

RESPIRATORY DISTRESS SYNDROME or Hyaline membrane disease (same) COMPLICATIONS (7)

A

Septicaemia

Necrotizing enterocolitis (NEC)

Retinopathy of prematurity (ROP)

Hypertension

Failure to thrive

Intraventricular hemorrhage (IVH)

Periventricular leukomalacia (PVL) - With associated neurodevelopmental and audio-visual handicaps

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59
Q

Transient Tachypnoea of the Newborn FOLLOW-UP INVESTIGATIONS

A
  1. **CXR **IF:
  • Meconium aspiration syndrome suspicion
  • Neonatal pneumonia suspicion
  • Respiratory status worsens
  1. Echocardiogram IF:
  • Persistent tachypnea > 5-6 days. Rule out
    congenital cardiac anomalies and function.
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60
Q

Neonatal Pulmonary Alveolar Proteinosis - General Features (2):

A
  • Baby at term w/ sibling that died of the same, and now have severe resp distress

Physiopathology: Over-production of surfactant proteins within the alveoli.

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61
Q

Neonatal Pulmonary Alveolar Proteinosis - Etiology:

A

*Autoimmune (90%)
*Secondary (4%)
*Congenital (1%), depending on the gene involved:
- Autosomal dominant
- Autosomal recessive
- X-linked recessive

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62
Q

Neonatal Pulmonary Alveolar Proteinosis - Treatment (2):

A
  1. Bronchoalveolar lavage.
  2. Lung transplant.
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63
Q

Sudden infant death syndrome RISK FACTORS (7)

A
  • Smoking parents (passive smoking)
  • Parental narcotic/cocaine abuse
  • Prone position during sleep
  • Artificial feeding
  • Hyperthermia
  • Extreme prematurity
  • URTI
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64
Q

PNEUMONIA: Most common causes (microorganisms)

A
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65
Q

What are the (5) Signs of withdrawal in kids with:
Neonatal Abstinence Syndrome

A
  1. High-pitched cry
  2. Hyperreflexia.
  3. Tremors.
  4. Seizures.
  5. Hypertonia.
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66
Q

What are the (2) onsets of: Neonatal Abstinence Syndrome

A

Heroine (2-3 days)
Methadone (up to 1-2w)

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67
Q

Neonatal Abstinence Syndrome - Treatment

A

Morphine to assist with gradual withdrawal, then decrease slowly.

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68
Q

Neonatal Overdose Syndrome (narcotics/opioid) - Clinical Features (3)

A
  • Pinpoint pupils
  • Lethargy
  • Mom’s use of opioids: Meperidine (Demerol), pethidine & heroine
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69
Q

Neonatal Overdose Syndrome (narcotics/opioid) - First Treatment (1) and then Best Treatment (1)

A

Treatment:
- Next: Bag and mask ventilation

  • Best: Naloxone is tx. Should only be
    given if the mother has received narcotics < 2 hrs of delivery
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70
Q

Apnoea after birth in a term neonate SUSPECTED CAUSE

A

Neonatal overdose syndrome.
(History of Mom’s use of opioids)

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71
Q

Neonatal Hypoglycaemia - Clinical features & Associations:

A

Clinical features:
- Jitteriness
- Peripheral cyanosis
- Irritability
- Poor feeding
- Seizures
- High pitched cry
- Lethargy
- Hypotonia (rare)

Association with:
- Hepatomegaly
- Micropenis
- Macrosomia
- Cleft lip

Investigations???
Treatment???

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72
Q

NEONATAL JAUNDICE - Bilirubin concentration

A

Jaundice may not be visible in the neonate’s skin until the bilirubin concentration exceeds 70-100 micromol/L.

Infants that are not jaundiced to the naked eye do not need routine bilirubin checking.

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73
Q

Transcutaneous bilirubinometer indications (TCB)

A
  • > 35 weeks gestation
  • > 24 hours old for the first measurement.
  • TCB can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment

NOTE: If the patient is not a good candidate for TCB, SERUM BILIRUBIN should be performed

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74
Q

NEONATAL JAUNDICE: Kramer’s RULE

A

Still, send the child for serum bilirubin (SBR) ASAP - despite Kramer rule results

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75
Q

Phototherapy and Exchange transfusion Indications

A

NICE treatment threshold graph

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76
Q

Phototherapy Procedure

A

There are different types:
 Single Light - Double Lights w/ Bili blanket or even Triple Lights.
 They are all the same methods just different intensity of exposure.

Give the baby eye protection

Cease phototherapy when SBR is at least 50 micromol/L below the phototherapy range for the age.

SUNLIGHT EXPOSURE IS NOT RECOMMENDED AS A TREATMENT FOR JAUNDICE

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77
Q

Name 8 complications of Phototherapy

A

 overheating
 water loss
 diarrhoea
 ileus (preterm infants)
 rash (no specific treatment required)
 retinal damage (theoretical)
 parental anxiety/separation
 ‘bronzing’ of infants with conjugated hyperbilirubinemia.

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78
Q

Rh disease: Exchange transfusion - Indications: (3)

A

 have cord blood haemoglobin < 100 g/L
 have cord bilirubin > 80 micromol/L
 are visibly jaundiced within 12 hours of birth.

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79
Q

Exchange transfusion Procedure

A

During:
* Continuing multiple phototherapy
* Perform a double-volume exchange

After:
* Maintain continuous multiple phototherapy
* Measure serum bilirubin level within 2 hours and manage according to threshold table

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80
Q

Exchange transfusion COMPLICATIONS (8)

A
  • apnoea
  • bradycardia
  • cyanosis
  • vasospasm
  • air embolism
  • infection
  • thrombosis
  • necrotising enterocolitis
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81
Q

Kernicterus Definition

A

Permanent clinical sequelae of bilirubin toxicity (UNCONJUGATED)

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82
Q

Kernicterus Definition Clinical Features (5)

A
  • Athetoid/Dyskinetic cerebral palsy (abnormal posturing, tone, and involuntary movements)
  • Developmental and intellectual delay
  • Hearing deficit
  • Dental dysplasia
  • Oculomotor disturbance
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83
Q

Kernicterus Risk Factors (4)

A

 Serum bilirubin >340 micromol/L in term neonates

 Preterm infants may be at risk at lower SBR < 300
micromol/L

 Rapidly rising bilirubin level of greater than 8.5 micromol/L per hour

 Clinical features of acute bilirubin encephalopathy

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84
Q

Acute bilirubin encephalopathy Clinical Features (8)

A

Initially:
- Decreased feeding (poor suck reflex)
- Lethargy
- Abnormal tone: hypotonia

Progress to:
- High-pitched cry
- Abnormal tone: Hypertonia
- Retrocollis and opisthotonus
- Setting-sun sign (upward-gaze paresis)
- Fever
- Seizures

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85
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Mechanism (3)

A
  • Shorter lifespan of neonatal red blood cells
  • Immature liver function at birth
  • A relatively high concentration of β-glucuronidase in the small intestine
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86
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Risk factors (4)

A
  1. Preterm babies (higher bilirubin levels)
  2. Exclusive breastfed babies
  3. Babies with significant bruising or cephalohaematoma: The breakdown of RBCs within the cephalohaematoma causes higher bilirubin levels and predisposes to jaundice.
  4. Previous sibling with neonatal jaundice requiring phototherapy
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87
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Characteristics

A
  • Day 2-14 (> 21 in preterm)
  • Mild
  • Diagnosis of exclusion
  • Resolves in 2w
  • Rarely exceeds 220 micromol/L
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88
Q

PATHOLOGICAL NEONATAL JAUNDICE: Characteristics

A
  • Too early < 24 hours of age
  • Too Long > 10 - 14 days of age (term: 2 weeks / preterm: 3 weeks)
  • Too high > 220 micromol/L
  • CONJUGATED Hyperbilirubinemia
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89
Q

NEONATAL JAUNDICE: UNconjugated (INDIRECT) Hyperbilirubinemia CAUSES

A
  • Physiological
  • Breast milk jaundice
  • Sepsis
  • Metabolic:
  • Gilbert’s syndrome
  • Congenital hypothyroidism
  • Crigler-Najjar syndrome
  • Hemolytic:
  • ABO/Rh incompatibility
  • Spherocytosis
  • G6PD deficiency
  • Sickle cell anemia
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90
Q

NEONATAL JAUNDICE: Conjugated (DIRECT) Hyperbilirubinemia CAUSES

A
  1. Biliary atresia
  2. Neonatal hepatitis
  • TORCH infection
  • Idiopathic
  • Metabolic: Galactosemia, Wilson, alpha 1antitripsine.

NOTE:
Always > 24 h
Conjugated bilirubin level >25 micromol/L because this may indicate serious liver disease

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91
Q

Biliary atresia VS Idiopatic Neonatal hepatitis

A
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92
Q

NEONATAL JAUNDICE + unwell state, suggests:

A

Sepsis OR GIT obstruction

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93
Q

NEONATAL JAUNDICE < 24-48 H UNCONJUGATED suggests:

A

Hemolysis

  1. ABO incompatibility (Most common)
    - Mother: O group; Child: A or B
    - Direct Coombs (+)
    - Peripheral smear: Spherocytes (some)
  2. Spherocytosis
    - Peripheral smear: Predominant spherocytes
    - Direct Coombs (-)
    - FBE:↑ MCHC
    - FxHx: Anemia/spherocytosis/gallstones
  3. Sickle Cell
    - Peripheral smear: Sickle and target cells
    - Direct Coombs (-)
    - African descendants
  4. Rh incompatibility (Most severe)
    - Peripheral smear: NO spherocytes
    - Direct Coombs (+)
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94
Q

NEONATAL JAUNDICE > 24-48 H ↑UNCONJUGATED, suggests:

A
  1. Physiological jaundice
    Most Common cause in the first week:
    - Term: 50%
    - Preterm: 80%
    finishes in 1-2 weeks (preterm 3 weeks)
  2. Breast milk jaundice
    Lasts up to 6 weeks
    Diagnose: Suspending breastfeeding for 24-48 hrs = ↓ serum bilirubin
  3. Neonatal sepsis
    End of the first week (4-7 days old)
    Lethargic + jaundice + hepatosplenomegaly
    ↑ BOTH, Direct and Indirect bilirubin.
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95
Q

NEONATAL JAUNDICE + Family history of hemolytic disease, suggests:

A

G6PD deficiency

OR

Spherocytosis (FxHx of gall stones)

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96
Q

NEONATAL JAUNDICE + Dark urine or pale stools OR ↑ DIRECT bilirubin, suggests:

A

Biliary obstruction (Biliary atresia)

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97
Q

JAUNDICE + Plethora, suggest:

A

Polycythaemia

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98
Q

NEONATAL JAUNDICE + Hepatosplenomegaly, suggest:

A

Hepatitis (↑ liver enzymes)

OR

Metabolic problems (Galactosemia)

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99
Q

NEONATAL JAUNDICE: Sepsis Management

A

1st Hemocultures

2nd ATB: Wich??

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100
Q

NEONATAL JAUNDICE: Gilbert’s Syndrome Clinical Features

A

Inheritance: Autosomal recessive

Deficit of glucuronyl transferase => ↑ unconjugated bilirubin

Triggers: fasting, intercurrent illness, menstruation, stress, and dehydration

Other blood tests are normal

No treatment required.

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101
Q

NEONATAL JAUNDICE: Gilbert’s Syndrome Contraindicated drugs

A

Amoxiclav
Flucoxaciline
Erythromycin
Rifampicin

Radiographic agent

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102
Q

NEONATAL JAUNDICE: Gilbert’s syndrome Diagnostic methods

A

Fasting bilirubin

Bilirubin after nicotinic acid

Liver biopsy (normal)

NOTE: Diagnostic tests are NOT performed in the majority of patients.

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103
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Clinical features (11)

A

listless

 Goitre

 prominent tongue

 hoarse cry

 puffy face

 constipation

 umbilical hernia

 hypothermia

 bradycardia

 dry skin

 failure to thrive

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104
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Risk factors (3)

A

Mother with:

  • Diet: Iodine deficiency
  • Medication history: Amiodarone, methimazole
  • Auto-immune disease: Hashimoto
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105
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Investigations (3)

A
  1. T4 and TSH levels
  2. Serum bilirubin (SBR) if clinically indicated.
  3. Thyroid scan: showing absent, lingual or increased uptake of radioisotope
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106
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Management (4)

A

 Referral to Endocrine team

 Thyroxine replacement therapy ASAP

 Growth and development must be closely monitored.

 Hearing tests should be done.

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107
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Medical Treatment

A

Levotiroxine

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108
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Prognosis

A

Normal intellectual and physical development if the treatment is commenced promptly (<2 weeks old) and monitored closely.

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109
Q

NEONATAL JAUNDICE: Crigler Najjar syndrome Type 1

A

Inheritance: Autosomal recessive

UDP-G Absent

Unconjugated bilirubin > 340 micromol/L

Complication: Kernicterus, unless rapid treatment

Management:
Phototherapy, exchange transfusion, etc.
Phenobarbital doesn’t help

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110
Q

NEONATAL JAUNDICE: Crigler Najjar syndrome Type 2

A

Inheritance: Autosomal recessive

UDP-G Decreased

Unconjugated bilirubin < 340 micromol/L

Management: Phenobarbital help

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111
Q

NEONATAL JAUNDICE: Spherocytosis CLINICAL FEATURES

A

Inheritance: Autosomal dominant

  • English – Irish – Scottish descendants.
  • Gallstone family history
  • Splenomegaly
  • FBE: ↓ Hb ↑ MCHC
  • Blood smear: Abnormally shaped RBC or Spherocytes
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112
Q

NEONATAL JAUNDICE: Spherocytosis FIRST INVESTIGATION

A

Osmotic fragility test

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113
Q

NEONATAL JAUNDICE: Spherocytosis BEST INVESTIGATION

A

Eosin-5-maleimide test

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114
Q

NEONATAL JAUNDICE: G-6PD Deficiency Inheritance

A
  • X-linked Recessive (only boys)
  • Sudanese, African descents
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115
Q

NEONATAL JAUNDICE: G-6PD Deficiency Clinical Features (4)

A

Hemolytic anemia

Jaundice

Lethargy

Dark urine

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116
Q

NEONATAL JAUNDICE: G-6PD Deficiency FIRST investigations

A
  1. FBE: ↓ RBC count, ↓ Hb level, ↑ reticulocytes
  2. Peripheral blood smears:* Heinz bodies (bite cell): Inclusions within red blood cells composed of denatured hemoglobin
  3. LFT: ↑Total Bilirubin ↑Unconjugated (Haemolysis)
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117
Q

NEONATAL JAUNDICE: G-6PD Deficiency Diagnostic/BEST investigation

A
  1. G6PD Assay

NOTE: Beutler fluorescent spot test is for screening

  1. Genetic Screening is recommended to all 1st degree relatives – also to exclude other haemolytic anaemias like Sickle that is also common in the same community
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118
Q

NEONATAL JAUNDICE: G-6PD Deficiency Management (3)

A
  1. Avoid oxidative stress triggers:
  • Infections
  • Cold weather
  • Hypoxia
  • Dehydration
  • Acidosis
  • Surgery
  • Certain foods like fava beans
  • Antioxidant drugs: Sulphonamides, antimalarial, nitrofurantoin, naphthalene, aspirin, high dose of Vit. C and K and
  1. Vit E
  2. SEVERE CASES: RCB TRANSFUSIONS
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119
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Definition

A

Obliteration of the extra-hepatic bile ducts
- Fetal (20%)
- Perinatal: after birth (80%)

Type III it’s the most common (90%), and involves all biliary ducts.

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120
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Clinical Features (6)

A
  • Presentation: since the 1st week
  • Prolonged Jaundice (> 14 days in term and > 21 in preterm)
  • Dark urine
  • Clay-colored stools (even meconium is pale)
  • Abdominal pain (crying on changing diapers)
  • Hepatosplenomegaly ( >2cm below costal margin)
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121
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Investigations (4)

A
  • LFT (all kids with JAUNDICE)
  • Total & Direct Bilirubin (↑CONJUGATED)
  • Full Blood exam: Haemoglobin level
  • Urgent: Abdominal US and GE review.
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122
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Best Investigation

A

Percutaneous biopsy (gold-standard):

Bile ductular proliferation (>specific), bile plugging, multinucleated giant cells, focal necrosis of liver parenchyma, extramedullary hemopoiesis, and inflammatory cell infiltrate.

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123
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Management

A
  • Surgery:
  • Portoenterostomy (Kasai procedure)
    *Within 70 days to prevent biliary cirrhosis

OR

  • Liver Transplant
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124
Q

Galactosemia: Clinical features (4)

A
  1. Cataracts
  2. Chronic liver failure
  3. Failure to thrive (FTT): fails to gain weight or height.
  4. Delay: Slower than normal development of motor, cognitive, social, and emotional skills.
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125
Q

Galactosemia: Management

A
  1. Lactose-free formula
  2. Screen family members
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126
Q

Breast Milk Jaundice Clinical features

A

Very common

Develops within 2-4 days of birth, may peak at 7-15 days of age, and may persist for many weeks.

No need to stop breastfeeding

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127
Q

Lactose Intolerance: Clinical features (7)

A
  • Watery or foamy stools
  • Farty baby (LOL)
  • Excoriation of buttocks
  • Normal growth
  • Abdominal bloating
  • Gurgling stomach
  • Presentation after an episode of viral gastroenteritis
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128
Q

Lactose intolerance FIRST MANAGEMENT

A

TRIAL: Cut lactose from the diet for 2 weeks.

RESULTS:
* Successful: Lactose should be cut out from the diet for 8 weeks and then gradually re-introduced over a week.

  • Unsuccessful: Other causes should be suspected.
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129
Q

Lactose intolerance: First Investigation

A

Stool acidity test: Unabsorbed lactose is fermented by colonic bacteria into lactic acid, which lowers the stool pH.

130
Q

Lactose intolerance: Best Investigation

A

Endoscopy with Small bowel biopsy

131
Q

Lactose intolerance: Treatment

A
  • Continue breastfeeding unless severe excoriation or inadequate weight gain
  • Formula-fed infants should be placed in soy formula.
132
Q

Cow’s Milk allergy - Clinical Features (3)

A

Clinical features:
- Diarrhea
- Malabsorption
- Failure to thrive (FTT)

133
Q

Cow’s Milk allergy - First Investigation

A

Complete elimination of cow’s milk protein (CMP) challenge test.

134
Q

Cow’s Milk allergy - Treatment (4):

A
  • Breastfeeding: The mother should eliminate all foods containing cow’s milk protein (cheese, yogurt, and butter)
  • Extensively hydrolyzed hypoallergenic formulas.
  • Supplements of vitamin D and riboflavin.
  • It doesn’t improve with soy, sheep’s or goat’s milk
135
Q

cow’s milk micronutrient deficiencies

A
  • Iron
  • Vit C
136
Q

Toddler diarrhoea

A

Age: 1 - 3 yo

Diarrhea with undigested food
(a piece of carrot)

Reassure and explain

137
Q

Infantile colic - Clinical Features (5):

A

Clinical features:
- Crying for 3 hours in late afternoon and early evening
- Flexing legs
- Clenching fists
- Appears in pain
- Everything else is normal

138
Q

Infantile colic - Management (3*):

A
  1. Exclude organic causes
  2. Reassure
  3. Infacol colic relief drops

Note: Severe cases can trial CMP elimination

139
Q

DIARRHEA PART 1:
Viral
Typhoid – Enteric Fever Salmonella
Giardiasis
Amoebiasis

A
140
Q

DIARRHEA PART 2:
Salmonella sp. (non-Typhoidal)
Shigella
E. coli
Campylobacter jejuni

A
141
Q

DIARRHEA PART 3:
Clostridium difficile
Staph Aureus
Bacillus cereus
Clostridium sp
Clostridium botulinum
Vibrio Cholerae - Cholera

A
142
Q

Bilious Vomiting in
Neonate CAUSES (5)

A
  • Malrotation and volvulus
  • Duodenal atresia
  • Meconium ileus
  • Meconium plug
  • Hirschsprung’s disease
143
Q

DD TABLE: Obstruction with bilious vomiting

A
144
Q

Milk-stained vomiting in
Neonate CAUSES (3)

A
  • Pyloric stenosis
  • Transoesophageal atresia
  • Gastro-Oesophageal Reflux Disease (GORD)
  • Infections: Gastroenteritis, UTI, Otitis media.
145
Q

Malrotation of the Gut GENERAL FEATURES* (4)

*Don’t answer with clinical features

A

 Abnormal rotation of the gut during embryogenesis.
 1:6000 live births
 Associated with duodenal atresia-stenosis, abdominal wall
defects, choanal atresia
 Most patients will develop volvulus within the first week of life.

146
Q

Malrotation of the Gut Clinical Features* (3)

*Don’t answer with general features

A

 Bilious vomiting
 Abdominal Distension is minimal (very late symptom)
 Abdominal x-ray may be normal.

147
Q

Malrotation of the Gut - Diagnosis (2):

A
  • Abdominal xray is grally(-)
  • USG: Malposition of the superior mesenteric vessels
148
Q

Malrotation of the Gut - Treatment:

A

Requires urgent surgery

149
Q

Duodenal Atresia GENERAL FEATURES

A

 In 80% of cases, the obstruction is distal to the papilla of
Vater => bilious vomiting

 Incidence: 1:5000 - 10000

 M > F

 Associated with Down syndrome in 25% of cases

 Antenatal: Polyhydramnios

 X-ray: ‘double-bubble’

 Mx: referral for surgery

150
Q

Meconium ileus GENERAL FEATURES & Presentation:

A

Thick tenacious meconium in the bowel causes obstruction.

 15% of newborns with cystic fibrosis

 90% of patients with meconium ileus have cystic fibrosis.

Presentation:
 Acute early marked bowel distension within first 24hs w/ bilious vomiting. DRE: mucus plugs is still present.

151
Q

Meconium ileus - Complications (2):

A

 Volvulus
 Bowel perforation and/or meconium peritonitis

152
Q

Meconium ileus - Investigation

A

Xray
 distended loops of the intestine with thickened bowel walls
 meconium mixed with swallowed air produces a ‘ground-glass’ sign typical of meconium ileus
 Free air, very large air-fluid levels => bowel perforation.

153
Q

Meconium ileus - Management

A

Plan:
 uncomplicated meconium ileus: hypertonic enemas & IV fluids
 Immediate surgery for infants with complicated meconium ileus – perforations.

154
Q

Meconium plug syndrome GENERAL/Clinical FEATURES

A

Most common form of functional distal intestinal obstruction in the neonate (1:500-1:1000). Caused by meconium in the distal colon or rectum.

Clinical Features:
* Acute marked abdominal distension and failure to pass meconium in the first 24hs of life.

155
Q

Meconium plug syndrome - Investigation

A

 X-Ray: Generalised intestinal dilatation (LBO)

156
Q

Meconium plug syndrome - Management

A

 Enema or digital exam is usually curative.

157
Q

Hirschsprung’s Disease GENERAL FEATURES

A

 Causes 15-20 % of newborn intestinal obstructions - 1:4000
 Abnormal innervation of the colon => absence of ganglion cells in the Auerbach and Meissner Plexus
 Distal spastic zone (contracted) w/ Proximal dilated zone (normal)

158
Q

Hirschsprung’s Disease - Clinical Features

A
  • 80% in the first 6 weeks of life - male > female
  • Failure to pass meconium in the first 24 hours but w/ gradual onset of abdominal distension of days to weeks.
  • Persistent and progressive constipation.
  • Vomiting late

 On digital rectal examination we have explosive poo.
 The most serious complication is enterocolitis
 Enemas should be avoided during episodes of enterocolitis because of the possibility of perforating the
colon

159
Q

Hirschsprung’s Disease - Diagnosis

A

 Rectal suction biopsy – Gold standard

160
Q

Hirschsprung’s Disease - Management

A

 Laxatives (mild cases)
 Surgery

161
Q

Necrotising Enterocolitis (NEC) GENERAL FEATURES

A

Rapidly progressive disease in (premature) newborns or w/low APGAR score.

  • Causes extensive bowel necrosis, infection and perforation
  • 10 -12 days after birth
  • Associated with RDS

TIP: represents mesenteric
ischemia in adult

162
Q

Necrotising Enterocolitis (NEC) - Clinical Features (5)

A
  • Gastric retention
  • Bilious vomiting
  • Ileus
  • Abdominal distension
  • Bloody stools – red currant
163
Q

Necrotising Enterocolitis (NEC) - Diagnosis (2)

A
  • Abdominal X-Ray => Dilated bowel loops
  • Pneumatosis intestinalis
164
Q

Necrotising Enterocolitis (NEC) - Management (2)

A

 Gastric decompression & IV fluids
 Surgery for perforation, Clinical deterioration, metabolic acidosis (ischemia)

165
Q

Necrotising enterocolitis -
Investigations and diagnosis

A

Laboratory investigations:
 Baseline blood tests (FBC, CRP): CRP may be raised and there may be** thrombocytopenia and neutropenia.**

 Blood cultures: non-specific in NEC and are commonly reported as negative. However, if a bacterial, viral or fungal agent is isolated this
can be useful for guiding treatment.

 Blood gas: may show a raised lactate
or acidosis.

Imaging
Abdominal ultrasound: ultrasound is a safe first choice of imaging due to the lack of exposure to ionising radiation. Signs that are indicative of NEC include air in the portal system, ascites and perforation.

** Abdominal X-ray**: may show thickening of the bowel wall, dilated bowel loops filled with gas and distended bowel.
 If the bowel has perforated, Rigler’s sign may be visible. This occurs when both sides of the bowel wall are visible due to the presence of gas inside the lumen and within the peritoneal cavity.

166
Q

Pyloric Stenosis GENERAL FEATURES

A

 Symptoms presents at 2 - 6 weeks of age

Clinical features:
* Projectile vomiting
* Baby appears HUNGRY
* FTT
* Visible gastric peristalsis
* Pyloric mass (olive-shaped)

167
Q

Pyloric Stenosis - Diagnosis (3):

A

 First: Palpation during test feed
 USG
 FBE, electrolytes, ABGs.

168
Q

Pyloric Stenosis - Metabolic Complications:

A

 Loss of H2O and HCl
 Dehydration causes conservation of H2O and Na+ in exchange for H+ and K+

Result: Hypovolemia, metabolic alkalosis

169
Q

Pyloric Stenosis - Management:

A

 Shock: NS 20 ml/kg
 IV Fluid replacement: 0.45% NS + 5% Dextrose
 Potassium replacement once baby passes urine (KCl)
 Surgery: Refer for Pyloromyotomy
 Good prognosis

170
Q

Transoesophageal atresia GENERAL FEATURES

A

Vomiting from first feeding

As the narrowing is above the level of the biliary duct, the vomit would also appear the same color as the milk ingested.

171
Q

GORD GENERAL FEATURES

A
  • Peaks at 4 months
  • Self-limiting – usually resolves by 18 months

 Clinical features:
* Irritability
* Crying
* Milky vomitus
* Spontaneous effortless regurgitation of gastric contents

172
Q

Intussusception GENERAL FEATURES / AGE / Clinical Presentations:

A

 Invagination of the proximal segment of bowel into the distal bowel lumen.
 The commonest is segment of ileum
 colon through the ileocecal valve.

Most common age: 3m - 1yo.
HSP kid or teen w/ skin
Preutz-Jeger px – at any age

Clinical Presentation:
* Intermittent abdominal pain which is colicky, and severe. The child may draw up the legs.
* Episodic 2-3 times/hour, increasing over next 12-24 hours.
* Pallor and lethargy - Vomiting
* Diarrhoea- blood or mucus - classic red currant jelly stool is a late sign

173
Q

Intussusception - Management (Long Answer):

A

MX
 On PE: Abdominal mass - sausage shaped mass RUQ or crossing midline in epigastrium or behind umbilicus, palpable in about 60% of children and signs of an acute bowel obstruction will be present.
* Plain abdominal Xray is the 1st step in Dx:
* Target sign - 2 concentric circular radiolucent lines usually in the right upper quadrant or Crescent sign - a crescent shaped lucency usually in the left upper quadrant with a soft tissue mass
* Ultrasound scan next step in Dx – also preferred in HSP Abd pain.
* Barium or Air enema: best step - is both diagnostic and therapeutic, as long as there is a paeds surgical team available on site as there is a risk of perforation.

Mx plan:
 Gas or barium enema only in a setting where there is a pediatric
surgeon available in case of perforation.
 Hydrostatic reduction under USG.
 Surgery: If enema failed, peritonitis or septicemia

174
Q

Neonatal Lupus - Clinical Features (2):

A
  • BradIcardia (AV block) in newborn.
  • Mums with primary Sjogren or undifferentiated SLE
175
Q

Neonatal Lupus - Investigation:

A

AntiRo antibodies

176
Q

Ophthalmia Neonatorum (Neonatal conjunctivitis) - (2):

A
  1. Gonorrhoea
    - Most dangerous.
    - Complication: Corneal perforation.
    - Presentation: 1-5d after birth.
    - Tx: IV Cefotaxime for 7d.
  2. Chlamydia:
    - Most common
    - Presentation: 10- 14d after birth.
    - Tx: Erythromycin for 21d + eye toilet
177
Q

Blocked Naso-Lacrimal Duct - Clinical Features (4)

A
  • Mucopurulent discharge
  • Watery eye
  • Worse on waking
  • Conjunctiva not inflamed
178
Q

Blocked Naso-Lacrimal Duct - Treatment Acute (1):

A
  • Acute: Birth-neonates: Immediate
    referral
179
Q

Blocked Naso-Lacrimal Duct - Treatment Chronic 2-12mm (4):

A
  1. Massage the nasolacrimal sac
  2. Wash with salt water
  3. Warm compress
  4. Chloramphenicol drops until tears
    clear
180
Q

Umbilical Granuloma - Clinical features (4):

A
  • Umbilical mass in neonates
  • Swelling
  • Non-mucopurulent discharge
  • The cord is swollen and pink
181
Q

Umbilical Granuloma - Treatment (2):

A

1st: Salt
2nd: Silver Nitrate for 5 days

182
Q

Umbilical Discharge: Omphalomesenteric duct anomalies Differential diagnoses

A

CA

Urine discharge

Differential diagnoses:
Fistula
Urachal cyst
Umbilical calculus
Patent urachus

183
Q

Umbilical Discharge: Omphalomesenteric duct anomalies INVESTIGATIONS (2)

A
  • Creatinine and urea levels from discharge -> confirm it’s a urinary discharge
  • U/S: Rule out patent urachus
184
Q

Umbilical Discharge: Omphalomesenteric duct anomalies Management

A

Clean debris

Apply dressing (wound)

Swab for culture and sensitivity A/B

Refer for surgical correction

185
Q

Umbilical Discharge: Omphalomesenteric duct anomalies COMPLICATIONS (4)

A

Urinary Tract Infection (UTI) (especially in the case of full patency and bladder diverticulum)

Cyst infection

Abdominal pain

Haematuria

186
Q

Umbilical Discharge: Omphalitis CLINICAL FEATURES

A

Infection of the umbilicus and/or surrounding tissues.

Purulent (±bloody) discharge from the umbilical cord
Surrounding: induration, erythema, and tenderness.

Systemic signs such as fever, lethargy or poor feeding are suggestive of a more severe infection.

187
Q

Umbilical Discharge: Omphalitis Risk factors (5)

A

Unplanned home birth or septic delivery

Low birth weight

Prolonged rupture of membranes (PROM)

Umbilical catheterization

Chorioamnionitis

188
Q

Umbilical Discharge: Omphalitis MOST COMMON BACTERIA

A

Staphylococcus aureus (MCC)

Streptococci group A and group B

Gram-negative bacilli

189
Q

Umbilical Discharge: Omphalitis Management and ATB Treatment

A
  • Admission

*Septic workup

  • Cultures (including dry swab of the discharge)
  • IV antibiotics:
    <1 month: Refer to neonatal
    > 1 month: Flucloxacillin OR Gentamicin
190
Q

Umbilical Hernia Clinical Features

A

Soft swelling, varying in size, of the
umbilical area – usually easily reduced.

More prominent during coughing, crying, or straining and could
became larger in the first 6 months of life.

Presentation:
- Most cases are asymptomatic.
- Incarcerated or strangulated umbilical hernias are extremely rare.

191
Q

Umbilical Hernia Risk factors (5)

A
  • Prematurity
  • Low birth weight
  • African descent
  • Congenital Hypotiroidism
  • Certain syndromes: Patau (13), Edwards’ (18), and Down syndrome (21).
192
Q

Umbilical Hernia Treatment (Asymptomatic & Symptomatic)

A

Asymptomatic:
Observation until 4-5 years of age is preferred since the closure of the umbilical ring is complete in most children by the age of 5-6 years old.

Symptomatic: SURGERY
Incarceration (Firm, irreducible, tender, red, associated with vomiting)
or
Very large/persistently growing hernias

NOTE: Surgical correction in children < 4 years old has a higher complication

Spontaneous closure is less likely in cases of a hernia >1.5 cm, older age, underlying predisposing condition
(e.g. Ehlers Danlos syndrome).

193
Q

Balanitis (Infection of the foreskin) - Clinical features (3):

A
  • Swelling
  • White exudate
  • Redness
194
Q

Balanitis Treatment (3):

A
  1. Local penile toilet
  2. Mupirocin
  3. Penis shaft skin swollen to the pubis = IV atbs
195
Q

Phimosis Clinical Features:

A

Scarring of preputial opening. Tight ring or “rubber band” of foreskin around the tip of the penis, preventing full retraction.

196
Q

Phimosis Treatment (2):

A
  • Mild: Steroid topical cream
  • Severe: Circumcision
197
Q

Circumcision Indications (2):

A

Phimosis & balanitis

Absolute CI: Hypospadias

198
Q

Circumcision Treatment:

A

Dorsal penile nerve block

199
Q

Botulism Clinical features (6):

A
  • Dysarthria (MC symptom)
  • Descending paralysis
  • Low reflexes
  • Dry mouth
  • Blurry vision
  • Urinary retention
200
Q

Botulism Best Investigation:

A
  • Blood test for toxin
201
Q

Botulism Management (2):

A
  1. Antitoxin
  2. Notifiable disease
202
Q

Nephroblastoma (Wilms Tumour) Clinical features (3):

A
  • 2 to 5 years old
  • Does not cross the midline
  • Asymptomatic abdominal mass (maybe abdominal pain, HTA, and gross hematuria)
203
Q

Nephroblastoma (Wilms Tumour) Next Investigation

A

Ultrasound

204
Q

Nephroblastoma (Wilms Tumour) Best Investigation:

A

Best Investigation: CT/MRI to stage

205
Q

Nephroblastoma (Wilms Tumour) Treatment:

A

Nephrectomy + Chemo

206
Q

Neuroblastoma Clinical features (5):

A
  • < 2 years old
  • Crosses the midline
  • Painful abdominal mass (adrenal medulla)
  • Racoon eyes (retroorbital metastasis)
  • Associated with Horner syndrome (cervical ganglia)
207
Q

Neuroblastoma Next Investigation:

A

Bone Scan

208
Q

Neuroblastoma Best Investigation: CT/MRI

A

CT/MRI

209
Q

Neuroblastoma Treatment:

A

Qx + chemo and radio

210
Q

Hepatoblastoma Clinical features (3):

A
  • < 5years old
  • Abdominal mass with intermittent abdominal pain
  • Hx of Familial adenomatous polyposis (FAP)
211
Q

Hepatoblastoma Best Investigation:

A

CT/MRI

212
Q

Hepatoblastoma Treatment:

A

Chemo

213
Q

Hereditary Angioedema

A

Autosomal dominant

Clinical features:
1. Edema in:
- Respiratory tract (cough)
- Eyelids (swelling)
- Intestines (abd pain)

  1. The attacks last 2 to 5 days, usually slowly increasing. Are preceded by prodromal symptoms, including a rash (erythema marginatum)
  2. Triggers: Trauma, infections, stress or procedures, ACE inhibitors, and estrogens.
214
Q

Hereditary Angioedema First Investigation:

A

Complement test (Low C3 & C4)

215
Q

Hereditary Angioedema Best Investigation:

A

C1-inhibitor protein (low) and function

216
Q

Mongolian spots (Dermal Melanocytosis) Clinical features

A

Bluish grey lesion in buttocks,
lower back, extensor surfaces of extremities.

Common in black, Asian, and Latin kids.

Disappears by 1- 2 years old

217
Q

Strawberry Tongue Causes (4)

A
  1. Kawasaki Disease
  2. Scarlet fever
  3. Allergies
  4. Toxic shock syndrome (associated with tampons, diaphragms, skin inf, pneumonia, osteomyelitis)
218
Q

Strawberry Tongue Investigation

A

Toxic shock syndrome: S. Aureus TSS1-toxin

219
Q

Cystic fibrosis Clinical features

A

Autosomal Recessive

Defects in the ion protein channel
CFTR.

Viscoid secretions in the lungs, pancreas, and gut.

Clinical features:
- Meconium Ileus
- Prolonged neonatal jaundice
- Failure to thrive and poor weight gain
- Chronic lung diseases
- Bronchiectasis
- Fat globules on feces examination (Diff from fatty crystals in celiac and CMPA)
- Vas deferens atrophy
- Increase sweat

CI: Hyponatremic, hypochloremic, metabolic alkalosis

220
Q

Cystic fibrosis Investigations

A
  1. Newborns: Heel Prick
    test.
  2. If (-) but parental
    concern: Do test for gene
    mutations:

1 mutation: Sweat chloride
test. If (+) CF clinic, if (-) healthy carrier

≥2 mutations: CF clinic

221
Q

Cystic fibrosis Treatment (2)

A
  1. Fix nutritional deficiencies: High-calorie and high-fat diets with supplemental fat-soluble vitamins to compensate for malabsorption and maintain a healthy weight.
  2. Minimize chest infections.
222
Q

WEEZES CAUSES

A
223
Q

BRONCHIOLITIS Deshidratation treatment

A
224
Q

BRONCHIOLITIS : Referral and transfer indications

A

Bronchiolitis peaks between the age of 3-6 months

225
Q

Asthma DIAGNOSE

A

ALSO:
Otherwise, unexplained low FEV1 or PEF (historical or serial readings)

Otherwise, unexplained peripheral blood eosinophilia

226
Q

TYPES OF ASTHMA

A
227
Q

Caries in kids Clinical Features

A

Adult teeth replace baby teeth between 6-12yo

228
Q

Caries in kids Management

A
  • Babies and toddlers: brush teeth 2x/day
  • 18m-6y: brush with LOW fluoride toothpaste
229
Q

Enuresis Clinical Features:

A
  • Daytime control: 4yo
  • Nighttime control: ≥7yo
  • Primary: Never was dried
  • Sec: Dried for 6m and wet again

MCC: Bladder infection

230
Q

Enuresis Management (3):

A
  1. Urotherapy: Increasing daytime fluid intake (50 ml/kg/day). Regular voiding every 2–3 hours.
  2. Bedwetting Alarm: Start from 7yo.
    Do for 6-8w, overlearn for 2w more.
  3. Desmopressin: If the kid is going to school camp, prefer oral or sublingual. Is not recommended because of the high risk of HypoNa.
231
Q

Male puberty

A

Pubertal Changes Secuence:

  1. Enlargement of testes & scrotum (>2.5cm or >4ml)
  2. Pubic hair (6 m)
  3. Lengthening of penis (12 - 18 m)
  4. Axillary hair > medial thigh hair and Growth spurt. Deepening of the voice (2 y after initial signs of puberty)

TANNER STAGES

Stage 1: kid (< 9 yo)

Stage 2: scrotal and testicular growth (9 -11 yo)

Stage 3: gynaecomastia and voice break (11 - 13 yo)

Stage 4: Axillary hair and acne (13 - 15 yo)

Stage 5: Adult (> 15 yo)

Delayed: >14 yo (testis and axillary hair) Ix: Bone age

Preconscious: 9.5 yo
1st Ix: FSH and LH
2nd Ix: MRI of brain

Management: Refer to the endocrinologist

232
Q

Females Puberty

A

Pubertal Changes Secuence:

  1. Boobs
  2. Grow
  3. Pubes
  4. Flow

TANNER STAGES

Stage 1 Telarche: 2 y till menarche

Stage 2 Adrenarche: Axillary and pubic hair, body odor (9 -11 yo)

Stage 3: Menarche (11 - 13 yo)

Stage 4: Pubic hair (13 - 15 yo)

Stage 5: Adult (> 15 yo)

Delayed: > 13 -14 yo (Bubs, axillary and pubic hair)
1st Ix: Bone age

Preconscious: < 8 yo
1st Ix: FSH and LH
2nd MRI of brain

Management:
1. If only isolated growth public hair
< 8yo: Follow up in 6 months

  1. Refer to the endocrinologist
233
Q

Short stature Clinical Features

A
  • Males <1.62 Females <1.52
  • If constitutional delay BA<CA (Bone Age less than chronological age)
234
Q

Short stature Investigations

A
  1. Bone age x-ray (left hand wrist)
  2. TFT, LFT, IGF-1
235
Q

Short stature Management

A

GH Tx only if height<1st centile for age, or Growth velocity <25th centile

236
Q

Sexual abuse Clinical Features

A
  • Clinical features: guilt, anger, sexual behavior with other kids, unexplained physical symptoms, sleep disturbance, poor school performance.
  • Org dx: Chlamydis, syphilis, gonorrhea, and HIV.
237
Q

Sexual abuse Investigations

A
  • Prepubertal: Visual examination
  • Postpubertal: Speculum
238
Q

Sexual abuse Management

A

Refer to CPS

239
Q

Tourette Sx - Clinical features (6)

A
  • Blinking
  • Eye twitch
  • Facial grimacing
  • Shoulder shrugging with sniffing
  • Coprolalia
  • Echolalia
240
Q

Tourette Sx - Management (2)

A
  1. Behavioural therapy
  2. Risperidone
241
Q

Prodrome Schizophrenia Clinical features:

A

Difficulty concentrating, social withdrawal, decline in school performance, becoming superstitious

242
Q

Breath Holding Spell Clinical features:

A

1-3yo
Frustration->breath hold-> cyanosis ->LOC

DD: In seizures it’s LOC->Cyanosis

243
Q

Breath Holding Spell Management:

A

Behavioural therapy

244
Q

Attention Deficit Hyperactivity Disorder (ADHD) Clinical Features: (4)

A
  • Child 4 - 7yo (NO <2yo)
  • Most common in boys
  • Social, academic, and occupational impairment
  • Slurred speech
245
Q

Attention Deficit Hyperactivity Disorder (ADHD) - Assessment (3)

A
  • School reports
  • Psychoeducational Assessment
  • Audiology - vision Assessment
246
Q

Attention Deficit Hyperactivity Disorder (ADHD) - Management (2)

A
  1. Behavioral modification
  2. Methylphenidate (MOA: inhibition of Dopamine and NE reuptake). If bad compliance use the slow release
247
Q

Autism Clinical Features (3):

A
  • Low inteligence
  • Bad social interaction and communication
  • Repetitive stereotype behaviors - - - Enjoys being alone
248
Q

Autism Management:

A

Risperidone (if aggressive)

249
Q

Asperger’s syndrome Clinical Features (3)

A
  • Normal to superior intelligence
  • Impaired social and communication skills
  • Seek friendships
250
Q

Asperger’s syndrome Management:

A

Behavioral therapy

251
Q

Oppositional Defiant Disorder Clinical Features:

A
  • Since > 6 m
    -Defiant, negative, and disobedient.
  • Hostile behavior toward authority figures that are present
  • Interfere with academic, social, and occupational functioning
  • No violent or aggressive behaviour
252
Q

Oppositional Defiant Disorder Management:

A

Best: Family therapy

253
Q

Conduct Disorder Clinical Features:

A

<18yo
Violation of rules, theft, destruction of property, aggression cruelty toward people and animals

254
Q

Night terrors Clinical Features:

A

Child 5-7yo.
Wakes up, cannot be consoled by parents, cannot remember anything the day after

255
Q

Night terrors Management

A

Family reassurance

256
Q

Obstructive sleep apnea (OSA) Clinical Features (4):

A
  • Daytime sleepiness
  • Disturbed sleep
  • HTN
  • Narcolepsy
257
Q

Obstructive sleep apnea (OSA) Best Investigation:

A

Polysomnography

258
Q

Obstructive sleep apnea (OSA) Management (4):

A
  1. Adenotonsillectomy
  2. Weight loss
  3. IN steroids for rhinitis
  4. CPAP
259
Q

Slipped Capital Femoral Epiphysis (SCFE) Clinical Features (5):

A
  • Obese pre or adolescent
  • Atraumatic hip, thigh, or knee (medial obturator nerve) pain
  • Limping
  • Inability to bear weight
  • Limited internal rotation (Drehmann sign)
260
Q

Slipped Capital Femoral Epiphysis (SCFE) Risk Factors (4):

A
  • Obesity
  • Male sex
  • Periods of rapid growth
  • Prior radiation therapy
261
Q

Slipped Capital Femoral Epiphysis (SCFE) Investigation:

A

Hip XR AP and frog-leg lateral views

262
Q

Slipped Capital Femoral Epiphysis (SCFE) Management:

A

Surgical: Open Reduction and Internal Fixation

263
Q

Slipped Capital Femoral Epiphysis (SCFE) Complication:

A

Femoral head osteonecrosis

264
Q

Developmental dysplasia of the hip (DDH) Clinical Features (5):

A
  • Barlow maneuver: Gentle ABDUCT and “Hip clicks”
  • Ortolani maneuver: ADDUCT the hip DD: In dislocated hip: jerk or clunk
  • Trendelenburg gait
  • Toe walking
  • Leg length discrepancies
265
Q

Developmental dysplasia of the hip (DDH) Risk Factors (7):

A
  • Breech position (most significant)
  • Female sex
  • Family history
  • Oligohydramnios
  • Multiple pregnancy (twins)
  • Delivery by C-Section
  • Large for gestational age (LGA)
266
Q

Developmental dysplasia of the hip (DDH) Screening:

A

US 3–4 months

267
Q

Developmental dysplasia of the hip (DDH) Investigation:

A

X-ray: AP of the pelvis

268
Q

Developmental dysplasia of the hip (DDH) Management:

A

< 18 m: Hip spica cast (close reduction) Complication: Avascular necrosis of the femoral head.
> 18 m: Surgery, Open reduction.

269
Q

Perthes Disease - Definition & Clinical Features

A

Idiopathic avascular necrosis of the capital femoral epiphysis of the femoral head

  • Male (MC) between 4 - 9 yo
  • Limping
  • Pain localized to the hip or referred to the knee or thigh
  • Limited abduction and internal rotation
  • Asoc w/ coagulopathies (Haemophilia)
270
Q

Perthes Disease - Investigation

A

US: Widening of joint space (epiphyseal cartilage hypertrophy)
X-ray: AP of the pelvis ????

271
Q

Perthes Disease - Management

A

Immobilize and refer immediately

272
Q

Transient Synovitis Clinical Features:

A
  • Age: 3 - 8 yo (MC 6 yo)
  • Male sex
  • Fever (30%)
  • Unilateral hip pain and limping.
  • Refusal to bear weight.
  • Presentation with the hip flexed, abducted, and externally rotated.
  • PE: Limited abduction and internal rotation, Patrick test (Pain on the ipsilateral anterior side)
  • Preceding: URTI, trauma, or bacterial infection (post-streptococcal toxic synovitis)
273
Q

Transient Synovitis First Investigation:

A

Rule out Septic Arthritis
1. WBC, CRP, ESR
2. Hip X-ray

274
Q

Transient Synovitis Best Investigation:

A

US w/ join aspiration:
Diagnostic and therapeutic. Intracapsular effusion.
SA:
- Positive gram stain
- PMN > 90%
- glucose < 40 mg/dL

275
Q

Transient Synovitis Management:

A

supportive care and rest from activity.
NSAIDs can be used forpaincontrol.
Complete resolution of symptoms often takes up to 1to2weeks (sometimes within 48 hours) <3

276
Q

Foot Deformity

A

NORMAL:
- 0-1y: Metatarsus varus
- 1-3y: Internal tibial torsion
- 5-6yr: Medial femoral torsion

277
Q

List 3 Acyanotic + 3 Cyanotic Congenital Heart Diseases

A

Acyanotic {Left to the right}
1. VSD - Ventricular Septal Defect*
2. ASD - Atrial Septal Defect
3. PDA - Patent Ductus Arteriosus

Cyanotic {Right to the left}
1. TOF - Tetralogy of Fallot
2. HLHD - Hypoplastic Left Heart Dx
3. TGV - Transposition of the great vessels

278
Q

Congenital Heart Disease: VSD - Details & Clinical Features: Hint: different sizes may have varying clinical features

A

Most common congenital heart disease.
Asoc w/ Turner Sx
Presentation age: Infant 5 to 6 weeks

Clinical Features:
2-3/6 harsh holosystolic murmur heard along the LSB more prominent with small VSD and absent with very Large VSD

SMALL - Moderate: 3-6mm
- Asymptomatic
- 50% will close spontaneously at 2y

Mod - LARGE
- Symptomatic & require Sx repair
- SOB with feeding & crying
- Recurrent chest infections
- Heart failure from 3 months of age
- FTT

279
Q

Congenital Heart Disease: VSD - Management & Indications for Surgical Closure:

A
  • Small VSD: No physical restrictions, reassurance, periodic follow-up & endocarditis prophylaxis.
  • Symptomatic VSD: Medical treatment initially with afterload reducers & diuretics.
  • Indications for Surgical Closure:
     Large VSD w/ medically uncontrolled symptomatology &
    continued FTT.
     Ages 6-12 mo w/ large VSD & Pulmonary HT
280
Q

Congenital Heart Disease: ASD - Details & Clinical Features:

A

Secundum ASD – Fossa Ovalis, most common
Primum ASD – lower in position, more serious

Clinical Features:
- Initial: NO MURMUR
- PS: Systolic ejection murmur - LSB
- RV heave.
- Fixed widely split S2 (Ao then Pulm Valve closes)
- Asymptomatic or easy fatigability or mild growth failure.

High risk of developing right heart failure with pulmonary HT

281
Q

Congenital Heart Disease: ASD - Management:

A
  • Surgical or device closure for Secundum ASD
  • Closure performed between ages 2 & 5 years
  • Sx correction is done earlier in children w/ CHF or significant
    pulmonary HTN.

 NOT Endocarditis prophylaxis

282
Q

Congenital Heart Disease: PDA - Details & Clinical Features:

A
  • Persistence of the Ductus Arteriosus (PA to the Aorta)
  • Normally closes in the 1st wk of life.
  • Associated with Turner Sx
  • Associated with Ao coarctation, VSD, and TORCH inf Rubella!!)

Clinical Features:
- Continuous machinery systolic murmur: Gibson Murmur
- Small PDA: Asymptomatic
- Large PDA: CHF, growth restriction, and FTT.

283
Q

Congenital Heart Disease: PDA - Management:

A
  1. Indomethacin
  2. Surgical: Ligation or catheter closure by insertion of a device or embolization coils.
284
Q

Congenital Heart Disease: TOF - Details & Clinical Features:

A

Most common cyanotic CHD

  1. Pulmonary stenosis (1st worse)
  2. VSD (2nd worse)
  3. Overriding Ao
  4. Right ventricular hypertrophy

Clinical Features:
- Cyanosis after the neonatal period (4m approx) and progressive
- Clubbing fingers(Scharmoth’s sing)
- Hypoxemic spells (“Tet spells”)
- Systolic ejection murmur - LSB (PS)

285
Q

Congenital Heart Disease: TOF - Management:

A

Corrective Sx at about 6 months

286
Q

Congenital Heart Disease: HLHD (3)

A
  • LV and aorta are abnormally small (hypoplastic).
  • Early days (2-7d) of life & need urgent Sx to survive.
  • HLH is dependent on PDA for survival
287
Q

Congenital Heart Disease: TGV

A

The aorta arises from the RV & receives “blue” blood, whilst the Pulmonary Artery arises from the LV.

Immediately after birth, and needs urgent treatment.

Survival depends on the PDA or the FO remaining open in the early days of life until treatment.

288
Q

TGV Management

A
  1. The FO can be enlarged with a catheter procedure, called Balloon
  2. Septostomy
289
Q

TGV 1st Investigation & Diagnosis

A

Hyperoxia Test:

ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise

290
Q

Hyperoxia Test: Differences between Acyanotic CHD & TGV

A

TGV: ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise

◦ Pulmonary disease (not cyanotic CHD) is suspected if the PaO2 increases to more than 150 mm Hg with oxygen.

291
Q

Cerebral Palsy

A

Clinical features: Persistent and non-progressive.

  1. Delayed motor milestones
  2. Unexplained irritability
  3. Muscle tone abnormalities:
    - Stiffness (most common) or Floppy
    - Preference for one side of the body

Differentiate from spinal muscular atrophy (SMA): Intelligence is
unaffected

292
Q

Pain in Kids Treatment Protocol

A
  1. Paracetamol
  2. NSAIDs
  3. Oxycodone
  4. IN Fentanyl

CI: Codeine<18yo because can cause respiratory depression

293
Q

Aspirin in Children Indications (3)

A

o Kawasaki
o Rheumatic fever
o Juvenile rheumatic arthritis

(otherwise, always Paracetamol)

294
Q

Infective Diseases School Exclusion

A
295
Q

Down syndrome CLINICAL FEATURES

A

typical facies + hypotonia + single palmar crease

Down syndrome (trisomy 21) is based on typical facial features (flat facies, slanting eyes, prominent epicanthic folds, small ears), hypotonia, intellectual disability, and a single palmar crease.

296
Q

Down Syndrome: Associated disorders (8)

A
  • Seizures (usually later onset)
  • Impaired hearing
  • Leukaemia
  • Hypothyroidism
  • Congenital anomalies (e.g. heart, duodenal atresia, Hirschsprung, TOF) Alzheimer-like dementia (fourth–fifth decade)
  • Atlantoaxial instability
  • Coeliac disease
  • Diabetes
297
Q

CHARGE syndrome CLINICAL FEATURES

A

chromosome 8

Coloboma
Heart abnormalities
Choanal atresia
Development retardation
GU anomalies
Ear abnormalities

298
Q

Edward syndrome CLINICAL FEATURES (4)

A

Trisomy 18

  • Microcephaly
  • Facial abnormalities, e.g. cleft lip/palate
  • Malformations of major organs, e.g. heart
  • Malformations of hands and feet—clenched hand posture neural tube defect

Prognosis is poor—about one-third die in first month, <10% live beyond 12 months.

Prenatal diagnosis is available.

299
Q

Patau syndrome Clinical features (5)

A

Trisomy 13

  • Microcephaly
  • Brain and heart malformation
  • Cleft lip/palate
  • Polydactyly
  • Neural tube defect

Prognosis is poor—50% die within first month.

300
Q

Fragile X syndrome (FXS) CLINICAL FEATURES

A

characteristic facies + intellectual disability + large testes

Large prominent ears
Long narrow face
Macro-orchidism
Intellectual disability.

Most common inherited cause known of developmental disability

M:F ratio 2:1
Females may appear normal but may be affected
Variable spectrum of characteristic features, making detection difficult

301
Q

Fragile X syndrome (FXS): Associated disorders (9)

A

X chromosome

Intellectual disability (IQ <70)

Autism or autistic-like behaviour

Attention deficit in 10% (with or without hyperactivity)

Seizures (20%)

Connective tissue abnormalities

Learning disability and speech delay

Coordination difficulty

Primary ovarian insufficiency

Late-onset tremor/ataxia syndrome

Big testis

Long Face

Strabismus

Flat feet

Hypotonia

302
Q

Prader–Willi syndrome Clinical features

A

neonatal hypotonia + failure to thrive + obesity (later)

chromosome 15

Hypotonic infants with weak suction and failure to thrive, then voracious appetite causing morbid obesity

Usually manifests at 3 years

Intellectual disability

Narrow forehead and turned-down mouth

Small hands and feet

Hypogonadism

303
Q

Williams syndrome Clinical Features

A

‘elfin’ face + intellectual disability + aortic stenosis

chromosome 7

Elfin facial appearance

Mild pre- and postnatal growth retardation

Mild microcephaly

Mild-to-moderate developmental delay.

In the first 2 years of life, feeding problems, vomiting, irritability, hyperacusis, constipation and failure to thrive may lead to presentation, but children are rarely diagnosed at this stage.

304
Q

Marfan syndrome Clinical Features (8)

A

tall stature + dislocated lens and myopia + aortic root dilatation

  • Disproportionally tall and thin
  • Long digits—arachnodactyly
  • Kyphoscoliosis
  • Joint laxity (e.g. genu recurvatum)
  • Myopia and ectopic ocular lens
  • High arched palate
  • Aortic dilatation and dissection
  • Mitral valve prolapse

If untreated, death in the 30s and 40s is common

Chromosome 15 Autosomal dominant

305
Q

Noonan syndrome: Clinical features

A

facies + short stature + pulmonary stenosis

chromosome 11

  • Characteristic facies—down-slanting palpebral fissures, widespread eyes, low-set ears ± ptosis
  • Short stature
  • Pulmonary valve stenosis
  • Webbed neck
  • Failure to thrive, usually mild
  • Abnormalities of cardiac conduction and rhythm ± Intellectual disability
306
Q

Angelman syndrome Clinical features (8)

A

Abnormal chromosome 15

  • Hand flapping
  • ‘Puppet’-like ataxia
  • Frequent laughter/smiling
  • Microcephaly by age 2 years
  • Developmental delay
  • Speech impairment
  • Seizures
  • Cannot live independently

Treatment with minocycline is promising.

307
Q

Klinefelter syndrome Clinical Features (10)

A

47, XXY genotype

lanky men + small testes + infertility

Approximately 2 out of 3 are never recognised

  • Marked variation but usually:
  • tall men with long limbs
  • small firm testes ≤2 cm (10 mL)
  • infertility (azoospermia)
  • sparse facial hair
  • reduced libido
  • learning difficulties, especially reading
  • intellectual ability may range from normal to disability
  • gynaecomastia
  • increased risk of DVT, breast cancer and diabetes (screening indicated)
308
Q

Klinefelter syndrome Diagnosis

A

Increased gonadotrophin

Low to normal testosterone

309
Q

Klinefelter syndrome Treatment

A

Transdermal testosterone

310
Q

Turner syndrome (gonadal dysgenesis)

A

short stature + webbed neck + facies

  • Short stature—average adult height 143 cm
  • Primary amenorrhoea in XO patient; infertility
  • Webbing of neck
  • Typical facies: micrognathia, low hairline
  • Lymphoedema of extremities
  • Cardiac defects (e.g. coarctation of aorta)

Mental deficiency is rare.

99% of conceptions are miscarried

311
Q

Turner syndrome (gonadal dysgenesis) Treatment

A

Hormone-based (e.g. growth hormone, hormone replacement therapy)

312
Q

Turner syndrome (gonadal dysgenesis) Genetic profile

A

45 chromosomes of XO karyotype (typical Turner karyotype in 50% of cases)

Many are mosaics (45X/46XX)

313
Q

Alagille Syndrome CLINICAL FEATURES

A
314
Q

DiGeorge Syndrome CLINICAL FEATURES

A
315
Q

Lesch-Nyhan Syndrome CLINICAL FEATURES (6)

A

Deficiency of the activity of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT)

X-linked recessive

Most often affects males

  • Uric acid levels are abnormally high
  • Impaired kidney function
  • Acute gouty arthritis
  • Self-mutilating behaviors such as lip and finger biting and/or head banging.
  • Involuntary muscle movements
  • Neurological impairment
316
Q

Peutz-Jeghers Syndrome GENERAL FEATURES

A

Autosomal dominant Chromosome 19
Intestinal polyposis syndrome

317
Q

Peutz-Jeghers Syndrome Clinical Features:

A

Hamartomatous polyps in the gastrointestinal tract

Hyperpigmented macules on the lips and oral mucosa (melanosis) - appear before 5 years of age

318
Q

Peutz-Jeghers Syndrome Complications:

A

Intrussusception
Substantial risk of cancer, especially of the breast and gastrointestinal tracts. Colorectal is the most common malignancy.

DD: Addison’s disease

319
Q

Peutz-Jeghers Syndrome First Investigations:

A

Barium enema radiograph showing multiple polyps (mostly pedunculated) and at least one large mass at the hepatic flexure coated with contrast in a patient with Peutz–Jeghers syndrome
Some suggestions for surveillance for cancer include the following…

320
Q

Peutz-Jeghers Syndrome Best Investigations:

A

Colonoscopy + Biopsy

321
Q

Peutz-Jeghers Syndrome Monitoring:

A

Small intestine with small bowel radiography every two years

Esophagogastroduodenoscopy and colonoscopy every two years

CT scan or MRI of the pancreas yearly

Ultrasound of the pelvis and testes yearly

Mammography from age 25 annually

Papanicolaou smear (Pap smear) annually beginning at age 18–20

AMC MCQ (55 decks)

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