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AMC MCQ - You Can Do It!!!!!❤️❤️ > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Rinne test

A

AC>BC = Normal/SNHL
BC>AC= CHL

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2
Q

Tanner stages

A

I:
- 0–15 years
- None
II:
- Commencement of puberty
-8–15
- Pubic hair first, along with breast budding
- Scrotal/Testicular growth, penis growth after a year
III:
- Increase in hair and pigmentation

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3
Q

Development of pubic hair

A

Boys: 9 years
Girls: 8 years

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4
Q

List of autosomal dominant diseases

A

D -dystrophy myotonia
O - osteogenisis imperfecta
M - Marfan’s
I - intermittent porphyria
N - Noonan’s
A - achondroplasia, familial adenomatous polyposis (FAP)
N - neurofibromatosis
T - Tuberous sclerosis

V- Von Willebrand
H - Huntington’s HNPCC
H - hereditary spherocytosis
H- familial hypocholesteraemia
R - retinoblastoma

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5
Q

List of autosomal recessive diseases

A

A - albinism
B - thalassaemia
C - cystic fibrosis
D - deafness
E - emphysema
F - Friederich’s ataxia (trinucleotide test, repeat GAA)
G - Gaucher’s disease
H Hemochromatosis, homocystinuria

S - sickle cell
P - phenylketonuria
N - Wilson’s
X - xeroderma pigmentosa

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6
Q

List of X-linked recessive diseases

A

D- diabetes insipidus
D - Duchenne’s
C - colour blindness
C - chronic granulomatous disease (membranous type)
F - Fabry’s disease (alpha- glucosidase deficiency)
F - fragile X syndrome (Martin Bell Syndrome)
2 blood - haemophilia. G6PD
2 syndrome Lesch Nylon syndrome, Wiskots Aldrich yndrome

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7
Q

SIADH in children

A
  • hyponatremia
  • excessive amount of ADH from hypothalamus-pituitary
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8
Q

SIADH in children symptoms

A
  • nausea and vomiting
  • headache
  • problems with balance
  • mental changes (confusion, memory problems)
  • seizures or worst case, coma
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9
Q

SIADH in children causes

A
  • type 2 DM medication:
  • antiepileptic
  • antidepressant
  • surgery under general anaesthesia
  • brain disorders, injury, infections, stroke
  • lung disease (pneumonia, tuberculosis, cancer, chronic infections)
  • cancer of lung, small intestine, brain, leukaemia
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10
Q

Addison’s disease in children

A
  • hyponatraemia with hyperkalaemia
  • 21-hydroxylase deficiency
  • Dehydration, hypotension, and shock
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11
Q

Lymphoblastic leukaemia in children

A
  • Live-attenuated vaccines contraindicated (MMRV, rotavirus, yellow fever)
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12
Q

Hyponatremia in children

A

Dehydration: hypernatremia
Cardiac: Pseudohyponatremia
Addisons:
- Low aldosterone
- Hyperkalaemia
- hypotension

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13
Q

Hyponatraemic seizures in children

A
  • increasing irritability
  • increasing lethargy, - increasing tonic-clonic generalised
    seizures
  • respond poorly to conventional anticonvulsants (phenytoin, phenobarbitone)
  • address hyponatraemia by 3% NaCl solution
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14
Q

Hypernatremia in children

A
  • “doughy” skin
  • Isotonic (normal) saline for an initial bolus
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15
Q

Most common long-term complication of streptococcus pneumonia meningitis in children

A

Deafness 11%

Intellectual disability (mental retardation)-4%.
-Spasticity and/or paresis-4 %.
-Seizure disorder-4 %

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16
Q

Weber’s test

A

Normal = lateralizes equally to both ears

CHL= lateralizes to abnormal ear

SNHL= lateralizes to the normal ear

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17
Q

Acute Otitis media risk factors

A
  • Age (6-18 months)
  • Lack of breastfeeding
  • Day care attendance
  • Smoke exposure
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18
Q

Pathogens that give arise to acute otitis media

A
  • Streptococcus pneumoniae (most common)
  • Nontypeable (?) Haemophilus influenzae
  • Moraxella catarrhali

The primary pathogens responsible for acute otitis media (AOM) include:

  1. Streptococcus pneumoniae: This is the most common bacterial cause of AOM.
  2. Haemophilus influenzae (non-typeable): Another frequent bacterial pathogen.
  3. Moraxella catarrhalis: Less common but still a significant cause.
  4. Group A Streptococcus: Can also cause AOM, though less frequently than the above pathogens.

These bacteria often follow viral upper respiratory tract infections, which can set the stage for secondary bacterial infections in the middle ear oai_citation:1,Otitis Media: Rapid Evidence Review | AAFP oai_citation:2,Clinical Practice Guidelines : Acute otitis media.

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19
Q

Complications of Otitis media

A

Acute mastoiditis

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20
Q

Acute mastoiditis pathogen

A

Streptococcus pneumoniae

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21
Q

Acute mastoiditis initial treatment

A

sample from the ear discharge should be taken for culture DONE BY ENT

flucloxacillin + a third-generation cephalosporin

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22
Q

Acute otitis media treatment

A
  • Amoxicillin 1st choice (used for 1 week)
  • 2nd line: amoxicillin-clavulanate
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23
Q

Acute otitis media treatment px that’s allergic to penicillin

A
  • clindamycin
  • azithromycin
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24
Q

Chronic suppurative otitis media treatment

A

Assess if tympanic membrane intact or perforated:
If intact: ciprofloxacin ear drops to treat on going infection
If perforated: initial treatment ear toilet with povidone-iodine solution, followed by
dry mopping with rolled toilet papers2 to 3 times a day using 20ml syringe with plastic tubing. In addition, ciprofloxacin ear drops

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25
Q

Untreated a tympanic membrane perforation secondary to chronic otitis media

A
  • Marginal perforation with discharge
  • Perforation that is surrounded by granulation tissue
  • Continuously discharging central perforation
  • Perforation associated with a cholesteatoma
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26
Q

Cholesteatoma risk factors

A
  • history of recurrent acute otitis media
  • chronic middle ear effusion
  • tympanostomy tube placement
  • history of cleft palate
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27
Q

Bilateral sensorineural deafness in children

A

Congenital sensorineural deafness.

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28
Q

Lymph nodes red flags

A

Weight loss
Sustained fever
Night sweats Generalized lymphadenopathy
Signs and symptoms of pancytopenia
Mass persisting> 6 weeks
Lymph node> 3 cm
Thyroid mass
Supraclavicular mass
Hard, irregular mass
Fixed mass

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29
Q

1 standard deviation above/below the 50th percentile

A

Weight: overweight/underweight

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30
Q

2 standard deviation above/below the 50th percentile

A

Weight: obese/severely underweight

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31
Q

Marfan’s syndrome (MFS) features

A
  • autosomal dominant connective tissue
    disorder (FBN1)
  • affects height
  • does not affect weight
  • aortic aneurysm
    dissection, aortic regurgitation (Decrescendo high-pitched diastolic murmur at the left sternal edge)
  • Myopia and ectopic ocular lens.
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32
Q

Marfan’s syndrome (MFS) investigation

A

echocardiogram

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33
Q

Most common neurological cancers in children

A
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34
Q

Most common neurological symptoms in children with cancer

A
  • Nausea
  • Vomiting
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35
Q

Lymphadenopathy in children

A

viral upper respiratory tract infection

TB, Infectious
mononucleosis cytomegalovirus infection
Cat scratch disease
haematological and nonhematological malignancies, Kawasaki
disease.

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36
Q

Kawasaki disease features

A
  • acute onset of fever more than 39C
    -inadequate response to paracetamol
  • sole, palm and tongue erythema
  • desquamation of fingertips (vasculitis)
  • tender mass in the right hypochondrium
  • elevated CRP and ESR
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37
Q

Kawasaki disease in children complications

A
  • vasculitis leading to coronary artery aneurysm 17-31% (second week and second month
    of illness)
    -
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38
Q

Kawasaki disease in children management

A
  • aspirin and immunoglobulins
    -Steroids must be avoided
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39
Q

< 6 months + > 7 days fever + systemic
inflammation but no other explanation for febrile illness

A

Atypical Kawasaki

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40
Q

Growing pains

A

Growing pains refers to pain in the lower
extremities of growing active children.

children between 2 and 12 years with the peak
incidence in preschool children.

mostly felt in the thighs, calves and
behind the knee.

intermittent and in mostly present in the afternoon and evening after activity during the day.

Pain may also wake up the child at night.

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41
Q

male adolescent athlete + pain below the knee + tenderness

A

Osgood-Schlatter disorder

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42
Q

Osgood-Schlatter disorder management

A

Gentle quadriceps stretching exercises
- self limiting up to 12 months

NOTE: Corticosteroids are absolutely contraindicated

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43
Q

Perthes

A
  • avascular necrosis of the femoral head.
    4 -8 years of age
    associated with hip pain and intermitent limp.
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44
Q

Perthes features

A
  • Normal Caucasian boy
  • 4 and 10 years, peak incidence at 5 to 7 years
  • 15% bilateral
  • widening of joint hip space
    Hip pain result of necrosis of the involved bone
    -pain may be referred to the medial aspect of the ipsilateral knee or to the lateral thigh.
  • The quadriceps muscles and adjacent thigh soft tissues may atrophy, and the hip may develop adduction flexion contracture
  • antalgic gait with limited hip motion, or a Trendelenburg gate (abductor lurch).
  • Pain may be present with passive range of motion and
    limited hip movement, especially internal rotation and abduction
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45
Q

Perthes disease management

A
  • refer to surgeon

Surgeon will make call on conservative or surgical
- conservative: brace
- surgical: osteotomy/femoral head fixation, hip replacement worst case

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46
Q

slipped capital femoral
epiphysis (SCFE)

A
  • Overweight adolescent of 10 to15 years
  • bilateral in 20%
  • Limp and irritability of hip on movement
  • Knee pain — referred from the affected hip
  • On flexion of the hip, it rotates externally. Hip
    is often in external rotation on walking.
  • Most movements restricted, especially
    internal rotation.
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47
Q

slipped capital femoral epiphysis (SCFE) management

A
  • Cease weight-bearing and refer urgently.
  • lf acute slip, gentle reduction via traction is
    better than manipulation for prevention of
    later avascular necrosis.
  • Once reduced, perform pinning
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48
Q

Developmental dysplasia (DDH) of the hip features

A
  • neonates from breech delivery
  • Female 6xt more likely
  • unilateral or bilateral (positive family hx)
  • Diminished abduction in flexion of the
    affected hip
  • Apparent inequality of legs: affected
    leg being shortened and externally rotated
  • Asymmetrical skin creases of the groin and
    thigh
  • ‘clicking’ on hip movements
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49
Q

Developmental dysplasia (DDH) of the hip dx

A

Barlow test —‘telescoping’ movements in the long axis of the flexed and abducted thighs.

Ortolani test — flexed hips are abducted. thighs are the grasped between the thumbs in front and other fingers behind. The child’s knees are flexed and hip flexed to a right
angle. **positive sign makes audible and palpable ‘jerk’ or ‘clunk’ (not a click). **
- Ortolani and Barlow tests but is usually negative after two months
- Ultrasound is excellent especially up to 3-4 months

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50
Q

Henoch-Schönlein purpura (HSP) in children

A
  • Autumn, winter and spring months
  • IgA mediated vaculitis
  • anaphylactoid purpura
  • arthralgia (not arthritis),
  • non-thrombocytopenic purpura (the purpura is vascular due to leukocratic activity)
    -typical symmetrical distribution over legs and buttock.
  • colicky abdominal pain 2 to 4 weeks
  • melena
  • ankle swelling
  • nephritis
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51
Q

Henoch-Schönlein purpura (HSP) in children Dx

A

-Clinical presentation + urinalysis for nephritis

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52
Q

Henoch-Schönlein purpura (HSP) in children complication

A

Intussusception (due to intestinal oedma and bleeding)

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53
Q

Transient synovitis

A
  • 3-8 years
  • URTI hx
  • sudden onset unilateral hip or groin pain most common sx
  • medial thigh or knee
    pain 2nd common sx
    Arthralgia and arthritis secondary to synovium inflammation
  • no fever, or only a mild fever
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54
Q

Transient synovitis

A
  • NSAIDs 48 hours
  • bed rest
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55
Q

Features of Epiglottitis

A

– H. influenzae
High fever, sore throat,
dysphagia, odynophagia,
drooling due to inability to swallow the saliva because swallowing
is painful and difficult.
child miserable adopts a tripod position with a hyperextended neck to maintain the airway open. Muffled voice (hot potato voice)
Lungs are clear on auscultation initiallt later expiratory stridor (ominous sign.)

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56
Q

Epiglottitis treatment

A
  • supplemental oxygen
  • intubate
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57
Q

age of epiglottitis

A

more common between
ages 2 and 4 years;

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58
Q

Thumb sign in X-ray

A

Acute epiglottitis
- intubation at hospital

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59
Q

Foreign body

A

U/L wheeze

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60
Q

Asthma in children definitive dx

A
  • 2 and 5 years
    -Bilateral wheezing
  • viral wheezing, pre-school wheeze, episodic viral wheeze and multiple
    trigger wheeze
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61
Q

Infrequent Intermittent asthma in children

A
  • less than one episode of asthma in 6
    weeks and no symptoms in between the flare-ups
  • inhaled short-acting beta2 agonist
    (SABA)
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62
Q

Asthma short-acting beta2 agonist SABA

A

salbutamol

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63
Q

Asthma LABA

A
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64
Q

CXR in bronchiolitis

A

B/L perihilar infiltrates

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65
Q

Expiratory wheeze + RSV URTI + barking cough

A

Croup

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66
Q

Croup management

A

mild: no treatment
moderate/severe:
-Dexamethasone 0.3 mg/kg orally (first-line);
- Prednisolone 1mg/kg orally, or
- Budesonide 2mg by nebulizer
most severe with significant airway obstruction/fatigue: Adrenaline 1% (1:100, 10mg/ml) solution 0.05ml/kg/dose

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67
Q

Cervical masses in children

A
  1. Congenital
  2. Inflammatory/ infective
  3. Neoplastic
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68
Q

Posterior triangle of the neck mass

A

CCP
- Cystic hygroma
- Cervical rib
- Pancoast tumour
- (Naso/oropharyngeal squamous cell carcinomas)

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69
Q

Cervical masses in neonatal period

A
  • thyroglossal duct cyst (TDC)
  • teratomas
  • sternocleidomastoid tumours of infancy
  • vascular or lymphatic malformations.
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70
Q

Complications of thyroglossal duct cyst (TDC)

A
  • Infection
    -Malignancy 1%
  • Overgrowth and pressure of the underlying
    structures.
  • Rupture and fistula formation
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71
Q

Anterior triangle of the neck mass

A

BCC
- Branchial cyst
- Carotid body tumour
- Carotid aneurysm

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72
Q

Midline of the neck mass

A

**TTD **
- Thyroid nodule
- Thyroglossal cyst
- Dermoid cyst

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73
Q

Acute rheumatic fever high risk population (JONES)

A

Major criteria:
- Carditis
-Polyarthritis
-Chorea.
-Subcutaneous nodules.
-Erythema marginatum
- Polyarthritis or aseptic mono-arthritis or
polyarthralgia

Minor criteria
-Fever more than 38c
-Previous rheumatic fever
-Arthralgia
-Raised ESR/CRP more than 30
-ECG shows prolonged PR interval

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74
Q

Acute rheumatic fever treatment

A
  • benzathine penicillin IM
    -Roxithromycin if allergic to penicillin/NSAIDs
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75
Q

Treatment of Perthes disease

A

Conservative: Splinting
Surgery: osteotomy

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76
Q

Features of Acute rheumatic fever (ARF)/ erythema marginatum.

A

2 major and 2 minor criteria
- history of sore throat 3 weeks
-migratory arthralgia/arthritis
- Erythema marginatum - well demarcated bright red/pink macules rash

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77
Q

Initial ARF dx

A

2 major criteria OR one major and two minor criteria + Evidence of preceding GAS infection

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78
Q

recurrent attack of ARF dx

A

Two major criteria OR one major and two minor criteria OR three minor criteria + Evidence of preceding GAS infection

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79
Q

ARF dx

A

Cultures for GAS are the gold standard (Throat swab)

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80
Q

Most common cause of vaginal bleeding in children

A

vaginal foreign body

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81
Q

nonspecific vulvovaginitis

A
  • caused by chemical
    irritants such as bubble baths or by poor hygiene
  • stop bubble baths and use only cotton underwear
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82
Q

vulvovaginitis management in children

A

no voiding difficulties: reassure
voiding difficulties: topical oestrogen or oestradiol cream applied twice daily
severe obstruction to urinary flow with retention or recurrent infections: Manual or surgical separation

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83
Q

Causes of vaginal bleeding in children

A
  • Vaginal foreign body
  • Severe vulvovaginitis
  • Trauma (including straddle injury and sexual
    abuse)
  • Excoriation associated with threadworms
  • Onset of first menstruation
  • Haematuria
  • Urethral prolapse
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84
Q

Enuresis management in children

A
  • Spontaneous resolution <5 years (84%)
  • Bed wetting alarms >5 years and conservative methods (fluid
    intake, toileting, reward system) failed + wetting >2 per week
  • nasal desmopressin alternative bed wetting alarm.
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85
Q

Gastroenteritis in children causes

A
  • Norovirus 95% aus
  • faecal–oral route
  • Contaminated food and water (cold meats)
  • 12 to 24/48 hour incubation period
  • noninflammatory, nonbloody, non-mucoid
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86
Q

Norovirus Gastroenteritis in children dx

A

PCR stool

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87
Q

Gastroenteritis in children clinical features

A

Common:
- Nausea
- Vomiting
- Diarrhoea
- Abdominal cramps

Not common:
- Headache
- Low-grade fever
- Chills
- Muscle aches
- Malaise

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88
Q

Gastroenteritis in children management

A

Symptomatic

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89
Q

anal fissure features

A
  • passage of hard stools
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90
Q

anal fissure management in children

A
  • anusol cream (lignocaine)
  • pain for anal fissure is under control, laxatives and fibre diet
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91
Q

Hirschsprung disease (HD)

A
  • 15-20 % of newborn intestinal obstructions
  • 80% in the first 6 weeks of life
  • male > female
  • congenital anomaly by absence of ganglia in a segment of colon and paralysis of this aganglionic segment
    -starts at the anus and progresses up
    the rectum towards the colon. (Delayed meconium passage)
  • 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
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92
Q

Hirschsprung disease (HD) complication

A

enterocolitis

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93
Q

Hirschsprung disease (HD) Dx

A

Rectal suction biopsy – Gold standard

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94
Q

3 months

A
  • hold the neck
  • recognize mother’s face
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95
Q

Hirschsprung Disease (HD) Mx

A
  • Laxatives (mild cases)
  • Surgery
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96
Q

intestinal malrotation with volvulus

A
  • 6 months
    -bilious vomiting
  • crampy abdominal pain
  • abdominal distention
  • bloody, mucoid stool
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97
Q

Hypertrophic Pyloric Stenosis features in children

A
  • 2 and 6 weeks of age
  • gastric outlet narrowing
  • projectile vomiting a few minutes after feeding
  • non bloody, non bilious vomiting
  • delayed capillary refill > 2 seconds
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98
Q

Hypertrophic Pyloric Stenosis risk factors in children

A

-Formula feeding
-Male
-Caucasian background
-Firstborn
-Maternal smoking during pregnancy
-Positive family history
-Both erythromycin and azithromycin < 2weeks

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99
Q

Hypertrophic Pyloric Stenosis in children mananament

A

Initial: Fluid resuscitation
Best: Ramstedts Pyloromyotomy

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100
Q

Proteinuria in children

A

> 1+ protein on urine dipstick exam
- perform urinalysis for confirmation

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101
Q

Abnormal UA in children

A
  • Asymptomatic microscopic hematuria
  • Repeat UA after fever settles if no UTI (2 positive UA)
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102
Q

UTI in children

A
  • Fever, nausea, vomiting
  • abdominal pain
  • Leukocytes and nitrites on urinalysis
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103
Q

UTI in children investigation

A
  • suspect vesicoureteric reflux
  • < 3 years (2-36 months) US of the kidney, ureter & bladder
  • If US normal then voiding cystoureterogram (VCU)
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104
Q

UTI hospital admission indication

A
  • Most of children less than 3 months.
  • Children who are seriously unwell such as
    those with toxic appearance or
    dehydration.
  • Oral antibiotics cannot be tolerated.
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105
Q

UTI in children Managment

A

1st line: trimethoprim
cephalexin

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106
Q

UTI in infants < 1 year

A
  • 1st: US
  • micturating cystourethrogram (MCU): rule out vesicoureteric reflux
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107
Q

tachycardia + sunken eyes + >3 sec capillary resuscitation

A

severe dehydration

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108
Q

severe dehydration management

A

10-20ml/kg boluses of 0.9% normal saline

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109
Q

Renal scarring in children

A
  • Recurrent urinary tract infections (more than
    2 times during childhood)
  • Dimercaptosuccinic acid scintigraphy (DMSA) - Gold Standard
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110
Q

DMSA indications

A
  • Clinical suspicion of renal injury
  • Reduced renal function
  • Suspicion of VUR
  • Suspicion of obstructive uropathy on ultrasound in older toilet-trained children
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111
Q

post-streptococcal Glomerulonephritis (PSGN) in children symptoms

A
  • hypertension 50-90%
  • haematuria 30-50%
  • oedema 60%
  • Decreased complement (C3) levels
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112
Q

post-streptococcal Glomerulonephritis (PSGN) management

A
  • Fluid restriction
  • Loop diuretics/dialysis
  • Steroids (caution, could be wrong)
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113
Q

Minimal Change Disease (MCD) in Children

A
  • nephrotic syndrome
  • <6 years
  • Absence of hypertension
    Absence of hematuria by Addis count
  • Normal complement levels
  • Normal renal function
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114
Q

Minimal Change Disease (MCD) in Children dx

A

1. Nephrotic range proteinuria-urinary protein excretion greater than 50 mg/kg per
day.
2. Hypoalbuminemia-serum albumin
concentration less than 30 g/L.
3. Edema.
4. Hyperlipidaemia

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115
Q

Nephrotic disease management

A
  • Corticosteroid (Prednisolone)
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116
Q

Causes of obesity in children

A
  • Hypothyroidism (check TSH)
  • Excessive caloric intake
  • Cushing’s disease (ACTH, cortisol)
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117
Q

Autistic disorder features

A
  • preoccupations with activities
  • objects
  • delayed speech language development
  • Aggression and irritability
  • poor communication with friends and avoiding eye contact
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118
Q

Characteristic features of autistic disorder

A
  1. Onset during infancy and early childhood
  2. Lack of socila interactions
    least two of the following:
    - No awareness of the feelings of others
    - No or abnormal comfort seeking in
    response to distress
    - No imitation
    - No social play
    - cannot socialize, (no eye contact )

3- Impaired communication
least one of the following:
- No babbling, gesture, mime or spoken
language
No non-verbal
communication
- abnormal form of
speech
- inability to make conversation
-abnormal speech

4- Restricted or repetitive activities, interests and
imaginative development, shown in at least one of
the following:
- stereotyped body movements
- persistent preoccupations and
rituals with objects or activities
- gets troubled over changes in routine or
surroundings
- No imaginative and symbolic play

5- Behavioral problems:
- tantrums
- hyperactivity
- risk-taking activity

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119
Q

Autism treatment

A

Atypical antipsychotics (Risperidone)

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120
Q

Relationship between ADHD & ODD

A

In more than 50% of px with ADHD, ODD is also a part of the clinical picture

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121
Q

kidney scarring features in children

A
  • one kidney smaller than the other
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122
Q

nutshell diagnosis of autistic disorder requires
the presence of core features by the
age of 3 years:

A
  1. Impairment of social interaction
  2. Impairment of communication
  3. Restricted, repetitive and stereotyped patterns of activities, behavior and interest
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123
Q

kidney scarring investigation of choice in children

A

DMSA (gold standard)

  • Clinical suspicion of renal injury
  • Reduced renal function
  • Suspicion of VUR
  • Suspicion of obstructive uropathy on ultrasound in older toilet-trained children
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124
Q

6 weeks

A
  • good head control
  • head stabilises when sitting
  • track objects
  • startes at loud noise
  • social smile
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125
Q

2 months

A

social smile 6 weeks

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126
Q

3 months

A
  • hold the neck
  • recognize mother’s face
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127
Q

4 months

A
  • eye contact with people
  • look for mother when she speaks
  • happy or settled most of the time
    -follow activities with eyes
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128
Q

6 months

A
  • Sits without support
  • Rolls from prone to supine vice versa
  • palmar grasp
  • hand to hand transfer
  • turns head to loud noise
  • understands bye bye and no
  • puts object to mouth (stops at 1 year)
  • shakes rattle
    reaches for bottle/breast
  • Ability to explore things by holding, looking at them and putting them in mouth
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129
Q

8 months

A
  • sits without support
  • repeats syllables ‘mama/dada’
  • enjoys peekaboo
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130
Q

9 months

A
  • crawls
  • stranger anxiety
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131
Q

12 months

A
  • ‘Cruises’
    -thumb grasp
  • imitates speech with meaning
  • waves goodbye
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132
Q

14 months

A
  • pulls string on toy
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133
Q

15 months

A
  • neat pincer grasp
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134
Q

18 months

A
  • walks without support
  • can build 2 tower blocks
  • say 3 words
  • drinks from cup
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135
Q

2 years child expected to

A
  • walking upstairs
  • Scribbling
  • points to body part
  • knowing 2 pronouns
    -Toilet trained
  • self feeding by spoon/cup
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136
Q

2.5 years

A
  • runs/jumps
  • throws ball
  • build 4 blocks
  • 2 word sentences
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137
Q

3 years

A
  • ride tricycle
  • copes vertical line/ circle
  • can use scissors
  • 3-word sentences
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138
Q

4 years

A
  • learns bicycle
    -copies square
  • first and last name
  • dress with supervision
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139
Q

5 years

A
  • hops on one foot
  • draw a person with 3 parts triangles
  • knows colours
  • dress without supervision
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140
Q

Encoperesis

A

voluntary or involuntary passageof stools
- place
other than the toilet
- >1/month for 3months
- >4years

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141
Q

Social & emotional developmental milestones

A
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142
Q

Emotional development milestones

A
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143
Q

Types of encoperesis

A

primary- child has never been
continent

secondary- previously
continent.

144
Q

Cognitive development milestones

A
145
Q

Staphylococcal scalded skin syndrome

A

Ritter disease, also known as Staphylococcal Scalded Skin Syndrome (SSSS), is a serious skin condition typically seen in infants and young children. Here’s a simple breakdown:

  1. Cause: It’s caused by a toxin produced by certain strains of the Staphylococcus aureus bacteria.
  2. Symptoms:
    • Red, painful skin: The skin looks like it’s been burned or scalded.
    • Blisters: Large, fluid-filled blisters appear, usually on areas like the face, neck, armpits, and groin.
    • Skin peeling: The top layer of the skin peels off easily, leaving raw, red areas underneath.
    • Fever and irritability: The child may also have a fever and be very irritable.
  3. Who is at risk?: It mainly affects newborns and young children because their immune systems are still developing. Adults with weakened immune systems or kidney disease can also be affected.
  4. Treatment:
    • Antibiotics: To kill the bacteria causing the infection.
    • Skin care: The affected skin is treated with gentle care to prevent infection and help it heal.
    • Fluids: In severe cases, fluids may be given to prevent dehydration due to the skin damage.
  5. Prognosis: With prompt treatment, most children recover fully within a couple of weeks. However, it can be serious, so quick medical attention is important.

In short, Ritter disease is a severe skin condition caused by a bacterial toxin, leading to red, blistered, and peeling skin, primarily in young children. It’s treatable with antibiotics and proper skin care.

known as Ritter disease
commonly in children less than 5 years of age
fever,
irritability, erythema,tender skin
Circumoral
erythema
crusting of the eyes, mouth, and nose
blisters on the skin
Postive Nikolsky sign- Peeling of the epidermis in
response to mild shearing forces

146
Q

With constipation and overflow
Incontinence:

A

<3/week bowel movements
-stool partially emptied remaining
- stool leak out, often during the child’s daily
activities.
- if constipation resolves encoperesis resoleves

147
Q

Language development milestones

A
148
Q

Encoperesis with No constipation overflow Incontinence:

A

there’s no constipation, and the child’s faeces have normal consistency. Unlike in cases associated with constipation and overflow, soiling of this type is intermittent. Feces may be emitted in
a prominent location (e.g., as an act of defiance) or
may be an unintentional consequence of anal selfstimulation (e.g., a variety of masturbation).
Encopresis without constipation and overflow
incontinence is less common than the first type of
encopresis, and is often associated with
oppositional defiant disorder and conduct disorder.
It has been estimated that 3% of children with
psychiatric issues may have encopresis.

149
Q

Oppositional Defiant Disorder (ODD) in Children

A
  • 10-12 years
150
Q

Oppositional Defiant Disorder (ODD) in Children Treatment

A

1st line: Antipsychotics (risperidone)
2nd line: mood stabilisers (sodium valproate) SSRIs

151
Q

‘hand, foot
and mouth (HFM) disease’

A
  • Self-limiting
  • Coxsackie A virus. - Erythematous macular rash,
    progressing to gray
    vesicles
    vesicles seen in buccal mucosa,
    gums and tongue.
  • doesn’t involve the buttocks and the genitalia
  • no scarring.

School Exclusion: until lesions dried up

152
Q

Parvovirus B19

A
  • Fifth disease (erythema infectiosum)
  • Low haemoglobin patients with
    haemolytic conditions (such as sickle-cell anaemia) thus develop a transient aplastic
    crisis
  • poorly functioning bone marrow (for a week or more)
153
Q

Conductive disorder

A
  • 12-18
154
Q

Features of partial seizures

A
  • no loss of consciousness
  • no pos ictus
155
Q

vertigo in children

A
  • CNS tumours (medulloblastoma)
  • temporal lobe epilepsy
156
Q

cyanosed baby + No murmur at birth

A

Transposition of great vessels

157
Q

Absent seizures ion children

A
  • loss of consciousness
    -pos ictus
  • 30-60s duration
158
Q

Febrile seizures/ convulsions

A

Simple:
- duration of less than 15 minutes
- do not occur more than once in 24 hours

Complex seizures:
- MAY last for longer than 15 minutes
- recur in
the course of 24 hours

159
Q

Febrile seizures/ convulsions management

A

If seizure is of short duration and doesn’t reoccur = reassurance
if the following situations:
1. A child with a pattern of prolonged seizures (usually longer than ten mins.) which
have previously responded to intravenous or rectal diazepam.
2. A child with clusters of repeated seizures in whom oral treatment is inappropriate.
3. A child with severe epilepsy who is remote from emergency services.
=
Rectal diazepam

160
Q

Neurocysticercosis (NCC)

A
  • raw meat consumption
  • Tapeworm Taenia solium
  • MRI single focal white matter lesions
  • Blood test serology
  • Albendazole
161
Q
A
162
Q

Temporal lobe seizures in children

A
163
Q

Features of infantile spasms

A
  • 3-7 months
    sudden bending of the trunk and flexion of upper limbs
  • Corticosteroids (prednisolone) 1st line for 8 to 10 week. Vigabatrin
  • Clonazepam for acute presentation?
164
Q

Tics in children

A
  • also known as habit spasms
  • individually recognisable, intermittent movements
  • aware in the urge to perform the movement
  • blinking,
  • facial grimacing,
  • shoulder shrugging,
  • head jerking
165
Q

Unknown seizures

A
  • resistant to
    treatment with
    intravenous calcium
  • test Serum magnesium level
166
Q

BPPV child

A
  • variant of migraine
    preceeds - migraine in future
167
Q

cyanosed baby + murmur at birth

A

Tetrology of fallot

168
Q

Roseola infantum

A

exanthem subitum/sixth disease/three-day
fever

169
Q

Roseola infantum features

A

3 to 5 days of high
fever may exceed) 40°C.
fever resolves abruptly
rash develops

170
Q

cyanosed baby + No murmur at 2-7 days of life

A

Hypoplastic left heart

171
Q

Features of diarrhoea

A
  • opposite of vomiting
172
Q

Roseola infantum causes

A

human herpes virus 7 (HHV-7),
enteroviruses (coxackievirus A and B, echovirus),
adenovirus, and parainfluenza virus type 1.

173
Q

Austin-Flint murmur

A

mid-diastolic
rumbling murmur best heard over the apex.
In Severe Aortic Regurgitation
In MFS

174
Q

MFS treatment

A

1st -beta blockers
2nd- verapamil, ACEinhibitors

175
Q
A
176
Q

Drugs closing ductus arteriosus

A

NSAIDS

177
Q

most
common cause of failure to breastfeed?

A

Reduced frequency of
breastfeeding.

178
Q

ureteropelvic junction (UPJ)
obstruction features

A
  • most common cause
    of paediatric hydronephrosis
  • periodic abdominal pain with vomiting
  • exacerbation on UPJ can also lead to pelvic distention, flank pain or even tenderness
179
Q

Drug keeping the ductus arteriosus open or patent

A

PGE2

180
Q

COUGH

A

acute (<3 weeks),
subacute (3-8 weeks)
chronic or persistent (>8
weeks).

181
Q

ureteropelvic junction (UPJ)
obstruction diagnosis

A

US during painful episode

182
Q

Idiopathic (immune) thrombocytopenic purpura (ITP)

A
  • preceding viral infection
  • s frequently < 20,000/μL
  • ## other lab tests normal
183
Q

Idiopathic (immune) thrombocytopenic purpura (ITP) in children management

A
  • If not bleeding: monitoring/observation
  • If bleeding: IVIG and corticosteroids (prednisone)
184
Q

Isolated thrombocytopenia features

A
  • following an URTI
  • acute (~90%) or chronic (~10%)
  • no pallor, lymphadenopathy
    or hepatosplenomegaly.
  • if platelets > 20 x 109/L: bed rest
  • if platelets < 20 x 109/L: oral steroids (prednisolone)
185
Q

Colon polyp

A
  • benign hamartomas
  • ages 2 and 8 years, peak at 3 to 4 years
  • mostly painless
    rectal bleeding
    palpable polyp
    on rectal examination >60%
186
Q

anal fissure

A
  • most common cause of painful rectal bleeding in children
  • associated with constipation
  • bright blood on the
    surface of stool, on the nappy or toilet paper
187
Q

retinoblastoma

A
  • most common intraocular tumor in children
  • Leukocoria (white cornea or Cat’s eye)
    -strabismus
  • initial: US (intraocular calcification)
  • best dilated indirect
    ophthalmoscopic examination under anesthesia
188
Q

Chronic cough cause in children

A

asthma

189
Q

separation anxiety in child features

A
  • Want to stay at home with parents
  • Get upset about going to school
    aches or headaches, or do
    not feel well without a physical cause -Do not have any serious behavior problems
  • Do not try to hide their wish regarding not going to school from their parents
  • Are more likely to be the youngest memberof a family
190
Q

acute or subacute cause of cough

A

Post viral cough

191
Q

diagnosis and staging of the VUR.

A

Voiding cystoureterogram

192
Q

Bordetella pertussis (whooping cough) hospital admission

A
  • Infants less than 6 months of age
  • Any child with complications (i.e. apnoea,
    cyanosis, pneumonia, encephalopathy, pneumothorax)
193
Q

Bordetella pertussis (whooping cough) school exclusion

A

3 weeks start of symptoms
2 weeks start of cough
<5 days of antibiotics

194
Q

Bordetella pertussis (whooping cough) investigation

A

Children: Nasopharyngeal aspiration
Adults: nasopharyngeal swab

195
Q

Lobar Pneumonia in children

A
  • streptococcus pneumoniae
  • high fever
  • chest auscultation
    deceitfully normal
    -high fever
  • pallor
    -respiratory distress
196
Q

expiratory stridor

A
197
Q

Lobular (atypical) Pneumonia in children

A
  • fever is not often that high.
  • insidious onset
  • prodromal
    state
198
Q

inspiratory
stridor

A

suggests obstruction above the glottis.

199
Q

Pneumonia in children investigation

A

initial step: chest X-ray (to see consolidation)

200
Q

Choanal atresia features

A
  • failure of canalization of the bucconasal membrane.
    CHARGE SYNDROME
  • coloboma
  • heart defect,
  • atresia choanae
  • retarded growth
  • genital abnormality
  • ear abnormality
201
Q

Choanal atresia dx

A

pass nasogastric tube (also managment)
no use in giving oxygen

202
Q

Choanal atresia management

A

Mild hypoxemia: nasogastric tube
Severe hypoxemia: intubation and ventilation

203
Q

CHARGE SYNDROME

A

-bilateral choanal atresia

coloboma
- heart defect,
- atresia choanae
- retarded growth
- genital abnormality
- ear abnormality

204
Q

Laurence-Moon-Biedl syndrome

A
  • autosomal
    recessive
    -Obesity
  • mental retardation
  • hypogonadism
  • retinitis
    pigmentosa with night blindness
  • polydactyly
205
Q

Fröhlich syndrome

A
  • adiposogenital dystrophy
  • obesity associated with a hypothalamic tumour
206
Q

Noonan’s (Male Turner’s) syndrome features

A
  • Affects males
  • An autosomal disorder involving mutation in chromosome 11
  • Pulmonary valve stenosis
  • Webbed neck
  • Abnormalities in cardiac conduction and rhythm
  • flat nasal bridge
  • single palmar crease
  • protruding tongue
  • eyes that are apart more than usual
  • low set ears
207
Q

Turner Syndrome features

A
  • Affects females
    -Madelung deformity
  • short stature,
  • webbed neck
  • low-set ears
  • low hairline at the back of the neck
  • epicanthal folds
208
Q

Turner Syndrome complications

A
  • aortic coarctation
  • Complete atrioventricular septal defect (CAVSD) – 37 percent
  • Ventricular septal defect (VSD) – 31 percent
  • ASD – 15 percent
  • Partial atrioventricular septal defect (PAVSD) – 6 percent
  • Tetralogy of Fallot (TOF) – 5 percent
  • PDA – 4 percent
209
Q

prominent ulnar head and apparent volar subluxation of the wrist on the forearm

A

Madelung deformity

210
Q

vesicoureteral reflux (VUR)

A

Grade I: Reflux into the nondilated ureter
2. Grade II — Reflux into the ureter and renal calyces without dilation
3. Grade III — Reflux with mild to moderate dilation
and minimal blunting of the fornices
4. Grade IV — Reflux with moderate ureteral
tortuosity and dilation of pelvis and calyces
5. Grade V — Reflux with gross dilation of ureter,
pelvis and calyces, loss of papillary impressions,
and ureteral tortuosity NEED SURGERY

211
Q

vesicoureteral reflux (VUR) management

A

management depends on grading:

Grade I-IV: continuous antibiotics
Grade V: Surgery

212
Q

Tetralogy of Fallot (TOF)

A

4 defects
- blood going from left to right ( acyanotic)
- all have VSD (systolic murmur)
- pulmonary stenosis
- right ventricle hypertrophy
- overriding aorta

213
Q

Patent ductus arteriosus. (PDA)

A

-acyanotic
- pansystolic machinery murmur (harsh) at the left sternal border
- wide pulse pressure.
- Definite treatment surgical closure

214
Q

Ventricular septal defect (VSD)

A
  • holosystolic murmur at left sternal border
  • acyanotic
215
Q

Atrial Septal Defect (ASD)

A
  • acyanotic
  • mid-systolic murmur at the pulmonary area, a split-second heart sound and a loud P2

2 main types:
- Ostium Primum: most dangerous type, can lead to pulmonary hypertension and heart failure, Prophylactic antibiotics recommended
- Ostium Secundum: most common type, e hole is higher in the septum, not serious, symptoms uncommon in infancy

216
Q

Transposition of the great arteries (TGA)

A
  • central cyanotic after 10-12 hours
    Aorta and pulmonary arteries are reversed
  • no murmur as there is no hole
  • prescribe PG e1
  • definite treatment: surgery to correct the transposition
217
Q

Innocent murmur

A

7S
-soft
- systolic
- short duration
- sounds (S1 &S2)
- symptomless
- Special tests normal (X-ray, ECG)
- Standing/Sitting changes (not fixed) (increased when supine)

218
Q

Pathological murmurs

A

Family hx of sudden cardiac death or
congenital heart disease
- in utero exposure to certain medications (lithium) or
alcohol
- Maternal diabetes mellitus
- History of rheumatic fever
- History of Kawasaki disease

  • Grade 3/6 or higher murmurs
  • Harsh quality
  • Abnormal S2
  • The presence of a systolic click
  • Increased intensity with decreased venous
    return (e.g., when the patient stands)
  • The patient has any symptoms that could be
    related to a cardiac condition (e.g. shortness
    of breath, chest pain, poor feeding, etc.)
219
Q

murmurs that increase in
intensity when the venous return to the heart is
decreased:

A
  1. hypertrophic obstructive
    cardiomyopathy (HOCM)
  2. mitral valve prolapse
  3. venous hum (low-pitched continuous
    murmurs produced by blood returning from
    the great veins to the heart)
220
Q

most common
allergens that can cause allergy and asthma

A

dust mites 90%
sheepskin 2nd most common

221
Q

Duodenal atresia features

A
  • Neonate w/ vomiting (after first feeds)
  • Down syndrome 5%
    distal obstruction to the papilla of Vater 80%
    -bilious vomiting
  • M > F
    -X-ray: ‘double-bubble’
  • drooling
  • abdominal distension (very late symptom)
222
Q

Down syndrome in children

A
  • short stature
  • microcephaly
  • centrally placed hair whorl
  • small ears
  • redundant skin on the nape of the neck
  • flat nasal bridge
  • Cardiac lesions 30% to 50% (endocardial cushion defect, VSD, tetralogy of Fallot (all 30%)
  • Duodenal atresia
223
Q

Edwards syndrome in children

A
  • Mortality is 50% in the first week and 90% in the first year
  • low-set ears,
  • a prominent
    occiput,
  • a short sternum,
  • a closed hand with overlapping fingers,
  • cardiac defects,
    rocker-bottom (rounded) feet,
  • cleft lip and/or palate
224
Q

Müllerian agenesis

A
  • Female gonads do not secrete Müllerian-inhibiting factor (MIF)
  • Male testes secrete MIF
  • empty scrotum
  • testes are impalpable in inguinal canal
225
Q

Oxygen saturation in children

A
  • > 93%
  • RR 50
226
Q

Bronchiolitis

A
  • acute LRTI <12 months (2 weeks to 9 months)
  • respiratory syncytial virus (RSV)
  • irritating cough and rhinorrhoea
  • distressed wheezing breathing
  • Hyper-inflated chest (barrel-shaped)
  • Use of accessory muscles and subcostal
    recession
  • fine inspiratory crackles
  • supportive with oxygen and hydration
  • bilateral perihilar congestion on X-ray (not necessary)
227
Q

Bronchiolitis management

A

100% oxygen via nasal prongs.
- severe bronchiolitis and requires rehydration
using intravenous fluids or nasogastric tube.

228
Q

bronchiolitis high risk of airway compromise

A
  • Infants younger than 3 months of age
  • Preterm or low birth weight infants.
    – Infants with chronic lung disease.
    – Infants with congenital acyanotic heart disease.
229
Q

Pulmonary hypoplasia

A
  • Oligohydramnios
  • Kidney US (bilateral renal agenesis)
230
Q

Laryngomalacia in children

A
  • congenital softening of the tissues of the larynx
  • **noisy breathing ** worsens when agitated, feeding, crying or sleeping
    on back
  • High pitched sound
  • symptoms present at
    birth, can become more obvious within the first
    few weeks
  • outgrow by 18 to 20 months
231
Q

most common cause of failure to thrive

A

inadequate caloric intake

232
Q

Tonsillitis management

A
  • Perform throat swab+ start antibiotics
  • If swab+ve = continue antibiotics
  • if swab-ve = discontinue antibiotics
233
Q

tonsillectomy in children

A
  • Hemorrhage common complication, also life thereatening
  • bleeding may occur in the early post-operative
    period or may be as delayed as 5 to 10 days
  • bleeding secondary to tonsillar fossae infection
234
Q

post-tonsillectomy haemorrhage management

A
  • Resuscitation - 2 large bore cannula with
    bloods
  • Reservation of cross-matched packed red
    cells
  • IV antibiotics: with 1.2g Benzyl Penicillin, 6-hourly + 500mg of metronidazole, 12-hourly
  • NSAIDs
  • Hydrogen peroxide gargle - 20mls of
    hydrogen peroxide diluted with water in a
    ratio of 1:6.
235
Q

Retropharyngeal abscess

A
  • inflamed prevertebral soft tissue
  • inability to extend the neck
  • lateral neck film demonstrates a widened prevertebral soft tissue strip
  • typically not present with airway compromise and hypoxia
236
Q

What Vitamin is given to babies after birth?

A
  • Vitamin K IM injection to avoid intercranial haemorrhage
237
Q

Aboriginal Australians are deficient in what vitamin

A

Vitamin D

238
Q

umbilical granuloma

A
  • most common umbilical mass
  • overgrowth of tissue during the healing process
  • soft pink or red lump
  • leaks small amounts of clear or yellow fluid
  • presence of non-purulent discharge
239
Q

umbilical granuloma management

A

topical silver nitrate
- cauterisation may need to be repeated at 3-day intervals if drainage persists

240
Q

Most common organism causing ophthalmia neonatorum

A

Chlamydia trachomatis
- notifiable disease

•	Neisseria gonorrhoeae: One of the most serious causes, potentially leading to corneal ulceration and blindness if not treated promptly.
•	Chlamydia trachomatis: The most common infectious cause. Symptoms may appear 5-14 days after birth.
241
Q

ophthalmia neonatorum treatment

A

oral erythromycin and sulfacetamide eye drops

242
Q

Neisseria gonorrhoea infection in a child

A

Vaginal non-bloody pus-like discharge 95%

243
Q

Bacterial conjunctivitis in children

A
  • gonorrhoea: fast and aggressive (3 and 7 days after birth)
  • chlamydia: slow and less aggressive (end of 1st week - 1 month after birth)
244
Q

Bacterial conjunctivitis in children school exclusion

A
  • Excluded until discharge has resolved
245
Q

congenital adrenal
hyperplasia (CAH)

A
  • ## 21-hydroxylase deficiency
246
Q

congenital adrenal
hyperplasia (CAH) dx

A

Palpable gonads:
-Pelvic ultrasound
-Testosterone and dihydrotestosterone (DHT) ratio.
-LH and FSH.
-ACTH stimulation test.
-hCG stimulation test

No palpable gonads:
- markedly elevated 17-hydroxyprogesterone 90%
-Serum electrolytes.
-Plasma renin activity

247
Q

Hereditary angioedema

A
  • recurrent angioedema without pruritis in:
  • upper respiratory tract
  • gastrointestinal tract
  • subcutaneous tissues
  • autosomal dominant reduced C-1 esterase
    inhibitor levels (HAE type I) or poorly functional (HAE type II)
248
Q

Meningitis in children features

A
  • < 1 month old
  • fever
  • poor feeding
  • jaundice
  • bulging fontanelle
  • seizures
  • nuchal rigidity
  • irritability/lethargy
  • Usually GBS
249
Q

Meningitis management in children

A

CSF analysis/Lumbar puncture FIRST:
- turbidity
- low glucose (less than 1.7 mmol/L)
- elevated proteins
- elevated white cells (20 to 30 cells/microL)
- Gram stain may be negative 60%

> 7 days E. Coli most
common

IF signs of ICP (seizure, papilledema) then CT head

250
Q

Immediate management of acute meningitis in chidren

A

-Airway, Breathing, Circulation, Disability, Exposure (Primary Survey).
-Obtain immediate intravenous access (an intraosseous needle may be required).
-Administer intravenous dexamethasone (0.15 mg/kg).
-Intravenous ceftriaxone (100 mg/kg).
-Take blood cultures.

251
Q

Aortic coarctation in children

A
  • 90% of blood is shunted across ductus arteriosus (well tolerated)
  • low cardiac output and shock once the ductus arteriosus closes
252
Q

Aortic coarctation symptoms in children

A
  • hypotension,
  • cyanosis,
  • respiratory distress,
  • **shock with normal or weak upper extremity pulses **
  • absent femoral pulses
  • Metabolic acidosis is seen as compensation to respiratory alkalosis
  • prostaglandin E1 infusion to maintain a patent ductus
    arteriosus and surgical repair
253
Q

incidence of congenital heart disease in children

A

1 child: 2% to 6%
2 children: 20% to 30%

254
Q

indications for preventer therapy in asthama

A

symptoms at night
>1 canister beta 2 aginists every 3mon
using beta 2 agonists >2days /week
asthma attacks >2/month
infrquent asthma attacks but severe
spirometry with reversible airflow obstruction

255
Q

most common congenital heart disease in infants?

A

Ventricular Septal Defect (VSD) 1 in 100 Australian infants

256
Q

Hepatoblastoma

A

-<5 years
- mass in right upper quadrant
- abdominal distension
- right-sided abdominal pain
- familial adenomatous polyposis high risk
- lost appetite and weight
- vomiting and jaundice (very rare)

257
Q

infant < 2 years + low-grade fever + abdominal distension + loss of appetite + limb pain + abdominal mass that crosses the midline

A

Neuroblastoma
- originates from adrenal glands

258
Q

3-4 years of age + kidney claw sign + abdominal mass does not cross midline

A

nephroblastoma (Wilm’s tumour)

259
Q

most common cause of sinus bradycardia in
neonates

A

secondary to Respiratory failure and hypoxia

260
Q

Most common allergy in children

A

Food allergy 80%

261
Q

most common cause of short stature in children

A

Constitutional delay of growth and puberty
- lack of breast development-thelarche in girls above 13 years
- testicular volume less than 4ml by the age of 14 years

262
Q

Growth investigations to consider prior to referral

A
  • FBC
  • urea & electrolytes
  • ESR
  • Coeliac serology

NOTE: GH is pulsatile therefore not diagnostic

263
Q

bacterial balanitis ( bacterial infection of the
foreskin) treatment

A
  • topical antibiotics mupirocin
  • mild inflammation without pus or other signs of cellulitis = topical
    steroids
264
Q

best method of anaesthesia for neonatal circumcision

A

Dorsal penile nerve block

265
Q

most common cause of jaundice in a neonate
within 24 hours after birth?

A

Haemolysis due to ABO incompatibility
- always pathological

266
Q

most common cause of hyponatremia in children

A
  • diarrhoea
267
Q

hyponatremia in children

A

-Gastrointestinal fluid losses.
-Administration of hypotonic fluids.
-Severe infections-meningitis, encephalitis, pneumonia, bronchiolitis, sepsis etc can lead to SIADH

268
Q

persistent hyponatremia in children

A

– Congenital Adrenal Hyperplasia.
– Addison’s Disease.
– Psychogenic polydipsia.
– Obstructive uropathy

269
Q

Chronological age and bone age

A

-should be equal
- difference <2 years = normal (reassure)
- difference > 2 years = constitutional delay

270
Q

Guillain-Barré syndrome in children

A
  • Campylobacter infection
  • 10 days after a nonspecific viral illness
  • acute polyneuropathy
  • progressive, mostly symmetric muscle weakness (days or weeks) beginning in the lower
    extremities and progressing toward the trunk
  • absent or depressed deep
    tendon reflexes
271
Q

Guillain-Barré syndrome dx in children

A
  • spinal fluid protein measurement (elevated protein 2x normal)
  • glucose and cell counts are normal
272
Q

Guillain-Barré syndrome management in children

A
  • observation (24-48 hours)
  • intravenous immunoglobulin,
    steroids, or plasmapheresis (respiratory failure)
273
Q

Charcot-Marie-Tooth disease in children

A
  • peroneal and intrinsic foot muscle atrophy (strange feet)
  • extending to the intrinsic hand muscles and proximal leg
274
Q

Fragile X syndrome in children

A
  • inherited disorder
  • Fragile X Mental Retardation 1 (FMR1) gene expansion
  • associated primary ovarian
    insufficiency & tremor ataxia syndrome
  • All males with the full mutation
  • Relative macrocephaly
  • Strabismus
    *Pale blue irises
    *Midface hypoplasia with sunken eyes
    *Arched palate
    *Mitral valve prolapse (seemingly benign)
    *Joint hyperlaxity (particularly of the thumbs, fingers, and wrists)
    *Hypotonia
    *Doughy skin over the dorsum of hands
    *Flexible flat feet
275
Q

Tay Sachs disease in children features

A
  • 2 to 6 months
  • Retinal cherry red spots 90%
  • progressive weakness and loss of motor skills
  • with hypotonia
  • hyperreflexia
  • retinal ganglion cells become distended with glycolipid• Cherry-Red Spot in the Eyes: One of the hallmark signs is a “cherry-red spot” that can be seen on the retina during an eye exam.
276
Q

Tay Sachs disease in children investigation

A

Fundoscopy: retinal cherry red spots in 90%

277
Q

Tay Sachs disease in children blood test

A

Hexosaminidase A & B enzyme

Tay-Sachs disease is a genetic disorder that primarily affects the brain and nervous system. It’s caused by a deficiency of a specific enzyme called Hexosaminidase A.

  1. What Does Hexosaminidase A Do?
    • Hexosaminidase A is an enzyme that helps break down fatty substances in the brain and nerve cells. Without this enzyme, these fatty substances (called GM2 gangliosides) build up to toxic levels, damaging the brain and nervous system.
  2. Why Test for Hexosaminidase A & B?
    • Hexosaminidase A is the enzyme specifically deficient in Tay-Sachs disease. By testing the levels of this enzyme in the blood, doctors can diagnose Tay-Sachs disease.
    • Hexosaminidase B is another related enzyme that usually works alongside Hexosaminidase A. Testing both helps doctors understand whether the deficiency is specific to Hexosaminidase A (which indicates Tay-Sachs) or if there’s a broader issue affecting both enzymes.
  3. What the Test Shows:
    • Low Hexosaminidase A: If the blood test shows very low or absent levels of Hexosaminidase A, it indicates Tay-Sachs disease.
    • Normal Hexosaminidase B: In classic Tay-Sachs disease, Hexosaminidase B levels are usually normal, which helps confirm that the problem is specific to Hexosaminidase A.
  • Tay-Sachs disease is caused by a deficiency in the enzyme Hexosaminidase A.
  • Blood tests measuring Hexosaminidase A & B levels help diagnose the disease by showing whether the specific enzyme needed to break down fatty substances in the brain is missing or low. Without this enzyme, harmful substances build up in the brain, leading to the symptoms of Tay-Sachs disease.
278
Q

Mumps meningitis in children

A
  • occurs in the post-pubertal male 25%, usually unilateral
  • Paramyxovirus isolated from CSF,
    saliva and nasopharynx
  • fever,
  • lethargy,
  • bilateral parotid swelling
  • parasternal oedema
279
Q

Mumps meningitis in children complications

A
  • Aseptic meningitis
  • testes causing orchitis, usually unilateral,
280
Q

Tetanus vaccinations in children

A
  • 3 vaccinations at 2,4 and 6 months
  • 1st booster at 4 years
  • 2nd booster between 12-17 years
281
Q

Clean laceration tetanus

A
  • no immunoglobulins required
  • check to see vaccination status and vaccinated in indicated
282
Q

Dirty laceration tetanus

A
  • immunoglobulins required
283
Q

DTPa minimum dose
duration

A

4 weeks
- booster doses 10 years and 20 years after primary course

284
Q

Oral polio vaccine (OPV) in children

A

Preterm babies should not get vaccinated until after leaving hospital (might spread the live vaccine virus to other babies in the hospital)
- inactivated polio vaccine can be used instead

285
Q

Hydrocele in children

A
  • scrotal swelling
  • A bluish discoloration of the skin if the hydrocele is large.
  • Fluctuation in the size of the swelling (mainly in infants).
  • The area of the hydrocoele is clearly defined.
  • Hydroceles are not painful but may cause discomfort if they are large.
286
Q

Hydrocele in children investigation

A

positive transillumination test

287
Q

Hydrocele in children management

A
  • wait until 18 months (resolve spontaneously)
  • surgery if not resolved after 18 months
288
Q

cystic fibrosis in children

A
  • autosomal recessive
  • 1:3700
  • Sweat chloride test
  • DNA testing (CFTR) diagnostic 72%
289
Q

Kernicterus in children

A

pathogenic sign of bilirubin staining of the brain stem nuclei and
cerebellum

– Athetoid cerebral palsy with or without seizures.
– Developmental delay.
– Hearing deficit.
– Oculomotor disturbances including paralysis of upward gaze.
– Dental dysplasia.
– Intellectual impairment.

290
Q

Vitamin A deficiency

A

night blindness
drying of the conjunctivas and sclera
dry skin
Poor growth and impaired cognition

291
Q

Duchenne’s muscular dystrophy in children

A
  • X-linked recessive trait
  • after
  • deficiency of dystrophin
    beginning to walk features become more evident
  • Pseudohypertrophy limited to the calf muscle
  • hip girdle weakness at 2 years
  • Gower sign (use of the hands to “climb up” the legs in order to assume the upright position) at 3-5 years
  • use of a wheelchair after 12 years
  • mental impairment and cardiomyopathy
  • Death respiratory failure, heart failure, pneumonia, or aspiration
292
Q

Klumpke paralysis

A
  • C7, C8 & T1 injury
  • affects elbow
  • hand palsy
293
Q

Acute disseminated encephalomyelitis (ADEM)

A

autoimmune-demyelinating
<10 years of age
preceeding URTI
high-dose corticosteroids to treat

294
Q

Neonatal hypoglycaemia features

A
  • Mid-line defects (Congenital pituitary deficiency)
  • Hepatomegaly (glycogen storage diseases and fatty acid oxidation
    disorders)
  • Micro penis (congenital gonadotropin deficiency, possible pituitary, cortisol deficiency)
    abnormalities
  • Macrosomia (maternal history of
    gestational diabetes)
295
Q

Hypoglycaemia IV infusion

A

2ml/kg of 10% dextrose IV

296
Q

benign haemangioma

A
  • strawberry naevus
  • around 1 to 4 weeks of age, then get bigger, for a few months
  • stop growing between 6-12 months
  • gradually disappear over the next few years
  • if naevus at eyes, nose, ears or trachea then laser therapy
  • If anywhere else, then observation
297
Q

ABO hemolytic disease in this infant

A

positive direct Coombs test

298
Q

Brain tumours in children

A
  • account for 25% -
    30% of all paediatric malignancies
  • 1 to 10 years infratentorial (posterior fossa)
  • After 10 years of age, supratentorial tumour’s (eg, diffuse astrocytoma)
299
Q

infratentorial tumours in children

A

cerebellar and brainstem tumours (medulloblastoma, cerebellar astrocytoma)
- ICP
- nausea
- vomiting,
- ataxia,
- vertigo,
- papilloedema
- Cranial nerve VI to X palsies

300
Q

Phenylketonuria,

A

Phenylketonuria (PKU) Made Easy

What is Phenylketonuria?

•	Definition: PKU is a genetic disorder that results in the body’s inability to break down an amino acid called phenylalanine, leading to its accumulation in the blood.

Cause

•	Genetics: PKU is an autosomal recessive disorder caused by mutations in the gene that codes for the enzyme phenylalanine hydroxylase (PAH). This enzyme is needed to convert phenylalanine into tyrosine.
  • autosomal recessive
  • absence of an enzyme that metabolizes
    phenylalanine to tyrosine
    mental retardation
  • Treatment consists of a diet that maintains phenylalanine at levels low enough to
    prevent brain damage but adequate to support normal physical and mental
    development.
301
Q

supratentorial tumours in children

A
302
Q

Seborrheic dermatitis in children

A
  • Erythema toxicum 50% of term newborns
  • commonly greasy, scaly, and erythematous rash
  • face, neck, axilla, and diaper area
303
Q

Mongolian spot in children

A
  • a bluish-grey lesion over
    buttocks, lower back, and occasionally extremities extensor surfaces
  • blacks, Asians, and Latin Americans
  • tend to disappear by
    1 to 2 years
304
Q

Biotinidase

A

autosomal
recessive trait
dermatitis, alopecia, ataxia,
hypotonia, seizures, developmental delay, deafness, immunodeficiency, and
metabolic acidosis
Treatment is lifelong administration of free biotin.

305
Q

Sickle cell anaemia in children

A
  • pneumonia,
  • pulmonary thromboemboli
  • sepsis

NOTE: with sickle-cell anaemia, these can be rapidly progressive and quickly fatal
- require hospitalisation

306
Q

causes of iron deficiency anaemia in
children

A

– Excessive intake of cow’s milk.
– Prematurity.
– Low birth weight.
– Coeliac disease.
– Lead poisoning.

307
Q

inguinal hernia ‘6-2’ rule

A

birth to 6 weeks, surgery is recommended within 2 days, 6 weeks to 6 months-surgery within 2 weeks and over 6 months surgery within 2 months

308
Q

Diaphragmatic hernia in children

A
  • Mortality 50%
  • transmittal of abdominal contents across a
    congenital or traumatic defect in the diaphragm
  • profound respiratory distress
  • birth at a tertiary-level
    centre
  • scaphoid abdomen
  • bowel sounds in the chest
309
Q

Diaphragmatic hernia in children management

A
  • high-frequency oscillatory ventilation
  • extracorporeal membrane oxygenation (ECMO)
310
Q

Holt-Oram syndrome

A

hypoplastic radii, thumb abnormalities, and cardiac anomalies.
pectoralis major muscle is missing

Holt-Oram Syndrome is a genetic disorder that primarily affects the bones in the arms and hands (upper limbs) and the heart. Here’s a simplified way to understand and remember it:

  1. Key Features:• “Heart-Hand Syndrome”: Holt-Oram is often called “heart-hand syndrome” because it affects both the heart and the hands.
    • Upper Limb Abnormalities:
    • These can range from mild to severe and usually affect the thumb, wrist, or forearm.
    • Common issues include underdeveloped or missing thumbs, short or fused bones in the forearm, and sometimes abnormalities in the shoulder.
    • Heart Defects:
    • The most common heart problems are atrial septal defects (ASD) and ventricular septal defects (VSD), which are holes in the walls separating the heart chambers.
    • Some people might have a conduction disease that affects the heart’s electrical system, leading to arrhythmias.
311
Q

Opioid intoxication in children

A

maternal analgesic narcotic drug (meperidine)
- depression of the newborn via crossing of the placenta
- administration
of naloxone, 0.1 mg/kg, IM, IV, or endotracheal

312
Q

Rickets in children

A
  • failure of bone mineralization
  • Vitamin D deficiency
  • a flattened occiput
  • prominent forehead
    -significant dental caries,
  • bumpy ribs
  • bowed extremities
313
Q

maternal infection with mumps or rubella virus

A

may produce aqueductal stenosis hydrocephalus

314
Q

Vitamin C deficiency

A
  • irritability
  • low-grade fever
  • swelling
  • tachypnoea
  • and poor appetite
  • impaired wound healing
  • diffuse tenderness, worse in legs
315
Q

Coombs test

A

Direct = autoimmune haemolytic anaemia
Indirect = antibodies in blood to see if there’s reaction to blood transfusion

316
Q

Pseudohematuria

A

beets, blackberries, and rhubarb
chloroquine
metronidazole
phenytoin
rifampinsulfasalazine

317
Q

Galactosemia in children

A
  • galactose-l-phosphate uridyl transferase enzyme deficiency
  • ## serious damage to liver, brain, and eyes after being fed lactose milk
318
Q

Galactosemia in children symptoms

A

-lethargy,
vomiting and diarrhoe,
-hypotonia,
-hepatomegaly
- jaundice (liver failure)
-failure to thrive
- cataracts

319
Q

Galactosemia in children treatment

A
  • elimination
    of lactose-containing milk from the diet
  • exclusion of foods that contain casein, dry milk solids, whey, or curds
320
Q

Prader willi syndrome

A
  • hypotonia, hypogonadism
  • hyperphagia after the newborn period - hypomentia
  • obesity
  • deletion of a
    portion of chromosome 15
  • Feeding difficulties and failure to thrive in 1st year
  • defect in the satiety center in the hypothalamus.
  • Stringent caloric
    restriction is the only known treatment
321
Q

Night terrors

A
  • 5 and 7 years
  • awaken suddenly, appear frightened and unaware of surroundings
  • cannot recall the
    event in the morning
  • Sleepwalking is common
  • reassurance
322
Q

Pseudohypoparathyroidism

A

(Pseudohypoparathyroidism is a condition where the body looks like it has low parathyroid hormone (PTH) effects, but the problem isn’t with the hormone itself—it’s with how the body responds to it.

  1. What is PTH?
    • PTH is a hormone produced by the parathyroid glands that helps regulate calcium levels in the blood by controlling how much calcium is absorbed from the diet, released from bones, or excreted by the kidneys.
  2. What Happens in Pseudohypoparathyroidism?
    • In this condition, the parathyroid glands produce normal (or even higher) levels of PTH, but the body’s tissues are resistant to it. This means that even though there is enough hormone, the body doesn’t respond to it properly.
  3. Resulting Symptoms:
    • Because the body doesn’t respond to PTH, calcium levels in the blood stay low, and phosphorus levels remain high, similar to what happens in true hypoparathyroidism (where there’s an actual deficiency of PTH).
  4. Key Signs and Symptoms:
    • Low Calcium Levels: This can lead to muscle cramps, spasms (tetany), or tingling in the hands, feet, and face.
    • High Phosphorus Levels: This happens because PTH normally helps the body get rid of excess phosphorus, but in this condition, that process doesn’t work correctly.
  5. Why “Pseudo”?
    • The term “pseudo” means false, indicating that the problem isn’t with the hormone production but rather with the body’s response to the hormone.

In pseudohypoparathyroidism, the body can’t properly use the parathyroid hormone, leading to symptoms similar to those of hypoparathyroidism, such as low calcium levels, even though the hormone itself is present in normal or high amounts.

low serum calcium and high serum phosphorus
levels
- high
levels of endogenous parathyroid hormone
short,round-faced, and mildly retarded.
- Metacarpals and metatarsals are shortened
- subcutaneous and basal ganglia -
- calcifications
- cataracts can be present.
- Treatment: large doses of vitamin D and reduction of the
phosphate load.

323
Q

Abetalipoproteinemia in children

A
  • Microsomal triglyceride transfer protein (MTP) gene mutation
  • impaired VLDL formation
  • decreased
    vitamin E delivery to PNS/CNS
    -
  1. What Is It?• “Fat Transport Problem”: Abetalipoproteinemia is essentially a problem with how the body transports and absorbs fats, including important fat-soluble vitamins (A, D, E, K).
    • Gene Involved: It’s caused by mutations in the MTTP gene, which is responsible for producing a protein needed to form lipoproteins (which carry fats in the blood).
324
Q

Duchenne dystroph

A
  • Pseudohypertrophy routinely is limited to the calf muscles
  • lordotic posture as weakness evolves in the hip girdle
    musculature
  • ## waddling gait
325
Q

normal infants show the following

A
  • Coarse, tremulous movements accompanied by ankle
    clonus
  • harlequin color change (a
    transient, longitudinal division of a body into red and pale halves)
    softness of
    parietal bones at the vertex (craniotabes)
    a liver that is palpable down to 2 cm
    below the costal margin
326
Q

adolescent + fever >38.5C + ↑WBC, ESR, CRP + Acute painful, tender and warm joint + limited movement + refusal to bear weight

A

Septic arthritis

327
Q

septic arthritis in children

A
  • S aureus
  • joint aspiration
328
Q

septic arthritis management

A
  • Joint drainage & debridement
  • IV antibiotics
  • orthopaedic surgeon referral
329
Q

Indication for urgent referral in children

A
  • Green vomiting: gangrene of
    the bowel
330
Q

Autosomal dominant

A

Most are affected: males and femailes

331
Q

congenital motor neuron disease in newborn/infant

A

Werdnig-Hoffmann disease
hypotonia, and muscle atrophy
Anterior horn cell
disease

Congenital motor neuron disease in newborns or infants refers to a group of genetic disorders that affect the nerves controlling muscles from birth. These conditions lead to muscle weakness and other serious health problems.

  1. What Are Motor Neurons?
    • Motor neurons are nerve cells in the brain and spinal cord that send signals to muscles, telling them to move. They control voluntary movements like crawling, walking, and even breathing.
  2. What Happens in Congenital Motor Neuron Disease?
    • In these diseases, the motor neurons are either not working properly or are dying off, which means the muscles don’t get the signals they need to move.
    • This leads to muscle weakness, which is noticeable from birth or early infancy.
  3. Common Types:
    • Spinal Muscular Atrophy (SMA): The most well-known congenital motor neuron disease. Babies with SMA have severe muscle weakness and may have difficulty moving, swallowing, and breathing.
    • Other Rare Forms: There are other, rarer types of congenital motor neuron diseases, but SMA is the most common and widely recognized.
  4. Symptoms in Newborns/Infants:
    • Floppy Baby Syndrome: Babies might be very “floppy” or have low muscle tone, which means their muscles are very weak.
    • Delayed Milestones: They may not reach typical milestones like holding up their head, sitting, or crawling at the usual ages.
    • Breathing and Swallowing Problems: Weak muscles can make it hard for the baby to breathe or swallow properly.
  5. Why It’s Serious:
    • These diseases are progressive, meaning they tend to get worse over time.
    • Because muscles control so many important functions (like breathing and swallowing), children with severe forms of these diseases often need special medical care.

Congenital motor neuron disease in newborns or infants is a genetic condition where the nerves controlling muscles don’t work properly from birth. This leads to severe muscle weakness, making it hard for the baby to move, breathe, or swallow. The most common type is Spinal Muscular Atrophy (SMA). Early diagnosis and treatment are crucial to manage symptoms and improve quality of life.

332
Q

Autosomal recessive

A

A few are affected: males and females

333
Q

congenital motor neuron disease in older children

A

Kugelberg-Welander disease
Anterior horn cell
disease
hypotonia, and muscle atrophy

334
Q

X- linked recessive

A

A few are affected: only males

335
Q

Wiskott-Aldrich syndrome

A
  • X-linked recessive
  • Thrombocytopenia
  • Eczema
  • Increased susceptibility to infection
  • bloody diarrhea and easy bruising
  • impaired humoral
    immunity
  • low serum IgM and a normal or slightly low IgG
  • low T cells and lymphocyte
  • Few live past their teens, frequently succumbing to malignancy caused by
    EBV infection.

Wiskott-Aldrich Syndrome (WAS) is a rare genetic disorder that mainly affects boys and impacts the immune system and blood clotting. Here’s a simple explanation:

  1. Immune System Problems:
    • Weak Immune System: Children with WAS have a weak immune system, which makes it hard for them to fight off infections. This means they get sick more often and may have more severe infections than other children.
    • Eczema: Many children with WAS also develop eczema, a skin condition that causes itchy, red, and irritated skin.
  2. Blood Clotting Problems:
    • Low Platelets: Platelets are cells in the blood that help it clot, so when you get a cut, the bleeding stops. In WAS, the body doesn’t produce enough platelets, and the ones it does produce are often too small.
    • Easy Bruising and Bleeding: Because of the low platelet count, children with WAS bruise easily, get nosebleeds, and may have prolonged bleeding even from small cuts.
  3. Autoimmune Issues and Cancer Risk:
    • Autoimmunity: The immune system may mistakenly attack the body’s own tissues, leading to autoimmune diseases.
    • Increased Cancer Risk: Children with WAS have a higher risk of developing certain types of cancer, particularly blood cancers like lymphoma.
  • Genetic Cause: WAS is caused by a mutation in a specific gene (WAS gene) on the X chromosome, which is why it primarily affects boys. The mutation affects the production of a protein needed for proper immune system and platelet function.
  • Managing Symptoms: Treatment often involves managing infections with antibiotics, treating eczema, and sometimes giving platelet transfusions to help with bleeding.
  • Bone Marrow Transplant: The most effective treatment for WAS is a bone marrow transplant, which can help restore a healthy immune system.

Wiskott-Aldrich Syndrome is a genetic disorder that makes it hard for children to fight infections and causes problems with blood clotting. Children with WAS bruise and bleed easily, often have eczema, and are at higher risk for infections and certain cancers. The condition is caused by a gene mutation and is usually treated with supportive care or, in some cases, a bone marrow transplant.

336
Q

Adenosine deaminase (ADA)
deficiency

A
  • Type of severe combined immunodeficiency (SCID)
  • Lymphopenia from birth
  • Platelets are not affected
337
Q

Toxic shock syndrome (TSS) in children

A
  • S aureus
  • “menstrual” TSS (associated with
    intravaginal devices like tampons, diaphragms, and contraceptive sponges)
  • “nonmenstrual” TSS associated with pneumonia
  • skin infection
  • bacteremia
  • osteomyelitis
338
Q

Toxic shock syndrome (TSS) in children treatment

A

Antibiotics against S aureus (penicillin)

339
Q

Epstein-Barr virus (EBV) in children

A

PE:
- diffuse adenopathy
- tonsillar enlargement
- enlarged spleen
- small haemorrhages on the soft palate
- periorbital swelling
Blood:
- predominance of atypical lymphocytes with at least 10%
- heterophil antibodies present (may not be present in young
children)

340
Q

Epstein-Barr virus (EBV) in children management

A
  • Self-limiting symptomatic management
  • avoid contact sports to protect spleen
341
Q

VATER/VACTERL

A

V- vertebral defect,
A- anal atresia,
C- cardiac defects,
TE- tracheoesophageal fistula
-R renal/radial defect
L- limb defects

VATER/VACTERL is a collection of birth defects that often occur together in a baby. It’s not a single condition but rather a group of abnormalities that affect different parts of the body. The name VATER/VACTERL comes from the first letters of the organs or systems that are affected.

  1. What Does VATER/VACTERL Stand For?
    • V: Vertebral defects – Problems with the bones of the spine (vertebrae), which might be missing, shaped differently, or fused together.
    • A: Anorectal malformations – Abnormalities of the anus and rectum, like an imperforate anus (where the anus is missing or blocked).
    • C: Cardiac defects – Heart problems, such as holes in the heart (septal defects) or other structural issues.
    • T: Tracheo-Esophageal fistula – An abnormal connection between the windpipe (trachea) and the food pipe (esophagus), often seen with esophageal atresia (where the esophagus doesn’t develop properly).
    • E: Esophageal atresia – The esophagus is incomplete or blocked, so food can’t pass from the mouth to the stomach properly.
    • R: Renal (kidney) defects – Problems with the kidneys, such as missing or abnormally formed kidneys.
    • L: Limb abnormalities – Issues with the arms or legs, like missing or extra fingers or toes, or bones that are abnormally shaped.
  2. How Does It Affect the Baby?
    • Babies with VATER/VACTERL association might have some or all of these defects. The combination of problems can vary widely from one child to another.
    • For example, a baby might have spine problems, a heart defect, and issues with the kidneys, while another baby might have different combinations of the abnormalities.
  3. Why Is It Important?
    • Because VATER/VACTERL can affect many different parts of the body, babies with these defects often need a team of specialists (like surgeons, cardiologists, and orthopedists) to help manage their care.
    • Early diagnosis is important so that each of the defects can be treated as needed, helping the child lead a healthier life.

VATER/VACTERL is a group of birth defects that can affect the spine, anus, heart, windpipe, esophagus, kidneys, and limbs. The name comes from the initials of the affected areas. Babies with these conditions might have one or more of these problems and often require specialized care to address the different issues.

342
Q

Undescended testes

A

descend into the scrotum during the
first two weeks of life
- the descent is unlikely to take place after the age of 1year
- 20 percent of premature males
- Orchidopexy is best performed by 12-18 month
- 5-10 times greater risk of developing a malignancy

343
Q

Hx of travel to South Asia + fever + dry cough + dull frontal headache + gastroenteritis

A

Salmonella Typhi

344
Q

Salmonella Typhi treatment

A
  • South/South East Asia: azithromycin 1 g (child: 20 mg/kg up to 1 g)
    Not India: ciprofloxacin 500 mg
345
Q

Early onset neonatal sepsis risk factors

A

– Maternal group B streptococcus colonization in current pregnancy.
– A previous baby with GBS infection.

346
Q

Late onset neonatal sepsis risk factors

A

– Artificial ventilation with an endotracheal tube.
– Extreme prematurity.
– Total parenteral nutrition.
- Central catheter

347
Q

Coeliac disease assessment

A

gluten challenge for 4-6 weeks and then should have coeliac serology performed

348
Q

Diabetic ketoacidosis in a young patient

A
  • type 1 diabetes mellitus
  • autoimmune (diseases celiac, autoimmune thyroiditis)
349
Q

HPV contraindications

A
  • egg and yeast allergy
350
Q

strawberry like red mass on cheek

A

infantile haemangioma

351
Q

infantile haemangioma management

A

reassure
-Gradual regress in size

352
Q

< 8 girl + tall + pubic hair & breast development Tanner stage 3 + inappropriate sexual behaviour

A

Precocious puberty

353
Q

Precocious puberty investigation

A
  • serum FSH & LH estradiol
  • MRI
  • Bone age
354
Q

dry eyes and mouth + low urine output + dilated pupils + decreased bowel sounds/constipation + sinus tachycardia + QRS interval
prolongation

A

anticholinergic toxicity (TCA)

355
Q

anticholinergic toxicity (TCA) managment

A

Sodium bicarbonate Sodium bicarbonat

AMC MCQ - You Can Do It!!!!!❤️❤️ (50 decks)

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