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Year 5 > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Typical number of resp infections per year in Young childen

A

6-12 per year with self limiting cough within 1 to 3 weeks

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2
Q

Red flags for cough

A

lasted >8 weeks
Cough since birth
Sudden inset/history of choking
Feeding associated
Severe respiratory illness (previous ICU admission)
Signs of ill health
Clubbing

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3
Q

Polyphonic wheeze indicates…

A

diffuse and variable obstruction in smaller airways

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4
Q

Causes of cough to consider in infant

A

Structural airway abnormalities
Tracheo-esophageal fistula
Vascular ring

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5
Q

Causes of cough to consider in toddlers

A

foreign body, viral induced wheeze

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6
Q

Causes of cough to consider in children

A

asthma, chronic rhinitis

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7
Q

Causes of cough to consider in adolescents

A

asthma, upper airway hyper responsiveness, psychogenic factors, smoking

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8
Q

Asthma prevalence in children

A

About 15-20% but about 50% will have an episode of non asthma wheeze

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9
Q

Wheeze clinical cause and differentials

A

bronchial smooth muscle contraction and airway wall inflammation(asthma and VIW)
Excessive secretions (bronchiolitis)
Airway lumen obstruction (foreign body, endobronchial mass)
Floppy airway wall (tracheomalacia, bronchomalacia)
Extrinsic compression (vascular structures, mediastinal mass)

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10
Q

Examining for wheeze severity

A

wheeze intensity not a good marker of severity
Best measurs:general appearance, WOB and mental State
SpO2 in air, HR, ability to talk
Beware tachycardia as a SE of beta agonists
Silent chest = indicates imminent respiratory collapse

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11
Q

Initial management of wheeze

A

monitor vitals and resp distress
Give O2 if says >92%
High flow, further resp intervention
If possibly anaphylaxis, give adrenaline

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12
Q

Severe asthma attack criteria

A

SpO2 <92%
PEF 33-50% best or predicted
Too breathless to talk or feed
HR > 125 (>5yrs) OR >140 (1-5)
RR >30 breaths per min (>5), >40 (1-5years)
Use of accessory necl muscles

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13
Q

Life threatening asthma attack criteria

A

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

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14
Q

Management of asthma exacerbation/VIW

A

Salbutamol via spacer, up to 10 puffs. Or nebs
Consider steroids (oral or IV)
Involve seniors for IV MgSO4, aninophylline or IV salbutamol

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15
Q

Long terms asthma management strategy

A

Step up approach if continue to be poorly controlled
SABA - short acting beta agonist
+ ICS (low dose inhaled corticosteroid)
+ LTRA (leukotriene receptor agonist)
+ LABA (long acting beta agonist) and stop LTRA if not of use

Then: SABA + switch to MART (maintenance and reliever, includes low dose ICS)
Next: SABA + pediatric moderate dose ICS MART
Then: SABA + EITHER incr dose ICA to high, either as fixed dose regime or as a MART
OR trial of additional drug (eg theophylline)

Management is slightly different in under 5s

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16
Q

Management of bronchiolitis

A

supportive care, NG feeds and IV fluids
Humidified O2 wafting
Worse day typically 4-5 so be aware of progression
Section sometimes used for excessive upper airway secretions

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17
Q

Risks for bronchiolotis

A

age <6 weeks
Prematurity
Underlying health issues

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18
Q

Bronchiolitis cause

A

acute bronchiolar inflammation.
Typically RSV (75-80%)
Most common cause LRTI in under 1s
Higher incidence in winter

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19
Q

Fearures of bronchiolitis

A

coryzal symptoms (incl fever) preceding
Dry cough
Increasing breathlessness
Wheeze, fine inspiratory crackles (sometimez)
Feeding difficulties associated with increasing dyspnoea are often reason for hospital admission

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20
Q

Red flags for immediate admission to hospital with bronchiolitis

A

Apnoeas
Child looks seriously unwell to Healthcare professional
Severe resp distress, eg grunting, marked chest recession, resp rate over 70 breaths /min
Central cyanosis
Persistent O2 says <92% on air
Significant dehydration

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21
Q

Inhaled foreign body features

A

May have classic history
Cough, stridor, dyspnea
CXR abnormality in 80%

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22
Q

inspiratory stridor cause

A

typically extrathoracic airway narrowing

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23
Q

Biphasic stridor cause

A

intrathoracic tracheal narrowing

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24
Q

Causes of stridor in infants

A

Layngomalacia,
Tracheomalacia
Subglottic stenosis
Vascular ring

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25
Q

What is stridor

A

An externally audible, harsh, high pitched monophonic sound heard on inspiration and possibly also expiration

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26
Q

Infective causes of stridor in a child

A

Croup
Epiglottitis
Quinsy
Deep neck space infections
Bacterial tracheitis

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27
Q

Non infective causes of stridor in a child

A

foreign body inhalation
Anaphylaxis
Burns/trauma
Vocal cord fysfunction

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28
Q

Signs of mild airway obstruction

A

Intermittent stridor
Able to speak or cry, may be hoarse
Minimal or no resp distress
Good air entry

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29
Q

Signa of moderate airway obsrtruction

A

tachypnoea
Stridor even at rest
Nasal flaring
Grunting
Paradoxical chest movement
Decreased air entry

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30
Q

Signs of severe airway obstruction

A

hypoxia (late on)
Slow resp rate, or marked tachypnoea
Sniffing/tripod position
Agitated or drowsy
Severe WOB
Markedly reduced or no air movement
Silent gagging or coughing

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31
Q

initial management of acute stridor

A

Do not upset or examine the child. Decompensation of obstruction fan be rapid
Give parent oxygen msdk to hold near child
Nebulised adrenaliine may give temporary relief
IM adrenaline if possible anaphylaxis
Consider oral/IV decamethasone or neb budesonide
Escalate

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32
Q

Features of acute epiglottitis

A

rapid onset
High temp, generally unell
Stridor
Drooling of saliva
Tripod position

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33
Q

CXR difference between acute epiglottitis and crojp

A

Lateral view in acute epiglottitis will show swelling of epiglottis
Posterior anterior view in croup will dhow subglottic narrowing

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34
Q

What is croup

A

respiratory tract infection seen in infants and toddlers.
Laryngeal oedema and secretions lead to strida
Parainfluenza viruses most common cause
Peal 6 months to 3 years

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35
Q

Features of croup

A

stridor
Barking cough (worse at night )
Fever
Coryzal symptoms

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36
Q

Need for admission for croup if

A

frequent barking cough
Easily audible stridor at rest
suprasternal and sternal wall retraction at rest
Any sort of distress
<6 months of ge
Known upper airway abnormalities

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37
Q

Croup management

A

single dose oral dexamethasome (0.15mg/kg) to all children regardless of severity
If bad: High flow O2, nebulised adrenaline

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38
Q

Peritonsillar abscess (quinsy)

A

Typically abscess as complication of bacterial tonsillitis
Features: Severe throat pain lateralising to one side, deviation of uvula to unaffected side, difficulty opening mouth, reduced neck mobility.

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39
Q

Diphtheria pathophysiology

A

caused by gram + Corynebacterium diphtheriae
Releases exotoxin which inhibits pretein synthesis
Typically causes diphtheria membrane on tonsils caused by necrotic mucosal cells

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40
Q

Presentation of diphtheria

A

unvaccinated
Poss recent visit to Eastern Europe/Russia/Asia
Sore throat with grey pseudomembrane on posterior pharyngeal wall
Bulky cervical lymphadenopathy
Neuritis or heart block (secondary things)
Husky voice and brassy cough
Unilateral profuse nasal discharge and crusting

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41
Q

Tetanus pathophysiology

A

caused by exotoxin from Clostridium tetani, preventing release of GABA
features: Prodrome of fever, lethargy, tiredness
Trismus, facial spasms, opisthotonud
Spasms

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42
Q

Pertussis pathhysiolovy

A

caused by Bordatella pertussos Nd around 1000 cased per hear in the UK

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43
Q

Features of pertussis

A

catarrhal phase : Symptoms similar to viral URTI, lasting 1-2 weeks
Paroxysmal phase: Cough increases in sevrity
Bouts of coughing worse at night and after feeding
Inspiratory whoop(not always oresent)
Apnoeic spells
Persistent coughing may cause subconjunctival haemorrhage
Lasts 2-8 weeks
Convalescent phae: Cough subsided over weeks to months.

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44
Q

Management of pertussis

A

Admit if under 6 nonths
Notify PHE
Oral macrolide if cough onset within last 3 weeks
Household contacts get a antibiotic prophylacis
School excludion for 48 hours after starting symptoms, of not vaccinated can’t go back until 72 hours since start of placement

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45
Q

Mumps features

A

spread by droplets, then incubation period 14-21 days
Fever, malaise, muscular pain
Paris swelling
Parotitis (earache or pain on eating) unilaterally initially then bevomes bilateral in 70%
Not had MMR
Generally mild and self limiting

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46
Q

Complications of mumps

A

orchitis - uncommon in prepubertal males, but in around 25-35% of post pubertal. Typically 4-5 days after start of parototis
Hearing loss -usually unilateral and transient
Meningoencephalotis
Pancreatitis

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47
Q

Measles features

A

Caused by RNA paramyxoviris, super infectious
Infective from prodrome until 4 days after rash starts
Incubation period 10-14 days
Prodrome: Irritable, conjunctivitis, fever
Koplok spots: Typifally before rash, white spots (grains of salt) on buccal mucosa
Rash: Starts behind ears then to whole body. Discrete maculopapular rash becoming blotchy and confluent
Diarrhoea in 10% of patients

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48
Q

Management of measles

A

mainly supportive
Admission considered in immunosuppressef or pregnant patients
Inform public health
Immunize non vaccinated contacts within 72 hours

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49
Q

Complications of measles

A

otitis media (common)
Pneumonia
Encephalitis (1-2 week after onset)
Subacute sclerosing panencephalitis (very rare, and may present 5-10years after illness’ but very bad)
Febrile convulsions
Keratoconjunctivitis
Diarrhoea
Incr incidence appendicitis
Myocarditis

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50
Q

Most common cause of gastroenteritis in children in thr UK

A

Rotavirus

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51
Q

Should do a stool culture for gastroenteritis if any of…

A

suspect septicemia
Blood and/or mucus in stool
Child is imminocompromised
Child has recently been abroad
Child has not improved by day 7

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52
Q

Risk factors for congenital heart disease

A

Family history of CHD (1st degree relativr)
Trisomy
Abnormal antenatal cardiac scan
Maternal exposure to viruses during preg
Maternal conditions (DM, epilepsy, SLE, PKU)
Teratogenic drugs during pregnancy (AED, warfarin, diazepam, retinoids for acne, ibuprofen after 30wks geztation)

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53
Q

Possible presentations of congenital heart disease

A

40-50% antenatal diagnosis
Murmur
Cyanosis
Chest pain
Palpitations
Dyspnea
Fatigue (in babies = feeding difficultied)
Recurrent RTI
Faltering growth
Syncope, seizures, brain abscess, myopathy
Fever
Tiredness

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54
Q

Examination with congenital heart diseaese

A

Dysmorphism
Pulse, saturation
Cyanosis And clubbing
Precordial bulge, Apex beat, scars
Auscultstion

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55
Q

Development of clubbing

A

soft tissue growth under nail bed related to megakaryocyte trapping and releasing growth factors
After 6 months hypoxia, and first in thumb

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56
Q

Hallmarks of innocent murmurs

A

aSymptomatic, Soft blowing, Systolic, left Sternal edge. And no thrills or radiation

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57
Q

Incidence of congenital heart disease

A

1/125 live births
1000 newborns leave hospital every year with undetected significant defect

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58
Q

Acyanotic congenital heart disease

A

ventricular septal defects
Atrial septsl defects
Patent ductus arteriosus
Coarctation of the aorta
Aortic valve stenosis

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59
Q

Cyanotic congenital heart disseases

A

Tetralogy of Fallot
Transposition of the great vessels
Tricuspid atresia

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60
Q

Features of atrial septal defects

A

Ejection systolic murmur, foxed splitting of S2
Possible for embolism to pass from venous system to left side of heart causing stroke

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61
Q

Holt Oram Syndrome

A

Autosomal dominant condition assoc w
-abnormalities to bones of hand and arm (inch absence of radius)
-CHD, partic ostium secundum atrio-septal defects, and also VSDs

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62
Q

Investigations for ASD

A

ECG: RBBB with either RAD (ostium secundum) or LAD (ostium primum)
CXR: Cardiomegsly, enlarged pulmonary arteries

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63
Q

Aetiology of VSDs

A

most common cause of congenital heart disease. Close spontaneously in about 50%
Associated with chromosomal disorders, eg Down’s, Edward’s, Patau, cri-du-chat syndrome
And also congenital infections

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64
Q

Murmur in VSD

A

classically pansystolic murmur which is louder in smaller defects. Left lower sternal border

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65
Q

Murmur in PDA

A

Medium pitch, high grade continpus ‘machinery’ murmur

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66
Q

Patent foramen ovale murmur

A

faint systolic murmur

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67
Q

TOF murmur

A

ejection systolic murmur loudest at pulmonary area (as due to pulmonary stenosis)

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68
Q

Complications of VSD

A

Aortic regurgitation
Infective endocarditis
Eisenmenger’s complex
right heart failure
Pulmonary hypertension (such that pregnancy is contraindicated)

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69
Q

Eisenmenger’s complex

A

prolonged pulmonary hypertension from left to right shunt results in right ventricular hypertrophy and incr right ventricular pressure. Eventually exceeds left ventricular pressure leading to reversal of blood flow
Get cyanosis and clubbing
Indication for heart and lung transplant

70
Q

Patent ductus arteriosus pathophysiology

A

Duct between pulmonary artery and aorta
usually closes with first breaths due to increased pulmonary flow which enhances prostaglandins clearance
Patency more common in premarure babies, born at high altitude or maternal rubella in first trimester

71
Q

Features of PDA

A

Left subclavicular thrill
Continuous machinery murmur
Large volume, bounding, collapsing pulse
Wide pulse pressure
Heaving apex beat

72
Q

Management of PDA

A

Indomethacin or ibuprofen: Given to neonate, inhibits prostaglandin synthesis, closes in majority f cases
If assoc w another congentical heart defect amenable to surgery then useful to keel OPEN with prostaglanding E1 until after repair

73
Q

Atrioventricular septal defect (AVSD) fearures

A

Loud S1 and S2, pansystoloc murmur of left AV valve regurg, ejection systolic murmur in pulmonary area

74
Q

Noonan Syndrome

A

Autosomal dominant condition associated with normal karyotype, but defect in gene on chromosome 4.
SIM fearures to Turner’s, eg webbed neck, widely spaced nipples, short stature, pectus carinatum and excavatum
+ pulmonary valve stenosis
Ptosis
Triangular shaped face
Low set ears
Factor XI deficiency

75
Q

Presentation of coarctation of aorta

A

Neonates can present w acute circulatory collapse when duct shuts
Less severe forms then hypertension in Young patients or intermittent vlaudicatioon in exercise

76
Q

Hypertension in Young patient think…

A

could this be aortic coarctation??

77
Q

Features of aortic coarctation

A

pulse: Absent femoral or weak femorals with brachionfemoral delay
BP high in arms and low in legs
Legs desaturated
May or may not have a murmur, but if moderate than can have ejection systolic murmur on left sternal edge.

78
Q

Turner’s synfro,e

A

Presence of only one X chromosome, or deletion of short arm of one of the X chromosomes
features:
Short stature
Shield chest with widely spaced nipples
Webbed neck
Bicuspid aortic valve 15% and coarctation aorta 5-10%
Primary amenorrhoea
High arched palate
Short fourth metacarpal
Multiple pigmented naevi
Lymphodoema partic of feet in neonates
Often hypothyroidism

79
Q

Transposition of the great arteries

A

aorta leaves right ventricle and pulmonary trunk leaves left ventricle
Feat: Cyanosis, tachypnoea, loud single s2, prominent right ventricular impulse, egg on side appearance on CXR
Need surgical correction and meantime maintain ductus arteriorsus with prostaglandins.

80
Q

Tetralogy of Fallot Four things

A

Ventricular septal defect
Right ventricular hypertrophy
Pulmonary stenosis
Overriding aorta
Typically presents st 1-2 months

81
Q

Features of TOF

A

Cyanosis. And periods of hypercyanosis (‘tet’ spells) due to near occlusion of right ventricular outflowr tract
During this then have tachypnoea and poss LOC if infant is upset, in pain or has fever
Ejection systolic murmur due to pulmonary stenosis
CXR boot shaped heart
ECG RV hypertrophy

82
Q

Marfan syndrome pathophys

A

Autoxomal dominant caused by defect in thr FBN1 gene which encodes for fibrillin-1, which is a connective tissue protein. Approx 1/3000

83
Q

Fearures of Marfan syndrome

A

Tall stature with arm span to heigh ratio >1.05
High arched palate
Arachnodactyly
pectus excavatum
Pes planus
Scoliosis
Heart: Dilation of aortic sinuses, may lead to aortic aneurysms, dissection, regurg. 75% have mitral valve prolapse
Lungs: Repeated pneumothoraces
Eyes: Upward lens dislocation, blue sclera, myopia
Dural ectssia
Life expectancy 40-50yrs due to cardiac issues

84
Q

Cystic fibrosis pathophys

A

autosomaL recessive disorder due to defect in CFTR gene which encodes a cAMP regulated chloride channel. Increased viscosity of secretions.
In the UK, 80% of CF cases are due to delta F508 on long arm of chromoosome 7. Affects 1/2500 births.

85
Q

Features of cystic fibrosis

A

prwsenting:
Neonate: Meconium ileus, prolonged jaundice
Recurrent chest infections
Malabsorption, failure to thrive
5% diagnosed much later
Also: Short stature, diabetes mellitus, delayed puberty, rectal prolapse, nasal polyps, male infertility.

86
Q

Fragile X syndrome

A

Trinucleotide repeat disorder
Features in M: Learning difficulties
Large low set ears, long thing face, high arched palate
Macroirchidism
Hypotonia
Autism more common
Mitral valve prolaps

Features in females normally normal to mild
Diagnosis: Vis CVS or amnio, analysis of CGG repeats

87
Q

Features of Down’s synfrome

A

up slanting palpebral fissures
Epicanthic folds
Brushfield spots in iris
Protruding tongue
Small low set ears
Rojnd/Flat face
Flat occiput
Single Palmar crease
Sandal gap between toe 1 and 2
Hypotonia
40-50% congenital heart defects
Duodenal atresia
Hirschsprung’s disease

88
Q

Later complications of Down’s syndrome

A

Infertility in M, and subfertility in F with incr problems pregnancy and labour
Learning difficulties
Short stature
Repeated resp infections
ALL
hypothyroidism
Alzheimer’s disease
Atlantoaxial instability

89
Q

Trisomy 18=

A

Edward syndrome

90
Q

Trisomy 13=

A

Patau syndrome

91
Q

DiGeorge ssyndrome

A

22qq11 deletion
Characteristic face
Heart defect
Cleft palate
decr T cells /hypoplastic thymus
Hypocalcaemia
Renal anomalies
Incr risk psychiatric illness

92
Q

Williams syndrome

A

7q11 deletion
Characteristic face: Periorbital fullness, full cheeks and lips, wide mouth, bulbous nasal tip, long smooth philtrum
Short stature
Sloping shoulders
Mild to mod learning difficulties
Cocktails party manner
Supravalvukar aortic stenosis in 50%

93
Q

Crouzon syndrome

A

Premature fusion of the cranial sutures
Autosomal domiman
Craniosynostosis-» frontal bossing, hypertelorism, proptosis, maxillary hypoplasia
Normal intelligence
Complications:raised ICP, conductive hearing loss

94
Q

Prader Willi Syndrome

A

absence of PATERNAL 15q11-13
Feat: hypotonia during infancy
Dysmorphic fearures
Short stature
Hypogonadism and infertility
Learning difficulties
Childhood obesity
Mamagememt: Growth hormone, dietary management

95
Q

Angelman syndrome

A

Absence of MATERNAL 15q11-13
Severe learning difficulties
Delayed development
“happy puppet” movements
Microbrachycephaly
Often seizures

96
Q

Cephalohaematoma

A

swelling on newborn head (a few hours after birth), typically due to bleeding between periosteum and skull
Most commonly in parietal region doesnt cross suture lines
jaundice may develop as complication.
Tales up to three months to resolve

97
Q

Caput succedaneum

A

present at birth
Oedema of the scalp at the presenting part, due to mechanical trahmz of scalp pushing through cervix in prolonged delivery or following ventouse
Typically forms over vertex and crosses suture lines
Managed conservatively

98
Q

Cystic fibrosis drug

A

Lumacaftor/ivacaftor = new drug if homozygous for delta F508 mutation
Increases number or pltentiates CFTR at cell surface

99
Q

Management of CF

A

regular chest Physio and postural drainage
High calorie diet incl high fat intake
Minimize contact with other CF patients to prevent cross infection eg with pseudomonas
Vitamin supplementation
Pancreatic enzyme supplements (creon) taken with meals
lung transplant

100
Q

Risks for developmental dysplasia of hip

A

female sex (6x incr)
Breech presentation
Positive FH
Firstborn child
Oligohydramnios
Big baby

Slightly more common in left hip

101
Q

Barlow test

A

attempt to dislocate an articulated femoral head
Flex and adduct hips, then apply light pressure to the knee and direct force posteriorly

102
Q

Ortolani test

A

attempts to relocate a dislocated femoral head
Flex hips and knees at 90 degrees, and then abduct out of Barlow’s relocating femoral head back into acetabulum with an audible clunk

103
Q

Managing unstable hips

A

Most spontaneously stabilize by 3-6 weeks
Pavlik harness if younger than 4-5 months
Once older, may require surgery.

104
Q

Adult height prediction calculation (M)

A

(Father height+mother height +13)/2

105
Q

Adult height prediction calculation (F)

A

(Father height + mother height - 13)/2

106
Q

features of familial short stature

A

unremarkable history
NormL examination
Normal height velocity
Within parental target range

107
Q

Constitutional delay of growth and puberty features

A

short stature during later childhood
Height drops below parental target range
Reduced height velocity in later childhood, but not in puberty
Delayed bone age

108
Q

Tanner stages

A

Measure stage of puberty for M and F.
Genitalia, breast and pubic hair rated independently
Genitalia and breast from 1 to 5 (adult)
Testicular volume measured using an orchidometer

109
Q

normal testicle sizes through puberty

A

3ml = prepubertal (stage 1)
10ml = stage 3
25ml = mature adult size (stage 5)

110
Q

Delayed puberty with short stature

A

Turner’s syndrome
Prader Willi Syndrome
Noonan’s syndrome

111
Q

Delayed puberty with normal stature

A

PCOS
Androgen insensitbity
Kallman’s syndrome
Klinefelter’s syndrome

112
Q

Low gonadotrophins cause of delayed puberty

A

chronic disease
Malnutrition/eating disorder

113
Q

ICD definition of learning disability/disorders of intellectual development

A

a group of aetiologically diverse conditions
originating in the developmental period
Characterized by significantly below average intellectual functioning (>2 SD below the mean =2.3rd percentile)
And adaptive behaviour (daily living skills)

114
Q

Triad of symptoms in autism

A

Social interaction and social communication
Restricted interests and repetitive behaviours
Sensory sensitivities

115
Q

Risk factors for Autism

A

sibling with ASD
Older parents
Genetic conditions (Downs syndrome, fragile X, Rett syndrome)
Prematurity
Low birth weight

116
Q

Possible alterations in development in preverbal child with autism

A

Avoidant/brief gaze rather than reciprocal
No social smile
Not aware of where adult is looking
Odd sounds/unusual tone not expressive
No babble, odd prosody
Not responding to name
Reduced gestures, not integrated
Reduced copying/shared enjoyment
Plays independently
Repetitive okay with narrow unusual interests

117
Q

Possible alterations in development in verbal child with autism

A

plays independently/conyrols
Limited interaction
Ignores questions
No initiation of conversation/favourite subjects
Difficult to make verbal choices
No sharing enjoyment
Less able to offer comfort
Limited repetitive odd interests, lining up
Difficulties with change

118
Q

Comorbidities with autism

A

very common, 70% at least one
Delayed language
Learning problems, specific ore genzl
Coordination difficulty
ADHD
epilepsy
Tics/tourettes
ARFID
constipation/disrrhoea
Mood disorders
Sleep difficulty

119
Q

Supporting children with autism

A

Support parents
Support Childs behaviour/communicarion - modifications, speech and language, picture communication, specific approaches
Support/change environment
Address comorbidities

120
Q

ADHD triad of impaired symptoms

A

attention and concentration
Impulsivity
Huperactivity

121
Q

Risk factors for ADHD

A

genetic (strongly 70% heritability)
Any neurobiological abnormality
Alcohol and tobacco
Low birth weight and prematurity
Psychosocial adversity
Institutional care
Genetic conditions dg fragile x
TBI

122
Q

Problems assoc w ADHD

A

Sleep issues
Disruptive behaviour disorder
Mood disorder
Learning difficulty
Fine/gross motor coordination difficulties
Executive funvtion/planning and organizing issues
Tics/tourettes

123
Q

Management of ADHD

A

non pharmacological: Psychoeducation, behaviour therapy, sleep/exercise/routine, school accommodation
Pharmacological: Sleep/stimulants eg methylphenidate
Treat comorbidity eg anxiety

124
Q

Management of ADHD

A

non pharmacological: Psychoeducation, behaviour therapy, sleep/exercise/routine, school accommodation
Pharmacological: Sleep/stimulants eg methylphenidate
Treat comorbidity eg anxiety

125
Q

Incidence of cerebral palsy

A

2/1000 live births
ssociated with gestation <28 weeks
Birth weight <1500g

126
Q

Aetiology of cerebral palsy

A

Any brain injury before 2 years
Prenatal: Abnormality brain development, structural, vascular, genetic, infection (80%)
Postnatsl: Hypoxic ischemic encephalopathy (10%) or other

127
Q

Early warning signs of cerebral palsy

A

Floppy baby (neonate)
Incr muscle home in older children, reflexes may be brisk
Feeding difficulties - due to poor coordination, eg slow feeding, vomiting, gagging/weight gain
Delayed motor milestones
Asymmetric hand movement
Persistence of primitive reflex eg stepping reflex/Moro

128
Q

Hb range in neonate

A

137-200g/L

129
Q

Hb range in 3 month baby

A

95-145g/L

130
Q

Hb range from 1.5-6yrs

A

105-140g/L

131
Q

Hb range in 7-12yrs

A

110-140g/L

132
Q

Symptoms of anaemia in infants

A

tiring easily
Slow feeding
Maybe pallor, but partic pale conjunctiva/tongue/palmar creases
‘Pica’ - which is inappropriate eating of non food materials eg soil, chalk, gravel

133
Q

80% childhood leukaemias caused by…

A

acute lymphoblastic leukaemia

134
Q

Features of ALL

A

Anaemia: Lethargy and pallor
Neutropaenia: Frequent or severe infections
Thrombocytopenia: Easy bruising, petechiae
Bone pain
Splenomegaly
Hepatomegaly
Fever in 50% of new cases
testicular swelling

135
Q

Poor prognostic factors for ALL

A

age <2 or >10 years
WBC >20 at diagnosis
T or B cell surface markers
Non Caucazian
Male sex

136
Q

Iron deficiency anaemia in children

A

common in infants and toddlers
Usually dietary cause (partic cows milk has v know iron)
High iron requirements for growth, nutrition and body store
Easily avoided if weaned at 6 months onto mixed diet
Hypochromic microcytic anaemia with low serum ferritin
Treat with dietary advice and oral iron

137
Q

Red cell aplasia features

A

low reticulocyte count despite low Hb
Normal bilirubin =not bleeding
Negative direct antiglobulin test (Coombs)
Absent red cell precursors on bone marrow exam

138
Q

Causes of red cell aplasia

A

Congenital red cell aplasia (Diamond-Blackfan) - very serious and presents at 2-3 months
Transient erythroblastopenia of childhood - triggered by viral infection and recovering within a few weeks
Parvovirus B19 infection - if they have an inherited haemolytic anaemia. Not in healthy children.

139
Q

Hereditary spherocytosis

A

Autosomal dominant, but 25% have no FHx
Often early severe jaundice in newborn infants
Often asymptomatic but may cause anaemia, jaundice, splenomegaly, aplastic crisis and gallstones
Usually diagnose on film
Treat with folic acid, splenectomy if symptomatic

140
Q

Beta thalassaemia major

A

mutation of beta globin gene ->cannot produce HbA
Clinical feat: Severe anaemia, faltering growth, heoatosplemomegaly
Fatal without regular blood transfusion, which goes with iron chelation to minimise iron overload

141
Q

G6PD deficiency

A

especially people of Mediterranean, middle East, far east and Central African ethnicity
X linked so predominantly males
May present with neonatal jaundice
Acute intermittent haemolysis precipitated by: Infection, some drugs, fava beans (broad), naphthalene in mothballs
Parents should be given list of things to avoid

142
Q

Haemophilia A factor deficiency

A

factor 8 deficiency

143
Q

Haemophilia B factor defocoency

A

Factor 9 deficiency

144
Q

Features of von Willebrand dizease

A

Bruising
Excessive prolonged bleeding after surgery
Mucosal bleeding eg epipstaxia and menorrhagia
Bleeding into soft tissue eg large haematomas and haemarthroses are uncommon

145
Q

Treatment of vonWillebrand disease

A

if mild with DDAVP
If severe with plasma derived factor 8 concentrate
Avoid IM injections, aspirin, NSAIDs

146
Q

Acquired disorders of coagulation

A

Vitamin k deficiency
Liver disease
ITP
DIC

147
Q

Clinical feat of ITP

A

between 2-10yars typically
1-2 weeks following a viral illness or vaccination
Possibly bruising, petechiae and it purpura
Profuse bleeding uncommon even tho platelet count mat be below 10
Self limiting and benign in 80%, remitting spontaneously after about 6-8weeks
Important to disringuidb from ALL and aplastic anaemia, so needs FBC and film

148
Q

Treatment of ITP

A

Not needed unless platelets really low or bf complication eg intracranial bleed
Oral pred or IVIG
Platelet transfusions only if life threatening

149
Q

Red flags for development

A

loss of developmental skills at any age
concerns about vision
Hearing loss at any age
Persistently low muscle tone or floppiness
No speech at 18mo esp if no other attempt to communicated
Asymmetry of movements
Persistent toe walking
Head circumference above 99.6th centile or below 0.4th.

150
Q

factors increasing risk of preterm labour

A

multiple pregnancies
Asymptomatic intrauterine infection
Preterm rupture of membranes age <17/>35
Low or high BMI
Lower socioeconomic status
Smoking, alcohol and substance misuse
Cervical incompetence (previous terminations, later miscarriages, surgery on cervix)
Uterine abnormalities

151
Q

Glucocorticoids for preterm babies

A

IM betamethasone or dexamethasone prior to delivery reduces incidence of lots of complications
Two doses given 12 hours apart
Tocolyrics often used to allow time for steroids

152
Q

pathophysiology of respiratory distress syndrome

A

Lack of endogenous surfactant
Distal alveoli collapse (atelectasis)
Decreased functional residual capacity
Require higher ooenning pressure then damaging lining of endothelial and epithelial cells
Protein exudate then layed down in alveoli (hyaline membranes)
Plus cytokine inflammatory response

153
Q

Symptoms of respiratory distress syndrome

A

Tachypnoea
Grunting (from partial closure of glottis to maintain own PEEP)
Recession (intercostal, subcostal, tracheal tug)
Head bobbing
Nasal flaring
Cyanosis
Apnoea

154
Q

Management of respiratory distress synfrome

A

CPAP
Surfactant as per current rescue guideline
Lie prone, minimal handling
Trophic feeds (full stomach pushes up on stomach-))
May need intubation and ventilation
Risk of spontaneous pneumothorax

155
Q

Intraventricular haemorrhage in the premature baby

A

fragile and vascular choiroid plexus at risk of rupture into the ventricular system. Most common in first 3 days, and uncommon after 1 week.

156
Q

Factors increasing risk of intraventricular haemorrhage

A

extreme prematurity
Vascular instability
Pneumothorax
Oscillatons on pCO2, BP, intravascular volume

157
Q

Factors increasing risk of necrotising enterocolitis

A

low gestation, esp birth weight <1000g
IUGR esp with abnormal flow antenatally in umbilical cessels
Compromised gut perfusion eg twin twin transfusion, IUGR, critically ill, large PDA
Feeding: Formula feeds, hypertonic feeds, withholding feeds?
Infection: Bacterial flora, empirical antibiotics
RARE in term babies

158
Q

Triad of necrotising enterocolitis

A

loss of mucosal integrity, milk feeds, bacteria

159
Q

Symptoms of necrotosing enterocolitis

A

quiet, feeding intolerance
Abdo distension
Bloody stools
Rapid progression to: Abdominal discolouration, intestinal perforation and peritonitis, systemic hypotension

160
Q

AXR of necrotosing enterocolitis

A

dilated bowel loops
Paucity of gas
A fixed loop filled with gas
Pneumatosis intestinalis (pathognomic)
Portal venous gas
Pneumoperitoneum

161
Q

Management of necrotising enterocolitis

A

supportive: NBM, TPN, antibiotics for 10-14 days
Early intubation, volume and inotropic support
In aggressive cases need laparotomy and resection of necrotic bowel

162
Q

Chronic lung disease in prems

A

either O2 requirement >28 days of life, or >36 weeks corrected gestation
Baso fragile and underdeveloped preterm lungs can easily become damaged, inflamed and scarred.
Basically really want to avoid this by managing preventable risks and ensure adequate nutrition

163
Q

Risks for chronic lung disease

A

extreme preterm esp <26 weeks
Ventilator induced injury
Hiigh oxygen requirements
Chorioamnionitis
Sepsis including NEC
Pulmonary haemorrhage

164
Q

Perinatal asphyxia causes

A

altered placental perfusion, eg maternal hypotension
Altered placental gas exchange eg insufficiency
Cord accident (compression, prolapse)
Delayed delivery

165
Q

Pathophysiology of hypoxic ischemic encephalopathy

A

Insult leads to primary energy failure within minutes, immediate necrotic cell death
Cerebral metabolism then transiently recovers, Nd then 6-72hours post insult then secondary phase of apoptotic cell death -> hypoxic ischemic brain injury

166
Q

Therapeutic cooling

A

used for moderate and severe hypoxic ischemic encephalopathy, specific requrenenrs eg Agpar <5 at birth, continued need for rescue, acidosis within hour or high base deficit

167
Q

Managing HIE

A

Ventilate as required, not allowing pCO2 to drop low
Maintain cerebral perfusion by maintaining BP w inotropes if necessary
Fluid: Restrict and maintain neutral balance, incr glucose concentration ro maintain blood level
Anticipate and look for multi organ involvement

168
Q

Symptoms of paracetamol poisoning

A

early abdominal pain and vomiting
12-24h later: Liver failuee

169
Q

Treatment of paracetamol poisoning

A

risk assess by measuring plasma paracetamol concentration
IV acetylcysteine if concentration high or liger function abnormal

170
Q

Button battery inhestion

A

can form electrical circuits leading to corrosion of guy wall
Abdominal pain followed by gut perforation and stricture formation
X ray chest and abdo to confirm ingestion
Endoscopic removal if in oesophagus, fails to pass or symptoms

Year 5 (11 decks)

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