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MY REVISION - ALL TO DO > TO DO PAEDS PART 1 > Flashcards

TO DO PAEDS PART 1 Flashcards

1
Q

FOETAL CIRCULATION
What is the flow of foetal blood?

A
  • Oxygenated + nutrients at placenta for rest of body (umbilical vein) + disposes waste like CO2 + lactate (umbilical artery)
  • Umbilical vein > ductus venosus > RA > foramen ovale > LA > LV > rest of body > umbilical artery
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2
Q

FOETAL CIRCULATION
What are physiological (innocent flow) murmurs?

A

4S’s –
- Soft blowing murmur
- Symptomless
- left Sternal edge
- Systolic murmur only

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3
Q

FOETAL CIRCULATION
What are the main cyanotic heart diseases?

A

4Ts –
- ToF
- TGA
- Tricuspid atresia
- Truncus arteriosus
(Complete AVSD too)

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4
Q

ATRIAL SEPTAL DEFECT
What signs would you find on clinical examination in ASD?

A
  • Fixed + widely split S2 (split does not change with inspiration/expiration)
  • ES murmur at upper L sternal edge (pulmonary) as increased flow across pulmonary valve by L>R shunt
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5
Q

VSD
What are the features of the pansystolic murmur in VSD?

A
  • Left lower sternal edge
  • Loud murmur = smaller VSD (larger = quieter)
  • May have systolic thrill on palpation
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6
Q

PDA
What are the signs of PDA?

A
  • Collapsing or bounding pulse as increased pulse pressure
  • Continuous ‘machinery’ murmur heard loudest beneath the L clavicle
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7
Q

PDA
What is the management of PDA?

A
  • Monitor until 1y with ECHOs (treat early if Sx or heart failure)
  • NSAIDs (indomethacin) facilitates closure of PDA as inhibits prostaglandins
  • After 1y unlikely to resolve so trans-catheter or surgical closure to reduce IE risk
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8
Q

TOF
What abnormalities are described in tetralogy of fallot (TOF)?

A
  • Large VSD
  • Pulmonary stenosis (RV outflow obstruction)
  • RVH
  • Overriding aorta
    (If ASD present too = pentad of Fallot)
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9
Q

TOF
What is the management of a hyper-cyanotic tet spell in TOF?

A
  • Morphine for sedation + pain relief
  • IV propranolol as peripheral vasoconstrictor
  • IV fluids, sodium bicarbonate if acidotic
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10
Q

TOF
What is the management of TOF?

A
  • Neonates = prostaglandin infusion to maintain ductus arteriosus to allow blood to flow from aorta > pulmonary arteries
  • Early surgical repair with closure of VSD + correction of pulmonary stenosis at 6m
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11
Q

TGA
What are the investigations for TGA?

A
  • May be Dx antenatally, pre (R arm) + post duct (foot) sats
  • CXR may show narrow mediastinum with ‘egg on its side’ appearance
  • ECHO confirms Dx
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12
Q

TGA
What is the management of TGA?

A
  • Neonates = prostaglandin E1 infusion to maintain ductus arteriosus
  • Balloon atrial septostomy to create hole between 2 atria for mixing
  • Arterial switch procedure = open heart surgery, definitive Mx
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13
Q

COARCTATION OF AORTA
What is the clinical presentation of coarctation of aorta?
How may it present if severe?

A
  • Weak femoral pulses + radiofemoral delay
  • Systolic murmur between scapulas or below L clavicle
  • Heart failure, tachypnoea, poor feeding, floppy
  • LV heave (LVH)
  • Acute circulatory collapse at 2d as duct closes (duct dependent)
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14
Q

COARCTATION OF AORTA
What are the investigations for coarctation of the aorta?

A
  • 4 limb BP (R arm > L arm), pre + post-duct sats
  • CXR may show cardiomegaly + rib notching (often teens + adults)
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15
Q

COARCTATION OF AORTA
What is the management of coarctation of aorta?

A
  • ABCDE if collapse
  • Prostaglandin E1 infusion if critical
  • Stent insertion or surgical repair
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16
Q

EBSTEIN’S ANOMALY
What is Ebstein’s anomaly associated with?

A
  • Wolff-Parkinson-White syndrome + lithium in pregnancy
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17
Q

EBSTEIN’S ANOMALY
What is the clinical presentation of Ebstein’s anomaly?

A
  • Evidence of heart failure
  • SOB, tachypnoea, poor feeding, collapse or cardiac arrest
  • Gallop rhythm with S3 + S4
  • Cyanosis few days after birth if ASD when ductus arteriosus closes
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18
Q

EBSTEIN’S ANOMALY
What are the investigations for Ebstein’s anomaly?

A
  • ECG = arrhythmias, RA enlargement (P pulmonale), LAD + RBBB
  • CXR = cardiomegaly + RA enlargement
  • ECHO diagnostic
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19
Q

AORTIC STENOSIS
What is the normal clinical presentation of aortic stenosis?

A
  • Most asymptomatic with ejection-systolic murmur at upper right sternal edge (aortic area) radiating to neck (carotid thrill)
  • Ejection click before murmur
  • Palpable systolic thrill
  • Slow rising pulses + narrow pulse pressure
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20
Q

PULMONARY STENOSIS
What is the clinical presentation of pulmonary stenosis?

A
  • Ejection systolic murmur at upper left sternal edge with ejection click
  • ?RV heave due to RVH
  • Critical PS = duct-dependent pulmonary circulation so cyanosis in first few days of life
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21
Q

RHEUMATIC FEVER
How is rheumatic fever diagnosed?

A

Jones criteria –
- Evidence of recent strep infection plus 2 major or 1 major + 2 minor criteria

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22
Q

RHEUMATIC FEVER
What are the major criteria in rheumatic fever?

A

JONES –

  • Joint arthritis (migratory as affects different joints at different times)
  • Organ inflammation (pancarditis > pericardial friction rub)
  • Nodules (subcut over extensor surfaces)
  • Erythema marginatum rash (pink rings of varying sizes on torso + proximal limbs)
  • Sydenham chorea
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23
Q

RHEUMATIC FEVER
What are the minor criteria in rheumatic fever?

A

FEAR –

  • Fever
  • ECG changes (prolonged PR interval) without carditis
  • Arthralgia without arthritis
  • Raised CRP/ESR
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24
Q

RHEUMATIC FEVER
What are the investigations for rheumatic fever

A
  • Throat swab for MC&S
  • Anti-streptococcal antibodies (ASO) titres = anti-DNase B +ve indicates strep infection (repeat after 2w to check if negative)
  • Echo, ECG + CXR to check cardiac involvement
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25
Q

RHEUMATIC FEVER
What is the management of rheumatic fever?

A
  • Prevention by treating strep infections with 10d phenoxymethylpenicillin
  • Specialist Mx (NSAIDs for joint pain, aspirin + steroids for carditis)
  • Prophylactic 1/12 IM benzathine penicillin most effective to prevent recurrence (if not daily PO penicillin)
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26
Q

PDA
What are some risk factors of PDA?

A

Prematurity is key + association with maternal rubella

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27
Q

HEART FAILURE
What are the causes of heart failure in infants?

A

High pulmonary blood flow (VSD, AVSD, large PDA)

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28
Q

TOF
What are some risk factors?

A
  • Rubella,
  • maternal age >40,
  • alcohol in pregnancy,
  • maternal DM
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29
Q

TGA
What is it associated with?

A

Duct dependent lesion, associated with PDA, ASD + VSD

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30
Q

TRICUSPID ATRESIA
How is it managed?

A

Shunt between subclavian + pulmonary artery with surgery later

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31
Q

CROUP
What are the investigations for croup?

A
  • Clinical but if CXR done PA view shows subglottic narrowing (steeple sign)
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32
Q

CROUP
What is the management of croup?

A
  • PO dexamethasone 0.15mg/kg 1st line, can repeat at 12h
  • Nebulised budesonide (steroid)
  • High flow oxygen + nebulised adrenaline (more severe/emergency cases)
  • Monitor closely with anaesthetist + ENT input, intubation rare
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33
Q

ACUTE EPIGLOTTITIS
What is the investigation for acute epiglottitis?

A
  • Clinical Dx but if CXR done lateral view show epiglottis swelling = thumb sign
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34
Q

ACUTE EPIGLOTTITIS
What is the management of epiglottitis?

A
  • Prevention HiB vaccine, rifampicin prophylaxis for close household contacts
  • Do NOT examine throat, anaethetist, paeds + ENT surgeon input
  • Intubation if severe, may need tracheostomy
  • IV ceftriaxone + dexamethasone given once airway secured
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35
Q

BRONCHIOLITIS
What are some criteria for admission?

A
  • Apnoea
  • Severe resp distress (RR>60, marked chest recession, grunting)
  • Central cyanosis
  • SpO2 < 92%
  • Dehydration
  • 50–75% usual intake
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36
Q

PNEUMONIA
What is the management of pneumonia?

A
  • Newborns = IV broad-spec Abx (amoxicillin)
  • Older = PO amoxicillin with broad-spectrum Abx (co-amoxiclav) if unresponsive or influenza
  • Macrolides (erythromycin) to cover for mycoplasma, chlamydia or if unresponsive
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37
Q

ASTHMA
What is the purpose of spirometry?

A
  • Obstructive pattern = FEV1 <80%, FEV1/FVC < 70%
  • Bronchodilator responsiveness = FEV1 ≥12% improvement
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38
Q

ASTHMA
What is the stepwise management of chronic asthma in <5y?

A
  1. SABA + low dose ICS (trial for 8-12 weeks)

IF SYMPTOMS RESOLVE
2. stop SABA + low dose ICS for 3 months
3. if symptoms recur restart SABA + low-dose ICS and titrate up to moderate dose ICS as needed
4. consider further trial without treatment
5. SABA + moderate dose ICS + LTRA
6 stop LTRA + refer to specialist

IF SYMPTOMS DO NOT RESOLVE
2. check inhaler adherence, review if alternative diagnosis is likely
3. refer to specialist

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39
Q

ASTHMA
What is the stepwise management of chronic asthma 5-12yrs?

A
  1. SABA + ICS
  2. decide whether MART pathway or conventional pathway is more suitable

MART PATHWAY
3. SABA + low dose MART
4. SABA + moderate dose MART
5. refer to specialist

CONVENTIONAL PATHWAY
3. SABA + ICS + LTRA (trial for 8-12 weeks)
4. SABA + low dose ICS/LABA (+/- LTRA)
5. SABA + moderate dose ICS/LABA (+/- LTRA)

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40
Q

ASTHMA
What are some reasons for failure to respond to treatment for asthma?

A

ABCDE –
- Adherence (#1)
- Bad disease (dose inadequate for severity)
- Choice of drug/device (different pts respond differently)
- Diagnosis (?correct)
- Environment (?trigger)

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41
Q

ASTHMA
What is classed as a severe asthma exacerbation?

A
  • PEFR 33–50% predicted
  • Unable to complete full sentences
  • RR>50 (2-5y), or >30 (>5y)
  • HR >130 (2-5y) or >120 (>5y)
  • Signs of resp distress (chest recessions)
  • SpO2 <92%
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42
Q

ASTHMA
What is classed as a life-threatening asthma exacerbation?

A
  • PEFR 33% predicted
  • Exhaustion/cyanosis
  • Poor respiratory effort
  • Altered consciousness, hypotension
  • Silent chest (airways so tight no air entry)
  • SpO2 <92%
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43
Q

ASTHMA
What is the management of severe exacerbations of asthma?

A

stepwise approach:
1. salbutamol inhalers via spacer with 10 puff every 2 hrs
2. nebulisers with salbutamol/ipratropium bromide
3. oral prednisolone (for 3 days)
4. IV hydrocortisone
5. IV magnesium sulphate
6. IV salbutamol
7. IV aminophylline
8. call ICU

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44
Q

CROUP
What are the causes?

A
  • Parainfluenza viruses (#1), less so RSV, metapneumovirus, influenza
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45
Q

CROUP
When would you admit a patient to hospital?

A
  • Mod-severe croup,
  • <3m old
  • upper airway issues (laryngomalacia)
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46
Q

CROUP
How do you assess croup severity?

A

Westley score for severity
(chest wall retractions, stridor, cyanosis, air entry + consciousness)

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47
Q

VIRAL INDUCED WHEEZE
What is the management?

A

1st line = PRN salbutamol
2nd line = Montelukast or ICS or both

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48
Q

PNEUMONIA
What are the common causes of pneumonia in infants + young children?

A

RSV most common,
pneumococcus #1 bacterial,
H. influenzae,
Bordatella pertussis,
chlamydia trachomatis

(S. aureus rarely but = serious)

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49
Q

PNEUMONIA
What are the common causes of pneumonia in children >5?

A

Pneumococcus,
mycoplasma pneumoniae,
chlamydia pneumoniae

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50
Q

ASTHMA
what is the management of mild-moderate exacerbations of asthma?

A
  • salbutamol inhaler via spacer - give 1 puff every 30-60 seconds upto maximum 10 puffs

if symptoms are not controlled, refer to hospital

  • oral prednisolone (for 3 days)
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51
Q

PYLORIC STENOSIS
What is the management of pyloric stenosis?

A

1st line
- nil-by-mouth and NG tube insertion (to decompress stomach)
- IV fluids (rehydration + correct electrolyte imbalances)
- ramstedt pyloromyotomy (laparoscopic)

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52
Q

MECKEL’S DIVERTICULUM
What are the investigations for Meckel’s diverticulum?

A
  • Technetium scan will demonstrate increased uptake by ectopic gastric mucosa
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53
Q

CONSTIPATION
What are some causes of constipation?

A
  • Usually idiopathic
  • Meds (opiates)
  • LDs
  • Hypothyroidism
  • Hypercalcaemia
  • Poor diet (dehydration, low fibre)
  • Occasionally forceful potty training
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54
Q

CONSTIPATION
What is the medical management of constipation?

A
  • 1st = MACROGOL (osmotic) laxative like polyethylene glycol + electrolytes (Movicol)
  • 2nd = stimulant laxative if no effect like Senna, bisocodyl ± osmotic laxative (lactulose) or stool softener (docusate) if hard stools
  • 3rd = consider enema ± sedation or specialist manual evacuation
  • Continue for several weeks after regular bowel habit then gradual dose reduction
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55
Q

GORD
What are some complications of GORD?

A
  • Failure to thrive from severe vomiting
  • Oesophagitis = haematemesis, discomfort on feeding or heartburn, Fe anaemia
  • Aspiration > recurrent pneumonia, cough/wheeze
  • Sandifer syndrome = dystonic neck posturing (torticollis)
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56
Q

GASTROENTERITIS
What are some complications of gastroenteritis?

A
  • Isonatraemic + hyponatraemic dehydration
  • Hypernatraemic dehydration
  • Post-infective lactose intolerance (remove lactose + slowly reintroduce)
  • Guillain-Barré
  • Dehydration #1 cause of death
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57
Q

BILIARY ATRESIA
What is the clinical presentation of biliary atresia?

A

SYMPTOMS
- prolonged jaundice >2 weeks
- pale stools
- dark urine
- irritability

SIGNS
- hepatomegaly
- scleral icterus
- failure to thrive
- abdominal distention
- signs of portal hypertension (if severe)

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58
Q

BILIARY ATRESIA
What is the management of biliary atresia?

A

1st line
- Kasai portoenterostomy
- ursodeoxycholic acid

2nd line
- liver transplant

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59
Q

NEONATAL HEPATITIS
What are 4 main causes of neonatal hepatitis?

A
  • Congenital infection
  • Alpha-1-antitrypsin (A1AT) deficiency
  • Galactosaemia
  • Wilson’s disease
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60
Q

NEONATAL HEPATITIS
What is galactosaemia?

A
  • Deficiency of galactose-1-phosphate uridyltransferase (GALT) involved in galactose metabolism (lactose breaks down into galactose)
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61
Q

NEONATAL HEPATITIS
What is the management of galactosaemia?

A
  • Stop cow’s milk, breastfeeding C/I
  • Dairy-free diet
  • IV fluids
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62
Q

NEONATAL HEPATITIS
What is Wilson’s disease?

A
  • Reduced synthesis of caeruloplasmin (normally binds to copper + allows it to be excreted with bile)
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63
Q

NEONATAL HEPATITIS
How does Wilson’s disease present?

A

Sx of copper accumulation

  • Eyes (Kayser-Fleischer rings)
  • Brain (Parkinsonism + psychosis)
  • Kidneys (vit D resistant rickets)
  • Liver (jaundice)
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64
Q

FAILURE TO THRIVE
How does NICE define faltering growth in children by weight?

A
  • ≥1 centile spaces if birth weight was <9th centile
  • ≥2 centile spaces if birth weight was 9th–91st centile
  • ≥3 centile spaces if birth weight was >91st centile
  • Current weight is below 2nd centile for age, regardless of birth weight
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65
Q

CMPA
What are the investigations for cows milk protein allergy (CMPA)?

A
  • IgE mediated = skin prick tests + RAST for cow’s milk protein
  • Gold standard if doubt = elimination diet under dietician supervision
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66
Q

CMPA
What is the management for cows milk protein allergy (CMPA)?

A

FORMULA FED
- 1st line = extensive hydrolysed formula milk
- 2nd line = amino acid-based formula

BREASTFED
- continue breastfeeding
- eliminate cows milk protein from maternal diet. (consider prescribing calcium supplements to mother)
- use extensively hydrolysed milk when breastfeeding stops, until 12 months of age and at least for 6 months

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67
Q

CHOLEDOCHAL CYST
How may it present?

A
  • Cholestatic jaundice
  • abdominal mass
  • pain in RUQ
  • nausea and vomiting
  • fever
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68
Q

CHOLEDOCHAL CYST
what are the investigations?

A

can be detected on ultrasound before the child is born

after the baby is born, the parent’s may notice lump in RUQ, the following tests are then done:
- CT scan
- cholangiography

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69
Q

CHOLEDOCHAL CYST
What are the complications?

A
  • Cholangitis
  • small risk of malignancy
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70
Q

CHOLEDOCHAL CYST
What is the management?

A

Surgical cyst excision

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71
Q

CHOLEDOCHAL CYST
what are the different types?

A

Type 1 - cyst of extrahepatic bile duct (most common)
Type 2 - abnormal pouch/sac opening from duct
Type 3 - cyst inside the wall of the duodenum
Type 4 - cysts on both intrahepatic and extrahepatic bile ducts

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72
Q

HIRSCHSPRUNG’S DISEASE
How is Hirschsprung associated enterocolitis (HAEC) managed?

A

Urgent Abx, fluid resus + decompression of obstructed bowel

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73
Q

MECKEL’S DIVERTICULUM
What is the management of Meckel’s diverticulum?

A

Surgical resection, may need transfusion if severe haemorrhage

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74
Q

GASTROENTERITIS
what is the management for shigella infection?

A

severe = azithromycin or ciprofloxacin

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75
Q

GASTROENTERITIS
What is hyponatraemic dehydration?

A
  • Child with diarrhoea drinks large quantities of water, Na+ loss greater than water so fall in plasma Na+
    – Fluid shifts from ECF>ICF + can result in convulsions
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76
Q

BILIARY ATRESIA
What genetic mutation is biliary atresia associated with?

A

Associated with CFC1 gene mutations

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77
Q

NEONATAL HEPATITIS
What is the cause of A1AT deficiency?

A

AR on chromosome 14

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78
Q

NEONATAL HEPATITIS
What are the genetics for Wilson’s disease?

A

AR on chromosome 13

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79
Q

FAILURE TO THRIVE
What are some causes of inability to process nutrients properly?

A
  • T1DM,
  • inborn errors of metabolism
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80
Q

CMPA
What is cow’s milk protein allergy (CMPA) associated with?

A
  • More common in formula fed babies
  • those with personal or FHx of atopy
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81
Q

GASTROENTERITIS
How does hypernatraemic dehydration present?

A

Jittery movements,
increased muscle tone,
hyperreflexia,
convulsions,
drowsiness/coma

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82
Q

GASTROENTERITIS
How is hypernatraemic dehydration managed?

A

Slow rehydration over 48h

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83
Q

INTUSSUSSEPTION
what are the risk factors?

A
  • young children
  • male gender
  • preceding viral illness
  • henoch-schonlein purpura (HSP)
  • meckel’s diverticulum
  • lymphoma
84
Q

HSP
What is Henoch-Schönlein purpura (HSP)?

A
  • IgA mediated small vessel vasculitis leading to inflammation affecting the skin, joints, GI tract + kidneys
85
Q

HSP
What is the clinical presentation of HSP?

A

SYMPTOMS
- joint pain
- abdominal pain
- bloody stools
- haematuria

SIGNS
- palpable purpuric rash (typically on legs)
- joint swelling
- joint tenderness

86
Q

HSP
What are some investigations for HSP?

A
  • serum U&Es = may have rising creatinine
  • serum clotting screen
  • urinalysis = proteinuria, haematuria + RBC cast cells
  • stool analysis

to consider
- skin biopsy
- renal biopsy

87
Q

HSP
What is the management of HSP?

A

1st line:
- supportive care (rest, hydration + monitoring for complications
- NSAIDs (for pain relief + joint symptoms, use with caution in renal injury)

2nd line
- corticosteroids
- immunosuppressive agents (AZATHIOPRINE or CYCLOPHOSPHAMIDE)

88
Q

HAEMOLYTIC URAEMIC SYNDROME
What is haemolytic uraemic syndrome (HUS)?

A
  • Thrombosis within small blood vessels throughout the body, usually triggered by a bacterial toxin (shiga)
89
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the classic HUS triad?

A
  • Microangiopathic haemolytic anaemia (due to RBC destruction)
  • AKI (kidneys fail to excrete waste products like urea)
  • Thrombocytopenia
90
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the clinical presentation of HUS?

A

SYMPTOMS
- bloody diarrhoea
- fever
- abdominal pain
- vomiting
- reduced urine output

SIGNS
- dehydrated (delayed CRT, tachycardic/hypotensive, mottled skin)
- pyrexia
- pallor

91
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some investigations for HUS?

A
  • FBC = anaemia, thrombocytopaenia
  • blood film = schistocytes due to microangiopathic haemolysis
  • LDH = raised
  • LFTs = raised bilirubin
  • urinalysis = microscopic haematuria + proteinuria
  • U&Es = raised creatinine + reduced eGFR, often hyperkalaemia
  • stool culture = e.coli 0157:H7
  • PCR shiga toxin
92
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the management of HUS?

A

SUPPORTIVE
- IV fluids
- red cell transfusion
- dialysis (if refractory acidosis, hyperkalaemia, fluid overload or oliguria)

2ND LINE
- antibiotics (only in non-e.coli HUS)
- plasma exchange
- eculizimab

93
Q

HAEMATURIA
What investigations for haematuria should all patients get?

A
  • Urinalysis + urine MC&S
  • FBC, platelets, clotting + sickle cell screen
  • U+Es, creatinine, albumin, Ca2+, phosphate
  • USS kidneys + urinary tract
94
Q

HAEMATURIA
What investigations would you do if you suspected glomerular haematuria?

A
  • ESR, C3/4 + anti-DNA antibodies
  • Throat swab + antistreptolysin O/anti-DNAse B titres
  • Hepatitis B/C screen
  • Renal biopsy if recurrent haematuria, abnormal renal function/complement levels or significant persistent proteinuria
95
Q

UTI
In terms of performing ultrasounds scans in UTI, what are the guidelines?

A
  • USS within 6w if 1st UTI + <6m but responds well to Tx within 48h or during illness if recurrent or atypical bacteria
96
Q

UTI
Admission criteria for UTI?

A
  • Admission if <3m, systemically unwell or significant risk factors
97
Q

UTI
What is the management of UTI for >3m with upper UTI?

A

?Admission for IV, if not PO co-amoxiclav or cefalexin for 7–10d

98
Q

UT ABNORMALITIES
Name 6 urinary tract abnormalities

A
  • Renal agenesis
  • Multicystic dysplastic kidney
  • Polycystic kidney disease
  • Pelvic/horseshoe kidney
  • Posterior urethral valves
  • Prune-belly syndrome
99
Q

UT ABNORMALITIES
How can posterior urethral valves present in utero?
What is a complication of posterior urethral valves?

A
  • Oligohydramnios + potentially pulmonary hypoplasia
  • Risk of dysplastic kidneys, at its worse if bilateral could lead to potter syndrome
100
Q

UT ABNORMALITIES
What are the 2 first steps in management of urinary tract abnormalities?
How is the management split after that?

A
  • Antenatal Dx + start prophylactic Abx to prevent UTI
  • Bilateral hydronephrosis and/or dilated lower urinary tract in a male
  • Unilateral hydronephrosis in male or any anomaly in female
101
Q

UT ABNORMALITIES
What is the management of bilateral hydronephrosis and/or dilated lower urinary tract in a male?

A
  • Bilateral seen in bladder neck obstruction or posterior urethral valves
  • USS within 48h of birth to exclude posterior urethral valves
    – Abnormal = MCUG + surgery if required (ablation during cystoscopy)
    – Normal = stop Abx, repeat USS after 2-3m
102
Q

UT ABNORMALITIES
What is the management of unilateral hydronephrosis in male or any anomaly in female?

A
  • Unilateral seen in pelviureteric or vesicoureteric junction obstruction
  • Abnormal = further investigations
  • Normal = stop Abx, repeat USS after 2-3m
103
Q

CHRONIC KIDNEY DISEASE
What is the management of CKD?

A
  • Diet + NG or gastrostomy feeding may be needed for normal growth
  • Phosphate restriction + activated vitamin D to prevent renal osteodystrophy
  • May need recombinant growth hormone
  • Recombinant erythropoietin to prevent anaemia
  • Dialysis + transplantation if in ESRF (GFR <15ml/min/1.73m^2)
104
Q

VESICOURETERIC REFLUX
how is it graded?

A

graded using International Reflux Study grading system

105
Q

VESICOURETERIC REFLUX
how is it diagnosed?

A
  • micturating cystourethrogram: radiocontrast medium introduced to catheterised bladder, reflux is detected on voiding
  • indirect cystogram
106
Q

NEPHROTIC SYNDROME
what can cause minimal change disease?

A
  • NSAIDs,
  • Hodgkin’s lymphoma,
  • infectious mononucleosis
107
Q

HAEMATURIA
What are some non-glomerular causes of haematuria?

A
  • Wilm’s tumour,
  • trauma,
  • stones (esp if FHx),
  • sickle cell disease
  • other bleeding disorders
108
Q

UTI
What are the investigations for recurrent + atypical UTIs?

A
  • USS within 6w in all children with recurrent UTIs
  • DMSA (dimercaptosuccinic acid) scan (renal scarring 4-6m)
  • Micturating cystourethrogram (<6m) if FHx of vesico-ureteric reflux, dilatation of ureter on USS, poor urinary flow (catheterise + inject contrast into bladder)
109
Q

UTI
What is the management of children under 3m in UTI?

A

ALL children <3m + fever get immediate IV cefuroxime + full septic screen (blood cultures, FBC, CRP lactate, LP etc)

110
Q

UTI
What is the management of UTI for >3m with lower UTI?

A

3d PO trimethoprim, nitrofurantoin, amoxicillin or cephalosporin with follow-up if still unwell after 24-48h

111
Q

PYELONEPHRITIS
what are the risk factors?

A
  • vesicoureteral reflux (VUR) = most common + most important
  • previous history of UTI
  • siblings with a history of UTI
  • female sex
  • indwelling urinary catheter
  • intact prepuce in boys
  • structural abnormalities of the kidneys and lower urinary tract
112
Q

PYELONEPHRITIS
what is the management?

A
  • empirical antibiotics (co-amoxiclav or cefalexin) then targeted based on cultures
  • severe = hospitalisation and IV antibiotics
113
Q

PYELONEPHRITIS
how can it be prevented?

A

children <2yrs diagnosed with a UTI should have a renal USS

114
Q

NOCTURNAL ENURESIS
what are the causes?

A
  • not waking to bladder signals
  • inadequate levels of vasopressin (ADH)
  • overactive bladder
  • constipation
  • UTIs
  • Family history
  • Anxiety/stress
  • poor bedtime routines
115
Q

NOCTURNAL ENURESIS
what is the presentation of inadequate levels of vasopressin?

A
  • large volumes of urine passed at night
  • wet in the early part of the night
  • wet more than once per night
116
Q

NOCTURNAL ENURESIS
what is the presentation of an overactive bladder?

A
  • damp patches that occur at night also occur during the day
  • the volume of urine passed is variable
  • children often wake after wetting at night
117
Q

NOCTURNAL ENURESIS
what is the medical management?

A
  • antibiotics for infection
  • laxatives for constipation
  • alarms
  • desmopressin
  • anticholinergic medications (oxybutynin + tolterodine) for detrusor relaxation
118
Q

ALPORT’S SYNDROME
what are the 3 types?

A

X-linked Alport syndrome (XLAS)
Autosomal recessive Alport syndrome (ARAS)
Autosomal dominant Alport syndrome (ADAS)

119
Q

ALPORT SYNDROME
what is the clinical presentation?

A
  • haematuria
  • oedema
  • hypertension
  • loss of kidney function
  • progressive hearing loss
  • proteinuria
  • vision problems
120
Q

ALPORT SYNDROME
what is the management?

A

ACE inhibitors
dialysis
kidney transplant

121
Q

RDS
What are some risk factors of RDS?

A
  • Prematurity #1
  • Maternal DM
  • 2nd premature twin
  • C-section
122
Q

RDS
What is the investigation for RDS?

A

CXR –

  • Reticular “ground-glass” changes
  • Heart borders indistinct
  • Air bronchograms
123
Q

NEC. ENTEROCOLITIS
What are some risk factors for necrotising enterocolitis?

A
  • Very LBW + premature
  • Formula feeds (breast milk protective)
  • RDS + assisted ventilation
  • Sepsis
  • PDA + other CHD
124
Q

NEC. ENTEROCOLITIS
What are some investigations for necrotising enterocolitis?

A
  • FBC = thrombocytopaenia and neutropenia
  • U&Es = deranged electrolytes
  • CRP = raised
  • blood gas = acidosis, raised lactate
  • abdominal x-ray = bowel wall thickening, gas filled loops, gaseous distention

to consider
- bowel USS = increased bowel wall thickness + echogenicity, free fluid collection, loss of bowel wall perfusion

125
Q

NEC. ENTEROCOLITIS
What would an AXR show in necrotising enterocolitis?

A
  • Dilated loops of bowel
  • Bowel wall oedema (thickened bowel walls)
  • Pneumatosis intestinalis (intramural gas)
  • Pneumoperitoneum (free gas in peritoneum = perf)
  • Football sign = air outlining falciform ligament
  • Rigler’s sign = air both inside/outside bowel wall
  • Gas in portal veins
126
Q

NEC. ENTEROCOLITIS
What is the management of necrotising enterocolitis?

A

STAGE 1
- conservative = NG tube, IV fluids, parenteral nutrition
- medical = IV antibiotics (triple therapy), paracetamol +/- morphine

STAGE 2 & 3
- conservative = NG tube, discuss with surgical team
- medical = correct electrolytes, IV morphine, IV antibiotics (triple therapy)
- surgical = laparotomy +/- bowel resection

127
Q

JAUNDICE
What are some risk factors for jaundice?

A
  • LBW
  • Breastfeeding
  • Prematurity
  • FHx
  • Maternal diabetes
128
Q

JAUNDICE
Jaundice can be split into 3 aetiological time categories.
What are these?

A
  • <24h = always pathological, usually haemolytic disease
  • 24h–2w = common
  • > 2w = also bad
129
Q

JAUNDICE
What are some causes of jaundice 24h–2w after birth?

A
  • Physiological + breast milk jaundice (common)
  • Infection (UTI, sepsis)
  • Haemolysis, polycythaemia, bruising
  • Crigler-Najjar syndrome (rare inherited disorder with no UGT enzyme)
130
Q

JAUNDICE
What are some causes of jaundice >2w after birth?

A
  • Unconjugated = physiological or breast milk, UTI, hypothyroid, high GI obstruction (pyloric stenosis), Gilbert syndrome
  • Conjugated (>25umol/L) = bile duct obstruction (biliary atresia), neonatal hepatitis
131
Q

JAUNDICE
What is Gilbert’s syndrome?
How does it present?

A
  • AR deficiency of UDP-glucuronyltransferase = defective bilirubin conjugation
  • Unconjugated hyperbilirubinaemia (not in urine), jaundice may only be present if ill, exercising or fasting
132
Q

JAUNDICE
What investigations would you perform in neonatal jaundice?

A
  • FBC + blood film (polycythaemia, G6PD, spherocytosis)
  • Bilirubin levels
  • Blood type testing of mother + baby for ABO/Rh incompatibility
  • Direct Coombs (antiglobulin) test for haemolysis
  • TFTs, LFTs + urine MC&S
133
Q

HIE
What happens as a result of cardiorespiratory depression?

A
  • Hypoxia, hypercarbia + metabolic acidosis
  • Compromised cardiac output reduces tissue perfusion > hypoxic ischaemic injury to brain
134
Q

HIE
What is used to stage the severity of HIE?
What are the stages?

A

Sarnat staging –

  • Mild = poor feeding, generally irritable + hyperalert, resolves in 24h
  • Moderate = poor feeding, lethargic, hypotonic, seizures, can take weeks to resolve
  • Severe = reduced GCS, apnoeas, flaccid + reduced/absent reflexes, half die
135
Q

TORCH
What are the TORCH conditions?

A

Main congenital conditions
- Toxoplasmosis,
- Other (HIV),
- Rubella,
- CMV,
- Herpes + Syphilis

136
Q

TORCH
What are the characteristic features of toxoplasmosis?

A
  • Cerebral calcification, chorioretinitis + hydrocephalus
137
Q

TORCH
What is the clinical presentation of CMV?

A
  • 90% normal at birth
  • 5% = hepatosplenomegaly, petechiae at birth, growth issues, neurodevelopmental disabilities (cerebral palsy, epilepsy, microcephaly)
  • 5% = problems later in life, mainly sensorineural hearing loss
138
Q

TORCH
How does syphilis present?

A
  • Rash on soles of feet + hands
  • Hutchinson’s triad = keratitis, deafness, small + pointed teeth
139
Q

MECONIUM ASPIRATION
What are some risk factors for meconium aspiration?

A
  • Post-term deliveries at 42w
  • Maternal HTN or pre-eclampsia
  • Smoking or substance abuse
  • Chorioamnionitis
140
Q

MECONIUM ASPIRATION
What is a complication of meconium aspiration?
What are some other risk factors for that complication?

A
  • Persistent pulmonary HTN of the newborn due to high pulmonary vascular resistance
  • RDS, sepsis, congenital diaphragmatic hernia, maternal SSRI use, maternal NSAID use in 3rd trimester (early closure of DA)
141
Q

MECONIUM ASPIRATION

What is the management of meconium aspiration?

A
  • Artificial (positive pressure) ventilation with oxygenation
  • Suction if no breathing
142
Q

GASTROSCHISIS
What is the management of gastroschisis?

A
  • May attempt vaginal delivery
  • Urgent repair (theatre within 4h)
143
Q

BRONCHOPULMONARY DYSPLASIA
How can bronchopulmonary dysplasia be prevented?

A
  • Corticosteroids to mothers in premature labour <34w
  • CPAP rather than intubation where possible
  • Use caffeine to stimulate resp effort
  • Do not over oxygenate
144
Q

DUODENAL ATRESIA
What is the clinical presentation?

A
  • most appear well at birth
  • when they atart to feed they are sick (vomit is green)
  • jaundice
  • not pass meconium in first day
145
Q

GROUP B STREP INFECTION
which babies are at more risk of becoming infected with group B strep?

A
  • preterm labour
  • premature rupture of membranes
  • a long time between rupture of membranes and birth
  • internal foetal monitor
  • fever
  • past pregnancy with baby who had strep B
  • african-american/hispanic
  • group B strep in urine during pregnancy
146
Q

GROUP B STREP INFECTION
what are the investigations?

A
  • blood cultures
  • FBC, CRP
  • blood gas
  • urine microscopy
  • lumbar puncture
  • sputum culture
147
Q

GROUP B STREP INFECTION?
what is the management?

A
  • IV antibiotics (IV benzylpenicillin with gentamicin)
  • NICU admission
148
Q

PREMATURITY
What are some neuro complications of prematurity?

A
  • Cerebral palsy,
  • hearing/visual impairment,
  • intraventricular haemorrhage
149
Q

PREMATURITY
What are some metabolic complications of prematurity?

A
  • Hypoglycaemia,
  • hypocalcaemia,
  • electrolyte imbalance,
  • fluid imbalance
  • hypothermia
150
Q

PREMATURITY
What causes hypocalcaemia?

A

Kidneys + parathyroid not fully developed

151
Q

JAUNDICE
How does kernicterus present?
What are the outcomes?

A
  • Lethargy, poor feeding > hypertonia, seizures + coma
  • Permanent damage = dyskinetic cerebral palsy, LD + deafness
152
Q

TORCH
How is CMV managed?

A

No therapy so no screening

153
Q

TORCH
How is syphillis managed?

A
  • If fully treated ≥1m before delivery = no treatment
  • Any doubts = benzylpenicillin
154
Q

OESOPHAGEAL ATRESIA
What is it associated with?

A
  • Tracheo-oesophageal fistula + polyhydramnios
155
Q

EXOMPHALOS
What is the management?

A

C-section at 37w, staged repair as primary closure difficult

156
Q

LISTERIA INFECTION
what is the management?

A

ampicillin + aminoglycoside (gentamycin)

157
Q

HIE
what are the risk factors?

A

MATERNAL
- HTN
- diabetes
- substance abuse
- infection

OBSTETRIC
- prolonged labour
- meconium-stained amniotic fluid
- placental abruption
- umbilical cord prolapse

INFANT
- prematurity
- low birth weight
- congenital abnormalities

158
Q

HIE
what are the investigations?

A
  • blood gas
  • blood tests
  • cranial USS

to consider
- MRI
- EEG

159
Q

SIDS
what are the risk factors?

A
  • not prone sleeping
  • parental smoking
  • prematurity
  • bed sharing
  • hyperthermia
  • head covering

other risk factors
- LBW
- male sex
- maternal drug use
- multiple births
- incidence increases in winter

160
Q

SIDS
what are protective factors?

A
  • breastfeeding
  • room sharing
  • use of dummies
161
Q

SIDS
what measures can be taken to reduce the risk of SIDS?

A
  • put baby on their back when not directly supervised
  • keep head uncovered
  • place feet at foot of the bed to prevent them sliding down under blanket
  • keep cot clear of toys and blankets
  • maintain a comfortable room temperature (16-20 degrees)
  • avoid smoking (avoid handling baby after smoking)
  • avoid co-sleeping (particularly on sofa or chair)
  • if co-sleeping avoid drugs, alcohol, sleeping tablets or deep sleepers
162
Q

HSV ENCEPHALITIS
what is the cause?

A
  • neonates = HSV-2 (genital herpes)
  • older children = HSV-1 (cold sores)
163
Q

HSV ENCEPHALITIS
what are the complications?

A
  • lasting fatigue + prolonged recovery
  • changes to personality or mood
  • changes to memory and cognition
  • learning disability
  • headaches
  • chronic pain
  • movement disorder
  • sensory disturbance
  • seizures
  • hormonal imbalance
164
Q

CONGENITAL HYPOTHYROIDISM
what are the causes?

A
  • primary congenital hypothyroidism
  • thyroid dysgenesis
  • dyshormonogenesis
  • secondary or central congenital hypothyroidism
165
Q

CONGENITAL HYPOTHYROIDISM
what are the risk factors?

A
  • medication use during pregnancy
  • maternal advanced age
  • family history of thyroid disease
  • low birth weight
  • preterm birth
  • multiple pregnancies
166
Q

CONGENITAL HYPOTHYROIDISM
what are the clinical features?

A
  • prolonged neonatal jaundice
  • poor feeding + weight gain
  • hypothermia
  • macroglossia
  • large fontanelle
  • distended abdomen with umbilical hernia
  • dry skin
  • hoarse cry
  • myxoedema
  • bradycardia
167
Q

CEREBRAL PALSY
What are the causes of cerebral palsy?

A
  • Antenatal (80%) = genetics, congenital malformations or infections
  • Intrapartum (10%) = hypoxic-ischaemic injury
  • Postnatal (10%) = IV haemorrhage (prems), meningitis/encephalitis, trauma (NAI), hydrocephalus, kernicterus
168
Q

CEREBRAL PALSY
What are some early features of cerebral palsy?

A
  • Abnormal limb/trunk tone + posture with delayed motor milestones
  • Feeding issues > oromotor incoordination, slow feeding, gagging + vomiting
  • Abnormal gait when walking achieved
  • Hand preference before 12m + primitive reflexes after 6m
169
Q

CEREBRAL PALSY
What are the stages of the Gross Motor Function Classification System?

A
  • I = walks without limitation
  • II = with limitation
  • III = handheld mobility device
  • IV = III with limitation
  • V = wheelchair
170
Q

VISION
What are some causes of severe visual impairment?

A

Genetic –

  • Congenital cataracts
  • Albinism
  • Retinal dystrophy
  • Retinoblastoma
171
Q

HEARING
What are some causes of conductive hearing loss?

A
  • # 1 = congestion behind eardrums (viral URTI)
  • Glue ear, ear wax, middle ear infection, perforated ear drum
  • Structural abnormality of the outer ear (syndromes)
172
Q

HEARING
What are some causes of sensorineural hearing loss?

A
  • Genetic or syndromes
  • Perinatal (trauma, infection, hypoxia)
  • Congenital infections (rubella, CMV)
  • Meningitis (pneumococcus can cause ossification of cochlear)
173
Q

HEARING
What are some risk factors for conductive hearing loss?

A
  • Down’s syndrome,
  • craniofacial syndromes
  • cleft palate
174
Q

HEARING
What 2 types of hearing tests are part of the newborn hearing screening programme (NHSP)?

A
  • Evoked otoacoustic emission (EOAE)
  • Auditory brainstem response (ABR) audiometry if EOAE fails
175
Q

HEARING
What is evoked otoacoustic emission?
What are the pros?
What are the cons?

A
  • Earphone produces sound which evokes an echo from ear if cochlear function normal
  • Simple + quick
  • Misses auditory neuropathy, cochlear test not hearing, high false +ve in first 24h
176
Q

HEARING
What is auditory brainstem response audiometry?
What are the pros?
What are the cons?

A
  • Computer analysis of EEG waveforms evoked in response to auditory stimuli
  • Screens hearing pathway ear>brainstem, low false +ve rate
  • Affected by movement (time consuming), electrodes on infant’s head, complex computerised gear
177
Q

HEARING
What testing might be done in children 6–9m?

A
  • Distraction testing
  • Relies on baby locating + turning appropriately to high + low frequency sounds out of field of vision
  • 2x trained staff
178
Q

HEARING
What testing might be done in children 10–18m?

A
  • Visual reinforcement audiometry
  • Hearing thresholds are established using visual rewards (illumination of toys) to reinforce the child’s head turn to stimuli of different frequencies
  • First test that does single ear measures
179
Q

HEARING
What hearing tests are done at…

i) >2y?
ii) >2.5y?
iii) 4y?

A

i) Performance testing = child performs an action when hear a noise
ii) Speech discrimination tests (McCormick toy test)
iii) Pure tone audiometry at school entry = child responds to pure tone stimulus with headphones

180
Q

HEARING
What does Rinne’s test show you?

A
  • Normal = louder at EAM
  • Conductive = louder on mastoid
  • Sensorineural = both decreased
181
Q

HEARING
What does Weber’s test show you?

A
  • Normal = vibrations equal in both ears
  • Conductive = louder in abnormal ear
  • Sensorineural = louder in normal ear
182
Q

EPILEPSY
What are 4 epilepsy syndromes seen in children?

A
  • Infantile spasms (West’s syndrome)
  • Lennox-Gastaut syndrome
  • Juvenile myoclonic epilepsy
  • Benign Rolandic epilepsy = M>F, paraesthesia (unilateral face, tongue, twitching) during sleep, EEG shows centrotemporal focal spike waves
183
Q

EPILEPSY
Who is affected by infantile spasms?

A
  • Early life (4-6m), M>F, often secondary to serious neuro abnormality (tuberous sclerosis, encephalitis, birth asphyxia)
184
Q

EPILEPSY
What are the 3 components to infantile spasms?

A
  • Violent flexor spasms of head, trunk + limbs followed by extension of arms (salaam spasms) for 1-2s, can repeat up to 50 times
  • Progressive mental handicap
  • EEG shows hypsarrhythmia
185
Q

EPILEPSY
What is Lennox-Gastaut syndrome?
How does it present?
Management?

A
  • Can be extension of infantile spasms, 1-5y
  • Atypical absences, falls, jerks + 90% have mod-severe mental handicap
  • EEG shows slow spike, ketogenic diet may help
186
Q

EPILEPSY
Who is juvenile myoclonic epilepsy more common in?
How does it present?
Management?

A
  • Teens, F>M
  • Infrequent generalised seizures (often morning), daytime absences, sudden shock-like myoclonic seizures (can happen before seizures)
  • Good response to valproate
187
Q

EPILEPSY
What is the management of generalised seizures?

A
  • 1st line = sodium valproate
  • 2nd line = lamotrigine, carbamazepine (TC), clonazepam (myoclonic)
188
Q

EPILEPSY
What is the management of focal seizures?

A
  • 1st line = carbamazepine or lamotrigine
  • 2nd line = levetiracetam or sodium valproate
189
Q

EPILEPSY
What is the management of absence seizures?

A
  • Ethosuximide or sodium valproate
190
Q

DISORDERS
Name 2 neurocutaneous disorders
What is the mode of inheritance for these conditions?

A
  • Neurofibromatosis (type 1 + 2) + tuberous sclerosis
  • AD
191
Q

NEUROFIBROMATOSIS
What is the clinical presentation of neurofibromatosis 1?

A
  • No intellectual problems but lots of skin involvement
  • > 5 café-au-lait spots
  • Axillary freckling in skin folds
  • Iris hamartomas, scoliosis + pheochromocytomas
  • Peripheral neurofibromas
192
Q

NEUROFIBROMATOSIS
What is the clinical presentation of neurofibromatosis 2?

A
  • Hearing problems with no skin involvement
  • Bilateral vestibular schwannomas > sensorineural hearing loss then tinnitus + vertigo
193
Q

TUBEROUS SCLEROSIS
What are the cutaneous features of tuberous sclerosis?

A
  • Hypopigmented ‘ash-leaf’ spots which fluoresce under UV light
  • Roughened (Shagreen) patches of skin over lumbar spine
  • Angiofibromas (butterfly distribution over nose)
  • Subungual fibromata
194
Q

TUBEROUS SCLEROSIS
What are some other features of tuberous sclerosis?

A
  • Neuro = epilepsy (infantile spasms or partial), developmental delay + intellectual impairment
  • Retinal hamartomas,
  • polycystic kidneys,
  • rhabdomyomata of heart
195
Q

NEURAL TUBE DEFECTS
What are 5 different types of neural tube defects?

A
  • Spina bifida occulta (#1)
  • Meningocele
  • Myelomeningocele (most severe)
  • Anencephaly
  • Encephalocele
196
Q

GLUE EAR
What is the management?

A
  • Insertion of ventilation tubes (grommets) to drain excess fluid
  • Adenoidectomy as adenoids can harbour organisms + obstruct Eustachian tube so poor ventilation + drainage
197
Q

GLUE EAR
What investigations would you do?

A
  • Otoscopy (TM appears dull + retracted, often with visible fluid level)
  • Flat trace on tympanometry + evidence of conductive loss on pure tone audiometry (or reduced hearing on distraction test if younger)
198
Q

DEAFNESS
what are the causes of sensorineural hearing loss?

A

Inherited/genetic - ushers syndrome, Waardenburg syndrome

Acquired
- perinatal - birth asphyxia, hyperbilirubinemia, congenital infection (rubella, CMV, syphilis)
- postnatal - drugs, meningitis, head injury, labyrinthitis, acoustic neuroma

199
Q

DEAFNESS
what are the causes of conductive hearing loss?

A

External - ear canal atresia/stenosis

Middle ear - acute/chronic otitis media, glue ear

200
Q

EPILEPSY
What is the management of infantile spasms?

A

Vigabatrin or corticosteroids (poor prognosis)

201
Q

EPILEPSY
What is the management of myoclonic seizures?

A
  • 1st line = sodium valproate
  • 2nd line = clonazepam
202
Q

‘FUNNY TURNS’
What is the clinical presentation of reflex anoxic seizures?

A
  • Child becomes pale + falls to floor,
  • hypoxia may induce generalised tonic-clonic seizure which is brief + child RAPIDLY recovers
203
Q

‘FUNNY TURNS’
What are the investigations for reflex anoxic seizures?

A
  • Ocular compression under controlled conditions often lead to asystole
  • paroxysmal slow-wave discharge on EEG
204
Q

TUBEROUS SCLEROSIS
What are the investigations?

A

CT/MRI will detect calcified subependymal nodules + tubers from 2nd year of life

205
Q

DEVELOPMENTAL DELAY
what are the referral points?

A
  • doesn’t smile at 10 weeks
  • cannot sit unsupported at 12 months
  • cannot walk at 18 months
206
Q

DEVELOPMENTAL DELAY
what problems can indicate fine motor problems?

A

hand preference before 12 months - can indicate cerebral palsy

MY REVISION - ALL TO DO (21 decks)

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