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B TO REVISE - PHASE 3A > B PAEDS PART 1 TO DO > Flashcards

B PAEDS PART 1 TO DO Flashcards

1
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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2
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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3
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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4
Q

HYPOPLASTIC LEFT HEART
What is the clinical presentation of HLHS?

A
  • Sickest neonates with duct-dependent circulation
  • No L side flow so ductal constriction > profound acidosis + rapid CV collapse
  • Weakness or absence of all peripheral pulses
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5
Q

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

A
  • Wolff-Parkinson-White syndrome + lithium in pregnancy
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6
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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7
Q

AORTIC STENOSIS
What is aortic stenosis associated with?

A
  • Bicuspid aortic valve + William’s syndrome (supravalvular)
  • Also may be mitral stenosis + coarctation of aorta too
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8
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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9
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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10
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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11
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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12
Q

SUPRAVENTRICLAR TACHYCARDIA
What is the management of a supraventricular tachycardia?

A
  • 1st line = Vagal stimulation (carotid sinus massage, cold ice pack to face)
  • 2nd line = IV adenosine
  • 3rd line = Electrical cardioversion
  • Long term = ablation of pathway or flecainide
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13
Q

INFECTIVE ENDOCARDITIS
What is the management?

A

High dose IV Abx (penicillin with aminoglycoside like vancomycin) for 6w

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14
Q

TOF
What are some risk factors?

A
  • Rubella,
  • maternal age >40,
  • alcohol in pregnancy,
  • maternal DM
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15
Q

TGA
What is it associated with?

A

Duct dependent lesion, associated with PDA, ASD + VSD

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16
Q

TRICUSPID ATRESIA
How is it managed?

A

Shunt between subclavian + pulmonary artery with surgery later

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17
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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18
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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19
Q

PNEUMONIA
How can CXR indicate what the causative organism may be?

A
  • Lobar consolidation (dense white area in a lobe) = pneumococcus
  • Rounded air-filled cavities (pneumatoceles) + multi-lobar = S. aureus
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20
Q

PNEUMONIA
What is the management of pneumonia?

A
  • Newborns = IV broad-spec Abx
  • 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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21
Q

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

A
  1. SABA
  2. SABA + 8-week trial of MODERATE dose ICS
  3. SABA + LOW dose ICS + LTRA
  4. stop LTRA and refer to paeds asthma specialist
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22
Q

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

A
  1. SABA
  2. SABA + LOW dose ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA
  5. SABA + MART (includes LOW dose ICS)
  6. SABA + MART (includes MODERATE dose ICS) / SABA + MODERATE dose ICS + LABA
  7. SABA + HIGH dose ICS/theophylline and seek advise from expert
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23
Q

ASTHMA
What is the management of exacerbations of asthma?

A

O SHIT ME –
- Oxygen (SpO2 94–98%)
- Salbutamol (spacer or neb B2B, IV if no response to this + ipratropium as 2nd line)
- Hydrocortisone IV or PO pred
- Ipratropium bromide (neb if poor response to salbutamol)
- Theophylline (IV)
- Magnesium sulfate (IV)
- Escalate early > ICU if not improving for ventilation ± intubation

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24
Q

CYSTIC FIBROSIS
What is the pathophysiology of cystic fibrosis?

A
  • Decreased Cl- excretion into airway lumen + increased reabsorption of Na+ into epithelial cells means less excretion of salt (+ so water) > increased viscosity of airway secretion
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25
Q

CYSTIC FIBROSIS
How does cystic fibrosis present in older children + adolescents?

A
  • DM (pancreatic insufficiency)
  • Cirrhosis + portal HTN
  • Distal intestinal obstruction
  • Pneumothorax or recurrent haemoptysis
  • Sterility in males as absent vas deferens
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26
Q

CYSTIC FIBROSIS
What are some signs of cystic fibrosis?

A
  • Low weight or height on growth charts
  • Hyperinflation due to air trapping
  • Coarse inspiration crepitations ± expiratory wheeze
  • Finger clubbing
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27
Q

CYSTIC FIBROSIS
What are some typical causes of respiratory tract infections in cystic fibrosis?

A
  • S. aureus
  • H. influenzae
  • Pseudomonas aeruginosa
  • Bulkholderia cepacia associated with increased morbidity + mortality
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28
Q

ASTHMA
What are some risk factors for asthma?

A

LBW, FHx, bottle fed, atopy, male, pollution

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29
Q

VIRAL INDUCED WHEEZE
What are some risk factors?

A

Maternal smoking during/after pregnancy + prematurity

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30
Q

VIRAL INDUCED WHEEZE
What is the management?

A

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

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31
Q

ASTHMA
What are the important side effects of ICS?

A

Oral thrush,
adrenal + growth suppression,
DM,
osteoporosis

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32
Q

ASTHMA
What are the important side effects of theophylline?

A

Vomiting,
insomnia,
headaches

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33
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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34
Q

COELIAC DISEASE
What is the aetiology of coeliac disease?

A
  • Genetics = HLA-DQ2 + HLA-DQ8
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35
Q

COELIAC DISEASE
What are the characteristic features seen on small intestinal biopsy?

A
  • Villous atrophy
  • Crypt hyperplasia
  • Increased intraepithelial lymphocytes
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36
Q

COELIAC DISEASE
What are some complications of coeliac disease?

A
  • Anaemias
  • Osteoporosis
  • Lymphoma (EATL)
  • Hyposplenism
  • Lactose intolerance
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37
Q

ABDOMINAL PAIN
What are some causes of recurrent abdominal pain?

A
  • No structural cause in >90%
  • GI = IBS, abdominal migraine, coeliac
  • Gynae = ovarian cysts, PID, Mittelschmerz (ovulation pain)
  • Hepatobiliary = hepatitis, gallstones, UTI
  • Psychosocial = bullying, abuse, stress
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38
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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39
Q

CONSTIPATION
What are some red flags in constipation?

A
  • Delayed passage of meconium = Hirschsprung’s, CF
  • Failure to thrive = hypothyroid, coeliac
  • Abnormal lower limb neurology = lumbosacral pathology
  • Perianal bruising or multiple fissures = ?abuse
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40
Q

CONSTIPATION
What is the medical management of constipation?

A
  • 1st = macrogol (osmotic) laxative like polyethylene glycol + electrolytes (Movicol)
  • 2nd = lactulose (osmotic) if movicol is not tolerated +/- stimulant e.g. Senna
  • 3rd = consider enema ± sedation or specialist manual evacuation
  • Continue for several weeks after regular bowel habit then gradual dose reduction
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41
Q

GORD
What are the investigations for GORD?

A
  • Usually clinical but if atypical Hx, complications or failed Tx…
    – 24h oesophageal pH monitoring
    – Endoscopy + biopsy to identify oesophagitis
    – Contrast studies like barium meal
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42
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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43
Q

GORD
What is the management of more significant GORD?

A
  • Acid suppression = H2 receptor antagonists (ranitidine) or PPI (omeprazole)
  • Surgical Mx (fundoplication) if complications, unresponsive to intensive medical treatment or oesophageal strictures
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44
Q

GASTROENTERITIS
What is a complication of E. coli 0157?

A
  • Destroys blood cells + can lead to haemolytic uraemic syndrome
  • Abx increase this risk so avoid
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45
Q

BILIARY ATRESIA
What is the clinical presentation of biliary atresia?

A
  • Prolonged jaundice >2w
  • Pale stools + dark urine (obstructive pattern)
  • Failure to thrive
  • Hepatosplenomegaly
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46
Q

BILIARY ATRESIA
What is the management of biliary atresia?

A
  • Kasai portoenterostomy (attach section of small intestine to opening of liver where bile duct attaches)
  • Some will need full liver transplant
  • Success decreases with age so early Dx crucial
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47
Q

NEONATAL HEPATITIS
What are some investigations for neonatal hepatitis syndrome?

A
  • Deranged LFTs with raised unconjugated + conjugated bilirubin
  • Liver biopsy = multinucleated giant cells + Rosette formation
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48
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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49
Q

FAILURE TO THRIVE
How is failure to thrive defined by height?

A
  • Mild = fall across 2 centile lines on growth chart
  • Severe = fall across 3 centile lines on growth chart
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50
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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51
Q

KWASHIOKOR
what are the clinical features?

A
  • growth retardation
  • diarrhoea
  • anorexia
  • oedema - defining characteristic
  • skin/hair depigmentation
  • abdominal distension with fatty liver
52
Q

KWASHIOKOR
what are the investigations?

A

bloods - FBC, U+E, serum protein, urine dipstick
- hypoalbuminaemia
- normo/microcytic anaemia
- low calcium, magnesium, phosphate and glucose

53
Q

HERNIA
what are the risk factors for developing a hernia?

A
  • premature, underweight babies
  • male gender
  • family history
  • medical conditions - undescended testes, CF
  • African descent
54
Q

CHOLEDOCHAL CYST
How may it present?

A
  • Cholestatic jaundice
  • abdominal mass
  • pain in RUQ
  • nausea and vomiting
  • fever
55
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

56
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

57
Q

LIVER FAILURE
what are the causes?

A
  • chronic hepatitis
  • biliary tree disease
  • toxin induced
  • A1AT deficiency
  • autoimmune hepatitis
  • wilson’s disease
  • CF
  • budd-chiari syndrome
  • primary sclerosing cholangitis
58
Q

IBD
what is the histology of ulcerative colitis?

A
  • Increased crypt abscesses,
  • pseudopolyps,
  • ulcers
59
Q

COELIAC DISEASE
What is the pathophysiology?

A

Autoimmune response to alpha-gliadin portion of protein gluten causes inflammation in small intestine (particularly jejunum)

60
Q

NEONATAL HEPATITIS
How does it present?

A
  • Intruterine growth restriction (IUGR),
  • hepatosplenomegaly at birth,
  • failure to thrive
  • dark urine
61
Q

NEONATAL HEPATITIS
What is the cause of A1AT deficiency?

A

AR on chromosome 14

62
Q

NEONATAL HEPATITIS
What is the presentation of A1AT deficiency?

A
  • Prolonged neonatal jaundice (cholestasis), worse on breast feeding,
  • can have (prolonged) bleeding due to vitamin K deficiency,
  • COPD
63
Q

NEONATAL HEPATITIS
How does galactosaemia present?

A
  • Poor feeding,
  • vomiting,
  • jaundice + hepatomegaly when fed milk
64
Q

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

A

AR on chromosome 13

65
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
66
Q

NEONATAL HEPATITIS
What is the management of Wilson’s disease?

A

Penicillamine for copper chelation

67
Q

PROTEINURIA
What are some causes of proteinuria?

A
  • Transient (febrile illness, after exercise = no investigation)
  • Nephrotic syndrome
  • HTN
  • Tubular proteinuria
  • Increased glomerular perfusion pressure
  • Reduced renal mass
68
Q

NEPHROTIC SYNDROME
What are some complications of nephrotic syndrome?

A
  • Hypovolaemia as fluid leaks from intravascular to interstitial space
  • Thrombosis due to loss of antithrombin III
  • Infection due to leakage of immunoglobulins, weakening the immune system + exacerbated by Tx with steroids
69
Q

NEPHRITIC SYNDROME
What is the clinical presentation of nephritic syndrome?

A
  • Haematuria (often macroscopic) + proteinuria of varying degree
  • Impaired GFR (rising creatinine), decreased urine output + volume overload
  • Salt + water retention > HTN (?seizures) + oedema (eyes)
70
Q

HSP
What are some investigations for HSP?

A
  • Exclude DDx of non-blanching rash
    – FBC + blood film (thrombocytopenia, sepsis + leukaemia), CRP, cultures, HSP = afebrile
  • Urinalysis for proteinuria + haematuria
  • PCR to quantify proteinuria
  • Renal biopsy if severe renal issues to determine if Tx
71
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some causes of HUS?

A
  • Mostly E. Coli 0157 producing Shiga toxin, can be Shigella (?Petting zoo)
  • Use of Abx + antimotility agents to treat gastroenteritis caused by these pathogens can increase risk of HUS
72
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the clinical presentation of HUS?

A
  • Prodrome of bloody diarrhoea
  • Urine > reduced output, haematuria or dark brown
  • Abdo pain, lethargy
  • Oedema, HTN, bruising
73
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some investigations for HUS?

A
  • FBC (anaemia, thrombocytopenia), fragmented blood film
  • U+Es reveal AKI
  • Stool culture
74
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the management of HUS?

A
  • ABCDE as emergency
  • Often self-limiting so supportive > refer to paeds renal unit for ?dialysis
  • Anti-hypertensives, careful fluid balance, blood transfusions
  • Plasma exchange if severe + not associated with diarrhoea
75
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
76
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
77
Q

UTI
When is a UTI classified as atypical?

A
  • Septicaemia
  • Poor urine flow
  • Non-E. Coli
  • Failure to respond
78
Q

UTI
What are some risk factors for UTI?

A
  • Incomplete bladder emptying
  • Vesico-ureteric reflux
  • Structural abnormality (horseshoe kidney, ureteric strictures)
  • Inadequate toilet hygiene
79
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
80
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)

81
Q

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

A

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

82
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

83
Q

UTI
What is a recurrent UTI?

A
  • ≥2 UTIs with ≥1 with systemic Sx (or ≥3 without)
84
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
85
Q

UT ABNORMALITIES
What are some complications of autosomal recessive polycystic kidney disease?

A

Often liver involvement with portal + interlobular fibrosis

86
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
87
Q

ACUTE KIDNEY INJURY
What is acute kidney injury (AKI)?
What is it characterised by?

A
  • Spectrum of potentially reversible, reduction in renal function
  • Rapid rise in creatinine + development of oliguria (<0.5ml/kg/h)
88
Q

ACUTE KIDNEY INJURY
What are some renal causes of AKI?

A
  • Vascular = HUS, vasculitis, embolus)
  • Glomerular = glomerulonephritis
  • Interstitial = interstitial nephritis, pyelonephritis
  • Tubular = acute tubular necrosis
89
Q

ACUTE KIDNEY INJURY
What are some investigations for AKI?

A
  • FBC, U+Es (high urea), high creatinine, USS to identify if obstruction
  • Can have hyperkalaemia, hyperphosphataemia + metabolic acidosis
90
Q

CHRONIC KIDNEY DISEASE
What are some causes of chronic kidney disease (CKD)?

A
  • Structural malformations (congenital dysplastic kidney)
  • Glomerulonephritis
  • Hereditary nephropathies
  • Systemic diseases
91
Q

CHRONIC KIDNEY DISEASE
What is the clinical presentation of CKD?

A
  • Failure to thrive, anorexia + vomiting
  • HTN, acute-on-chronic renal failure, anaemia
  • Bony deformities from renal osteodystrophy
  • Incidental proteinuria, polydipsia + polyuria
92
Q

CHRONIC KIDNEY DISEASE
What are some investigations for CKD?

A
  • Monitor growth
  • FBC = anaemia due to reduced EPO
  • U+Es + electrolytes (Ca2+ low, phosphate high)
93
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)
94
Q

VESICOURETERIC REFLUX
what is the management?

A

aim is to prevent renal scarring

  • antibiotic prophylaxis
  • surgery - not commonly recommended
95
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
96
Q

PYELONEPHRITIS
what is the management?

A
  • empirical antibiotics then targeted based on cultures
  • severe = hospitalisation and IV antibiotics
97
Q

PYELONEPHRITIS
how can it be prevented?

A

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

98
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
99
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
100
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
101
Q

NOCTURNAL ENURESIS
what are the investigations?

A
  • physical examination (back, genitalia + lower limbs)
  • urinalysis + MS&C
  • bladder scan
  • uroflowmetry
  • ultrasound
102
Q

ALPORT SYNDROME
what is the clinical presentation?

A
  • haematuria
  • oedema
  • hypertension
  • loss of kidney function
  • progressive hearing loss
  • proteinuria
  • vision problems
103
Q

ALPORT SYNDROME
what is the management?

A

ACE inhibitors
dialysis
kidney transplant

104
Q

ALPORT SYNDROME
what are the investigations?

A
  • genetic testing
  • tissue biopsy
  • urinalysis
  • hearing tests
105
Q

RDS
What are some risk factors of RDS?

A
  • Prematurity #1
  • Maternal DM
  • 2nd premature twin
  • C-section
106
Q

RDS
What are the short and long term complications of RDS?

A
  • Short = pneumothorax, infection, apnoea, necrotising enterocolitis
  • Long = bronchopulmonary dysplasia, retinopathy of prematurity
107
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
108
Q

JAUNDICE
What are some risk factors for jaundice?

A
  • LBW
  • Breastfeeding
  • Prematurity
  • FHx
  • Maternal diabetes
109
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
110
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
111
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
112
Q

TORCH
What are the characteristic features of toxoplasmosis?

A
  • Cerebral calcification, chorioretinitis + hydrocephalus
113
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
114
Q

TORCH
How does syphilis present?

A
  • Rash on soles of feet + hands
  • Hutchinson’s triad = keratitis, deafness, small + pointed teeth
115
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
116
Q

BRONCHOPULMONARY DYSPLASIA
What investigations would you do for bronchopulmonary dysplasia?

A
  • CXR = widespread areas of opacification, cystic changes, fibrosis
  • Formal sleep study to assess SpO2 during sleep supports Dx + guides Mx
117
Q

PREMATURITY
What are some metabolic complications of prematurity?

A
  • Hypoglycaemia,
  • hypocalcaemia,
  • electrolyte imbalance,
  • fluid imbalance
  • hypothermia
118
Q

JAUNDICE
How does kernicterus present?
What are the outcomes?

A
  • Lethargy, poor feeding > hypertonia, seizures + coma
  • Permanent damage = dyskinetic cerebral palsy, LD + deafness
119
Q

JAUNDICE
What are some side effects of phototherapy?

A
  • Temp instability,
  • macular rash,
  • bronze discolouration
120
Q

NEONATAL HYPOGLYCAEMIA
What are some risk factors for neonatal hypoglycaemia?

A
  • Preterm + intrauterine growth restriction (IUGR) = lack of glycogen stores
  • Maternal DM = infantile hyperinsulinaemia
  • LGA, polycythaemia or ill
  • Transient hypoglycaemia common in first hours after birth
121
Q

LISTERIA INFECTION
what is the clinical presentation?

A

symptoms are similar to sepsis - listlessness, irritable, poor feeding
- Early onset = low birth weight, obstetric complications, evidence of sepsis soon after birth
- late onset = usually full-term, previously healthy neonates, present with meningitis/sepsis

122
Q

LISTERIA INFECTION
what is the management?

A

ampicillin + aminoglycoside (gentamycin)

123
Q

IBD
How do you treat flares of crohns disease?

A

PO prednisolone or IV hydrocortisone

124
Q

IBD
How do you induce remission in Ulcerative colitis?

A

Mild to moderate disease
- 1st line = aminosalicylate (e.g. mesalazine oral or rectal)
- 2nd line = corticosteroids (e.g. prednisolone)

Severe disease
- 1st line = IV corticosteroids (e.g. hydrocortisone)
- 2nd line = IV ciclosporin

125
Q

IBD
How do you maintain remission in Ulcerative colitis?
What should be cautioned?

A
  • PO/PR mesalazine, azathioprine or mercaptopurine
  • Mesalazine can cause acute pancreatitis
126
Q

IBD
How do you induce remission in crohns disease?

A

1st line = steroids (e.g. oral prednisolone or IV hydrocortisone).

If steroids alone don’t work, consider adding immunosuppressant medication under specialist guidance:

Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab

127
Q

IBD
How do you maintain remission in crohns disease?

A

1st line = Azathioprine or Mercaptopurine

Alternatives:
Methotrexate
Infliximab
Adalimumab

B TO REVISE - PHASE 3A (9 decks)

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