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B TO REVISE - PHASE 3A > PAEDS EXTRA CONDITIONS > Flashcards

PAEDS EXTRA CONDITIONS Flashcards

1
Q

TONSILLITIS

What is tonsillitis?

A
  • Form of pharyngitis where there’s intense inflammation of the tonsils, often with purulent exudate
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2
Q

TONSILLITIS

What criteria can be used to distinguish if tonsillitis is bacterial or viral?

A

CENTOR –
- Tonsillar exudate, tender ant. cervical lymphadenopathy, fever, absence of cough (≥3 ?strep)
FeverPAIN score –
- Fever, Purulence, Attend rapidly (3d after Sx), severely Inflamed tonsils, No cough/coryza (2–3 consider delayed, ≥4 consider Abx)

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3
Q

TONSILLITIS

What is the main complication of tonsillitis?

A
  • Quinsy (peritonsillar abscess)
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4
Q

TONSILLITIS

What is the management of tonsillitis?

A
  • Phenoxymethylpenicillin if bacterial (or erythromycin)

- Tonsillectomy last resort if quinsy (in 6w), recurrent severe (≥5/year) or OSA

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5
Q

TONSILLITIS
Other than tonsils, what else might cause airway issues?
What are indications for management?

A
  • Adenoids grow faster than airway so narrow lumen greatest between 2–8y (regress)
  • Otitis media with effusion with hearing loss or OSA for adenotonsillectomy
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6
Q

CHRONIC LUNG INFECTION

When would you investigate for chronic lung infection?

A
  • Any child with persistent cough that sounds wet (i.e. excess sputum in chest) or productive
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7
Q

TONSILLITIS

What causes it?

A
  • Strep pyogenes,

- viral more common but cannot clinically distinguish

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8
Q

TONSILLITIS

How does quinsy present?

A

Severe sore throat (unilateral), uvula deviation, lockjaw

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9
Q

TONSILLITIS

What is the management for quinsy?

A

Incision + drainage + IV Abx

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10
Q

SINUSITIS

What is the management?

A

Abx, topical decongestants + analgesia

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11
Q

WHOOPING COUGH

What causes the inspiratory whoop?

A

Forced inspiration against a closed glottis

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12
Q

CHRONIC LUNG INFECTION

What can cause it?

A

May have bronchiectasis (may show on CXR but CT chest best) due to CF, primary ciliary dyskinesia, immunodeficiency or chronic aspiration

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13
Q

INTESTINAL MALROTATION
What is intestinal malrotation?
What is the outcome?

A
  • During rotation of small bowel in foetal life, if mesentery not fixed at the duodenojejunal flexure or in the ileocaecal region, its base is shorter than normal
  • Predisposed to volvulus > obstruction > ischaemia
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14
Q

INTESTINAL MALROTATION
What can contribute to the obstruction in intestinal malrotation?
How may it present?

A
  • Ladd bands may cross the duodenum

- Obstruction or obstruction with compromised blood supply

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15
Q

INTESTINAL MALROTATION

What is the clinical presentation of intestinal malrotation?

A
  • First week of life bilious vomiting (below ampulla of vater) = malrotation until proven otherwise
  • Abdo pain
  • Tenderness (peritonitis, ischaemic bowel)
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16
Q

INTESTINAL MALROTATION

What is the investigation + management of intestinal malrotation?

A
  • Urgent upper GI contrast study is Dx, abdo USS

- Urgent surgical correction = Ladd’s procedure rotates bowel anti-clockwise

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17
Q

MESENTERIC ADENITIS

What is non-specific abdominal pain?

A
  • Abdo pain which resolves in 24–48h
  • Similar Sx to appendicitis but pain less severe + RIF tenderness variable
  • Often accompanied with viral URTI + cervical lymphadenopathy
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18
Q

MESENTERIC ADENITIS

What is the management of mesenteric adenitis?

A
  • Conservative

- Laparoscopy if abdo Sx persist = Dx mesenteric adenitis if large mesenteric nodes + normal appendix

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19
Q

ABDOMINAL MIGRAINE

What is an abdominal migraine?

A
  • Pain >1h, midline, paroxysmal + associated with facial pallor + vomiting
  • Can be associated with headache, photophobia + aura
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20
Q

ABDOMINAL MIGRAINE
What is the acute management of abdominal migraine?
What is the prophylaxis?
What is a caution?

A
  • Sumatriptan + paracetamol ± NSAID (ibuprofen)
  • Pizotifen (serotonin receptor antagonist) or propranolol
  • Withdraw pizotifen slowly as can cause depression, anxiety, poor sleep + tremor
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21
Q

FUNCTIONAL DYSPEPSIA

What is functional dyspepsia?

A
  • Epigastric pain, early satiety, bloating + postprandial vomiting
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22
Q

FUNCTIONAL DYSPEPSIA

What is the management of functional dyspepsia?

A
  • C-13 Urea breath test for H. pylori + upper GI endoscopy if Sx recur, if normal = Dx
  • Hypoallergenic diet
  • Eradicate H. pylori if suspected with triple therapy > omeprazole, amoxicillin + metronidazole or clarithromycin
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23
Q

VOMITING
Define…

i) posseting
ii) regurgitation
iii) vomiting

A

i) Non-forceful return of small amounts of milk usually accompanied by wind (normal)
ii) Non-forceful return of milk, larger + more frequent losses than in posseting + usually indicates reflux
iii) forceful ejection of gastric contents

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24
Q

VOMITING

What are some common causes of vomiting in infants?

A
  • GOR (v common)
  • Infection (gastroenteritis, pertussis, UTI, meningitis)
  • Dietary protein intolerances + feeding problems
  • Intestinal obstruction (pyloric stenosis, malrotation)
  • Inborn errors of metabolism, CAH
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25
Q

VOMITING

What are some common causes of vomiting in preschool children?

A
  • Gastroenteritis + infections
  • Appendicitis
  • Intestinal obstruction (intussusception, volvulus)
  • Raised ICP
  • Torsion
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26
Q

VOMITING

What are some common causes of vomiting in school-age children and adolescents?

A
  • Gastroenteritis, infection
  • Peptic ulceration + H. pylori
  • Appendicitis, raised ICP, DKA, alcohol/drugs
  • Bulimia/anorexia nervosa
  • Pregnancy
  • Torsion
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27
Q

VOMITING
What are some differentials for the below red flags…

i) bile-stained vomit?
ii) haematemesis?
iii) abdo distension?
iv) PR bleed?
v) severe dehydration + shock?
vi) failure to thrive?

A

i) Obstruction (malrotation, atresia, meconium ileus)
ii) Oesophagitis, peptic ulceration, oral/nasal bleed
iii) Obstruction incl. strangulated inguinal hernia
iv) Intussusception, gastroenteritis
v) Severe gastroenteritis, systemic infection, DKA
vi) GOR, coeliac, IBD, CMP allergy

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28
Q 
THREADWORMS
What are threadworms?
How does it present?
How is it investigated?
How is it treated?
A
  • Enterobius vermicularis
  • V common, perianal itching (esp. at night), girls may have vulval Sx
  • Sellotape perianal area + send to lab to visualise eggs
  • Anti-helminthic (mebendazole if >6m stat) + hygiene measures for WHOLE family
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29
Q

NEPHROTIC SYNDROME
What is focal segmental glomerulosclerosis?
Pathophysiology?
Management?

A
  • Most common, familial or idiopathic
  • Injury to podocytes that alters permeability of the glomeruli
  • May progress to ESRF, some respond to cytotoxic meds
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30
Q

NEPHROTIC SYNDROME
What is membranous nephropathy?
Associations?

A
  • Immunologically mediated disease of glomerular basement membrane
  • Associated with hep B, may precede SLE, most remit spontaneously in 5y
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31
Q

NEPHRITIC SYNDROME
What is IgA nephropathy?
How does it present?

A
  • IgA deposits in the nephrons of the kidney causes inflammation
  • Teenagers/young adults, related to HSP
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32
Q

NEPHRITIC SYNDROME

How does Goodpasture’s syndrome present?

A
  • Anti-glomerular basement membrane antibodies against type 4 collagen, also causes pulmonary haemorrhage
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33
Q

NEPHRITIC SYNDROME
What antibodies would you screen for?
What would renal biopsy show in IgA nephropathy?

A
  • Anti-dsDNA if SLE, ANCA in vasculitides

- IgA deposits + glomerular mesangial proliferation

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34
Q

VARICOCELE
What is a varicocele?
Which side is most likely?
How does it present?

A
  • Abnormal dilatation of the testicular veins
  • L sided due to angle of L testicular vein entering the L renal vein
  • ‘Bag of worms’, dragging or aching sensation, associated with subfertility
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35
Q

VARICOCELE

What is the management of varicocele?

A
  • Confirm with USS + Doppler studies

- Conservative unless pain

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36
Q

HYDROCELE
What is a hydrocele?
What are the 2 types?

A
  • Accumulation of fluid within the tunica vaginalis
  • Communicating = patency of processus vaginalis > peritoneal fluid draining into the scrotum (newborn males, often resolves within first few months)
  • Non-communicating = excess fluid production within the tunica vaginalis
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37
Q

HYDROCELE

What is the clinical presentation of hydrocele?

A
  • Soft, non-tender swelling of hemi-scrotum
  • Swelling is confined to scrotum + you can get ‘above’ the mass on examination
  • Transilluminates with a pen torch
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38
Q

HYDROCELE

What is the management of hydrocele?

A
  • USS to confirm

- Repair if not resolved by 2y

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39
Q

INGUINAL HERNIA
What is an inguinal hernia and what causes it?
Epidemiology?

A
  • Almost always indirect + due to patent processus vaginalis

- More common in boys + prematures infants

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40
Q

INGUINAL HERNIA

What is the clinical presentation of an inguinal hernia?

A
  • Intermittent swelling in groin/scrotum on crying or straining
  • Unable to get ‘above’ it on examination, often is reducible
  • If strangulated may have N+V, severe pain
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41
Q

INGUINAL HERNIA

What is the management of an inguinal hernia?

A
  • Surgical repair to avoid risk of strangulation (bowel obstruction + perforation)
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42
Q

DIABETES MELLITUS

What is the physiology of insulin?

A
  • Lowers blood glucose by stimulating uptake from blood into muscle, kidney + fat cells as well as targeting the liver to convert glucose to glycogen
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43
Q

DIABETES MELLITUS

What is the pathophysiology of insulin in T1DM?

A
  • Absolute insulin deficiency means that glycogenolysis, gluconeogenesis + lipolysis are not suppressed + there is reduced peripheral glucose uptake > hyperglycaemia
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44
Q

DIABETES MELLITUS

What causes T1DM?

A
  • Autoimmune destruction of the pancreatic beta cells

- Associated with HLA-DR3 + HLA-DR4 genetics + environment

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45
Q

DIABETES MELLITUS

What is the clinical presentation of T1DM?

A
  • Can be incidental finding
  • Polydipsia, polyuria (+ nocturia, weight loss, fatigue
  • Less commonly secondary enuresis or recurrent infections
  • Left untreated > DKA
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46
Q

DIABETES MELLITUS

How can T1DM be diagnosed?

A
  • Symptomatic = 1 reading, asymptomatic = 2 separate readings
  • Fasting glucose ≥7.0mmol/L
  • Random glucose ≥11.1mmol/L (or 2h after 75g OGTT)
  • HbA1c ≥48mmol/mol (long-term impression of control)
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47
Q

DIABETES MELLITUS

What are the subthreshold measurements for TD1M?

A
  • Impaired fasting glucose 6.1-6.9mmol/L
  • Impaired glucose tolerance 7.8-11.1mmol/L
  • Pre-diabetes 42-47mmol/mol (HbA1c)
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48
Q

DIABETES MELLITUS
What can cause poor glycaemic control in T1DM?
What is the impact?

A
  • Many factors can increase glucose (sex hormones at puberty, stress, illness, food) or decrease (insulin, exercise, alcohol, some drugs)
  • May have hyperglycaemia + need insulin dose increased or hypoglycaemia or worst case DKA
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49
Q

DIABETES MELLITUS

What are some complications of T1DM?

A
  • Macrovascular
  • Microvascular
  • Increased risk of illnesses (UTIs, pneumonia, fungal infections)
  • Screen for other autoimmune conditions (TFTs + TPO Ab, anti-TTG, insulin Abs)
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50
Q

DIABETES MELLITUS

What are some macrovascular complications of T1DM?

A
  • IHD
  • Peripheral ischaemia > poor healing ulcers + “diabetic foot”
  • Stroke + HTN (check BP annually)
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51
Q

DIABETES MELLITUS

What are some microvascular complications of T1DM?

A
  • Peripheral neuropathy = good foot care with treating infections early
  • Retinopathy = annual check-up after 5y of diabetes or after puberty
  • Renal disease (esp. glomerulosclerosis) = annual screening for microalbuminuria
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52
Q

DIABETES MELLITUS

What is the main conservative management for T1DM?

A
  • Diet = reduced refined carbs, carb counting, high fibre
  • Adjust diet + insulin for exercise, ‘sick-day rules’
  • BMs = capillary BM to adjust insulin or continuous glucose monitoring like FreeStyle Libre (lag in results mean confirm hypo with capillary BM)
  • Recognising + treating hypos
  • Support groups (Diabetes UK)
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53
Q

DIABETES MELLITUS
What is the mainstay medical management of T1DM?
What regime is often used?

A
  • Insulin
  • Basal bolus = basal > long-acting insulin like Lantus given in evening as background, bolus > short-acting insulin like Actrapid before meals according to carb counting
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54
Q

DIABETES MELLITUS
What may be offered to individuals who struggle to control their blood sugars with basal bolus regime?
What are the pros/cons?

A
  • Insulin pump to continuously infuse insulin at different rates
  • Better at glucose control, more eating flexibility + less injections
  • But attached constantly, can have blockages + small risk of infection
55
Q

DIABETES MELLITUS

What are some negatives about insulin therapy in general?

A
  • Lipohypertrophy (rotate site)
  • Risk of hypoglycaemia
  • Weight gain
56
Q

DIABETES MELLITUS
When would you suspect T2DM in children?
How may it present?

A
  • V uncommon, suspect if FHx, from Indian subcontinent + severely obese
  • Can have signs of insulin resistance (acanthosis nigricans, skin tags or PCOS)
57
Q

DIABETIC KETOACIDOSIS

What is the pathophysiology of diabetic ketoacidosis (DKA)?

A
  • Absence of insulin leads to uncontrollable lipolysis

- Increased production of free fatty acids which are oxidised in the liver to ketone bodies leading to ketoacidosis

58
Q

DIABETIC KETOACIDOSIS

How does the body respond to ketoacidosis?

A
  • Initially, kidney produces bicarbonate to counteract but this is used up > acidotic
  • Hyperglycaemia overwhelms the kidneys + glucose starts being filtered into the urine + draws water out with it in the process (osmotic diuresis) leading to polyuria + severe dehydration, stimulating thirst centre (polydipsia)
59
Q

DIABETIC KETOACIDOSIS

What is the effect on potassium in DKA?

A
  • Kidneys excrete K+ in urine so overall body K+ is low so when treatment with insulin starts can develop severe hypokalaemia as insulin drives K+ into cells
60
Q

DIABETIC KETOACIDOSIS

What is the clinical presentation of DKA?

A
  • Smell of acetone on breath (pear drops)
  • Vomiting, dehydration, abdominal pain
  • Hyperventilation due to acidosis (Kussmaul’s breathing)
  • Drowsiness, coma + hypovolaemic shock
61
Q

DIABETIC KETOACIDOSIS

What are some investigations for DKA?

A

Diagnosis –
- Glucose >11mmol/L
- Blood ketones >3mmol/L
- Blood gas pH <7.3 or bicarb <15mmol/L (metabolic acidosis)
ECG = signs of hypokalaemia (U waves, small/absent T, long PR, ST depression)
- U+Es + creatinine show dehydration, hypokalaemia

62
Q

DIABETIC KETOACIDOSIS

What are some complications of DKA?

A
  • Cerebral oedema (neuro obs)
  • VTE
  • Hypokalaemia > arrhythmias
  • AKI
63
Q

DIABETIC KETOACIDOSIS

What is the initial management of DKA?

A
  • ABCDE = ?airway, 100% oxygen by face mask, IV cannula + bloods, cardiac monitor, BP + HR
  • Aggressive IV fluid resus over 48h is first CRUCIAL step
64
Q

DIABETIC KETOACIDOSIS

How do you calculate how dehydrated someone is in DKA?

A
  • 5% if pH 7.2–7.29 or bicarbonate <15 (mild)
  • 7% if ph 7.1–7.19 or bicarbonate <10 (mod)
  • 10% if pH <7.1 or bicarbonate <5 (severe)
65
Q

DIABETIC KETOACIDOSIS
What fluids do you give in DKA for…

i) shock?
ii) not shocked but needs fluids?
iii) maintenance?

A

i) 1st bolus = 0.9% NaCl 20ml/kg, subsequent 10ml/kg, do NOT subtract bolus from deficit
ii) 0.9% NaCl 10ml/kg over 1 hour, DO subtract bolus from deficit
iii) 0.9% NaCl with 40mmol/L KCl (20mmol in 500ml bag)

66
Q

DIABETIC KETOACIDOSIS
Why do you rehydrate slowly over 48h?
Management?

A
  • Risk of cerebral oedema = headache, altered behaviour or GCS
  • CT head, IV mannitol + hypertonic saline if suspect
67
Q

DIABETIC KETOACIDOSIS

What is the further management of DKA after fluid resus has been commenced?

A
  • Insulin infusion 1-2h after IV fluids = Actrapid 0.05-0.1 unit/kg/h
  • Once blood glucose <15mmol/L, add 5% dextrose to fluids
  • Monitor ketones, glucose, plasma electrolytes, GCS, obs, strict fluid balance hourly
68
Q

HYPOGLYCAEMIA
What is hypoglycemia?
What can it be due to?

A
  • Low blood sugar level, defined as <2.6mmol/L

- Too much insulin, lack of carbs or not processing the carbs properly (diarrhoea, vomiting, malabsorption)

69
Q

HYPOGLYCAEMIA

What is the clinical presentation of hypoglycaemia?

A
  • Tremor, sweating, irritability, nauseous, dizzy, pale, confused, drowsy
  • More severe = reduced GCS, coma, seizures + even death
  • Hypo phenomena
70
Q

HYPOGLYCAEMIA

What are some hypo phenomena?

A
  • Hypo unawareness
  • Reactive hypoglycaemia (after meal)
  • Somogyi = post-hypoglycaemic hyperglycaemia
  • Dawn phenomena = morning rise in blood sugar
71
Q

HYPOGLYCAEMIA

What is the management of mild-moderate hypoglycaemia?

A
  • Check BM to confirm + lab confirmation
  • PO if can tolerate with rapid acting glucose (sugary drink)
  • Follow up with longer acting carb (biscuits, toast)
  • Glucogel if cannot tolerate, check BM after 15m
72
Q

HYPOGLYCAEMIA

What is the management of severe hypoglycaemia?

A
  • Do NOT attempt to give anything orally
  • IV dextrose (2ml/kg bolus then infusion)
  • IM glucagon (<5y = 0.5mg, >5y 1mg)
  • Wait 10m + if conscious give longer-acting carb
73
Q

APNOEA OF PREMATURITY

What is apnoea of prematurity?

A
  • Periods where breathing stops spontaneously for >20s (or shorter periods with oxygen desaturation or bradycardia
  • Common, esp <28w
74
Q

APNOEA OF PREMATURITY
What causes apnoea of prematurity?
What are some underlying causes?

A
  • Immature autonomic nervous system as brainstem not fully myelinated until 32–34w so pontine resp centre not fully developed
  • Hypoxia, infection, CNS pathology, GOR
75
Q

APNOEA OF PREMATURITY

What is the management of apnoea of prematurity?

A
  • Gentle tactile stimulation when alerted by apnoea monitors
  • Resp stimulant like IV caffeine
  • May need CPAP if frequent
76
Q

IV HAEMORRHAGE
What is an intraventricular haemorrhage?
When is it more common?

A
  • Haemorrhage in the ventricular system

- Following perinatal asphyxia + in infants with severe RDS

77
Q

IV HAEMORRHAGE
Where do intraventricular haemorrhages occur?
What is a complication?

A
  • Typically germinal matrix above caudate nucleus which contains fragile network of blood vessels
  • Large haemorrhages may impair drainage + reabsorption of CSF > hydrocephalus
78
Q

IV HAEMORRHAGE

What is the management of intraventricular haemorrhage?

A
  • Cranial USS
  • Sx relief with removal of CSF by LP or ventricular tap
  • Ventriculoperitoneal shunt may be needed for hydrocephalus
79
Q

RETINOPATHY
What is the pathophysiology of retinopathy of prematurity?
What may this lead to?

A
  • Affects developing blood vessels at junction of the vascular + non-vascularised retina
  • Retinal blood vessel formation is stimulated by hypoxia so hyperoxic insult can prevent this
  • Retina responds with vascular proliferation which may progress to retinal detachment, fibrosis + blindness
80
Q

RETINOPATHY
What are some risk factors for retinopathy of prematurity?
What is the clinical presentation?

A
  • Use of high oxygen conc, very LBW (<1.5kg), premature babies <32w
  • Plus disease describes other findings like tortuous vessels + hazy vitreous humour
81
Q

RETINOPATHY

What is the management of retinopathy of prematurity?

A
  • Regular eye screening by ophthalmologist for susceptible preterm infants (<1.5kg or <32w), must visualise all retinal areas
  • Transpupillary laser photocoagulation to halt + reverse neovascularisation
82
Q

CDH
What is congenital diaphragmatic hernia?
Most common type?

A
  • Failure of pleuroperitoneal cavity to close completely

- Most common is Bochdalek hernia (L sided posterior-lateral)

83
Q

CDH

What is the clinical presentation of congenital diaphragmatic hernia?

A
  • Resp distress, lung hypoplasia (prevents lungs to develop throughout pregnancy) + pulmonary HTN
  • Heart sounds louder on R, poor air entry on L
  • Tinkling bowel sounds
84
Q

CDH

What is the management of congenital diaphragmatic hernia?

A
  • Often Dx on antenatal USS, CXR = bowel in lungs

- NG feeding, intubation + ventilation prior to surgery

85
Q

NEONATAL SEPSIS

What are some risk factors of neonatal sepsis?

A
  • Vaginal GBS colonisation
  • GBS sepsis in previous baby
  • Maternal sepsis
  • Fever >38
  • Chorioamnionitis
  • PPROM
  • Preterm babies
86
Q

NEONATAL SEPSIS

What are some causes of neonatal sepsis?

A
  • GBS (strep. agalactiae) from genital tract #1 (mostly pneumonia, also meningitis)
  • E. Coli, Klebsiella, S. aureus
  • Listeria monocytogenes (unpasteurised milk, soft cheese, undercooked poultry)
    – Can also cause spontaneous abortion + preterm delivery
87
Q

NEONATAL SEPSIS
What is the likely source of infection if it develops…

i) <48h?
ii) >48h?

A

i) Birth canal

ii) Environment (catheters, tracheal tubes, bloods) = mostly strep epidermidis

88
Q

NEONATAL SEPSIS

What is the clinical presentation of neonatal sepsis?

A
  • Fever or hypothermia
  • Poor feeding + vomiting, hypoglycaemia
  • Apnoea, resp distress (grunting, nasal flaring) + tachycardia
  • Seizures, jaundice
89
Q

NEONATAL SEPSIS

What are the investigations for neonatal sepsis?

A

Septic screen –

  • FBC, CRP, blood cultures
  • Blood gas (metabolic acidosis worrying)
  • Urine MC&S
  • CXR
  • LP for CSF sample
90
Q

NEONATAL SEPSIS

How can neonatal sepsis be prevented?

A
  • High risk GBS women are screened or offered intrapartum Abx
91
Q

NEONATAL SEPSIS

What is the management of neonatal sepsis?

A
  • Treatment before culture results
  • IV benzylpenicillin (gram +ve) + gentamycin (gram -ve) = 1st line
  • Consider 3rd gen cephalosporin (IV cefotaxime) if lower risk
  • Maintain oxygenation, normal fluid + electrolytes, prevent/manage metabolic acidosis + hypoglycaemia
92
Q

NEONATAL SEPSIS

How can response to treatment be monitored in neonatal sepsis?

A
  • Check CRP 24h after presentation, re-check at 5d if still on treatment
  • At 48h if cultures negative + CRP <10mg/L = stop Abx
93
Q 
DUODENAL ATRESIA
What is duodenal atresia?
What can confirm it?
What is it associated with?
What is the management?
A
  • Congenital absence or complete closure of duodenum > intestinal obstruction
  • AXR shows ‘double bubble’ from distension of stomach + duodenal cap
  • Third have Down’s
  • Correct fluid + electrolyte depletion > surgical Mx
94
Q

EXOMPHALOS

What is exomphalos, or omphalocele?

A
  • Abdominal contents protrude through umbilical ring, covered with a transparent sac formed by the amniotic membrane + peritoneum
95
Q

EXOMPHALOS
What is exomphalos associated with?
What is the management?

A
  • Other major congenital abnormalities, antenatal Dx

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

96
Q

NEONATAL CONJUNCTIVITIS
What is neonatal conjunctivitis?
What is the management?

A
  • Common starting day 3–4
  • Usually just cleaning with water or saline
  • More troublesome discharge or redness of eye may be staph/strep so topical Abx eye ointment like neomycin
97
Q

NEONATAL CONJUNCTIVITIS
In terms of neonatal conjunctivitis, how would…

i) gonococcal infection
ii) chlamydia infection

present and what is the management of both?

A

i) Purulent discharge, conjunctival injection, eyelid swelling, within 48h
– Gram stain, IV ceftriaxone + cleanse frequently (can lose vision)
ii) Purulent discharge, eyelid swelling, 1-2w
– Immunofluorescent staining, PO erythromycin for 2w

98
Q

SIDS

What are some major risk factors for SIDS?

A
  • Baby sleeping prone
  • Parental smoking (during pregnancy or in same room)
  • LBW + prematurity
  • Sharing a bed
  • Hyperthermia (over wrapping) or head covering (blanket moving)
99
Q

SIDS

What are some other risk factors for SIDS?

A
  • M>F
  • Low socioeconomic status
  • Infant pillow use
  • Maternal drug use
100
Q

SIDS

What are some protective factors from SIDS?

A
  • Breastfeeding
  • Room (NOT bed) sharing
  • Use of dummies
101
Q

SIDS

What is the management of SIDS?

A
  • Following cot death screen siblings for sepsis + inborn errors of metabolism
  • Infants sleep on backs, ‘feet-to-foot’ position
  • Do not smoke near them
  • Bedroom for first 6m
102
Q

TRANSIENT TACHYPNOEA
What is transient tachypnoea of the newborn?
What is it caused by?

A
  • Commonest cause of resp distress in term infants
  • Delay in resorption of lung fluid, commoner after c-section ?fluid not ‘squeezed out’ during passage through birth canal
103
Q

TRANSIENT TACHYPNOEA

What is the clinical presentation?

A
  • Tachypnoea after birth which resolves usually 48h
104
Q

TRANSIENT TACHYPNOEA

What is the management of transient tachypnoea of the newborn?

A
  • CXR may show hyperinflation + fluid in horizontal fissure
  • Dx after other causes excluded
  • Supplementary oxygen may be needed to maintain SpO2
105
Q

NUTRITION

What are the advantages of breastfeeding?

A
  • Free
  • Helps bonding
  • Lactational amenorrhoea
  • Reduces risk of NEC in preterm infants + SIDS
  • Antibodies to protect neonate against infection
  • Reduced maternal risk of breast + ovarian cancer
106
Q

NUTRITION

What are the disadvantages of breastfeeding?

A
  • Breast milk jaundice
  • Unknown intake so ?eating adequately
  • Discomfort for mother
  • Transmission of drugs or infections to baby
  • Insufficient vitamin D + K (reason for vitamin K IM injection at birth)
107
Q

NUTRITION
What is weaning?
When is it typically done?

A
  • Gradual transition from milk to normal food

- 6m with pureed foods that are easy to palate, swallow + digest > normal, healthy diet

108
Q

ROSEOLA INFANTUM
What is roseola infantum?
How is it spread?

A
  • Caused by human herpes virus 6+7

- Classically most children infected by age 2, often from oral secretions of a family member

109
Q

ROSEOLA INFANTUM
What is the clinical presentation of roseola infantum?
What is a key feature of roseola infantum?

A
  • High fever (up to 40) with malaise lasting a few days + then settles suddenly
  • As fever settled, followed by generalised macular rash (chest > limbs)
  • Common cause of febrile convulsions
110
Q

ROSEOLA INFANTUM

What is the management of roseola infantum?

A
  • Often full recovery in a week with no school exclusion if well
111
Q

COMMON KNEE ISSUES
What is chondromalacia patellae?
How does it present?
What is the management

A
  • Softening of the cartilage of the patellar, common in teenage girls
  • Anterior knee pain on walking up/downstairs + rising from prolonged sitting
  • Usually responds to physiotherapy
112
Q

COMMON KNEE ISSUES
What is patellar tendonitis?
Who is it more common in?

A
  • Chronic anterior knee pain that worsens after running, tender below patellar on examination
  • More common in athletic teenage boys
113
Q

COMMON KNEE ISSUES
What is…

i) osteochondritis dissecans?
ii) patellar subluxation?

A

i) Pain after exercise with intermittent swelling

ii) Medial knee pain due to lateral subluxation of the patellar, knee may give way

114
Q

ACHONDROPLASIA
What is achondroplasia?
How does it occur?

A
  • Skeletal dysplasia leading to disproportionate short stature (dwarfism)
  • Abnormal function of epiphyseal (growth) plates which restricts bone growth
115
Q

ACHONDROPLASIA

What is the aetiology of achondroplasia?

A
  • Autosomal dominant, abnormal fibroblast growth factor receptor 3 (FGFR-3) gene
  • Always heterozygous as homozygous is fatal
116
Q

ACHONDROPLASIA

What is the clinical presentation of achondroplasia?

A
  • Short stature from marked shortening of limbs + fingers
  • Large head with frontal bossing + depression of nasal bridge
  • ‘Trident’ hands + marked lumbar lordosis
117
Q

ACHONDROPLASIA

What are some complications of achondroplasia?

A
  • Foramen magnum stenosis > cervical cord compression + hydrocephalus
  • Recurrent otitis media (cranial abnormalities)
  • Obstructive sleep apnoea
  • Obesity
118
Q

ACHONDROPLASIA

What is the management of achondroplasia?

A
  • No cure but MDT approach to maximise functioning = paeds, specialist nurses, PT/OT, geneticists
  • ?Leg lengthening (controversial)
119
Q

TALIPES
What is talipes?

A
  • Fixed abnormal ankle position
120
Q

TALIPES
What causes talipes equinovarus?

A
  • Idiopathic or secondary to oligohydramnios
121
Q

SEBORRHOEIC DERMATITIS

What is seborrhoeic dermatitis?

A
  • Inflammatory skin condition that affects sebaceous glands which produce oil
  • Sebaceous glands plentiful at scalp, nasolabial folds + eyebrows
122
Q

SEBORRHOEIC DERMATITIS

What are the 3 types of seborrhoeic dermatitis?

A
  • Infantile (cradle cap) = erythematous scaly eruption, yellow, not itchy
  • Scalp = flaky, itchy skin on scalp (dandruff)
  • Face + body = widespread red, flaky, crusted itchy skin > eyelids, nasolabial folds, upper chest + body
123
Q

SEBORRHOEIC DERMATITIS
What is the management of…

i) infantile seborrhoeic?
ii) scalp seborrhoeic?
iii) face + body seborrhoeic?

A

i) 1st line = baby shampoo + olive oil (petroleum jelly can be used overnight to soften + wash in morning), severe = mild topical steroids (1% hydrocortisone)
ii) Ketoconazole shampoo or topical steroids
iii) 1st line = anti-fungal creams (clotrimazole) or topical steroids

124
Q

HEAD LICE
What are head lice?
How do they spread?

A
  • Pediculus capitis = parasitic insects that infest hairs + feed on blood from scalp
  • Direct head-head contact so often schools
125
Q

HEAD LICE

What is the clinical presentation of head lice?

A
  • Infestation causes itchy scalp
  • Suboccipital lymphadenopathy
  • Nits (eggs) + lice visible with Dx on fine-toothed combing of hair
126
Q

HEAD LICE

What is the management of headlice?

A
  • Dimeticone 4% or malathion 0.5% lotions, leave overnight then wash off (repeat 7d later to kill any head lice hatched since)
  • Special fine combs + wet combing (bug-busting) every 3–4d for 2w
127
Q

SCABIES

What is scabies?

A
  • Infestation of mites (Sarcoptes scabiei) that burrow under skin + lay eggs
  • Can take 8w for Sx (delayed type 4 hypersensitivity reaction)
128
Q

SCABIES
What is the clinical presentation of scabies?
Classic location?
When would you suspect it?

A
  • Very itchy burrows, papules + vesicles (may be track marks from mites)
  • Classic location between finger webs, can spread to whole body
  • Suspect if child + family itching
129
Q

SCABIES

What are some complications of scabies?

A
  • Crusted scabies = serious infestation in immunocompromised
    – Patches of red skin > scaly plaques, may not itch
    – Rx inpatient with PO ivermectin + isolation (v contagious)
  • Scratching leads to excoriation + secondary bacterial infection
130
Q

SCABIES

What is the management of scabies?

A
  • Very contagious so ALL close contacts Tx > school exclusion until treated
  • Wash bed linen, towels, clothes + clean furniture to destroy mites
  • 5% permethrin cream to cover whole body for 8–12h then wash it off, repeat in 1w
  • Malathion 0.5% cream second line
131
Q

HYPERTHYROIDISM
What is the most common cause of hyperthyroidism?
What causes it in neonates?

A
  • Graves’ disease (autoimmune) secondary to production of thyroid stimulating immunoglobulins
  • Transplacental IgG exchange if mother has Graves’ disease
132
Q

HYPERTHYROIDISM

What is the clinical presentation of hyperthyroidism?

A
  • Sweating, increased appetite, weight loss
  • Diarrhoea, psychosis, tremor, tachycardia
  • Rapid growth in height + advanced bone maturity
  • Eye disease less common in children
133
Q

HYPERTHYROIDISM

What are the investigations for hyperthyroidism?

A
  • TFTs = T3/4 high, TSH low

- TSH receptor stimulating antibody (TRAb) in Graves’ disease

134
Q

HYPERTHYROIDISM

What is the management of hyperthyroidism?

A
  • 1st line = carbimazole or propylthiouracil (either dose titration or block + replace with thyroxine)
  • Radioiodine can be used too
  • May need subtotal thyroidectomy to give permanent remission
  • Beta-blockers for symptomatic relief

B TO REVISE - PHASE 3A (9 decks)

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