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
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)
3
Q
TONSILLITIS
What is the main complication of tonsillitis?
A
- Quinsy (peritonsillar abscess)
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
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
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
7
Q
TONSILLITIS
What causes it?
A
- Strep pyogenes,
- viral more common but cannot clinically distinguish
8
Q
TONSILLITIS
How does quinsy present?
A
Severe sore throat (unilateral), uvula deviation, lockjaw
9
Q
TONSILLITIS
What is the management for quinsy?
A
Incision + drainage + IV Abx
10
Q
SINUSITIS
What is the management?
A
Abx, topical decongestants + analgesia
11
Q
WHOOPING COUGH
What causes the inspiratory whoop?
A
Forced inspiration against a closed glottis
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
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
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
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)
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
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
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
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
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
21
Q
FUNCTIONAL DYSPEPSIA
What is functional dyspepsia?
A
- Epigastric pain, early satiety, bloating + postprandial vomiting
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
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
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
25
VOMITING
| What are some common causes of vomiting in preschool children?
- Gastroenteritis + infections
- Appendicitis
- Intestinal obstruction (intussusception, volvulus)
- Raised ICP
- Torsion
26
VOMITING
| What are some common causes of vomiting in school-age children and adolescents?
- Gastroenteritis, infection
- Peptic ulceration + H. pylori
- Appendicitis, raised ICP, DKA, alcohol/drugs
- Bulimia/anorexia nervosa
- Pregnancy
- Torsion
27
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?
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
28
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THREADWORMS
What are threadworms?
How does it present?
How is it investigated?
How is it treated?
```
- 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
29
NEPHROTIC SYNDROME
What is focal segmental glomerulosclerosis?
Pathophysiology?
Management?
- Most common, familial or idiopathic
- Injury to podocytes that alters permeability of the glomeruli
- May progress to ESRF, some respond to cytotoxic meds
30
NEPHROTIC SYNDROME
What is membranous nephropathy?
Associations?
- Immunologically mediated disease of glomerular basement membrane
- Associated with hep B, may precede SLE, most remit spontaneously in 5y
31
NEPHRITIC SYNDROME
What is IgA nephropathy?
How does it present?
- IgA deposits in the nephrons of the kidney causes inflammation
- Teenagers/young adults, related to HSP
32
NEPHRITIC SYNDROME
| How does Goodpasture's syndrome present?
- Anti-glomerular basement membrane antibodies against type 4 collagen, also causes pulmonary haemorrhage
33
NEPHRITIC SYNDROME
What antibodies would you screen for?
What would renal biopsy show in IgA nephropathy?
- Anti-dsDNA if SLE, ANCA in vasculitides
| - IgA deposits + glomerular mesangial proliferation
34
VARICOCELE
What is a varicocele?
Which side is most likely?
How does it present?
- 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
35
VARICOCELE
| What is the management of varicocele?
- Confirm with USS + Doppler studies
| - Conservative unless pain
36
HYDROCELE
What is a hydrocele?
What are the 2 types?
- 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
37
HYDROCELE
| What is the clinical presentation of hydrocele?
- 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
38
HYDROCELE
| What is the management of hydrocele?
- USS to confirm
| - Repair if not resolved by 2y
39
INGUINAL HERNIA
What is an inguinal hernia and what causes it?
Epidemiology?
- Almost always indirect + due to patent processus vaginalis
| - More common in boys + prematures infants
40
INGUINAL HERNIA
| What is the clinical presentation of an inguinal hernia?
- 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
41
INGUINAL HERNIA
| What is the management of an inguinal hernia?
- Surgical repair to avoid risk of strangulation (bowel obstruction + perforation)
42
DIABETES MELLITUS
| What is the physiology of insulin?
- Lowers blood glucose by stimulating uptake from blood into muscle, kidney + fat cells as well as targeting the liver to convert glucose to glycogen
43
DIABETES MELLITUS
| What is the pathophysiology of insulin in T1DM?
- Absolute insulin deficiency means that glycogenolysis, gluconeogenesis + lipolysis are not suppressed + there is reduced peripheral glucose uptake > hyperglycaemia
44
DIABETES MELLITUS
| What causes T1DM?
- Autoimmune destruction of the pancreatic beta cells
| - Associated with HLA-DR3 + HLA-DR4 genetics + environment
45
DIABETES MELLITUS
| What is the clinical presentation of T1DM?
- Can be incidental finding
- Polydipsia, polyuria (+ nocturia, weight loss, fatigue
- Less commonly secondary enuresis or recurrent infections
- Left untreated > DKA
46
DIABETES MELLITUS
| How can T1DM be diagnosed?
- 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)
47
DIABETES MELLITUS
| What are the subthreshold measurements for TD1M?
- Impaired fasting glucose 6.1-6.9mmol/L
- Impaired glucose tolerance 7.8-11.1mmol/L
- Pre-diabetes 42-47mmol/mol (HbA1c)
48
DIABETES MELLITUS
What can cause poor glycaemic control in T1DM?
What is the impact?
- 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
49
DIABETES MELLITUS
| What are some complications of T1DM?
- Macrovascular
- Microvascular
- Increased risk of illnesses (UTIs, pneumonia, fungal infections)
- Screen for other autoimmune conditions (TFTs + TPO Ab, anti-TTG, insulin Abs)
50
DIABETES MELLITUS
| What are some macrovascular complications of T1DM?
- IHD
- Peripheral ischaemia > poor healing ulcers + "diabetic foot"
- Stroke + HTN (check BP annually)
51
DIABETES MELLITUS
| What are some microvascular complications of T1DM?
- 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
52
DIABETES MELLITUS
| What is the main conservative management for T1DM?
- 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)
53
DIABETES MELLITUS
What is the mainstay medical management of T1DM?
What regime is often used?
- 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
54
DIABETES MELLITUS
What may be offered to individuals who struggle to control their blood sugars with basal bolus regime?
What are the pros/cons?
- 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
DIABETES MELLITUS
| What are some negatives about insulin therapy in general?
- Lipohypertrophy (rotate site)
- Risk of hypoglycaemia
- Weight gain
56
DIABETES MELLITUS
When would you suspect T2DM in children?
How may it present?
- V uncommon, suspect if FHx, from Indian subcontinent + severely obese
- Can have signs of insulin resistance (acanthosis nigricans, skin tags or PCOS)
57
DIABETIC KETOACIDOSIS
| What is the pathophysiology of diabetic ketoacidosis (DKA)?
- 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
DIABETIC KETOACIDOSIS
| How does the body respond to ketoacidosis?
- 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
DIABETIC KETOACIDOSIS
| What is the effect on potassium in DKA?
- 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
DIABETIC KETOACIDOSIS
| What is the clinical presentation of DKA?
- Smell of acetone on breath (pear drops)
- Vomiting, dehydration, abdominal pain
- Hyperventilation due to acidosis (Kussmaul's breathing)
- Drowsiness, coma + hypovolaemic shock
61
DIABETIC KETOACIDOSIS
| What are some investigations for DKA?
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
DIABETIC KETOACIDOSIS
| What are some complications of DKA?
- Cerebral oedema (neuro obs)
- VTE
- Hypokalaemia > arrhythmias
- AKI
63
DIABETIC KETOACIDOSIS
| What is the initial management of DKA?
- 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
DIABETIC KETOACIDOSIS
| How do you calculate how dehydrated someone is in DKA?
- 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
DIABETIC KETOACIDOSIS
What fluids do you give in DKA for...
i) shock?
ii) not shocked but needs fluids?
iii) maintenance?
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
DIABETIC KETOACIDOSIS
Why do you rehydrate slowly over 48h?
Management?
- Risk of cerebral oedema = headache, altered behaviour or GCS
- CT head, IV mannitol + hypertonic saline if suspect
67
DIABETIC KETOACIDOSIS
| What is the further management of DKA after fluid resus has been commenced?
- 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
HYPOGLYCAEMIA
What is hypoglycemia?
What can it be due to?
- 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
HYPOGLYCAEMIA
| What is the clinical presentation of hypoglycaemia?
- Tremor, sweating, irritability, nauseous, dizzy, pale, confused, drowsy
- More severe = reduced GCS, coma, seizures + even death
- Hypo phenomena
70
HYPOGLYCAEMIA
| What are some hypo phenomena?
- Hypo unawareness
- Reactive hypoglycaemia (after meal)
- Somogyi = post-hypoglycaemic hyperglycaemia
- Dawn phenomena = morning rise in blood sugar
71
HYPOGLYCAEMIA
| What is the management of mild-moderate hypoglycaemia?
- 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
HYPOGLYCAEMIA
| What is the management of severe hypoglycaemia?
- 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
APNOEA OF PREMATURITY
| What is apnoea of prematurity?
- Periods where breathing stops spontaneously for >20s (or shorter periods with oxygen desaturation or bradycardia
- Common, esp <28w
74
APNOEA OF PREMATURITY
What causes apnoea of prematurity?
What are some underlying causes?
- 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
APNOEA OF PREMATURITY
| What is the management of apnoea of prematurity?
- Gentle tactile stimulation when alerted by apnoea monitors
- Resp stimulant like IV caffeine
- May need CPAP if frequent
76
IV HAEMORRHAGE
What is an intraventricular haemorrhage?
When is it more common?
- Haemorrhage in the ventricular system
| - Following perinatal asphyxia + in infants with severe RDS
77
IV HAEMORRHAGE
Where do intraventricular haemorrhages occur?
What is a complication?
- Typically germinal matrix above caudate nucleus which contains fragile network of blood vessels
- Large haemorrhages may impair drainage + reabsorption of CSF > hydrocephalus
78
IV HAEMORRHAGE
| What is the management of intraventricular haemorrhage?
- Cranial USS
- Sx relief with removal of CSF by LP or ventricular tap
- Ventriculoperitoneal shunt may be needed for hydrocephalus
79
RETINOPATHY
What is the pathophysiology of retinopathy of prematurity?
What may this lead to?
- 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
RETINOPATHY
What are some risk factors for retinopathy of prematurity?
What is the clinical presentation?
- Use of high oxygen conc, very LBW (<1.5kg), premature babies <32w
- Plus disease describes other findings like tortuous vessels + hazy vitreous humour
81
RETINOPATHY
| What is the management of retinopathy of prematurity?
- 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
CDH
What is congenital diaphragmatic hernia?
Most common type?
- Failure of pleuroperitoneal cavity to close completely
| - Most common is Bochdalek hernia (L sided posterior-lateral)
83
CDH
| What is the clinical presentation of congenital diaphragmatic hernia?
- 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
CDH
| What is the management of congenital diaphragmatic hernia?
- Often Dx on antenatal USS, CXR = bowel in lungs
| - NG feeding, intubation + ventilation prior to surgery
85
NEONATAL SEPSIS
| What are some risk factors of neonatal sepsis?
- Vaginal GBS colonisation
- GBS sepsis in previous baby
- Maternal sepsis
- Fever >38
- Chorioamnionitis
- PPROM
- Preterm babies
86
NEONATAL SEPSIS
| What are some causes of neonatal sepsis?
- 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
NEONATAL SEPSIS
What is the likely source of infection if it develops...
i) <48h?
ii) >48h?
i) Birth canal
| ii) Environment (catheters, tracheal tubes, bloods) = mostly strep epidermidis
88
NEONATAL SEPSIS
| What is the clinical presentation of neonatal sepsis?
- Fever or hypothermia
- Poor feeding + vomiting, hypoglycaemia
- Apnoea, resp distress (grunting, nasal flaring) + tachycardia
- Seizures, jaundice
89
NEONATAL SEPSIS
| What are the investigations for neonatal sepsis?
Septic screen –
- FBC, CRP, blood cultures
- Blood gas (metabolic acidosis worrying)
- Urine MC&S
- CXR
- LP for CSF sample
90
NEONATAL SEPSIS
| How can neonatal sepsis be prevented?
- High risk GBS women are screened or offered intrapartum Abx
91
NEONATAL SEPSIS
| What is the management of neonatal sepsis?
- 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
NEONATAL SEPSIS
| How can response to treatment be monitored in neonatal sepsis?
- Check CRP 24h after presentation, re-check at 5d if still on treatment
- At 48h if cultures negative + CRP <10mg/L = stop Abx
93
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DUODENAL ATRESIA
What is duodenal atresia?
What can confirm it?
What is it associated with?
What is the management?
```
- 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
EXOMPHALOS
| What is exomphalos, or omphalocele?
- Abdominal contents protrude through umbilical ring, covered with a transparent sac formed by the amniotic membrane + peritoneum
95
EXOMPHALOS
What is exomphalos associated with?
What is the management?
- Other major congenital abnormalities, antenatal Dx
| - C-section at 37w, staged repair as primary closure difficult
96
NEONATAL CONJUNCTIVITIS
What is neonatal conjunctivitis?
What is the management?
- 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
NEONATAL CONJUNCTIVITIS
In terms of neonatal conjunctivitis, how would...
i) gonococcal infection
ii) chlamydia infection
present and what is the management of both?
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
SIDS
| What are some major risk factors for SIDS?
- 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
SIDS
| What are some other risk factors for SIDS?
- M>F
- Low socioeconomic status
- Infant pillow use
- Maternal drug use
100
SIDS
| What are some protective factors from SIDS?
- Breastfeeding
- Room (NOT bed) sharing
- Use of dummies
101
SIDS
| What is the management of SIDS?
- 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
TRANSIENT TACHYPNOEA
What is transient tachypnoea of the newborn?
What is it caused by?
- 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
TRANSIENT TACHYPNOEA
| What is the clinical presentation?
- Tachypnoea after birth which resolves usually 48h
104
TRANSIENT TACHYPNOEA
| What is the management of transient tachypnoea of the newborn?
- CXR may show hyperinflation + fluid in horizontal fissure
- Dx after other causes excluded
- Supplementary oxygen may be needed to maintain SpO2
105
NUTRITION
| What are the advantages of breastfeeding?
- 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
NUTRITION
| What are the disadvantages of breastfeeding?
- 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
NUTRITION
What is weaning?
When is it typically done?
- Gradual transition from milk to normal food
| - 6m with pureed foods that are easy to palate, swallow + digest > normal, healthy diet
108
ROSEOLA INFANTUM
What is roseola infantum?
How is it spread?
- Caused by human herpes virus 6+7
| - Classically most children infected by age 2, often from oral secretions of a family member
109
ROSEOLA INFANTUM
What is the clinical presentation of roseola infantum?
What is a key feature of roseola infantum?
- 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
ROSEOLA INFANTUM
| What is the management of roseola infantum?
- Often full recovery in a week with no school exclusion if well
111
COMMON KNEE ISSUES
What is chondromalacia patellae?
How does it present?
What is the management
- 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
COMMON KNEE ISSUES
What is patellar tendonitis?
Who is it more common in?
- Chronic anterior knee pain that worsens after running, tender below patellar on examination
- More common in athletic teenage boys
113
COMMON KNEE ISSUES
What is...
i) osteochondritis dissecans?
ii) patellar subluxation?
i) Pain after exercise with intermittent swelling
| ii) Medial knee pain due to lateral subluxation of the patellar, knee may give way
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ACHONDROPLASIA
What is achondroplasia?
How does it occur?
- Skeletal dysplasia leading to disproportionate short stature (dwarfism)
- Abnormal function of epiphyseal (growth) plates which restricts bone growth
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ACHONDROPLASIA
| What is the aetiology of achondroplasia?
- Autosomal dominant, abnormal fibroblast growth factor receptor 3 (FGFR-3) gene
- Always heterozygous as homozygous is fatal
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ACHONDROPLASIA
| What is the clinical presentation of achondroplasia?
- Short stature from marked shortening of limbs + fingers
- Large head with frontal bossing + depression of nasal bridge
- 'Trident' hands + marked lumbar lordosis
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ACHONDROPLASIA
| What are some complications of achondroplasia?
- Foramen magnum stenosis > cervical cord compression + hydrocephalus
- Recurrent otitis media (cranial abnormalities)
- Obstructive sleep apnoea
- Obesity
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ACHONDROPLASIA
| What is the management of achondroplasia?
- No cure but MDT approach to maximise functioning = paeds, specialist nurses, PT/OT, geneticists
- ?Leg lengthening (controversial)
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TALIPES
What is talipes?
- Fixed abnormal ankle position
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TALIPES
What causes talipes equinovarus?
- Idiopathic or secondary to oligohydramnios
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SEBORRHOEIC DERMATITIS
| What is seborrhoeic dermatitis?
- Inflammatory skin condition that affects sebaceous glands which produce oil
- Sebaceous glands plentiful at scalp, nasolabial folds + eyebrows
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SEBORRHOEIC DERMATITIS
| What are the 3 types of seborrhoeic dermatitis?
- 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
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SEBORRHOEIC DERMATITIS
What is the management of...
i) infantile seborrhoeic?
ii) scalp seborrhoeic?
iii) face + body seborrhoeic?
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
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HEAD LICE
What are head lice?
How do they spread?
- Pediculus capitis = parasitic insects that infest hairs + feed on blood from scalp
- Direct head-head contact so often schools
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HEAD LICE
| What is the clinical presentation of head lice?
- Infestation causes itchy scalp
- Suboccipital lymphadenopathy
- Nits (eggs) + lice visible with Dx on fine-toothed combing of hair
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HEAD LICE
| What is the management of headlice?
- 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
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SCABIES
| What is scabies?
- Infestation of mites (Sarcoptes scabiei) that burrow under skin + lay eggs
- Can take 8w for Sx (delayed type 4 hypersensitivity reaction)
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SCABIES
What is the clinical presentation of scabies?
Classic location?
When would you suspect it?
- 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
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SCABIES
| What are some complications of scabies?
- 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
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SCABIES
| What is the management of scabies?
- 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
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HYPERTHYROIDISM
What is the most common cause of hyperthyroidism?
What causes it in neonates?
- Graves' disease (autoimmune) secondary to production of thyroid stimulating immunoglobulins
- Transplacental IgG exchange if mother has Graves' disease
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HYPERTHYROIDISM
| What is the clinical presentation of hyperthyroidism?
- Sweating, increased appetite, weight loss
- Diarrhoea, psychosis, tremor, tachycardia
- Rapid growth in height + advanced bone maturity
- Eye disease less common in children
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HYPERTHYROIDISM
| What are the investigations for hyperthyroidism?
- TFTs = T3/4 high, TSH low
| - TSH receptor stimulating antibody (TRAb) in Graves' disease
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HYPERTHYROIDISM
| What is the management of hyperthyroidism?
- 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
