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Phase 3A > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

principles of neonatal resuscitation

A
  1. warm baby - drying, heat lamp, plastic bag still wet
  2. calc APGAR score at 1.5 and 10mins
  3. stim breathing - drying, check for obstruction
  4. inflation breaths - 2 cycles of 5 (3s each), air +O2 in prem, if no response then 30s ventilation breaths, still no response then chest compressions
  5. chest compressions - 3:1 with ventilation breaths if HR<60
  6. severe situations may need IV drugs and intubation
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2
Q

APGAR score

A
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3
Q

Vitamin K in newborn

A
  • Vit K IM given
  • all babies born with vit K deficiency (needed for blood clotting)
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4
Q

blood spot screening in the neonate and conditions tested for

A

done on day 5 to screen for 9 congenital conditions (sickle cell, CF, congenital hypothyroidism, phenylketonuria, MCADD, MSUD, IVA, GA1, homocystin)

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5
Q

respiratory distress syndrome overview

A
  • common <32w due to inadequate surfactant = lung collapse (hypoxia, hypercapnia, resp distress)
  • ground glass appearance on CXR
  • prevent with antenatal steroids
  • may need intubation, O2, endotracheal surfactant
  • short term complications (pneumothorax, infection, apnoea, intraventricular haemorrhage, pulmonary haemorrhage, necrotising enterocolitis)
  • long term complications (chronic lung disease of prematurity, retinopathy of prematurity, sensory/neuro impairment
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6
Q

Chronic lung disease of prematurity overview

A
  • bronchopulmonary dysplasia
  • most <28w - RDS then diagnose from CXR and O2 requirement
  • prevent via antenatal steroids, CPAP>intubation, caffeine, not over-oxygenating
  • may need home O2, 1m injection of palivizumab to prevent RSV
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7
Q

meconium aspiration syndrome overview

A
  • if meconium aspirated inflammatory response in lungs - RDS, pneumonitis, pneumonia, pneumothorax
  • present with meconium-stained liquor, RDS, CXR (hyperinflation, patchy opacification, consolidation), increased O2 requirements
  • investigations - pre and post ductal oxygen saturations, capillary gas, FBC, CRP, cultures, CXR
  • may need suction to unblock, monitor for sepsis, O2 and ventilation
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8
Q

Hypoxic ischaemic encephalopathy overview

A
  • brain damage from prolonged hypoxia (maternal shock, haemorrhage, prolapsed cord etc)
  • sarnat staging for mild (resolves in 24h), moderate (40% get CP), severe (90% CP)
  • supportive care on NICU - optimal ventilation, nutrition, therapeutic hypothermia (33/34 degrees for 72h)
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9
Q

what are the TORCH infections

A
  • cause vide variety of complications in neonate
  • Toxoplasma gondii
  • Other agents, such as Treponema pallidum, varicella zoster virus (VZV), parvovirus B19, and human immunodeficiency virus (HIV)
  • Rubella
  • Cytomegalovirus (CMV)
  • Herpes simplex virus (HSV)
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10
Q

symptoms shared by TORCH infections

A

fever, lethargy, cataracts, jaundice, red/brown spots on skin, hepatosplenomegaly, congenital heart disease, microcephaly, low birth weight, hearing loss, blueberry muffin rash

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11
Q

Toxoplasma gondii (TORCH infection )

A
  • parasite - undercooked meats/cat faeces
  • inflammation to eyes, hydrocephalus, rash, intracranial calcifications
  • treat with pyrimethamine (antiparasitic)
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12
Q

features of congenital rubella syndrome

A

deafness
cataracts
rash
heart disease

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13
Q

physiological jaundice

A
  • fetal RBC break down quicker and less developed liver function
    -normal rise in bilirubin from 2-7d after birth - resolves by day 10
  • jaundice in first 24h or lasting >14d (term), >21d (prem) is pathological
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14
Q

causes of neonatal jaundice

A
  • increased production of bilirubin (HDOTN, haemorrhages, polycythaemia, sepsis, G6PD deficiency)
  • decreased clearance of bilirubin (prem, breast milk jaundice, neonatal cholestasis, extrahepatic biliary atresia, endocrine disorders)
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15
Q

jaundice in premature neonates

A
  • physiological jaundice exaggerated so higher risk of complications (kernicterus)
  • need treatment
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16
Q

breast milk jaundice

A
  • breast milk contains components that inhibit livers processing of bilirubin, also at higher risk of dehydration and inadequate feeding slows down bowels causing more bilirubin to be reabsorbed
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17
Q

investigations for neonatal jaundice

A
  • FBC, bilirubin (conjugated/unconjugated), blood type testing, TFT
  • Direct Coombs test for haemolysis
  • blood and urine cultures
  • G6PD levels
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18
Q

management of neonatal jaundice

A
  • bilirubin monitored and plotted on chart
  • phototherapy - blue light breaks down conjugated bilirubin, rebound bilirubin levels after 12-18h
  • exchange transfusion if severe
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19
Q

necrotising enterocolitis in neonate overview

A
  • life threatening emergency in prem neonate
  • bowel becomes necrotic (can cause perforation and peritonitis)
  • poor feeding, vomiting green bile, unwell, no bowel sounds, blood in stool, shock
  • FBC, CRP, cap blood gas (metabolic alkalosis), blood culture, abdo XR (distended bowel, oedema, gas in bowel wall/peritoneum/portal veins)
  • Nil by mouth, IV fluids, total parenteral nutrition, antibiotics, NG tube to drain fluid/gas
  • Surgical emergency
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20
Q

gastroschisis in neonate overview

A
  • birth defect
  • hole in abdo wall (R side of umbilicus) some bowel/organs can be outside
  • irritation from amniotic fluid causes bowel to shorten/twist/swell
  • surgery
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21
Q

oesophageal atresia

A
  • oesophagus doesn’t attach to stomach (may end in pouch)
  • often alongside trachea-oesophageal fistula (acid into lungs - life threatening)
  • antenatal polyhydramnios or poor feeding after birth
  • surgery, may need PEG
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22
Q

bowel atresia in the neonate overview

A
  • birth defect, most small bowel, intestines not connected/blocked/partially bloked
  • Present antenatally or after birth with poor feeding, green bile vomit, absence of meconium, jaundice
  • abdo XR to diagnose
  • Treated surgically
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23
Q

effect of gestational diabetes on the neonate

A
  • struggles to keep up large supply of glucose from oral feeding - hypoglycaemia
  • risk of hypoglycaemia, polycythaemia, jaundice, congenital heart disease, cardiomyopathy
  • close monitor of BM >2mmol/L, frequent feds
  • may need IV dextrose or NG feeding
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24
Q

effect of maternal hypothyroidism on neonate

A
  • if undertreated can lead to preterm birth, low birth weight, RDS
  • thyroxine important in fetal brain development (learning difficulties and developmental delay)
  • fetus starts making own thyroid hormone at 12w
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25
Q

hypoglycaemia in the neonate overview

A
  • Glucose <2.6mmol/l is pathological
  • Causes – deficient glycogen stores, delayed feeding, hyperinsulinemia, infection
  • Present with tachycardia, cyanosis, seizures, apnoea, lethargic
  • Diagnosed with glucose testing
  • Treatment depends on cause/severity but may include IV dextrose, enteral feeding, IM glucagon
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26
Q

common causes of neonatal sepsis

A

GBS, e.coli, listeria, klebsiella, staph aureus

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27
Q

clinical features of neonatal sepsis

A

fever, reduced tone/activity, poor feeding, resp distress, vomiting, tachycardia or bradycardia, hypoxia, jaundice within 24h, seizures, hypoglycaemia

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28
Q

red flags for neonatal sepsis

A
  • Confirmed or suspected sepsis in the mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting more than 4 hours after birth
  • Presumed sepsis in another baby in a multiple pregnancy
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29
Q

treatment of sepsis in neonate

A
  • low threshold for treatment - >1 risk factor, clinical feature or red flag
  • blood culture, FBC, CRP, lumbar puncture
  • Benzylpenicillin and gentamycin
  • recheck CRP at 24h
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30
Q

listeria infection in neonate

A
  • granuloma formation (skin, liver, adrenal glands, lymphatic tissue, lungs, brain) and infection (sepsis)
  • contracted trans placentally or during birth
  • contaminated dairy products, raw veg, deli meats
  • 14d benpen and gentamycin
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31
Q

HSV encephalitis in the neonate

A
  • presents in first 4w
  • Encephalitis manifested by neurologic findings, cerebrospinal fluid pleocytosis, and elevated protein
  • Diagnosis from PCR, lumbar puncture
  • high mortality if untreated
  • IV aciclovir for 21d then oral for 6m
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32
Q

Cleft lip and palate overview

A
  • congenital
  • associated syndromes
  • complications with feeding, speech, swallowing, psycho-social
  • Management – referral to cleft lip services, MDT, specially shaped bottles, cleft lip surgery (at 3m), cleft palate surgery (6-12m)
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33
Q

characteristic chest signs of pneumonia

A
  • bronchia breath sounds
  • focal course crackles
  • dullness to percussion
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34
Q

most common causes of pneumonia

A
  • bacterial: streptococcus, s.aureus, mycoplasma (atypical)
  • viral: RSV, parainfluenza, influenza
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35
Q

management of pneumonia

A
  • amoxicillin + macrolide (erythromycin, clarithromycin)
  • IV if sepsis
  • O2 if low sats
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36
Q

croup overview

A
  • acute URTI causing oedema of larynx
  • 6m-2y
  • most common cause parainfluenza virus
  • presentation: increased work of breathing, barking cough in clusters, stridor, hoarse voice
  • supportive management
  • oral dexamethasone, O2, nebulisers (budesonide, adrenaline), intubation
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37
Q

long term management of asthma under 5

A
  1. SABA prn
  2. low dose ICS or leukotriene antagonist
  3. other from step 2
  4. refer to specialist
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38
Q

long term management of asthma in 5-12y

A
  1. SABA
  2. low dose ICS
  3. LABA
  4. medium dose ICS and leukotriene receptor antagonist
  5. high dose ICS
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39
Q

long term management of asthma in >12y (same as adults)

A
  1. SABA
  2. low dose ICS
  3. LABA
  4. medium dose ICS, LAMA or LRA
  5. high dose ICS
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40
Q

assessing severity of acute asthma exacerbation

A
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41
Q

management of moderate/severe acute asthma

A

o Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours
o Nebulisers with salbutamol / ipratropium bromide
o Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days)
o IV hydrocortisone
o IV magnesium sulphate
o IV salbutamol
o IV aminophylline

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42
Q

viral induced wheeze overview

A
  • mostly <3, younger children have smaller airways so more likely
  • causes wheeze and resp distress, higher risk of developing asthma
  • coryzal symptoms preceded by SOB, resp distress, expiratory wheeze throughout chest
  • manage same as acute asthma
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43
Q

signs of resp distress

A
  • Raised respiratory rate
  • Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
  • Intercostal and subcostal recessions
  • Nasal flaring
  • Head bobbing
  • Tracheal tugging
  • Cyanosis (due to low oxygen saturation)
  • Abnormal airway noises
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44
Q

abnormal airway noises

A
  • Wheezing – whistling during expiration caused by narrowed airways
  • Grunting – caused by exhaling with the glottis partially closed to increase positive end-expiratory pressure
  • Stridor – high pitched inspiratory noise caused by obstruction of the upper airway
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45
Q

bronchiolitis overview

A
  • inflammation of bronchioles, mostly RSV, winter, <1y
  • URTI symptoms, chest symptoms (resp distress, dyspnoes, tachypnoea, apnoeas, wheeze) peak day 3/4, lasts 7-10d, poor feeding, mild fever
  • assess ventilation from cap blood gas from toe
  • supportive – adequate intake (oral/NG/IV), saline nasal drops, nasal suction, O2, ventilatory support
  • palivizumab monoclonal ab in monthly injection if at risk baby
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46
Q

cystic fibrosis presentation and diagnosis

A
  • AR mutation in cystic fibrosis transmembrane conductase regulatory geen (c7) - affects cl channels
  • thick pancreatic and biliary secretions, low volume thick airway secretions, congenital absence of vas deferens (infertile males)
  • present at screening (newborn), meconium ileus (blocked), childhood (recurrent infection, steatorrhoea, FTT, pancreatitis)
  • diagnosis - screening, sweat test (for high cl), genetic test
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47
Q

microbial colonisers in cystic fibrosis

A
  • Staph aureus – long term prophylactic flucloxacillin
  • H.influenza, klebsiella pneumoniae, e.coli
  • Pseudomonas aeruginosa - hard to treat and worse prognosis – often become resistant to multiple abx – treat with long term nebulised abx (tobramycin) and oral ciprofloxacin
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48
Q

management of cystic fibrosis

A
  • chest physio, exercise
  • High calorie diet for malabsorption, CREON tablets (digest fats with pancreatic insufficiency)
  • Prophylactic flucloxacillin
  • Bronchodilators (salbutamol), nebulised DNase (dornase alfa – makes secretions less viscous), nebulised hypertonic saline
  • Others – lung transplant, liver transplant, fertility treatment (sperm extraction), genetic counselling
  • Monitoring every 6 months – screen for sputum colonisation, diabetes, vit D deficiency, liver failure
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49
Q

epiglottitis overview

A
  • inflam/swelling of epiglottis from HIB (haemophilus influenza type B)
  • sore throat, stridor, drooling, tripod position, high fever, quiet and unwell, difficulty swallowing
  • DON’T DISTRESS or move
  • alert senior and anaesthetist
    -ensure airway secure - may need intubation or tracheostomy
  • IV abx and steroids (dex)
  • can be fatal or develop epiglottic abscess
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50
Q

breathless congenital heart disease

A
  • L to R shunt (increased blood to lungs)
  • ventricular septal defects, atrial septal defects, patent ductus arteriosus
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51
Q

ventricular septal defect

A
  • most common
  • Can lead to Eisenmenger syndrome
  • Signs – tachycardia, tachypnoea, FTT, HF, pansystolic murmur (L lower sternal edge), may be systolic thrill on palpation)
  • Mx – small will close spontaneously, large needs surgical closure and diuretics
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52
Q

atrial septal defect

A
  • increase risk of stroke from DVT
  • leads to pulmonary htn and can get Eisenmenger syndrome
  • HF in adulthood, tachypnoea, FTT, wheeze, ejection/mid-systolic murmur (L upper SE) with fixed split second heart sound
  • mx - large will need surgical repair
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53
Q

patent ductus arteriosus

A
  • normally closes by 4w, increased risk if prem
  • Signs – tachypnoea, FTT, continuous crescendo-decrescendo machine-like murmur (below L clavicle), bounding pulse
  • Mx – NSAIDS (indomethacin) or surgical ligation at 1y (unless symptomatic/HF before)
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54
Q

cyanotic congenital heart disease

A
  • R to L shunt (deox blood around body)
  • Tetralogy of Fallot, transposition of the great arteries, Ebstein’s anomaly
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55
Q

Tetralogy of Fallot

A

*4 components – pulmonary stenosis, VSD, overriding aorta, RVH
*Signs – severe cyanosis, hypercyanotic/Tet spells on exertion (crying, defecating etc), ejection systolic murmur (second intercostal space, LSE), clubbing of fingers/toes (late)
*CXR shows boot shaped heart due to RV thickening
*Mx – surgery at 6 months but has mortality of 5% (close VSD, relieve pulmonary outlet obstruction)
*Treatment of Tet spells – squat to increase systemic vascular resistance

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56
Q

transposition of the great arteries

A
  • PA and aorta swap (relies on DA staying open)
  • Signs – often presents on day 2 (when DA closes) with severe life threatening cyanosis
  • Mx – maintain PDA (prostaglandin infusion), surgery (atrial septostomy and correction)
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57
Q

Ebstein’s anomaly

A
  • tricuspid valve lower = RA >RV = poor blood flow to lungs
  • Often present few days after birth (when DA closes) with HF symptoms and gallop rhythm (additional 3rd and 4th heart sounds)
  • Manage arrhythmias (associated with wolff-parkinson-white syndrome) and HF then surgery
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58
Q

innocent murmur (flow murmur)

A
  • common in children, caused by fast blood flow in systole
  • 5 S’s (soft, short, systolic, symptomless, situation dependant)
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59
Q

pan-systolic murmurs

A
  • Mitral regurgitation heard at the mitral area (fifth intercostal space, mid-clavicular line)
  • Tricuspid regurgitation heard at the tricuspid area (fifth intercostal space, left sternal border)
  • Ventricular septal defect heard at the left lower sternal border
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60
Q

ejection systolic murmur

A
  • Aortic stenosis heard at the aortic area (second intercostal space, right sternal border)
  • Pulmonary stenosis heard at the pulmonary area (second intercostal space, left sternal border)
  • Hypertrophic obstructive cardiomyopathy heart at the fourth intercostal space on the left sternal border
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61
Q

Coarctation of the aorta overview

A
  • Narrowing of the aorta, commonly at DA
  • Symptoms become more severe with age – asymptomatic then SOB, arterial hypertension, intermittent claudication
  • Ejection systolic murmur (L upper SE), radial:radial or radial:femoral delay
  • Mx – stent and surgical repair
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62
Q

Heart failure overview

A
  • breathlessness, sweating, poor feeding, recurrent chest infections, FTT, tachycardia, tachypnoea, heart murmur, hypertrophy, peripheral cyanosis
  • causes: neonates (obstructed systemic circulation), infants (high pulmonary blood flow), older children (R or L, same as adult)
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63
Q

Rheumatic Fever

A
  • multisystem autoimmune response to GAS infection
  • 5-15y, may lead to rheumatic heart disease (scarring to valves - mitral)
  • After a latent interval of 2-6 weeks following GAS pharyngitis or streptococcal pyoderma there is an acute febrile illness with polyarthritis and often carditis
  • Jones criteria used for diagnosis (2 major or 1major+2minor)
  • carditis, migratory arthritis, sydenham chorea, erythema marginatum, subcut nodules
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64
Q

management of rheumatic fever

A
  • NSAID
  • Penicillin for GAS
  • Prevent further episodes with abx prophylaxis for 10y or until 21 (IM benzathine penicillin once monthly or daily oral penicillin)
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65
Q

long QT syndrome

A
  • Ventricles take too long to contract and release
  • Signs – may be asymptomatic or have syncope, irregular heart rate, palpitations/fluttering, may get worse on exertion
  • Mx – beta blockers, surgical (implantable cardioverter defibrillator)
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66
Q

premature contractions arrhythmia

A
  • Can be atrial or ventricular
  • Common in normal children or can be result of disease or injury
  • No treatment required normally
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67
Q

tachycardia

A
  • Sinus tachycardia – normal increase in HR occurring with fever, excitement or exercise but can be with underlying cause (eg anaemia)
  • Supraventricular tachycardia – electrical signals fire abnormally from atrium (SA node)
    o Mx – meds, ablation, cardioversion
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68
Q

wolff-parkinson-white syndrome

A
  • Electrical pathway between atria and ventricles malfunction allowing signals to reach ventricles prematurely and can bounce back causing fast HR
  • Medications, catheter ablation and surgery
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69
Q

sick sinus syndrome

A
  • SA node doesn’t fire properly (fast or slow)
  • Tired, dizzy and faint
  • Unusual in children but more common after heart surgery, may need pacemaker
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70
Q

infective endocarditis

A
  • most at risk if CHD with turbulent blood flow or prosthetic material
  • suspected in anyone with a sustained fever, malaise, raises ESR, unexplained anaemia or haematuria
  • fever, anaemia, splinter haemorrhages, clubbing, necrotic skin lesions, changing cardiac signs, splenomegaly, neurological signs from cerebral infarction, retinal infarcts, arthritis/arthralgia, haematuria (microscopic)
  • diagnosis from multiple cultures, detailed echo (vegetations)
  • Mx - IV high dose penicillin + aminoglycoside for 6w, may need surgery
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71
Q

otitis media overview

A
  • normally follows viral URTI, most common bacteria is H.influenza
  • if perforated tympanic mem then discharge from ear
  • can be non-specific symptoms in children
  • <3m temp >38 or 3-4m temp>39 refer to specialist
  • Most will resolve in 3-7d without abx, complications rare (mastoiditis), give analgesia
  • Immediate antibiotics – co-morbidities or immunocompromised, <2y with bilateral otitis media, discharge or perforation
  • Delayed prescription – collect in 3 days if not improving
  • amoxicillin for 5d
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72
Q

Glue ear overview

A
  • otitis media with effusion, fluid in middle ear causing hearing loss
  • audiometry, normally resolve in 3m, grommets if not resolving
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73
Q

audiogram and types of hearing loss

A
  • Sensorineural hearing loss – both air and bone conduction will be above 20dB
  • Conductive hearing loss – bone conduction normal, air above 20dB
  • Mixed hearing loss – both above 20dB but a difference of >15dB between (bone>air)
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74
Q

Periorbital cellulitis overview

A
  • fever with erythema/tenderness/oedema of skin near eye, most unilateral
  • treat promptly with IV abx (ceftriaxone) to prevent orbital cellulitis
  • urgent CT/MRI if suspect orbital cellulitis
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75
Q

squint

A
  • strabismus (misaligned eyes) caused double vision, one eye becomes dominant and one lazy (amblyopia)
  • need treatment under 8 from ophthalmologist
  • occlusive patch over good eye or atropine drops causing vision blurring
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76
Q

UTI

A
  • fever may be only symptom in young
  • acute pyelonephritis if temp>38 and loin pain/tenderness
  • urine dip - anything positive then send for MCS
  • <3 months with fever - IV abx (ceftriaxone) and full septic screen
  • Other children may have oral abx if otherwise well or IV if symptoms of pyelonephritis or sepsis
  • Trimethoprim, nitrofurantoin, cefalexin, amoxicillin
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77
Q

investigating recurrent UTI

A
  • USS (<6m with first, others with recurrent, immediately during atypical)
  • DMSA (dimercaptosuccinic acid) scan – 4-6m after to assess for damage
    -Micturating Cystourethrogram (MCUG) – in children under 6 months or if family hx of VUR, dilation of ureters on USS or poor urine flow, used to diagnose VUR
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78
Q

nocturnal enuresis

A
  • involuntary urination at night , abnormal after 4 or if after previous dry nights (secondary)
  • causes of primary - slower development, overactive bladder, fluid before bed, failure to wake, psychological stress, constipation, UTI
  • causes of secondary - UTI constipation, T1DM, psychological, maltreatment
  • 2w bladder diary, urine culture etc
  • reassure, lifestyle changes, treat underlying cause, enuresis alarms, meds (desmopressin)
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79
Q

AKI

A
  • Sudden potentially irreversible reduction in renal function
  • Oliguria (<5ml/kg per hour) is normally present
  • Stratified into levels of severity by the pRIFEL (changes in estimated creatinine clearance) and KDIGO criteria (serum creatinine and changes in urine output)
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80
Q

causes of AKI

A

*Prerenal – hypovolaemia (gastroenteritis, burns, sepsis, haemorrhage, nephrotic syndrome), circulatory failure, HF
*Renal – vascular (haemolytic uraemic syndrome, vasculitis, embolus, renal vein thrombosis), tubular (acute tubular necrosis, ischaemic, toxic, obstructive), glomerular (glomerulonephritis), interstitial (interstitial nephritis, pyelonephritis)
*Postrenal – obstruction (congenital, acquired)

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81
Q

management of AKI

A
  • circulation and fluid balance monitoring
  • reduce meds affecting kidneys
  • USS
  • prerenal - urgent fluid replacement
  • renal - restrict fluids, high calorie diet, balance acid/base and electrolytes
  • post renal - unblock obstruction, correct fluid and electrolytes
  • renal replacement therapy if management fails or severe
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82
Q

chronic renal failure / CKD

A
  • progressive loss of renal function, 5 stages
  • most caused by congenital abnormalities, less common (glomerular disease, hereditary, systemic disease etc)
  • anorexia, lethargy, polydipsia/uria, FTF, bony deformities (renal osteodystrophy), htn, proteinuria
  • management - nutrition (NG/PEG), phosphate restriction, vit D, salt supplements, erythropoietin (prevent anaemia), GH, dialysis, transplant
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83
Q

nephrotic syndrome

A
  • basement mem becomes permeable to protein
  • triad of low albumin, oedema and high proteinuria
  • 90% caused by minimal change disease (no clear pathology)
  • secondary to intrinsic kidney disease or systemic illness (AHSP, diabetes, infection)
  • Mx - high dose prednisolone for 4w then weaned slowly, low salt diet, diuretics, albumin infusions, abx prophylaxis
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84
Q

minimal change disease

A
  • nephrotic syndrome
  • no clear reason why
  • renal biopsy and microscopy don’t detect abnormality
  • urinalysis - protein and hyaline casts
  • Mx - prednisolone - most make full recovery
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85
Q

nephritic syndrome

A
  • nephron inflammation causing decreased renal function, haematuria, proteinuria (less than nephrotic s)
  • most common causes in children: post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease).
  • can also be caused by SLE and Alport syndrome
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86
Q

Post-streptococcal glomerulonephritis

A
  • 1-3w after beta haemolytic strep infection (eg tonsilitis)
  • immune complexes get stuck in glomeruli causing inflammation and AKI
  • supportive Mx - 80% full recovery
  • if worsening then Tx with antihypertensives and diuretics
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87
Q

IgA nephropathy (Berger’s disease)

A
  • causes nephritic syndrome
  • Related to Henoch Schoenlein purpura (IgA vasculitis)- purple purpuric rash in lower legs and buttocks from blood vessels leaking, arthritis, GI problems, condition usually improves on its own
  • IgA deposits in the nephrons and glomerular mesangial proliferation on biopsy
  • teenagers
  • supportive Tx and immunosuppression (steroids and cyclophosphamide)
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88
Q

SLE

A
  • mostly female teenagers
  • inflammatory autoimmune connective tissue disease
  • multiple anti-nuclear autoantibodies against double stranded DNA
  • haematuria and proteinuria indicate biopsy
  • malar rash (butterfly over cheeks/nose)
  • immunosuppression needed
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89
Q

Alport syndrome

A
  • genetic condition with kidney disease, sensorineural hearing loss and eye abnormalities
  • progression could be slowed by ACEi, avoid NSAIDs, healthy lifestyle, may eventually need dialysis or transplant
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90
Q

hypospadias

A
  • males, urethral meatus is displaced to the ventral side of penis, most just to bottom of glans but can be anywhere on penis
  • epispadias if on top side
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91
Q

phimosis

A
  • Inability to retract foreskin over glans penis
  • Physiologic – normal in children and resolves around age 5-7
  • Pathological – occurs due to scarring, infection or inflammation – may need surgery
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92
Q

renal agenesis

A
  • no kidneys
  • severe oligohydramnios = Potter sequence (pulmonary aplasia causing resp failure, fetal compression, FATAL)
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93
Q

Multicystic dysplastic kidney

A
  • result of failure of union of ureteric bud and nephrogenic mesenchyme
  • non-functioning with large fluid filled cysts - no renal tissue or connection to bladder
  • only survive if unilateral
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94
Q

cystic dysplastic kidneys

A
  • Caused by autosomal recessive polycystic kidney disease (ARPKD), or dominant (ADPKD), renal cysts or diabetes
  • some normal renal tissue but both always affected
  • ADPKD = childhood htn and CKD - associated with liver/pancreas cysts, cerebral aneurysms and mitral valve prolapse
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95
Q

Duplex kidney

A

Vary from simply a bifid renal pelvis to complete division of the two ureters. May have abnormal drainage and can lead to reflux in the lower one. One may drain into vagina or urethra directly.

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96
Q

Vesico-ureteric reflux

A
  • reflux of urine up dilated ureters
  • predisposes to infection and renal scarring (reflux nephropathy)
  • diagnose by MCUG
  • Mx - avoid constipation, avoid excessively full bladder, prophylactic abx, surgery
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97
Q

haemolytic uraemic syndrome

A
  • thrombosis in small vessels in body
  • triggered by shiga toxin (e.coli 0157 or shigella)
  • traid of: haemolytic anaemia, AKI, thrombocytopenia
  • risk increased by use of abx and anti-motility Tx for diarrhoea
  • follows gastroenteritis, starting on day 5
  • Reduced urine output, haematuria, abdo pain, lethargy, confusion, oedema, hypertension, bruising
  • emergency (10% mortality) needs to be under specialist, self-limiting needs supportive management (dialysis, antihypertensives, fluid balance, blood transfusions)
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98
Q

immunisation schedule (8w, 12w, 16w, 12m, 3y4m, teenage)

A
  • 8w: 6-in-1 (1st - diphtheria, tetanus, pertussis (whooping cough), polio, Hib disease and hepatitis B), rotavirus (1st), MenB (1st)
  • 12w: 6-in-1 (2nd), rotavirus (2nd), pneumococcal conjugate vaccine (PCV)(1st)
  • 16w: 6-in-1 (3rd), MenB (2nd)
  • 12m: Hib/MenC, MMR (1st), PCV booster, MenB booster
  • Preschool (3y4m): MMR booster, Pre-school booster 4-in-1 (diphtheria, tetanus, pertussis (whooping cough) and polio)
  • 2y up to year 6: nasal flu vaccine
  • Teenage: HPV (2 doses around 12/13), teenage booster (tetanus, diphtheria and polio), MenACWY
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99
Q

calculating maintenance fluid

A
  • Children >28d – Holliday-Segar formula
    o 100 ml/kg/day for the first 10kg of weight
    o 50 ml/kg/day for the next 10kg of weight
    o 20 ml/kg/day for weight over 20kg
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100
Q

calculating fluid replacement

A
  • Calculate % dehydration – signs of dehydration but no red flags (5%), red flags (10%)
  • Fluid deficit (mL) = % dehydration x weight (kg) x 10
  • Total fluid requirement (mL) = maintenance fluids (mL) + fluid deficit (mL)
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101
Q

resuscitation fluids

A

0.9% sodium chloride with no additives via intravenous (IV) or intraosseous (IO) in a standard bolus of 10 mL/kg over <10 minutes

102
Q

Leukaemia

A
  • cancer of line of stem cells in bone marrow, reduction of other cells (pancytopenia)
  • ALL most common (2-3y, 80% cure), then AML (<2y), CML rare
  • Non-specific, fatigue, fever, FTT, weight loss, night sweats, pallor, petechiae/unexplained bleeding (thrombocytopenia), abdo pain, lymphadenopathy, bone/joint pain, hepatosplenomegaly
  • Dx - very urgent FBC in 48h if suspected (anaemia, leukopenia, thrombocytopenia and abnormal white cells), blood film (blast cells), bone marrow biopsy, lymph node biopsy
  • may have CXR, CT, lumbar puncture, genetic analysis etc
  • Mx- MDT, chemo, radiotherapy, bone marrow transplant, surgery
103
Q

types of brain tumours

A
  • Choroid plexus carcinoma – malignant, mostly <2y
  • Craniopharyngioma – benign, begins near pituitary, may have effect on pit (vision changes, poor growth etc)
  • Embryonal tumours – malignant, start in embryonic cells in brain, mostly in babies, many types including medulloblastoma
  • Ependymoma – in ependymal cells that line brain and spinal cord, most often young children, can cause headaches and seizures
  • Glioma – begin in glial cells (produce myelin sheath), classified depending on cell type etc, include ependymoma, astrocytoma, oligodendroglioma
  • Medulloblastoma – malignant, starts in cerebellum, tends to spread through CSF, rare but most common cancerous brain tumour in children
  • Pineoblastoma – malignant, starts in pineal gland (affects melatonin), grows quickly,
104
Q

Wilms tumour

A
  • nephroblastoma, tumour of kidney in <5s
    -Presentation – consider in any child <5 with mass in abdo, abdo pain, haematuria, lethargy, fever, hypertension, weight loss
  • USS to diagnose, CT/MRI to stage, biopsy for histology and definite diagnosis
  • surgical excision of tumour and kidney, adjuvant chemo or radiotherapy
    – early stage has cure of 90%, metastatic has poorer prognosis
105
Q

neuroblastoma

A
  • cancer from immature nerve cells in body, most in adrenal gland in <5s
  • some may resolve spontaneously but others need treatment
  • symptoms depend on location
  • Dx - urine and blood tests, imaging, biopsy, staging CT/MRI
  • Mx could include surgical excision, chemo, radio, bone marrow transplant
106
Q

Retinoblastoma

A
  • malignant tumour of retinal cells (causes 5% of severe visual impairment), mostly <3y
  • screened if family hx, white pupillary reflex, squint
  • MRI and examination under GA
  • Mx could include chemo to shrink then laser therapy or surgery
  • most cured but some visual impairment, sig risk of future malignancies (sarcoma)
107
Q

bone tumours

A
  • malignant rare before puberty
  • osteosarcoma more common than Ewing sarcoma
  • mostly limbs, persistent localised bone pain, mass
  • XR, MRI, bone scan
  • Mx = chemo then surgery , radio tx may be used in Ewing sarcoma
108
Q

osteosarcoma

A
  • Ages 10-20
  • Persistent bone pain normally worse at night
  • XR - poorly defined lesion in bone, destruction of normal bone, fluffy appearance, periosteal reaction (sun burst appearance)
  • raised ALP
109
Q

hepatoblastoma

A
  • rare, mostly <5y
  • increased risk if pre, low birth weight, genetic conditions
  • abdo mass, weight loss, abdo pain, vomiting, jaundice, fever, itchy skin, anaemia, back pain from compression of tumour
  • Dx - biopsy, FBC, LFT, XR, CT/MRI, USS
  • Mx - chemo, surgery
110
Q

Kleinfelter’s syndrome

A
  • male has extra X (47XXY)
  • normal males until puberty - taller, wider hips, gynaecomastia, weaker muscles, small testicles, reduced libido, shyness, infertility, subtle learning difficulties
  • Mx- MDT, testosterone, fertility treatment, breast reduction surgery
111
Q

Turner’s syndrome

A
  • female has single X (45XO)
  • short, webbed neck, high arching palate, downward sloping eyes with ptosis, broad chest with widely spaced nipples, cubitus valgus (abnormal extension of elbow), underdeveloped ovaries, late/incomplete puberty, most are infertile
  • Mx - GH, oestrogen and progesterone replacement, fertility treatment, monitoring for associated conditions (hypothyroid, diabetes, htn, coarctation of the aorta)
112
Q

Down syndrome

A
  • trisomy 21, life expectancy 60
  • hypotonia, brachycephaly (small head with a flat back), short neck, short stature, flattened face and nose, prominent epicanthic folds, upward sloping palpebral fissures, single palmar crease
  • lots of complciations - learning dis, sensory problems, hypothyroid, cardiac defects, leukaemia, dementia
  • antenatal screening
  • Mx- MDT supportive acre, routine montoring (TFT 2y, echo, regular audiometry and eye checks)
113
Q

Edwards syndrome

A
  • Trisomy 18
  • Rare, most die in infancy
  • Features – low birth weight, prominent occiput, small mouth and chin, short sternum, flexed/overlapping fingers, rocker-bottom feet, cardiac and renal malformations
114
Q

patau syndrome

A
  • Trisomy 13
  • Rare, most die in infancy
  • Features – structural defect of the brain, scalp defects, small eyes/other defects of the eye, cleft lip and palate, polydactyly, cardiac and renal malformations
115
Q

Fragile X syndrome

A
  • X linked AD mutation in the FMR1 (fragile X mental retardation 1) gene - plays role in cog development
  • developmental delay, disability, long face, large ears, hypermobile joints, ADHD, autism, seizures
  • supportive Mx, MDT
116
Q

Muscular dystrophy

A
  • Umbrella term for genetic conditions that cause gradual weakening and wasting of muscles
  • Main one is Duchennes muscular dystrophy
  • gower’s sign - specific way of getting up (hands and knees then walk hands up)
  • no cure but supportive management from MDT
117
Q

Duchennes muscular dystrophy

A
  • X-linked AR, defective gene for dystrophin (protein holds muscles together)
  • Boys present around 3-5y with weakness in muscles around pelvis
  • usually wheelchair bound by teens with life expectancy of 25-35y
  • oral steroids slow progression of muscle weakness by up to 2y, creatinine supplements can improve muscle strength
118
Q

angelman’s syndrome

A
  • loss of function of UBE3A gene (c15) from mothers copy
  • happy demeanour, fascination with water, widely spaced teeth, developmental delay, ataxia, innappropriate laughing, epilepsy, ADHD, dysmorphic features, fair skin/light hair/blue eyes
119
Q

prader willi syndrome

A
  • loss of functional genes on proximal arm of c15 from farther
  • insatiable hunger leads to obesity, hypotonia, learning dis, hypogonadism, soft skin prone to bruising, MH problems, dysmorphic features (narrow forehead, almond shaped eyes etc)
  • GH to improve muscle development, close diet control
120
Q

noonan syndrome

A
  • AD, many diff genes
  • short stature, broad forehead, downward sloping eyes with ptosis, hypertelorism (wide spaced eyes), prominent nasolabial folds, low set ears, webbed neck, widely spaced nipples
  • associated with congenital heart disease, infertility, learning dis, bleeding disorders, increased risk of leukaemia
121
Q

William syndrome

A
  • deletion of genes on one copy of c7
  • broad forehead, starburst eyes, wide mouth, very sociable trusting personality, small chin, learning dis
  • complications - supraventricular aortic stenosis, htn, hypercalcaemia
  • supportive mx, ECG and BP monitoring
122
Q

osteogenesis imperfecta

A
  • brittle bones - genetic condition affecting collagen
  • Px - recurrent/inappropriate fractures, hypermobility, blue/grey sclera, bone deformities, pain, dental problems
  • manage with bisphosphonates (increase bone density), vit D and MDT
123
Q

Rickets

A
  • defective bone mineralisation = soft deformed bones
  • caused by vit D/Ca deficiency or hereditary hypophosphataemic rickets
  • Px - bone pain, deformities, poor growth, fractures, dental problems
  • Ix - XR, FBC, ESR/CRP, U&E, LFT, TFT, autoimmune tests
  • Serum 25-hydroxyvitamin D (<25nmol/L is deficiency), calcium (low), phosphate (low), alkaline phosphatase (high), parathyroid hormone (high)
  • prevent with supplement vit D and Ca (especially if breastfed)
124
Q

transient synovitis

A
  • irritable hip, common cause of hip pain in 3-10y
  • temporary inflammation of the synovial membrane
  • often few weeks after viral URTI
  • don’t have fever and otherwise well
  • Mx - analgesia, safety netting, follow up at 48h and 1w
  • most improve after 24-48h and resolve in 1-2w
125
Q

septic arthritis

A
  • most common <4
  • hot/swollen/painful joint, reduced range of movement, systemic symptoms
  • s.aureus most common
  • Mx - joint aspiration for MC&S, IV abx for 3-6w, may need surgical drainage
126
Q

osteomyelitis

A
  • s.aureus, typically in metaphysis of long bones
  • chronic or acute
  • Ix - XR (MRI best), raised inflammatory markers, blood culture
  • Mx - prolonged abx, may need surgical debridement
127
Q

Perthes disease

A
  • impaired blood flow to epiphysis of femur causing necrosis (most between 5-8y)
  • remodels overtime but can still result in deformed/soft femoral head
  • slow onset hip pain, reduced movement, limp
  • XR (MRI best), technetium bone scan, bloods all normal
  • Mx - conservative if less severe, bed rest, traction, crutches, analgesia, physio, regular xr, surgery if severe
128
Q

Discoid meniscus

A
  • Meniscus – 2 pieces of cartilage, crescent-shaped, shock absorber
  • Discoid meniscus – ticker, different shape and texture
  • More likely to be injured (twisting motion) but may never have problems
  • If torn they will feel pain, stiffness, inability to straighten knee, locking, buckling knee
  • May need surgery if symptomatic
129
Q

Slipped femoral epiphysis

A
  • head of femur displaced along growth plate
  • boys, 8-15, obese, typically during growth spurt
  • Ix - XR, blood tests normal, technetium bone scan, CT/MRI
  • Mx - surgery to correct and fix in place
130
Q

osgood schlatter’s disease

A
  • inflammation at tibial tuberosity where patella tendon inserts
  • anterior knee pain, 10-15y, boys more common
  • Stress from running/jumping etc at the same time as growth in the epiphyseal plate result in inflammation on the tibial epiphyseal plate
  • results in bony lump under knee
  • Mx - reduce pain and inflammation - rest/ice/NSAIDs
  • rare complication is a full avulsion fracture = surgery
131
Q

developmental dysplasia of the hip

A
  • structure abnormality at birth with instability of hips
  • most found on NIPE
  • treated to prevent problems in adulthood
  • ortilani test and barlow test for dislocations
  • USS hips
  • Mx - pavlik harness if <6m for 6-8w, surgery if >6m
132
Q

JIA

A
  • autoimmune inflammation of joints lasting >6m in <16s
  • 5 key subtypes (systemic, polyarticular, oligoarticular, enthesitis related, juvenile psoriatic arthritis)
  • Mx - MDT, steroids, DMARDS, biologics (TNF inhibitors, etanercept, infliximab)
133
Q

systemic JIA

A
  • still’s disease
  • salmon pink rash, high swinging fevers, joint inflammation, weight loss, enlarged lymph nodes, pleuritis/pericarditis
  • ANA/RF negative, raised inflammatory markers
  • key complication is macrophage activation syndrome (acute unwell child, DIC, anaemia, thrombocytopenia, bleeding, non-blanching rash, low ESR, life threatening)
134
Q

polyarticular arthritis

A

> 5 joints
- symmetrical
- minimal systemic symptoms
- equivalent of RA in adults
- Most are seronegative (no RF) but can be seropositive (tend to be older)

135
Q

oligoarticular JIA

A

<4 joints
* Classic associated feature is anterior uveitis – needs ophthalmology referral
* Tend not to have systemic symptoms with normal inflammatory markers, antinuclear antibodies often positive but RF negative

136
Q

enthesitis-related arthritis

A
  • boys >6
  • paeds version of spondyloarthropathies (HLA B27)
  • arthritis and enthesitis (tender on palpation)
137
Q

torticollis

A
  • wry neck - head rotated and tilted at odd angle
  • Most common cause in infants is a sternomastoid tumour (congenital muscular torticollis) – present in first weeks of life with a mobile, non-tender nodule in the muscle – usually resolves in 2-6m passive stretching is advised
  • Most common acquired cause is injury or inflammation of the sternocleidomastoid or trapezius muscle groups, infections of ENT, spinal tumours
138
Q

medical causes of abdo pain

A

– constipation, UTI, coeliac, IBD, irritable bowel syndrome, mesenteric adenitis, abdominal migraine, pyelonephritis, Henloch-Shlonlein purpura, tonsilitis, diabetic ketoacidosis, infantile colic (in girls = dysmenorrhea, Mittelschmerz (ovulation pain), ectopic pregnancy, PID, ovarian torsion, pregnancy

139
Q

surgical causes of abdo pain

A
  • Appendicitis causes central abdominal pain spreading to the right iliac fossa
  • Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools
  • Bowel obstruction causes pain, distention, absolute constipation and vomiting
  • Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting
140
Q

red flags for abdo pain

A

persistent or bilious vomiting, severe chronic diarrhoea, fever, PR bleeding, weight loss, poor growth, dysphagia, night-time pain, abdo tenderness

141
Q

recurrent abdo pain

A
  • Repeated episodes with no identifiable cause
  • Often corresponds to stressful life events
  • Theory is increased sensitivity and inappropriate pain signals from the visceral nerves (the nerves in the gut) in response to normal stimuli.
  • Management is explanation and reassurance, distraction, reduce stress, good diet
142
Q

abdominal migraine

A
  • may happen before they have a migraine
  • Episodes of central abdo pain lasting >1h with a normal examination, may be nausea, anorexia, pallor, headache, photophobia, aura
  • Treat acute attack – paracetamol, ibuprofen, sumatriptan
  • Preventative meds – pizotifen (serotonin agonist needs to be withdrawn slowly), propranolol (bb), cyproheptadine (antihistamine)
143
Q

constipation

A

<3 stools/week, hard, straining, abdo pain, rectal bleeding, faecal impaction (overflow soiling), loss of sensation to open bowels (desensitisation of the rectum)
- encopresis (faecal incontinence, pathological >4y)
- Mx - lifestyle and diet, laxatives (movicol - osmotic laxative) for long term until bowel habit formed, may need disimpaction regimen

144
Q

red flags for constipation

A
  • Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
  • Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
  • Vomiting (intestinal obstruction or Hirschsprung’s disease)
  • Ribbon stool (anal stenosis)
  • Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
  • Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
  • Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
  • Acute severe abdominal pain and bloating (obstruction or intussusception)
145
Q

GORD

A
  • normal after large feeds until 1y
  • chronic cough, hoarse cry, reluctance to feed, pneumonia
  • Mx - reassurance and advice, gaviscon with feeds, thickened formula etc
146
Q

red flags for vomiting

A
  • Not keeping down any feed (pyloric stenosis or intestinal obstruction)
  • Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
  • Bile stained vomit (intestinal obstruction)
  • Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
  • Abdominal distention (intestinal obstruction)
  • Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
  • Respiratory symptoms (aspiration and infection)
  • Blood in the stools (gastroenteritis or cows milk protein allergy)
147
Q

sandifer’s syndrome

A

rare condition causing brief episodes of abnormal movements (torticollis, dystonia) associated with GORD – tends to resolve when reflux is treated

148
Q

pyloric stenosis

A
  • thickening and narrowing of pylorus = peristalsis after feed caused projectile vomiting
  • present in first few weeks with FTF
  • Ex - peristalsis can be seen, ‘large olive’ mass in upper abdomen (pylorus), blood gas may show hypochloric metabolic alkalosis
  • Mx - USS and laparoscopic pyloromyotomy
149
Q

viral gastroenteritis

A
  • most common cause is viral
  • dehydration is main concern
  • viral - rotavirus, norovirus
150
Q

E.coli gastroenteritis

A
  • E. coli 0157 produces the Shiga toxin - causes abdominal cramps, bloody diarrhoea and vomiting - destroys blood cells and leads to haemolytic uraemic syndrome (HUS).
  • ABX increases risk of HUS
151
Q

campylobacter jejuni gastroenteritis

A
  • travellers diarrhoea, most common bacterial cause worldwide, gram negative bacteria that has curved shape
  • Spead by raw poultry, untreated water, unpasteurised milk
  • Incubation normally 2-5d, symptoms resolve after 3-6 (cramps, diarrhoea often with blood, vomiting fever)
  • Abx (azithromycin or ciprofloxacin) after isolating organism in patients with severe symptoms or with risk factors (HIV, HF etc)
152
Q

shigella gastroenteritis

A

contaminated water, swimming pools, food; incubation 1-2d, symptoms resolve within a week; causes bloody diarrhoea, cramps and fever; can produce shiga toxin causing HUS; treat severe cases with azithromycin or ciprofloxacin

153
Q

salmonella gastroenteritis

A

raw eggs or poultry or food contaminated with infected faeces of small animals; incubation 12h-3d, symptoms normally resolve withing a week; watery diarrhoea, abdo pain, vomiting; abx rarely necessary but should be guided by stool culture and sensitivities

154
Q

bacillus cereus gastroenteritis

A
  • gram positive rod spread through inadequately cooked food. It grows well on food not immediately refrigerated after cooking (rice)
  • produces toxin called cereulide – causes cramping and vomiting within 5h
  • when it arrives in intestines it produces different toxins that cause watery diarrhoea >8h
  • all symptoms usually resolve within 24h
155
Q

staphylococcus aureus toxin gastroenteritis

A

enterotoxins made when growing on food (eggs, dairy, meat) – cause small intestine inflammation, vomiting, cramps fever within hours then settle in 12-24h

156
Q

coeliac disease

A
  • autoimmune (anti-TTG and anti-EMA) in response to gluten
  • Inflammation, particularly in jejunum causes villous atrophy = malabsorption
  • Dx - test antibodies while on gluten containing diet, IgA levels (deficiency can cause false negative), endoscopy and biopsy (crypt hypertrophy, villous atrophy)
  • Mx - gluten free diet
157
Q

appendicitis

A
  • can quickly rupture = peritonitis
  • peak incidence 10-20y
  • central abdo pain moving to RIF, tenderness at McBurney’s point, vomiting, Rovsing’s sign (LIF palpation caused pain in RIF), guarding, rebound tenderness
  • Dx - raised inflammatory markers, CT, USS (rule out ovarian torsion)
  • Mx - emergency laparoscopic appendicectomy
158
Q

hernias

A
  • Umbilical hernias – doesn’t close properly, left until age of 3 to close naturally but may need op if causing discomfort
  • Epigastric hernias – surgical repair if causing discomfort
  • Inguinal hernia – fairly common especially in preterm infants, needs surgical treatment, caused when processus vaginalis doesn’t close which can cause bowel or ovary/testicle to become trapped
159
Q

inflammatory bowel disease

A
  • Umbrella term for ulcerative colitis and Chron’s disease – both involve inflammation of walls of GI tract and associated with periods of remission and exacerbation
  • perfuse diarrhoea, abdo pain, bleeding, weight loss, anaemia, may be systemically unwell during flares
  • Ix - bloods (FBC, ESR/CRP, TFT, U&E, LFT), faecal calprotectin (bowel inflammation), endoscopy with biopsy (GOLD standard), imaging for complications
  • Mx - MDT, monitor growth, induce remission and maintain it
160
Q

Chron’s features (crows NESTS)

A
  • N – No blood or mucus (these are less common in Crohns.)
  • E – Entire GI tract
  • S – “Skip lesions” on endoscopy
  • T – Terminal ileum most affected and Transmural (full thickness) inflammation
  • S – Smoking is a risk factor (don’t set the nest on fire)
161
Q

ulcerative colitis features (CLOSEUP)

A
  • C – Continuous inflammation
  • L – Limited to colon and rectum
  • O – Only superficial mucosa affected
  • S – Smoking is protective
  • E – Excrete blood and mucus
  • U – Use aminosalicylates
  • P – Primary sclerosing cholangitis
162
Q

management of crohns

A
  • Inducing remission – steroids (oral prednisolone or IV hydrocortisone), add immunosuppressant of not working
  • Maintaining remission – may not need anything, immunosuppressants (first line azathioprine, mercaptopurine) (second line methotrexate, infliximab, adalimumab)
  • Surgery – if only affects the distal ileum then can resect this area.
163
Q

management of ulcerative colitis

A
  • Inducing remission:
    o Mild to moderate disease = aminosalicylate (e.g. mesalazine oral or rectal) or corticosteroids
    o Severe disease = IV corticosteroids or IV ciclosporin
  • Maintaining remission – aminosalicylate (mesalazine), azathioprine, mercaptopurine
  • Surgery – removal of colon and rectum (panproctocolectomy) will remove the disease and leave them with an ileostomy or an ileo-anal anastomosis (J-pouch)
164
Q

failure to thrive

A
  • 1+ centile space if <9th centile, 2+ if 9-91st, 3+ if >91st
  • causes: inadequate nutritional intake, difficulty feeding, malabsorption, increased energy requirements, inability to process nutrients properly
  • Ix - urine dip (UTI, ketones), coeliac screen
  • Mx - MDT, treat cause, dietitian, supplements, enteral tube feeding
165
Q

kwashiorkor and marasmus

A
166
Q

intestinal obstruction

A
  • causes: meconium ileus, Hirschsprung’s disease, oesophageal atresia, intussusception, imperforate anus, malrotation of intestines, strangulated hernia
  • Px: persistent vomiting, pain and distention, failure to pass stools or wind, abnormal bowel sounds
  • Urgent abdo XR – dilated loops of bowel proximal to obstruction, collapsed after
  • Nil by mouth (IV fluids) and NG tube to drain stomach and emergency to surgical unit
167
Q

Hirschsprung’s disease

A
  • congenital - nerve cells of myenteric plexus are absent in distal bowel and rectum = parasympathetic aganglionic section loses peristalsis and motility = constricts causing obstruction
  • Px - obstruction, FTF, constipation since birth
  • Mx - abdo XR, rectal biopsy confirms, surgical removal of aganglionic section
168
Q

Hirschsprung-associated enterocolitis

A

inflammation and obstruction in around 20%; typically presents in first 2-4w with fever, distention, diarrhoea (often bloody), sepsis; life threatening and can lead to perforation; need urgent abx, fluid resuscitation and decompensation of the obstructed bowel

169
Q

intussusception

A
  • bowel telescoped into itself = thins lumen = mass and obstruction
  • infants 6m-2y with redcurrant jelly stool, severe abdo pain, unwell, lethargic, sausage shaped mass, vomiting, obstruction
  • Mx - USS, therapeutic enemas, surgical reduction, may need removing if gangrenous
170
Q

Meckel’s diverticulum

A
  • malformation of distal ileum caused by incomplete obliteration of omphalomesenteric duct
  • most common congenital GI disorder
  • most asymptomatic but can bleed, become inflamed, rupture or cause a volvulus or intussusception
  • Abnormal sac or pouch in ileum – normally contains all 3 layers of bowel.
  • Diagnosis via stool smear for blood, CT
171
Q

Toddler’s diarrhoea

A
  • Common cause of chronic nonspecific diarrhoea in children age 1-5
  • Resolves as child ages, normally child is well
  • Normally resoles with diet – good amount of fat, low fruit juice, normal fibre
  • 3 + watery stools a day – often smellier and paler, mild tummy pain rare, other wise well and growing normally
172
Q

colic

A
  • cry more than 3 hours a day, 3 days a week for at least 1 week but are otherwise healthy – often gets worse in evening, may bring knees up, clench fists, gassy, hard to sooth
  • Normally gets better around 3-4 months of age
173
Q

cows milk protein allergy

A
  • mostly babies <1
  • 2 types of CMPA: IgE-mediated (immediate reaction with allergic symptoms) and non-IgE mediated (delayed reaction 48h-1w after)
  • mostly clinical diagnosis with possible trial without cow’s milk
  • treat immediate reaction if anaphylaxis – epinephrine
  • cut out cows milk
  • 75% have resolved by age 3 so challenge every 6-12m
174
Q

Biliary atresia

A
  • congenital = section of bile duct narrowed or absent causing cholestasis = no excretion of conjugated bilirubin = jaundice
  • persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies
  • bilirubin levels (high conjugated)
  • Mx - “Kasai portoenterostomy” involves attaching a section of the small intestine to the opening of the liver, liver transplant to fully resolve
175
Q

choledochal cysts

A
  • congenital cysts in bile ducts (inside or outside liver) = backup of bile
  • Pain, jaundice, nausea, abdo mass, pancreatitis
  • Diagnosed via bloods (high conjugated bilirubin), USS
  • surgical treatment
  • different types depending on location: 1=cyst in bile duct, 2=sac on bile duct, 3= cyst in wall of duodenum or pancreas, 4=syst extends into liver
    5=multiple cysts along bile duct inside liver
176
Q

neonatal hepatitis syndrome

A
  • inflammation of liver in neonate
  • Viral (20%)– from mothers infection rubella, CMV, hepatitis A,B, C
  • Idiopathic (80%) – damage to developing liver, cholestasis, unknown
  • Genetic – alpha 1-antitrypsin deficiency
    – USS, liver biopsy (multinucleated giant cells signify cholestatic liver disease), serum bilirubin levels, LFT
  • Mx: Ursodeoxycholic acid increased bile production, may need liver transplant, optimise nutrition
177
Q

liver failure

A
  • uncommon, high mortality
  • massive hepatic necrosis with loss of function
  • May present in hours or weeks with jaundice, encephalopathy (irritability, confusion, drowsiness), coagulopathy, hypoglycaemia and electrolyte disturbance.
  • , transaminases +++, ALP +, coag abnormal, plasma ammonia +, EEG, CT head
  • Mx: bm >4mmol/L, prevent sepsis with abx and antifungals, prevent haemorrhage (IV vit K, H2-blocking drug/PPI), prevent cerebral oedema by fluid restriction and treat with mannitol
178
Q

causes of acute liver failure

A
  • Children <2 – infection (herpes simplex), metabolic disease, seronegative hepatitis, drug induced, gestational autoimmune liver disease
  • Children >2 – seronegative hep, paracetamol overdose, mitochondrial disease, Wilson disease, autoimmune hepatitis
179
Q

causes of chronic liver failure

A

– postviral hep B/C, autoimmune hep and sclerosing cholangitis, drug induced (NSAID), CF, Wilson disease, fibropolycystic liver disease, non-alcoholic fatty liver disease, alpha 1 antitrypsin deficiency

180
Q

undescended testes

A
  • develop in abdo then migrate through inguinal canal
  • longer they take to descend less likely they are to
  • after puberty have higher risk of torsion, infertility and testicular cancer
  • Mx: watch and wait in newborns, urologist at 6m, orchidopexy at 6-12m
181
Q

retractile testes

A

normal in boys before puberty for testes to move into inguinal canal when its cold or the cremasteric reflex is activated. Occasionally may fully retract or fail to descend again which will require surgery (orchidopexy)

182
Q

testicular torsion

A
  • teenage boys most common
  • emergency
  • Bell-clapper deformity (horizontal testicles) risk actor
  • USS = whirlpool sign
  • Mx - nil by mouth, analgesia, orchiopexy, orchidectomy if necrosis
183
Q

premature sexual development

A
  • Development of puberty <8y girls, <9y boys
  • Thelarche – prem breast development, 6m-2y/o, no other signs of puberty, normally self limiting
  • Adrenarche (pubarche) – pubic hair development
  • Gonadotrophin-dependent precocious puberty
  • Isolated premature menarche
184
Q

precocious puberty

A
  • gonadotrophin dependant: premature activation of normal pathway
  • gonadotrophin independent: excess sex steroids produced outside of pituitary, sequence of puberty abnormal
  • more common in girls without pathology, more often pathological in boys
185
Q

hypothyroidism

A
  • if undiagnosed can lead to neurodevelopmental and intellectual disability
  • congenital: dysgenesis or dyshormonogenesis, screened on blood spot test, prolonged jaundice, FTF, lethargy
  • acquired: autoimmune thyroiditis (Hashimotos)
  • Ix: TFT, USS, thyroid antibodies
  • Mx: Levothyroxine orally once daily titrated up
186
Q

gonadotrophin deficiency

A
  • hypogonadotropic hypogonadism (low LH and FSH)
  • causes delayed puberty
  • causes: hypothalamus/pituitary damage, GH def, hypothyroidism, hyperprolactinaemia, excessive exercise/dieting, constitutional delay in growth and development, Kallman syndrome
  • Ix: Early morning serum FSH and LH (low), TFT, FBC, GH testing (insulin like growth factor 1), serum prolactin, imaging, genetic testing
  • Mx: treat cause, sex hormone replacement
187
Q

Kallmann syndrome

A
  • Genetic condition causing hypogonadotropic hypogonadism, resulting in failure to start puberty
  • Associated with reduced or absent sense of smell (anosmia)
  • hypothalamus fails to secrete the bursts of GnRH in utero, during infancy, and at puberty – during development part of hypothalamus forms part of nose resulting in anosmia
188
Q

hypothalamic tumours

A
  • most are gliomas – abnormal growth of glial cells
  • symptoms – failure to thrive, headache, hyperactivity, cachexia, puberty problems
  • reduced production of GnRH leading to hypogonadotropic hypogonadism
189
Q

congenital adrenal hyperplasia

A
  • AR genetic deficiency of the 21-hydroxylase enzyme
  • enzyme converts progesterone into aldosterone and cortisol (not used for progesterone to testosterone) = low aldosterone, low cortisol, high testosterone
  • Px: severe = poor feeding, vomiting, dehydration, enlarged clitoris, hyponatraemia, hyperkalaemia, hypoglycaemia
  • hyperpigmentation - anterior pit makes more ACTH, byproduct is melanocyte stimulating hormone
  • Mx: cortisol replacement, aldosterone replacement, corrective surgery for virilised genitalia
190
Q

eczema

A
  • chronic atopic condition - defects in skin barrier allow irritants in = immune response
  • Mx: maintenance (emollients), flares (emollients, topical steroid, treat infections)
  • topical steroids - weakest steroids for shortest time (start hydrocortisone)
191
Q

Stevens-Johnson syndrome

A
  • SJS (affects <10% of body)and toxic epidermal necrolysis spectrum of same pathology
  • causes: medications (anti-epileptics, abx, allopurinol, NSAIDs), infections (HSV, mycoplasma pneumonia, cytomegalovirus, HIV)
  • can be fatal - medical EMERGENCY
  • start with non-specific symptoms - purple/red rash - blisters - skin breaks away leaving raw skin, shedding of mucous membranes - eyes become inflamed and ulcerated - can affect urinary tract, lungs and organs
  • Mx: supportive care, steroids, immunoglobulins, immunosuppressant
192
Q

anaphylaxis - principles of management

A

oA – Airway: Secure the airway
oB – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.
oC – Circulation: Provide an IV bolus of fluids
oD – Disability: Lie the patient flat to improve cerebral perfusion
oE – Exposure: Look for flushing, urticaria and angio-oedema
*IM adrenalin, repeated after 5 minutes if required
*Antihistamines, such as oral chlorphenamine or cetirizine
*Steroids (IV hydrocorticone)

193
Q

vascular birth marks

A
  • Macular stains (salmon patches, angel kisses or stork bite) – faint red marks mainly around the head/neck, most fade by end of infancy
  • Haemangiomas – can be slightly raised and bright red or bluish and usually appear a few days/weeks after birth, grow quickly in first 6m then shrink, most on head/neck
  • Port-wine stain – grow only as child grows, darken and thicken over time, may need MRI as can be same pattern in meninges
194
Q

pigmented birthmarks

A
  • Café-au-lait spots – very common, having many can be a sign of neurofibromatosis
  • Mongolian blue spots – often on lower back or buttocks, more common on darker skin, usually fade by 4y
  • Moles (congenital naevi etc)
195
Q

macular rash

A

a non-palpable rash with colour change in limited areas
measles, rubella

196
Q

papular rash

A

a palpable rash with raised, solid lesions and colour changes in limited areas up to 0.5cm
pityriasis rosea

197
Q

vesicular rash

A

elevated lesions that are filled with clear fluid <0.5cm
chicken pox, herpes simplex, herpes zoster

198
Q

nodule

A

a circumscribed swelling or an elevated lesion

199
Q

petechiae

A

small red/purple spot that is not elevated and doesn’t blanch.
meningococcal septicaemia

200
Q

viral causes of rashes

A
  • 1 – smallpox
  • 2 – chickenpox – beware in immunocompromised & eczema. Reactivation = shingles.
  • 3 – measles – remember prodromal CCCK – cough, coryza, conjunctivitis, Koplik spots.
  • 4 – rubella – beware congenital form –teratogenic, multi-organ inflammation.
  • 5 – parvovirus –slapped cheek.
  • 6 – roseola infantum – retrospective diagnosis, HHV6.
  • Hand-foot & mouth – coxsackie.
  • Mumps –parotitis
  • Herpes stomatitis – painful – reactivation = cold sore
  • Warts, verrucas & molluscum contagiosum
201
Q

bacterial causes of rashes

A
  • Impetigo (Staph aureus) – contagious ++.
  • Abscess, boils, carbuncles (Staph).
  • Scalded skin – reaction to staph toxin.
  • Cellulitis – staph (usually) in soft tissues.
  • Meningococcaemia – rapid multi-organ failure.
  • Contrasted with – HSP (Henoch-Schonlein purpua)
  • Erisypelas (Strep) & lymphangitis.
  • Scarlet fever – reaction to strep toxin (glomerulonephritis, rheumatic fever etc).
  • Acne.
202
Q

fungi and yeast rashes

A
  • Tinea – capitis/corporis (ringworm) / unguium / athletes foot.
  • Candida – spreading nappy rash –in mouth too.
203
Q

protozoa and insects causing rashes

A
  • Toxoplasmosis – from cat poo – beware congenital form.
  • Nits & lice.
  • Scabies – spreading eruption in infants.
  • Toxocara – from dog poo.
204
Q

Kawasaki’s disease

A
  • mucocutaneous lymph node syndrome, Systemic medium sized vessel vasculitis, <5y, no clear cause
  • key complication = coronary artery aneurysm
  • Px: persistent fever >39 for >5d, unwell, wide spread erythematous maculopapular rash, desquamation on palms and soles, strawberry tongue, cracked lips, cervical lymphadenopathy, bilateral conjunctivitis
  • Ix: FBC (anaemia, leukocytosis, thrombocytosis), LFT (hypalbuminaemia, elevated liver enzymes), raised inflammatory markers, urinalysis (WBC but no infection)
205
Q

management of Kawasaki’s disease

A
  • High dose aspirin to reduce the risk of thrombosis (one of few scenarios where aspirin used in children as normally avoided due to risk of Reye’s syndrome)
  • IV immunoglobulins to reduce the risk of coronary artery aneurysms
  • Need close follow up with echos
206
Q

kawasaki’s disease course

A
  • Acute phase: The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.
  • Subacute phase: The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.
  • Convalescent stage: The remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks
207
Q

measles

A
  • less common due to vaccination
  • PCR or serological confirmation = notifiable diasease
  • 10-14d incubation, Fever, cough, runny nose, conjunctivitis, malaise, Koplik spots (white spots on buccal mucosa), maculopapular rash (spreads downwards from behind the ears and becomes blotchy and confluent)
  • Mx: supportive, isolation, ribavirin (antiviral) in immunocompromised
208
Q

Chicken pox

A
  • varicella zoster virus
  • incubation 10d-3w vesicular rash (widespread, erythematous, raised, stop being contagious once scabbed over)
  • complications - bacterial superinfection, dehydration, encephalitis
  • Mx: usually self-limiting, aciclovir in immunocompromised and neonates, calamine lotion for itching
209
Q

Rubella

A
  • german measles, mild infection in childhood
  • causes congenital abnormalities if infected pregnant woman
    – low fever, maculopapular rash on face then spreads and fades in 3-5d, lymphadenopathy (suboccipital and postauricular)
210
Q

diphtheria

A
  • Corynebacterium diphtheriae usually affecting mucous membranes of nose and throat
  • rare now, used to be deadly in children
  • can cause damage to heart, kidneys and CNS
  • Sx: thick gray membrane covering tonsils, sore throat, swollen lymph nodes, difficulty breathing, nasal discharge, fever, fatigue
  • Mx: abx (penicillin or erythromycin), an antitoxin
211
Q

Scalded skin syndrome

A
  • type of s.aureus that produce epidermolytic toxins (protease enzymes), <5y
  • starts with generalised patches of erythema – looks thin and wrinkled – formation of fluid filled blisters (bullae) – burst and leave very sore erythematous skin below
  • Nikolsky sign – gentle rubbing causes skin to peel away
  • Systemic symptoms – if untreated an lead to sepsis and death
  • Mx: admission and IV abx, fluid/electrolyte balance to avoid dehydration
212
Q

Whooping cough

A
  • URTI caused by Bordetella pertussis (gram negative bacteria) 100 DAY COUGH
  • severe coughing fits start after 1w, unable to breath = inspiratory whoop when out of breath
  • Can cough so hard they faint, vomit or develop pneumothorax
  • infants can have apnoeas instead of cough
  • Mx: notifiable disease, supportive care, macrolide abx (azithromycin), close contacts prophylactic abx
  • complication is bronchiectasis
213
Q

polio

A
  • poliovirus.
  • Non-paralytic polio – mild flu like illness lasting up to 10d
  • Paralytic polio – hyporeflexia, weakness, muscle aches, flaccid paralysis – may be temporary or permanent
  • Post-polio syndrome – cluster of disabling signs that develop years after infection
  • Dx: throat swab, stool swab, lumbar puncture
  • Mx: no cure, supportive, contact tracing
214
Q

testing in children born to HIV+ parents

A
  • viral load test at 3m (if negative then not contracted during birth)
  • HIV antibody test at 24m (should be negative if 3m test negative and not breastfed)
215
Q

bacteria meningitis causes

A
  • in children and adults most common are Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).
  • In neonates = group B strep (GBS)
216
Q

investigations for meningitis

A
  • Lumbar puncture for all children: <1m with fever, 1-3m fever and unwell, <1y with unexplained fever and features of illness
  • kernig’s test (flex hip and knee then straighten)
  • brudzinski’s test (lie on back, slowly pick head up flexing neck)
217
Q

management of meningitis

A
  • Community – urgent IM/IV benzylpenicillin then hospital
  • Hospital – blood culture and lumbar puncture if possible to do quickly – blood test for meningococcal PCR (quicker to come back), abx, steroids (dexamethasone)
    o Under 3 months – cefotaxime plus amoxicillin
    o Above 3 months – ceftriaxone
  • Notifiable disease
218
Q

post exposure prophylaxis for meningitis

A

for people with prolonged contact with patient from 7 days before symptoms – single dose of ciprofloxacin within 24h of diagnosis

219
Q

viral meningitis

A
  • herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV)
  • sample of CSF from lumbar puncture should be sent for viral PCR testing
  • tends to be milder – supportive treatment, aciclovir for HSV or VZV
220
Q

lumbar puncture results for bacterial vs viral meningitis

A
221
Q

encephalitis

A
  • infective or autoimmune
  • most common cause is HSV (1 from coldsores in children, 2 from genital herpes in neonates)
  • Px: altered consciousness, unusual behaviour, acute onset, focal seizures, fever
  • Dx: lumbar puncture, CT (if not lumbar puncture), MRI, EEG, swabs for causative agent, HIV test
  • Mx: IV antimicrobials (aciclovir), repeat lumbar puncture before stopping, follow up, rehab
222
Q

slapped cheek syndrome

A
  • Human Parvovirus B19 infection - Causes erythematous infectiosum/fifth disease/slapped cheek syndrome
  • Infects the erythroblastoid red cell precursors in the bone marrow
  • characteristic rash on face 1w later – progresses to maculopapular ‘lace’ like rash on trunk and limbs
223
Q

impetigo

A
  • superficial skin infection, normally caused by s.aureus
  • golden crust characteristic of staph infection
  • kept off school until all lesions healed or on abx for 48h
  • classified as bullous or non-bullous
  • Complications – cellulitis, sepsis, scarring, post-strep glomerulonephritis, scalded skin syndrome, scarlet fever
224
Q

non-bullous impetigo

A
  • Typically around nose or mouth
  • The exudate from lesions dries into golden crust
  • Normally no systemic symptoms
  • Topical fusidic acid for localised non-bullous impetigo
  • antiseptic cream (hydrogen peroxide 1% cream) first line
  • oral flucloxacillin if severe
225
Q

bullous impetigo

A
  • always caused by s.aureus – can produce epidermolytic toxins that break down proteins holding skin together – causes 1-2cm fluid filled vesicles which grow then burst forming golden crust – can be painful and itchy but heal without scarring
  • more common in neonates and children <2
  • may have systemic symptoms
  • in severe infections/widespread its called staphylococcus scalded skin syndrome
  • swabs to confirm diagnosis and abx sensitivities
  • abx – fluclox oral or IV
  • need isolating where possible
226
Q

candida infection

A
  • yeast infection
  • candida normally causes no harm as part of flora in skin, vagina and GI tract but can overgrow causing a rash, itching etc
  • overgrowth due to warm, moist conditions such as wet nappies; recent use of abx or corticosteroids; immunocompromise
  • swab for confirmation
  • treated with creams (eg clotrimazole) , suppositories, mouthwash etc
  • oral anti-yeast meds (fluconazole) if immunocompromised and severe
227
Q

toxic shock syndrome

A
  • caused by toxin producing s.aureus and GAS
  • fever >39, hypotension, diffuse erythematous macular rash
  • acts as a superantigen causing organ dysfunction such as mucositis, vomiting/diarrhoea, renal impairment, liver impairment, clotting abnormalities, altered consciousness
  • Mx: intensive care for shock, area of infection surgically debrided, abx (ceftriaxone + clarithromycin), IV Ig to neutralise toxins
  • 1-2w after infection = desquamation of pals and soles
228
Q

scarlet fever

A
  • caused by an exotoxin from GAS pharyngitis
  • Diffuse, erythematous macular-papular rash, sandpaper texture, appears shortly after pharyngitis – spreads rapidly to whole body with increased density on neck, axilla and groin
  • Circumoral pallor – rash spares area around mouth
  • Tongue initially white but desquamates leaving a red strawberry tongue with prominent papillae
  • May be desquamation of palms/soles
  • Throat swab
  • Mx:10 days of abx (such as penicillin or erythromycin) to prevent complications such as rheumatic fever, glomerulonephritis etc
229
Q

coxsackie’s disease

A
  • coxsackie A virus, incubation 3-5d
  • starts with viral URTI symptoms - small mouth ulcers day 1-2 - blistering red spots across body (most on hands, feet and around mouth), may be itchy and painful
  • Mx: supportive, resolved without treatment in 7-10d
230
Q

causes of global developmental delay

A
  • Down’s syndrome
  • Fragile X syndrome
  • Fetal alcohol syndrome
  • Rett syndrome
  • Metabolic disorders
231
Q

causes of gross motor delay

A
  • Cerebral palsy
  • Ataxia
  • Myopathy
  • Spina bifida
  • Visual impairment
232
Q

causes of fine motor delay

A
  • Dyspraxia
  • Cerebral palsy
  • Muscular dystrophy
  • Visual impairment
  • Congenital ataxia (rare)
233
Q

causes of language delay

A
  • Specific social circumstances, for example exposure to multiple languages or siblings that do all the talking
  • Hearing impairment
  • Learning disability
  • Neglect – needs safeguarding referral
  • Autism
  • Cerebral palsy
234
Q

causes of personal and social delay

A
  • Emotional and social neglect
  • Parenting issues
  • Autism
235
Q

febrile convulsions

A
  • seizure due to high fever between 6m-5y
  • Simple = generalised tonic clonic seizures lasting <15m and only occur once during the illness
  • Complex = partial or focal seizures, >15m, multiple times
  • Mx: find infection, analgesia, further investigations for complex, parenting advice of seizure safety (call ambulance if >5m)
236
Q

generalised tonic-clonic seizures

A

o May be associated with tongue biting, incontinence, groaning, irregular breathing
o Prolonged post-ictal period
o Management – 1st line sodium valproate, 2nd line lamotrigine or carbamazepine

237
Q

focal seizures

A

o Start in temporal lobes and affect hearing, speech, memory and emotions
o Can present in many ways eg: hallucinations, memory flashbacks, déjà vu, doing strange things on autopilot
- lamotrigine or carbamazepine

238
Q

absence seizures

A

o Typically in children and >90% grow out of it
o Becomes blank and stares into space then abruptly returns to normal in 10-20s
o Management – first line sodium valproate

239
Q

atonic seizures

A

o Drop attacks – brief lapses in muscle tone usually lasting <3m
o May be indicative of Lennox-Gastaut syndrome
o Management – 1st sodium valproate, 2nd lamotrigine

240
Q

myoclonic seizures

A

o Sudden brief muscle contractions, usually remains awake
o May occur in children as part of juvenile myoclonic epilepsy
o Management – sodium valproate

241
Q

infantile spasms

A

o West syndrome
o Rare disorder starting in infancy characterised by clusters of full body spasms
o Poor prognosis: 1/3 die by age 25, however 1/3 are seizure free
o Management: prednisolone, vigabatrin

242
Q

status epilepticus

A

> 5m or 2+ without regaining consciousness
* Secure the airway
* Give high-concentration oxygen
* Assess cardiac and respiratory function
* Check blood glucose levels
* Gain intravenous access (insert a cannula)
* IV lorazepam, repeated after 10 minutes if the seizure continues

243
Q

causes of microcytic anaemia TAILS

A
  • T – Thalassaemia
  • A – Anaemia of chronic disease
  • I – Iron deficiency anaemia
  • L – Lead poisoning
  • S – Sideroblastic anaemia
244
Q

investigations for anaemia

A
  • Full blood count for haemoglobin and MCV
  • Blood film
  • Reticulocyte count
  • Ferritin (low iron deficiency)
  • B12 and folate
  • Bilirubin (raised in haemolysis)
  • Direct Coombs test (autoimmune haemolytic anaemia)
  • Haemoglobin electrophoresis (haemoglobinopathies)
245
Q

thalassemia

A
  • AR defect in hb chains (alpha or beta)=more haemolysis = splenomegaly, bone marrow expands = fractures, pronounced forehead/malar eminences
  • Ix: FBC (microcytic anaemia), hb electrophoresis, DNA testing
  • Mx: thalassemia minor (monitor), intermedia (2 abnormal copies, occasional blood transfusion), major (2 deletion genes, regular transfusions, iron chelation, splenectomy)
  • beware iron overload
246
Q

iron overload

A
  • due to faulty RBC, recurrent transfusions and increased gut iron absorption
  • Need serum ferritin level monitoring
  • Mx: limiting transfusions and performing iron chelation
  • Causes fatigue, liver cirrhosis, infertility, impotence, HF, arthritis, diabetes, osteoporosis
247
Q

sickle cell anaemia

A
  • AR abnormal gene for beta-globin on c11 leading to HbS
  • Symptoms evolve as HbF disappears
  • tested on newborn blood spot
  • Mx: avoid dehydration and triggers for crises, abx prophylaxis (phenoxymethylpenicillin), hydroxycarbamide stimulated production of HbF , transfusions for anaemia, bone marrow transplant can be curative
248
Q

Fanconi anaemia

A
  • AR mutations in FANC genes
  • Majority will have congenital abnormalities such as short stature, abnormal thumbs, renal malformations, microphthalmia and pigmented skin
  • Signs of bone marrow failure normally present around age 5-6y
  • Genetic testing for diagnosis
  • High risk of mortality from bone marrow failure or transformation into leukaemia
  • Treatment with bone marrow transplant
249
Q

haemophilia

A
  • X linked AR - A=factor VIII deficiency, B= factor IX def
  • Sx: severe= crippling arthritis from joint/muscle bleeds, most present with excessive bleeding (after heel prick, intercranial haemorrhage)
  • Mx: IV prophylactic factor VIII/IX every 2-3d if severe, during bleed= recombinant factor concentrate
  • avoid IM injections, aspirin, NSAIDs
250
Q

von willebrands disease

A
  • von willebrand factor produced in vascular endothelium - facilitates platelet adhesion and is a carrier protein for FVIII
  • AD
  • bruising, excessive bleeding, mucosal bleeding
  • Mx: depends on severity, Type 1 treated with DDAVP which causes secretion of vWF and FVIII into plasma
251
Q

immune thrombocytopaenia

A
  • most common cause of low platelets in children 2-10y
  • destruction of platelets by antiplatelet IgG autoantibodies
  • It is acute, benign, and self-limiting in 80% of children, usually clearing in 6-8w
  • most present 1-2w after viral infection or vaccination
  • petechiae, purpura, bruising, epistaxis
  • Mx: most don’t need treatment, oral prednisolone or IV Ig for severe bleeding, platelet transfusion in life-threatening haemorrhage

Phase 3A (6 decks)

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