Paeds Flashcards
HUS triad
- Low platelet count (thrombocytopenia)
- consumption of platelets for blood clots - Haemolytic anaemia (normocytic - HHAAA)
- blood clots within the small vessels chop up the red blood cells as they pass by (haemolysis), causing anaemia - Acute kidney injury
- blood flow through the kidney is affected by the clots and damaged red blood cells, leading to acute kidney injury
HUS presentation
Brief gastroenteritis (bloody diarrhoea)
5 days after:
Reduced urine output
Haematuria
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising
Causes of HUS
Most common cause: toxin produced by E.coli called the shiga toxin
- shigella also produces this toxin and can cause HUS
The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis INCREASE THE RISK of developing HUS
Infective mononucleosis causative organism
Epstein Barr Virus (EBV)
Features of infectious mononucleosis
Fever
Sore throat
Fatigue
Lymphadenopathy
Tonsillar enlargement with white coating
Splenomegaly (and in rare cases splenic rupture)
intensely itchy maculopapular rash in response to AMOXICILLIN or cefalosporins in 99% of patients
Infectious mononucleosis tests
‘Mono spot test’ for heterophile antibodies (produced in response to EBV infection)
- can take up to 6 weeks for these antibodies to be produced
Anti-viral capsid antigen (VCA) antibody test
- IgM antibody: rises early and suggests acute infection
- IgG antibody: persists after the condition and suggests immunity
5 signs of leukaemia
Failure to thrive
Pallor (anaemia)
Neutropenia (infection)
Petechiae + abnormal bleeding/bruising (secondary to thrombocytopenia)
Lymphadenopathy
Hepatosplenomegaly
Main investigations leukaemia
FBC - 1st line
Bone marrow biopsy - diagnostic
Blood film - to look for abnormalities
Leukaemia associated with Down’s syndrome
ALL
4 complications of chemotherapy
- Stunted growth and development in children
- Infertility
- Neurotoxicity
- Tumour lysis syndrome
Explain the pathophysiology of congenital adrenal hyperplasia
- Deficiency of 21-hydroxylase enzyme
- 21-hydroxylase enzyme usually converts progesterone into aldosterone and cortisol = underproduction of aldosterone and cortisol
- unconverted progesterone = converted into testosterone = overproduction of androgens
Why does hypoglycaemia, hyponatraemia and hyperkalaemia occur in CAH
Low cortisol = Hypoglycaemia
Low aldosterone = Hyponatraemia, Hyperkalaemia
Why does skin hyperpigmentation occur in CAH
Anterior pituitary responds to low cortisol by increasing ACTH
By product of ACTH = melanocyte stimulating hormone
Characteristics of CAH in cases presenting later in childhood
Tall for age
Deep voice
Early puberty
Females: absent periods, facial hair
Males: large penis, small testicles
CAH management
Corticosteroids:
Hydrocortisone (CORTISOL replacement)
Fludrocortisone (ALDOSTERONE replacement)
Female patients with virilised genitalia may require corrective surgery
Risk factors for further febrile convulsions
Age of onset < 18 months
Fever < 39
Shorter duration of fever before the seizure
FHx of febrile convulsions
Features of a simple febrile seizure
Generalised tonic clonic seizure
Lasts less than 15 mins
Only occur once during a single febrile illness
management following febrile convulsion
Treat underlying cause (usually viral or bacterial infection)
Reassurance and parental education
Complex - further investigation
Eye muscle controlled by cranial nerve 6 (abducens) and action
Lateral rectus
‘ABDuction’ = “out”
Eye muscles controlled by cranial nerve 3 (oculumotor) and action
Medial rectus - adduction
Superior rectus - elevates + turns medially
Inferior rectus - depresses + turns medially
Inferior oblique - elevates + turns laterally
Eye muscle controlled by cranial nerve 4 (trochlear) and action
Superior oblique
Depresses :( and turns laterally “down” :(
Other than “down and out” in a third nerve palsy, name 2 other presentations (usually indicating a ‘surgical’ cause of compression against the 3rd nerve)
Ptosis (levetor palpebrae superioris is not innervated)
Dilated fixed (non-reactive) pupil (parasympathetic nerves of iris sphincter not innervated)
Name 4 causes of a third nerve (oculomotor) palsy
Microvascular (diabetes, HTN, ischaemia)
Tumour
Cavernous sinus thrombosis
Posterior communicating artery aneurysm
Types of microcytic anaemia
TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency anaemia
Lead poisoning
Sideroblastic anaemia
Types of normocytic anaemia (3)
Increased reticulocyte count:
Acute blood loss
Haemolytic anaemia
Decreased reticulocyte count:
Aplastic anaemia
Causes of megaloblastic (impaired DNA synthesis) macrocytic anaemia
B12 deficiency
Folate deficiency
4 causes of normoblastic macrocytic anaemia
Drugs
Alcohol
Hypothyroidism
Liver disease
Causes of anaemia in infancy
Physiological (most common cause)
Anaemia of prematurity
Blood loss
Haemolysis
Twin-twin transfusion (shared placenta)
Test for haemolytic disease of the newborn
Direct coombs test (DCT)
Investigations show increased reticulocytes - 2 differentials
Haemolysis
Blood bloss
Causes of anaemia in older children
Iron deficiency anaemia secondary to dietary insufficiency (most common cause)
Blood loss e.g. menstruation in older girls
Four general symptoms of anaemia
Fatigue
Shortness of breath
Headache
Dizziness
Four general signs of anaemia
Pale skin
Conjunctival pallor
Tachycardia
Increased resp rate
Specific symptoms of iron deficiency anaemia
Pica (dirt cravings)
Hair loss
Specific signs of iron deficiency anaemia
Koilonychia (spoon shaped nails)
Angular chelitis (inflammation around mouth)
Atrophic glossitis (smooth tongue)
Brittle hair and nails
Inheritance pattern sickle cell anaemia
Autosomal recessive
When is sickle cell anaemia screened for (2)
High risk pregnant women are offered testing during pregnancy
Newborn screening heel prick test at 5 days of age
General management of sickle cell anaemia
Antibiotic prophylaxis (penicillin V) - due to splenectomy
Hydroxycarbamide (stimulates production of HbF) - prevents vaso-occlusive complications
Blood transfusion (for severe anaemia)
Bone marrow transplant (curative but high risk)
Avoid NSAIDs in complications of CKD
Name the four sickle cell crises
Vaso-occlusive crisis (> priapism)
Splenic sequestration crisis (> hypovolaemic shock)
Aplastic crisis (+ triggered by parvovirus B19)
Acute chest syndrome (= fever or resp symptoms WITH new infiltrates on CXR)
Factor deficiency in Haemophilia A and Haemophilia B
A = VIII (8)
B = IX (9)
8 is B and it’s the opposite way round
Presentation of haemophilia
Neonatal intracranial haemorrhage, haematomas + cord bleeding
Spontaneous bleeding into joints + muscles = joint damage and deformity, bruising
1st line investigation haemophilia
Clotting screen:
PT
APTT
fibrinogen
Management of haemophilia
IV infusion replacement of clotting factors (prophylactic or in response to bleeding)
In acute settings:
- IV infusion
- Desmopressin (to stimulate VWF)
- Antifibrinolytics e.g. tranexamic acid
APGAR score
Appearance
Pulse
Grimace
Activity
Respiratory
Presentation of biliary atresia (4)
prolonged jaundice (present > 14 days of age)
Dark urine and pale stools
hepatomegaly
splenomegaly
Appetite and abnormal growth
Investigatory blood test for biliary atresia
Serum bilirubin: total bilirubin may be normal with abnormally high conjugated bilirubin
Ebstein’s anomaly definition
congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle
Hirschprung’s disease definition
aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses
Definitive management Hirschsprung’s
surgery to affected segment of the colon (Swenson procedure)
3 bronchiolitis red flag signs
Severe respiratory distress e.g. grunting
Central cyanosis
Apnoea
Thalassaemia definition
Genetic defect in the protein chains of haemoglobin (alpha or beta)
Thalassaemia inheritance pattern
Autosomal recessive
Three key presentations of thalassaemia
Splenomegaly: fragile RBCS break down and collect in the spleen
Pronounced forehead and malar eminences + susceptibility to fractures: bone marrow expands to produce extra RBC to compensate
Diagnostic testing thalassaemia (3) + who is offered screening?
FBC: Microcytic anaemia
Haemoglobin electrophoresis: globin abnormalities
DNA testing: genetic abnormalities
Pregnant women are offered screening
A complication of thalassaemia (and recurrent infusions) + management of the complication
Iron overload
Management:
- serum ferritin monitoring
- limit transfusions
- iron chelation
Management of alpha thalassamia and beta thalassaemia major (4)
Regular blood transfusions
Iron chelation due to iron overload in transfusions
Splenectomy
Bone marrow transplant
Most likely demographic of patient with Kawasaki disease
Under 5 years old
Japanese or Korean
Male
Key complication of Kawasaki disease
Coronary artery aneurysm
Ix = transthoracic echocardiogram
Clinical features of Kawasaki disease
CRASH & BURN
Conjunctivitis (bilateral) 👀
Rash (widespread erythematous maculopapular)📍📍📍
Adenopathy (cervical lymphadenopathy)
Strawberry tongue 🍓
Hands: desquamation (skin peeling) on palms and soles
BURN (Persistent fever: >39c for >5 days 🥵)
Diagnostic criteria: fever for > 5 days PLUS 4 out of 5 of CRASH
Management Kawasaki disease
High dose aspirin (to reduce risk of thrombosis)
AND
IV immunoglobulins (to reduce risk of coronary artery aneurysm)
Close follow up using echocardiograms
Why is aspirin not usually used in the treatment of children?
Risk of Reye’s syndrome (acute increase in pressure within the brain)
Patient age group most likely to get septic arthritis
< 4 years old
Presentation of septic arthritis
Usually a single joint (often knee or hip)
Rapid onset:
- hot, red, swollen, painful joint
- refusing to weight bear
- stiffness and reduced range of motion
- systemic symptoms E.g. fever, lethargy, sepsis
usually results from haematological spread from a bacterial infection
elsewhere in the body, although it can occur following a skin wound such as chickenpox scar
Most common causative bacteria of sepsis arthritis
Staph aureus
Differential diagnosis septic arthritis
Transient sinovitis
Perthes disease
SUFE
Juvenile idiopathic arthritis
Management of septic arthritis
Aspiration: gram staining, crystal microscopy, culture, antibiotic sensitivities,
- joint fluid may be purulent
Empirical Abx given until microbial sensitivities known (Abx given 3-6 wks)
Severe cases = surgical drainage + washout
Bimodal age distribution in Hodgkin’s lymphoma
20 + 75
Risk factors for Hodgkin’s lymphoma
HIV
EBV
Autoimmune conditions (RA/sarcoidosis)
FHx
Describe the lymphadenopathy seen in Hodgkin’s (key presentation)
Cervical / Axilla / Inguinal
Non tender + “rubbery”
Pain when drinking alcohol
Hodgkin’s B symptoms
Unexplained Fever
Unexplained Weight loss
Drenching Night sweats
‘B’ symptoms = associated with B-cell abnormalities
Investigations Hodgkin’s lymphoma
Lactate dehydrogenase (LDH) = raised but not specific
Lymph node biopsy = diagnostic
- Reed Sternberg cells
CT/MRI/PET = diagnosing + staging
Ann Arbor staging
S1: one region of lymph nodes
S2: more than one region but same side of diaphragm
S3: above + below
S4: non-lymphatic (lungs/liver etc)
Management of Hodgkin’s lymphoma and risks of management options
Chemo: risk of leukaemia + infertility
Radiotherapy: risk of cancer, damage to tissues + hypothyroidism
Name 3 Non-Hodgkin lymphomas
Burkitt lymphoma
MALT lymphoma
Diffuse large B cell lymphoma
Non-Hodgkin management options
Watchful waiting
Chemo
Monoclonal antibodies E.g. rituximab
Radiotherapy
Stem cell transplant
Perthe’s disease definition
Avascular necrosis of the femoral head
It is idiopathic
Most common gender / age of onset Perthes disease
Boys aged 5-10
Presentation of Perthes disease
Younger than 10
Slow onset of:
- Pain in the hip or groin
- Limp
- Restricted in hip movements
- Possible referred pain to knee
No history of trauma (SUFE more likely if minor trauma history)
Associated with hyperactivity and short stature
Investigations for Perthes disease
1st line: X Ray (can appear normal)
Other:
- Blood tests (typically normal - useful for DDx)
- Technetium bone scan
- MRI scan
Four conservative management option for a Perthes disease patient who is under 6 years old/less severe disease
Bed rest
Traction
Crutches
Analgesia
Slipped upper femoral epiphysis definition
Head of the femur is displaced (slips) along the growth plate
Typical patient presentation of SUFE
Obese 12 year old boy undergoing growth spurt and may be history of minor trauma that triggers onset
Bilateral (75%)
Investigations for SUFE
1st line: X ray
Other:
- Bloods (typically normal - useful for DDx)
- Technetium bone scan
- CT scan
- MRI scan
Management of SUFE
Surgery to correct position and fix it in place
Surgery: Internal fixation across the growth plate
Developmental dysplasia of the hip definiton
Structural abnormality in the hips caused by abnormal development of the fetal bones during pregnancy - causes instability in the hips and a tendency for dislocation
Risk factors for DDH
Fs
Family history (1st degree)
Female
First born children
Feet first (Birth in breech position from 28 weeks onward)
Fat (high birth weight)
Fluid (oligohydramnios)
+ prematurity
What two tests are done in the NIPE to check for DDH
Barlow test (dislocation of an articulated femoral head / adduction and downward pressure)
Ortoloni test (relocation of a dislocated femoral head / abduction and upward pressure)
Diagnostic investigation of DDH in < 4.5 months
Ultrasound
>4.5 months = X-ray
Management of DDH
Pavlik harness if presentation <6 months (flexed and abducted)
Surgery if >6 months or if harness fails
Associated genetic condition of duodenal atresia
Down’s syndrome
Name 5 causes of intestinal obstruction
Intussusception
Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
X ray sign of duodenal atresia
Double bubble
Name 4 dysmorphic features of Down’s syndrome
Hypotonia
Brachycephaly
Prominent epicanthic folds
Upslanted palpebral fissures
Small ears + round face
Brushfield spots in the iris
Name 5 complications of Down’s syndrome
Learning disability
Visual problems (myopia, cataracts)
Recurrent otitis media
Deafness (eustachian tube abnormality)
Obstructive sleep apnoea
Cardiac defects (1 in 3): ASD, VSD, PDA, Tet of F
brain > eyes > ears > mouth > heart
How is Down’s syndrome primarily screened for
Combined test: ultrasound + maternal blood test
How is Down’s syndrome diagnosed prenatally (2)
Week 9 to 11: chorionic villus sampling
Week 14 to 18: amniocentesis
What is intussusception
The bowel telescopes into itself which thickens the overall size of the bowel and narrows the lumen
This causes a palpable mass + obstruction
Typical presentation of a patient with intussusception
More common in boys and typically 6 months - 2 years
Recent viral upper respiratory tract infection
Pale, lethargic and unwell
Features of intestinal obstruction (vomiting, absolute constipation, abdo distention)
Drawing legs up to abdomen
Redcurrant jelly stool
RUQ palpable mass (sausage shaped)
Key Investigation for intussusception
Ultrasound abdomen: shows ‘target sign’ or ‘doughnut sign’ which confirms diagnosis
Management of intussusception
Therapeutic enema/rectal air insufflation: force the folded bowel out
If therapeutic enema fails or if there is gangrenous bowel or perforation = surgical reduction
4 complications of intussusception
Obstruction
Gangrenous bowel
Perforation
Death
as the obstruction worsens, mesentery is stretched leading to venous obstruction. This then causes strangulation of the bowel, leading to necrosis of the bowel, generalised peritonitis and shock over time
Hirschsprung’s definition
Congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel + rectum
Pathophysiology of Hirschsprung’s
Absence of parasympathetic ganglion cells in the myenteric plexus
What increases the risk of Hirschsprung’s
Family history
Presentation of Hirschsprung’s associated enterocolitis
20% of neonates with Hirschsprung’s get HEC
2-4 weeks after birth
Fever, abdominal distention, diarrhoea with blood + septic features
LIFE THREATENING
Investigation of Hirschsprung’s
Diagnostic: full thickness suction rectal biopsy (shows absence of ganglion cells in mesenteric plexus)
Abdominal X-Ray can be used in addition to diagnose intestinal obstruction + HAEC: dilated loops of bowel with fluid levels
Definitive management of Hirschsprung’s
Surgical removal of the aganglionic section of bowel
How does NEC lead to death
Death of bowel tissue > perforation > peritonitis > shock > death
Presentation of NEC
first 2 weeks of life in neonates
Intolerance to feeds
Vomiting (milk from feeding particularly w/ green bile)
Distended, tender abdomen
Visible intestine loops lacking peristalsis
Absent bowel sounds
Blood in stools
Generally unwell/lethargic
Initial Investigations NEC
Bloods:
- FBC (thrombocytopenia + neutropenia)
- CRP
- capillary blood gas (to determine metabolic acidosis)
- blood culture (sepsis)
Diagnostic investigation NEC
Abdominal X-Ray
- dilated loops of bowel
- bowel wall oedema (thickened)
- pneumatosis intestinalis (intramural gas) = pathognomonic
Management of NEC
Suspected NEC: Nil by mouth with IV fluids, TPN + broad spectrum antibiotics to stabilise
- a nasogastric tube can be inserted to drain fluid + gas from the stomach intestines
SURGICAL EMERGENCY 🚨
May be left with a temporary stoma if significant bowel is removed
Risk: short bowel syndrome
Where is unconjugated bilirubin found
RBCs
Where is unconjugated bilirubin conjugated
Liver
How is conjugated bilirubin excreted
- Via the biliary system into the GI tract / stool
- urine
Common presentation of Hirschsprung’s in neonates
Failure or delay in passing meconium within 48 hours
Vaccines: 2 months
6 in 1 (1st)
Rotavirus (1st)
Men B (1st)
Vaccines: 3 months
6 in 1 (2nd)
Rotavirus (2nd)
Pneumococcal
Vaccines: 4 months
6 in 1 (3rd)
Men B (2nd)
Vaccines: 1 year
Pneumococcal (2nd)
Men B (3rd)
Hib/Men C (1st)
MMR (1st)
Vaccines: 3 years + 4 months
MMR (2nd)
4 in 1 pre-school booster
Inheritance pattern of Haemophilia
X-linked recessive disorder = only boys develop it and can only get it from their mother’s being carriers
von Willebrand = Women too
commonest lymphoma in childhood
non-Hodgkin
Hodgkin more common in adolescence
Most important differential diagnoses of limp in children 1-3 years
developmental dysplasia of the hip
septic arthritis
transient synovitis
trauma
leukaemia
Most important differential diagnoses of limp in children 11-16 years (3)
slipped upper femoral epiphysis (SUFE)
reactive arthritis
mechanical/overuse injuries (sports related)
3 causes of bilious vomiting in neonates
bilious vomiting = intestinal obstruction
Duodenal atresia
Meconium ileus
NEC
Meconium ileus presentation
Thick and sticky stool that causes obstruction
Typically presents 24-48 hours after birth with bilious vomiting and abdo distention
Associated with cystic fibrosis
Hirschprung’s disease associations (2)
3 times more common in males
Down’s syndrome
DKA triad
Hyperglycaemia i.e. blood glucose > 11mmol/l
Ketonaemia i.e. blood ketones > 3 mmol/l
Acidosis i.e. pH < 7.3
DKA key signs and symptoms
Fruity-smelling breath (due to presence of acetone)
Vomiting
Dehydration (due to glucose taking fluid out in urine)
Abdominal pain
Kussmaul respiration
Altered mental status (drowsiness/coma)
signs of DM e.g. weight changes, polyuria, polydipsia before DKA starts
DKA investigations
Blood glucose >11.1
Blood ketones >3
Urinary glucose + ketones
Bicarbonate < 15
Blood gas analysis (pH < 7.3)
Blood cultures (if infection is suspected)
U&Es (high potassium due to acidosis/lack of insulin)
Creatinine (mildly raised in dehydration)
Management of DKA: alert patient, not significantly dehydrated and can tolerate oral intake w/o vomiting
Encourage oral intake of fluids
Administer subcutaneous insulin
Major complication of treating DKA
Cerebral oedema caused by rapid correction of dehydration with IV fluids
Common precipitating factors causing DKA
Untreated type 1 diabetes
Infection
Dehydration
Myocardial infarction
Fasting
Management of DKA: patient is vomiting, confused, or significantly dehydrated
IV fluids (initial bolus of 10ml/kg 0.9% NaCl)
1 hour after starting IV fluids: Insulin infusion (0.1 units/kg/hour)
Once blood glucose falls below 14mmol/l: IV 10% dextrose at 125 mls/hour
correct dehydration evenly over 48 hours to reduce risk of cerebral oedema
monitor and correct hypokalaemia + cardiac signs after insulin administration
Does regular insulin treatment continue in the management of DKA
Long acting insulin should be continued
Short acting insulin should be stopped
DKA pathophysiology
uncontrolled lipolysis which results in an excess of free fatty acids that are ultimately converted to ketone bodies
DKA resolution defined values
pH > 7.3
Blood ketones < 0.6
Bicarbonate > 15
How soon should DKA be resolved
within 24 hours or a senior review is needed from an endocrinologist
Does insulin transport potassium into or out of cells
Into cells
pathognomonic sign for measles
Koplik spots on oral mucosal membranes
measles features
incubation period: 10-14 days
prodrome: irritable, conjunctivitis, fever
2 days after fever: koplik spots
3-15 days after fever: rash starts behind ears and spreads downwards
management of measles
self-resolving after 7-10 days of symptoms
children should be isolated until 4 days after symptoms resolve
most common complication of measles infection
Otitis media
most common cause of death in measles infection
pneumonia
4 complications of measles infection
otitis media
pneumonia
encephalitis (1-2 weeks after)
subacute sclerosing panencephalitis (5-10 years after)
1st investigation for suspected measles
measles-specific IgM and IgG serology
scarlet fever associated bacterial infection
group A streptococcus (streptococcus pyogenes)
usually tonsilitis
scarlet fever features
red-pink, blotchy, rough sandpaper rash that starts on the trunk and spreads outwards
strawberry tongue
lymphadenopathy
sore throat
fever
management of scarlet fever/strep throat
phenoxymethylpenicillin (penicillin V) for 10 days
children should be kept off school until 24 hours after starting antibiotics
2 complications of scarlet fever
otitis media
post-streptococcal glomerulonephritis (typically 10 days after infection)
acute rheumatic fever (typically 20 days after infection)
rubella 2 key features
rash lasting 3 days
lymphadenopathy behind the ears and back of the neck
management of rubella
supportive/self-limiting
children should stay off school for at least 5 days after the rash appears
congenital rubella syndrome triad
deafness, blindness, congenital heart disease
parvovirus b19 presentation
prodrome (mild fever, coryzal)
rash appears 2-5 days after symptoms begin: diffuse bright red rash on both cheeks and a few days later a reticular rash on trunk and limbs
when is parvovirus b19 infectious
until the rash appears
3 groups at risk of complications from parvovirus b19
immunocompromised
pregnant women
sickle cell anaemia (cause of aplastic crisis)
roseola infantum causative virus
human herpes virus 6
roseola infantum presentation
Most common in children 6 months - 2 years
high fever that comes on suddenly, lasts for 3-5 days then suddenly disappears
followed by mild non-itchy maculopapular lace-like rash on the trunk for 1-2 days
roseola infantum key complication
febrile convulsions due to high temperature
1st feature of chickenpox infection
pyrexia
stages of chickenpox lesions
papules > vesicles > pustules > crusts
Henoch-schoenlein purpura (HSP) patho
IgA mediated small vessel vasculitis
4 features of HSP
Palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
Joint pain
Abdominal pain
Renal involvement
Turner syndrome chromosomal abnormality
Female with single X chromosome (45 XO)
presentation of Turner’s syndrome (4)
Short stature
Primary amenorrhoea
Widely spaced nipples
Webbed neck
+ Infertility later in life due to underdeveloped ovaries
sign of Turner’s syndrome in neonates
lymphoedema
which hormones are elevated in Turner’s (1)
Gonadotrophins (LH and FSH)
(Caused by low levels of osteogen = negative feedback)
Hypo or hyper thyroidism in Turner’s
Hypothyroidism
Most common cardiac defect seen in Turner’s
Bicuspid aortic valve (15%) = ejection systolic murmur
Turner’s is also associated with coarctation of the aorta but it is not as common
Major long-term health complication in Turner’s syndrome
Aortic dilation and dissection
Rocker bottom feet sign (2 disorders)
Soles of the feet are convex
Patau syndrome (trisomy 13)
Edwards syndrome (trisomy 18)
Patau’s syndrome presentation
Holoprosencephaly (failure of the cerebral hemispheres to divide)
Microcephaly
Cleft lip and palate
Polydactyly (extra digits)
Congenital heart disease
Edward’s syndrome presentation
Low-set ears
Macrognathia (undersized jaw)
Microcephaly
Overlapping 4th and 5th fingers
Rocked bottomed feet
Congenital heart disease
Klinefelter’s syndrome karyotype
47, XXY
Klinefelter’s syndrome characteristics
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia
elevated gonadotrophin levels but low testosterone
Rash for > 5 days non-infective differentials
Kawasaki disease
Still’s disease
Rheumatic fever
Leukaemia
Juvenile idiopathic arthritis
Chronic autoimmune disease that causes arthritis < 16 years old for > 6 weeks
Joint pain, swelling, stiffness
Still’s disease
Systemic onset JIA
Features of systemic onset JIA/Still’s disease
Intermittent febrile episodes
salmon-pink rash
lymphadenopathy
arthritis
uveitis
Reduced appetite and weight loss
Most common subtype of JIA
oligoarticular JIA (4 or less joints affected) accounts for 60% of cases
most frequently occurs in girls under the age of 6 years
Classic associated feature of oligoarticular JIA
chronic anterior uveitis (eye redness, pain, vision loss)
seen in 1/3 of children with JIA
Joints affected in JIA
large joints e.g. knee, ankle, wrist
5 key onset subtypes of JIA
Systemic
polyarticular > 4 joints
oligoarticular < 4 joints
enthesitis related (key complication: anterior uveitis)
juvenile psoriatic (nail pitting, plaques of psoriasis, dactylitis)
Still’s disease investigations
ANA negative
rheumatoid factor negative
Raised inflammatory markers (raised CRP, ESR, platelets, and serum ferritin)
Key complication of Still’s disease
Macrophage activation syndrome (acutely unwell child with DIC, anaemia, thrombocytopenia, bleeding, non-blanching rash)
Key investigation finding: low ESR
Medical management of JIA
NSAIDs e.g. ibuprofen
Steroids (oral, intramuscular, or intra-articular in oligoarthritis)
Disease modifying anti-rheumatic drugs (DMARDs) e.g. methotrexate, hydroxychloroquine
Biologic therapy e.g. anti-TNFa e.g. infliximab
1st line treatment for oligoarticular JIA
intra-articular steroid injection
Stephen-Johnson syndrome
flu-like symptoms followed by a red/purple target-like rash that spreads and forms blisters
triggered by viral infection (mumps, flu, HSV, EBV) or reaction to medicines
4 medications that can cause stephen-johnson syndrome
Penicillin
Lamotrigine
Phenytoin
Allopurinol
Red flags in developmental milestone assessment
Not able to hold an object at 5 months
Not sitting unsupported at 12 months
Not standing independently at 18 months
No words at 18 months
No interest in others at 18 months
Not walking independently at 2 years
Not running at 2.5 years
Four major domains of child development
Gross motor and Fine motor
Language and communication
Cognitive
Personal and social
milestones in gross motor development:
4 months
9 months
12 months
15 months
head downwards
4 months: support their head
7-8 months months: sit unsupported, crawling
12 months: cruising
15 months: walk unaided
milestones in fine motor development:
8 weeks
6 months
9 months
12 months
8 weeks: fixes their eyes on an object
6 months: palmar grasp
9 months: scissor grasp (squashes it between thumb and forefinger)
12 months: pincer grasp (with the tip of the thumb and forefinger)
what age should a baby be able to say single words in context e.g. mama
12 months
at what age should a baby smile responsively
6 weeks
West syndrome
Infantile spasms starting at around 6 months of age (repeated flexion of head/arms/trunk followed by extension of arms)
More common in male infants
Poor prognosis
Juvenile myoclonic epilepsy
Bilateral myoclonic jerks in upper and lower limbs often in the morning/following sleep deprivation
periods of absence
Age of onset: 10-20 years
If left untreated, may progress to generalised tonic-clonic seizures
Lennox-Gastaut syndrome
atypical absences, falls, jerks
90% moderate-severe mental handicap
onset: 1-5 years
Absence seizures management
1st line in men: sodium valproate
Girls: ethosuximide, lamotrigine
Management of general tonic-clonic seizures
1st line: sodium valproate
2nd line: lamotrigine or carbamazepine
Management of focal seizures
remember opposite to general tonic-clonic
1st line (for men and women): carbamezepine or lamotrigine
2nd line: sodium valproate
1st line investigation after 2nd seizure
electroencephalogram (EEG)
categorises epilepsy type and aids diagnosis before deciding which anti-epileptic would be appropriate
when would an MRI be indicated in epilepsy diagnosis
Unclear history/atypical features
1st seizure in child under 2 years
Focal seizures
Hand foot and mouth disease virus
coxsackie A
Wilms’ tumour
Nephroblastoma
One of the most common childhood malignancies
Typically presents under 5 years old (median age 3)
WAGR syndrome
Wilms’ tumour
Aniridia
Genitourinary malformations
mental Retardation
Wilms’ tumour features
unilateral in 95% of cases
Palpable abdominal mass (most common presenting feature)
painless haematuria
flank pain
Unexplained enlarged abdo mass in a child = arrange paediatric review within 48 hours
Fragile X syndrome features
MALES are always affected (X-linked)
learning difficulties
large ears, long thin face, high-arched palate
macrocephaly
macroorchidism
autism
ADHD
hypotonia
mitral valve prolapse
Prader-Willi syndrome
hypotonia
faltering growth
developmental delay
learning difficulties
facies: almond shaped eyes, narrow bridge of nose, narrowing of forehead at temples, thin upper lip
Noonan syndrome
mild learning difficulties
short webbed neck
pectus excavatum (ribs + sternum grow inwards)
pulmonary stenosis
short stature
congenital heart disease
facies: broad forehead, drooping eyelids, wide distance between eyes
Williams syndrome
short stature
congenital heart disease (supravalvular aortic stenosis)
mild-moderate learning difficulties
facies: broad forehead, short nose, full cheeks, wide mouth
Kallman syndrome
genetic condition causing delayed puberty secondary to hypogonadotropic hypogonadism
Kallman syndrome features
‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
Hypogonadotropic Hypogonadism
deficiency of LH and FSH (hypogonadotropic)
leads to a deficiency of the sex hormones testosterone and oestrogen (hypogonadism)
Hypergonadotropic Hypogonadism
gonads fail to respond to stimulation from the gonadotrophins (LH and FSH) (hypogonadism)
no negative feedback from the sex hormones (testosterone and oestrogen), therefore the anterior pituitary produces increasing amounts of LH and FSH (hypergonadtropic)
2 chromosomal abnormalities that cause hypergonadotropic hypogonadism
Kleinfelter’s Syndrome (XXY)
Turner’s Syndrome (XO)
Impetigo rash
small pustules that develop a honey-coloured crusted plaques
usually begins on face
no surrounding erythema
often not itchy
the rash starts as erythematous macules that progress to vesicles, pustules or bullae. rupture of these causes the crusting over plaques
highly contagious, children should stay off school until the lesions have dried out
Status epilepticus management
ABCDE (rule out hypoxia and hypoglycaemia) then benzodiazepine
Benzodiazepine indication:
pre-hospital: buccal midazolam or PR diazepam
IV access: lorazepam (max 2 doses) if still no response IV phenytoin
Status epilepticus definition
a single seizure lasting >5 minutes
or
>2 seizures within a 5-minute period without the person returning to normal between them
Nephrotic syndrome triad
Proteinuria (> 3g / 24 hr)
causing
Hypoalbuminaemia
and
Oedema
complications of nephrotic syndrome (6)
Hypercoagulable state (increased risk of VTE): Prophylactic LMWH required - due to loss of antithrombin-III
Hyperlipidaemia (increased risk of ACS, stroke)
Hypovolaemia (during initial phase of oedema formation)
Hypocalcaemia (vit D and binding protein lost in urine)
Chronic kidney disease
Infection (due to urinary immunoglobulin loss)
which condition causes 80% of nephrotic syndrome cases in children
Minimal change glomerulonephritis
Treatment nephrotic syndrome
High dose oral corticosteroids e.g. prednisolone
how many cases of nephrotic syndrome will have frequent relapses
1/3
pathophysiology minimal change disease
foot process effacement causes proteins to pass through the glomerular membrane
SUFE presenting features (3)
Hip, groin, thigh or knee pain
Restricted range of hip movement (particularly internal rotation in flexion)
Painful limp
commonest cause of vomiting in infancy
GORD (can be physiological)
Risk factors for GORD in infancy
Preterm delivery
Neurological disorders e.g. cerebral palsy
Down syndrome
Features of GORD in infancy
typically develops before 8 weeks
vomiting/regurgitation (milky vomits after feeds, after being laid flat)
excessive crying esp. while feeding
Aspiration/hoarseness/wheezing
complications of GORD in children
distress
failure to thrive
Iron deficiency anaemia
Oesophagitis
recurrent pulmonary aspiration
frequent otitis media
in older children dental erosion may occur
Sandifer syndrome (unusual movements)
1st line treatment for GORD in infancy
1st for Breast- fed baby: Gaviscon (alginate therapy)
1st for Bottle-fed baby: Feed thickener e.g. Carobel
When should a PPI be used to treat GORD in infancy
where the child doesn’t respond to alginates/thickened feeds and:
-
unexplained feeding difficulties (for example, refusing feeds, gagging or choking)
Or -
distressed behaviour
Or - faltering growth
Scoring system for likelihood of strep throat
FeverPAIN
Fever in past 24 hours
Purulent tonsils
Attend rapidly (under 3 days)
Inflamed tonsils
No cough or coyza
Common causes of bacterial otitis media
Streptococcus pneumonaie
Haemophilus influenzae
Moraxella catarrhalis
Streptococcus pyogenes
Features of otitis media
Otalgia (tug or rubbing ear)
fever (50%)
hearing loss
recent viral URTI symptoms are common
ear discharge (if tympanic membrane perforates)
Otoscopy findings in otitis media
bulging tympanic membrane → loss of light reflex
opacification or erythema of the tympanic membrane
perforation with purulent otorrhoea
Diagnostic criteria otitis media (3)
- acute onset of symptoms (otalgia or ear tugging)
-
presence of a middle ear effusion (bulging of the tympanic membrane, or
otorrhoea, decreased mobility on pneumatic otoscopy) - inflammation of the tympanic membrane i.e. erythema
Management of otitis media if antibiotics are not indicated
majority of patients do not require an antibiotic prescription
Analgesia
Safety net: seek medical help if symptoms worsen or do not improve after 3 days
Indications for the use of antibiotics in otitis media (5)
- Symptoms lasting more than 4 days or not improving
- Systemically unwell but not requiring admission
- Immunocompromise or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease
- Younger than 2 years with bilateral otitis media
- Otitis media with perforation and/or discharge in the canal
1st line antibiotic for otitis media
5-7 day course of amoxicillin
penicillin allergy: erythromycin, clarithromycin
chronic suppurative otitis media (CSOM)
perforation of the tympanic membrane with otorrhoea for >6 weeks
4 complications of otitis media
complications are rare
mastoiditis
meningitis
brain abscess
facial nerve paralysis
presentation of acute mastoiditis
presence of a tender boggy swelling behind the pinna with loss of the post-auricular sulcus & auricular proptosis
presentation of otitis media with effusion/glue ear on otoscopy
grey tympanic membrane
loss of cone of light reflex
visible fluid level behind the tympanic membrane
Naevus flammeus birth mark
Port wine stain
present from birth and grows with infant
Cavernous haemangioma
Strawberry naevus birth mark
often not present at birth but appears in the first month of life
Erythema toxicum
(neonatal urticaria)
common rash appearing at 2-3 days of age, consisting of white pinpoint papules at the centre of an erythematous base, concentrated on the trunk
Mongolian blue spots
blue/black macular discolouration at the base of the spine and on the buttocks
these can be misdiagnosed as bruises
Management of constipation in children (disimpaction regimen)
1st line: Movicol Paediatric Plain (Macrogol laxative e.g. polyethylene glycol + electrolytes)
If a macrogol laxative is not tolerated: osmotic laxative e.g. lactulose
2nd line (if no improvement after 2 weeks): stimulant laxative e.g. senna can be added
ensure adequate fluid + fibre intake
Secondary causes of constipation in children
Hirschsprung’s
Cystic fibrosis
Hypothyroidism
Red / amber flags constipation
Reported from birth or first few weeks of life
> 48 hours (CF / Hirschsprung’s)
Faltering growth (hypothyroidism, coeliac)
‘ribbon’ stools (anal stenosis)
Previously unknown or undiagnosed weakness in legs/locomotor delay (cerebral palsy)
Distention (obstruction or intussusception)
Disclosure or evidence that raises concerns (child abuse)
Immune (idiopathic) thrombocytopenia purpura (ITP) management
typically runs a benign course and 80% of cases will have resolved spontaneously after 6-8 weeks
If the platelet counts needs to be raised: prednisolone
Chronic and unremitting ITP for 12-24 months with severe symptoms: splenectomy
What should be avoided in ITP
NSAIDs and aspirin
Contact sports
What kind of hypersensitivity reaction is ITP
Type II
immune-mediated reduction in the platelet count (usually following infection). Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex
Major differential in child presenting with petechiae, purpura (non-blanching) and no fever
ITP
When would a bone marrow examination be indicated in ITP
Atypical features
- lymph node enlargement
- splenomegaly
- high/low WCC
- failure to resolve/respond to treatment
Most common cause of bronchiolitis
Respiratory Syncytial virus (80%)
Age of onset bronchiolitis
90% are 1-9 months (peak incidence 3-6 months)
3 conditions where bronchiolitis is more complicated
Bronchopulmonary dysplasia e.g. premature
Congenital heart disease
Cystic fibrosis
Key symptom that leads to hospital admission in bronchiolitis
Feeding difficulties associated with increasing dyspnoea
signs of respiratory distress
grunting
marked chest recession
resp rate of > 70 breaths/min
SpO2 <94%
nasal flaring
cyanosis
fluid intake <50%
Bronchiolitis investigation
immunofluorescence of nasopharyngeal secretions may show RSV
Management bronchiolitis
supportive
Pyloric stenosis presentation
2-4 weeks of age
4 times more common in males
Non-bilious projectile vomiting (typically 30 mins after a feed)
Palpable mass in the upper abdomen, visible peristalsis as stomach pushes contents past obstruction
hypochloraemic, hypokalaemic alkalosis due to persistent vomiting
Meckel’s diverticulum
congenital abnormality of the small intestine caused by incomplete obliteration of the vitelline (omphalomesenteric) duct
most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
Meckel’s diverticulum
Management Meckel’s diverticulum
wedge excision or small bowel resection and anastomosis
Most common cause of cyanotic congenital heart disease
Tetrology of fallot
4 characteristic features of ToF
Right ventricular outflow tract obstruction (pulmonary stenosis) determines the degree of cyanosis
VSD
Overriding aorta
Right ventricular hypertrophy
= R to L shunt
CXR sign of T of F
Boot shaped heart (due to right ventricular thickening)
1 symptom and 1 sign of Tet of F
Hypercyanotic ‘Tet’ spells (usually after crying etc.)
Ejection systolic murmur due to pulmonary stenosis
cyanotic episodes can be helped by beta-blockers
4 risk factors for Tet of F
Rubella infection
Increased age of the mother (over 40 years)
Alcohol consumption in pregnancy
Diabetic mother
What can be given to maintain the ductus arteriosus
Prostaglandin infusion
when does TOF generally present
1-2 months
Atrial septal defect
Acyanotic (left to right shunt)
2 types: secundum ASD and partial AVSD
Coarctation of the aorta
Acyanotic
narrowing of the aorta in the region of the ductus arteriosus (proximal, distal or at DA)
Patent ductus arteriosis
Acyanotic
persistence of the connection between the aorta and pulmonary artery which would normally close physiologically after birth
if uncorrected can become cyanotic
Commonest congenital heart disease
Ventricular septal defect
VSD murmur
loud, hard pansystolic murmur best heard at the lower left sternal border
(High to low pressure)
ASD murmur
ejection systolic
Guthrie test
Heel prick test
Newborn screening test to identify 9 potentially life threatening genetic conditions (including sickle cell anaemia and cystic fibrosis
Immediate first step when a child presents in respiratory distress
Acute emergency: ABCDE
Which viruses account for the majority of croup cases
Parainfluenza viruses
Croup peak incidence
6 months - 3 years
More common in autumn
4 features of croup
Stridor
Barking cough (worse at night)
Fever
Coryzal symptoms
Audible stridor at rest in a child management
Admission to hospital
admit any child with moderate or severe croup
Medical management croup
Single dose oral dexamethasone to all children regardless of severity
Alternative: prednisolone
Severe/no response to steroids: high-flow oxygen, nebulised adrenaline
ADHD defining criteria
6 x diagnostic features
Symptoms present before age 12
Clear impact on function
Developmentally inappropriate
Management after initial presentation of ADHD
10 week watch and wait before being referred to a specialist
Medical management of ADHD
Drug therapy is a last resort, after parental educational training etc, and is only available to those ages 5+
1st line: Methylphenidate (given on 6 week trial bias)
2nd line: Lisdexamfetamine
3rd line: Dexamfetamine (if the child benefited from Lisdexamfetamine but couldn’t tolerate the side effects)
All of these drugs are cardiotoxic - perform baseline ECG
Measure height and weight
Methylphenidate mechanism of action
CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor
Anaphylaxis definition
ABC
A - airway (swelling of throat and tongue = hoarse voice and stridor)
B - breathing (respiratory wheeze and dyspnoea)
C - circulation (hypotension and tachycardia)
Most important drug given in anaphylaxis
Intramuscular adrenaline
Repeated every 5 minutes if necessary
Best site = anterolateral aspect of the middle third of the thigh
Why is discharge risk-stratified in anaphylaxis
20% of patients experience bisphasic reactions
Management of a child with dehydration without shock
Give low osmolarity oral rehydration solution (ORS) over 4 hours
Continue breastfeeding (if relevant)
Signs of hypernatraemic dehydration
jittery movements
increased muscle tone
hyperreflexia
convulsions
drowsiness or coma
Most common cause of gastroenteritis in children in the UK
Rotavirus
Most common cause of obstruction in infants after the neonatal period
Intussusception
Causes of cerebral palsy
antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
intrapartum (10%): birth asphyxia/trauma, prematurity
postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma, kernicterus
4 signs cerebral palsy
abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties
4 classifications of cerebral palsy
spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
dyskinetic
+/- dystonia, +/- athetosis
athetoid movements and oro-motor problems
ataxic
caused by damage to the cerebellum with typical cerebellar signs
mixed
Viral induced wheeze vs asthma
Presenting before 3 years of age
No atopic history
Only occurs during viral infections
both will present with wheeze throughout the chest, a focal wheeze could indicate blockage
Life threatening sign in acute asthma
silent chest (e.g. no wheezing or coughing heard on ausculation)
Severe acute asthma attack features
Peak flow < 50 % predicted
Saturations < 92%
Unable to complete sentences in one breath
Signs of respiratory distress
RR > 40 in 1-5, > 30 in > 5
HR > 140 in 1-5, > 125 in > 5
Life threatening acute asthma attack features
Peak flow < 33 % predicted
Saturations < 92 %
Exhaustion and poor respiratory effort
Normal pCO2 = no longer compensating
Hypotension
Silent chest
Cyanosis
Altered consciousness/confusion
medical management options in viral induced wheeze (3)
If sats <94% = Supplementary oxygen
1. short acting bronchodilators e.g. salbutamol
2. leukotriene receptor antagonist e.g. montelukast or inhaled corticosteroids
stepwise management in moderate to severe cases of acute asthma
- Salbutamol inhaler via spacer
- Inhaled or nebulised salbutamol or ipratropium bromide
- Oral prednisolone
- IV hydrocortisone
- IV magnesium sulphate
- IV salbutamol
- IV aminophylline
Red flags for acute asthma or viral induced wheeze
Central cyanosis
Child becoming floppy
Tracheal tug
Costal recession
Too breathless to feed/finish a sentence
What is not recommended whilst awaiting surgery for a strangulated inguinal hernia
Manually reducing the strangulated hernia as this can cause more generalised peritonitis
Strangulated hernia symptoms
Pain (as apposed to unpainful incarcerated)
Fever
Increase in the size of a hernia or erythema of the overlying skin
Peritonitic features such as guarding and localised tenderness
Bowel obstruction e.g. distension, nausea, vomiting
Bowel ischemia e.g. bloody stools
Incarcerated hernia definition
where a hernia cannot be reduced
Stepwise 1-3 chronic asthma management for all paediatric ages
1 (newly diagnosed): SABA
2 (not controlled or newly diagnosed with symptoms 3/week or night time waking): SABA + paediatric dose ICS (8 week trail if under 5)
3: SABA + ICS + LTRA e.g. monteleukast
4. SABA + ICS + LABA e.g. salmeterol
Which causal organism is impetigo normally caused by
Staph aureus
May also be caused by Group A strep
Impetigo management
Localised/non-bullous lesions: short course of hydrogen peroxide cream or topical antibiotic creams
Widespread/non-bullous lesions: 1st line topical or oral antibiotics
Bullae/unwell child/risk of complications: 1st line oral antibiotics e.g. flucloxacillin
bullae = raised, clear fluid-filled lesions > 0.5 cm
3 types of cryptorchidism
Retractile (not present in the scrotum but can be manipulated back before retracting again)
Palpable (palpated in the groin but cannot be manipulated back)
Impalpable (no testis can be felt)
Why is cryptorchidism more common in premature infants
descent occurs in the 3rd trimester
When would referral be needed in an infant with cryptorchidism
If the testes are still undescended at 3 months of age
When would hormonal testing and karyotyping be done in undescended testes
Bilateral impalpable testes
Benefits of an orchidopexy in cryptorchidism
Orchidopexy = surgical placement of the testis in the scrotum
- Improving fertility
- Potential reduced risk of malignancy
- Cosmetic and psychological benefits
Volvulus definition
Loop of intestine twists around itself and the mesentery that supplies it, causing bowel obstruction
Most commonly presents in the first few days of life
First sign of puberty in males
Testicular growth (around 12 years of age)
First sign of puberty in males
Testicular growth (around 12 years of age)
First sign of puberty in females
Breast development (around 11.5)
4 causes of jaundice in the first 24 hours of life
first 24 hours = always pathological + always a haemolytic disorder:
- Rhesus haemolytic disease
- ABO haemolytic disease
- Hereditary spherocytosis
- Glucose-6-phosphodehydrogenase
Physiological jaundice
Jaundice between 2-14 days (caused by more RBCs, more fragile RBCs, less developed liver function)
more commonly seen in breastfed babies
Causes of prolonged jaundice (after 14 days)
Hypothyroidism
Breast milk jaundice
Prematurity
Congenital infections
Biliary atresia
Measles causative organism
RNA paramyxovirus
Gillick competence
A young person is able to make decisions regarding their medical treatment if they are deemed to be mentally competent
Used in cases where they don’t want their parents involved, or they can’t be involved
Fraser = specifically relating to contraception and sexual health
Pyloric stenosis on examination
Olive sized mass
Varicocele
Dilated testicular veins which causes scrotal swelling
Most common presentation of varicocele
Asymptomatic
Causes of jaundice 24h-14d
Physiological/breastfeeding
Polycythaemia
Haemolysis
Infection
4 side effects of topical steroids
Acne
Striae
Telangiectasia
Thinning of the skin
Coeliac presentation
Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
GI symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Anaemia
4 key drivers for failure to thrive
- Inadequate intake: can be caused by issues with feeding and may be associated with maternal depression and socio-economic background
- Inadequate retention: including vomiting or severe GORD
- Malabsorption: diseases such as coeliac disease
- Increased requirements: thyrotoxicosis, congenital heart failure or malignancy
Coeliac biopsy findings
atrophy of the villi with flat mucosa and marked crypt hyperplasia and Intraepithelial lymphocytosis
ADHD triad
Hyperactivity, impulsivity and inattentiveness
Modified Kocher criteria septic arthritis
Fever > 38 .5
Inability to weight bear
CRP > 20
WBC > 12
Transient synovitis of the hip typical age group
3-8 years
Transient synovitis presentation (1)
Acute hip pain following recent viral infection
Commonest cause of hip pain in children
Transient synovitis
Management transient synovitis
Self-limiting (rest and analgesia)
Causative organism epiglottis
Haemophilus influenza B
Whooping cough causative organism
Bordatella pertussis
Gram-negative
Pyloric stenosis definitive management
Ramstedt pyloromyotomy
Pyloric stenosis diagnostic investigation
Ultrasound
Pyloric stenosis U&E / ABG
Blood gas values:
- raised bicarbonate (metabolic)
- high pH (alkalosis)
- raised CO2 (partial compensation as still alkalosis)
Electrolyte values:
- Low Cl- (hypochloraemic)
- Low K+ (hypokalaemic)
due to persistent vomiting
Duchenne and Becker muscular dystrophy inheritance patter
X-linked recessive
Dystrophinopathies
Duchenne muscular dystrophy features
Progressive proximal muscle weakness from 5 years old - most children cannot walk by 12 years old and will need a wheelchair
Calf pseudohypertrophy (fat + fibrosis)
Gower’s sign: child uses arms to stand up from a squatted position
30% have intellectual impairment
Dilated cardiomyopathy
Survival = 25-30 years
Investigations Duchenne muscular dystrophy
Diagnostic: genetic testing for dystrophin mutations
Other: Raised CK
Duchenne vs Becker
Becker develops after the age of 10 (Duchenne is earlier from 5) and intellectual impairment is much less common in Becker
Treatments for spasticity in cerebral palsy (4)
Oral diazepam
Oral and Intrathecal Baclofen
Botulinum toxin type A
Orthopaedic surgery
Most common causative organism of early onset neonatal sepsis (within 72 hours of birth)
GBS infection
Most common causative organisms of late-onset sepsis (between 7-28 days of life)
Staphylococcus epidermidis
Pseudomonas aeruginosa
Klebsiella
Enterobacter
Risk factors for neonatal sepsis
- INFECTION: Previous baby with GBS infection, current GBS colonisation from prenatal screening, current bacteruria, intrapartum temp >38, membrane rupture >18 hours, or current infection throughout pregnancy
- Premature (<37 weeks) - 85% of cases
- Low birth weight (<2.5kg) - 80% of cases
Most common presenting feature of neonatal sepsis
Respiratory distress (grunting, nasal flaring, use of accessory resp muscles, tachypnoea)
1st line treatment neonatal sepsis
IV Benzylpenicillin with gentamicin
CRP should be re-measured 18-24 hours after presentation
Transient tachypnoea of the new born (TTN)
Delayed resorption of fluid in the lungs
More common following C-sections possibly due to lung fluid not being ‘squeezed out’ during birth canal passage
Commonest cause of respiratory distress in the newborn period
CXR in transient tachypnoea of the newborn
Hyperinflation of the lungs and fluid in the horizontal fissure
Management transient tachypnoea of the newborn
Supportive care (usually settles within 1-2 days)
5 non-lifestyle causes of obesity in children
GH deficiency
Hypothyroidism
Down’s syndrome
Cushing’s syndrome
Prayer-Willi syndrome
Cystic fibrosis inheritance pattern
Autosomal recessive
Genetic defect seen in cystic fibrosis
Delta F508 in chromosome 7 causes a defect in the Cystic fibrosis transmembrane conductance regulator gene (CFTR)
4 organisms that may colonise CF patients
Staph aureus
Pseudomonas aeruginosa
Burkholderia cepacia
Aspergillus
3 presenting features of cystic fibrosis
Meconium ileus
Recurrent chest infections
Malabsorption (steatorrhoea, failure to thrive)
features of cystic fibrosis that may present later in childhood/adulthood
Short stature
Diabetes Mellitus
Delayed puberty
Rectal prolapse
Nasal polyps
Male infertility
Diagnostic test for cystic fibrosis
Sweat test
Management cystic fibrosis
- Chest physiotherapy and postural draining (x2/day)
- High calorie, high fat diet
- minimise contact with other CF patients to prevent cross infection with Burkholderia cepacia and Pseudomonas aeruginosa
- Vitamin supplements
- Pancreatic enzyme supplements
- Lung transplantation (chronic infection with Burkholderia is a C/I)
Which medication can be used for cystic fibrosis in patients who are homozygous for the delta F508 mutation
CFTR modulators i.e. Lumacaftor + Ivacaftor
Most causative organism of pneumonia in children
Strep pneumoniae
Treatment of pneumonia in children
1st line: Amoxicillin
2nd line: Macrolides if no response or if mycoplasma or chlamydia is suspected
Pneumonia associated with influenza: co-amoxiclav
Features of acute epiglottis
Rapid onset
High temperature
Stridor
Saliva drooling
Tripod position (easier to breathe by leaning forward in seated position)
Diagnosis of epiglottis
Direct visualisation by airway trained staff
Management of acute epiglottis
Endotracheal intubation
Do not examine the throat (risk of acute airway obstruction)
Oxygen
IV antibiotics
Features of CMPA
Regurgitation and vomiting
Diarrhoea
Urticaria, atopic eczema
‘Colic’ symptoms (irritability, crying)
Wheeze, chronic cough
Diagnosis CMPA
Often clinical i.e. improvement with cows milk protein elimination
Other investigations:
Skin prick/patch testing
Total IgE and specific IgE (RAST) for cows milk protein
Management CMPA
Failure to thrive = refer to paediatrician
1st line replacement for mild-moderate symptoms: extensively hydrolysed formula
Severe or no response to eHF: amino acid-based formula
Prognosis of CMPA
IgE mediated intolerance: tolerant by age 5
Non-IgE mediated intolerance: tolerant by age 3
Causes of snoring in children
Obesity
Nasal problems e.g. polyps
Recurrent tonsillitis
Down’s syndrome
Hypothyroidism
Threadworm organism
Enterobius vermicularis
How does transmission occur of threadworms
Swallowing eggs that are present in the environment
Features of threadworms
Asymptomatic (90%)
Perianal itching (particularly at night)
Girls may have vulval symptoms
Management of threadworms
Combination of anthelmintic with hygiene measures for all members of the household
Children over 6 months = 1st line anthelmintic is mebendazole
Who requires a routine ultrasound examination at 6 weeks to screen for DDH (3)
- 1st degree family history of hip problems in early life
- Breech presentation at or after 36 weeks gestation (regardless of birth)
- Multiple pregnancy
Rovsing’s sign
Appendicitis: Palpation in the LIF causes pain in the RIF
Diagnosis of appendicitis
Raised inflammatory markers coupled with compatible history and examination findings
+ neutrophil-predominant leucocytosis
Management appendicitis
Laparoscopic appendicectomy
Prophylactic IV antibiotics reduces wound infection rates
Periorbital cellulitis + epidemiology
Infection of the soft tissues anterior to the orbital septum (includes the eyelids, skin and subcutaneous tissue of the face but not the contents of the orbit)
Infection spreads from nearby sites e.g. breaks in the skin or local infections (sinusitis, URTIs)
80% of patients are under 10 (peak 21 months)
More common in the winter (due to increased URTIs)
Most frequent causative organisms of periorbital/preseptal cellulitis
Staph aureus
Staph epidermidis
Streptococci
Presentation of periorbital cellulitis
Erythema and oedema of the eyelids which can spread to surrounding skin
Partial or complete ptosis of the eye due to swelling
ABSENT: Orbital signs (pain on movement etc.) if these are present it would indicate orbital cellulitis
Investigations periorbital cellulitis
- Raised inflammatory markers
- Swab of any discharge present
- Contrast CT for orbital cellulitis differential diagnosis
Management of periorbital cellulitis
- Oral antibiotics - usually co-amoxiclav
- All cases should be referred to secondary care for assessment
Squint (strabismus)
Imbalance in extraocular muscles of one eye
Convergent is more common than divergent
How can a squint be detected
Hirschberg test: Corneal light reflection test (holding a light source 30cm from the child’s face to see if the light reflects symmetrically on the pupils)
Cover test
Management of squint in GP setting
Refer to ophthalmology
Squint definition
Misalignment of the eyes which causes double vision
Amblyopia
The affected eye in a squint becomes passive and has reduced function compared to the dominant eye
If uncorrected, becomes a lazy eye
Squint treatment options (2)
Occlusive patch over good eye
Atropine drops in good eye
Presentation of UTI infants
Poor feeding, vomiting, irritability
Presentation of UTI in younger children
Abdominal pain, fever, dysuria
Presentation of UTI in older children
Dysuria, frequency, haematuria
Features of pylonephritis
Temperature > 38, loin pain/tenderness
NICE criteria for checking urine sample in a child
- Any symptoms or signs of UTI
- Unexplained fever of 38 or higher (test urine within 24 hours)
- Alternative site of infection but remain unwell (test urine within 24 hours)
Urine collection method for children
1st: Clean catch
2nd: urine collection pads
If non-invasive methods are not possible: suprapubic aspiration
Management of infant less than 3 months old with UTI
Immediate referral to paediatrician
IV cefotaxime and urine sample for urgent microscopy and culture
Management child over 3 months with pyelonephritis
Consider admission to hospital
Start oral antibiotics e.g. cefotaxime or co-amoxiclav for 7-10 days
Management of child over 3 months old with lower UTI
Oral antibiotics for 3 days:
1st: trimethoprim or nitrofurantoin
2nd: cefalexin or amoxicillin
Advise parents to bring child back if they remain unwell after 24-48 hours
Enuresis definition (4)
- Involuntary discharge of urine
- Day/night/both
- Child aged 5 years or older
- Absence of congenital or acquired defects of the nervous system or urinary tract
Primary nocturnal enuresis
The child has never achieved continence
Secondary nocturnal enuresis
The child has been dry for at least 6 months before
Management options for nocturnal enuresis
1st line: Enuresis alarm
2nd line: desmopressin (particularly useful for short-term control e.g. sleepover)
+ Reward systems e.g. star charts (give for agreed behaviour e.g. using the toilet before bedtime rather than dry nights)
Nephritic syndrome / glomerulonephritis presentation
inflammation within the glomeruli
- haematuria
- renal impairment
- hypertension
- variable proteinuria
Commonest cause of glomerulonephritis worldwide
IgA nephropathy
Classical presentation of IgA nephropathy / Bergers disease
Recurrent episodes of macroscopic haematuria in a young boy following URTI
nephrotic range proteinuria is rare
Pathophysiology of IgA nephropathy
Mesangial deposition of IgA immune complexes
- considerable overlap with Henoch-Schoenlein purpura (IgA vasculitis)
IgA nephropathy vs Post-streptococcal glomerulonephritis
Post-strep = low complement levels
Main symptom of post-strep = proteinuria (although haematuria can occur)
Post strep has an interval between URTI and onset of renal problems
Management of IgA nephropathy
Minimal proteinuria or normal GFR: no treatment needed other than follow-up
Persistent proteinuria: ACE inhibitors
Active disease e.g. falling GFR or no response to ACEi: Immunosuppression with corticosteroids
Poor prognosis indicators of IgA nephropathy
Male gender
Proteinuria
Hypertension
Hyperlipidaemia
Phimosis
Inability to retract the foreskin
Age dependent management of phimosis
Under 2: expectant approach
Over 2 with recurrent balanoposthitis or UTI: consider treatment e.g. circumcision
Most common inherited bleeding disorder
Von Willebrand’s disease
Inheritance pattern of Von Willebrands (type 1 and 2)
Autosomal dominant
2 common features of vWD
Epistaxis
Menorrhagia
Investigation results vWD (3)
Prolonged bleeding time
APTT may be prolonged (intrinsic pathway)
Factor VIII levels may be moderately reduced
Management of vWD (3)
- Transexamic acid for mild bleeding
- Desmopressin (raises levels of vWF)
- Factor VIII concentrate
What age does atopic eczema in children usually present by
Before the age of 2 years
Clears in around 50% of children by 5 years and 75% by 10 years
Features of eczema (by age)
Itchy, erythematous rash
Infants: face and trunk
Younger children: extensor surfaces
Older children: more typical distribution of flexor surfaces and creases of face and neck
Management of eczema in children
Avoid irritants
Simple emollients (apply before topical steroid if using one)
Topical steroids
Wet wrapping (large amounts of emollient under wet bandages)
Severe cases: oral ciclosporin
Management of allergic rhinitis (hayfever)
Allergen avoidance
Mild to moderate intermittent: oral or intranasal antihistamines
Moderate to severe persistent: intranasal corticosteroids
4 features of allergic rhinitis
Sneezing
Clear nasal discharge
Nasal pruritis
Post nasal drip
Urticaria features
Pale, pink raised skin
Pruritic
Management of urticaria
1st line: non-sedating anti-histamines
Severe or resistant episodes: prednisolone
Neuroblastoma
Tumour which arises from neural crest tissue of the adrenal medulla (most common site) and abdominal sympathetic chain
Median age of onset: 20 months (most common cancer in children under 1)
Features of neuroblastoma
Abdominal mass
Pallor, weight loss
Bone pain, limp
Hepatomegaly
Paraplegia
Proptosis
Neuroblastoma investigations
Urinalysis (vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels)
Calcification on abdominal X-Ray
Biopsy
Most common ocular malignancy found in children
Retinoblastoma
Average age of diagnosis: 18 months
Hereditary cases of retinoblastoma inheritance pattern
Autosomal dominant
RB1 gene
Features of retinoblastoma
Absence of red-reflex, replaced by white pupil (leukocoria) most common presenting symptom
Strabismus/squint
Visual problems
Most common primary brain tumour in children
Astrocytoma (develop from glial cells)
3 risk factors for CNS malignancies
Neurofibromatosis 1 and 2
Tuberous sclerosis 1 and 2
Personal or family history of brain tumour, leukaemia
Red flags of brain tumours in children
Most common bone affected in osteosarcoma
Femur
(Other sites are tibia and humerus)
Main presenting feature osteosarcoma
Persistent bone pain worse at night time
Osteosarcoma associations
Retinoblastoma (Rb gene)
Paget’s disease of the bone
Radiotherapy
Ewing’s sarcoma
Small round blue cell tumour occurring most frequently in the pelvis and long bones
Causes severe pain
X-ray: onion-skin appearance
Causes of non-transient/severe hypoglycaemia
Preterm birth (<37 weeks)
Maternal DM
IUGR
Hypothermia
Neonatal sepsis
Features of neonatal hypoglycaemia
May be asymptomatic
Autonomic: jitteriness, irritable, tachypnoea, pallor
Neuroglycopenic: poor feeding/sucking, weak cry, drowsy, hypotonia, seizures
Asymptomatic management of neonatal hypoglycaemia
Encourage normal feeding (breast or bottle)
Monitor blood glucose
Symptomatic/severe neonatal hypoglycaemia management
Admit to neonatal unit
IV infusion of 10% dextrose
Acute respiratory distress syndrome pathology
Increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli i.e. non-cardiogenic pulmonary oedema
Mortality = 40% / significant morbidity in those who survive
Causes of ARDS
Acute pancreatitis
Infection (sepsis, pneumonia)
Massive blood transfusion
Trauma
Smoke inhalation
Covid-19
Cardio-pulmonary bypass
4 ARDS features typical of acute and severe onset
- Dyspnoea
- Elevated respiratory rate
- Bilateral lung crackles
- Low oxygen saturations
2 key investigations ARDS
Chest X-ray = pulmonary oedema (bilateral infiltrates)
Arterial blood gas = low pO2
Diagnostic criteria ARDS
Clinical (acute onset within 1 week of a known risk factor) + CXR (pulmonary oedema) + low pO2 + exclude cardiogenic causes
Management of ARDS
ITU management
Oxygenation/ventilation to treat hypoxaemia
General organ support e.g. vasopressors
Treat underlying cause e.g. Abx for sepsis
Newborn resuscitation
- Dry baby and maintain temperature
- Assess tone, respiratory rate, heart rate
- If gasping or not breathing give 5 inflation breaths
- Reassess (chest movements)
- If the heart rate is not improving and <60bpm start compressions and ventilation breaths at a rate of 3:1
Meconium aspiration syndrome
Respiratory distress in the newborn as a result of meconium in the trachea (occurs in the immediate neonatal period)
When do most cases of meconium aspiration syndrome occur
In post-term deliveries (after 42 weeks)
Risk factors meconium aspiration syndrome
Maternal hypertension
Pre-eclampsia
Chorioamnionitis
Smoking
Substance abuse
Signs of meconium aspiration syndrome
Dark green streaks in amniotic fluid (meconium staining)
Cyanosis
Grunting
Limpness
Bradycardia
Kernicterus
Brain damage (cerebral palsy, learning disability, deafness) resulting from untreated jaundice in babies
Risk factors for haematogenous osteomyelitis resulting from bacteraemia (most common form in children)
Sickle cell anaemia
Immunosuppression
Infective endocarditis
Most common causative organism of osteomyelitis
Staph aureus except in sickle cell patients where Salmonella species predominates
Gold standard imaging modality for osteomyelitis
MRI
Management osteomyelitis
Flucoxacillin for 6 weeks
Clindamycin if penicillin-allergic
Osteogenesis imperfecta
brittle bone disease
Group of disorders of collagen metabolism resulting in bone fragility and fractures
Inheritance pattern osteogenesis imperfecta
Autosomal dominant
Features of osteogenesis imperfecta
Fractures following minor trauma
Blue sclera
Deafness secondary to otosclerosis
Dental imperfections
Investigations osteogenesis imperfecta
Normal calcium, phosphate, parathyroid hormone and ALP results
Rickets definition
Inadequately mineralised bone in developing and growing bones resulting in soft and easily deformed bones
Usually due to vitamin D deficiency
In adults it is termed osteomalacia
Predisposing factors for rickets (4)
- Dietary deficiency of calcium e.g. in developing countries
- Prolonged breastfeeding
- Unsupplemented cow’s milk formula
- Lack of sunlight
Features of rickets
Aching bones and joints
Lower limb abnormalities: toddlers = genu varum (bow legs), older children = genu valgum (knock knees)
‘Rickety rosary’ - swelling at the costochondral junction causing widening of the wrist joints
Rickets investigations
Low Vit D levels
Reduced serum calcium (symptoms may result from hypocalcaemia)
Raised alkaline phosphatase
Management of rickets
Oral vitamin D
6 in 1 vaccine
Diphtheria
Hepatitis B
Haemophilus influenzae type B
Polio
Tetanus
Whooping cough
Features of whooping cough
1-2 weeks: URTI symptoms
2-8 weeks:
1. cough increases in severity, usually worse at night and after feeding, associated vomiting and central cyanosis
2. inspiratory whoop (not always present, caused by forced inspiration against a closed glottis) instead may have spells of apnoea
Diagnostic criteria whooping cough
Acute cough lasting for 14 days or more without another apparent cause and one or more of the following features:
- Paroxysmal cough
- Inspiratory whoop
- Post-tussive vomiting
- Undiagnosed apneoic attacks
Diagnosis whooping cough
Nasal swab culture for Bordetella pertussis + PCR
Management of whooping cough (5)
- Infants under 6 months should be admitted
- Onset within last 21 days: Oral macrolide e.g. clarithromycin or azithromycin
- Household contacts should be offered antibiotic prophylaxis
- School exclusion: 48 hours after commencing antibiotics (or 21 days from onset of symptoms)
- Notifiable disease
Complications of whooping cough
Subconjunctival haemorrhage
Pneumonia
Bronchiectasis
Seizures
When should pregnant women be offered the pertussis vaccine
16-32 weeks pregnant
Testicular torsion features
Pain usually severe and sudden onset - may refer to lower abdomen
Nausea + vomiting
O/E: swollen, tender testis retracted upwards, reddened skin
Stroking the thigh does not raise the ipsilateral testicle (Cremasteric reflex is lost)
Elevation of the testis does not ease the pain (Prehn’s sign is lost)
Management testicular torsion
SURGICAL EMERGENCY - urgent surgical exploration and both testis should be fixed
Total fluid requirement
First 10kg: 100ml/kg/day
Second 10kg - 50ml/kg/day
Over 20kg - 20ml/kg/day
Most common cause of admissions to child and adolescent psychiatric wards
Anorexia nervosa
DSM-5 diagnostic criteria for anorexia nervosa (3)
- Restriction of energy intake relative to requirement leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health
- Intense fear of gaining weight or becoming fat, even though underweight
- Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight
1st line treatment for children and young people with anorexia nervosa
Anorexia focused family therapy
2nd line = CBT
DSM-5 diagnostic criteria of bulimia nervosa (6)
- Recurrent episodes of binge eating
- Sense of lack of control over eating during the episode
- Recurrent inappropriate compensatory behaviour in order to prevent weight gain e.g. self induced vomiting
- Binge eating + compensatory behaviour occur at least once a week for 3 months
- Self evaluation is unduly influenced by body shape and weight
- The disturbance does not occur exclusively during episodes of anorexia nervosa
Signs of recurrent vomiting in bulimia nervosa
Erosion of teeth
Russell’s sign (calluses on the knuckles or back of the hand)
Bacteria that contributes to development of acne
Propionibacterium acnes
1st line treatment of mild to moderate acne
12 week course of topical combination therapy e.g. retinoids, benzoyl peroxide, topical clindamycin
1st line treatment for moderate-severe acne
12 week course of topicals +/- oral antibiotics i.e. oral lymecycline or oral doxycycline
What can be used instead of tetracyclines in pregnancy
Erythromycin
management to prevent antibiotic resistant developing in acne
Topical retinoid or benzoyl peroxide should always be co-prescribed (never monotherapy)
Topic and oral antibiotics should not be used in combination
Alternative option for women wanting acne medication
COC
Contraindication to topical and oral retinoid treatment
Pregnancy
When should referral for acne be considered
Non-responders
Scarring
Persistent pigment are changes
Persistent psychological distress caused by acne
4 viral causes of otitis media
RSV
Rhinovirus
Adenovirus
Influenza virus
Commonest cause of conductive hearing loss in childhood
Glue ear
Treatment for glue ear
Grommet insertion
Seizure definition
Transient episodes of abnormal electrical activity in the brain
Advice after first seizure
Shower rather than bath
Take caution when swimming
Take caution with heights
Record any further episodes
If > 5 minutes ring 999
Follow up after first seizure
Paediatric neurologist 2 week urgent referral
2 factors to monitor when a patient is admitted with life threatening asthma
Oxygen saturations
PEFR
Features of a complex febrile seizure
partial or focal, >15 mins, can occur multiple times during same febrile illness
Phototherapy
Converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the liver
Treatment threshold charts for neonatal jaundice
Age of baby x Total bilirubin level
Phototherapy usually adequate for correction
Extremely high levels = exchange blood transfusion
Fluid deficit calculation for a dehydrated patient
% dehydration x weight (kg) x 10
How to calculate amount of fluids for dehydrated patient without signs of shock
Work out maintenance
Work out fluid deficit
Maintenance + fluid deficit = hourly rate
TORCH infection
When is a childs hearing first formally tested
Newborn hearing screening programme
Test: Otoacoustic emission test
features of growing pains in a child
never present at the start of the day
no limp
no limitation of physical activity
systemically well
normal physical exam
intermittent symptoms, worse after a day of vigorous activity
Rumination
Frequent regurgitation of ingested food that is largely behavioural
Regurgitation
Effortless expulsion of gastric contents e.g. in healthy infants
Possetting
Small volume vomiting during or between feeds in an otherwise well child
Intestinal atresia presentation
Delayed passage of meconium
Bilious vomiting
Abdominal distention
3 signs of food intolerance
Vomiting
Stool changes
Eczema
Presentation of appendicitis in older child
Anorexia
Central abdominal pain migrating to RIF
Vomiting fever
Precocious puberty diagnosis
Before age 8 in girls
Before age 9 in boys
Stimulation of puberty
High amplitude pulses of GnRH
Pseudopuberty
Gonadotropin-independent puberty / low FSH and LH
CAH, tumours of the adrenals, ovaries, McCune Albright syndrome (cafe au last spots)
Score for acute presentation of perinatal mental illness
Mental state examination
Testes signs in precocious puberty (bilateral, unilateral, small)
bilateral enlargement = gonadotrophin release from intracranial lesion
unilateral enlargement = gonadal tumour
small testes = adrenal cause (tumour or adrenal hyperplasia)
Vesicoureteric reflux
Abnormal back flow of urine from the bladder into the ureter and kidney
Causes UTIs
Investigation vesicoureteric reflux
Micturating cystourethrogram
Management of mild to moderate acute asthma (exacerbation)
Bronchodilator therapy (salbutamol via spacer)
Steroid therapy (give to all children with asthma exacerbation for 3-5 days)
4 features which may be present in a sexually abused child
STIs, recurrent UTIs
Anal fissure, bruising
Enuresis
Behavioural problems, self harm
Autosomal recessive condition
Both parents carriers
Chance of affected child ?
Chance of carrier child ?
Chance of unaffected child ?
25% homozygous affected child
50% heterozygous carrier child
25% unaffected genotypical child
Fetal alcohol syndrome features
Short palpebral fissure
Smooth philtrum
Hypoplastic upper lip
Learning difficulties
Microcephalic
Cardiac malformations
Epicanthic folds
Paediatric BLS
5 rescue breaths
Circulation check (infants use brachial or femoral, children use femoral)
15:2 chest compressions:rescue breaths (100-120/min)
- children: compress lower half of sternum
- infants: two-thumb encircling technique
Risk of using NSAIDs in chickenpox
Risk of necrotising fasciitis
All the milestones in gross motor development (grid)
4 indications for immediate CT scan (within 1 hour) of a child with head injury
LOC > 5 minutes
3 or more vomiting episodes
Amnesia > 5 minutes
Seizure with no history of epilepsy
Initial treatment of suspected cyanosis congenital heart disease
Prostaglandin E1 e.g. alprostadil (maintains patent duct arteriosus)
Test to differentiate cardiac from non-cardiac causes in a cyanosed baby
Nitrogen washout test (100% oxygen then ABG)
2 signs that point to pneumonia in a child
High fever (over 39C)
Persistently focal crackles
Features of bronchiolitis
Corzyal symptoms / mild fever preceding:
Dry cough
Increased breathlessness
Wheezing, fine inspiratory crackles
Feeding difficulties (associated with dyspnoea)
How may an older child (2-3 yrs) with missed DDH present
Trendlenberg gait
Leg length discrepancy
Osgood-Schlatter disease
Aged 10-15
Unilateral inflammation/swelling of the area below the knee which can be exacerbated by exercise and relieved by rest
Gradual in onset and can become severe
Self-resolving
Steroid treatment in meningitis
> 3 months = dexamethasone if high WCC
< 3 months = do not give steroids!
Chickenpox school exclusion
Until all the lesions are dry and have crusted over
Definitive treatment biliary atresia
Surgical intervention
Intestinal malrotation
High caecum at the midline
Presents with: bilious vomiting, abdominal distention
Associated with: exomphalos (below pic), congenital diaphragmatic hernia, intrinsic duodenal atria
Complications: volvulus
Urgent upper GI contrast study and ultrasound
Reflex anoxic seizures typical features
child goes very pale
falls to floor
secondary anoxic seizures are common
rapid recovery
Later complications of Down’s syndrome
Alzheimer’s disease
Hypothyroidism
ALL
Repeated respiratory infections
Subfertility
Management of chickenpox
Supportive
Calamine lotion
Common complication of chickenpox infection
Secondary bacterial infection of the lesions
NSAIDs may increase this risk
Invasive group A strep soft tissue infections can occur resulting in necrotising fasciitis
GORD investigations
PH testing
Barium swallow and meal
Endoscopy
2 components of milk that cause CMPA
Casein and whey
Encopresis
Involuntary faecal soiling or incontinence secondary to chronic constipation
Functional constipation
Withhold from going to the toilet because defecation is painful but this only increases pain
Clinical signs of dehydration
Prolonged capillary refill time
reduced skin turgor
Thirst
Sunken eyes
Irritability
lethargy
Chronic diarrhoea definition
> 2 weeks
3 features more typical of functional abdominal pain than organic
Stressful life event
Vague pain with gradual onset
Prolonged duration with few effective interventions
3 subgroups of children at increased risk of developing cancer
Neurofibromatosis 1
Down’s syndrome
Immunocompromised
Features of CNS tumour
Headache worse lying down
Early morning vomiting
Papilloedema
Squint
Nystagmus
Ataxia
Personality or behaviour change
Features that would indicate head scan for child with headaches
< 3 y/o
Underlying risk factors e.g. NF1
Presence of any CNS tumour red flag symptoms
5 requirements for Fraser guidelines
Understands the advice
Understands the implications of treatment
Likely to have sex regardless
Likely to suffer physically or mentally without treatment
It is in their best interests to receive advice and treatment without consent
National child measurement programme
Measures BMI in children in reception and year 6
Mild, moderate, severe DKA
pH under 7.3 or BiC under 15
PH under 7.2 or BiC under 10
pH under 7.1 or BiC under 5
Grams of carb per unit insulin
15g
Management of mild-moderate hypoglycaemia
Check BG to confirm hypo
Give glucose tablet, gel, food or drink
Check BG in 15 mins
Follow up with longer acting carb e.g. bread
Top 2 GI emergencies in babies
Sepsis - antibiotics
Malrotation - upper GI contrast (barium meal)
4 most common causes of vomiting in a 4 week old baby
Overfeeding
GORD
Sepsis
Pyloric stenosis
Top 3 differential diagnoses for intussusception
Infantile colic, gastroenteritis, sepsis
Red flags NICE paeds traffic light system
Abnormal skin colour
Appears ill to a healthcare professional
Grunting
RR > 60
Intercostal recession
Reduced skin turgor
Age < 3 months with temp > 38
Signs of meningitis
Management: ADMIT/REFER URGENTLY TO PAEDIATRIC SPECIALIST
CF infection with pseudomonas aeruginosa Abx
Oral ciprofloxacin
1st line management of jaundiced newborn in first 24 hours
Measure and record serum bilirubin level
What age does persistence of primitive reflexes become concerning
6 months e.g. cerebral palsy
Vesicoureteric reflux risk factor
Family Hx
White
Female
Spina bifida
3 investigations minimal change disease
Urinalysis
24 hour urinary protein
Serum albumin
CAH ABG
Metabolic acidosis
Cause of purpura in meningococcal septicaemia
disseminated intravascular coagulation
Differential diagnoses for an unwell neonate
Infective: Sepsis
Cardiac: Congenital heart disease
NAI
Metabolic: Hypoglycaemia, Congenital adrenal hyperplasia
Surgical: Hirschsprungs, Necrotising enterocolitis, pyloric stenosis
Stridor definition
high-pitched respiratory sound produced by irregular airflow in a narrowed airway during the inspiration phase
DDx wheeze = expiratory
Patent ductus arteriosus murmur
machinery murmur (continuous crescendo-decrescendo) at the upper left sternal edge
2 risk factors for PDA
rubella infection
Prematurity
4 presentations of PDA
Shortness of breath
Difficulty feeding
Poor weight gain
LRTI
PDA investigation
Echocardiogram: right + left hypertrophy
monitored with echos until 1 year - resolves spontaneously or need surgery
PDA medications
IV indomethacin or ibuprofen
5 causes of failure to thrive
Inadequate nutritional intake e.g. iron deficiency anaemia, neglect
Difficulty feeding e.g. cerebral palsy, pyloric stenosis
Malabsorption e.g. cystic fibrosis, coeliac, CMPA
Increased energy requirements e.g. hypothyroidism, infection
Inability to process nutrients e.g. T1DM
2 key investigations failure to thrive
Urine dipstick for UTI
Coeliac screen (anti-TTG)
Neonatal respiratory distress syndrome
Surfactant deficiency
Key signs: rapid, laboured breathing, ground class on CXR
Management: corticosteroids pre-delivery, artificial surfactant via intratracheal instillation, high pressure oxygen
4 causes of diarrhoea in infants/children
Infection (gastroenteritis)
Cow milk intolerance
Toddler’s diarrhoea
Coeliac
Post-gastro lactose intolerance
Antibiotic treatment
Anxiety/stress
IBD
Fecal impaction
Constipation and overflow diarrhoea (loose, watery stool comes around the stuck fetal matter), often affects the child’s ability to sense and respond to the presence of stool in the rectum
Cerebral palsy is a clinical diagnosis, what further investigations could you do?
MRI brain
Professionals involved in care of cerebral palsy
Occupational therapy
Physiotherapy
Speech therapy
GP
Neurology
3 indications for Botox prescription in cerebral palsy
Salivary glands to stop drooling
Bladder in overactive bladder
Lower limb spasticity and dystonia
Differential diagnoses Neonatal RDS
Meconium aspiration
Sepsis
Pneumothorax
Complication of building up feeds too quickly in neonatal hypoglycaemia
Necrotising enterocolitis
Severe complications of neonatal hypoglycaemia (4)
Retinopathy of prematurity
Sensorineural hearing loss
Chronic lung disease
Cerebral palsy
rhesus disease of the newborn
1st baby: rhesus D negative, 2nd baby: rhesus D positive
Mothers anti-D antibodies from 1st pregnancy cross the placenta into the rhesus D positive 2nd baby = haemolysis (anaemia + jaundice)
What condition can maternal antenatal labetalol use increase the risk of
Neonatal hypoglycaemia
investigations in infants younger than 3 months with fever
Full blood count
Blood culture
C-reactive protein
Urine testing for urinary tract infection
Chest radiograph only if respiratory signs are present
Stool culture, if diarrhoea is present
Management of child < 3 years with acute limp
Urgent specialist assessment
One parent has an autosomal dominant disease (Aa or AA)
One parent does not have the disease (aa)
Chance of the patient’s children inheriting the disease?
50%
Parallel play milestone
2 years
Corrected age of a premature baby
Age minus the number of weeks born early from 40 weeks
Intestinal obstruction e.g. meconium ileus X-ray
Dilated bowel loops proximal to impaction
Shaken baby syndrome triad
Retinal haemorrhages
Subdural haematoma
Encephalopathy
4 delayed motor milestones that should elicit urgent referral for cerebral palsy if there are risk factors e.g. low birth weight
Not sitting by 8 months
Not walking by 18 months
Early asymmetry of hand function before 12 months
Persistent toe-walking
Otherwise well infant with inspiratory strider
Laryngomalacia
Congenital softening of the cartilage of the larynx, causing collapse during inspiration
Usually self-resolves before 2 years of age
Cystic fibrosis positive heel prick test results
Raised level of immunoreactive trypsinogen (IRT)
Duchenne muscular dystrophy associated cardiac pathology
Dilated cardiomyopathy
Toddler’s diarrhoea
Stools vary in consistency and often contain undigested food
Cephalohaematoma (DDx from caput)
Typically develops several hours after birth
Most commonly in parietal region
Doesn’t cross the suture lines
May take months to resolve
Caput succedaneum (DDx from cephalohaematoma)
Present at birth
typically forms over the vertex and crosses suture lines
Resolves within days
Caput succedaneum + Cephalohaematoma (3 similarities)
Swelling on the head of a newborn
more common following prolonged, difficult deliveries
Managed conservatively
Major risks for sudden infant death syndrome
Prone sleeping (face down)
Parental smoking
Bed sharing
Hyperthermia and head covering
Prematurity
Smooth midline lesion, round, located just below the hyoid bone
Rises on protrusion of the tongue
Thyroglossal cyst
Cause of spastic cerebral palsy
increased tone resulting from damage to upper motor neurons
Cause of dyskinetic cerebral palsy
damage to the basal ganglia and the substantia nigra
Mesenteric adenitis
Inflamed lymph nodes within the mesenteric
Often follows a recent viral infection
DDx: appendicitis
Congenital diaphragmatic hernia O/E
Displaced apex beat and decreased air entry
Scaphoid abdomen
Vitamin K in neonates
Offered by IM route as a once-off injection shortly after birth
Neonatal death definition
Between 0-28 days of birth
3 complications of undescended testis
Infertility
Torsion
Testicular cancer
2 options for head lice management
Treatment is only indicated if living lice are found when combing inc household contacts unless they are affected
- Malathion
- Wet combing
Premature baby vaccinations: gestational or chronological age?
Chronological age
Antibiotic whooping cough
Onset within last 21 days: Oral macrolide e.g. clarithromycin or azithromycin
Congenital diaphragmatic hernia
Herniation of abdominal viscera into the chest cavity due to incomplete formation of the diaphragm
= pulmonary hypoplasia and hypertension resulting in respiratory distress shortly after birth
What should be prescribed for all patients presenting with an asthma attack for 5 days
Prednisolone
Myoclonic Tx
Levetiracitam
complication minimal change disease
Hypovolaemia
Thrombosis
Infection
