paeds level 2 conditions (pack 1) Flashcards

Question 1

Q

Birth Asphyxia/ Hypoxic Ischaemic encephalopathy (HIE):

what is it?
groups of causes? 5 (with example causes)

Answer

A

HIE = Clinical syndrome of brain injury – secondary to hypoxic ischaemic insult (2/1000 live births)

Decreased Umbilical blood flow e.g. Cord prolapse
Decreased placental gas exchange e.g. placental abruption
Decreased maternal placental perfusion e.g. abruption, Accreta
Maternal hypoxia
Inadequate postnatal cardiopulmonary circulation

Question 2

Q

SIGNS OF Hypoxic Ischaemic encephalopathy (HIE):

mild? 5
moderate? 6
severe? 10

(also rough prognosis of each)

Answer

A

MILD

muscle tone increased
tendon reflexes brief
poor feeding
excessive crying
sleepiness

(typically resolves in 24hrs)

MODERATE

lethargy
hypotonia
apnoeic periods
diminshed deep tendon reflexes
grasp, moro + sucking reflexes poor / absent
seizures within 24hrs of birth

(full recovery 1-2 weeks is possible)

SEVERE

hypotonia
coma / stupor
depressed deep tendon reflexes
neonatal reflexes absent
bulging fontanelle
irregular breathing
irregular HR and BP
disturbed ocular motion (eg nystagmus, skewed deviation)
pupils dilated, fixed, poorly reactive to light
seizures (may be resistant to treatment, generalised, freq may increase in early period - with progression seizures subside)

Question 3

Q

Hypoxic Ischaemic encephalopathy (HIE):

how to detect abnormalities intrapartum?
test done on all babies at birth to screen for HIE?
additional test done at birth for babies at risk of HIE?
additional bloods which can consider?
additional other investigations which can consider?

Answer

A

may be CTG abnormalities
- can also do scalp blood test

All babies get APGAR score

if risk of HIE, do cord gases after birth (pH <7.0 = encephalopathy)

additional bloods to consider
- U+Es
- cardiac enzymes
- LFTs
- coagulation screen
^basically to see how much damage done to these organs

other tests to consider

MRI head
echo of heart
EEG

Question 4

Q

APGAR score

What does it stand for? (ie what features does it look at)?
max possible score? healthy score?
how many minutes after birth is it done? 2

Answer

A

ACTIVITY (muscle tone)

0 = absent
1 = arms + legs flexed
2 = active movement

PULSE

0 = absent
1 = below 100 bpm
2 = over 100 bpm

GRIMACE (reflex irritability)

0 = flaccid
1 = some flexion of extremities / grimace
2 = cries on stimulation / sneezes / coughs

APPEARANCE (skin colour)

0 = blue or pale
1 = body pink, extremities blue
2 = completely pink

RESPIRATORY EFFORT

0 = absent
1 = slow, irregular
2 = vigorous cry

max score is 10

7-10 is normal
4-6 is moderately depressed
0-3 is severely depressed

done at:

1 min
5 mins

nb DON’T BOTHER LEARNING INS AND OUTS! JUST GET THE GIST OF THIS AND WHAT A NORMAL SCORE

Question 5

Q

Hypoxic Ischaemic encephalopathy (HIE):

treatment with most efficacy? how long for?
other thing to treat? 1
important things to monitor? 3

Answer

A

THERAPEUTIC HYPOTHERMIA

33-33.5 deg for 72 hours
followed by slow and controlled rewarming
stops glutamine and free radicals from being released

treat seizures

MONITOR

blood glucose
EEG
fluid levels (mild fluid restriction

Question 6

Q

Possible complications of HIE? 6

Answer

A

death
dyskinetic cerebral palsy
severely reduced IQ
epilepsy
cortical blindness
hearing loss

Question 7

Q

BIRTHMARKS

definition?
two main groups?

Answer

A

Coloured marks that are visible on the skin – present at birth or develop soon after birth

VASCULAR

Often red, purple or pink
Caused by abnormal blood vessels in or under the skin
Often on head and neck area – mainly the face
If affected vessels are deep, birthmark can appear blue.

PIGMENTED

Usually brown
Caused by clusters of pigmented cells.

Question 8

Q

NEVUS SIMPLEX

Two other names for them?
appearance? (incl location)
what % of babies will have?
prognosis?

Answer

A

AKA

stork mark
salmon patch

Flat red/ pink patches that appear on eyelids, neck or forehead at birth
- more noticeable when baby cries

50% of babies will have
- most common type of vascular birth mark

will fade within months (up to 4 years if on forehead)

Question 9

Q

INFANTILE HAEMANGIOMA

aka?
appearance?
when treat? 3
what is treatment?
prognosis?

Answer

A

strawberry mark

usually not present at birth but may develop rapidly in the first month of life. They appear as erythematous, raised and multilobbed tumours

Raised red mark anywhere on body
- 5% of babies, esp girls

TREAT IF:

grows rapidly
interferes with feeding
interferes with vision

treatment = systemic propranolol (or topical beta blockers)

typically increase in size until around 6-9 months then regress over next few years
- 95% resolve before age 10

Question 10

Q

PORT WINE STAIN

appearance?
what to rule out? how?
prognosis?
treatment option?

Answer

A

Permanent, flat, red or purple marks

Often on one side of body
is a capillary malformation

Rule out Sturge-Weber syndrome: seizures, learning disorders, glaucoma, port wine mark
- DO MRI!!

Permanent, may deepen in colour over time
- is also sensitive to hormones (puberty, pregnancy, menopause)

can have multiple sessions of laser therapy to reduce appearance
- or use camouflage make up

Question 11

Q

CAFE AU LAIT SPOTS

appearance?
what’s normal?
when get suspicious that could be due to an underlying condition? which condition?

Answer

A

Coffee coloured skin patches

One or two is normal – if >6 develop by age 5, review needed

Rule out neurofibromatosis type 1

(Growth of tumours along nerves in the skin)

Question 12

Q

MONGOLIAN BLUE SPOTS:

appearance?
who most commonly seen in?
prognosis?
what can be mistaken for?

Answer

A

Blue/grey or bruised looking birthmarks

Present from birth
Occur over lower back or buttocks

Commonly seen in darker-skinned people

May last for months – years (usually disappear by 4)

Important new baby check – may be mistaken for bruises later on

Question 13

Q

CONGENITAL MELANOCYTIC NAEVI

appearance?
what is there a risk of them becoming? what increases the risk?

Answer

A

Congenital moles
- Large, black or brown moles from birth

Fairly common

May change over time

Risk of skin cancer is low
- Risk with increased size

Question 14

Q

What are the three types of extra-cranial head injury that can occur due to trauma at birth?
- How do you tell the difference between then? (when appear, appearance and findings on palpation, cross suture lines or not)

Answer

A

CAPUT SUCCEDANUM

most superficial
localised scalp oedema
fluid collection is greatest immediately following delivery (and will then decrease)
soft to touch with irregular margins
cross suture lines

CEPHALOHAEMATOMA

rupturing of blood vessels between periosteum and bone
firm, tender mass
appears hours to days after birth and can increase in size for 2-3 days
DON’T cross suture lines (even when increases in size)

SUBGALEAL HAEMORRHAGE

damage to veins between the scalp and intracranial venous sinuses
boggy fluid collection with ballotable fluid wave beneath the scalp + bleeding extending to above the eyes and back to the insertion of trapezius muscle
occiptal frontal circumference will increase (potential for large blood loss - need to be monitored)
cross suture lines
vacuum procedure gives highest risk of this

nb these can all happen in any birth but all are more likely in instrumental delivery

Question 15

Q

CEPHALOHAEMATOMA:

how long will it take to resolve?
when should you do a CT head? 2

Answer

A

resolves over a few weeks

do CT head if:

neurological impairment seen
concern for skull fracture

Question 16

Q

HAEMOLYTIC DISEASE OF THE NEWBORN:

describe the pathophysiology
how is it prevented?

Answer

A

Foetus Rh positive

Mother Rh Negative

(Father usually Rh Positive)

Sensitising event makes mother produce anti bodies to Rh positive blood

On second exposure anti-Rh antibodies cross the placenta and destroy foetal RBCs

Effect seen on delivery, when baby cannot cope with haemolysis.

PREVENTION

all mothers tested for rhesus antibodies
rhesus -ve mothers given anti-D at 28wks and any sensitising events (eg bleeding after 24wks, miscarriage, amniocentesis etc)

Question 17

Q

HAEMOLYTIC DISEASE OF THE NEWBORN:

antenatal presentation? (incl latin name)
postnatal presentation?

Answer

A

ANTENATAL (ie on USS)
- hydrops fetalis: abnormal accumulation of fluid in two or more foetal compartments (eg ascites, pleural effusion, skin oedema)

POSTNATAL

early jaundice (in first 24hrs)
hepatosplenomegaly
coagulopathy
thrombocytopaenia
anaemia (may be a later sign)

Question 18

Q

main groups of DDx for jaundice in first 24hrs of birth? 4

Answer

A

nb almost always HAEMOLYTIC cause in first 24hrs of life:

1) ABO incompatibility
2) rhesus or other isoimmunisation
3) red cell defects (eg G6PD deficiency, spherocytosis)

4) congenital infection (eg TORCH)

Question 19

Q

HAEMOLYTIC DISEASE OF THE NEWBORN:

bloods from mother? 1
bloods from infant? 3

Answer

A

MOTHER
- group and rhesus status

INFANT (can do as cord blood)

FBC (low Hb, increased reticulocytes, low platelets)
coombs test
LFTs (increased bilirubin)

Question 20

Q

HAEMOLYTIC DISEASE OF THE NEWBORN:

symptomatic management options? 2
other management? 1

Answer

A

TREATMENT FOR JAUNDICE
- plot on line (make sure using correct chart for gestational age) then UV light and/or exchange transfusion

consider IV Ig as definitive treamtent
- this may not be necessary though, but monitor closely!!

Question 21

Q

PREMATURITY:

definition?
at what gestation are most problems seen though?
If an infant is born prematurely, what full history should be taken?
risk factors for prematurity? 11 (as identified in the hx)
what percentage of premature births are idiopathic? (ie have no risk factors)

Answer

A

birth before 37 wks gestation (8%)

most problems seen in infants born <32 wks (2%)

TAKE FULL OBSTETRIC Hx

RISK FACTORS:

young maternal age
previous premature birth
cervical incompetence
multiple pregnancies
gestational HTN / pre-eclampsia
antepartum haemorrhage
congenital infection (TORCH)
certain medications during pregnancy
maternal smoking
maternal alcohol
domestic violence

40% have no known risk factors

Question 22

Q

COMPLICATIONS ASSOCIATED WITH PREMATURITY:

CNS? 4
metabolic? 4
blood? 2
cardiovascular? 2
respiratory? 3
GI? 5
other? 2
later? 4

Answer

A

CNS

intraventricular haemorrhage (bleeding into ventricular system, can lead to cerebral palsy)
periventricular leukomalacia (white matter surrounding ventricle deprived of blood and oxygen -> softening)
cerebral palsy
retinopathy of prematurity (ROP)

(also higher risk of HIE during delivery)

METABOLIC

hypoglycaemia
electrolyte imbalance
hypocalcaemia (poor renal function)
osteopenia of prematurity (w risk of fractures)

BLOOD

anaemia of prematurity
neonatal jaundice

CARDIOVASCULAR

hypotension
patent ductus arteriosus

RESPIRATORY

surfactant deficiency -> resp distress syndrome (RDS)
recurrent apnoea
chronic lung disease (broncho-pulmonary dysplasia)

GI (incl nutriution)

inability to suck (lack of reflex)
poor milk tolerance
Necrotising enterocolitis (NEC)
Gastro-oesophageal reflux
inguinal hernia

OTHER

hypothermia (poor temp regulation)
immunocompromised (increased risk of infection)

LATER

increased risk of adverse neurodevelopment
behavioural problems
sudden infant death syndrome (SIDS)
non-accidental injury (stress of long-term complications)

Question 23

Q

How to antenatally prevent resp distress syndrome?

at what gestation is this given?

Answer

A

IM corticosteroids to mother
- 2 doses, 12-24 hrs apart

give if <34 weeks gestation

Question 24

Q

Management of preterm birth:

where to deliver?
who present at birth?
cord clamping?
how to keep warm if small?
what resp support can be provided if needed? 3

Answer

A

delivery in centre with preterm facilities

<28 weeks, senior paediatrician present at birth

Delay cord clamping for 1 min where possible

to prevent heat loss: can put in polytheme bag at birth to prevent evaporative loss of fluid and heat

ie if really preterm, do this before drying them
also warm them

RESP SUPPORT OPTIONS

PEEP
intubation
surfactant replacement therapy (through endotracheal tube)

Question 25

Q

PRETERM INFANTS

how to manage poor thermoregulation?
how to minimise risk of infection? 2
how to manage hypoglycaemia?
how to feed? (which also reduces risk of NEC)
how to manage patent ductus arteriosus?
how to manage retinopathy of prematurity?

Answer

A

put baby in incubator
minimal handling of baby
low threshold for starting broad spec abx
start feeding as soon as possible, can also add glucose to milk
get mother to express breast milk and (norm) feed through nasogastric tube (breast milk reduces risk of NEC)

can give NSAIDs (eg iboprofen) to close PDA
- check no duct-dependant heart disease first though

all premature babies are screened for ROP
- if have, treat with laser treatment to the extra blood vessels

Question 26

Q

RESPIRATORY DISTRESS IN THE NEWBORN:

what RR?
other signs? 5
aside

Answer

A

tachypnea, RR = >66

intercostal recession
subcostal recession
grunting (endogenous PEEP)
nasal flaring
cyanosis

Question 27

Q

RESP DISTRESS SYNDROME:

what other risk factors? 5 (aside from prematurity)
Imaging? 1 (incl findings)
what things to monitor? 2

Answer

A

OTHER RISK FACTORS

caesarian section
hypothermia
meconium aspiration
maternal diabetes
family Hx

CXR

ground glass appearance in all lung fields
generalised atelectasis = a complete or partial collapse of a lung or a lobe
air bronchograms
reduced lung volume

MONITOR

spo2
blood gasses

Question 28

Q

RESPIRATORY DISTRESS SYNDROME

management? 5 (1 treatment, 3 supportive, 1 prevention)
prognosis?
how long does condition normally take to resolve?
most common complication?

Answer

A

nb also antenatal steroids if poss

1) sufficient oxygen + supporting respiration
- CPAP
- intubation

2) surfactant replacement therapy down endotracheal tube

3) abx - penicillin and gentamicin
- until congenital pneumonia excluded (can mimic or co-exist with RDS)

4) IV fluids
5) NG tube feeding (mothers expressed milk if poss)

generally good prognosis (mortality is 5-10%)

norm resolves over 3-7 days as surfactant production increases

most common complication = bronchopulmonary dysplasia (require O2 at home)

Question 29

Q

What are the two different types of IUGR?

causes of each?

which tends to have better prognosis?

Answer

A

SYMMETRICAL GROWTH RESTRICTION

= head circum and weight equally reduced
= EARLY insult

genetic
foetal abnormality
congenital viral infection (eg TORCH)
early foetal malnutrition
early teratogen exposure

ASYMMETRICAL GROWTH RESTRICTION

= head circum significantly higher on centiles than weight
= LATE insult
- tend to have better prognosis (ie less likely to have developmental delay etc)

late foetal malnutrition
pre-eclampsia
smoking

Question 30

Q

Potential complications for IUGR:

immediate? 4
late? 2

Answer

A

hypoglycaemia
hypothermia
polycythaemia
bone marrow / hepatic compromise (thrombocytopenia, neutropenia, coagulopathy)

LATE

poor post-natal growth
neurodevelopment impairments

Question 31

Q

TALIPES:

also known as?
what is the deformity seen? (describe it)
two different types? how to tell difference? which needs treatment?
when is it normally picked up / examined for?

Answer

A

aka neonatal club foot (talipes equinovarus)
- nb bilateral in 50% of cases

inversion + adduction of forefoot
- plantarflexion deformity

TWO TYPES
= postural: CAN be passively everted and dorsiflexed through full range of motion (not concerning)
= structural: can NOT be passively everted and dorsiflexed through full range of motion (needs treatment)

newborn exam OR 6/8 week exam

Question 32

Q

STRUCTURAL TALIPES:

- two management options?

Answer

A

Ponseti Method – foot manipulated over 6 weeks, held in long leg plaster cast. Gradual correction

Operation if Ponseti doesn’t work – from 2 years old

Question 33

Q

CHICKEN POX:

virus it’s caused by?
first sign / symptom?
other symptoms?
appearance and distribution of rash?

Answer

A

varicella zoster virus (VZV)

FIRST SIGN = fever (about 2 days before rash)

other symptoms:

ITCHY RASH
headache
anorexia
signs of URTI (sore throat, coryza, cough)

RASH:

predominantly starts on torso (also perineum + scalp) then may go over whole body
lesions evolve: red macules, papules, VESICLES, pustules then crusting/scabs (will have lesions at different stages)

Question 34

Q

CHICKEN POX:

how is it spread?
incubation period?
when most infective?
when tell parents that children can go back to school?
how diagnosed?

Answer

A

spread by respiratory droplets or direct contact with lesion

incubation of 10-21 days (norm 14 days)

most infective 4 days before the rash to 5 days after rash first appeared (ie norm when lesions are all crusted over)

should be excluded from school and then can go back when all lesions have crusted over

diagnosed clinically (based on appearance and distribution of rash) 
- though can do test of vesicular fluid for virus - but very rarely done!

Question 35

Q

CHICKEN POX:

most common complication? 1
rarer, more serious complications? 4

Answer

A

most common complication is secondary bacterial infected of lesions (eg impetigo)

RARE COMPLICATIONS

conjunctival lesions
encephalitis (presents as ataxia about a week after rash appears, good prognosis)
pneumonia (esp in infants)
necrotising fascitis

Question 36

Q

CHICKEN POX:

who is most at risk if infected? 3
what give them as prophylaxis if have contact? 1
what give them if they get infected? 1

Answer

A

pregnant women
infants under 1 year
immunocompromised children

Varicella Zoster Immunoglobulins – prophylaxis following contact e.g. when pregnant or on chemo (or give to newborn if antenatal exposure)

Aciclovir if get infected (also use for anyone else who gets complications)

Question 37

Q

MANAGEMENT OF UNCOMPLICATED CHICKEN POX:

advice to parents?
options to try to reduce itching? 2
option if distressing fever?
who to give antivirals to? 4

Answer

A

cut children’s nails (to prevent itching + scarring)

to reduce itching

calamine lotion
chlorphenamine (if >1 year)

antipyretics if child is distressed by the fever

GIVE ANTIVIRALS (acyclovir)

immunosuppressed
pregnant
infants <1 year
get any complications

Question 38

Q

INFECTIVE CONJUNCTIVITIS:

key features? 3
how to tell difference between bacterial and viral?
main differential for infective conjunctivitis?

Answer

A

sore
red eyes
discharge

BACTERIAL:

purulent discharge
Eyes may be ‘stuck together’ in the morning

VIRAL:

Serous discharge
Recent URTI
Preauricular lymph nodes

main differential = allergic conjunctivitis (ie norm w hayfever)

Question 39

Q

MANAGEMENT OF CONJUNCTIVITIS:

viral?
bacterial? (incl name of abx)
advice given to parents? 1
school exclusion needed?

Answer

A

viral if norm self-limiting within 1-2 wks

bacterial
= chloramphenicol drops OR ointment multiple times a day

ADVICE

don’t share towels while have symptoms
school exclusion not necessary

(also don’t wear contact lenses while have symptoms)

Question 40

Q

NEONATAL CONJUNCTIVITIS:

likely cause if <48hrs after birth? management?
likely cause if day 3-4 after birth? management?
likely cause if >7 days after birth? management?

Answer

A

GONORRHOEA
= within 48hrs of birth
- purulent discharge + swelling of eyelids
- treat w cephalosporin

NEONATAL CONJUNCTIVITIS
= day 3-4
- simple cleaning normally sufficient

CHLAMYDIA
= suspect if after day 7
- diagnosis with monoclonal antibody text
- treat w abx

nb gonorrhoea and chlamydia are vertical transmission

Question 41

Q

ALLERGIC CONJUNCTIVITIS:

features? 5
1st line management?

Answer

A

Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)

1ST LINE
= topical or systemic antihistamines

Question 42

Q

Common food allergies? 8

which tend to grow out of?

Answer

A

TEND TO GROW OUT OF:

cow’s milk protein
soya
eggs
wheat

TEND TO HAVE FOR LIFE:

fish
shellfish
peanuts
tree nuts

Question 43

Q

Possible symptoms of a food allergy:

most serious presentation?
other possible symptoms / presentations? 8

Answer

A

ANAPHYLAXIS

dysphagia
Diarrhoea +/- blood or mucus
Vomiting
Abdominal pain
Failure of growth/ weight loss
Eczema
Erythematous rash – esp. peri-orbital
Asthma symptoms

nb always think of cow’s milk protein allergy if weaning infant starts getting rash or blood in stools and doesn’t seem acutely unwell

Question 44

Q

Food allergy:

two possible ways of testing for it? 2
if these are negative but allergy still suspected, what investigation to do?

Answer

A

skin prick test
blood test for IgE specific to that allergen

if negative: can do controlled exposure in hospital

Question 45

Q

Food allergy:

dietary advice?
what give for emergencies? how to describe how to give to parents?
medication to give if mild reaction?

Answer

A

AVOID FOOD ALLERGIC TO!

give epipen (one for home and one for school nursery)

teach how to use:

remove blue cap then hold with a fist around and stab into thigh (don’t put thumb over end)
‘orange to the thigh, blue to the sky’
hear a click
hold in for 5 secs then remove

can give antihistamines if mild reaction

Question 46

Q

GLANDULAR FEVER:

other name for it?
most common virus that causes it?
which age group most common in?

Answer

A

infectious mononucleosis
- ‘mono’ in the US

90% is ebstein-barr virus (EBV)
- rarer causes: CMV, HHV-6

most common in teenagers and young adults

Question 47

Q

GLANDULAR FEVER:

three classical features?
other possible features? 6 (3 symptoms, 3 clinical signs)
describe the typical course of the disease?

Answer

A

1) SORE THROAT
2) LYMPHADENOPATHY
3) FEVER

nb lymphadenopathy may be present in the anterior and posterior triangles of the neck
- tend to be firm and non-tender

OTHER POSSIBLE FEATURES:

malaise
anorexia
headache
palatal petechiae
splenomegaly (50%, may rarely lead to rupture)
hepatitis (transient rise in ALT)

PRESENTATION IS VERY VARIABLE

may be gradual with malaise, anorexia + low-grade fever for 1-2 weeks
may begin abruptly with high fever and headache

Question 48

Q

what is the main DDx for glandular fever?

How is the pattern of lymphadenopathy differ between these two conditions?

other rarer, but more serious, DDx? 2

Answer

A

TONSILITIS
- typically only upper anterior chain are enlarged

glandular fever
- may be present in anterior and posterior triangles of neck

other DDx

hodgkins lymphoma
other haem or solid tumours

Question 49

Q

GLANDULAR FEVER:

two investigations to order if suspect?
when to order?
findings on these?

Answer

A

FBC

increased lymphocytes and monocytes
may be thrombocytopenia
may get a haemolytic anaemia

MONOSPOT

test for antibody to the virus
takes 1-2 weeks to become positive

order both in 2ND WEEK of illness (may get false negatives if ordered before this)

Question 50

Q

GLANDULAR FEVER:

non-pharm management advice? 3
medication for symptomatic management?
what medication to avoid? why?
what else to avoid? why? for how long?
how long norm take symptoms to resolve?

Answer

A

rest during early stages
drink plenty of fluid
avoid alcohol
simple analgesia for aches + pains

AVOID ampicillin or amoxycillin when glandular fever suspected
- will cause a maculopapular rash in 99% of pts with glandular fever (may be misdiagnosed as an allergy)

AVOID contact sports for 8 weeks
- to reduce risk of splenic rupture

Symptoms typically resolve after 2-4 weeks

Question 51

Q

KAWASAKI DISEASE:

pathophysiology?
age group normally affected?

Answer

A

systemic vasculitis of unknown aetiology

- affects children under age of 5 years

Question 52

Q

KAWASAKI DISEASE:

- What are the 6 diagnostic criteria? (how many do you need to diagnose?)

Answer

A

1) high grade FEVER which lasts >5 DAYS
- nb fever is characteristically resistant to antipyretics

2) bilateral CONJUNCTIVITIS
- non-purulent

3) inflamed + red mouth, CRACKED LIPS, red pharynx
- also STRAWBERRY TONGUE

4) polymorphous RASH
5) changes to extremities: HAND/FOOT palm/soles reddening, oedema and later desquamation (ie PEELING)
6) cervical LYMPHADENOPATHY

“Think:

fever, nodes, rash
eyes, mouth, hands/feet”

need at least 5 of the 6 criteria to diagnose kawasaki

nb kawasaki is a clinical diagnosis, there’s no specific diagnostic test

Question 53

Q

KAWASAKI DISEASE:

- what is the main two DDx? 2

Answer

A

main DDx

scarlet fever
atypical infection (eg if someone has a sore throat and persistant fever not responding to 1st line abx then maybe try macrolides)

Question 54

Q

KAWASAKI DISEASE

medications for management? 2
when do you need to treat by?
most important complication?
investigation used to screen for this complication?

Answer

A

MANAGEMENT:

high dose aspirin
IV immunoglobulins

treat within 10 days of start of fever! - ie treat fast!

complication = CORONARY ARTERY ANEURYSMS
- screen for with echo

nb this is the most common cause of acquired heart disease in the UK

Question 55

Q

MEASLES:

describe the course of the disease (incl symptoms, what first symptoms to occur, where does rash start and spread, features of rash)
also incubation period and when infective from

Answer

A

incubation = 7-14 days (average 10 days)

infective from prodrome until 4 days after rash starts

1st) PRODROME (about 3 days)
- fever
- miserable
- cough
- coryza
- conjunctivitis
^”all the C’s”

2nd) KOPLIK SPOTS
- white spots (‘grain of salt’) on buccal mucosa
- nb doesn’t occur in any other condition

3rd) RASH (about day 4)
- starts BEHIND EARS
- then spreads to face + trunk
- discrete maculopapular rash, becoming blotchy and confluent

Question 56

Q

MEASLES:

mainstay of management? 2
investigation you can do?
who may need admission to hospital? 2
what should you do whenever you see someone with measles?
school exclusion required?
what should contacts do?

Answer

A

fluids
antipyretics

can test for IgM antibodies within a few days of rash onset

may need admission:

pregnant women
immunosuppressed

NOTIFY PUBLIC HEALT

exclude from school (?how long for**)
unvaccinated contacts should get urgent MMR vaccine

Question 57

Q

MEASLES:

age group most common in?
who at increased risk? 1
most common complication?
most common cause of death?
other possible complications?

Answer

A

pre school + young children

increased risk if have Vit A deficiency

most common
= OTITIS MEDIA

most common cause of death
= PNEUMONIA

OTHER COMPLICATIONS:

encephalitis: typically 1-2 wks following onset of illness
subacute sclerosing panencephalitis: very rare, may present 5-10 years after illness
febrile convulsions
keratoconjunctivitis, corneal ulceration
diarrhoea
increased incidence of appendicitis
myocarditis

Question 58

Q

PERIORBITAL CELLULITIS:

also known as?
what is it?
which age group most common in?

Answer

A

aka preseptal cellulitis

an infection of the soft tissues anterior to the orbital septum - this includes the eyelids, skin and subcutaneous tissue of the face, but not the contents of the orbit
- nb this is in contrast to orbital cellulitis, which is an infection of the soft tissues behind the orbital septum, and is a much more serious infection

most common in children under 5

80% of patients are under 10
median age of presentation is 21 months

Question 59

Q

PERIORBITAL CELLULITIS:

common causes / mechanisms of infection?
common causative organisms? 4

Answer

A

MECHANISMS OF SPREAD:

= sinus or respiratory infection

= cut, scratch, or foreign object in or near the eye

bite from an insect or animal
skin infection, such as impetigo
stye (eyelid bumps) or swelling of the gland that makes tears

CAUSATIVE ORGANISMS:

Staph. aureus
Staph. epidermidis
streptococci
anaerobic bacteria

nb is more common in winter dt increased prevelence of resp pathogens

Question 60

Q

PERIORBITAL CELLULITIS:

local symptoms?
main systemic symptom?
findings on examination?
what examination should be performed?
what signs should NOT be found, but should be examined/tested for? 6 (what would they indicate)

Answer

A

red, swollen, painful eye

acute onset
fever

O/E

erythema and oedema of the eyelids, which can spread onto the surrounding skin
partial or complete ptosis of the eye due to swelling

PERFORM CRANIAL NERVE EXAM (just ones that affect eye)

SIGNS INDICATIVE OF ORBITAL CELLULITIS:

pain on eye movement
restriction of eye movements
proptosis
chemosis (oedema of conjunctiva)
visual disturbance
RAPD (ie fail swinging light test)

Question 61

Q

PERIORBITAL CELLULITIS:

main two differentials?
how to differentiate between?

Answer

A

ORBITAL CELLULITIS

do neuro exam: will have painful and reduced eye movement, proptosis, visual disturbance and RAPD
can do imaging to differentiate if not sure

ALLERGIC REACTION

more likely to be bilateral
ask about other allergy symptoms (incl PMH + FH)
ask about any new exposures etc

Question 62

Q

PERIORBITAL CELLULITIS:

bloods? 2
other bedside investigation?
imaging to do if suspect orbital cellulitis? 1

Answer

A

FBC (raised inflam markers)
CRP

swab discharge from eye

if suspect orbital cellulitis
= contrast CT of head

Question 63

Q

PERIORBITAL CELLULITIS:

where should it be managed?
oral or IV abx? which abx?
other medication to give?
main complication to look out for?

Answer

A

All cases should be referred into hospital for assessment

Oral antibiotics are frequently sufficient - usually co-amoxiclav

Children may require admission for observation

give analgesia / anti-pyretics

Monitor for signs of orbital cellulitis
- also, rarely, meningitis

Question 64

Q

BRAIN TUMOURS IN CHILDREN:

concerning characteristics of a headache?
other symptoms / signs of raised ICP?
other symptoms / signs? 3

Answer

A

CONCERNING HEADACHE

worse on coughing / sneezing
worse in the morning
present on walking
recent onset, worsening or persistent
any associated neuro and/or focal symptoms

SIGNS OF RAISED ICP

headache
vomiting
seizures
new-onset squint
blurred vision

OTHER SYMPTOMS

new-onset ataxia, clumsiness
incoordination
nystagmus

nb brain tumours can often be in cerebellum, hence ataxic etc symptoms

Answer 65

A

ANY AGE

abnormal eye movements
fits / seizures
behavioural change (lethargy under 5)
abnormal balance / walking / coordination
persistent / recurren t vomiting

YOUNG CHILDREN
- abnormal head position such as: wry neck, head tilt or stiff neck

OLDER CHILDREN:

persistent / recurrent headache
blurred or double vision
delayed or arrested puberty

nb can also get symptoms similar to a stroke but with more insidious onset (eg weakness or loss of sensation down one side of arm

nb if on spinal cord can also present with symptoms of spinal cord compression

nb can also have endocrine effects

Answer 66

A

brain abscess
meningitis
encephalitis
brain tumour
seizures / post-ictal
trauma (incl non-accidental injury)
idiopathic intracranial hypertension (esp teenagers)

Answer 67

A

ophthalmoscope to look for papilloedema

CT head

Answer 68

A

GLIOMAS = most common

either astrocytomas or medulloblastomas
astrocytomas have best survival rates

nb in children most brain tumours are primary (whereas in adults, most are mets)

Answer 69

A

Haemophilia A = factor 8
- VIII

Haemophilia B = factor 9

IX
aka christmas disease

both are X-linked recessive

1/3rd have no FHx

nb carrier females are rarely symptomatic

nb haemophilia A is 5x more common than haemophilia B (B is less serious)

Answer 70

A

excessive bruising / joint swelling as child learns to crawl / walk (haemarthrosis, haematomas)
prolonged bleeding following circumcision, tooth eruption

nb rare to present in neonates - the more severe the disease is, the earlier it is likely to present

Answer 71

A

von willebrand disease
platelet disorder
non-accidental injury (look at pattern of bruises etc)

Answer 72

A

APTT (activated partial thromboplastin time) is prolonged
- nb bleeding time, thrombin time and prothrombin time will all be normal

FBC
factor 8 and factor 9 assay

consider doing:

head + neck CT/MRI (if injury)
abdominal / joint USS (if injury / bruising / swelling)

Answer 73

A

avoid NSAIDs (they interfere with platelets)

avoid contact sports (but can do other sports)

give IV injections of of factor concentrate (either 8 or 9)

most families manage this at home
portacaths are useful
frequency of injection depends on severity of disease and what doing (eg have more before surgery/dental procedures)

Desmopressin may allow mild haemophilia A to be managed without use of blood products – stimulates endogenous release of factor 8 and Von Willebrand factor
- nb this doesn’t work for haemophilia B

nb there is a huge range of disease from mild (who rarely bleed and only need only need prophylaxis for surgery) and severe disease who have spontaneous bleeds and need constant prophylactic factor concentrate
- always ask pts how often take factors, how bad symptoms are etc

Answer 74

A

aka IgA vasculitis

HSP is an IgA-mediated small vessel vasculitis

most common aged 2-10 years

normally follows an infection (eg an URTI)

There is a degree of overlap with IgA nephropathy (Berger’s disease)

Answer 75

A

1) SKIN
- begins as a maculopapular, red rash which gradually becomes a palpable purpuric rash (w localised oedema)
- BUM, ANKLES, EXTENSOR surfaces

2) GUT
- colicky abdo pain (can be mistaken for an acute abdomen)
+/- diarrhoea / vomiting (common)
+/- haematemesis / meleana (less common)
- intussception (may occur)
- perforation (very rare)

3) JOINTS (60%)
- arthralgia of of medium-sized joints
- may progress to an obvious arthritis with red, swollen, tender joints

4) KIDNEYS (50%)
- haematuria is common (concerning if accompanied by proteinuria)
- if severe, can cause acute nephritic or nephrotic syndrome (AKI or CKD follow in a minority)
- renal complications are responsible for majority of morbidity + mortality

nb renal injury is caused by deposition of IgA immune complexes

Answer 76

A

urine dipstick
FBC (nb pa
U+E (for renal function)

do USS with biopsy if suspect renal involvement

do relevant abdo investigations, eg USS if suspect intussusception

nb also do obs to rule out more serious causes of purpuric rash

Answer 77

A

simple analgesia for arthritis
- can use nsaids only if no kidney involvement

repeat for a few weeks at home to screen for renal complications:

dipstick for blood + protein
BP

self-limiting, normally resolves in 1-3 weeks

around 1/3rds of patients relapse

Answer 78

A

acute lymphoblastic leukaemia (ALL)

Malignant proliferation of pre-B or T-cell lymphoid precursors in the bone marrow

nb ALL accounts for 85% of all leukaemias in childhood and 25% of all cancers in childhood

peak incidence ages 2-5 years
- affects boys slightly more than girls

increased likelihood in pts with Downs

nb also get AML but rarer, is more common n adults

Answer 79

A

thrombocytopenia -> BRUISING, PETECHIAE

anaemia -> LETHARGY, PALLOR

neutropenia -> frequent or severe INFECTIONS

OTHER SYMPTOMS

bone pain (secondary to bone marrow infiltration)
^ may present as a limp
hepatosplenomegaly
lymphadenopathy
fever

may also see testicular swelling in boys

nb can also get AML in kids but is rarer (the lymphadenopathy tends to be less prominent than in ALL)

Answer 80

A

age < 2 years or > 10 years
WBC > 20 * 109/l at diagnosis
T or B cell surface markers
non-Caucasian
male sex

Answer 81

A

MALIGNANCY UNLIKELY

smooth, mobile, <2cm
cervical or small inguinal
well child (or signs of URTI / otitis media etc)

MALIGNANCY LIKELY

hard, craggy, tethered, >2cm
more widespread distribution
bruising, pallor, fever, hepatosplenomegaly

Answer 82

A

FBC
LFTs

bone marrow biopsy

Answer 83

A

chemotherapy (to remove blast cells from circulation
- then intermittent cycles of chemo for 2 years

intrathecal methotrexate +/- cranial irradiation to prevent spread to CNS

nb may also need steroids

80% at 5 years (rare to relapse after that)

Answer 84

A

intensive myeloablative chemo

relapse is common

bone marrow transplant offers best chance of cure

overall survival is about 60%

Answer 85

A

HODGKIN’S
= young adults

NON-HODGKINS
= 7-10years

nb also get both of these in elderly as well

Answer 86

A

Pts commonly have previous EBV infection

Reed-Sternberg cells in reactive lymph node

MAIN PRESENTATION:
- Progressive, painless lymph node enlargement – norm cervical and mediastinal

B-SYMPTOMS (get in 25%)
- weight loss
- night sweats
- fever
- (pruritis)
nb presence of B symptoms at presentation is a poor prognostic sign (but prognosis for HL is very good so is all relative)

may get pain in lymph nodes when drink alcohol in hodgkins

NON-HODGKINS:
symptoms are similar, although B symptoms occur later in disease
- in addition, more likely to present with extranodal disease:
- gastric (dyspepsia, dysphagia, abdo pain)
- bone marrow (pancytopenia, bone pain)
- lungs
- skin
- CNS (nerve palsies)

Answer 87

A

lymph node biopsy to diagnose

FURTHER TESTS TO ASSESS SPREAD:

bone marrow biopsy
chest x-ray
CT scan (neck, chest, abdo, pelvis)
PET scan

ANN ARBOR STAGING

I = single lymph node region
II = two or more regions on same side of the diaphragm
III = involvement of lymph node regions on both sides of the diaphragm
IV = involvement of extra-nodal sites

^then add A if no B symptoms present and B if B symptoms present

nb LDH is often done too as is a good prognostic marker

Answer 88

A

chemo
radiotherapy to affected areas of nodes

stage I disease is associated with 85% survival at 5 years

POOR PROGNOSTIC FACTORS:

advancing age
male sex
stage IV disease

Answer 89

A

lymph node biopsy to diagnose

OTHER INVESTIGATIONS TO CONSIDER (to assess spread)

bone marrow biopsy
LP
pleural + peritoneal fluid
CT scan
PET scan

also do basic bloods

ANN ARBOR STAGING

I = single lymph node region
II = two or more regions on same side of the diaphragm
III = involvement of lymph node regions on both sides of the diaphragm
IV = involvement of extra-nodal sites

^then add A if no B symptoms present and B if B symptoms present

nb LDH is often done too as is a good prognostic marker

MANAGEMENT
- normally intensive chemo, but depends on the subtype

70% of children will have prolonged remission (nb worse prognosis in adults)

Answer 90

A

Sickle haemoglobin, it sickles at low oxygen concentrations -> increased viscosity of blood, reducing flow through small vessels -> tissue infarction

sickle RBCs are destroyed early = haemolytic anaemia

hyposplenic (dt repeat infarction) -> increased risk of infection (esp in infants)

autosomal recessive condition
- trait is prtective against malaria

most common in afro-carribean ethnicity

screened for in newborn blood spot at 5-9 days old

presents age 3months - 6 years if not picked up
- ie when foetal hb switches over to adult (sickled) hb

Answer 91

A

dactylitis (sausage fingers)

first 3 years of life = increased risk of pneumococcal sepsis

infections from encapsulated organisms and parvovirus

definitive diagnosis of sickle cell disease is by haemoglobin electrophoresis

Answer 92

A

THROMBOTIC (painful)
- aka painful crises or vaso-occlusive crises
- precipitated by infection, dehydration, deoxygenation
- infarcts occur in various organs including the bones (e.g. avascular necrosis of hip, hand-foot syndrome in children, lungs, spleen and brain
(stroke is a big cause of death)

SEQUESTRATION
- sickling within organs such as the spleen or lungs causes pooling of blood with worsening of the anaemia

ACUTE CHEST SYNDROME

dyspnoea, chest pain, pulmonary infiltrates, low pO2
most common cause of death after childhood

APLASTIC CRISIS

caused by infection with parvovirus
sudden fall in haemoglobin

HAEMOLYTIC

rare
fall in haemoglobin due an increased rate of haemolysis

boys can get priapism as a form of painful crisis

Answer 93

A

FBC
U+E
LFT
blood culture
CRP
Group + save
consider CXR if chest symptoms

FOR ALL CRISES (“a who)

1) Analgesia
2) Warmth
3) Hydration (give 150% normal maintenance)
4) Oxygen

antibiotics if suspect infection

Blood transfusion for aplastic crisis, sequestration, anaemia.

Answer 94

A

AVOID PRECIPITATING FACTORS:

dehydration
cold
hypoxia
lifetime oral penicillin V prophylaxis
vaccination to pneumococcal
hydroxycarbamide (chemo drug) to prevent vaso-oclussive crisis
daily oral folic acid (as chemo drug reduces this)

can have bone marrow transplant

Answer 95

A

URTI
- throaty

BRONCHIOLITIS
- unpleasant with ‘wet’ sound

PNEUMONIA
- productive of phlegm (but kids normally swallow this)

CROUP
- barking

PERTUSSIS
- paroxysms of coughing, ending with inspiratory ‘whoop’, persists many days (nb mild cases may not have the ‘whoop’)

ASTHMA
- worse at night

Answer 96

A

COMMON

post-infective
run of recurrent URTIs
postnasal drip
asthma (exercise, night)
cigarette smoke
habit (psychogenic)

UNCOMMON

foreign body
GORD
pertussis
TB
cystic fibrosis
immune deficiency

Answer 97

A

ACUTELY

‘croupy’ cough + splutter
choking noises
stridor
dyspnea

1/3rd present after a few days when infection, collapse or obstructive emphysema present
- so suspect in any child (esp toddler) with new resp symptoms

ASK ABOUT FOREIGN BODY INHALATION:

1) persistent cough
2) chest infection not resolving

Answer 98

A

lodge in bronchus in:
- right middle or lower lobe

do CXR

may demonstrate if radio-opaque object
or may just show associated changes

DIRECT LARYNGOSCOPY + BRONCHOSCOPY
- diagnostic and can remove object at same time

Answer 99

A

otitis media with effusion

middle ear fills with fluid instead of air
- can occur insidiously or following acute otitis media

any age can be affected but norm toddlers

more commonly affected:

down’s
cleft palate
atopy

Answer 100

A

HEARING LOSS

kids may speak louder than normal, ask people to repeat what they say or appear to not be listening
this is CONDUCTIVE hearing loss

YOUNG
- speech delay

OLDER

feeling of fullness in ear
tinnitus

Answer 101

A

otoscopy (GP can do)
- drum is dull and retracted in glue ear

give abx if sign of infection

TREAT IF:

no improvement after 3 months (most are self-limiting)
symptoms are affecting their learning and development
already have severe hearing loss before glue ear
have down’s or cleft palate, as glue ear less likely to resolve by itself

GROMMETS

small temporary tubes placed in ear drum
will fall out within 6-12 months

(can also ‘pop ears’ to help clear - ie autoinflation - but not recommended in under 3s)

can also give temporary hearing aids

Answer 102

A

INFANTS

high fever
rolling heads from side to side
rubbing ears

OLDER KIDS
- ear ache

A mildly pink dull drum may be present in any URTI

Answer 103

A

OTOSCOPY

mild inflammation of pars flaccida with dilated vessels running down the handle of the malleus, and an an absent light reflex
can progress to a red, bulging, painful tympanic membrane, perforation and pus discharge

SIMPLE ANALGESIA for all

GIVE ABX:

child is very unwell
immunosuppression
premature
symptoms for >4 days

PREVENTION

avoid passive smoking
don’t use dummies
don’t feed supine

Answer 104

A

MASTOIDITIS:

systemically unwell
swelling, erythema + tenderness over mastoid process
external ear may protrude forward

CEREBRAL ABSCESS:

signs of raised ICP
systemic infection

LATERAL SINUS THROMBOSIS
- rare

MENINGITIS
- see other flashcard

Answer 105

A

RESP

asthma
foreign body inhalation
bronchiolitis
pneumonia

(also tracheomalacia, pulm hypoplasia, neuromuscular probs)

CARDIOASCULAR

congenital heart disease
anaemia

OTHER

sepsis
DKA (and other acidosis)
anxiety
medications

Answer 106

A

LOOK FOR SIGNS OF RESP DISTRESS

inter/subcostal indrawing
tracheal tug
accessory muscle use (arms and shoulders, incls tripoding)

INFANTS

head bobbing
expiratory grunting
nasal flaring

Answer 107

A

any congenital abnormalities of the pharynx, larynx or trachea (may be audible from birth)

most common = CONGENITAL LARYNGEAL STRIDOR (aka laryngomalacia)

dt floppy aryepiglottic folds
does not cause obstruction + gradually disappears as laryngeal cartilage becomes firmer during first year of life

nb laryngomalacia often presents with stridor at about 4 weeks

do laryngoscopy if:

intercostal + suprasternal recession
feeding problems
no sign of improvement in first few weeks

Answer 108

A

ACUTE LARYNGOTRACHEITIS

(aka croup)
also have barking cough
coryzal symptoms
6months - 3 years
louder stridor

FOREIGN BODY IN LARYNX

hx of inhalation
coughing
choking
vomiting
no signs of infection (eg fever)

EPIGLOTITIS

likely have drooling too
child sits upright and doesn’t move
unwell looking
softer stridor
2-6 years

DON’T EXAMINE THROAT (unless intubating)

Answer 109

A

MOST COMMON

constipation
mesenteric adenitis
gastroenteritis

OTHER GI

appendicitis
intusssuception
bowel obstruction (incl volvulus in neonates, also meckels)
peptic ulcer (pain at night, relief with milk)
inflammatory bowel disease

(also cholecystitis + pancreatitis are rare but can happen)

URINARY

pyelonephritis / UTI
henoch schonlein purpura

OTHER
- lower-lobe pneumonia
- DKA
- anxiety / stress / migraine
(- sickle cell)

TEENS

ectopic pregnancy
ovarian cyst
pelvic inflam disease
ovarian / testicular torsion

nb could also be an acute presentation of a chronic problem - always ask if had before!

Answer 110

A

SOCRATES!

site
onset (incl any viral illness before!)
character
radiation (incl to testes)
associated symptoms
timing (does it wake from sleep)
exacerbating / relieving factors
severity

RED FLAGS

bilious vomiting
blood in stool or vomit
pain waking up child at night
haemodynamic instability / shock
peritonitis / guarding

GI

nausea
vomiting (blood? green?)
diarrhoea / constipation (ask re freq + consistency)
blood in stools

URINARY

pain on urination
new nocturnal enuresis (DM, UTI)
blood in urine
polyuria (also polydipsia)

OTHER

girls: periods started? painful? heavy?
vaginal / penile discharge (think STI)
resp symptoms (incl SOB, cough)
joint pain / swelling (HSP, IBD))

SYSTEMIC - AW FS FIN

appetite loss (or gain if DM)
weight loss
fatigue
sleep
fever
itch (incl jaundice, RASH, skin probs)
night sweats

ANY CHILD = check glucose

ANY TEENAGE GIRL = pregnancy test

Answer 111

A

RECURRENT ABDO PAIN OF CHILDHOOD
Irritable bowel syndrome
non-ulcer dyspepsia
abdominal migraine
constipation
GORD / oesophagitis
IBD
coeliac disease
recurrent UTIs (could be dt anatomical problem or ureteric reflux)
dysmenorrhoea / endometriosis

RARE

eosinophilic oesophagitis
h. pylori infection / peptic ulcer disease
hiatal hernia
pancreatitis
giardiasis
mittelschmertz
ovarian cyst
pelvic inflammatory disease
ureteropelvic junction obstruction
kidney stones
nerve entrapment
spinal tumour
transverse myelitis
porphyria
familial meditierranean fever
lead posioning
lymphoma
sickle cell disease

Answer 112

A

RAP in children is defined as abdominal pain which occurs at least four times a month over a period of two months or more, which is severe enough to limit a child’s activities and which, after appropriate evaluation, cannot be attributed to another medical condition
- nb childhood IBS is a subtype (pain is associated with change in bowel habits and pain relieved by defecation)

about 90% of recurrent abdo pain is functional (ie an organic cause can only be found 10% of the time)

Answer 113

A

take a full hx
examine
plot growth on chart
urine dipstick

(can also consider doing some bloods - eg FBC, ESR)

SITE

Functional = CENTRAL
Organic = not central, more localised

ONSET

F = erratic pattern
O = related to food

CHARACTER
- varies with both

RADIATION

F = NO radiation
O = may be radiation

ASSOCIATED SYMPTOMS

F = often get nausea, may be quiet and pale w pain
O = vomiting/diarrhoea, generalised illness, dysuria, daytime enuresis, growth failure

TIMING

F = does not wake at night
O = can wake at night

EXACERBATING/ RELIEVEING

F = maybe stress
O = maybe food

SEVERITY

F = can be severe
O = can be severe

Answer 114

A

RED FLAGS ON HX

pain that is not-central
wake child at night?
any GROWTH FAILURE/weight loss?
diarrhoea or vomiting?
any GI blood loss?
dysuria?
secondary nocturnal enuresis
unexplained fever
joint inflammation
skin rashes
FHx of IBD

RED FLAGS ON EXAM

any perianal or oral lesions
palpable mass
jaundice

Answer 115

A

Rare in children under 2 (if do get, often present with perforation)

1) central abdo pain which moves to RIF
2) low grade fever
3) minimal vomiting

under 2: vomiting and abdo distension

older children may have diarrhoea and constipation

children with abdo pain caused by appendicitis often walk bent in the middle or curl up in a ball - movement aggravates the pain

pts often have anorexia too

symptoms can be similar to gastroenteritis or food poisoning (important to ask about sick contacts to help rule these out)
- but also UTI, dysmenorrhoea, HSP, mesenteric adenitis etc

ALWAYS CONSIDER APPENDICITIS IN ANY CHILD W ACUTE ABDO PAIN!

Do USS (or CT) if not sure!

do urine dipstick to exclude infection + pregnancy in teenage girls!

Answer 116

A

1) poor growth
2) abnormal stools
3) nutrient deficiency

potential causes:

coeliac
CF
worms
IBD

Answer 117

A

assess diet
assess growth

send stool sample for fat content and culture

sweat test
coeliac disease antibodies

Answer 118

A

CLASSICALLY:

anaemia (pale)
miserable, poor appetite
abdo distension
muscle wasting
fatty diarrhoea + vomiting

NOW PEOPLE PRESENT WITH one or all of:

1) variety of GI symptoms
2) variable growth failure
3) iron-deficient anaemia

CAN PRESENT AT ANY AGE!!! - very non-specific, have in back of head!
- BUT most present before 3 years

nb won’t present before child weans as obviously no wheat in the diet yet

Answer 119

A

RULE OUT:

cystic fibrosis (sweat test)
giardia lamblia infection (stool culture)

1st line = ANTI-TISSUE TRANSGLUTAMINASE (coeliac disease antibodies)

need jejunal biopsy to confirm diagnosis

Answer 120

A

gluten-free diet
replace any deficient fat-soluable vitamins

consider referral to dietician

bowel lymphoma is a long-term complication

Answer 121

A

GROWTH CHART
- weigh and measure accurately

MAY PRESENT WITH:

vomiting
disturbed bowel habit
unsatisfactory weight gain
crying

1) QUANTITY of food
- both under and over-feeding may lead to vomiting and crying
- bottle fed babies are often over fed
- CHECK how parents are making up the formula

2) KIND of food
- early mixed feeding may lead to vomiting, diarrhoea + crying
- introduce solids slowly and gradually

3) feeding TECHNIQUE
- watch how baby is bottle or breast fed, may be in wrong position, teet too small or large

REFER TO DIETITICIAN!

Answer 122

A

BABY:

bonding
best composition (consistent quality + quantity)
less collick and reflux
antibodies, reduce risk of infections
reduced risk of atopy + allergies
reduced risk of future obesity/DM/heart disease
better neurodevelopment (compared to formula-fed kids)

MOTHER:

bonding
sense of achievement
convenience
free
burns about 500 calories a day
reduces risk of breast cancer

Answer 123

A

Successful breast feeding

About 20-40mins of feeding
Feed fully from one breast before offering other
Don’t switch too must (get the watery foremilk first then calorific hindmilk later)
1) Whey = thirst quenching
2) Casein = calories/protein

But do switch from one to other between feeds or higher chance of mastitis

On demand
Cluster feeding

nb hard to overfeed a breast fed infant

Answer 124

A

Successful bottle feeding

Demand or by the clock
First 6 wks expect to feed every 3-4 hours (incl night feeding)

Standard infant formula
- Approx 150ml/kg/day to meet requirements for growth

Avoid over overfeeding (vomiting)

Babies stomach is size of an egg so can’t take big feeds

Answer 125

A

first steps nutrition

Answer 126

A

HIGH ENERGY (eg SMA high energy)

For use in faltering growth / increased energy requirements
Requirements met in lower volume
Not for use in IUGR

PRETERM FORMULA

For infants born <37 wks
Increased protein and micronutrients required by preterm infants
Not for faltering growth as not high energy formula

EXTENSIVELY HYDROLYSED (eg similac alimentum)

Extensively hydrolysed proteins for treatment of CMPA and gut disorders / malabsorption
Some contain lactose / MCT fats
Taste vs age

AMINO ACID (eg alfamino)

Broken down into amino acids
For severe allergy and gut disorders / malabsorption
MCT fat content

nb probs don’t need to know this much detail but just be aware

Answer 127

A

Ideally 6 months but definitely not before 4 months

Start with puree (slightly thicker than milk)
Needs to be quite a consistent texture
Baby rice, puree fruit and veg, baby porridge

Normal food by 1 year

FOODS TO AVOID BY:
- No honey
- No soft cheeses
- No whole nuts, but can chop it up then fine (just a choking risk)
- No added salt and sugar
(even after a year, avoid added salt and sugar)

Nb don’t avoid egg or peanuts!

Make meal times fun

Let them be messy, don’t constantly wipe hands etc
Be relaxed - or they’ll become fussy

Answer 128

A

periods of crying that last for more than 3 hours for more than 3 days a week

abdo pain
tends to be worse at night (norm between 6-10pm

usually occurs between 4-12 weeks
- resolves around 12-16wks

nb worse in bottle fed than breast fed babies

NO OTHER SYMPTOMS!

MANAGEMENT

reassurance
monitor growth (as long as this is fine, no need to worry)

lots of treatment but little evidence for anything

wind baby well
can try things: change bottle, colic drops, change formula

tends to be that parents find a ‘management’ thing that works for them then it works

Answer 129

A

Turn off TV: mealtime must be the focus and ideally family members all eat together with child in high or other safe chair and table

Answer 130

A

either make only one meal for all the family, or offer child a choice of two things and, if appropriate, allow child to help in preperation

Answer 131

A

If weight satisfactory, reassure parent that child won’t starve

don’t hurry child or force feed

present food for an agreed fixed period of time and then remove it

Answer 132

A

gives drink and snacks after, not before, meals

Answer 133

A

DIRECT

affects adults
“punches directly through the superficial inguinal ring”

INDIRECT

affects infants / children
due to patent PROCESSES VAGINALIS
“indirectly goes through deep and then superficial inguinal rings”
8x more common in boys
more likely to occur on RIGHT side (dt later descent of R testes)
but can be bilateral

PRETERM infants at greater risk

Answer 134

A

small or large swelling in groin or testicular sac

appears / increases in size when child cries
can be reduced when child is quiet

does NOT transilluminate
- a hydrocele would

UNDER 1 YEAR

operate within days
herniotomy

OVER 1 YEAR
- still operate but less urgency, can be done electively

nb paediatric hernias do not spontaneously resolve like adult ones do and have a high chance of complications

Answer 135

A

‘telescoping of the bowel’

invagination of one portion of the bowel, into the lumen of the immediately adjoining section
normally around illeocaoecal region

ages 6 - 36 months
- less common under 3 months or over 3 years

normally preceded by a viral infection or change in diet -> hypertrophy of Peyer’s patches
- or viral illness may be intercurrent

Answer 136

A

paroxysmal abdominal colic pain

during paroxysm the infant characteristically draws their knees up and turns pale
spasms occur about every 15 mins (become more frequent + severe)
child screams and is very anxious on examination
vomiting
passing of blood/mucus in stool (redcurrant jelly - only in 25%)

(may have abdominal distension)

sausage shaped mass in RUQ (not always palpable)

poor prognosis: signs of peritonitis (ie guarding, tense woody abdomen)
- means perforated

look for signs of DEHYDRATION!

eg high HR, long CRT, high RR
kids with intussusception are often dehydrated and hypovolaemic

Answer 137

A

USSS
- ‘target sign’

can do abdo X-ray for signs of obstruction

1st line = REDUCTION by AIR INSUFFLATION under radiological guidance (ie and air enema)

success of air enema is determined by speed at which done: if air enema is performed within 12 hours of start of symptoms then success in 90%
- diagnostic delay makes surgery more likely!

if reduction unsuccessful or signs of peritonitis, need surgery

GIVE FLUIDS

20ml/kg bolus if severely dehydrated
maintenance fluids if mildly dehydrated (20ml/kg/day first 10kg, 50ml/kg/day second 10kg, 100ml/kg/day after that)

also potentially NG tube too - ie drip + suck

Answer 138

A

PRE-HEPATIC
- normally haemolytic

HEPATIC
- eg in hepatitis (Hep A is common in children)

POST-HEPATIC
- norm obstructive (eg cholangitis)

COMMON IN CHILDREN:

haemolytic (norm genetic probs)
hepatitis (norm Hep A)
obstructive - eg gall stones (in older children)

also can get jaundice in severe epstein barr virus infection

Answer 139

A

abdo pain
colour and consistency of stools (incl blood)
urine colour (incl blood)
vomiting (also nausea)
fatigue
any rash or bruises (blanching or non)

(also do a full systems review)

OTHER HISTORY

any FHx of jaundice or any bleeding problems?
travel history (eg malaria, Hep A)

(also sexual hx if teenager - think help B/C)

Answer 140

A

FBC (anaemia)
U+E (kidney func + dehydration)
LFT
clotting
coombs test
peripheral blood smear

Answer 141

A

do it when someone is ill or jaundice and you suspect a haemolytic anaemia

to look for antibodies that are attached to red blood cells

eg in:

transfusion reaction
haemolytic disease of newborn (rh or ABO)
autoimmune haemolytic anaemia (incl SLE, mononucleosis etc)

if you have anaemia but a negative coombs test it means that the cause of your anaemia is something else (ie not due to antibodies against RBCs)

an indirect coombs test is of the plasma and looks for the antibodies (ie when not attached to RBCs)
- this is part of ‘group + save’ blood test, done to test if you will be able to receive blood (or if rh -ve mother etc)

Answer 142

A

inflammation of abdominal lymph nodes

children and teenagers

Answer 143

A

ABDO PAIN (esp in RIF)
- can be severe

caused by a viral illness, often have:

swollen lymph nodes in other areas
red throat or ears
fatigue / malaise
vomiting / diarrhoea
fever

often confused with appendicitis:

in mesenteric adenitis, often have a viral illness beforehand whereas appendicitis often comes out of nowhere
pain may also be more generalised in mesenteric adenitis

RED FLAGS

blood in stool
peritonitis (guarding, rebound tenderness)
haemodynamically unstable

nb 1 in 5 children who go for laprascopy for appendicitis actually have mesenteric adenitis

MANAGEMENT:

analgesia
reassurance and safety-netting

nb intussusception can occur following mesenteric adenitis so make sure to safety net well!

if not sure if appendicitis, do USS

Answer 144

A

projectile vomiting AFTER feeds (nb is initially non-projectile)
crying more than usual
always hungry
not opening bowels or seeing as much as usual
child stops gaining weight and then starts to loose weight

present at 2-7 WEEKS
(never from birth)

EXAM:

irritable
weight loss
dehydration (mucus membranes, CRT, HR, nappies, cool peripheries)
hard non-tender mobile mass in epigastric area (olive-shaped - rarely feel)
prominent peristaltic waves

common DDx = OVERFEEDING
- if child is growing normally (or gaining centiles) then more likely to be this!

RED FLAG = BILE-STAINED VOMIT

points to a different aetiology (pyloric stenosis never produces bile-stains)
always ask what vomit looks like!

nb more common in first born males and does seem to be some familial link

Answer 145

A

TEST FEED

can see peristaltic waves in epigastrium
then see projectile vomit

ALWAYS MEASURE GROWTH

height and weight
plot on chart

1) BLOOD GAS
2) U+Es
- hypokalaemia
- hypochloraemia
- alkalosis
(also dehydration)

USS
- large pylorus and narrowed canal

Answer 146

A

1) HYDRATION
- to correct electrolytes and dehydration!
- norm also give NG tube to stop vomiting

2) PYLORIC MYOTOMY
- only when electrolytes and alkalosis normalised!

Answer 147

A

spermatic cord becomes twisted, cutting off blood flow to the testes -> ischaemia + necrosis

most common in ages 10-30
- peak incidence 13-15 years

Answer 148

A

acute, severe unilateral testicular pain
abdominal pain
nausea + vomiting
‘walk like woody from toy story’
hurts to urinate

DDx

epidymo-orchitis
UTI
idiopathic scrotal oedema

nb urine dipstick cannot rule out torsion

always ask SEXUAL HISTORY!!! (may be an STI causing nepidydymo-orchitis)

Answer 149

A

“BELL-CLAPPER” deformity
- plus lots of erythema and scrotal swelling

cremesteric reflex is LOST
elevation of testis does NOT ease the pain (Prehn’s sign)

can do USS doppler to measure blood flow to testes
- but don’t delay surgery for this!!!

URGENT surgical exploration and fixation of BOTH testes! (even if only one affected
- need to do within 6 hours to salvage testes!

Answer 150

A

aka cryptorchidism

2-3% of term male infants
- much more common if preterm

25% are bilateral

COMPLICATIONS

infertility
torsion
testicular cancer
psychological

Answer 151

A

key DDx is retractile testes

very common and normal
an active cremaster muscle withdraws the testes into the inguinal canal or higher, esp if examined with cold hands

RED FLAGS
- testes cannot be palpated in inguinal canal
- bilateral undescended testes
REFER URGENTLY to senior paediatrician, may need imaging + urgent endocrine or genetic investigation

if no concerning features, REFER TO SURGEON at 3 months of age (many will have fully descended before then)
- ideally want to see a surgeon by 6 months and have surgery (OCRHIDOPEXY) at around a year old!

Answer 152

A

CONGENITAL ADRENAL HYPERPLASIA
- only in females (male genitalia is normal)

other causes:
- intersex
- maternal ingestion of androgen
(loads of rarer conditions too)

Answer 153

A

do NOT assign sex of baby if unsure!!
- causes distress if incorrectly assigned and may misdiagnose CAH

refer to:

paeds endocrinologist
genetics

INITIAL INVESTIGATIONS:

steroid hormone levels
karyotyping
USS

Answer 154

A

gene mutation (autosomal recessive) leading to a block in the production of hydrocortisone -> increased pituitary ACTH (to try and stimulate cortisol production) -> adrenal cortical hypertrophy -> increase in androgens (but still no/little hydrocortisone, though loads of androgenic cortisol precursors produced)

1) AMBIGUOUS GENITALIA (in girls)
- enlarged clitoris
- labia fusion
this is aka virilisation

2) 60-70% have a SALT-LOSING CRISIS
- norm 1-3 weeks of age
- vomiting and markedly dehydrated
- some are severely ill (fatal if untreated)

nb can also rarely present as precocious puberty in boys if no salt crisis occurs

nb there is a very rare subtype which can cause males to be intersex, but normally they have normal genetalia

think of a salt crisis like addisons crisis - not exactly the same but helpful to think about it

Answer 155

A

DDx for salt-loss crisis is neonatal sepsis!!
- look at temp and signs of infection!!

elevated level of cortisone precursors (17-hydroxyprogesterone)

if salt-loss crisis:
- LOW sodium
- HIGH potassium
ie do U+Es

MANAGEMENT:

lifelong hormone replacement therapy (increase dose when ill or stressed)
girls may require genital plastic surgery

Answer 156

A

chromosomal sex
gonadal sex
surgical aspects
psychosexual development / adult sexual function
fertility issues

NEED AN MDT DECISION WITH FMAILY INVOLVED

Answer 157

A

Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome
- nb you can have partial/mild androgen insensitivity syndrome (can present with male genetalia but then adolescent gynaecomastia or infertility later in life)

X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype
- is an abnormality in the androgen receptor

1) bilateral inguinal / labial swellings in a ‘female’ infant
2) primary amenorrhoea in adolescence (develop normal secondary sex characteristics though)

karyotype reveals 46XY chromosome with a female phenotype

MANAGEMENT:

counselling (raise child as female, will be infertile)
bilateral orchidectomy (increased risk of testicular cancer)
oestrogen therapy (if needed)

Answer 158

A

45 X

lymphedema in neonates (especially feet)
- other characteristics develop later

CARDIAC DEFECTS:

bicuspid aortic valve (15%)
coarctation of aorta (5-10%)
webbed neck
shield chest, widely spaced nipples
short stature
no secondary sex characteristics (are infertile!)

(nb also have high arch palate)

horseshoe kidney
recurrent otitis media
autoimmune conditions (esp autoimmune thyroiditis + crohns) - screen for these regularly!

nb breast development and periods can be induced using hormone therapy

most don’t grow above 1.5m (although GH therapy can sometimes increase height a bit)

nb have normal intelligence

Answer 159

A

47 XXY

often taller than average
lack of secondary sex characteristics (normally infertile)
small, firm testes
gynaecomastia (increased incidence of breast cancer)

nb normally slightly lower than average intelligence

Answer 160

A

TANNER STAGING

GIRLS:

Tanner stage 1 (ie pre-pubertal)
- No sign of pubertal development

Tanner stage 2-3

Breast enlargement (1st sign)
Pubic or axillary hair
Growth spurt

Tanner stage 4-5

Started periods (menarche)
Signs of pubertal development

BOYS

Tanner stage 1 (ie pre-pubertal)

High voice
No signs of pubertal development

Tanner stage 2-3

Testicular / penis enlargement (1st sign)
Deepening of voice
Early pubic / axillary hair

Tanner stage 4-5

Voice broken
Facial hair
Growth spurt
Adult size penis, pubic + axillary hair

Answer 161

A

onset of secondary sexual characteristics

before age 8 in girls
before age 9 in boys

In girls this is less concerning
- Is normally ‘true’ precocious puberty

In boys it is more concerning as more likely to be an underlying pathology
- also a lot more rare than in females

always consider + address psychological + behavioural effect of this!! - has big effect on child’s life

Answer 162

A

GONADOTROPHIN DEPENDENT (aka central or true)
= early activation of hypothalamic-pituatory-gonadal axis
= high FSH + LH
- normal sequence of pubertal development observed
- may be idiopathic + familial (esp in females)
- boys more likely to be due to intracranial tumours etc

GONADOTROPHIN INDEPENDENT (aka peripheral or false)
= excess of sex hormone (either endogenous or exogenous)
= low FSH + LH
- more likely to be abnormal sequence of pubertal development observed

Answer 163

A

do a full near exam to look for any focal signs

BLOODS

estradiol / testosterone
pituitary function test
TFTs
bone age (x-ray hand + wrist of non-dominant hand) - do to see if correct bone age for age of child, if not is more concerning
scan pelvis and adrenals
MRI head

Answer 164

A

TESTICULAR SIZE can provide a clue (in addition to FSH/LH levels)

bilateral enlargement
= gonadotrophin release from intracranial lesion

unilateral enlargement
= testicular tumour

small testes
= adrenal cause (tumour or congenital adrenal hyperplasia)

GIRLS
- norm idiopathic or familial

CAUSES FOR BOTH

intracranial tumours
hydrocephalus
encephalitis or meningitis

always look for near symptoms!

nb don’t worry about this too much - main points to remember is age of definition of precocious puberty and general causes for male and female - don’t need to know this much detail

Answer 165

A

thelarche (the first stage of breast development)

adrenarche (the first stage of pubic hair development)

nb isolated thelarche in girls is common and commonly resolves and then have normal puberty

nb gynaecomastia in adolescent boys is almost always physiological + self-limiting
- still embarrassing for the boy

Answer 166

A

lack of initiation and progress of pubertal development
- more than 2 standard deviations than average onset of puberty of the population

GIRLS:
- no signs of puberty, ie no breast development (ie still tanner stage 1) by age 13
OR
- no menarche by age 15

BOYS:
- no signs of puberty, ie no testicular enlargement (ie still tanner stage 1) by age 15

Answer 167

A

CENTRAL (low LH/FSH)

constitutional delay
chronic disease (eg CF)
poor nutrition
pituitary problem

PERIPHERAL (high LH/FSH)
- testicular / ovarian damage or underdevelopment

Most common cause is constitutional delay (esp in boys)
- This is more common if FHx of delayed puberty

ALWAYS ASK WHAT AGE PARENTS HAD MENARCHE ETC

exclude TURNERS in girls
- will also have short stature

Delayed puberty with short stature

Turner’s syndrome
Prader-Willi syndrome
Noonan’s syndrome

Delayed puberty with normal stature

polycystic ovarian syndrome
androgen insensitivity syndrome
Kallman’s syndrome
Klinefelter’s syndrome

Answer 168

A

BLOODS

FBC
U+Es
TFTs
coeliac screen
FSH/LH
testosterone / estradiol

KARYOTYPE (exclude turners/klinefelters)

Bone age (x-ray of hand + wrist of non-dominant hand)
- if constitutional delay then bone age will ALSO be delayed!

consider imaging: MRI, pelvic ultrasound

Answer 169

A

CONSTITUTIONAL DELAY

Long-standing short stature during childhood
Poor growth most noticeable 9-11yrs
Slow progression through puberty
Bone age delay
Exclude organic cause eg coeliac / thyroid screen

reassurance, moral support and patience
- also ensure good nutrition (and no developmental concerns)

can give exogenous sex steroid therapy to induce puberty

Answer 170

A

normally due to absence of thyroid gland (or a small or ectopic gland is present)

picked up in heel prick blood test (5-8 days)

puffy face, macroglossia
hypotonia
prolonged neonatal jaundice
delayed mental & physical milestones
short stature

if not picked up, can cause severe learning disability (as well as growth restriction)

lifelong thyroid hormone replacement!
- prolonged follow up as will need to adjust levels as child grows

Answer 171

A

Hashimoto’s autoimmune thyroiditis

more common in:

diabetes
down’s
turner’s

other causes:

post total-body irradiation (e.g. if previous treated for ALL)
iodine deficiency (most common cause in developing world)

nb pituitary causes of hypothyroidism are incredibly rare in children

nb children with downs are norm screened annually for hypothyroidism and coeliac disease (as both are harder to spot)

Answer 172

A

SHORT STATURE
= most common presenting symptom

drop in school performance
delayed puberty
constipation
dry skin

presents pretty similarly to in adults

ASK ABOUT PMHx and FHx of autoimmune conditions

Answer 173

A

TFTs

low T4 (thyroxine)
high TSH

antithyroid antibodies
- positive if autoimmune cause

Thyroid hormone replacement – lifelong
- Prognosis is good

Answer 174

A

use BMI percentile charts for children under 18

overweight = over 91st centile

obese = over 98th centile

nb a 1/3rd of children leaving primary school are overweight or obese

NUTRITIONAL OBESITY

family Hx
social / emotional difficulties
early puberty

Answer 175

A

Kids under 18 need 60mins of activity a day that makes them breathless

reduce sugar intake
- kids need fat but sugar is just empty calories

fizzy drinks have a lot of calories in which kids don’t realise

Use non-food items as a reward
Eg star charts to earn a trip to the park

most effective if get whole family on board
- also dietician if needed (most effective if see every wk or fortnight)

nb don’t cut out snacks, unlike adults, kids need snacks, but just make them healthy snacks

Answer 176

A

RED FLAG = obesity but with short stature
- most obese children are also tall

growth hormone deficiency
hypothyroidism
cushing’s syndrome
down’s syndrome
trader-willi syndrome

Answer 177

A

Slipped upper femoral epiphyses
Blount’s disease (developmental abnormality of the tibia = resulting in bowing of legs)
MSK pain
low-self esteem
bullying / problems at school
^ALWAYS ask how kids are getting on at school
asthma
sleep apnoea
idiopathic intracranial hypertension

INCREASE ADULTHOOD RISK OF:

diabetes
HTN
dyslipidaemia (+IHD)
PCOS

Answer 178

A

autosomal recessive mutation

deficiency of phenylalanine hydroxylase: this is the enzyme that converts phenylalanine to tyrosine

therefore get high levels of phenylalanine in the blood ->

intellectual disability
behavioural problems
seizures (typically infantile spasms)

many PKU children have fair hair and blue eyes
- also ‘musty’ odour to urine and sweat

have higher rates of eczema

Answer 179

A

GUTHRIE heel prick test
- at 5-9 days of life

if not picked up on heel prick test then usually presents by 6 months eg with developmental delay and/or seizures

(nb this is one reason why you should always ask about developmental delay if child has seizures)
- a DDx is West Syndrome

phenyl ketones in urine
phenylketonuria in blood

if detected early, child can develop normally and live normal life

MANAGEMENT:

Restriction on phenylalanine intake
Supplements of tyrosine

Especially important when mother with PKU is pregnant as child may be genetically normal but get brain damage from high phenylketonuria level in maternal blood going through placenta

Answer 180

A

familial (ie tall family)
early puberty
overweight/obese
klinefelter syndrome
marfan syndrome

Answer 181

A

PHYSIOLOGICAL

constitutional (COMMONEST)
delayed puberty (norm have a FHx)

MALNUTRITION (height is norm first feature of growth to be lost)

social + emotional deprivation
coeliac
IBD
chronic disease (eg kidney)
(also CF)

ENDOCRINE

deficiency of growth hormone
hypothyroidism

GENETIC

turners (look for in girls)
downs
skeletal dysplasias (eg achondroplasia)

IATROGENIC
- steroid use (eg in asthma)

also remember rare things like malignancy

Answer 182

A

birth hx (where they prem?)

FULL systems review

any anaemia (could be coeliac)
any bowel symptoms
any sign of cancer
DO FULL TOP TO TOE!
PMHx (any known comorbidities)
DHx (any steroids)
FHx (are parents short? any familial conditions?)
SHx (any deprivation, social services etc)
diet!!!!

if teenagers, ask about signs of puberty / menarche etc

Answer 183

A

plot growth and height on growth chart
calculate mid-parental height (MPH) and target centile range (TCR) based on that

BLOODS

FBC (anaemia)
TFTs
cortisol studies
GH stimulation test

BONE AGE
- x-ray of hand/wrist of non-dominant hand

Answer 184

A

height is below TCR (which is based on MPH)
reduced height velocity (drop of >2 centiles is bad)
obesity
other symptoms/signs (eg anaemia, GI symptoms etc)

Short & Fat = Pathological problem

Short & thin = chronic disease / malnutrition

Answer 185

A

steady growth below centiles (within TCR)
delayed onset of puberty
FHx of delay
delayed bone age
not obese

Answer 186

A

If boy:

(Mothers height + fathers height + 13) / 2

If girl:

(Mothers height + fathers height - 13) / 2

This tells you what the estimated adult height for child
- can calculate TCR (target centile range) from this

Answer 187

A

AGE 1-4

reflex anoxic seizures
breath-holding attacks
GOR, writhing or back-arching

AGE 4-8

self-gratification ‘fits’
benign paroxysmal vertigo of childhood
night terrors

AGE 9-16

syncope
migraine
habit spasms (tics)
behavioural disorders - psychosomatic
dissociative seizures

ANY AGE

day dreaming
hypoglycaemia

DON’T FORGET TO CHECK GLUCOSE!!

Answer 188

A

febrile seizure
meningitis
encephalitis

Answer 189

A

Brief episodes of asystole triggered by pain, fear or anxiety

Child becomes suddenly pake, limp, loses consciousness (ie syncope), followed by tonic clonic phase
Episodes usually resolves in 30-60secs, after which kids are tired

These are non-epileptic events

Can occur at any age, but most common between 6 months and 2 years of age

Diagnosis is usually based on the history, with a normal ECG

1) Once diagnosis has been made, parents should be reassured
2) If further attacks, put in recovery position

Good prognosis, majority grow out of it by age 5

Answer 190

A

common

occur in 1-2% of children up to age 5
normally resolves in 18 months (can be up to 4 years)

often precipitated by frustration or pain

after one lusty yell the child holds their breath, goes red in the face, and may later become cyanosed and briefly loose conciseness

they then start breathing again and is soon back to normal
- sometimes the cerebral hypoxia is sufficient to cause brief generalised twitching

careful history can normally differentiate this from epileptic seizure

BLUE SPELLS

most common
cry or scream -> breathe out forcefully -> breath hold + turn blue (esp around lips) -> floppy + LOC

PALE SPELLS:

less common
caused by a slow heart rate
open their mouth as if to cry but no sound comes out
faint and look very pale
brief period where their arms + legs become stiff or lose control of their bladder / bowel

Answer 191

A

RED FLAGS:

very frequent spells (more than once a day or several times a week) - may be normal but should still see a dr
lasts longer than a couple of minutes and child then confused/drowsy for several hours after
any head injury prior to attack
any neurodevelopment delay

MANAGEMENT

attacks are benign and self-limiting
- brain will trigger breath even without parent shaking child

1) reassure and explain to parents
2) should ignore attacks as much as possible, distraction at the right moment may help (as kids may then start doing it deliberately)

make sure parent does not scold or give child lots of attention after attack or they may start doing it on purpose

also DON’T put anything in mouth!!

Answer 192

A

young children
enjoy the feeling of tensing up or shaking
not doing it to get out of school etc

Answer 193

A

most frequent in boys age 8-11 years

repetitive
not rhythmical
involuntary
stereotypic (the same each time)
often head + neck

eg forceful blinks, neck twist

worse with stress

likely to improve with time
low-key supportive approach usually all that’s needed

Answer 194

A

nb pseudo seizures is the old term

now say non-epileptic or dissociative seizures! but this is less helpful
actually dissociative seizures are not someone “faking it” but is just not ‘epileptic’, they are not under conscious control

true ‘fake seizures’, ie what kids/teenagers sometimes do to get out of school

movements are random (in seizures, movements are rhythmic)
eyes closed shut (in seizures, eyes are rolled back or look to the left)
can distract them or give them saline and will improve

can also have pelvic thrusting

also less likely to bite tongue

MANAGEMENT

really careful social Hx, any problems at home, school, other behavioural problems etc
careful counselling with parents
get a seniors help to help explain to parents

Answer 195

A

a whole variety of fits that occur, often mimic epileptic seizures but are due to a psychological cause, eg a traumatic event in childhood (can sometimes be hard to identify the trigger)
- ie sort of like PTSD

commonly misdiagnosed as epilepsy!

often diagnosed when someone is treated for epilepsy with anti-epileptics and there is no change in their seizures!
- also have no changes on EEG during seizures

often begin in teens/young adults
more common in women
often have comrobid mental health conditions and/or hx of trauma, chronic disease, stressful life events etc

MANAGEMENT:

CBT, psychotherapy, counselling
manage stress
improve sleep hygiene

nb dissociative seizures can go on longer than epileptic seizures

only need to call an ambulance etc if someone hurts themselves while having a seizure

Answer 196

A

Differentiate between this and an absent seizure!

In daydreams they keep doing what they’re doing but just ‘zone out’ absence seizures stop all activity

Answer 197

A

SEIZURE:

any age
day or night
commonly occur during inactivity
brief prodrome (twitching, hallucinations, automatisms)
variable duration
tonic-clonic movement common
may be cyanosis
tongue biting (on side)
urinary incontinence common
drowsiness, confusion or headache afterwards for at least 30 mins
rarely partial paralysis

SYNCOPE

8-15 years most common
occur during day
occur while standing
long prodrome (dizziness, sweats, nausea)
duration under 5 mins
tonic -clonic movements are rare
often get pallor
tongue biting may occur on tip but not side
urinary incintinence is rare
quick full recovery
never paralysis

Answer 198

A

VASOVAGAL

common in teens, rare in children
standing, warm, no breakfast, fright, anxiety

CARDIAC

more worrying
commonest cause in children is long QT syndrome (always ask about FHx of this)

NEED AN ECG

Answer 199

A

SEIZURE
= Paroxysmal, excessive / hypersynchronus (usually self-limited) neuronal activity causing a change in the patient’s clinical state

EPILEPSY
= 2 or more unprovoked seizures at least 24 hours apart
- ie unrelated to fever or acute cerebral insult
- usually idiopathic but can be due to chronic cerebral insult or anatomical lesion

febrile seizures
infection (eg meningitis, sepsis)
trauma / injury
space occupying lesions
electrolyte abnormality (eg hypoglycaemia)
ingestion of drugs

nb also always consider seizure mimics (see other flashcards)

Answer 200

A

GENERALISED

tonic clonic
atonic
tonic
myoclonic
epileptiform spasms (ie infantile spasms)

NON-GENERALISED

focal aware (formerly known as partial)
focal impaired awareness (formerly known as complex partial)

Answer 201

A

BEFORE:
- unwell before (incl fever, other symptoms)
- taken any drugs (teens)
- what were you doing?
any collateral hx (eg did they turn pale)

DURING:

how long
any LOC?
what happened (get collateral to describe / film if possible)
colour change?
eyes rolling?
tongue biting
incontinence
any treatment given

AFTER:
- sleepy/confused/amnesic after? for how long?

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paeds level 2 conditions (pack 1) Flashcards

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