paeds level 2 conditions (pack 2) Flashcards

Question 1

Q

Primary headaches in children? 2 (which is most common)

Common secondary causes of headaches in children? 4

rare, but serious, secondary causes of headaches in children? (3 more acute in onset, 2 more insidious)

Answer

A

PRIMARY
- stress / tension
= migraine

migraine without aura is most common cause of primary headache in children
- aura is rare in children!

COMMON SECONDARY

eye strain
dental problems
sinusitis
analgesic headache (overuse: esp in teens)

nb headaches are rare in younger children!

RARE SECONDARY

ACUTE:
= meningitis (only get in older kids)
= trauma
- carbon monoxide posioning

INSIDIOUS

space occupying lesion
hypertension (esp overweight teenagers)

Question 2

Q

Features of a stress headache in children?

go through socrates

Answer

A

S = frontal, often bilateral

O

gradual
occurs during the day
not present on waking

C = pressing / tightening

R = no radiation

A = no associated symptoms

T = timing relates to stress (school etc)

E

not aggravated by routine physical activity
stress exacerbates

S

mild or moderate
may inhibit but does not prohibit activity

no nausea or vomiting

may have photophobia OR photophobia but not both

Question 3

Q

Features of a migraine without aura in children?

go through socrates

what is the diagnostic criteria in children?

Answer

A

nb 80% of children with migraines don’t have an aura (so 20% do! - so always ask!)

S

bilateral or unilateral
frontal

O = variable

C = pulsating

R = no radiation

A

nausea and/or vomiting
photophobia + photophobia (may be inferred from behaviour)

T = lasts 4-72 hours

E

aggravated by routine physical activity
may be brought on by chocolate, cheese, food additives etc

S
- moderate to severe intensity

DIAGNOSTIC CRITERIA:

A)
>= 5 attacks fulfilling features B to D

B)
Headache attack lasting 4-72 hours

C)
Headache has at least two of the following four features:
- bilateral or unilateral (frontal/temporal) location
- pulsating quality
- moderate to severe intensity
- aggravated by routine physical activity

D)
At least one of the following accompanies headache:
- nausea and/or vomiting
- photophobia AND phonophobia (may be inferred from behaviour)

nb also often have a positive FHx for migraines!

nb don’t bother learning exact diagnostic criteria! - just be aware

Question 4

Q

Paediatric migraine without aura:

acute management? 2
options for prophylaxis? 2

Answer

A

ACUTE MANAGEMENT

ibuprofen
nasal triptans (if over 12)

nb nasal triptans are poorly tolerated by children (dt taste in back of mouth) but oral triptans aren’t licensed under age 18

nb side effects of triptans:

tingling
heat
heaviness / pressure sensation

PROPHYLAXIS

migraine diary to identify triggers
no clear guidelines, use medications if severe
in practice PIZOTIFEN and PROPRANOLOL are often used first line

(2nd line: valproate, topiramate + amitryptiline)

Question 5

Q

RED FLAGS FOR HEADACHES IN CHILDREN:

features of headache? 5 (incl exacerbating features)
associated symptoms? 6
findings on exam? 4
PMHx? 3
what to consider doing if find these?

Answer

A

acute onset of severe pain
pain wakes child at night
pain present on waking or worse in early morning
pain worse on lying
pain worse on coughing, sneeze, exercise

ASSOCIATED SYMPTOMS

blurred vision
vomiting
fever (with worsening headache)
non-blanching rash
impaired consciousness
developmental regression or personality change

nb neck stiffness and photophobia may indicate meningitis but, in kids the former could just indicate a viral infection, and the latter a migraine

SIGNS:

HTN
papilloedema
increasing head circumference
focal neuro signs

PMHx

hx of head trauma (in last 3 months)
hx of seizures
bleeding disorder

consider head imaging if suggestive of raised ICP
- consider investigation (eg LP) + management of meningitis if suspect that

Question 6

Q

What should you always consider when a child presents with a head injury?

How do you rule this in/out?

other questions to ask about in head injury:

symptoms to ask about? 7
What PMHx to ask about? 1
what examinations to do? 3

Answer

A

whether it could be a non-accidental injury (NAI)

by taking a thorough history from child + parents and making sure the story and mechanism matches with the symptoms + signs found on exam
- also any signs of a delay in presentation may also make you suspicious (if any delay, ask why!)

mechanism of injury?
any LOC? (if witnessed, how long?)
any seizures? (if so, ask about epilepsy hx)
any amnesia? (how long)
abnormal drowsiness
vomiting? (how many
discrete episodes)
any blood or fluid from ears or nose?
ANY INJURIES TO ANYWHERE ELSE?

PMHx
- Any bleeding disorders

EXAMS

full neuro exam
opthalmascope to see funds (also check pupils)
examine whole head for bruising, size, fontanelle etc

Question 7

Q

When to perform a CT head scan on a child presenting with a head injury:

if have any of these risk factors, how fast should a CT scan be done?
mechanism of injury?
symptoms following the injury?
GCS score?
other findings on exam? (incl 2 just for age under 1 year)
which of these are indications for immediate CT on their own and which need 2 or more? if latter, how long do they need to be observed for?

Answer

A

perform CT scan within an hour (and provisionally report within an hour of scan being done)

MECHANISM
= suspicion of non-accidental injury (NAI)
- dangerous mechanism of injury (see definition below)

dangerous mechanism:

high-speed road traffic accident either as pedestrian, cyclist or vehicle occupant
fall from a height of greater than 3 metres
high-speed injury from a projectile or other object

SYMPTOMS
= post-traumatic seizure (with no PMHx of epilepsy)
- LOC lasting more than 5 mins (witnessed)
- abnormal drowsiness
- three or more discrete episodes of vomiting
- Amnesia (antegrade or retrograde) lasting more than 5 minutes (assessment of amnesia will not be possible in preverbal children and is unlikely to be possible in children aged under 5 years)

GCS
= GCS <14 on initial assessment in ED (or <15 for infants under 1)
= GCS <15 at 2 hours after the injury

OTHER FINDINGS ON EXAM

= suspected open or depressed skull fracture
= any signs of basal skull fracture (see other flashcard)

= tense fontanelle
= for children under 1, presence of bruise, swelling or laceration of >5cm on head

= focal neurological deficit

For risk factors with ‘=’, just need one to do an urgent CT, for risk factors with ‘-‘ need 2 or more, if only 1, observe in ED for 4 hours and if, during observation, you see:

GCS <15
further vomiting
further episode of abnormal drowsiness

then order urgent CT

nb don’t learn this totally off by heart (if in ED etc, google nice head injury guidelines) but good to be aware - and ask these questions in a Hx

Question 8

Q

What are the signs of a possible basal skull fracture? 5

Answer

A

blood from ears (haemotympanum)
CSF from ears
CSF from nose
‘panda’ eyes
battle’s sign (bruising behind ear)

Question 9

Q

HYDROCEPHALUS:

what are the two mechanisms / groups of causes? (give 3 causes of each)
what congenital condition are they more common in?

Answer

A

OBSTRUCTIVE
- aka non-communicating)
= dt a structural pathology blocking the flow of CSF, dilatation of the ventricular system is seen superior to site of obstruction

OBSTRUCTIVE CAUSES:

developmental abnormalities (eg aqueduct stenosis)
tumours
acute haemorrhage (eg SAH or intraventricular haemorrhage)

NON-OBSTRUCTIVE
- aka communicating
= due to an imbalance of CSF production and/or absorption
- either caused by an increased production of CSF or, more commonly, a failure of reabsorption at the arachnoid granulations

COMMUNICATING CAUSES
- meningitis
- post-haemorrhagic
- choroid plexus tumour (very rare)
^top 2 are reduced absorption, last one is increased production

MORE COMMON if have SPINAL BIFIDA (or other neural tube defects)

Question 10

Q

HYDROCEPAHLUS:

most common presenting complaint in infants?
other possible symptom in infant?
symptoms in older children? 2
what two examinations to do?
signs on examination? 6
simple bedside investigations to do? 2 (and findings with these)

Answer

A

most commonly = CONCERNS ABOUT INCREASING HEAD CIRCUMFERENCE
- also developmental delay

OLDER CHILDREN (ie after sutures fused)

headache
vomiting (and other symptoms of raised ICP)

EXAMS

full neuro exam
developmental assessment

FINDINGS

full anterior fontanelle (may also be large)
prominent scalp veins
downward turned eyes (sun setting sign)
hyperreflexia
spasticity
poor head control (also other developmental delay)

INVESTIGATIONS

measure (+ plot) head circumference (increasing rate of growth)
fundoscopy with opthlmascope (papilloedema)

Question 11

Q

HYDROCEPHALUS:

main DDx? how to differentiate?
first line imaging?
when to do an LP?

Answer

A

constitutionally big head

commonest cause of a big head is having parents with big heads (ask about parental head size!)
rate of head growth is important - if it’s following centile line then is fine

CT is first line
- although may need MRI later down the line

LUMBAR PUNCTURE

can be useful as samples CSF, measure opening pressure and relieve symptoms BUT can only use if non-obstructive/communicating cause
if obstructive then the difference in cranial and spinal pressures induced by CSF drainage may result in brain herniation!!

Question 12

Q

HYDROCEPHALUS:

management if acute and severe?
longer-term management?

Answer

A

An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside

A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum
- is tunnelled under skinned can be felt behind ear

In obstructive hydrocephalus, the treatment may involve surgically treating the obstructing pathology

Question 13

Q

NORMAL PRESSURE HYDROCEPHALUS:

what is it?
what age does it affect?
classic triad of symptoms
DDx? 2

Answer

A

Normal pressure hydrocephalus is a unique form of non-obstructive hydrocephalus characterised by large ventricles (ie on CT scan) but normal intracranial pressure

affects older individuals (gradual onset over age 40years)
- ie irrelevant to paeds but good to know!

SYMPTOMS:

1) dementia
2) disturbed gait
3) incontinence

DDx

Parkinson’s (dt gait changes)
alzheimers (dt cognitive dysfunction)

Question 14

Q

PLAGIOCEPHALY:

what is it?
what causes it?
red flags to ask about? 3

Answer

A

Very common asymmetry of the skull with normal head circumference
- parents may also complain that they only have head to one side

Flat area on the back or one side of the head – caused by remaining supine for too long: baby sleeping position – or neglect? Lack of interaction?

should be no associated symptoms
does not affect the brain, is cosmetic

RED FLAGS

any neuro symptoms
any developmental delay
any increase in rate of head circumference growth

Question 15

Q

PLAGIOCEPHALY:

how to explain to parents?
management? 3

Answer

A

REASSURE PARENTS

very normal
due to lying on back a lot
the asymmetry will become less with growth and does not cause problems (though management can speed up the changes)

MANAGEMENT

increase ‘tummy time’
alter position of sleeping + position of toys (children will turn to what’s interesting!)
alleviate pressure for head whilst in car seat

nb head-shaping helmets preserve head but have no medical benefit and are a pain! - other options are better and less invasive!

ask parents if child sleeps in same room as them, what side are they to the cot, babies will often favour this side, so switch it around a bit!

Question 16

Q

HAEMATURIA:

two broad types?
things which may mimic one of these types, but dipstick will be negative? 2

Answer

A

VISIBLE (aka macroscopic)
- ie can see with naked eye a dark urine

NON-VISIBLE (aka microscopic)
- urine looks normal but blood found on dipstick

if urine looks dark but no blood on dipstick think:

food (beetroot, rhubarb)
drugs (rifampicin, doxorubicin)

Question 17

Q

DDx of HAEMATURIA in children:

transient causes? 3
infection related? 2
autoimmune/inflammatory causes? 3
oncological causes? 1
genetic causes? 4
other causes? 4

Answer

A

TRANSIENT

rigorous exercise
fever
foreign bodies / trauma
menses (in girls)

INFECTION

UTI
Haemolytic ureic syndrome (HUS)

AUTOIMMUNE / INFLAM

IgA nephropathy (aka Berger disease)
Henoch-Schonlein purpura
post-infective glomerulonephritis
goodpasture syndrome (rare autoimmune attack of lung and kidney basement membranes)

ONCOLOGY
- Wilms tumour

GENETIC

Sickle cell trait
benign familial haematuria (aka thin-basement membrane nephropathy)
Alport syndrome
polycystic kidneys

OTHER

medications
coagulopathy (nb this could be genetic)
kidney / urinary stones (rare in kids, unless familial)
recurrent haematuria syndrome

Question 18

Q

BRIEF DESCRIPTION OF:

IgA nephropathy (aka Berger disease)
Henoch-Schonlein purpura
post-infective glomerulonephritis

including how to differentiate between them

Answer

A

IgA NEPHROPATHY
- aka Berger disease
- commonest cause of chronic glomerulonephritis
= visible painless, intermittent haematuria, followed by on-going non- visible haematuria
- visible develops 1-2 days after URTI (or UTI or gastroenteritis)
- proteinuria is rare
- renal failure seen in a minority (at this stage can see IgA complexes if do renal biopsy)
- no effective treatment, although immunosuppressives can help some

HENOCH-SCHONLEIN PURPURA

triad of: acute joint swelling, abdominal pain, purpuric rash
40% will also have renal involvement (from mild haematuria to AKI)
is an IgA-mediated vasculitis
HSP is self-limiting

POST-INFECTIVE GLOMERULONEPHRITIS

occurs 1-3 weeks after streptococcal throat infection (or skin infection)
often have proteinuria and low complement as well as haematuria (coca cola urine)
thus can get oedema, HTN and oliguria as well
creatinine is raised in 2/3rds of patients
treatment is supportive, 80-90% have complete recovery

Both IgA nephropathy and post-infective glomerulonephritis have haematuria and follow an URTI, but IgA is 1-3 days after, instead of 1-3 weeks

also post-infective often have proteinuria and low complement too
also IgA have repeatedly with alternating visible and non-visible

although both IgA nephropathy and HSP are about IgA antibodies, HSP is a vasculitis (so you get the main triad of rash, joints, abdo pain) whereas IgA is more chronic and only affects kidneys

Question 19

Q

benign familial haematuria (aka thin-basement membrane nephropathy)

short description?
incl how to diagnose

Answer

A

autosomal dominant
get microscopic haematuria due to an abnormally thin glomerular basement membrane
is benign

to make diagnosis

evidence of haematuria in 3 generation
with NO family history of renal failure, dialysis and/or transplantation

Question 20

Q

Alport syndrome:

how inherited?
triad of features?

Answer

A

X-linked disease which causes problems with collagen

1) glomerulonephritis
2) end-stage kidney disease
3) hearing loss

Hematuria is usually discovered in childhood in boys with Alport syndrome

Proteinuria develops later in childhood and 90% will reach end-stage renal failure by the age of 40

Hearing loss and ocular abnormalities become apparent by late childhood or early adolescence

Question 21

Q

Transient haematuria:

investigations to consider?
management (if sure no other cause)?

Answer

A

INVESTIGATION

urine culture
screening for bleeding disorders
USS

^nb these may not always be done!

if history is negative for anything else and haematuria can be explained by exertion, fever or intercurrent illness then send away and REPEAT DIPSTICK in a few weeks to see if gone

nb if proteinuria as well as haematuria then take this more seriously

Question 22

Q

HAEMOLYTIC URAEMIC SYNDROME (HUS)

age group normally in?
by far the most common cause?
what proceeded by?
triad of features?
symptoms that may present with? / to ask about? 4 (think about what symptoms that triad would give)

Answer

A

most common cause of AKI in children (followed by dehydration/sepsis)
- older infants + toddlers (ie under 5)

90% are secondary to toxin-producing e.coli 0157 infection (‘typical’)

nb can also rarely be secondary to pneumococcal infection, HIV, SLE, drugs and cancer

also can get primary HUS (‘atypical’) which is due to complement dysregulation

E COLI 0157
Initial symptoms typically include bloody diarrhoea (though not always bloody), fever, vomiting, and weakness. Kidney problems and low platelets then occur as the diarrhoea is improving.

1) haemolytic anaemia
2) thrombocytopenia
3) AKI

pale + fatigue
unexplained bleeding or bruising (eg purpuric rash)
reduction in urine output

nb unlike most other causes of haematuria - these kids are normally clinically really quite ill!!!
- way to differentiate from HSP!

Question 23

Q

HAEMOLYTIC URAEMIC SYNDROME (HUS)

investigations? (2 bedside, 2 bloods)
management options? 3
possible complications?

Answer

A

urine dipstick
stool culture
FBC (anaemia, thrombocytopenia, fragmented blood film)
U+Es (show AKI)

MANAGEMENT:
- mainly supportive (may need dialysis)
- plasma infusion + plasma exchange (if severe)
(- monoclonal antibodies if severe or CNS involvement)

80% recover completely

nb antibiotics not needed (even though caused by a bacteria initially but have no effect as symptoms are due to toxins which have already been produced)

POSSIBLE COMPLICATIONS

chronic renal failure
encephalopathy

Question 24

Q

Qs to ask child presenting with HAEMATURIA:

associated urinary symptoms?
other localised symptoms?
other systemic features?
general PMHx? 5
recent PMHx? 1
FHx? 4

Answer

A

ASSOCIATED SYMPTOMS:

what is urine like: smelly? visible blood? frothy?
pain on urination (UTI)
nocturia (UTI)
reduced urinary output (AKI dt HUS)
abdo pain (HSP, kidney stones, UTI, Wilms tumour)
diarrhoea (any blood? - HUS)
vomiting (UTI)
fever (UTI, HUS)
fatigue (HUS)
rash (HSP, HUS)
joint pain (HSP)

PMHx

ever had this before?
started periods yet??? (if girl)
sickle cell
coagulopathies
hearing problems (alport)
any recent infection? (URTI or GI) how long ago?
(IgA is 1-3 days after, post- strep 1-3 weeks)

FHx

haematuria or kidney problems (aport, thin basement membrane, polycystic kidneys, IgA nephropathy)
kidney stones
sickle cell
bleeding disorders

ANY CONSANGUINITY (a lot are recessive so more common if related)

also keep suspicion for NAI as may all be due to trauma

Question 25

Q

HAEMATURIA

exam to do?
what may find on exam? 8 (and what does each sign point towards)

Answer

A

vitals may find temp and/or HTN

ABDO EXAM

pale (HUS)
dry mucus membranes (dehydration secondary to HUS, UTI)
purpuric rash (HUS, around bum for HSP)
abdo tenderness (HSP)
abdominal mass (Wilms, polycystic, hydronephrosis secondary to stones)
ascites (post-strep)
joint swelling / tenderness (HSP)
legs for oedema (post-strep)

nb in all kids you must also check:

ear
nose
throat
listen heart
listen lungs

Question 26

Q

First line investigations for haematuria:

bedside? 3
bloods? 3
imaging to consider?

Answer

A

urine dipstick
urine culture
urine PCR
FBC (platelets in HUS, bleeding disorder)
U+Es (AKI)
CRP (infection)
(can also do albumin if any proteinuria)

USS is norm first line to pick up stones, polycystic, hydronephrosis, Wilms etc

can do CT or more fancy studies, even a renal biopsy

Question 27

Q

HAEMATURIA

red flags in history? 5
red flags on examination? 5
red flag on dipstick? 1

Answer

A

HISTORY

child is also unwell / dehydrated
urine is frothy and bloody
reduction in urine output
history of trauma to abdomen
positive FHx for any inherited conditions (except thin basement membrane)

EXAM

raised BP
pale
unwell with purpuric rash
palpable kidneys / abdominal mass
ascites / facial swelling / oedema (post-strep, nephrotic)

RED FLAG if proteinuria AND haematuria on dipstick

Question 28

Q

NEPHROTIC SYNDROME:

triad of features?
how normally present?
other possible features?
most common cause in children?
peak age of onset of this condition?

Answer

A

1) heavy proteinuria
2) hypo-albuminaemia
3) oedema

norm present with gradual onset of generalised oedema and slightly pale
- may also get discomfort from the oedema and SOB (if pleural effusion)

facial oedema and pallor
ascites
sacral + leg oedema
genital oedema
small volume of frothy urine

OTHER POSSIBLE FEATURES:

hyperlipidaemia
hypercoaguable (dt loss of antithrombin III)
predisposition to infection (dt loss of antibodies)

nb may have Hx of recurrent UTIs

MINIMAL CHANGE GLOMERULONEPHRITIS

80% of children under 5
if over 10 then more likely to be from a different underlying pathology

peak onset of minimal change disease is age 2-5 years

Question 29

Q

NEPHROTIC SYNDROME DDx?

Answer

A

post-strep glomerulonephritis (have hx of URTI a couple of weeks ago)
liver sclerosis
severe malnutrition (ie kwashiorkor)
cushings syndrome

(also maybe could be confused for obesity…)

Question 30

Q

NEPHROTIC SYNDROME:

bedside investigations? 2
bloods? 3
other investigation to consider?

Answer

A

urine dip (protein, not much/if any blood, hyaline casts)
urine protein
FBC
LFT (looking at the albumin)
U+Es (kidney function)
(may also find raised triglycerides)

can do renal biopsy to confirm
- this will be normal in minimal change disease (hence the name)

Question 31

Q

MINIMAL CHANGE DISEASE:

management?
prognosis?

Answer

A

high dose steroids (4-6 wks)
reduce fluid + salt intake
diuretics
prophylactic abx until proteinuria clears (as higher risk of infection)

most kids go into remission within 2 weeks of starting steroids
- a large proportion will relapse within the next year though

can be given further courses of steroids, but if relapses are common may need cyclophosphamide

relapses gradually reduce in frequency and severity as child ages
- most children grow out of condition by the time they’re adults

a few develop renal insufficiency (mainly those initially unresponsive to steroids)

Question 32

Q

differences between acute nephritic and nephrotic syndrome:

oedema?
blood pressure?
urine albumin?
urine RBC?
urine WBC?
cast morphology?
urine bacteria?
serum albumin?

Answer

A

ACUTE NEPHRITIC:

mild facial oedema
raised BP
albumin ++
RBC ++++
WBC ++
cellular / granular casts
0 bacteria
normal serum albumin

NEPHROTIC:

gross oedema
normal BP
albumin ++++
RBC 0 or +
WBC 0
hyaline casts
0 bacteria
low serum albumin

Question 33

Q

IMPETIGO:

causative organisms? 2
describe the rash (incl typical location)
what increases risk of getting it?
how spread?

Answer

A

staph aureus
prep progenies (ie group A strep)

Thin-roofed vesicles surrounded by narrow margin of erythema. The vesicles rupture to release thin cloudy yellow fluid. Dries to form thick ‘golden’ crusts.

typically found on face (esp around nose + mouth)
- can be on flexures + limbs not covered by clothing too

bacteria get in through a break in the skin, so anything that causes this:

eczema
insect bites
scabies
spots
herpes simplex

Spread is by direct contact with discharges from the scabs of an infected person. The bacteria invade skin through minor abrasions and then spread to other sites by scratching. Infection is spread mainly by the hands, but indirect spread via toys, clothing, equipment and the environment may occur. The incubation period is between 4 to 10 days.

Question 34

Q

IMPETIGO:

management if localised? 1
management if extensive lesions? 1
management advice for parents? 4
exclusion from school required? 1

Answer

A

if localised:
- topical fusidic acid cream

if extensive:
- oral fluclox

nb don’t give both oral and topical abx together

wash affected areas with soap + water
wash hands regularly, esp after touching the impetigo
avoid scratching
avoid sharing towels, face cloths, thoroughly clean potentially contaminated toys + play equipment

exclude from school until all lesions crusted and healing or 48 hours after start abx

reassure parents that impetigo usually heals completely without scarring

Question 35

Q

DDx for ‘nappy rash’:

caused / worsened by the diaper? 3
independent of the diaper? 3

Which is most common?

how to tell difference between them (ie briefly describe rash + distribution of each)

Answer

A

CAUSED / WORSENED BY DIAPER

IRRITANT CONTACT DERMATITIS
- inguinal creases are spared
= most common

CANDIDA

involves inguinal creases
discrete satellite pustules + papules
scaling along margins

IMPETIGO

superficial pustule which ruptures to form honey-crusted lesion
(if neonatal this could be mistaken for HSV)

NOT CAUSED BY DIAPER

SEBORRHAEIC DERMATITIS

caused by sebaceous gland dysfunction
salmon-pink patches with greasy scale
also on face, scalp, axilla, neck, posterior ear
involves creases!
no satellite lesions or pustules
treat with mild steroids
can be confused with psoriasis

PSORIASIS

less common
erythematous scaly rash
also present elsewhere on body

ATOPIC ECZEMA
- other areas will also be affected

Question 36

Q

QUESTIONS TO ASK IN HX OF ‘NAPPY RASH’:

HPC? (use operates)
key Qs in FHx? 2
other key aspect that important to ask in Hx?

nb also obvs do full paeds Hx incl DHx, PMHx, BINDS etc

Answer

A

O - onset (any changes: food, diapers, environment, recent illness)

P - progression

E - exacerbating
- HOW OFTEN CHANGE DIAPER?

R - relieving (what already tried?)

A

fever?
unwell in themselves?
pain
bleeding
discharge
size
any other affected areas of the body?

T
E
S

FHx

autoimmune disorders
skin conditions (eg eczema, psoriasis)

REVIEW OF SYSTEMS
- do head to toe!

Question 37

Q

EXAMINATION OF NAPPY RASH:

what should you do for EVERY paeds exam?
what to look for under nappy? 2
what other body parts to check? 4

Answer

A

measure + plot:

weight
height
head circum

perineum

creases / inguinal folds
perianal and buttocks

ALSO CHECK

skin over WHOLE body
scalp
nails
mucous membranes

Question 38

Q

IRRITANT CONTACT DERMATITIS (type of ‘nappy rash’)

what causes it / makes it worse?
classical distribution of rash?
management? 4
safety net? 1

Answer

A

soiled diapers (long periods between changing)
scented / harsh soaps
other chemicals / detergents

is where the nappy touches the skin
- spares inguinal creases

MANAGEMENT:

frequent diaper changes (even if doesn’t feel full)
use water-soaked cloth and dabbing instead of wiping with wipes
when dry use thick barrier creams: zinc oxide based, glacial based, petroleum jelly)
use more absorbent diapers (overnight ones are better, cloth diapers are worse)

SAFETY NET:
- come back if not improving after a couple of weeks or getting worse

nb can use a mild steroid cream if not getting better

nb nappy rashes don’t mean poor care, some babies just have more sensitive skin
- but chronic or grossly ulcerated rashes may raise suspicions of bad care!

Question 39

Q

CANDIDA DERMATITIS (type of ‘nappy rash’):

describe rash (incl distribution)
management? 2

Answer

A

Typically an erythematous rash which INVOLVE the flexures and has characteristic satellite lesions

discrete satellite pustules + papules
scaling along margins

MANAGEMENT

topical imidazole
cease use of barrier cream until candida has settled

Question 40

Q

STEVENS JOHNSON SYNDROME:

what normally triggered by? 2
describe the presentation (incl systemic signs and appearance and distribution of the rash)
common DDx? how to differentiate it?
severe form of it called?

Answer

A

normally triggered by:

reaction to medication (anticonvulsants, NSAIDs,
infection (esp if have HIV)

Begins with flu-like symptoms
- Followed by painful RED or PURPLE rash that spreads + BLISTERS

Fever >38C, headache, photophobia, aching joints
Starts as target lesions – dark central blister - before increasing in size + spreading
Affected skin eventually dies and peels off- Blistering mucosae: conjunctival, oral, genital

ie child is systemically unwell with blistering rash all over body with blistering mucosal membranes
- nb rash is norm not itchy but is very painful!

differentiate from erythema multiforme (similar but DOESN’T affect mucous membranes)

severe form = TOXIC EPIDERMAL NECROLYSIS (TEN)

high mortality
large loss of epidermis

Question 41

Q

STEVENS JOHNSON SYNDROME:

possible investigation? 1
supportive management? 3
medical management options? 5

Answer

A

norm just done on hx + exam but can also do skin biopsy

cool, moist compresses on skin +/or sterile dressings
replacement fluids (often get dehydrated)
anaesthetic mouthwashes (make swallowing easier)
strong painkillers
emollients
topical steroids
abx (if secondary infection suspected)
eye drops (for eye symptoms)

if severe: systemic steroids or immunoglobulin

Question 42

Q

Developmental dysplasia of the hip:

risk factors? 4 (what should these babies get)
clinical tests used for screening? 2 (describe them)
investigation if suspicion of DDH?
investigation if suspicion of DDH over 4 months?

Answer

A

RISK FACTORS

breech (after 36 wks)
positive FHx
multiple pregnancy
neuromuscular or joint problems (eg spina bifida, talipes)

^ GET USS AT 6 WKS

(nb girls get 6x more frequently than boys)
- also high birth weight and oligohydramnios

–> Barlow’s Test – push back, to see if hip pops out – attempt to dislocate the hip
–> Ortolani’s Test – push legs out to see if hips clunk into place. – reduction of dislocated hip

also look for asymmetry of skin creases on thigh / buttocks

nb these tests aren’t very sensitive or specific, so have a high index of suspicion

USS hips

do X-ray of hip if over 4 months old

Question 43

Q

Developmental dysplasia of the hip (DDH):

management if picked up early?
how can older children present if not picked up early? 3
management in older children?
potential longer term complication if picked up late?

Answer

A

splinting and pavlik harness (dynamic flexion-abduction orthosis) for 3 months

Delay in walking
Waddling gait
Shortened affected leg

older children may require surgery
- and at risk from early osteoarthritis

Question 44

Q

DDx of a limp:

under 3 years? 2
3-10 years? 4
10-18 years? 3
any age? 4
rarer groups of causes? 4

Answer

A

UNDER 3 YEARS

DDH
septic arthritis

3-10 YEARS

transient synovitis
septic arthritis
JIA
perthes disease

10-18 YEARS

slipped upper femoral epiphysis (SUFE)
osgood-schlatter disease
JIA

ANY AGE

fracture or soft tissue injury (?NAI esp if under 3)
osteomyelitis (nb may not show on x-ray initially)
malignancy (sarcoma, lymphoma, leukaemia)
Reactice arthritis (mumps, rubella, imms)

RARER CAUSES:

HAEM conditions (eg sickle cell)
METABOLIC (rickets)
NEUROMUSCULAR diseases (cerebral palsy, spina bifida, muscular dystrophy)
OTHER (HSP, rheumatic fever)

Question 45

Q

Common knee problems in children + young adults?

briefly describe features / classical presentation of each

what must you always examine if have knee pain?

Answer

A

CHONDROMALACIA PATELLAE:

Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy

OSGOOD-SCHLATTER DISEASE
(tibial apophysitis)
- Seen in sporty teenagers
- Pain, tenderness and swelling over the tibial tubercle

OSTEOCHONDRITIS DISSECANS

Pain after exercise
Intermittent swelling and locking

PATELLAR SUBLUXATION

Medial knee pain due to lateral subluxation of the patella
Knee may give way

PATELLAR TENDONITIS - More common in athletic teenage boys

Chronic anterior knee pain that worsens after running
Tender below the patella on examination

Referred pain may come from hip problems such as SUFE
- always examine joint above and below!

Question 46

Q

Hx of a child with limp:

features of HPC? (operates - incl 2 Qs about what may have proceeded in onset)
associated symptoms? (3 local, 7 systemic)

(see other flashcard for rest of hx Qs)

Answer

A

O

when came on / duration (also sudden or gradual onset)
any trauma?
preceding viral illness?

P
- getting worse?

E

worse in morning? (morning stiffness)
can they weight bear?

R
- tried anything to make it better?

A

joint pain
joint swelling / redness / heat
muscle weakness

AW FS FIN

appetite
weight loss
fatigue
sleep - waking up at night?
fever
itch / rash
night sweats

if joint pain, do socrates of the pain!!

T / E
- there all the time? is more worrying

S
- impact on life

Question 47

Q

Hx of child presenting with limp:

PMHx? 2
BINDS (what specifically to look for risk factors for)
FHx? 3
SHx? 4

nb did HPC in prev flashcard

Answer

A

PMHx

ever had before?
any autoimmune conditions?

BIRTH HX

risk factors for DDH (breech, FHx of DDH, multiple pregnancy)
any ischaemic damage (cerebral palsy)

IMMS - up to date

NUTRITION (rickets)

DEVELOPMENT

any delays in walking? (DDH, muscular dystrophy)
any other delays?

SOCIAL SERVICES Hx

previous injuries
child protection concerns

FHx

autoimmune conditions
joint problems
DDH

SHx - ASD OHA DOT

diet (ricketts)
exercise (osgood-schlatter)
who live with
how interfering with life

Question 48

Q

EXAMINATION OF CHILD WITH A LIMP:

what initial exams to do? 2
other things to examine / look for on exam? 5

Answer

A

EXAM OF AFFECTED JOINT

swelling, erythema, tenderness
range of motion

pGALS

knee pain can be referred from the spine
sacro-iliac joints and spine in joint assessment - look for pain on flexion and/or midline tenderness which may be present in discitis
Hip ABDUCTION and INTERNAL ROTATION are often the most restricted movements in hip pathology

nb also get them to run - it may exagerrate a limp!

GENERAL INSPECTION
- septic / temp

BRIEF NEURO EXAM
- look for ataxia, weakness

FEEL FOR LYMPHADENOPATHY

viral infection
haem / onc cause

FEEL FOR ORGANOMEGALY

LOOK AT SKIN
- extensive bruising or bruising in unusual place may indicate: NAI, haem

Question 49

Q

RED FLAGS FOR CHILD WITH LIMP:

age of child?
history? 7
exam? 5

what could each indicate?

Answer

A

AGE UNDER 3 YEARS
- septic arthritis more common in this age

Pain waking the child at NIGHT
- ?malignancy.

? malignancy, infection, inflamm

anorexia / appetite loss
weight loss
fatigue
sleep (waking at night)
fever
night sweats

Limp and stiffness WORSE in the MORNING
- ?inflammatory joint disease.

SYSTEMICALLY UNWELL
- ?infection

SEVERE PAIN, anxiety, and agitation after a traumatic injury (also reduced peripheral pulses or muscle weakness
- ? evolving compartment syndrome

Signs of REDNESS, SWELLING, or stiffness of the joint or limb
- ?infection or inflammatory joint disease

Unexplained rash or BRUISING
- ?haematological or inflammatory joint disease, or NAI

HEPATOSPLENOMEGALY
- ?oncology

Question 50

Q

TRANSIENT SYNOVITIS:

what is it?
age group most common in?
normal cause?
describe presentation
DDx to rule out? how?

Answer

A

aka irritable hip

most common cause of hip pain in 3-10 year olds
- is a diagnosis of exclusion

cause

1/3 preceding viral illness
1/3 preceding trauma
1/3 no cause found
limp (can have difficulty weight bearing)
single joint pain (rarely bilateral)
no pain on passive movement
NO systemic symptoms

eg if hip: pain on movement, pain in groin

main DDx is septic arthritis
- this also has systemic signs (eg fever, high HR etc)

Question 51

Q

TRANSIENT SYNOVITIS:

imaging to consider? 2 findings?
bloods? 2
other investigation to consider?
management? 3
safety net? 2
who should you always admit with suspected transient synovitis?

Answer

A

USS
- may show joint effusion

X-RAY
- normal

can do joint aspiration to rule out septic arthritis

bloods
- FBC
- CRP
both should be normal (if abnormal, may be septic arthritis)

MANAGEMENT

nsaids
rest
bring back for follow up in a couple of days

SAFETY NET

come back if fever
come back if symptoms worsen

always admit if UNDER 3 YEARS

transient synovitis rare in this age group
much more likely to be septic arthritis or trauma from NAI!

Question 52

Q

JUVENILE IDIOPATHIC ARTHRITIS:

diagnostic definition? (ie length of time, age etc)
just LIST the 5 subtypes! (describe in a later flashcard)
bloods to do? 5

Answer

A

arthritis (pain, swelling, red, hot, reduced range of motion) lasting at least 3 MONTHS in children UNDER 16

after exclusion of other primary diseases
also get MORNING STIFFNESS

1) oligoarthritis / pauciarticular
2) polyarticular
3) systemic (still’s)
4) psoriatic
5) enthesitis-related

FBC
CRP
ESR
RF
ANA

nb do more extensive bloods if have systemic signs (eg may do blood culture if infection is on Ddx)

Question 53

Q

JUVENILE IDIOPATHIC ARTHRITIS:
- describe features of the five subtypes? (3 main ones and 2 much less common)

^ incl how to deferential between them, blood results etc

what other part of body may be affected in some subtypes?

Answer

A

1) OLIGOARTHRITIS / PAUCIARTICULAR
- most common
- affects young children
- 1-4 joints affected initially (though may increase)
- knees, ankles, elbows
- muscle wasting
- risk of UVEITIS (30%), norm asymptomatic

2) POLYARTICULAR
- affects all ages
- 5 or more joints affected
- norm a mix of large + small joints
- norm RF negative but can be RF positive (like adult RA - so is treated as such)
- ANA and ESR may be positive
- risk of UVEITIS (30%), norm asymptomatic

3) SYSTEMIC (STILL’S)
- unwell
- swinging, high fever
- lymphadenopathy
- hepatosplenomegaly
- erythematous (salmon pink) rash
- arthritis may be absent at presentation in 30% of pts
- high CRP
- ANA + RF negative

4) PSORIATIC
- associated with psoriasis but arthritis and rash may not be present at the same time (arthritis may come first)
- norm also have nail changes (pitting), dactylitis
- often have FHx of psoriasis
- risk of UVEITIS (20%), norm asymptomatic

5) ENTHESITIS-RELATED
- enthesitis is pain at tendon insertion into bone
- more common in boys and over 10 years
- typically lower extremities (hips, midget, toes)
- may have FHx of ankolysing spondylitis and/or psoriasis (HLA B27 type)
- in contrast to others, are more likely to have acute, SYMPTOMATIC (pain, red, photophobia) uveitis or iritis

nb 5-10% have ‘undifferentiated JIA’ - ie don’t fit neatly into any one subtype

Question 54

Q

Ddx for systemic JIA (Still’s disease)? 4

Answer

A

infection
malignancy
kawasaki (look like have lipstick on)
SLE (v rare before adolescence)

so if a child presents with systemic, do a more thorough work up!

Question 55

Q

DIFFERENTIATING BETWEEN TYPE OF JIA:

Qs in Hx? 2
findings on exam? 8

Answer

A

any FHx of psoriasis
any FHx of ankylosing spondylitis (enthesitis)

EXAM

rash (systemic or psoriatic)
nail pitting (psoriatic)
systemically unwell / fevers (systemic)
lymphadenopathy (systemic)
hepatosplenomegaly (systemic)
muscle wasting (oligo)
which joints?
how many joints (1-4 is oligo)

Question 56

Q

MANAGEMENT OPTIONS FOR JIA:

for all? 1
oligo / pauciarticular? 2
polyarticular? 2
systemic? 3
psoriatic? 3
enthethesis-related? 4

also incl prognosis

Answer

A

ALL (well most) need to be seen by ophthalmologist with regular check ups for asymptomatic UVEITIS (which can lead to blindness)

1) OLIGOARTHRITIS / PAUCIARTICULAR
- best prognosis for remission
- NSAIDs
- steroid joint injections
(nb methotrexate + biologics often not necessary)

2) POLYARTICULAR
- methotrexate (more aggressive if RF +ve)
- biologics (more likely to need if RF +ve)

3) SYSTEMIC (STILL’S)
- NSAIDs
- steroids (for systemic symptoms)
- newer biologics
- 50% recover completely, 50% develop significant poly arthritis after systemic features have gone (is often resistant to methotrexate, so use newer biologics)

4) PSORIATIC
- NSAIDs
- methotrexate (may also help skin rash)
- biologics (if severe)

5) ENTHESITIS-RELATED
- NSAIDs
- methotrexate
- sulfasalazine
- biologics

nb do NOT need to know this level of detail (I just found it interesting and got carried away!)
- don’t forget the risk of uveitis though!!!

PROGNOSIS OVERALL

depends on subtype
generally 50% may full recovery and ‘grow out of’ condition, while 50% have progressive and crippling disease

Question 57

Q

‘GROWING PAINS’

technical name?
what age normally affect?
describe them
DDX? 2
red flags to ask about? 6

Answer

A

benign nocturnal limb pains of childhood

very common

age 3-5 years
age 8-12 years

intermittent crampy pain in calves, thighs or shin in evening or at night

DDX
- JIA
- cancer
(also osteoid osteoma - a rare benign tumour)

RED FLAGS

pain is always in exactly the same place (think malignancy)
pain during the day
swelling
weight loss
fever
night sweats

may do bloods and x-ray if unsure of diagnosis (but norm can be diagnosed from hx and exam)

Question 58

Q

MALNUTRITION:

- main four groups of causes in the UK?

Answer

A

neglect
diets low in protein, energy or specific nutrients (eg strict vegan/vegetarien or fussy eater)
eating disorders
diseases causing malnutrition (GORD, chronic infection, crohns/coeliac)

Question 59

Q

name of condition caused by energy (calorie) AND protein deficiency?

name of condition caused by JUST protein deficiency?

describe the characteristics of each

Answer

A

MARASMUS

= calorie AND protein deficiency

basically just very skinny
in UK, main cause is severe neglect (caused by famine, war etc elsewhere in world)
even if managed, high chance of permanent intellectual handicap
high chance of intercurrent infection
height is relatively preserved
wasted appearance
muscle atrophy
listlessness
diarrhoea
constipation

KWASHIORKOR:
= protein deficiency

normally occurs when a child stops breastfeeding and then has a high carb, low protein diet
rare in UK
growth retardation
diarrhoea
apathy
anorexia
oedema
skin / hair pigmentation
abdominal distension with fatty liver
norm + microcytic anaemia

Question 60

Q

SUSPECTED MALNUTRITION:

initial investigation to do before anything else?
what to extensively question parent / child about in hx? 3
what three aspects of social Hx are really important?

Answer

A

PLOT SERIAL WEIGHT + HEIGHT MEASUREMENTS

falling across 2 centiles or below 3rd centile may indicate malnutrition
can also work out expected weight for height

MAIN Qs

diet (how much? what?)
any GI symptoms (also do a full systems review)
any FHx of coeliac, crowns etc

nb can do a 7 day food diary

Social Hx

home situation (any problems with money, buying food, knowing what food is nutritious etc)
any problems at school (bullying, screen for mental health problems etc, esp if teen)
any involvement from social services?

Question 61

Q

SUSPECTED MALNUTRITION:

possible bloods? 5
management options if severely malnourished? 5
what management to always consider?

Answer

A

obvs after plotting weight and height!

FBC
U+E
LFT
other micronutrients
coeliac screen

MANAGEMENT

1) correct dehydration + electrolyte imbalance
2) treat any infection / parasite
3) treat concurrent / causative disease (eg coeliac)
4) treat specific nutritional deficiency
5) reintroduce oral feeding, really slowly (avoid re-freeding syndrome)

CONSIDER INVOLVING SOCIAL SERVICES

nb see elsewhere how to manage eating disorders and fussy eaters

Question 62

Q

OSTEOMALACIA

what called if in kids?
what is commonest cause?
who is at greatest risk from this cause? w
other rarer causes? 3

Answer

A

RICKETS
- if before end of bone growth

OSTEOMALACIA
- if after epiphysis fusion

dietary fit D deficiency and lack of sunlight

commonest in asian children dt skin colour and lack of calcium in traditional diets
also exclusively breast fed babies older than 6 months (need vit A, C + D supplements after this!)

rare causes

renal disease
drug induced (eg anticonvulsants)
liver disease (eg cirrhosis)

Question 63

Q

Presentation / features of:

rickets? 4
osteomalacia? 4

Answer

A

RICKETS
- thickening of metaphases at wrists, ankles + costchondral junctions
- bow-legged in toddler, older children get knocked knees
- hypotonia
(may produce acutely with hypocalcaemic fits)

OSTEOMALACIA

bone pain
fractures
muscle tenderness
proximal myopathy

Question 64

Q

RICKETS / OSTEOMALACIA:

blood tests? 4 (incl findings)
imaging? 1
management? 1

Answer

A

U+E (30% have low calcium + phosphate, also see if kidney cause)
LFT (90-100% have raised ALP)
vitamin D (low, by definition)
parathyroid hormone

X-RAY
- widened metaphases in distal radius / ulna
(- translucent bands in adults)

MANAGEMENT

high dose vitamin D and calcium supplements
also parental advice on diet + sunlight exposure

Answer 65

A

APPROPRIATE SITUATION

1) Has features of genetic disorder e.g. ?Down’s syndrome
2) Asymptomatic, but at risk of genetic condition for which there are therapeutic measures
3) Child at risk of genetic condition with paediatric onset

INAPPROPRIATE MEASURES

1) At risk of genetic condition with adult onset, for which prevention/ treatment not available e.g. Huntington’s
2) Testing carrier status
3) Genetic testing for benefit of another family member (unless testing necessary to prevent significant harm to family member)

Answer 66

A

families are often helped by having a diagnosis
prognosis
early intervention during or before worst of disease (eg cardiac surgery)
genetic counselling

dysmorphic features is often first sign

be vigilant
compare child’s features to parent’s

Answer 67

A

recurrence risk in a family
carrier detection in healthy parents, siblings and extended family
paternity
predictive testing of children who may be asymptomatic
reproductive choices, incl foetal intervention

Answer 68

A

square = male
circle = female
diamond = unknown gender
triangle = foetus

fully coloured in = person is affected by condition

partially coloured in = person is carrier (or heterozygous)

line through shape = person is deceased

two lines connecting parents = cosanguinity

Answer 69

A

lots of members of same generation
- esp if parents are consanguineous!

“remember that a lot of metabolic conditions in Bradford, where there are higher rates of consanguinity”

if both parents are carriers:

25% have disease
50% carrier
25% healthy

most recessive conditions are METABOLIC!

The following conditions are autosomal recessive:

Albinism
Ataxic telangiectasia (nb this is exception, this is structural)
Congenital adrenal hyperplasia
Cystic fibrosis
Cystinuria
Familial Mediterranean Fever
Fanconi anaemia
Friedreich's ataxia (nb this is exception, is structural)
Gilbert's syndrome (may be dominant)
Glycogen storage disease
Haemochromatosis
Homocystinuria
Lipid storage disease: Tay-Sach's, Gaucher, Niemann-Pick
Mucopolysaccharidoses: Hurler's
PKU
Sickle cell anaemia
Thalassaemias
Wilson's disease

nb don’t need to know all these conditions, just remember that recessive tend to be metabolic and dominant tend to be structural! (and know inheritance chances)

Answer 70

A

tend to manifest in multiple generations

if one parent has:

50% will have disease
50% will be unaffected

(remember no such thing as a carrier in dominant disease)

if both parents have:

25% will be homozygous (norm die)
50% will have disease (heterozygous)
25% will be unaffected

most dominant conditions are STRUCTURAL

The following conditions are autosomal dominant:

Achondroplasia
Acute intermittent porphyria
Adult polycystic disease
Antithrombin III deficiency
Ehlers-Danlos syndrome
Familial adenomatous polyposis
Hereditary haemorrhagic telangiectasia
Hereditary spherocytosis
Hereditary non-polyposis colorectal carcinoma
Huntington's disease
Hyperlipidaemia type II (nb is an exception, is metabolic)
Hypokalaemic periodic paralysis (nb is an exception, is metabolic)
Malignant hyperthermia
Marfan's syndromes
Myotonic dystrophy
Neurofibromatosis
Noonan syndrome
Osteogenesis imperfecta
Peutz-Jeghers syndrome
Retinoblastoma
Romano-Ward syndrome
tuberous sclerosis
Von Hippel-Lindau syndrome
Von Willebrand's disease (rare, severe form is recessive)

nb don’t need to know all these conditions, just remember that recessive tend to be metabolic and dominant tend to be structural! (and know inheritance chances)

Answer 71

A

if mother is carrier

50% of females will be carrier
50% of sons will be affected

if father is affected

50% of females will be carrier
0% of sons will be affected

NON MALE TO MALE TRANSMISSION OCCURS!

The following conditions are inherited in a X-linked recessive fashion:

Androgen insensitivity syndrome 
Becker muscular dystrophy
Colour blindness
Duchenne muscular dystrophy
Fabry's disease
G6PD deficiency
Haemophilia A,B
Hunter's disease
Lesch-Nyhan syndrome
Nephrogenic diabetes insipidus
Ocular albinism
Retinitis pigmentosa
Wiskott-Aldrich syndrome

nb don’t need to know all these conditions, just know inheritance chances

The following conditions are inherited in a X-linked dominant fashion*** what does this mean?:

Alport’s syndrome (in around 85% of cases - 10-15% of cases are inherited in an autosomal recessive fashion with rare autosomal dominant variants existing)

Rett syndrome

Vitamin D resistant rickets

Answer 72

A

1) restricted, repetitive BEHAVIOURS and interests (RRB)
2) reciprocal SOCIAL INTERACTION difficulties
3) COMMUNICATION difficulties

DIAGNOSIS

need evidence of features from all three domains which are severe enough to have an impact on daily life
changes noted before age 3 years
not explained by another diagnosis (beware of multiple diagnoses - also deafness etc)
diagnosis made by an MDT meeting

Answer 73

A

1) restricted, repetitive BEHAVIOURS and interests (RRB)
- inflexible, non-functional rituals (distress if routine is changed)
- stereotyped motor mannerisms (hand flapping, rocking)
- preoccupied with parts of objects (try to logically understand a small thing + not see the ‘big picture’)
- abnormally intense and restricted interests
- attachment to unusual objects (eg vacuum cleaners, door handles - may not know normal things like music / TV programmes appropriate to their age)
- distress over small environmental changes (meltdowns if something changes, may intially present when a younger sibling is born)

Answer 74

A

2) reciprocal SOCIAL INTERACTION difficulties
- failure or delay in use of gaze or gesture (incl eye contact - too much or too little - laughing may also appear awkward)
- failure in peer relationships (sitting in playground on their own, parents often say they struggle to ‘fit in’ with groups of people)
- rarely seeking others or offering affection at times of stress (tend to be solitary, can’t read other’s emotions + recognise when they’re sad etc + know how to respond to that)
- lack of shared enjoyment of own or others happiness (don’t like peek a boo, play on their own with their toys, not showing / bringing/pointing)
- lack of modulation of behaviour to fit social context (if person asks what they think of dress person with ASD will be honest, even if that’s not what’s expected of them)

Answer 75

A

3) COMMUNICATION difficulties
- delay or lack of functional speech development (50% fail to develop functional speech)
- failure in reciprocal conversation (often interrupt)
- stereotypes or idiosyncrasies of speech (eg hand socks, instead of gloves, repeating phrases from TV out of context, concrete thinking, don’t get metaphors)
- speech abnormalities in pitch, rate + rhythm (eg more monotonous, can’t control volume)
- pronoun reversal (eg referring to self as you or him, eg he wants to eat now, not I want to eat)
- echolalia (also echopraxia: mimicking others actions)
- neologisms (eg hand sock)
- lack of man believe or social imitative play

Answer 76

A

90% primary (idiopathic) and 10% secondary to known cause

known causes

Rett syndrome
Fragile X syndrome
Tuberous sclerosis
Down’s syndrome
Cerebral Palsy

risk factors:

older paternal age
premature birth

60-70% of people who have ASD will also have a LD

nb prevalence of autism increases with greater severity of learning disability or lower verbal IQ

Answer 77

A

MILD ASD / ASPERGERS

less severe autistic behaviour
normal or high IQ
norm acquire spoken language at same time as peers
may eg be good at maths but struggle with English etc
may appear odd or eccentric
often have difficulties at school with peers
distress can be greater than with severe ASD as child has greater insight
may present with mental health conditions in adolescence

Answer 78

A

ALWAYS ASK ABOUT WHEN PROBLEM STARTED

routine (what happens if deviate from)
language (repetitive)
interests (intense, repetitive)
food (same things/textures)
light + noise sensitivities (also textures of clothes)
how get on with children their own age
how do they get on at school / nursery
eye contact
turn taking in convos

Answer 79

A

learning difficulties
anxiety
depression (esp in adolescence)
ADHD

also check hearing impairment (more to prevent misdiagnosis of deaf pts)

think about anxiety in child with recurrent ‘tummy ache’

nb consider ASD in a child who is not speaking, esp if they are silent and don’t communicate non-verbally (eg eye contact + pointing)

Answer 80

A

special education support
speech therapy
behavioural interventions, if needed
management of mental health conditions
parental education and support (+ respite)

Answer 81

A

visual acuity of <3/60 in the eye with the best vision in a child under 16
- ie the child can’t see something 3ft away that another child could see if it was 60ft (about 20m) away

also blind if education can only be provided by methods such as braille that do not involve sight

partially sighted if educational methods such as large print books can be used

Answer 82

A

optic atrophy
congenital cataracts
choroidoretinal degeneration

Answer 83

A

ABSENT RED REFLEX

cataracts
retinoblastoma
psychomotor development will be abnormal
early smiling is inconsistent
no turning towards sound
no fixing and following
reaching for objects and pincer grip are delayed
early language may be normal but complex language will be delayed
eyes may look abnormal
nystagmus or purposeless eye movements
‘blindisms’ (eye poking, eye rubbing, rocking)

commonly associated with:

hearing deficit
learning difficulties

Answer 84

A

experienced home advisors from RNIB or local authority come around and support with advice like: wear noisy shoes and give a running commentary about all your household activities so that they can understand and learn about the things they can hear, smell etc but never see

early intervention is focused on optimising development

then education support with either large font or braille
- can often go to mainstream school but may need to go to a special school for blind

Answer 85

A

FACTORS FOR RISK OF DEAFNESS

FHx of deafness (norm sensorineural)
cleft palate (conductive)
cerebral palsy (sensorineural)
Hx of meningitis (sensorineural)
Hx of recurrent otitis media (conductive)

IMPORTANT TO ASK ABOUT:

birth Hx
PMHx (esp otitis media + meningitis)
FHx

nb most mild to moderate hearing loss is conductive, resulting from secondary otitis media. Sensorineural hearing loss may be genetic, result from pre or perinatal problems or follow a cerebral insult

Answer 86

A

lack of response to sound (ie not moving head to sound)
delayed speech
behavioural problems (if mild, may not be picked up until school)

all neonates are screened with otoautistic emissions (OAE) to pick up congenital sensorineural hearing loss

audiological testing is done:

any child with significantly delayed or unclear speech
any parental concern
following meningitis
following recurrent otitis media

common co-morbid conditions:

learning disabilities
neurological disorders
visual deficits

Answer 87

A

hearing impairment
ASD
learning disability
child is not being spoken to enough (neglect)

Answer 88

A

grommets for conductive hearing loss

sensorineural hearing loss

hearing aids
cochlear implants
early involvement from speech + language therapists
education for parents and child on sign language
may be able to go to mainstream school or special school

Answer 89

A

variant of normal
cerebral palsy
neuromuscular disorder (eg duchesses)

Answer 90

A

ANY AGE

parental concern
regression in prev acquired skills

10 WEEKS
- no smiling

6 MONTHS

persistent primitive reflexes
persistent squint
hand preference
little interest in people, toys, noises

10-12 MONTHS

no sitting
no double syllable babble
no pincer grasp

18 MONTHS

not walking independently
less than 6 words
persistent mouthing and drooling

5 YEARS
- no 2-3 word sentences

4 YEARS
- unintelligible speech

don’t forget to correct for prematurity!!!

Answer 91

A

PRENATAL INJURY

foetal alcohol syndrome
intrauterine infections (TORCH)

PERINATAL INJURY

asphyxia / HIE
birth trauma

POSTNATAL INJURY

meningitis
non-accidental injury
neglect

CNS MALFORMATION

neural tube defects
hydrocephalus

ENDOCRINE + METABOLIC
- congenital hypothyroidisim
- phenylketonuria
(also other inborn error of metabolism - always ask about consanguinity)

NEURODEGENERATIVE
- leucomalacia

NEUROCUTANEOUS

sturge-weber (port wine stain)
neurofibromatosis
tubero sclerosis

CHROMOSOMAL

down’s syndrome
Fragile X

IDIOPATHIC

autism spectrum disorder
various dysmorphic syndromes

Answer 92

A

enquire systematically about milestones for the FOUR developmental areas
ascertain the extent of delay and which areas are affected
ask if any concerns about hearing or vision

nb remember to adjust for prematurity up to 2 years (after this catch up rarely occurs)

nb loss in skills suggest a neurodegenerative condition

PMHx

alcohol consumption, medical problems, medication during pregnancy
any prematurity and neonatal complications

^ ie birth and prenatal hx is SO important

FHx

learning difficulties
consanguinity

Answer 93

A

1) DEVELOPMENTAL ASSESSMENT
- assess each developmental area in turn (fine motor + dight, gross motor, language + hearing, social)
- attempt to evaluate vision and hearing
- assess factors such as alertness, responsiveness, interest in surroundings, determination + concentration (these all have positive influences on a child’s attainment)
2) GENERAL EXAMINATION
- DYSMORPHIC signs suggest genetic, chromosomal or teratogenic effect
- MICROCEPHALY at birth suggest foetal alcohol syndrome or TORCH
- POOR GROWTH could be organic, eg hypothyroidism, or you,d be environmental (eg neglect)
- look at SKIN: cafe au last spots, depigmented lesions, port wine stains all indicative of neurocutaneous lesions
- HEPATOSPLENOMEGALY suggests a metabolic disorder
3) NEURO EXAM

look for abnormalities in:

tone
strength
coordination
deep tendon reflexes
clonus
cranial nerves
primitive reflexes
ocular abnormalities

Answer 94

A

GLOBAL DEVELOPMENTAL DELAY

chromosome analysis
TFTs
urine screen for metabolic defects

other more sophisticated metabolic investigations + brain imaging may be indicated for some

HEARING TEST if any language delay

Answer 95

A

thoughts going round and round
thoughts of impending doom
faint / dizziness
headaches
heart racing / palpitations
rapid breathing
nausea / butterflies
abdominal pain
sweating
muscle tension

Answer 96

A

generalised anxiety disorder
panic disorder
specific phobia
social anxiety disorder
separation anxiety disorder
obsessive compulsive disorder

Answer 97

A

depression
ADHD
child abuse / neglect

Answer 98

A

CBT
hierarchical desensitisation

reserve medication for no or incomplete response to therapy
- 1st line = fluoxetine (then sertraline)

if affecting SCHOOL WORK / ATTENDENCE then need more help
- equally always risk assess children for self/harm suicide

and always consider neglect in your mind - ask about home situation!

Answer 99

A

young children need to develop at least ONE secure attachment
- though may have several

within the attachment relationship are a typical sequence of behaviours that occur again and again:

1) child has a need and it (CARE-ELICITING)
- eg baby cries when hungry, runs to parent when frightened

2) patient recognises the need and responds (CARE-GIVING)
- baby is fed, child is comforted

3) the child styles, their need met and their internal balance restored

over the years this repeated sequence builds into the child a model of their world that affects future relationships

with ‘good enough’ parenting, a secure attachment forms and child learns fundamental concepts eg:

I am loveable
people will be there for me
people can be trusted

if care-giving is inconsistent, or even abusive, then other attachment styles occur (see other flashcard)

Answer 100

A

DISINHIBITED ATTACHMENT
= associated with early institutional style of care or multiple care givers
- unduly friendly with strangers
- forms superficial relationships early
- overactive / aggressive / emotional lability / poor tolerance of frustration

INSECURE OR REACTIVE ATTACHMENT
= parental abuse, neglect + severe maltreatment
- failure to respond appropriately to social interaction
- displays fearfulness + hyper vigilance that is not responsive to reassurance

Answer 101

A

stranger anxiety starts at about 6 months, is maximal at around a year then slowly recedes as a child reaches school age

nb this is why young children should always be examined close to their parents (eg on parent’s knee)

a lack of this may indicate attachment problems
- a child who has not formed secure attachments may be either suspicious and hostile or overly familiar with strangers

Answer 102

A

ADHD
ASD
conduct disorder
social phobia
learning disability / developmental delay

Answer 103

A

take a long, detailed hx from parents about social situation
- document everything

refer to social services

also screen for other signs of neglect but ALSO screen for Ddx (eg ADHD, ASD, learning disability etc)

Answer 104

A

1) INATTENTION
2) HYPERACTIVITY
3) IMPULSIVITY

nb sleep is often also disrupted but this is not required for diagnosis

DIAGNOSIS

need features of all 3 domains
which are excessive compared to norm for child of that age or developmental ability
present from an early age
PERVASIVE - ie present in more than one social setting (ie school AND home)

nb many normal children are ‘always on the go’, ‘never still’ and need relatively little sleep
- becomes ADHD when these features are so pronounced that they interfere with learning and development

RISK FACTORS

boys
evidence of brain damage (ask about birth hx)

Answer 105

A

poor attention to tasks
avoids tasks requiring sustained mental effort
doesn’t finish tasks (looses homework etc)
poor self organisation
poor attention to detail
apparently not listening
easily distracted
appears forgetful (but memory fine when tested)

QUESTIONS

get bored easily?
how easily distracted are they? (do teachers complain of this?)
ever have difficulty in organising an activity or task needing to get done? (eg poor time management, fails to meet deadlines, difficulty managing sequential tasks, messy + disorganised work)
ever have difficulty listening to someone, even when spoken to directly? (like their mind is elsewhere)
close attention to detail or do they make careless mistakes in homework, chores etc?

Answer 106

A

fidgets and squirms
runs / climbs rather than walks
leaves seat in class, at meals etc
noisy, cannot play or work quietly
persistent over-activity not moderated by social demands

QUESTIONS

how long can they sit still for?
can they play / work quietly?
ever run or climb in situations where it is inappropriate?

Answer 107

A

blurts out answers
fails to wait turn
interrupts and intrudes on others activities
talks excessively without response to social constraints
frequent accidents
thoughtless rule-breaking

QUESTIONS

able to take their turn? weight in a queue
do they interrupt people?
do they raise their hand in class or just blurt out answers?
cross the road on their own or do they jump out into the road without looking?

Answer 108

A

difficulties / bullying at school or dyslexia (if probs only at school)
chaotic or unsupportive household (if probs only at home)

HENCE REALLY IMPORTANT TO ASK IF SYMPTOMS AT HOME AND SCHOOL!

age or developmentally appropriate boisterousness or disobedience (ie normal!)
conduct disorder
disinhibited attachment
anxious inattentiveness (norm secondary to stress)
over-activity caused by prescribed drugs (eg thyroxine, salbutamol)

TAKE A THOROUGH DRUG Hx (inc inhalers)

over-activity associated with ASD

nb rarely:

depression
psychosis
bipolar
closed head injury

Answer 109

A

hitting milestones in all domains (ask age-appropriate ones)
when did parents first notice that child was different to other children?
any problems at school?
any issues in pregnancy (smoking, alcohol, infections)
any problems in labour or neonatally

PMHx

head injury
epilepsy
any developmental conditions (LD, ASD)
any mental health conditions
DHx (incl inhalers)
any FHx of behavioural problems

SOCIAL Hx

who lives at home
relationship with child
any alcohol or drug use in fam
any post-natal depression or psychosis
any involvement with social services

Answer 110

A

anxiety
tourettes
scholastic skill disorder (dyslexia, dyspraxia, dis-maths one)
language impairment
conduct disorder
global learning disability (GLD)

Answer 111

A

BEHAVIOURAL MANAGEMENT

structured tasks
simple instructions
praise for concentrating on and completing tasks (incl star charts etc)
time out regimes for unacceptable behaviour (basically ignore them)
school intervention programmes
parental education (and sometimes respite) about how to manage child’s behaviour

MEDICATION

used as a last resort after trying behavioural interventions (and only if over 5 years)
only used on school days
METHYLPHENIDATE (aka ritalin) is first line drug (is a CNS stimulant)
may need drug therapy for years (as get older may grow out of the ‘hyperactivity’ but still have the inattention)

nb no clear evidence about diet for ADHD though some may find evidence from excluding certain foods

Answer 112

A

Ritalin
- 1st line medication for ADHD

SIDE EFFECTS:

reduced appetite / nausea
difficulty sleeping
stomach pains + headaches (often transient)
occasionally slowed growth
rarely cardiac conditions

do a baseline ECG before starting
- and ask about FHx of heart problems

monitor height + weight ever 6 months while on medication

also be aware that it is a drug of misuse and may be used by siblings / parents etc

Answer 113

A

intentional, direct injury to body tissue, done WITHOUT suicidal intentions

7% of 15-16 year olds have self-harmed in previous year
10% lifetime risk

4x more common in females

cutting
poisoning
depriving food
burning

Answer 114

A

HPC

before (why do it, any trigger)
during (what do? what did it feel like)
after (why stop? who raised alarm, did you try to conceal)

^ideally take this hx with teenager on their own (and then interview parents separately)

PMHx

prev self-harm
presence / absence of mental health problems (screen for anxiety + depression)

HEADS

home
eating
education / employment (bullying?)
activities outside of school
drugs (incl alcohol + tobacco)
suicidality (incl depression + anxiety)
sexuality (sexually active, sexual orientation/gender)
safety (safe at home etc)

RISK ASSESS BEFORE THEY GO!!

risk of self-harming again (see management flashcard for tips to prevent)
suicide risk
risk to others

EXAMS

examine injury
mental state exam (do while taking hx)

Answer 115

A

treat injury / poisoning
risk assess (before send home)
refer to CAHMS
treat psychiatric co-morbidities
individual support / counselling
family support
involvement at school (if secondary to bullying)

Answer 116

A

use a pen to draw on skin
holding ice cube against skin
hitting a pillow to vent
creative things (music/art)
going on a walk
having big scream /cry
writing thoughts/feelings on a bit of paper and then tearing it up
keeping a diary
talking to a friend
self-help apps which aim to distract!

Answer 117

A

bullying
social media
certain sports
perfectionist traits
malnourishment - triggers food anxiety
female

Answer 118

A

Restriction of energy intake relative to requirements 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

nb neither a specific BMI or amenorrhoea are required for diagnosis

mortality is 5-10%
- ie this is a serious condition!!!

common DDx = depression

in contrast to children who eat poorly because they are depressed, children with AN appear to have an abundance of energy strangely at variance with their low food intake + falling weight
they may look ill but insist that they are well!

Answer 119

A

BRAIN / NERVES

can’t think right (concrete thinking)
fear of gaining weight
sad/moody
irritable
bad memory
fainting

HAIR + SKIN

hair thinning + brittle
fine hair growth over body
bruise easily
yellow skin
dry skin
brittle nails
get cold easily

HEART

low BP
low HR
palpitations
heart failure

BLOOD + ELECTROLYTES

anaemia
low potassium
low magnesium
low sodium

MUSCLES + JOINTS

weak muscles
swollen joints
osteoporosis
fractures

KIDNEYS

kidney stones
kidney failure

INTESTINES

constipation
bloating

HORMONES

periods stop
trouble getting pregnant
stop growing

nb if do get pregnant, higher risk of:

miscarriage
needing a c-section
low birth weight
post natal depression

Answer 120

A

1) slow REFEEDING
- under section + through NG tube if required

only once have a decent BMI can start cognitive therapy etc (as brain becomes too concrete in its thinking when has so little energy)

2) THERAPY
- family therapy if first line
- CBT focused on eating disorders is 2nd line

screen for (and treat) comorbid mental health conditions as these are common

Answer 121

A

DSM 5 diagnostic criteria for a diagnosis of bulimia nervosa:

recurrent episodes of binge eating (eating an amount of food that is definitely larger than most people would eat during a similar period of time and circumstances)
a sense of lack of control over eating during the episode
recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise.

the binge eating and compensatory behaviours both occur, on average, at least once a week for three months.

self-evaluation is unduly influenced by body shape and weight.

the disturbance does not occur exclusively during episodes of anorexia nervosa.

RISK FACTORS:

Adverse life events
FHx obesity
parental substance misuse
FHx affective disorders
High expression of emotion+ impulsivity
chaotic lifestyle

Answer 122

A

BRAIN

depression
anxiety
fair of gaining weight
shame
low self-esteem
dizziness

CHEEKS

swelling
soreness

MOUTH

cavities / tooth enamel erosion
gum disease
sensitive teeth (to hot + cold)

THROAT + OESOPHAGUS

sore + irritated
can tear + rupture (blood in vomit)

STOMACH

pain
ulcers (incl rupturing)
delayed emptying

INTESTINES

constipation / irregular bowel movements
diarrhoea
bloating
abdominal cramping

HEART

low BP
low HR
palpitations / arrhythmias
heart failure / weakened heart muscle

BLOOD + ELECTROLYTES

anaemia
low potassium
low magnesium
low sodium

HORMONES
- irregular or absent periods

SKIN

abrasions on knuckles
dry skin

nb all of these may not be present if someone purges using laxatives instead of inducing vomiting

Answer 123

A

bulimia-nervosa-focused family therapy (FT-BN)

2nd line= trial of fluoxetine

Answer 124

A

SCOFF questionnaire

S = do you make yourself SICK because you feel uncomfortably full?

C = do you worry that you have lost CONTROL over how much you eat?

O = have you recently lost more than ONE STONE in a 3 month period?

F = do you believe yourself to be FAT when others say you are too thin?

F = would you say that FOOD dominates your life?

score of 2 or more suggests likely anorexia or bulimia (or other eating disorder)

100% sensitive
87.5% specific

Answer 125

A

acronym = arthritis

A = Acute septic arthritis
R = Reactive: to infection (transient synovitis)
T = Trauma
H = Haematological: haemophilia / leukaemia
R = Rheumatological: JIA/JDM/lupus
I = Immunological: HSP
T = Tuberculosis
I = Inflammatory bowel disease
S = Sarcoidosis