paeds level 2 conditions (pack 2) Flashcards
(125 cards)
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)
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)
2
Q
Features of a stress headache in children?
go through socrates
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
3
Q
Features of a migraine without aura in children?
go through socrates
what is the diagnostic criteria in children?
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
4
Q
Paediatric migraine without aura:
- acute management? 2
- options for prophylaxis? 2
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)
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?
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
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
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
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?
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
8
Q
What are the signs of a possible basal skull fracture? 5
A
- blood from ears (haemotympanum)
- CSF from ears
- CSF from nose
- ‘panda’ eyes
- battle’s sign (bruising behind ear)
9
Q
HYDROCEPHALUS:
- what are the two mechanisms / groups of causes? (give 3 causes of each)
- what congenital condition are they more common in?
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)
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)
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)
11
Q
HYDROCEPHALUS:
- main DDx? how to differentiate?
- first line imaging?
- when to do an LP?
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!!
12
Q
HYDROCEPHALUS:
- management if acute and severe?
- longer-term management?
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
13
Q
NORMAL PRESSURE HYDROCEPHALUS:
- what is it?
- what age does it affect?
- classic triad of symptoms
- DDx? 2
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)
14
Q
PLAGIOCEPHALY:
- what is it?
- what causes it?
- red flags to ask about? 3
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
15
Q
PLAGIOCEPHALY:
- how to explain to parents?
- management? 3
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!
16
Q
HAEMATURIA:
- two broad types?
- things which may mimic one of these types, but dipstick will be negative? 2
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)
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
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
18
Q
BRIEF DESCRIPTION OF:
- IgA nephropathy (aka Berger disease)
- Henoch-Schonlein purpura
- post-infective glomerulonephritis
including how to differentiate between them
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
19
Q
benign familial haematuria (aka thin-basement membrane nephropathy)
- short description?
- incl how to diagnose
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
20
Q
Alport syndrome:
- how inherited?
- triad of features?
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
21
Q
Transient haematuria:
- investigations to consider?
- management (if sure no other cause)?
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
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)
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!
23
Q
HAEMOLYTIC URAEMIC SYNDROME (HUS)
- investigations? (2 bedside, 2 bloods)
- management options? 3
- possible complications?
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
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
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
25
HAEMATURIA
- exam to do?
- what may find on exam? 8 (and what does each sign point towards)
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
26
First line investigations for haematuria:
- bedside? 3
- bloods? 3
- imaging to consider?
- 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
27
HAEMATURIA
- red flags in history? 5
- red flags on examination? 5
- red flag on dipstick? 1
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
28
NEPHROTIC SYNDROME:
- triad of features?
- how normally present?
- other possible features?
- most common cause in children?
- peak age of onset of this condition?
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
29
NEPHROTIC SYNDROME DDx?
- 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...)
30
NEPHROTIC SYNDROME:
- bedside investigations? 2
- bloods? 3
- other investigation to consider?
- 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)
31
MINIMAL CHANGE DISEASE:
- management?
- prognosis?
- 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)
32
differences between acute nephritic and nephrotic syndrome:
- oedema?
- blood pressure?
- urine albumin?
- urine RBC?
- urine WBC?
- cast morphology?
- urine bacteria?
- serum albumin?
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
33
IMPETIGO:
- causative organisms? 2
- describe the rash (incl typical location)
- what increases risk of getting it?
- how spread?
- 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.
34
IMPETIGO:
- management if localised? 1
- management if extensive lesions? 1
- management advice for parents? 4
- exclusion from school required? 1
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
35
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)
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
36
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
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!
37
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
measure + plot:
- weight
- height
- head circum
perineum
- creases / inguinal folds
- perianal and buttocks
ALSO CHECK
- skin over WHOLE body
- scalp
- nails
- mucous membranes
38
IRRITANT CONTACT DERMATITIS (type of 'nappy rash')
- what causes it / makes it worse?
- classical distribution of rash?
- management? 4
- safety net? 1
- 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!
39
CANDIDA DERMATITIS (type of 'nappy rash'):
- describe rash (incl distribution)
- management? 2
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
40
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?
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
41
STEVENS JOHNSON SYNDROME:
- possible investigation? 1
- supportive management? 3
- medical management options? 5
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
42
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?
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
43
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?
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
44
DDx of a limp:
- under 3 years? 2
- 3-10 years? 4
- 10-18 years? 3
- any age? 4
- rarer groups of causes? 4
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)
45
Common knee problems in children + young adults?
briefly describe features / classical presentation of each
what must you always examine if have knee pain?
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!
46
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)
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
47
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
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
48
EXAMINATION OF CHILD WITH A LIMP:
- what initial exams to do? 2
- other things to examine / look for on exam? 5
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
49
RED FLAGS FOR CHILD WITH LIMP:
- age of child?
- history? 7
- exam? 5
what could each indicate?
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
50
TRANSIENT SYNOVITIS:
- what is it?
- age group most common in?
- normal cause?
- describe presentation
- DDx to rule out? how?
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)
51
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?
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!
52
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
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)
53
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?
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
54
Ddx for systemic JIA (Still's disease)? 4
- 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!
55
DIFFERENTIATING BETWEEN TYPE OF JIA:
- Qs in Hx? 2
- findings on exam? 8
- 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)
56
MANAGEMENT OPTIONS FOR JIA:
- for all? 1
- oligo / pauciarticular? 2
- polyarticular? 2
- systemic? 3
- psoriatic? 3
- enthethesis-related? 4
also incl prognosis
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
57
'GROWING PAINS'
- technical name?
- what age normally affect?
- describe them
- DDX? 2
- red flags to ask about? 6
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)
58
MALNUTRITION:
| - main four groups of causes in the UK?
- 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)
59
name of condition caused by energy (calorie) AND protein deficiency?
name of condition caused by JUST protein deficiency?
describe the characteristics of each
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
60
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?
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?
61
SUSPECTED MALNUTRITION:
- possible bloods? 5
- management options if severely malnourished? 5
- what management to always consider?
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
62
OSTEOMALACIA
- what called if in kids?
- what is commonest cause?
- who is at greatest risk from this cause? w
- other rarer causes? 3
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)
63
Presentation / features of:
- rickets? 4
- osteomalacia? 4
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
64
RICKETS / OSTEOMALACIA:
- blood tests? 4 (incl findings)
- imaging? 1
- management? 1
- 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
65
GENETIC TESTING IN CHILDREN:
- indications / appropriate situations for genetic testing in children? 3
- situations where genetic testing in children is inappropriate? 3 (ie should wait till child old enough to consent)
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)
66
Benefits of early diagnosis of genetic disease? 4
what is often the first sign of a chromosomal abnormality?
- 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
67
What are some issues / topics of discussion that may come up during genetic counselling? 5
- 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
68
What do these symbols mean in a family pedigree:
- square?
- circle?
- diamond?
- triangle?
- shape fully coloured in?
- shape partially coloured in?
- line through shape?
- two lines connecting parents?
```
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
69
AUTOSOMAL RECESSIVE
- do conditions tend to manifest in multiple generations or in lots of members of same generation?
- chance of child having condition / being carrier if both parents are carriers?
- what do most of these conditions affect?
- examples? (just list as many as you can)
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)
70
AUTOSOMAL DOMINANT
- do conditions tend to manifest in multiple generations or in lots of members of same generation?
- chance of children getting if one parent has? what if both parents have?
- what do most of these conditions affect?
- examples? (just list as many as you can)
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)
71
X-LINKED RECESSIVE
- if mother is carrier, chance of male sons being affected / girls being carriers?
- if father is affected, chance of chance of male sons being affected / girls being carriers?
- examples? (just list as many as you can)
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
72
AUTISM SPECTRUM DISORDER (ASD):
- three core domains / groups of features?
^just list them (in depth features are on other flashcards)
what is needed to make a diagnosis of ASD?
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
73
Give examples of features that come under the 'behaviours' domain of ASD? 6
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)
74
Give examples of features that come under the 'social interaction' domain of ASD? 5
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)
75
Give examples of features that come under the 'communication' domain of ASD? 8
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
76
AUTISM SPECTRUM DISORDER:
- what % are primary (ie idiopathic) and what % are secondary to a known cause?
- known causes? 5
- other risk factors? 2
- what % of children with ASD also have learning difficulties?
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
77
List some differences between severe ASD (prev autism) and mild ASD (prev aspergers)
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
78
What things can you ask about in a child with suspected ASD? 9
nb this is not an exhaustive list
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
79
co-morbid conditions to screen for in ASD? 4
- 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)
80
Management options for ASD? 5
- special education support
- speech therapy
- behavioural interventions, if needed
- management of mental health conditions
- parental education and support (+ respite)
81
BLINDNESS:
| - definition in children?
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
82
Three commonest causes of blindness?
- optic atrophy
- congenital cataracts
- choroidoretinal degeneration
83
- what is a red flag for blindness in a newborn infant check? 1
- what will be the affect on developmental milestones? 6
- other signs/symptoms children may show? 3
- other conditions which are commonly associated with visual impairment? 2
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
84
management of visual impairment?
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
85
HEARING IMPAIRMENT:
- risk factors for deafness? 5
- what three aspects of the history is really important if suspect hearing impairment?
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
86
HEARING IMPAIRMENT:
- clinical features which raise suspicion of impairment? 3
- what screening is available?
- what gets tested? 4
- co-morbid conditions which are associated with deafness? 3
- 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
87
Main four DDx for language delay?
- hearing impairment
- ASD
- learning disability
- child is not being spoken to enough (neglect)
88
HEARING IMPAIRMENT:
- management of conductive hearing loss?
- management options to correct sensorineural hearing loss? 2
- management to help with development? 3
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
89
common DDx for isolated gross motor delay? 3
- variant of normal
- cerebral palsy
- neuromuscular disorder (eg duchesses)
90
DEVLOPMENTAL RED FLAGS:
- at any age? 2
- at 10 weeks? 1
- at 6 months? 4
- at 10-12 months? 3
- at 18 months? 3
- at 2.5 years? 1
- at 4 years? 1
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
2. 5 YEARS
- no 2-3 word sentences
4 YEARS
- unintelligible speech
don't forget to correct for prematurity!!!
91
CAUSES OF DEVELOPMENTAL DELAY:
- prenatal injury? 2
- perinatal injury? 2
- postnatal injury? 3
- central nervous system malformation? 2
- endocrine + metabolic defects? 2
- neurodegenerative disorders? 1
- neurocutaneous syndromes? 3
- chromosomal abnormalities? 2
- idiopathic? 2
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
92
When taking a hx from a child with concerns about development:
- what points do you need to make sure you cover when specifically asking about developmental milestones? 3
- Qs for PMHx? 2
- Qs for FHx? 2
- 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
93
If a child presents with suspected developmental delay, what THREE examinations should you perform?
what might you look for / find in each?
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
94
1st line investigations for global developmental delay? 3
mandatory investigation if any language delay? 1
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
95
Possible symptoms of anxiety in children/teens? 10
- thoughts going round and round
- thoughts of impending doom
- faint / dizziness
- headaches
- heart racing / palpitations
- rapid breathing
- nausea / butterflies
- abdominal pain
- sweating
- muscle tension
96
ANXIETY DISORDERS? 6
- generalised anxiety disorder
- panic disorder
- specific phobia
- social anxiety disorder
- separation anxiety disorder
- obsessive compulsive disorder
97
Ddx for anxiety in children? 3
- depression
- ADHD
- child abuse / neglect
98
Management options for anxiety?
- which med is first line for children?
- what to always ask about? (and get more help if present)
- 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!
99
How many 'attachment figures' does a child need?
describe how 'secure attachment' is formed
what are the long-term psychological consequences of secure attachement
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)
100
What are the two main types of 'insecure attachment' that can form?
- features / red flags for these?
- what are often the causes of these?
consequences of these later in life?
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
101
STRANGER ANXIETY
- when does it normally develop and then start to go away?
- what may it indicate if not present?
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
102
Ddx for attachment problems? 5
- ADHD
- ASD
- conduct disorder
- social phobia
- learning disability / developmental delay
103
Management of suspected attachment disorder? 2
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)
104
ADHD:
- three core features?
- what do you need for a diagnosis?
- risk factors for ADHD? 2
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)
105
Give examples of features that come under the 'inattention' domain of ADHD? 8
include Qs that can ask parents to elicit these
- 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?
106
Give examples of features that come under the 'hyperactivity' domain of ADHD? 5
include Qs that can ask parents to elicit these
- 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?
107
Give examples of features that come under the 'impulsivity' domain of ADHD? 6
include Qs that can ask parents to elicit these
- 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?
108
Ddx of ADHD? 8
what is it really important to establish when asking about symptoms to differentiate? 2
- 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
109
QUESTIONS TO ASK IN A CHILD WITH SUSPECTED ADHD:
- Developmental hx? 3
- birth hx? 2
- PMHx? 5
- FHx? 1
- Social Hx? 5
- 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
110
Conditions which often co-occur with ADHD? 6
- anxiety
- tourettes
- scholastic skill disorder (dyslexia, dyspraxia, dis-maths one)
- language impairment
- conduct disorder
- global learning disability (GLD)
111
What are the two mainstays of treatment for ADHD?
describe each
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
112
METHYLPHENIDATE:
- aka?
- side effects? 5
- what investigation must be done before starting child on this?
- what must be monitored while child on this?
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
113
DELIBERATE SELF HARM:
- definition?
- prevalence amongst teenagers?
- forms which it can take?
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
114
history of someone with deliberate self-harm:
- HPC? 3
- PMHx? 2
- SHx (use one for teens!) 8
- examinations to do? 2
- what part of history to always do before you let them leave?
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)
115
MANAGEMENT OF DELIBERATE SELF-HARM:
- immediate management? 3
- ongoing management options? 4
- 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)
116
What ideas to give to teens for alternatives to self-harm? 10 (ie when they get the urge)
- 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!
117
EATING DISORDERS:
| - risk factors / triggers? 6
- bullying
- social media
- certain sports
- perfectionist traits
- malnourishment - triggers food anxiety
- female
118
ANOREXIA NERVOSA:
- three features for diagnosis?
- mortality?
- common DDx for anorexia nervosa? (+ how to differentiate)
1. 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
2. Intense fear of gaining weight or becoming fat, even though underweight
3. 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!
119
EFFECTS OF ANOREXIA NERVOSA:
- brain + nerves? 6
- hair + skin? 7
- heart? 4
- blood + electrolytes? 4
- muscles + joints? 4
- kidneys? 2
- intestines? 2
- hormones? 3
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
120
MANAGEMENT OF ANOREXIA:
- initial management?
- management after initial management? 2
- what to screen for?
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
121
BULIMIA NERVOSA:
- diagnostic criteria?
- risk factors? 6
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
122
EFFECTS OF BULIMIA NERVOSA:
- brain? 6
- cheeks? 2
- mouth? 3
- throat + oesophagus? 2
- stomach? 3
- intestines? 4
- heart? 4
- blood + electrolytes? 4
- hormones? 1
- skin? 2
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
123
MANAGEMENT OF BULIMIA NERVOSA:
- 1st line?
- 2nd line?
bulimia-nervosa-focused family therapy (FT-BN)
2nd line= trial of fluoxetine
124
Screening questions (incl acronym) for eating disorders? 5
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
125
Ddx for swollen joint? 9 (use acronym)
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
```
