Paediatrics Flashcards
What is the common age group that DDH presents and what the signs / clinical tests to screen for it?
0-3 years: Developmental dysplasia of the hip (DDH) = congenital dysplasia of the acetabulum and partial dislocation of the femoral head from the acetabulum. Predominantly effects females.
All newborns should be screened for DDH within the first 24-72 hours after birth.
First assess for risk factors: breach presentation at or after 36 weeks even if successful ECV, family history in 1st degree relative, fixed foot deformity (if a twin/triplet pregnancy and any of the babies have a risk factor they should all get USS)
Then Look, Feel, Move assessment
LOOK: look for asymetrical groin creases or leg length discrepancy
FEEL: Flex both hips and knees and assess for knees being at unequal lengths (postive galeazzi sign)
MOVE: 1) Gentle abduction test: with hips and knees flexed and with thumbs on inner thighs and forefingers over greater trochanters and gently abduct both hips at the same time. Assess for assymetrical or restricted hip abduction.
2) Barlow’s test: gentle push posteriorly with the hips and knees flexed in a neutral abd/adduction position. Assess for if hip slips posteriorly.
3) Ortolani test: abduct the hips in a flexed position and feel for the greater trochanter popping back anteriorly from a posteriorly displaced position.
Need USS within 2-4 weeks if positive examination finding (asymmetrical leg lengths / groin creases, asymmetrical /restricted abduction, positive Barlow’s or Ortolani’s).
Need USS within 4-6 weeks if no positive examination findings but risk factors (breach at or after 36 weeks, first degree relative, fixed foot deformity).
Can only really USS until 4-6 months. Then use X rays as the femoral head starts to ossify.
Early Mx = Pavlik harness (main risk is avascular necrosis of the femoral head). If conservative Mx fails or late presentation (>6-18 months) = surgical reduction.
Differential diagnoses in the limping child at different ages?
At any age:
- INFECTION: septic arthritis (can affect any joint but most commonly lower limb, FEVER +/- raised inflam markers, refusal to weightbear), osteomyelitis (pain on palpation over the bone)
- TRANSIENT SYNOVITIS: non infective inflammation of the joint synovium, sometimes a preceding history of viral illness but not always. Features that suggest septic arthritis rather than TS: 1) Fever 2) Raised ESR 3) Raised WCC 4) Refusal to weight-bear on affected site.
TRANSIENT SYNOVITIS IS VERY RARE IN CHILDREN UNDER 3.
- Fracture / soft tissue trauma
- Child abuse
0-3:
- Missed DDH
- Toddler’s fracture (undisplaced tibial shaft fracture commonly after unwitnessed fall)
3-10:
- Perthes disease (idiopathic avascular necrosis of the femoral head, higher risk in males, tend to present with several month onset of groin/thigh/knee pain especially after physical activity, limp + stiff joint. Mx over 50% self resolve within a couple of years, advise to avoid physical activity / contact sport during acute phase, some may need physio / crutches and arthrogram to assess if surgery needed for more severe cases.)
10-19:
- Slipped capital femoral epiphysis (SCFE): displacement of the femoral epiphysis from the metaphysis. presents with insidious hip/knee pain, antalgic gait, limited internal rotation, externally rotated + shortened affected limb. Risk factors = male, overweight, prev radiotherapy, hormonal issues (eg hypothyroidism, growth hormone deficiency). Mx: insitu screw fixation (if very unstable / severe might need to do an open reduction).
What are the major risk factors for Sudden Infant Death Syndrome
1) Sleeping on their front / prone
2) Parental smoking
3) Co-sleeping
4) Hyperthermia and head covering
5) Prematurity
When should vaccinations be given to premature infants ?
According to chronological age (Ie number of months from their delivery) NOT adjusted for gestational age.
They are at especial risk of infection so don’t want to delay until they are gestationally 2 months.
How should you manage nocturnal enuresis (bed wetting) in children <5
Reassurance, advice on reducing fluids in the evening, and toileting hygiene. Nocturnal enuresis in children <5 can be managed with reassurance
What are risk factors for surfactant deficient lung disease in neonates?
- the earlier the gestation the higher the risk
- male gender
- diabetic mothers
- c-section
- being the 2nd born of premature twins
What are the 4 defects of tetralogy of fallot?
1) Pulmonary stenosis
2) Right ventricular hypertrophy
3) Ventricular septal defect
4) Over-riding aorta
Cyanotic, presents at birth, boot-shaped heart
What are the 5x types of CYANOTIC congenital heart defect?
1) Tetralogy of Fallot
2) Transposition of the great arteries
3) Tricuspid Atresia
4) Truncus arteriosus
5) Total anomalous pulmonary venous return
What are absolute contraindications to the MMR vaccine?
For all live attenuated vaccines: immunosuppression, prev anaphylactic reaction to MMR vaccine, prev anaphylactic reaction to gelatin or neomycin, pregnancy, yellow fever vaccination within the past 4 wks
(need at least a 4 week window between yellow fever and MMR or varicella vaccination
What doses of IM adrenaline should be given in anaphylaxis in the child
<6 = 150 micrograms of 1:1000
6-12 = 300 micrograms
>12 + adults = 500 micrograms
What are the sequalae associated with being SGA /IUGR?
Hypoglycaemia Polycythaemia Thrombocytopenia Necrotising enterocollitis hypocalcaemia
What are the 1st line drug treatments for ADHD?
1st line = Methylphenidate (ritalin)
2nd line = Dexamfetamine
What is the typical presentation of lymphoma in children?
NON-PAINFUL LYMPHOMA initially may be without other prodrome, can later develop B symptoms of fever, weight loss and nightsweats
Non-hodgkins = much more common than hodgkins
What is the typical presentation of acute lymphoblastic leukaemia (ALL)
Relatively sudden onset across several weeks
Overgrowth of immature lymphocytes in the bone marrow, liver, spleen and lymph nodes = anaemia, thrombocytopenia (bruising, petechia, nose bleeds), neutropenia (recurrent infections, hrpatosplenomegaly, lymphadenopathy
What are the associated conditions / sequelaea of cystic fibrosis?
- Pancreatitis -> diabetes
- Liver cirrhosis
- Nasal polyps
- Reduced fertility (absence of vas deferens in males, reduced fertility in females)
What drug is first line for absence seizures in children?
Sodium valproate
What is the classical presentation of Di-George syndrome?
CATCH-22
C - conotruncal cardiac defects (TETRALOGY OF FALLOT + truncus arteriosus)
A - abnormal faces (long face)
T - thymic hypoplasia (hypoparathyroidism + hypocalcaemia)
C - cleft palate
H - Hypocalcaemia
22 - due to deletion of part of chromosome 22
ALSO HAVE HIGHER RATES OF SCHIZOPHRENIA
What is the peak incidence of febrile seizures?
18 months
When is a febrile seizure considered complex?
- > if it lasts >15 mins
- > if there is recurrence within 24 hrs
- > if the seizure is focal at onset or at any time during the convulsion
What is the subsequent risk of epilepsy in a child presenting with a febrile seizure?
2%
seizures that occurred with a lower fever is associated with a higher chance of recurrence
What is functional abdominal syndrome?
periumbilical abdominal pain that occurs in otherwise well children around school-age
What is the typical presentation of cri de chat syndrome?
= chromosome 5p deletion (Five for Feline)
= cat-like cry, small jaw, small head (microcephaly), hypertelerism (eyes spaced far apart), learning difficulties
What is the typical presentation of Patau syndrome?
= trisomy 13
= poor survival, only 1 in 10 live longer than 5 years
= microcephaly, polydactyl (extra fingers/ toes), undescended testes, may have cyclopia (one eye, may have 1x cerebral hemisphere which isn’t survivable)
13 for unlucky -> don’t live very long
What is the typical presentation of Edward syndrome?
= trisomy 18
8dward syndrome
= neural tube defects, small jaw, prominent occiput, overlapping fingers, chroroid plexus cysts
Eighten for Edward
What is the typical presentation of Pierre-Robin syndrome?
= SOX-9 mutation
= cleft palate + posterior tongue displacement + small jaw
Pierre Robin = all about the face
What is the typical presentation of Prader-willi syndrome?
= deletion in paternal copy of 15q-11-15 (genetic imprinting)
= obesity + behavioural difficulty + HYPOgonadism + hypotonia
What is the typical presentation of William’s syndrome?
= chromosome 7 deletion
Wi7iam syndrome
Short stature + learning difficulties + VV FRIENDLY + EXTROVERTED + supravalvular aortic stenosis
What is the typical presentation of Fragile X syndrome?
trinucloetide repeat of the X chromosome (XXY)
= micrcephaly + large ears + large testicles (macro-orchidism) + mitral valve prolapse + high arched palate
What is the typical presentation of Noonan’s syndrome?
Autosomal DOMINANT
- Webbed neck
- Pulmonary stenosis
- Pectus excavatum
What is the typical presentation of Turner’s syndrome?
Turners = 45X0 (Girl’s only, lack of a second X chromosome)
- PRIMARY AMENORRHOEA (due to only rudimentary ovarian development)
- Aortic co-arctation
- bicuspid Aortic valve
- widely spaced nipples
What is the typical presentation of Down’s syndrome?
= trisomy 21
Presents w/:
* Flat occiput and flat nasal bridge + round face
* Brushfield spots in the eyes (little white dots)
* Atrioventricular septal defect is the most common congenital heart defect associated with downs
(also associations with tricuspid atresia, VSD, PDA and tetralogy of fallot)
What is the typical presentation of Klinefelter Syndrome?
= 47XXY
= men with an extra X chromosome (thus more oestrogen in their body!)
- Slim and tall with feminine build
- Hypogonadism
- Gynaecomastia
- ^ risk of breast cancer and osteoporosis
What are the typical presentations of cyanotic congenital heart defects?
Tetralogy of fallot; the MOST COMMON CYANOTIC congenital heart defect in children
Risk factors: Di George syndrome
Pulmonary stenosis, RV hypertrophy, VSD, overiding aorta
Presents w/ cyanosis AFTER the week of life, tet spells (hypercyanotic when crying or feeding), ejection systolic murmur radiating to axilla
CXR - boot-shaped heart
Truncus arteriosus: the aorta and PT are joined as one -> so circulating blood is much lower in 02 -> presents w/ cyanosis, poor feeding and growth, excessive sleepiness
Tricuspid atresia: associated w/ DOWN’S SYNDROME -> failure of right tricuspid valve to develop = no communication between right atria and ventricle. Must have an ASD or patent PDA for survival - Presents initially well then becomes breathless and increasingly cyanosed, ejection systolic murmur loudest upper left sternal edge
Mx - prostaglandin to maintain PDA and surgery
Transposition of the great arteries: aorta comes out of the right side of heart, pulmonary trunk comes out of the left side. Presents w/ immediate cyanosis on first day / week of life, loud S2 heart sound, CXR (egg on a string - narrow mediastinum + large cardiac shadow)
Mx -> IV prostaglandin to maintain PDA patency -> surgery
Total anomalous pulmonary venous return: shunt between pulmonary vein and SVC -> oxygenated blood goes back into SVC rather than the left atrium.
Need a patent foramen ovale for survival
Presents w/ cyanosis after the 1st wk of life (like ToF)
CXR - figure of 8 appearance
Typical presentation of acyanotic congenital heart defect?
ASD: left->right shunt -> ^ pulmonary pressures = ej syst murmur left upper sternal edge + recurrent chest infections + breathlessness
VSD: risk factors -> Down’s, fetal alcohol syndrome
-> pansystolic murmur -> Eisenmenger syndrome (reversal of the shunt, when right-sided pressure ^ and shunt becomes right to left -> presents with cyanosis on fingertips and lips
AVSD - presents w/ signs of heart failure - AVSD IS THE MOST COMMON HEART DEFECT ASSOCIATED WITH DOWNS
Patent DA -> left to right shunt from aorta into PA -> CONTINUOUS MACHINERY LIKE MURMUR + left subclavicular thrill, collapsing bounding pulse, faltering growth and poor feeding
Can also develop eisenmenger syndrome -> right to left shunt ->
(DA normally closes ~ day 2/3)
Mx -> premature (<37 wks) -> ibuprofen/indomethacin to close the DA. If term baby -> surgery
What is the typical presentation of roseola infantum / exanthem subitum
Young infants, prodrome of being feveish then PINK maculopapular rash
Likely viral in origin -> contagious. self-limiting
What is the definition of delayed puberty in boys ?
testicular volume <4ml in a boy > 14
warrants a paediatric referral
Guttate psoriasis?
Common in children, often follows a viral or strep URTI
A defect in what leads to recurrent meningococcal infections?
a defect in complement proteins
( a defect in T cell immunity -> atypical fungal and viral infections, in B cell immunity -> recurrent bacterial infections but not so much meningococcal -> defect in neutrophils -> recurrent abscesses)
Presentation of motor sensory neuropathy in children?
Most common = charcot-marie-tooth
DISTAL SYMMETRICAL muscular wasting + PES CAVUS + DISTAL SENSORY LOSS / LOSS OF ANKLE REFLEXES
When is neonatal jaundice considered abnormal?
If in the first 24 hours OR persists after 2 weeks in term babies or 3 weeks in preterm babies.
Differentials for neonatal jaundice?
1) Pre-hepatic -> haemolysis eg rhesus disease of the newborn
2) Heptic -> hepatocellular infection
3) Post-hepatic -> biliary atresia
Breast milk jaundice -> occurs in exclusively breast fed babies
Typical presentation of congenital CMV infection?
Sensorineural hearing loss
Intracranial calcification + cerebral palsy
Typical presentation of Pendred syndrome?
autosomal recessive
sensorineural hearing loss + goitre with hyPO thyroidism
Typical presentation of henoch-schonlein purpura?
Post strep or viral infection
Arthralgia + purpuric rash + haematuria (IgA-mediated vasculitis)
Self-limiting
1 in 4 recur, 1 in 10 get CKD
HSP / Ignephropathy v post-infectious glomerulonephritis??
IgA pathologies (HSP and Ig nephropathy/Berger's syndrome) = at the same time as the URTI (IgA = At the same time) Post-infectious glomerulonephritis = delay of a few weeks
Acute infection-related renal syndromes in children?
Henoch-schonlein purpura -> Ig A vasculitis DURING an URTI -> arthralgia + purpuric rash + haematuria
Ig nephropathy / bergers syndrome -> DURING an URTI but nephritic syndrome without the rash/arthralgia
Post-infectious GN -> a several week delay between the URTI and the nephritic syndrome
haemolytic uraemic syndrome -> haemolytic anaemia + thrombocytopenia + acute renal failure with haematuria associated with E.COLI GI INFECTION
What does the Coomb’s test test for?
IMMUNE-MEDIATED haemoylsis
typical presentation of salicylate posioning?
Mild -> dizziness, tinnitus, vomiting
Severe -> deafness, ^ RR, profound sweating
Sources -> paracetamol, tiger balm/deep heat, bonjela
Neonatal jaundice -> differentials?
Physiological jaundice = an unconjugated bilirubinaemia between day 1 -> day 14 (in term, day 21 in preterm)
Unconjugated hyperbilirubinaemia -> ^ haemolysis
- > w/ positive coombs test (immune-mediated RCC destruction):
- ABO incompatibility (common)
- Rh incompatibility
- Hereditary spherocytosis
- > w/ negative coombs test
- G6PD deficiency (enzymatic deficiency that shortens the lifespan of the RBCs)
- sepsis
- > polycythaemia
- > Breast feeding jaundice -> in 1st week, with failure to establish BF -> dehydration + reduced stool output = reduced clearance of bilirubin in the stool
- > Breast milk jandice -> presents in 2/3rd week, enzyme in breast milk increases enterohepatic recirculation of bilirubin
Conjugated hyperbilirubinaemia (ALWAYS pathological) * Biliary atresia
Complications of hyperbilirubinamia?
acute bilirubin encephalopathy -> high pitched cry, seizures
kernicterus -> long-term issues from it -> cerebral palsy, hearing loss, gaze abnormalities
Vomiting child differentials?
GORD -> vomiting after feeds, non-bilious vomiting, feeding difficulty / faltering growth -> CLINICAL diagnosis but can use 24 hr oesophageal impedance for a concrete diagnosis
Duodenal atresa: linked to Down’s syndrome, get a stricture in the duodenum -> BILIOUS vomiting in the first few days of life.
Abdo XR -> double bubble sign (gastric bubble + a duodenal bubble)
Tx - IVI, NG for decompression, duodenoduodenostomy
Hirschsprung’s disease: underdevelopment of the ganglion cells / parasympathetic supply to the distal bowel.
Presents w/ delayed presentation of meconium (>48hrs), bilious vomiting, unable to pass flatus, loose stools.
Dx: rectal punch biopsy
Mx - rectal washout / bowel irrigation and then an anorectal pullthrough
Gastroenteritis:
e.coli -> TRAVELLERS diarrhoea -> watery diarrhoea and cramps
giardiasis -> water-transmitted -> PROLONGED non-bloody diarrhoea
cholera -> EXTREME WATERY DIARRHOEA + DEHYDRATION
shigella -> BLOODY DIARRHOEA + vomiting + abdo pain
staph aureus -> EXTREME VOMITING
campylobacter -> initial flu-like prodrome then BLOODY diarrhoea + FEVER (linked to guillain-barre syndrome.
bacillus cereus -> rapid onset (6 hrs) after eating rice / take-aways
amoeibis -> gradual blood diarrhoea + abdominal pain that lasts for several weeks
Differentials for a child with a mass?
Necrotising enterocollitis -> necrosis + perforation across the large bowel
Presents w/ DISTENDED ABDOMEN, abdominal pain, BLOODY STOOLS and BILIOUS VOMITING
risk factor -> prematurity, low BW, hypotension, sepsis
Dx - abdo XR -> may have pneumoperitoneum + bowel wall oedema + pneumatosis intestinalis
Mx -> broad spectrum abx (cefotaxime + vancomycin) + NG decompression + NBM
Intussuception -> part of the intestine ‘telescopes’ into the distal part, blocking flow -> risk factors = viral infection, intestinal malrotation, burketts lymhoma
Presents w/ SAUSAGE-like mass in the RIF + REDCURRENT JELLY STOOLS + BILIOUS VOMITING + draws knees upto chest
Dx -> 1st line = abdominal USS (target sign / doughnut sign)
Tx -> IVI + abx + rectal air insufflation to push the bowel back into place
Pyloric stenosis -> presents 2 wks -> 2 month = projectile NON-BILIOUS vomiting, olive-shaped mass RUQ, visible gastric peristalsis wave after eating, blood gas shows HYPOCHLORAEMIC HYPOKALAEMIA metabolic alkalosis.
1st line Dx -> USS
Tx -> IVI + NG decompression + Ramsted’s pyloromyotomy
Neuroblastoma -> tumour in the adrenal medulla . sympathetic nerve system
Presents w/ abdominal mass crossing the midline, blueberry muffin rash, periorbital bruising, short stature/underweight
Dx - urinary catecholamines (VMA + HVA)
Wilm’s tumour (nephroblastoma) -> PAINLESS unilteral mass that doesn’t cross the midline + haematuria + hypertension
Dx - renal biopsy
Mx - nephrectomy + chemo
Routine childhood vaccination schedule?
8 weeks:
- 6 in 1 (Diptheria, Polio, Pertussis, Tetanus, Hib, Hep b)
- Men B
- oral Rotavirus
12 weeks:
- 6 in 1 booster
- Pneumococcal
- oral Rotavirus
16 weeks:
- 6 in 1 booster
- Men B booster
1 year:
- Hib + Men C
- Men B booster
- MMR
- Pneumococcal
3 years + 4 months:
- 4 in 1 (Dip, tetanus, petussis, polio)
- MMR 2nd dose
12/13 years:
* HPV (2 doses 6-24 months apart)
14:
* 3 in 1 (diptheria, tetanus and polio)
* combined meningococcal (A, C, W and Y)
Paediatric developmental milestones?
GROSS MOTOR
Newborn - flexed limbs, head lag when pulled up
6-8 weeks - lift their head 45 degrees when lying on their stomach
6-8 months - sit without support
9 months- crawling
10 months - crusing
12 months - walking (upper limit 18 months!)
15 months - walking STEADILY
Running and jumping by 2.5
VISION + FINE MOTOR
By 3 months (limit age) it should fix and follow
By 6 months (limit age) it should reach out for toys and have a palmar grasp
by 9 months (limit age) it should transfer toys from one hand to the other
By 12 months (limit age) it should have a mature pincer grip
by 18 months should mark with crayons and build a tower of 3
by 2 years should build tower of 6
by 2.5 years should build tower of 8
bridge @ 3 and steps @ 4
DRAWING Line - 2 Circle - 3 Cross - 3.5 Square - 4 Triangle - 5
HEARING, SPEECH AND LANGUAGE Newborn - startle to loud noises by 4 months - coo by 7 months - babble by 10 months - mamma and dadda by 12 months - a few words other than mamma and dadda by 2 years - can make simple phrases by 3 years - can make joined commands
SOCIAL
By 8 weeks (limit age) should smile responsively
By 8 months - can put food in their mouth
By 12 months - can wave bye bye and drink a cup with 2 hands
By 18 months bring a spoon to the mouth
By 2 years -> symbolic play and be dry by day
By 3 years -> parallel and interactive play
Mx of a UTI in a child < 6 months?
If responds to abx and no atypical features -> USS within 6 weeks
If atypical features, recurrent or no response to abx -> USS during the acute infection
Urgent paeds referral needed if <3 months old OR high risk of serious illness
Neonate resuscitation guidelines?
If < 32 weeks wrap undried in plastic under radiant heat
1) Assess airway + breathing -> if gasping or not-breathing = 5 INFLATION BREATHS (with PEEP if possible, on air initially)
2) Asses for ^ in HR (the best indicator of successful aeration) -> If no increase in heart rate -> assess for chest movements -> if no chest movement consider ^ the inflation pressure of the PEEP / repeating the inflation breaths
3) If HR remains <60 or undetectable after 30 secs = commence CPR at a ratio of 3:1 and ^ inspired 02 to 100%
most common cause of bacterial pneumonia in children > 2?
Streptococcus pneumonia
The APGAR score?
0-10
A - appearance (pink = 2, peripheral cyanosis = 1 all-over pallor / cyanosis = 0)
P - pulse -> pulse 100-140 bpm = 2, pulse <!00 bpm = 1, no pulse = 0
G - grimace -> strong cry when stimulated = 2, grimace/weak cry = 1, no reaction to stimulation = 0
A - activity -> well-flexed = 2, some flexion = 1, floppy = 0
R - respiration -> strong cry = 2, slow irregular breathing = 1 apnoeic = 0
Congenital spinal muscular atrophy?
Kugelberg Welander -> mutation in chromsome 5
Werdnig-Hoffman / infantile onset -> presents <6 months -> mutation in chromosome 5
Becker muscular dystrophy -> inherited muscular atrophy in males
Treatment of MS?
Steroids reduce the severity and duration of the attack but DO NOT reduce the frequency of relapses or long-term disability
Disease-modifying agents (that reduce the freq of relapses) -> Interferon, Natalizumab, Azathioprine, Glatiramer
which inherited condition is associated with development of acoustic neuromas and meningiomas?
Neurofibromatosis type II
Delayed puberty differentials in boys and girls ?
Considered delayed when puberty hasn’t started by 13 in females or 14 in males.
1) PRIMARY HYPOGONADISM: (hypergonadotrophic hypogonadism = low oestrogen/progesterone/testosterone but high FSH and LH to try and compensate)
Congenital -> Turner’s syndrome, Klinefelter’s
Acquired - radio/chemotherapy or trauma to the gonads
2) SECONDARY HYPOGONADISM
(hypogonadotrophic hypogonadism -> low LH + FSH)
Acquired - radio/chemotherapy, excess exercise, chronic illness, coeliac disease, obesity, stress, malnutrition
Congenital -> Kallmann syndrome (hypothalamic and olfactory neurones fail to develop in embryo -> impaired sense of smell and a failure of pulsatile GnRH release = delayed or absent puberty) Panhypopituitarism (either due to congenital underdevelopment of the pituitary gland or due to compression on the pituitary due to tumour / hydrocephalus)
3) CONSTITUTIONAL DELAY
temporary delay in puberty that typically runs in family, may have a lower GnRH than someone their age but often will have normal puberty but at a later stage.
What conditions are tested for in the Guthrie test / blood spot screening at 1 week of age?
Phenylketonuria
Cystic fibrosis
Sickle cell disease
Congenital hypothroidism
Below what age is puberty considered precocious in boys and girls?
Boys <9
Girls < 8
What is thelarche?
Breast development
Central versus peripheral causes of precocious puberty?
CENTRAL (due to loss of inhibition from the hypothalamus / pituitary)
- Hypothalamic hamartoma (GnrH-secreting tumour)
- Angelman syndrome
PERIPHERAL (excess androgens) Endogenous: * Congenital adrenal hyperplasia (insufficiency of 21-hydroxylase) = EXCESS ANDROGENS (get female virilisation) + LOW CORTISOL * Gonadal / adrenal tumours Exogenous -
