Paeds Flashcards

1
Q

def live attenuated vaccine

A

version of living microbe that has been weakened

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2
Q

def inactivated vaccine

A

killed microve

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3
Q

when should you not administer a vaccine

A
  • below age set
  • acutely unwell
  • anaphylaxis reaction to drug previously
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4
Q

different classification of children by age group

A
  • neonates: birth- 1m
  • infants: 1m-2y
  • young child: 2-6y
  • child: 6-12y
  • adolescent 12-18y
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5
Q

red flags of child development

A

not:

  • smiling by 8 weeks
  • following objects/face by 3 months
  • holdinh head up and turning to sound by 4 months
  • reaching for toys by 6 months
  • babbling by 8 months
  • transfer toys from one hand to another by 9 months
  • sitting without support by 9 months
  • wave goodbye by 10 months
  • mature pincer grip by 12 months
  • first word by 15 months
  • walking and feeding themselves by 18 months
  • symbolic play not reached by 2-2.5y
  • talking in sentences by 36 months
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6
Q

causes of stridor

A
  • croup
  • epiglottitis
  • bacterial tracheitis
  • foreign body (laryngeal or oesophageal)
  • anaphylaxis
  • inhalation of smoke
  • trauma
  • retropharyngeal abscess
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7
Q

epidemiology of croup

A

usually 6months to 6years

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8
Q

causes of croup

A

viral:

  • parainfluenza
  • adenovirus
  • RSV
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9
Q

presentation of croup

A
  • sudden onset, seal like barking cough
  • stridor: harsh, rasping
  • chest wall and/or sternal indrawing
  • typically worse at night and increase with agitation
  • hoarse voice
  • prodomal: 12-49h prior: non specific URTI
  • in moderate to severe cases: child showing signs of resp distress or failure
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10
Q

investigations for croup

A

clinical diagnosis but

CXR: subglottic narrowing

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11
Q

management of croup

A
  • analgesia
  • consider admission if moderate to severe illness or resp rate high with fever
  • dose of oral dexamethasone
  • emergency: nebulised adrenaline and high flow O2
  • safenetting (cant talk, drooling, wants to sit instead of lying, skin between ribs being pulled in, child pale/blue/grey for more than few sec)
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12
Q

cause of epiglottitis

A

haemophilus influenzae type B (Hib vaccine)

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13
Q

features of epiglottitis

A
  • rapid onset
  • high T, generally unwell
  • stridor: soft, whispering
  • drooling of saliva
  • ‘tripod’ position
  • voice: muffled, reluctant to speak
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14
Q

investigations for epiglottitis

A
  • direct visualisation

- XRAY if worried about foreign body: thumb sign, swollen epiglottitis

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15
Q

management of epiglottitis

A
  • immediate senior involvement
  • DO NOT EXAMINE THROAT (if so, make sure facilities for immediate intubation)
  • oxygen
  • IV antibiotics
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16
Q

presentation of foreign body inhalation

A
  • sudden onset resp distress

- associated with choking/gagging, coughing, stridor, vomiting

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17
Q

management of foreign body inhalation

A

assess severity
do they have effective/ineffective cough?
- if effective: encourgae cough
- if ineffective: 5 back blows/5 thrusts (if conscious), open airways 5 breats and start CPR (if unconscious)

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18
Q

what is anaphylaxis

A

type 1 hypersensitivity reaction

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19
Q

presentation of anaphylaxis

A
  • wheeze
  • stridor
  • pallor and sweating
  • hypotension, tachycardia
  • generalised pruritis
  • rash
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20
Q

management of anaphylaxis

A
  • adrenaline pen
  • antihistamines
  • advice on allergen avoidance
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21
Q

haemangioma

A
  • slowly progressive airway obstruction/stridor since birth
  • can have capillary haemangiomas (strawberry marks)
  • natural course: enlarge over first 12-24 months of life
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22
Q

presentation of GORD in infants

A
  • intermittent breathing difficulties with symptoms of stridor, episodes of colour changes and/or recurrent chest infections
  • reduced feeding
  • crying on or after feeding or on lying flat
  • vomiting
  • green faeces
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23
Q

treatment of GORD in infants

A
  • small regular feeds
  • correct feeding/burping technique
  • meds: carobel feed thickened, gaviscon, omeprazole
  • surgery
    (tends to resolve with weening)
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24
Q

which groups are high risk for GORD

A
  • neurological or muscular problems
  • pre-term
  • severe allergy
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25
which sign points towards upper resp tract infection compared to LTRI
wheeze: lower stridor: upper
26
signs of increased work on breathing
``` tracheal tug recession increased resp rate abdominal breating cyanosis 'tripod' position - stridor/hoarse voice/drroling ig upper airway obstruction ```
27
def acute, chronic and reccurent cough
acute <3 weeks chronic: 4-8 weeks reccurent: 2+ times a year
28
differentials of cough in children
- congenital heart disease - asthma - infection (ie pneumonia) - pneumothorax (mainly teenagers) - sarcoidosis - foreign body inhalation - CF - parental cig smoking - functional ie tics, anxiety
29
def asthma
reversible, paroxysmal inflammation of the airwyas, accompanied by wheezing, coush, SOB and exacerbated at night and early morning
30
pathophysiology of asthma
- airway obstruction - smooth muscle hyperplasia and hyperactivity - inflammation (histamine bvia IgE mediated allergens: increase mucus prod)
31
def status asthmaticus
asthma attack that does not respond to immediate medical treatment and is life threatening
32
types of asthma
- atopic/extrinsic: allergic reaction from extrinsic source | - non-atopic/intrinsic: drug related, exercise, stress, occupational
33
precipitants of asthma
- cold air and exercise - emotion - allergens - pollution and irritant dust, fumes, vapours - drugs (NSAIDs, beta blockers) - diet - infection, smoking
34
asthma: grading severity
Moderate: - PEFR > 50-75% best or predicted with normal speech - with no features of acute severe or life threatening asthma Acute Severe: - PEFR 33-50% best predicted OR - Resp rate > 5-10 resp/min of normal for each age group OR - increased HR OR - inability to complete sentences OR - inability to feed in infants w/ O2sats > 92% Life Threatening: - PEFR < 33% best or predicted OR - O2sats < 92% OR (any of the following individually - altered consciousness, exhaustion, cardiac arrhythmias, hypotension, cyanosis, poor resp effort, silent chest, confusion
35
what are predicters of good control of asthma
- no day symptoms - no night waking - no rescue meds - no asthma attacks - normal lung function - minimal side effects
36
management of asthma (chronic)
- control of asthma: treat when needed and decrease treatment when control is good, check asthma technique - non pharmacological (quit smoking, lose weight, breathing exercises, avoid allergens, info and support advice, assess for depression and anxiety) - pharmacological: SABA (PRN), ICS (if use SABA/have symptoms > 3*week, wake up at night at least once a week due to symptoms), LTRA (added to ICS), LABA (if LTRA not controlling it, replace LTRA with LABA)
37
management of acute exacerbation of asthma
- O2: maintain 94-98% - SABA: 1 puff every 30-60s, up to 10 puffs, repeat 10-20s (if life threatening or hypocis: nebulised 5mg) (monitor K+) - ipratropium bromide nebs if poor response to salbutamol - IV magnesium sulfate (monitor BP)
38
following acute exacerbation of asthma, what is the discharge plan
- any current change in meds - review by GP 48h later, weaning off plan - clinic appointment 2 months later
39
diagnosis of asthma
- under 5s: clinical - spirometry with bronchodilator reversibility test (BDR) - FeNO (fractional exhaled nitric oxide): levels rise in inflammatory cells - check not occupational
40
assessment of child with suspected pneumonia
- severity assessment: PEWS, physical exam, degree of agitation and consciousness (signs of hypoxia), signs of exhaustion and hydration status - refer to hospital if seriously ill
41
epidemiology of CF
- autosomal recessive condition - most common in caucasians - affects 1:2500 births
42
pathophysiolofy of CF
abnormal ion transport across epithelial memebranes: - in airways: reduction of airway surface liquid layer - dysregulation of inflammation and defence against infecction - sweat glands, pancreatic ducts, intestine affected
43
which organisms colonise CF patients
- staphylococcus aureus - pseudomonas aeruginosa - burkholderia cepacia - aspergillus
44
diagnosis of CF
- screening; heel prick test: raised immunoreactive trypsinogen - check common CF gene mutations: if 2 present: - sweat test to confirm diagnosis
45
clinical features of CF
- lungs: thick, sticky mucus buildup, bacterial infection and widened airways - skin: salty sweat - sinusitis - blocked biliary ducts (cirrhosis and portal hypertension) - blocked pancreatic ducts (DM) - maldigestion and absoprtion (pancreas insufficiency) + mecomium ileus and distal intestinal obstruction - vas deferens and fallopian tube blockage: sterility
46
Management in CF
- ohysio x2 daily for airway clearance and postural drainage - high calorie diet (including fat intake), vit supplements and pancreatic enzyme supplements with each meal - prophylaxis oral antibiotics - minimise contact with other CF patients - nebulised d>Nase or hypertonic saline helps with mucus viscosity - lung transplant
47
different types of Heart problems in children
- congenital: acynotic cyanosis - aquired: myocarditis, rheumatic heart disease - Inherited: HOCM, Marfan's syndome
48
types of acynotic congenital heart disease
- septal defect (ventricular and atrial) - aortic/pulmonary stenosis - coarctation of the aorta - patent ductus arteriosus - mitral/tricuspid stenosis
49
types of cyanotic congenital heart disease
5Ts - Fallot's Tetralogy - TGA (transposition of great arteries) - complete atrio-venTricular septal defect - tricuspid atresia - truncal arteriosus
50
non specific symptoms in CHD
- poor feeding/weight loss - SOB/increased work on breathing - clammy when breathing - increased sleepiness - irritability
51
non specific signs of CHD
- cyanosis - tachycardia - tachypnoea - murmurs - enlarged liver - crackles
52
specific symptoms/signs in coarctation of the aorta
- cold feet/legs - femoral pulse weak/Absent - systolic hypertension of upper limbs, BP arms >>> legs - headaches and abdo/leg cramps
53
specific signs in patent ductus arteriosus
- bounding pulses | - increased systolic BP
54
Fallot's tetralogy parts
- ventricular septal defect - large overriding aorta - right ventricular hypertrophy - pulmonary artery narrowing
55
specific signs of Fallot's tetralogy
clubbing
56
TGA presentation
central cyanosis at birth
57
tricuspid atresia problem
no tricuspid valve: no blood flow from RA to RV
58
truncus arteriosus problem
connection between aorta and pulmonary artery
59
risk factors for CHD
- maternal factors: anti seizure meds or lithium during pregnancy, uncontrolled DMT1, lupus, rubella in T1 - FH - chromosomal abnormalities (trisomy 13 or 18, Down's syndrome, turner's, Karageners, DiGeorge, cri du chat)
60
management of CHD
- oxygen if cyanotic - digoxin, diuretics - adequate nutrition (if poor feeding) - catherisation or surgical repair - prostaglandin with TGA and prostaglandin inhibitors with PDA
61
neonatal blood spot screening
- congenital hypothyroidism - CF - sickle cell disease - phenylketonuria - MCADD (medium chain acyl-CoA dehydrogenase deficiency) - maple syrup urine disease (MSUD) - isovaleric acidaemi - glutarix aciduria type 1 - homocysturia (HCU)
62
risk factors involved in child maltreatment
child: - younger, increased needs, low birth weight, multiple births parental: - younger, mental illness, drug/alcohol abuse, domestic violence, low SES, parents were abused, criminal hx, chaotic/socially isolated families, vulnerable/unsupported parents, previous child maltreatment in other member of family, known maltreatment of animals
63
what is the toxic trio of maltreatment
- domestic violence/abuse - parental mental illness - parental substance misuse
64
elements in Hx pointing towards NAI
- no mechanism offered/mechanism not consistent with injury - delay in reporting the injury/seeking medical attention - inconsistent Hx from parents - inappropriate reaction from parents - recurrent injuries - injury inconsistent with child's age, development, mobility
65
NAI fractures presentation
- metaphyseal fractures - posterior rib fractures - fractures of different ages - complex skull fractures - long bone shaft fractures in non-mobile child
66
NAI bruises presentation
- face, back, buttocks (soft tissues) - bruises outline particular object - pattern of bruising ie fingertips
67
NAI burns presentation
uniform shape | glove-stocking distribution
68
presentation of NAI in a baby
- irritability - poor feeding - increased head circumference - seizures - reduced GCS - full frontanelle - anaemia - retinal haemorrhage
69
fabricated or induced illness presentation
- often background of existing disease - bizzare illness events - strnage new symptoms - parental reportage out of keeping with physical signs - symptoms not witnessed by others - unneeded operations
70
management of fabricated or induced illness
FII (fabricated or induced illness) pathway
71
neglect presentation
- failure to thrive - inadequate hygiene - poor development or emotional attachment to child's caregiver - delay in development in speech and language - poor attendance in school and health appointments - failure to supervise/unsupervised young children at home
72
how to do child protection medical assessment
- must be done by registar + level paediatrician and have named consultant on sheet - full Hx, exam, growth chart, obs, body map, photography, investigations as appropriate - child must be questions away from carers
73
differentials to NAI bruising
- accidental injury - mongolian blue spots - leukaemia or aplastic anaemia - platelet and coag pb: immune thrombocytopaenic purpura, haemophilia A, vWd, chrismas disease - meningococcal septicaemia, Henoch schonlein purpura
74
differentials to broken bone
- NIA - accidental injury - osteogenesis imperfecta - copper, vit D or vit C deficiency - ehler danlos or other hypermobility syndromes - JOBs syndome
75
differentials for abdo pain and diarrhoea
common: - constipation - infectious gastroenteritis - acute appendicitis - UTI - abdominal trauma - primary dysmenorrhea - pneumonia - functional (IBS or abdominal migraine) - coeliac disease less common - intussusception - Merkel's diverticulum - mesenteric adenitis - Hirschprung's disease - IBD - small/large bowel obstruction - volvulus - necrotising enterocolitis - peptic ulcer disease - GORD - DKA - neoplasm: neurobladtoma or Willms nephroblastoma
76
differentials of meleana
- bacterial diarrhoea - IBD - tearing from anal vein - polyp - intussusception
77
presentation of IBD
- diarrhoea (non bloody (crohns) /bloody (UC)) - abdo pain - pyrexia - oral ulcers (crohns) - abdo mass in RIF - PR bleeding (UC) - mucus/pus - tenesmus - perianal disease - weight loss - malabsorption
78
coeliac disease presentation
symptoms coincide with introduction to cereals - failure to thrive - diarrhoea - abdominal distention and cramping - nausea and vomiting - anaemia - weight loss
79
Willms nephroblastoma presentation
- abdominal mass (unilateral) - painless haematuria - flank pain - anorexia - fever
80
management of willms nephroblastoma
- refer for paediatric review within 48h | - nephrectomy, chemotherapy, radiotherapy
81
investigations for IBD
- serum FBC, inflam markers, U&Es, LFTs, TFTs, ferritin, B12, folayte, vit D and coeliac serology - stool microscopy and culure (C diff toxin and faecal calprotectin) - colonoscopy with biopsies - CT for staging (Crohns) - AXR if obstruction, absecesses, fistulas and strictures
82
treatment of Crohns disease
may require hospital admission - stop smoking - oral/IV corticosteroids for flare ups (mesalazine as second line) - enteral feeding with elemental diet - azathioprine ot mercaptopurine to maintain remission - surgery
83
treatment of ulcerative colitis
- topical (rectal) or oral aminosalicylate | - oral corticosteroids (second line)
84
investigation of coeliac disease
- serology: tissue transglutaminase (TTG) antibodies (IgA) - endoscopic intestinal biopsy (villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina, propria infiltration with lymphocytes)
85
treatment of coeliac disease
- gluten free diet | - pneumococcal vaccine
86
pyloric stenosis presentation
- projectile non bile stained vomiting at 4-6 weeks of life - FH - males> females
87
intussusception presentation
- 6-9 months of age - colicky pain, diarrhoea and vomiting - suasage shape mass, red jelly stool
88
when do you need to worry about refeeding syndrome
if patient has not eaten in > 5 days
89
cause of refeeding syndrome
switch from gluconeogenesis (catabolic state) to insulin release: stimulates glycogen, fat and protein synthesis (anabolic state) results in rapid intracellular uptake of cofactors of potassium, magnesium and phosphate --> electrolyte imbalance can be fatal
90
clinical features of refeeding syndrome
- electrolyte abnormalities (hypophosphotaemia, hypokalaemia, hypomagnesaemia, hyponatraemia, metabolic acidosis, thiamine deficiency - clinical manifestations: muscle weakness, seizures, peripheral oedema, cardiac arrhythmias, hypotensionn delirium
91
management of refeeding syndrome
- replacement of fluid and electrolytes - start feeding cautiously - frequent electrolyte monitoring - thiamine replacemtn (to avoid beri beri delirium)
92
what are the risk of rapid weight loss
- refeeding syndrome - hypoglycaemia - risk of infection - cardiac arrythmias
93
aetiology of anorexia nervosa
- genetic factors - events around puberty - cultural promotion of thinness
94
presentation of anorexia nervosa
behavioural/psychological: - pre occupied with food - dysmorphia/feeling fat - wont eat in front of others - hiding food - may be compulsive exerciser clinical features: - low BMI - amenorrhea - headaches - cool peripheries/hypothermia - constipation - dry skin - hair loss - fainting/dizziness/hypotension - lethargy - bradycardia - peripheral oedema
95
what are the significant mortality in anorexia nervosa
- sudden cardiac death - suicide - chronic emaciation and pneumonia
96
issues with laxative abuse
short term: - K+ and Na+ de^pletion - severly dehydrated - cardiac arrest long term: - loss of bowel motility if try to stop: - oedema due to refeeding syndrome: CHF and psychological distress of weight gain
97
diagnosis of anorexia nervosa
- restriction of energy intake relative to requirements leading to low BMI - intense fear of gaining weight - dysmorphia
98
management of anorexia nervosa
physical stabilisation - commence vitamins (thiamine, vit B complex, multivitamins) - if not drinking: IV 10% dextrose - diet plan: aim for 0.5-1kg weight gain a week MDT apprach: - child psychiatrist - dietatictian - therapists - paediatrician relapse prevention: - transitional phases (ie uni) - 3rd sector ie BEAT charity
99
diagnosis of bullimia nervosa
- recurrent episodes of bing eatinf - sense of lack of control - recurrent inappropriate compensatoery mechanisms to prevent wieght gain (self vomiting, misuse of laxatives, diuretics) - binge eating and comensory mechanisms occur at least once a week for 3 months - self evaluation is influenced by body shape and weight - disturbance does not occur excusively during episodes of anorexia nervosa
100
management of bullimia nervosa
- refer to specialist | - bulimia nervosa focused family therapy
101
differentials of rapid weight loss
- coeliac diease - IBD - oesophageal pb ie achalasia - T1DM - hyperthyroidsim - malignancy - anorexia nervosa - severe depression/OCD/autism - juvenile arthritis - addisons
102
risk factors for dehydration
- low birth weight - <1 year - 2+ vomiting episodes and more than 5 diarrhoeal episodes in previous 24h - malnourished children
103
presentation of dehydration
- sunken anterior fontanelle - dry mucus membrane - tachycradia - reduced cap refill - reduced skin turgor
104
causes of gastroenteritis
viral: - rotavirus - adenovirus - calcivirus - astrovirus bacteria: - campylobacter - C diff - E coli - salmonella - shigella - cholera parasite: - giardia lambia - cryptosporidium
105
what pathogens are associated with blood in stool in gastroenteritis
- campylobacter - shigella - e coli - rotavirus - salmonella
106
main causes of gastroenetiritis in young children
rotavirus | adenovirus
107
causes of food poisoning
- campylobacter (found in raw/uncooked meat esp poultry) - salmonella (raw/uncooked meat, raw eggs, milk - listeria (chilled, ready to eat foods)
108
cows allergy presentation
- failure to gain weight - abdominal pain and crying - diarrhoea and vomiting - rash and wheeze
109
differentials of poor feeding
- difficulty latching on - infection (resp) - physical malformations - neurological (swallowing pb) - cardiovascular (congenital cardiac conditions) - cows milk allergy/lactose intolerance - GORD
110
abdominal migraine presentation
- sudden onset episodic midline abdominal pain lasting between 1 and 72h - anorexia, nausea, vomiting, pallor and other vasomotor symptoms are common
111
what additional symptoms do you have in viral gastroenteritis
- fevers - headaches - chills - fatigue
112
modes of transmission of gastroenteritis
viral: - contaminated water/food - contact with vomit/fomites (faecal/oral) bacterial: - as above - improperly prepareed and stored food
113
E coli presentation
- associated with diarrhoea with blood in stools and HUS | - occurs in clusters after ingestion of contaminated food
114
complications of gastroenteritis
- dehydration - HUS - post infective IBS - IBD - reactive arthritis
115
causes of secondary (typical) HUS
- E coli - pneumocooccal infection - HIV - rare: SLE, drugs, cancer
116
presentation of haemolytic uraemix syndrome
triad: - microangiopathic haemolytic anaemia - thrombocytopaenia - renal insufficiency symptoms: - abdo pain - bloody diarrhea - fever - seizures - lethargy
117
what investigations to do when suspected HUS
FBC: anaemia, thrombocytopaenia, fragmented blood film - U&Es: AKI - stool culture: STEC infection and shiga toxin (from E coli)
118
management of HUS
- supportive treatment (fluids, blood transfusion, dyalisis) - no antibiotics needed - plasmapharesis/IVIG
119
management of gastroenteritis
- rehydration (fluids or ORS) - education about infection control (4Cs: cleaniless, cooking, chilling, cross contamination) - stool culture - do not attend school until 48h after last episode of D&V - notify healthprotection team if due to food - explain that D can last up to 2 weeks and V up to 3 days - specific treatment with campylobacter, C diff, shigela
120
red flags for dehydration
- becomes suddenly unwell - pale/mottled - persistent vomiting - decreased urine output/wet nappies - irritable/lethargy - cold extremities
121
severly ill child red flags
- fever >38 (if aged <3 months), or > 39 (if aged 3-6 months) - colour: pale, mottled, cyanosed - level of consciousness reduced, stiff neck, bulging fontanelle, status epilepticus, focal neurological signs or seizures, rash - significant resp distress (grunting, nasal flarring, use of acc muscles, tachypnoea) - bile stained vomiting - severe dehydration/shock
122
causes of bacterial meningitis by age group
0-3 months: - group B strep (neonates) - E coli - listeria monocytogenes 3 months- 6 years - neisseria meningitidis - streptococcus peumonia - haemophilus influenzae B 6 years above: - neisseria meningitidis - streptococcus pneumlonia
123
causes of viral meningitis
- enterovirus (coxsachie and echovirus) - adenovirus - mumps - EBV - CMV - varicella zoster - herpes simplex - HIV
124
risk factors for meningitis
- low family income - children with facial cellulitis, periorbital cellulitis, sinusitis and septic arthritis - asplenia - basal skull fracture - attendance at day care/overcrowding - maternal infection and pyrexia at time of delivery
125
epidemiology of meningitis in paeds
- neonates | - adolescents
126
presentation of meningitis in neonates
``` poor feeding lethargy irritability apnoea listlessness fever hypothermia seizures jaundice pallor bulging fontanelle high pitched cry floppiness ```
127
presentation of meningitis in infants/young children
``` fever lethargy irritability nausea and vomiting bulging fontanelle neck stiffness altered consciousness opisthotonus poor apetite seizures hypothermia ```
128
presentation of meningitis in older children
``` fever headache nausea/vomiting neck stiffness photophobia altered alertness seizures poor apetite opisthotonus hypothermia ``` positive kernig's sign (pain on lowering leg extension with hip flex) and brudzinski's sign (involuntary flexion of knees and hips with neck flexion)
129
investigations in suspected meningitis
- bloods: FBC, CRP, coagulation screen - blood culture - urine culture - blood glucose - blood gas - LP for CSF
130
diagnosis of meningitis
- clinical: symptoms § pos kernig and brudinski sign | - CSF results
131
management of meningitis
ANTIBIOTICS - under 3 months: IV cefotaxime and amoxicillin/ampicin - over 3 months: IV ceftriaxone and vancomycin (if recent abroad travel) IM if before hospital transfer VIRAL: - antiviral - dexamethasone: adjuvent to antibiotics to reduce incidence of neuro and audio complications (MUST be given before or with first dose of antibiotics) prophylaxis offered to household audiology assesmment as follow up
132
complications of meningitis
acute: - seizures - raised ICP - metabolic disturbances - coagulopathy - anaemia - coma - death long term: - hearing impairement - psychological problems - epilepsy - developmental/learning difficulties - neurological impairement
133
septic sceen
- blood cultures - urine sample - bloods: FBC, CRP, lactate if indicated: - CXR - LP - rapid antigen screen on blood/CSF/urine - meningococcal and pneumococcal PCR on blood/CSF - PCR for viruses in CSF
134
risk factors for sepsis (general to paeds)
- congenital heart failure - chronic steroid dependency - burns - asplenia - neonates - presence of central line or vascular access device - malignancy or bone marrow transplant or impaired immune function - neutropaenia - complex urogenital anatomy or repair - neuro impairement - technology dependent (ie ventilated)
135
red flag sepsis for children
- hypotension - tachycardia - high lactate - prolonged cap refill - pale/mottled/cyanoses or rash - O2 needed to maintain O2sats > 92% - resp rate > 60 min or grunting - AVPU: V, P or U - dry nappies, lack of response to social cues, decreased activity, high pitched or continuous cry
136
management of neonatal sepsis
- IV benzypenicillin with gentamicin - maintain adequate O2, fluid and elctrolytes - prevent/manage hypoglycaemoa and metabolic acidosis
137
prevention of group B strep infection in neonates
give antibiotics to mother during mabout if : - previous group B strep baby - group B strep in urine during pregnancy - fever during labour - goes into labour before 37 weeks
138
prevention of meningitis
vaccination MenB at 2, 4 and 12 months Hib/menC at 12 month MenACWY at 14 years
139
kawasaki disease presentation
- usually in under 5s - persistent (>5days) fever - lymphadenopathy - bright red cracked lips - strawberry tongue - bilateral non infective conjunctivitis - desquamating rash
140
third generation cephalosporin examples
cefotaxime cefixime cedtazidime ceftriaxone
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side effects of penicillins
- D&V, nausea - hypersensitivity - skin reaction - thrombocytopaenia rare but important: - agranulocytosis, angioedema, haemolytic anaemia, neutropaniea, seizures, SCARs
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what class of drugs does vancomycin belong to
glycopeptide antibacterials
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SE of vancomycin
back pain, bradycardia, cardiac arrest, cardiogenic shock , chest pain, dyspnoea, hearing loss, hypotension, nephrotoxicity agranulocytosis, dizziness, drug fever, oesinophilia, hypersensivity
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presentation of transient synovitis
- acute onset limp, with or without pain - reduced hip movements - child systemically well, self limiting - often preceded by viral inf (URTI or gastroenteritis)
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epidemiology of transient synoviitis
boys > girls | age 4-8
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management of transient synovitis
- self limiting - rest - analgesia (OTC)
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septic arthritis/osteomyelitis persentation
- acute onset pain - non weight bearing - extreme pain on movement - erythema and heat over site - fever - systemic upset
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fracture presentation
acute onset pain reduced/non weight bearing typical: 0-3 y
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perthes disease epidemiology
boys > girls | age 4-8
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presentation of perthes disease
- gradual onset limp - painless - stiffness and reduced hip movements - can be bilateral
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pathophysilogy of perthes disease
- avascular necrosis due to interrupted blood flow to femoral epiphysis - remodelling occurs but can result in deformity
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epidemiology of slipped upper femoral epiphysis (SUFE)
boys > girls | age > 10
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risk factors for SUFE
- obesity | - hypothyroidism
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presentation of SUFE
different presentation - sudden onset pain and non weight bearing or - gradual onset vague pain that may be referred to knee and a limp
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cause of SUFE
proximal femoral growth plate becoming unstable | epiphsis and diaphysis can slip
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development dysplasia of the hip presentation
girls > boys | usually detected at birth
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risk factors for DDH
``` female breech position positive FH firstborn children oligohydramnios birth weight > 5 kg congenital calcaneovalgus foot deformity ```
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presentation of DDH
- asymmetrical skin folds - leg length disparity - buttocks flattened - walking with affected leg in external rotation - older children: fradual onset of painless limp
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management of DDH
-ultrasound to confirm diagnosis (if child > 4.5 months: XRay) - spontaneous stabilisation by 3-6 weeks of age - Pavlik harness in children < 4-5 months - surgery in older childrenn
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SUFE management
- AP and lateral views Xray (frog legs) | - internal fixation
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Perthes disease management
- plain Xray or technetium bone scan or MRI - if less than 6: observation, or cast or brace to keep femoral head in acetabulum. - older: surgical management
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septic arthritis management
- joint aaspiration for culture, blood culture, bloods | - antibiotics, joint washout, arthrotomy
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types of juvenile idiopathic arthritis
- oligoarthritis (<5 joints affected in 6/12, ANA pos) - polyarthritis (>5 joints affected in 6/12, can be RH pos or neg) - enthesitis related arthritis (inflam where tendons attach to bone) - psoriatic arthritis (mainly fingers and toes + dactilitis and psoriasis) - systemic onset JIA (fever and rash) - undifferentiated arthritis (symptoms don't fit with anything else)
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JIA management
referral to rheumatology - NSAIDs - corticosteroids - methotrexate
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presentation of JIA
<16y, >3months duration - join pain and swelling (usually medium sized jointss) - limp
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indications for specialist assessment
Pain waking the child at night ○ Malignancy Redness, swelling or stiffness of the joint or limb ○ Infection or inflammation Weight loss, anorexia, fever, night sweats or fatigue ○ Malignancy, infection or inflammation Unexplained rash or bruising ○ Haematological or inflammatory joint disease or child maltreatment Limp and stiffness worse in the morning ○ Inflammory joint disease Unable to weight bear or painful limitaion of range of motion ○ Trauma or infection Severe pain, anxiety, agitation afrer traumatic injury ○ Neurovascular compromise or impending compartment syndrome Palpable mass ○ Malignancy or infection
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epidemiology of UTI
girls > boys highest incidence in first year life (boys>girls) e coli most common pathogen
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presentation of UTI in children <3 months
most common to least common - fever, vomiting, lethargy, irritability - poor feeding, failure to thrive - abdominal pain, jaundice, haematuria, offensive urine
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presentation of UTI in children > 3months
from most common to least common: preverbal: - fever - abdominal pain, loin tenderness, vomiting, poor feeding - lethargy, irritability, haematuia, offensive urine, failure to thrive verbal: - frequency, dysuria - dysfunctional voiding, changes in continence, abdo pain, loin tenderness - malaise, fever, vomiting, haematuria, offensive cloudy urine
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risk factors for underlying pathology in UTI
- poor urine flow, dysfunctional voiding - Hx of previous UTI - recurrent fever of uncertain origin - antenatally diagnosed renal abnormality - FH of vesicouretic reflux or renal disease - constipation - enlarged bladder - abdominal mass - spinal lesion - poor growth - high BP
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management of UTI
- if <3 months, urgent paeds referral - for upper UTI/cystitis: reconsider referral and start on oral cefalexin or co-amoxiclav - for lower UTI/cystitis: trimethoprim or nitrofurantoin
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further investigations for UTI
- USS: if recurrent UTI > 6months, atypical infection, >6 months and first UTI that responds to treatment - DMSA scan (renal function and scarring) if <3y with typical or reccurent UTI or >3y with reccurent UTI - MCUG (micturating cystogram) to identify VUR, bladder abnormalities or posterior urethral valves if <6m with atypical/reccurent UTI or >6m if dilation on ultrasound, poor renal flow, no E coli inf of FH VUR
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pathogen of UTI in children
- E coli - proteus mirabilis (mainly boys) - staphylococcus saprophyticus (adolescents) - pseudomonas (in urinary tract malformation or dysfunction) - klebsiella aerogenes and enterococcus species - adenovirus (rare) - cadidal UTI (immunocompromised)
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def vesicoureteric reflux (VUR)
abnormal backflow of urine from bladder into ureter and kidneys
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epidemiology of VUR
- found in 30% of children presenting with UTI | - 35% will develop renal scarring
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pathophysiology of VUR
- ureters are displaced laterally, entering bladder perpendicular fashion - shortened intramural course - vesicoureteric junction cannot function adequately
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presentation of VUR
- antenatal period (hydronephrosis on USS) - recurrent childhoof UTI - reflux nephropathy (chronic pyelonephritis secondary to VUR)
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investigations when suspecting VUR
- voiding cystourethrogram (VCUG) | - DMSA scan to look for renal scarring
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treatment of VUR
- self improvement | - surgery to remove blockage or repair valve
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what are the different co ngenital abnormalities of kidney and urinary tract in childhood
- renal hypoplasia, dysplasia and agenesis - infantile polycystic kidney disease (IPKD), ADPKD, ARPKD - pelvic kidney/horseshoe kidney/ renal fusion - posterior urethral valves - ectopic kidney
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def Henoch Schonlein purpura
IgA mediated small vessel vasculitis: inflammation and leaking of blood
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which organs does HSP affect
kidneys GIT skin
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which organs does HSP affect
kidneys GIT skin joints
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features of HSP
- palpable purpuric rash (with lov
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features of HSP
- palpable purpuric rash (with localised oedema) over buttocks and extensor surface of arms and legs (non blanching, severe: ulceration and necrosis) - abdominal pain (severe: haemorrhage, intussusception and bowel infarction) - polyarthritis: mostly knees and ankles - features of IgA nephropathy: haematuria, renal failure, proteinuria
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investigations for HSP
BLOODS - FBC and film (exclude thrombocytopenia, sepsis, leukaemia) - CRP and blood cultures (sepsis) - renal function - albumin - urine sample and protein:creatinine ratio - BP
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differentials of HSP
- meningococcal septicaemia - leukaemia - idiopathic thrombocytopenic purpura - HUS
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diagnosis of HSp
palpable purpura with one of the following: - difuse abdo pain - arthritis and arthralgia - IgA deposits on histology - proteinuria/haematuria
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treatment of HSP
- analgesia for arthritis - supportive for nephropathy - monitoring (urine dip for renal impairement and BP for hypertension)
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complications of HSP
intussusception pancreatitis acute renal impairement arthritis/arthralgia esp knees and ankles
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prognosis of HSP
- self limiting condition: 4-6 weeks - 1/3 patients relapse - some develop end stage renal failure
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def of immune thrombocytopenic purpura (ITP)
immune mediated reduction in platelet count
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epidemiology of ITP
- more acute than with adults - equal sex incidence - may follow infection/vaccination - usually self limiting course: 1-2 weeks
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symptoms of ITP
- assymptomatic - purpura - frequent mucosal bleeding (if severe) ie epixtasis
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diagnosis of ITP
- clinical/diagnosis of exclusion | - isolated thrombocytopenia
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treatment of ITP
- if asymptomatic: observed | - symptomatic: corticosteroids and IVIG, platelets transfusion
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def intussusception
invagination of one portion of bowel into lumen of adjacent bowel
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epidemiology of intussusception
infants 6-18 months boys > girls - associated conditions: CF, HSP, crohns, coeliac, abnormal intestinal formation at birth
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features of intussusception
- paroxysmal abdominal colic pain - draws knees up and turns blue - vomiting - blood stained stool (red current jelly) - sausaged shaped mass in RUQ
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def testicular torsion
twist of spermatic cord resulting in testicular ischemia and necrosis - most common in 10-30 year olds - peak incidence: 13-15y
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symptoms of testicular torsion
- pain (severe, sudden onset, can be referred to lower abdomen, elevation of testes does not ease the pain) - nausea and vomiting - swollen, tender testis, retracted upwards - reddened skin - cremasteric reflex is lost
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management of testicular torsion
urgent surgical exploration of both testis
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def epididymo-orchitis
infection of epididymis +/- testes resulting in pain and swelling
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cause of epididymo-orchitis
local spread of infection from genital tract or bladder
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features of epididymo-orchitis
- unilateral testicular pain and swelling - urethral discharge may be present - gradual onset
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management of epididymo-orchitis
antibiotics if organism unknown: -ceftriaxone and doxycycline
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when do yu send a stool for MS&C
If diarrhoea AND - suspect septicaemia - blood or mucus in stool - child is immunocompromised - Hx of travel - diarrhoea > 7days - uncertain about diagnosis of gastroenteritis
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diagnosis Kawasaki disease
clinical
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treatment of Kawasaki disease
- high dose aspirin - IVIG - coronary angiography to check for aneurysms
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presentation of Lyme's disease
- early: fever, arthralgia, malaise, rash - second stage (weeks later): aseptic meningitis, facial palsy, arthritis, carditis - third stage (couple of years later): neuropsychiatric manifestations, chronic fatigue
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treatment of lyme's disease
cefuroxime and amoxicilin
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differentials of prolonged fever
INFECTIVE: - localised infection (ie osteomyelitis) - bacterial infection - deep absecess - infective endocarditis - TB - nontuberculous mycobacterial infections - viral infections (EBV, CMV, HIV) NONINFECTIVE - systemic onset juvenile idiopathic arthritis - SLE - vasculutis - IBD - sarcoidosis - malignancy - macrophage activation syndromes - drug fever - FII
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epidemiology of febrile seizure
- aged 6 months- 5 years - occurs during febrile illness - most common seizure disorder in childhood
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presentation of simple febrile seizure
- short (<15min) generalised seizure - not recurring within 24h - not resulting from acute disease of CNS
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presentation of complex febrile seizure
- focal or generalised and prolonged seizure - duration 15-30 mins - reccuring more than once in 24h and/or - associated with postictal neurological abnormalities ie todds palsy
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def febrile status epilepticus
- complex febrile seizure w/ duration > 30min OR | - shorter serial seizures witout regaining consciousness at interictal state
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what treatment to give in acute management of generalised seizures
- buccal midazolam - rectal diazepam - IV lorazepam - IV phenytoin do not give more than 2 doses of benzos
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diagnosis of epilsepsy
- primarily from Hx from child and eyewitnesses video - triggers aand impairementq (educational, psychological, social) - clinical exam: skin markers of neuro-cutaneous syndrome/neuro pb - EEG - MRI for structural abnormalities - ECG (convulsive syncope)
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challenges of long term management in seizures
- avoid swimming unsupervised and deep baths due to life threatening consequences - driving, contraception and pregnancy an issue - alcohol and poor sleep routines can precipitate seizures - do less well educationally, socially and in future employment
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def inborn errors of metabolism
disorders of enzymatic reactions that degrade, synthesise, or interconvert molecules within cells
221
epidemiology of IEM
- commonly affects the brain | - autosomal recessive inheritance
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different categories of neonatal sepsis
- early-onset (within 72h of birth) | - late-onset: between 7-28 days of life
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cause of neonatal sepsis
- GBS and Ecoli are most common - early onset sepsis: GBS - late onset: staphylococcus epiderlidis, pseudomonas aeruginosa, Klebsiella, enterobacter
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investigations in neonatal sepsis (and how to differentiated between different causes)
- blood culture - urine MS&C: rarely pos for EOS, more useful for LOS - LP
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how does IEM present
- screening - unexpectedly severe presentation of an otherwise common illness - significant metabolic acidosis - unexplaied resp alkalosis - hypoglycaemia - cardiac failure/cardiomyopathy - hepatomegaly/hepatosplenomegaly/liver dysfunction - unexplained drowsiness, coma or irritability - early onset seizures - dysmorphic features - developmental regression or loss of skills - sudden unexplained death
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problem in pheylketonuria
unable to convert phenylalanine inro tyrosine due to enzyme deficiency : excess phenylalanine which is toxic to the brain (developmental delays + regression or loss of skills) + decreased tyrosine
227
management of PKU
very low protein diet supplements of all amino acids except PHE - monitoring of blood PHE levels
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outcomes of PKU
- good - women with PKU need strict diet for pregnancy, or bad outcomes - but as adults, can come off diet
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def global development delay
significant delay in milestones in + areas
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what are the main causes of profound disability in paeds
- chromosomal abnormalities - genetic factors (microduplications, deletions) - cerebral palsy - IEM
231
what investigations for developmental delays
- observation of child - neuro and ear exam - genetic blood test ( CGH microarray and karyotype) - standard blood test (TFTs, CK, urate, chloride, FBC and ferritin, U&Es, LFTs, calcium, lactate, ammonia)
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differentials of fever
- meningococcal disease - bacterial meningitis - herpes simplex encephalopathy - Kawasaki disease - UTI - septic arthritis - pneumonia
233
def cerebral palsy
group of lifelong conditions of motor and coordination dysfunction (tone, posture, movement) caused by non progressive brain lesion in developing brain
234
risk factors for cerbral palsy
- prematurity/low birth weight - intrauterine infections: TORCH - multiple gestations - complications in pregnancy (thrombophilias, haemorrhage, preeclampsia) - birth asphyxia - complicated labour and delivery - kernicterus (from neonatal jaundice) - NAI/head trauma - meningitis/encephalitis - cardiac-pulmonary arrest
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presentation of cerbral palsy
- delays in reaching developmental milestones - hypotonia/hypertonia - weakness in limbs - fidgety, clumsy, jerky mvnt - walking on tiptoes - dysphagia - learning disability - fisting
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treatment of cerbral palsy
- physio - speech therapy - occupational therapy - meds for stiffness: baclofen, diazepam, botulin toxin - surgery: orthopaedics and neurosurgical
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prevention of cerebral palsy
- phototherapy for neonatal jaundice (kernicterus) - vaccinations - buckle children into car seats
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prognosis of cerebral palsy
- most children live into adulthood - can limit activities/independance - may need special school - can cause strain on body - can cause psychiatric pb ie depression
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presentation of autism
- social communication pb - social understanding and interaction pb - social imagination young childre: tandrums, active, difficult to engage with older children: difficult making/maintaining relationship - social cues diff - difficult taking turns - edge of groups
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suumptoms of ADHD
- inattention - impulsivity - hyperactivity
241
clinical features of DMT1
``` hyperglycaemia polyuria polydipsia weight loss excessive tiredness ``` secondary nocturnal enureis skin sepsis candida and othe infections
242
management of DMT1
- insulin theray (one long acting and short acting before meals OR continuous subcutaneous insulin infusion with insulin pump therapy) - monitoring ( at least 5 cap blood glucose test per day and HbA1c 4x/year) - hypos: fast acting glucose by mouth or IM glucagon)
243
complications of diabetes type 1
- increase risk of hypothyroidism, addison's disease, coeliac disease, rheumatoid arthritis - diabetic retinopathy, kidney disease, neuropathy - hypertension
244
symptoms of DKA
- smell of acetones on breath - vomiting - dehydraarion - abdo pain - hyperventilation - hypovolaemic shock - drowsiness - coma and death
245
diagnosis of DKA
- symptoms - acidosis (blood pH<7.3 or high bicarb) - ketanaemia
246
management of DKA
fluids | insulin