Paediatrics Flashcards

(257 cards)

1
Q

Developmental Milestones 2 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

coos and gurgles. turns head to sound

Begins to smile at people. Tries to look at parents. Sucks on hand to sooth

Begins to follow things with eyes
Begins to act bored

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2
Q

Developmental Milestones 8 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Understands no. Mamama/dadada sounds

Stranger awareness. Has favourite toy

Transfers from one hand to another
Picks up cereal between thumb and index finger
Plays peek a boo

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3
Q

Developmental Milestones 18 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Says 10 words
Says no and shakes head

Temper tantrums
Points to show something interesting

Follows 1 step verbal command
Scribbles on own

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4
Q

Developmental Milestones 3 years
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Understands words such as in/on/under
Carries on a conversation using 2 to 3 sentences

Copies adults and friends
Takes turns in games
Shows concern friend crying

Does jig saw 3-4 pieces
Copies a circle with a pencil

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5
Q

cpr in children

A

15 compression s to 2 breaths

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6
Q

Croup (laryngotracheobronchitis) presentation and management

A

Common cause of acute respiratory distress in children 6 months to 3 years

Acute onset of seal-like barky cough in moderate to severe cases accompanied by stridor and sternal/intercostal indrawing
Fever
Viral cause (parainfluenza usually)
note majority of cases mild but if needed…

  • oral dexamethasone 0.15 mg/ kg as a single dose
  • Nebulised Adrenaline 5mls 1:1000 (mod or severe)
  • senior input
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7
Q

symptoms and management of foreign body aspiration

A

sudden onset of respiratory distress associated with coughing, gagging, or stridor. Unilateral wheezing suggests partial obstruction of the main or distal bronchi

management with flexible bronchoscopy or rigid if fails

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8
Q

signs of respiratory distress

A
  • increased RR
  • stridor
  • tracheal tug; retraction at the suprasternal notch
  • intercostal recession
  • subcostal recession
  • head bobbing
  • grunting
  • posture

impending respiratory failure and exhaustion will develop a low respiratory rate (for their age) and breath sounds including added sounds can diminish

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9
Q

differentials child in upper respiratory distress

A

Viral Croup
Epiglottitis (unlikely with haemophilia influenza vaccine)
Foreign body aspiration
Anaphylaxis
Bacterial tracheitis

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10
Q

laryngeal capillary haemangioma

A

slowly progressive airway obstruction / stridor since birth, particularly if the child has other capillary haemangiomas

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11
Q

gastro-oesophageal reflux disease in infants

A

silent symptoms or intermittent distress commonly after feeds and on lying flat, intermittent breathing difficulty with symptoms including stridor, episodes of colour change and / or recurrent chest infections, and behavioural changes such as back arching

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12
Q

stridor present since birth

A

Laryngomalacia or floppy larynx
soft stridor that worsens with feeds

monitor feeding and growth

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13
Q

epiglottitis

A

very rare cause of airway obstruction seen most in children 2-7

sudden onset of distressed child with muffled cough and voice, normal temp, drooling and leaning forward

needs emergency airway management
usually bacterial cause

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14
Q

bacterial tracheitis

A

differenital for epiglottis
younger age; 6 months to 14 months

fever present
sudden onset
hoarse voice and cough
drooling

needs emergency airway
broad spec Abx once airway secured

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15
Q

anaphylaxis presentation

A

Hypotension, Bronchoconstriction or Airway compromise in the setting of an allergic reaction

child pale and sweating (hypotensive), wheeze, stridor

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16
Q

what type of allergic reaction is a food allergy

A

type I hypersensitivity

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17
Q

sensitisation to allergen

A

for an allergy to occur a child must have previously encountered the allergen

Following exposure to an antigen the protein causes cross binding of two bound IgE molecules on the Mast Cell or Basophil surface. This process results in degranulation of the Mast Cell.

Histamine is released immediately causing the reaction

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18
Q

actions of histamine

A

localised irritation

vasodilation

bronchoconstriction

endothelial cell separation - resulting in urticarial rash

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19
Q

criteria for prescribing an Adrenaline Pen

A
  • History of Anaphylaxis
  • Previous cardiovascular / Respiratory involvement
  • Evidence of airway obstruction
  • Poorly controlled Asthma requiring regular inhaled corticosteroids
  • Reaction to a small amount of allergen
  • Ease of allergen avoidance

in less severe allergy, having antihistamine available can be sufficient

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20
Q

what is bronchiolitis

A

acute inflammation of the bronchioles usually caused by RSV
affects infants

initially subtle symptoms which worsen over 3-4 days

usually self limiting and needs supportive care but infants can become more unwell and need admission

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21
Q

symptoms of bronchiolitis

A

initial coryzal symptoms

progress to some or all of (day3-6)
- increased work of breathing
- typical cough
- poor/reduced feeding
- pallor
- exhaustion
- widespread wheeze and crackles
- fever (low grade)
- apnoea
- reduced oxygen sats
- tachycardia of bradycardia (more worrying)

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22
Q

symptoms bronchiolitis requiring admission

A
  • 50% feeding intake
  • pre-existing condition such as prematurity, CF
  • RR>70
  • O2 sats <92%
  • moderate resp distress
  • apnoeas
  • clinical dehydration
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23
Q

management of bronchiolitis in hospital

A

maintain oxygen sats

NG feed

if severely worsening; NBM, FBC, blood gas, biochem
IV fluids
orogastric decompression

consider CPAP if very severe
PICU?
consider Abx ?concurrent bac infection

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24
Q

accurate assessment of feeding in an infant

A

calculate the amount in mls/kg/day not ounces as reported by parents

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25
minimum milk requirement for growth
150ml/kg/day in first month 100ml/kg/day after as long as meeting growth requirements
26
antenatal Hx
important in early childhood illness maternal health delivery post delivery
27
systolic paediatric murmurs
Tetralogy of Fallot VSD pul/aortic stenosis
28
diastolic murmurs
pul or aortic valve regurge mitral stenosis
29
symptoms/signs of HF in children
shortness of breath; tachypnoea and dyspnoea poor feeding; can't breathe and feed comfortably tachycardia hepatomegaly poor pulses acidosis sweating oedema only in children 3years+
30
management of HF in children
diuretics ACEi oxygen; with caution can close ducts prostaglandins; prostin, to keep duct open monitor diet/fluid intake inotropes such as dopamine sometimes catheter interventions, surgery last resort
31
diet in infants in HF
have higher energy requirements but need to control volume - high calorie feeds, supplements, frequent feeds less volume sometimes need NG or if long term gastronomy
32
embryology of heart
forms from mesenchymal cells 4 chamber heart forms by 40 days
33
types of heart problems in children
congenital - cyanotic - acyanotic acquired (rare) - myocarditis (coxsackie B virus) - viral pericarditis - rheumatic heart disease inherited - HOCM - marfans etc
34
presentation of congenital heart disease
antenatal; routine scan or FHx initiated scan postnatal; routine check, symptomatic (cyanotic)
35
acyanotic CHD
majority septal defects; VSD, ASD also - aortic/pulmonary stenosis - PDA - coarctation of aorta - mitral/tricuspid stenosis rare
36
VSD murmur
pansystolic
37
PDA murmur
continuous + bounding pulses
38
coarctation (narrowing) of aorta presentation
femoral pulses weak/absent hypertension upper limbs commonly associated with other heart defects in newborns risk of necrotising enterocolitis presents around 3 days. needs surgery and give prostin to keep a PDA open
39
cyanotic CHD
many but most important are - fallot's tetralogy - transposition of great arteries (TGA) - complete atria-ventricular septal defects
40
atrial-ventricular septal defect
atrial and ventricular septal defect can be partial (no ventricular) or complete higher incidence in trisomy 21 LAD on ECG
41
CHD and chromosomal syndromes
trisomy 21; 40% have CHD trisomy 13 (Patau's); 80% have CHD trisomy 18 (Edward's; 80-100% have CHD
42
DiGeorge syndrome
autosomal dominant condition. DiGeorge syndrome is associated with congenital heart disease.
43
sex chromosome aneuploidies
Turners 45XO Klinefelters 47XXY Triple X 47XXX + others
44
what is tested for on heel prick test
MCAD HCU Sickle cell Isovalaric acidaemia Cystic fibrosis Hypothyroidism Phenylketonuria
45
Kawasaki disease
inflammatory condition swinging fevers resistant to paracetamol lymphadenopathy red eyes and tongue rash swollen feet and hands platelet rise in 2 weeks can cause coronary artery aneurysms; cardiac complications reduced by early aspirin and IV gammaglobulin
46
what can happen if VSD not treated
may close spontaneously but if left reversal of the shunt from L-R to R-L can occur which can lead to permanent pulmonary hypertension VSD needs medical or surgical management
47
ASD management
needs closure long term can result in arrhythmias or shunt reversal
48
pre term PDA
use NSAIDS for first 2-3 weeks may close if not surgery
49
4 components of tetralogy of fallot
pulmonary outflow obstruction right ventricular hypertrophy VSD overriding aorta baby presents with blue spells. needs surgery
50
innocent flow murmur
Many children will have an innocent flow murmur when they are pyrexic
51
differentials acutely breathless school age child
asthma pneumonia pneumothorax (unlikely) foreign body aspiration cardiac failure
52
acute severe asthma examination findings
Severe recession; sc/ic/ tracheal tug Posture sitting forward; ‘Tripod’ position Wheeze may be audible from end of bed Hyperexpanded chest; Symmetrical expansion; poor expansion if severe trachea central cardiac apex in usual position liver pushed down; edge palpable. Resonant but equal Air entry symmetrical; poor Air entry indicates increasing severity
53
severe pneumonia O/E
Respiratory distress with recession and tracheal tug Wet cough; +/- Grunting Expansion may be asymmetrical if severe unilateral pneumonia Dullness over consolidation may be present Reduced air entry +/- Bronchial breathing / crackles over area of infection
54
what is Harrison's sulcus
groove under ribcage seen in children with chronic respiratory disease e.g. severe asthma
55
sputum MC&S children
usually over 7 years can if younger or cannot do a cough swab
56
investigations for chronic lung disease in a child e.g. bronchiectasis
CT chest Measurement of serum immunoglobulin levels; assesses for primary immune deficiencies Sweat chloride test; for CF
57
organs affected by cystic fibrosis
sinuses lungs skin - saltier sweat liver pancreas - exocrine and endocrine insufficiency intestines - malabsorption reproductive organs
58
CFTR protein
ion channel at cell membrane transporting ions such as chloride loss of function results in altered secretions
59
diagnosis of CF
heel prick test approx day 5 in UK - measures a pancreatic trypsinogen elevated in CF babies sweat test more accurate diagnosis esp in children >6 weeks genetic testing analysis done to confirm
60
CF GI and liver complications
- Meconium ileus (often first sign) - Constipation - Distal Intestinal obstruction - Neonatal cholestasis - fatty liver - cirrhosis - gallstones - cholecystitis
61
CF pulmonary management
Abx; oral/nebs/IV, prophylactic (start at birth) and treatment mucolytics physiotherapy wheeze treatment anti-fungals
62
extra pulmonary CF management
Creon for enzyme support + vitamins A, E, D, K (fat soluble) management of constipation insulin for CF diabetes liver; ursodeoxycholic acid, vit K salt supplements (lost in sweat)
63
presentation of CF if not diagnosed as neonate
poor growth and failure to thrive fatty stools recurrent respiratory problems (not in firth few months)
64
fetal circulation shunts
ductus arteriosus - between pulmonary artery and aorta to bypass lungs foramen ovale - between R to L atria ductus venosus - between umbilical vein and inferior vena cava to bypass liver ducts are aided by high pulmonary vascular resistance in the foetus
65
how do fetal shunts change at birth
at first breath - alveoli fill with air and vascular resistance of the pulmonary circulation decreases LA pressure exceeds RA pressure and the foramen ovale closes circulating prostaglandins drop due to increased blood oxygenation - ductus arteriosus closes ductus venous closes after cord clamped
66
PDA - diagnosis - management
may be picked up at birth with a murmur can also present with failure to thrive, SoB, difficulty feeding - the L-R shunt causes increased pul pressure and HF needs echo to diagnose typically monitored until 1 year by which point may have closed or catheter surgery is performed
67
ASD symptoms/complicaitons
L-R shunt causes right heart strain and pul hypertension but is acyanotic because blood is always being oxygenated eventually in Eisenmenger syndrome the pul pressure can exceed systemic and the shunt reverses to R-L causing cyanosis murmur:mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound may be picked up antenatally or later with symptoms/complciations other complications are AF, stroke
68
VSD presentation
may be picked up antenatally or a murmur at newborn baby check can also present with symptoms such as Poor feeding Dyspnoea Tachypnoea Failure to thrive
69
CXR tetralogy of fallot
typically boot shaped heart due to RVH
70
"Tet spells" tetralogy of fallot
intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode usually when a child is physically exerting themselves, crying, laughing etc. management: can try knees to chest/squatting. if failed - oxygen - IV fluids - beta blockers/adrenaline/morphine
71
tetralogy of fallot management
prostaglandins can maintain ductus arteriosus then heart surgery needed - mortality from surgery 5%
72
differentiating viral induced wheeze and asthma
factors favouring asthma - personal or FHx of atopy - interval symptoms (between viral infections ) of coughing at night, when playing or in cold
73
management of acute asthma child
Oxygen to maintain sats>94% Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours Nebulisers with salbutamol / ipratropium bromide Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days) IV hydrocortisone IV magnesium sulphate IV salbutamol IV aminophylline if still not controlled contact ICU work back down ladder as they get better Antibiotics only if bacterial cause suspected
74
long term medical asthma therapy age <5
Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required Add a low dose corticosteroid inhaler or a leukotriene antagonist (i.e. oral montelukast) Add the other option from step 2. Refer to a specialist.
75
long term medical asthma therapy age 5+
Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required Add a regular low dose corticosteroid inhaler Add a long-acting beta-2 agonist inhaler (e.g. salmeterol). Continue salmeterol only if the patient has a good response. Titrate up the corticosteroid inhaler to a medium dose. Consider adding: Oral leukotriene receptor antagonist (e.g. montelukast) Oral theophylline Increase the dose of the inhaled corticosteroid to a high dose. Referral to a specialist. They may require daily oral steroids.
76
whooping cough symptoms
URTI caused by pertussis (children and pregnant women are vaccinated against) typically starts with mild coryzal symptoms, a low grade fever and possibly a mild dry cough. more severe coughing fits start after a week or more
77
whooping cough diagnosis
A nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks later can be tested for anti-pertussis toxin immunoglobulin G
78
whooping cough management
notifiable disease management usually supportive macrolide Abx can be helpful in early stages close contacts are given prophylactic Abx usually resolves in 8 weeks but can be long lasting and key complication is bronchiectasis
79
pyrexia and sepsis in children
apyrexia does not exclude sepsis septic children often have normal or low temperatures
80
investigations suspected shaken baby
CT head - intracerebral haemorrhage? skeletal survey ophthalmology review - retinal haemorrhages? metabolic testing - exclude glutaric aciduria associated with ICH coagulation
81
clinical features of non-accidental head injury
Irritability Poor Feeding Increasing head circumference Seizures Reduced GCS Full fontanelle Anaemia Retinal Haemorrhages
82
how does shaking baby cause injury
esp in a child under 6 months shaking can cause rupture to the small vessels crossing the subdural space, causing a subdural haemorrhage
83
What action should a doctor take if they have a child protection concern?
Refer to Social Services Social Services will consider whether the child (and potentially siblings) requires a child protection medical assessment and needs to be safeguarded from impending harm.
84
child with bruising differentials
accidental injury non accidental injury immune thrombocytopenia meningococcal septicaemia leukaemia Haemophilia A Von Willebrands Disease
85
child with fractures differentials
accidental injury non accidental injury Osteogenesis Imperfecta Copper Deficiency Vit D defiency Vit C deficiency Ehlers Danlos and other hypermobility syndromes JOBs syndrome
86
child with burns/scalds differentials
Accidental Injury Non accidental injury Bullous Impetigo Scalded Skin Syndrome
87
red flag symptoms that indicate unlikely to be functional GI disorder of childhood
age <5years weight loss/poor growth blood in stools regularly waking at night due to symptoms
88
causes of blood in stool in children
Infective – bacterial diarrhea eg campylobacter, salmonella Inflammatory bowel disease Tearing from anal vein Polyp Intussusception – acutely unwell
89
investigations IBD suspected
Hx and examination bloods; FBC, U+E, LFT, CRP/ESR Coeliac tests stool MC&S faecal calprotectin if still suggestive; colonoscopy +/- small bowel barium studies
90
what typically causes Haemolytic Uraemia Syndrome classical history
E Coli Hx of severe diarrhoea, progressing to anaemia, thrombocytopenia, haematuria and raised creatinine
91
Kartagner’s triad
describes the three key features of primary ciliary dyskinesia. Not all patients will have all three features. Paranasal sinusitis Bronchiectasis Situs Inversus
92
surgical causes abdo pain children
Appendicitis causes central abdominal pain spreading to the right iliac fossa Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools Bowel obstruction causes pain, distention, absolute constipation and vomiting Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting
93
abdominal migraine
more likely in children compared to traditional migraine abdo pain lasting >1 hour with possible associated Nausea and vomiting Anorexia Pallor Headache Photophobia Aura management similar to migraine in adults acute; analgesia, low stimulus environment, triptan preventative; Pizotifen, a 5-HT antagonist, consider propranolol
94
causes of constipation
majority idiopathic but consider CF, Hirschprungs, hypothyroidism idiopathic contributed to by lifestyle factors including diet, activity, psychosocial problems
95
Encopresis/faecal incontinence
not pathological until >4years usually a sign of chronic constipation where rectum loses sensation other rarer causes include learning disability, abuse, psychosocial stress, cerebral palsy
96
constipation red flags
Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease) Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion) Vomiting (intestinal obstruction or Hirschsprung’s disease) Ribbon stool (anal stenosis) Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse) Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis) Failure to thrive (coeliac disease, hypothyroidism or safeguarding) Acute severe abdominal pain and bloating (obstruction or intussusception)
97
management idiopathic constipation
diagnose without investigations if red flags excluded - correct reversible lifestyle factors - laxatives (movicol first line) should be weaned off as returns to normal - impaction may require disimpaction regime - encourage and praise toiletting
98
causes of vomiting
Overfeeding Gastro-oesophageal reflux Pyloric stenosis (projective vomiting) Gastritis or gastroenteritis Appendicitis Infections such as UTI, tonsillitis or meningitis Intestinal obstruction Bulimia
99
red flags of vomiting
Not keeping down any feed (pyloric stenosis or intestinal obstruction) Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction) Bile stained vomit (intestinal obstruction) Haematemesis or melaena (peptic ulcer, oesophagitis or varices) Abdominal distention (intestinal obstruction) Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure) Respiratory symptoms (aspiration and infection) Blood in the stools (gastroenteritis or cows milk protein allergy) Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis) Rash, angioedema and other signs of allergy (cows milk protein allergy) Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment
100
physical risks of rapid weight loss
Refeeding syndrome risk, hypoglycaemia, risk of infection, cardiac arrhythmia.
101
What conditions can cause rapid weight loss in adolescents?
Coeliac disease Type 1 diabetes mellitus Hyperthyroidism Malignancy Anorexia nervosa Inflammatory bowel disease Oesphageal problems eg achalasia Severe depression/OCD/autism Juvenile arthritis Addisons
102
what assessments/tests would you want in a child with rapid weight loss?
Weight, height HR, BP, BM, RR, CRT ECG, U+E, phosphate, calcium, magnesium, LFTS, CRP, WCC, TFTS, coeliac screen, ESR.
103
course of action severe weight loss concerns of eating disorder
Admit to stabilise physically, commence vitamins (thiamine, Vitamin B complex, multivitamins) to prevent refeeding syndrome, regular observations + BM, monitoring bloods. Contact local eating disorders team, diet plan. IV fluids if hypoglycaemic or not drinking (10% dextrose+045% saline).
104
Lanugo hair
fine hair growth in anorexia in response to loss of insulating fat
105
short term treatment/weight gain plan anorexia nervosa
if weight height ratio <75% commence thiamine, Vitamin B complex and multivitamins Aim for 0.5 kg-1kg per week weight gain monitor blood especially phosphate; drop indicates refeeding syndrome regular ECGs Discharge when vital signs stable and weight gain occurring
106
medium term plan anorexia nervosa
Multi-disciplinary treatment package in the community - child psychiatrist oversees care + role of antidepressants for comorbidities - dietician - therapists + family therapist - paediatrician to mentor physical health (risks of osteopenia/porosis esp if amenorrhea)
107
main types of eating disorder young people
anorexia nervosa bulimia nervosa EDNOS - eating disorder not otherwise specified)
108
What is weight for height ratio?
A method of assessing how appropriate that persons weight is for their height at a given age. more accurate in children than BMI
109
most significant mortality risks in anorexia nervosa
Sudden cardiac death Suicide Chronic emaciation + pneumonia
110
causes of short stature in children/adolescents
- familial note hypochondroplasia - constitutional/delay - psychosocial - chronic physical disease - malabsorption - endocrine - genetic/syndrome
111
short stature; approach to diagnosing cause
general Hx + Hx of family ?diarrhoea ?abdo pain ?energy examination: ?dysmorphic, ?limb size, ?skin lesions parental heights + mid parental centile blood pressure - renal failure can be missed cause investigations; thyroid, creatinine, bone and liver profiles, FBC, CRP, glucose, coeliac screen chromosomes esp girl ?turners bone age vs actual age; is there just delay
112
follow up short stature
usually not immediate medical diagnosis follow up every 4 months and if cause identified can treat keep safeguarding in mind
113
first signs of puberty girls/boys
girls; breast development then pubic hair boys; testicular enlargement followed by genital changes. later age than girls
114
definition of delay puberty
no signs age 14 in boy or age 13 in girl in boys testosterone to kickstart puberty sometimes offered
115
precocious puberty
any signs before age of 8 in girl and 9 in boy more likely to be pathological if under age 6 can be psychological distressing and can stunt adult height can offer blockade with GnRH antagonist e.g. zoladex every 12 weeks injection
116
thyroid disorders causing stunted growth
congenital hypothyroidism - should be detected on newborn heel prick test 2/3 of these have absent or ectopic thyroid gland - need lifelong replacement other 1/3 gland is present but not producing - usually still needs replacing but sometimes starts producing thyroxine; trial cessation at age 3 acquired hypothyroidism - autoimmune condition can be seen in adolescent females
117
physical features of dehydration in an infant
Sunken anterior fontanelle dry mucous membrane tachycardia reduced capillary refill time reduced skin turgor
118
common causes of gastroenteritis in young children
1. rotavirus - particularly winter and early spring 2. adenovirus if bacterial campylobacter is most common
119
what infections can cause blood in the stool associated with diarrhoea and vomiting
Rotavirus Intussusception E. coli Campylobacter Shigella
120
definition and typical presentation of intussusception
invagination of proximal bowel into a distal segment commonly involving invagination of ileum into caecum through the ileocecal valve age 3 months to 2 years paroxysmal severe colicky pain pallor during painful episodes followed by lethargy child may refuse to feed, vomit, and pass red currant jelly stools
121
what infection is associated with haemolytic uraemia syndrome management
E.Coli associated with diarrhoea and blood in stool can progress to HUS which is the most common cause of acute renal failure in children treatment is mainly supportive; may include dialysis +/- IVIG if severe
122
red flag features of vomiting
blood in vomit bilious vomiting projectile vomiting abdominal tenderness or distention blood in stool bulging fontanelle
123
young child vomiting with persistent or associated fever
may be associated with infections such as urinary tract infection or meningitis
124
what does bilious vomiting indicate
intestinal obstruction
125
what does haematemesis indicate
Oesophagitis, gastric ulcer, oral or nasal bleeding and vomiting up swallowed blood
126
projectile vomiting under 2mo
pyloric stenosis
127
vomiting with abdominal distention/tenderness
Intestinal obstruction, strangulated inguinal hernia, surgical abdomen
128
vomiting with severe dehydration/shock
Severe gastroenteritis, systemic infection – UTI, meningitis, diabetes ketoacidosis
129
vomiting with bulging fontanelle or fits
Raised intracranial pressure due to meningitis/ hydrocephalus
130
vomiting with faltering growth
Gastroesophageal reflux, coeliac disease, chronic gastrointestinal conditions
131
vomiting with paroxysmal cough
whooping cough
132
what is a fluid challenge
if at risk of dehydration, give oral bolus of rehydration solution frequently in small amounts 5ml/kg of ORS after each large watery stool in children who are at risk of dehydration - consider giving via NG continue to monitor input and output continue breast feeding and other milk feeds
133
what children are at risk of dehydration
low birth weight, age less than 1 year, had more than 2 vomiting episodes and more than 5 diarrhoeal episodes in the previous 24 hours
134
usual duration of diarrhoea illness in children + how to manage simple illness
5-7 days and in most children, it stops in 2 weeks. The family should continue encouraging intake of usual fluids (breast milk or formula) and give 5ml/kg of ORS after passage or each loose stool not attend nursery until 48 hours after last vomit or diarrhoea
135
safety net simple gastroenteritis
contact healthcare professionals if child becomes unwell, appears pale/mottled, starts to vomit again (vomiting should not last longer than 3 days) has decreased urine output/wet nappies, irritable/lethargic and has cold extremities.
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mechanisms of infectious diarrhoea
Secretory mechanism: ↓ absorption, ↑ secretion & electrolyte transport --> Watery stool. caused by Cholera, E. coli , Clostridium difficile and cryptosporidium (in HIV infection) Mucosal Invasion: Inflammation, ↓ mucosal surface area and/or colonic reabsorption and ↑ motility --> stool with Blood and ↑ WBC’s. Caused by Rotavirus, campylobacter, Salmonella, shigella, Yersinia
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features of a gastroenteritis that suggest another diagnosis
- Fever – temperature >38 degrees or higher in children younger than 3 months & >39 degrees or higher in children aged 3 months and older - Tachypnoea - Altered consciousness level -Neck stiffness - Bulging fontanelle in infants - Non-blanching rash - Blood and /or mucus in stool - Bilious vomit - Severe or localised abdominal pain - Abdominal distension or rebound tenderness
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mechanisms/causes of dehydration
isonatraemic - proportional loss of water and sodium hyponatraemic - intake of large quantity of water, fall in serum sodium, resulting is shift of water form extracellular to intracellular compartment causes brain oedema and marked extracellular dehydration and shock hypernatraemic - water loss exceeds the sodium loss with resultant increase in plasma sodium concentration. This can happen when there is low sodium diarrhoea or high insensible water loss. There is shift of water from intracellular to extracellular compartment and therefore less signs of dehydration and more features of hypertonia, hyperreflexia, convulsions, drowsiness
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when is stool microscopy and culture indicated in gastroenteritis what other investigations are done
Recent travel abroad The diarrhoea is not improving by day 7 Suspected septicaemia Blood and /or mucus in stool Immunocompromised child blood culture if starting Abx U+Es and glucose if dehydrated/starting fluids
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IV fluid treatment of shock
treat with fluid bolus 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion. Give a second bolus of 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion if shock persists. Considers other causes of shock. Once symptoms and signs of shock resolve, start rehydration using intravenous fluids
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what fluid is generally used for maintenance
0.9 % sodium chloride and 5 % dextrose
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how do you calculate volume of maintenance fluids for 24 hours
100ml/kg first 10kg 50ml/kg second 10kg over 20kg 20ml/kg
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how should weight and U+Es be monitored in fluid therapy
Weight and u&e’s should be measured prior to commencing intravenous fluids and then at least every 24 hours if u&e’s are normal. Measure blood glucose when starting intravenous fluids and at least every 24 hours or more frequently if there is risk of hypoglycaemia.
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when and what Abx are given for treatment of diarrhoea
Campylobacter – Erythromycin shortens the duration of illness and shedding of bacteria Clostridium difficile – metronidazole or vancomycin Nontyphoid salmonella, shigella , vibrio cholerae, Giardia, Yersinia and cryptosporidium
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what fluid is typically used for acute resuscitation
0.9% saline
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pyloric stenosis - presentation - investigation - management
first few weeks of life, pale hungry baby with FTT and projectile vomiting + crying after feeds diagnosis is by abdominal USS which shows pyloric hypertrophy blood gas shows hypochloric metabolic alkalosis treatment is laparoscopic pyloromyotomy (known as “Ramstedt’s operation“) - excellent prognosis
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post-gastroenteritis complications
Lactose intolerance Irritable bowel syndrome Reactive arthritis Guillain–Barré syndrome
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coeliac disease presentation
can often be asymptomatic may present when weaning starts possible symptoms Failure to thrive in young children Diarrhoea Fatigue Weight loss Mouth ulcers Anaemia secondary to iron, B12 or folate deficiency Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
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coeliac disease diagnosis
Investigations must be carried out whilst the patient remains on a diet containing gluten Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies: Raised anti-TTG antibodies (first choice) Raised anti-endomysial antibodies Endoscopy and intestinal biopsy show: “Crypt hypertrophy” “Villous atrophy”
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when to suspect IBD in children
children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration may have extraintestinal features such as eye, joint and skin symptoms
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when to suspect IBD in children
children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration may have extraintestinal features such as eye, joint and skin symptoms
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what is biliary atresia when to suspect management
where a section of the bile duct is either narrowed or absent resulting in cholestasis babies with a persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies measure the bilirubin and conjugated only will be elevated management is surgical
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causes of intestinal obstruction
Meconium ileus Hirschsprung’s disease Oesophageal atresia Duodenal atresia Intussusception Imperforate anus Malrotation of the intestines with a volvulus Strangulated hernia
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presentation of intestinal obstruction
Persistent vomiting. This may be bilious, containing bright green bile Abdominal pain and distention Failure to pass stools or wind Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later
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investigation is suspected intestinal obstruction
abdominal X-ray is first line - absence of air in rectum
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initial management intestinal obstruction
emergency referral to paediatric surgical unit NBM, insert NG tube, IV fluids
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what is Hirschsprung’s disease
congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel and rectum - absence of parasympathetic ganglion cells length of lost innervation varies
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what family pattern does Hirschsprung's disease occur in
usually in isolation but does have genetic associations Downs syndrome Neurofibromatosis Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair) Multiple endocrine neoplasia type II
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how does Hirschsprung's disease present
varies significantly depending on length of gut affected can present with acute intestinal obstruction shortly after birth or more gradually developing symptoms: - Delay in passing meconium (more than 24 hours) - Chronic constipation since birth - Abdominal pain and distention - Vomiting - Poor weight gain and failure to thrive
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what is Hirschsprung-associated enterocolitis (HAEC)
inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease. It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis. It is life threatening and can lead to toxic megacolon and perforation of the bowel. It requires urgent antibiotics, fluid resuscitation and decompression of the obstructed bowel.
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diagnosis and management of Hirschsprung's
definitive diagnosis is with rectal biopsy management is surgical removal of the affected bowel
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Intussusception - diagnosis - management - complications
diagnosis; USS or contrast enema management; therapeutic enemas can be used. if failed, surgical management Obstruction Gangrenous bowel Perforation Death
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appendicitis - signs and symptoms - diagnosis - management
S&S - anorexia, N&V - Rovsing’s sign; palpation of LIF causes pain in RIF - guarding - rebound and percussion tenderness (suggest rupture and peritonitis) diagnosis: clinical presentation and raised inflammatory markers but CT/USS can be used to rule out differentials management: appendicectomy; better by laparoscopic
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when to suspect Kawasaki's disease
fever >5 days additional features: - bilateral conjunctival injection without exudate - erythema and cracking of lips, strawberry tongue, or erythema of oral and pharyngeal mucosa - oedema and erythema in the hands and feet - polymorphous rash - cervical lymphadenopathy
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causes of non-blanching petechial/purpuric rash
meningococcal septicaemia Henoch-Schonlein Purpura Idiopathic thrombocytopaneia purpura Non-accidental injury
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suspected meningitis actions
A-E and sepsis 6 obtain IV access and call seniors fluid, Abx and oxygen IN blood cultures, lactate and urine output OUT bloods for FBC, CRP, Blood culture, lactate, whole blood real-time PCR testing for Meningococcus and Pneumococcus LP if not contraindicated but shouldn't delay Abx being given - third gen cephalosporin
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suspected meningitis Abx - under 3 months - over 3 months
under 3 mo - IV ceftriaxone with amoxicillin for listeria cover over 3 mo - IV ceftriaxone
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What bacterial causes of meningitis are more prevalent in - under 3 mo - 3 mo to 5 years - over 5 years
under 3 mo - listeria, E. coli, Group B strep 3mo-5yrs; Niesseria Meningitides, Streptococcus pneumoniae, Haemophilus influenza B over 5 (same as adults) - niesseria or strep pneumonia
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what are the most likely viral causes of meningitis
enteroviruses (85%, especially coxsackie and echovirus). Other viruses include adenovirus, mumps, EBV, CMV, Varicella zoster, Herpes Simplex virus, HIV.
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risk factors for bacterial meningitis
- asplenia - basal skull fracture - attendance at daycare/crowding - low family income - children with facial cellulitis, periorbital cellulitis, sinusitis, and septic arthritis - maternal infection and pyrexia at delivery
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Indications for Dexamethasone in suspected/confirmed Meningitis
- Frankly purulent pus - CSF wcc > 1000/microlitre - Raised CSF wcc with CSF Protein > 1g/l - Bacteria on Gram stain give with first dose of Abx and never more than 12 hours after usually given qds for 2-4 days under senior clinician
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where should the needle enter in an LP
into the L4/L5 intervertebral space, With the child on his/her side with the child’s back in a vertical position then the L5 vertebrae is vertically below the iliac crest. The L4 L5 disc space is just above
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when is LP contraindicated
- unstable child; signs of shock or respiratory insufficiency - signs or symptoms of raised ICP - extensive or spreading purpuric rash - bleeding disorder - after convulsions if not yet stabilised - local infection at the LP site
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acute complications of meningitis
- seizures - raised ICP - metabolic disturbance - coagulopathies - anaemia - coma - death
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long term complications meningitis
- hearing impairment - psychosocial problems - epilepsy - developmental/learnign difficulties - neurological impairment children need general paediatrician follow up + audiology assessment within two weeks
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which pathogen in meningitis has the worst prognosis
group B streptococcus pneumonia highest mortality and highest res of neurological complications
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slapped cheek syndrome
fever and bright red clearly demarcated rash on cheeks otherwise generally well caused by parovirus
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antenatal Hx and UTI risk
abnormalities such as renal pelvis dilatation, cysts, or poor production of amniotic fluid (oligohydramnios) may indicate antenatal renal abnormalities predisposing to infection. Prematurity may indicate an increased overall infection risk
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how can urine be obtained from an infant
clean catch sample is best method if not possible can catheterise or suprapubic aspiration which should be ultrasound guided
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management if UTI detected on dipstick
if nitrites and leukocytes +ve start antibiotics if one positive start if clinical UTI send samples for microscopy, culture and sensitivity (M,C&S)
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what is checked for on a dipstick
- leukocytes - nitrites - blood (tumour, trauma, infection) - protein (tubular or glomerular disease) - ketones
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In Renal disease, what are the significant levels of proteinuria?
>20 mmol/ml - This may be significant, and may indicate tubular disease >200 mmol/mg - This is nephrotic range
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complications of minimal change nephrotic syndrome are recognised in childhood?
- spontaneous bacterial peritonitis - infection with streptococci - recurrence
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what parameters make a diagnosis of Minimal Change Nephrotic Syndrome less likely (meaning further investigations would be indicated)?
- abnormal renal function - haematuria - hypertension
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when in gestation do the kidneys form?
5 weeks with glomeruli still forming until 34 weeks
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What is the commonest congenital renal anomaly?
renal hypoplasia
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Definition of atypical UTI; increased risk of renal screening
- seriously ill - poor urine flow - abdominal or bladder mass - raised creatinine - septicaemia - failure to respond within 48 hours - non E coli
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Definition of recurrent UTI; requires investigations for an underlying cause
2 or more upper UTI 1 upper and 1 or more lower UTI 3 or more lower UTI
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what features make an upper UTI more likely compared to lower?
Bacteriuria and fever of 38oC or higher +/- loin tenderness Bacteriuria, loin pain/tenderness and fever of less than 38oC Age less than 3 months usually no systemic features in lower UTI
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what developmental anomaly can underly UTIs
vesoureteric reflux - in 35% of cases in children others; hydronephrosis, duplex system or obstructive lesions
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management simple lower UTI
oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours
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management upper UTI
considered for admission to hospital. If not admitted oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days
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antibiotic prophylaxis UTI
not after first one but consider for recurrent or if structural abnormality such as VUR
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investigations in atypical or recurrent UTI symptoms
3 investigations are used selectively depending on the age of the child and presence of atypical or recurrent UTI symptoms: Ultrasound scan, MCUG and DMSA.
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indications for renal ultrasound in UTI
- Infants less than 6 months with confirmed UTI (acutely if infant has atypical or recurrent UTI) - Children more than 6 months old only in the presence of atypical UTI
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when is Micturating cystogram (MCUG) used in UTI
identify any vesicoureteric reflux (VUR), bladder abnormalities and posterior urethral valves within a few weeks after treatment of UTI catheterizing the child in order to fill the bladder with a radio-contrast agent then taking x-rays as the infant voids urine.. Indications: Infants younger than 6 months with atypical or recurrent UTI Consider in children older than 6 months if dilatation on ultrasound, poor urine flow, non-E coli infection or family history VUR
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when is DMSA used in UTI
DMSA in 4-6 months after infection radionucleotide scan used to assess renal function and identify any scarring of the kidneys due to the UTI - predisposes to HTN Healthy renal tissue takes up the isotope. Unhealthy or scarred tissue doesn’t take up the isotope and appears as a filing defect on DMSA scan. DMSA may be inaccurate if performed shortly after an infection. Indications: All children with recurrent UTI Children under 3 years with atypical UTI
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how do urinary infections present in children
can be quite non-specific more specific with age - older children more classic triad of dysuria, frequency and haematuria Abdominal pain Haematuria Bedwetting/enuresis Constipation Febrile convulsion Dysuria
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definition of enuresis
involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract
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how is nocturnal enuresis defined
primary - child never achieved continence secondary - child was dry for at least 6 months before
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possible underlying causes of enuresis
- neglect/abuse - disturbed sleep/wake cycle - constipation - diabetes mellitus - UTI if recent onset - rarely neurological disease
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enuresis management techniques
- general fluid intake management and toileting patterns - reward systems for agreed behaviours (not for dry nights) - enuresis alarm - desmopressin can be used for short term eg. sleepovers
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bilateral dilated kidneys in a neonate
in a male child can mean posterior urethral valves – this is a very serious condition which if untreated can cause renal failure due to obstruction
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scarlet fever presentation immediate management
reaction to group A strep toxins most common age 2-6 years presentation: fever: typically lasts 24 to 48 hours malaise, headache, nausea/vomiting sore throat 'strawberry' tongue rash commence Abx immediately 10 days of pen V
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complications of scarlet fever
otitis media: the most common complication rheumatic fever: typically occurs 20 days after infection acute glomerulonephritis: typically occurs 10 days after infection invasive complications (e.g. bacteraemia, meningitis, necrotizing fasciitis) are rare but may present acutely with life-threatening illness
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presentation of immune thrombocytopenia purpura
petechial and purpura often after a viral illness
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surgical sieve for anaemia
V-acute bleed? haemorrhgaic disease of newborn? I- malaria, helminth infection, transient aplastic anaemia secondary to parvovirus, inflammatory bowel disease, severe cow’s milk protein enteropathy T- acute bleed i.e. following an accident or non-accidental injury worsened by a clotting disorder A- pernicious anaemia very rare in children , coeliac, haemolytic anaemia, haemolytic uraemic syndrome M- G6PD deficiency I- IDA N- leukaemia C- inherited pure red cell aplasia (Diamond Blackfan Anaemia), thalassaemia sickle cell, spherocytosis, fanconis anaemia, clotting disorders, congenital infectionsions ie parvo B19 D- physiological anaemia of the newborn E - menstruation, medication ie nitrofurantoin
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when does sickle cell disease present
after 6 months when fatal haemoglobin is replaced
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what is Henoch Schonlein Purpura
an IgA vasculitis that presents with a purpuric rash affecting the lower limbs and buttocks in children often triggered by a recent infection and most common under 10 years 4 main features: - purpuric rash (100%) - joint pain (75%) - abdominal pain (50%) - renal involvement (50%)
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abdominal complications HSP
gastrointestinal haemorrhage, intussusception and bowel infarction
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renal involvement HSP
affects the kidneys in around 50% of patients, causing an IgA nephritis. This can lead to microscopic or macroscopic haematuria and proteinuria. If there is more than 2+ of protein on the urine dipstick the child has developed nephrotic syndrome and will have a degree of oedema
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HSP management
exclude other causes of purpura! then supportive management: - steroids debatable for abdo pain/renal involvement - closely monitor urine dip and BP for 6 months most fully recover 4-6 weeks. small proportion develop renal failure
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what are Kernigs and Brudzinkis signs
Kernigs +ve = Pain on lower leg extension with hip flexed Brudzinkis +ve = Involuntary flexion of the knees and hips with neck flexion
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differentials child with seizure and reduced consciousness
febrile seizure encephalopathy encephalitis/meningitis sepsis/shock brain tumour metabolic disorder epilepsy poisoning/intoxication could be post ictal - only if returns to normal within an hour
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Indications for urgent head CT or MRI in seizure
Encephalopathic or coma Suspected raised intracranial pressure Progressive neurological deficit
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Indications for elective MRI head in seizure
- In a child under 2 year of age at onset - hard focal neurological signs - a focal epilepsy - associated significant learning difficulties - an epilepsy resistant to full doses of 2 appropriate drugs
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EEG urgent and non urgent indications in seizure
Urgent Indications: suspected non-convulsive status Non traumatic encephalopathy Coma of unknown cause Elective standard EEG if: strong suspicion of epilepsy (to support classification) developmental or language regression NOT generally after a first afebrile seizure or febrile seizures
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causes of delayed walking
central - delayed maturation, global developmental delay, any cause of hemiplegia, cerebral palsy peripheral - spinabifida muscular and neuromuscular e.g. DMD environmental orthopaedic e.g. DDH metabolic/hormonal - hypoT, rickets
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what is cerebral palsy
Static brain injury pre or shortly post birth, causing a motor and coordination dysfunction, usually with neuroimaging changes
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neonatal causes of tachypnoea
sepsis cardiac respiratory metabolic pain - either acidosis causing compensatory tachypnoea or a raised ammonia which acts as a respiratory stimulant causing tachypnoea
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main groups of inborn errors of metabolism causing hyperammoniaemia
urea cycle disorders and the organic acidaemias
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Urea cycle disorders
ammonia level is markedly raised and often over 1000 micromols/L and there is liver dysfunction blood gas often shows a respiratory alkalosis due to the ammonia acting as a respiratory stimulant
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organic acidaemia
mixed picture of metabolic acidosis and hyperammonaemia - less high than urea cycle disroders The first pointer to diagnosis is a metabolic acidosis that does not respond to standard fluid resuscitation and then the finding of a raised anion gap caused by the presence of the abnormal organic acid. Methylmalonic acidaemia and propionic acidaemia are the 2 most common organic acid disorders.
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presentation in born errors of metabolism
presents neonatally often reduced consciousness blood gas abnormalities and often altered anion gap can be very sick and need specialist review
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definition of global developmental delay
A child has global developmental delay if they have a significant delay in milestones in two or more areas
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definition of cerebral palsy
A disorder of tone, posture and movement, caused by a non-progressive brain lesion in a developing brain
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types of cerebral palsy
spastic (UMN signs) ataxic dyskinetic aka choreoathetoid in reality is often mixed
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medications which can be used to help manage increase tone in children with cerebral palsy?
Baclofen Diazepam Botulinum toxin
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what is Gower's sign
pt uses hands and arms to walk to and then up the body in order to stand sign of weakness of the proximal muscles seen in Duchenne Muscular Dystrophy
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Duchenne Muscular Dystrophy
most common muscular dystrophy in northern Europe and is due to an abnormality of the dystrophin gene X linked disorder measure CK +genetic testing to diagnose Steroid treatment has been shown to delay the progression can also present with early neurological signs due to expression of dystrophin protein in the brain
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long term complications of conditions such as DMD
Reduced mobility, loss of ambulation Scoliosis – spinal surgery will be needed if scoliosis significant Feeding problems – may cause malnutrition – gastrostomy feeds may be required Cardiac involvement (depending on condition, but common in DMD) Respiratory weakness- nocturnal non-invasive ventilation may be required
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side effects of steroids in children
Increased appetite – with weight gain Behavioural deterioration – especially if pre-existing problems Hypertension Growth failure Gastrointestinal irritation Bone thinning
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at what times are DKA most likely to occur in T1 DM
At diagnosis During a growth spurt/puberty Insulin omission for any reason (DKA usually develops over 24 hours but can develop faster particularly in young children or patients on insulin pumps)
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how does DKA present
may initially have polyuria, polydipsia, weight loss, excessive tiredness more specific to DKA symptoms are nausea or vomiting, abdominal pain, hyperventilation, dehydration and reduced level of consciousness
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when should a suspected DKA be sent immediately to an acute paediatric facility (HDU) what needs measuring on arrival
child not known to have diabetes with glucose level is above 11 mmol/litre and suggestive symptoms child known to have diabetes with any symptoms of DKA - but only need transfer if ketones elevated or can't measure on arrival measure capillary blood glucose, capillary blood ketones (beta-hydroxybutyrate) capillary or venous pH and bicarbonate
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DKA diagnostic criteria
1. Acidosis (indicated by blood pH below 7.3 or plasma bicarbonate below 18 mmol/litre) and 2. Ketonaemia (indicated by blood beta-hydroxybutyrate above 3 mmol/litre Diagnose severe DKA in children and young people with DKA who have a blood pH below 7.1.
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what is the main cause of morbidity and mortality in childhood DKA
from cerebral oedema due to rapid correction The aim of therapy is very gentle and slow correction to avoid cerebral oedema
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initial management DKA
- inform senior clinician - explain to child and parents - fixed rate insulin infusion - IV fluids - may need potassium - avoid hypo by adding dextrose when glucose is coming down - monitor for signs of cerebral oedema can give O2, consider ABX and consider NG tube
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what is Kussmaul breathing
deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. In metabolic acidosis, breathing is first rapid and shallow but as acidosis worsens, breathing gradually becomes deep, labored and gasping. It is this latter type of breathing pattern that is referred to as Kussmaul breathing.
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what needs recording once DKA diagnosed
blood gas - pH and pCO2, lactate monitor ketones level of consciouss vital signs clinical evidence of dehydration + weight plasma sodium, potassium, urea and creatinine plasma bicarbonate
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when should you think about sepsis in a child with DKA
has any of the following: fever or hypothermia, hypotension, refractory acidosis, lactic acidosis.
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what fluids and when should be given in DKA how much
only give oral fluids if alert, not nauseated or vomiting, and not clinically dehydrated otherwise give IV and if IV don't let them have oral until ketosis is resolving give the fluid gradually - not a bolus unless can consider in severe Use 0.9% sodium chloride without added glucose until the plasma glucose concentration is below 14 mmol/litre. Ensure that all fluids (except any initial bolus) administered to children and young people with DKA contain 40 mmol/litre potassium chloride, unless they have renal failure. first 48 hours adding the estimated fluid deficit to the fluid maintenance requirement assume if pH>7.1 5% deficit if <7.1 assume 10% deficit maintenance if they weigh less than 10 kg, give 2 ml/kg/hour if they weigh between 10 and 40 kg, give 1 ml/kg/hour if they weigh more than 40 kg, give a fixed volume of 40 ml/hour - this is reduced volume to avoid cerebral oedema
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when should insulin be started and how
fixed rate insulin infusion start 1-2 hours after fluids started use a soluble insulin infusion at a dosage between 0.05 and 0.1 units/kg/hour
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when should normal insulin be restarted
subcut at least 30 minutes before stopping intravenous insulin. For a child or young person with DKA who is using insulin pump therapy, restart the pump at least 60 minutes before stopping intravenous insulin
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signs of cerebral oedema when to treat and how
assess for oedema if any of headache, agitation/irritability, increased BP or fall in HR treat with mannitol or hypertonic sodium chloride if a child with DKA has any of deterioration in level of consciousness abnormalities of breathing pattern (for example respiratory pauses), oculomotor palsies, pupillary inequality or dilatation escalate
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potassium in DKA
insulin moves potassium which can lead to hypokalaemia if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU
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potassium in DKA
insulin moves potassium which can lead to hypokalaemia if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU
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basic types of insulin regimen in T1DM
1. Multiple daily injection basal–bolus insulin regimens: injections of short-acting insulin before meals, together with 1 daily injection of long-acting insulin. 2. Continuous subcutaneous insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid-acting insulin analogue or short-acting insulin) by a subcutaneous needle or cannula.
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optimal target ranges for short-term plasma glucose control
Fasting plasma glucose level of 4–7 mmol/litre on waking a plasma glucose level of 4–7 mmol/litre before meals at other times of the day a plasma glucose level of 5–9 mmol/litre after meals a plasma glucose level of at least 5 mmol/litre when driving measure 5x a day - more in illness or activity
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management of mild to moderate hypoglycaemia
Give fast-acting glucose (for example, 10–20 g) by mouth and recheck BM within 15 minutes repeat if persists once resolved give oral complex long-acting carbohydrate to maintain blood glucose levels
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treatment of severe hypoglycaemia
if in hospital with IV access; give 10% intravenous glucose. if no access give intramuscular glucagon or a concentrated oral glucose solution (for example Glucogel). Do not use oral glucose solution if the level of consciousness is reduced as this could be dangerous
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what complications monitoring should children with T1DM have
Thyroid disease at diagnosis and annually thereafter until transfer to adult services Diabetic retinopathy- annually from 12 years Moderately increased albuminuria (albumin:creatinine ratio [ACR] 3–30 mg/mmol; ‘microalbuminuria’) to detect diabetic kidney disease- annually from 12 years Hypertension- annually from 12 years. Be aware of the following rare complications and associated conditions with type 1 diabetes: Juvenile cataracts Necrobiosis lipoidica Addison’s disease. In addition Children and Young People with Type 1 DM get screened for Coeliac Disease at diagnosis
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what is Meckel's diverticulum
congenital diverticulum of the small intestine most common cause of massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years presents with rectal bleeding, can cause obstruction and may be painful
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investigation and management of Meckel's diverticulum
'Meckel's scan' should be used if haemodynamically stable uses 99m technetium pertechnetate mangamenet is surgical removal
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traffic light system paediatric history
- colour - activity; playing normally? - respiratory; any difficulty breathing? - hydration/circulation; feeding? drinking? nappies? - other; have they felt hot? recorded temperatures? rashes?
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APGAR score + what are the domains
assesses health of newborn baby at 1, 5 and 10 minutes looking at pulse, respiratory effort, colour, tone and irritability A score of 0-3 is very low score, between 4-6 is moderate low and between 7 - 10 means the baby is in a good state
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when is neonatal jaundice physiological or pathological
first 24 hours pathological 2-14 days physiological >14 days (21 in premature) pathological if pathological screen for haemolytic anaemia and sepsis screen