Paediatrics Flashcards

(495 cards)

1
Q

Paediatric Life support?

A

5 rescue breaths
15:2 chest compressions and breaths

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2
Q

Immunisations for babys?

A

2,3 and 4 months - get the 6-1 vaccine.
Men B given at 2, 4 and 12

MMR given at 12

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3
Q

Vaccinations given to children?

A

3-4 years - get the 4 in 1 pre school booster

12-13 = HPV vaccination

13-18 = 3 in 1 teenage booster

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4
Q

Whats in the 6-1 vaccine

A

Diphtheria
Tetanus
Whooping cough
Polio
HiB
Hepatitis B

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5
Q

What sin the 4 in 1 pre school booster

A

Diptheria, tetanus, whooping cough, polio

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6
Q

Wheeze - ages

A

<1 = bronch
1-4 = viral induced
5+ = asthma

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7
Q

What is bronchiolitis?

A

Inflammation and infection of the bronchioles
Viral induced usually - RSV most common
Higher incidence in winter
Mostly in children under 1
Worse on day 5 then tails off

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8
Q

Features of bronchiolitis?

A
  • Corzal symptoms - viral resp tract symptoms e.g. running noses, sneezing, mucus in throat, watery eyes
  • Resp distress
  • Dry cough
  • Dyspnoea
  • Tachycardia
  • Wheeze and crackles
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9
Q

Signs of respiratory distress?

A

Raised respiratory rate
Use of accessory muscles
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis

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10
Q

Abnormal airway noises?

A

○ Wheezing - tightened airways
○ Grunting - exhaling with the glottis partially closed to increase positive end expiratory pressure
○ Stridor - obstruction of the upper airway

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11
Q

Investigations for bronchiolitis?

A

Immunofluorescence of nasopharyngeal secretions may show RSV

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12
Q

Management of bronchiolitis?

A

Supportive
Oxygen if <90%
Ventilation support if required
Saline nasal drops/suctioning
NG feeding

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13
Q

What is palivizumab?

A
  • Monoclonal antibody that targets the RSV
  • Monthly injection given as prevention against bronchiolitis caused by RSV
  • Given to high risk babies such as ex premature and those with congenital heart disease
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14
Q

What is viral induced wheeze?

A

Acute wheezy illness caused by viral infection
Inflammation, swelling and constriction of the airway
Usually between 1-4
SOB, coryzal symptoms, expiratory wheeze

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15
Q

What is poiseulles law?

A

Flow rate is proportional to the radius of the tube to the power of 4 = because small children have small diameter of airway, a slight narrowing leads to a proportionally larger restriction in airway

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16
Q

Management of viral induced wheeze?

A

Same as acute asthma in children

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17
Q

Presentation of acute asthma?

A
  • Progressively worsening SOB
  • Signs of resp distress
  • Tachypnoea
  • Expiratory wheeze on auscultation heard throughout the chest
  • Tight chest and reduced air entry
    Where airways are so tight they cant move enough air through the airways to create a wheeze - might be associated with reduced respiratory effort due to fatigue.
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18
Q

Moderate asthma

A

Peak flow >50 % predicted

Normal speech

No features listed across

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19
Q

Severe asthma

A

Peak flow <50% predicted

Saturations <92%

Unable to complete sentences in one breath

Signs of resp distress

Resp rate:
>40 in 1-5 years
>30 in >5 years

Heart rate
>140 in 1-5 years
>125 in >5 years

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20
Q

Life threatening asthma

A

Peak flow <33% predicted

Saturations <92%

Exhaustion and poor respiratory effort

Hypotension

Silent chest

Cyanosis

Altered consciousness and confusion

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21
Q

Management of asthma

A

O sad map!
1. Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours
2. Nebulisers with salbutamol / ipratropium bromide
3. Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days)
4. IV hydrocortisone
5. IV magnesium sulphate
6. IV salbutamol
7. IV aminophylline

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22
Q

What is whooping cough?

A
  • Upper resp tract infection caused by Bordetella pertussis ( gram negative bacteria)
  • Whooping because coughing fits are so severe they cant take in enoguh air between coughs= loud whooping sound as they forecefully suck in air

Children and pregnant women( 16-32 weeks) are vaccinated

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23
Q

What are the features of whooping cough?

A

Catarrhal phase
- Mild coryzal symptoms, low grade fever and possibly a mild dry cough

Paroxysmal phase
- Cough increases in severity
- Coughing bouts usually worse at night and after feeding
- Inspiratory whoop
- Spells of apnoea
- 2-8 weeks

Convalescent phase
- Subsides over weeks to months

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24
Q

Diagnosis of whooping cough?

A

Suspected if have acute cough for 14 days or more without another apparent cause:
Have one or more of the following features;
- paroxysmal cough
- inspiratory whoop
- post tussle vomiting
-apnoea attacks

Nasal swab for bordetella pertussis

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25
Management of whooping cough
Notifiable disease Supportive care Oral macrolide if onset of cough is within 21 days - clarithromycin. Give household contacts prophylactic abx school exclusion 48 hours until after commencing ABX
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Complications of whooping cough?
Subconjunctival haemorrhage Bronchiectasis Seizures Pneumonia
27
What is croup?
Upper respiratory tract disease = oedema in the larynx Parainfluenza viruses Characterised by an inspiratory stridor Peak incidence at 6 months
28
Features of croup?
Cough - worse at night Stridor Fever Coryzal symtpoms Increased work of breathing
29
Management of croup?
- Single dose of oral dexamethasone 0.15mg/kg to all children regardless of severity - Prednisolone as an alternative - Adrenaline - Oxygen
30
What is pneumonia?
Infection of lung tissue Inflammation of the lung tissue and sputum filling the airways and alveoli Can be seen as consolidation on CXR Bacteria, virus, or atypical bacteria such as mycoplasma
31
Presentation of pneumonia?
- Cough ( wet and productive) - High fever - Tachypnoea - Tachycardia - Increased work of breathing - Lethargy - Delirium
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Signs of pneumonia?
- Tachypnoea - Tachycardia - Hypoxia - Hypotension - Fever - Confusion Bronchial breath sounds - equally loud on EXPIRATION AND INSPIRATION. Caused by consolidation of lung tissue - Focal coarse crackles - Dullness to percussion
33
Bacteria pneumonia - whats the most common cause?
Strep pneumonia
34
Viral pneumonia most common cause?
RSV
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Investigations for pneumonia?
CXR but not routinely required Viral PCR, throat swab for causative organism
36
Management of pneumonia?
Amoxicillin first line Macrolides will cover atypical pneumonia Oxygen if sats are <92%
37
Recurrent LRTI - what to do?
Full blood count to check levels of various white blood cells. Chest xray to screen for any structural abnormality in the chest or scarring from the infections. Serum immunoglobulins to test for low levels of certain antibody classes indicating selective antibody deficiency. Test immunoglobulin G to previous vaccines (i.e. pneumococcus and haemophilus). Some patients are unable to convert IgM to IgG, and therefore cannot form long term immunity to that bug. This is called an immunoglobulin class-switch recombination deficiency. Sweat test to check for cystic fibrosis. HIV test, especially if mum’s status is unknown or positive.
38
What is epiglottitis?Cause?
Inflammation and swelling of the epiglottis Caused by infection, typically with haemophiliac influenza type B Can swell to the point of obstructing the airway completely
39
Presentation of epiglottitis?
Rapid onset High temperature Sore throat and stridor Drooling of saliva Tripod position - leaning forward and extending neck in a seated position
40
Diagnosis of epiglottitis?
Direct visualisation LAteral XRAY - thumb sign- caused by oedematous and swollen epiglottis
41
Management of epiglottitis?
- Immediate senior involvmenet - Don’t distress patient - Endotracheal intubation - DO NOT examine the throat - Oxygen - IV ABX- Ceftriaxone - Steroids -Dexamethasone
42
Complications of epiglottitis?
Epiglottic abscess!
43
What is cystic fibrosis?
Autosomal recessive condition affecting the mucus glands Genetic mutation of the cystic fibrosis transmembrane conductor gene on chromosome 7 Most common variant = delta F508 mutation - coding for cellular Channels ( chloride)
44
KEY consequences of cystic fibrosis?
- Thick pancreatic and biliary secretions that cause blockage of the ducts = lack of digestive enzymes such as pancreatic lipase in digestive tract - Low volume thick airway secretions that reduce airway clearance resulting in bacterial colonisation and susceptibility to airway infections Congenital bilateral absence of vans deferens in males ---> sperm have no way of getting from the testes to ejaculate = male infertility
45
Initial presentation of cystic fibrosis?
Screened at birth with new born spot test Meconium ileus - in 20% of babies with CF, the meconium is thick and sticky and gets stuck and obstructs the bowel.
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Symptoms of cystic fibrosis?
Chronic cough Thick sputum production Recurrent respiratory tract infections Stetorrhoea - due to lack of fat digesting enzymes Abdominal pain and bloating Parents may report the child tastes salty Poor weight and height gain Delayed puberty Nasal polyps Short DM Rectal prolapse due to bulky stools
47
Signs of cystic fibrosis?
- Low weight or height on growth charts - Nasal polyps - Finger clubbing - Crackles and wheezes on auscultation Abdominal distention
48
Causes of clubbing in children?
- Hereditary clubbing - Cyanotic heart disease - IE - Cystic fibrosis - TB - IBD - Liver cirrhosis
49
Diagnosis of cystic fibrosis?
- New-born blood spot tests - Sweat test is the gold standard for diagnosis ○ Pilocarpine is applied to skin ○ Electrodes. Causes skin to sweat and chloride concentration is measured Diagnostic = more than 60mmol/L
50
Examples of microbial colonisers in CF?
* Staphylococcus aureus * Pseudomonas aeruginosa - particuarly hard to get rid of. Treated with nebulised abx such as tobramycin / cipro * Burkholderia cepacia* * Aspergillus
51
Management of cystic fibrosis?
Chest physiotherapy (at least twice daily) to clear mucus High calorie diet Creon tablets to digest fats in patients with pancreatic insufficiency Prophylactic fluclox to reduce risk of bacterial infections Bronchiodilators such as salbutamol inhalers can treat bronchoconstriction Vaccinations - pneumococcal, influenzai and varicella Lung transplant in end stage respiratory failure Kaftrio! - homozygous for mutation. Lumacaftor/ invacaftor
52
Monitoring in CF?
DM, osteoporosis, vitamin D deficiency and liver failure
53
What is chronic lung disease of prematurity
Bronchopulmonary dysplasia Occurs in premature babies typically before 28 weeks gestation Respiratory distress syndrome and require o2 therapy or intubation and ventilation at birth
54
Features of chronic lung disease of prematurity?
Low o2 sats Increased work of breathing Poor feeding and weight gain Crackles and wheezes on chest auscultation Increased susceptibility to infection
55
Prevention of chronic lung disease of prematurity?
Giving corticosteroids e.g. betamethasone to mothers that show signs of premature labour at less than 36 weeks gestation can speed up development
56
Once neonate is born ( if have chronic lung disease of prematurity)...
- Use CPAP rather than intubation and ventilation - Use caffeine to stimulate the resp effort
57
Management of chronic lung disease of prematurity?
- Sleep stid to assess oxygen sats during sleep - Protection against RSV to reduce risk and severity of bronchiolitis Monthly injections of a monoclonal antibody - palvizumab
58
What is cerebral palsy?
Permanent neurological problems resulting from damage to the brain around the time of birth NOT a progressive condition
59
Causes of cerebral palsy?
Antenatal eg cerebral malformation, congenital infection Intrapartum - birth asphyxia Post natal - intraventricular haemorrhage, meningitis, head trauma
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Presentation of cerebral palsy
Abnormal tone, early infancy Delayed motor milestones Abnormal gait - hemiplegic, diplegia gait Increased tone and spasticity in the legs Feeding difficulties Signs of UMN lesion = good muscle bulk, increased tone, brisk reflexes, reduced power Non motor problems- learning difficulties, epilepsy, squints and hearing problems
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Classification of cerebral palsy?
Spastic - Dyskinetic Ataxic Mixed
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Management of cerebral palsy?
Physio Speech and language Dieticians Spasticity OT Antiepileptic Glycopyronium bromide
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Upper motor neurone - findings?
Muscle bulk preservation, hypertonia, power is slightly reduced, and reflexes are brisk
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Lower motor neurone - findings?
Reduced muscle bulk with fasciculation, hypotonia, dramatically reduced power, reduced reflexes
65
What are febrile convulsions?
Seizures provoked by fever Typically occur between ages of 6 months and 5 years
66
Clinical features of febrile convulsions?
Occur early in viral infection Last less than 5 minutes Tonic clonic
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Simple Febrile Convulsions?
<15 minutes Generalised seizure Typically no reoccurrence within 24 hours Once during single febrile illness Complete recovery within an hour
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Complex febrile convulsions?
15-30 minutes Partial or focal seizures Repeat seizures within 24 hours/ multiple times during febrile illness
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What is febrile state epileptics?
>30 minutes of seizure
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Management of febrile convulsions?
Control fever Stay with child, pillow under their head Call ambulance if lasting more than 5 minutes If recurrent - benzodiazepine rescue medication may be considered
71
Prognosis of febrile convulsions?
Typically no lasting damage Slightly higher risk of developing epilepsy
72
What are seizures?
Transient episodes of abnormal electrical activity
73
Generalised tonic clonic seizures?
tonic= muscle tensing clonic = muscle jerking Tonic before the clonic May be associated tongue biting, incontinence, groaning or irregular breathing Prolonged post ictal period - where confused, drowsy, irritable or low
74
Management of generalised tonic clonic seizures?
First line - sodium valproate Second line - lamotrigine or carbamezepine
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What are focal seizures?
Start in temporal lobes Affect speech, hearing, memory and emotion Hallucinations, memory flashbacks, deja vu
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Management of focal seizures?
Reverse of tonic clonic? First line = carbamazepine or lamotrigine Second line = sodium valproate
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Absence seizures - what are they?
Becomes blanks, stares into space for 10-20 seconds Most stop having these as they get older
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Management of absence seizures?
Sodium valproate or ethosuximide
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What are atonic seizures?
Drop attacks Lapses in muscle tone Don't usually last for more than 3 minutes - may be indicative of Lennox gastaut syndrome
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Management of atonic seizures?
First line - sodium valproate Second line - lamotrigine
81
Myoclonic seizures - what are they?
Sudden brief muscle contractions Remain awake Juvenile myoclonic epilepsy
82
Treatment for myoclonic seizures?
First line - sodium valproate Second line - Iamotrigine, levetiracetam or topiramate
83
Infantile spasms - features
West syndrome Starting around 6 months Clusters of full body spasms Poor prognosis
84
Treatment of infantile spasms?
Prednisolone or igabatrin
85
Investigations for epilepsy?
EEG- after the second simple tonic clonic seizure MRI brain considered when first seizure is in children under 2, focal seizures or no response to first line anti epileptic medications
86
What does sodium valproate do?
Increases activity of GABA, which relaxes the brain
87
Side effects of sodium valproate?
Teratogenic, liver damage, hepatitis, hair loss, tremors
88
Side effects of carbamazepine?
Agranulocytosis, aplastic anaemia, induces the p450 system = drug interactions
89
Side effects of phenytoin?
Folate and vitamin D deficiency, megaloblastic anaemia ( folate deficiency), osteomalacia ( vitamin D deficiency)
90
Ethosuximide side effects?
Night terrors and rashes
91
Lamotrigine side effects
SJS
92
Status epilepticus? Treatment?
Seizure lasting more than 5 minutes, or 2 or more seizures without regaining consciousness in the interim IV lorazepam, high concentration o2, check blood glucose levels IV phenobarbital or phenytoin if seizures persist
93
What is syncope?
Transient loss of consciousness due to a disruption of blood flow to the brain, often leading to a fall Vasovagal episodes/ fainting
94
What is a vasovagal attack?
Problem with the autonomic nervous system regulating blood flow to the brain. When the vagus nerve receives a strong stimulus Can stimulate the parasympathetic nervous system Blood pressure in the cerebral circulation drops = hypoperfusion of brain tissue = faint
95
Primary syncope?
Dehydration Missed meals Response to stimuli
96
Secondary causes of syncope?
- Hypoglycaemia - Dehydration - Anaemia - Infection - Anaphylaxis - Arrythmias - Valvular heart disease - HOCM
97
Reflex syncope?
Vasovagal Situational - cough, micturition Carotid sinus syncope
98
Orthostatic syncope?
Primary autonomic failure e..g Parkinson's, lewy body Secondary autonomic failure e..g diabetic neuropathy Drug induced e.g. alcohol, diuretics Volume depletion e.g. haemorrhage, diarrhoea
99
Cardiac syncope
- Arrythmias - bradycardias, tachycardias - Structural - MI, HOCM - Ohers- PE
100
Investigations for syncope?
- CV exam - ECG - Echo - structural hear disease - Bloods NOTE: patients with typical features, no postural drop and a normal ecg don’t require further investgiations
101
What is a breath holding spell? when do they usually occur
Breath holding attacks Involuntary episodes when a child holds their breath Usually triggered by something upsetting or scarring them 6-18 months old
102
Cyanotic breath holding spells
Occur when a child is really upset, worked up and crying After letting out a long cry - loose consciousness. Within a minute they regain it
103
What are reflex anoxic seizures
Occur when a child is startled heart stops beating Pale, consciousness los Within 30 seconds, the heart restarts and child becomes conscious again
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Management of breath holding spells
- Iron deficiency anaemia is linked? Exclude other pathology, educate parents
105
Migraine management
Paracetamol, sumatriptan, antiemetics
106
Prophylaxis of migraines
Propranolol, pizotifen, topiramate
107
What is misalignment of the eyes
When the eyes are not aligned, experience double vision May lead to amblyopia - when one eye becomes more dominant and other ignores ( lazy eye)
108
Concomitant squints
Differences in control of extra ocular muscles
109
Paralytic squints
Due to paralysis of extra ocular muscles
110
Causes of squint
Usually idiopathic Hydrocephalus Cerebral palsy Space occupying lesions e.g. retinoblastoma Trauma
111
Examination of squint?
Cover test - observing movement of uncovered eye Corneal light reflecting test - holding a light source from 30cm from the child's face to see if the light reflects symmetrically on teh pupils
112
Management of squint(strabismus)
Referral to secondary care Eye patches
113
What is craniosytnosis?
When skull sutures close prematurely Results in abnormal head shapes and restriction to the growth of the brain If left untreated - leads to raised ICP, resulting symptoms of developmental delay, cognitive impairment, vomiting, irritability XRAY skull and surgical reconstruction
114
What is muscular dystrophy?
Genetic conditions that cause gradual weakening and wasting of muscles X linked recessive
115
What is Gowers sign?
Children with proximal muscle weakness use a specific technique to stand up from a lying position Get up from downward dog, muscles around pelvis aren't strong enough without the help of their arms
116
Management of muscular dystrophy's
Lots of OT, physio and medical appliances
117
Duchenne muscular atrophy?
Defective gene for dystrophin on the X chromosome Dystrophin is a protein that holds muscles together at cellular level Calf psuedohypertrophy Life expectancy 25-35 years Investigations = raised CK and genetic testing
118
what is spinal muscular atrophy?
Autosomal recessive condition that causes a progressive loss of motor neurones, leading to progressive muscular weakness Affects the lower motor neurones in the spinal cord.
119
Lower motor signs seen in SMA?
Fasciculations, reduced muscle bulk, reduced tone, reduced power and reduced or absent reflexes.
120
Types of SMA?
Type 1 - onset in the first few months of life, usually progressing to death within 2 years Type 2 - onset within the first 18 month . Most never walk but survive to adulthood Type 3 - Onset after first year of life. Most walk without support, but subsequently loose the ability. Respiratory muscles are less affected and life expectancy is close to normal Type 4- onset in the 20s, most retains ability to walk short distances, but require a wheelchair for mobility
121
Management of SMA?
- No cure - Physiotherapy can help to maximise strength of muscles - Resp support - PEG feeding when weak swallow = unsafe swallow
122
What is hydrocephalus?
CSF build up within the brain and spinal cord overproduction of CSF or problem with draining CSD
123
Where is CSF created and absorbed?
CSF created in the 4 choroid plexusus ( one in each ventricle) CSF absorbed into the venous system by the arachnoid granulations
124
Congenital causes of hydrocephalus?
Aqueductal Stenosis - most common, insufficient drainage of CSF, Cerebral aqueduct that connects the 3rd and 4th ventricle is stenosed Blocks normal flow of CSF out of the 3rd = builds up in the lateral and 3rd ventricles Arachnoid cysts Arnold-chiari malformation -where cerebellum herniates downwards through the foramen magnum, blocking CSF outflow Chromosomal abnormalities and congenital malformations can cause obstruction to CSF damage
125
Presentation of hydrocephalus?
Cranial bones in babies arent fused at sutures till 2 Skull can expand, get and enlarged and rapidly increasing head circumference. Bulging anterior fontanelle Poor feeding and vomiting Poor tone Sleepiness
126
Treatment for hydrocephalus
Ventriculoperitoneal shunt VP shunt that drains CSF from ventricles into antoher body cavity = mainstay
127
What is eczema?
Chronic atopic condition Inflammation, defects in the barrier that the skin provides Dry Typically presents before 2 years Flexor - insides of elbows and knees
128
Management of eczema?
- Avoid irritants - Emollients ○ E45, aveeno, hydromol, - Topical steroids ○ Hydrocortisone, eumovate, betnovate, demovate ○ Be careful of skin thinning - Wet wrapping ○ Severe cases Large amounts of emollient under wet bandages
129
What Is eczema herpeticum?Treatment?
- Severe infection caused by HSV 1 or 2 OR VZV - Rapidly progressing painful rash, often in children that have eczema - Monomorphic, circular, depressed ulcerated, punched out erosions, usually 1-3mm IV aciclovir
130
What is psorasis?
Chronic autoimmune condition Red scaly patches on skin Genetic - associated with HLA-b13 EXTENSOR - knees and elbows, also scalp
131
What is plaque psoriasis?
: the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
132
What is flexural psoriasis?
In contrast to plaque psoriasis the skin is smooth
133
What is guttate psoriasis?
Transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
134
What is pustular psoriasis?
Commonly occurs on the palms and soles
135
Presentation of psoriasis?
Ausptiz sign - bleeding when plaques are scraped off Keobner phenomenon - development of psoriatic lesions to areas of skin affected by trauma Residual pigmentation of the skin after the lesions resolve
136
Management of psoriasis?
- Topical potent corticosteroid once daily + vitamin D anaolgue once daily - Topical vitamin D analogues - calcipotriol - Topical dithranol Tacrolimus in adults
137
What is acne vulgaris?
- Chronic inflammation in the pilosebaceous unit - Increased production of sebum which traps keratin and blocks unit - Comedones - swollen and inflammed units inflammatory lesions form when the follicle bursts releasing irritants Papules and pustules
138
How do you decide which treatment path for acne?
Mild acne: open and closed comedones with or without sparse inflammatory lesions Moderate acne: widespread non inflammatory lesions and numerous papules and pustules Severe acne: extensive inflammatory lesions, may include nodules, pitting and scarring
139
Mild to moderate acne treatment?
* 12 week course of topical combination therapy e.g. a fixed combination of topical adapalene with topical benzoyl peroxide
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Moderate to severe acne - treatment?
2 week course of: - a fixed combination of topical adapalene with topical benzoyl peroxide - a fixed combination of topical tretinoin with topical clindamycin - a fixed combination of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline - a topical azelaic acid + either oral lymecycline or oral doxycycline
141
Measles rash characteristics, treatment, etc
- Highly contagious via respiratory droplets - 10-12 days post exposure - get symptosm - Fever, coryzal symptosm and conjunctivitis - Kopli spots = greyish white spots on the buccal mucosa - Rash starts on the face, erythematous macular rash - Notifiable - Resolves on its own. - Isolate until 4 days after symptoms resolve
142
Scarlet fever - features
- Group A strep infection, usually tonsilitis - Red pink blotchy macular rash with rough sandpaper skin - Strawberry tongue, lymphadenopathy - Pen V - Notifiable - Off school until 24 hours after starting abx
143
Rubella symptoms
- Resp droplets - Milder erytehmatous rash - Lymphadenopathy - Notifiable. Avoid pregnant women - Stay off school till at least 5 days post rash resolving
144
Parovirus b19 features
Red rash on cheeks - slapped cheeks Don’t need to stay off school Reticular(net like) midly erythematous rash on trunk and limbs Mild fever, and coryszal symptoms Complications = aplastic anaemia
145
Roseola infantum features
- Caused by HHV 6 - HIGH FEVER!!. Rash on trunk arms, legs, not itcy Complication = febrile convulsions
146
What is erythema multiforme? Causes?
Erythematous rash caused by hypersensitivity reaction Herpes simplex virus is most common cause. Also - mycoplasma, penicillin, nsaids, SLE, sarcoid Itchy, erythematous rash.
147
Features of erythema multiform?
Target lesions Initially seen on the back of the hands/feet before spreading to the torso Upper limbs more commonly affected than lower limbs Pruritus is occasionally seen and is usually mild Stomatitis - sore mouth Erythema multiforme major is associated with mucosal involvement
148
Management of erythema multiforme?
Identify underlying cause - e.g. CXR to check for e.g. mycoplasma pneumonia Most of the time resolves spontaneously, may be assoicatd with recurrent soldsores IV fluids and analgesia if affecting mucosa - e.g. oral mucosa
149
Features of urticaria?
Hives! Features - Pale, pink raised skin - Pruitic - Histamine release Can be acute or chronic
150
Management of urticaria?
- Non sedating antihistamines - loratadine or certirizine - Sedating antihistamine might be considered at night time - chlorphenamine Prednisolone used for severe or resistant
151
What is chicken pox?
- Generalised vesicular rash. - Highly infectious.. Spread via respiratory route/ direct contact with lesions - Shingles = reactivation of the dormant virus in dorsal root ganglion
152
Presentations of chickenpox?
- Fever often first symptoms - Infectivity = 4 days before rash until 5 days after - Itch, rash starting on head/trunk before spreading. Vesciular blistering
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Complications of chickenpox?
- Bacterial superinfection - Dehydration - Conjunctival lesions - Pneumonia - Encephalitis - presenting as ataxia
154
Management of chickenpox?
- Calamine lotion - Infectivity continues until all the lesions are dry and crusted over = school exclusion - Aciclovir may be considered in immunocompromised - Chlorphenamine ( antihistamine Common complication is secondary bacterial infection of the lesions - NSAIds may increase the risk - On small number - invasive group A streptococcal soft tissue infections may occur = necrotising fasciitis
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What is hand foot and mouth? How does it present?
Coxsackie A virus Presentation Viral upper resp tract symptoms After 1-2 days - small mouth ulcers, followed by blistering red spots Painful mouth ulcers
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Management of hand, foot and mouth?
Supportive! HIGHLY contagious- advise about sharing towels etc
157
Complications of hand, foot and mouth?
- Dehydration - Encephalitis - Bacterial superinfection
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What is molluscum contagiosum? Features?
Skin infection caused by molluscum contagiosum virus - poxvirus Features - Small, flesh coloured papules that each have a central dimple - Crops! - Spread through direct contact or sharing towels/ bedsheets
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Management of mollucscum contagiosum?
- Resolve by themselves - Exclusion from school etc not necessary - If bacterial superinfection occurs - then you might give oral fluclox - Refer for people with HIV who have extensive lesions.
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What is pityriasis rosea?Features?
thought that herpes hominis virus 7 may play a role Generalised, self limiting rash Minority may have prodromal history of headache/ erecent viral infection Herald patch, usually on the trunk FIR TREE APPERANCE! (arrangement following lines of the ribs) - faint pink oval lesions.
161
Management of pityriasis rosea?
Usually disappears after 6-12 weeks
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What is seborrheic dermatitis?
Inflammatory skin condition affecting the sebaceous glands Affects areas that have these glands - scalp, nasolabial folds, eyebrows Cradle cap = crusted dry flaky scalp.
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Management of sebhorreic dermatitis?
Reassurance, usually resolves in a few weeks Baby oil, petroleum jelly on scalp For body and face - clotrimazole anti fungal cream may be used
164
What is ring worm? Features?
Fungal infection. Athletes foot/ tine capitits/ tine corpus Itchy rash that is erythematous, scaly and well demarcated One or several ring or circular shaped areas that spread outwards
165
Management of ring worm?
- Anti fungal medications Creams - Clotrimazole and miconazole Shampoos - ketoconazole for tinea capitis Oral anti fungal medcations e.g. flucanozone
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Risk factors for nappy rash?
Delayed changing of nappies Irritant soap products Certain types of nappies Diarrhoea Oral abx predispose to candida infection Pre term infants
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Nappy rash vs candidal infections
- Rash extending into the skin folds - Larger red macules - Well demarcated scaly border - Circular pattern to the rash spreading outwards, similar to ringworm Satellite lesions, which are small similar patches of rash or pustules near the main rash
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Management of nappy rash?
Switching to highly apsobent nappies Change nappy and clean after wetting or soiling Maximise time not wearing one Barrier cream Infection with candida or bacteria = clotrimazole or fusidic acid cream/ oral fluclox
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What is scabies?
Caused by a mite Sarcoptes scabiei and is spread by prolonged skin contact Typically affects children and young adults Can take up to 8 weeks for any symptoms/ rash to occur Itchy small red spots, tack marks where mites have burrowed Finger webs!
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Management of scabies?
- Permethrin 5% - Mathathion is second line - Oral ivermectin is a single dose that can be repeated if difficult to treat - All household contacts should be treated even if asymptomatic - Pruitis persists for up to 4-6 weeks post eradication - WASH CLOTHES
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What is norweigan crusted scabies?
- Serious infestation with scabies in patients that are immunocompromised - Extremely contagious - Scaly plaques - May not have an itch - Oral ivermectin admission and isolation
172
What is headlice management?
- Malathion - Wet combing - Dimeticone 4% lotion can be put on head left overnight - Houshold contacts don’t need to be treated unless they are also affected
173
What is non blanching rash?
Bleeding under the skin! Doesn’t fade when pressed
174
Differentials for a non blanching rash?
Meningococcal septicaemia HSP - purpuric rash on the legs and buttocks, may have associated abdo/joint pain ITP - develops over several days, in otherwise well child Acute leukaemia HUS - associated with oliguria Mechanical - strong coughing, vomiting etc can produce petechiae in superior vena cava distribution Traumatic - tight pressure Viral illness - influenza/ enterovirus
175
What is erythema nodosum?
Inflammation of the subcutaneous fat on the shins Inflammation of fat = panniculitis Caused by a hypersensitivity reaction Usually over the shins, usually resolves within 6 weeks and lesions heal without scarring
176
Causes of erythema nodosum
- Infection ○ Streptococci ○ TB - Systemic disease ○ Sarcoidosis ○ IBD - Malignancy - Drugs ○ Penicillin's ○ COCP - Pregnancy
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Investigations for erythema nodosum?
- Inflammatory markers - ESR and CRP - Throat swab for strep infection - CXR - Stool microscopy and culture - Faecal calprotectin for IBD
178
Management for erythema nodosum?
Management dependent on underlying cause Managed conservatively May use steroids to settle inflammation
179
Impetigo - what is it?
Superficial bacterial skin infection usually cased by either staph aureus or streptococcus pyogens Primary infection or complication of an existing skin condition CONTAGIOUS - no school until lesions are crusted or 48 hours after commencing abx Either bullous or non bullous
180
Features of impetigo?
- Golden crusted lesions typically round the mouth - Very contagious - Exudate - Bullous is always caused by staph aureus = fluid filled vesicles
181
Management of impetigo?
- Hydrogen peroxide 1% cream for people who are not systemically unwell - If not suitable - topical fusidic acid - Extensive disease - oral fluclox / erithyromycin if penicillin allergic
182
Complications of impetigo?
- Cellulitis - Sepsis - SSSS - Post streptococcal glomerulonephritis
183
What is SSSS?
Condition caused by a type of staphylococcus aureus that produces epidermyoltic toxins Protease enzymes that break down the proteins that hold skin cells together. Often children <5
184
Presentation of SSSS?
Patches of erythema on the skin Skin looks thin and wrinkled. Formation of fluid filled blisters called bullae- these burst and leave sore erythema skin Nikolsky sign - gentle rubbing of the skin causes it to peel away. Systemic symptoms- fever, irritability, lethargy, dehydration, sepsis
185
Management of SSSS?
Admission and treatment with IV ABX Electrolyte balances and fluids
186
SJS vs TEN
SJS = <10% of body surface area TEN = >10 %
187
Causes of SJS/TEN
Pheyntoin (TEN) Penicillins Sulponamides ( SJS) NSAIds HSV HIV
188
Features of SJS/TEN
Rash maculopapular with target lesions being characteristic Nikolsky sign positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently Mucosal involvement Systemic symptoms
189
Management of SJS/TEN
- Hospital admission - May have volume loss and electrolyte derangement IV immunoglobulins
190
What is Kawasaki?
Muocutaenous lymph node syndrome Systemic, medium sized vessel vasculitis Affects young children under 5
191
Features of Kawasaki?
Persistent high fever for more than 5 days CRASH +burn C- conjunctivitis R- rash A - adenopathy ( lymph nodes swollen) S - strawberry tongue H - hand and feet swelling + demarcation ( desquamation = skin peeling) And burn / fever for more than 5 days NOTE coronary artery aneurysms as a complication
192
3 phases of Kawasaki?
Acute - most unwell, with fever, rash and lymphadenopathy. Lasting 1-2 weeks Subacute - acute symptoms settle. Desquamation and arthralgia occur and risk of coronary artery aneurysms forming Convalescent - remaining symptoms settle, blood tests slowly return to normal and coronary aneurysms may regress
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Management of Kawasaki?
High dose aspirin to reduce thrombosis risk IV immunoglobulins to reduce risk of coronary artery aneurysms Echocardiogram
194
Why is aspirin rarely used in children?
Risk of Reyes syndrome
195
What is juvenile idiopathic arthritis?
Autoimmune inflammation Arthritis without any other cause, lasting more than 6 weeks in a patient under the age of 16 Joint pain, swelling and stiffness
196
What is systemic juvenile idiopathic arthritis (still's disease)?
Inflammatory Subtle salmon pink rash, high swinging fevers, enlarged lymph nodes, weight loss, joint inflammation, splenomegaly, muscle plain, pleuritis and pericarditis
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What is a key complication of systemic Juvenile arthritis? (stills)
Macrophage activation syndrome (MAS) … severe activation of the immune system with massive infalmmatory resonse = DIC, anaemia thrombocytopenia, bleeding, low ESR, non blanching rash
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What is polyarticular arthritis?
Idiopathic inflammatory arthritis in 5 joints or more Symmetrical, can affect the small joints of the hand and feet+ large joints such as hips and knees Can get mild fever, anaemia and reduced growth Equivilent of RA in adults. Most children negative for rheumatoid factor and described as seronegative.
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What is oligoarticular arthritis?
4 joints or less Usually only affects a single joint Anterior uveitis ANA often positive, Rheumatoid factor negative No systemic symptoms or inflammatory markers
200
What is enthestits related arthritis?
More common in male children over 6 years Inflammatory arthritis Enthesis's - inflammation of the point where the tendon inserts into a bone HLA b27 gene Psoriasis, IBD, anterior uveitis
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Management of juvenile idiopathic arthritis?
- NSAIDs - Steroids - oral, intramuscular, intraarticular - DMARDs - methotrexate, sulfasalazine Biological therapy e..g inflixamab
202
What is henoch shonlein purpura?
IgA mediated small cell vasculitis - presents with purpuric rash affects lower limbs and buttocks in children Inflammation occurs in affected organs due to IgA deposits in the blood vessels Degree of overlap with IgA nephropathy Affects skin, kidneys and GI tract Usually seen post infection
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Features of Henoch Schonlein Purpura?
Palpable purpuric rash ( with localised oedema) over buttocks and extensor surfaces in arms and legs Abdo pain - note Gi haemorrhage, intususcpetion and bowel infarction Polyarthritis Kidneys - IgA nephritis
204
Investigations for HSP?
- Exclude: meningogoccoal septicaemia, leukaemia, ITP and haemolytic uraemic syndrome - FBC - Renal profile Serum albumin - CRP - Urine dipstick - BP
205
Management of HSP?
Supportive Analgesia Monitor BP and urinalysis should be monitored Around 1/3 of patients have a relapse
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What is Ehlers Danlos Syndrome?
Group of genetic conditions involving defects in collagen, causing hyper mobility of the joints and elasticity of the skin Type III collagen affected
207
Features and complications of Ehlers danlos?
Elastic, fragile skin Joint hypermobility - recurrent dislocation Easy bruising Stretch marks Aortic regurgitation, aortic dissection and mitral valve prolapse SAH Chronic pain
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What is POTs?
Can occur with hypermobile EDS resulting from autonomic dysfunction Tachycardia occurs on sitting/standing and symtoms include: Presyncope Syncope Headaches Disorientation Nausea Tremor
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What is the. Beighton score?
Used in EDS for assessing hypermobility Maximum score of 9 Hyperextending
210
Management of EDS?
Physiotherapy to strengthen and stabilise the joints OT Moderating activity to minimise flares Psychology
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What is rheumatic fever?
Develops following an immunological reaction to a recent (2-4 weeks) streptococcus pyrogens infection Autoimmune! Caused by antibodies created against the streptococcus bacteria that also target tissues in the body
212
What causes rheumatic fever?
Rheumatic fever is caused by group A beta haemolytic streptococcal - typically streptococcus pyogens causing tonsilitis. Immune system creates antibodies to fight the infection. They not only target the bacteria, but also match antigens on the cells of the persons body eg the muscle cells in the myocardium in the heart. Type 2 hypersensitivity reaction. Immune system begins attacking cells throughout the body. Process is usually delayed 2-4 weeks after the initial infection
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Presentation of Rheumatic Fever?
Sore throat, rash, arthritis, murmur Often 2-4 weeks post tonsillitis SOB, nodules Joint involvement - migratory joints become inflamed and improve at different times Carditis - tachycardia, murmurs from valvular heart disease, pericardial rub on auscultation Skin involvement - subcutaneous nodules Nervous system - chorea (irregular, uncontrolled and rapid movements of the limbs)
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Investigations for rheumatic fever?
Throat swab for bacterial culture ASO antibody titres Echocardiogram, ECG
215
What is jones criteria?
A RF diagnosis can be made when theres evidence of a recent streptococcal infection 2 major criteria OR one major and 2 minor criteria
216
Mneumonic for the jones criteria?
JONES- FEAR Major criteria J- joint arthritis O- organ inflammation N- nodules E- erythema marginatum rash S - synedra chorea Minor criteria F- fever E- ECG changes ( prolonged PR interval ) without carditis A- arthralgia without arthritis R - raised inflammatory markers ( CRP and ESR)
217
Management of rheumatic fever?
Pen V Anti inflammatory - NSAIDs Treatment of complications e.g. HF
218
Complications of rheumatic fever?
Reoccurrence Valvular heart disease - notably mitral stenosis Chronic HF
219
What is coeliac?
Autoimmune condition where exposure to gluten causes immune reaction that creates inflammation in the small intestine Develops in early childhood Autoantibodies are created in response to exposure of gluten - anti TTG and anti EMA.
220
Presentation of a child with coeliac?
Often asymptomatic Failure to thrive Diarrhoea, fatigue, weight loss, mouth ulcers, anaemia secondary to iron, b12 or folate deficiency Dermatitis herpetiformis on the abdomen RARELY can present with neurological symptoms: peripheral neuropathy, cerebellar ataxia, epilepsy
221
What should new diagnosis of T1DM be tested for?
Coeliac disease! As they are often linked
222
Genetic associations - coeliac disease
HLA - DQ2 gene HLA - DQ8 gene
223
Investigations for coeliac?
MUST continue the investigations while the patient is on a gluten diet Check IgA Anti TTG anitbodies Anti EMA Endoscopy and intestinal biopsy will show crypt hypertrophy and villous atrophy
224
Complications of untreated coeliac disease
* Vitamin deficiency * Anaemia * Osteoporosis * Ulcerative jejunitis * Enteropathy-associated T-cell lymphoma (EATL) of the intestine * Non-Hodgkin lymphoma (NHL) * Small bowel adenocarcinoma (rare)
224
Coeliac disease associated conditions?
* Type 1 diabetes * Thyroid disease * Autoimmune hepatitis * Primary biliary cirrhosis * Primary sclerosing cholangitis Down’s syndrome
225
Treatment of coeliac disease?
A lifelong gluten free diet is essentially curative. Relapse will occur on consuming gluten again. Checking coeliac antibodies can be helpful in monitoring the disease.
226
Presentation of constipation?
Less than 3 stools a week Hard stools difficult to pass Rabbit dropping Straining and painful Holding an abnormal posture - retentive posturing Rectal bleeding associated with hard stools Faecal impaction causing overflow soiling with incontinence of particularly loose stools May be able to palpate in abdomen
227
What is encopresis?
Faecal incontinence Not pathological until 4 years of age Sign of chronic constipation where the rectum becomes stretched and looses sensation Hard stools remain in the rectum, and only loose stools are able to bypass the blockage and leak out = soiling
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Rarer causes of encopresis?
Spina bifida, Hirschsprungs disease, cerebral palsy, learning disability, psychosocial stress, abuse
229
What is desensitisation of the rectum?
- Developing a habit of not opening bowels and ignoring sensation - Over time loose the sensation - Start to retain faeces - Faecal impaction- rectum stretches as it fills - Desensitisation of the rectum - More difficult to treat the constipation and reverse the problem
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Secondary causes of constipation?
Hirschsprungs, CF (particuarly meconium Ileum), hypothyroidism, spinal cord lesions, sexual abuse, intestinal obstruction, anal stenosis, cows milk intolerance
231
Red flags - constipation
Not passing meconium within 48 hours of birth - CF or hirschsprungs disease Neurological signs Vomiting - obstruction or hirschsprungs Ribbon stool - stenosis Abnormal anus - stenosis, IBD, sexual abuse Failure to thrive - coeliac, hypothyroid, safe guarding Acute severe abdo pain and bloating- obstruction or intussuspection
232
Management of constipation?
- Treat underlying cause - High fibre diet and good hydration - MOVICOL is first line laxative - Faecal impaction may require dis impaction regimen with high dose laxatives Encourage and praise visiting toilet
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medical causes of abdominal pain in children?
- Constipation - UTI - Coeliac - IBD - IBS - Mesenteric adenitis - Abdominal migraine - Pyelonephritis - Henoch schonlein purpura DKA
234
Surgical causes of abdominal pain in children?
Appendicitis- spreads from central to right iliac fossa Intussusception - colicky non specific abdo pain, redcurrant jelly stool Bowel obstruction - pain, distention, constipation and vomiting Testicular torsion - sudden onset, unilateral testicular pain, nausea and vomiting
235
Red flags for abdominal pain?
Persistent or bilious vomiting, severe chronic diarrhoea, fever, rectal bleeding, weight loss, dysphagia, night-time pain, abdominal tenderness
236
What is an abdominal migraine?
- Episodes of central abdomianl pain lasting more than 1 hour - Nausea and vomiting, anorexia, pallor, headache, photophobia, aura May occur in young children before developing traditional migraines as they get older
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Management of abdominal migraine?
Management : explanation, education, treating acute attacks, preventative measures Acute attack: low stimulus, paracetemol, ibuprofen Prevention: pizotifen ( serotonin antagonist, withdraw slowly as associated with withdrawal symptoms eg depression, anxiety, poor sleep and tremor), propranolol etc
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What is GORD?
The contents of the stomach reflux through the lower oesophageal sphincter into the oesphaegous, throat and mouth In babies - there's a immaturity of the lower oesphageal sphincter which allows stomach contents to easily reflux. NORMAL for babies if theres normal growth, usually improves as they grow.
239
Risk factors for GORD?
- Preterm delivery - Neurological disorders
240
Presentation of GORD?
Normal for babies to have some reflux after larger feeds, becomes more troublesome when this causes them to become distressed Signs of problematic reflux: - chronic cough - hoarse cry - distress - reluctance to feed - pneumonia - poor weight gain
241
Management of GORD?
- Small frequent feeds - Burping - Not over feeding Keep upright
242
Complications of GORD?
- Distress - Failure to thrive - Aspiration Frequent otitis media
243
RED FLAGS for vomiting in children/ babies?
* 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 assessmen
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What is a pyloric stenosis?
Presents in 2nd to 4th weeks of life with vomiting Caused by hypertrophy of the circular muscles of the pylorus Pyloric sphincter is a ring of smooth muscle that forms the canal between the stomach and duodenum. Hypertrophy of the pylorus = pyloric stenosis. After feeding, powerful peristalsis in the stomach as it tried to push food into the duodenum and eventually it comes so powerful it ejects the food into the oesophagus
245
Presentation of pyloric stenosis?
- Projectile vomiting 30 mins after feed - Peristalsis palpable mass - Hypochoraemic, hypokalaemia alkalosis due to persistent vomiting ( as HCL is going ) Constipation/ dehydration
246
Diagnosis of pyloric stenosis?
USS to visualise
247
Treatment for pyloric stenosis?
Ramstedt Pyloromyotomy
248
What is biliary atresia?
Bile duct is either narrowed or absent Cholestasis = bile cannot be transported from the liver to the bowel Prevents excretion of conjugated bilirubin
249
Presentation of biliary atresia?
Presents shortly after birth with significant jaundice Appetite and growth disturbance Jaundice Hepatomegaly
250
Investigations for biliary atresia?
Conjugated bilirubin is abnormally high LFTs Sweat test ?CF
251
Treatment for biliary atresia?
Surgical management IS THE ONLY DEFINITIVE TREATMENT Kasai portoenterostomy - Attaching a small section of the intestine to the opening of the liver where the bile duct normally attaches.
252
What are causes of intestinal obstruction?
Meconium ileus Hirschsprungs Oesophageal atresia Intusscpetion
253
Presentation of intestinal obstruction
Persistent vomiting, may be bilious Abdo pain and distention Failure to pass stool or wind Abnormal bowel sounds, can be high pitched an tinkling in the early obstruction and absent later
254
What is Hirschsprung's?
Congenital condition where nerves of myenteric plexus are absent in the distal bowel and rectum Brain of the gut Nerve plexus runs all the way along the bowel in the bowel wall, responsible for stimulating peristalsis
255
Genetics of hirschsprungs?
More common in males Family history Downs syndrome, NF, MEN II
256
Presentation of Hirschsprung's?
Delay in passing meconium Constipation, abdominal distention, abdominal pain, vomiting and poor weight gain
257
What is Hirschsprung associated enterocolitis? What is the management?
- Inflammation and obstruction of intestine - Presents within 2-4 weeks of birth - Fever, abdo distention and diarrhoea and features of sepsis - Toxic megacolon and perforation of the bowel can occur Requires urgent ABX, fluid resuscitation and decompression of the obstructed bowel
258
Investigations for Hirschsprungs?
- Abdo xray Rectal biopsy - absence of ganglionic cells
259
Management of Hirschsprungs?
Initially - rectal washouts/ bowel irrigation Definitive = surgery to affected segment of the colon
260
Symptoms of appendicitis?
Central abdominal pain, moves to the right iliac fossa. Mcburneys point. Loss of appetite Nausea and vomiting Rovsigns sign - palpation of the left iliac fossa causes pain in the RIF Guarding on abdominal palpation Rebound tenderness - peritonitis
261
Differentials for appendicitis?
Ectopic, ovarian cyst, meckels diverticulum, mesenteric adentiis, appendix mass
262
What is intusscpetion?
Telescoping of the bowel Most common in the ileocaecal region Boys are more affected
263
Associated conditions- intusseption
Concurrent viral illness Henoch schleim purpura Cystic fibrosis Intestinal polys Meckel diverticulum
264
Presentation of intusscepetion?
Severe colicky abdominal pain Pale, lethargic and unwell child Redcurrant jelly stool - late sign Right upper quadrant mass on palpation - sausage shaped Vomiting
265
Investigations for intussception?
USS
266
Management of intussception?
AIr insufflation under radiological control If fails or signs of peritonitis ---> surgical
267
Complications of intusception?
Obstruction Gangrenous bowel Perforation Death
268
When does tetralogy of fallot usually present?
Around 1-2 months.
269
4 characteristics of teralogy of fallot?
VSD Right ventricular hypertrophy - from trying to pump the blood against resistance of the light ventricle and pulmonary stenosis Right ventricular outflow tract obstruction - pulmonary stenosis = more resistance - blood would rather take the VSD route = more cyanosis Overriding aorta = Entrance to the aorta is further right. When the right ventricle contracts and sends blood upwards, the aorta is in the direction of the travel meaning more deoxygenated blood enter the aorta from the right side of the heart
270
Effect of tetralogy of fallot?
Right to left cardiac shunt Blood bypasses the child's lungs Cyanosis Degree depends on severity of pulmonary stenosis
271
Risk factors for teratology of fallot?
Rubella infection Increased age of mother Alcohol consumption at pregnancy Diabetic mother
272
Presentation of tetralogy of fallot?
Cyanosis - hyper cyanotic tet spells Right to left shunt Ejection systolic murmur - pulmonary stenosis Boot shaped heart on CXR, ECG shows right ventricular hypertrophy Echocardiogram - doppler flow
273
Management of tetralogy of fallot?
Surgical repair Cyanotic episodes - use prostaglandin infusion to maintain the ductus arterisosus in neonates
274
What is ASD?
Most likely congenital heart defect to be found at adulthood Defect in septum between the 2 atria Left and right are connected during pregnancy and get a problem with them
275
Types of ASD?
Patent foramen ovale - when it fails to close Ositum secundum - where the septum secundum fails to close Otisum primum - where the septum primum fails to close
276
Complications of ASD
Stroke - in the context of DVT- normally when patients have a DVT that becomes an embolus it travels through right side of heart to the lungs and becomes a PE With ASD, the clot is able to travel across the left side of heart = systemic circulation =- brain and stroke!!!!
277
Presentation of ASD?
Ejection systolic murmur Fixed split second heart sound SOB, difficulty feeding, poor weight gain, LRTI
278
Management of ASD?
Echocardiogram Active monitoring, percutaneous catheter closure via femoral vein or open heart surgery
279
What is VSD?
Congenital hole between 2 ventricles Commonly associated with downs syndrome and turners syndrome
280
Presentation of VSD?
May be picked up on antenatal scans Typical symptoms: Poor feeding Dyspnoea Tachypnoea Failure to hive PAN SYSTOLIC MURMUR - louder in smaller defects
281
Treatment of VSD?
Nutritional support Medication for HF - e.g diuretics
282
What is a patent ductus arterisosus?
Connects the pulmonary artery with the aorta allowing blood to bypass the lungs Stops functioning within 3 days of birth and closes entirely within the first 3 weeks of life - PDA is when it fails to close
283
Associations with patent ductus arteriosus
More common In premature babies, born at high altitude or maternal rubella infection in the first trimester May be related to genetic - downs syndrome Prostaglandins keep it open during pregnancy - note
284
Features of a patent ductus arteriosus
SOB Small - may not have have any abnormal heart sounds Larger = continuous machinery murmur Large volume, bounding, collapsing pulse Left sub clavicular thrill Wide pulse pressure Apex beat heaving Difficulty feeding Poor weight gain
285
Management of a patent ductus arteriosus
Echocardiogram Medical closure = indomethacin or ibuprofen.. inhibits prostaglandins synthesis. Endovascular procedures/ open surgery
286
What heart defects cause right to left shunt, and therefore cyanotic heart disease?
VSD, ASD, PDA, transposition of the great arteries
287
What is eisenmenger syndrome?
Reversal of left to right shunt in congenital heart defect due to pulmonary hypertension Occurs when an uncorrected left to right leads to remodelling of the pulmonary micro vasculature - eventually leads to obstruction in pulmonary blood and pulmonary hypertension. Deoxygenated blood bypasses the lungs and enters the body Cyanosis
288
3 lesions that can result in eisenmengers
ASD VSD Patent ductus arteriosus
289
Examination findings for eisenmenger syndrome?
- Right ventricular heave - Loud p2 - Raised JVP - Peripheral oedema
290
What is aortic valve stenosis?
Restricting blood flow from left ventricle into the aorta Can be asymptomatic May get fatigue, SOB, dizziness, fainting Symptoms worsen on exertion
291
Signs of aortic valve stenosis?
Ejection systolic murmur
292
Management of aortic valve stenosis?
Echocardiogram Surgery
293
What is pulmonary valve stenosis?
When the pulmonary valve becomes thickened
294
Presentation of pulmonary valve stenosis ?
Often completely asymptomatic adn discovered as an incidental finding of a murmur Can get fatigue, SOB and dizziness
295
Signs of pulmonary valve stenosis?
EJS heard loudest at pulmonary area Palpable thrill in pulmonary area Right ventricular heave due to right ventricular hypertrophy Raised JVP with giant a waves
296
Management of pulmonary valve stenosis?
Echocardiogram Watch and wait for mild Surgery for symptomatic /sever
297
What is ebstein's abnormaly?
Tricuspid valve is set lower to the right side of the heart, causing a bigger right atrium and a smaller right ventricle Leads to poor flow from the right atrium to the right ventricle = poor flow to teh pulmonary vessels
298
Clinical features of ebstein's abnomaly?
Evidence of heart failure - gallop rhythm - poor feeding - cyanosis - collapse/ cardiac arrest
299
What is transposition of the great arteries?
When the attachments of the aorta and pulmonary trunk are swapped Right ventricle pumps blood into the aorta ada the left ventricle pump blood into the pulmonary vessels 2 separate circles don’t mix! After birth the condition is immediately life threatening as there's no connection between the systemic circulation and pulmonary circulation. Baby will be cyanosed Immediate survival depends on shunt between systemic circulation and pulmonary circulation to allow blood to get oxygenated by the lungs - e.g. ASD or VSD or PDA
300
Presentation of transposition of the great arteries?
- Often diagnosed during pregnancy with antenatal USS - Cyanosis - Tachycardia - Loud single S2 - Prominent right venticular impulse
301
Management of transposition of the great arteries?
- Maintenance of the ductus arteriosus with prostaglandins Surgical correction
302
Most common organism - otitis media?
Streptococcus pneumoniae
303
Symptoms of otitis media?
Ear pain, reduced hearing, upper airway infection symptoms eg fever, cough, core throat Balance issues and vertigo Buldging inflamed red tympanic membrane Middle ear effusion
304
Treatment of otitis media?
DOESN'T REQUIRE ABX USUALLY - Seek medical help if symptoms don’t improve after 3 days Prescribe immediately if: - Symptoms last more than 4 days or not improving - Systemically unwell - Immunocompromise - Perforation and or discharge 5-7 day course of amoxicillin
305
Complications of otitis media
Mastoiditis, meningitis, brain abscess, facial nerve palsy
306
What is otitis externa? Organisms?
Infection of the outer ear Recent swimming is a common trigger Infection: bacterial or fungal, contact dermatitis Fungal - candidias.. Especially if recurrent
307
Features of otitis externa?
Ear pain, itch and discharge Otoscope shows red, swollen and eczematous canal
308
Treatment of otitis externa?
Topical antibiotic or combined topical antibiotic with steroid NOTE THAT ahminoglycosides are contraindicated e.g. gentamicin If dont respond to topical ABX then refer to ENT
309
Most common cause of tonsillitis?
Most common cause is viral infection Most common cause of bacterial is group A strep which is treated with pen V
310
Fever pain...
Fever during previous 24 hours P- purulence ( pus on tonsils) A- attended within 3 days of onset of symptoms I- inflamed tonsils N - no cough or coryza FeverPAIN score of 0 or 1: Do not prescribe antibiotics. FeverPAIN score of 2 or 3: Consider a delayed antibiotic prescription FeverPAIN score of 4 or 5: Consider an immediate antibiotic prescription.
311
Treatment for bacterial tonsillitis?
Pen V for 10 days is first line Clarithromycin if allergic
312
Complications of tonsillitis?
Otitis media Quinsy Rheumatic fever
313
Tonsillectomy indications?
7 or more in 1 year 5 per year in 2 years 3 per year in 3 years Other indications = recurrent tonsillar abscesses, swallowing or snoring or breathing problems
314
Post tonsillectomy bleeding ....
STRAIGHT BACK TO THEATRE!
315
What is a quinsy?
Peritonsillar abscess Bacterial infection with trapped pus, forming an abscess in the tonsils
316
Features of a quinsy
Severe throat pain, lateralising to one side Deviation of the uvula to the unaffected side Trismus - can't open their mouth Change in voice due to pharyngeal swelling - hot potato voice Swelling and erythema
317
Most common cause of quinsy ?
Streptococcus pyogens ( group A strep)
318
Management of quinsy?
Needle aspiration or incision and drainage + IV abx URGENT REVIEW BY ENT SPECIALIST
319
What is glue ear?
Otitis media with effusion = middle ear full of fluid. Eustachian tube gets blocked
320
Risk factors for glue ear?
Male Siblings with glue ear Winter and spring Parental smoking
321
Features of glue ear?
Peaks at 2 years of age Hearing loss = presenting feature Secondary problems e.g. speech and language delay, behavioural and balance problems Otoscopy shows dull tympanic membrane with air bubbles or fluid
322
Management of glue ear?
Refer to audiometry to establish hearing loss Resolves without treatment in 3 months usually May require grommet insertion
323
Congenital causes of hearing loss?
Maternal rubella or CMV infection during pregnancy Genetic deafness Associated syndromes e..g Downs
324
Perinatal causes of hearing loss?
Prematurity, hypoxia during or after birth
325
What is the newborn hearing screening programme?
Tests hearing in all neonates
326
Audiometry?
Younger children ( under 3) tested by looking for response to sound e.g. turning towards a sound Results are recorded on an audiogram§
327
Epistaxis?
Keisselbachs plexus ( littles area) Area of nasal mucosa in the front of the nasal cavity that contains a lot of blood vessels Unilateral bleeding
328
Management of epistaxis?
Sit up, tilt head forwards Squeeze the cartiliginous part of the nostrils for 10-15 minutes - if the bleeding doesn't stop after 10-15 minutes - nasal cautery, nasal packing, if failed ----> sphenopalatin ligation in theatre
329
What is naspetin?
Antiseptic, chlorhexidine, neomycin Reduces inflammation and infection Caution in peanut allergy
330
What is cleft lip?
Congenital condition - split or open section of the upper lip Clift lip results from failure of the front-nasal and maxillary processes to fuse
331
What increases the risk of cleft lip?
Maternal anti epileptic use
332
What is a thyroglossal cyst?
Thyroid gland starts at the base of the tongue during foetal development Travels down neck during development to its final position in front of trachea Leaves a track called thyroglossal duct, which then disappears, but when part of it persists ---> gives rise to fluid filled cyst
333
Main complication of thyroglossal cyst?
Infection, causing a hot, tender and painful lump
334
Presentation of thyroglossal cyst?
Usually midline Moves upwards with protrusion of the tongue, as thyroglossal duct and base of the tongue are connected Mobile, non tender, soft and fluctuant
335
Management of thyroglossal cyst?
USS or CT can confirm the diagnosis Surgical removal
336
What is a branchial cyst?
Congenital abnormality arising when the second branchial cleft fails to properly form during foetal development Leaves a space around by ezhithelial tissue in the left lateral aspect of the neck Presents as a soft, round, cystic swelling around the angle of the jaw and the sternocleidomastoid muscle in the anterior triangle of the neck
337
Features of a branchial cyst?
Present as a round, soft, cystic swelling around the angle of the jaw and the sternocleidomastoid muscle in the anterior triangle of the neck Present on infection Round, soft, non tender. Don’t transilluminate
338
Management of a branchial cyst?
Consider and exclude malignancy Referral to ENT USS Fine needle aspiration or surgery
339
What is ADHD?
Hyperactivity and inability to concentrate Affects persons ability to carry out everyday tasks, develop normal skills and perform well at school Factors should be consistent across settings
340
Features of ADHD?
- Short attention span - Quickly moving from one activity - Quickly loosing interest in one task and not being able to persist - Constantly moving or fidgeting - Impulsive behaviour Disruptive or rule breaking
341
Medications for ADHD>
Medications - CNS stimulants E.g. methyphenidate - ritalin Dexamfetamine Atomextine
342
First line medication for children with depression?
Fluoxetine
343
What is ketogenesis?
When theres an insufficient supply of glucose and glycogen stores are exhausted May happen during prolonged fasting or low card diet Liver takes fatty acids and coverts them to ketones. Ketones are water soluble. Fatty acids that can be used as fuel Ketones are buffered in normal patients dont become acidotic, but when underlying pathology e.g. T1DM causes extreme ketosis = metabolic acidosis
344
What is DKA?
Diabetic ketoacidosis occurs in type 1 diabetes, where the person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when they body does not have enough insulin to use and process glucose Ketoacidosis Dehydration - hyperglycaemia overwhelms the kidney Potassium imbalance - insulin normally drives potassium into cells, kidneys continue to balance the blood potassium so serum can be high or normal ,but total body potassium is low as theres none stored in cells
345
Cerebral oedema in DKA?
Dehydration + high blood sugar concentration = water moves from intracellular to extracellular space in the brain Causes brain cells to shrink and become dehydrated Rapid correction of dehydration and hyperglycaemia causes rapid shift in water from extracellular to intracellular - causes brain to become oedematous
346
Cerebral oedema treatment?
Slow the IV fluids, IV mannitol and IV hypertonic saline
347
Features of DKA?
Abdominal pain Polyuria, polydipsia and dehydration Kussmaul respiration = deep breathing Acetone smelling breath
348
Diagnosis of DKA?
Hyperglycaemia Ketosis Acidosis
349
Management of DKA?
Fluid replacement ○ Isotonic saline used. Insulin ○ IV infusion started 0.1 unit/kg.hour ○ Once blood glucose is <14 mmol/l an infusion of 10% dextrose should be started at 125 ml/hr in addition to 0.9% sodium chloride ○ Long acting insulin should be continued, short acting shouild be stopped Correction of electrolyte disturbances Serum potassium often high on admission despite total body potassium being low - falls quickly following treatment = hypokalaemia. Monitor cardiac things ( add about 40 mmol to the saline if the potassium is between 3.5 -5.5 - if higher seek senior review)
350
When should ketonaemia and acidosis have resolved - dka- and what can they switch onto?
Both the ketonaemia and acidosis should have been resolved within 24 hours If its resolved,( and patient is eating and drinking) can switch to subcutaenous insulin
351
Addison disease?
Adrenal glands are damaged Autoimmune Reduced secretion of cortisol and aldosterone Primary adrenal insufficiency
352
Causes of primary adrenal insufficiency?
Addisons TB Metastases Meningococcal septicaemia HIV APS
353
Secondary adrenal insufficiency?
Inadequate ACTH stimulating the adrenal glands, resulting in low levels of cortisol being released Result of loss or damage to the pituitary e..g congenital underdevelopment, surgery, loss of blood flow or radiotherapy
354
Tertiary adrenal insufficiency?
Inadequate CRH release by the hypothalamus Result of patients being on long term oral steroids causing suppression of the hypothalamus When steroids are suddenly withdrawn the hypothalamus doesn't wake up quick enough and steroids are adequately produced
355
Features of adrenal insufficiency?
Lethargy, vomiting, anorexia, hypoglycaemia, weight loss, salt craving, jaundice, failure to thrive, abdominal pain, developmental delay Hyperpigmentation - associated with Addisons as high ACTH Vitiligo, hypoglycaemia, hyponotraemia, hyperkalaemia
356
Management of adrenal insufficiency?
Hydrocortisone - 20-30mg a day. Majority given in first half of day Fludrocortisone (used to replace aldosterone)
357
Sick days - adrenal insufficiency
Glucocorticoid dose should be doubled and fludrocortisone dose stay the same With diarrhoea or vomiting, IM injected!
358
Addisonian crisis?
Acute presentation of severe Addisons with absence of steroid hormones Reduced consciousness Hypotension Hypoglycaemia, hyponatraemia, hyperkaelaemia
359
Management of addisonian crisis?
IV hydrocortisone 100mg IV fluids Correct the hypoglycaemia
360
What is chronic adrenal hyperplasia?
Congenital deficiency of the 21 hydroxylase enzyme Causes underproduction of cortisol and aldosterone and overproduction of androgens from birth Autosomal recessive!
361
Presentation of chronic adrenal hyperplasia?
Female patients present with vitalised genitalia, enlarged clitoris due to high testosterone Hyponatreamia Hyperkalaemia Hypoglycaemia Milder cases --->females who are tall, facial hair, absent periods, deep voices and males with large penis, early puberty, deep voice and tall
362
What does excess ACTH cause?
hyperpigmentation
363
Management of chronic adrenal hyperplasia?
Management - Cortisol replacement - hydrocortisone - Aldosterone replacement - fludrocortisone May require corrective surgery
364
Growth hormone deficiency?
Gh produced in the anterior pituitary gland Responsible for stimulating cell production and growth of organs muscles, bones and height Stimulates release of insulin like growth factor by the liver
365
Presentation of growth hormone deficiency?
At birth: - micropenis - hypoglycaemia - serve jaundice Later - Poor growth - Short stature - Slow development of movement and strength - Delayed puberty
366
Treatment for growth hormone deficiency?
Daily subcutaneous injections of growth hormone - somatropin Treatment of other associated deficiency
367
Investigations for growth hormone deficiency?
Seeing response to medications that normally stimulate the release of GH MRI brain and genetic testing
368
Congenital hypothyroidism
When cild is born with underactive thyroid Newborn blood spot screening test Prolonged jaundice, poor feeding, constipation and reduced activity
369
Acquired hypothyroidism?
Autoimmune thyroiditis ( hashimotos) anti TPO antibodies and antithyroglobulin antibodies Fatigue, poor growth, weight gain, poor school performance, dry skin, hair loss
370
Management of hypothyroidism?
TFTs Thyroid USS Levothyroxine can be used to replace thyroid hormones
371
Symptoms of a UTI?
Infants - poor feeding, vomiting and irritability Younger children - abdo pain, fever, dysuria Older children - dysuria, frequency, haematuria
372
Urine dipstick for a UTI?
Nitrites - gram negative bacteria break down nitrates ( normal wast product in urine) into nitrites Leukocytes - result of an infection/another cause of inflammation
373
Management of UTI?
Infants <3 months should be referred immediately to a paediatrician and started on IV ABX( ceftriaxone) Oral Abx can be considered in children over 3 months if otherwise well ○ Trimethoprim ○ Nitro ○ Cefalexin Amoxicillin
374
Recurrent UTIs in children- what to do?
USS All children under 6 months with their first UTI should have an abdo USS within 6 weeks, or during the illness if there are recurreent UTIs or atypical bacteria Children with recurrent UTIs should have an abdo USS within 6 weeks Children with atypical UTIs should have an abdo USS during the ilness DMSA scan - 4-6 months post ilness to assess for damage from reucrrent or atypical UTIs VUR - Where urine has the tendency to flow from the bladder back into the ureters. This predisposes patients to developing upper UTIs and subsequent renal scarring. MCUG
375
Management of vesico-uteric reflux?
Avoid constipation Avoid an excessively full bladder Prophylactic abx Surgical input from paediatric urology
376
Causative organisms - uti
* E. coli (responsible for around 80% of cases) * Proteus Pseudomonas
377
Predisposing factors to UTis in children
Incomplete bladder emptying * infrequent voiding * hurried micturition * obstruction by full rectum due to constipation * neuropathic bladder Vesicoureteric reflux * a developmental anomaly found in around 35% of children who present with a UTI Poor hygiene e.g. not wiping from front to back in girls
378
What is vulvovaginitis?
Inflammation and irritation of the vulvac and vagina Condition often affecting girls between ages of 3-10 years Irritation caused by sensitive and thin skin and mucosa Oestrogen helps to keep the skin and vaginal mucosa healthy and resistant to infection = much less common after puberty.
379
Presentation of vulvovaginitis?
Soreness, itching, erythema around the labia, vaginal discharge, dysuria, constipaiton
380
Urine dipstick - vulvovaginitis?
Leukocytes but no nitrites
381
Management for vulvovaginitis
Management Often patients have already been treated for urinary tract infections and thrush, usually with little improvement in symptoms. It is unusual for girls to develop thrush before puberty. Generally no medical treatment is required and management focuses on simple measures to improve symptoms: Avoid washing with soap and chemicals Avoid perfumed or antiseptic products Good toilet hygiene, wipe from front to back Keeping the area dry Emollients, such as sudacrem can sooth the area Loose cotton clothing Treating constipation and worms where applicable Avoiding activities that exacerbate the problem In severe cases an experienced paediatrician may recommend oestrogen cream to improve symptoms.
382
What is nephrotic syndrome?
When basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from the blood into the urine Most common between 2 and 5 Frothy urine, generalised oedema and pallor
383
SYMPTOMS of nephrotic syndrome ?
TRIAD: - Low serum albumin - High urine protein content ( >3+ protein on urine dipstick) - Oedema Other features: deranged lipid profile ( high levels of cholesterol, triglycerides and low density lipoproteins), high BP, hypercoagulability ( increased tendency to form blood clots), loss of thyroxine binding globulin lowers the total, but not free, thyroxine levels.
384
Causes of nephrotic syndrome?
Most common = minimal change disease Secondary to intrinsic kidney disease e..g FSGS or membranoproliferazive glomerulonephritis Secondary to underlying systemic illness e..g HSP, diabetes, infection such as HIV, hepatitis and malaria
385
What is minimal change disease?
Small molecular weight proteins and hyaline casts on urinalysis Management = corticosteroids
386
Management of nephrotic syndrome
High dose steroids - given for 4 weeks and then gradually weaned over the next 8 If steroid resistant - ACEi and immunosuppressants e.g. cyclosporine, tacrolimus or rituximab Low salt diet Diuretics may be used to treat oedema
387
Complications of nephrotic syndrome?
- Hypovolaemia - occurs as fluid leaks from the intravascular space into the interstitial space causing oedema and low BP Thrombosis - proteins that normally prevent blood clotting are lost in the kidney, and the liver responds to low albumin by producing pro thrombotic proteins Infection - kidneys leak immunoglobulins Acute or chronic renal failure Relapse
388
Nephritis vs nephrotic syndrome?
Nephritis = insalmation of the kidneys Blood in urien, high bP, mild to moderate protienurea, often autoimmune diseases / infection Nephrotic syndrome = damage to glomeruli leading to protein loss, severe proteinurea, oedema, no haematuria
389
What is nephritis?
Inflammation within the nephrons of the kidney... Reduction in kidney function Haematuria: invisible or visible amounts of blood in the urine Proteinuria ( but less than in nephrotic syndrome)
390
Causes of nephritis In children?
Post streptotoccal glomeruloneprhtiis and IgA nephropathy ( Burgers )
391
Post streptotoccal glomerulonephritis features?
- 1-3 weeks after a B haemolytic streptococcus infection such as tonsilitis caused by streptococcus pyogens - Features: headache, malaise, porteinuria, haematuria, HTN, raised anti streptolysin O titre - Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation - leads to acute deterioration in renal function causing AKI - **** THINK WITH RECENT TONSILITIS + STREPTOCOCCUS Often just supportive management, but may need antihypertensives and diuretics
392
IgA nephropathy feautures ( bergers)
- Bergers disease - Related to HSP and igA nephropathy - IgA depsoits in the nephrons of the kidney causes inflammation Management = supportive and immunosuppressants e.g. steroids and cyclisphosphamide. Develops 1-2 days after URTI Macroscopic haematuria
393
What is haemolytic uraemic syndrome?
Thrombosis in the small vessels throughout the body, usually triggered by shiga toxins from either E coli or shigella Often affects children following an episode of gastroenteritis. Also abx and anti motility medication ( e.g. loperamide) used to treat gastroenteritis caused by E. coli 0157 or shigella increase the risk of HUS
394
Triad in haemolytic uraemia syndrome?
- AKI - MAHA (microangiopathic haemolytic anaemia) - Thrombocytopenia - formation of blood clots consumes platelets = thrombocytopenia, blood flow through the kidney is affected by thrombi and damaged RBCs leading to AKI
395
Presentation of haemolytic uraemic syndrome?
- E coli 0157 and shigella causes gastroenteritis - Diarrhoea is the first symptom, which turns bloody within 3 days. - Around a week after the onset of diarrhoea, the features develop: ○ Fever ○ Abdo pain ○ Lethargy ○ Pallor ○ Oliguria ○ Haematuria ○ HTN ○ Bruising ○ Jaundice ( due to haemolysis) Confusion
396
Investigations for haemolytic uraemia syndrome?
Blood film is most useful initial diagnostic test Stool culture U + E - aki
397
Management of haemolytic uraemia syndrome?
- Supportive treatment - MEDICAL EMERGENCY = admission and supportive management with treatment of: ○ Hypovolaemia ○ HTN ○ Severe anaemia ( e.g. blood transfusions ) ○ Severe renal failure e.g. haemodialysis NO ROLE FOR ABX
398
What is MAHA?
Type of anaemia caused by destruction of red blood cells as they pass through small blood vessels ( microangiopathy) Associated with mechanical destruction of RBCs in damaged blood vessels
399
Causes of MAHA ?
○ TTP (characterised by formation of small blood clots through the microcirculation). Get a thrombocytopenia too (low platelet count) ○ HUS ○ DIC - when widespread clotting causes RBC fragmentation. Triggered by severe infections, trauma, malignancy or pregnancy complications ○ SLE ○ Malignant hypertension ○ Pre-eclampsia and eclampsia ○ Vasculitis Bone marrow disorders
400
What is enuresis?
Involuntary urination Can be either primary = child has never achieved continence Or secondary = child has been dry for at least 6 months before
401
When do most children get control of urination?
Most children can control daytime urination by 2 years and night time urination by 3-4 years
402
Primary nocturnal causes of enuresis?
- Variation on normal development, if younger than 5 -family history - Overactive bladder - frequent small volume urination prevents the development of bladder capacity - Fluid intake prior to bedtime - Failure to wake due to deep sleep - Psychological distress Secondary causes e.g. chronic constipation, UTI, learning disability
403
Management of primary enuresis?
MANAGEMENT: 2 week diary. Lifestyle Enuresis alarm.
404
Secondary nocturnal enuresis causes?
- When previously dry for 6 months - Causes: ○ UTIs ○ Constipation ○ T1dm ○ Psychosocial MALTREATMENT - safeguarding!
405
Causes for diurnal enuresis?
UTI's, psychosocial problems, constipation
406
Role for desmopressin?
Enuresis For short term control e.g. sleepovers or na enuresis alarm hasn't been affective
407
What is polycystic kidney disease/ARPKD?
Defect in gene located on chromosome 6 which encodes fibrocystic - responsible for creation of the tubules and maintenance of healthy epithelial tissue in kidneys, liver and pancreas
408
Features of polycystic kidney disease?
- Cystic enlargement of the renal collecting ducts - Oligohydramnios, pulmonary hypoplasia and potter syndrome - Congenital liver fibrosis Usually presents in antenatal period with oligohydramnios and polycystic kidneys seen on antenatal scans Oligohydramnios is lack of amniotic fluid - caused by reduced urine production by the foetus
409
What is potter syndrome?
Lack of amniotic fluid - Dysmorphic features e.g. Underdeveloped ear Cartlidge, low set ears, flat nasal bridge and abnormalities of the skeleton Underdeveloped fetal lungs resulting in respiratory failure shortly after brith - Large cystic kidneys ca take up so much space in abdomen that its hard for neonates to breath adequately - Renal dialysis may be needed
410
Problems that PCKD causes?
- Liver failure due to fibrosis - Portal HTN ---> oesphageal varices - Progressive renal failure - HTN due to renal failure Chronic lung disease
411
What is Wilms tumour?
Childhood malignancy Presents under 5 years old
412
Features of Wilms tumour?
Abdominal mass Abdomianl pain Haematuria Lethargy Fever HTN Weight loss Unilateral communal Metastases found in 20% - most commonly lung
413
Referral - wilms tumour
children with an unexplained enlarged Abdo mass - possibly Wilms tumour- arrange paediatric review within 48 hours
414
Diagnosis of wilms tumour?
- USS of the abdomen to visualise kidneys - CT or MRI scan used to stage the tumour Biopsy to identify the histology
415
Management of Wilms tumour?
- Nephrectomy - Chemotherapy - Radiotherapy if advanced disease - Prognosis = 80% cure rate!
416
What is a posterior urethral valve?
Where there is a tissue at the proximal end of the urethra that causes obstruction of urine output Occurs in new born boys Can create back pressure into the bladder, ureters and up to the kidney= hydronephrosis
417
Presentation of posterior urethral valve
Difficulty urinating Weak urinary system Chronic urinary retention Palpale bladder Recurrent UTIS Impaired kidney function
418
What can posterior urethral valve lead to...?
Obstruction to urine outflow in the developing foetus resulting in bilateral hydronephrosis and oligohydramnios ( low amniotic fluid volume). This leads to underdeveloped foetal lungs ( pulmonary hypoplasia) with respiratory failure shortly after birth.
419
Investigations for posterior urethral valve?
Severe cases may be picked up on antenatal scans as oligohydramnios and hydronephrosis After birth ○ Abdominal USS - thickened, enlarged bladder + bilateral hydronephrosis ○ MCUG - shows location of the extra urethral tissue and reflux of urine back into the bladder - Cystoscopy
420
Management of posterior urethral valve
Mild cases may just be observed and monitored If required a temporary urinary catheter may be inserted to bypass the valve Ablation or removal of the extra urethral tissue during cystoscopy
421
What are undescended testes/cryptoorchidism
The testes develop in the abdomen and gradually migrate down, through the inguinal canal and into the scrotum When they fail to reach the bottom of the scrotum by 3 months of age = congenital undescended testes
422
Risk factors for undescended testes?
FH of undescended testes Low birth weight Small for gestational age Prematurity Maternal smoking during pregnancy
423
Management of undescended testes/ cryptorchidism
Watch and wait for the first 3-6 months Orchidoplexy ( surgical correction of undescended testes) Should be carried out between 6-18 months of age
424
What is retractile testes?
Normal for boys that havent reached puberty for the testes to move out of the scrotum into the inguinal canal when its called or the cremasteric reflex is activated Resolves as they go through puberty and the testes settle into the scrotum
425
Hypospadias
Congenital abnormality where the urethral meatus is abnormally displaced to the ventral side of the penis
426
Features of hypospadias?
Ventral urethral meatus Hooded prepuce Chordee = ventral curvature of the penis
427
Associations with hypospadias?
Cryptoorchidism ( present in 10%) and inguinal hernia
428
Management of hypospadias?
Referral to urology Corrective surgery at around 12 moths of age Do NOT circumsise prior to surgery
429
What is testicular torsion?
Twist of the spermatic cord resulting in testicular ischaemia and necrosis Most common in males aged between 10 and 30
430
Features of testicular torsion
Pain is usually severe and sudden onset Pain may be referred to the lower abdomen N+V Swollen, tender testes retracted upwards Cremasteric reflex lost Elevation of the testes doesn't not ease pain (Prehn's sign) and in epidymitits it does
431
Management of testicular torsion? Investigations?
- Urgent surgical exploration - If a torted testis is identified then both should be fixed as the condition of bell clapper testis is often bilateral ○ Bell clapper = when the fixation between testicle and tunica vaginalis is absent, so the testicle hangs in a more horizontal position. Able to rotate - twisting the spermatic cord. As it rotates it twists the vessels and cuts off the blood supply USS shows whirlpool sign
432
What is orchiopexy vs orchidectomy?
Orchiopexy (correcting the position of the testicles and fixing them in place) Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis
433
What is a hydrocele?
Collection of fluid within the tunica vaginalis that surrounds the testes Tunica vaginalis = sealed pouch of membrane that surrounding the testes.
434
Communicating vs non communicating hydrocele?
Communicating - Caused by patency of the processes vaginalis allowing peritoneal fluid to drain into the scrotum -Common in newborn males and usually resolves in the first few months of life Non communicating - caused by excessive fluid production within the tunica vaginalis May develop secondary to: epididymo-orchitis, torsion, testicular tumours
435
Features of hydrocele?
Soft, non tender, smooth swelling around one of the testes Can get above the mass on examination Transilluminates
436
Management of hydrocele?
Infantile will resolve within 2 years usually USS to exclude underlying cause e.g. tumour
437
What is Perth's disease? Whos it more common in? What age?
Avascular necrosis of the femoral head, specifically the femoral epiphysis Occurs in children between 4-8. More common in boys!!! Idiopathic - Main complication is a soft and deformed femorla head = osteoarthritis = totoal hip replacement artificial
438
Presentation of Perthes disease?
Hip pain develops progressively over a few weeks Limp Restricted hip movements Referred pain to the knee No history of trauma
439
XRAY - perthes disease
Early changes include widening of joint space, later changes = decreased femoral head size/ flattening
440
Investigations for Perthes?
XRAY Blood tests are normal Technetinum blood scan or MRI
441
Complications of Perth's?
Osteoarthritis Premature fusion of the growth plates
442
Management of Perthes?
Femoral head within acetabulum = casts and braces Physiotherapy If less than 6 years - observation If older - surgical management
443
What is transient synovitis? Most common age?
Irritable hip Caused by temporary irritation and inflammation of the synovial membrane 3-8 years old Most common cause of hip pain in children Associated with recent viral respiratory tract infection
444
Features of transient synovitis?
- Limp/ refusal to weight bear - Groin or hip pain - Low grade fever present in minority of patients High fever should raise suspicion of other causes such as septic arthritis
445
Management of transient synovitis?
Symptomatic management Analgesia and rest BUT make sure to both safety net and exclude other significant pathology - especially septic arthritis
446
What is slipped upper femoral epiphysis? Who gets it?
Slipped capital femoral epiphysis OBESE BOYS 10-15 years Head of femur slips along the growth plate
447
Features of slipped upper femoral epiphysis?
Hip, groin, medial thigh or knee pain Loss of internal rotation of the leg in flexion Bilateral slip in 20% of cases
448
Investigations for slipped upper femoral epiphysis?
AP and lateral views on XRAY Blood tests normal
449
Management of slipped upper femoral epiphysis
Internal fixation - single cannulated screw placed in the centre of the epiphysis
450
Complications of slipped upper femoral epiphysis?
Osteoarthritis AVN of the femoral head Chondrolysis Leg length discrepancy
451
What is osteomyelitis?
Infection of the bone Typically occurs in the metaphysis of the long bones Commonly staph aureus May be introduced directly into the bone, for example during an open fracture. Or it may have travelled to the bone through the blood - after entering the body through another route such as skin or gums
452
Haematogenous vs non haematogenous osteomyelitis?
- Haematogenous ○ Results from bacteraemia ○ Most common form in children - Non haematogenous Results from continuous spread of infection from adjacent soft tissues to the bone or from direct injury/ trauma to the bone
453
Risk factors for osteomyelitis?
Open bone fracture Orthopaedic surgery Immunocompromised Sickle cell anaemia HIV TB
454
Presentation of osteomyelitis?
Can present acutely or more chronically refusing to use the limb or weight bear Pain Swelling Tenderness
455
Microbiology - osteomyelitis?
Staph aureus most common In sickle cell patients though- salmonella is more common
456
Investigations for osteomyelitis?
MRI Blood tests show raised inflammatory markers and WBCs in response to infection
457
Management of osteomyelitis?
Flucloxacillin Clindamycin if penicillin allergic
458
What is osteosarcoma?
Type of bone cancer Usually presents in adolescents and younger adults aged 10-20 Most common bone to be affected is the femur
459
Presentation of osteosarcoma?
Persistent bone pain Worse at night time May disturb them of wake them from sleep Other symptoms = bone swelling, palpable mass, restricted joint movements
460
Diagnosis of osteosarcoma?
- Urgent direct access XRAY within 48 hours for children presenting with unexplained boen pain or swelling - If it suggests a possible sarcoma, they need an urgent specialist assessment within 48 hours - Raised ALP
461
What does osteosarcoma show on XRAY?
Poorly defined lesion in the bone Destruction of the normal bone and a fluffy appearance Periosteal reaction = irritation of the lining of the bone - described as a sun burst appearance
462
Management of osteosarcoma?
Resection of the lesion Adjuvant chemotherapy used alongside
463
What is developmental dysplasia of the hip?
Structural abnormality in the hips caused by abnormal development of the foetal bones during pregnancy Leads to instability in the hips and tendency or potential for subluxation or dislocation Potential to persist into adulthood, leading the weakness, recurrent subluxation or dislocation, abnormal gait and early degenerative changes
464
When do you usually detect developmental dysplasia of the hip?
During new born examinations or later when the child presents with hip asymmetry, reduced range of movement in the hip or a limp
465
Risk factors for developmental dysplasia of the hip?
Female Breech presentation Positive family history Birth weight >5kg Oligohydramnios
466
Screening for developmental dysplasia of the hip?
DDH is screened for on neonatal examination at birth and 6-8 weeks USS for infants with: - First degree family history or hip problems in early life - Breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery - Multiple pregnancy - All infants screened at both the newborn check and also 6 week baby check using Barlow and Ortolanti tests
467
Barlow and Orlanti tests?
Barlow - attempts to dislocate an articulated femoral head Orlanti - attempts to relocate a dislocated femoral head
468
Investigations for Developmental dysplasia
USS BUT If >4.5 months then XRAY is first line
469
Management of developmental dysplasia of the hip?
Most unstable hips will spontaneously stabilise by 3-6 weeks of age Palvik harness if baby presents at less than 6 months Older children may require surgery
470
What is rickets?
Inadequately mineralised bone in developing and growing bones Results in soft and easily deformed bones Osteomalacia in adults
471
Causes of rickets?
Deficiency in calcium or vitamin D - vitamin D is produced by the body in response to sunlight or obtained through diet - Calcium found in dairy/ green vegetables - Rare form caused by genetic defects that result in low phosphate in the blood --hereditary hypophosphatemia rickets - X linked dominant
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Presentation of vitamin D deficiency/ rickets?
- Lethargy - Aching bones and joints - Swollen wrists - Bone deformity - Poor growth - Dental problems - Muscle weakness - Bowing legs, knock knees - Rickety rosary - ends of the ribs expand at the costochondral junctions - Craniotabes - soft skull, with delayed closure of the sutures and frontal bossing Delayed teeth with under development of the enamel
473
Investigations for rickets?
Reduced Serum vitamin D Reduced serum calcium Raised ALP PTH high
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Management of rickets?
Prevention is key Breastfeeding women should take vitamin D supplement Vitamin D oral - ergocalicefrol
475
What is achondroplasia?
Autosomal dominant disorder associated with dwarfism. Abnormal cartilage Achondroplasia gene, FGFR3 is on chromosome 4. Mutation in this gene
476
Features of achondroplasia?
Disproportionate short stature. Average height around 4 feet. Limbs mostly affected by reduced bone length The femur and humerus- Proximal limbs- more affected than bones of the forearm and lower leg Normal trunk Short digits Bow legs Disproportionate skull
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Associations of achondroplasia?
Recurrent otitis media due to cranial abnormalities Kyphoscoliosis Spinal stenosis OSA Obesity Foramen magnum stenosis can lead to cervical cord compression and hydrocephalus
478
Management of achondroplasia ?
MDT involvement Leg lengthening surgery can add height
479
What is Osgood Schlatter's?
Inflammation at the tibial tuberosity where the patella ligament inserts Common cause of anterior knee pain in adolescents Typically occurs in patients aged 10-15 years and more common in males usually unilateral but can be bilateral
480
Presentation of osgood schlatters?
Palpable hard or visible tender lump at the tibial tuberosity Pain in the anterior aspect of the knee Pain exacerbated by physical activity, kneeling and on extension of the knee
481
Management of osgood schlatters?
Focuses on reducing pain and inflammation Reduction in physical activity Ice NSAIDs for symptomatic relief
482
What is osteogenesis imperfecta?
Genetic condition where you get brittle bones that are prone to fractures Collagen metabolism Autosomal dominant
483
Features of osteogenesis imperfecta?
Hypermobility Blue/grey sclera Triangular face Short stature Deafness from early adulthood Dental problem Bone deformities and joint pain
484
Investigations and management for osteogenesis imperfecta?
Investigations - Adjusted calcium, phosphate, PTH, alp are usually NORMAL Management - XRAYs for diagnosing fractures - Bisphosphates to increase bone density - Vitamin D supplementation to prevent deficiency MDT
485
Septic arthritis features?
Single painful joint: - Hot, red, swollen, painful - Refusing to weight bear - Stiffness and reduced range of motion - Systemic symptoms e.g. fever, lethargy and sepsis - Can be subtle in young children
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Septic arthritis criteria?
Kocher criteria Fever >38.5 degrees Non weight bearing Raised ESR Raised WCC
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Investigations and management for septic arthritis ?
Investigations - Joint aspiration for culture - will show raised WBC - Raised inflammatory markers - Blood culture's SEPSIS 6! May drain.
488
SALTR Harris fractures - growth plate
Type 1 - Straight across Type 2 - Above Type 3 - BeLow Type 4 - Through Type 5 - CRush
489
Pain management in children
Pain management - Paracetamol Morphine do not give codeine, tramadol or aspirin in fractures - risk of Reyes
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Causes of hip pain - 0-4
Septic arthritis Developmental dysplasia of the hip Transient sinovitis
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Causes of hip pain 5-10
Septic arthritis Transient sinovitis Perthes disease
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Causes of hip pain 10-16
Septic arthritis Slipped upper femoral epiphysis Juvenile idiopathic arthritis
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Red flags for hip pain?
child under 3 years Fever Waking at night with pain Weight loss Anorexia Night sweats Fatigue Persistent pain Stiffness in the morning Swollen or red joint
494