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phase 3a medicine > paediatrics > Flashcards

paediatrics Flashcards

1
Q

what is leukaemia?

A

cancer of the stem cells in the bone marrow

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2
Q

what are the risk factors for leukaemia?

A
  • Down’s syndrome
  • Kleinfelters syndrome
  • Radiation exposure during pregnancy
  • Noonan syndrome
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3
Q

what are the clinical symptoms of leukaemia?

A
  • Persistent fatigue
  • Unexplained fever
  • Faltering growth
  • Weight loss
  • Night sweats
  • Anaemia
  • Petechiae and abnormal bruising
  • Unexplained bleeding
  • Abdominal pain
  • Generalised lymphadenopathy
  • Hepatosplenomegaly
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4
Q

Which type of leukaemia peaks in 2-3 year olds?

A

ALL

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5
Q

Which type of leukaemia peaks in under 2 year olds?

A

AML

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6
Q

What would require a specialist assessment in suspected leukaemia?

A

unexplained petechiae or hepatomegaly

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7
Q

What would an FBC show in leukaemia, and when should it be done?

A

anaemia, leukopenia and thrombocytopenia
within 48 hours

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8
Q

which investigations are needed to diagnose leukaemia?

A

Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
Blood film, which can show blast cells
Bone marrow biopsy
Lymph node biopsy

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9
Q

what is the management of leukaemia?

A

CHEMOTHERAPY
+/- radiotherapy
+/- bone marrow transplant
+/- surgery

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10
Q

What is the prognosis for ALL?

A

overall cure rate is 80%

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11
Q

what are the complications of chemotherapy for leukaemia?

A

Failure to treat the leukaemia
Stunted growth and development
Immunodeficiency and infections
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity

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12
Q

what is a Wilm’s Tumour?

A

originates from embryonal renal tissue, usually presenting before the age of 5

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13
Q

How do Wilm’s tumours present?

A
  • Large abdominal mass, often incidentally found in an otherwise well child
  • Abdominal pain
  • Anorexia
  • Haematuria
  • HTN
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14
Q

What investigations can confirm Wilm’s Tumour?

A

CT/ MRI

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15
Q

What is the management of Wilm’s Tumour?

A

Initial chemotherapy followed by delayed nephrectomy

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16
Q

what are the possible causes of jaundice <24 hours after birth?

A

Always pathological
- G6PD deficiency
- spherocytosis
- Rhesus disease
- blood group incompatibility

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17
Q

what are the possible causes of jaundice over 14 days (21 in preterm infants)?

A

Prolonged jaundice
- biliary atresia
- hypothyroidism
- breast milk jaundice
- UTI/ infection

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18
Q

what tests should be done in neonatal jaundice?

A

TCB for gestation over 35 weeks
Serum bilirubin (conj. and unconj.)
Coombs test
Infection screen

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19
Q

what is biliary atresia?

A

obstruction of the biliary tree due to sclerosis of the bile duct, reducing bile flow

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20
Q

what are the risk factors for biliary atresia?

A
  • female
  • cholestasis at 2-8 weeks
  • CMV infection
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21
Q

how does biliary atresia present?

A

Jaundice post 2 weeks
dark urine
pale stools
appetite disturbances
hepatosplenomegaly

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22
Q

what is caput succedaneum?

A

boggy superficial scalp swelling that can cross suture line

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23
Q

what can cause caput succedaneum or cephalohaematoma?

A

traumatic, prolonged or instrumental delivery

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24
Q

what is a cephalohematoma?

A

a collection of blood between the skull and the periosteum

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25
Q

how can a caput succedaneum be differentiated from a cephalohematoma?

A

CS crosses suture lines, CH does not.

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26
Q

what are the risks of caput succedaneum or cephalohematoma?

A

anaemia and jaundice

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27
Q

what are the 2 main reasons for neonatal jaundice?

A
  • increased bilirubin production, foetal haemoglobin has 70 day lifespan compared to adult 120
  • decreased bilirubin conjugation due to liver immaturity
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28
Q

what is the pathophysiology behind breastmilk jaundice?

A

feeding difficulties => dehydration + impaired bilirubin elimination

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29
Q

what is kernicterus?

A

acute bilirubin encephalopathy caused by unconjugated bilirubin deposition in the basal ganglia and brainstem after it exceeds albumin binding capacity

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30
Q

how can kernicterus present?

A

less responsive, floppy, drowsy baby with poor feeding
later, seizures, hypertonia, opisthotonos

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31
Q

what are the long term risks of kernicterus?

A

cerebral palsy, learning disabilities and sensorineural deafness

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32
Q

what are the possible treatments of neonatal jaundice?

A

phototherapy or exchange transfusion if over threshold

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33
Q

what are the prenatal signs of oesophageal atresia?

A

polyhydramnios- the baby cannot swallow the amniotic fluid

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34
Q

what are postnatal signs of oesophageal atresia?

A

blowing bubbles
salivation and drooling
cyanotic episodes on feeding
respiratory distress and aspiration

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35
Q

how does bowl obstruction present?

A

Persistent vomiting. This may be bilious, containing bright green bile.
Abdominal pain and distention
Failure to pass stools or wind
Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later.

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36
Q

when would malrotation/ volvulus typically present?

A

later at 2-30 days, will have passed meconium normally

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37
Q

what sign on x-ray would indicate duodenal atresia?

A

double bubble sign

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38
Q

what sign would indicate volvulus on x-ray?

A

coffee bean sign

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39
Q

what can help pass meconium in CF?

A

therapeutic contrast enema (gastrografin)

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40
Q

what is hirschsprung’s disease?

A

congenital absence of ganglia (both myenteric and submucosal plexus in a segment of the colon

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41
Q

where does Hirschsprung’s most commonly affect?

A

rectosigmoid junction (75%)

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42
Q

what are the clinical features of Hirschsprung’s?

A

failure to pass meconium within 24-48 hours
abdominal distension and late bilious vomiting

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43
Q

what would a PR reveal in Hirschsprung’s?

A

contracted distal segment followed by a rush of liquid stool and temporary relief of symptoms

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44
Q

what does an abdominal X-ray show in Hirschsprung’s?

A

contracted distal segment and dilated proximal segment

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45
Q

what is the gold standard investigation for Hirschsprung’s?

A

rectal suction biopsy

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46
Q

how common are undescended testes?

A

common:
5% of term babies
20% of preterm babies

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47
Q

when in pregnancy does testicular descent occur?

A

the 8th month, requires testosterone

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48
Q

how will most undescended testes resolve?

A

will spontaneously descend by 6 months to 1 year

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49
Q

how will undescended testes be managed if not dropped by 1 year?

A

orchidopexy

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50
Q

what is a hydrocele?

A

a hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes

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51
Q

what is the most common heart defect?

A

ventricular septal defect

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52
Q

what are the risk factors for VSD?

A

premature birth
genetic conditions such as Down’s, Edward’s and Patau’s
family history

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53
Q

how does VSD present?

A
  • Often can by symptomless
  • Pansystolic murmur at the lower left sternal border
  • Poor feeding
  • Tachypnoea
  • Dyspnoea
  • Failure to thrive
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54
Q

How is VSD diagnosed?

A
  • Echo
  • ECG
  • X- ray which may show cardiomegaly
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55
Q

what is the treatment for VSD?

A
  • Diuretics to relieve pulmonary congestion
  • ACE inhibitors to reduce systemic pressure
  • Surgical repair
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56
Q

what are the complications of VSD?

A
  • Eisenmenger’s
  • Endocarditis
  • Heart failure
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57
Q

what are the risk factors for atrial septal defect?

A
  • maternal smoking in 1st trimester
  • family history of CHD
  • maternal diabetes
  • maternal rubella
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58
Q

how does atrial septal defect present?

A
  • Tachypnoea
  • Poor weight gain
  • Recurrent chest infections
  • Soft, systolic ejection murmur heard in 2nd intercostal space
  • Wide, fixed split S2 sound
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59
Q

how is atrial septal defect managed?

A
  • If small, can be managed conservatively and will close within 12 months of birth
  • Surgical closure, usually if ASD >1cm
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60
Q

what are the complications of ASD?

A
  • Stroke from DVT
  • Atrial fibrillation
  • Pulmonary HTN
  • Eisenmenger’s syndrome
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61
Q

what is the most common congenital CYANOTIC heart disease?

A

tetralogy of fallot

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62
Q

what are the four features of tetralogy of fallot?

A
  • Overriding aorta
  • Large VSD
  • Pulmonary stenosis
  • Right ventricular hypertrophy
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63
Q

what are the risk factors for tetralogy of fallot?

A
  • More common in males
  • Rubella
  • Increased age of the mother (>40)
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64
Q

How does tetralogy of fallot present?

A
  • Clubbing
  • Poor feeding
  • Poor weight gain
  • Ejection systolic murmur in pulmonary region (caused by pulmonary stenosis)
  • Tet spells
  • Irritability
  • Cyanosis
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65
Q

What would X-ray show in tetralogy of fallot?

A

boot shaped heart

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66
Q

what is the treatment of tetralogy of fallot?

A
  • Prostaglandin infusion PGE1 to maintain ductus arteriosus
  • Beta blockers
  • Morphine to reduce respiratory drive
  • Surgical: repair under bypass 3 months - 4 years but needs ICU post op
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67
Q

what is transposition of the great arteries?

A

aorta rises from the right ventricle and pulmonary artery from the left, meaning deoxygenated blood is delivered systemically.

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68
Q

what must be present with transposition of great arteries for the baby to survive?

A

Mixing must occur- patent foramen ovale, VSD or PDA

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69
Q

what is the clinical presentation of transposition of the great arteries?

A
  • Cyanosis in the first 24 hours of life
  • Right ventricular heave
  • Loud S2 heart sound
  • Systolic murmur if VSD present
  • Sometimes PD/VSD can make symptoms however within a few weeks they will
    develop respiratory distress, poor feeding etc
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70
Q

what would an X-ray show in transposition of great arteries?

A

egg on string’- narrowed mediastinum and cardiomegaly

71
Q

what is the treatment of transposition of great arteries?

A

PGE1 infusion to ensure PDA and mixing of blood
Surgical correction before 4 weeks

72
Q

what is patent ductus arteriosus?

A

persistent connection between aorta and pulmonary artery

73
Q

what are the risk factors for PDA?

A

female, premature

74
Q

how does PDA present?

A
  • Respiratory distress
  • Apnoea
  • Tachypnoea
  • Tachycardia
  • Continuous machinery murmur at the left sternal edge
75
Q

what is the management of PDA?

A
  • Cardiac catheterisation to close around 1 years old or sooner in more severe cases
  • Premature infants: Indomethacin or Ibuprofen inhibits prostaglandin and stimulates
    closure
76
Q

when is croup most common?

A

children: 6 months to 3 years old
peak incidence at 3 years
common in autumn and spring

77
Q

what are the common causative organisms of croup?

A

Parainfluenza virus mainly, Adenovirus, Rhinovirus,
Enterovirus

78
Q

how will croup present?

A
  • 1-4 days history of non-specific rhinorrhea (thin, nasal discharge), fever and barking
    cough
  • Worse at night
79
Q

what will examination findings be in croup?

A
  • Stridor
  • Decreased bilateral air entry
  • Tachypnoea
  • Costal recession
80
Q

how should a croup diagnosis be made?

A
  • FBC, CRP U+E
  • CXR to exclude foreign body
81
Q

how should croup be managed?

A
  • Symptoms can last 48 hours - 1 week
  • Paracetamol/Ibuprofen for fever/sore throat
  • Admission if moderate/severe and consider if dehydrated
  • Single dose dexamethasone 0.15mg/kg or prednisolone
  • Nebulised adrenaline for relief of severe symptoms
  • Oxygen if required
  • Monitor for needed ENT intervention if suspected airway blockage
82
Q

what is bronchiolitis?

A

a viral infection of the bronchioles

83
Q

who does bronchiolitis affect?

A
  • Affects under 2’s
  • Very common
  • Peaks in the winter and spring months
84
Q

what is the main cause of bronchiolitis?

A

Respiratory Syncytial virus

85
Q

what are the risk factors for bronchiolitis?

A
  • Breastfeeding for < 2 months
  • Smoke exposure
  • Older siblings who attend nursery/school
  • Chronic lung disease of prematurity
86
Q

what would a chest x-ray show in bronchiolitis?

A

hyperinflation, air trapping and flattened diaphragm

87
Q

how could RSV be diagnosed?

A

nasopharyngeal aspirate for RSV culture

88
Q

when should palvizumab vaccine be considered?

A
  • Children <9 months with chronic lung disease of prematurity
  • Children < 2 years with severe immunodeficiency require long term ventilation
89
Q

what would indicate need for urgent hospital admission in bronchiolitis?

A
  • Apnoea
  • Resp Rate > 70
  • Central cyanosis
  • SpO2 < 92%
90
Q

what would indicate need for non-urgent admission in bronchiolitis?

A
  • Resp Rate > 60
  • Clinical dehydration
91
Q

what is the inpatient management of bronchiolitis?

A
  • oxygen, fluids
  • CPAP if in respiratory failure, suctioning of secretions
  • rivabarin for severe cases
92
Q

what is the most common cause of pneumonia in neonates?

A

Group B Strep
E coli, Klebsiella, Staph Aureus

93
Q

What is the most common cause of pneumonia in infants?

A

Strep pneumoniae, chlamydia

94
Q

what is the most common cause of pneumonia in school age children?

A

Strep pneumoniae
Staph Aureus, group A Step, Mycoplasma pneumoniae

95
Q

what would you find on examination in pneumonia?

A

dullness to percuss, crackles, decreased breath sounds,
bronchial breathing

96
Q

would wheeze and hyperinflation suggest viral or bacterial pneumonia?

A

viral

97
Q

what bacteria would be suggested by pneumatocoeles and consolidations in multiple lobes?

A

staphylococcus aureus

98
Q

what tests could be considered in a child with recurrent pneumonia?

A

FBC
Chest X-ray
Serum immunoglobulins
IgG to previous vaccines
Sweat test for CF
HIV test

99
Q

what is the causative organism of whooping cough?

A

Bordetella pertussis- gram -ve bacillus

100
Q

when are vaccines for whooping cough given?

A

2,3,4 months and booster at 3 years 4 months

101
Q

what is the first phase of whooping cough infection?

A

catarrhal phase, lasts 1-2 weeks, coryzal symptoms

102
Q

what is the second phase of whooping cough?

A

paroxysmal phase: lasts 3-6 weeks, characteristic whooping cough

103
Q

what would whooping cough be described like?

A

seal-like/ barking on inspiration
worse at night
can lead to vomiting

104
Q

what test can be done for whooping cough?

A

nasal-pharyngeal swab with pertussis

105
Q

what antibiotic is given for whooping cough?

A

macrolide e.g. clarithromycin

106
Q

give two measures to stop the transmission of whooping cough

A
  • prophylactic antibiotics to close contacts in high health risk group
  • isolation for 21 days or 5 days after antibiotics
107
Q

what wheeze would be heard in asthma?

A

bilateral widespread ‘polyphonic’ wheeze

108
Q

what tests can be used to make a diagnosis of asthma?

A

Spirometry with reversibility testing (in children aged over 5 years)
Direct bronchial challenge test with histamine or methacholine
Fractional exhaled nitric oxide (FeNO)
Peak flow variability measured by keeping a diary of peak flow measurements several times a day for 2 to 4 weeks

109
Q

what is the first line therapy in asthma?

A

SABA e.g. salbutamol

110
Q

what can be used in combination with SABA in <5s?

A

low dose corticosteroid inhaler or leukotriene antagonist
if not successful, add the other option
then refer to specialist

111
Q

when does respiratory distress syndrome commonly occur?

A

below 32 weeks

112
Q

what does a chest x-ray show in respiratory distress syndrome?

A

ground-glass appearance

113
Q

how is respiratory distress syndrome prevented?

A

antenatal steroids i.e. dexamethasone given to mothers with suspected of confirmed pre-term labour

114
Q

what are the possible short term complications of respiratory distress syndrome?

A

Pneumothorax
Infection
Apnoea
Intraventricular haemorrhage
Pulmonary haemorrhage
Necrotising enterocolitis

114
Q

what support can be given to neonates with respiratory distress syndrome?

A

-intubation and ventilation
-endotracheal surfactant
-CPAP
-supplementary oxygen

115
Q

what are the long term complications of respiratory distress syndrome/ CLDP?

A

Chronic lung disease of prematurity
Retinopathy of prematurity occurs more often and more severely in neonates with RDS
Neurological, hearing and visual impairment

116
Q

how is a diagnosis of bronchopulmonary dysplasia/ CLDP made?

A

chest x-ray changes
infant requiring oxygen therapy after 36 weeks gestational age

117
Q

what are the features of bronchopulmonary dysplasia/ CLDP?

A

Low oxygen saturations
Increased work of breathing
Poor feeding and weight gain
Crackles and wheezes on chest auscultation
Increased susceptibility to infection

118
Q

how can bronchopulmonary dysplasia/ CLDP risk be reduced?

A

Using CPAP rather than intubation and ventilation when possible
Using caffeine to stimulate the respiratory effort
Not over-oxygenating with supplementary oxygen

119
Q

what is pyloric stenosis?

A

Progressive hypertrophy of the pyloric sphincter causing gastric outlet obstruction

120
Q

how does pyloric stenosis typically present?

A

first 4-6 weeks of life
hungry baby, thin, pale and failing to thrive
‘projective vomiting’ 30 minutes after every feed, non-bilious

121
Q

what would be found on examination of pyloric stenosis?

A

visible peristalsis
dehydration
palpable olive sized pyloric mass

122
Q

what would a blood gas show in pyloric stenosis?

A

Blood gas analysis will show a hypochloric (low chloride) metabolic alkalosis as the baby is vomiting the hydrochloric acid from the stomach.

123
Q

how can pyloric stenosis be diagnosed?

A
  • Test feed with NG tube and empty stomach to feel for visible peristalsis and olive
    shaped mass
  • USS - Hypertrophy of the muscle
124
Q

how is pyloric stenosis managed?

A
  • Correct metabolic imbalances - NaCl
  • Fluid bolus for hypovolemia
  • NG tube and aspiration of the stomach
  • Ramstedt’s Pyloromyotomy - feeding can commence 6 hours after procedure
125
Q

what is hirschsprung’s disease?

A

Nerve cells of the myenteric plexus are absent in the distal bowel and rectum,
specifically the parasympathetic ganglionic cells resulting in lack of peristalsis.

126
Q

what are the risk factors for Hirschsprung’s disease?

A

FAMILY HISTORY
Downs syndrome
Neurofibromatosis
Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
Multiple endocrine neoplasia type II

127
Q

How does Hirschsprung’s present?

A

Delay in passing meconium (more than 24 hours)
Chronic constipation since birth
Abdominal pain and distention
Vomiting
Poor weight gain and failure to thrive

128
Q

what is a life threatening complication of Hirschsprung’s?

A

Hirschsprung-associated enterocolitis (HAEC), leading to toxic megacolon and perforation of bowel.

129
Q

How does HAEC present?

A

affects 20% of Hirschsprung’s babies
It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis.

130
Q

what is the most common type of hirshsprung’s disease?

A

short segment- disease is confined to rectosigmoid part of the colon

131
Q

What tests can be used to diagnose Hirschsprung’s?

A

abdominal x-ray with contrast enema shows obstruction
rectal suction biopsy (GS)- will show absence of ganglionic cells

132
Q

what is the management of Hirschsprung’s?

A

surgical removal of the aganglionic section of bowel
if unwell/ enterocolitis: fluid resuscitation and manage obstruction
if HAEC- IV Abx

133
Q

how does intestinal obstruction present?

A

Persistent vomiting. This may be bilious, containing bright green bile.
Abdominal pain and distention
Failure to pass stools or wind
Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later.

134
Q

how is intestinal obstruction diagnosed?

A

abdominal x-ray showing dilated loops of bowel proximally and collapsed loops distally
absence of air in the rectum

135
Q

what is the most common age of presentation of intussusception?

A

mainly <1 (3 months to 3 years)

136
Q

what conditions are associated with intussusception?

A

Concurrent viral illness
Henoch-Schonlein purpura
Cystic fibrosis
Intestinal polyps
Meckel diverticulum

137
Q

how does intussusception present?

A

Severe, colicky abdominal pain
Pale, lethargic and unwell child
“Redcurrant jelly stool”
Right upper quadrant mass on palpation. This is described as “sausage-shaped”
Vomiting
Intestinal obstruction

138
Q

how is intussusception diagnosed?

A

ultrasound scan or contrast enema

139
Q

how is intussusception managed?

A

therapeutic enema or surgical reduction

140
Q

what is necrotising enterocolitis?

A

Acute inflammatory disease affecting preterm neonates leading to bowel necrosis
and multi system organ failure

141
Q

what are the risk factors of NEC?

A

Very low birth weight or very premature
Formula feeds (it is less common in babies fed by breast milk feeds)
Respiratory distress and assisted ventilation
Sepsis
Patient ductus arteriosus and other congenital heart disease

142
Q

how does NEC present?

A

Intolerance to feeds
Vomiting, particularly with green bile
Generally unwell
Distended, tender abdomen
Absent bowel sounds
Blood in stools

143
Q

what would blood tests show in NEC?

A

Full blood count for thrombocytopenia and neutropenia
CRP for inflammation
Capillary blood gas will show a metabolic acidosis
Blood culture for sepsis

144
Q

what is the diagnostic investigation in NEC and what does it show?

A

Abdominal X-ray
Dilated loops of bowel
Bowel wall oedema (thickened bowel walls)
Pneumatosis intestinalis is gas in the bowel wall and is a sign of NEC
Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
Gas in the portal veins

145
Q

how is NEC managed?

A

Nil by mouth with IV fluids, total parenteral nutrition (TPN) and antibiotics to stabilise them. A nasogastric tube can be inserted to drain fluid and gas from the stomach and intestines.
Some may require surgery to remove dead bowel.

146
Q

What is Meckel’s diverticulum?

A
  • Congenital diverticulum of the small intestine containing ileal, gastric and pancreatic
    mucosa
  • Occurs in 2% of the population
  • Is 2cm from the ileocecal valve
147
Q

What is Meckel’s diverticulum supplied by?

A

omphalomesenteric artery

148
Q

what is the risk with Meckel’s diverticulum?

A

peptic ulceration- can lead to intussusception and volvulus

149
Q

what is biliary atresia?

A

Biliary atresia is a congenital condition where a section of the bile duct is either narrowed or absent. This leads to cholestasis.

150
Q

what is type 1 biliary atresia?

A

common duct is obliterated

151
Q

what is type 2 biliary atresia?

A

atresia of the cystic duct in the porta hepatis

152
Q

what is type 3 biliary atresia?

A

Most common atresia of the right and left ducts at the level of the porta hepatis

153
Q

how does biliary atresia present?

A
  • Jaundice post 2 weeks
  • Dark urine
  • Pale stools
  • Appetite disturbance
  • Hepatosplenomegaly
  • Abnormal growth
154
Q

what type of bilirubin would be raised in biliary atresia?

A

conjugated bilirubin

155
Q

what is the management of biliary atresia?

A

surgery- the ‘Kasai portoenterostomy’, a section of the small intestine is attached to the opening of the liver

156
Q

what would ‘ribbon stool’ in constipation raise worries of?

A

red flag for anal stenosis

157
Q

what is the first line laxative for constipation?

A

movicol

158
Q

what can be used to manage faecal impaction?

A

faecal disimpaction regimen with a high dose of laxatives at first

159
Q

what is epiglottitis?

A

inflammation and swelling of epiglottis, typically caused by haemophilus influenza B

160
Q

how does epiglottitis present?

A

Patient presenting with a sore throat and stridor
Drooling
Tripod position, sat forward with a hand on each knee
High fever
Difficulty or painful swallowing
Muffled voice
Scared and quiet child
Septic and unwell appearance

161
Q

what investigation can confirm epiglottitis and what will it show?

A

lateral x-ray of neck, shows characteristic ‘thumb print’ sign
also excludes foreign body

162
Q

what is the management of epiglottitis?

A

DO NOT distress the patient
alert senior paediatrician and anaesthetist
ensure airway is secure
IV ABx e.g. ceftriaxone
steroids e.g. dexamethasone
Oxygen

163
Q

what is the middle ear?

A

the space between the tympanic membrane and the inner ear, where the cochlea, vestibular apparatus and nerves are

164
Q

how do bacteria get to the middle ear?

A

eustachian tube from the throat

165
Q

what is the most common cause of otitis media?

A

STREP PNEUMONIAE
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus

166
Q

how does otitis media present?

A

ear pain, reduced hearing and general illness

167
Q

what is the first line antibiotic choice of otitis media?

A

amoxicillin for 5 days
otherwise erythromycin and clarithromycin

168
Q

when should you consider antibiotics in otitis media?

A

significant co-morbidities, systemically unwell or immunocompromise
less than 2 years with bilateral otitis media and otorrhoea

169
Q

what are febrile convulsions?

A

seizures which occur in children with a high fever between 6 months and 5 years

170
Q

what are simple febrile convulsions?

A

Simple febrile convulsions are generalised, tonic clonic seizures. They last less than 15 minutes and only occur once during a single febrile illness.

171
Q

what are complex febrile convulsions?

A

Febrile convulsions can be described as complex when they consist of partial or focal seizures, last more than 15 minutes or occur multiple times during the same febrile illness.

172
Q
A

phase 3a medicine (4 decks)

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