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NP- Phase 3a Medicine > Paeds- Resp, ENT and Ophthalmology > Flashcards

Paeds- Resp, ENT and Ophthalmology Flashcards

1
Q

what viruses commonly cause respiratory infections in children?

A
  • Respiratory syncytial virus (RSV)
  • rhinovirus
  • parainfluenza
  • metapneumovirus
  • adenoviruses
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2
Q

what are some host and environmental factors that can increase the risk fo respiratory infection?

A
  • maternal/ parental smoking
  • poor socioeconomic status
  • poor nutrition
  • underlying disease- CF
  • male
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3
Q

what does the term upper respiratory tract infection (URTI) encompass?

A
  • common cold (rhinitis)
  • sore throat (pharyngitis, tonsilitis)
  • acute ottitis media
  • sinusitis
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4
Q

how does the common cold present and what patohgens typically cause this?

A
  • clear/ mucopurulent nasal discharge and nasal blockage

- rhinovirus, coronaviruses, RSV

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5
Q

how is the common cold managed and what advice is given to patients?

A
  • self-limiting- no need for ABx
  • paracetamol and ibuprofen
  • vapour rob, steam inhalation can help
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6
Q

what viruses (and which bacteria) typically cause pharyngitis?

A

common cold viruses

adenoviruses

EBV

bacteria- group A B- haemolytic strep

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7
Q

how is pharyngitis managed?

A

paracetamol and ibuprofen for symptomatic relief

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8
Q

what is tonsilitis?

A

form of pharyngitis where there is intense inflammation of the tonsils with a purulent exudate

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9
Q

what common pathogens can cause tonsilitis?

A
  • viral- adneoviruses, EBV, rhinovirus

- bacterial- group A- B- haemolytic strep

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10
Q

what symptoms does tonsillitis present with?

A
  • headache
  • abdo pain
  • tonsillar exudate and cervical lymphadenopathy- if bacterial
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11
Q

what is the CENTOR criteria for tonsillitis?

A

Cervical lymphadenopathy
Exudate (tonsilar)
No cough
Temperature

3+ of the above= strep infection (so need ABx)

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12
Q

what are some potential complications of tonsililtis?

A
  • peritonsillar abscess
  • otitis media
  • sinusitis
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13
Q

how is tonsillitis managed?

A
  • symptoms- paracetamol and ibuprofen
  • penicillin V or erythromycin if strep infection (if Patient has met CENTOR criteria 3+)
  • hospital admission if severe
  • tonsillectomy if recurring cases
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14
Q

what is acute otitis media?

A

infection/ inflammation of the middle ear

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15
Q

what is chloesteatoma?

A

collection of skin cells in the middle ear- leads to infection and an offensive discharge from the middle ear (and some hearing loss)

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16
Q

when and why does otitis media typically present?

A
  • 6-12 months

- prone to otitis media as the eustachian tubes are short and function poorly

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17
Q

what are some predisposing factors that can lead to otitis media?

A
  • male
  • passive smoking
  • immune deficiency
  • URTI
  • asthma
  • bottle-feeding
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18
Q

how does a patient with otitis media present clinically?

A
  • rapid onset pain in ear
  • pyrexia, fever, irritability
  • ottorhoea
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19
Q

what are some potential complications of otitis media?

A
  • mastoiditis
  • petrosis
  • facial nerve palsy
  • meningitis
  • labrynthitis
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20
Q

what common pathogens can cause otitis media?

A
  • S. pneumoniae
  • H. influenza
  • Moraxella catarrhalis
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21
Q

how is otitis media managed?

A
  • paracetamol/ ibruprofen for pain
  • most resolve spontaneously within 24h
  • immediate ABx if systemicaly unwell/ if patient is immunocompromised- amoxicillin/ erythromycin
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22
Q

what can cause conductive hearing loss?

A
  • glue ear
  • ear wax
  • ottitis media
  • perforated ear drum
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23
Q

what is the name for ottitis media + effusion?

A

glue ear

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24
Q

what causes glue ear and give some risk factors for this?

A

infection

  • older sibling
  • male
  • attending nursery
  • parental smoking
  • allergies
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25
Q

how is conductive hearing loss managed?

A
  • watch and wait
  • Grommet insertion
  • temporary hearing aid
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26
Q

what is the function of a grommet?

A

keeps the middle ear aerated and prevents the accumulation of fluid in the middle ear

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27
Q

when might a grommet by indicated clinically?

A
  • reccurent acute ottitis media

- chronic ottitis media + effusion (glue ear)

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28
Q

how does sinusitis occur?

A
  • initially viral infection of paranasal sinuses lasting <10 days
  • secondary bacterial infection may occur- pain, swelling and tenderness over cheek from infection of maxillary sinus
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29
Q

how is sinusitis diagnosed?

A

clinical examination- mucosal inflammation, discharge, oedema

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30
Q

how is sinusitis managed?

A

98%- viral and self limiting

  • if bacterial- amoxicillin/ doxycycline
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31
Q

what is stridor?

A

rasping sound heard predominantly on inspiration

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32
Q

what is Croup?

A

Laryngotracheobronchitis- mucosal inflammation and increased secretions affecting the airway.

Oedema of the subglottic area is also present

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33
Q

what viruses typically cause croup?

A
  • parainfluenza 1,2,3
  • metapneumovirus
  • RSV
  • influenza
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34
Q

when does croup typically occur?

A

6 months- 6 years

peak is at age of 2

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35
Q

how does croup present clinically?

A
  • barking cough- worse at night
  • harsh stridor
  • hoarseness
  • preceding non-specific viral URTI
  • severe- restlessness, cyanosis, recession, altered consciousness, rising HR/RR
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36
Q

how is mild croup managed?

A

oral dexamethasone/ oral prednisolone

ABC+/- oxygen

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37
Q

what can be given and done in severe cases of croup?

A

nebulised epinephrine and tracheal intubation

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38
Q

what organism causes acute epiglottitis?

A

haemophilus influenza B

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39
Q

why is acute epiglottitis a life-threatening emergency?

A

high risk of respiratory obstruction

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40
Q

how does acute epiglottitis present clinically?

A
  • swelling of epiglottis and surrounding tissues (septicaemia)
  • acute onset
  • high fever, in an ill, toxic looking child
  • painful throat- cannot speak or swallow (muffled voice)
  • drooling
  • soft inspiratory stridor
  • child sits upright with open mouth
  • MINIMAL COUGH/ ABSENT- DIFFERENTIATES FROM CROUP
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41
Q

what must be avoided when assessing a patient with suspected epiglottitis?

A

must not examine the throat with a spatula or lie child down

do not cannulate

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42
Q

how is acute epiglottitis managed?

A
  • intubate under general anaesthetic
  • IV ABx- cefotaxime
  • tracheostomy if complete obstruction
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43
Q

what is bacterial tracheitis and how does it present clinically?

A

pseudomembranous croup is an uncommon but dangerous disease very similar to croup but with :
- high fever

  • toxic appearance
  • tracheal tenderness
  • rapidly progressive airway obstruction- thick exudate
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44
Q

what organisms cause bacterial tracheitis and how is it managed?

A

S. aureus, Strep A, haemophilus

IV ABx

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45
Q

what is whooping cough (pertussis)?

A
  • bronchitis in childhoold

acute, highly contagious respiratory infection- 2 weeks of cough associated with paroxysms, whoops or post-cough vomiting

46
Q

how is whooping cough transmitted?

A

respiratory droplets

47
Q

what organism causes whooping cough?

A

bordetella pertussis- gram negative coccobacillus

48
Q

what are the 2 stages of the clinical presentation of whooping cough?

A
  • catarrhal phase

- paroxysmal coughing phase

49
Q

what are the symptoms of the ‘catarrhal phase’ of whooping cough?

A
  • malaise
  • conjuctivitis
  • nasal discharge
  • sore throat
  • dry cough
  • mild fever
  • lasts 1-2 weeks before progressing to paroxysmal coughing stage
50
Q

how long do symptoms of whooping cough last?

A

even with treatment commonly lasts 6-8 weeks

51
Q

what happens during the paroxysmal coughing phase of whooping cough?

A
  • dry hacking cough, brought on by a sudden startle, worse at night/ after feeding
  • prolonged coughing episodes followed by a characteristic ‘whoop’
  • post-cough vomiting
  • apnoea +/- cyanosis
52
Q

what causes the characteristic ‘whoop’ in whooping cough?

A

inspiration against closed glottis

53
Q

how is whooping cough diagnosed?

A

NOTIFIABLE DISEASE !

  • PCR- nasal swab
  • culture swabs
  • serology testing for anti-pertussis IgG
  • marked lymphocytosis
54
Q

when is hospital admission required in a patient with whooping cough?

A
  • infant <6 months

- respiratory difficulties

55
Q

how is whooping cough managed?

A

macrolides- azithromycin, clarithromycin, erythromycin

  • erythromycin to close contacts
  • patient must remain off school for 48 hours after commencement of Abx
56
Q

what causes bronchiolitis in infants?

A
  • RSV- majority
  • metapneumovirus
  • parainfluenza
  • rhinovirus
  • adenovirus
57
Q

risk factors for bronchiolitis

A
  • premature infant/ low birth weight
  • CF
  • congenital heart disease
  • Down’s
58
Q

how does bronchiolitis present clinically?

A
  • Coryza precedes dry cough
  • increasing breathlessness
  • subcostal and intercostal recession +/- cyanosis and fever
  • wheezing + fine end inspiratory crackles
  • hyperinflation of chest
  • tachycardia
  • feeding difficulties
59
Q

what clinical signs and symptoms, if present, indicate that a patient with bronchiolitis needs to be admitted?

A
  • inadequate feeding and fluid intake
  • respiratory distress
  • hypoxia
  • apnoea
  • persistent O2<92%
60
Q

how is bronchiolitis diagnosed?

A
  • pulse oximetry
  • viral throat swab
  • CXR in severe
61
Q

how is bronchiolitis managed?

A
  • self-limiting- symptoms peak at 3-5 days

- support pt- fluid, nutrition, high flow O2

62
Q

what is given as a preventative medicine against bronchiolitis in immunocompromised patients?

A

ribavarin

63
Q

aetiology of pneumonia in newborns and infants

A

newborn- group B strep (maternal), gram negative enterococci

infants- strep pneumoniae, heamophilus influenza B

64
Q

viral causes of pneumonia

A

RSV
Influenza A and B
Parainfluenza
Adenovirus

65
Q

clinical presentation of pneumonia

A
  • cough
  • fever >38.5
  • respiratory distress- tachypnoea, cyanosis, grunting, intercostal recession, use of accessory muscles, nasal flaring
  • lethargy
  • poor feeding
66
Q

what features of pneumonia may present in older children?

A
  • end inspiratory crackles
  • bronchial breathing
  • pleuritic pain
67
Q

what investigations would be done in severe cases of pneumonia?

A
  • blood cultures
  • sputum culture
  • FBC, CRP
  • CXR- dense, fluffy opacity, blunting of costophrenic angle
68
Q

how is pneumonia managed?

A
  • O2<92%= ADMIT !
  • supportive- oxygen, analgesia, IV fluids, Abx
  • 1st line- amoxicillin (or clarithromycin, co-amoxiclav, azithromycin)
  • drain empyema
69
Q

what are the 2 types of wheeze seen in asthma?

A

transient early wheeze

persistent and recurrent wheezing

70
Q

what is a transient early wheeze in asthma?

A
  • viral associated- RSV
  • small airway obstructed due to inflammation
  • more common in males and resolves by the age of 5
71
Q

what is a persistent and recurrent wheeze in asthma?

A
  • presence of IgE to common inhalant allergens (atopic asthma)
  • common in FH and associated with eczema, hayfever and food allergies
72
Q

in asthma, what does bronchial inflammation lead to?

A
  • airway narrowing and reversible airflow obstruction
  • oedema
  • excessive mucous production
  • infiltration of cells
73
Q

in asthma, what cells infiltrate the bronchials?

A

eosinophils

neutrophils

mast cells

lymphocytes

74
Q

risk factors for the development of asthma?

A
  • ADAM33 gene
  • low BW
  • FH
  • bottle fed
  • atopy
  • male
  • pollution
75
Q

what tests are done in a patient with suspected asthma?

A
  • CXR- rule out other causes
  • spirometry
  • peak flow- diurnal variation
  • skin prick test for common allergens
76
Q

how does asthma present clinically?

A
  • polyphonic expiratory wheeze (due to obstruction)
  • coughing
  • SOB
  • symptoms worse at night and morning
77
Q

what is the main red flag for a severe asthma exacerbation?

A

silent chest on auscultation

78
Q

what is the treatment pathway for patients between 5-16 with asthma?

A

Step 1: SABA (salbutamol)

Step 2: SABA + low dose ICS (beclomethasone)

Step 3: SABA+ ICS + LTRA (Montelukast)

Step 4: SABA+ ICS + LABA (salmeterol)

Step 5:
SABA + low dose MART
(ICS and fast acing LABA- formoterol)

Step 6: SABA + moderate dose MART

79
Q

what pneumonic can be used to remember what must be given to a patient with a severe asthma attack?

A

OSHITME

Oxygen
Salbutamol (nebulised)
Hydrocortisone IV 
Iproatropium bromide (nebulised)
Theophylline IV
Magnesium sulphate IV
Escalate
80
Q

how is asthma treated in patients under 5?

A
  • SABA
  • 8 week moderate dose ICS trial
  • stop trial at 8 weeks and monitor, add back if controlling well
  • if ICS not working, and LRTA
81
Q

what is primary ciliary dyskinesia?

A

congenital abnormality in the structure or function of cilia, leading to the impairment of mucociliary clearance

82
Q

how does primary ciliary dyskinesia present clinically?

A
  • recurrent infections of the upper and lower and respiratory tract
  • recurrent productive cough
  • purulent nasal discharge
  • chronic ear infections
  • dextrocardia and situs inversus
83
Q

how is primary ciliary dyskinesia diagnosed?

A

lab- examination of structure of cilia

84
Q

how is primary ciliary dyskinesia managed?

A
  • physiotherapy to clear secretions

- proactive treatment of infections with Abx and ENT follow up

85
Q

what is cystic fibrosis?

A

alteration of the viscosity and tenacity of mucous produced at epithelial surfaces

86
Q

what is the classical form of cystic fibrosis?

A

bronchiopulmonary infection and pancreatic insufficiency with a high sweat sodium and chloride concentration

87
Q

where are the mutations that cause cystic fibrosis located?

A

cystic fibrosis transmembrane conductance regulator gene (CFTR) on chromosome 7

88
Q

how are the features of cystic fibrosis caused?

A
  • mutation in CFTR gene
  • decreased excretion of chloride into the airway lumen and an increased reabsorption of sodium into epithelial cells
  • with less excretion of salt there is less excretion of water and increased viscosity/ tenacity of airway secretion
89
Q

aetiology of cystic fibrosis

A

autosomal recessive inherited disorder

specific deletion at position 508 results in defect in transmembrane regulator protein

90
Q

how does cystic fibrosis affect the:

Respiratory system?

A
  • structurally normal
  • frequent resp infections
  • sinusitis
  • nasal polyps
  • breathlessness
  • airflow limitation + bronchiectasis
  • spontaneous pneumothorax
  • late onset problems- haemoptysis, resp failure and cor pulmonale
91
Q

how does cystic fibrosis affect the:

  • GI system
A
  • symptomatic steatorrhoea (due to pancreatic dysfunction)
  • meconium ileus
  • cholesterol gallstones
  • peptic ulcers
  • GI malignancy risk
92
Q

how does cystic fibrosis affect:

  • Nutritional balance
A
  • malnutrition; malabsorption and maldigestion
  • risk of pulmonary sepsis
  • failure to thrive + slow growth
93
Q

other than affecting the respiratory and GI systems, what other effects does cystic fibrosis have on the body?

A
  • puberty and skeletal maturity delayed
  • males infertile
  • females- can conceive but develop secondary amenorrhoea
  • arthropathy and DM- rare but can happen
94
Q

how is cystic fibrosis screened for?

A

all newborns screened- for abnormally raised immunoreactive trypsinogen and 29 CTFR mutations on Guthrie Card

95
Q

how is cystic fibrosis diagnosed?

A
  • sweat test- sodium concentration >60mmol/L
  • CXR- hyperinflation
  • random glucose
  • malabsorption screen
  • spirometry
96
Q

what are some pitfalls with the use of the sweat test to diagnose cystic fibrosis?

A
  • false positives- common for newborns to have a high sodium
  • sodium concentration naturally falls 2nd day after birth
97
Q

how is cystic fibrosis managed?

A
  • education- nutrition etc
  • general care- stop smoking, keep up-to-date with vaccinations etc
  • oxygen therapy if necessary
  • physiotherapy
98
Q

what drug therapy is used in cystic fibrosis?

A
  • B2 agonists
  • ICS

symptomatic relief only

99
Q

how is airway clearance assisted in CF?

A
  • inhalation of recombinant human deoxyribonuclease (rhDNAse)
  • hypertonic saline by inhalation
  • amiloride
  • acetylcysteine
100
Q

how are pancreatic insufficiency and GI problems managed in CF?

A

pancreatic insufficiency:

  • PERT (pancreatic enzyme replacement therapy)
  • older children- Creon

GI:
- omeprazole

101
Q

what are some complications of CF?

A
  • haemoptysis
  • pneumonia
  • pneumothorax
  • pulmonary osteoarthropathy
  • diabetes
  • cirrhosis
  • cholesterol gallstones
  • fibrosing colonopathy
  • male infertility
102
Q

what type of squint may require neuro-imaging?

A

paralytic squint- may be due a SOL

103
Q

what can cause a squint?

A
  • idiopathic
  • refractive error
  • visual loss
  • opthlamoplegia
  • SOL
104
Q

what are the 2 types of squint?

A
  • non-paralytic (concomitant)

- paralytic (non-concomitant)

105
Q

what is a non-paralytic (concomitant) squint?

A

common and usually due to a refractive error in one or both eyes

106
Q

what is a paralytic (non-concomitant) squint?

A

rare and usually due to cranial (motor) nerve palsy. Can also be caused by a SOL

107
Q

how is a squint managed?

A
  • correct refractive error with glasses
  • eye patch- wear over good eye to train weaker eye
  • eye muscle exercises
108
Q

what is periorbital cellulitis?

A

infection of the eyelid.

109
Q

what are the complications of periorbital cellulitis?

A
  • intracranial infection (meningitis etc)
  • cavernous sinus thrombosis
  • vision loss
110
Q

how does periorbital cellulitis present clinically?

A

unilateral eyelid swelling and erythema, along with pain and tenderness

111
Q

what are some red flags in periorbital cellulitis?

A
  • painful/ restricting eye movements
  • visual impairment
  • severe headache
112
Q

how is periorbital cellulitis treated?

A

flucloxacillin/ ceftriaxone

NP- Phase 3a Medicine (22 decks)

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