Clinical Infections: Respiratory Flashcards

1
Q

What does the URT consist of?

A

Nose, sinuses, mouth, pharynx and larynx

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2
Q

What does the LRT consist of?

A

Trachea, bronchi, bronchioles and lungs

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3
Q

What are the key points in taking a patient history for an acute sore throat?

A
  • Rapidity of onset of sore throat
  • Difficulty breathing/speaking
  • Ability to eat/drink/swallow
  • Associated neck pain/swellings
  • Symptoms of systemic infection e.g. fever, chills, rigors, general malaise
  • Travel history
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4
Q

What 4 things should immediately be considered when a patient presents with an acute sore throat?

A
  1. Pharyngitis
  2. Acute tonsillar pharyngitis
  3. Infectious mononucleosis (EBV)
  4. Epiglottitis
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5
Q

What is pharyngitis?

A

inflammation of the back of the throat (pharynx), resulting sore throat and fever

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6
Q

How does acute tonsillar pharyngitis?

A

Symmetrically inflamed tonsils and pharynx (+/- fever +/- headache)

Severe infection: patient has marked systemic symptoms of infection and/or unable to swallow.

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7
Q

How does infectious mono present?

A

symmetrically inflamed tonsils / soft palate inflammation and posterior cervical lymphadenopathy

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8
Q

How does epiglottitis present?

A

sudden onset of severe sore throat and fever. Inflammation of the epiglottis and surrounding tissue leading to obstruction of the airway.

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9
Q

How are pharyngitis and tonsillar pharyngitis caused?

A

Commonly caused by viruses, however in a third of people, no cause can be found.

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10
Q

Are viral or bacterial infections the more common cause of sore throats?

A

Viral

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11
Q

What are the viral causes of pharyngitis and tonsillar pharyngitis (i.e. sore throat)?

A
o	Rhinovirus
o	Coronavirus
o	Parainfluenza
o	Influenza (A & B)
o	Adenovirus etc
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12
Q

What is the most common bacterial cause of sore throat?

A

Group A beta-haemolytic Streptococcus (GABHS) aka Streptococcus pyogenes

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13
Q

What are 3 rarer causes of sore throat?

A

o Neisseria gonorrhoeae (Gonococcal pharyngitis)
o HIV-1 (can be the first presentation of HIV infection)
o Corynebacterium diphtheriae (Diptheria)

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14
Q

What criteria can help you distinguish if a sore throat is due to a bacterial infection?

A

Centor criteria

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15
Q

What are the 4 components of Centor criteria?

A

o Tonsillar exudate
o Tender anterior cervical lymphadenopathy
o Fever over 38°C
o Absence of cough

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16
Q

How can the Centor criteria give an indication of the likelihood of a sore throat being due to bacterial infection?

A
  • If 3 or 4 of Centor criteria are met, the positive predictive value is 40% to 60%
  • The absence of 3 or 4 of the Centor criteria has a fairly high negative predictive value of 80% (i.e. non-bacterial infection)
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17
Q

In a patient presenting with a sore throat (but a non-severe infection), when is the only time it would be investigated?

A

If infectious mononucleosis is suspected

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18
Q

In suspected infectious mononucleosis, what investigation is done to confirm?

A

blood sample for Monospot or EBV serology

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19
Q

In severe infections of sore throats, what investigations should be done?

A

o Throat swab for culture

o Blood cultures, (blood tests: full blood count, urea and electrolytes and liver function tests)

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20
Q

Management for majority of sore throats?

A

Oral analgesics (paracetamol, ibuprofen)

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21
Q

When would you consider antibiotics for a sore throat?

A

o Consider antibiotics in non-severe acute tonsillar pharyngitis if symptoms present for 1 week and getting worse
o Give antibiotics in severe acute tonsillar pharyngitis, quinsy or epiglottitis

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22
Q

What 3 diseases presenting with a sore throat require antibiotics?

A
  1. severe acute tonsillar pharyngitis
  2. quinsy
  3. epiglottitis
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23
Q

Viral pathogen behind infectious mono?

A

EBV (80%) or CMV (20%)

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24
Q

Who does infectious mono tend to affect?

A

Teenagers, often asymptomatic

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25
Q

Classic triad of symptoms of infectious mono?

A

1) fever
2) tonsillar pharyngitis
3) cervical lymphadenopathy

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26
Q

Which antibiotic should be avoided in infectious mono?

A

ampicillin

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27
Q

Why should ampicillin be avoided in infectious mono?

A

This can result in a maculopapular rash which can then be confused with allergic reaction; patient would then have a FALSE penicillin allergy label

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28
Q

What is epiglottitis?

A

inflammation of structures above the glottis

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29
Q

What USED to be the commonest cause of epiglottitis?

A

Haemophilus influenzae type b (Hib) was the commonest cause in >90% of paediatric cases but the Hib vaccine has significantly reduced the rate of Hib epiglottis (still do see Hib cases in adults & rarely in children)

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30
Q

What are other causative organisms of epiglottitis?

A

Streptococcus pneumoniae and Group A Streptococcus

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31
Q

What investigations should be done in suspected epiglottitis?

A

Blood cultures and epiglottic swabs

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32
Q

Why should care be taken when taking epiglottic swabs?

A

Attempting to examine the throat may result in total airway obstruction (only do when anaesthetic support present)

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33
Q

How can epiglottitis lead to death within 24 hours? What is the important factor in management of epiglottitis?

A

Acute epiglottitis and associated upper airway obstruction have significant morbidity and mortality and may cause respiratory arrest and death within 24 hours.

Securing the airway & oxygenation is a priority!!

Then;
o IV antibiotics (usually 3rd generation cephalosporin)
o Analgesia

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34
Q

If a case of Hib epiglottitis is confirmed, what should be done?

A

Inform public health

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35
Q

What is the only skin-lined cul-de-sac in the body?

A

Ear canal

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36
Q

What is otitis externa (OE)?

A

Inflammation of the external ear canal

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37
Q

What 3 features does OE present with?

A
  1. Otalgia (ear pain)
  2. Pruritus (unpleasant itch)
  3. Non-mucoid ear discharge
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38
Q

What separates acute from chronic OE?

A

Symptoms < 3/52 = acute OE

Symptoms >3/52 = chronic OE

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39
Q

What are some risk factors for OE?

A

o Swimming (or other water exposure)
o Trauma (e.g. ear scratching, cotton swabs)
o Occlusive ear devices (e.g. hearing aids, earphones)
o Allergic contact dermatitis (e.g. due to shampoos, cosmetics)
o Dermatologic conditions (e.g. psoriasis).

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40
Q

Is acute OE typically unilateral or bilateral?

A

Unilateral

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41
Q

What are the different types of acute OE?

A
  • Mild/moderate/severe

- Necrotising malignant OE

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42
Q

What makes up 90% of causes of acute OE?

A

Bacterial causes!!

Pseudomonas aeruginosa and Staphylococcus aureus are most common

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43
Q

What makes up only 2% of causes of acute OE?

A

Fungal causes

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44
Q

Investigations for acute OE?

A

History and otoscopic examination

Ear swab or pus sample for culture

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45
Q

What additional investigations are required necrotising otitis externa?

A
  • CT temporal bone (and bone biopsy)

- Blood cultures (if systemically unwell)

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46
Q

Non-antimicrobial management for acute OE?

A

o Remove/modify precipitating factors (e.g. cosmetics, shampoo)
o Remove pus and debris from ear canal
o Analgesia

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47
Q

Antimicrobial management for acute OE?

A

o Topical agents for mild-moderate

o Topical plus systemic antibiotic such as flucloxacillin for severe AOE

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48
Q

What is malignant necrotising OE?

A

Occurs when external otitis spreads to the skull base (soft tissue, cartilage, and bone of the temporal region and skull).

Can be life threatening!

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49
Q

Who does malignant necrotising OE typically affect?

A

Most commonly develops in elderly diabetic or other immunocompromised patients

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50
Q

Symptoms of malignant necrotising OE?

A

Severe pain, otorrhoea, granulation tissue in the canal floor, and cranial nerve palsies may be present.

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51
Q

Treatment for malignant necrotising OE?

A

o These patients should be promptly referred ENT

o Treat for a minimum of 6 weeks e.g. with iv ceftazidime then po ciprofloxacin

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52
Q

Is chronic OE typically unilateral or bilateral?

A

Bilateral

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53
Q

How does chronic OE typically present?

A
  • Pruritus
  • Mild discomfort
  • Erythematous external canal that is usually devoid of wax
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54
Q

Over time, the external ear canal may become narrowed in chronic OE? Why?

A

White keratin debris may fill the ear canal and over time the canal wall skin may become thickened narrowing the external ear canal

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55
Q

What are common causes of chronic OE?

A

o Allergic contact dermatitis (e.g. from chemicals in cosmetics or shampoos).
o Generalised skin conditions such as atopic dermatitis or psoriasis can also predispose to chronic OE

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56
Q

Treatment of chronic OE?

A

Treat underlying cause

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57
Q

What is otitis media (OM)?

A

Middle ear inflammation. Fluid present in middle ear.

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58
Q

Who is OM common in?

A

Children

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59
Q

What defines ‘uncomplicated’ acute OM?

A

Mild pain <72hours duration, an absence of severe systemic symptoms, with a temperature of less than 39°C and no ear discharge.

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60
Q

What defines ‘complicated’ acute OM?

A

severe pain, perforated eardrum and/or purulent discharge, bilateral infection, mastoiditis

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61
Q

What are the 3 most common pathogens behind OM?

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Moraxella catarrhalis
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62
Q

Investigations for OM?

A

Swab any pus

63
Q

Treatment for OM?

A

o If not unwell; watch and treat symptomatically (analgesia, decongestant etc.) and review earl
o If unwell; amoxicillin

64
Q

Which antibiotic is recommended in unwell patients with OM?

A

Amoxicillin

65
Q

What is mastoiditis a complication of?

A

The most common complication of acute OM

66
Q

What is mastoiditis?

A

Infection of the mastoid bone and air cells

67
Q

What significantly reduces the incidence of mastoiditis?

A

Incidence significantly reduced with the use of antibiotics for OM

68
Q

How common is mastoiditis?

A

Very rare;
• Mastoiditis and other severe complications of AOM are very rare in adults
• Occurs in <1 in 1000 children with untreated AOM

69
Q

Features of mastoiditis?

A

o Fever
o Posterior ear pain and/or local erythema over the mastoid bone
o Oedema of the pinna
o A posteriorly and downward displaced auricle

70
Q

What investigation is always required in mastoiditis?

A

CT scan

71
Q

Treatment for mastoiditis?

A

o Analgesia
o IV antibiotics +/-
o Mastoidectomy

72
Q

Pinna cellulitis vs pericondritis?

A

Pinna cellulitis can occur as a complication of acute otitis externa, a complication of eczema or psoriasis, or from an insect bite.

Pinna perichondritis is usually a result of penetrating trauma, including ear piercing.

73
Q

Define cellulitis

A

inflammation of subcutaneous connective tissue.

74
Q

Define perichondritis

A

an infection of the skin and tissue surrounding the cartilage of the outer ear

75
Q

What is the ‘pinna’?

A

Outer ear (the only visible part of the ear)

76
Q

Usual organisms behind Pinna Cellulitis/Perichondritis?

A

Pseudomonas aeruginosa and/or Staphylococcus aureus

77
Q

Empirical treatment for Pinna Cellulitis/Perichondritis?

A

ciprofloxacin + flucloxacillin (or vancomycin if penicillin allergy)

78
Q

What is pneumonia?

A

Infection affecting the most distal airways and alveoli. Involves the formation of inflammatory exudate.

79
Q

What are the 2 anatomical patterns of pneumonia?

A
  1. Bronchopneumonia

2. Lobar pneumonia

80
Q

What is the pattern of bronchopneumonia?

A

Characteristic patchy distribution centred on inflamed bronchioles & bronchi then subsequent spread to surrounding alveoli

81
Q

What is the pattern of lobar pneumonia?

A

Affects a large part, or the entirety of a lobe

82
Q

Which organism is 90% of all lobar pneumonias due to?

A

S. pneumoniae

83
Q

What are the 4 main groups of pneumonia?

A

1) Community acquired pneumonia (CAP)
2) Hospital acquired pneumonia (HAP)
3) Ventilator acquired pneumonia (VAP)
4) Aspiration pneumonia

84
Q

What defines ‘hospital acquired pneumonia (HAP)’?

A

Pneumonia developing >48hrs after hospital admission

85
Q

Hospital acquired pneumonia (HAP) has additional causative organisms to CAP, especially if >5days after admission.

What are these?

A

Enterobacteriaceae (e.g. E. coli)

S. aureus (including MRSA)

86
Q

What is ventilator acquired pneumonia (VAP)?

A
  • Subgroup of HAP
  • Pneumonia developing >48hrs after ET intubation & ventilation
  • Pseudomonas spp. may be implicated
87
Q

What is aspiration pneumonia?

A

Pneumonia resulting from the abnormal entry of fluids e.g. food, drinks, stomach contents, etc. into the lower respiratory tract

(Patient usually has impaired swallow mechanism)

Anaerobes may be implicated

88
Q

What are the 3 major routes of acquisition of organisms in CAP?

A
  1. Person-to-person or from a person’s existing commensals (S.pneumoniae, H.influenzae)
  2. From the environment (L. pneumophilia)
  3. From animals (C.psittaci)
89
Q

The bacterial causes of CAP can be split into 2 main groups. What are they?

A

Atypical and typical

90
Q

What is ‘atypical’ pneumonia?

A

Caused by atypical organisms; clinical presentation and treatment are slightly different

91
Q

What are 5 ‘typical’ bacteria which cause pneumonia?

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Klebsiella pneumoniae
92
Q

What are 5 ‘atypical’ bacteria which cause pneumonia?

A
  • Mycoplasma pneumoniae
  • Legionella pneumophilia
  • Chlamydophila pneumoniae
  • Chlamydophila psittaci
  • Coxiella burnetii
93
Q

Symptoms of bacterial CAP?

A
	Usually rapid onset
	Fever / chills
	Productive cough
	Mucopurulent sputum
	Pleuritic chest pain
	General malaise: fatigue, anorexia
94
Q

Signs of bacterial CAP?

A

Tachypnoea, tachycardia, hypotension

Examination findings consistent with consolidation:
• Dull to percuss
• Reduced air entry, bronchial breathing

95
Q

What is atypical pneumonia caused by Chlamydophila psittaci associated with?

A

Exposure to birds (history!!)

96
Q

What are outbreaks of Legionella pneumophilia typically associated with?

A

Colonise water piping systems:

  • Showers
  • Air conditioning units
  • Humidifiers
97
Q

What score is used to assess the severity of CAP?

A

CURB-65 score

98
Q

Explain the CURB-65 score

A

C: Confusion
U: Urea >7 mmol/l
R: Respiratory rate >30
B: Blood pressure

Age >65

99
Q

What should the CURB-65 score be used in conjuction with when assessing the severity of a pneumonia case?

A

Clinical judgement

100
Q

Why is a chest x-ray not a good measure of an immediate response to pneumonia treatment?

A

can take 6 weeks+ for radiological changes to resolve

101
Q

What investigations are recommended for all moderate-severe CAP based on CURB65 score >2?

A
  • Sputum culture
  • Blood culture
  • Pneumococcal urinary antigen
  • Legionella urinary antigen
  • PCR or serology
102
Q

What pathogens are being looked for in PCR or serology in CAP?

A
  • Viral pathogens e.g. influenza or COVID-19
  • Mycoplasma pneumoniae
  • Chlamydophila sp.
103
Q

What 2 other tests should be routinely done in CAP?

A

HIV test

COVID-19 test

104
Q

Why should an HIV test be performed in CAP?

A

CAP is an HIV indicator condition; a condition in which the prevalence of undiagnosed HIV is more than 0.1%

105
Q

Management for all types of pneumonia?

A

ABC!!

o Airway: Ensure an open, patent and maintained airway

o Breathing:

  • Assess respiratory rate and saturations
  • Provide supplemental oxygen to reach prescribed target

o Circulation:

  • Assess blood pressure and heart rate
  • Gain IV access and give IV fluids if haemodynamically unstable
  • Urinary catheter to monitor urine output

THEN –> prompt empirical antibiotic therapy

106
Q

What are 3 potential complications of pneumonia?

A
  1. Pleural effusion
  2. Empyema
  3. Lung abscess
107
Q

What viruses typically cause pneumonia?

A
Adults:
	Influenza A & B 
	Adenovirus 
	VSV
	COVID-19

Children:
 RSV
 Parainfluenza

108
Q

What viruses typically cause pneumonia in IMMUNOCOMPROMISED hosts?

A

Normal ones PLUS:

	Measles
	Herpes simplex (HSV)
	Cytomegalovirus (CMV)
	Varicella zoster virus (VZV)
	HHV-6
109
Q

Typical presentation of influenza infection?

A

o Fever, headache, myalgia, dry cough, sore throat
o Convalescence takes 2-3 weeks

Usually uncomplicated disease.

110
Q

Who does primary viral pneumonia occur more commonly in?

A

In patients with pre-existing cardiac & lung disorders

111
Q

Symptoms of primary viral pneumonia?

A

Cough, breathlessness, cyanosis

112
Q

What can develop post primary viral pneumonia?

A

Secondary bacterial pneumonia then may develop after initial period of improvement

113
Q

Which bacteria are largely responsible for secondary bacterial pneumonia?

A

S.pneumoniae, H.influenzae, S.aureus

114
Q

What is VSV pneumonia a complication of?

A

VSV (chickenpox) infection

115
Q

Who is a significant morbidity and mortality rate of VSV pneumonia seen in?

A

Adults, immunocompromised, chronic lung disease patients, smokers, pregnant women

116
Q

Presentation of VSV pneumonia?

A

Insidious onset 1-6 days after the rash has appeared with symptoms of progressive tachypnoea, dyspnoea, and dry cough.

117
Q

Treatment of VSV pneumonia?

A

Supportive and prompt administration of IV acyclovir

118
Q

Which organism is responsible for most ‘common colds’?

A

Rhinovirus

119
Q

Can rhinovirus lead to an LRTI?

A

Yes

120
Q

Who can CMV pneumonia cause severe illness in?

A

o Is rarely described in immunocompetent hosts

o Can cause severe illness in transplant recipients & HIV patients (uncommon)

121
Q

What should be considered in transplant recipients with CMV pneumonia?

A

consider immunosuppression reduction

122
Q

What is bronchiectasis?

A

Acquired disorder of the major bronchi and bronchioles that is characterised by permanent abnormal dilatation and destruction of bronchial walls

123
Q

Symptoms of LRTI with bronchiectasis?

A

o Chronic cough
o Mucopurulent sputum production
o Recurrent infections

124
Q

Which organisms are responsible for recurrent infections seen in bronchiectasis?

A

S.aureus, H.influenzea, Pseudomonas aeruginosa, viruses

125
Q

What investigations should be done during exacerbations of bronchiectasis?

A

SpO2, CXR, FBC, U&Es, LFTs, CRP, review previous sputum culture

126
Q

When would antibiotics be required during exacerbations of bronchiectasis?

A

Antibiotics are recommended for exacerbations with acute deterioration with worsening symptoms

127
Q

Non-antimicrobial management for LRTI with bronchiectasis?

A
  • Effective clearance of respiratory secretions e.g. physiotherapy, postural drainage
  • Nutritional support
  • Identification and treatment of underlying cause
  • Annual influenza vaccination
128
Q

What is CF?

A

An inherited disease caused by a genetic mutation on chromosome 7 resulting in abnormal production and function of the cystic fibrosis transmembrane conductance regulator (CFTR).

The defective CFTR chloride channel function results in viscous secretions.

129
Q

Which organisms are responsible for infection in CF;

a) in childhood
b) in childhood/early adolescence

A

a) Staphylococcus aureus

b) Pseudomonas aeruginosa

130
Q

Which RESISTANT and TRANSMISSIBLE organism can cause LRTI in CF patients?

A

Burkholderia cepacia complex

131
Q

General measures for treating LRTIs in CF patients?

A

o Prolonged antibiotic courses (3-4 weeks not uncommon)
o Postural drainage, deep breathing, coughing, exercise, aerosolised DNAase etc+ Influenza and Pneumococcal vaccinations. Lung transplant.

132
Q

Which 3 vaccinations are available which can help prevent LRTIs?

A

1) Pneumococcal vaccination for certain groups (S. pneumoniae)
2) Influenza vaccination for vulnerable groups (annually)
3) COVID-19

133
Q

What is aspergillosis?

A

An infection caused by Aspergillus, a common mould (a type of fungus) that lives indoors and outdoors

134
Q

Who is susceptible to apergilllosis?

A

o Most people breathe in Aspergillus spores every day without getting sick
o Immunocompromised patients & those with lung disease are at a higher risk of developing health problems due to Aspergillus

135
Q

Typical health problems caused by Aspergillus?

A

Include allergic reactions, lung infections, and infections in other organs

136
Q

Who does Allergic Bronchopulmonary Aspergillosis (ABPA) occur in?

A

Occurs in people with a background of atopy, asthma & cystic fibrosis

137
Q

How does ABPA present?

A

with worsening asthma & lung function

138
Q

Diagnosis of ABPA?

A

o A high total IgE, specific IgE to Aspergillus and positive serum IgG Aspergillus
o CT imaging of the thorax may demonstrate central bronchiectasis

139
Q

Treatment of ABPA?

A

corticosteroids and antifungal therapy

140
Q

What is an aspergilloma (pulmonary)?

A

Mobile mass (of Aspergillus) within a pre-existing lung cavity

141
Q

Cause of aspergilloma (pulmonary)?

A

Old cavities left by previous TB or sarcoidosis become colonised with Aspergillus spp.

142
Q

Symptoms of aspergilloma (pulmonary)?

A

Cough, haemoptysis, weight loss, wheeze & clubbing. Some are asymptomatic.

143
Q

Diagnosis of aspergilloma (pulmonary)?

A

o Can be demonstrated on either chest X-ray or CT thorax
o The diagnosis can be confirmed by a positive test for Aspergillus IgG antibody +/- Aspergillus antigen
o Sputum culture may be positive for Aspergillus spp.

144
Q

Potential complication of aspergilloma (pulmonary)?

A

: Massive haemoptysis

145
Q

What is Pneumocystis pneumonia (PCP)?

A

A serious infection caused by the fungus Pneumocystis jiroveci.

146
Q

Transmission of Pneumocystis pneumonia (PCP)?

A

Airborne

147
Q

What is a classic finding of Pneumocystis pneumonia (PCP)?

A

o Reduced exercise tolerance (induced hypoxia)

o Non-productive cough

148
Q

What is Nocardia Asteroides?

A

Nocardia is a genus of bacteria found in the environment.

Pulmonary nocardiasis is acquired through inhalation of the organism

149
Q

Who is pulmonary nocardiasis more common in?

A

More common in the immunosuppressed and those with pre-existing lung disease (esp. alveolar proteinosis) – but still rare!

150
Q

Transmission of mycobacterium tuberculosis?

A

Infection is acquired by inhalation of infected respiratory droplets –> the bacilli lodge in alveoli & multiply

151
Q

What is a Ghon focus?

A

A Ghon focus is a primary lesion usually sub-pleural, often in the mid to lower zones, caused by Mycobacterium tuberculosis developed in the lung of a non-immune host.

152
Q

The risk of disease progression of tuberculosis is highest in which groups?

A

At the extremes of age and in the immunocompromised (inc. HIV)

153
Q

Reactivation of TB can occur later in life. Who is this most common in?

A

Immunocompromised

154
Q

Presentation of TB?

A

Pulmonary tuberculosis is the most common presentation:
 Chronic productive cough, haemoptysis
 Weight loss, fever, night sweats

Can disseminate (miliary TB) or affect almost any other organ