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respiratory > Lecture 14- Lower respiratory tract infections and pneumonia > Flashcards

Lecture 14- Lower respiratory tract infections and pneumonia Flashcards

1
Q

Lower respiratory tract infections (LRTI) are a leading cause of death in the

A

elderly

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2
Q

Course of typical infection

A
  1. Alveolar macrophages fails to stop pathogen
  2. Cytokines to recruit more macrophages
  3. Inflammation= increased permeability
  4. More WBC/proteins
    1. Neutrophils
    2. Lymphocytes
    3. Antibodies to aid macrophage
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3
Q

course of typical infection outside the lungs

A
  • Inflammatory mediators (cytokines) into systemic circulation
  • Physiological- activates bone marrow/more CO and raised body temp
  • Dysregulation/ pathological inflammation– signs of tissue injury/ organ injury (multi-organ failure- low BP due to vasodilation of blood vessels in response to inflammation e.g. liver and kidney failure due to low BP
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4
Q

Inflammation=

A

increases blood supply and increases WBC to the site of infection via the release of cytokines

  • Damages lung tissue
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5
Q

common microbiota of the resp tract

A
  • Viridians streptococci
  • Neisseria sp
  • Anaerobes candida sp
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6
Q

Less common microbiota of respiratory tract

A
  • Streptococcus’s pneumoniae
  • Streptococcus pyrogens
  • Haemophilus influenzae

Others

  • Pseudomonas
  • E.coli
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7
Q

Upper resp tract=

A

nasal cavity to the larynx

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8
Q

lower resp tract

A

trachea –> lungs

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9
Q

lungs are not

A

sterile

  • normal alveolar microbiota
  • aspiration
  • blood stream spread
  • direct spread
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10
Q

Defences of resp tract

A
  • Muco-ciliary clearance mechanisms nasal hairs, ciliated columnar epithelium of the resp tract
  • Cough and sneezing
  • Respiratory mucosal immune system
    • Lymphoid follicles of the pharynx and tonsils, alveolar macrophages, secretary IgA and IgG
  • Alveolar microbiota
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11
Q

what causes dyrefulation of inflammation

A
  • the pathogens virulence factors
  • host factors
  • drugs
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12
Q

pathogen virulence factors

A
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13
Q

What causes dysregulation of inflammation: host factors

A
  • Over 75
  • Lifestyle
    • Smoking (abnormal ciliary function)
    • Alcohol/drugs
  • Chronic lung disease e.g. bronchiectasis, CF
  • Aspiration
    • Change in level of consciousness
    • Dysphagia
    • Wearing dentures whilese sleeping
  • Immunocompromised
    • DM
    • HIV
  • Metabolic
    • Malnutrition
    • Hypoxaemia
    • Acidosis
    • Uraemia
  • Co-infection with viruses (abnormal ciliary function)
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14
Q

What causes dysregulation of inflammation: drugs

A
  • Antacids
  • Antipsychotics
  • ACE inhibitors
  • Glucocorticoids
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15
Q
  • Antacids
A
  • PPI- increases risk for pneumonia
  • H2 antagonist- myelosuppression (rare, long term)
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16
Q
  • ACE inhibitors-
A

associated reduced risk but only seen in observational studies with reporting bias

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17
Q
  • Glucocorticoids-
A

use of inhaled corticosterois

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18
Q

types of URTI

A
  • Rhinitis
  • Pharyngitis
  • Epiglottis
  • Laryngitis
  • Tracheitis
  • Sinusitis
  • Otitis media
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19
Q

URTI are most commonly caused by

A

viruses

  • Rhinovirus
  • Coronavirus
  • Influenza/parainfluenza
  • Respiratory syncytial virus (RSV)
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20
Q

Bacterial superinfection (after viral infection)

*

A
  • Common with
    • Sinusitis and otitis media–> can lead to mastoiditis, meningitis, brain abscess
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21
Q

Lower respiratory tract infections

A
  • bronchitis
  • pneumonia
  • bronchiolitis
  • empyema
  • bronchiectasis
  • lung abscess
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22
Q
  • Bronchitis =
A

infection of the bronchi

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23
Q
  • Pneumonia=
A

infection of the lung parenchyma

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24
Q

LRTI definittions (inflammation of the lungalveoli)

A
  • community acquired pneumonia (CAP)
  • hospital acquired pneumonia (HAP)
  • venitalted acquired pneumonia (VAP)
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25
Q

community acquired pneumonia (CAP)

A

outside healthcare setting

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26
Q

HAP

A

48 hours post admission

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27
Q

VAP (ventilator)

A

48h post intubation

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28
Q

acute bronchitis

A
  • Inflammation (infection *chronic bronchitis is just inflammation not infection*) of medium sized airways
  • Mainly in smokers
29
Q

symptoms of acute bronchitis

A
  • Symptoms
    • Cough
    • Fever
    • Increase SoB
    • Increased sputum
30
Q

investigations for acute nronchitis

A
  • Investigations- CXR normal (don’t expect changes – in pneumonia we do)
31
Q

organisms that cause acute bronchitis

A
  • Organisms
    • S.pneumoniae
    • H.influenzae
    • M. Cararrhalis
32
Q

treatment of acute bronchitis

A
  • Bronchodilation (symptomatic)
  • Remove secretions with physiotherapy
  • If bacterial antibiotics
33
Q

Chronic bronchitis

A

NOT primarily infection

  • Exacerbations have been associated with many organisms, but the role of infections remain controversial
34
Q

what is penumonia

A
  • Inflammation of the lung alveoli
  • Alveoli become full of fluid and neutrophils and macrophages (fluid in lungs-dull sound and crackles on stethoscope)
35
Q

pathology is the same for all types of pneumonia

A
  1. Acute inflammatory response
  2. Exudation of fibrin-rich fluid
  3. Neutrophil infiltration
  4. Macrophage infiltration
36
Q

Lobar pneumonia–>

A

pneumonia involving 1 lobe

37
Q

Bronchopneumonia–>

A

patchy

38
Q

Symptoms of pneumonia

A
  • Shortness of breath
  • Coughing
  • Difficulty breathing
39
Q

Signs of pneumonia

A

ABG- hypoxic

40
Q

Community acquired pneumonia causative organisms

*

A
  • No microbiological ID made in most cases
  • True prevalence difficult to establish due to use of indirect methods /mixed infections
  • Typical and atypical organisms
41
Q

typical causative (85%) organisms for CAP

A
  • Strep pneumonia is commonoist
  • haemophilis influenzae if COPD
42
Q

atypical organisms (15%)

A

mycoplasma commonest

legionella- contaminated water sources

43
Q

Diagnosing CAP

A

Clinical symptoms +imaging finding

  • Clinical
    • Cough (with/without sputum)
    • Dyspnoea
    • Pleurisy
    • Fever
    • Tachycardia
    • Organ dysfunction (e.g. hypotension/mental status change)
    • Crackles
    • Bronchial breathing
  • Imaging
    • Consolidation/infiltrate/cavitation’s
  • When to admit? Use CURB-65
44
Q

Assessing severity of CAP

*

A
  • CURB-65 score
    • Confusion
    • Urea >7mmol/l
    • Respiratory rate>30
    • Blood pressure <90 systolic <60 diastolic
    • Over 65
45
Q

CURB- 65 score 2

A

admit

46
Q
  • Score 2-5=
A

manage as severe

47
Q

CAP investigations

A

Investigations

  • FBC
  • U &E
  • CRP
  • ABG
  • Chest Xray
  • Microbiological
    • Sputum
    • Blood culture
    • Bronchoalveolar lavage fluid (BAL)
    • Nose and throat swabs or NPAs (viruses)
    • Urine (antigen test for legionella, pneumococcus)
    • Serum (antibody test) acute and convalescent sera (usually collected at presentation and 10-14 days
48
Q

management of CAP

A

Management

  • Mild CAP- treat empirically
  • Moderate CAP
    • Blood culture/sputum culture
    • Urinary streptococcal antigen
    • Legionella +PCR
    • Viral screen
  • Serve CAP
    • Same as moderate management + bronchoscopic specimens
49
Q

Differential diagnoses for CAP

*

A
  • Heart failure and pulmonary oedema
  • Pulmonary embolism
  • Atelectasis
  • Aspiration/ chemical pneumonitis
  • Drug reactions
  • Lung cancer
  • Vasculitis acute exacerbation of bronchiectasis
  • Interstitial lung disease
50
Q

Treatment of CAP

*

A
  • Abx treatment
  • Empirical regimes can differ in hospitals/ allergy status/ comorbidities
    *
51
Q

how many days of Abx for mild CAP

A

5-7 days

52
Q

how many days of Abx for severe CAP

A

7-10 days

53
Q

which type of Abx for mild-moderate CAP

A
  • amoxicillin
  • or doxycyclin or erythromycin
54
Q

which type of Abx for moderate-severe CAP

A

needing hospital admission

  • co-amoxiclav and clarithromycin
55
Q

give amoxicillin because

A

commonest cause is S.pneumoniae

56
Q

Complications of CAP

*

A
  • Initial infection progression
    • Empyema- infection of pleural cavity
    • Lung abscess
    • Bacteraemia
  • Non- resolving CAP
    • Delayed clinical response
    • Closed space infections
    • Bronchial obstruction e.g. a tumour
    • Subacute chronic CAP (TB/Fungal)
    • Incorrect initial diagnosis
57
Q

causative organisms of hospital acquired pneumonia

A
  • S.aureus
  • MRSA
  • enterobacteriaciae (E.coli and klebsiella spp_
  • Pseudomonas spp
  • Fungi (candida)
58
Q

Management of HAP

A
  • Cover S.aureus and gram negative enteric bacilli (e.g. klebsiella) + typical/atypical pathogens
    • Co-amoxiclav
  • Pseudomonas risk
    • Antipseudomonal beta lactam or anti-pseudomonal fluoroquinolone (ciprofloxacin)
  • MRSA risk- vancomycin/linezolid
59
Q

first line treatment for HAP

A

co-amoxiclav

60
Q

second line treatment of HAP

A

piperacillin or meropenem

61
Q

Aspiration pneumonia

*

A

Aspiration of exogenous material or endogenous secretions into the resp tract

62
Q

Aspiration pneumonia most common in

A
  • Common in pts with neurological dysphagia
    • Strokes
    • Epilepsy
    • Alcoholics
    • Drowning
    • At risk groups
      • Nursing home residents and drug overdose
63
Q

what sort of infections can aspiration pneumonias be

A
  • Mixed infection e.g. viridians streptococci and anaerobes
64
Q
  • Moderate to severe aspiration pneumonia treated with
A

Co-amoxiclav (broad spectrum)

65
Q

Immunosuppression and LRTI

A
  • HIV
    • Pneumocystis jirovecci
    • TB
    • Atypical mycobacteria
  • Neutropenia
    • Fungi e.g. aspergillus spp
  • Bone marrow transplant: cytomegaly virus
  • Splenectomy: encapsulated organism e.g. Pneumonia, H. influenzae, malaria
66
Q

prevention of pneumonia

A
  • immunisation
  • chemoprophylaxis
  • smoking advice
67
Q
  • Immunisation
A
  • Flu vaccine- given to high risk pts
  • Pneumococcal vaccine- every 5 years
68
Q

chemoprophylaxis e.g.

A

respiratory (27 decks)

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