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Phase 2a Green Conditions > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What 2 conditions make up COPD?

A
  • chronic bronchitis
  • emphysema
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2
Q

What is COPD?

A
  • non-reversible long term deterioration in air flow through the lungs
  • caused by damage to lung tissue
  • SOB and prone to infection
  • not reversible with bronchodilators
  • exacerbations occur → if due to infection, these are called IE COPD
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3
Q

What are the classic presenting features of COPD?

A
  • long term smoker
  • SOB
  • cough
  • sputum production
  • wheeze
  • recurrent respiratory infections
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4
Q

How do you classify COPD?

A

MRC dyspnoea scale

  1. breathless on strenuous exercise
  2. breathless on walking up hill
  3. breathless that slows on flat
  4. stop to catch breath after 100m walking on flat
  5. unable to leave house due to breathlessness
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5
Q

Risk factors for COPD

A
  • smoking
  • 40-60
  • secondhand smoke exposure
  • occupational exposure → mining, dust, cotton, wood
  • pollution → heating fuel, outdoor pollutants
  • alpha-1-antitrypsin deficiency
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6
Q

Why is A1AT implicated in COPD?

A
  • protein made by liver
  • protects lung from damage
  • deficiency can lead to earlier onset and increased severity of COPD
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7
Q

Diagnosis of COPD

A
  • clinical presentation
  • spirometry
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8
Q

What can be seen in COPD spirometry?

A
  • shows obstructive picture
  • lung capacity > ability to forcefully expire air quickly
  • FEV1/FVC <0.7
  • does not respond to reversibility testing with SABA
  • severity of obstruction can be measure using FEV1
  • compare patient to predicted
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9
Q

What other tests can be done for COPD?

A
  • chest xray → exclude others
  • FBC
  • BMI
  • ECG
  • serum A1AT
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10
Q

What is emphysema?

A

Symptoms

  • dyspnoea/tachypnoea
  • minimal cough
  • pink skin, pursed lip breathing
  • accessory muscle use
  • cachexia
  • hyperinflammation → barrel chest
  • weight loss

complications = pneumothorax due to bullae

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11
Q

What is chronic bronchitis?

A

symptoms

  • chronic productive cough → purulent sputum
  • dyspnoea
  • cyanosis = hypoxaemia
  • peripheral oedema
  • obesity
  • haemoptysis
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12
Q

General management of COPD

A
  • stop smoking
  • pneumococcal vaccine
  • annual flu vaccine
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13
Q

Stepwise management of COPD

A
  1. SABA or SAMA
  2. if no asthmatic/steroid response → LABA/LAMA, if asthmatic/steroid response → LABA, ICS
  3. long term oxygen therapy
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14
Q

Presentation of IE COPD

A
  • acute worsening of symptoms
  • SOB, sputum, wheeze
  • usually triggered by infection
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15
Q

Investigations for IE COPD

A
  • ABG
  • chest xray
  • sputum culture and sensitivities for Ab therapy
  • FBC and U&E
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16
Q

What does ABG show in IE COPD

A
  • CO2 retention = acidosis
  • are they in type 1 or 2 RF
    normal pCO2 and low pO2 = T1RF
    raised pCO2 and low pO2 = T2RF
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17
Q

Management of IE COPD

A
  • steroids AND
  • nebulised bronchodilators
  • Abs
  • physiotherapy → sputum clearance
  • if severe = IV aminophylline (bronchodilator), NIV (CPAP/BIPAP)
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18
Q

What bronchodilators are used in IE COPD?

A
  • salbutamol
  • ipratropium bromide
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19
Q

How does A1AT deficiency affect the lungs and liver?

A

lungs

  • lack of normal A1AT
  • excess protease enzymes → attack lung tissue

liver

  • mutant A1AT builds up
  • tissue damage → cirrhosis → HCC
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20
Q

Signs and symptoms of A1AT deficiency

A

lungs
- COPD symptoms

liver

  • loss of appetite
  • weight loss
  • oedema
  • jaundice
  • haematemesis
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21
Q

Diagnosis of A1AT deficiency

A
  • low serum A1AT
  • liver biopsy
  • A1AT mutant gene
  • CT thorax
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22
Q

Management of A1AT

A
  • no cure
  • stop smoking
  • symptomatic treatment
  • organ transplant for end-stage liver/lung disease
  • monitor for HCC
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23
Q

What is asthma?

A
  • chronic inflammatory condition
  • episodes of reversible airway obstruction due to:
    bronchoconstriction
    excessive secretion production
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24
Q

Causes of asthma

A

hypersensitivity of the airways triggered by:

  • cold air, exercise
  • cigarette smoke
  • air pollution
  • allergens → pollen, cats, dogs, horses, mould
  • time of day → early morning, night
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25
Q

Presentation of asthma

A

episodes of

  • wheeze → widespread, polyphonic
  • breathlessness
  • chest tightness
  • dry cough
  • family/personal history of atopy = eczema, asthma, hayfever
  • diurnal variability
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26
Q

Investigations for asthma

A

spirometry with reversibility testing

  • obstructive pattern
  • FEV1 <80% of predicted normal
  • FEV1/FVC ratio <0.7

peak flow measurement

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27
Q

Treatment for asthma

A
  1. SABA eg salbutamol
  2. inhaled corticosteroid eg budesonide
  3. leukotriene receptor antagonist eg montelukast
  4. LABA eg salmeterol
  5. increase ICS dose
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28
Q

Epidemiology of TB

A
  • majority of cases in Africa and Asia
  • cause of death for most people with HIV
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29
Q

Features of TB

A
  • aerobic, non-motile, non-sporing, slightly curved bacilli with a thick waxy capsule
  • acid-fast bacilli → turns red/pink with Ziehl-neelsen stain
  • slow growing
  • resistant to phagolysosomal killing
  • able to remain dormant
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30
Q

Pathophysiology of TB

A

spread via respiratory droplets → airborne infection

  1. alveolar macrophages ingest bacteria and rods proliferate inside
  2. drain into hilar lymph nodes
  3. delayed hypersensitivity reaction
  4. tissue necrosis and granuloma formation = caseating
    - primary ghon focus
    - ghon complex = ghorn focus and lymph nodes
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31
Q

Systemic symptoms of TB

A
  • low grade fever
  • anorexia
  • drenching night sweats
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32
Q

Pulmonary symptoms of TB

A
  • productive cough
  • haemoptysis
  • cough >3 weeks (dry or productive)
  • breathlessness
  • sometimes chest pain
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33
Q

Signs of TB

A
  • signs of bronchial breathing
  • dulness to percuss
  • decreased breathing
  • fever
  • crackles
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34
Q

What are signs of bronchial breathing?

A
  • loud harsh breathing sounds
  • mid range pitch
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35
Q

Investigations for TB

A
  • chest xray → fibronodular opacities on upper lobes
  • sputum culture for acid-fast bacilli → ZN stain on Lowenstein-Jensen agar
  • biopsy → caseating granuloma
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36
Q

Diagnosing latent TB

A

Mantoux

  • tuberculin injected intradermally
  • inspect skin for signs of local skin reaction over 2-3 days

Interferon gamma release assay
- blood test that detects WBC response to TB antigens

37
Q

Treatment for TB

A

RIPE

  • rafampicin → 6 months
  • isoniazid → 6 months
  • pyrazinamide → 2 months
  • ethambutamol → 2 months
38
Q

Side effects of TB medication

A
  • rifampicin = orange tears/urine
  • ethambutol = optic neuritis
  • all = liver failure
39
Q

What is pneumonia?

A
  • inflammation of the substance of the lungs
  • acute LRT infection
  • typically caused by bacterial infection of distal airways and alveoli
  • inflammatory exudate formed
40
Q

What are the types of pneumonia

A
  • CAP
  • HAP
  • atypical
  • in immunocompromised patients
41
Q

Pathophysiology of pneumonia

A
  • invasion and overgrowth of a pathogen in lung parenchyma
  • overwhelming of host immune defences
  • production of intra-alveolar exudates
42
Q

Clinical features of pneumonia

A
  • fever
  • productive cough
  • increased resp and heart rate
  • low BP
  • dyspnoea, rigors
43
Q

Signs of pneumonia

A
  • dull to percussion
  • decreased air entry
  • bronchial breath sounds
44
Q

Diagnosis of pneumonia

A
  • FBC → elevated WBC
  • sputum culture
  • chest xray
45
Q

What can be seen on a chest x-ray in pneumonia?

A
  • multi-lobar → strep pneumoniae, s.aureus
  • multiple abscesses → s.aureus
46
Q

How is the severity of pneumonia assessed

A

CURB-65 score → 1 point each for:

  • confusion
  • urea >7
  • resp rate >30
  • BP <90 systolic and/or <60 diastolic
  • age >65
0-1 = outpatient 
2 = short stay inpatient/hospital supervised outpatient 
3-5 = manage as high severity pneumonia
47
Q

Treatment for pneumonia

A
  • maintaining O2 sats between 94-98% (88-92 for COPD)
  • analgesia → paracetamol/NSAIDs
  • IV fluids
48
Q

CURB-65 guided treatment for pneumonia

A 
0-1 = oral amoxicillin at home 
2 = consider hospitalising, amoxicillin (IV/oral) and macrolide 
3+ = consider ITU, IV co-amoxiclav and macrolide

macrolide → clarithromycin/erythromycin

49
Q

What is CAP?

A
  • pneumonia acquired outside hospital/healthcare facilities
  • commoner in extremes of age
50
Q

What is HAP?

A
  • pneumonia acquired at least 48 hours after admission to hospital and no incubating at time of admission
51
Q

Causes of CAP

A
  • strep pneumoniae
  • haemophilus influenzae
  • mycoplasma pneumoniae

rusty sputum = characteristic of strep pneumoniae

52
Q

Causes of HAP

A

most cases caused by gram -ve bacilli

  • pseudomonas
  • e coli
  • klebsiella pneumoniae
53
Q

What is atypical pneumonia

A

bacterial pneumonia caused by atypical organisms not detectable on gram stain/cannot be cultured using standard methods

common organisms

  • mycoplasma pneumoniae
  • chlamydophila pneumoniae
  • legionella pneumophila
54
Q

What is a pneumothorax?

A

air in the pleural space

can be

  • spontaneous
  • traumatic → penetrating/blunt injury to chest
  • iatrogenic → central line/mechanical ventilation
  • tension
  • lung pathology
55
Q

Risk factors of PTX

A
  • smoking
  • family history
  • male
  • tall and slender build
  • young age
  • presence of underlying lung disease
56
Q

Clinical presentation of PTX

A
  • stable patient
  • sudden onset pleuritic chest pain, dyspnoea, cough

on examination look for

  • evidence of trauma
  • features of tension PTX
57
Q

Diagnosis of PTX

A
  1. erect chest xray
    - reduced/absent lung markings between lung margin and chest wall
    - visible rim between lung margin and chest wall
  • bloods → clotting
  • US
  • CT → if chest xray uncertain
  • ABG
58
Q

Management for PTX

A

small primary spontaneous PTX and not SOB

  • consider discharge
  • follow up chest xray in review

large primary spontaneous PTX and/or SOB

  • needle aspiration
  • if not <2cm on repeat chest xray, insert chest drain and supplemental O2 if needed
  • admission

secondary PTX

  • large = chest drain
  • small = needle aspiration
  • admission and high flow O2
59
Q

What is a tension PTX?

A
  • one way valve mechanism → air enters pleural space but cannot leave
  • increased +ve pressure in chest
  • collapse of ipsilateral lung
  • compression of contralateral, trachea, heart etc.
60
Q

Clinical presentation of tension PTX

A

cardiopulmonary deterioration

  • hypotension → imminent cardiac arrest
  • respiratory distress
  • low sats
  • tachycardia
  • shock

severe chest pain

61
Q

Physical examination of tension PTX

A
  • tracheal deviation to contralateral side
  • ipsilateral reduced breath sounds
  • hyperresonance on percussion
  • hypoxia
62
Q

Management of tension PTX

A
  • put out cardiac arrest call
  • start high flow O2
  • immediate decompression
  • insert large bore cannula into pleural space through the second intercostal space in the mid-clavicular line
  • hiss sound confirms diagnosis
63
Q

What is cystic fibrosis?

A
  • condition affecting mucus glands
  • autosomal recessive
  • defect in CFTR gene
64
Q

What are the key consequences of CF?

A
  • thick pancreatic and biliary secretions that cause blockage of ducts
  • low volume thick airway secretions that reduce airway clearance → susceptible to airway infections
  • congenital bilateral absence of vas deferens in male → infertile
65
Q

Symptoms of CF

A
  • chronic cough
  • thick sputum production
  • recurrent respiratory tract infections
  • steatorrhoea
  • abdominal pain and bloating
  • parents report child’s sweat tastes salty
  • failure to thrive
66
Q

Signs of CF

A
  • low height/weight on growth charts
  • nasal polyps
  • finger clubbing
  • crackles and wheezes on auscultation
  • abdominal distention
67
Q

Diagnosis of CF

A
  • newborn blood spot testing/heel-prick test
  • genetic testing for CFTR gene during pregnancy or as blood test after birth
  • GOLD STANDARD = sweat test → diagnostic Cl conc >60
68
Q

What organisms commonly colonise in CF patients?

A
  • s.aureus
  • haemophilus influenza
  • klebsiella pneumoniae
  • e.coli
  • psudomonas aeruginosa
69
Q

Management of CF

A

specialist MDT

  • chest physiotherapy
  • exercise
  • high calorie diet
  • CREON tablets → digest fats
  • prophylactic flucloxacillin
  • treat chest infections
  • bronchodilators
  • lung transplant in end stage resp failure
  • liver transplant in liver failure
  • fertility treatment
  • genetic counselling
70
Q

What is bronchiectasis?

A

permanent dilation of airways

71
Q

Causes of bronchiectasis

A
  • post-infection
  • CF
  • lung cancer
72
Q

Signs and symptoms of bronchiectasis

A
  • dyspnoea
  • cough
  • haemoptysis
  • recurrent chest infections
73
Q

Investigations for bronchiectasis

A
  • chest xray → kerly B lines
  • sputum → H.influenzae most common
74
Q

Management of bronchiectasis

A
  • physical training
  • postural drainage
  • prophylactic Abs
  • surgery if disease localised
75
Q

What is pleural effusion?

A

collection of fluid in the pleural cavity → space between parietal ad visceral pleura

76
Q

Types of pleural effusion

A
  • exudative → high protein count
  • transudative → lower protein count
77
Q

Causes of exudative pleural effusion

A

related to inflammation
- proteins leak out of tissue into pleural space

  • lung cancer
  • pneumonia
  • RA
  • TB
78
Q

Causes of transudative pleural effusion

A

related to fluid moving across pleural space

  • congestive cardiac failure
  • hypoalbuminaemia
  • hypothyroidism
  • Meig’s syndrome
79
Q

What is Meig’s syndrome?

A

right sided pleural effusion with ovarian malignancy

80
Q

Presentation of pleural effusion

A
  • SOB
  • cough
  • stony dull percussion over effusion
  • reduced breath sounds
  • tracheal deviation away from effusion if large
81
Q

Investigations for pleural effusion

A
  1. chest xray
    - pleural US
    - thoracocentesis → diagnoses underlying cause
82
Q

What would you see on a chest xray with pleural effusion?

A
  • blunting of costophrenic angle
  • fluid in lung fissures
  • meniscus
  • tracheal and medial deviation
83
Q

What is idiopathic pulmonary fibrosis?

A

formation of scar tissue in lungs with no known cause

84
Q

Presentation of IPF

A
  • dyspnoea
  • dry cough
  • bibasal crackles
85
Q

Treatment of IPF

A
  • prifenidone
  • nintedanib
  • treatments for ILD
86
Q

What is sarcoidosis?

A
  • granulomatous inflammatory condition
  • varied severity
87
Q

Presentation of sarcoidosis

A

affects any organ in body

most common = lung

  • mediastinal lymphadenopathy
  • pulmonary fibrosis
  • pulmonary nodules
88
Q

Investigations for sarcoidosis

A

GOLD STANDARD = histology from biopsy
- non-caseating granulomas with epithelioid cells

89
Q

Treatment for sarcoidosis

A
  • if mild, resolves spontaneously
  1. oral steroids, bisphophonates
  2. methotrexate/azathrioprine
  • lung transplant if severe

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