Respiratory Flashcards

1
Q

What is the aetiology of hospital-acquired pneumonia?

What are examples of atypical and aspiration

A

(48 hours in hospital or 7 days after leaving hospital)

Staphylococcus aureus (often post-viral URTI, can cause empyema & abscess)

Gram-negative enterobacteria (Pseudomonas, Klebsiella)

Anaerobes (due to aspiration pneumonia)

Atypical pneumonia - interstitial inflammation rather than consolidation

Mycoplasma pneumonia - 2nd most common, often in young adults (results in a rise of cold agglutinins - clumping of RBCs at low temperatures, commonly seen in close-community settings e.g. universities)

Chlamydia pneumonia

Legionella pneumophilia - A/C (can occur anywhere with air conditioning)

Coxiella burnetti

Chlamydia psittaci (causes psittacosis) - linked to exotic pet birds

Pneumocystis jiroveci - opportunistic fungal infection, AIDS defining illness

Aspiration pneumonia - anaerobes from gut, likely to affect right lower lobe

Klebsiella pneumoniae (commonly right lower lobe, redcurrant, foul-smelling jelly sputum, affects alcoholics, diabetics and those with poor swallow)

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2
Q

What is pneumoconiosis and what are the types?

A

Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts

  • Simple: Coalworker’s pneumoconiosis or silicosis (symptom free)
  • Complicated: Pneumoconiosis (progressive massive fibrosis) results in loss lung function
  • Asbestosis: A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos (associated with mesothelioma, lung carcinoma, benign pleural effusion, pleural plaques and diffuse pleural thickening)
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3
Q

What are the signs of idiopathic pulmonary fibrosis on examination?

A

Clubbing (50%)

Bibasal fine end-inspiratory crackles

Signs of right heart failure in advanced stages of disease

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4
Q

What are the signs of aspergillus lung disease on examination??

A
  • Tracheal deviation in large aspergillomas - Dullness in affected lung, reduced breath sounds, wheeze in ABPA - Cyanosis may develop in invasive aspergillosis
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5
Q

What are the signs and symptoms of TB in the skin?

A
  • Lupus vulgaris (jelly like reddish-brown glistening plaques)
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6
Q

What is the epidemiology of pulmonary embolisms?

A
  • Relatively common, especially in hospitalised pts
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7
Q

Mx on TB?

A

ACTIVE : RIPE

Inactive 2 options:

3m isoniazid + rifmapicin

6months isoniazid

RIFAMPICIN

ISONIAZID

PYRAZINAMID

ETHAMBUTAMOL

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8
Q

What are presenting symptoms of aspergillus lung disease?

A

Aspergilloma ASYMPTOMATIC Haemoptysis (potentially massive) Lethargy and weight-loss CXR - apical, round opacity within cavity ABPA Difficult to control asthma Recurrent episodes of pneumonia with wheeze, cough, fever and malaise Wheeze, cough, fever, malaise CXR - Segmental collapse and bronchiectasis Invasive Aspergillosis Dyspnoea Rapid deterioration Headache and seizure, altered mental state - may indicate intracranial disease/ space occupying lesion Septic picture CXR - consolidation and abscess

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9
Q

What is the aetiology of COPD?

A

Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke).

A1-antitrypsin deficiency is rare cause

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10
Q

What is the aetiology of extrinsic allergic alveolitis?

A

Inhalation of antigenic organic dusts containing microbes or animal proteins induce a hypersensitivity response in susceptible individuals

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11
Q

What are the presenting symptoms of asthma?

A
  • Episodes of wheeze, breathlessness, cough, worse in the morning and at night - Ask about interference with exercise, sleeping, days off school and work
  • In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity -
  • Precipitating factors: Cold, viral infection, drugs (B-blockers, NSAIDs), exercise, emotions
  • May have a history of allergic rhinits, uticaria, eczema, nasal polyps, acid reflux and family history
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12
Q

What are the risk factors for pneumoconiosis

A
  • Occupational exposure: in coal mining, quarrying iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders.
  • Risk depends on extent of exposure, size and shape of particles and individual susceptibility, as well as co-factors such as smoking and TB
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13
Q

What are the signs of a pneumothorax on examination?

A

There may be NO signs if the pneumothorax is small

Reduced chest expansion

Hyper-resonance to percussion ipsilaterally

Reduced breath sounds ipsilaterally

Tachycardic & tachypnoeic

Tension Pneumothorax

Hyper-expanded chest

Contralateral tracheal deviation

Severe respiratory distress

Hypotension - circulatory shock

Cyanosis

Distended neck veins

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14
Q

What are are the presenting symptoms of a pneumothorax?

A

May be ASYMPTOMATIC if the pneumothorax is small

Sudden-onset breathlessness (dyspnoea)

Pleuritic chest pain

Sweating, tachypnoea, tachycardia

Distress with rapid shallow breathing in tension pneumothorax

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15
Q

What are the investigations for aspergilloma?

A
  • Aspergilloma: CXR: Round opacity may be seen with a crescent of air around it (usually in the upper lobes) - CT or MR imaging if CXR does not clearly delineate a cavity - Cultures of the sputum may be negative if there is no communication between the cavity and the bronchial tree. Also Aspergillus is a common common coloniser of an abnormal respiratory tract
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16
Q

What is the pathogenesis of asthma with regards to the late phase?

A
  • After 6-12 hours - Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness - Structural cells may also release cytokines, profibrogenic and proliferative growth factors and contibute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodelling’)
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17
Q

What is a pneumothorax?

A

Air in the pleural space (the potential space between visceral and parietal pleura) Other variants depend on the substance in the pleural space (e.g. blood: haemothorax: lymph: chylothorax) - Tension pneumothorax: Emergency when a functional valve lets air enter the pleural space during inspiration but not leave during expiration

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18
Q

What is the pathogenesis of asthma with regards to the early phase??

A

Early phase (up to 1 hour): Exposure in inhaled allergens in a presensitised individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These induce bronchoconstriction, mucous hypersecretion, oedema and airway obstruction

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19
Q

How is a tension pneumothorax managed?

A
  • Emergency - Maximum 02, insert large-bore needle into second intercostal space, midclavicular line, on side of pneumothorax to relieve pressure, insert chest drain soon after, 5TH ics mcl
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20
Q

What are the possible complications of asthma?

A
  • Growth retardation - Chest wall deformity (e.g. pigeon chest) - Recurrent infections - Pneumothorax - Respiratory failure - Death
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21
Q

What are the signs and symptoms of primary tuberculosis?

A
  • Mostly asymptomatic - May have fever - Malaise - Cough - Wheeze - Erythema nodosum - Phlyctenular conjunctivits (allergic manifestiations
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22
Q

How to treat acute exacerbation of COPD?

A

Controlled oxygen:

Via 24% O2 via Venturi mask , aim for SpO2 88-92% if hypercapnic on ABG, otherwise aim for 94-98%

Nebulised bronchodilators: salbutamol, ipratropium bromide

Corticosteroids (usually 5 day course)

Start empirical antibiotic therapy if evidence of infection (e.g. amoxicillin & doxycycline)

Theophylline if inadequate response to nebulisers

Respiratory physiotherapy to clear sputum

Ventilation if evidence of worsening respiratory acidosis:

  • BiPAP
  • Mechanical ventilation if BiPAP fails
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23
Q

What is the epidemiology of aspergillosis?

A
  • Uncommon - Most common in elderly and immunocompromised
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24
Q

How do mesothelioma spread?

A

Mesotheliomas usually spread through one pleural cavity then invade into the contiguous lung and chest wall

Also spread to the other pleural cavity, pericardial cavity and peritoneal cavity

Hilar nodes are involved by lymphatic spread

Death is usually due to lung/pleural involvement.

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25
Q

What are the possible complications of a pneumothorax?

A
  • Recurrent pneumothoraces - Bronchopleural fistula
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26
Q

What are the investigations for invasive aspergillosis?

A
  • Detection of Aspergillus in cultures or by histological examinations - Chest CT scan may show nodules surrounded by a ground-glass appearance (halo sign)
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27
Q

What are the investigations for pneumonia?

A
  • Blood: FBC (abnormal WCC) U&E (reduced Na+, especially with Legionella, LFT, blood cultures (sensitivity 10-20%, ABG (assess pulmonary function), blood film - CXR: Lobar or patchy shadowing, may lag behind clinical signs, pleural effusion, Klebsiella often affects upper lobes, repeat 6-8 weeks. May detect complications: Abscess - Sputum/pleural fluid: Microscopy, culture & sensitivity, acid fast bacilli - Urine: Pneumococcus and Legionella antigens - Atypical viral serology - Bronchoscopy
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28
Q

What are the investigations for obstructive sleep apnoea?

A

Assessment of sleepiness:

Epworth sleepiness scale (questionnaire completed by patient/partner) (0-6 is normal, 9-24 points is abnormal sleepiness)

Multiple sleep latency test - MSLT (measures how quickly one falls asleep, the sleepier you are the faster you should fall asleep)

Sleep Study/polysomnography (PSG) - diagnostic

Ranges from monitoring pulse oximetry at night, to full polysomnography (measures respiratory airflow, thoracoabdominal movement, EEG, ECG, capnography, snoring and pulse oximetry)

DIAGNOSIS IF APNOEA-HYPOPNOEA INDEX (AHI) > 15 episodes/hour

Portable multichannel sleep tests

Used for patients with a higher probability of OSA

DIAGNOSIS IF Respiratory-event index (REI) > 15 episodes/hour

Awake fibreoptic endoscopy - performed to exclude nasal polyps/laryngeal/pharyngeal tumours

Bloods

TFTs - thyroid cancer could be pressing on and obstructing airways

ABG

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29
Q

What would be seen on a CXR in post-primary TB?

A
  • Upper love shadowing - Streaky fibrosis and cavitation - Calcification - Pleural effusion - Hilar lymphadenopathy
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30
Q

What is extrinsic allergic alveolitis?

A

DEFINITION: Non-IgE mediated interstitial inflammatory disease of the distal gas-exchanging parts (alveoli and bronchioles) of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis. Type 3 hypersensitivity in acute phase, type 4 in chronic phase

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31
Q

What are the signs and symptoms of TB in the gastrointestinal system?

A
  • Subacute obstruction - Change in bowel habit - Weight loss - Peritonitis - Ascites
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32
Q

What is the aetiology of a pneumothorax?

A
  • Spontaneous: In individuals with previously normal lungs, typically tall thin males. Probably caused by rupture of a subpleural bleb
  • Secondary: Pre-existing lung disease (COPD, asthma, TB, pneumonia, lung carcinoma, cystic fibrosis, diffuse lung disease)
  • Traumatic: Penetrating injury to chest, often iatrogenic causes e.g. during subclavian or jugular venous cannulation, thoracocentesis, pleural or lung biopsy, or positive pressure-assisted ventilation -

Collagen disorders (e.g. Marfan’s syndrome, Ehlers-Danlos syndrome)

Pre-existing lung disease (Asthma, COPD - due to rupture of bulla)

Diving & flying (due to changes in pressure)

Mechanical ventilation

Smoking

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33
Q

What would be seen on a CXR in miliary TB?

A

Fine shadowing

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34
Q

What is the aetiology of idiopathic pulmonary fibrosis?

A

Occurs in genetically predisposed individuals

Recurrent injury to alveolar epithelial cells results in secretion of cytokines and growth factors

This leads to fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and increased collagen synthesis and deposition

Certain drugs can produce similar illness (e.g. methotrexate, amiodarone)

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35
Q

What are the possible complications of a pulmonary embolism?

A
  • Death - Pulmonary infarction - Pulmonary hypertension - Right heart failure
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36
Q

What are the signs and symptoms of TB in the lymph nodes

A
  • Suppuration of cervical lymph nodes leading to abscesses or sinuses which discharge pus and spread to skin (scrofuloderma)
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37
Q

What is the epidemiology of obstructive sleep apnoea?

A
  • Common
  • Affects 5-20% men
  • Affects 2-5% of women
  • Over 35 yrs
  • Prevalence increases with age
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38
Q

What are the investigations for extrinsic allergic alveolitis?

A
  • Blood: FBC

FBC - neutrophilia, lymphopenia, anaemia - NO EOSINOPHILIA

ESR - elevation indicates inflammation

Albumin - may be low in chronic disease

  • Serology: Precipitating IgG to fungal or avian antigens in serum, however, these are not diagnostic as are often found in asymptomatic individuals
  • CXR: Often normal in acute episodes, may see fibrosis
  • High resolution CT thorax: Detects early change before CXR. Patchy ‘ground glass’ shadowing and nodules
  • Pulmonary function tests: Restrictive ventilatory defect (Reduced FEV1, FVC with preserved or increased ratio)
  • Bronchoalveolar lavage: Increased cellularity with increased CD8+ suppressor T cells. Lung biopsy.
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39
Q

What are the investigations for a pulmonary embolism?

A
  • Low probability:

D-Dimer blood test

  • High probability: Requires imaging
  • Additional initial investigations: ABG, ECG (tachy, right avis dev. RBBB), CXR
  • Spiral CT pulmonary angiogram - Ventilation-perfusion (VQ) scan - Pulmonary angiography - Doppler USS of lower limb - Echocardiogram
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40
Q

What are the presenting symptoms of bronchoiectasis?

A
  • Productive cough with purulent sputum or haemoptysis - Breathlessness, chest pain, malaise, fever, weight loss - Symptoms usually begin after an acute respiratory illness
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41
Q

What is chronic ‘stepwise’ therapy for asthma?

A

Start on step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3-6 months

  1. SABA , if needed more than 1 day move to 2
  2. SABA+ Low dose steroid
  3. SABA+Low dose steroid+LTRA
  4. SABA+LOW DOSE STEROID+LABA
  5. SABA +-LTRA
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42
Q

What are the possible complication of bronchiectasis?

A
  • Life-threatening haemoptysis - Persistent infections - Empyema - Respiratory failure - Cor pulmonale - Multi-organ abscesses
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43
Q

What is the prognosis of asthma?

A
  • Many children improve as they grow older - Adult-onset asthma is usually chronic
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44
Q

What is pneumonia?

A
  • infection of distal lung parenchyma (inflammation of the alveoli). Most commonly a bacterial pneumonia
  • Several ways of categorisation:
  • Community-acquired, hospital acquired or nosocomial -
  • Aspiration pneumonia, pneumonia in the immunocompromised
  • Typical and atypical ( (Mycoplasma, Chlamydia, Legionella))
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45
Q

What are the the investigations for a pneumothorax?

A
  • CXR(skip if tension): A pneumothorax is seen as a dark area of film where lung markings do not extend to. Fluid may be seen be seen if there is blood present. In small pneumothoraces, expiratory films may make it more prominent
  • ABG: May be necessary to determine if there is any hypoxaemia, particularly in secondary disease

CT CHEST: DIAGNPOSTC

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46
Q

What is the epidemiology of tuberculosis?

A
  • Annual mortality 3 million - Incidence in Asian immigrants more than 30x UK white population?
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47
Q

What are the signs and symptoms of post-primary tuberculosis?

A
  • Fever/night sweats - Malaise - Weight loss - Breathlessness - Cough - Sputum - Haemoptysis - Pleuritic pain - Signs of pleural effusion - Collapse - Consolidation - Fibrosis
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48
Q

What are examples of extrinsic allergic alveolitis?

A
  • Famer’s Lung & mushroom worker’s lung - caused by mouldy hay containing thermophilic actinomycetes
  • Pigeon Fancier’s Lung - caused by blood on bird feathers and excreta - avian protein antigen
  • Maltworker’s Lung - caused by barley or maltlings containing Aspergillus clavatus
  • SOME DRUGS CAN CAUSE HYPERSENSITIVITY PNEUMONITIS e.g. methotrexate, amiodarone, rituximab and nitrofurantoin
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49
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on size and site of the pulmonary embolus?

  • Small: May be asymptomatic
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain
  • Large: All of above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death - Multiple small recurrent: Symptoms of pulmonary hypertension
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50
Q

What is the prognosis of a pulmonary embolism?

A
  • 30% untreated mortality - 8% with treatment - Pts have an increased risk of future thromboembolic disease
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51
Q

What are the investigations for TB?

A
  • Sputum/pleural/bronchial washings: Microscopy (Ziehl-Neelson stain), culture - Tuberculin tests: Positive in previous exposure to M.tuberculosis or BCG - Mantoux test - Heaf test - Interfreron-gamma tests - CXR - HIV testing - CT, lymph nodes, pleural biopsy, sampling of other affected systems
52
Q

What is the aetiology of tuberculosis?

A

M. tuberculosis is an intracellular organism which survives after being phagocytosed by macrophages

53
Q

What is the aetiology of asthma?

A
  • Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy. - Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens
54
Q

What is the epidemiology of COPD?

A
  • Very common (prevalence up to 8%) - Presence in middle age or later - More common in males, but likely to change with increasing female smokers
55
Q

What are the presenting symptoms of obstructive sleep apnoea?

A
  • Excessive daytime sleepiness (at work, driving) - Unrefreshing or restless sleep - Morning headaches or dry mouth, difficulty concentrating, irritability or mood changes - Partner reporting snoring, nocturnal apnoeic episodes or nocturnal choking
56
Q

What are the investigations for chronic asthma?

A
  1. FeNO (fractional exhaled nitric oxide)
  • FIRST
  • Inflammatory cells produce nitric oxide (>40ppb)
  1. Spirometry
  • Obstructive picture
  • FEV1% (FEV1/FVC)
  • Bronchodilator Reversibility: 12% pre- and post- bronchodilator spirometry
  1. PEFR monitoring:
  • Used if spirometry does NOT show variability
  • Often shows diurnal variation
  • PEFR varies by at least 20% for 3 days in a week over at least 2 weeks or PEFR increases by at least 20%
    4. Airway hypersensitivty testing :histamine or methacholine direct bronchial challenge
    5. Allergy testing (skin prick tests and RAST (radioallergosorbent) testing) - for allergic asthma

Bloods - check:

Eosinophilia

IgE level

Aspergillus antibody titres

57
Q

What is the prognosis of a pneumothorax?

A
  • After 1 spontaneous pneumothorax, at least 20% will have another - Frequency increasing with repeated pneumothoraces
58
Q

What is the prognosis of bronchiectasis?

A

Most patients continue to have the symptoms after 10 yrs

59
Q

What are the signs and symptoms of miliary tuberculosis?

A
  • Fever - Weight loss - Meningitis - Yellow caseous tubercles spread to other organs (e.g. in bone and kidney may remain dormant dormant for years
60
Q

What is obstructive sleep apnoea?

A

Characterised by recurrent collapse of the pharangeal airway and apnoea (cessastion of airflow for more than 10s) during sleep, followed by arousal from sleep. Also known as Pickwickian syndrome

61
Q

What are the presenting symptoms of COPD?

What are the symptoms during exacerbations?

A

Chronic productive cough

Breathlessness (initially at exercise - reducing exercise tolerance, eventually at rest)

Fatigue

In severe cases, chronic changes in the vascular beds causing pulmonary hypertension –> right sided heart failure (cor pulmonale) –> peripheral oedema

Pink puffers(emphysema) and blue bloaters( bronchitis)

Exacerbations:

  • Dyspnoea
  • Sputum purulence
  • sputum volume
  • cough
62
Q

What is the epidemiology of asthma?

A
  • Affects 10% of children and 5% of adults - Prevalence is increasing - Male=Female
63
Q

What are the investigations for COPD?

A

Pulse oximetry

Spirometry and Pulmonary Function Tests

  • Obstructive picture
  • Reduced PEFR, serial measurements to exclude asthma
  • Reduced FEV1/FVC <70% & lack of reversibility
  • Decreased carbon monoxide gas transfer coefficient - Tlco, perform if symptoms disproportionate to spirometry results
  • CXR:

May appear NORMAL

Hyperinflation (> 6 anterior ribs or 10 posterior ribs, flattened diaphragm)

Reduced peripheral lung markings

Elongated cardiac silhouette

bullae

  • Blood:

FBC: increased Hb and heamatocrit due to secondary polycythaemia ( Heamtaocrit > 55%)

  • ABG - may show hypoxia, normal/raised PCO2 (if acutely unwell) - type 2 respiratory failure

ECG and Echocardiogram - check for cor pulmonale (RBBB & right axis deviation) risk factors for COPD are similar to those for IHD (so co-morbidities common)

  • Sputum and blood cultures -

Consider a1-antitrypsin levels: in young pts or minimal smoking history

64
Q

What is the epidemiology of idiopathic pulmonary fibrosis?

A

RARE

6/100,000

More common in MALES

65
Q

How is bronchiectasis managed?

A

Maintenance therapy:

Conservative: exercise, good diet and pulmonary rehabilitation.

Airway clearance: oral hydration, chest physio, nebulised hyperosmolar agents

Treatment of exacerbations (presents with change in sputum colour, increase in volume, worsening cough, fever, malaise)

  • Outpatient care - oral antibiotic for 14 days (amoxicillin, or clarithromycin or trimethoprim)
  • Patients with known pseudomonas infection or severe exacerbation - IV antibiotics for 14 days minimum (aminoglycoside or a fluoroquinolone)

Prophylactic courses of antibiotics for those with frequent exacerbations

  • Inhaled corticosteroids (e.g. fluticasone) have been shown to reduce inflammation and volume of sputum, although it does not affect the frequency of exacerbations or lung function - Bronchodilators - Maintain hydration - Consider flu vaccination - Physiotherapy - Bronchial artery embolisation - Surgical
66
Q

What is the epidemiology of bronchiectasis?

A
  • Most often arises initially in childhood - Incidence has reduced with use of antibiotics
67
Q

How is asthma managed on discharge?

A
  • When PEF more than 75% predicted or pts best, diurnal variation less than 25%, inhaler technique checked, stable on discharge medication for 24h, pt own a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up
68
Q

What is asthma?

A

Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation

69
Q

What is aspergillus lung disease?

A

Lung disease associated with Aspergillus fungal infection

70
Q

What are the investigations for Allergic bronchopulmonary aspergillosis (ABPA)?

A
  • Immediate skin test reactivity to Aspergillus antigens - Eosinophilia - Increased serum total IgE - Increased serum specific IgE and IgG to A. fumigatus or precipitating antibodies to A. fumigates - CXR: Transient patchy shadows, collapse, distended mucus-filled bronchi producing tubular shadows - CT: Lung infilitrates and central bronchiectasis - LFT: reversible airflow limitation
71
Q

How is acute asthma managed?

A
  • Resuscitate, monitor 02 sats, ABG and PEFR
  • High flow oxygen
  • Nebulized B2-agonist bronchodilator salbutamol, ipatropium
  • Steroid therapy, hydrocortison 100mg
  • IV - If no improvement: IV Mg sulphate. Consider IV salbutamol
    • Summon anaesthetic help if pt is getting exhausted (PC02 increasing). Treat any underlying cause (infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, increased WCC, fever). Monitor electrolytes closely - May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early
72
Q

What is tuberculosis?

A

Granulomatous disease caused by Mycobacterium tuberculosis. Primary: Initial infection may be pulmonary (acquired by inhalation from the cough of an infected patient) or, occasionally, gastrointestinal - Miliary TB: Results when there is haematogenous dissemination - Post-primary: Caused by infection or reactivation

73
Q

How is pneumonia managed?

A

CAP= AMOXICILLIN

IF NOT TREATED THEN AMOXICILLIN+CLARITHYMYOCIN

HAP-> co-amoxiclav

Aspiration= metrinadaxole

Atypical= clarithymoucine

74
Q

What is a pulmonary embolism?

A

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site

75
Q

What are the signs and symptoms of TB in the genitourinary system?

A
  • UTI symptoms - Renal failure - Epididymitis - Endometrial or tubal involvement - Infertility
76
Q

What are the investigations for pneumoconiosis?

A
  • CXR: Simple (micronodular mottling is present). Complicated (Nodular opacities in the upper lobes, micronodular shadowing, eggshell calcification of hilar lumph nodes is characteristic of silicosis - CT scan: Fibrotic changes can be visualised early - Bronchoscopy: Visualises changes. Allows for bronchoalveolar lavage - Lung function test: Restrictive ventilatory defect, impaired diffusion
77
Q

What is the aetiology of pneumoconiosis?

A

Caused by inhalation of particles of coal dust, silica or asbestos (two main types of fibre: white asbestos and blue asbestos or crocidolite, the latter is more toxic)

Asbestos (asbestosis) - shipbuilding, construction, textiles & insulation manufacturing, boiler makers, heating engineers, electrical engineers

78
Q

What is chronic obstructive pulmonary disease (COPD)?

A

Chronic, progressive lung disorder characterised by airflow obstruction with the following - Chronic bronchitis and/or - Emphysema

79
Q

What advice should be given to pts with asthma?

A

Educate on proper inhaler technique and routine monitoring of peak flow Develop an individualised management plan, with emphasis on avoidance of provoking factors

80
Q

What advice should be given to patients with a pneumothorax?

A
  • Avoiding air travel until follow-up CXR confirms resolution of pneumothorax - Avoid diving unless bilateral surgical pleurectomy
81
Q

What are the signs and symptoms of TB in the CNS?

A
  • Meningitis - Tuberculoma
82
Q

What are the presenting symptoms of pneumoconiosis?

A

Occupational history is important, there may be a long latency between exposure and expression - Asymptomatic:

Picked up on routine CXR (simple coal or silica pneumoconiosis)

  • Symptomatic: There is usually insidious onset of shortness of breath and a dry cough.

Chest-tightness and wheeze

Occasionally, black sputum (melanoptysis) is produced in coalworker’s.

Workers exposed to asbestos may develop pleuritic chest pain many years after first exposure as a result of acute asbestos pleurisy

83
Q

What is the prognosis of pneumonia?

A

Most resolve with treatment (1-3 weeks). High mortality of severe pneumonia Markers of Severe pneumonia

(CURB-65 score) - Confusion - Urea more than 7mmol/L - Respiratory rate more than 30 mins - BP: Systolic less than 90mmg or diastolic less than 60 mmHg - Age: More than 65 tears

confusion and RR signs of sepsis

84
Q

What are the signs and symptoms of TB in the bones/joints?

A
  • Osteomyelitis - Arthritis - Paravertebral abscesses and vertebral collapse (Pott’s disease) - Spinal cord compression from abscesses
85
Q

What are the investigations for acute asthma?

A
  • Peak flow
  • Pulse oximetry
  • ABG
  • CXR (to exclude other diagnoses e.g. pneumothorax, pneumonia)
  • FBC (increased WCC if infective exacerbation)
  • CRP, U&E, blood and sputum cultures: (charcot leyden crystals are eosinophilic)
86
Q

What is the aetiology of aspergillus lung disease?

A

Inhalation of Aspergillus spores can produce THREE different clinical pictures: Aspergilloma Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess) Allergic Bronchopulmonary Aspergillosis (ABPA) Colonisation of the airways by Aspergillus leads to IgE and IgG-mediated immune responses Usually occurs in asthmatics & CF patients The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage and central bronchiectasis Invasive Aspergillosis Invasion of Aspergillus into lung tissue and fungal dissemination This can occur in immunosuppressed patients (e.g. neutropenia, steroids, AIDS), and after broad spectrum antibiotics

87
Q

How is a pulmonary embolism managed?

A
  • Primary prevention: Graduated pressure stockings (TEDs) and heparin prophylaxis in those at risk (e.g. post surgery). Early mobilisation and adequate hydration post surgery
  • If haemodynamically stable: 02 anticoagulation with heparin of LMW heparin, changing to oral warfarin therapy for min 2 months. Analgesics for pain
  • If haemodynamically unstable: Resuscitate, give oxygen, IV fluic resuscitation, thrombolysis with tPa can be considered on clinical grounds alone if cardiac arrest is imminent - Surgical or radiological: Embolectomy. IVC filters for recurrent pulmonary emboli
88
Q

What is the aetiology of bronchiectasis?

A

Severe inflammation in the lung causes fibrosis and dilation of the bronchi.

This is followed by pooling of mucous, predisposing to further cycles of infection, damage, and fibrosis to bronchial walls

  • Can be idiopathic and post-infectious (after severe pneumonia, whooping cough, tuberculosis)

Congenital:

Cystic fibrosis

CF is an autosomal recessive condition

Failure to pass meconium/meconium ileus

Failure to thrive

Recurrent infection

Absence of vas deferens –> infertility

Organisms in CF: S. Aureus, H. Influenza, P. Aeruginosa

Alpha-1 anti-trypsin disease

Ciliary dyskinetic syndromes e.g. kartagener’s syndrome (PCD + situs inversus), PCD (primary ciliary dyskinesia)

PCD is an autosomal recessive condition

Affects the protein machinery used by epithelial cells to rhythmically beat their cilia and by spermatozoa to beat their tails

Causes: bronchiectasis, serous otitis media (glue ear), rhinitis and sinusitis, male infertilitiy and situs inversus (dextrocardia)

Obstruction of bronchi

  • Foreign body
  • Enlarged lymph nodes
  • Tumour
  • GORD
  • Inflammatory disorders (e.g. rheumatoid arthritis)
  • Yellow nail syndrome (lymphoedema, yellow dystrophic nails and pleural effusions)
  • Allergic bronchopulmonary aspergillosis
  • HIV
89
Q

What are the signs of a pulmonary embolism on examination?

A
  • Clinical probability assessment
  • Small: Often no clinical signs. Earliest sign is tachycardia or tachypnoea
  • Moderate: Tachypnoea, tachycardia, pleural rub, low saturation 02 (despite oxygen supplementation) - Massive PE: Shock, cyanosis, signs of right heart strain (raised JVP, left parasternal heave, accentuated S2 heart sounds) - Multiple recurrent PE: Signs of pulmonary hypertension and right heart failure
90
Q

What are the signs of obstructive sleep apnoea on examination?

A
    • Large tongue, enlarged tonsils, long or thick uvula, retrognathia (pulled back jaws) -
  • Neck circumference (more than 42cm in males but 40cm in females) is correlated with presence of disease -
  • Obesity and hypertension common
91
Q

What are the signs and symptoms of TB in the adrenal system?

A

Insufficiency

92
Q

What is the epidemiology of extrinsic allergic alveolitis?

A
  • Uncommon - Marked geographical variation reflecting dependence on occupational causes
93
Q

What are the signs and symptoms of TB in the heart?

A
  • Pericardial effusion - Constrictive pericarditis
94
Q

What is the aetiology of community-acquired pneumonia?

A

Streptococcus pneumoniae (80%) - MOST COMMON

Haemophilus influenzae - rare except in COPD patients

Staph aureus

Moraxella catarrhalis (occurs in COPD patients)

Coxiella burnetii (causes Q fever)

95
Q

What are the investigations for bronchiectasis?

A
  1. CXR
  2. high-resolution chest CT : DIAGNOSTIC
  3. FBC - WBC may help identify presence of superimposed infection, eosinophilia may suggest ABPA
  4. sputum culture and sensitivity
  • Sputum: Culture and sensitivity, common organisms in acute exacerbations. P. auruginosa, H. influenzae, S. aureus, S. pneumoniae, Klebsiella, M. catarrhalis, Mycobacteria -

CXR: Dilated bronchi may be seen as parallel line radiating from hilum to diaphragm (tramline shadows). May show fibrosis, atelactasis, pneumonic consolidations or may be normal

  • High res CT: Dilated bronchi with thickened walls. Best diagnostic method
  • Bronchography: Determine extent of disease before surgery - Other: sweat electrolytes, serum immunoglobulins, sinus X-ray, mucociliary clearance study
96
Q

What are the signs of pneumoconiosis on examination?

A
  • Examination may be normal
  • Decreased breath sound in coalworker’s pneumoconiosis or silicosis
  • End-inspiratory crepitations and clubbing in asbestosis
  • Signs of a pleural effusion or right heart failure (cor pulmonale)
97
Q

How are recurrent pneumothoraces managed?

A

Chemical pleurodeces (visceral and parietal pleura fusion with tetracycline or talc) - Surgical pleurectomy

98
Q

What would be seen on a CXR in Primary TB?

A
  • Peripheral consolidation - Hilar lymphadenopathy
99
Q

What are the presenting symptoms of idiopathic pulmonary fibrosis?

A

Gradual-onset, progressive dyspnoea on exertion

Dry irritating cough

NO wheeze

Symptoms may be preceded by a viral-type illness

Fatigue and weight loss are common

IMPORTANT: take a full occupational and drug history

100
Q

What are the risk factors for pneumonia?

A
  • Age - Smoking - Alcohol - Pre-existing lung disease - Immunodeficiency - Contact with pneumonia
101
Q

how are penumothorax managed

A

Tension Pneumothorax (EMERGENCY)

High flow O2

Analgesia as needed

DECOMPRESS before imaging if high clinical suspicion

Insert large bore needle (14 gauge iv catheter) into 2nd intercostal space MCL

Insert above upper border of rib to avoid neurovascular bundle

Up to 2.5 L of air can be aspirated

Stop if patient coughs or resistance is felt

Follow-up CXR 2 hrs and 2 weeks later

Chest Drain with Underwater Seal

Inserted in the 5th intercostal space midaxillary line, triangle of safety

Performed if:

Aspiration fails

Fluid in the pleural cavity

After decompression of a tension pneumothorax

Primary pneumothorax

Advise to stop smoking

< 2cm & patient NOT SOB –> discharge

> 2cm and/or patient is SOB –> aspiration (with 16-18G cannula)

If this fails –> chest drain

Secondary pneumothorax

< 1cm - oxygen and admit for 24 hrs for monitoring

1-2cm - aspiration

> 2cm or breathless –> chest drain

102
Q

What are the signs and symptoms of non-pulmonary tuberculosis?

A

Particularly in immunocompromised

103
Q

What is the epidemiology of pneumoconiosis?

A
  • Incidence increasing in developing countries, disability and mortality from asbestosis will increase for the next 20-30 yrs
104
Q

How is discharge planned for pneumonia?

A
  • Presence of 2 or more features of clinical instability (raised temperature, heart rate, respiratory rate and reduced BP, oxygen saturation, mental status and oral intake) predict a significant change of re-admission or mortality. Thus this assessment should be considered when planning for discharge - Non-resolving pneumonia: Consider other causes - Prevention: Pneumococcal, H influenzae, type B vaccination in vulnerable groups
105
Q

What are the signs of bronchiectasis on examination?

A

Early inspiratory course crackles and squeaks

Coarse crepitations (usually at lung bases)

These shift with coughing

Wheeze

Clubbing

106
Q

What is the aetiology of a pulmonary embolism?

A
  • Thrombus (more than 95% originating from DVT of lower limbs and rarely from right atrium in pts with AF - Other agents that can embolise to pulmonary vessels include amniotic fluid embolus, fat emboli, tumour emboli and mycotic emboli from right-sided endocarditis - Groups at risk include surgical pts, immobility, obesity, OCP, heart failure, malignancy
107
Q

What is the aetiology of obstructive sleep apnoea?

A
  • Obstructive apnoeas occur when the upper airway narrows because of collapse of the soft tissues of the pharynx
  • when tone in pharangeal dilators decreases during sleep.
  • Associated with:
  • Weight gain

Smoking

Alcohol

Sedative use

Enlarged tonsils and adenoids in children

Macroglossia (hypothyroidism, amyloidosis and acromegaly)

Marfan’s syndrome

Craniofacial abnormalities

108
Q

What is the epidemiology of a pneumothorax?

A
  • Mainly affects 20-40 year olds - 4x more common in males
109
Q

How is COPD managed?

A
  • Stop smoking
  • Bronchodilators: delivered by inhalers or nebulizers
  • Steroids
  • Pulmonary rehabilitation
  • Oxygen therapy
110
Q

What are the possible complications of pneumonia?

A
  • Pleural effusion
  • Empyema (pus in the pleural cavity - Localised suppuration-> lung abscess (especially staphylococcal, Klebsiella pneumonia, presenting with swinging fever, persistent pneumonia, copious/foul-smelling sputum), septic shock, ARDS, acute renal failure
  • M. pneumonia: Erythema multiforme, myocarditis, haemolytic anaemia, meningoencephalitis, transverse myelitis,

Guillain-Barre syndrme

111
Q

What is the supportive treatment of pneumonia?

A
  • Oxygen (maintain p02 more than 9kPa - Parenteral fluids for dehydration or shock, analgesia, chest physiotherapy - CPAP, BiPAP or ITU care for respiratory failure - Surgical drainage may be needed for empyma/ abscesses
112
Q

What is emphysema?

A

Pathological diagnosis of permanent destructive enlargement of the airways, distal to the terminal bronchus

Destruction and enlargement of alveoli

Leads to loss of elasticity that keeps small airways open in expiration

Progressively larger spaces develop called bullae (diameter > 1 cm)

113
Q

What are the signs of COPD on examination?

A

Inspection

  • Respiratory distress
  • Use of accessory muscles
  • Barrel-shaped over-inflated chest
  • Decreased cricosternal distance
  • Cyanosis
  • Pursed-lip breathing
  • Tar staining

Percussion

  • Hyper-resonant chest
  • Loss of liver and cardiac dullness

Auscultation

  • Quiet breath sounds
  • Prolonged expiration
  • Wheeze
  • Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions
  • Early inspiratory coarse crackles (infective exacerbation)

Signs of CO2 Retention

  • Bounding pulse
  • Warm peripheries
  • Asterixis - RARE

LATE STAGES: signs of right heart failure (cor pulmonale)

  • Right ventricular heave
  • Raised JVP
  • Ankle oedema
114
Q

What are the presenting symptoms of chronic extrinsic allergic alveolitis?

A
  • Poorly reversible manifestation i some
  • Slowly increasing breathlessness and decreasing exercise tolerance, weight loss
  • Exposure is usually chronic, low level and may be no history of previous acute episodes
  • Full occupational history and enquiry into hobbies and pets important
115
Q

What is bronchiectasis?

A

Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections

116
Q

What is the epidemiology of pneumonia?

A

Community-acquired causes, more than 60,000 deaths in the UK per year

117
Q

What is chronic bronchitis?

A

Chronic cough and sputum production on most days for at least 3 months per year over 2 years

Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis)

Bronchial mucosal oedema

Mucous hypersecretion

Squamous metaplasia

118
Q

What are some features with this and investaigations?

A

Features Patients who manifest disease usually have PiZZ genotype Lungs: panacinar emphysema, most marked in lower lobes Liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children Investigations A1AT concentrations spirometry: obstructive picture

119
Q

What are the presenting symptoms of pneumonia?

A

Productive cough, haemoptysis

Sputum

Dyspnoea/ SOB

Fever

Pleuritic chest pain

Confusion (in severe cases or in the elderly)

Atypical Pneumonia Symptoms: (flu-like) Headache

Myalgia - muscle pains

Diarrhoea/abdominal pain

DRY cough for prolonged time

Hepatitis

Bullous myringitis - RARE (indicates mycoplasma pneumonia, ear infection)

120
Q

What is alpha-1 antitrypsin deficency?

A

Alpha-1 antitrypsin (AAT) is a protein that protects the lungs. The liver makes it. If the AAT proteins aren’t the right shape, they get stuck in the liver cells and can’t reach the lungs.

121
Q

What are the presenting symptoms of acute extrinsic allergic alveolitis?

A

Present 6-18 hrs after exposure

Flu-like illness

REVERSIBLE episodes of:

Dry cough

Dyspnoea

Malaise

Fever

Myalgia

122
Q

What are the signs of pneumonia on examination?

A
  • Signs of systemic inflammation: pyrexia, tachycardia, tachypnoea, hypotension (if septic)
  • Cyanosis + reduced oxygen sats
  • Decreased chest expansion
  • Dull to percussion
  • Increased vocal & tactile fremitus over affected area
  • Bronchial breathing over affected area
  • Coarse crepitations on affected side
  • Chronic suppurative lung disease (empyema, abscess) –> clubbing
123
Q

What are the signs of asthma on examination and the signs of acute asthma attack

A
  • Tachypnoea
  • Use of accessory muscles
  • Prolonged expiratory phase
  • Polyphonic expiratory wheeze on auscultation
  • Hyperinflated chest and hyper-resonant percussion, decreased air entry
  • Harrison’s sulcus in chronic asthma

Severe asthma attack
* Cyanosis, absent chest sound, RR>25, BP>110, cant complete sentences, reduced consciouness , arrythmia and low BP

124
Q

What are the investigations for idiopathic pulmonary fibrosis?

A

CXR :

  • Usually NORMAL at presentation
  • Early disease may show bilateral interstitial shadowing (ground glass)
  • Later stage disease shows signs of cor pulmonale and eventually honeycombing

High-Resolution CT

  • More sensitive in early disease than CXR

Blood tests:

  • Rheumatoid factor
  • ANA - anti nuclear antibodies
  • Anti-cyclic citrullinated peptide

Myositis panel

Pulmonary Function Tests

  • Restrictive features (reduced FEV1 and FVC, with preserved or increased FEV1/FVC)
  • Decreased lung volumes
  • Decreased lung compliance
  • Decreased total lung capacity

Bronchoalveolar Lavage - exclude infections and malignancy

Lung Biopsy - accomplished by video-assisted thoracoscopy

Echocardiography - to check for pulmonary hypertension

125
Q

What is idiopathic pulmonary fibrosis?

A

DEFINITION: inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium. Previously known as cryptogenic fibrosing alveolitis.

126
Q

What are the signs of extrinsic allergic alveolitis on examination?

A

Acute: Rapid shallow breathing, pyrexia, inspiratory crepitations Chronic: Fine inspiratory crepitations. Finger clubbing is rare

127
Q

What are the possible complications of COPD?

A
  • Acute respiratory failure - Infections (particularly S. pneumoniae, H. influenzae - Pulmonary hypertension and right heart failure, - Pneumothorax (resulting from bullae rupture) - Secondary polycythaemia