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Flashcards in Respiratory pathology Non-neoplastic Deck (29)
1

The respiratory system

Upper airways: nose, accessory air sinuses, nasopharynx, larynx
Lower airways: trachea, bronchi, bronchioles, terminal bronchioles, alveoli
Pleura

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Infection upper airways

acute inflammatory process that affects mucous membranes of the respiratory tract
Includes: rhinitis, laryngitis, tonsilitis sinusitis
Symptoms: malaise, headache, sore throat, discharge
Aetiology
Commonly viral
Can get secondary bacterial infection

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Lower airways: infectionPNEUMONIA

Inflammation of the lung parenchyma
- Consolidation of the affected part
- Exudate with inflammatory cells and fibrin in the alveolar air spaces
Causes: infectious agents
inhalation of chemicals
chest wall trauma
Setting:
Community acquired
Hospital acquired
Aspiration pneumonia
Chronic pneumonia
Necrotizing pneumonia and lung abscesses
Pneumonia in the immunocompromised host

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Pneumonia clinical features

Fever, rigours, SOB, pleuritic chest pain, purulent sputum, cough

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Pneumonia Morphology

Lobar
Multifocal/lobular (bronchopneumonia)
Interstitial (focal diffuse)

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Community acquired pneumonia

Relatively common, especially in elderly population
Strep. pnuemoniae most common organism
Haemophilus influenzae
Staph aureus- complicates viral infection and in IVDU
Lobar or bronchopneumonia

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Hospital acquired pneumonia

Aka nosocomial pneumonia
Any pneumonia contracted by patient at least 48-72hrs after admission
Usually bacterial- gram negative bacilli and Staph aureus
Severe and can be fatal- most common cause of death in ITU
Fever
Increased white cell count
Cough with purulent sputum
Chest X-ray changes

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Aspiration pneumonia

Develops after inhalation of foreign material.
Elderly, Strokes, Dementia, Anaesthetic
Usually right middle and right lower lobe
Oral flora +/- other bacteria

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Obstructive disease

Characterised by partial or complete obstruction at any level from the trachea to respiratory bronchioles
PFT: limitation of maximal airflow rate during forced expiration FEV1

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Restrictive disease

Characterised by reduced expansion with decreased total lung capacity,
FVC is reduced: amount of air that can be blown out after maximal inspiration

11

COPD - Emphysema

Irreversible enlargement of the airspaces distal to the terminal bronchiole - destruction of their walls without obvious fibrosis
Types: centriacinar / panacinar / paraseptal / irregular
Pathogenesis:
mild chronic inflammation throughout the airways
protease – antiprotease imbalance hypothesis
+ imbalance of oxidants and antioxidants
role of smoking and genetics

12

Emphysema- morphology and clinical course

Morphology: voluminous lungs large alveoli, large apical bullae or blebs
Clinical course - symptoms:
dyspnoea, cough, wheezing, weight loss
expiratory airflow limitation – “pink pufferrs”
death due to cor pulmonale,
congestive heart failure, pneumothorax

13

COPD – chronic bronchitis

persistent cough with sputum production
for at least 3 months in at least 2 consecutive years
without any other identifiable cause
- long-standing irritation by inhaled substances (e.g tobacco smoke, dust from grain, cotton, silica)
- hypertrophy of submucosal glands in trachea and bronchi, increase in goblet cells
- mucus hypersecretion + alterations in the small airways chronic airway obstruction

14

Chronic bronchitis - Morphology and clinical course

Morphology
mucous membrane hyperaemia, swelling, oedema
excessive mucous/mucopurulent excretions,
narrowing of the bronchioles caused by mucus plugging, inflammation and fibrosis,
may cause obliteration in severe cases
Clinical course
persistent cough productive of sputum
dyspnea on exertion
hypercapnia, hypoxemia, mild cyanosis (“blue bloaters”)
Leads to cor pulmonale, cardiac failure, may cause atypical metaplasia/dysplasia

15

Asthma

Chronic inflammatory disorder of the airways
recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning.
widespread but variable bronchoconstriction and airflow limitation
At least partly reversible (spontaneously/with treatment).
Hallmarks: increased airway responsiveness  episodic bronchoconstriction, inflammation of bronchial walls, increased mucus secretion
Types: extrinsic (response to inhaled antigen – atopic, occupational) intrinsic (non-immune mechanisms – cold, exercise,aspirin). Atopic best understood

16

Asthma - morphology and clinical course

Morphology
lung overinflation + small areas of atelectasis,
thick mucus plugs in bronchi and bronchioles,
airway remodelling
Clinical course
chest tightness, wheezing, dyspnea, cough +/- sputum
status asthmaticus
increase in airflow obstruction, difficulty with exhalation

17

Bronchiectasis

Permanent destruction and dilatation of the airways associated with severe infections or obstructions:
Aetiology: CF, kartageners, post infectious: TB, measles, bronchial obstruction eg TB/FB
Morphology: dilated, inflamed airways.
Clinical course: persistent cough, purulent sputum +++, haemoptysis,

18

Restrictive lung disease

Heterogenous group of diseases
Characterised by inflammation and fibrosis of the pulmonary connective tissue (eg interstitium of the alveolar walls)
most common causes- sarcoidosis and occupational/environmental

19

Restrictive lung disease - morphology and clinical features

Morphology
Xray: bilateral infiltrative lesions - small nodules, irregular lines, ground-glass shadows
Scarring and gross destruction of the lung - end-stage/honeycomb lung
Clinical features
dyspnea, tachypnea, end-inspiratory crackles,
eventual cyanosis, without wheezing
reductions in gas diffusing capacity, lung volume, and compliance
May lead to secondary pulmonary hypertension and right-sided heart failure with cor pulmonale

20

Pulmonary Embolism

Blockage of a main or branch pulmonary artery by an embolus –
Usual source of emboli are deep venous thrombi of the leg (95% of cases)
Pathophysiology: respiratory compromise and haemodynamic compromise

21

Pulmonary embolism - morphology and clinical course

Morphology
central/peripheral emboli
pulmonary haemorrhage
pulmonary infarction
Clinical course
abrupt onset pleuritic chest pain,
shortness of breath
hypoxia
increased pulmonary vascular resistance –
right ventricular failure

22

Pulmonary oedema

Accumulation of fluid in the air spaces and parenchyma of the lungs
- Haemodynamic oedema
Increased venous pressure
Eg left ventricular failure
Decreased oncotic pressure
Eg nephrotic syndrome
Liver failure
- Oedema due to alveolar injury
infections
Shock/trauma
- Oedema of undetermined origin
Eg neurogenic/high altitude

23

Pulmonary oedema - morphology and clinical features

Morphology
initial fluid accumulation in basal regions – dependent oedema
engorged alveolar capillaries, intra-alveolar granular pink precipitate
alveolar microhaemorrhages, hemosiderin-laden macrophages
heavy, wet lungs
Clinical features
SOB, pink frothy sputum, characteristic CXR findings

24

Pneumothorax

Pneumothorax
Air in the pleural cavity
Associated with ephysema, asthma, TB, trauma, idiopathic

25

Atelectasis

Incomplete expansion of lungs
Reduces oxygenation and predisposes to infection
reversible

26

Respiratory failure Type 1

Type I -Hypoxia with a normal or low PCO2
Pneumonia
Pulmonary oedema
Asthma
PE
Pulmonary fibrosis
ARDS

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ARDS

Acute respiratory distress syndrome (ARDS) is a life-threatening medical condition where the lungs can't provide enough oxygen for the rest of the body

28

Respiratory failure Type 2

Type II -Hypoxia with high PCO2
Asthma, COPD, OSA
Reduced respiratory drive
Neuromuscular disease
Thoracic wall disease eg kyphoscoliosis

29

OSA

Obstructive sleep apnoea (OSA) is a condition where the walls of the throat relax and narrow during sleep, interrupting normal breathing