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Respiratory Pathology Flashcards

1
Q

What is rhinitis?

A
  • Inflammation of the nasal mucosa.
  • May be acute of chronic.
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2
Q

Describe the aetiology of acute rhinitis.

A
  • Acute rhinitis is either:
    • Infective
    • Allergic
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3
Q

Describe infectious rhinitis.

A
  • Usually viral.
  • Virally-induced inflammation of the surface epithelial cells is followed by exudation of fluid and mucus from the damaged surface (‘runny nose’).
  • Later, submucosal oedema produces swelling, which may lead to a partial blockage of the nasal airways.
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4
Q

Describe allergic rhinitis.

A
  • Type 1 (IgE mediated) hypersensitivity reaction to inhaled materials, producing a mixed serous-mucous exudate and submucosal oedema leading to nasal blockage.
  • Eosinophils are prominant in the inflammatory infiltrate.
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5
Q

What is chronic rhinitis?

A
  • Chronic rhinitis can be caused by repeated attacks of acute rhinitis, which often develop a secondary bacterial infection.
  • It may result in the development of nasal polyps.
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6
Q

What is sinusitis?

A
  • Inflammation of the paranasal sinuses, usually secondary to acute or chronic rhinitis.
    • Usually results in the inflammation of the sinus linings; swelling of the mucosa around the drainage foramen of the maxillary sinus secretions.
    • Stasis predisposes to secondary bacterial infection with alteration of the static maxillary fluid from seromucous to purulent.
  • Chronic sinusitis is characterised by chronically thickened and inflammed mucosa of the sinuses and by persistent fluid accumulation.
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7
Q

What are Wegener’s granulomatosis?

A

Autoimmune granulomatosis vasculitis which frequently presents with nasal lesions.

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8
Q

What is acute laryngitis?

A
  • Acute inflammation of the larynx which may be caused by viruses, bacteria, irritants (cigarette smoke), mechanical factors (endotracheal intubation), or overuse of the voice.
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9
Q

What is the sequeale of acute laryngitis?

A
  • Resolution - infective causes typically resolve without complications.
  • Spread of infection may occur throughout the respiratory tract with the development of tracheobronchitis, bronchopneumonia or lung abscesses; this is more common in the elderly or debilitated due to poor cough reflex.
  • Airway obstruction - laryngeal oedema can result in a life-threatening narrowing of the airway especially in children suffering from H. influenza epiglottitis or in cases of corrosive chemical ingestion.
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10
Q

What is chronic laryngitis?

A
  • Chronic inflammation of the larynx is most commonly seen in heavy cigarette smokers.
  • It may lead to a permanent thickening of the laryngeal mucosa and submucosa, particularly where there is associated excess production of keratin (smokers keratosis).
  • Overlying epidermis may also undergo keratotic thickening with dysplastic change in the basal layer; this is a predisposing factor in the development of squamous carcinoma of the larynx.
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11
Q

What is acute laryngotracheobronchitis?

A
  • Croup
  • Croup is a life-threatening acute inflammation and obstruction of the respiratory tract involving the larynx, trachea and epiglottis.
  • Typically caused by viral infection.
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12
Q

What is atelectasis?

A
  • A defective expansion and collapse of the lung. It may occur as a result of:
    • Obstruction
    • Compression
    • Scarring
    • Surfactant loss
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13
Q

What are the obstructive causes of atelectasis?

A
  • Obstruction of the larger bronchial tubes leads to resorption of air from the lung distal to the obstruction.
  • Causes of obstruction can be within the lung (e.g. mucous plugs in bronchiectasis, inhaled foreign bodies) or outside the lung (enlarged lymph nodes as in tuberculosis or lung cancer).
  • Patchy atelectasis describes the pattern of atelectasis associated with chronic obstructive airway diseases.
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14
Q

What are the compressive causes of atelectasis?

A
  • Compressive atelectasis is the compression of the lung caused by the accumulation of fluid or air in the pleural cavity e.g. following a pneumothorax.
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15
Q

What are obstructive lung diseases?

A
  • Obstructive lung diseases are those in which there is obstruction to the flow of air within the lungs, although the lungs themselves may be hyperinflated.
  • Disorders include emphysema, chronic bronchitis, bronchiectasis and asthma.
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16
Q

What is COPD?

A
  • Emphysema and chronic bronchitis which occur together, almost always as the result of long-term cigarette smoking.
  • It is a chronic, slowly progressive disease of airflow limitation caused by an abnormal inflammatory response of the lungs to noxious substances.
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17
Q

What are restrictive lung diseases?

A
  • Restrictive lung diseases are those in which there is obstruction to the expansion of the lungs (e.g. due to fibrosis or oedema) such that they can only take in a limited amount of air.
  • In these diseases, although the lungs are often underinflated, the rate of air flow is unaffected.
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18
Q

Describe the pathological changes which occur in COPD.

A
  • Chronic bronchitis - this causes hyperplasia of the bronchial submucosal glands, leading to an increased Reid index.
  • Emphysema - abnormal dilation of the air spaces with destruction of alveolar walls.
  • Bronchiolitis - this describes inflammation of the small airways (bronchioles).
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19
Q

What is emphysema?

A
  • Emphysema is permanent dilation of any part of the air spaces distal to the terminal bronchiole, occuring with tissue destruction but without fibrosis.
  • Usually COPD but may occasionaly present alone.
  • Risk factors are the same as for COPD.
  • The inherited disorder α1-antitrypsin deficiency predisposes to early emphysema.
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20
Q

Describe the pathogenesis of emphysema.

A
  • In normal individuals, extracellular elastases secreted into the lungs by inflammatory cells are inhibited by protease inhibitors (particularly α1-antitrypsin).
  • In emphysema, these inhibitors are either inactivated (e.g. by cigarette smoke) or absent (inherited disorder), resulting in continued activity of the elastases with destrution of lung parenchyma.
  • Destruction of respiratory tissue leads to a loss of elastic recoil in the lungs and a decreased area available for gaseous exchange.
  • About 1/3 of lung capacity must be destroyed before clinical symptoms of emphysema appear.
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21
Q

What is chronic bronchitis?

A
  • Defined as a cough productive of sputum on most days for 3 months of the year for at least 2 successive years.
  • It typically affects middle-aged men and normally forms part of COPD, most cases are due to cigarette smoking.
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22
Q

Describe the pathogenesis of chronic bronchitis.

A
  • Constant irritation by cigarette smoke causes chronic inflammation of the respiratory bronchioles (bronchiolitis) and increased mucous secretion.
  • Hypersecretion of mucous is associated with hyperplasia of the submucosal mucous-secreting glands.
  • Proteases stimulate this hypersecretion following their release by neutrophils recruited as part of the inflammatory response.
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23
Q

What is the Reid index?

A

The Reid index gives the ratio of gland to wall thickness in the bronchus, and it is significantly increased in cases of chronic bronchitis.

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24
Q

What is asthma?

A

Asthma is increased iritability of the bronchial tree with paroxysmal narrowing of the airways, which may reverse either spontaneously or after treatment with bronchodilators.

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25
Q

Describe the pathogenesis of asthma.

A
  • There are 3 key features in both types of asthma (atopic and non-atopic):
    • Airflow limitation - obstruction is caused by a combination of bronchospasm, oedema and mucous plugging. This may be spontaneously reversible, or reversible with bronchodilator treatment.
    • Airway hyper-responsiveness to bronchoconstrictor trigger factors.
    • Airway inflammation - it appears that the allergic inflammation process of extrinsic (atopic) asthma is driven by type 2 helper T cells (Th2). With time, airway remodelling occurs so that the smooth muscles of the bronchial wall become hypertrophied, increasing airflow limitation.
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26
Q

Describe the structural changes which occur in asthma.

A
  • Immune cell infiltration - the bronchial mucosa is infiltrated by eosinophils, mast cells, lymphoid cells nd macrophages.
  • Mucosal oedema - extravasation of plasma into submucosal tissues produces a narrowing of the airways.
  • Mucous hypersecretion leads to plugging of airways.
  • Hypertrophy of bronchial smooth muscle due to recurrent bronchoconstriction.
  • Focal necrosis of the airway epithelium, caused by prolonged inflammation.
  • Deposition of collagen beneath the bronchial epithelium in long-standing cases.
  • Sputum contains Charcot-Leyden crystals (derived from eosinophil granules) and Curschmann’s spirals (composed of mucous plugs from small airways).
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27
Q

What is cor pulmonale?

A

Pulmonary vasoconstriction caused by chronic alveolar hypoventilation results in pulmonary hypertension leading to right ventricular hypertrophy.

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28
Q

What is bronchiectasis?

A
  • There is irreversible dilataion of the bronchi or their branches. It is causes are:
    • Congenital - CF, primary ciliary dyskinesia.
    • Acquired - infection (especially whooping cough, necrotising pneumonia or measles in childhood) and obstruction (either by inhaled foreign body or by tumour).
  • Widened bronchi are more prone to infections.
  • Patients often cough up purulent sputum, which may contain blood.
29
Q

What is cystic fibrosis?

A
  • Hereditary multisystem disease characterised by the production of abnormally thick mucous, and primarily affects the lung and the pancreas.
  • Autosomal recessive mode of inheritance.
30
Q

Describe the pathogenesis of cystic fibrosis.

A
  • The mutated gene is found on chromosome 7 and encodes for a protein termed the cystic fibrosis transmembrane regulator (CFTR).
  • In CF, defective CFTR results in impaired chloride transport, which prevents the release of sodium and water to liquefy mucous.
  • The net result is the production of extremely thick and viscous mucous by the exocrine glands.
  • The epithelial dysfunction of CF affects the following systems:
    • Bronchi - abnormally viscid mucous cannot be cleared from the lungs.
    • Intestine - causing meconium ileus in newborn babies and distal intestinal obstruction syndrome later in life.
    • Pancreas - causing deficiency of the pancreatic enzymes, resulting in malabsorption and failure to thrive.
    • Liver - causing biliary cirrhosis.
    • Vas deferens - failure to develop leads to male infertility.
31
Q

In cystic fibrosis the respiratory tract, the bronchi and bronchioles become obstructed by abnormally viscid mucous, which leads to 4 main problems. What are they?

A
  1. Infections - obstruction and stagnation of secretions leads to repeated bouts of infection, particularly with S. aureus.
  2. Bronchiectasis - frequent complication.
  3. Hyperinflation of the lungs due to air trapping behind mucin plugs; increased risk of developing spontaneous pneumothorax.
  4. Hypoxia, scarring and destruction of the pulmonary vascular bed, leadog to pulmmonary hypertension and cor pulmonale.
32
Q

What are interstitial lung diseases?

A
  • A group of non-infectious, non-malignant disorders in which there is inflammation of the alveolar walls with a thickening of the interstitium between the alveoli, usually with fibrosis.
  • This large group of diseases occurs with a mainly restrictive pattern.
  • Most important interstitial lung diseases:
    • Idiopathic pulmonary fibrosis
    • The pneumoconioses
      • Coal-worker’s pneumoconiosis
      • Silicosis
      • Asbestosis
    • Sarcoidosis
33
Q

Describe the basic pathogenesis of the pneumoconioses.

A
  • This is a group of interstitial lung diseases resulting from chronic exposure to inorganic dust.
  • In the normal lung, inhaled dust is coughed out, or ingested by macrophages.
  • However, if the dust is toxic to macrophages there is local inflammation, secretion of cytokines and stimulation of fibrosis.
  • The end result is a restrictive pattern of respiratory dysfunction.
34
Q

What is pneumonia?

A
  • Pneumonia is defined as the infection of alveolar tissue resulting in the consolidation of lung tissue with an intra-alveolar inflammatory exudate.
35
Q

What are the predisposing factors for pneumonia?

A

Immunosuppression

Neurological impairment of the cough reflex

Secretion retention

Pulmonary oedema

Impaired mucociliary clearance

Respiratory tract infection (viral)

Antiobiotics and cytotoxics

Tracheal instrumentation

Impaired alveolar macrophages

Other

Neoplasia

36
Q

What is bronchopneumonia?

A
  • Infection is centred on the bronchi but with the extension of the inflammatory exudate into the alveoli, causing patchy consolidation of the lung (lobar distribution).
  • Often hospital-acquired due to underlying disease.
37
Q

Describe the pathogenesis of bronchopneumonia.

A
  • Patients develop retention of secretions, which gravitate to dependent parts of the lungs and become infected, hence bronchopneumonia most commonly involves lower lobes.
  • Macroscopically, multiple areas of consolidation usually occur distributed bilaterally around bronchi / bronchioles in dependent parts of the lung.
  • Affected areas are firm and airless and have dark red or grey appearance.
  • Bronchial mucosa is inflammed and pis may be present in the more peripheral bronchi.
  • Patchy collapse is associated with bronchial obstruction.
  • Involvement of the pleura is common with purulent pleuritis.
  • Microscopically, there is acute inflammation of the bronchi and bronchioles with an acute inflammatory neutrophil-rich exudate present in the lumina and extending into the peribronchial alveoli.
38
Q

What are the complications and sequelae of bronchopneumonia?

A
  • Resolution - complete resolution occurs only if treatment is instituted early, before the onset of structural damage.
  • Bronchial damage - imperfect repair of the bronchial mucosa results in scarring of the bronchial wall, with increased predisposition to further infection and to bronchiectasis.
  • Lung fibrosis - inflammatory exudate is often not completely absorbed but is organised with residual fibrous scarring.
  • Lung abscesses - single or multiple areas of suppurationa.
  • Empyema - pus in the pleural cavity as a result of extension of infection into the pleaural cavity.
  • Pericarditis - direct extension of infection to the pericardium.
  • Death - very common cause of death, particularly as a terminal manifestation of debilitating diseases.
39
Q

What is lobar pneumonia?

A
  • Uniform or homogenous consolidation of part of a lobe or of the whole lobe caused by infection.
  • Often called streptococcus pneumoniae.
40
Q

Describe the pathogenesis of lobar pneumonia.

A
  • Organisms gain entry to distal air spaces without colonisation of bronchi.
  • Infection spreads rapidly through the alveolar spaces and bronchioles, causing acute inflammatory exudation into air spaces.
  • Macroscopically, the whole lobe becomes consolidated and airless.
  • Microscopically, the alveoli are filled with an acute inflammatory exudate, which is limited by the pulmonary fissures.
41
Q

What are the 4 pathological stages of lobar pneumonia?

A
  1. Congestion - outpouring of protein-rich exudate into the alveolae.
  2. Red hepatisation - massive accumulation of red cells and polymorphs in the alveolar spaces, giving a liver-like consistency.
  3. Grey hepatisation - accumulation of fibrin in the lung spaces with red-cell disintegration.
  4. Resolution - most patients recover with their lungs returning to normal structure and function.
42
Q

What are the complications and sequelae of lobar pneumonia?

A
  • Lung fibrosis - inflammatory exudate is often not completely absorbed but is organised with residual fibrous scarring and permanent lung dysfunction.
  • Bacteraemia - bacterial dissemination of organisms can lead to septicaemia with meningitis, arthritis, endocarditis or pyemic abscesses.
  • Lung abscesses - single or multiple areas of suppuration.
  • Empyema - pus in the pleural cavity as a result of extension of infection into the pleural cavity.
  • Pleural effusion - non-infected effusion is common.
  • Death
43
Q

What is primary atypical pneumonia?

A
  • This is an inflammation of the alveolar septa by inflammatory cells (acute interstitial pneumonia) in the absence of any consilidation.
  • Patients develop fever, dry cough and dyspnoea, but there is little sputum and few signs of consolidation.
44
Q

What is pulmonary tuberculosis?

A

Chronic granulomatous infection of the lung caused by myobacterium tuberculosis.

45
Q

Describe the spread of pulmonary tuberculosis.

A
  • Inhalation of myobacterium tuberculosis in the form of droplets (most common).
  • Ingestion of food or milk.
  • Inoculation of the skin.
  • Transplacental spread (i.e. congenital TB).
46
Q

What are the predisposing factors for pulmonary tuberculosis?

A
  • Close contact with infected individuals.
  • Immunosuppression.
  • Malnourishment.
  • Other diseases.
47
Q

Describe the sequence of pathogenesis in primary atypical pneumonia.

A
  • 0-10 days - myobacteria excite a transient but marked acute inflammatory response. Neutrophils phagocytose the organisms but are unable to deestroy them, as the cell walls are resistant to degradation. Instead, engulfed bacteria are drained into local lymph nodes.
  • After 10 days - development of T-cell-mediated immune response (type IV hypersensitivity reaction) to the bacilliary cell wall constituents results in cytokine release and macrophage activation. Gradually, a chronic inflammatory pattern develops, which is dominated by aggregates of macrophages called epithelioid cells, which form variable numbers of granulomas with a central core of necrotic caseous tissue containing variable myobacteria. TB granulomas are termed tubercles.
48
Q

Describe the macroscopic and microscopic appearance of TB granulomas.

A
  • Macroscopically:
    • ​the granulomas appear as pinhead-sized white or greyish foci (tubercles) in the tissues.
  • Microscopically:
    • ​granulomas are the histological hallmark of TB infection.
    • A granuloma consists of an amorphous caseous necrosis, surrounded by 3 cellular layers:
    1. An inner layer of activated macrophages (epithelioid cells) with Langerhans’ giant cells.
    2. A middle layer of lymphocytes.
    3. An outer layer of fibroblastic tissue, which merges with surrounding structures and increases with the age of the lesion.
49
Q

What is primary tuberculosis?

A
  • The first encounter with the organism, resulting in the development of a small parenchymal peripheral focus with a large response in the draining lymph nodes.
  • Inhaled organisms proliferate in the alveoli at the periphery of the lung, often, often just beneath the pleura.
  • This primary parenchymal tubercle is termed the Ghon focus.
  • It is often associated with enlarged caseous hilar lymph nodes.
  • The combination of lung and lymph node lesions together constitutes the primary complex or Gohn complex.
50
Q

What is secondary tuberculosis?

A
  • Occurs as a result of the reactivation of a quiescent but viable myobacteria in hosts with weakened immune responses, or as a result of reinfection by additional organisms.
  • Reinfection occurs in 5-10% of those with latent infection, usually in the lungs.
  • Caseous granulmoas typically develop in the apical segments of the lungs, spreading directly and locally but without lymph node lesions.
  • The initiating apical lesion is often called Assmann focus, and it is histologically similar to te Gohn focus.
51
Q

What is pulmonary fibrosis?

A

Lung lesions typically heal with fibrosis, which may be extensive, producing localised honeycombing. This is common in relapsing and progressive untreated disease.

52
Q

What are the 4 main types of bronchogenic (lung) carcinoma?

A
  1. Squamous cell carcinoma - 35%
  2. Small cell carcinoma - 20%
  3. Adenocarcinoma - 30%
  4. Large cell anaplastic carcinoma - 15%
  • Tumours may be central (all types) or peripheral (mainly adenocarcinomas).
53
Q

What are the routes of spread of lung carcinoma?

A
  • Local - central tumours invade locally either through the bronchial wall into the surrounding lung or along the outside of the bronchi (peribronchial spread) to distant parts of the lung. Direct extension into pleura and and adjacent mediastinal structures is a feature of advanced disease. Apical lung tumours (Pancoast tumours) may invade local sympathetic ganglia and produce Horner’s syndrome (ptosis, miosis and anhydrosis).
  • Lyphatic spread - carcinomas spread to the ipsilateral and contralateral peribronchial and hilar lymph nodes. Compression of adjacent tissues by infiltrated nodes may then cause symptoms.
  • Transcoelomic spread - tumour cells may seed within the pleural cavity, causing a malignant pleural effusion.
  • Haematogenous spread - most commonly to the brain, bone, liver, adrenal glands and skin.
54
Q

What is pulmonary oedema?

A

Pulmonary oedema is defined as an increase in extravascular fluid in the alveolar walls (pulmonary interstitium), which, if severe, subsequently affects alveolar spaces.

55
Q

Describe the pathogenesis of pulmonary congestion and oedema.

A
  • Normally, a balance exists between hydrostatic pressure and colloid osmotic (oncotic) pressure such that only a small amount of fluid passes into the interstitium.
  • This fluid is drained from the lung via lymphatic channels.
  • Pulmonary oedema can result from increased hydrostatic pressure (left ventricular failure) or increased alveolar capillary permeability (inflammatory alveolar reactions) where the lymphatic drainage capacity is exceeded, resulting in a net accumulation of fluid within the interstitium.
  • Macroscopically, the lungs are heavy and congested. In fatal cases, fluid flows from the cut surfaces and it can often be seen in the large airways.
  • Microscopically, the interstitium is widened, the capillaries are congested and the alveoli are filled with proteinaceous fluid.
56
Q

What is acute respiratory distress syndrome?

A

ARDS is a clinical syndrome of diffuse alveolar capillary damage, characterised by pulmonary exudation and oedema with widespread systemic metabolic derangements.

57
Q

What is a pulmonary embolism?

A

PE is the occlusion of a pulmonary artery, most commonly by thromboemboli originating in the systemic veins.

58
Q

Describe the pathogenesis of pulmonary congestion and oedema.

A
  • Normally, a balance exists between hydrostatic pressure and colloid osmotic (oncotic) pressure such that only a small amount of fluid passes into the interstitium.
  • This fluid is drained from the lung via lymphatic channels.
  • Pulmonary oedema can result from increased hydrostatic pressure pressure (left ventricular failure) or increased alveolar capillary permeability (inflammatory alveolar reactions) where the lymphatic drainage capacity is exceeded, resulting in a net accumulation of fluid within the interstitium.
  • Macroscopically, the lungs are heavy and congested. In fatal cases, fluid flows from the cut surfaces and it can often be seen in the large airways.
  • Microscopically, the interstitium is widened, the capillaries are congested and the alveoli are filled with proteinaceous fluid.
59
Q

Describe pulmonary infarction.

A
  • Infarction of the lung tissue is usually associated with embolism. The lower lobes are involvd in 75% of cases.
  • Macroscopically, pulmonary infarcts are typically haemorrhagic (because of blood entering from the bronchial circulation) and wedge-shaped, and there is often an associated pleural reaction, which causes chest pain.
  • With time, the infarct becomes organised to form a fibrous scar.
  • Microscopically, there is extravasation of blood into the necrotic lung.
60
Q

What are the common sequelae of pulmonary infarction?

A
  • Pulmonary dysfunction due to loss of lung tissue.
  • Pulmonary vascular obstruction leading to right heart failure (cor pulmonale).
  • Pleurisy and pleural effusion.
  • Healing, with fibrous scarring.
  • Septic infarction due to either a primary septic embolism or secondary infection leading to abscess formation.
61
Q

Describe the irreversible structural changes caused by pulmonary hypertension.

A
  • Pulmonary vasculature - medial hypertrophy of the muscular arteries (increased smooth muscle) and pulmonary veins (arterialisation); occlusion of the pulmonary arteries caused by intimal proliferation.
  • Lungs - interstitial fibrosis.
  • Right side of the heart - increased workload of the right side of the heart causes ultimate development of right heart failure (cor pulmonale).
62
Q

Describe serofibrinous pleuritis.

A
  • Acute inflammation of the pleura which is accompanied by an accumulation of high-protein fluid (30g protein /L) containing fibrinogen / fibrin between the pleural surfaces.
  • The condition is commonly due to infection, infarction or tumour.
63
Q

Describe the pathogenesis of serofibrinous pleuritis.

A
  • Effusion is the result of movement of fluid through damaged vessel walls.
  • In serofibrinous pleuritis, the effusion is typically unilateral, with the pleural surface covered by a fibrinous exudate.
  • The fluid consists of a straw-coloured fibrinous fluid containing mesothelial cells, lymphocytes and polymorphs.
  • In neoplastic diseases, malignant cells can also be identified within the pleural field.
64
Q

What are the common sequelae of serofibrinous pleuritis?

A
  • Atelectasis - compression of the lungs causes pulmonary collapse and respiratory impairment.
  • Adhesions - formation of fibrous adhesions between the visceral and parietal pleura.
  • Fibrosis - obliteration of the pleural space by fibrosis, which is common in long-standing effusions.
  • Empyema
65
Q

What is suppurative pleuritis?

A
  • Empyema.
  • Acute inflammation of the pleura with accumulation of pus in the pleural cavity.
  • Typically caused by pulmonary infection (pneumonia, TB, lung abscess), it can also complicate thoracic surgery or penetrating chest wall injury.
66
Q

What are the common sequelae of empyema?

A
  • Septicaemia (haematogenous spread of infection to other organs).
  • Atelectasis (lung collapse as a result of compression).
67
Q

What is haemorrhagic pleuritis?

A

Acute inflammation of the pleura which occurs with the accumulation of blood-stained exudate and is often caused by tumour or pulmonary infarcts.

68
Q

What is a hydrothorax?

A
  • A type of non-inflammatory pleural effusion.
  • Collection of low-protein fluid (<30g protein / L) which is due to the movement of excess fluid through normal vessel walls.
  • Common causes are:
    • Cardiac failure (most common) - increased hydrostatic pressure in pulmonary hypertension.
    • Hypoalbuminaemia - decreased oncotic pressure.
  • Effusions are usually bilateral and the pleural surface appears normal. Fluid is straw coloured and contains occasional lymphoctes and mesothelial cells.
  • The condition can cause pulmonary collapse (compression of the lungs causing respiratory impairment) or it may resolve completely (resorption of fluid on correction of the cause with no structural alterations).
69
Q

What is a haemothorax?

A
  • Bleeding into the chest is called haemothorax.
  • It is most commonly the result of:
    • Trauma, especially with rib fractures
    • Surgery
    • Pulmonary infarction
    • Spontaneous rupture of diseased arteries e.g. atheromatous and dissecting aortic aneurysm.
  • If blood remains within the plerual cavity. Air that enters the cavity in inspiration is unable to escape during expiration.

Respiratory (13 decks)

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