Pulmonary vascular disease and pleural disease Flashcards

1
Q

What makes up the duel supply for pulmonary circulation?

A

pulmonary arteries

bronchial arteries

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2
Q

Low pressure systems

A

Thin walled vessels

low incidence of atherosclerosis

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3
Q

what is Pulmonary oedema and what does it cause?

A

accumulation of fluid in the lung in the interstitium and alveolar spaces
Can cause a restrictive pattern of disease

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4
Q

What causes Pulmonary oedema?

A

Haemodynamic (increase in hydrostatic pressure)
Due to cellular injury (alveolar lining cells or alveolar endothelium), localised - pneumonia, generalised - adult respiratory distress syndrome

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5
Q

What is ARDS (Adult respiratory distress syndrome)

A

Diffuse alveolar damage syndrome (DADS)

Shock lung - causes include sepsis, diffuse infection, severe trauma, oxygen

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6
Q

what is the pathogenesis of ARDS

A
Injury (eg: bacterial endotoxin)
infiltration of inflammatory cells
cytokines
oxygen free radicals
injury to cell membranes
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7
Q

what is the pathology of ARDS

A

Fibrinous exudate lining alveolar walls (hyaline membranes)
Cellular regeneration
Inflammation

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8
Q

outcome of ARDS

A

death
resolution
fibrosis (chronic restrictive lung disease)

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9
Q

neonatal RDS

A

Premature infants
Deficient in surfactant (type 2 alveolar lining cells)
Increased effort in expanding lung - physical damage to cells

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10
Q

What is an embolus

A

A detached intravascular mass carried by the blood to a site in the body distant from its point of origin

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11
Q

What are most types of emboli

A

Thrombi

others include: gas, fat, foreign bodies and tumour clumps

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12
Q

example: pulmonary embolus

A

Common, often subclinical, an important cause of sudden death and pulmonary hypertension
most of these emboli are thromboemboli

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13
Q

source of most pulmonary emboli

A

deep venous thrombosis (DVT) of lower limbs

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14
Q

Risk factors for PE (same for DVT)

A
  1. Factors in vessel wall (Eg: endothelial hypoxia)
  2. abnormal blood flow (venous stasis)
  3. Hypercoagulable blood (cancer patients, post-MI etc.)
    Virchow’ triad
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15
Q

What is Virchow’s triad

A

The 3 factors for PE

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16
Q

Effects of PE

A

Sudden death
Severe chest pain/dyspnoea/haemoptysis
Pulmonary infarction
pulmonary hypertension

17
Q

Effects of PE depend on

A

Size on embolus
cardiac function
respiratory function

18
Q

pulmonary infarct (ischaemic necrosis)

A

embolus necessary but not sufficient

bronchial artery supply compromised (eg in cardiac failure)

19
Q

pulmonary hypertension

A

primary (rare, young women)

Secondary

20
Q

mechanisms of pulmonary hypertension

A

Hypoxia (vascular constriction)
increased flow through pulmonary circulation (congenital heart disease)
blockage (PE) or loss (emphysema) of pulmonary vascular bed
back pressure from left sided heart failure

21
Q

morphology of pulmonary hypertension

A
medial hypertrophy of arteries
intimal thickening (fibrosis)
atheroma
right ventricular hypertrophy
extreme cases (congenital heart disease etc.)
22
Q

Cor pulmonale

A

pulmonary hypertension complicating lung disease
Right ventricular hypertrophy
Right ventricular dilatation
Right heart failure

23
Q

what is the pleura

A

a mesothelial surface lining the lungs and mediastinum
mesothelial cells designed for fluid absorption
hallmark of disease is the effusion

24
Q

types of pleural effusion

A

transudate (low protein)

Exudate (high protein)

25
examples of transudate pleural effusions
cardiac failure | hypoproteinaemia
26
examples of exudate pleural effusions
pneumonia TB connective tissue disease malignancy (primary or metastatic)
27
purulent effusion
full of acute inflammatory cells empyema can become chronic
28
pneumonthorax
air in pleural space due to trauma or rupture of bulla
29
pleural neoplasia
primary (benign or malignant mesothelioma) or secondary (common- adenocarcinomas - lung, GIT, ovary)
30
mesothelioma
Asbestos related Increasing incidence Mixed epithelial/mesenchymal differentiation Dismal prognosis
31
differential diagnosis of malignant effusions
cytology, biopsy difficult immunohistochemistry for lineage specific antigens may help medicolegal importance