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week 6 resp > Pulmonary vascular disease and pleural disease > Flashcards

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
Q

examples of transudate pleural effusions

A

cardiac failure

hypoproteinaemia

26
Q

examples of exudate pleural effusions

A

pneumonia
TB
connective tissue disease
malignancy (primary or metastatic)

27
Q

purulent effusion

A

full of acute inflammatory cells
empyema
can become chronic

28
Q

pneumonthorax

A

air in pleural space due to trauma or rupture of bulla

29
Q

pleural neoplasia

A

primary (benign or malignant mesothelioma) or secondary (common- adenocarcinomas - lung, GIT, ovary)

30
Q

mesothelioma

A

Asbestos related
Increasing incidence
Mixed epithelial/mesenchymal differentiation
Dismal prognosis

31
Q

differential diagnosis of malignant effusions

A

cytology, biopsy
difficult
immunohistochemistry for lineage specific antigens may help
medicolegal importance

week 6 resp (6 decks)

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