Lecture 3 Vascular and Pleural

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Transcript Lecture 3 Vascular and Pleural

1.Pulmonary Vascular Disease
2.Pleural Disease
Prof. Frank Carey
Pulmonary Circulatuion
 Dual


supply
Pulmonary arteries
Bronchial arteries
 Low
pressure system
 Pulmonary artery receives entire cardiac
output (a filter)
Low pressure system….
 Thin
walled vessels
 Low incidence of atherosclerosis
At normal pressures
Pulmonary Oedema
 Accumulation


of fluid in the lung
Interstitium
Alveolar spaces
 Causes
a restrictive pattern of disease
Pulmonary Oedema (causes)
Haemodynamic ( hydrostatic pressure)
Due to cellular injury
1.
2.
Alveolar lining cells
ii.
Alveolar endothelium
Localised – pneumonia
Generalised – adult respiratory distress syndrome
(ARDS)
i.
ARDS
 Diffuse
alveolar damage syndrome (DADS)
 Shock lung

Causes include sepsis, diffuse infection (virus,
mycoplasma), severe trauma, oxygen
Pathogenesis of ARDS
Injury (eg bacterial endotoxin)
 Infiltration of inflammatory cells
 Cytokines
 Oxygen free radicals
 Injury to cell membranes
Pathology of ARDS
 Fibrinous
exudate lining alveolar walls
(hyaline membranes)
 Cellular regeneration
 Inflammation
ARDS with hyaline membrane
ARDS – cellular reaction
Outcome of ARDS
 Death
 Resolution
 Fibrosis
(chronic restrictive lung disease
Neonatal RDS
 Premature
infants
 Deficient in surfactant (type 2 alveolar
lining cells
 Increased effort in expanding lung
physical damage to cells
Embolus
 A detached
intravascular mass carried by
the blood to a site in the body distant from
its point of origin
 Most emboli are thrombi – others include
gas, fat, foreign bodies and tumour clumps
Pulmonary Embolus
 Common
 Often
subclinical
 An important cause of sudden death and
pulmonary hypertension
95% + of emboli are thromboemboli
Source of most pulmonary
emboli…..
 Deep
limbs
venous thrombosis (DVT) of lower
Risk factors for PE are those for DVT….
1.
2.
3.
Factors in vessel wall (eg endothelial
hypoxia)
Abnormal blood flow (venous stasis)
Hypercoaguable blood (cancer patients,
post-MI etc)
- Virchow’s triad
Effects of PE
 Sudden
death
 Severe chest pain/dyspnoea/haemoptysis
 Pulmonary infarction
 Pulmonary hypertension
Effects of PE depend on…
 Size
of embolus
 Cardiac function
 Respiratory function
Effect of embolus size…

Large emboli



Death
Infarction
Severe symptoms

Small emboli


Clinically silent
Recurrent
pulmonary
hypertension
Pulmonary Infarct (ischaemic
necrosis)
 Embolus
necessary but not sufficient
 Bronchial artery supply compromised (eg in
cardiac failure)
Pummonary Embolus
Pulmonary infarct – tumour embolus
Pulmonary Hypertension
 Primary
(rare, young women)
 Secondary
Pulmonary Hypertension
(mechanisms)
 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
Morphology of pulmonary
hypertension
 Medial
hypertrophy of arteries
 Intimal thickening (fibrosis)
 Atheroma
 Right ventricular hypertrophy
 Extreme cases (congenital heart disease,
primary pulmonary hypertension) –
plexogenic change/necrosis
Pulmonary artery – intimal fibrosis
Plexiform lesion – primary pulmonary
hypertension
“Cor Pulmonale”
 Pulmonary
hypertension complicating lung
disease
 Right ventricular hypertrophy
 Right ventricular dilatation
 Right heart failure (swollen legs, congested
liver etc)
Cardiomegaly due to right ventricular
dilatation
Right ventricular hypertrophy and
dilatation
The Pleura
 A mesothelial
surface lining the lungs and
mediastinum
 Mesothelial cells designed for fluid
absorption
 Hallmark of disease is the effusion
Pleural Effusion

Transudate (low
protein)


cardiac failure
hypoproteinaemia

Exudate (high protein)




pneumonia
TB
connective tissue
disease
malignancy (primary
or metastatic)
Pleural effusion
Purulent Effusion
Full of acute inflammatory cells
 Empyema
 Can become chronic
Pneumothorax
Air in pleural space
 Trauma
 Rupture of bulla
Large bullae
Pleural Neoplasia
 Primary


benign (rare)
malignant mesothelioma
 Secondary

common (adenocarcinomas - lung, GIT, ovary)
Mesothelioma
 Asbestosis
related
 Increasing incidence
 Mixed epithelial/mesenchymal
differentiation
 Dismal prognosis
Mesothelioma
Pleural biopsy - mesothelioma
Metastases in Pleura
Differential diagnosis of
malignant effusions…..
 Cytology,
biopsy
 Difficult
 Immunohistochemistry
for lineage specific
antigens may help
 Medicolegal importance