Week 14 Pathology - Lungs II

Question 1

What is pneumonia defined as?

Answer 1

Any infection in the lungs, which can present as 1 of 2 radiographic patterns

1. Lobar pneumonia (affected contiguous airspaces)
2. Bronchopneumonia (distribution of inflammation involving >1 lobe, usually initial infection of bronchi and bronchioles with extension into the alveoli –> most frequently bilaterally lower lobes

Question 2

What is the pathogenesis of pneumonia?

Answer 2

Attachment of organism to respiratory epithelium followed by necrosis of the cells and inflammatory response, which when occurring in the alveoli causes interstitial inflammation

Question 3

What lobe is most commonly affected in CAP?

Answer 3

R middle lobe (due to aspiration of pharyngeal flora)

Question 4

What are potential complications of pneumonia?

Answer 4

Abscess formation
Empyema
Tissue fibrosis
Bacteraemia post dissemination

Question 5

What are the pathological/histological stages of pneumonia?

Answer 5

1. Congestion: vascular congestion/oedema (Days 1-2)
2. Red hepatisation: alveolar spaces filled with RBCs, neutrophils, fibrin (Days 3-4)
3. Grey Hepatisation: alveolar spaces dry, grey, firm, lysed RBCs, but ongoing fibrinosuppurative exudate present (Days 5-7)
4. Resolution: exudates enzymatically cleared Days 8 to 3 weeks)

Question 6

What is clinically different with atypical CAP?

Answer 6

Moderate sputum production, however absence of any findings on CXR of consolidation, more mild WCC elevation.

Characterised by dyspnoea out of proportion to the clinical and radiological signs

Question 7

What histologically is different with atypical CAP?

Answer 7

Inflammatory response confined to walls of alveoli, with alveolar spaces relatively free of exudate

Question 8

What are ‘typical organisms’ in CAP?

Answer 8

S. pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
S. aureus
Legionella
Klebsiella

Question 9

What are ‘atypical’ organisms in CAP?

Answer 9

Chlamydia
Q fever (Coxiella burnettii)

Question 10

What are HAP pathogens”?

Answer 10

Klebsiella
Serratia marcescens
E. coli
Pseudomonas
MRSA

Question 11

What 2 factors can contribute to developing acute pulmonary oedema?

Answer 11

1. Haemodynamic disturbance –> increased hydrostatic pressure or decreased oncotic pressure
2. Changes in capillary permeability –> infectious/inflammatory in nature

Question 12

What are causes of increased hydrostatic pressure or decreased oncotic pressure APO?

Answer 12

HYDROSTATIC
Left ventricular failure
Mitral stenosis
Fluid overload
Pulmonary vein obstruction

LOW ONCOTIC
Hypoalbuminaemia
Nephrotic syndrome
Liver disease/ascites
Enteropathies

Question 13

What are causes of changes in capillary permeability APO?

Answer 13

Infection
Inhaled gases
Aspiration
Shock/trauma
Radiation
DIC
Transfusions related
ARDS

Question 14

How do you categorise a pleural effusion?

Answer 14

Transudative (protein poor) vs exudative (protein rich)

Question 15

What is the most common cause of transudative pleural effusion?

Answer 15

CCF

Question 16

What are the most common causes of exudative pleural effusion?

Answer 16

Infection/microbial invasion (i.e. parapneumonic effusion)
Cancer
Pulmonary infarction
Uraemia
Viral pleuritis

Question 17

Where do the majority of PE originate from?

Answer 17

Deep veins, generally from popliteal vein and above

Question 18

What percentage of PE are clinically ‘silent’?

Answer 18

60-80% - cleared by fibrinolytic activity

Question 19

What are morphological changes in the lung associated with PE?

Answer 19

If acute and causing heart failure and shock, death is sudden and no morphological change

If peripheral emboli, can cause wedge shaped infarct, haemorrhagic necrosis

Question 20

What are the complications of PE?

Answer 20

1) Increased pulmonary arterial pressure, reduced cardiac output and cardiogenic shock

2) Ischaemia of downstream pulmonary parenchyma

Question 21

How does PE cause hypoxia?

Answer 21

Atelectasis in ischaemic areas due to reduction of surfactant production + reduced inspiratory effort due to pain

Decreased cardiac output, widening difference in alveolar and arterial oxygen saturation

Right to left shunting of blood through PFO (present in 30% normal people)

Question 22

Why does PE not always cause pulmonary infarct?

Answer 22

Bronchial arteries and oxygen directly diffusing can maintain oxygenation of lung tissue, but this can be compromised if reduced cardiac output or bronchial circulation, or if under ventilated due to underlying pulmonary disease