Respiratory Tutorial

Pulmonary oedema

• Causes– Haemodynamic

• Increased hydrostatic pressure – (heart failure, mitral stenosis, volume overload)

• Decreased oncotic pressure– Hypoalbuminaemia

• Lymphatic obstruction

– Microvascular injury• Infections (sepsis/viral/Mycoplasma)• Toxic injury (gases/aspirated liquids/drugs/chemotherapy)• Trauma, shock, DIC, emboli, heat• Uraemia, pancreatitis• Extracorporeal circulation

Pulmonary oedema

• Gross findings

Pulmonary oedema

• Microscopic findings

Pulmonary oedema

• Microscopic findings

ARDS/Diffuse Alveolar Damage

• Damage to what?– Diffuse alveolar capillary damage

• Presentation– Oedema, resp failure, hypoxia resistent to O2

• Pathogenesis– Endothelial damage– Increased vasc permeability

• Fibrin exudation – membrane formation• Inflammatory cell infiltrate in alveolar septum

• Causes

ARDS/Diffuse Alveolar Damage

• Gross findings

ARDS/Diffuse Alveolar Damage

• Microscopic findings

Pulmonary Emboli

• Types of emboli?• Majority thromboemboli

– Majority from deep leg veins

• Risk factors– Surgery, immobility, old age– Hypercoagulability, pregnancy, OCP,

malignancy, esp gynae malignancy– Trauma, burns, fracture

Saddle embolus; sudden death

Large embolus; acute right heart failure

Medium embolus; pulmonary infarct

Small embolus; +/- infarct depending on circulatory status

Pulmonary Emboli

• Consequences– Embolus

• Resolution• Organization• Vascular sclerosis• Pulm HTN• Chronic cor pulmonale

– Infarct• Organization

Pulmonary Hypertension

• Causes– Chronic lung disease (interstitial or COPD)– Chronic left heart failure– Recurrent pulmonary emboli– Primary / idiopathic

• Pathogenesis– Endothelial injury– Vasoconstriction– Medial hypertrophy– Intimal fibrosis

Pulmonary Hypertension

• Histology– Large arteries: Atheroma– Medial and small arteries

COPD

• Emphysema• Abn. Enlargement of airways distal to terminal bronchioles with

destruction of walls

• Bronchitis• Persistent cough with sputum x 3/12 x 2 conseq years

• Asthma• Chronic inflammatory disorder with hyper-responsiveness &

paroxysmal contraction of bronchial tree

• Bronchiectasis• Chronic necrotizing infection of bronchi & bronchioles with abn

permanent dilatation of their walls

What type?

Pathogenesis?

Emphysema

• Microscopic findings

Bronchitis

• Pathogenesis– Chronic irritation of airways

• Inflammation, congestion, edema• Increased mucus secretion

– Mucous gland hypertrophy in bronchi– Goblet cell metaplasia in bronchioles

• Secondary infection

– Morphology• Inflamed bronchi with thickening of mucus layer• Mucous plugs• Fibrosis• Squamous metaplasia• Squamous dysplasia

Asthma

• Types– Extrinsic (atopic)– Intrinsic (non-atopic)

• Pathogenesis– Atopic:

• Antigen binding to IgE on mast cell – acute phase• Cytokine release – late phase

• Morphology– Gross:

• Overinflation with mucus plugging

– Micro:• Edema, inflammation, mucous gl and smooth m hypertrophy

What type of COPD?

Causes?

Pathogenesis?

Obstruction

Atelectasis

Infection

Necrosis of bronchial walls

Irreversible dilation

What is this?

Causes?

Morphology?

Consequences?

What is this?

Causes?

Morphology?

Consequences?

What is this?

Morphology?

Consequences?

Secondary TB Cavitating Miliary TB

Adenocarcinoma Squamous cell carcinoma Small cell carcinoma

Adenocarcinoma Squamous cell carcinoma Small cell carcinoma

Bronchioloalveolar carcinoma

Hamartoma

Mesothelioma