9. Respiratory pathology Non-neoplastic

Question 1

Normal respiratory tree

Answer 1

Trachea
Bronchi
Right Lung: Upper, middle and lower lobe
Left Lung: Upper and lower lobe
Diaphragm

Question 2

The respiratory system

Answer 2

Upper airways: nose, accessory air sinuses, nasopharynx, larynx
Lower airways: trachea, bronchi, bronchioles, terminal bronchioles, alveoli
Pleura

Question 3

Trachea and bronchi

Answer 3

Trachea and bronchi have cartilage in wall.

Bronchioles have smooth muscle in the wall.

Question 4

Mechanics of breathing

Answer 4

Upper airways warm, humidify and filter air, air carried through the respiatory tree down into trachea, through bronchioles, into alveoli, where gas exchnage takes place….

Question 5

General overview

Answer 5

Obstructive disorders
Infections
Restrictive
Vascular disorders
Expansion disorders
Miscellaneous

Question 6

Obstructive disorders

Answer 6

COPD – bronchitis/emphysema
Asthma
Bronchiectasis

Question 7

Infections

Answer 7

Uri/sinusitis
Flu
Pneumonia

Question 8

Restrictive

Answer 8

Chest wall abnormalities
Connective tissue disorders
pneumoconioses

Question 9

Vascular disorders

Answer 9

Pulmonary oedema

Pulmonary embolism

Question 10

Expansion disorders

Answer 10

Atelectasis

pneumothorax

Question 11

Miscellaneous

Answer 11

Respiratory failure

Question 12

Infection upper airways

Answer 12

Definition: acute inflammatory process that affects mucous membranes of the respiratory tract
Includes: rhinitis, laryngitis, tonsilitis sinusitis

Symptoms: malaise, headache, sore throat, discharge
Aetiology
Commonly viral
Can get secondary bacterial infection

Question 13

Lower airways: infectionPNEUMONIA

Answer 13

Definition: Inflammation of the lung parenchyma
 - Consolidation of the affected part
 - Exudate with inflammatory cells and fibrin in the alveolar air spaces
Causes:  infectious agents
	 inhalation of chemicals
	 chest wall trauma
Categories 
Setting:  
 Community acquired
Hospital acquired
Aspiration pneumonia
 Chronic pneumonia
 Necrotizing pneumonia and lung abscesses
Pneumonia in the immunocompromised host

Question 14

Pneumonia

Answer 14

Clinical features/course
Fever, rigours, SOB, pleuritic chest pain, purulent sputum, cough
Morphology:
Lobar	
Multifocal/lobular (bronchopneumonia)
Interstitial (focal diffuse)

Question 15

Community acquired pneumonia

Answer 15

Relatively common, especially in elderly population

Strep. pnuemoniae most common organism
Haemophilus influenzae
Staph aureus- complicates viral infection and in IVDU
Lobar or bronchopneumonia

Question 16

Hospital acquired pneumonia

Answer 16

Aka nosocomial pneumonia
Any pneumonia contracted by patient at least 48-72hrs after admission
Usually bacterial- gram negative bacilli and Staph aureus
Severe and can be fatal- most common cause of death in ITU
Fever
Increased white cell count
Cough with purulent sputum
Chest X-ray changes

Question 17

Aspiration pneumonia

Answer 17

Develops after inhalation of foreign material.
Elderly, Strokes, Dementia, Anaesthetic
Usually right middle and right lower lobe
Oral flora +/- other bacteria

Question 18

Obstructive disease

Answer 18

Characterised by partial or complete obstruction at any level from the trachea to respiratory bronchioles
PFT: limitation of maximal airflow rate during forced expiration FEV1

Question 19

Restrictive disease

Answer 19

Characterised by reduced expansion with decreased total lung capacity,
FVC is reduced: amount of air that can be blown out after maximal inspiration

Question 20

Obstructive disease

Asthma

Answer 20

Reversible airways obstruction

common

Question 21

Obstructive disease

COPD

Answer 21

Emphysema

Chronic bronchitis

Question 22

Obstructive disease

Bronchiectasis

Answer 22

chronic infection leading to destruction and dilatation of the airways

Question 23

COPD - Emphysema

Answer 23

Irreversible enlargement of the airspaces distal to the terminal bronchiole - destruction of their walls without obvious fibrosis
Types: centriacinar / panacinar / paraseptal / irregular
Pathogenesis:
mild chronic inflammation throughout the airways
protease – antiprotease imbalance hypothesis
+ imbalance of oxidants and antioxidants
role of smoking and genetics

Question 24

Emphysema

Answer 24

Morphology: voluminous lungs
large alveoli, large apical bullae
or blebs

Clinical course - symptoms:
dyspnoea, cough, wheezing, weight loss
expiratory airflow limitation – “pink pufferrs”
death due to cor pulmonale,
congestive heart failure, pneumothorax

Question 25

COPD – chronic bronchitis

Answer 25

persistent cough with sputum production for at least 3 months in at least 2 consecutive years without any other identifiable cause

Question 26

Chronic bronchitis cont.. (1)

Answer 26

long-standing irritation by inhaled substances (e.g tobacco smoke, dust from grain, cotton, silica) hypertrophy of submucosal glands in trachea and bronchi, increase in goblet cells mucus hypersecretion + alterations in the small airways  chronic airway obstruction

Question 27

Chronic bronchitis cont… (2)

Answer 27

Morphology mucous membrane hyperaemia, swelling, oedema excessive mucous/mucopurulent excretions, narrowing of the bronchioles caused by mucus plugging, inflammation and fibrosis, may cause obliteration in severe cases Clinical course persistent cough productive of sputum dyspnea on exertion hypercapnia, hypoxemia, mild cyanosis (“blue bloaters”) Leads to cor pulmonale, cardiac failure, may cause atypical metaplasia/dysplasia

Question 28

Asthma (1)

Answer 28

Chronic inflammatory disorder of the airways recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning. widespread but variable bronchoconstriction and airflow limitation At least partly reversible (spontaneously/with treatment). Hallmarks: increased airway responsiveness  episodic bronchoconstriction, inflammation of bronchial walls, increased mucus secretion Types: extrinsic (response to inhaled antigen – atopic, occupational) intrinsic (non-immune mechanisms – cold, exercise,aspirin). Atopic best understood – IgE mediated hypersensitivity……

Question 29

Asthma (2)

Answer 29

genetic predisposition + exposure to environmental triggers early phase reaction: bronchoconstriction, increased mucus production, vasodilation + increased vascular permeability late phase reaction: inflammation, epithelial damage, more bronchoconstriction

Question 30

Asthma (3)

Answer 30

Morphology lung overinflation + small areas of atelectasis, thick mucus plugs in bronchi and bronchioles, airway remodelling Clinical course chest tightness, wheezing, dyspnea, cough +/- sputum status asthmaticus increase in airflow obstruction, difficulty with exhalation

Question 31

Bronchiectasis

Answer 31

Permanent destruction and dilatation of the airways associated with severe infections or obstructions: Aetiology: CF, kartageners, post infectious: TB, measles, bronchial obstruction eg TB/FB Morphology: dilated, inflamed airways. Clinical course: persistent cough, purulent sputum +++, haemoptysis,

Question 32

Restrictive:

Answer 32

Heterogenous group of diseases | Characterised by inflammation and fibrosis of the pulmonary connective tissue (eg interstitium of the alveolar walls)

Question 33

Restrictive lung disease

Answer 33

Morphology Xray: bilateral infiltrative lesions - small nodules, irregular lines, ground-glass shadows Scarring and gross destruction of the lung - end-stage/honeycomb lung Clinical features dyspnea, tachypnea, end-inspiratory crackles, eventual cyanosis, without wheezing reductions in gas diffusing capacity, lung volume, and compliance May lead to secondary pulmonary hypertension and right-sided heart failure with cor pulmonale

Question 34

Pulmonary Embolism (1)

Answer 34

Blockage of a main or branch pulmonary artery by an embolus – Usual source of emboli are deep venous thrombi of the leg (95% of cases) Pathophysiology: respiratory compromise and haemodynamic compromise

Question 35

Pulmonary embolism (2)

Answer 35

Morphology central/peripheral emboli pulmonary haemorrhage pulmonary infarction ``` Clinical course abrupt onset pleuritic chest pain, shortness of breath hypoxia increased pulmonary vascular resistance – right ventricular failure ```

Question 36

Pulmonary oedema (1)

Answer 36

``` Accumulation of fluid in the air spaces and parenchyma of the lungs Haemodynamic oedema Increased venous pressure Eg left ventricular failure Decreased oncotic pressure Eg nephrotic syndrome Liver failure Oedema of undetermined origin Eg neurogenic/high altitude Oedema due to alveolar injury infections Shock/trauma ```

Question 37

Pulmonary oedema (2)

Answer 37

Morphology initial fluid accumulation in basal regions – dependent oedema engorged alveolar capillaries, intra-alveolar granular pink precipitate alveolar microhaemorrhages, hemosiderin-laden macrophages heavy, wet lungs Clinical features SOB, pink frothy sputum, characteristic CXR findings

Question 38

Expansion

Answer 38

Pneumothorax Air in the pleural cavity Assd with ephysema, asthma, TB, trauma, idiopathic Atelectasis Incomplete expansion of lungs Reduces oxygenation and predisposes to infection reversible

Question 39

Respiratory failure (1)

Answer 39

``` Type I -Hypoxia with a normal or low PCO2 Pneumonia Pulmonary oedema Asthma PE Pulmonary fibrosis ARDS ```

Question 40

Respiratory failure (2)

Answer 40

``` Type II -Hypoxia with high PCO2 Asthma, COPD, OSA Reduced respiratory drive Neuromuscular disease Thoracic wall disease eg kyphoscoliosis ```

Question 41

Infections

Answer 41

``` URTI Pneumonia Infection and inflammation Viral, bacterial Fungal ```

Question 42

Obstructive

Answer 42

COPD Asthma Bronchiectasis Airway obstruction +/- destruction

Question 43

Restrictive

Answer 43

Heterogenous | Inflammation and fibrosis of connective tissue of lung

Question 44

Vascular

Answer 44

PE – VQ mismatch | Pulmonary oedema – different mechanisms

Question 45

Expansion

Answer 45

Pneumothorax air in the pleural cavity | atelectasis

Question 46

Respiratory failure

Answer 46

Type I vs II | Caution with oxygen in II