9. Respiratory pathology Non-neoplastic Flashcards Preview

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Flashcards in 9. Respiratory pathology Non-neoplastic Deck (46)
1

Normal respiratory tree

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

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The respiratory system

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

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Trachea and bronchi

Trachea and bronchi have cartilage in wall.
Bronchioles have smooth muscle in the wall.

4

Mechanics of breathing

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….

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General overview

Obstructive disorders
Infections
Restrictive
Vascular disorders
Expansion disorders
Miscellaneous

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Obstructive disorders

COPD – bronchitis/emphysema
Asthma
Bronchiectasis

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Infections

Uri/sinusitis
Flu
Pneumonia

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Restrictive

Chest wall abnormalities
Connective tissue disorders
pneumoconioses

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Vascular disorders

Pulmonary oedema
Pulmonary embolism

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Expansion disorders

Atelectasis
pneumothorax

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Miscellaneous

Respiratory failure

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Infection upper airways

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

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Lower airways: infectionPNEUMONIA

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

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Pneumonia

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

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Community acquired pneumonia

Relatively common, especially in elderly population

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

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Hospital acquired pneumonia

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

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Aspiration pneumonia

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

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Obstructive disease

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

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Restrictive disease

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

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Obstructive disease
Asthma



Reversible airways obstruction
common

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Obstructive disease
COPD

Emphysema
Chronic bronchitis

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Obstructive disease
Bronchiectasis

chronic infection leading to destruction and dilatation of the airways

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COPD - Emphysema

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

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Emphysema

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

25

COPD – chronic bronchitis

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

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Chronic bronchitis cont.. (1)

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

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Chronic bronchitis cont… (2)

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

28

Asthma (1)

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……

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Asthma (2)

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

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Asthma (3)

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

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Bronchiectasis

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,

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Restrictive:

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

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Restrictive lung disease

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

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Pulmonary Embolism (1)

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

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Pulmonary embolism (2)

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

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Pulmonary oedema (1)

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

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Pulmonary oedema (2)

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

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Expansion

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

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Respiratory failure (1)

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

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Respiratory failure (2)

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

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Infections

URTI
Pneumonia
Infection and inflammation
Viral, bacterial
Fungal

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Obstructive

COPD
Asthma
Bronchiectasis
Airway obstruction +/- destruction

43

Restrictive

Heterogenous
Inflammation and fibrosis of connective tissue of lung

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Vascular

PE – VQ mismatch
Pulmonary oedema – different mechanisms

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Expansion

Pneumothorax air in the pleural cavity
atelectasis

46

Respiratory failure

Type I vs II
Caution with oxygen in II