Respiratory pathology Non-neoplastic Flashcards

1
Q

The respiratory system

A

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

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2
Q

Infection upper airways

A

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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3
Q

Lower airways: infectionPNEUMONIA

A
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
Setting:  
 Community acquired
Hospital acquired
Aspiration pneumonia
 Chronic pneumonia
 Necrotizing pneumonia and lung abscesses
Pneumonia in the immunocompromised host
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4
Q

Pneumonia clinical features

A

Fever, rigours, SOB, pleuritic chest pain, purulent sputum, cough

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5
Q

Pneumonia Morphology

A

Lobar
Multifocal/lobular (bronchopneumonia)
Interstitial (focal diffuse)

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6
Q

Community acquired pneumonia

A

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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7
Q

Hospital acquired pneumonia

A

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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8
Q

Aspiration pneumonia

A

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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9
Q

Obstructive disease

A

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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10
Q

Restrictive disease

A

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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11
Q

COPD - Emphysema

A

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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12
Q

Emphysema- morphology and clinical course

A

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

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13
Q

COPD – chronic bronchitis

A

persistent cough with sputum production
for at least 3 months in at least 2 consecutive years
without any other identifiable cause
- 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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14
Q

Chronic bronchitis - Morphology and clinical course

A

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

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15
Q

Asthma

A

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

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16
Q

Asthma - morphology and clinical course

A

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

17
Q

Bronchiectasis

A

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,

18
Q

Restrictive lung disease

A

Heterogenous group of diseases
Characterised by inflammation and fibrosis of the pulmonary connective tissue (eg interstitium of the alveolar walls)
most common causes- sarcoidosis and occupational/environmental

19
Q

Restrictive lung disease - morphology and clinical features

A

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

20
Q

Pulmonary Embolism

A

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

21
Q

Pulmonary embolism - morphology and clinical course

A
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
22
Q

Pulmonary oedema

A
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 due to alveolar injury
infections
Shock/trauma
- Oedema of undetermined origin
Eg neurogenic/high altitude
23
Q

Pulmonary oedema - morphology and clinical features

A

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

24
Q

Pneumothorax

A

Pneumothorax
Air in the pleural cavity
Associated with ephysema, asthma, TB, trauma, idiopathic

25
Q

Atelectasis

A

Incomplete expansion of lungs
Reduces oxygenation and predisposes to infection
reversible

26
Q

Respiratory failure Type 1

A
Type I -Hypoxia with a normal or low PCO2
Pneumonia
Pulmonary oedema
Asthma
PE
Pulmonary fibrosis
ARDS
27
Q

ARDS

A

Acute respiratory distress syndrome (ARDS) is a life-threatening medical condition where the lungs can’t provide enough oxygen for the rest of the body

28
Q

Respiratory failure Type 2

A
Type II -Hypoxia with high PCO2
Asthma, COPD, OSA
Reduced respiratory drive
Neuromuscular disease
Thoracic wall disease eg kyphoscoliosis
29
Q

OSA

A

Obstructive sleep apnoea (OSA) is a condition where the walls of the throat relax and narrow during sleep, interrupting normal breathing