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1Principles of Biomedicine - MD1 > 81 > Flashcards

81 Flashcards

1
Q

Causes of disease

A 
I DIVINE TIME
Congenital/Genetic
• Acquired
– Infectious
– Degenerative
– Inflammation/Immune reactions
– Vascular
– Iatrogenic
• Drugs
• Surgery
• Radiotherapy
– Neoplastic
– Environmental
– Trauma
– Idiopathic
– Metabolic
– Endocrine
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2
Q

Difference between a bronchus and a bronchiole

A

Bronchioles lack cartilage

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3
Q

Acinus

A

Respiratory bronchiole
Alveolar ducts
Alveolar sacs
Alveoli

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4
Q

Lobule

A

3-5 acini

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5
Q 
Epithelial lining of airways
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A

Tall, columnar, pseudostratified, ciliated.
Goblet cells
Neuroendocrine cells
Basal cells

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6
Q 
Cells comprising normal alveoli
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A 
Alveolar macrophages
Type I, II pneumocytes
Fibroblasts
Inflammatory cells
Endothelial cells
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7
Q

Examples of obstructive lung disease
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3

A

Asthma
COPD (chronic bronchitis, emphysema, small airways disease/chronic bronchiolitis
Bronchiectasis

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8
Q 
Examples of restrictive lung disease
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A

Idiopathic pulmonary fibrosis
Pneumoconiosis
Sarcoidosis
‘Honeycomb lung’

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9
Q

Spirometry of obstructive lung disaese

A

Decreased FEV1, normal FVC

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10
Q

Spirometry of restrictive lung disaese

A

Decreased FEV1, decreased FVC

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11
Q

Obstructive lung diseases associated with smoking

A

Emphysema
Chronic bronchiolitis
Small airway disease

Collectively called COPD

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12
Q

How is asthma diagnosed?

A

Physiologically and clinically, not histologically

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13
Q

Different types of asthma
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A

Atopic/allergic (increased serum IgE, specific external allergens)
Non-allergic asthma (normal serum IgE, non-specific triggers)

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14
Q

Acute phase of asthma
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A

Increased vascular permeability leading to oedema
Increased mucus production
Bronchospasm

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15
Q

Late phase of asthma
1
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3

A

4-8 hours later.
Chemotaxis of eosinophils, mast cells, lymphocytes, macrophages. This leads to ongoing inflammation.
Epithelial damage

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16
Q

Which aspects of acute phase asthma do bronchodilators work on?

A

Only on bronchospasm (smooth muscle)

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17
Q

Which aspects of late-phase asthma do bronchodilators work on?

A

None (patient can have early symptoms relieved, but then get worse when late-phase response begins kicking in)

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18
Q

Short-term complications of asthma
1
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3

A

Death
Atelectasis
Spontaneous pneumothorax and/or pneumomediastinum (rare)

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19
Q

Long-term complications of asthma
1
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A 
Airway remodelling (fibrosis and irreversible obstruction)
Chronic hypoxia leads to pulmonary hypertension leads to cor pulmonale
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20
Q

Cor pulmonale

A

Right heart failure from pulmonary artery hypertension from pulmonary artery constriction in response to hypoxia

21
Q

Status asthmaticus

A

Acute severe asthma not responding to bronchodilators

22
Q

Emphysema

A

Abnormal, permanent enlargement of air spaces distal to
the terminal bronchiole
From destruction of the alveolar wall
without fibrosis

23
Q 
Types of emphysema
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A

Centriacinar (centrilobular, caused by smoking)
Panacinar (panlobular)
Distal acinar (Paraseptal)
Irregular

24
Q

Aetiology of centriacinar emphysema

A

Smoking leads to an imbalance between proteases and antiproteases in the lungs.
Smoke leads to recruitment of inflammatory cells which release proteases.
ROS generated by smoke inactivate antiproteases

25
Q

How does emphysema lead to obstruction?

A

Loss of elastic recoil

26
Q

Effect of loss of elastic recoil on the lungs

A

Loss of supporting elastic tissues around small airways leads to collapse, with dynamic airway collapse on expiration (the harder you try to expire, the more compressed the lungs become)

27
Q

Complications of emphysema
1
2
3

A

Hypoxia (caused by airflow obstruction, loss of diffusion capacity (rare, only happens in late emphysema)
Pulmonary hypertension–>Cor pulmonale
Pneumothorax

28
Q

Bullous emphysema

A

Emphysema with cysts on the outside of the lung.
Risk of bursting, cause pneumothorax.
More an appearance of the disease, doesn’t tell you anything of pathogenesis

29
Q

Clinical definition of chronic bronchitis

A

Persistent cough productive of sputum for
at least 3 months in 2 consecutive years.
No other cause

30
Q

Pathogenesis of chronic bronchitis
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A

Chronic irritation of large airways by inhaled substances.
Increased mucus production in larger airways.
Airways inflammation, scarring, narrowing in smaller airways.

31
Q 
Histological appearance of chronic bronchitis
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A

Excessive mucus (hypertrophy of mucus-secreting glands, Reid index over 0.4)
Increased goblet cells
Mild increase in lymphocytes, macrophages and plasma cells, and oedema
Peribronchial fibrosis in small airways
+/-Squamous metaplasia

32
Q

Complications of chronic bronchitis

A

Superimposed infective exacerbations (most common complication)
Hypoxia, pulmonary hypertension, cor pulmonale
Squamous metaplasia, squamous dysplasia (premalignant)

33
Q

Is there squamous epithelium in the lungs?

A

No. Squamous is tough, impermeable, which is why it’s on the skin, and unsuitable for the lungs

34
Q

What is small airways disease?

A

Caused by cigarette smoke
Chronic inflammation, fibrosis, obstruction of terminal bronchioles (<2mm)
Important component of COPD

35
Q

Differences in parts of lungs affected by COPD diseases

A

Chronic bronchitis affects large airways.
Emphysema affects acini.
Small airways disease affects very small airways.

36
Q

Why are bronchodilators often prescribed for COPD?

A

Because there is a small aspect of bronchospasm to COPD, even though primary problems with COPD are non-responsive to bronchodilators

37
Q

Two broad types of COPD

A

Predominant bronchitis and predominant emphysema

38
Q

Predominant bronchitis

A

A lot of cough, a lot of sputum, not much shortness of breath.

‘Blue bloaters’ - Tolerate cyanosis better than predominant emphysemics. Become cyanotic, develop cor pulmonale

39
Q

Predominant emphysema

A

Not much cough or sputum, a lot of shortness of breath.

Breathe hard, quickly. Look sort of pink because of this (don’t look cyanosed) (‘pink puffers’)

40
Q

Cause of most smoking-related deaths

A

COPD

41
Q

Bronchiectasis

A

Irreversible, abnormal dilation of bronchi/bronchioles

42
Q

Appearance of bronchiectasis

A

Huge, dilated airways present at the lung hila

43
Q

Pathogenesis of bronchiectasis
1
2
3

A

Severe destructive inflammation of airways (severe recurrent infection is common)
Loss of surrounding elastic tissue and muscle exceeds contraction of fibrous tissue.
Clearance of organisms and fluid is impaired (bronchiectasis will only get worse)

44
Q

Causes of bronchiectasis

A

Necrotising infections (S aureus, influenza, aspergillus)
Obstruction with infection
Cystic fibrosis
Cilia disorders

45
Q

Contents of dilated airways in bronchiectasis

A

Pus

46
Q 
Clinical course of bronchiectasis 
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A 
Severe cough productive of copious amounts of foul-smelling sputum.
Episodic fever
SOB and cyanosis
Cor pulmonale
Metastaic infection (rare)
Amyloidosis (rare)
47
Q

Common features of restrictive lung disaese

A

Chronic, diffuse, non-infectious
Restrictive spirometry
Inflammation and fibrosis in inter-alveolar septa (interstitium)

48
Q

Idiopathic pulmonary fibrosis
1
2
3

A

Cause unknown
Interstitial inflammation, fibrosis at varying stages of development.
Mean survival is three years
A restrictive lung disease

1Principles of Biomedicine - MD1 (157 decks)

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