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BDS2; FHHD > SP2: Lung Diseases > Flashcards

SP2: Lung Diseases Flashcards

1
Q

What is an acinus

A

The terminal respiratory unit; functional unit where gaseous exchange occurs

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2
Q

Describe the anatomy of trachea

A
  • C-shaped cartilage rings to give support when there is negative pressure created for inspiration to ensure the trachea remains open; these are open ended so that the oesophagus and vertebral body is not obstructed so that food can easily be swallowed
  • Mucous glands; these remove dirt on inhalation
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3
Q

Describe the anatomy of bronchi

A
  • Discontinuous cartilage plates

- Mucous glands to remove inhaled dirt

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4
Q

Describe the anatomy of bronchioles

A
  • No cartilage
  • No mucus
  • Terminal bronchioles <2mm diameter
  • Respiratory bronchioles is where gas exchange begins
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5
Q

Describe the anatomy of alveolar ducts and sacs

A
  • Flat epithelium

- No glands/cilia

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6
Q

What are the three types of pneumonia

A
  1. Lobar pneumonia
  2. Bronchopneumonia
  3. Atypical pneumonia
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7
Q

What is lobar pneumonia

A
  • it affect part or entire lobe
  • it commonly affects healthy males age 20-50
  • it is community acquired
  • it is caused by streptococcus pneumoniae
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8
Q

What are the clinical features of lobar pneumonia

A
  • high grade fevers with rigors
  • productive cough (brings up sputum)
  • rusty (blood streaked) sputum
  • pleuritic chest pain
  • signs of consolidation (solid texture on percussion)
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9
Q

What are the 4 stages of progression for lobar pneumonia and the characteristic features of these stages

A
  1. Congestion (24 hrs)
    - engorged vessels due to more blood and inflammatory cells
    - oedema in alveoli
    - heavy and red lungs
  2. Red hepatisation (2-4 days)
    - outpouring of neutrophils and RBCs into alveoli
    - red, solid, airless liver like appearance
  3. Grey hepatisation (4-8 days)
    - fibrin and macrophages replace neutrophils and RBCs
    - grey, solid airless lungs
  4. Resolution (8-10 days)
    - gradual return to normal; there is no scarring due to inflammation being acute
    - there is no functional change
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10
Q

What complications can occur with lobar pneumonia

A
  1. Lung abscesses in parenchyma
  2. Empyema in pleural cavity

These abscesses require surgical interventions to drain

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11
Q

Which infections can cause complications for lobar pneumonia

A
  1. Klebsiella infection

2. Staphylococcus infections

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12
Q

What is bronchopneumonia

A

This is acquired secondary to other factors e.g.

  • chronic debilitating illnesses
  • viral infections
  • infancy
  • old age

It begins as bronchitis and bronchiolitis and then spreads to alveoli and isn’t associated with a specific bacterium; low virulence staph., strep. viridans, H. influenzae, coliforms

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13
Q

Describe the pathology of bronchopneumonia

A
  • bilateral and commonly basal (lower lung)
  • grey or grey-red spots of consolidation
  • small white patches present in lung parenchyma
  • acute inflammatory infiltrate in bronchioles and alveoli
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14
Q

What are the complications of bronchopneumonia

A

Can result in death due to further complicating an already debilitating illness

  • scarring is rare
  • abscess/empyema (pockets of pus) is rare
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15
Q

What is atypical (interstitial) pneumonia

A

This is where inflammation is restricted to alveolar septa and interstitial tissue; there is no alveolar exudate thus it is atypical

This is a chronic response involving lymphocytes and plasma cells and is clinically generalised rather than just localised symptoms

The lungs appear normal due to little exudate or consolidation

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16
Q

What is pulmonary tuberculosis

A

Infection of lungs by Mycobacterium tuberculosis; this is an air-borne bacterium; the infection occurs in childhood through droplet infection and the clinical disease represents reinfection or reactivation by the same bacterium and is a result of the immune reaction

This can be prevented via the BCG vaccine

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17
Q

What is primary TB

A

This represents response to first contact with tubercule bacilli and is usually asymptomatic

A Ghon complex is formed which has a 1cm midzone with draining lymph node - it is a small well defined calcified deposit at the edge of the lung

It heals with fibrosis and calcification and is now called a Ranke complex

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18
Q

What is secondary TB

A

This is where there is reinfection/reactivation due to bacterial exposure

  • this affects lung apex
  • there is visible white regions of caseous necrosis
  • lesions are around 3cm
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19
Q

Describe the microscopic pathology of TB

A

There are characteristic changes resulting from the Type IV hypersensitivity reaction

  • Granulomas present (collection of activated macrophages)
  • Caseous necrosis (shown by homogenous pink region)
  • Langerhan’s giant cells present (multi nucleated horse-shoe appearance)
  • Epithelioid macrophages
20
Q

What is the difference between an immune reaction and a hypersensitivity reaction

A 
Immune = protects against pathogen 
Hypersensitive = goes beyond protection and causes harm to the host
21
Q

Which stain is used to identify the characteristic cells of TB

A

Ziehl-Neelsen stain reveals the characteristic acid-fast bacilli; it will show red rods against a blue background
- definitive diagnosis is by sputum culture

22
Q

What complications can arise from pulmonary TB

A
  • progressive fibrocavitary TB due to granulomatous activity
  • this gradually destroys the parenchyma through caseous necrosis, cavitation and necrosis
  • miliary TB
23
Q

What is miliary TB

A

Bloodborne dissemination within the lung or throughout the body; seed-like foci consisting of granulomas: meninges, bone marrow, liver or any other organ

24
Q

What happens to the lung parenchyma in infections

A

It is blocked off because it aims to destroy the bacterial or fungal infections, but this also removes tissue via the granulomatous inflammation and central necrosis - this results in cavity formation and scarring of the lung tissue

25
Q

What are chronic obstructive airway diseases and give examples of these

A

Those characterised by obstruction to air flow including

  1. Chronic bronchitis
  2. Emphysema
  3. Bronchial Asthma
  4. Bronchiectasis
26
Q

Describe chronic bronchitis

A
  • Productive cough for >3 months in 2 consecutive years
  • There is mucous gland hypertrophy and mucus hyper secretion causing obstruction
  • This is progressive and due to smoking
  • Causes hypoxia, hypercapnia and cyanosis-prone (blue colouration)
27
Q

Describe emphysema

A
  • Permanent dilation of airways distal to terminal bronchiole
  • Elastin destruction occurs leading to loss of elastic recoil and is associated with smoking
  • Tend to hyperventilate
  • Blood gasses are normal - relies on forced expiration
28
Q

What is bronchial asthma

A

Increased irritability of bronchial tree classified by paroxysms of reversible bronchospasm

  • Commonly Type I hypersensitivity to allergens
29
Q

What is bronchiectasis

A

Permanent dilation of bronchi and bronchioles with necrosis of their walls; usually follows obstruction or childhood viral pneumonia

30
Q

Outline the clinical features of bronchiectasis

A
  • sac like airways filled with foul smelling pus
  • chronic paroxysmal cough brought on by change in posture
  • copious foul smelling sputum
31
Q

How do changes in the respiratory epithelium result in lung cancer

A

Ciliated, mucus-secreting, pseudo stratified, columnar epithelium changes into stratified squamous via squamous metaplasia

Metaplastic tissue is a site of cancer formation due to oncogenes being activated/deactivated

This causes squamous dysplasia and so carcinoma

32
Q

What are the four types of lung cancer that can occur

A
  1. Squamous cell carcinoma
  2. Adenocarcinoma
  3. Large cell carcinoma
  4. Small cell (oat cell) carcinoma
33
Q

What is the treatment of small cell carcinoma

A
  • not surgically treatable
  • widely disseminated at time of diagnosis
  • systemic treatments are given
  • radiotherapy
34
Q

What is the treatment of non-small cell carcinoma

A
  • surgically treatable

- new molecular targets are available for use

35
Q

What are the clinical features of lung cancer

A

Local : cough, haemoptysis (blood in sputum, pain)

General : wight loss, clubbing, hypertrophic pulmonary osteoarthropathy

Paraneoplastic syndromes : due to ectopic hormone production by tumour cells - hypercalcaemia, SIADH syndrome inappropriate ADH

36
Q

What is pulmonary oedema

A

It is haemodynamic, usually cardiogenic when the LHS of heart is not working properly there is clogging in the LV resulting in heavy wet lungs - the alveolar pink granular fluid may contain

  • haemosiderin-laden macrophages
  • resolution /brown induration if long-standing
37
Q

What is diffuse alveolar damage

A
  • oedema caused by injury to alveolar capillary endothelium
  • this is rapidly developing life-threatening respiratory insufficiency
  • oedema fluid and fibrinous membranes lining alveoli; fibrin deposition within the alveolar space
  • doesn’t resolve but proceeds to severe scaring
38
Q

What are large saddle emboli

A

Fatal lodges of circulating clots at the bifurcation of the pulmonary trunk

39
Q

What results from the peripheral lodging of smaller emboli

A

Characteristic wedge-shaped infarcts

40
Q

What is pulmonary hypertension

A
  • pulmonary circulation is low resistance
  • increase in pressure can be secondary to COPD, left heart valvular disease or recurrent thromboemboli
  • this causes right ventricular hypertrophy and failure
41
Q

Complications of bronchiectasis

A 
Abscess
Fibrosis
Amyloid
Clubbing
Cor pulmonale
42
Q

What is the most important determinant of lung cancer outcome

A

Staging

43
Q

List the two broad mechanisms of occupational lung injury caused by inhalation of dust, minerals or organic substances due to occupational exposure

A

Occupational lung diseases are diffuse interstitial and restrictive - they occur via

  1. Scarring from chronic irritation
  2. Hypersensitivity to organic dust
44
Q

Give examples of occupational lung diseases

A
  • Coal workers pneumoconiosis: anathracosis, macule, progressive massive fibrosis
  • Silicon: silicosis, Caplan’s syndrome
  • Asbestos: asbestosis, pleural plaques, Caplan’s syndrome, mesothelioma, lung, stomach and colon cancers
  • Farmer’s lung, baggassosis, byssinosis, bid breeders’ lung
45
Q

Why does pulmonary artery occlusion usually occur

A

From the lower limb veins in bed ridden patients

BDS2; FHHD (26 decks)

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