SP2: Lung Diseases Flashcards

(45 cards)

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
What are chronic obstructive airway diseases and give examples of these
Those characterised by obstruction to air flow including 1. Chronic bronchitis 2. Emphysema 3. Bronchial Asthma 4. Bronchiectasis
26
Describe chronic bronchitis
- 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
Describe emphysema
- 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
What is bronchial asthma
Increased irritability of bronchial tree classified by paroxysms of reversible bronchospasm - Commonly Type I hypersensitivity to allergens
29
What is bronchiectasis
Permanent dilation of bronchi and bronchioles with necrosis of their walls; usually follows obstruction or childhood viral pneumonia
30
Outline the clinical features of bronchiectasis
- sac like airways filled with foul smelling pus - chronic paroxysmal cough brought on by change in posture - copious foul smelling sputum
31
How do changes in the respiratory epithelium result in lung cancer
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
What are the four types of lung cancer that can occur
1. Squamous cell carcinoma 2. Adenocarcinoma 3. Large cell carcinoma 4. Small cell (oat cell) carcinoma
33
What is the treatment of small cell carcinoma
- not surgically treatable - widely disseminated at time of diagnosis - systemic treatments are given - radiotherapy
34
What is the treatment of non-small cell carcinoma
- surgically treatable | - new molecular targets are available for use
35
What are the clinical features of lung cancer
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
What is pulmonary oedema
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
What is diffuse alveolar damage
- 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
What are large saddle emboli
Fatal lodges of circulating clots at the bifurcation of the pulmonary trunk
39
What results from the peripheral lodging of smaller emboli
Characteristic wedge-shaped infarcts
40
What is pulmonary hypertension
- 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
Complications of bronchiectasis
``` Abscess Fibrosis Amyloid Clubbing Cor pulmonale ```
42
What is the most important determinant of lung cancer outcome
Staging
43
List the two broad mechanisms of occupational lung injury caused by inhalation of dust, minerals or organic substances due to occupational exposure
Occupational lung diseases are diffuse interstitial and restrictive - they occur via 1. Scarring from chronic irritation 2. Hypersensitivity to organic dust
44
Give examples of occupational lung diseases
- 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
Why does pulmonary artery occlusion usually occur
From the lower limb veins in bed ridden patients