pathology of lung disease Flashcards

0
Q

which cells in the lungs make mucus

A

goblet cells

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1
Q

what epithelium is found in the lungs

A

pseudostratified ciliated columnar epithelium

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2
Q

whats the difference between type 1 and 2 pneumocytes

A

type 1 are flattened and make up 95% of the alveolar surface. type 2 are rounded and make surfactant.

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3
Q

define FEV1

A
  • Forced expiratory volume in 1 sec. the volume that can be forcibly exhaled in the first second of forced expiration.
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4
Q

define FVC

A

forced vital capacity. the maximum volume of air that can be forcibly exhaled out of the lung until no more can be expired.

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5
Q

whats the lung TLC

A

total lung capacity.

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6
Q

whats the lung PEFR

A

peak expiratory flow rate. max flow achieved during forced expiration.

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7
Q

6 causes of obstructive lung disease

A

acute - foreign bodies, bronchiolitis

recurrent acute - asthma

chronic - chronic brochitis, emphysema, bronchiectasis.

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8
Q

define chronic bronchitis

A

chronic sputum production usually accompanied by chronic cough, occuring on most days for three months of the year, for 2 or more consecutive years.

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9
Q

pathogenesis of chronic bronchitis

A

1 - chronic irritation eg cigarrette smoke or air pollution
2 - mucus hypersecretion to protect, submucosal gland hypertrophy and hyperplasia in the larger airways, increased numbers of goblet cells in small airways.
3 -damage and death of ciliated cells (reduced mucociliary action), secondary infection, inflammation and fibrosis.

  • partially reversible on stopping smoking.
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11
Q

what is cor pulmonale

A

Pulmonary heart disease (New Latin pulmōnāle, of the lungs), also known as Cor pulmonale (Latin cor, heart + of the lungs) is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs (pulmonary hypertension).

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12
Q

what is emphysema

A

Definition is Pathological:

An abnormal permanent increase in the size of air spaces beyond the terminal bronchioles with destruction of their walls but without fibrosis

In a highly compliant lung, as in emphysema, the elastic tissue is damaged by enzymes. These enzymes are secreted by leukocytes (white blood cells) in response to a variety of inhaled irritants, such as cigarette smoke. Patients with emphysema have a very high lung compliance due to the poor elastic recoil, they have no problem inflating the lungs but have extreme difficulty exhaling air. In this condition extra work is required to get air out of the lungs. Compliance also increases with increasing age.

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13
Q

what are the subclassificatiojns of emphysema

A
---Centriacinar (centrilobular) 
> common
-cigarette smoking
-chronic bronchitis
-upper zones of lung
-secondary to airway inflammation (increased protease activity)

—-Panacinar (panlobular)
-α1 – antitrypsin deficiency
(decreased anti-protease activity)
-lower zones of lung
-Homozygotes (PiZZ) onset <40 yrs
-Heterozygotes must smoke

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14
Q

histopath appearance of end stage empysema

A

End-stage
emphysema has
cystic alveolar spaces
visible macroscopically

  • alevoli are dilated and their boundaries broken.
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15
Q

Lung Function Tests n empysema

A

Reduced FEV1 to <0.7)

Reduced PEF

Increased TLC

Also reduced diffusion capacity

loss of the elastic recoil causes premature closure of the small airways (decreased radial traction causes collapse).

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16
Q

what is COPD

A

Chronic obstructive pulmonary disease

Defined by lung function tests

Combination of bronchitis & emphysema

Secondary to smoking

Most have mixture of symptoms

‘Pure’ disease at each end of spectrum

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17
Q

COPD Treatment and Prognosis

A

Prevention & supportive therapy
Stop smoking

Oxygen therapy if hypoxic
Pulmonary rehabilitation (exercise & education programme for patients to increase mobility, understand their disease, cope with their breathlessness by pacing their activities, improve anxiety and depression)

5-10% of all deaths in UK

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18
Q

COPD complications

A

Pneumonia

Respiratory failure

Pulmonary hypertension

Cor pulmonale

Polycythaemia

Pneumothorax

19
Q

asthma definition, hallmarks and incidence.

A

Definition is largely clinical:

Paroxysmal wheezing and shortness of breath caused by acute, reversible narrowing of airways

Hallmarks:
hyper-reactive airways
inflammation (bronchial walls)
increased mucus secretion

Affects 8% of the population and incidence increasing

20
Q

subclassification of asthma

A
Extrinsic (Immune)
Atopic (allergic) asthma
Occupational asthma
Drug-induced asthma
Allergic bronchopulmonary aspergillosis
Non-atopic asthma 

Intrinsic (Non-immune)

21
Q

what is atopic asthma

A
Most common type of asthma
Type I hypersensitivity reaction
Environmental antigens
Dust, Pollen, Animal dander, Food
M >F, childhood onset
Family history of atopy
Gene as yet unknown 
Skin test positive - ‘Wheal & flare’
22
Q

what is intrinsic asthma

A
2nd most common type of asthma
Hyper-irritability of airways
Triggered by diverse, non-immune mechanisms 
pollution, viral infection etc
 F>M, adult-onset
No family history or other atopy
IgE levels normal
Skin test negative
23
Q

WHAT IS Occupational asthma

A

Type I & III hypersensitivity
Various inhaled agents:
Formalin, Plastics, Wood, Platinum

24
Q

what is Drug-induced asthma

A

Aspirin

Also have nasal polyps & skin urticaria

25
Q

what is Allergic bronchopulmonary aspergillosis

A

Type I & III hypersensitivity

Inhalation of aspergillus spores

26
Q

3 stages of asthma

A
Priming or Sensitization 
(1st exposure) 
Th2 response
IgE production
Eosinophil recruitment

Re-exposure

Immediate
Mast cell degranulation
Bronchospasm
vascular permeability
Oedema

Late
Eosinophils & Inflammation
Epithelial damage
Airway constriction

27
Q

how is the airway obstructed in asthma

A

Acute response - immediate
Smooth muscle spasm
Mucosal oedema

Late phase reaction – 12-24 hours
Epithelial damage and inflammation
Mucous exudation

Chronic Phase – with repetition
Mucous gland hyperplasia
Smooth muscle hypertrophy
Bronchial BM thickening

28
Q

generic treatment of asthma

A

Inhaled steroids (mainstay of treatment)
Bronchodilators (symptom relief)
Avoidance of allergen
+ systemic steroids for acute exacerbations

29
Q

complications of asthma

A

Status asthmaticus
Pneumonia
Bronchiectasis
Cor pulmonale

30
Q

define bronchiectasis

A

Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotizing infections.

31
Q

3 causes of bronchiectasis

A

Congenital or hereditary conditions
Postinfection
Bronchial obstruction

32
Q

morphology of the lungs with bronchiectasis

A

Usually affects the lower lobes bilaterally

Bronchial dilatation
Most severe in distal bronchi and bronchioles

Spectrum of histological changes
varies with the activity and chronicity of the disease
Inflammation
Ulceration
Necrosis
Fibrosis (bronchiolitis obliterans)

Superimposed infection

33
Q

complications of bronchiectasis

A

Respiratory insufficiency

Cor pulmonale

Brain abscess

Amyloidosis

34
Q

what are interstitial lung diseases?

A

A heterogenous group of diseases

Mostly immune mediated

Share interstitial inflammation & fibrosis

CXR shows an bilateral infiltrative pattern
small nodules, irregular lines or ground-glass shadows

Restrictive pattern on lung function tests
reduced lung compliancy and gas exchange

35
Q

8 causes/associations of interstitial lung diseases

A
Pneumoconioses 
Systemic CT (auto-immune) diseases
Sarcoidosis
Post radiation or chemotherapy 
Post ARDS	
Idiopathic pulmonary fibrosis
Wegener’s granulomatosus	
Goodpasture’s Syndrome
36
Q

what is pneumoconosis

A

Term originally for inorganic particles only

Now also includes organic particles & chemical fumes

Inorganic particles cause direct interstitial fibrosis

Organic particles cause inflammation then fibrosis

Fumes cause ARDS then fibrosis

Organic particles & fumes can also cause asthma

37
Q

what is inorganic pneumoconiosis

A

Coal dust: Anthracosis
Silica: Silicosis
Asbestos: Asbestosis

Often clinically insignificant

Progressive massive fibrosis when significant respiratory compromise

Most common with coal & silica

Caplan’s syndrome if associated RA

Nodules of fibrosis and chronic inflammation in interstitium
38
Q

what is organic pneumoconiosis

A

Farmer’s lung: Actinomycetes in mouldy hay

Bird fancier’s lung: Animal proteins from faeces

aka extrinsic allergic alveolitis
aka hypersensitivity pneumonitis
Sensitisation to organic inhaled antigen
Initial type III hypersensitivity reaction
Later type IV hypersensitivity reaction

Interstitial inflammation by lymphocytes & often also
granulomas, then later fibrosis

39
Q

what is sarcoidosis

A
Systemic disease of unknown aetiology
F>M, Black>>White>>Asian 
Probable response to antigen
Activated T-cells & macrophages
Hilar LN or lung involvement in 90%
Skin, LN & kidney involvement common
Raised serum ACE & often high calcium

Non-necrotising granulomatous inflammation

40
Q

what is idiopathic pulmonary fibrosis

A
aka cryptogenic fibrosing alveolitis
aka usual interstitial pneumonitis
aka Hamman-Rich syndrome when rapidly progressive
M>F, 60+ years
Interstitial pneumonitis & fibrosis
Cause unknown

Extensive interstitial fibrosis with alveolar distortion and interstitial expansion

41
Q

what happens in the end stage of interstitial fibrosis?

A

End stage ‘honeycomb’ lung:
Interstitial fibrosis leading to cystic air-spaces

cystic air spaces are smaller than those seen in bronchiectasis but far far more frequent. literally like a honeycomb.

42
Q

complications of pulmonary fibrosis

A

Respiratory failure
Pulmonary hypertension
Cor pulmonale

43
Q

treatment of interstitial lung diseases

A

Pneumoconiosis:
Stop exposure to stop progression
Any damage irreversible

Other interstitial lung diseases:
Steroid or further immunosuppression
Response variable
Often progress to significant fibrosis