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Cardio > Histopathology Respiratory Pathology 1 and 2 > Flashcards

Histopathology Respiratory Pathology 1 and 2 Flashcards

1
Q

Microscopic structure of alveolar walls consist (from blood to air) of the following:

A

The capillary endothelium
The basement membrane
The alveolar epithelium

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2
Q

The alveolar epithelium

A

Type 1 pneumocytes – 95%

Type II pneuomocytes – secrete surfactant and rapidly replicate after injury.

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3
Q

The Pluera consists of

A

A double layer of fibrous connective tissue lined with mesothelial cells.

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4
Q

Diseases due to immaturity →

A
  • Hyaline membrane disease

* Bronchopulmonary dysplasia

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5
Q

Hyaline Membrane Disease: Description

A

Complication of prematurity, less than 36 weeks gestation. Also associated with maternal diabetes, caesarean section, and amniotic fluid aspiration.

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6
Q

Hyaline Membrane Disease:Due to

A

Deficiency of pulmonary surfactant (type II not developed).

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7
Q

Hyaline Membrane Disease: Symptoms

A

Tachypnoea
Dyspnoaea
Develops within hours after birth followed by cyanosis

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8
Q

Hyaline Membrane Disease:Histologically

A

There is diffuse alveolar damage with formation of hyaline membrane.
Alveoli lined by fibrosis with inflammatory cells – produce hyaline membrane.

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9
Q

Hyaline Membrane Disease:Treatment

A

Oxygen
Surfactant
Artificial ventilation

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10
Q

Hyaline Membrane Disease: Prognosis

A

If infant survives resolution follows within next few days

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11
Q

Respiratory Infections → Types

A

Primary – with no underlying predisposing condition.

Secondary – when local or systemic defences are weakened

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12
Q

Respiratory Infections → Secondary causes

A

Loss or suppression of cough reflex
Ciliary defects
Mucus disorders
Acquired or congenital hypogammaglobulinaemia - reduced antibodies
Immunosuppression
Pulmonary oedema with flooding of alveoli

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13
Q

Bronchitis Acute epi and causes

A

More severe in children (larygo-tracheo-bronchitis)
Usually causes by RSV.
Other causative agents include Haemophillia influenza and strept pneumonia

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14
Q

Bronchitis Chronic

A

Is a clinical term defined as cough and sputum for 3 months in 2 consecutive years.

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15
Q

Pneumonia: Definition

A

This is usually due to infection affecting lower air ways and can be classified according to various criteria

  1. Clinical circumstances
  2. Aetiological agent
  3. Anatomical pattern
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16
Q

Pneumonia: Clinical circumstances

A

Primary

Secondary

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17
Q

Pneumonia: Aetiological Agent

A

Bacterial
Viral
Fungal
Others

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18
Q

Pneumonia:Anatomical pattern

A

Lobar Pneumonia

Bronchopneumona

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19
Q

Pneumonia: Complications of pneumonia

A
  • Abscess formation (type 3 pmneumococci and klebsiella) – collection of pus
  • Empyema – neutrophillic exudate (can be seen in lung and gallbladder)
  • Organisation of the exudate with fibrosis
  • Bacteraemia dissemination to other organs e.g. heart valves causing metastatic abscess (transient presence of bacteria in blood).
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20
Q

Pulmonary Tuberculosis: Definition

A

It is a major cause of death globally. It’s incidence is again increasing. With increase in incidence of HIV disease.

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21
Q

Pulmonary Tuberculosis: Caused by

A

M tuberculosis:

  • Mycobacterium T hominis (human human transfer via air droplets)
  • Mycobacterium T Bovis (unpastuerised milk)
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22
Q

Pulmonary Tuberculosis: Types

A

Primary (1st occurrence)
Secondary (increased infection @ site of entry → lung)
Miliary (serious medically emergency – multiple seeds throughout body)

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23
Q

Pulmonary Tuberculosis: Important features which differentiate TB from other infections

A
  • Organisms
  • Pathogenesis and histology
  • Clinical features
  • Investigations
  • Treatment
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24
Q

Pulmonary Tuberculosis: Staining

A
  • Zihl neilson staining
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25
Q

Pulmonary Tuberculosis: Culture

A
  • 5/6 weeks to grow for TB v. different to other organisms
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26
Q

Pulmonary Tuberculosis: Pathogenesis and histology

A
  • Granuloma forms (inflammation)
  • Neutrophillic exudate
  • Histocytes and giant cell
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27
Q

Pulmonary Tuberculosis: Clinical features

A
  • Strep → high grade
  • TB → low grade fever + night sweats
  • Haemoptysis
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28
Q

Pulmonary Tuberculosis: Investigations

A
  • FBC –Increased WCC, increased neutrophils
  • Culture – sensitivity (afp culture)
  • Skin test – eve’s test (purified protein on skin – check sensitivity)
  • TB immunisation
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29
Q

Diseases of Vascular Organs: Types

A

Pulmonary congestion and oedema
Pulmonary embolism and infarction
Pulmonary Hypertension

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30
Q

Pulmonary congestion and oedema

A

Oedema: accumulation of abnormal amounts of fluid in the intercellular tissues or body cavities.

Congestion: Increased volume of blood in an affected tissue or part.

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31
Q

Congestion histology

A

Dilated in bloodstreams

RBC containing increased

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32
Q

Oedema histology

A

Leakage of fluid into interstitium

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33
Q

Two types of congestion and oedema

A

Hemodynamic oedema

Oedema due to micro-vascular injury (ARDs)

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34
Q

Normal fluid exchange is regulated by following forces:

A

Hydrostatic pressure
Colloid osmotic pressure
Crystalloid osmotic pressure
Tissue tension

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35
Q

Causes of hemodynamic oedema

A

Increased hydrostatic pressure
Decreased osmotic pressure
Lymphatic obstruction

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36
Q

Increased hydrostatic pressure (back pressure from neins)

A

Left sided heart failure
Mitral stenosis
Volume overload
Pulmonary vein obstruction

37
Q

Decreased osmotic pressure (cant bring fluid back in)

A

Hypoalbuminaemia:

  • Nephrotic syndrome
  • Liver diseases
  • Protein-losing enteropathy
38
Q

Oedema due to micro-vascular injury→ causes

A
  • Infectious agents: viruses and Mycoplasma
  • Inhaled toxins: O2, SO2, Smoke
  • Liquid aspiration: gastric contents
  • Drugs: Busulphan
  • Shock, trauma and sepsis
  • Radiation
39
Q

Pulmonary Embolism and Infarction → Description

A

Occlusion of pulmonary artery is almost embolic in origin

40
Q

Pulmonary Embolism and Infarction → Consequences of pulmonary artery occlusion depends upon

A
  • Size of the embolic mass

- General state of the circulation

41
Q

Pulmonary Embolism and Infarction → Smaller emboli and consequence

A
  • In patients with heart diseases who have already impaired circulation produce infarction.
  • In patients with adequate cardiovascular circulation the bronchial artery sustain the lung parenchyma and there is no infarction.
42
Q

Tidal Volume (TV)

A

Amount of air inhaled/exhaled during each normal/quiet respiration.

43
Q

Vital capacity (VC)

A

Amount of air exhaled after maximum inspiration.

44
Q

Residual Volume (RV)

A

Amount of air left in lung after expiration.

45
Q

Total lung cancer capacity

A

Vital capacity and residual volume.

46
Q

Forced expiratory volume 1 in 1 Second (FEV1)

A

The maximum volume of air exhaled from the lungs within the 1st second after a previous maximum inspiration. Reduced with obstructed airways, pulmonary fibrosis or oedema, or muscle weakness.

47
Q

Forced Expiratory Ratio (FEV1/VC)

A

Low in obstructive defects. Normal or high in restrictive defects.

48
Q

Transfer Factor for Carbon Monoxide (TCO)

A

Air containing a known concentration of carbon monoxide is inhaled; the breath is held for 15 seconds and then exhaled. The amount of CO absorbed is a measure of pulmonary gas exchange. TCO is reduced in pulmonary fibrosis, oedema, embolism and anaemia.

49
Q

Restrictive Airway Disease: characterised by

A

Reduced lung capacity – two groups
• Acute or chronic interstitial or infiltrative lung diseases e.g. ARDs, Pneumoconiosis (fibrosis of lung post exposure to particles e.g. asbestos
• Chest wall disorders e.g. poliomyelitis (resp muscle trunk), kyphoscoliosis, severe obesity and pleural diseases.

50
Q

Pulmonary function tests

A

Reduced vital capacity (VC)

Normal or increased FEV1/VC ratio

51
Q

Chronic Bronchitis → Defined clinically as

A

Cough with sputum for at least 3 months in 2 consecutive years.

52
Q

Chronic Bronchitis → Two factors are important in the genesis of chronic bronchitis

A

Chronic irritation by inhaled substances: cigarette smoking

Microbiologic infection: H. influenza and strept. Pneumonia.

53
Q

Chronic Bronchitis → Smoking predisposes to infection in different ways:

A

Interferes with ciliary action of the respiratory epithelium
Causes direct damage to airway epithelium
Inhibits the ability of bronchial and alveolar leukocytes to clear bacteria (macrophages can’t phagocytose)

54
Q

Chronic Bronchitis → Pathogenesis

A
  • Respiratory bronchitis affecting airways of less than 2mm
  • Leads to destruction of the wall and surrounding parenchymal elastin with the development of centri-lobular emphysems
  • Hyper-secretion of mucus secondary to hypertrophy of submucosal glands in bronchi and increased number of goblet cells of small airways
55
Q

Chronic Bronchitis → Severe cases symptoms

A

• Hypercapnia
• Hypoxaemia
• Cyanosis
‘BLUE BLOATERS’

56
Q

Emphysema → Description

A

This is an anatomical term defined as permanenet enlargement of airspaces distal to the terminal bronchioles together with destruction of their walls (hyperinflation if no destruction).

57
Q

Emphysema → 6 different types of emphysema

A 
Centrilobular emphysema
Panlobular emphysema
Paraseptal emphysema
Irregular emphysema
Bullous emphysema
Interstitial emphysema
58
Q

Emphysema → Centrilobular Emphysema

A
  • Mostly seen in heavy cigarette smokers
  • It involves respiratory bronchioles (central part of lobules) particularly of upper lobes.
  • Dust laden macrophages are seen in the wall with inflammation around bronchi and bronchioles.
59
Q

Emphysema →Panlobular Emphysema

A
  • Mostly seen in patients with α1 antitrypsin deficiency: acute phase serum protein which inhibitis the action sof collagenase, elastase and other proteases (secreted by dying macrophages and macrophages).
  • It involves all air spaces distal to the terminal bronchioles particularly in lower lobes.
60
Q

Emphysema → α1 antitrypsin deficiency:

A

• Death: alveolar macrophages → contain lysosomal bags with enzymes when macrophages die, the enzymes are released in alveoli. Normally α1 antitrypsin neutralises those enzymes to prevent damage from enzymes to alveoli.

61
Q

Emphysema → Paraseptal Emphysema

A

• It involves air spaces at the periphery of the lobules typically adjacent to the pleura. Upper lobes are most frequently involved.

62
Q

Emphysema → Irregular Emphysema

A
  • It irregularly involves the respiratory acinus.
  • Commonly seen around old healed scars at lung apices therefore pathogenesis thought o be air trapping caused by fibrosis.
63
Q

Emphysema → Bullous emphysema

A

• Not a separate category but refers to the presence of balloon-like foci of emphysema over 10mm in diameter
→ Spontaneous pneumothorax (young adult male with isolated bullous burst causing a collapse.

64
Q

Interstitial Emphysema

A
  • This is inflation of the interstitium of the lung by air, commonly due to traumatic rupture of an airway. It may extend into the mediastinum or sub-cutis.
  • → air present in the soft tissues (surgical emergency)
65
Q

Bronchiectasis: Definition

A

This is a chronic necrotizing infection of the bronchi and bronchioles leading to, or associated with, abnormal and permanent dilation of these airways, particularly in lower lobes.

66
Q

Bronchiectasis: Clinical manifestations

A

Cough

Fever and the expectoration of copious amounts of foul-smelling purulent sputum.

67
Q

Bronchiectasis: Develops in association with following conditions

A
  • Bronchial obstruction due to tumour or foreign body
  • Congenital or hereditary condition e.g. cystic fibrosis and immobile cilia and Kartagener’s syndrome
  • Necrotizing pneumonia.
68
Q

Bronchiectasis: Pathophysiology

A

There is dilation of bronchi and bronchioles with inflammatory infiltration especially polymorphs during acute exacerbation. The inflammation and associated fibrosis extends into the adjacent lung tissue.

69
Q

Bronchial Asthma: Definition

A

Is a disease characterised by hyperactive airways leading to episodic, reversible bronchoconstriction, owing to increased responsiveness of the trachea-bronchial tree to various stimuli.
→ Transient constriction of bronchioles: Type 1 hypersensitivity (Ige) – mast cells

70
Q

Bronchial Asthma: Hypersensitivity

A 
Mast cells (FC) receptors of mast cells – release histamine (vasodilation, bronchoconstriction).
The next time the body recognises the antigens: antigen-antibody reaction takes place.
71
Q

Bronchial Asthma: Epi

A

Begins in childhood
Triggered by – a variety of environmental agents including dust, pollens, food and animal dander.
Often a family history of atopy.

72
Q

Bronchial Asthma: Mediated by a

A

Type 1 hypersensitivity reaction.

73
Q

Bronchial Asthma: Release of histamine and othe chemical mediators leads to

A
  • Bronchoconstriction – causing wheezing, tachypnoea and dyspnoea
  • Increased vascular permeability – oedema
  • Mucus hyper-secretion
74
Q

Bronchial Asthma: Serum:

A

• IgE levels are raised

75
Q

Bronchial Asthma: Investigations

A

• Skin test with offending antigen results in an immediate wheel and flare reaction

76
Q

Bronchial Asthma: Symptoms

A
  • Rarely symptoms persist for days (status asthamaticus) leading to respiratory failure and even death.
  • Grossly the lungs are overdistended; bronchi and bronchioles are occluded by mucus plugs.
77
Q

Bronchial Asthma: Pathophysiology

A
  • Mucus plgus contains crushmann spirals (whorls of shed epithelium), large number of eosinophils and charcot – leyden crystals.
  • Mucus glands hypertrophy
  • Thickening of BM
78
Q

Bronchial Asthma: Types

A
  • Atopic
  • Non-atopic
  • Aspirin induced
  • Occupational
  • Allergic broncho-pulmonary aspergillosis
79
Q

Bronchogenic Carcinoma →Epi

A

One of the commonest malignancies
Accounts for one third of all cancer deaths in males
Occurs between ages 40-70 years
Overall 5 year survival rate is 4-7%

80
Q

Bronchogenic Carcinoma →Risk factors

A

Cigarette smoking
Abestos
Radiation
Oncogenes

81
Q

Bronchogenic Carcinoma →Cigarette smoking

A

Increased risk of lung cancer
• Average smoker 10x increased risk
• Heavy smoker 20x increased risk

82
Q

Bronchogenic Carcinoma →Substances harmful in smoking

A

Polycyclic aromatic hydrocabons such as benzo(a)oyrene
Phenol derivative
Radioactive elements: polonium – 210, carbon-14

83
Q

Bronchogenic Carcinoma →Asbestos

A
  • Lung cancer is the most frequent malignancy in persons exposed to asbestos
  • Abestos workers who do not smoke have a five times increased risk and those who smokes have a 50-90 times greater risk of developing lung cancer.
  • Among asbestos workers one death in five is due to lung cancer and one death in ten is due to mesothelioma
  • A latent period of 20 years between exposure and development of cancer.
84
Q

Bronchogenic Carcinoma → Radiation

A
  • Increased incidence of lung cancer among survivors of the Haroshima and Nagaski atomic bombs blasts.
  • Lung cancer rates among non-smoking uranium minor is four times higher than those of general population.
  • Exposure to radon gas is also linked to increased lung cancer risk.
85
Q

Bronchogenic Carcinoma →Oncogenes

A
  • C mymc in small cell carcinoma

* K-ras in adenocarcinoma

86
Q

Bronchogenic Carcinoma →Scarring

A

• Controvertial

87
Q

Bronchogenic Carcinoma →Clinical Features

A
  • Weight loss, cough and haemophtysis are common presenting features.
  • Patients may present with metastisi and common sites include lymph node, bone, brain, liver and adrenals.
  • Paraneoplsatic effects are common and are due to ectopic hormones.
88
Q

Bronchogenic Carcinoma Paraneoplastic ectopic hormones

A
  • ACTH and ADH from small cell carcinoma
  • PTH from squamous cell carcinoma
  • Finger-clubbing and hypertrophic pulmonary osteoarthropathy
89
Q

Bronchogenic Carcinoma Classification of lung Carcinoma

A 
Squamous cell carcinoma
Adenocarcinoma
Bronchio-alveolar carcinoma
Large cell undifferentiated carcinoma
Neuroendocrine tumours:
•	Carcinoid
•	Atypical carcinoid
•	Small cell carcinoma
•	Large cell neuroendocrine carcinoma

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