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Clinical Pathology > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

What 3 M’s define respiratory pathology

A

morbidity, mortality, money.

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2
Q

What 2 parts make up the lungs and respiratory system

A

conducting portion- trachea to terminal bronchioles.

Respiratory portion- respiratory bronchioles, alveolar ducts, sacs and alveoli

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3
Q

What type os epithelium lines the conducting part of the reparatory system

A

Pseudo stratified ciliated columnar (mucus secreting)

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4
Q

What types of cells line the alveoli

A

Flat type 1 pneumocytes (gas exchange) and type 2 pneumocytes (surfactant production)

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5
Q

Problems in what 3 functions can lead to respiratory failure

A

ventilation
perfusion
gasexchange

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6
Q

define type 1 respiratory failure

A

low oxygen but co2 is normal (

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7
Q

define typ 2 respiratory failure

A

low oxygen and high co2 (>6.3kPa)

hypercapnic drive

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8
Q

signs and symptoms which indicated a respiratory problems

A 
sputum
cough
stridor-proximal airway obstruction.
wheeze- distal airway obstruction.
pleuritic pain
dysponea
cyanosis
clubbing
weight loss.
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9
Q

signs on respiratory examination

A

Auscultation-crackles, wheeze, bronchial breathing, pleural rub
Percussion
dull (consolidation or effusion), hyperresonanat (pneumothorax or emphysema)

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10
Q

Are most primary lung tumours benign or malignant

A

90% are malignant.

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11
Q

what are the risk factors of primary lung tumours.

A

smoking, secondary cigarette smoke, asbestos, lung fibrosis, nickel, hematite, arsenic and mustard gas

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12
Q

define asbestosis

A

pulmonary interstitial fibrosis cause by asbestos.

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13
Q

Is asbestos related disease occupational

A

yes if proven to have a history of over 5 years in a high absestos exposure job.

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14
Q

what are benign primary lung tumours called

A

adenochondroma

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15
Q

what is the most common type of malignant primary tumour

A

non-small cell carcinoma.

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16
Q

what type of tumours are carcinoid tumours

A

malignant primary tumours

low grade, neuroendocrine epithelial tumours.

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17
Q

what type of lung tumour is the commonest

A

secondary lung tumour (usually from a primary source)

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18
Q

How do you distinguish between a primary and a secondary lung tumour.

A

histology, morphology, antigen expression

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19
Q

what antigens are expressed in lung non-mucinous adenocarcinoma and small cell.

A

cytokeratin and thyroid transcription factor postivie.

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20
Q

most common sites of lung carcinoma

A

central, main or upper lobe bronchus (bronchogenic).

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21
Q

are adenocarcinomas found centrally or peripherally.

A

peripherally.

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22
Q

what type of epithelium does respiratory epithelium become after metaplastic change.

A

pseudostratified columnar epithelium – stratified squamous type which may keratinize.

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23
Q

what irritant causes metaplastic change to occur in the epithelium

A

smoke

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24
Q

define dysplasia.

A

One metaplastic cell undergoes irreversible genetic changes (a series of sequential somatic mutations of oncogenes & anti-oncogenes) producing the first neoplastic cell

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25
Q

define neoplasm

A

An abnormal tissue that grows by cellular proliferation more rapidly than normal and continues to grow after the stimuli that initiated the new growth cease

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26
Q

define metaplastic

A

change from 1 cell type to another.

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27
Q

Why does squamous cell carcinoma cause hypercalcaemia

A

parathyroid hormone related peptide.

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28
Q

how does sqaumous cell carcinoma metasize

A

nfiltrate lymphatic and blood vessel

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29
Q

what common respiratory condition does bronchioalveolar carcinoma mimic

A

pneumonia

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30
Q

Is bronchioalveolar carcinoma invasive.

A

No.

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31
Q

How are neuroendocrine cells detected in lung tumours

A

immunochemistry
neural cell adhesion molecule
neurosecretory granule protein.

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32
Q

What cells are associated with typical carcinoid tumours

A

bland cells

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33
Q

what syndrome is typical carcninoid tumour associated with

A

multiple endocrine neoplasia syndrome type 1

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34
Q

which is more aggressive atypical or typical carcinoid tumours

A

atypical

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35
Q

What is a common peptide hormone secreted by small cell carcinoma.

A

Neurosecretory granules with peptide hormones such as ACTH

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36
Q

can carcinomas have multiple differentiation

A

NSCLC, small cell carcinoma.

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37
Q

What common factor do large cell carcinomas express

A

thyroid transcription factor

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38
Q

common paraneoplastic effects of lung carcinomas

A
  • Cachexia
  • Skin
  • Hypertrophic pulmonary osteoarthropathy.
  • Coagulopathies.
  • Encephalomyelitis, neuropathies & myopathies
  • Endocrine effects
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39
Q

what is acanthosis nigricans

A

hyperpigmentation of the skin- thick dark patches

thickening of palms and soles

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40
Q

New drug which has been introduced to treat lung cancer.

A

epidermal growth factor receptor tyrosine kinase inhibitors

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41
Q

How does this drug work

A

– Inhibition of EGFR TK mediated protein phosphorylation and activation of the mitotic cycle

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42
Q

What does ALK gene stand for

A

anaplastic lymphoma kinase-
Important gene in cell maturation and differentiation
rearrangements in this gene can lead to tumours.

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43
Q

what drug inhibits ALK

A

crizotinib

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44
Q

Types of pleural diseases

A 
Pneumothorax
Pleural effucison
Haemothorax
Chylothorax-lymph
empyema-pus
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45
Q

what is a common fusion gene which results in respiratory cancer

A

ALK-EML

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46
Q

what are the inflammatory causes of pleural effusion

A

serous/fibrinous exudate

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47
Q

what causes non inflammatory pleural effusion

A

congestive cardiac failure

transduate

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48
Q

what conditions can affect the pleura

A

– inflammation (pleurisy, pleuritis)
• collagen vascular diseases
• pneumonia, tuberculosis
• lung infarct, usually secondary to pulmonary embolus
• lung tumour
– asbestos
• effusion, fibrous plaques, diffuse fibrosis

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49
Q

Are pleural tumours likely to be benign or malignant

A

malignant

benign e.g. fibroma is rare.

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50
Q

common pleural tumour

A

malignant mesothelioma.

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51
Q

what chemical is malignant mesothelioma associated with

A

asbestos

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52
Q

how long is the latency period for malignant mesothelioma

A

15-60 years

53
Q

How does malignant mesothelioma progress

A

1-nodule and effusion
2-invades chest wall and lung.
3-nodal and distal metastases less common than with carcinomas.

54
Q

which pleura does early malignant mesothelioma effect

A

parietal pleura

55
Q

where are fibrous pleural plaques typically found and what chemical are they associated with

A

lower thoracic wall & diaphragmatic parietal pleura and asbestos

56
Q

What condition is PE secondary to

A

DVT

57
Q

Risk factors of PE

A

virchow’s triad (stasis, hypercoagubale blood, endothelial wall injury), recent surgery, low flow, reduced mobility

58
Q

what syndrome is a result of cillary dysmotility

A

Kartageners syndrome

59
Q

what causes acute bronchitis

A

– Viral (RSV), H. influenzae, Strep. pneumoniae

60
Q

2 clinical signs associated with cute bronchiolits

A

– Croup- viral infection which causes swelling of the windpipe
– Exacerbations of COAD-chronic obstructive airway disease.

61
Q

define bronchiolitis obliterans

A

bronchioles compressed and narrowed.

62
Q

what 2 main factors lead to respiratory infections

A

mucocillary escalator problem

immunity problem e.g. hypogammaglobulinaemia

63
Q

what is pneumonia

A

• Inflammatory exudate (seeped out of blood or organ) in alveoli & distal small airways - consolidation

64
Q

what are the 4 main classifications for pneumonia

A

clinical
Aetiology
Anatomical
reaction

65
Q

what are 2 main types of respiratory infections.

A

primary

secondary- compromised defences

66
Q

is bronchopneumonia caused by a primary or secondary infection

A

secondary infection

67
Q

what causes bronchopnemonia

A

low virulence bacteria or occasionally fungi

68
Q

is lobarpneumoniae primary or secondary

A

primary

69
Q

which type of pneumonia affect full lobes and which type has a pathcy distribution

A

full lobes-lobarpneumoniae

pathcy-bronchopneumoniae

70
Q

most common atypical pneumonia’s in the non-immunosuppressed.

A
  • Viral - flu, varicella, RSV, rhino, adeno, measles
  • Mycoplasma pneumoniae - Mild, chronic, fibrosis
  • Chlamydia (psittacosis), Coxiella burnetti (Q-fever)
  • Legionella pneumophilla - Systemic, 10- 20% fatal
71
Q

clinical signs and symptoms of atypical pneumonia

A

– Intersitial lymphocytes, plasma cells, macrophges
– Intra-alveolar fibrinous cell-poor exudate
– Diffuse alveolar damage (DAD)

72
Q

most common atypical pneumonia in the immunsuppressed patient

A

• Opportunistic infections by low virulence or non-virulent organisms
– Fungi - candida, aspergillus, Pnumocystis carinii
– Viruses - CMV, HSV, measles

73
Q

3 types of non-infective pneumonias

A

aspiration pneumonia
lipid pneumonia
Cryptogenic organising pneumonia and bronchiolotis obliterans organising pneumonia

74
Q

what causes pulmonary TB

A

Mycobacterium tuberculosis

75
Q

what vaccine is used to prevent TB

A

BCG

76
Q

primary Tb reaction symotomatic or asymtomatic

A

aymptomatic

77
Q

where does reactivation of TB typically occur

A

apically.

78
Q

effects of TB on the lungs

A

Primary infection: Asymptomatic, Ghon complex in peripheral lung & hilar nodes, usually resolves
Scarring - fibrous calcified scar.
Granulomas with multinucleated Langhans’ giant cells & caseous necrosis

79
Q

3 conditions which cause pulmonary vasculitis.

A
  • Necrotising granulomatous vasculitis - Wegener’s granulomatosis (kidneys & nose, elevated serum ANCA) Churg-Strauss syndrome (eosinophilia & asthma)
  • Goodpasture’s syndrome - Anti-glomerular basement membrane antibody, Intra-alveolar haemorrhage & glomerulonephritis
  • Microvascular damage - ARDS & DAD, SLE
80
Q

common causes for emboli to forms

A

DVT, fat, air amniotic fluid, tumour, foreign bodies.

81
Q

define obstructive pulmonary disease.

A

localised of diffuse obstruction of air flow.

82
Q

causes of obstructive pulmonary disease

A

tumour or foreign body
distal alveolar collapse
distal retention pnemonitis
distal bronchiectasis

83
Q

define bronchiectaisis

A

• Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue

84
Q

cause of brochiectasis

A

• Results from chronic necrotizing infection

85
Q

signs and symptoms of bronchiectais

A

Cough, fever, copious amounts of foul smelling sputum

86
Q

Chronic Obstructive Pulmonary Disease is a combination of what 2 conditions

A

chronic bronchitis & emphysema

87
Q

pathology of chronic bronchitis

A

Mucus gland hyperplasia and hypersecretion, secondary infection by low virulence bacteria, chronic inflammation

88
Q

define emphysema

A

Abnormal permanent dilation of airspaces distal to the terminal bronchiole, with destruction of airspace wall, without obvious fibrosis

89
Q

how do we classify emphysema

A

– Centrilobular (centiacinar) Coal dust, smoking
– Panlobular (panacinar) - >80% a1 antitrypsin deficient (rare, autosomal dominant) , severest in lower lobe bases
– Paraseptal (distal acinar) - Upper lobe subpleural bullae adjacent to fibrosis. Pneumothorax if rupture

90
Q

pink puffer and blue bloater describe which 2 conditions

A

emphysema-pink puffer

brochioloits- blue bloater

91
Q

is asthma reversible

A

yes

92
Q

which hyper of hypersensitivity reaction is asthma

A

type 1 -caused by an allergen

93
Q

what chemical initiates bronchoconstriciton and mucus production is asthma

A

histamine initiated bronchoconstriction and mucus production obstructing the airways.

94
Q

what are the main changes to the airways in asthma.

A

– bronchiolar wall smooth muscle hypertrophy
– mucus gland hyperplasia
– respiratory bronchiolitis leading to centrilobular emphysema

95
Q

Is intersitial lung disease more commonly restrictive or obstructive

A

restrictive.

96
Q

signs of chronic interstitial disease

A
  • Dyspnoea increasing for months to years

* Clubbing, fine crackles, dry cough

97
Q

what does the lung look like in chronic interstitial disease

A

honeycomb

98
Q

example of chronic interstitial disease

A

– idiopathic pulmonary fibrosis,
– many pneumoconioses (dust diseases)
– sarcoidosis,
– collagen vascular diseases-associated lung diseases

99
Q

Idiopathic pulmonary fibrosis

is also known as

A

cryptogenic fibrosing alveolitis

100
Q

what lobes of the lungs are effected more in Idiopathic pulmonary fibrosis

A

lower

101
Q

what do the lungs look like in idiopathic pulmonary fibrosis

A

– Interstitial chronic inflammation & variably mature fibrous tissue
– Adjacent normal alveolar walls
– Similar pattern of fibrosis in collagen vascular disease associated interstitial lung disease and in asbestosis
• Bosselated (“cobblestone”) pleural surface due to contraction of interstitial fibrous tissue accentuates lobular architecture

102
Q

what structure is typically involved in sarcoidosis

A

• Hilar nodes

103
Q

what other organs are typically affected in Sarcoidosis

A

skin, heart, and brain.

104
Q

are the granulomas caseating or non-caseating in Sarcoidosis

A

non-caseating

105
Q

what chemical in the body is elevated in sarcodoisis

A

calcium (hypercalcaemia)

106
Q

Pneumonconises are also known as

A

the dust diseases

107
Q

what causes pneumoconioses

A

inhalation of mineral dusts

108
Q

common 3 Pneumonconises

A

coal-workers
silicosis
asbestosis

109
Q

what condition that silicosis reactivate

A

tuberculosis

110
Q

what is the pathology of silicosis

A

Kills phagocytosing macrophages

111
Q

which pneumonconises increase the occurrence of lung cancer

A

Asbestosis, Silicosis

112
Q

what is hypersensitivity pnemonitis also known as

A

extrinsic allergic alveolitis

113
Q

what type of hypersensitivity reaction is pnemonitis

A

Type 3

114
Q

what condition are
– farmers’ lung - actinomycetes in hay
– pigeon fanciers’ lung - pigeon antigens
associated with

A

hypersensitivity pneumonitis

115
Q

define CF

A

• An inherited multiorgan disorder of epithelial cells affecting fluid secretion in exocrine glands and the epithelial lining of the respiratory, gastrointestinal and reproductive organs

116
Q

What cause CF

A

• Mutation in CFTR gene

117
Q

Is CF recessive or dominant condition

A

recessive

118
Q

what are the main organs which CF affects

A

lungs, pancreas and bowel

119
Q

treatments for CF

A
  • Mucolytics
  • Heart/lung transplants
  • Not genre therapy currently.
  • Physiotherapy
120
Q

diagnosis test for CF

A
  • Part of Newborn screening in UK
  • Sweat test
  • Genetic testing
121
Q

How does CF affect the lungs

A
  • Bronchioles distended with mucus
  • Hyperplasia mucus secreting glands
  • Multiple repeated infections
  • Severe chronic bronchitis and bronchiectasis
122
Q

How does CF affect the pancrease

A
  • Exocrine gland ducts plugged by mucus
  • Atrophy and fibrosis of gland
  • Impaired fat absorption, enzyme secretion, vitamin deficiencies ( pancreatic insufficiency)
123
Q

common symptoms of CF

A

reccurent chest infections

124
Q

are hypersensitive pneumonitis granuolomas caveating or non caveating

A

poorly formed non-caseating granulomas extends alveolar walls

125
Q

what type of inflammation occurs in hypersensitivity pneumonitis

A

• Peribronchiolar inflammation

126
Q

coal workers’s pneumoconiosis is also known as

A

• Anthracosis

127
Q

Coal workers’ pneumoconiosis is associated with causing which respiratory condition

A

COPD

via ling fibrosis

128
Q

2 main types of Coal workers’ pneumoconiosis

A
  • Simple (macular) CWP

* Nodular CWP

129
Q

4 main types of inhaled dust are

A
  • inert
  • fibrogenic
  • allergenic
  • oncogenic

Clinical Pathology (45 decks)

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