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SBCP Pathology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Difference between bronchi and bronchioles?

A

Bronchioles do not have glands or cartilage

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2
Q

Type of epithelium lining respiratory system?

A

Pseudostratified ciliated columnar epithelium which contains goblet cells

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3
Q

How many alveoli in each acinus?

A

2000

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4
Q

Type of epithelium making up the lung pleura?

A

Single layer of mesothelium covering strands of collagen and elastin

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5
Q

Key cell type involved in any form of acute bacterial pneumonia?

A

Neutrophil polymorph

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6
Q

Difference between bronchopneumonia and lobar pneumonia? (simple)

A

Different morphological patterns

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7
Q

Bronchopneumonia pattern?

A

Focal inflammation centred on airways

Often bilateral/lower lobes

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8
Q

Aetiological factors for bronchopenumonia

A 
Old age/infants
Underlying organ failure
Acute bronchitis/CF
Post op
Steroids
HIV/AIDS
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9
Q

Complications of pneumonia?

A

Pleurisy
Abscess
Sepsis

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10
Q

Histology of bronchopneumonia

A

Acute inflammation CENTRED ON bronchioles and surrounding alveoli

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11
Q

Healing of bronchopneumonia?

A

Healing with organisation or scarring

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12
Q

Pattern of lobar pneumonia?

A

Entire lobe affected by inflammatory infiltrate

Inflammation extends to pleura or to a major fissure

FREQUENTLY ASSOCIATED WITH PLEURAL EFFUSION

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13
Q

What organsism most commonly causes lobar pneumonia?

A

Streptococcus pneumoniae (may also cause bronchopneumonia, depends on virulence serotype)

Normally present in throats of healthy people

Therefore viewed as ENDOGENOUS infection due to weakening of host immunity

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14
Q

Clinical presentation of lobar pneumonia

A

Sudden onset

High fever
High RR
Cough with RUSTY sputum
Pleuritic chest pain

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15
Q

Healing in lobar pneumonia?

A

Healing by crisis rather than lysis at 8-10 days in untreated cases

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16
Q

Morphology of lung in congested phase of lobar pneumonia?

A

Infected lobe is heavy, red and boggy with vascular congestion, outpouring of fluid, relatively few neutrophil polymorphs and bacteria

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17
Q

3 stages of lobar pneumonia?

A

Congestion
Red hepatisation
Grey hepatisation

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18
Q

Morphology of lung in red hepatisation

A

Liver like consistency where the alveolar spaces are packed with neutrophils, RBCs, and fibrin

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19
Q

Morphology of lung in grey hepatisation

A

Firm lung, RBCs are lysed and fibrinous exudate persists in alveoli

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20
Q

Most common causes of community aqcuired pneumonia?

A

Strep. pneumoniae-most common

  • H influenzae
  • Legionella
  • Mycobacterium
  • TB
  • Staph. aureus
  • Mycoplasma pneumoniae

<1% Klebsiella

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21
Q

What percentage of hospital acquired pneumonias are gram negative?

A 
60%:
Klebsiella
E coli
Pseudomonas
Proteus
Enterobacter
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22
Q

Causes of interstitial/atypical pneumonia?

A

Inflammation in alveolar septa

Viruses, chlamydia, Ricketts, Herpes, RSV

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23
Q

When is alveolar epithelial necrosis seen?

A

Well recognised in viral pneumonias

Gives rise to pattern of diffuse alveolar damage

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24
Q

Who gets pneumocystis pneumonia? Pathological appearance?

A

People with AIDS

Pink frothy exudate in alveoli

Silver stain will show round or crescent organisms

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25
Q

Why type of organism is Lengionella pneumophilia?

A

Aerobic gram negative

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26
Q

Functions of type 1 and 2 pneumocytes?

A

Type 1: Gas exchange

Type 2: surfactants

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27
Q

True/false: The lungs develop from ectoderm

A

True

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28
Q

How much fluid is in the pleural space?

A

Only a few mls

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29
Q

What is a lung abcess?

A

A collection of pus walled off by chronic inflammatory granulation tissue and fibrous tissue

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30
Q

Aetiology of primary lung abscess?

A

Caused by aspiration of infectied oropharyngeal contents

Risks:
LOC, dysphagia

Most common right side

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31
Q

Aetiology of secondary lung abscesses?

A

-Airway obstruction eg by carcinoma, foreign body in airway, bronchiectasis, pneumonia

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32
Q

Complications of lung abscess?

A
  • Spontaneous rupture into bronchus
  • Spread throughout rest of lung
  • Cyst formation following drainage
  • Pneumatocele formation
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33
Q

Definition of chronic bronchitis?

A

Cough with sputum for 3 months in 2 consecutive years

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34
Q

Histological appearance of which disease?: Mucous hypersecretion and mucous gland hyperplasia

A

Chronic Bronchitis

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35
Q

What disease will increase the Reid index? (Ratio of thickness of gland layer to thickness of bronchial wall)

A

Normal value 0.3, may double in Bronchitis

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36
Q

What is emphysema?

A

Permanent dilatation of any air spaces distal to the terminal bronchiole WITHOUT fibrosis

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37
Q

Two forms of emphysema? (just recognise)

A

Centrilobular: Involves respiratory bronchioles and destroys alvelar septa. CIGARETTE SMOKING. In upper lobes.

Panlobular: Involves entire acinus (cotton candy lungs). ALPHA 1 ANTITRYPSIN DEFICIENCY. In lower lobes, widespread destruction.

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38
Q

Histology of which disease: mucous plugs in bronchi/oles are infiltrated with eosinophils and Charcot-Leyden crystals. Curshmann spirals appear as coiled mucous fragments.

A

Asthma

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39
Q

Lung morphology in asthma?

A

Ballooned lungs that meet in the midline of the anterior mediastinum

Due to air trapping as a result of mucous plugs

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40
Q

What produces Charcot leyden crystals?

A

Eosinophils in asthma

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41
Q

What are Creola bodies?

A

Clumps of respiratory epithelium that have been shed from mucosa

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42
Q

Histology features of asthma?

A

Marked eosinophil infiltration

Thickening of sub epithelial basement membrane

Hypertrophy of bronchial smooth muscle due to sustained contraction

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43
Q

Most common organism causing TB in developed countries?

A

Mycobacterium tuberculosis

44
Q

How is mycobacterium tuberculosis stained for?

A

Acid fast and alcohol fast RODS

Stained using Ziehl-Neelsen stain

3-6 wks for microbial culture

45
Q

Pathological hallmark of TB?

A

Caseating Granulomatous inflammation

Epitheliod macrophages surrounded by lymphocytes (secretes many interleukins leading to chronic infection)

46
Q

Clinical features of TB

A 
Cough with sputum/blood
Chest pain
Night sweats
Weight loss
Fatigue
47
Q

Describe (a) Primary TB (b) Secondary TB

A

(a) Occurs in patient not infected with TB before. Ghon focus (caseous necrosis) may occur in any lobe in subpleural distribution. The bacteria then spreads to hilar lymph nodes to form GHON COMPLEX. Most patients heal well but bacteria may remain dormant.
(b) dormant mycobacteria become active. Cavitary lesions appear in APICES.

48
Q

Potential complications of secondary TB?

A

Miliary TB (Many granulomas spread thoughout brain, lungs and kidneys)

Tuberculosis pneumonia

Bronchopleural fistula

Infection of granulomas by Aspergillus

Infection may be coughed up and swallowed- terminal ileum to cause ulcers and inflammation

Systemic amyoidosis (rare)

49
Q

Treatment of TB (simple)

A

More than 1 drug needed

50
Q

Clinical features of restrictive lung disease?

A

SOB
Reduced FV1/FVC
Bilateral CT shadowing
Hypoxia

51
Q

What may cause parenchymal lung disease?

A

Interstitial oedema
Cellular infiltration
Fibrosis

52
Q

What may cause parenchymal lung disease?

A

Interstitial oedema
Cellular infiltration
Fibrosis

53
Q

Pathology of parenchymal lung restrictive disease?

A

Chronic inflammation leads to fibrosis and thickening of ALVEOLAR CAPILLARY WALL

Gas exchange is impaired

Destruction of alveoli and decreased expansibility of lung

54
Q

Histology of which disease: Intra-alveolar fibrosis, obliterative fibrosis and interstitial fibrosis leading to END STAGE honeycomb lung

A

Lung fibrosis

55
Q

What is intra-alveolar fibrosis?

A

Fibrosis within alveoli

Accounts for condition called “cryptogenic organising pneumonia” where you see granulation tissue in the alveoli. Responds to STEROIDS

Leads to interstial fibrosis

56
Q

What is obliterative fibrosis?

A

Destruction of multiple alveoli due to fibrosis (end stage)

Example is DIFFUSE ALVEOLAR DAMAGE (DAD) which leads to ARDS. Causes include viruses, smoke inhalation, shock, aspiration of gastric contents etc.

57
Q

Interstitial fibrosis can be classified into which two groups?

A

Group 1: Caused by exudate or transudate which becomes incorporated into the alveolar walls to produce fibrosis. Affects BASE of lung.

  • Asbestosis
  • RA, SLE
  • Longstanding interstitial oedema

Group 2: GRANULOMATOUS inflammatory process due to macrophages.

  • SPARES base of lung
  • Sarcoidosis
  • Extrinsic allergic alveolitis
  • Chronic beryllosis
  • Silicosis
58
Q

Define pneumocosis

A

Permanent change in lung structure due to inhalation of mineral dust

Can be due to ether exudates/transudates or granulomatous inflammation

Eg, Asbestosis, sSilacosis (silica), coal workers pneumocosis

59
Q

How is asbestosis diagnosed?

A

Lung biopsy: Fibrosis and asbestos bodies (asbestos fibres coated by protein and iron)

60
Q

What percentage of people with sarcoidosis develop interstitial fibrosis?

A

5-15%

61
Q

Organs affected in sarcoidosis?

A

90%- lung and mediastinal lymph node involvement

Also:

  • Eyes: Iritis, choroiditis, retinitis
  • Liver
  • Skin, erythema nodosum
  • Marrow
  • Kidneys
62
Q

Histology of which disease: Tight, non-caseating granulomata. Firbosis with bulla formation.

A

Sarcoidosis

63
Q

What type of condition is extrinsic allergic alveolitis?

A

Hypersensitivity pneumonitis which leads to interstitial fibrosis

64
Q

Examples of extrinsic allergic alveolitis?

A

Farmer’s lung-mouldy hay

Bird-Fanciers lung- Bird serum and excreta

Chicken lung- Feathers

Detergent packers lung- bacillus form biological washing powder

65
Q

Pathology of extrinsic allergic alveolitis?

A

Poorly formed non-caseating GRANULOMAS (resolve within 6 months)

Background of diffuse chronic interstitial fibrosis

May progress to honeycomb lung

66
Q

What is Cryptogenic (idiopathic) fibrosing alveolitis?

A

Number of conditions with different histology patterns

Different treatments required for each.

Diagnosed with high contrast CT

Subtype examples:

  • Idiopathic pulmonary fibrosis
  • Cryptogenic organising pneumonia (COP)
67
Q

Hallmark of ARDS?

A

Diffuse pattern of alveolar damage

Causes:

  • Refractory hypoxaemia
  • CXR- Bilateral opacification
  • Multiorgan failure due to hypoxia
68
Q

3 phases of diffuse alveolar damage?

A

Exudation (1 wk): Lungs are heavy, dark and have copius amounts of bloodstained fluid exudates. Changes mostly in basal regions.
-Under microscope, capillaries are congested, and there are numerous RBCS. HYALINE MEMBRANE!!

Regeneration: Prolif. of type II pneumocytes. Epitheium regenerates below hyaline membrane.

Repair(scarring or fibrosis) or resolution (exudate broken down and absorbed, no scarring)

69
Q

Histological hallmark of diffuse alveolar damage?

A

HYALINE MEMBRANE (mixture of fibrin and necrotic alveolar cells which have formed into thin layers)

70
Q

Causes of DAD (diffuse alveolar damage) and ARDS? (many, just recognise a few)

A 
Major trauma
Sepsis
Near drowning
Gastric aspiration
Smoke/fumes
Major burns
Chemo
Pneumonia
DIC
Blood transfusion
Acute pancreatitis!!
Cardiac surgery bypass
71
Q

Type of hypersensitivity in acute exposure of extrinsic allergic alveolitis?

A

Type III

SOB, fever,cough a few hours post exposure

72
Q

Type of hypersensitivity in repeated exposure of extrinsic allergic alveolitis?

A

Type 4 (eg man with one pigeon) cell mediated

Granulomas, interstitial fibrosis

Progressive respiratory failure, slow

73
Q

Most common population affected by sarcoidosis?

A

Age 20-40

COmmon in scandanavians and black population in USA

74
Q

Electrolyte abnormality in sarcoidosis?

A

Hypercalcaemia, 1 in 5

75
Q

Symptoms of sarcoidosis?

A

Fatigue, fever, weight loss, SOB, erythema nodosum, exercise intolerance

Anterior uvetitis or iritis

Obscure neurological symptoms

76
Q

Pathogenesis of pulmonary oedema?

A
  1. Increased lung capillary hydrostatic pressure (LVF, tachycardia, mitral valve disease, pericarditis, IV fluid overload, severe anaemia, veno-occlusive disease)
  2. Increased pulmonary capillary permeability (ARDS)

Both: Cerebral bleed, high altitude, renal failure

77
Q

Macroscopic lung findings in pulmonary oedema?

A

Lungs are heavy and wet

Copius amounts of frothy fluid in airways

Distended subpleural lymphatics

Enlarged hilar lymph nodes

78
Q

CXR features of pulmonary oedema

A

Kerley B lines
Upper lobe diversion
Prominent hilar regions (bats wing)

79
Q

Histology of which disease: Pink staining FLUID in alveolar spaces. Congested capillaries amongst alveoli with “beads on string” appearance. “heart failure” cells which are macrophages with yellow-brown granules of haemosiderin due to haemorrhage

A

Pulmonary oedema

80
Q

Types of embolism?

A

Thromboembolism (>90%)

Others:

  • atheromatous
  • amniotic fluid
  • gas (trauma)
  • fat (trauma, long bone fractures)
  • tumour mets
  • Foreign material (IV drugs)
  • Infective agents (IE)
81
Q

Effects of PE depending on size?

A

Small: may go unnoticed, or minor reduction over time unless there are multiple

Medium: Significant SOB, haemoptosis, Heart failure due to VQ mismatch

Large: Saddle emboli can cause sudden death

82
Q

Difference between transudates, exudates, and empyema?

A

Transudates: Low protein, few cells, due to FAILURE eg CCF, cirrhosis, nephrotic syndrome

Exudates: High protein: LDH ratio. Due to irritation of lung lining due to infections or cancer or autoimmune disease. MALIGNANT EXUDATE IS BLOODSTAINED

Empyema: Collection of pus in pleural cavity

83
Q

Risk factors for lung cancer

A

Smoking (95% cases)
Occupational (asbestos causing adenocarcinoma, arsenic, cadmium, coal, silica, nickel)

Pollution
Fibrosis
Radon

84
Q

Overall 5 year survival of lung Ca?

A

4-7%

85
Q

Symptoms of lung cancer

A 
Cough
SOB
Haemoptysis
Weight loss
Chest pain

PARANEOPLASTIC SYNDROMES IN SMALL CELL

86
Q

Local effects of lung tumour?

A

Hoarseness
Diaphragm paralysis
Superior vena cava syndrome
Horner’s

87
Q

Examples of paraneoplastic syndromes caused by lung tumour?

A

Lambert-Eaton syndrome

Acanthosis nigricans
Hypertrichosis

Cushing;s

SIADH

Hypertrohic pulmonary osteoarthropathy

88
Q

Types of non-small cell cancers?

A

85% of lung cancers

Adenocarcinoma most common
Squamous cell
Large cell

89
Q

Patterns of spread of lung adenocarcinoma?

A

May have multiple patterns in ONE tumour

Adenocarcinoma in situ

Lepidic spread (abnormal cells use alveoli like scaffolding) may lead to adenocarcinoma

90
Q

Well vs poorly differentiated lung adenocarcinoma?

A

Well: Evident gland formation

Poor: Little glands

Use of IHC might help if pattern unclear.

91
Q

How to tell if lung adenocarcinoma is primary or secondary?

A

IHC staining with thyroid transcription factor (TTF-1). If positive, its primary.

If primary, do mutation testing: Test for ALK or EGFR mutations

92
Q

Are adenocarcinomas central or peripheral?

A

Can be both

93
Q

Are squamous cell carcinomas central or peripheral?

A

Central

94
Q

Hallmark feature of squamous cell carcinoma in lung?

A

Areas of necrosis in the centre. Tumour grows so fast that blood supply cannot keep up.

95
Q

Histology of which disease: Lung tumour showing keratinisation and intracellular bridges.

A

Squamous CC of lung

96
Q

Are large cell lung carcinomas central or peripheral?

A

Central

97
Q

Histology of which lung carcinoma: Large cells, pleomorphic nuclei. No squamous or glandular features

A

Large cell carcinoma

98
Q

Types of neuroendocrine tumours of lung (3 in a spectrum)

A

Carcinoid (more orderly cells)

Atypical carcinoid

Small cell (less orderly cells)

99
Q

Carcinoid tumours histology?

A

Low grade, central, obstructing bronchus

Malignant potential but good prognosis

Nested growth pattern, granular chromatin

100
Q

Small cell carcinoma central or peripheral?

A

Also called OAT CELL carcinoma

Usually central and has metastasised at presentation

Poor prognosis

101
Q

Histology of which lung carcinoma: Hyperchromatic nuclei, smudge chromatin (AZZOPARDI PHENOMENON), nuclear moulding, indistinct nucleoli

A

Small cell carcinoma

102
Q

Which are more common, primary or secondary lung tumours?

A

Secondary, tend to present as multiple nodules

Carcinomas from breast, kidney, GIT

Also, sarcomas, melanoma, lymphoma

103
Q

Why do we use molecular testing for EGFR in primary lung tumours?

A

Epidermal growth factor receptor mutation may respond to TKIs! (tyrosine kinase inhib.)

104
Q

Example of primary pleural tumour

A

Malignant mesothelioma

105
Q

Medial survival time of malignant mesothelioma?

A

11 months

Very aggressive

Long lag time between asbestos exposure and diagnosis

106
Q

Histology of which pleural cancer: Biphasic histology as cells can differentiate along epitheliod or sarcomatoid roots. Therefore can look like sarcoma and adenocarcinoma

A

Malignant mesothelioma

Difficult to diagnose even with IHC staining to help

SBCP Pathology (24 decks)

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