Respiratory Flashcards
1
Q
Difference between bronchi and bronchioles?
A
Bronchioles do not have glands or cartilage
2
Q
Type of epithelium lining respiratory system?
A
Pseudostratified ciliated columnar epithelium which contains goblet cells
3
Q
How many alveoli in each acinus?
A
2000
4
Q
Type of epithelium making up the lung pleura?
A
Single layer of mesothelium covering strands of collagen and elastin
5
Q
Key cell type involved in any form of acute bacterial pneumonia?
A
Neutrophil polymorph
6
Q
Difference between bronchopneumonia and lobar pneumonia? (simple)
A
Different morphological patterns
7
Q
Bronchopneumonia pattern?
A
Focal inflammation centred on airways
Often bilateral/lower lobes
8
Q
Aetiological factors for bronchopenumonia
A
Old age/infants Underlying organ failure Acute bronchitis/CF Post op Steroids HIV/AIDS
9
Q
Complications of pneumonia?
A
Pleurisy
Abscess
Sepsis
10
Q
Histology of bronchopneumonia
A
Acute inflammation CENTRED ON bronchioles and surrounding alveoli
11
Q
Healing of bronchopneumonia?
A
Healing with organisation or scarring
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
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
14
Q
Clinical presentation of lobar pneumonia
A
Sudden onset
High fever
High RR
Cough with RUSTY sputum
Pleuritic chest pain
15
Q
Healing in lobar pneumonia?
A
Healing by crisis rather than lysis at 8-10 days in untreated cases
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
17
Q
3 stages of lobar pneumonia?
A
Congestion
Red hepatisation
Grey hepatisation
18
Q
Morphology of lung in red hepatisation
A
Liver like consistency where the alveolar spaces are packed with neutrophils, RBCs, and fibrin
19
Q
Morphology of lung in grey hepatisation
A
Firm lung, RBCs are lysed and fibrinous exudate persists in alveoli
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
21
Q
What percentage of hospital acquired pneumonias are gram negative?
A
60%: Klebsiella E coli Pseudomonas Proteus Enterobacter
22
Q
Causes of interstitial/atypical pneumonia?
A
Inflammation in alveolar septa
Viruses, chlamydia, Ricketts, Herpes, RSV
23
Q
When is alveolar epithelial necrosis seen?
A
Well recognised in viral pneumonias
Gives rise to pattern of diffuse alveolar damage
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
25
Why type of organism is Lengionella pneumophilia?
Aerobic gram negative
26
Functions of type 1 and 2 pneumocytes?
Type 1: Gas exchange
| Type 2: surfactants
27
True/false: The lungs develop from ectoderm
True
28
How much fluid is in the pleural space?
Only a few mls
29
What is a lung abcess?
A collection of pus walled off by chronic inflammatory granulation tissue and fibrous tissue
30
Aetiology of primary lung abscess?
Caused by aspiration of infectied oropharyngeal contents
Risks:
LOC, dysphagia
Most common right side
31
Aetiology of secondary lung abscesses?
-Airway obstruction eg by carcinoma, foreign body in airway, bronchiectasis, pneumonia
32
Complications of lung abscess?
- Spontaneous rupture into bronchus
- Spread throughout rest of lung
- Cyst formation following drainage
- Pneumatocele formation
33
Definition of chronic bronchitis?
Cough with sputum for 3 months in 2 consecutive years
34
Histological appearance of which disease?: Mucous hypersecretion and mucous gland hyperplasia
Chronic Bronchitis
35
What disease will increase the Reid index? (Ratio of thickness of gland layer to thickness of bronchial wall)
Normal value 0.3, may double in Bronchitis
36
What is emphysema?
Permanent dilatation of any air spaces distal to the terminal bronchiole WITHOUT fibrosis
37
Two forms of emphysema? (just recognise)
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.
38
Histology of which disease: mucous plugs in bronchi/oles are infiltrated with eosinophils and Charcot-Leyden crystals. Curshmann spirals appear as coiled mucous fragments.
Asthma
39
Lung morphology in asthma?
Ballooned lungs that meet in the midline of the anterior mediastinum
Due to air trapping as a result of mucous plugs
40
What produces Charcot leyden crystals?
Eosinophils in asthma
41
What are Creola bodies?
Clumps of respiratory epithelium that have been shed from mucosa
42
Histology features of asthma?
Marked eosinophil infiltration
Thickening of sub epithelial basement membrane
Hypertrophy of bronchial smooth muscle due to sustained contraction
43
Most common organism causing TB in developed countries?
Mycobacterium tuberculosis
44
How is mycobacterium tuberculosis stained for?
Acid fast and alcohol fast RODS
Stained using Ziehl-Neelsen stain
3-6 wks for microbial culture
45
Pathological hallmark of TB?
Caseating Granulomatous inflammation
Epitheliod macrophages surrounded by lymphocytes (secretes many interleukins leading to chronic infection)
46
Clinical features of TB
```
Cough with sputum/blood
Chest pain
Night sweats
Weight loss
Fatigue
```
47
Describe (a) Primary TB (b) Secondary TB
(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
Potential complications of secondary TB?
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
Treatment of TB (simple)
More than 1 drug needed
50
Clinical features of restrictive lung disease?
SOB
Reduced FV1/FVC
Bilateral CT shadowing
Hypoxia
51
What may cause parenchymal lung disease?
Interstitial oedema
Cellular infiltration
Fibrosis
52
What may cause parenchymal lung disease?
Interstitial oedema
Cellular infiltration
Fibrosis
53
Pathology of parenchymal lung restrictive disease?
Chronic inflammation leads to fibrosis and thickening of ALVEOLAR CAPILLARY WALL
Gas exchange is impaired
Destruction of alveoli and decreased expansibility of lung
54
Histology of which disease: Intra-alveolar fibrosis, obliterative fibrosis and interstitial fibrosis leading to END STAGE honeycomb lung
Lung fibrosis
55
What is intra-alveolar fibrosis?
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
What is obliterative fibrosis?
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
Interstitial fibrosis can be classified into which two groups?
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
Define pneumocosis
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
How is asbestosis diagnosed?
Lung biopsy: Fibrosis and asbestos bodies (asbestos fibres coated by protein and iron)
60
What percentage of people with sarcoidosis develop interstitial fibrosis?
5-15%
61
Organs affected in sarcoidosis?
90%- lung and mediastinal lymph node involvement
Also:
- Eyes: Iritis, choroiditis, retinitis
- Liver
- Skin, erythema nodosum
- Marrow
- Kidneys
62
Histology of which disease: Tight, non-caseating granulomata. Firbosis with bulla formation.
Sarcoidosis
63
What type of condition is extrinsic allergic alveolitis?
Hypersensitivity pneumonitis which leads to interstitial fibrosis
64
Examples of extrinsic allergic alveolitis?
Farmer's lung-mouldy hay
Bird-Fanciers lung- Bird serum and excreta
Chicken lung- Feathers
Detergent packers lung- bacillus form biological washing powder
65
Pathology of extrinsic allergic alveolitis?
Poorly formed non-caseating GRANULOMAS (resolve within 6 months)
Background of diffuse chronic interstitial fibrosis
May progress to honeycomb lung
66
What is Cryptogenic (idiopathic) fibrosing alveolitis?
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
Hallmark of ARDS?
Diffuse pattern of alveolar damage
Causes:
- Refractory hypoxaemia
- CXR- Bilateral opacification
- Multiorgan failure due to hypoxia
68
3 phases of diffuse alveolar damage?
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
Histological hallmark of diffuse alveolar damage?
HYALINE MEMBRANE (mixture of fibrin and necrotic alveolar cells which have formed into thin layers)
70
Causes of DAD (diffuse alveolar damage) and ARDS? (many, just recognise a few)
```
Major trauma
Sepsis
Near drowning
Gastric aspiration
Smoke/fumes
Major burns
Chemo
Pneumonia
DIC
Blood transfusion
Acute pancreatitis!!
Cardiac surgery bypass
```
71
Type of hypersensitivity in acute exposure of extrinsic allergic alveolitis?
Type III
| SOB, fever,cough a few hours post exposure
72
Type of hypersensitivity in repeated exposure of extrinsic allergic alveolitis?
Type 4 (eg man with one pigeon) cell mediated
Granulomas, interstitial fibrosis
Progressive respiratory failure, slow
73
Most common population affected by sarcoidosis?
Age 20-40
| COmmon in scandanavians and black population in USA
74
Electrolyte abnormality in sarcoidosis?
Hypercalcaemia, 1 in 5
75
Symptoms of sarcoidosis?
Fatigue, fever, weight loss, SOB, erythema nodosum, exercise intolerance
Anterior uvetitis or iritis
Obscure neurological symptoms
76
Pathogenesis of pulmonary oedema?
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
Macroscopic lung findings in pulmonary oedema?
Lungs are heavy and wet
Copius amounts of frothy fluid in airways
Distended subpleural lymphatics
Enlarged hilar lymph nodes
78
CXR features of pulmonary oedema
Kerley B lines
Upper lobe diversion
Prominent hilar regions (bats wing)
79
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
Pulmonary oedema
80
Types of embolism?
Thromboembolism (>90%)
Others:
- atheromatous
- amniotic fluid
- gas (trauma)
- fat (trauma, long bone fractures)
- tumour mets
- Foreign material (IV drugs)
- Infective agents (IE)
81
Effects of PE depending on size?
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
Difference between transudates, exudates, and empyema?
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
Risk factors for lung cancer
Smoking (95% cases)
Occupational (asbestos causing adenocarcinoma, arsenic, cadmium, coal, silica, nickel)
Pollution
Fibrosis
Radon
84
Overall 5 year survival of lung Ca?
4-7%
85
Symptoms of lung cancer
```
Cough
SOB
Haemoptysis
Weight loss
Chest pain
```
PARANEOPLASTIC SYNDROMES IN SMALL CELL
86
Local effects of lung tumour?
Hoarseness
Diaphragm paralysis
Superior vena cava syndrome
Horner's
87
Examples of paraneoplastic syndromes caused by lung tumour?
Lambert-Eaton syndrome
Acanthosis nigricans
Hypertrichosis
Cushing;s
SIADH
Hypertrohic pulmonary osteoarthropathy
88
Types of non-small cell cancers?
85% of lung cancers
Adenocarcinoma most common
Squamous cell
Large cell
89
Patterns of spread of lung adenocarcinoma?
May have multiple patterns in ONE tumour
Adenocarcinoma in situ
Lepidic spread (abnormal cells use alveoli like scaffolding) may lead to adenocarcinoma
90
Well vs poorly differentiated lung adenocarcinoma?
Well: Evident gland formation
Poor: Little glands
Use of IHC might help if pattern unclear.
91
How to tell if lung adenocarcinoma is primary or secondary?
IHC staining with thyroid transcription factor (TTF-1). If positive, its primary.
If primary, do mutation testing: Test for ALK or EGFR mutations
92
Are adenocarcinomas central or peripheral?
Can be both
93
Are squamous cell carcinomas central or peripheral?
Central
94
Hallmark feature of squamous cell carcinoma in lung?
Areas of necrosis in the centre. Tumour grows so fast that blood supply cannot keep up.
95
Histology of which disease: Lung tumour showing keratinisation and intracellular bridges.
Squamous CC of lung
96
Are large cell lung carcinomas central or peripheral?
Central
97
Histology of which lung carcinoma: Large cells, pleomorphic nuclei. No squamous or glandular features
Large cell carcinoma
98
Types of neuroendocrine tumours of lung (3 in a spectrum)
Carcinoid (more orderly cells)
Atypical carcinoid
Small cell (less orderly cells)
99
Carcinoid tumours histology?
Low grade, central, obstructing bronchus
Malignant potential but good prognosis
Nested growth pattern, granular chromatin
100
Small cell carcinoma central or peripheral?
Also called OAT CELL carcinoma
Usually central and has metastasised at presentation
Poor prognosis
101
Histology of which lung carcinoma: Hyperchromatic nuclei, smudge chromatin (AZZOPARDI PHENOMENON), nuclear moulding, indistinct nucleoli
Small cell carcinoma
102
Which are more common, primary or secondary lung tumours?
Secondary, tend to present as multiple nodules
Carcinomas from breast, kidney, GIT
Also, sarcomas, melanoma, lymphoma
103
Why do we use molecular testing for EGFR in primary lung tumours?
Epidermal growth factor receptor mutation may respond to TKIs! (tyrosine kinase inhib.)
104
Example of primary pleural tumour
Malignant mesothelioma
105
Medial survival time of malignant mesothelioma?
11 months
Very aggressive
Long lag time between asbestos exposure and diagnosis
106
Histology of which pleural cancer: Biphasic histology as cells can differentiate along epitheliod or sarcomatoid roots. Therefore can look like sarcoma and adenocarcinoma
Malignant mesothelioma
Difficult to diagnose even with IHC staining to help
