Respiratory system Flashcards
1
Q
Sarcoidosis
A
- Seen in females»_space; males
- Type IV hypersensitivity, so CD4 TH1 cells can be seen ➡️ granuloma
- Immunologically mediated, associated with HLA-A1, HLA-B8
2
Q
Presenting complaints of sarcoidosis
A
- Eye: uveitis
- Salivary gland’s: Sicca syndrome/ Sjögren’s syndrome
- Lung is most commonly affected
- Hillary lymph node enlargement
- Skin, genitals and bone marrow can be affected
3
Q
Sarcoidosis, on histological examination
A
1. Non caseating/ naked granuloma: Lymphocytes collar absent 2. Asteroid bodies: Star shaped inclusions in giant cells 3. Schaumann bodies: Basophilic Ca+2 concretions
4
Q
Investigation findings of sarcoidosis
A
- Increased ACE levels
- Increased Ca+2 ➡️ metastatic calcification
- Increased CD4:CD8 ratio (normal is 2:1)
- Kveim’s test positive
5
Q
Hypersensitivity pneumonitis
A
It is an example of (both type III and) Type IV hypersensitivity
Honey combing and fibrosis of lung is seen
6
Q
Histoplasmosis
A
Caused by Histoplasma capsulatum
Seen in pigeon/ bird breeders (because fungus lives in bird droppings)
Grossly:
Tree bark appearance (like syphillitic aneurysm)
H&E:
caseating granuloma (like TB)
7
Q
Acid fast bacteria
Mycolic acid
A
My. Mycobacterium tuberculosis Nose. Novartis Is. Isospora Cold. Cryptosporidium and Hot. Hooklets of hydatid cyst
8
Q
Virulence factor of Mycobacterium tuberculosis
A
Cord factor
This bacteria can be seen in necrotic area
9
Q
Primary tuberculosis
A
Occurs on 1st exposure
Lesion in lower part of upper lobe and upper post of lower lobe subpleurally: Ghon’s focus
Ghon’s focus + lymph node involvement ➡️ Ghon’s complex
If calcified, Ranke complex
10
Q
Secondary or activation tuberculosis
A
Affects apex
Supraclavicular region of lung- Puhl’s focus
Infraclavicular region - Assmann’s focus
11
Q
Disseminated/ military tuberculosis
A
1-2 mm disseminated lesions all over
12
Q
Most common cause of community acquired pneumonia
A
Streptococcus pneumonia
13
Q
Pathological classification of pneumonia
A
- Lobar pneumonia
2. Lobular (bronchial) pneumonia
14
Q
4 stages of lobar pneumonia
A
1. Congestion : 1-2 days Full of RBC and exudate fluid 2. Red hepatisation: 2-4 days Fibrin and RBC 3. Grey hepatisation: 4-8 days RBC disintegration 4. Resolution: 9-10 days Most common outcome
15
Q
Etiological classification of pneumonia
A
1. Typical: bacterial Lots of exudate Purulent cough 2. Atypical: Vital, mycoplasma, respiratory syncytial virus, chlamydia pneumonia Less exudate Non purulent cough
16
Q
TB infects
Type of cells which are increased after TB infection
A
Macrophages
Lymphocytes
17
Q
Features of viral pneumonia
A
- Presence of interstitial inflammation
- Bronchiolitis
- Deficiency of alveolar exudate
- Multinucleate giant cells in bronchial wall
18
Q
Most common malignancy of lung
A
Metastasis
Most common is from breast carcinoma
19
Q
Most common benign lung tumour
A
Pulmonary hamartoma
Abnormal proliferation of cells
X-rays: coin shaped lesions
20
Q
Classification of lung tumours
A
- Small cell lung cancer
- Non-small cell cancer:
a) adenocarcinoma
Precursor lesson:
• atypical adenomatous hyperplasia
• bronchoalveolar carcinoma (BAC/ adenocarcinoma in situ)
b) squamous cell carcinoma
Precursor lesion: squamous cell carcinoma in situ
21
Q
Squamous cell carcinoma of lung
A
Centrally located Cavitary lesions formed Smoking associated Males > females Paraneoplastic syndrome: hypercalcemia due to PTHrp (related peptide) Pathogenesis: p53 gene mutations
22
Q
Microscopy and immunohistochemistry of squamous cell carcinoma
A
Microscopy: 1. Keratin pearls 2. Desmosomes (adhere 2 squamous cells) Immunohistochemical markers: 1. CK+ (cytokeratin) 2. p63 3. p40
23
Q
Adenocarcinoma of lung
A
M/C lung cancer in women and in non smokers
Peripherally lesions
Paraneoplastic syndrome: migratory thrombophlebitis
H&E: glands lined by malignant cells
IHC markers: TTF-1, NAPSIN-A
24
Q
Bronchoalveolar carcinoma
A
Adenocarcinoma in situ
• Good prognosis
• Tumour cells grow along the bronchoalveolar lining
• Butterflies in a fence/ lepidic/ filigree pattern
25
Small cell carcinoma of lung
```
Strongest association with smoking
Males> females
Paraneoplastic syndrome: Cushing syndrome, SIADH (M/C PNS)
Produces maximum PNS
Starts centrally ➡️ peripheral, worst prognosis
Metastasises to brain
Chemosensitive
Pathogenesis: L-MYC mutation
```
26
Microscopy of small cell carcinoma of lung
1. Small cells
2. Nuclear moulding
3. Azzopardi effect:
Tumour cells (fragile) break ➡️ release nuclear chromatin ➡️ deposited in blood vessel wall ➡️ basophilic blood vessel walls
4. Salt and pepper chromatin
On electron microscopy: dense core neurosecretory granules
27
IHC markers for small cell carcinoma of lung
1. NSE: neuron specific enolase
2. Chromogranin
3. Synaptophysin
28
The H&E , IHC and electron microscopy findings are same for neuroendocrine tumours like
1. Pheochromocytoma
2. Carcinoid tumour
3. Paraganglioma
4. Carotid body tumours
5. Small cell carcinoma of lung
29
Large cell carcinoma of lung
```
Large pleomorphic cells
Aggressive tumour
PNS: gynaecomastia
Clinically:
Cough, haemoptysis
Weight loss
Dyspnoea
```
30
Pancoast tumour
```
Lung cancer at the apex
Compresses cervical sympathetic chain ➡️ Horner’s syndrome
Punjabi. Ptosis
M. Miosis
E. Enophthalmos
A. Anhidrosis
L. Loss of ciliospinal reflex
```
31
Spread of lung carcinomas
1. Directly: to recurrent laryngeal nerve ➡️ hoarseness
2. Metastasis to brain (adrenals)
3. To lymph nodes (hilar)
32
Carcinoid tumour
```
Arises from Kulchitsky cells of lungs
Clinical presentation:
1. Flushing
2. Sweating
3. Diarrhoea
Microscopy, electron microscopy and IHC are same as all neuroendocrine tumours like small cell carcinoma
```
33
Classification of carcinoid tumour
```
1. Typical:
<2 mitosis/10 HPF
No necrosis
2. Atypical:
2-10 mitosis/10 HPF
Necrosis present
```
34
Most common cause of pleural malignancy
Metastasis
| Commonly from lung
35
Malignant mesothelioma
Most specific lung carcinoma associated with asbestos exposure
• duration of exposure:>25 years (otherwise lung adenocarcinoma)
IHC markers:
1. Calretinin (best marker)
2. CK 5/6
3. WT-1
36
Microscopy of malignant mesothelioma
```
Three types of cells:
1. Spindle cells
2. Epitheloid cells
3. Sarcomatoid cells
Electron microscopy:
Long slender microvilli/ tonofilaments
(Opp of lung adenocarcinoma where short plump microvilli are seen)
```
37
Acinus
Combination of respiratory bronchiole, alveolar duct and alveolar sac
38
Type 2 pneumocytes
5% of cells
| Involved in repair and produce surfactant
39
Part of respiratory tract not lined by pseudostratified ciliated columnar epithelium
Vocal cords is lined by stratified squamous epithelium
40
Adult respiratory distress syndrome is also called as
| Its properties
1. Acute lung injury- ALI
2. Diffuse alveolar damage- DAD
3. Hyaline membrane disease
Microscopy:
Hyaline production and deposition in sacs
X-ray:
B/L diffuse infiltrate ➡️ white-out appearance
41
Pathogenesis of adult respiratory distress syndrome/ALI/DAD
1. Toxin in alveoli
2. Macrophage activation
3. IL-1, IL-6 and TNF-α secretion
4. Neutrophil recruitment in capillaries
5. Protease secretion:
• endothelial damage
• procoagulase activation ➡️
6. Production of fibrin
7. Fibrin leaks out of capillaries
8. Hyaline membrane
Macrophage activation also causes TGF-β secretion
42
Obstructive lung diseases
```
1. COPD:
• Chronic bronchitis
• Emphysema
2. Bronchiectasis
3. Bronchial asthma
```
43
Emphysema
```
Irreversible dilation and destruction of air spaces distal to the terminal bronchioles
Involves:
1. Respiratory bronchioles
2. Alveolar ducts
3. Alveolar sac
Gross: bullae due to destruction of walls
C/F:
Pursed lip breathing
Pink puffers
```
44
Pathogenesis of emphysema
1. Smoking
2. α-1 Antitrypsin deficiency, which is an anti-elastase/anti-protease
• Both increases elastase ➡️ tissue damage
45
Types of emphysema
```
1. Centriacinar:
Central acinar affected
2. Panacinar:
Entire acinus affected
3. Distal acinar/ paraseptal :
Alveolar sacs/ducts affected
4. Irregular:
M/C histologically
```
46
Differences between centriacinar and panacinar emphysema
```
1. Centriacinar:
• M/C clinically
• Smoking associated
• Upper lobes affected
2. Panacinar:
• α-1 Antitrypsin deficiency associated
• Lower lobes affected
```
47
Type of emphysema associated with spontaneous pneumothorax
Distal acinar/ paraseptal emphysema where alveolar sacs/ ducts are affected
Rupture in alveolar sacs leads to spontaneous pneumothorax
48
Definition of chronic bronchitis
Persistent productive cough for at least 3 months, in at least 2 consecutive years in absence of any other identifiable cause
49
Reid’s index
Ratio of thickness of mucus glands layer to thickness of basement membrane between epithelium and cartilage =bc/ad
Normal: 0.4
Increased in chronic bronchitis
50
Chronic bronchitis pathogenesis
1. Smoking (in 90%)
2. Epithelial irritation
3. Increased mucous production:
• Increased Reid’s index
• increased risk of 2° infections
• goblet cell hyperplasia
Chronic bronchitis is a pre malignant condition
It is not associated with amyloidosis unlike other chronic inflammations
51
Bronchial asthma
Reversible bronchoconstriction and inflammation of airways
Type I hypersensitivity reaction
Airway remodelling occurs
52
Bronchial asthma types
```
1. Allergic/ Atopic/ Extrinsic:
• Type I hypersensitivity
• increased IgE
• in children usually
• family history maybe present
2. Intrinsic/ Non-atopic:
• IgE not raised
• in adults usually
• no family history
```
53
Bronchial asthma genetics
1. IL-13 gene polymorphism
2. ADAM 33 polymorphism
3. Gene for atopy ➡️ chromosome 5q
4. Increased YKL 40 leads to increased severity
54
Bronchial asthma sputum microscopy
```
1. Curschmann’s spirals:
Whorled mucus plugs
2. Charcot Leyden crystals:
Eosinophilic membrane protein Galectin 10
3. Creola bodies:
Slighted mucus epithelium
```
55
Airway remodelling
1. Increased fibrosis
2. Increased vascularity
3. Increased smooth muscles
56
Bronchiectasis
Abnormal permanent dilation of bronchi and bronchioles
HRCT is taken for diagnosis
Complications:
1. Empyema
2. Lung abscess
3. Amyloidosis
Probe reaches almost upto pleura (rather than stopping 1-4 cm before)
57
Causes of bronchiectasis
1. Kartagener’s syndrome
2. Cystic fibrosis
3. Obstruction
4. Infection
The last 3 affects the lower lobes
58
Kartagener’s syndrome/ Immotile cilia syndrome/ 1° ciliary dyskinesia
```
Mutation in dynein arm of cilia
Triad:
1. Sinusitis
2. Situs inversus
3. Bronchiectasis
Infertility
```
59
Restrictive lung disorders
```
1. Fibrosing lung disorders:
• Usual interstitial pneumonia
• Non-specific interstitial pneumonia
• Cryptogenic organising pneumonia
2. Pneumoconiosis / occupational lung disease:
• Coal worker’s pneumoconiosis
• Caplan syndrome
• Silicosis
• Asbestosis
```
60
Factors for development of pneumoconiosis
1. Size of particles: <5 microns are dangerous
2. Solubility of particles: inversely
3. Duration of exposure
4. Synergistic factors like smoking
61
Coal worker’s pneumoconiosis
```
Usually affects upper lobes
Three types:
1. Asymptomatic anthracosis
2. Simple coal worker’s pneumoconiosis:
• coal macules and nodules
3. Complicated coal worker’s pneumoconiosis:
• progressive massive fibrosis
```
62
Caplan syndrome
Coal worker’s pneumoconiosis + rheumatoid arthritis
63
Grinder’s disease/ Silicosis/ Miner’s disease
* M/C occupational lung disease in the world
* M/C particle causing silicosis is quartz
* increased risk of TB and cancer
* X-ray: egg cell calcifications of lymph nodes
* produces nodular fibrosis of lung
