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Pathology MBBS > Respiratory system > Flashcards

Respiratory system Flashcards

1
Q

Sarcoidosis

A
  • Seen in females&raquo_space; males
  • Type IV hypersensitivity, so CD4 TH1 cells can be seen ➡️ granuloma
  • Immunologically mediated, associated with HLA-A1, HLA-B8
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2
Q

Presenting complaints of sarcoidosis

A
  1. Eye: uveitis
  2. Salivary gland’s: Sicca syndrome/ Sjögren’s syndrome
  3. Lung is most commonly affected
  4. Hillary lymph node enlargement
  5. Skin, genitals and bone marrow can be affected
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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
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4
Q

Investigation findings of sarcoidosis

A
  1. Increased ACE levels
  2. Increased Ca+2 ➡️ metastatic calcification
  3. Increased CD4:CD8 ratio (normal is 2:1)
  4. Kveim’s test positive
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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

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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)

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7
Q

Acid fast bacteria

Mycolic acid

A 
My. Mycobacterium tuberculosis
Nose. Novartis
Is. Isospora
Cold. Cryptosporidium 
and
Hot. Hooklets of hydatid cyst
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8
Q

Virulence factor of Mycobacterium tuberculosis

A

Cord factor

This bacteria can be seen in necrotic area

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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

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10
Q

Secondary or activation tuberculosis

A

Affects apex
Supraclavicular region of lung- Puhl’s focus
Infraclavicular region - Assmann’s focus

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11
Q

Disseminated/ military tuberculosis

A

1-2 mm disseminated lesions all over

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12
Q

Most common cause of community acquired pneumonia

A

Streptococcus pneumonia

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13
Q

Pathological classification of pneumonia

A
  1. Lobar pneumonia

2. Lobular (bronchial) pneumonia

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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
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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
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16
Q

TB infects

Type of cells which are increased after TB infection

A

Macrophages

Lymphocytes

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17
Q

Features of viral pneumonia

A
  1. Presence of interstitial inflammation
  2. Bronchiolitis
  3. Deficiency of alveolar exudate
  4. Multinucleate giant cells in bronchial wall
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18
Q

Most common malignancy of lung

A

Metastasis

Most common is from breast carcinoma

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19
Q

Most common benign lung tumour

A

Pulmonary hamartoma
Abnormal proliferation of cells
X-rays: coin shaped lesions

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20
Q

Classification of lung tumours

A
  1. Small cell lung cancer
  2. 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
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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
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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
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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

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24
Q

Bronchoalveolar carcinoma

A

Adenocarcinoma in situ
• Good prognosis
• Tumour cells grow along the bronchoalveolar lining
• Butterflies in a fence/ lepidic/ filigree pattern

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25
Q

Small cell carcinoma of lung

A 
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
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26
Q

Microscopy of small cell carcinoma of lung

A
  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
Q

IHC markers for small cell carcinoma of lung

A
  1. NSE: neuron specific enolase
  2. Chromogranin
  3. Synaptophysin
28
Q

The H&E , IHC and electron microscopy findings are same for neuroendocrine tumours like

A
  1. Pheochromocytoma
  2. Carcinoid tumour
  3. Paraganglioma
  4. Carotid body tumours
  5. Small cell carcinoma of lung
29
Q

Large cell carcinoma of lung

A 
Large pleomorphic cells
Aggressive tumour
PNS: gynaecomastia
Clinically:
 Cough, haemoptysis
 Weight loss
 Dyspnoea
30
Q

Pancoast tumour

A 
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
Q

Spread of lung carcinomas

A
  1. Directly: to recurrent laryngeal nerve ➡️ hoarseness
  2. Metastasis to brain (adrenals)
  3. To lymph nodes (hilar)
32
Q

Carcinoid tumour

A 
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
Q

Classification of carcinoid tumour

A 
1. Typical:
 <2 mitosis/10 HPF
 No necrosis
2. Atypical:
 2-10 mitosis/10 HPF
 Necrosis present
34
Q

Most common cause of pleural malignancy

A

Metastasis

Commonly from lung

35
Q

Malignant mesothelioma

A

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
Q

Microscopy of malignant mesothelioma

A 
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
Q

Acinus

A

Combination of respiratory bronchiole, alveolar duct and alveolar sac

38
Q

Type 2 pneumocytes

A

5% of cells

Involved in repair and produce surfactant

39
Q

Part of respiratory tract not lined by pseudostratified ciliated columnar epithelium

A

Vocal cords is lined by stratified squamous epithelium

40
Q

Adult respiratory distress syndrome is also called as

Its properties

A
  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
Q

Pathogenesis of adult respiratory distress syndrome/ALI/DAD

A
  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
Q

Obstructive lung diseases

A 
1. COPD:
• Chronic bronchitis
• Emphysema
2. Bronchiectasis
3. Bronchial asthma
43
Q

Emphysema

A 
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
Q

Pathogenesis of emphysema

A
  1. Smoking
  2. α-1 Antitrypsin deficiency, which is an anti-elastase/anti-protease
    • Both increases elastase ➡️ tissue damage
45
Q

Types of emphysema

A 
1. Centriacinar:
 Central acinar affected
2. Panacinar:
 Entire acinus affected
3. Distal acinar/ paraseptal :
 Alveolar sacs/ducts affected
4. Irregular:
 M/C histologically
46
Q

Differences between centriacinar and panacinar emphysema

A 
1. Centriacinar:
• M/C clinically
• Smoking associated
• Upper lobes affected
2. Panacinar:
• α-1 Antitrypsin deficiency associated
• Lower lobes affected
47
Q

Type of emphysema associated with spontaneous pneumothorax

A

Distal acinar/ paraseptal emphysema where alveolar sacs/ ducts are affected
Rupture in alveolar sacs leads to spontaneous pneumothorax

48
Q

Definition of chronic bronchitis

A

Persistent productive cough for at least 3 months, in at least 2 consecutive years in absence of any other identifiable cause

49
Q

Reid’s index

A

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
Q

Chronic bronchitis pathogenesis

A
  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
Q

Bronchial asthma

A

Reversible bronchoconstriction and inflammation of airways
Type I hypersensitivity reaction
Airway remodelling occurs

52
Q

Bronchial asthma types

A 
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
Q

Bronchial asthma genetics

A
  1. IL-13 gene polymorphism
  2. ADAM 33 polymorphism
  3. Gene for atopy ➡️ chromosome 5q
  4. Increased YKL 40 leads to increased severity
54
Q

Bronchial asthma sputum microscopy

A 
1. Curschmann’s spirals:
 Whorled mucus plugs 
2. Charcot Leyden crystals:
 Eosinophilic membrane protein Galectin 10
3. Creola bodies:
 Slighted mucus epithelium
55
Q

Airway remodelling

A
  1. Increased fibrosis
  2. Increased vascularity
  3. Increased smooth muscles
56
Q

Bronchiectasis

A

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
Q

Causes of bronchiectasis

A
  1. Kartagener’s syndrome
  2. Cystic fibrosis
  3. Obstruction
  4. Infection
    The last 3 affects the lower lobes
58
Q

Kartagener’s syndrome/ Immotile cilia syndrome/ 1° ciliary dyskinesia

A 
Mutation in dynein arm of cilia
Triad:
1. Sinusitis
2. Situs inversus 
3. Bronchiectasis
Infertility
59
Q

Restrictive lung disorders

A 
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
Q

Factors for development of pneumoconiosis

A
  1. Size of particles: <5 microns are dangerous
  2. Solubility of particles: inversely
  3. Duration of exposure
  4. Synergistic factors like smoking
61
Q

Coal worker’s pneumoconiosis

A 
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
Q

Caplan syndrome

A

Coal worker’s pneumoconiosis + rheumatoid arthritis

63
Q

Grinder’s disease/ Silicosis/ Miner’s disease

A
  • 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

Pathology MBBS (17 decks)

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