Lung: Pneumoconiosis, Tumors Flashcards

1
Q

Silicosis increases chances of

A

TB and Lung cancer

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2
Q

6 disease processes of ASBESTOSIS

A
  1. Pleural plaques: local and diffused
  2. Pleural effusion: recurrent
  3. Parenchymal interstitial fibrosis
  4. Lung cancer
  5. Mesothelioma: pleural and peritoneum
  6. Laryngeal cancer
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3
Q

Smoking in asbestosis increases risk of what cancer, and has no effect on what?

A

Increases- lung cancer

No effect- mesothelioma

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4
Q

Pneumoconiosis definition

A
  1. Non neoplastic reaction
  2. To inhalation of
  3. MINERAL DUST
  4. inorganic, organic particulates, chemical fumes, vapours
  5. Encountered at work place
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5
Q

What is Caplan syndrome

A

Rheumatoid pneumoconiosis

Combination of RA and pneumoconiosis especially with

  1. Anthracosis
  2. Silicosis
  3. Asbestosis
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6
Q

What causes

  1. Siderosis
  2. Baritosis
  3. Stannosis
  4. Farmers lung
  5. Bagassosis
  6. Bird breeders lung
  7. Byssinosis
A
  1. Iron oxide
  2. BaSO4
  3. Tin oxide
  4. Mouldy hay
  5. Bagasse: fibrous remains after juice extraction from SUGARCANE and SORGHUM
  6. 🐦 droppings
  7. Cotton, flax, hemp
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7
Q

Most dangerous particle size

Why?

A

1-5 um

Because they can reach terminal airways and settle in their lining

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8
Q

Effect of particle size on pneumoconiosis

A

Small- rapid onset acute lung injury

Large- resist dissolution and may persist within parenchyma for years and cause chronic disease

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9
Q

Spectrum of coal workers pneumoconiosis

A
  1. Asymptomatic anthracosis
  2. Simple CWP
  3. Complicated CWP/ PMF (progressive massive fibrosis)
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10
Q

Silica admixed with coal dust favours which disease of CWP spectrum

A

PMF

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11
Q

Asymptomatic anthracosis

A
  1. Inhaled carbon pigment engulfed by alveolar/interstitial macs
  2. Accumulate in connective tissue along lymphatics
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12
Q

Simple CWP: histology, location, complications

A

HISTOLOGY

  1. Coal macules: 1-2 mm and consist of carbon laden macs
  2. Coal nodules: larger and consist of carbon laden macs and delicate network of collagen fibres

LOCATION

  1. More commonly affects upper lobes and upper zones of lower lobes
  2. Adjacent to respiratory bronchioles

COMPLICATIONS
1. Centrilobular emphysema

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13
Q

Complicated CWP/ progressive massive fibrosis (PMF)

Gross, histo

A

Associated with lung dysfunction

Gross

  1. Blackened scars: 1-10cm
  2. Usually multiple

Histology

  1. Dense collagen and pigment
  2. Center of lesion is necrotic, because of ischemia
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14
Q

Clinical presentation of CWP

A
  1. PMF: pulmonary dysfunction, pulmonary hypertension, cor pulmonale
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15
Q

Silicosis definition

A

An occupational lung disease caused by inhalation of Proinflammatory crystalline silica

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16
Q

Crystalline silica examples

A

Quartz- most common
Cristobalite
Tridymite

More dangerous than amorphous because MORE FIBROGENIC

17
Q

Acute silicosis histology

A

Accumulation of abundant lipoproteinaceous material in the alveoli

18
Q

Inflammatory cytokines made be macs ie implicated in silicosis

A

IL 1 and IL 18

19
Q

Silicosis Gross and microscopic morphology

A

Gross:

  1. Initially, in the hilar lymph nodes and upper parts of lung, tiny nodules
  2. The nodules later COALESCE to form Hard collagenous (fibrous) scars
  3. Nodules also might also undergo central cavitation secondary to TB or ischemia
  4. Fibrotic lesions in hilar LN or pleura
  5. Egg shell calcification
  6. Later, PMF

Micro:

  1. Hallmark lesion: central area of whorled collagen fibres and peripheral area of silica laden macs
  2. Birefringent silicates
20
Q

Onset of silicosis

A
  1. Slow, insidious: 10-30 years (most common)
  2. Accelerated: within 10 years of exposure
  3. Rapid: weeks or months of exposure
21
Q

Classify lung tumours

A

Add picturer page 714

21
Q

Adenocarcinoma precursor lesions

A
  1. Atypical adenomatous hyperplasia
    A. <5mm small lesion
    B. Has dysplastic pneumocytes lining alveolar walls
  2. Adenocarcinoma in situ
    A. <3cm
    B. Dysplastic cells growing along alveolar septae (lepidic pattern)
    C. May or May not have mucin
22
Q

Adenocarcinoma histology

A
  1. Malignant epithelial tumor with glandular differentiation or mucin production
  2. Patterns : PALMS (papillary, acinar, lepidic, micropapillary, solid)
23
Q

Adenocarcinoma IHC

A
  1. TTF-1:thryroid trans factor needed for normal lung maturation
  2. Napsin A
24
Q

Microinvasive Adenocarcinoma

A
A special type of Adenocarcinoma where
   A. Tumor size =3cm
   B. Invasion =5mm
   C. A/w scarring
   D. Peripheral lepidic growth pattern
25
Q

Mucinous Adenocarcinoma

A

Adenocarcinoma that produces mucin
A. Spreads aerogenously and has satellite tumours
B. Worse prognosis
C. Resembles lobar pneumonia

26
Q

At what earliest stage can SQUAMOUS cell carcinoma be detected in SPUTUM by cytology ?

A

Carcinoma in situ

Despite being Asymptomatic and undetectable on radiograph

27
Q

Ways for squamous cell carcinoma to grow? And resultant complications?

A
  1. Exophytic mass> obstructs lumen> ATELECTASIS and INFECTION >if partially, focal EMPHYSEMA
  2. Penetrate bronchial wall> infiltrate adjacent carina and mediastinum> PERICARDITIS, PLEURITIS
  3. Along a broad front> parenchymal mass
28
Q

Squamous cell carcinoma Gross and histology

A

Gross: LIKE ALMOST ANY OTHER LUNG CANCER

  1. Gray White
  2. Firm to hard
  3. Focal areas of hemorrhage and necrosis (esp when bulky)
  4. Necrotic areas might cavitate
Histology :
   1. Signs of keratinisation 
      A. Keratin pearls
      B. Intense eosinophilic cytoplasm
   2. Intercellular bridges
29
Q

AZZOPARDI effect

A

Basophilic staining of venule walls due to encrustation (being covered) by DNA from necrotic tumor cells in SMALL CELL CARCINOMA

31
Q

Small cell carcinoma histology

A
  1. Small cells ( <3 times the size of resting small lymphocyte)
  2. Scant cytoplasm, irregular margins
  3. SALT AND PEPPER nuclear appearance (finely granular nuclear chromatin)
  4. Cells are round/oval/spindle-shaped
  5. Nuclear moulding present
  6. High miṭotic count
  7. Necrosis common : AZZOPARDI EFFECT
32
Q

Paraneoplastic syndromes a/w lung cancers

A
1. Small cell carcinoma
   A. ACTH-Cushing's
   B. ADH-SIADH, hyponatremia
2. Squamous cell carcinoma 
   A. PTH, PTHRP, PG-E, cytokines-hypercalcemia
3. Gonadotropins-gynecomastia
4. Serotonin, bradykinin-carcinoid syndrome
5. Calcitonin-hypocalcemia
33
Q

Systemic manifestations of lung cancers (other than para neo)

A
  1. Lambort Eaten syndrome- tumor cells calcium channels cause auto-antibody production
  2. Peripheral neuropathy
  3. Acanthosis
  4. Horner syndrome- called PANCOAST tumor
  5. Trousseau syndrome- DVT, VTE
  6. HPOA- a/w clubbing
  7. Leukamoid reaction
34
Q

Pancoast tumor

A

These are apical lung cancers that invade the cervical sympathetic plexus to produce

  1. Intense pain in the distribution of ulnar nerve
  2. Horner syndrome ( MAPLE - ipsilaterally)
36
Q

What carcinoma has better prognosis and which has worse?

A

Better:
Squamous CC
Adenocarcinoma

Worse:
Undifferentiated eg large cell

45
Q

Mutation with worse prognosis

A

KRAS

46
Q

Types of asbestos fibres

A

Serpentine
Amphibole-worse
1. Elongated
2. Solubility

47
Q

Asbestos in cancer

A
  1. Tumor initiator
  2. Tumor promotor
  3. Generate ROS
    4.