Module 8-Environmental Pathology Flashcards

1
Q

Coal Worker’s Pneumoconiosis is due to what?

A

Inhalation of coal dust which leads to black lung disease

also in the stem look for coal workers

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2
Q

In coal workers pneumoconiosis there are 3 types, each card will go through the types. Type 1 —

A

Asymptomatic: accumulation of carbon in perilymphatic regions and lymph nodes

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3
Q

2nd type of coal workers pneumoconiosis is…

A
  1. Simple: aggregation of carbon-laden macrophages in nodules and macules
    - -occurs in the upper lobes
    - -Macules: macrophages containing coal
    - -Nodules: multiple macrophages with fibrosis, more common
    - -may cause dilation of alveoli (focal dust emphysema)
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4
Q

3rd type of coal workers pneumoconiosis is…

A
  1. Complicated: progressive massive fibrosis
    –coalescence of modules into fibrosis scars
    –large blackened scars
    —significant resp impairment
    (note that as the coal miner is exposed to more and more coal then the pathology goes from simple to complicated)
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5
Q

Why is complicated pneumoconiosis more dangerous?

A

Because your exposed to more coal and macrophages (dust cells) start secreting TGFbeta and TGFbeta starts recruiting fibroblasts —- leads to fibrosis

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6
Q

What are the signs and symptoms of pneumoconiosis?

A

Interstitial dry cough and SOB

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7
Q

What would be the spirometry results for pneumoconiosis?

A
normal FEV/FVC (the air that is in can get out fine) (they are both decreases which is why the ratio is normal) 
TLC low (aka cant get the air in )
restrictive lung disease
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8
Q

What are complications for pneumoconiosis?

A
Cor pulmonale 
Contraction atelectasis (b/c of fibrosis)
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9
Q

Explain the coal rank

A

Ratio of carbon to other materials
–higher ratio of other materials associated with higher risk of CWP
aka you want a low rank!!!!

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10
Q

Asbestosis is due to inhalation of asbestos fibers, what common population?

A

SHIP YARD WORKERS (this will be in the stem)

—others mining, construction workers , milling or home insulation

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11
Q

What are the two shapes of the asbestosis fibers?

A

Amphobole: straight/stiff and more dangerous because it penetrates the lower lobes
Crystotile: curly/flexible and less pathogenic because more easily removed by mucociliary apparatus.

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12
Q

Asbestosis causes diffuse interstitial fibrosis (not nodular) in ________ lobes around bronchioles, alveolar ducts and interstitum

A

Lower

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13
Q

What does asbestosis look like on gross appearance?

A

Honeycomb lung: fibrosis

  • -thickening of the pleura
  • –see thickening of RV — cor pulmonale
  • -asbestos in the lymph nodes — bilateral hilar lymphadenopathy —carcinoma
  • –large pleural mass in the recess – obliteration of pleural space
  • –all indications of mesothelioma
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14
Q

What does asbestosis look like on histology?

A

Asbestos body —- Ferruginous bodies: macrophages + asbestos fibers

  • -macrophages attempt to phagocytize asbesto fiber – macrophages coat fiber with iron (from their own ferritin) – ferric state — beaded structures with translucent macrophages
  • -H & E: Golden Brown
  • –Prussian Blue: blue
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15
Q

Asbestosis is a restrictive lung disease so what would you expect on spirometry?

A

normal FEV1/FVC

low TLC

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16
Q

What are the complications of asbestosis?

A

HC lung —- fibrosis (Restrictive) —- contraction atelectasis
Peribronchiolar Fibrosis
Resp Failure
Cor Pulmonale

17
Q

In asbestosis there is an increased risk for cancer, what cancers?

A
  1. Bronchogenic Carcinoma (also called squamous cell lung carcinoma): (most common)
    - -associated with cig smoking
    - –smoking + asbestosis = greater risk of cancer
  2. Mesothelioma (quite rare)
    - -pleural cancer due to asbestosis
    - -neoplastic mesothelial cells: lungs unsheated with yellow-white firm (gelantinous) layer of tumor.
18
Q

So review time! If a patient presents with a bronchogenic carcinoma (Aka a squamous cell lung carcinoma) due to asbestosis, what paraneoplastic syndrome may you see in this patient?

A

Hypercalcemia due to PTH related peptide

19
Q

What are pleural plaques in regards to asbestosis?

A

Well circumscribes plaques of dense collagen and Ca2+ with dystrophic calcification

  • –found on anterior and posterolateral parietal pleura (not visceral) and domes of the diaphragm
  • –flat or nodular: does not contain asbestos bodies
20
Q

Silicosis is seen in what kind of patients and due to inhalation of what?

A

SANDBLASTERS
inhalation of silicia (silicon dioxide)
–crystaline form (quartz) – most fibrogenic

21
Q

What is the general progression of silicosis?

A

Slow, progressive nodular and fibrosing pneumoconiosis (not granulomatous) — 10-20 years — chronic silicosis
–nodular lesions may undergo central cavitation

22
Q

What is the pathogenesis for silicosis ?

A

Starts in the upper lobe

  • -macrophages engulf crystalline silica (w/SiOH) – H bonds with proteins and phospholipids of macrophages – damage cell membrane and kills macrophages
  • -macrophages release TGFbeta –produce collagen — whorls of collagen nodules (surrounded by lymphocytes and macrophages) –H and E looks pink
23
Q

What is the presentation for silicosis?

A

Dry cough

SOB

24
Q

What do you see on CXR and Stain with polarized microscopy and spirometry?

A

CXR: eggshell calcification in hilar LN (thin rims of calcification in hilar LN) – dystrophic calcification
Polarized Microscopy: weakly birefringent — white particles of silica glowing
Spirometry: Restrictive: FEV/FVC normal and TLC low

25
Q

What are the complications of silicosis?

A

Fibrosis with dystrophic calcification (contraction atelectasis)
Resp failure
Cor pulmonale
Increased risk for progressive TB: increase use of macrophages to digest silica – none available to form granulomatous inflammatory response (poor granuloma formation)

26
Q

On gross specimen slide 3a, what are the arrows pointing to?

A

Red: pleural thickening
Black: fibrosis (stained with trichrome, which is why it looks blue)

27
Q

Lead poisoning is more common in children, why?

A

Prone to eat paint

28
Q

What are the signs in children vs adults of lead poisoning?

A

Children: CNS —- low IQ, ADHD, learning difficulties
Adults: PNS most common is the common fibular and this leads to foot drop also radial nerve leads to wrist drop

29
Q

What is the best investigation for lead poisoning?

A

Lead Levels in the blood (Venous blood sampling)

30
Q

5 organ systems are involved in lead poisoning, each card will go through a system. First is blood

A

Blood:

  • -Iron has high affinity for sulfhydral groups, inhibits two enzymes in erythropoiesis —- impairs heme synthesis
  • –Inhibits iron incorporation into RBC – no heme synthesis
  • –Increased iron in blood but not in Hb — functional iron deficient anemia
  • -microcytic hypochromatic anemia with mild hemolytic anemia (hemolytic anemia is due to the shut down of the Na/K pump in cell membranes)
  • –Basophilic stippling: made up of ribosomal RNA because lead inhibits ribonucleus
31
Q

The second system involved in lead poisoning is skeletal system

A

Skeletal system:

  • –Xray of a kids knees: Lead lines (epiphyseal plates — lead competes with calcium)
  • –gums (blue/black lines)
  • -lead is competing with calcium for binding phosphate in bones
32
Q

The third system involved in lead poisoning is GI

A

GI:

–lead leads to colicky abdominal pain and constipation

33
Q

The fourth system involved in lead poisoning is Renal

A

Renal:

  • –acute renal tubular necrosis
  • -intranuclear inclusions in RT epithelium (insoluble protein)
  • -damages PCT: fanconi syndrome
34
Q

The fifth system involved in lead poisoning is CNS

A

CNS: leads to demyelination

  • -adults: PNS wrist and foot drop
  • -children: CNS: ADHD, Low IQ