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Week 4- Inhalational Lung Disease Flashcards

1
Q

What are some origins of pollutants that can cause lung disease?

A
  • natural (sand)
  • combustion (exhaust, cigarettes)
  • synthetic
  • agriculture
  • chemical reactions
  • unknown
  • indoor (cleaning products
  • outdoors (ozone)
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2
Q

What are some possible patterns of exposure to lung pollutants?

A
  • magnitude of exposure (insidious vs accidental?)
  • context
  • persistence (acute? chronic?)
  • duration (steady? intermittent? diurnal?)
  • geography
  • conditions (exertion? PPE?)
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3
Q

What 3 factors determine the lung response to an inhaled pollutant?

A
  1. Deposition
  2. Clearance/Detoxification
  3. Biological activity of the substance
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4
Q

What determines the deposition of noxious gases and particles in the respiratory tract?

A

Gases

  • depends on solubility (henry’s constant, e.g. gas:liquid ratio)
  • higher gas:liquid deposits in the alveoli
  • lower gas:liquid deposits in nasopharynx/upper resp (e.g. ammonia)

Particles

  • depends mostly on particle size (sizes: thoracic, coarse, fine, ultrafine). Exhaust and cigarette smoke is ultrafine
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5
Q

What are the 3 patterns of deposition and what do they depend on? How could a pollutant be absorbed systemically?

A

Impaction (large airwyas, upper airways)

Sedimentation: (small airways)

Diffusion (alvoeli) ***may be able to enter the blood through this route and be absorbed systemically**

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6
Q

What are the lung’s natural defences?

A
  • nasal filtering
  • cough/sneeze reflex
  • mucociliary escalator
  • alveolar macrophages
  • bactericidal enzymes
  • lymphatic system
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7
Q

What determines whether a pollutant is cleared/detoxified from the lungs?

A
  • the site of deposition
  • the health of natural lung defences
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8
Q

What are some pathophysiologic mechanisms by which pollutants cause lung disease?

A

Non-specific chemical reactivity

  • ROS
  • strong acid or base
  • inflammation–>necrosis–>fibrosis

Specific toxic effects

  • DNA mutation
  • invoke allergic response
  • change O2 carrying capacity
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9
Q

What are some disease states that can caused (and exacerbated) by pollutant exposure?

A

Upper resp tract:

  • rhinitis
  • laryngitis

Upper airways

  • bronchitis
  • bronchiolitis

Small airways:

  • asthma
  • COPD

Diffuse:

  • Cancer
  • interstitial disease
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10
Q

What are some strategies to diagnose an occupational/environmental disease?

A
  • acquire MSDS to know what you could be dealing with
  • take a thorough history
  • can send patient home with a spirometer and have them do PEF several times a day to establish whether the symptoms aer due to work exposure
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11
Q

How to minimize the incidence of diseases caused by environmental exposure?

A

Good industrial hygiene:

  • Engineering controls
  • administrative controls
  • PPE

Government control

  • regulations
  • surveilllance for sentinel cases
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12
Q

Classification of lung malignancies

A

Small-cell carcinoma (15%)

Non small cell carcinoma (85%)

  • adenocarcinoma
  • squamous cell carcinoma
  • large cell carcinoma

Mesotholioma

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13
Q

Pathologic characteristics of squamous cell carcinoma

A
  • central
  • often cavitate
  • keratinization
  • intracellular bridges
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14
Q

Pathologic features of adenocarcinoma

A
  • 2/3 peripheral, 1/3 central
  • gland formation +/- mucin production (PAS stain)
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15
Q

What is bronchoalveolar carcinoma? AKA?

A

AKA: adenocarcinoma in-situ (preferred name)

Tumour cells grow along the surface of the alveoli, BUT can have mixed AIS and invasive adenocarcinoma.

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16
Q

What are the pathologic features of small cell carcinoma?

A
  • central
  • small, dark cells with hyperchromatic nucleus (salt and pepper chromatin)
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17
Q

What are the pathologic features of large cell carcinoma?

A
  • peripheral
  • large polygonal cells, poorly differentiated
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18
Q

Why do we group lung cancers in small cell vs. non-small cell?

Within NSCLC, how and why do we group into squamous and non-squamous?

A

SCLC vs. NSCLC:

  • Non-small cancers are treated primarly by surgical resection.
  • Small cell cancers are more disseminated and are treated by chemotherapy

Squamous vs. Non-squamous

  • subtype using TTF-1 and p63 expression
  • no targeted therapy is available for squamous.
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19
Q

What targeted therapy is available for adenocarcinomas?

A

eGFR mutation positive –> tyrosine kinase inhibitor

ALK mutation positive –> crizotinib

**these are almost always mutually exclusive, and are not found in all patients**

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20
Q

What type of syndromes can local spread of lung cancer cause?

A

superior vena caval syndrome (facial swelling, cyanosis, protrusion of neck veins)

pancoast tumour (brachial plexus compression –> arm pain)

Horner syndrome (compression of cervical sympathetic chain –> unilateral ptosis, miosis, anhidrosis

pleural effusion

pericardial effusion

21
Q

What is the usual lymph node spread of lung cancer?

A

intrapulmonary–?hilar nodes–>tracheobronchial nodes –>mediastinal nodes–>cervical, supraclavicular, axillary, distance nodes

22
Q

What are the most common metastasis in lung cancer? How are they spread?

A

They are spread hematogenously

  • adrenals (50%)
  • liver (30-50%)
  • brain (20%)
  • bone (20%)
23
Q

What are the clinical procedures used to acquire tissue to make a diagnosis of lung cancer?

A
  • For central (squamous and small cell) can often do cytology on the sputum
  • Bronchoscopy: lavage, brush, biopsy and do cytology/histology on each.
  • Endobronchial ultrasound
  • Trans-throacic fine needle aspirate
  • Trans-thoracic core needle aspirate
24
Q

Are primary or metastatic tumours of the lung or pleura more common?

A

Metastatic tumours are more common for both

25
Define mesothelioma. What is it associated with? What are it's pathologic features?
Mesothioloma is a **primary** tumour involving the pleura, often associated with **asbestos** exposure. Distant metastasis occur late, but poor prognosis. It encases the lung, and can invade the thoracic wall (\*\*\*it doesn't usually invade the lung itself) It has three microscopic patterns: epithelial (gland like), sarcomatoid, mixed.
26
What is the differential for a pulmonary nodule?
* bronchogenic carcinoma * granuloma (TB, fungal) * lung abscess * hamartoma * metastatic cancer * arteriovenous malformation * rheumatoid nodule * carcinoid
27
How to differentiate mesothelioma and adenocarcinoma?
Have to sub-type. Adenocarcinoma will be TTF-1 positive,
28
What is the differential for mesothelioma?
* primary cancer * metastatic cancer * asbestos plaques * bronchogenic carcinoma invading the pleura etc.....
29
Describe the diagnostic algorithm or pathway in detection/diagnosis of lung cancer using imaging.
Nodule or mass discovered (CXR or CT) Nodule or mass tissue needs to be characterized (CT) Resectability of the mass needs to be determined (local tissue involvement) (CT, MR) (MR is good for determining if vessels are encased and if there is chest wall invasion) Search for distant metastases (PET-CT) (MR and CT aren't good at differentiating nodes enlarged by infection or metastatic disease) (Use MR for brain mets)
30
How to differentiate malignant from benign masses or nodules using imaging
* CXR with contrast allows you to see **vascularization** of the mass/nodule * compare with previous CXR to see if it is **growing** * is it obvisouly **calcified**? CT will differentiate between fat (harmatoma), calcium (TB/fungal) and soft tissue (neoplasm?) * Are the **margins** smooth (more likely benign) or spiculated ( more like neoplastic)? * Does it have **satellite nodules**? More likely past infection.
31
When is a lung cancer unresectable?
Stage IIIb or higher: * mediastinal involvement * contralateral nodes/masses * spinal cord involvement * distant metastasis * malignant pleural effusion
32
Where does the pleural fluid come from?
From intercostal microvessels and bronchial microvessels
33
How does the Starling equation relate to the formation of pleural fluid in the normal physiologic state
Flow= K (change in hydrostatic pressure-change in oncotic pressure) Transudation and absorption of fluid within the pleural space normally follow the Starling equation, which depends on **hydrostatic, colloid,** and **tissue pressures** in addition to **permeability** of the pleural membrane. \*\*net flow of fluid is from parietal to visceral pleura\*\*
34
Define exudative vs. transudative effusions
They can be distinguished by using Light's criteria. Exudative * results from an inflammatory process * contains high protein * contains high LDH * lymphocytosis Transudative * low protein, LDH * leaks across an intact membrane * results from low increased hydrostatic pressure or decreased oncotic pressure in the the pleural space.
35
What is the mnemonic for transudative effusions?
LUCKI ME Liver (hepatic hydrothorax) Urinothorax CHF Kidney (low protein state) Iatrogenic (e.g. central line into pleural space) Myxedema Embolism
36
What are 3 causes of exudative pleural effusion?
malignancy infection pulmonary embolism serositis due to connective tissue disease
37
What are 3 mechanisms by which lung cancer can cause pleural effusion?
Can be direct or indirect Indirect * tumour blocking lymphatic drainage * inflitration of vasculature --\>leaky (cytokine production?) * superior vena caval syndrome Direct * infiltration of cancer cells into the pleural space
38
How long does it take nicotine to reach the brain when inhaled? What is it's half-life? What is it's major metabolite? What is it's oral bioavailability?
* 10 s to reach the brain * t1/2=1-2 hours * metabolized by CYP2A6 into continine (used as a serum marker for nicotine * has very poor oral bioavailablity
39
How is nicotine addictive?
It is a nicotinic receptor agonist. It causes dopamine release, is a stimulant, and activates the reward pathway of the brain. Long term use result in nicotinic receptor upregulation
40
What are the withdrawal symptoms for nicotine?
irritability sleep disturbance poor concentration depression restlessness increased appetite
41
What kinds of nicotine replacement therapies are availability and what are the side effects/drawbacks?
Gum * craving rescue * gastric irritant Lozenges * craving rescue * gastric irritant Patch * nicotine maintenance * local irritation * night-time waking because of continous delivery of nicotine Inhaler * mimics behaviour of smoking * cough/local irritation Sublingual spray * faster absorption
42
What is Champix, how does it work, what are its main side effects and what is its safety?
Verenicline (Champix) * partial agonist at nicotinic receptor * provides small amount of stimulation * reduces reward from smoking because it competes for receptors with nicotine, but only has partial activity * S/E: nausea * may cause anxiety/depression/suicide * increases risk of CV event in people with CV history
43
What is Zyban, how does it work, what is its main side effects and what is its safety?
Bupropion * dopamine reuptake inhibitor * S/E: dry mouth, insomnia, nausae * Safety: not safe if Hx of seizures (may cause these), and welbutrin=zyban, and suicidal behaviour in youth
44
What is nortriptyline, what is its MOA, what are its main side-effects?
Nortriptyline: * inhibits serotonin and NE reuptake * anticholinergic side-effects
45
What is the efficacy of NRT, verenicline and bupropion?
* all NRT types more effective than placebo, but no clear advantage of one type over another * bupropion works about the same as NRT, verenicline works better. * success is still only ~20%
46
What is a carcinoid?
A type of neuroendocrine tumour. Usually benign and slow growing. Often found in GI tract and lungs.
47
What are common genomic alterations in lung cancer? Which ones are tested for and why?
SCLC: * Bcl-2, C-kit, MMP, VEGF * The usual culprits...targeted therapy has failed though NSCLC: * eGFR gain of function mutation * KRAS gain of function mutation (mutually exclusive of eGFR mutation, found dowstream) * EML4-ALK fusion (driver mutation, mutually exclusive with eGFR, poor prognostic variable) We test for eGFR and ALK mutations in NSCLC because targeted drug therapy improves patient outcomes
48
What are the different kinds of head and neck cancers? What kind of carcinoma are they usually? Is there targeted therapy for these?
* oral cavity * oropharynx * hypopharynx * larynx * primary cancer of unknown origin * nasopharynx (NPC) Usually squamous cell carcinoma. NPC is squamous, but morphologically different and associated with EBV EGFR is overexpressed in 80% of head and neck cancers, so can use cetuximab. No testing, they just use it.
49
What are the risks for oral cancer?
Smoking Spirits Sex (HPV 16) Syphillis Spices Socioeconomic

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