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PULM > PULM Week 4 PBL > Flashcards

PULM Week 4 PBL Flashcards

1
Q

what is considered to be one of the primary causes of lung and oral cancer

A

smoking

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2
Q

what percent of lung cancers worldwide are attributed to smoking

A

75%

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3
Q

which two types of lung cancer are particularly rare in the absence of smoking

A

squamous cell carcinoma and small cell carcinoma

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4
Q

what are the majority of non smoking related lung cancers?

A

adenocarcinomas (high in women)

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5
Q

what aspect of a persons smoking history is considered most important when determining his or her risk for lung cancer

A

LENGTH of time smoking

20 years and over is associated with the highest risk

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6
Q

what is the main toxic/carcinogenic chemical from cigarette smoking?

A

polycyclic aromatic hydrocarbons

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7
Q

what are some other causes of lung and oral cancer?

A
  1. environmental tobacco smoke
  2. residential radon
  3. cooking oil vapors
  4. indoor coal and woodburning
  5. genetic factors
  6. HOV 16 and 18
  7. EBV
  8. HIV
  9. pre-existing lung disease–COPD in particular
  10. asbestos, arsenic, chromium compounds
  11. infections like TB
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8
Q

how many carcinogens are there in cigarette smoke?

A

60 at least

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9
Q

what are the strongest carcinogens in cigarette smoke

A

polycyclic aromatic hydrocarbons and N-nitrosamines and aromatic amines

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10
Q

what are the most abundant carcinogens in cigarette smoke

A

aldehydes, benzene and butadiene

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11
Q

what are the most important carcinogens to lung cancer (from smoking)?

A

PAH, and tobacco specific, nicotine derived nitrosamine NNK

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12
Q

how do carcinogens in cig smoke exert their effect?

A

carcinogens are enzymatically transformed into a series of metabolites

initial steps are carried out by CP450 enzymes, encoded by the CYP family of genes, which oxidize the substrate

nicotine addiction–>cigarette smoking–> PAH, NNK and other carcinogens (–>metabolic detox and excretion)–>metabolic activation–>DNA adducts (–>repair–>normal DNA)–> persistence and miscoding–> (1) apoptosis or (2) mutations and other changes: RAS, MYC, p53, RB, FHIT, and other critical genes–> lung cancer

humans metabolize carcinogens similarly to how they metabolize other foreign compounds–> some intermediates are “metabolically activated” by CYP450–reactive, electrophilic and binds DNA covalently

in smokers there is a chronic barrage or metabolically activated carcinogens which cause changes–> cancer

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13
Q

what is hemoptysis

A

expectoration of blood or blood-stained sputum from bronchi, larynx, trachea or lungs

characterized by site of bleeding (airways, parenchyma, vasculature)

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14
Q

what types of airway disease cause hemoptysis

A
  1. inflammatory–bronchitis or brochiectasis
  2. neoplasm–primary bronchi carcinoma, endobrachial metastatic carcinoma
  3. foreign body (2nd most common cause in children after LRTI)
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15
Q

how does an inflammatory airway disease cause hemoptysis

A

i.e bronchitis or bronchiectasis

inflammation of the mucosa–> vascular enlargement, desquamation, atrophy, erosion

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16
Q

how does neoplasm in the airways cause hemoptysis

A

i.e primary bronchi carcinoma, endobrachial metastatic carcinoma

  • lung CA (23%)–bronchigenic carcinoma most common lung cancer causing hemoptysis
  • bleeding from malignant or benign tumor can be secondary to mucosal invasion, erosion into blood vessels
  • tissue invasion–resulting angiogenesis

**metastatic lung cancer rarely results in bleeding

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17
Q

what types of pulmonary parenchymal disease may cause hemoptysis

A
  1. infection
  2. inflammatory or immune disorders
  3. coagulopathy
  4. drug indiced
  5. catamenial hemoptysis due to intrathoracic endometriosis
  6. idiopathic
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18
Q

what types of infections are most likely to cause hemoptysis? how do they do this?

A
  • especially TB, pneumonia, aspergillosis, lung abcess
  • most COMMON cause of hemoptysis (60-70%)
  • causes superficial mucosal inflammation and edema and thus rupture of superficial blood vessels
  • most common agents are invasive bacteria–>

S. aureus
Pseudomonas aeruginosa
fungi (aspergillus)

  • viruses may also cause hemoptysis–> influenza, HIV, predisposed Kaposi sarcoma
  • most common cause in kids = LOWER RESP TRACT INFECTION
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19
Q

what inflammatory/immune disorders of the pulmonary parenchyma cause hemoptysis

A

autoimmune–Goodpastures, systemic lupus

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20
Q

what coagulopathies may cause hemoptysis

A

thrombocytopenia, use of anticoagulants

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21
Q

what drug induced causes in the parenchyma may there be for hemoptysis

A

cocaine-induced diffuse alveolar damage

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22
Q

how many patients have idiopathic hemoptysis

A

up to 30% of patients have no ID-ed cause after careful observation (good prognosis)

23
Q

how does vascular disease cause hemoptysis

A
  • massive hemoptysis is usually related to involvement of systemic circulation
  • vasculitis, pulmonary embolism (uncommon), pulmonary arteriovenous malformation, mitral stenosis, elevated pulmonary capillary pressure and significant LEFT VENTRICULAR FAILURE (most common CV condition causing hemoptysis)
  • often difficult to distinguish parenchymal and vascular disease
24
Q

what conditions may cause elevated pulmonary capillary pressure? how might this elevated pressure result in hemoptysis?

A

mutral stenosis or significant left ventricular failure

higher pressure leads to rupture of pulmonary veins or capillaries

25
Q

what is the general clinical presentation of bronchial carcinoma

A
  1. cough (75%)
  2. weight loss (40%)
  3. chest pain (40%)
  4. dyspnea (20%)
26
Q

what causes the general symptoms on clinical presentation of bronchial carcinoma

A

symptoms arise due to local tumor growth, invasion/obstruction of adjacent structures, growth into regional lymph nodes, growth in distant metastatic sites after hematogenous dissemination, or remote effects of tumor products (paraneoplastic syndrome)

27
Q

how would a central/endobronchial growth present clinically

A 
cough
hemoptysis
wheeze
stridor
dyspnea 
post-obstructive pneumonitis (fever, productive cough)
28
Q

how would peripheral growth of a primary broncial carcinoma tumor present clinically?

A

pain from pleural/chest wall spread, dyspnea on restrictive basis, symptoms of lung abscess

29
Q

how would a bronchial cancer’s regional spread to thorax present clinically

A
  1. tracheal obstruction
  2. esophageal compression
  3. recurrent laryngeal nerve paralysis with HOARSE VOICE
  4. phrenic nerve paralysis with elevated hemi-diaphragm and dyspnea
  5. malignant pleural effusion
30
Q

what is Horner’s syndrome?

A

sympathetic nerve paralysis (i.e from bronchial cancer regional spread to thorax)

  1. enophthalmos (recession of eyeball into orbit)
  2. ptosis (drooping upper eyelid)
  3. miosis (pupil constriction)
  4. ipsilateral loss of sweating
31
Q

what is Pancoast syndrome?

A

local extension of tumor growing in apex of lung with involvement of C8 and T1 nerves

shoulder pain–radiates in the ulnar distribution of the arm

32
Q

what is superior vena cava syndrome?

A

due to regional spread of tumor in the thorax

tumor causes vascular obstruction (edema of the face and neck with dilated veins in the neck and upper torso; headache, dizziness, stupor, syncope, visual disturbances)

33
Q

what is extrathoracic metastatic disease

A

various symptoms caused by metastasis to brain, bone, bone marrow, liver, lymph node, spinal cord, adrenal glands

34
Q

what is paraneoplastic syndrome?

A

refers to the disorders that accompany benign or malignant tumors but are not directly related to mass effects or invasion

neoplastic cells can produce a variety of peptides that can stimulate hormonal, hematologic, dermatologic, or neurologic responses

especially common in SCLC and carcinoids

anorexia, cachexia, weight loss, fever, suppressed immunity

endocrine symptoms: electrolyte disturbances in calcium, phosphate, sodium, K+

35
Q

what are the three mechanisms/routes of lung cancer spread

A
  1. local
  2. lymphatic
  3. hematogenous
36
Q

describe the process of local spread of lung cancer

A

-bronchial lumen obstruction causes PULMONARY COLLAPSE, accumulation of secretions, pneumonia, abscess formation and/or bronchiectasis distal to the obstruction

  • pleural involvement results in blood stained pleural effusion and can lead to chest wall invasion by tumor
  • superior vena cava compression (by lymph nodes) or invasion causes “superior vena cava syndrome”
  • invasion of nerves such as spread to the axilla with involvement of brachial plexus (pancoast tumor) or cervial sympathetic chain (horner’s syndrome)
  • pericardial involvement resulting in hemorrhagic pericardial effusion
  • direct spread to bone such as ribs, sternum, and spine causes pain
  • esophageal involvement causes dysphagia or bronchoesophageal fistula
37
Q

describe lymphatic spread of lung cancer

A
  • occurs early with invasion of regional intrapulmonary, hilar, and then extrapulmonary tracheobronchial and other mediastinal lymph nodes
  • further spread may occur to cervical, supraclavicular, axillary and more distant lymph node groups
  • nodal involvement can be MASSIVE and can be the presenting feature
38
Q

Describe hematogenous spread of lung cancer

A
  • widespread systemic involvement is common–not uncommonly the first clinical manifestation of lung cancer
  • may occur in any organ but mainly ADRENALS (50%), LIVER (30-50%), brain (20%) and bone (20%)
39
Q

what does the right lymphatic duct drain? where does it drain into?

A

drains R side of the head and R side of the thorax

drains into the right subclavian vein

40
Q

what does the thoracic duct drain? where does it drain into?

A

rest of body

into L subclavian vein

41
Q

why do we use the TNM method to stage cancers?

A

for

  1. communication
  2. prognosis
  3. to type of treatment
42
Q

what does the T indicate in TNM staging? the N? the M?

A

T = info on primary tumor–size and relationship to surrounding structures

N = info on regional lymph nodes

M = presence or absence of metastasis

43
Q 
in NSCLC staging, what does: 
T1
T2
T3
T4
indicate?
A

T1 = tumor less than 3 cm without pleural or main stem bronchus involvement

T2 = tumor 3-7 cm OR involvement of main bronchus 2 cm from carina, visceral pleura involvement or lobar atelectasis

T3 = tumor larger than 7 cm OR one with involvement of chest wall, diaphragm, mediastinal pleura, pericardium, or entire lung atelectasis or separate tumor nodule in the same lobe

T4 = tumor with invasion of mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina or separate tumor nodules in different ipsilateral lobe

44
Q 
in NSCLC TNM staging, what does: 
N0 
N1
N2
N3 
indicate?
A

N0 = no demonstrable metastasis to regional lymph nodes

N1 = ipsilateral hilar or peribronchial nodal involvement

N2 = metastasis to ipsilateral mediastinal or subcarinal lymph nodes

N3 = metastasis to contralateral mediastinal or hilar lymph nodes, ipsilateral or contralateral scalene or supraclavicular nodes

45
Q 
in NSCLC TNM staging, what does:
M0
M1
M1a
M1b 
indicate?
A

M0 = no distant metastasis

M1 = distant metastasis

M1a = separate tumor nodule in contralateral lobe or pleural nodules or malignant pleural effusion

M1b = distant metastasis

46
Q

stage Ia

A

T1N0M0

47
Q

stage Ib

A

T2N0M0

48
Q

stage IIa

A

T1N1M0

49
Q

stage IIb

A

T2N1M0

50
Q

stage IIIa

A

T1-3N2M0

T3N1M0

51
Q

stage IIIb

A

any T N3 M0

52
Q

stage IV

A

any T any N M1

53
Q

what is oral leukoplakia?

A

white lesion of oral mucosa that cannot be characterized as any other defined lesion, not readily removed

Dx of exclusion–confirmatory biopsy

some are benign lesions, many should be regarded as premalignancy lesions

chief concern is malignant transformation to oral squamous carcinoma (esp in floor of mouth)

54
Q

causes of oral leukoplakia

A

TOBACCO use–most important

smokeless/chewing tobacco

excess alcohol

chronic irritation due to ill-fitting dentures

infection with candida albicans

rarely tertiary syphilis, sanguinaria products (herbal toothpastes)

PULM (9 decks)

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