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MCM Test 4 > B2.059 Pathology of Tobacco Use > Flashcards

B2.059 Pathology of Tobacco Use Flashcards

1
Q

what percentage of adults in the US are smokers?

A

20%

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2
Q

how many years after smoking cessation do you see a reduction in mortality from CVD or cancer?

A

5 years

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3
Q

how does nicotine work?

A

addictive
binds to nicotinic acetylcholine receptors in brain with release of catecholamines from sympathetic neurons
increased HR, BP, cardiac output

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4
Q

what is the effect of carbon monoxide in cigarettes?

A

impaired oxygen transport and utilization

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5
Q

what is the effect of formaldehyde and nitrogen oxides in cigarettes?

A

toxic to cilia, mucosal irritation

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6
Q

what is the function of cilia?

A

help move toxins and bacteria from lungs to upper respiratory tract so that they can be expelled

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7
Q

what are the 3 major effects of smoking on the lungs?

A

mucosal irritation
leukocyte recruitment
carcinogenic agents

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8
Q

what is the effect of leukocyte recruitment in lungs?

A

tissue destruction by elastases

emphysema

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9
Q

what are two ways that smoking has carcinogenic effects?

A

source of carcinogens

increases cancer risk from OTHER exposures by 10x (asbestos, uranium)

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10
Q

what are effects of smoking on the cardiovascular system?

A

atherosclerosis
increased platelet aggregation
decreased oxygen supply
increased oxygen demand (myocardial work)

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11
Q

what are some risks of smoking on maternal/fetal health?

A

increased risk of spontaneous abortions, preterm birth

intrauterine growth retardation

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12
Q

what are some cancers linked to smoking?

A 
lung, larynx
esophagus
pancreas
bladder
oral cavity
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13
Q

how can second hand smoke exposure be measured?

A

blood levels of cotinine (nicotine metabolite)

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14
Q

where is secondhand smoke exposure primarily a concern?

A

at home

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15
Q

what is the primary chronic injury which leads to emphysema or chronic bronchitis?

A

smoking

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16
Q

characterize chronic bronchitis

A

persistent cough with sputum production for at least 3 months in at least 2 consecutive years with no identifiable cause

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17
Q

what is the pathogenesis of chronic bronchitis

A

damage to airway lining cells and interference with ciliary function

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18
Q

what are the outcomes of mucous hypersecretion in chronic bronchitis?

A

protective response

contributes to obstruction in smaller, lower parts of airways

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19
Q

what are the outcomes of inflammation in chronic bronchitis?

A

acute and chronic

damage>repair>increased collagen>less flexibility>obstruction of small airways

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20
Q

characterize the risk of infection in chronic bronchitis

A

higher

easier for microbes to get into an area with excess damage/mucous

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21
Q

what are other clinical feature of chronic bronchitis?

A

dyspnea on exertion
hypercapnia (elevated CO2), hypoxemia, mild cyanosis
blue bloater

22
Q

what are some complications associated with chronic bronchitis?

A 
superimposed infections (most common)
pulmonary hypertension and cor pulmonale (compression on vasculature causes pressure backup on heart)
23
Q

characterize emphysema

A

irreversible enlargement of airspaces distal to the terminal bronchiole with destruction of airspace wall

24
Q

what makes up respiratory epithelium?

A

columnar and ciliary epithelium

25
Q

bronchi: epithelium type, muscle/support, function

A

respiratory
prominent smooth muscle & cartilage
conduct air

26
Q

bronchioles: epithelium type, muscle/support, function

A

simple ciliated cuboidal to columnar
circular smooth muscle
conduct air, regulate airway size

27
Q

terminal bronchioles: epithelium type, muscle/support, function

A

simple ciliated cuboidal
thin smooth muscle
conduct air

28
Q

respiratory bronchioles: epithelium type, muscle/support, function

A

simple ciliated cuboidal and alveoli
few smooth muscle fibers
conduct air and some gas exchange

29
Q

alveolar duct: epithelium type, muscle/support, function

A

simple cuboidal
smooth muscle fibers around alveolar openings
conducts air and a lot of gas exchange

30
Q

alveoli: epithelium type, muscle/support, function

A 
alveolar cells (type 1 and 2 pneumocytes)
no muscle
gas exchange and surfactant production
31
Q

what are the 2 primary classes of emphysema?

A

centriacinar (centrilobular)

panacinar (panlobular)

32
Q

emphysema is also used as a descriptive term for lung disease w which 2 features

A

overinflation

bullae (dilated spaces)

33
Q

characterize overinflation

A

compensatory
after removal of part of a lung
obstructive, distal to the point of obstruction (backflow not possible)

34
Q

characterize bullous emphysema

A

large subpleural bullae >1 cm from a variety of causes
risk for rupture and pneumothorax
DOES NOT necessarily indicate emphysema is present throughout the lung (can occur on its own)

35
Q

characterize centriacinar (centrilobular) emphysema

A

95% of clinically significant cases
affects proximal/central portion of acini (respiratory bronchiole), sparing distal alveoli
dilated and normal airspaces co-exist in the same acinus
more common/severe in upper lobes
inflammation of bronchi/bronchioles

36
Q

characterize paracinar (panlobular) emphysema

A

clinically significant
affects entire acini from respiratory bronchiole to the distal alveoli
more common/severe in lower lobes
seen primarily in alpha-1-antitrypsin deficiency

37
Q

what is the pathogenesis of emphysema?

A

inflammation and parenchymal destruction

  • inflammatory mediators and leukocytes
  • protease/antiprotease imbalance
  • oxidative stress
  • infection
38
Q

what can cause protease/antiprotease imbalance?

A

extra protease formation (in locations of injury) or alpha-1-antitrypsin deficiency (happens everywhere)

39
Q

what is alpha-1-antitrypsin

A

acts against proteases to limit tissue destrcution

40
Q

what is the result of protease/antiprotease imbalance?

A

connective tissue breakdown

loss of elastic recoil leading to collapse of respiratory bronchioles

41
Q

what is the pathogenesis of an obstruction in emphysema?

A

loss of elastic recoil leading to collapse of respiratory bronchioles
small airway inflammation- mucous hypersecretion and plugging OR narrowing of lumen of bronchioles due to inflammatory infiltrates, smooth muscle hyperplasia, and fibrosis

42
Q

what % of patients with emphysema have an A1AT deficiency?

A

1%

43
Q

where is A1AT synthesized and where is it located?

A

synthesized by hepatocytes

present in plasma, tissue fluid, and macrophages

44
Q

what is the wildtype A1AT gene?

A

PiMM

45
Q

what is the genotype associated with A1AT deficiency?

A

PiZZ

46
Q

characterize PiZZ protein

A

abnormally folded/polymerized
defect in migration from ER to Golgi
accumulates in hepatocytes in ER- can induce apoptosis
decreases serum levels of A1AT

47
Q

besides emphysema, what is a clinical consequence of A1AT deficiency?

A

liver disease, seen in 10-15% of patients

48
Q

how can you recognize empysema due to A1AT deficiency?

A

younger age of onset
panacinar distribution
smoking markedly exacerbates consequences

49
Q

what are some clinical features associated w emphysema?

A 
dyspnea
wheezing
weight bloss
barrel chested appearance
breathing through pursed lips
overventilation with normal oxygen
pink puffer
50
Q

what are some complications associated with empysema?

A

pneumothorax and collapse of lung
respiratory failure
pulmonary hypertension and cor pulmonale is uncommon and usually a terminal event

MCM Test 4 (19 decks)

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