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Systems Pathology Final > Lungs Part 1 > Flashcards

Lungs Part 1 Flashcards

1
Q

How many breaths does one breath per minute?

A

12-20

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2
Q

How many lobes does each lung have?

A

right-3

left-2

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3
Q

What are the structures of the lung from largest to smallest?

A

trachea, bronchus, bronchioles, terminal bronchioles, acinus

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4
Q

What are acini?

A

structures distal to terminal bronchioles

alveolar duct and multiple alveoli

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5
Q

Describe Type I pneumocytes?

A

95% of alveolar surface, have pores of Kohn

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6
Q

What are pores of Kohn?

A

pores within the type I pneumocytes

this is where diffusion, edema and bacteria occur

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7
Q

What are Type II pneumocytes?

A

pneumocytes for surfactant and repair

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8
Q

What are pulmonary alveolar macrophages?

A

sparse macrophages within the lung

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9
Q

What parts of the lung do pathologies involve?

A

airways, vasculature, interstitum

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10
Q

What is atelectasis?

A

collapsed lung because of multiple alveoli collapse (decreases lung volume)

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11
Q

What happens to the blood with atelectasis?

A

blood from pulmonary arteries get shunted to pulmonary veins without oxygen, which can cause hypoxia

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12
Q

What are the different types of atelectasis?

A

resorption, compression, contraction

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13
Q

What is resorption atelectasis?

A

when an obstruction prevents air from reaching distal airways

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14
Q

What happens to the air left in the lungs?

A

it eventually becomes absorbed and the alveolae collapse

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15
Q

What part of the lung collpases in resorption atelectasis?

A

it depends on the level of obstruction, could be the entire lung, complete lobe or one or more segments

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16
Q

What is the most common cause of resorption atelectasis?

A

mucous or mucopurulent plug

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17
Q

When does resorption atelectasis occur?

A

postoperatively, can also complicate bronchialasthma, bronchiectasis, chronic bronchitis, tumor or foreign body aspiration

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18
Q

What is compression atelectasis also called?

A

passive or relaxation atelectasis

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19
Q

What is compression atelectasis?

A

when there is an accumulation of fluid, blood or air within the pleural cavity, which mechanically collapses the lung

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20
Q

What is compression atelectasis most commonly caused by?

A

CHF

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21
Q

What can compression atelectasis follow?

A

pleural effusion (fluid in the lungs)

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22
Q

What is basal atelectasis?

A

a condition from elevated position of the diaphragm

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23
Q

Who commonly gets atelectasis?

A

bed ridden patients, patients with ascites, during or after surgery

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24
Q

What is contraction atelectasis?

A

a condition when either lcoal or generalized fibrotic changes in the lungor pleura hamper expansion and increase elastic recoil during expiration

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25
Q

Which type of atelectasis is reversible?

A

compression and resorption, as long as it is prompt to prevent hypoxemia and superimposed infection of the lung

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26
Q

What does acute lung injury manifest as?

A

acute onset dyspnea, hypoxemia, development ofbilateral pulmonary infiltrates on the chest radiograph

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27
Q

What is acute respiratory distress syndrome?

A

a clinical syndrome caused by diffuse alveolar capillary and epithelial damage

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28
Q

What is ARDS characterized by?

A

usually characterized by rapidonset of life-threatening respiratory insufficiency, cyanosis and severe arterial hypoxemia that is refractory to oxygen therapy and can progress to multisystem organ failure
40% lethal, 6-12 month survival

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29
Q

What is the histologic manigestation of ARDS?

A

diffuse alveolar damage

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30
Q

How does ARDS occur?

A

a multitude of clinical settings or indirect injury

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31
Q

What are the two barriers that are compromised in ARDS?

A

microvascular endothelium and alveolar epithelium

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32
Q

What types of immune cells are seen in ARDS?

A

lots of neutrophil chemotactic and activating agent by pulmonary macrophages

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33
Q

What is obstructive pulmonary disease characterized by?

A

limitation of airflow, usually resulting from an increase in resistance caused by partial or complete obstruction at any level

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34
Q

What is restrictive pulmonary disease characterized by?

A

reduced expansion of lung parenchyma accompanied by decreased total lung capacity

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35
Q

What are the major diffuse obstructive disorders?

A

emphysema, chronic bronchitis, bronchiectasis, asthma

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36
Q

What is the forced vital capacity for those with diffuse obstructive disorders?

A

normal or slightly decreased

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37
Q

What is the expiratory flow rate for those with diffuse obstructive disorders?

A

significantly decreased

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38
Q

The ratio of expiratory flow rate to forced vital capacity is what?

A

decreased

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39
Q

What does expiratory obstruction result from?

A

anatomic airway narrowing, loss of elastic recoil

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40
Q

What is the ratio of diffuse restrictive diseases?

A

FVC is reduced, expiratory flow rate is normal or reduced or slightly lowered

the ratio is normal

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41
Q

What are the restrictive defects that occur during two general conditions?

A

chest wall disorders in the presence of normal lungs

acute or chronic interstitial lung diseases

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42
Q

What are the types of expiratory obstruction diseases?

A

emphysema, chronic bronchitis, bronchiectasis, asthma

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43
Q

What is emphysema characterized by?

A

abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis

44
Q

What is the diagnosis for emphysema?

A

morphologic tissue destruction

45
Q

What kind of inflammatory cells accumulate in emphysema?

A

increase in proteases, increase in ROS, decrease in normal anti-proteases, but no fibrosis

46
Q

What does emphysema do to the acini? What happens because of that?

A

enlarges the acini, resulting in decreased surface area which leads to decreased gas exchange which results in dyspnea

47
Q

What are the two types of emphysema?

A

centriacinar and panacinar

48
Q

Which type of emphysema is more common?

A

centriacinar

49
Q

What happens in centriacinar emphysema?

A

the central acini get destroyed, but spares the distal lobule

50
Q

Where is centriacinar emphysema located most commonly?

A

lung apices

51
Q

Who is at risk for centriacinar emphysema?

A

chronic smokers

52
Q

What happens in panacinar emphysema?

A

acini are uniformly destroyed, most commonly in lower lungs

53
Q

What deficiency do those with panacinar emphysema?

A

alpha1-antitrypsin deficiency

54
Q

What does alpha1-antitrypsin do?

A

normally functions as a protease inhibitor, but when there are less of them, there is an increase in protease activity

55
Q

What accelerates the destruction of panacinar emphysema?

A

smoking

56
Q

What are risks of emphysema?

A

smoking, genetics, air pollution

57
Q

What immune cells are seen in emphysema?

A

neutrophils, macrophages and lymphocytes

58
Q

Why is smoking a risk for emphysema?

A

ROS from smoke and released from WBCs, oxidant and antioxiant imbalances (causes tissue damage)

59
Q

What is a chemoattractant for WBCs?

A

nicotine

60
Q

What are the resulting symptoms of emphysema?

A

progressive dyspnea, cough, hyperventilation, wheezing, weight loss

61
Q

What kind of immune cells are seen in chronic bronchitis?

A

neutrophils, macrophages, lymphocytes

62
Q

What occurs during chronic bronchitis?

A

there is hypersecretion of mucus because of hypertrophy/hyperplasia of mucous glands and increased sputum

63
Q

What are the risks of chronic bronchitis?

A

smoking, air pollutants, males, age 40-65

64
Q

What are the symptoms of chronic bronchitis?

A

pronounced and productive cough lasting more than 3 consecutive months in more than 2 consecutive years
dyspnea, wheezing, cyanosis, cor pulmonale, recurrent infections, green/yellow sputum

65
Q

What is COPD?

A

a mix of chronic bronchitis and emphysema

66
Q

Describe the “pink puffer”

A

pathologic diagnosis, permanent enlargement and destruction of airspaces distal to the terminal bronchiole
older and thin, severe dyspnea, quiet chest, X-Ray, hyperinflation with flattened diaphragm

67
Q

Describe “blue bloater”

A

clinical diagnosis, daily productive cough for 3 months or more in at least two consecutive years
overweight and cyanotic, elevated hemoglobin, peripheral edema, wheezing

68
Q

Describe the symptoms of COPD that is predominantly bronchitis.

A 
40-45 years, 
mild dyspnea (late), 
copious sputum cough (late), 
infections common, 
repeated respiratory insufficiency, 
cor pulmonale, 
increased airway resistance, 
normal elastic recoil, 
blue bloater
prominent vessels, large heart
69
Q

Describe the symptoms of COPD that is predominantly emphysema?

A 
50-75 years
severe, early dyspnea
late scanty sputum of cough
occasional infection
terminal respiratory insufficiency
rare, terminal cor pulmonale
airway resistance is normal
low elastic recoil
hyperinflation, small heart
70
Q

What are the shared risks of COPD?

A

smoking and air pollution

71
Q

What happens to the airflow in those with COPD? What are symptoms that follow this?

A

irreversible obstruction to airflow, prominent wheezing, possible pulmonary HTN

72
Q

What kind of lung disease is asthma?

A

obstructive (bronchoconstriction)

73
Q

What happens to the lung tissue in asthmatics?

A

smooth muscle hypertrophies or is hyperactive, inflammation and increase in mucous

74
Q

What happens to the airflow in those with asthma?

A

reversible airway obstruction, wheezing, dyspnea, cough, chest tightness

75
Q

What are the characteristics of asthmatics?

A

difficulty inhaling and exhaling, occurs in morningand evening, curschmann spirals, charcot-leyden crystals, various stimuli

76
Q

Where is there an increased prevalence of asthma?

A

westernized world

77
Q

What is atopic asthma?

A

Type I hypersensitivity, caused by allergens

78
Q

What is non-atopic asthma?

A

bronchial hyper-responsiveness, non-allergic stimuli

79
Q

Which type of asthma is more common?

A

atopic asthma

80
Q

What are the triggers for atopic asthma?

A

environmental antigens like dust, dander, food, pollen

81
Q

What is atopy?

A

a common condition, eczema/urticaria, allergic rhinitis, hyperreactive skin test

82
Q

What causes non-atopic asthma?

A

viral URTI infection, pneumonia, exercise,cold air, aspirin, inhaled irritants, physiological stress

83
Q

What happens histologically with non-atopic asthma?

A

bronchial inflammation, hyper-responsiveness

84
Q

Do we know what causes non-atopic asthma?

A

no, it’s idiopathic, no allergen trigger, no family history

85
Q

What are the physiological symptoms of chronic asthma?

A

bronchial narrowing, hypertrophy of bronchial smooth muscles, fibrosis, increased submucosal glands, mucous plugs, increased submucosal vascularity

86
Q

What happens to the acini of chronic asthma?

A

progressive hyperinflation, dysfunctional expiration, can be lethal, no response to bronchodilators or steroids

87
Q

What can happen when there is obstruction in chronic asthmatics?

A

necrotizing infection, lung cancer, tuberculosis, chronic bronchitis, foreign bodies, impacted mucus, cystic fibrosis, permanent dilation of bronchial tree, destroys tissue (CT and musculature)

88
Q

Where is chronic asthma located?

A

lower lobes
localized: foreign bodies
bilateral cystic fibrosis, Kartagener syndrome

89
Q

What are features of chronic asthma?

A

episodes of severe coughing, hemoptysis and foul/purulent sputum

90
Q

What kind of lung disease is bronchiectasis?

A

an obstructive lung disease that is caused by necrotizing infections that destroy supporting elastic tissue and muscle

91
Q

Is bronchiectasis primary or secondary?

A

secondary because it is persisting to infection or obstruction caused by a variety of conditions

92
Q

Once bronchiectasis develops, what is the characteristic symptoms complex?

A

cough and expectoration of copious amounts of purulent sputum

93
Q

What does diagnosis of bronchiectasis depend on?

A

appropriate history, radiographic demonstration of bronchial dilation

94
Q

What are the conditions that commonly predispose to bronchioectasis?

A

bronchial obstruction, congenital or hereditary conditions, necrotizing or suppurative pneumonia

95
Q

What are common causes of bronchial obstruction for bronchioectasis?

A

tumors, foreign bodies, occasionally impaction of mucus

96
Q

What can bronchioectasis complicate?

A

atopic asthma and chronic bronchitis

97
Q

What are examples of congenital or hereditary conditions that can cause bronchiectasis?

A

cystic fibrosis, immunodeficiency, Kartagener syndrome

98
Q

What is cystic fibrosis?

A

widespread severe bronchiectasis that results from obstruction caused by secretion of abnormally viscid mucus, which predisposes them to infections of bronchial tree

99
Q

How is bronchiectasis associated with immunodeficiency states?

A

immunoglobulin deficiencies, localized or diffuse bronchiectasis is likely to develop of an increased susceptiblity to repeated bacterial infections

100
Q

What is Kartagener syndrome?

A

a rare autosomal recessive disorder that is frequently associated with bronchiectasis and sterility in males

101
Q

What are the structural abnormalities of Kartagener syndrome?

A

abnormal cilia,

102
Q

What happens when there are abnormal cilia in Kartagener syndrome?

A

this impairs mucociliary clearance in the airways, leading to persistent infections and reduce the mobility of spermatozoa

103
Q

What are the organisms that cause pneumonia in Kartagener syndrome?

A

staph aureus or kleibsella, this predisposes patients to bronchiectasis

104
Q

Which type of bronchiectasis is a significant cause of morbidity in endemic areas?

A

post-tuberculosis bronchiectasis

105
Q

What are the symptoms of Kartagener syndrome?

A

bronchiectasis, chronic sinusitis, situs inversus

106
Q

What is situs inversus?

A

inverted chest and abdominal organs

107
Q

What is ascites?

A

accumulation of fluid in the peritoneal cavity that causes abdominal swelling

Systems Pathology Final (5 decks)

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