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Pathoma KAM > CH9 - Respiratory Tract Pathology > Flashcards

CH9 - Respiratory Tract Pathology Flashcards

1
Q

What is rhinitis?

A

Inflammation of the nasal mucosa;

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2
Q

What is the most common cause of rhinitis?

A

adenovirus

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3
Q

What does rhinitis present with?

A

sneezing, congestion, and runny nose (common cold)

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4
Q

What is allergic rhinitis?

A

a subtype of rhinitis due to a type I hypersensitivity reaction (e.g. to pollen)

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5
Q

What is allergic rhinitis characterized by?

A

an inflammatory infiltrate with eosinophils

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6
Q

What is allergic rhinitis characterized by?

A

associated with asthma and eczema

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7
Q

What is a nasal polyp?

A

Protrusion of edematous, inflamed nasal mucosa

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8
Q

What is a nasal polyp usually secondary to?

A

repealed bouts of rhinitis; also occurs in cystic fibrosis and aspirin - intolerant asthma

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9
Q

What is aspirin-intolerant asthma characterized by?

A

the triad of asthma, aspirin induced bronchospasms, and nasal polyps;

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10
Q

What is the incidence of asprin-intolerant asthma in asthmatic adults?

A

seen in 10% of asthmatic adults

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11
Q

What is angiofibroma?

A

Benign tumor of nasal mucosa composed of large blood vessels and fibrous tissue

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12
Q

In whom is angiofibroma classically seen?

A

in adolescent males

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13
Q

What does angiofibroma present with?

A

profuse epistaxis

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14
Q

What is nasopharyngeal carcinoma?

A

Malignant tumor of nasopharyngeal epithelium

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15
Q

What is nasopharyngeal carcinoma associated with?

A

EBV

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16
Q

Who is nasopharyngeal carcinoma classically seen in?

A

African children and Chinese adults

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17
Q

What happens in a biopsy of nasopharyngeal carcinoma?

A

usually reveals pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes

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18
Q

How does nasopharyngeal carcinoma often present?

A

with involvement of cervical lymph nodes

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19
Q

What is acute epiglottitis?

A

Inflammation of the epiglottis

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20
Q

What is the most common cause of acute epiglottitis?

A

H. influenzae type b especially in nonimmunized children

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21
Q

What does acute epiglottitis present with?

A

high fever, sore throat, drooling with dysphagia, muffled voice, and inspiratory stridor; risk of airway obstruction

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22
Q

What is laryngotracheobronchitis?

A

(croup) Inflammation of the upper airway

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23
Q

What is the most common cause of laryngotracheobronchitis?

A

parainfluenza virus

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24
Q

What does laryngotracheobronchitis present with?

A

a hoarse, (barking) cough and inspiratory stridor

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25
Q

What is a vocal cord nodule?

A

(singer?s nodule) nodule that arises on the true vocal cord

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26
Q

What is a vocal cord nodule due to?

A

excessive use of vocal cords, usually bilateral

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27
Q

What is a vocal cord nodule composed of?

A

degenerative (myxoid) connective tissue

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28
Q

How does a vocal cord nodule present?

A

with hoarseness; resolves with resting of voice

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29
Q

What is laryngeal papilloma?

A

Benign papillary tumor of the vocal cord

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30
Q

What is laryngeal papilloma due to?

A

HPV 6 and 11

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31
Q

What is usually the difference between papillomas in adults children?

A

Papilloma are usually single in adults and multiple in children.

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32
Q

What does laryngeal papilloma present with?

A

hoarseness

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33
Q

What is laryngeal carcinoma?

A

squamous cell carcinoma usually arising from the epithelial lining of the vocal cord

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34
Q

What are the risk factors for laryngeal carcinoma?

A

alcohol and tobacco; can rarely arise from a laryngeal papilloma

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35
Q

What does laryngeal carcinoma present with?

A

hoarseness; other signs include cough and stridor

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36
Q

What are some pulmonary infections?

A

Pneumonia, lobar pneumonia, bronchopneumonia, interstitial (atypical pneumonia), aspiration pneumonia, tuberculosis

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37
Q

What is pneumonia?

A

Infection of the lung parenchyma

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38
Q

When does pneumonia occur?

A

when normal defenses are impaired (e.g.. impaired cough reflex, damage to mucociliary escalator, or mucus plugging)

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39
Q

What are the clinical features of pneumonia?

A

include fever and chills, productive cough with yellow-green (pus) or rusty (bloody) sputum, tachypnea with pleuritic chest pain, decreased breath sounds, dullness to percussion, and elevated WBC count

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40
Q

How is the diagnosis for pneumonia made?

A

by chest x-ray, sputum gram stain and culture, and blood cultures.

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41
Q

What are the three patterns that are classically seen on chest x-ray for pneumonia?

A

lobar pneumonia, bronchopneumonia, and interstitial pneumonia.

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42
Q

What is lobar pneumonia?

A

Characterized by consolidation of an entire lobe of the lung

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43
Q

What are the most common causes for lobar pneumonia?

A

Usually bacterial; most common causes are Streptococcus pneumoniae (95%) and Klebsiella pneumoniae

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44
Q

What are the classic gross phases of lobar pneumonia?

A

1) Congestion, 2) red hepatization, 3) gray hepatization, 4) resolution

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45
Q

In lobar pneumonia what is the congestion due to?

A

congested vessels and edema

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46
Q

In lobar pneumonia what is red hepatization due to?

A

exudate, neutrophils, and hemorrhage tilling the alveolar air spaces, giving the normally spongy lung a solid consistency

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47
Q

In lobar pneumonia what is gray hepatization due to?

A

degradation of red cells within the exudate

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48
Q

What is bronchopneumonia?

A

Characterized by scattered patchy consolidation centered around bronchioles; often multifocal and bilateral

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49
Q

What is bronchopneumonia caused by?

A

a variety of bacterial organisms

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50
Q

What is interstitial (atypical) pneumonia characterized by?

A

diffuse interstitial infiltrates

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51
Q

How does interstitial (atypical) pneumonia present?

A

with relatively mild upper respiratory symptoms (minimal sputum and low fever); atypical presentation

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52
Q

What is interstitial (atypical) pneumonia caused by?

A

bacteria or viruses

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53
Q

What is the most common cause of community-acquired pneumonia?

A

Streptococcus pneumoniae

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54
Q

What is streptococcus pneumonia usually seen in?

A

middleaged adults and elderly

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55
Q

Who does Klebsiella pneumoniae affect?

A

malnourished and debilitated individuals, especially elderly in nursing homes, alcoholics, and diabetics (enteric flora that is aspirated).

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56
Q

What does Klebsiella pneumoniae result in?

A

Thick mucoid capsule results in gelatinous sputum (currant jelly); often complicated by abscess

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57
Q

What are the causes of bronchopneumonia?

A

Staphylococcus aureus, haemophilus influenzae, Pseudomonas aeruginosa, Moraxella calarrhalis, Legionella pnemnophila

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58
Q

What is the most common cause of secondary pneumonia?

A

Staphylococcus aureus

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59
Q

What is secondary pneumonia?

A

bacterial pneumonia superimposed on a viral upper respiratory tract infection

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60
Q

What is secondary pneumonia caused by staphylococcus aureus often complicated by?

A

abscess or emphyzema

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61
Q

Haemophilus influenzae is the most common cause of what type of pneumonia?

A

secondary pneumonia and pneumonia superimposed on COPD

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62
Q

How does haemophilus influenzae affect COPD?

A

It results in exacerbation of COPD?

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63
Q

What does pseudomonas aeruginosa cause?

A

Pneumonia in cystic fibrosis patients

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64
Q

What high yield association should be made with moraxella calarrhalis?

A

Community-acquired pneumonia and pneumonia super imposed on COPD (leads to exacerbation of COPD)

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65
Q

What high yield association should be made with Legionella pnemnophila?

A

Community-acquired pneumonia, pneumonia superimposed on COPD, or pneumonia in immunocompromised states;

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66
Q

How is Legionella pnemnophila transmitted?

A

from water source

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67
Q

How is Legionella pnemnophila best visualized?

A

Its an intracellular organism best visualized by silver stain

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68
Q

What is the most common cause of atypical pneumonia?

A

Mycoplasma pneumonia

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69
Q

What is the high yield association with mycoplasma pneumoniae?

A

Most common cause of atypical pneumonia, usually affects young adults (classically, military recruits or college students living in a dormitory).

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70
Q

What are the complications for mycoplasma pneumoniae?

A

they include autoimmune hemolytic anemia (IgM against I antigen on RBCs causes cold hemolytic anemia) and erythema multiforme. Not visibie on gram stain due to lack of cell wall

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71
Q

What is the second most common cause of atypical pneumonia in young adults?

A

Chlamydia pneumoniae

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72
Q

What is the most common cause of atypical pneumonia in infants?

A

Respiratory syncytial virus (RSV)

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73
Q

What causes atypical pneumonia with posttransplant immunosuppressive therapy?

A

Cytomegalovirus (CMV)

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74
Q

What does influenza virus cause?

A

atypical pneumonia in the elderly, immunocompromised, and those with preexisting lung disease

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75
Q

What does Influenza virus also increase the risk for?

A

superimposed S aureus or H influenzae bacterial pneumonia

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76
Q

What does coxiella burnetii cause?

A

atypical pneumonia with high fever (Q fever);

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77
Q

Who is coxiella burnetii seen in?

A

farmers and veterinarians

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78
Q

What happens to coxiella spores?

A

They are deposited on cattle by ticks or are present in cattle placentas

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79
Q

What is coxiella?

A

it is a rickettsial organism,

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80
Q

How is coxiella distinct from most rickettsiae?

A

because it (1) causes pneumonia, (2) does not require an arthropod vector for transmission (survives as highly heat-resistant endospores), and (3) does not produce a skin rash.

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81
Q

What is aspiration pneumonia seen in?

A

patients at risk for aspiration (e.g., alcoholics and comatose patients)

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82
Q

What is aspiration pneumonia most often due to?

A

anaerobic bacteria in the oropharynx (e.g., Bacteroides, Fusobacterium, and Peptococcus)

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83
Q

What does aspiration pneumonia classically result in?

A

a right lower lobe abscess

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84
Q

What is the anatomical difference between the right and left main stem bronchus?

A

branches at a less acute angle than the left.

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85
Q

What is tuberculosis due to?

A

inhalation of aerosolized mycobacterium tuberculosis

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86
Q

What arises with initial tuberculosis exposure?

A

Primary TB

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87
Q

What does primary TB result in?

A

focal, caseating necrosis in the lower lobe of the lung and hilar lymph nodes that undergoes fibrosis and calcification, forming a Ghon complex

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88
Q

What are generally the symptoms for primary TB?

A

Generally asymptomatic but leads to a positive PPD

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89
Q

What does secondary TB arise with?

A

reactivation of mycobacterium tuberculosis

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90
Q

What is reactivation of mycobacterium tuberculosis in secondary TB commonly due?

A

AIDS; may also be seen with aging

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91
Q

Where does secondary TB occur?

A

at apex of lung (high oxygen tension)

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92
Q

What does secondary TB form?

A

cavitary foci of caseous necrosis; may also lead to miliary pulmonary TB or tuberculous bronchopneumonia

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93
Q

What are the clinical features of secondary TB?

A

include fevers and night sweats, cough with hemoptysis, and weight loss.

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94
Q

What does biopsy in secondary TB reveal?

A

caseating granulomas, AFB stain reveals acid-fast bacilli

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95
Q

How might secondary TB spread?

A

Systemic spread often occurs and can involve any tissue; common sites include meninges (meningitis), cervical lymph nodes, kidneys (sterile pyuria), and lumbar vertebrae (Pott disease).

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96
Q

What is COPD?

A

Group of diseases characterized by airway obstruction; lung does not empty, and air is trapped.

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97
Q

What happens to the FVC and FEV in COPD?

A

Volume of air that can be forcefully expired is decreased (FVC), especially during the first second of expiration (FEV) results in decreased FEV:FVC ratio

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98
Q

What happens to total lung capacity in COPD and why?

A

Total lung capacity (TLC) is usually increased due to air trapping.

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99
Q

What happens in chronic bronchitis?

A

Chronic productive cough lasting at least 3 months over a minimum of 2 years; highly associated with smoking

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100
Q

What characterizes chronic bronchitis?

A

hypertrophy of bronchial mucinous glands

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101
Q

What does chronic bronchitis lead to?

A

increased thickness of mucus glands relative to overall bronchial wall thickness (Reid index increases to > 50%; normal is < 40%).

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102
Q

What are the clinical features for chronic bronchitis?

A
  1. Productive cough due to excessive mucus production 2. Cyanosis (blue bloaters) Mucus plugs trap carbon dioxide; increased PaCO2, and decreased PaO2
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103
Q

In chronic bronchitis what is there an increased risk of?

A

infection and cor pulmonale

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104
Q

What is emphysema?

A

Destruction of alveolar air sacs

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105
Q

What does emphysema result in?

A

Loss of elastic recoil and collapse of airways during exhalation results in obstruction and air trapping.

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106
Q

What is emphysema due to?

A

imbalance of proteases and antiproteases

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107
Q

What does inflammation in the lung normally lead to?

A

release of proteases by neutrophils and macrophages.

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108
Q

What neutralizes proteases?

A

A1-antitrypsin (A1AT)

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109
Q

In emphysema what leads to destruction of the alveolar air sac?

A

Excessive inflammation or lack of A1AT

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110
Q

What is the most common cause of emphysema?

A

Smoking

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111
Q

How does smoking lead to emphysema ?

A
  1. Pollutants in smoke lead to excessive inflammation and protease-mediated damage. 2. Results in centriacinar emphysema that is most severe in the upper lobes
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112
Q

AIAT deficiency relate to emphysema?

A

It is a rare cause of emphysema.

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113
Q

How does A1AT deficiency lead to emphysema?

A
  1. Lack of antiprotease leaves the air sacs vulnerable to protease-mediated damage. 2. Results in panacinar emphysema that is most severe in the lower lobes 3. Liver cirrhosis may also be present.
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114
Q

What is A1AT deficiency due to?

A

misfolding of the mutated protein

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115
Q

What happens to mutant A1AT?

A

it accumulates in the endoplasmic reticulum of hepatocytes, resulting in liver damage.

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116
Q

What is a PAS stain?

A

Periodic acid-Schiff stain

117
Q

What does biopsy of A1AT reveal?

A

Pink, PAS-positive globules in hepatocytes

118
Q

In A1AT deficiency what is disease severity based on?

A

the degree of A1AT deficiency.

119
Q

For A1AT deficiency induced emphysema, what is the normal allele?

A

PiM; two copies are usually expressed (PiMM).

120
Q

For A1AT deficiency induced emphysema what is the most common clinically relevant mutation and what does it result in?

A

PiZ which results in significantly low levels of circulating A1AT

121
Q

What is usually seen in PiMZ heterozygotes?

A

they are usually asymptomatic with decreased circulating levels of A1AT

122
Q

In PiMZ what is there significant risk for?

A

emphysema with smoking exists

123
Q

What is seen in PiZZ homozygotes?

A

significant risk for panacinar emphysema and cirrhosis.

124
Q

What are the clinical features of emphysema?

A
  1. Dyspnea and cough with minimal sputum 2. Prolonged expiration with pursed lips (pink-pu lier) 3. Weight loss 4. Increased anterior-posterior diameter of chest (barrel-chest) 5. Hypoxemia and cor pulmonale (late complications)
125
Q

Why is there hypoxemia in emphysema?

A

due to destruction of capillaries in the alveolar sac)

126
Q

What is asthma?

A

Reversible airway bronchoconstriction

127
Q

What is asthma most often due to?

A

allergic stimuli (type I hypersensitivity)

128
Q

When does asthma present?

A

in childhood; often associated with allergic rhinitis, eczema, and a family history of atopy

129
Q

What is atopy?

A

(atopic allergy), a genetic predisposition toward the development of immediate hypersensitivity reactions against common environmental antigens

130
Q

For the Pathogenesis of asthma, what do the allegens induce?

A
  1. Allergens induce TH2 phenotvpe in CD4+ T cells of genetically susceptible individuals 2. TH2 cells secrete IL-4, IL-5, IL-10
131
Q

What does IL-4 do?

A

mediates class switch to IgE

132
Q

What does IL-5 do?

A

attracts eosinophils

133
Q

What does IL-10 do?

A

stimulates TH2 cells and inhibits THl

134
Q

For the Pathogenesis of asthma, what does reexposure to allergen lead to?

A

IgE-mediated activation of mast cells.

135
Q

What does activation of mast cells lead to?

A

Release of preformed histamine granules and generation of leukotrienes C4, D4, and E4

136
Q

For the Pathogenesis of asthma what does release of preformed histamine granules and leukotrine generation lead to?

A

bronchoconstriction, inflammation, and edema (early phase reaction),

137
Q

For the pathogenesis of asthma, describe inflammation after reexposure to allergen?

A

There is inflammation especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction (late-phase reaction).

138
Q

What are the clinical features of asthma?

A

They are episodic and related to allergen exposure. 1. Dyspnea and wheezing 2. Productive cough, classically with spiral-shaped mucus plugs (Curschmann spirals) and eosinophil-derived crystals (Charcot-Leyden crystals) 3. Severe, unrelenting attack can result in status asthmaticus and death.

139
Q

What are curschmann spirals?

A

Spiral shaped mucus plugs

140
Q

What are some nonallergic causes for asthma?

A

Asthma may also arise from nonallergic causes such as exercise, viral infection, aspirin (e.g., aspirin intolerant asthma), and occupational exposures.

141
Q

What is bronchiectasis?

A

Permanent dilatation of bronchioles and bronchi; loss of airway tone results in air trapping.

142
Q

What is bronchiectasis due to?

A

necrotizing inflammation with damage to airway walls.

143
Q

What are the causes for bronchiectasis?

A
  1. Cystic fibrosis 2. Kartagener syndrome 3. Tumor or foreign body 4. Necrotizing infection 5. Allergic bronchopulmonary aspergillosis
144
Q

What is Kartagener syndrome?

A

inherited defect of the dynein arm, which is necessary for ciliary movement.

145
Q

What is Kartagener syndrome associated with?

A

sinusitis, infertility (poor motility of sperm), and situs inversus (position of major organs is reversed, e.g., heart is on right side of thorax)

146
Q

What is allergic bronchopulmonary aspergillosis?

A

Hypersensitivity reaction to aspergillus leads to chronic inflammatory damage;

147
Q

Allergic bronchopulmonary aspergillosis is usually seen in whom?

A

individuals with asthma or cystic fibrosis

148
Q

What are the clinical features for bronchiectasis?

A
  1. Cough, dyspnea, and foul-smelling sputum
149
Q

What are the complications for bronchiectasis?

A

hypoxemia with cor pulmonale and secondary (AA) amyloidosis.

150
Q

What are the restrictive diseases?

A

1) idiopathic pulmonary fibrosis 2) pneumoconioses 3) sarcoidosis 4) hypersensitivity pneumonitis

151
Q

What characterizes restrictive diseases?

A

restricted filling of the lung; decreased TLC and decreased FVC; FEV:FVC ratio is increased.

152
Q

What are restrictive diseases most commonly due to?

A

interstitial diseases of the lung; may also arise with chest wall abnormalities (e.g., massive obesity)

153
Q

What is idiopathic pulmonary fibrosis?

A

Fibrosis of lung interstitium

154
Q

What is the etiology for idiopathic pulmonary fibrosis?

A

unknown. Likely related to cyclical lung injury; TGF-beta from injured pneumocytes induces fibrosis. Secondary causes of interstitial fibrosis must be excluded

155
Q

What are the secondary causes of interstitial fibrosis?

A

drugs (e.g., bleomycin and amiodarone) and radiation therapy

156
Q

What are the clinical features for idiopathic pulmonary fibrosis?

A
  1. Progressive dyspnea and cough 2. Fibrosis on lung CT; initially seen in subpleural patches, but eventually results in diffuse fibrosis with end-stage honeycomb lung
157
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

lung transplantation.

158
Q

What is pneumoconioses?

A

Interstitial fibrosis due to occupational exposure;

159
Q

What does pneumoconioses require in order to develop?

A

chronic exposure to small particles that are fibrogenic

160
Q

In pneumoconioses what induces fibrosis?

A

Alveolar macrophages engulf foreign particles and induce fibrosis.

161
Q

What is the exposure for Coal Workers Pneumoconiosis?

A

Carbon dust; seen in coal miners

162
Q

What are the pathological findings for Coal Workers’ Pneumoconiosis?

A

Massive exposure leads to diffuse fibrosis (black lung); associated with rheumatoid arthritis (Caplan syndrome)

163
Q

How is Coal Workers’ Pneumoconiosis related to anthracosis?

A

Mild exposure to carbon (e.g., pollution) results in anthracosis (collections of carbon-laden macrophages); not clinically significant

164
Q

In silicosis, what is the exposure?

A

Silica; seen in sand blasters and silica miners

165
Q

In silicosis what are the pathologic findings?

A

Fibrotic nodules in upper lobes of the lung

166
Q

In silicosis what is there an increased risk for?

A

TB; silica impairs phagolysosome formation by macrophages.

167
Q

In Berylliosis, what is the exposure?

A

Beryllium; seen in beryllium miners and workers in the aerospace industry

168
Q

In berylliosis what are the pathological findings?

A

Noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs

169
Q

In berylliosis what is there an increased risk for?

A

lung cancer

170
Q

In asbestosis, what is the exposure?

A

Asbestos fibers; seen in construction workers, plumbers, and shipyard workers

171
Q

In asbestosis what are the pathologic findings?

A

Fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma and mesothelioma;

172
Q

In asbestosis, which is more common in exposed individuals?

A

lung carcinoma is more common than mesothelioma

173
Q

What may the lesions in asbestosis contain?

A

Lesions may contain long, goldenbrown fibers with associated iron (asbestos bodies), which confirm exposure to asbestos

174
Q

In asbestosis what are seen in the cells?

A

Characteristic stellate inclusions (asteroid bodies) are often seen within giant cells of the granulomas

175
Q

What is sarcoidosis?

A

Systemic disease characterized by noncaseating granulomas in multiple organs

176
Q

In whom is sarcoidosis classically seen in?

A

African American females

177
Q

What is the etiology for sarcoidosis?

A

it is unknown; likely due to CD4+ helper T-cell response to an unknown antigen

178
Q

In sarcoidosis what do granulomas most commonly involve?

A

the hilar lymph nodes and lung leading to restrictive lung disease.

179
Q

In sarcoidosis what are other commonly involved tissues?

A

include the uvea (uveitis), skin (cutaneous nodules or erythema nodosum), and salivary and lacrimal glands (mimics Sjogren syndrome); almost any tissue can be involved,

180
Q

What syndrome does sarcoidosis mimic?

A

Sjogren syndrome

181
Q

What are the clinical features for sarcoidosis?

A
  1. Dyspnea or cough (most common presenting symptom) 2. Elevated serum ACE 3. Hypercalcemia
182
Q

In sarcoidosis, why is there hypercalcemia?

A

1-alpha hydroxylase activity of epithelioid histiocytes converts vitamin D to its active form

183
Q

In sarcoidosis what is the most common presenting symptom?

A

Dyspnea or cough

184
Q

What is the treatment for sarcoidosis?

A

steroids; often resolves spontaneously without treatment.

185
Q

What is hypersensitivity pneumonitis?

A

Granulomatous reaction to inhaled organic antigens (e.g., pigeon breeder’s lung)

186
Q

How does hypersensitivity pneumonitis present?

A

with fever, cough, and dyspnea hours after exposure; resolves with removal of the exposure

187
Q

In hypersensitivity pneumonitis what does chronic exposure lead to?

A

interstitial fibrosis.

188
Q

What is seen in pulmonary hypertension?

A

high pressure in the pulmonary circuit (mean arterial pressure > 25 mm Hg; normal is 10 mm Hg)

189
Q

What is pulmonary hypertension characterized by?

A

atherosclerosis of the pulmonary trunk, smooth muscle hypertrophy of pulmonary arteries, and intimal fibrosis;

190
Q

With pulmonary hypertension what are seen with severe, long-standing disease?

A

plexiform lesions

191
Q

What does pulmonary hypertension lead to?

A

right ventricular hypertrophy with eventual cor pulmonale

192
Q

What does pulmonary hypertension present with?

A

exertional dyspnea or right-sided heart failure

193
Q

What is pulmonary hypertension subclassified as?

A

primary or secondary based on etiology

194
Q

What is primary pulmonary hypertension classically seen in?

A

young adult females

195
Q

What is the etiology for primary pulmonary hypertension?

A

unknown; some familial forms are related to inactivating mutations of BA1PR2, leading to proliferation of vascular smooth muscle.

196
Q

What is secondary pulmonary hypertension due to?

A

hypoxemia (e.g., COPD and interstitial lung disease) or increased volume in the pulmonary circuit (e.g., congenital heart disease); may also arise with recurrent pulmonary embolism

197
Q

What are the respiratory distress syndromes?

A

1) acute respiratory distress syndrome 2) neonatal respiratory distress syndrome

198
Q

What is acute respiratory distress syndrome?

A

Diffuse damage to the alveolar-capillary interface (diffuse alveolar damage)

199
Q

What happens in acute respiratory distress syndrome?

A

Leakage of protein-rich fluid leads to edema and formation of hyaline membranes in alveoli

200
Q

What are the clinical features for acute distress syndrome?

A
  1. Hypoxemia and cyanosis with respiratory distress due to thickened diffusion barrier and collapse of air sacs (increased surface tension) 2. White-out on chest x-ray
201
Q

Acute respiratory distress syndrome is secondary to what disease processes?

A

sepsis, infection, shock, trauma, aspiration, pancreatitis, DIG, hypersensitivity reactions, and drugs.

202
Q

Why is acute respiratory distress syndrome secondary to so many diseases?

A

Activation of neutrophils induces protease-mediated and free radical damage of type 1 and II pneumocytes.

203
Q

What is the treatment for acute respiratory distress syndrome?

A
  1. Address underlying cause 2. Ventilation with positive end-expiratory pressure (PEEP)
204
Q

For acute respiratory distress syndrome what might complicate recovery?

A

interstitial fibrosis; damage and loss of type II pneumocytes leads to scarring and fibrosis.

205
Q

What is neonatal respiratory distress syndrome?

A

Respiratory distress due to inadequate surfactant levels

206
Q

Surfactant is made by what?

A

type II pneumocytes;

207
Q

What is the major component in surfactant?

A

phosphatidylcholine (lecithin)

208
Q

What does surfactant do?

A

decreases surface tension in the lung, preventing collapse of alveolar air sacs after expiration.

209
Q

What does lack of surfactant lead to?

A

collapse of air sacs and formation of hyaline membranes.

210
Q

What is neonatal respiratory distress syndrome associated with?

A

1) Prematurity 2) Cesarian section delivery 3) Maternal diabetes

211
Q

When does surfactant production begin?

A

28 weeks

212
Q

When are adequate levels of surfactant reached?

A

34 weeks

213
Q

What is used to screen for lung maturity?

A

Amniotic fluid lecithin to sphingomyelin ratio

214
Q

What is the relationship between phosphatidylcholine (lecithin) levels and surfactant?

A

phosphatidylcholine (lecithin) levels increase as surfactant is produced

215
Q

What is the relationship between sphingomyelin levels and surfactant?

A

sphingomyelin remains constant as surfactant is produced

216
Q

What does an amniotic fluid lecithin to sphingomyelin ratio >2 indicate?

A

adequate surfactant production

217
Q

Why is neonatal respiratory distress syndrome associated with caesarian section delivery?

A

due to lack of stress-induced steroids; steroids increase synthesis of surfactant,

218
Q

Why is neonatal respiratory distress syndrome associated with maternal diabetes?

A

Insulin decreases surfactant production

219
Q

What are the clinical features for neonatal respiratory distress syndrome?

A
  1. Increasing respiratory effort after birth, tachypnea with use of accessory muscles, and grunting 2. Hypoxemia with cyanosis 3. Diffuse granularity of the lung (ground-glass appearance) on x-ray
220
Q

What are the complications for neonatal respiratory distress syndrome?

A
  1. Hypoxemia increases the risk for persistence of patent ductus arteriosus and necrotizing enterocolitis. 2. Supplemental oxygen increases the risk for free radical injury. Retinal injury leads to blindness; lung damage leads to bronchopulmonary dysplasia,
221
Q

What is the most common cause of cancer mortality in the US?

A

Lung cancer; average age at presentation is 60 years.

222
Q

What are the key risk factors for lung cancer?

A

cigarette smoke, radon, and asbestos.

223
Q

What percentage of lung cancer occurs in smokers?

A

85% Cigarette smoke contains over 60 carcinogens

224
Q

For lung cancer what are are particularly mutagenic?

A

Polycyclic aromatic hydrocarbons and arsenic

225
Q

How does cancer risk and smoking relate?

A

Cancer risk is directly related to the duration and amount of smoking (packyears).

226
Q

What is radon formed by?

A

radioactive decay of uranium, which is present in soil

227
Q

Where does radon accumulate?

A

in closed spaces such as basements

228
Q

What is responsible for most of the public exposure to ionizing radiation?

A

radon

229
Q

What is the 2nd most frequent cause of lung carcinoma in US?

A

Radon

230
Q

In addition to smokers and radon increased risk of lung cancer is also seen in what population?

A

uranium miners.

231
Q

What are the presenting symptoms for lung cancer?

A

they are nonspecific (cough, weight loss, hemoptysis, and postobstructive pneumonia)

232
Q

In lung cancer, what does imaging often reveal?

A

a solitary nodule (coin-lesion); biopsy is necessary for a diagnosis of cancer. Benign lesions, which often occur in younger patients, can also produce a coin lesion

233
Q

What are some examples of benign lesions that appear as coin lesions on imaging?

A

Granuloma and bronchial hamartoma

234
Q

What is the benign lesion seen in a granuloma often due to?

A

TB or fungus (especially Hittoplasma in the Midwest)

235
Q

What is the benign lesion seen in bronchial hamartoma due to?

A

benign tumor composed of lung tissue and cartilage; often calcified on imaging

236
Q

Lung carcinoma is classically divided into what 2 categories?

A

1) small cell carcinoma 2) non-small cell carcinoma

237
Q

What usually happens in small cell carcinoma?

A

(15% of cases) usually not amenable to surgical resection (treated with chemotherapy)

238
Q

What usually happens in non-small cell carcinoma?

A

(85% of cases) treated upfront with surgical resection (does not respond well to chemotherapy)

239
Q

What are the subtypes of non-small cell carcinoma?

A

adenocarcinoma (40%), squamous cell carcinoma (30%), large cell carcinoma (10%), and carcinoid tumor (5%).

240
Q

What is TNM staging?

A
  1. T?Tumor size and local extension 2. N?spread to regional lymph nodes (hilar and mediastinal) 3. M?unique site of distant metastasis is the adrenal gland.
241
Q

Involvement of what is classically seen with adenocarcinoma?

A

pleura

242
Q

What is superior vena cava syndrome?

A

Obstruction of SVC leads to distended head and neck veins with edema and blue discoloration of arms and face

243
Q

In regard to TNM, what would hoarseness and diaphragmatic paralysis indicate?

A

Involvement of recurrent laryngeal (hoarseness) or phrenic (diaphragmatic paralysis) nerve

244
Q

How is Horner syndrome related to TNM staging?

A

Compression of sympathetic chain leads to Horner syndrome

245
Q

How is Horner syndrome characterized?

A

by ptosis (drooping eyelid), miosis (pinpoint pupil), and anhidrosis (no sweating);

246
Q

What is Horner syndrome usually due to?

A

an apical (Pancoast) tumor

247
Q

What does the N in TNM staging stand for?

A

spread to regional lymph nodes (hilar and mediastinal)

248
Q

What does the M in TNM stand for?

A

unique site of distant metastasis is the adrenal gland.

249
Q

What is the 5 year survival rate for lung cancer? Explain.

A

Overall, 15% 5-year survival; often presents late due to the absence of an effective screening method

250
Q

What is the characteristic histology for small cell carcinoma?

A

Poorly differentiated small cells; arises from neuroendocrine (Kulchitsky) cells

251
Q

Who is small cell carcinoma associated with?

A

Male smokers

252
Q

What is the location for small cell carcinoma?

A

Central

253
Q

What are some characteristics of small cell carcinoma?

A

Rapid growth and early metastasis; may produce ADH or ACTH or cause Eaton-Lambert syndrome (paraneoplastic syndromes)

254
Q

What is the characteristic histology for squamous cell carcinoma?

A

Keratin pearls or intracellular bridges

255
Q

What is the most common tumor in male smokers?

A

squamous cell carcinoma

256
Q

What is the location for squamous cell carcinoma?

A

Central

257
Q

What might squamous cell carcinoma produce?

A

PTHrP (parathyroid hormone ? related protein)

258
Q

What is the characteristic histology for adenocarcinoma?

A

Glands or mucin

259
Q

In whom does adenocarcinoma most commonly affect?

A

Most common tumor in nonsmokers and female smokers

260
Q

What is the location for adenocarcinoma?

A

Peripheral

261
Q

What is the characteristic histology for large cell carcinoma?

A

poorly differentiated large cells (no keratin pearls, intercellular bridges, glands, or mucin)

262
Q

What is large cell carcinoma associated with?

A

Smoking

263
Q

What is the location for large cell carcinoma?

A

Central or peripheral

264
Q

What is the prognosis for large cell carcinoma?

A

poor

265
Q

What is the characteristic for bronchioloalveolar carcinoma?

A

Columnar cells that grow along preexisting bronchioles and alveoli; arises from Clara cells

266
Q

From what does bronchioloalveolar carcinoma arise?

A

From Clara cells

267
Q

How is bronchioloalveolar carcinoma related to smoking?

A

Its not

268
Q

What is the location for bronchioloalveolar carcinoma?

A

Peripheral

269
Q

How might bronchioloalveolar carcinoma present?

A

May present with pneumonia-like consolidation on imaging;

270
Q

What is the prognosis for bronchioloalveolar carcinoma?

A

excellent prognosis

271
Q

What is the characteristic histology for Carcinoid tumor?

A

Well differentiated neuroendocrine cells; chromogranins positive

272
Q

How is carcinoid tumor related to smoking?

A

Its not

273
Q

What is the location for carcinoid tumor?

A

Central or peripheral

274
Q

What does a carcinoid tumor classically form?

A

A polyp-like mass in the bronchus

275
Q

Describe the malignancy of a carcinoid tumor?

A

Low-grade malignancy; rarely, can cause carcinoid syndrome

276
Q

What is the characteristic histology for metastasis to lung?

A

Most common sources are breast and colon carcinoma.

277
Q

What is the location for metastasis to lungs?

A

Multiple cannonball nodules on imaging

278
Q

Metastasis to lungs is more common than what type of tumor?

A

primary tumors

279
Q

What is a pneumothorax?

A

An accumulation of air in the pleural space

280
Q

What is a spontaneous pneumothorax due to?

A

rupture of an emphysematous bleb

281
Q

In whom do you see spontaneous pneumothorax?

A

seen in young adults

282
Q

What does spontaneous pneumothorax result in?

A

collapse of a portion of the lung;

283
Q

In a spontaneous pneumothorax, how can you tell which side collapsed?

A

trachea shifts to the side of collapse

284
Q

Tension pneumothorax arises with what?

A

penetrating chest wall injury

285
Q

What happens in a tension pneumothorax?

A

1) Air enters the pleural space, but cannot exit; trachea is pushed opposite to the side of injury. 2) Medical emergency; treated with insertion of a chest tube

286
Q

Regarding pneumothorax, what does a tracheal shift tell you?

A

Tension pneumothorax = opposite side of injury, spontaneous pneumothorax = shifts to the side of the collapse

287
Q

What is mesothelioma?

A

Malignant neoplasm of mesothelial cells

288
Q

Mesothelioma is highly associated with what?

A

Occupational exposure to asbestos

289
Q

What does mesothelioma present with?

A

recurrent pleural effusions, dyspnea, and chest pain; tumor encases the lung

Pathoma KAM (19 decks)

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