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My Pathoma Unit 4 > Chapter 9 Respiratory Tract > Flashcards

Chapter 9 Respiratory Tract Flashcards

1
Q

at its core, what is pneumonia?

A

Infection of the lung parenchyma

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2
Q

What types of impairments to normal defense mechanisms can lead to pneumonia? 3

A

impaired cough reflex
Damage to mucociliary escalator
mucus plugging

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3
Q

What are 7 clinical features of pneumonia?

A 
Fever
chills
tachypnea with pleuritic chest pain
decreased breath sounds
dullness to percussion
elevated WBC
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4
Q

How is diagnosis of pneumonia made?

A

CXR, sputum gram stain and culture, and blood cultures

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5
Q

What are three typical patterns seen on xray in pneumonia?

A

Lobular pneumonia, bronchopneumonia, interstitial pneumonia

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6
Q

What is lobular pneumonia characterized by?

A

Consolidation of an entire lobe of the lung

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7
Q

What is usually the cause of lobular pneumonia? bacteria vs viral

A

Usually bacteria

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8
Q

What are the classic gross phases of lobular pneumonia? 4

A

1 Congestion- due to congested vessels and edema
2 Red Hepatization - due to exudate, neutrophils, and hemorrhage filling the alveolar air spaces, giving the normally spongy lung a solid consistency
3 Gray Hepatization - due to degradation of red cells within exudate
4 Resolution (regeneration from type II pneumocytes

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9
Q

What is Bronchopneumonia characterized by?

A

Scattered patchy consolidation centered around bronchioles; often multifocal and bilateral

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10
Q

What is Bronchopneumonia caused by? bacteria vs virus

A

variety of bacterial orga

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11
Q

What is interstitial (atypical) pneumonia characterized by?

A

diffuse interstitial infiltrates without major consolidation. Increased lung markings on CXR

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12
Q

How does Interstitial pneumonia present?

A

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

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13
Q

What is interstitial pneumonia caused by? bacteria vs virus?

A

Caused by both bacteria and viruses

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14
Q

What are the two most common organisms that cause lobular pneumonia?

A 
Streptococcus pneumoniae (95%)
Klebsiella pneumoniae
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15
Q

What are the high yield associations for streptococcus pneumoniae in the setting of lobular pneumonia?

A

Most common cause of community acquired pneumonia and secondary pneumonia (bacterial pneumonia superimposed on a viral URI); usually seen in middle aged adults and the elderly

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16
Q

What are the high yield associations for klebsiella pneumoniae in the setting of lobular pneumonia?

A

Enteric flora that is aspirated; affects malnourished and debilitated individuals. especially elderly in nursing homes, alcoholics, and diabetics. Thick mucoid capsule results in gelatinous sputum (currant jelly); often complicated by abscess.

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17
Q

Name five organisms that cause bronchopneumonia?

A 
Staph aureus
Haemophilus influenzae
P. Aeruginosa
Moraxella catarrhalis
legionella pneumophila
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18
Q

What are the high yield associations of staph aureus?

A

Most common cause of secondary pneumonia; often complicated by abscess or empyema

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19
Q

What are the high yield associations of haemophilus influenzae?

A

Common cause of secondary and pneumonia superimposed on COPD (leads to exacerbation of COPD)

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20
Q

What are the high yield associations of pseudomonas aeruginosa?

A

pneumonia in CF patients

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21
Q

What are the high yield associations of moraxella catarrhalis?

A

Community acquired pneumonia and pneumonia superimposed on COPD (leads to exacerbation of COPD)

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22
Q

What are the high yield associations of legionella pneumophila?

A

Community acquired pneumonia, pneumonia superimposed on COPD, or pneumonia in immunocompromised states; transmitted from water source, intracellular organism that is best visualized by a silver stain

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23
Q

What are six organisms that cause interstitial pneumonia?

A 
Mycoplasma pneumoniae
chlamydia pneumonia
Respiratory syncytial virus (RSV)
Cytomegalovirus (CMV)
Influenza virus
Coxiella burnetii
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24
Q

What are the high yield associations of mycoplasma pneumoniae?

A

Most common cause of atypical pneumonia, usually affects young adults (classically military recruits or college students living in a dormitory). Complications include autoimmune hemolytic anemia (IgM against I antigen on RBCs causes cold hemolytic anemia) and erythema multiforme. Not visible on gram stain due to lack of cell wall.

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25
Q

What are the high yield associations of chlamydia pneumonia?

A

second most common cause of atypical pneumonia in young adults

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26
Q

What are the high yield associations of respiratory syncytial virus?

A

most common cause of atypical pneumonia in infants

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27
Q

What are the high yield associations of influenza virus?

A

Atypical pneumonia in the elderly, immunocompromised, and those with preexisting lung disease. Also increases the risk for superimposed S aureus or H influenzae bacterial pneumonia

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28
Q

What are the high yield associations of Coxiella burnetii

A

Atypical pneumonia with high fever (Q fever, normally have low fevers); seen in farmers and veterinarians (Coxiella spores are deposited on cattle by ticks or are present in cattle placentas). Coxiella is a rickettsial organism, but it is distinct from most rickettsiae because it 1 causes pneumonia, 2 does not require arthropods vectors for transmission (survives as highly heat resistant endospores), and 3 does not produce skin rash.

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29
Q

What patients is aspiration pneumonia typically seen in?

A

patients with risk for aspiration (eg. alcoholics and comatose patients)

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30
Q

What is aspiration pneumonia often due to?

A

anaerobic bacteria in the oropharynx (eg. bacteroides, fusobacterium, and peptococcus)

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31
Q

What does aspiration pneumonia classically result in?

A

Right lower lobe abscess

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32
Q

What is TB due to?

A

Inhalation of aerosolized mycobacterium tuberculosis

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33
Q

What does primary TB arise from and what does it result in?

A

Initial exposure, results in 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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34
Q

Where is a ghon complex usually seen?

A

Subpleural or hilar lymph nodes

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35
Q

Is primary TB symptomatic? what effect does it have on a PPD?

A

Usually asymptomatic and causes a positive PPD

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36
Q

What causes secondary TB?

A

reactivation of Mycobacterium tuberculosis

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37
Q

What is reactivation commonly due to in TB?

A

AIDS; may also be seen with agin

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38
Q

Where does secondary TB occur at?

A

Apex of the lung (relatively poor lymphatic drainage and high oxygen tension)

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39
Q

What does secondary TB form?

A

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

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40
Q

What are the clinical features of secondary TB?

A

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

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41
Q

What does biopsy reveal in secondary TB?

A

caseating granulomas; AFB stain reveals acid fast bacilli in cords.

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42
Q

What tissues can systemic spread of secondary TB affect? which are the most common?

A

can affect any tissue; common sites include meninges (menigitis), cervical lymph nodes, kidneys (sterile pyuria), and lumbar vertebrae (Pott Disease)

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43
Q

How does TB meningitis present?

A

Usually involves the base of the brain, so meningitis with granulomas in the base of the brain

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44
Q

What are COPD disease characterized by?

A

airway obstruction; lung does not empty air; and air is trapped.

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45
Q

Describe the changes in FVC, FEV1, FEV1:FVC, and TLC in COPD?

A

vFVC, vvFEV1, vFEV1:FVC, ^TLC

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46
Q

How is chronic bronchitis defined?

A

Chronic productive cough lasting at least 3 months over a minimum of 2 years\

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47
Q

What is chronic bronchitis highly associated with?

A

smoking

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48
Q

What is chronic bronchitis characterized by?

A

hypertrophy of bronchial mucinous glands (cough up buckets of mucus). leads to increased thickness of mucus glands relative to bronchial wall thickness (Reid index increases to >50%; normal is <40%)

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49
Q

What are the clinical features of Chronic Bronchitis?

A

productive cough due to excessive mucus production. cyanosis (‘blue bloaters’) - mucus plugs trap CO2; increase PaCO2 and decreased PaO2. Increased risk of infection and cor pulmonale.

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50
Q

What is cor pulmonale?

A

Diffuse hypoxia results in globally pulmonary vasoconstriction and leading to RV hypertrophy and eventually RV failure.

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51
Q

What happens in emphysema?

A

destruction of alveolar air sacs. Loss of elastic recoil and collapse of small airways during exhalation results in obstruction and air trapping

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52
Q

What is emphysema due to?

A

imbalance of proteases and antiproteases.

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53
Q

What leads to the imbalance in in proteases and antiproteases in ephysema?

A

1 inflammation in the lung normally leads to release of proteases by neutrophils and macrophages.
2 alph1-antitrypsin (A1AT, inhibited by cigarette smoke) neutralizes proteases
3 excessive inflammation or lack of A1AT leads to destruction of the alveolar air sacs

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54
Q

What is the most common cause of emphysema and why?

A

Smoking, pollutants in smoke lead to excessive inflammation and protease mediated damage.

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55
Q

What pattern of emphysema arises in smokers?

A

centriacinar emphysema that is most severe in the upper lobes

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56
Q

What pattern of emphysema is seen in people with an A1AT deficiency?

A

results in panacinar emphysema that is most severe in lower lobes

57
Q

What other complicaiton may be seen in A1AT deficient emphysema and what causes this?

A

Liver cirrhosis. A1AT, which is produced in the liver, deficiency is due to misfolding of the mutated protein. Mutant A1AT accumulates in the ER of hepatocytes, resulting in liver damage. Biopsy reveals pink, PAS positive globules in hepatocytes

58
Q

What is disease severity determined by in A1AT deficient emphysema? describe the clinical consequence of the various genotypes?

A

severity is based on the degree of A1AT deficiency. PiM is the normal allele and the normal genotype is PiMM. PiZ is the most common clinically relevant mutation. PiMZ are usually asymptomatic but at significant risk for emphysema if they smoke. PiZZ are at significant risk for panacinar emphysema and cirrhosis.

59
Q

Name 5 clinical features of emphysema?

A

1 dyspnea and cough with minimal sputum
2 prolonged expiration with pursed lips (pink puffer)
3 weight loss
4 increased AP chest diameter (barrel chest)
5 hypoxemia (due to destruction of capillaries in the alveolar sac) and cor pulmonale are late complications

60
Q

At what lung volume does the inward recoil of the lung come into equillibrium with th eoutward recoil of the chest wall?

A

Functional Residual Capacity

61
Q

What happens to the FRC in COPD and restrictive disease?

A

Increases in COPD and decreased in restrictive disease

62
Q

What is Asthma and what is it most often due to?

A

Reversible airway bronchoconstriction, most often due to allergic stimuli (atopic asthma).

63
Q

When does asthma usually present and what is it often associated with?

A

In Childhood; often associated with allergic rhinitis, eczema, and a family history of atopy.

64
Q

Describe the pathogenesis (type 1 hypersensitivity) of asthma.

A 
1 Allergens induce Th2 phenotype CD4+ Tcells of genetically susceptible individuals. 
2 Th2 cells secreate IL4 (mediates class switch to IgE), IL5 (attracts eosinophils), and IL10 (stimulates Th2 cells and inhibits Th1)
3 Reexposre to allergen leads to IgE mediated activation of mast cells.
65
Q

What happens when reexposure to an allergen activates mast cells in asthma?

A

1 (early phase) release of preformed histamine granules (vasodilalation in arterioles and increase vascular permeability in post-capillary venules) and generation of LT C4, D4, and E4 (vasoconstriction , increase in permeability by contraction of pericytes, and bronchoconstriction) lead to broncho constriction, inflammation, and edema
2 (late phase) inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction.

66
Q

What are the clinical features of asthma?

A

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 statues asthmaticus and death.

67
Q

What is Bronchiectasis?

A

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

68
Q

What are 5 caused of bronchiectasis?

A 
1 CF
2 Kartenger syndrome
3 Tumor or foreign body
4 necrotizing infection
5 allergic bronchopulmonary aspergillosis
69
Q

What is Kartenger syndrome?

A

inherited defect of the dynein arm, which is necessary for ciliary movement. Associated with sinusitis, infertility (shitty sperm) and situs inversus.

70
Q

What is allergic bronchopulmonary aspergillosis?

A

Hypersensitivity reaction to Aspergillus leads to chronic inflammatory damage; usually seen in individuals with asthma or CF

71
Q

Name 4 COPDs

A

Chronic bronchitis
emphysema
Bronchiectasis
Asthma

72
Q

What is the underlying problem in restrictive diseases?

A

Characterized by restricted filling of the lung

73
Q

What abnormalities in spirometry are seen in restrictive diseases?

A

decreased TLC, FEV1, and FVC

FEV1:FVC is INCREASED

74
Q

What is the most common cause of restrictive disease, whats another cause?

A

most commonly due to interstitial diseases of the lung; may also arise with chest wall abnormalities (eg massive obesity)

75
Q

What is idiopathic pulmonary fibrosis?

A

Fibrosis of lung interstitium

76
Q

What is the etiology of idiopathy pulmonary fibrosis? what is it likely related to?

A

etiology is unknown. Likely related to cyclical lung injury and healing; TGF-B from injured pneumocytes induces fibrosis

77
Q

What are some secondary causes of interstitial fibrosis?

A

drugs (bleomycin and amiodarone) and radiation therapy

78
Q

What are the clinical features of idiopathic pulmonary fibrosis? and what is the treatment?

A

1 progressive dyspnea and cough
2 Fibrosis on lung CT; initially seen in subpleural patches, but eventually results in diffuses fibrosis with end-stage ‘honeycomb’ lung
3 treatment is lung transplantation

79
Q

What is pneumoconioses and what happens in it?

A

Interstitial fibrosis due to occupational exposure; requires chronic exposure to small particles that are fibrogenic. alveolar macrophages engulf foreign particles and induce fibrosis

80
Q

Name four different types of pneumoconioses?

A

1 coal workers’ pneumonconiosis
2 silicosis
3 berylliosis
4 Asbestosis

81
Q

What is the exposure, pathogenic findings, and associations for Coal workers’ pneumoconiosis?

A

Exposure is carbon dust; seen in coal miners. Pathological Findings; massive exposure leads to diffuse fibrosis (‘Black lung’); associated with rheumatoid arthritis (Caplan syndrome)

82
Q

What is the exposure, pathogenic findings, and associations for silicosis?

A

Exposure is silica; seen in sandblasters and silica miners. Pathological findings are fibrotic nodules in upper lobes of the lung. Increased risk for TB; silica impairs phagolysosome formation by macrophages

83
Q

What is the exposure, pathogenic findings, and associations for Berylliosis?

A

Exposure is beryllium; seen in beryllium miners and workers in the aerospace industry. Noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs. Increased risk for lung cancer

84
Q

What is the exposure, pathogenic findings, and associations for Asbestosis?

A

exposure is asbestos fibers; seen in construction workers, plumbers, and shipyard workers. Fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma (more common) and mesothelioma (Less common). Lesions contain long, golden brown fibers with associated iron (asbestos Bodies) which confirm exposure to asbestos.

85
Q

What is sarcoidosis, who is it classically seen in?

A

Systemic disease characterized by noncaseating granulomas in multiple organs (granulomas in interstitium of lung cause restricted filling). Classically seen in african american females.

86
Q

What is the etiology of sarcoidosis? what is it likely due to?

A

Etiology is unknown; likely due to CD4+ helper Tcell response to an unknown antigen

87
Q

What are common sites for granulomas in sarcoidosis and what are they characterized by?

A

Granulomas most commonly invilve hilar lymph nodes and lung leading to restrictive lung disease. Characteristic stellate inclusions (asteroid bodies) are often seen within giant cells of the granulomas

88
Q

What are other commonly involved tissues of granulomas in sarcoidosis?

A

uvea (uveitis), Skin (cutaneous nodules or erythema nodosum), and salivary and lacrimal glands (mimics sjogrens syndrome); almost any tissue can be involved.

89
Q

What are the clinical features of sarcoidosis? what is the treatment?

A

1 Dyspnea and cough (most common presenting symptom)
2 Elevated ACE
3 Hypercalcemia (a-alpha hydroxylase activity of epitheliod histiocytes converts vitamin D to its active form

treatment is steroids; often resolves spontaneously without treatment

90
Q

What is hypersensitivity pneumonitis?

A

Granulomatous reaction (plus eosinophils) to inhaled organic antigens (eg pigeon breeders lung)

91
Q

How does hypersensitivity pneumonitis present?

A

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

92
Q

What does chronic exposure in hypersensitivity pneumonitis lead to?

A

interstitial fibrosis

93
Q

What is pulmonary hypertension defined by ?

A

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

94
Q

What is pulmonary HTN characterized by?

A

atherosclerosis of pulmonary arteries, and intimal fibrosis; plexiform lesions (tuft of capillaries) are seen with severe, long standing disease

95
Q

What does pulmonary HTN lead to?

A

RV hypertrophy and cor pulmonale

96
Q

How does pulmonary HTN present?

A

Exertional dyspnea or right sided heart failure

97
Q

How is pulmonary HTN subclassified?

A

Primary or secondary

98
Q

Who is primary pulmonary HTN classically seen in, what is the etiology, what are family forms related to?

A

Classically seen in young adult females. etiology is unknown. some familial forms are related to inactivating mutations of BMPR2, leading to proliferation of vascular smooth muscle and thickening of vessel walls.

99
Q

What is secondary pulmonary HTN due to?

A

Due to hypoxemia (eg COPD and interstitial lung disease) or increased volume in the pulmonary circuit ( congenital heart disease); may also arise from recurrent PE.

100
Q

What happens in ARDS?

A

Diffuse damage to alveolar capillary interface (diffuse alveolar damage). Leakage of protein rich fluid leads to edema that combines with necrotic epithelial cells to form hyaline membranes in alveoli.

101
Q

What are the clinical features of ARDS?

A

hypoxemia and cyanosis with respiratory distress - due to thickened diffusion barrier and collapse of air sacs (increased surface tension). ‘White-out” appearance on CXR

102
Q

Name some diseases that ARDS is secondary to? and what causes the damage?

A

sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, hypersensitivity reactions, and drugs. Activation of neutrophils induces protease and free radical mediated damage of type I and type II pneumocytes

103
Q

What does treatment of ARDS involve?

A

Treatment of the underlying cause

ventilation with PEEP

104
Q

What may complicate recovery from ARDS?

A

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

105
Q

What is neonatal respiratory distress due to ?

A

Inadequate surfactant levels

106
Q

What cell makes surfactant and what is the main component?

A

Type II pneumocytes. Phosphatidylcholine (lecithin) is the major component

107
Q

What is the function of surfactant in the lung?

A

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

108
Q

What does loss of surfactant lead to?

A

collapse of air sacs and formation of hyaline membranes

109
Q

What is Neonatal respiratory distress syndrome associated with?

A

1 Prematurity - surfactant production begins at 28 weeks; adequate surfactant levels are not reached until 34 weeks
2 cesarian section - due to lack of stress induced steroids which increase the synthesis of surfactant
3 Maternal diabetes - high insulin levels from the fetal pancreas decrease surfactant production

110
Q

What is used for screening lung maturity and how is it assessed?

A

Amniotic fluid lecithin to sphingomylein ratio is used. Lecithin levels increase as surfactant is produced; sphingmyelin remains constant. a ratio of > 2 idicates adequate surfactant production.

111
Q

What are the clinical features of neonatal respiratory distress syndrome?

A

Increased respiratory effort at birth, tachypnea with use of accessory muscles, and grunting
hypoxemia with cyanosis
diffuse granularity of the lung (‘ground-glass’ appearance) on X-ray

112
Q

What are 2 complications of neonatal respiratory distress syndrome?

A

1 Hypoxemia increases the risk for persistence of patent ductus arteriosus (normally closes with good oxygenation) and necrotizing enterocolitis
2 Supplemental oxygen increased the risk for free radical injury. Retinal injury leads to blindness; lung damage leads to bronchopulmonary dysplasia.

113
Q

What are 3 key risk factors for lung cancer?

A

cigarette smoke, radon, and asbestos

114
Q

What is cigarettes is particularly carcinogenic, how is cancer risk related to smoking?

A

Polycyclic hydrocarbons and arsenic (SCC). Cancer risk is directly related to the duration and amount of smoking

115
Q

What is radon formed from and where is it ubiquitously present?

A

Formed from radioactive decay of uranium, which is present in soil

116
Q

What do you know about radon and its relation to lung cancer?

A

accumulates in closed spaces such as basements.
responsible for most public exposure to ionizing radiation; 2nd most frequent cause of lung carcinoma in US.
Increased risk of lung cancer is also seen in uranium miners.

117
Q

What are the presenting symptoms of lung cancer?

A

nonspecific; cough, weight loss, hemoptysis, and postobstructive pneumonia

118
Q

What does imaging often reveal in lung cancer? what is the next logical step in care?

A

solitary nodules (‘coin-lesion’); biopsy is necessary for diagnosis. Next step is to go back and look at prior CXR and look for changes in size.

119
Q

What are a couple benign lesions, which often occur in younger patients, that can produce ‘coin-lesions’?

A

Granuloma - often due to TB or fungus (especially histoplasma in the midwest)
Bronchial hamartoma - benign tumor composed of lung tissue and cartilage; often calcified on imaging

120
Q

What are the two categories that lung cancer is classically divided into? describe their treatment and subtypes?

A

Small Cell Carcinoma (15%) - usually not amenable to surgical resection (treated with chemo)
non-small cell carcinoma (85%) - treated upfront with surgical resection (does not respond well to chemo); subtypes include adenocarcinoma (40%), Squamous cell carcinoma (30%), large cell carcinoma (10%), and carcinoid tumor (5%)

121
Q

Describe the Characteristic histology, associations, locations, and high yield info of small cell carcinoma?

A

poorly differentiated small cells that are mitotically active with necrosis; arises from neuroendocrine (kulchitsky) cells which are cromogranin positive. Seen in male smokers, in central location. rapid growth and early metastasis; may produce ADH or ACTH (cushings) or cause Lambert-Eaton Syndrome

122
Q

Describe the Characteristic histology, associations, locations, and high yield info of Squamous cell carcinoma

A

Keratin pearls or intracellular bridges. Most common tumor in male smokers. central location. May produce PTHrP (hypercalcemia) syndrome

123
Q

Describe the Characteristic histology, associations, locations, and high yield info of adenocarcinoma?

A

Glands or mucin. Most common tumor in nonsmokers and female smokers. Peripheral location. no paraneoplastic syndromes

124
Q

Describe the Characteristic histology, associations, locations, and high yield info of large cell carcinoma?

A

Poorly differentiated large cells (no keratin pearls, intracellular bridges, glands, or mucin). Seen in smokers, central or peripheral location. poor prognosis

125
Q

Describe the Characteristic histology, associations, locations, and high yield info of Bronchioloaveloar carcinoma?

A

Columnar cells that grow along preexisting bronchioles and alveoli’ arises from clara cells/ Not related to smoking. Peripheral location. May present with pneumonia like consolidation on imaging; excellent prognosis

126
Q

Describe the Characteristic histology, associations, locations, and high yield info of Carcinoid tumor?

A

Well differentiated neuroendocrine cells; chromogranin positive. Not related to smoking. Centra or peripheral; when central, classically forms a polyp like mass in the bronchus. low grade malignancy; rarely, can cause carcinoid syndrome

127
Q

Describe the most common source of mets to the lungs, how they present on imaging and their commonality.

A

Most common sources are breast and colon. Multiple cannonball nodules on imaging. more common than primary

128
Q

What is the staging system used for lung cancer?

A

Tumor size and local extension
N spread to regional lymph nodes
Metastasis to distant sites

129
Q

What form of lung cancer is pleural involvement classically seen in?

A

adenocarcinoma

130
Q

What does obstruction of the SVC lead to?

A

distended head and neck veins with edema and blue discoloration of arms and face (SVC syndrome)

131
Q

What does involvement of the recurrent laryngeal or phrenic nerves lead to?

A

hoarseness and diaphragmatic paralysis

132
Q

What does the compression of the sympathetic chain lead to? what type of lung tumor causes this?

A

horners syndrome. usually due to apical (pancoast) tumor)

133
Q

What is a unique site of metastasis of lung cancer?

A

adrenal gland

134
Q

What is a pneumothorax?

A

Accumulation of air in the pleural space.

135
Q

What is spontaneous pneumothorax due to and what does it result in?

A

due to rupture of an ephysematous bleb; seen in young adults. results in collapse of a portion of the lung; trachea shits to the side of collapse.

136
Q

What causes a tension pneumothorax and what does it result in?

A

Arises with penetrating chest wall injury. Air enters pleural space, but cannot exit; trachea is pushed to the opposite side of the injury. medical emergency; treated with insertion of a chest tube.

137
Q

What is mesothelioma? what is it associated with?

A

Malignant neoplasm of mesothelial cells; highly associated with occupational exposure to asbestos.

138
Q

How does mesothelioma present?

A

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

My Pathoma Unit 4 (3 decks)

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