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Pathology II Exam 1 > Lungs > Flashcards

Lungs Flashcards

1
Q

T-F- the apices of the lung rise above the clavicle?

T-F- the lung does not cover any portion of the mediastinum upon inhalation?

A

True

False

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2
Q

Of the conducting airways, which section is the weakest link and why?

A

bronchioles- they do not have cartilage like the trachea and bronchi do

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3
Q

What does a normal gross lung specimen look and feel like?

A

light red brown

spongy

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4
Q

The connective tissue of the visceral pleura is lined by what type of cells? What is their ultrastructural hallmark?

A

mesothelial cells- long slender microvilli

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5
Q

What type of cell comprises 90-95% of the alveolar lining? what shape are they?

A

Type I pneumocyte- flat epithelial- gas exchange

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6
Q

What is the type II pneumocyte shape? What happens to these cells during inflammation?

A

cuboidal- surfactant production and antimicrobials

increase in number

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7
Q

What are the 4 key mechanism (mechanical and cellular) for pulmonary defense?

A

Tracheobronchial clearance (cilia and goblet)
Cough
Alveolar macrophages
lymphatics

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8
Q

What are common ways to suppress the cough reflex?

A

stroke, post-operative

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9
Q

What are common ways to injure mucociliary clearance?

A

tobacco

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10
Q

What are the 4 common ways to lose/impair host defense mechanisms that she gives?

A

smoking, ethanol, stroke, heart failure

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11
Q

What are the histological findings [2] of classic bacterial pneumonia (strep pneumonia)?

A
  1. intra alveolar exudate- fibrin and neutrophils

2. Alveolar capillary congestion

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12
Q

What are the two basic patterns of bacterial pneumonia?

The pattern of involvement really depends on what two things?

A
  1. patch bronchopneumonia or whole lobe lobar pneumonia

2. bacterial virulence and innate defenses

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13
Q

In bronchopneumnia we know we see a plug of fibrin and neutrophils, but what happens to the wall of the bronchiole?

A

it gets inflamed as well

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14
Q

What are the 4 pathological stages of bacterial pneumonia?

A

congestion
red hepatization
gray hepatization
resolution

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15
Q

What pathological stage of pneumonia (bacterial) is characterized by vascular engorgement, alveolar fluid, few neutrophils, numerous bacteria?

A

congestion

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16
Q

What pathological stage of bacterial pneumonia is characterized by firm, airless, massive exudate, neutrophils and fibrin?

A

red hepatization

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17
Q

What pathological stage of bacterial pneumonia is characterized by a dry surface, disintegration of RBCs, and a strong fibropurulent exudate?

A

gray hepatization

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18
Q

During resolution of bacterial pneumonia- enzymatic digestion of the exudate produces granular semifluid debris. What 4 things can happen to it?

A
  1. resorbed
  2. ingested by macrophages
  3. expectorated
  4. organized by fibroblasts growing in it
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19
Q

What is the clinical presentation of bacterial pneumonia? Review[6]

A 
abrupt onset
high fever
shaking
chills
productive cough
pleuritis
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20
Q

What type of bacterial pneumonia is very important to find, but won’t show on a gram stain but shows up with a silver stain?

A

legionella

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21
Q

What does viral and atypical bacterial pneumonia primarily effect?

A

the interstitium- the damage can predispose to other bacterial pneumonias

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22
Q

What is the best example of atypical bacterial pneumonia?

A

Mycoplasma

but don’t forget chlamydia

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23
Q

Atypical pneumonia may have a moderate amount of sputum, but what doesn’t it have?

A

consolidation and significant alveolar exudate

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24
Q

Mycoplasm bronchiolitis looks like what?

A

inflammation of a bronchiole mucosa with patchy infiltrates and swelling in the peribronchial interstitial space, SURROUNDING ALVEOLI LOOK PRETTY NORMAL

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25
Q

Clinical speaking, what does viral/atypical pneumonia look like?

A 
'walking pneumonia'
chest cold
low grade fever
headache
muscle aches
insidious onset
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26
Q

What are the common pathogens for community acquired pneumonia? hospital acquired?

A
  1. strep pneumonia and haemophilus influzae

2. staph aureus and pseudomonas

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27
Q

Review the following common virus for CA pneumonia

A

parainfluenza
adenovirus
influenza
RSV

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28
Q

What should we remember when looking at a biopsy of an immunocompromised host?

A

low virulence/opportunistic pathogens may be the causing factor

tissue pathology or inflammation may be minimal

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29
Q

Review the following CD4 levels and the pneumonia causing agents

A

<200 PCP, Aspergillus

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30
Q

What virus shows both intranuclear and intracytoplasmic inclusions?

A

CMV

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31
Q

What do we see cellularly in the case of food particles (maybe from GERD) that have been aspirated in the lungs?

A

multinucleate giant cells within alveolar spaces trying to digest–> airway centered granulomatous inflammation

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32
Q

What are three common risk factors for aspiration pneumonia that have polymicrobial infectious agents?

A 
impaired consciousness (alcoholics)
severe reflux (GERD)
Poor swallowing (stroke, neck cancer etc.)
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33
Q

What are the common causative organisms in lung abcesses? What are the common etiologies 4 ?

A
  1. 60% are anaerobic bacteria

2. aspiration, poorly treated bacterial infection, septic emboli, neoplasia

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34
Q

On gross specimen, what should surround an abcess? What does the x ray look like? Microscopic?

A
  1. hyperemic rim
  2. AIR-FLUID LEVELS
  3. neutrophils and fibrin surrounded by granulation tissue
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35
Q

what creates a -frothy bubbly and lacks a cellular intra-alveolar infiltrate exudate?

A

PCP

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36
Q

How do we stain PCP?

A

Silver stain from bronchoalveolar lavage

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37
Q

Where do we find histoplasma?

A

soil with bird droppings or bat droppings

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38
Q

Histoplasmosis causes what type of lesion? What does it appear as on CXR?

A
  1. granulomatous nodule with central necrosis and fibrous wall (like TB)
  2. Coin lesion- if they contain calcifications they are almost always benign
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39
Q

In the histoplasmosis silver stain, are the organisms small or large?

A

small- 4 microns (may also see budding)

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40
Q

What populations are at risk for initial exposure to M. tuberculosis to cause primary pulmonary tuberculosis?

A

poor
homeless
incarcerated
southern latitudes

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41
Q

T-F- primary pulmonary tuberculosis is normally symptomatic? T-F– rates are decreasing

A

False and false

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42
Q

What percentage of TB infected people develop clinically significant disease?

A

5

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43
Q

Primary pulmonary tuberculosis looks like what in the gross lung?

A

peripheral granuloma with hilar adenopathy (hilar nodes will be dark-anthracosis- not in the areas of the granuloma)

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44
Q

At the edge of a necrotizing granuloma, what cells do we readily see?

A

multinucleate giant cells.

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45
Q

IF we have a CT scan of someone with nodules in their lung, what do we see that can tell us that they are benign?

A

central calcification

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46
Q

Where is the lesion primarily in secondary pulmonary tuberculosis? who gets it?

A
  1. apical and posterior (apical shadow)

2. reactivation of primary or new infection in previously sensitized host

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47
Q

What are the differential diagnosis usually seen with tuberculosis?

A

malignancy
fungal infection
lymphoma

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48
Q

T-F– PPD test need intact cell-mediated immunity?

A

True- it is a Type IV hypersensitivity test

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49
Q

What is defined as a rapid onset of severe life threatening respiratory insufficiency, cyanosis and severe arterial hypoxemia refractory to oxygen therapy?

A

ARDS

- remember that ARDS can be caused by infections, sepsis, toxic fumes, drug and medication reactions,etc

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50
Q

What does a CXR of ARDS look like? what is the mortality rate?

A
  1. extensive opacities in both lungs

2. 60% +

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51
Q

What is the difference of ARDS and diffuse alveolar damage (DAD)?

A

ARDS is a clinical diagnosis and DAD is pathological (DAD = hyaline membranous disease or acute lung injury)

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52
Q

What are the 4 characteristics of diffuse alveolar damage-pathology injury to capillary endothelium?

A

increased cap. permeability
interstitial and intra-alveolar edema
fibrin exudation
hyaline membrane formation

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53
Q

What are the 4 phases of DAD?

A

exudative–>transition–>proliferative–>fibrotic

Corresponds to

edema—> hyaline membrane–>inflammation–>fibroplasia

NOTE:hyaline formation happens very early in exudative stage

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54
Q

In DAD- what does diffuse mean?

A

The entire alveoli is damaged- not the whole lung or lobe is damaged

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55
Q

Alveolar spaces are filled with what in DAD?

A

balls of fibroblasts

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56
Q

Is bronchiectasis and pneumonitis obstructive pulmonary diseases or restrictive pulmonary disease?

A

bronchiectasis is obstructive

pneumonitis is restrictive

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57
Q

What is described as increase in resistance to airflow due to partial or complete obstruction at any level of airway?

A

Obstructive lung disease

- can get air in but can’t get it out

58
Q

What is described as a reduced expansion of lung parenchyma and decreased total lung capacity

A

Restrictive lung diseases

- can get the air out, but can’t get it in well.

59
Q

Most of the obstructive pulmonary diseases have the bronchus as their main anatomic site, which one has the acinus as its main site?

A

emphysema

60
Q

What obstructive disease characterized by airway dilation and scarring?

A

bronchiectasis

61
Q

What obstructive disease is characterized by mucous gland hyperplasia and hyper secretion? smooth muscle hyperplasia?

A

chronic bronchitis

ASthma

62
Q

What obstructive disease is characterized by airspace enlargement; wall destruction

A

emphysema

63
Q

What two lung diseases are grouped together for COPD?

A

emphysema and bronchitis

64
Q

In emphysema- there is destruction to the walls past the terminal bronchiole…is there fibrosis? what is it associated with [2]?

A

No

cigarette smoke and alpha-1 antitripsin deficiency

65
Q

What type of emphysema is the most common?

A

centriacinar 95%

  • central, more common in upper lobes, common in smokers
66
Q

What type of emphysema is associated with alpha 1 antitrypsin?

A

panacinar- uniform enlargement, more common in lower zones

67
Q

On a gross specimen- what would be the diff between panacinar and centriacinar?

A

panacinar does not have normal tissue between the problematic areas. ITS PRETTY MUCH THE SAME DEAL UNDER MICROSCOPE TOO

68
Q

What does smoking decrease that leads to higher levels of elastase?

A

alpha-1 antitrypsin

69
Q

What cells are releasing the elastase?

What where do we get the anti-protease?

A
  1. neutrophils and macrophages

2. in the serum and tissue fluids

70
Q

The critical event in emphysema is the loss of alveolar walls, what two things does this lead to?

A

decreases gas exchange and reduces the elastic tissue content of the lungs

71
Q

Symptoms of emphysema appear after how much of the parenchyma was damaged? what do they include?

A

1/3

dyspnea, weight loss, eventually overdistension

72
Q

What is an air filled space that measures more than 1cm in diameter in the distended state of emphysema? what can this lead to?

A
  1. subpleural bullae

2. pneumothorax

73
Q

What are the 3 major complications of emphysema?

A

respiratory acidosis and coma
right sided heart failure
pneumothorax and collapsed lung

74
Q

What is described as a persistent cough with sputum production for at least 3 consecutive months in at least two consecutive years?

A

chronic bronchitis

- smokers and smog laden cities

75
Q

What is the difference in chest radiograph of bronchitis and emphysema?

A

bronchitis will have prominent vessels and a large heart, emphysema will show hyperinflation and a small heart

76
Q

Is bronchitis the blue bloater or the pink puffer?

A

blue bloater

77
Q

How are the bronchioles narrowed in bronchitis?

A

mucous plugs
inflammation
fibrosis

78
Q

What are the clinical symptoms of chronic bronchitis?

A

persistent cough with mucous
dyspnea
hypercapnea, hypoxemia and mild CYANOSIS

79
Q

Review the complications of chronic bronchitis complications-

A

progression to COPD
cor pulmonale and HF
atypical metaplasia and dysplasia (cancer opportunity)

80
Q

what is characterized by recurrent episodes of wheezing, breathlessness, chest tightness, and cough?

A

asthma

81
Q

What can cause non atopic asthma?

A

cold or exercise

82
Q

T-F- in asthma there is an increase in smooth muscle cells, inflammatory cells, but less mucous secretion?

A

false- more mucous too

83
Q

In bronchial asthma, the attack is reversible, but overtime will permanently remodel. review the things that will happen upon remodeling

A

thickening of the airway wall
sub-basement membrane fibrosis
increased vascularity
increase in size of the submucosal glands
hypertrophy/hyperplasia of the bronchial wall muscle

84
Q

What is a curschmann spiral?

A

a mucous cast of a small bronchiole

85
Q

What is charcot-leyden crystal?

A

collections of crystalloid made up of an eosinophilic lysophospholipase binding protein galactic 10

86
Q

What are the main 4 symptoms of an asthma attack?

A

chest tightness
dyspnea
wheezing
cough

87
Q

Review the following major asthma complications

A

status asthmaticus
progressive hyperinflation
bacterial infections
cor pulmonale and heart failure

88
Q

What are the major etiologies of bronchiectasis (permanent dilation of conducting airway)?

A

bronchial obstruction with inflammation

congenital/hereditary conditions
cystic fibrosis, primary ciliary dyskinesia, necrotizing pneumonia

89
Q

Is bronchiectasis a whole lung or whole lobe thing?

A

No- just distal to the obstruction

90
Q

On a microscope, what should we look for in bronchiectasis?

A
  1. inflammation

2. dilation of airways with a much larger diameter than blood vessels- remember they should be the same.

91
Q

Why do bronchiectasis patients get so many infections?

A

they can not clear the pooled secretions from the affected portion

92
Q

In restrictive lung diseases, where is the fibrosis and inflammation taking place?

A

most peripheral and delicate interstitial in the alveolar walls

93
Q

How are the majority of chronic interstitial lung diseases diagnosed?

A

history, CT, PFTs and serology

RARELY IS TISSUE EXAMINATION NEEDED

94
Q

The clinical diagnosis of idiopathic pulmonary fibrosis is equal to what?

A

the pathological diagnosis of usual interstitial pneumonia

95
Q

What are the key his to features of usual interstitial pneumonia?

A
  1. patchy intersitial fibrosis w/ temporal heterogeneity
  2. fibroblasts!! fibroblastic foci
  3. honeycomb fibrosis
96
Q

IN idiopathic pulmonary fibrosis, where does the honeycombing and fibrosis begin?

A

in the periphery

97
Q

In usual interstitial pneumonia, what is found between the honeycombing and the uninvolved lung under a microscope

A

this is where you will find the fibroblastic foci

98
Q

What is the prognosis of UIP/IPF? what are the symptoms?

A
  1. mean survival is 3 years, transplantation is the only definitive therapy
  2. progression of dyspnea, dry cough, hypoxemia, cyanosis and clubbing
99
Q

What is a non-neoplastic lung reaction to inhalation of organic and inorganic particles, chemicals and fumes?

A

pneumoconiosis

asbestos, coal dust, silicosis

100
Q

What really distinguishes asbestos from UIP under the microscope?

A

asbestos bodies (golden brown, fusiform or beaded rods with translucent center)

101
Q

What other things are caused by asbestos but are not asbestosis?

A

mesothelioma and pleural plaques

102
Q

Does the presence of asbestos body diagnose asbestosis?

A

No- other changes (characteristic pattern of fibrosis) are necessary

103
Q

What is a systemic granulomatous disease of unknown cause? is it caseating? where is the distribution heavy?

A
  1. sarcoidosis
  2. no necrosis in the center
  3. lymphatics, bronchi, and blood vessels
104
Q

What do we see on gross specimen of patients with sarcoidosis?

A

tan areas- nodules with sclerosis

105
Q

What two things might we see under high magnification of sarcoidosis?

A

asteroid body- star shaped eosinophilic structure

schaumann body- concentric calcification

106
Q

What is characterized by an immunologically mediated, interstitial lung disorder caused by inhaled organic dusts in susceptible individuals?

A

hypersensitivity pneumonitis

107
Q

What are the two most common antigens for HP?

A 
Farmers lung (termophilic actinomycetes)
Bird Fancier's lung
108
Q

What are the 3 key his to findings in hypersensitivity pneumonia?

A
  1. poorly formed granulomas (non-caseating)- small clusters of histiocytes
  2. interstitial pneumonitis- lymphocytes, plasma cells, macrophages
  3. fibrosis and honeycombing
109
Q

Do metastasis to the lung outnumber primary lung neoplasms?

A

They are much more frequent.

110
Q

Are lung cancers the most common type of cancer in men and women? what about the most common deaths?

A

No- they are the 2nd in both

Yes they are the most common cancers for cancer deaths

111
Q

Why did lung cancer deaths in women lag behind men?

A

The pattern of heavy smoking in women started a couple decades behind men and quitting in large groups was the same.

112
Q

What is the overall 5 year survival for primary lung cancer?

A

15%

113
Q

What are the 4 major symptoms for primary lung cancer?

A

cough, weight loss, chest pain, dyspnea

114
Q

Besides smoking, what are a couple major risk factors for primary lung cancer?

A

radon gas

industrial hazards

115
Q

Is low dose CT or CXR better at reducing lung cancer mortality when used for screening?

A

LDCT by 20%

Risks- radiation exposure, high false positive rates, potential for over diagnosis

116
Q

What is required to make a confident diagnosis of lung cancer?

A

a piece of tissue from the primary tumor site!

sputum cytology, bronchoscopy, FNA, open lung biopsy, pleural fluid biopsy

117
Q

What two variables does lung cancer prognosis and treatment really on?

A

histological classification and stage.

118
Q

Is surgery a primary mode of treatment for small cell lung cancer?

A

no radiation and chemotherapy

119
Q

What are the three major things for staging?

A

Tumor, Nodes, Metastasis

120
Q

What are the two major types of non-small cel carcinomas in the lung?

A

squamous cell carcinoma and adenocarcinoma

121
Q

Who does 90% of squamous cell carcinomas occur in? where are they usually located? what are the key his to findings?

A
  1. cigarette smokers
  2. CENTRALLY in the main stem, lobar, segmental
  3. keratin pearls, keratinization, intercellular bridges
122
Q

What is the common cancer P63 and P40 stain for in immunohistochemistry? What about TTF-1?

A
  1. squamous cell carcinoma

2. lung adenocarcinoma

123
Q

What are the key his to findings in adenocarcinoma?

A

gland formation and mucin production

124
Q

Who do we see with adenocarcinoma of the lungs often?

A

non-smokers, women, asian

125
Q

What is a common gross finding in adenocarcinoma?

A

pleural puckering

126
Q

What are the 4 types of adenocarcinoma? which ones are more aggressive?

A
  1. papillary, micropapillary, solid, acinar

2. micropapillary and solid

127
Q

In adenocarcinoma of the lung, is EGFR mutations more common in people that have smoked or non-smokers? what mutation correlate with worse outcomes?

A
  1. Non-smokers are 40-50% while smokers are 10%

2. KRAS

128
Q

What are the two immunihistochemistry markers for adenocarcinoma?

A

TTF-1 (thyroid cancer also expresses)

Napsin

129
Q

What is a non-invasive adenocarcinoma of the lung that grows along the alveolar surfaces.?
What is the survival? is it related to smoking? 2 main subtypes?

A
  1. bronchoalveolar carcinoma
  2. 100% if small
  3. over represented in non-smokers
  4. mutinous and non-mucinous
130
Q

Bronchoalveolar carcinoma often mimics pneumonia, what is the appearance of the tumor in gross anatomy?

A

spongy because it lacks desmoplasia

remember it’s not invasive

131
Q

Which subtype of bronchoalveolar carcinoma often lacks TTF-1 marker? does BAC grow in single file lines on the alveolar walls? which type of BAC comes as a solitary mass? multifocal mass?

A
  1. mucinous
  2. yes
  3. non-mucinous
  4. mucinous
132
Q

What cancer is positive for TTF-1, chromogranin, and synaptophysin?

A

small cell carcinoma

133
Q

Review the key features of small cell carcinoma-

A 
small cells
scant cytoplasm
granular nuclear chromatin (salt/pepper)
high mitotic rate
nuclear molding.
(MORPHOLOGY CAN LOOK SIMILAR TO LYMPHOCYTES)
134
Q

T-F- in small cell carcinoma, most patients appear with metastasis to lymph nodes?

A

Yes- and diagnosis is often made from material aspirated from a lymph node

135
Q

What is it called when nuclei push up against each other?

A

nuclear molding

Also remember they are fragile and have a streaming effect when smeared on glass

136
Q

What neuroendocrine tumor is at the far end of the spectrum from small cell carcinoma?

A
  1. carcinoid tumor

- localized, low stage, amenable by surgery

137
Q

What do we find in a his to slide of carcinoid tumor?

A

trabecular pattern, round nuclei, decent amount of cytoplasm, ovoid to spindle shaped

138
Q

Which asbestos fiber type is more tumorigenic? less tumorigenic?

A
  1. amfibole

2. crysolite and crocidolite

139
Q

What is the latency period of malignant mesothelioma?

A

20-45 post exposure

140
Q

What lung tumor do we think of with WT-1, CK5/6, and D2-40 immunohistochemistry?

A

mesothelioma

141
Q

Is epithelial cells or sarcomatoid mesothelioma more common in histology of mesothelioma?

A

epithelial is 60%

142
Q

Does mesothelioma have a good prognosis?

A

No 50% die in 1st year the rest die within 2.

Pathology II Exam 1 (8 decks)

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