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Pathology I > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

what is atelectasis

A

refers to an area of airless pulmonary parenchyma due to collapse or incomplete expansion

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2
Q

what is resorption atelectasis

A
  • complete obstruction of an airway
  • air within the dependent lung is resorbed -> collapse
  • mediastinum shifts toward the affected lung
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3
Q

what is compression atelectasis

A
  • fluid, tumor, or air accumulate within the pleural space, preventing normal expansion
  • mediastinum shifts away from the affected lung
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4
Q

what is contraction atelectasis

A
  • pulmonary or pleural fibrosis preventing normal expansion
  • not reversible
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5
Q

what is hemodynamic pulmonary edema

A
  • intra alveolar fluid accumulation due to increased hydrostatic pressure in the pulmonary circulation
  • hemosiderin-laden macrophages may be seen within alveoli with chronic pulmonary edema
  • decreased oxygenation, increased chance of infection
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6
Q

what is edema secondary to microvascular (alveolar) injury

A
  • injury to and inflammation of alveolar vascular endothelium and/or respiratory epithelium
  • infectious or toxic insults
  • may be localized or diffuse
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7
Q

what is obstructive lung disease chracterized by

A

an increase in resistance to airflow due to partial or complete obstruction at any level from the trachea and larger bronchi to the terminal and respiratory bronchioles

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8
Q

what will pulmonary function tests show in obstructive lung diseases

A

decreased maximal flow rates during forced expiration

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9
Q

what are the diseases in obstructive lung diseases

A
  • emphysema
  • chronic bronchitis
  • asthma
  • bronchiesctasis
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10
Q

which groups are more susceptible to COPD

A

women and african americans

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11
Q

what is the association of COPD and smoking

A
  • strong
  • approximately 35-50% of heavy smokers develop COPD
  • 80% of COPD is due to smoking
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12
Q

what is emphysema

A

destruction of airway walls and irreversible enlargement of the airways distal to the terminal bronchiole

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13
Q

what are the classifications of emphysema

A
  • centriacinar
  • panacinar
  • distal acinar
  • irregular
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14
Q

describe centriacinar emphysema

A
  • occurs predominantly in heavy smokers, often along with chronic bronchitis (COPD)
  • the respiratory bronchioles are involved, sparing the distal alveoli
  • more lesions are seen in the upper lobes/ apical segments
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15
Q

describe panacinar emphysema

A
  • associated with alpha1 antitrypsin deficiency
  • alveoli distal to the respiratory bronchioles are involved
  • occurs more frequently in the lower and anterior aspects of the lungs - lung bases are most severely involved
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16
Q

what is the pathogenesis of emphysema

A
  • exposure to injurious particles in tobacco smoke stimulates inflammation
  • imbalance of proteases and antiproteases
  • oxidative stress
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17
Q

how does exposure to injurious particles in tobacco smoke stimulate inflammation

A
  • lung epithelial cells and macrophages release chemotactic factors to recruit inflammatory cells from circulation
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18
Q

what releass destructive proteases

A

inflammatory cells

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19
Q

what causes oxidative stress

A

smoke, inflammatory cell products containing oxidants, continuing the cycle of tissue damage and inflammation

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20
Q

what is alpha-1 antitrypsin deficiency

A
  • alpha 1 antitrypsin is a potent antiprotease, encoded by the Pi locus on chromosome 14
  • homozygotes for the Z allele (0.012% of US population) have a significant decrease in alpha 1 antitrypsin
  • 80% of homozygotes will develop symptomatic panacinar emphysema, accelerated and more severe if the patient smokes
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21
Q

how is emphysema an obstructive lung disease

A
  • small airways are normally held open by the elastic recoil of lung parenchyma
  • destruction of elastic alveolar walls surrounding respiratory bronchioles leads to the collapse of those bronchioles during expiration
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22
Q

describe the clinical course of emphysema

A
  • no symptoms until one third of lung tissue is affected
  • initial symptoms include dyspnea, cough and wheezing
  • with severe emphysema: weight loss, barrel chest, prolonged expiration
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23
Q

what might emphysema progress to

A

pulmonary hypertension and right sided heart failure

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24
Q

what is death from emphysema usually due to

A
  • respiratory failure
  • RHF
  • pneumothorax -> lung collapse
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25
Q

what is chronic bronchitis and what population is common

A
  • a chronic, persistent productive cough without any other identifiable cause
  • common in smokers and inhabitatns of polluted environments
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26
Q

what is the pathogenesis of chronic bronchitis

A
  • initiating factor is exposure of the bronchi to inhaled irritants
  • mucus hypersecretion
  • chronic inflammation -> damage and fibrosis of small airways
  • diminished ciliary action of respiratory epithelium, leading to stasis of mucus
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27
Q

what are the morphologic changes with chronic bronchitis

A
  • edema and swelling of the respiratory mucosa, often with squamous metaplasia
  • hyperplasia of submucosal mucous glands of the trachea and larger bronchi (thickness of the mucus gland layer increases)
  • increased goblet cells in small bronchi and bronchioles and extensive small airway mucous plugging
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28
Q

what is the clinical course of chronic bronchitis

A
  • persistent productive cough
  • dypsnea on exertion
  • classically: hypercapnia, hypoxia, mild cyanosis
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29
Q

what is asthma

A
  • chronic disorder of the conducting airways characterized by:
  • recurrent bronchoconstriction associated with a variety of stimuli
  • inflammation of bronchial walls
  • increased mucus secretion
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30
Q

what are the symptoms of asthma

A
  • recurent wheezing, shortness of breath/chest tightness, cough
  • more frequently at night/early morning
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31
Q

describe atopic asthma

A
  • type I (IgE mediated) hypersensitivity reaction
  • usually onset in childhood
  • triggered by a variety of allergens: dust, animal dander, dust, foods
  • patients may have high serum IgE, a positive skin test for the inciting allergen or may demonstrate IgE antibodies to specific allergens and often have a family history of asthma
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32
Q

what is atopic asthma pathogenesis

A
  • sensitization occurs when Th2 cell in response to antigen presentation stimulate producion of IgE (IL4, IL13) recruits eospinophils (IL5) and stimulates mucus production (IL13)
  • IgE binds to Fc receptors on mast cells
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33
Q

describe the reaction upon re exposure to antigen in atopic asthma pathogenesis

A

cross linking of IgE molecules on mast cells, triggering degranulation and inducing the immediate hypersensitivity reaction

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34
Q

the immediate phase of atopic asthma pathogenesis is characterized by:

A
  • bronchoconstriction
  • mucus secretion
  • increased vascular permeability
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35
Q

the late phase (hours) of atopic asthma is characterized by

A
  • recruitment of more inflammatory cells ( neutrophils, eosinophils, lymphocytes)
  • results in damage to the mucosal tissue
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36
Q

in non atopic asthma bronchoconstriction is triggered by:

A
  • respiratory viruses
  • inhalation of irritants
  • cold air
  • exercise
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37
Q

what are the morphologic changes in asthma

A
  • repeated allergen exposure and reaction induced airway remodeling which includes:
  • bronchial wall smooth muscle hypertrophy and hyperplasia
  • subepithelial fibrosis
  • submucosal gland hyperplasia; increased goblet cells
  • increased airway vascularity
  • increased thickness of the airway wall
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38
Q

what are the morphologic changes in severe cases of asthma

A

bronchi and bronchioles become occluded by thick mucus plugs, which may be expelled in sputum or BAL specimens (Curschmann spirals)
- sputum and BAL specimens may also contain numerous eosinophils and charcot- leyden crystals

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39
Q

what is the clinical course of asthma

A
  • attacks may last hours, but some patients may experience symptoms at a lower baseline level constantly
  • in severe acute asthma the attack may last for days and result in obstruction sufficient to cause death
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40
Q

what is bronchiectasis

A
  • chronic recurrent necrotizing infections eventually destroy smooth muscle and elastic tissue, leadig to permanent dilation of bronchi and bronchioles
  • the infection with associated inflammation and destruction may follow obstruction and impedance of normal drainage; of severe bronchial infections may cause enough inflammatory damage and necrosis to bring about the bronchiectatic changes
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41
Q

what are the predisposing conditions for bronchiectasis

A
  • conditions affecting mucus clearing (primary ciliary dyskinesia, cystic fibrosis, other bronchial obstruction)
  • immunodeficiency conditions
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42
Q

repeated attempts to resolve the inflammatory process in bronchiectasis may result in______

A

peribronchial fibrosis

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43
Q

what are pneumoconioses

A
  • nontumor lung diseases in the setting of exposure to mineral dusts, inorganic and organic particles and chemical fumes
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44
Q

what is particle pathogenicity influenced by

A
  • particle size (1-5um are most pathogenic)
  • particle solubility
  • level and duration of exposure. effectiveness of clearance
  • intensity of immune response
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45
Q

what is coal workers lung disease

A
  • simple coal workers pneumoconiosis
  • inhaled carbon dust is taken up by macrophages which accumulate in interstitial tissue along pulmonary lymphatic tissue
46
Q

what is anthracosis and what population is it seen in

A
  • black pigmented lesions formed by these coal dust containing macrophages
  • can also be seen in smokers and in urban dwellers
  • can occasionally cause centriacinar emphysema
47
Q

what is complicated coal workers pneumoconiosis characterized by

A

multiple anthracotic scars, which if extensive may lead to:
- respiratory failure
- pulmonary hypertension and RHF

48
Q

what is silicosis

A
  • caused by inhalaing crystalline silicon dioxide over long periods of time
  • most common occupational disease worldwide
  • crystalline particles are ingested by macrophages which then mount an inflammatory response
  • slowly growing nodular collagenous scars
  • over time these may coalesce -> progressive massive fibrosis
49
Q

describe silicosis morphology

A
  • the nodular scars may occur in the lungs or in hilar lymph nodes - calcified lymph nodes can sometimes be identified with x-ray
  • the nodules are characteristically formed of whorled balls of dense collagen fibers, surrounded by dust containing macrophages
  • initially more prominent apically
  • the silica particles are birefringent with plane polarized light
50
Q

what is the clinical course of silicosis

A
  • rate of onset and disease progression is extremely variable, progression may occur even after exposure ceases
  • silicosis leads to increased susceptibility to TB
  • patients with silicosis have twice the risk of lung cancer
51
Q

describe asbestos related pulmonary diseae

A
  • asbestos refers to a group of fibrous hydrated silicate crystals known to cause interstitial and pleural fibrosis and lead to lung carcinoma and malignant mesothelioma
52
Q

what are the two types of asbestos related pulmonary disease

A

serpentine and amphibole

53
Q

describe asbestos related lung disease

A
  • asbestos fibers are taken up by macrophages which then initiate an inflammatory response leading to interstitial fibrosis
  • may result in honeycomb lung
  • the lung bases are affected first and it progresses upward
54
Q

what does asbestos related lung disease look like

A
  • plaques of dense collagen, sometimes calcified may form on the pleura, particularly the parietal pleura
  • occasionally asbestos exposure may result in pleural effusion
55
Q

clinically, in asbestos related lung disease, patients presents with findings similar to:

A

pneumoconiosis or usual interstitial pneumonia

56
Q

pleural plaques are usually:

A

asymptomatic

57
Q

asbestosis complicated by ________carries a poor prognosis

A

lung or pleural malignancy

58
Q

what is the prevalence of pulmonary infections

A

very common- causes 1 out of 6 deaths in the US

59
Q

what are the systemic conditions which may predispose to pulmonary infection

A
  • immunodeficiency
  • chronic disease
60
Q

what defense mechanisms specific to the lungs will be compromised in pulmonary infections

A
  • cough reflex
  • impaired or diminished ciliary function
  • mucus stasis
  • decreased pulmonary macrophage activity
  • pulmonary edema
61
Q

what is community acquired bacterial pneumonia

A
  • infections of bacterial pathogens may be indistinguishable from viral, clinically and radiologically
  • bacterial pneumonia may follow a viral URI
62
Q

what are the predisposing conditions for community acquired bacterial pneumonia

A
  • age: young or old
  • chronic disease (COPD, diabetes, CHF)
  • absent splenic function - predisposes toward encapsulated bacterial infections)
63
Q

what are the causative organisms in community acquired bacterial pneumonia

A

-streptococcus pneumoniae:
- hemophilus influenzae:
- moraxella catarrhalis
- pseudomonas aureginosa
- legionella pneumophilia
- mycoplasma pneumonia

64
Q

what are the morphologic changes in pulmonary infections and what patterns does consolidation occur in

A

invasion of bacteria leads to alveolar filling with inflammatory cells and exudate, resulting in consolidation of the lung tissue
- consolidation occurs in two patterns: bronchopneumonia, lobar pneumonia

65
Q

what is bronchopneumonia

A
  • patchy involvement of lung parenchyma
  • consolidated areas may coalesce
  • formed of acute suppuration
  • basal, often multilobar, and frequently bilateral
66
Q

what are the morphologic changes in lobar pneumonia and what are the 4 stages

A
  • consolidation occupies an entire lobe
  • occurs in 4 stages:
  • congestion: vascular engorgement, cell poor intraalveolar fluid with bacteria
    -red hepatization: robust exudate with neutrophils, erythrocytes disintegration, early organization
  • resolution: organizing fibrosis admixed with macrophages
67
Q

what is the clinical course of community acquired bacterial pneumonia

A

-presents with abrupt fever, shaking chills, productive cough
- lobar pneumonia x ray: opaque lobe
- bronchopneumonia x-ray: focal opacities
- antibiotics: culture and sensitivity
- complications include: abscess, empyema, bacteremia

68
Q

what are the common organisms in community acquired viral pneumonia

A
  • influenza viruses A, B, and C, RSV, human metapneumovirus, adenovirus, rhinovirus, coronaviruses
69
Q

what are the predisposing factors to community acquired pneumonia

A

very young and elderly
- malnutrition/alcoholism
- chronic disease

70
Q

describe COVID 19 transmission and clinical course

A
  • SARS-CoV-2
  • transmission through respiratory droplets
  • variable clinical course: potential for abnormally increased cytokine response, potential for development of arterial and venous thrombosis
71
Q

Type A influenza virus infects:

A

humans, swine, birds and horses

72
Q

influenza virus genome is composed of:

A

8 segmnets

73
Q

why does constant antigenic drift occur with influenza virus

A

viral RNA polymerase lacks error detection capability

74
Q

how does a pandemic with influenza occur

A
  • recombination of segments of the genome may occur when an individual is coinfected with different types -> antigenic shift leading to a new viral strain -> pandemic
75
Q

what does the influenza virus infect

A
  • upper respiratory tract
  • respiratory epithelium
76
Q

lung infection in influenza virus may be:

A

patchy or extensive

77
Q

extent of influenza disease in host is affected by:

A
  • host immune status
  • virulence of the infecting strain
  • presence/absence of other complication conditions
78
Q

describe tuberculosis transmission and mechanism and causative organism

A
  • mycobacterium tuberculosis
  • transmission via airborne droplets
  • entry into macrophages -> replication within macrophages -> bacteremia and seeding of multiple sites
  • immune response: cell mediated (3 weeks) -> macrophage activation and development of tissue hypersensitivity
  • granulomatous inflammation/tissue damage
79
Q

describe primary tuberculosis

A
  • infection of a previously unexposed and unsensitized patient
  • development of a Gohn complex
  • results in a focus of pulmonary scarring
  • approximately 5% will develop significant disease at this point
80
Q

what is a Gohn complex

A

a focus in the lung parenchyma with consolidation/necrosis and hilar lymph nodes with caseating necrosis

81
Q

what does progressive primary tuberculosis most commonly occur in

A

immunocompromised host

82
Q

desscribe secondary tuberculosis

A
  • arises in a previously sensitized host, from dormant primary lesions
  • usually multiple lesions involving the apices of one or both lungs
  • spread through the blood may result in military TB
  • isolated organ TB: from hematogenous seeding- may be the presenting manifestation
83
Q

where is military TB most prominent

A

liver, bone marrow, spleen, adrenal glands

84
Q

what is Pott disease

A

involvement of vertebrae in secondary TB

85
Q

what is aspiration pneumonia

A

occurs in debilitated patient with diminished swallowing reflex
- aspirated gastric content-> abscess
- usually more than one organism, usually anaerobes

86
Q

what is hospital acquired pneumonia and what are the causative agents

A
  • patients typically very ill, often on a ventilator
  • often immunocompromised
  • enterobacteriaceae, pseudomonas, S. aureus
87
Q

what is a carcinoma

A
  • lung cancer is the most common cause of cancer mortality world wide
  • overall 5 year survival rate of 16%
  • closely related to smoking
  • most cases are between 40-70 with peak incidence in the 50-60s
88
Q

describe how smoking affects lung cancer

A
  • 80% of lung cancer occur in active or recent smokers
  • direct relationship between cancer frequency and pack year history
  • some people may be genetically susceptible to tobacco smoke: polymorphisms of cytochroms P-450 mono oxygenase
  • environmental exposure: asbestos, uranium, vinyl chloride
89
Q

describe squamous cell carcinoma

A
  • strong association with tobacco smoke
  • high frequency of p53 mutations and overexpression
  • often preceded in bronchial epithelium by squamous metaplasia, dysplasia, and carcinoma in situ
  • most often arise in the central lung/hilar region
90
Q

describe adenocarcinoma

A
  • may occur in smokers or non smokers
  • more likely to be peripheral
  • gain of function mutations involving growth factor receptor pathways: EGFR, ALK, ROS, MET, RET, KRAS
    -precursor lesions include: atypical adenomatous hyperplasia (less than or equal to 5mm). adenocarcinomma in situ (less than 3cm). cells are more atypical and may be mucinous
91
Q

describe small cell carcinoma

A
  • strongest association with smoking
  • frequent TP53 and RB mutations
  • aggressive very high rate of fatality
  • may arise centrally or peripherally likely from neuroendocrine cells in the bronchial epithelium
92
Q

what do cells in small cell carcinoma look like

A
  • tumor cells are small with little cytoplasm, closely arranged nuclei with molding and absent nucleoli
  • cells grow in clusters without any architectural pattern
  • necrosis may be marked
93
Q

describe large cell carcinoma

A
  • poorly differentiated subtype of NSCC without neuroendocrine squamous or glandular differentiation
  • diagnosis of exclusion and accounts for approximately 10% of cases
94
Q

describe metastatic lung carcinoma

A
  • any type of lung cancer may spread to the pleural space
  • may spread hematogenously or within lymphatics: mediastinal, bronchial, paratracheal nodes
  • metastasis may occur widely particularly to: adrenal glands (>50%), liver (30-50%), brain (20%), bone (20%)
95
Q

describe tumors metastatic to the lung

A
  • the lung is the most common site of tumor metastasis
  • may receive metastases via blood or lymphatics
  • most common growth pattern is multiple scattered nodules
96
Q

what are the common primary sites of tumors metastatic to the lung

A

breast
- colon
- kidney
- prostate
- urinary bladder

97
Q

describe carcinoid tumors

A
  • part of a spectrum of tumors arising from bronchial neuroendocrine cells: neuroendocrine tumorlets, carcinoid tumors, SCC
  • 1-5% of all lung tumors, M=F <40
  • low grade malignant neoplasm: typical and atypical
  • may be central or peripheral
  • organoid nests of regular cells containing moderately abundant cytoplasm and regular round nuclei
    -atypical carcinoids show more cell variability and higher mitotis activity
98
Q

which carcinoid tumor is more likely to invade lymphatic vessels

A

atypical carcinoids

99
Q

central carcinoids often protrude into:

A

the bronchial lumen

100
Q

what symptoms are associated with carcinoid tumor

A

-coughing
- hemoptysis
- impaired drainage

101
Q

carcinoid syndrome, caused by tumor cells secreting vasoactive amines resulting in:

A
  • flushing
  • diarrhea
  • cyanosis
102
Q

what is the 5 year survival rate for typical carcinoids and atypical carcinoids

A
  • typical: 95%
  • atypical: 70%
103
Q

what is malignant mesothelioma

A
  • increased incidence with asbestos exposure, compound by smoking
  • most common mutational abnormality is homozygous deletion of p16 seen in 80%
  • mesothelioma arises from visceral or parietal pleura, spreads in the pleural space, eventually ensheating and compressing the lung
  • may invade adjacent thoracic structures
104
Q

what are the types of malignant mesotheliom

A

epithelioid and sarcomatoid types

105
Q

what is used to differentiated between malignant mesothelioma and adenocarcinoma

A

IHC

106
Q

what are the symptoms of malignant mesothelioma

A
  • chest pain
  • dyspnea
  • recurrent pleural effusions
  • concurrent asbestos related interstitial fibrosis
107
Q

what is the survival of malignant mesothelioma

A
  • 1 year survival is about 50%
  • most do not survive 2 years
108
Q

describe squamous papillomas

A
  • squamous lined fronds with fibrovascular cores
  • may be single or multiple, and may occur in children and in adults
  • caused by HPV types 6 and 11
  • benign but may recur
109
Q

describe laryngeal carcinoma

A
  • squamous cell carcinoma typically in men, 50s, and smokers
  • thought to arise from dysplastic squamous epithelium: squamous hyperplasia> dysplasia > carcinoma
  • carcinoma often forms a bulky, fungating mass protruding from the laryngeal surface, often with ulceration
110
Q
A

Pathology I (24 decks)

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