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Pathology for Health Professionals > W8: Pulmonary > Flashcards

W8: Pulmonary Flashcards

1
Q

How many lobes to the left and right lung have?

A

Right lung: 3 lobes

Left lung: 2 lobes

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2
Q

Dsecribe the pleural surface of the lungs

A
  • the surface of the lungs are covered by a lining called pleura
  • the pleura covering the outer surface of the lungs: visceral pleura is continuous with the parietal pleura that covers inside the thoracic cage
  • pleural surfaces are moist to allow surfaces to slide over each other
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3
Q

Epithelia of the nasal cavity and paranasal sinuses

A
  • cuboid epithelium- composed of ciliated and mucus producing cells
  • function to keep nasal pasages moist and to filter air
  • mucus contains bacteriacidal substances
  • cilia helps remove muscu from nasal passages
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4
Q

Epithelium of pharynx and larynx

A
  • squamous epithelium (identical to mouth)
  • sturdy- provides protection to injury
  • mucosa of the pharynx is rich in lymphoid tissue. This is a source for antibodies, but also goes through hyperplasia during infection
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5
Q

Epithelium of the trachea

A

-trachea and bronchi are lined with cuboidal epithelium

contains 4 cell typies: ciliated, mucus producing, neuroendocine, and basal cells

-under pathologic conditions, basal cells proliferate, and become squamous. Most lung cancers originate from bronchial epithelium. 4 cell types, this is why there are several histolic types of lung cancer.

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6
Q

The alveoli are lined with

A
  • pneumocytes
  • type1: 90% of alveolar surface - very thin cells designed to allow passaege of air to the blood
  • type 2: cuboidal cells, specialize in the production of pulmonary surfactant (mix of lipids, protein, carbohydrates), which keeps the alveoli open and prevents them from collapsing
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7
Q

Histology of Bronchi and Alveoli: image

A
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8
Q

External surface of the lung is covered with

A
  • mesothelium and underlying connective tissue
  • mesothelium is an epithlial layer that lines both the visceral and parietal pleura
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9
Q

Pulmonary Circulation image

A
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10
Q

Describe Pulmonary Blood Supply

A
  • the lungs have dual blood supply
  • the pulmonary artery brings venous blood supply from right ventricle into the lungs to be oxygenated in the alveolar speta
  • the oxygenated blood leaves the lungs through the pulmonary veins which drain into the left atrium
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11
Q

how are nutrients brought to the lungs?

A

through bronchial arteries, which originate in the thoracic aorta

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12
Q

Preconditions for normal respiration

A
  • airways must be patent
  • lungs must be able to expand rhythmically during each respiratory movement
  • alveolar respiratory membrane must be in tact
  • action of control centers in CNS, thoracic muscles and diaphragm must be properly coordinated
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13
Q

Metabolic function of the lungs

A

-maintain acid/base balance

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14
Q

Facts to know about the respiratory system

A
  1. ) is an open-ended system with direct contact with the environment (risk for URI, bronchitis, pneumonia)
  2. ) exposed to many allergens in air (immunologic diseases)
  3. )Inhaled air contains pollutants, airborne particles, and gases which may cause disease
  4. ) Heart and lungs form a functional unit
  5. ) Inhaled air contains many potential carcinogens
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15
Q

Most common cause of death in the elderly, and people with cancer, and immune diseases

A
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16
Q

Upper Respiratory Infections

most recognised as, characterized by, tendency to

A
  • most often recognised as the common cold
  • characterized by acute inflamation of the nose, sinus, throat, larynx
  • tendency to extend to trachea and bronchi
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17
Q

Etiology of URI

A
  • most often caused by viruses, though impractical to isolate the virus in every case
  • short lived, heal spontaneously, are not helped by abx
  • common cold is most often caused by rhinovirus, up to 50%, common in spring or fall
  • influenza and parainfluenza can also cause colds in the winter
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18
Q

Pathology of URI

A
  • largely non-specific
  • mucosa of nose and upper resp. tract is congested, edematous, infiltrated with inflammatory cells
  • cells infiltrates lynphocytes, macrophages, and plasma cells
  • severe infections may cause ulceration of mucosal lining, causeing infection.
  • Bacterial infections elicit PMN’s which cause mucopurlent exudate
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19
Q

Clinical Features of URI

A
  • nasal congestion, inflammation and rhinorhea
  • throat pain, sneezing, cough
    systemic: malaise, fever, headache
  • last 2-3 days, even though fever may persist for a day or 2 longer
  • purulent nasal discharge, ear pain, deep throat expecteration are signs of bacterial superinfection
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20
Q

What are middle respiratory infections?

A
  • Infections of the larynx, trachea, and extrapulmonary bronchi
  • most common in children, and include isolated laryngitis presenting as croup, acute epiglotitis, and viral tracheobronchitis
  • can be an extention of URI, and are commonly associated with pneumonia
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21
Q

What is croup?

most common in, patho, caused by, mild or severe?

A

Infection of larynx and adjacent structures

  • most common in children under 3
  • spasm of the vocal chords, which causes inspiratory stridor= barking or brass cough
  • typically caused by parainfluenza virus
  • 80% mild form of disease
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22
Q

Epiglotitis

A
  • previously common, caused by haemophilis influenzae
  • school aged children and adolescents. Vaccine reduced
  • Sudden loss of voice and hoarseness, throat pain on swallowing
  • narrowing of air passage due to edema of epiglotis and inflammation of pharangeal mucosa
  • abx. and supportive therapy with humidified 02
  • severe cases tracheal intubation
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23
Q

Bronchiolitis

A
  • acute childhood disease involving bronchi and bronchioles but not alveolar spaces of the lungs
  • Viral infection, 80% RSV
  • virus invades epithelial cells of bronchi and bronchioles, causing cell death and desquamation
  • also incites inflammatory response with macrophages, plasma cells, lymphocytes
  • Desquamation and inflammatory infiltrate, dead cells, edema, cause obstruction of bronchi and bronchioli
  • occurs in epidemics from fall to spring, 1% of infants
  • wheezing respiration, low grade fever, SOB
  • unless bacterial infection, recovery in 7-10 days
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24
Q

Pneumonia: 2 major forms

A
  • inflammation of the lung
  • Alveolar pneumonia: caused by bacteria, focal or diffuse,. May be limited to the alveoli, or involve the bronchi.
  • Bronchopneumonia: limited to segmental bronchi and lung parenchyma
  • lobular pneumonia: widespread alveolar pneumonia

-Interstitial pneumonia: Diffuse, bilateral, caused by infections with viruses. Mycoplasma pneumonia.

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25
Q

Chronic Pneumonia is typical of…

A

TB

Fungal infections

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26
Q

Bacteria accounts for what percentage of pneumonias

A

-75%

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27
Q

Pneumonias can be classified etiologically by which causes

A

Upper respiratory flora: is a mixture of bacteria. When entered into the lower respiratory systems, will cause pneumonia. Most common -Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus.”

Enteric Saprophytes: Anaerobic bacteris such as e.coli or pseudomonas are part of normal enteric flora. Will cause bacteria if entered into resp.

Extraneous Pathogens: Bacteria such as legionella or TB

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28
Q
A
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29
Q

Routes that bacteria responsible for pneumonia enter the lungs

A
  • inhalation of pathogens in air droplets (virus)
  • Apiration of infected secretions from upper resp. tract (strep & staph)
  • Apiration of infected gastric contents, foods, drinks (anaerobic bacteria)
  • Hematogenous spread: transport to the lungs by blood. Common in bacteremia (sepsis)

-

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30
Q

Pathology of Alveolar Pneumonia

A

Broncho-pneumonia: typically begins with bacterial invasion of the bronchial or bronchiolar mucosa. Followed by exudation of PMNs into the lumen of the airways. The inflammation spreads from the bronchi into the adjacent alveoli. I

Hypostatic pneumonia: the infection is pre-ceded by pulmonary edema. In either case the inflammation may be limited to a small number of single lobules (lobular pneumonia), or it may be spread through large por-tions of the pulmonary parenchyma (lobar pneumonia).

As the intraalveolar exudate accumulates, it replaces the air, and the lung parenchyma becomes consolidated.

Because consolidated lung parenchyma is denser than normal lung, pneumonia can be recognized on x-ray studies as “infiltrates” or “consolidation of parenchyma.”

With appropriate treatment, the pulmonary infection can be brought under control and the pneumonia cured. The exudate is resorbed or coughed out with complete restitution of the normal alveolar spaces

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31
Q

Pathology of interstitial pneumonia

A

Interstitial pneumonia: usually diffuse and often bilateral, differ from alveolar pneumonias in that the inflammation primarily affects the alveolar septa and does not result in exudation of PMNs into the alveolar lumen.

In contrast to alveolar pneumonia, which is usually caused by bacteria, interstitial pneumonias are caused by viruses or M. pneumoniae that attach to the surface of respira-tory epithelial cells.

These pathogens cause cell necrosis and induce an infiltrate predominantly restricted to the alveolar septa. This accounts for the so-called reticular pattern, with no major consolidations typically seen on radiographic examination. Fortunately, most interstitial pneumonias cause only minor alveolar damage and resolve without consequence.

Som may result in chronic pneumonia- characterized by interstitial fibrosis and honeycomb appearance of lung

-atypical course- may pass undiagnosed

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32
Q

Most NB complications of bacterial pneumonia

A
  • Pleuritis: Etension of inflammation to the pleural surface leads to pleural effusion. Some-times, especially with purulent bacteria, pus fills the entire pleural cavity (pyothorax); more often pus is encapsulated by fibrous tissue into pockets called empyema. Suppurative pleuritis heals slowly and usually results in pleural fibrosis encasing the entire lung. Pleural fibrosis obliterates the pleural cavity. Because the lungs cannot expand during inspiration, restrictive lung disease results.
  • Abscess: highly virulent bacteria (staff), may destory lung parenchyma and suppuration
  • Chronic lung disease: Complication whe pneumonia is not responsive to tx. Pus inside bronchi causes destruction of their walls and broncial dilation (bronchiectasis). Honeycomb lung: desruction of parenchyma and fibrosis
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33
Q

Complication of viral pneumonia

A

Rare b/c most heal spontaneously

some will not resolve and then become chronic pneumonia. Intersitial fibrosis and bacterial superinfection

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34
Q

Pneumonia primarily affects which age groups?

A
  • under 5
  • over70
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35
Q

Primary vs. secondary pneumonia

A

-Primary: Community aquired, healthy people

Secondary: hospital aquired (nosocomal) or in people with pre-existing conditions

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36
Q

Risk factors for pneumonia

A

-elderly, alcoholism, smoking, immunosupression

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37
Q

Symptoms of pneumonia can be classified as

A
  • systemic signs of infection: high fever, chills, prostration
  • local signs of infection: related to bronchial inflammation that promote secretion of mucus. Plugging airways causes irritation, coughing, and expectoration. Pleural inflammation causes cp
  • airway obstruction: impaired gas exchange causes dyspnea and tachypnea
  • inflammation and tissue destruction: inflammatory exudate causes tissue destruction and bleeding. Mucupulrulent, blood tinged (rusty) sputum
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38
Q

Clinical Findings of Pneumonia

A
  • distress, SOB
  • relentless coughing
  • auscultation: rales, other symptoms of consolidation
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39
Q

Pneumonia is confirmed by

A
  • CXR
  • bacteriologic studies of sputum
  • peripheral blood sample:
  • bacterial pneumonia accompanied by leukocytosis
  • viral: may have elevated lymphocytes
  • hypercapnia, hypoxemia, respiratory acidosis (low ph)
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40
Q

Common form of atypical pneumonia

A

-mycoplasma pneumoniea

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41
Q

More than 50% of bacterial pneumonia is caused by

A

s. pneumoniae

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42
Q

Pneumonia with multiple abscesses is caused by

A

staph aureus

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43
Q

most common gram negative hospital aquired pneumonia

A

pseudamonas pneumoniae

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44
Q

most common cause of lung infection with cystic fibrosis

A

P.aeruginosa

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45
Q

Most common cause of pneumonia in immune compromised or AIDS

A

pneumocystitis jiroveci (fungus)

-alveolar contents must be aspirated with bronchial lavage

46
Q

Clinical Symptoms of atypical pneumonia

A
  • more mild
  • less fever, no chills
  • mild cough- no muculopurulent. Pts may be SOB
  • no leukocytosis
  • dx. made with blood sample looking for IgM antibodies to mycoplasma
47
Q

What is TB

A
  • chronic bacterial infection caused by M.Tuberculosis
  • incidence decreased since 1950s, when tb agents were introduced
  • affects 13,000 americans per year
  • does not attract PMNs so no purulent
  • elicits formation of granulomas (composed of lymphocytes and macrophages)
  • caseus necrosis
48
Q

What is Gohns complex? (image)

A
49
Q

Primary infection in TB

A
  • results in localized lung inflammation
  • gohons complex
  • in 95% of cases, healts spontaneously- ungoes calcification which can be seen on xray
  • calcifications contain M.TB and can become activated to form secondary infection
50
Q

Secondary TB

A
  • reactivation of primary dormant infection or reinfection
  • most cases are re-activation
  • bacteria spread to the apex of the lungs, causing granulomatous lobular pneumonia
  • confluent granulomas tend to produce cavities (cavernous TB)
  • pulmonary cavities are sources of hemoptysis, which may be fatal
51
Q

In TB, tissue destruction facilitates

A
  • additional intrapulmonary and extrapulmonary spread of infection
  • dissemination of bacilli occurs in lymphatics, pulmonary blood vessels, or in air spaces
52
Q

Complications from dissemination of tb include

A
  • miliary TB: widespread seeding of TB in the lungs or other organs in the form of granuloma
  • TB pneumonia: spread of bacteria through air spaces produces massive lobular pneumonia. May involve same lung, or contralateral lung.

Pleuritis: extention of infection in the pleura is accompanied by pleural effusion and formation of granuloma in visceral and parieta pleura. thick adhesions, obstructive pleural fibrosis.

Extrapulmonary TB: Expectorated tb may infect larynx, and if swallowed, gi TB. Hematogenous spread may go to any organ in the body. Extrapulmonary TB is rarely seen in western countries.

53
Q
A
54
Q

Clinical Features of TB

A
  • variety of non-specific symptoms
  • primary: mild pulmonary disease, low grade fever. Clinically unrecognized in 95% of cases.
    secondary: non-productive dry cough, low grade fever, loss of appetite, malaise, night sweats, weight loss. Hemoptysis from destructive cavitary lesions occurs later.
  • dyspnea may indicate spread, pulm destructive lesions, pleural effusions
55
Q

Diagnosis of TB

A

-bacteriologic culture is still gold standard for final diagnosis

56
Q

Fungal Lung infections

A

histoplasmosis (midwestern US) and coccidioidomycosis (southwest deserts)

  • inhaled dried fungi and spores
  • clinically resemble TB
57
Q

Lung Abscess

A
  • localized, destructive, suppurative lesion
  • most often by s.aureus
  • can be solitary or multiple
  • cavitary lesions filled with puss
  • In early stages the central pus is surrounded by granu-lation tissue, whereas in late stages it is surrounded by a capsule composed of hyalinized collagen.
  • In contrast to abscesses of other internal organs, which usually remain encapsulated, pulmonary abscesses tend to connect with the airways.

The expanding abscesses erode the bronchial wall and extrude their purulent content into the airways. Putrid malodorous expectoration is thus typical of lung abscesses.”

58
Q

Lung Abscess develop under the following conditions

A
  • as a complication of necrotizing staphylococcal pneumonia
  • after aspiration of infected material from alimentary or upper resp. tract.
  • distal bronchial obstruction by tumors
  • as result of septic lung emboli
59
Q

Definition of COPD

A
  • disease state which is characteried by airway limitation which is not fully reversible
  • progressive and associated with abnormal inflammatory response
  • 3 entities:
  • emphysema
  • chronic bronchitis
  • bronchiolitis (inflam of airways less than 2cm diameter)

Many cases where emphysema and bronchitis co-exist

60
Q

Chronic Bronchitis

A
  • excessive production of tracheobronchial mucus causing cough or expectoration for at least 3 months for the past 2 years
  • 90% due to smoking
  • extent correlates to number of cigarettes, cessation associated with improvement of clinical symptoms
  • other contributing factors include: polution, occupational exposure to toxic fumes, respiratory infections if recurrent. Single bout of viral pneumonia may predispose.
  • pathology is non-specific- walls of bronchi and bronchioles thickened and with mucus
  • inflammed with lympthocytes, macrophages, and plasma cells
  • surface of epithelium is usually preserved, but may contain ulcerations and metaplasia from cubular to squamous epithelium
  • most prominent changes are in submucosa -marked mucous gland hyperplasia, chronic inflammation and fibrosis.
61
Q

What is bronchiectasis

A
  • is a permanent dilation of the bronchi
  • common compliation of chronic bronchitis
  • associated with bronchiolectasis
  • occurs because of contact inflammation inside the airways
  • enzymes released from bacteria and leukocytes; mechanical pressure from the inside, exerted by the bronchial contents; and traction of the fibrous scars from the outside all contribute to the formation of bronchiectases
62
Q

Bronchiectasis Image

A
  • cannot be cleared by coughing
  • infection spreads to adjascent alveoli
  • hematogenous spread
  • pt.s have clubbing of fingers
63
Q

Emphysema

A
  • enlargement of air spaces distal to the terminal bronchioles with destruction of the alveolar walls
  • linked to pathogens in cigarette smoke
  • rare in non-smokers- genetic deficiency of alpha1-antitrypsin
64
Q

Pathogenesis of emphysema

A
  • exact mechinism of tobaco induced emphysema is not known
  • hypothesized that irritants in smoke provoke an influx of inflammatory cells into alveoli
  • then enzymes released from leukocytes destroy alveolar walls
  • oxygen radicals from cigarette smoke kill alveolar cells and leukocytes, which release more degrative enzymes
  • reduced activity of leukocyte derived elastase results in decreased elastic fibers of alveoli
65
Q

COPD table

A
66
Q

Centrilobular and Panacinar Emphysema

A

Centrilobular emphysema: marked by widening of the air space in the center of a lobule and involves predominantly the respiratory bronchioles. This is the most common form of emphysema. It is typically found in cigarette smokers. The remaining respiratory bronchioles are characteristically infiltrated with anthracotic macrophages and chronic inflammatory cells.

Panacinar emphysema involves all the air spaces distal to the terminal bronchioles. This form of emphysema typically occurs in α1-AT deficiency and is most prominent in lower parts of the lungs and anterior margins”

67
Q

Treatment of COPD

A
  • supportive
  • advanced pulmonary lesions are irreversible
  • even if patients stop smoking, symptoms often persist
68
Q

Clinical Features of COPD

A
  • chronic bronchitis results in prolonged bouts of coughing, expectoration of purulent mucus, and dyspnea. hypoxia caues blue bloating. pulmonary vasculature is affected by peribronchial firbosis, results in pulm HTN and cor pulmonale (R. ventricular failure). enlarged heart
  • pink puffer: no obstructions or irritations. b/c of reduced respiratory surface, they have compensatory dyspnea (hyperventilate not to develop cyanosis). Barrel chested CXR show overinflation with small heart
69
Q

Immune Diseases of the Respiratory Tract

A
  • allergic rhinitis
  • bronchial asthma
  • sarcoidosis
  • hypersensitivity pneumonitis
70
Q

Asthma:

characterized by

A
  • increased responsiveness of the bronchial tree, to a variety of stimuli that cause complex acute and chronic inflmmatory response and resversible airway obstruction
  • maked by wheezing, cough, and dyspnea

common- 10% of children and 5% of adults

  • most common childhood disease
  • in more than 50% of cases, starts in childhood, affects males 2x more than females
  • 30% develop by the age of 40, remaining have old age asthma
71
Q

Asthma: etiology

A
  • multifactoral, more than one cause, and mediated by more than one pathogenic mechanism
  • two major forms: atopic and nonatopic
72
Q

Atopic asthma

A

-mediated by exposure to exogenous allergens. Type 1 hypersensitivity, mediated by IgE and basophils

Th2 helper t cells play a mojor role with eosinophils and plasma cells

-affects children and is associated with other allergies such as atopic dermatitis and hay fever

73
Q

Non-atopic asthma

A
  • precipitated by non-immune mechanisms, which are non-specific, and would not produce symptoms if not for hyper-reactivity of bronchial tissue
  • physical factos (heat/cold)
  • exercise
  • physical stress
  • chemical irritants
  • aspirin
  • reasons for reactivity remain unknown
74
Q

mediators in inflammation in asthma

A
  • immediate: histamine, bradykinin, prostaglandins
  • delayed: leukotryenes, platelet activating factor, chemotaxic factors
  • form mucus plugs
75
Q

Pathology of Asthma

A

Histologically, the bronchi show chronic inflammation and overabundance of mucus in the lumen.

The mucosal infil-trates consist of nonspecific chronic inflammatory cells, but they often also contain prominent eosinophils

The bronchial walls also show bronchial gland hyperplasia, which correlates with overproduction of mucus.

Smooth muscle cells are increased in number and appear to be enlarged, reflecting frequent bronchial spasms.”

76
Q

Histopathology of Asthma: image

A
77
Q
A
78
Q

Clinical Features of Asthma

A
  • extrinsic asthma begins before the age of 10 and lasts for several years
  • many improve, 50% have lasting
  • characterized by wheezing, dyspnea, cough
  • precipitated by exposures to allergens
  • most have other allergies ex. eczema
  • serum: elevated IgE and esosinophils
79
Q

Features of intrinsic asthma

A
  • begins in adulthood, before age of 40
  • attacks occur at random, and associated with exposure to cold, encironmental polutants, aspirin, emotional stress
80
Q

Treatment of Asthma

A
  • preventing bronchospasm and bronchial inflammation
  • drugs that prevent degranulation of mast cells
  • bronchodilators with simpathomimmetics
  • inhaled corticosteroids
  • prognosis is good, most people have a normal life
81
Q

What is sarcoidosis?

A
  • multisystemic granulomatous disease of unknown etiology
  • presumabily mediated by cell mediated immunity
  • incidence of 50 per 100,000, affects African American most
  • twice as common in African American women than in men - possible hormonal
  • for some reason, the disease has a prediliction for the lungs and mediastinal lymph nodes
  • lungs are infiltated with t-lymphocytes, cd4 helper cells outnumber cd8 10:1
82
Q

Clinical Features of Sarcoidosis

A
  • granulomas may involve any organ of the body
  • lungs, lymphnode of the thorax and neck, and liver most often involved
  • granulomas of lacrimal and salivary gland found in 1/3 of patients
83
Q

Clinical Symptoms of Sarcoidosis

A
  • symptoms vary
  • 50% asymptomatic and dx. on routine visit
  • enlarged bronchial lymph nodes and lung abnormalities seen on xray - may be only finding in some patients
  • most common complaints pertain to lung involvement: cough, dyspnea, wheezing respiration. X-ray show pulmonary nodule and hilar lymph node enlargement
  • peripheral lymphadenopathy, spleen and liver enlargement, skin nodules found in some patients
84
Q

Definitive Dx. of Sarcoidosis

A
  • biopsy of lymph nodes, bronchi, liver, skin, or enlarged salivary glands
  • typical sarcoid granulomas composed of epithelioid macrophages, and giant cells surrounded at the periphery by a narrow rim of lymphocytes
  • do not show central necrosis (non-caseating granulomas)
  • lab: 60% of patients have elevated serum levels of ACE (released from macrophages in granulomas)
  • 10% hypercalcemia

-

85
Q

Therapy for sarcoidosis

A
  • nothing specific
  • more than 70% recover spontaneously in a year or two
  • 20% persist, but not serious
  • 10% lethal
86
Q

What is hypersensitivity pneumonitis

A
  • extrinsic, allergic, alveolitis
  • immune disorder caused by repeated inhalation of foerign antigens
  • mold or fungi: hay, tree bark, or a/c units, bird dropping
  • can be acute or chronic
87
Q

Acute pneumonitis

A
  • mediated by anibodies that react with inhaled antigen in the alveoli
  • formation of antigen-antibody complexes activates compliment, which causes chemotaxic signals, and influx of leukocytes
  • evolves over a period of several hours after exposure
88
Q

Chronic hypersensitivity pneumonitis

A
  • mediated by t-lymphocytes, characterized by typical cell-mediated interaction
  • granulomas in chronic disease primarily located in the alveolar speta, causing thickening or focal destruction
  • damaged tissue replaced by granulation tissue and fibrosis
  • loss of parenchyma, dilation, and fibrosis -honeycomb lung
89
Q

Clinical Features of hypersensitivity pneumonitis

A
  • dyspnea of sudden onset
  • removal of antigen improves clinical picture
  • chonic: has more omnious prognosis
90
Q

Acute hypersensitivity pneumonitis presents as

A

-dyspnea of sudden onset, removal of allergen usually improves clinical picture

91
Q

Chronic hypersensitivity pneumonitis

A
  • has more omnious prognosis
  • most cases lung biopsy shows signs of hypersensitivity, but antigen can not be identified
  • destructive lesions cause chronic dyspnea, hyperventilation, and ultimately resp. failure
  • can only be tx. with transplant
92
Q

Pneumoconioses

A
  • lung diseases caused by mineral dusts, fumes, and particulate matter
  • most are occupational and r/t long term exposure
  • Mineral dust (coal workers), asbestosis, and silicosis
  • this type of lung injur is complex, exact mechanism is unknown
  • extent of injury depends on: duration of exposure, concentration of particles, size of particles, biochemical composition
93
Q

Coal Workers Lung Disease and Anthracosis

A
  • anthracosis= black discoloration, accumilation of carbon. Not associated with significant pulmonary dysfunctoin
  • CWLD= black lung b./c appear black and fibrotic. Carbon but likely silica as well. From suboptimal conditions and poor gear
94
Q

Coal Workers Lung Disease Pathogenesis

A
  • Amorphous carbon get stuck in the nasal or bronchial mucus
  • carbon that does reach the lung is taken up by macrophages and expectorated. Problematic if burden of coal particles is overwhelming or contains other particles= macrophages can not eliminate.
  • Dust particles then accumilate in the interstitial part of the lung, incite fibrosis, conribute to destruction of normal parenchyma
  • not everyone who works in a coal mine gets this, could be due to amount of particle, or predisposition.
95
Q

CWLD: Pathology

A
  • prolonged inhalation of dust that is rich in carbon or other minerals
  • deposited particles into lobules cause fibrosis or centrilobular emphysema
  • fibrosis may become progressive
96
Q

Clinical Features of CWLD

A
  • mild to severe
  • no effective tx.
  • slow, and unrelenting course
  • does not predispose to cancer
97
Q

Silicosis

A
  • lung disease caused by inhaling small silica crystals, generated from stone blasting, sanding, cutting
  • usually only develops in exposures over 10-20 years
  • most common lung disease caused by mineral particles from the environment
98
Q

Pathology of Silicosis

A
  • characterized by fibronodular lesions in the lung parenchyma
  • taken up by macrophages which are damaged in this process and often killed
  • these dead macrophages release silica crystals and substances that stimulate fibroblasts to produce collagen nodules, most promanent along lymphatics
  • causes massive pulm fibrosis, indistinguishable from other fibrotic lung disease
  • TB is a common complication, b/c silica laden macrophages can not combat mycobacterial infections
99
Q

Clinical Features of Silicosis

A
  • symptoms usually mild unless progressive bilateral fibrosis or TB
  • once lesions develop they are irreversible
  • incapacitating disease, but does not cause cancer
100
Q

Asbestosis

A

-generic name for several fibrous silicates that form natural minerals divided into 2 major groups:

Serpentines: Crysotile accounts for 90%, curly and elongated, and usually produce no harm

Amphiboes: smaller, more fibrous and carcinogenic

Asbestos fibers vary in shape and size, and biochem composition

101
Q

Pathogenesis of asbestosis

A
  • unknown -
  • not known why some dev pleural changes and some mesothelioma.
  • short straight fibers are taken up by macrophages, but they dont die
  • macrphages stimulate fibrogenic cytokines and growth factors, therefore extensive pulmonary fibrosis, fibrous plaques
  • amphibole is carcinogenic promotion pleural and peritoneal malignant mesothelioma
102
Q

Pathology of Asbestosis

A
  • course bilateral pulmonary fibrosis, and pleural plaques
  • asbestos bodies- fibrous tissue with beaded bodies, covered in hemosiderin called ferruginous bodies
  • may be complicated by lung ca or malignant mesothelioma of the pleura
103
Q

Clinical Features of Asbestosis

A
  • presents as restrictive lung disease and dyspnea
  • dyspnea occurs for years, resp fail only rarely
  • solitar or small pleural plaques- asymptomatic
  • diffuse fibrosis= restrictive lung disease
  • malignant mesothelioma=most common neoplastic complication
  • Lung ca=5-6x more than in population
  • asbestosis and cirgarettes= lung ca risk x50
104
Q

What is ARDS?

A

-Acute respiratory distress syndrome- term used to describe changes that occur in the lungs under a variety of conditions that occur from acute lung injury, all of which result in respiratory failure

105
Q

How may ARDS develop?

A
  • usually beginning either as an injury to endothelial cells in pulmonary capillaries, or as an injury of the cells in the alveolar lining. Terminal airways are affected in both cases and function severely impaired.
  • Consequences: Increased permeability of alveolar blood vessels, loss of alveolar lining cells, and accumilation of fluid in the alveolar space=result in anoxia
  • Injury of alveolar lining cells: (viral pneumonia, or toxic fumes)
  • Endothelial cell injury: pt.s who are septic
106
Q

pathology of ARDS

A
  • regardless of cause, diffuse alveolar damage
  • lungs are heavy and filled with edema- called non-cardiac pulmonary edema
107
Q

Clinical Features of ARDS

A
  • symptoms reflect acute onset of respiratory failure
  • initial symptoms occur within 24hrs of inciting event
  • sever distress, SOB, gasping
  • hypoxemia, hypercapnia
  • diffuse consolitation on xray, airless lung
  • recovered have issues with fibrosis and damages alveolar septa
  • 1/3 die within days, 1/3 die of pneumonia within weeks, 1/3 recover
  • 40% recovered have residual symptoms
108
Q

Atalectasis

A
  • term to denote incomplete expansion, or more often collapse of alveoli
  • minor focal atelectasis is common in pulm diseases
  • massive atelectasis of entire lung is less common
109
Q

Most Common Causes of Atelectasis

A
  • Deficiency of surfactant
  • Compression of lungs from outside
  • resorption of air distal to bronchial obstruction
110
Q

Atelectasis: image

A
111
Q
A

Pathology for Health Professionals (14 decks)

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