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Pathology > Pulmonary Disease > Flashcards

Pulmonary Disease Flashcards

1
Q

Atelectasis

A

• Incomplete expansion of the lungs or the collapse of previously inflated lung substance, producing areas of relatively airless parenchyma

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2
Q

Resorption Atelectasis

A

• Consequence of complete obstruction of airway
• Resorption of oxygen in dependent acini
• Diminished lung volume
• Mediastinum shifts towards the atelectatic lung

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3
Q

Compressive Atelectasis

A

• Results when the pleural cavity is partially or completely filled by fluid, exudate, blood, or air (tension pneumothorax)
• Mediastinum is shifted away from the atelectatic lung

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4
Q

Contraction Atelectasis

A

• Occurs when local or generalized fibrotic changes prevent complete expansion

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5
Q

Pulmonary Edema

A

• Defined as the leakage of excessive interstitial fluid which accumulates in the alveolar space
• Causes include
– Hemodynamic (or Cardiogenic) – Direct microvascular injury

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6
Q

Hemodynamic Pulmonary Edema

A

• Caused by increased hydrostatic pressure
– Commonly seen in left sided heart failure
• Fluid initially accumulates in the basal regions of the lower lobes

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7
Q

Edema Caused by Microvascular Injury

A

• Primary injury to the vascular endothelium or alveolar septal epithelial cells
– Causing secondary microvascular injury

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8
Q

Diseases of Vascular Origin

A

Acute Lung Injury Pulmonary Hypertension

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9
Q

Acute Lung Injury***

A
  • Encompasses a spectrum of bilateral pulmonary damage
    – Endothelial
    – Epithelial
  • Manifests as:
    – Acute onset of dyspnea
    – Hypoxemia
    – Development of bilateral pulmonary infiltrates on chest radiograph. ( takes time) **
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10
Q

Acute Lung Injury

• AKA: Noncardiogenic pulmonary edema, Diffuse alveolar damage (histologic manifestations)

A

• Acute respiratory distress syndrome is a manifestation of severe acute lung injury

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11
Q

ALI / Acute (Adult) Respiratory Distress Syndrome

• Causes:

A

– Shock (septic, traumatic, other)
– Inhalation of oxygen, smoke, or other irritants
– Diffuse pulmonary infection
– Drug toxicity
– Aspiration, near-drowning
– Burns, ionizing radiation, fractures with fat embolism
– DIC (Disseminated intravascular coagulation)
– Pancreatitis, Uremia, Hypersensitivity reactions

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12
Q

Nomenclature

A
  • Acute Lung Injury
    – Early stage of ARDS

* Adult Respiratory Distress Syndrome
=Acute Restrictive Lung Disease

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13
Q

ARDS: Pathogenesis

A
  • Diffuse damage to the alveolar capillaries and epithelium
  • Causative agents may include:
    – O2 derived free radicals, aggregation of activated neutrophils, activation of pulmonary macrophages, loss of surfactant
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14
Q

Hemodynamic pul edem

A

Dec oncotic pressure- less common

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15
Q

ARDS: Pathogenesis

A
  • Resultant edema and atelectasis (due to loss of surfactant) result in poor lung aeration
  • Chemical mediators of inflammation play a role:
    – Chemotactic factors
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16
Q

ARDS: Morphology

A

• Acute Phase
– Boggy, firm lungs
– Hyaline membranes, edema, acute inflammation

• Proliferative/Organizing Phase
– Proliferation of type II epithelial cells
– Interstitial fibrosis

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17
Q

ARDS: Clinical Course

A

• ~85% of patients develop clinical S&S within 72 hours of initiating phenomenon

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18
Q

ARDS: Clinical Course. *******

• Initially no pulmonary symptoms

A

• Dyspnea and tachypnea, radiographs normal

• Increasing cyanosis, hypoxemia, respiratory failure, and radiographic appearance of diffuse bilateral infiltrates (ground glass)

• Hypoxia can be unresponsive to oxygen therapy
***

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19
Q

ARDS: Clinical Course

• Therapy difficult

A
  • Oxygen given to patient may further damage the lungs

* Mortality rate: ~40%

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20
Q

Pulmonary Hypertension

• Definition: sustained pulmonary artery systolic pressure > 25 mm Hg

A

• Most commonly secondary:

– Chronic obstructive or interstitial lung disease
– Antecedent congenital or acquired heart disease – Recurrent thromboemboli

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21
Q

Pulmonary Hypertension

• Caused by

A
  1. decrease in the cross- sectional area of pulmonary vasculature
  2. increased vascular flow
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22
Q

Pulmonary HTN: Pathogenesis

• In primary pulmonary hypertension

– Exact cause is unknown

A

– Felt to be idiopathic pulmonary endothelial cell dysfunction

– Vascular hyperreactivity

• In secondary pulmonary hypertension

– Dysfunction of pulmonary endothelial cells due to initiating process

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23
Q

Pulmonary HTN: Morphology

• Variety of vascular lesions

A
  • Some overlap between primary and secondary forms
  • If thromboemboli as pathogenesis: recanalized thrombi
  • Atheromatous deposits
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24
Q

Pulmonary HTN: Morphology

• Medial hypertrophy

A

• Intimal fibrosis
• Narrowed lumen
• Plexogenic pulmonary arteriopathy
– Tufts of capillary formations form webs, spanning the lumens

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25
Q

Pulmonary HTN: Clinical Course

• Primary – F>M

A

– 20–40yearsofage
– Dyspnea and fatigue when arterial lesions are advanced

  • Secondary
    – Same symptomatology
  • Both forms: severe cyanosis, respiratory distress, right ventricular hypertrophy (cor pulmonale)
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26
Q

Obstructive vs. Restrictive Pulmonary Disease ****

Definitions

A
  • Obstructive Disease
    – Increased resistance to airflow due to partial or complete obstruction of airways
  • Restrictive Disease
    – Reduced lung expansion with decreased total lung capacity
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27
Q

Obstructive Disease

A
  • Decreased FEV1 (forced expiratory volume at 1 sec.) and FEV1/FVC
  • Due to obstruction, airway narrowing, or loss of elastic recoil
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28
Q

Restrictive Disease

A
  • Expiratory flow rate is normal or reduced proportionately to reduced lung volume
  • Decreased FVC
  • Restrictive defect:
    – Chest wall disorders in the presence of normal lungs
    – Acute or chronic interstitial and infiltrative diseases
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29
Q

Chronic Obstructive Pulmonary Disease

A

Emphysema Chronic Bronchitis Asthma Bronchiectasis

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30
Q

Emphysema

A
  • A condition characterized by abnormal permanent enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of their walls
  • No obvious fibrosis
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31
Q

Emphysema: Types

• Classified according to its anatomic distribution within the lobule

• Centriacinar (centrilobular):

A

– The portion of the acinus formed by the respiratory bronchioles is affected
– Central or proximal
– Distal alveoli are spared
– More severe in upper lobes

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32
Q

Emphysema: Types

• Panacinar (panlobular):

A

– Acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli

– Associated with α1-antitrypsin deficiency

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33
Q

Emphysema: Types. ***

• Paraseptal (distal acinar):

A

– Involves the distal part of the acinus
– Occurs adjacent to areas of fibrosis, scarring, or atelectasis
– Spontaneous pneumothorax in young adults **

• Irregular:
– Acinus is irregularly involved
– Associated with scarring

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34
Q

Emphysema: Epidemiology

A

• Common
• M>F
• Associated with smoking
• Morphologic changes occur long before the disease becomes disabling

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35
Q

Emphysema: Pathogenesis **

• Imbalance between proteases and antiproteases result in alveolar wall destruction

– α1-antitrypsin(α1-AT)istheprimary antiprotease.

– Matrix metalloproteinases (MMP-9 and MMP-12)

A

• Other genes may play a role
– TGF-β gene
Certain polymorphisms increase susceptibility

• Mesenchymal cell

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36
Q

Protease-Antiprotease Mechanism

A
  • Homozygous patients with a genetic deficiency of the enzyme α1-AT have a marked tendency—emphysema
  • Worse if patient smokes
  • α1-AT: present in serum, macrophages, and tissue fluids. Major inhibitor of proteases, especially elastase
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37
Q

Protease-Antiprotease
Mechanism

A
  • Elastase is secreted by neutrophils and other inflammatory cells
  • How does smoking fit in???
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38
Q

Smoking

A
  • Increases number of inflammatory cells – Chemotactic factors
  • Stimulates the release of elastases from neutrophils
  • Increases elastolytic activity in macrophages (not inhibited by α1-AT)
  • Oxidants in cigarette smoke form O2 free radicals which inhibit α1-AT activity
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39
Q

Emphysema: Clinical Course

• No clinical manifestations until 1/3 of lung incapacitated

A

• Dyspnea, progressive
• Barrel chest
• Cough
• Prolonged expiration

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40
Q

Emphysema: Clinical Course
• Pulmonary Function Tests

A

– Reduced FEV1
– Normal or near normal FVC
– Ratio of FEV1/FVC is reduced

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41
Q

Chronic Bronchitis: Definition

A
  • Is present in any patient who has persistent cough with sputum production for at least three months in two consecutive years
  • Can be simple or obstructive
    – Simple: productive cough but no physiologic evidence of airflow obstruction
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42
Q

Epidemiology

A

• Incidence: common
• Most frequent in middle aged men • More common in urban population • Cigarette smoking is a risk factor

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43
Q

Chronic Bronchitis: Pathogenesis

A

• Chronic irritation by inhaled substances
– Hypersecretion of mucous
– Hypertrophy of submucosal glands
– Increased number of goblet cells
– Bronchiolitis

• Microbiologic infections
– secondary

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44
Q

Chronic Bronchitis: Morphology

A
  • Excessive mucous secretion
    • Hypertrophy of mucous glands

* Bronchiolar inflammation
• Mucous plugging
• Fibrosis

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45
Q

Chronic Bronchitis: Clinical Course

A

• Persistent cough productive of copious sputum
• Hypercapnia
• Hypoxemia
• Cyanosis
• Long-standing severe disease may result in cor pulmonale (pul hypertension) *******
• Dyspnea on exertion

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46
Q

Asthma

A
  • A chronic relapsing inflammatory disorder of airways
  • Characterized by: intermittent and reversible airway obstruction, chronic bronchial inflammation with eosinophils, bronchial smooth muscle cell hypertrophy and hyperreactivity, and increased mucus secretion
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47
Q

Types of Asthma

A

• Atopic Asthma

– Most common type
– Aka “extrinsic asthma”
– Type I hypersensitivity reaction *****
– Triggered by environmental antigens (pollen)

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48
Q

Non-Atopic Asthma

A

• No evidence of allergen sensitization
• Skin tests usually negative
• Respiratory infections and inhaled air pollutants common triggers

49
Q

Drug Induced Asthma

A
  • Aspirin, other NSAIDs
    – Felt to involve arachadonic acid metabolism
    • The cyclooxygenase pathway is inhibited
  • The lipoxygenase pathway is not
50
Q

Occupational Asthma

A

• Stimulated by fumes
– Epoxy resins, plastics
– Organic and chemical dusts
– Chemicals

51
Q

Types of Asthma

A

• All types of asthma may be precipitated by cold, stress, and exercise.

52
Q

Asthma: Pathogenesis

• Extrinsic asthma:

A

– Driven by sensitization of CD4+ cells of the TH2 type

– Release cytokines (IL-4, IL-5, and IL-13) which favor the synthesis of IgE, growth of mast cells, and the growth and activation of eosinophils

53
Q

Atopic Asthma: Pathophysiology

• Early phase (30 – 60 min)

A

– Antigen reacts with sensitized mast cells
– Mediator release opens tight junctions, deeper penetration of allergen
– Also allows direct stimulation of subepithelial vagal receptors—bronchoconstriction

54
Q

Mediators: Primary

• Histamine—bronchospams and vasodilitation

A
  • Leukotrienes C4, D4, and E4—prolonged bronchoconstriction
  • Prostaglandin D2 , E2 , F2α— bronchoconstriction and vasodilation
  • PAF (platelet aggregating factor)—platelet aggregation and release of histamine
55
Q

Mediators: Primary

A

• Mast cell tryptase—inactivates normal bronchodilatory peptide

56
Q

Mediators: Secondary

A
  • Eosinophilic and neutrophilic chemotactic factors – Including leukotriene B4
  • IL-4 and IL-5– augment the TH2 response
  • PAF– chemotactic for eosinophils in the presence
    of IL-5
  • TNF—upregulationofadhesionmoleculeson vascular endothelium and inflammatory cells
57
Q

Asthma: Morphology

A

• Bronchioccludedbythickmucousplugs
• Curshmann’s spirals: whorls of shed epithelium
• Charcot-Leyden crystals: crystaloids composed of eosinophil membrane protein
• Hypertrophyofsubmucousglandsandthickened basement membrane
• Overdistentionofthelungsduetooverinflation
• Airwayremodeling

58
Q

Asthma: Clinical Course

A

• Classic asthma attack: last up to several hours, followed by prolonged coughing and or wheezing
• Status asthmaticus: ventilatory function may be so severely impaired—cyanosis and death

59
Q

Bronchiectasis

A

• A chronic, necrotizing infection of the bronchi and bronchioles leading to or associated with abnormal dilation of these airways
• Dilation is permanent

60
Q

Bronchiectasis: Associated Conditions

A

• Bronchial obstruction – Tumor, foreign body
• Congenital or hereditary conditions
– Congenital bronchiectasis, cystic fibrosis, immotile cilia
• Necrotizing pneumonia
– Tuberule bacillus, staphylococci, or mixed infections

61
Q

Pathophysiology

A

• Obstruction • Infection

62
Q

Bronchiectasis: Morphology

A

• Dilated airways, usually lower lobes bilaterally
• Airways are dilated up to 4x normal diameter

63
Q

Bronchiectasis: Clinical Course

A
  • Severe, persistent cough
    • Expectoration of foul-smelling sputum
  • Dyspnea
    • Symptoms may be episodic
64
Q

Infection or Inflammation of the Lung

Pneumonia

A
  • Inflammatory reaction in the alveoli and interstitium caused by an infectious agent
  • Causes
    – Aspiration of oropharyngeal secretions
    composed of normal bacterial flora or gastric
    contents (25% to 35%)
    – Inhalation of contaminants
    – Contamination from the systemic circulation
65
Q

Pneumonia

A

• Classifications: either by the specific etiologic agent or by the clinical setting in which the infection occurs
– Community-acquired
– Community-acquired atypical
– Hospital-acquired
– Aspiration
– Chronic

66
Q

Pneumonia: Bacterial

A
  • Can have two anatomic and radiographic patterns:
    – Bronchopneumonia
    – Lobar pneumonia
  • These patterns can be blurred
67
Q

Bronchopneumonia

A

• Patchy exudative consolidation of lung parenchyma
• Occurs in infancy and old age

68
Q

Lobar Pneumonia

A

• Involves a large portion of or an entire lobe of the lung
• Less common today

69
Q

Viral and Mycoplasmal Pneumonia

A

• Patchy or lobar areas of congestion without consolidation
• Interstitial pneumonitis
• Hyaline membranes
• Secondary bacterial infection

70
Q

Pulmonary Abcess

A
  • Localized suppurative process
  • Necrosis of lung tissue
    • Aspiration
    • Antecedent bacterial infection
  • Septic emboli
    • Obstructive tumors
  • Other
71
Q

Cystic Fibrosis (Mucoviscidosis)

A

• A disorder in epithelial transport affecting fluid secretion in exocrine glands and the epithelial lining of the respiratory, gastrointestinal, and reproductive tracts
• AR
• Incidence: 1in 3,100 live births
• Most common lethal genetic disease in Caucasians

72
Q

Cystic Fibrosis: Pulmonary Complications

A

• Most serious of the complications
• Viscous mucous secretions
– Secondary obstruction
– Infection
• Resulting bronchitis and bronchiectasis and even
abcesses
• Cardiorespiratory complications are themost common COD (~80%)

73
Q

Restrictive (Diffuse Interstitial) Diseases

A

Sarcoidosis

Idiopathic Pulmonary Fibrosis

74
Q

Restrictive Pulmonary Diseases

A
  • A heterogeneous group of diseases characterized by diffuse involvement of the pulmonary connective tissue
  • Known causes: occupational, drugs, infections
  • Unknown causes: sarcoidosis, goodpastures syndrome, idopathic pulmonary fibrosis, associated with collagen-vascular disorders
75
Q

Sarcoidosis. *****

A

• Multisystem disease of unknown cause characterized by noncaseating granulomas
• May present many clinical patterns
• Lymphadenopathy or lung involvement visible on chest radiographs is present in 90% of cases

76
Q

Sarcoidosis: Epidemiology

A

• Occurs throughout the world
• Affects females slightly more than males
•

77
Q

Sarcoidosis: Pathogenesis

• Granulomas—suggest the presence of a persistent, poorly degradable antigen

A

• Deranged immune response:
– Cutaneous anergy to common skin test antigens
– Often decreased number of peripheral blood T lymphocytes
– Bronchoalveolar lavage with increased numbers of T cells

78
Q

Sarcoidosis: Morphology
• Noncaseating granulomas

A

• No demonstrable organisms
• Lymph nodes and lungs frequently involved
• Skin: 1/3 to 1/2: nodules, plaques, violatious lesions
• CNS may be affected **

79
Q

Sarcoidosis: Clinical Course
• May be asymptomatic

A
  • In ~2/3, gradual appearance of respiratory symptoms
    – SOB, cough, substernal discomfort
  • Constitutional symptoms
    – Night sweats – Fever
    – Fatigue
    – Anorexia
80
Q

Sarcoidosis: Clinical Course

• Diagnosis of exclusion. **

A

• Unpredictable course. **
– Remissions: steroid therapy, spontaneous
• 65 –70% recover
• 20% permanent lung dysfunction
• 10 –15% succumb to progressive pulmonary fibrosis and cor pulmonale

81
Q

Idiopathic Pulmonary Fibrosis

A
  • Typically used for restrictive lung diseases caused by thickening of the alveolar interstitium
  • Synonyms
    – Interstitial pneumonia
    – Idiopathic pulmonary fibrosis
    – Cryptogenic fibrosing alveolitis
82
Q

Idiopathic Pulmonary Fibrosis
• Exact cause unknown

A
  • Postulated to be caused by repeated cycles of epithelial activation/ injury by an unidentified agent. ***
  • Abnormal epithelial repair gives rise to exuberant fiboblastic/ myofibroblastic proliferation
  • This leads to fibroblastic foci
83
Q

Idiopathic Pulmonary Fibrosis:
Morphology

• Pattern of fibrosis in IPF is referred to as usual interstitial pneumonia (UIP)

A

• Fibroblastic foci
– Become more collagenous over time
• Early and late lesions co-exist
• Honeycomb fibrosis
– Collapse of alveolar walls and formation of cystic spaces lined by hyperplastic type II pneumonocytes

84
Q

Idiopathic Pulmonary Fibrosis: Diagnosis

A

• Chest radiograph demonstrates a honeycomb appearance and coarse reticular pattern
• Ground –glass haziness—presence of infiltrates
• PFTs (decreased VC, TLC, diffusing capacity)

85
Q

Idiopathic Pulmonary Fibrosis : Clinical Presentation

• Insidious

A

• Gradually increasing dyspnea on exertion with dry cough
• Hypoxemia, cyanosis, and clubbing occur later in the disease
• Bibasilar end-expiratory crackles
• Mean survival

86
Q

Idiopathic Pulmonary Fibrosis: Treatment

A

• Smoking cessation (if applicable)
• Avoidance of environmental pathogens
• Anti-inflammatory and immunosuppressive agents
• Lung transplantation

87
Q

Pulmonary Involvement in Collagen Vascular Diseases

A

• Can be seen in many collagen vascular diseases
– SLE
– RA
– Systemic sclerosis
– Dermatomyositis
-polymyositis

• Several histologic variants can be seen

88
Q

Pulmonary Involvement in Collagen Vascular Diseases

• Rheumatoid arthritis
– Pulmonary involvement can occur in 30 – 40% of patients

A
  • Chronic pleuritis with or without effusion
    • Diffuse interstitial pneumonitis and fibrosis
  • Intrapulmonary rheumatoid nodules
    • Follicular bronchiolitis
    • Pulmonary hypertension
89
Q

Pulmonary Involvement in Collagen Vascular Diseases

A

• Systemic sclerosis (scleroderma)
– Diffuse interstitial fibrosis with pleural involvement

90
Q

Pulmonary Involvement in Collagen Vascular Diseases

• Systemic lupus erythematosus

A

– Patchy, transient parenchymal infiltrates
• Occasionally severe lupus pneumonitis – Pleurisy
– Pleural effusions

91
Q

Pulmonary Involvement in Collagen Vascular Diseases

A

• Pulmonary involvement in these diseases has a variable prognosis
• determined by: – Extent
– Histologic pattern of involvement

92
Q

Tumors

A

Bronchogenic Carcinomas Bronchioloalveolar Carcinoma Bronchial Carcinoid Metastatic Carcinoma

93
Q

Bronchogenic Carcinoma

A
  • ~156,900 deaths/year projected for 2011
    • ~221,100 new cases diagnosed in 2011
    • M>F
    • Most common visceral malignancy of men
  • Leading cause of cancer death in women
    • 90 – 95% of primary lung tumors
94
Q

Etiology and Pathogenesis

A
  • Tobacco smoking

* Industrial hazards • Air pollution
• Genetic Factors
• Pulmonary scarring

95
Q

Etiology and Pathogenesis: Smoking Related Carcinomas

A
  • Arise by a stepwise accumulation of a multitude of genetic mutations resulting in the malignant transformation of a benign progenitor cell
  • Sequence of molecular changes is not random
  • Follows a predictable sequence
96
Q

Etiology and Pathogenesis

• About 90% of lung cancers arise active smokers or those who quit recently

A
  • A nearly linear correlation exists between the frequency of lung cancer and the pack-years of cigarette smoking
  • Risk of lung cancer is even greater in those who smoke and are also exposed to :
    – Asbestos, arsenic, chromium, uranium, nickle, etc.
97
Q

Etiology and Pathogenesis
• Not everyone who smokes or is exposed to cigarette smoke develops lung cancer

A

– The mutagenic effects of carcinogens is conditioned by hereditary (genetic) factors

• Among the histologic subtypes of lung cancer, squamous and small-cell carcinomas show the strongest association with tobacco exposure ***

98
Q

Histologic Classification

A
  • Squamous cell carcinoma

* Adenocarcinoma
• Small cell carcinoma
• Large cell carcinoma

99
Q

Squamous Cell Carcinoma

• Most common in men

A

• Production of keratin and intercellular bridges
• Arises in larger, more central bronchi
• Disseminate outside the thorax later than other histologic types
• Spreads locally and metastasizes later than other bronchogenic cancers

100
Q

Squamous Cell Carcinomas

A
  • Large lesions can undergo central necrosis – Cavitation
  • Preneoplastic lesions antedate the development of cancer
    – Squamous metaplasia, with or without dysplasia
    – Carcinoma in situ
101
Q

Adenocarcinoma

• Most common type in women and nonsmokers

A

• Usually more peripherally located (scar)
– May be centrally located
• Acinar, papillary, mucinous, and solid
elements may be present
• Grow slowly but tend to metastasize at an early stage ***
• Associated with scarring

102
Q

Adenocarcinoma: Precursor Lesions

A
  • Atypical adenomatous hyperplasia (AAH) – Cuboidal to low columnar cells
    – Cytologic atypia
    – Monoclonal
  • Adenocarcinoma in situ (bronchioloalveolar carcinoma)
    – Involves peripheral parts of the lung as a single nodule
    – Growth along pre-existing structures
    – Preservation of alveolar architecture
103
Q

Small Cell Carcinoma **

• Pale gray, centrally located masses

A

• Extend into the lung parenchyma with early involvement of hilar and mediastinal nodes
• Small cells with scanty cytoplasm
• May also be spindled or polygonal, nuclear molding
• Electron microscopy: dense-core neurosecretory granules

104
Q

Large Cell Carcinoma

A
  • Undifferentiated malignant epithelial tumor
    – Lacks the cytologic features of small-cell, glandular, or squamous differentiation
  • Large nuclei, prominent nucleoli, and a moderate amount of cytoplasm
  • Probably represent squamous and adenocarcinomas that are so undifferentiated they cannot be recognized
105
Q

Lung Cancer, Clinical Course
• Silent insidious

A

• Frequently have spread by the time of diagnosis
• Symptoms:
– Chronic cough, productive
– Hoarseness, chest pain, superior vena cava
syndrome, pleural effusion, segmental atelectasis or pneumonitis

106
Q

Lung Cancer: Prognosis

A

• Overall, NSCLCs have a better prognosis than SCLCs
• If NSCLCs are detected early, before lymph node involvement or metastasis
– Possible surgical cure
• SCLCs have usually spread by the time they are detected

(NSCLC-Non small cell lung cancer)

107
Q

Bronchial Carcinoma

• Overall 5 year survival rate for all stages combined is ~14%

A
  • 5 year survival rate for disease limited to the lung~45%

* SCLC, though sensitive to chemotherapy, recur
– Survival with treatment is typically 1 year

108
Q

Bronchial Carcinoid

• Neuroendocrine tumor **

A

• 1 – 5% of lung tumors
• Locallypenetrating,welldemarcated **
• Occasionallycapableofmetastasis ***
•

109
Q

Bronchial Carcinoid

A

• Clinical manifestations:
– Intralumenal growth
– Capacity to metastasize
– Elaboration of vasoactive amines – Carcinoid syndrome:
• Intermittent attacks of diarrhea, flushing, and cyanosis *****

110
Q

Metastatic Tumors

A
  • Lung is a frequent site for metastatic tumors

* Spread via blood or lymphatics. ***
• Contiguous spread may also occur

111
Q

Normal Lung

A

• Right lung: 3 lobes • Left lung: 2 lobes
• Right mainstream bronchus: more vertical

– More directly in line with the trachea
– More prone to aspiration

112
Q

Pleural Effusion

A
  • Common manifestation of both primary and secondary pleural disease
  • May be
    – Inflammatory
    – Noninflammatory
113
Q

Pleural Effusion
• Occurs in the following settings

A

– Increased hydrostatic pressure
– Increased vascular permeability
– Decreased osmotic pressure
– Increased intrapleural negative pressure (as in atelectasis
– Decreased lymphatic drainage

114
Q

Inflammatory Pleural Effusions

A

• Serous, serofibrinous, and fibrinous pleuritis
– Have an inflammatory basis
– Differ in intensity and duration
– Most common causes involve
infection/inflammation of the underlying pulmonary parenchyma *****

115
Q

Inflammatory Pleural Effusions

• Purulent pleural exudate (empyema)
– results from bacterial or mycotic seeding of the pleural space

A
  • Frequently due to contiguous spread from an infection of the pulmonary parenchyma
  • Occasionally through lymphatic or hematogenous dissemination
    – Usually large volumes of pus
    – Tends to organize into dense adhesions, which frequently obliterate the pleural space
116
Q

Inflammatory Pleural Effusion

A

• Hemorrhagic pleuritis
– Sanguineous inflammatory exudates
– Infrequent
– Typically found in hemorrhagic diatheses, rickettsial diseases, and neoplastic involvement
– Must be differentiated from hemothorax

117
Q

Noninflammatory Pleural Effusions

• Hydrothorax
– Collection of serous fluid in the pleural cavity
– Most common cause is cardiac failure

A

• Hemothorax
– Collection of blood in the pleural fluid
– Typically caused by vascular trauma or rupture of aortic aneurysm

118
Q

Noninflammatory Pleural Effusions

A

• Chylothorax
– An accumulation of milky fluid, usually from lymphatics
– Contains finely emulsified fats
– Most often caused by thoracic duct trauma or obstruction

Pathology (15 decks)

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