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
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
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
4
Q
Contraction Atelectasis
A
• Occurs when local or generalized fibrotic changes prevent complete expansion
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
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
7
Q
Edema Caused by Microvascular Injury
A
• Primary injury to the vascular endothelium or alveolar septal epithelial cells
– Causing secondary microvascular injury
8
Q
Diseases of Vascular Origin
A
Acute Lung Injury Pulmonary Hypertension
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) **
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
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
12
Q
Nomenclature
A
- Acute Lung Injury
– Early stage of ARDS
* Adult Respiratory Distress Syndrome
=Acute Restrictive Lung Disease
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
14
Q
Hemodynamic pul edem
A
Dec oncotic pressure- less common
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
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
17
Q
ARDS: Clinical Course
A
• ~85% of patients develop clinical S&S within 72 hours of initiating phenomenon
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
***
19
Q
ARDS: Clinical Course
• Therapy difficult
A
- Oxygen given to patient may further damage the lungs
* Mortality rate: ~40%
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
21
Q
Pulmonary Hypertension
• Caused by
A
- decrease in the cross- sectional area of pulmonary vasculature
- increased vascular flow
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
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
24
Q
Pulmonary HTN: Morphology
• Medial hypertrophy
A
• Intimal fibrosis
• Narrowed lumen
• Plexogenic pulmonary arteriopathy
– Tufts of capillary formations form webs, spanning the lumens
25
Pulmonary HTN: Clinical Course
| • Primary – F>M
– 20–40yearsofage
– Dyspnea and fatigue when arterial lesions are advanced
* Secondary
– Same symptomatology
* Both forms: severe cyanosis, respiratory distress, right ventricular hypertrophy (cor pulmonale)
26
Obstructive vs. Restrictive Pulmonary Disease **************
Definitions
* Obstructive Disease
– Increased resistance to airflow due to partial or complete obstruction of airways
* Restrictive Disease
– Reduced lung expansion with decreased total lung capacity
27
Obstructive Disease
* Decreased FEV1 (forced expiratory volume at 1 sec.) and FEV1/FVC
* Due to obstruction, airway narrowing, or loss of elastic recoil
28
Restrictive Disease
* 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
29
Chronic Obstructive Pulmonary Disease
Emphysema Chronic Bronchitis Asthma Bronchiectasis
30
Emphysema
* A condition characterized by abnormal permanent enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of their walls
* No obvious fibrosis
31
Emphysema: Types
• Classified according to its anatomic distribution within the lobule
• Centriacinar (centrilobular):
– The portion of the acinus formed by the respiratory bronchioles is affected
– Central or proximal
– Distal alveoli are spared
– More severe in upper lobes
32
Emphysema: Types
| • Panacinar (panlobular):
– Acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli
– Associated with α1-antitrypsin deficiency
33
Emphysema: Types. *******
| • Paraseptal (distal acinar):
– 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
34
Emphysema: Epidemiology
• Common
• M>F
• Associated with smoking
• Morphologic changes occur long before the disease becomes disabling
35
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)
• Other genes may play a role
– TGF-β gene
Certain polymorphisms increase susceptibility
• Mesenchymal cell
36
Protease-Antiprotease Mechanism
* 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
37
Protease-Antiprotease
Mechanism
* Elastase is secreted by neutrophils and other inflammatory cells
* How does smoking fit in???
38
Smoking
* 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
39
Emphysema: Clinical Course
| • No clinical manifestations until 1/3 of lung incapacitated
• Dyspnea, progressive
• Barrel chest
• Cough
• Prolonged expiration
40
Emphysema: Clinical Course
• Pulmonary Function Tests
– Reduced FEV1
– Normal or near normal FVC
– Ratio of FEV1/FVC is reduced
41
Chronic Bronchitis: Definition
* 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
42
Epidemiology
• Incidence: common
• Most frequent in middle aged men • More common in urban population • Cigarette smoking is a risk factor
43
Chronic Bronchitis: Pathogenesis
• Chronic irritation by inhaled substances
– Hypersecretion of mucous
– Hypertrophy of submucosal glands
– Increased number of goblet cells
– Bronchiolitis
• Microbiologic infections
– secondary
44
Chronic Bronchitis: Morphology
* Excessive mucous secretion
• Hypertrophy of mucous glands
| * Bronchiolar inflammation
• Mucous plugging
• Fibrosis
45
Chronic Bronchitis: Clinical Course
• Persistent cough productive of copious sputum
• Hypercapnia
• Hypoxemia
• Cyanosis
• Long-standing severe disease may result in cor pulmonale (pul hypertension) *********
• Dyspnea on exertion
46
Asthma
* 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
47
Types of Asthma
• Atopic Asthma
– Most common type
– Aka “extrinsic asthma”
– Type I hypersensitivity reaction *****
– Triggered by environmental antigens (pollen)
48
Non-Atopic Asthma
• No evidence of allergen sensitization
• Skin tests usually negative
• Respiratory infections and inhaled air pollutants common triggers
49
Drug Induced Asthma
* Aspirin, other NSAIDs
– Felt to involve arachadonic acid metabolism
• The cyclooxygenase pathway is inhibited
* The lipoxygenase pathway is not
50
Occupational Asthma
• Stimulated by fumes
– Epoxy resins, plastics
– Organic and chemical dusts
– Chemicals
51
Types of Asthma
• All types of asthma may be precipitated by cold, stress, and exercise.
52
Asthma: Pathogenesis
| • Extrinsic asthma:
– 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
Atopic Asthma: Pathophysiology
| • Early phase (30 – 60 min)
– 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
Mediators: Primary
| • Histamine—bronchospams and vasodilitation
* 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
Mediators: Primary
• Mast cell tryptase—inactivates normal bronchodilatory peptide
56
Mediators: Secondary
* 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
Asthma: Morphology
• Bronchioccludedbythickmucousplugs
• Curshmann’s spirals: whorls of shed epithelium
• Charcot-Leyden crystals: crystaloids composed of eosinophil membrane protein
• Hypertrophyofsubmucousglandsandthickened basement membrane
• Overdistentionofthelungsduetooverinflation
• Airwayremodeling
58
Asthma: Clinical Course
• 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
Bronchiectasis
• A chronic, necrotizing infection of the bronchi and bronchioles leading to or associated with abnormal dilation of these airways
• Dilation is permanent
60
Bronchiectasis: Associated Conditions
• Bronchial obstruction – Tumor, foreign body
• Congenital or hereditary conditions
– Congenital bronchiectasis, cystic fibrosis, immotile cilia
• Necrotizing pneumonia
– Tuberule bacillus, staphylococci, or mixed infections
61
Pathophysiology
• Obstruction • Infection
62
Bronchiectasis: Morphology
• Dilated airways, usually lower lobes bilaterally
• Airways are dilated up to 4x normal diameter
63
Bronchiectasis: Clinical Course
* Severe, persistent cough
• Expectoration of foul-smelling sputum
* Dyspnea
• Symptoms may be episodic
64
Infection or Inflammation of the Lung
| Pneumonia
* 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
Pneumonia
• 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
Pneumonia: Bacterial
* Can have two anatomic and radiographic patterns:
– Bronchopneumonia
– Lobar pneumonia
* These patterns can be blurred
67
Bronchopneumonia
• Patchy exudative consolidation of lung parenchyma
• Occurs in infancy and old age
68
Lobar Pneumonia
• Involves a large portion of or an entire lobe of the lung
• Less common today
69
Viral and Mycoplasmal Pneumonia
• Patchy or lobar areas of congestion without consolidation
• Interstitial pneumonitis
• Hyaline membranes
• Secondary bacterial infection
70
Pulmonary Abcess
* Localized suppurative process
* Necrosis of lung tissue
• Aspiration
• Antecedent bacterial infection
* Septic emboli
• Obstructive tumors
* Other
71
Cystic Fibrosis (Mucoviscidosis)
• 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
Cystic Fibrosis: Pulmonary Complications
• 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
Restrictive (Diffuse Interstitial) Diseases
Sarcoidosis
| Idiopathic Pulmonary Fibrosis
74
Restrictive Pulmonary Diseases
* 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
Sarcoidosis. *****
• 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
Sarcoidosis: Epidemiology
• Occurs throughout the world
• Affects females slightly more than males
•
77
Sarcoidosis: Pathogenesis
• Granulomas—suggest the presence of a persistent, poorly degradable antigen
• 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
Sarcoidosis: Morphology
• Noncaseating granulomas
• No demonstrable organisms
• Lymph nodes and lungs frequently involved
• Skin: 1/3 to 1/2: nodules, plaques, violatious lesions
• CNS may be affected ****
79
Sarcoidosis: Clinical Course
• May be asymptomatic
* In ~2/3, gradual appearance of respiratory symptoms
– SOB, cough, substernal discomfort
* Constitutional symptoms
– Night sweats – Fever
– Fatigue
– Anorexia
80
Sarcoidosis: Clinical Course
| • Diagnosis of exclusion. ****
• Unpredictable course. ****
– Remissions: steroid therapy, spontaneous
• 65 –70% recover
• 20% permanent lung dysfunction
• 10 –15% succumb to progressive pulmonary fibrosis and cor pulmonale
81
Idiopathic Pulmonary Fibrosis
* Typically used for restrictive lung diseases caused by thickening of the alveolar interstitium
* Synonyms
– Interstitial pneumonia
– Idiopathic pulmonary fibrosis
– Cryptogenic fibrosing alveolitis
82
Idiopathic Pulmonary Fibrosis
• Exact cause unknown
* 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
Idiopathic Pulmonary Fibrosis:
Morphology
| • Pattern of fibrosis in IPF is referred to as usual interstitial pneumonia (UIP)
• 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
Idiopathic Pulmonary Fibrosis: Diagnosis
• Chest radiograph demonstrates a honeycomb appearance and coarse reticular pattern
• Ground –glass haziness—presence of infiltrates
• PFTs (decreased VC, TLC, diffusing capacity)
85
Idiopathic Pulmonary Fibrosis : Clinical Presentation
| • Insidious
• Gradually increasing dyspnea on exertion with dry cough
• Hypoxemia, cyanosis, and clubbing occur later in the disease
• Bibasilar end-expiratory crackles
• Mean survival
86
Idiopathic Pulmonary Fibrosis: Treatment
• Smoking cessation (if applicable)
• Avoidance of environmental pathogens
• Anti-inflammatory and immunosuppressive agents
• Lung transplantation
87
Pulmonary Involvement in Collagen Vascular Diseases
• Can be seen in many collagen vascular diseases
– SLE
– RA
– Systemic sclerosis
– Dermatomyositis
-polymyositis
• Several histologic variants can be seen
88
Pulmonary Involvement in Collagen Vascular Diseases
| • Rheumatoid arthritis
– Pulmonary involvement can occur in 30 – 40% of patients
* Chronic pleuritis with or without effusion
• Diffuse interstitial pneumonitis and fibrosis
* Intrapulmonary rheumatoid nodules
• Follicular bronchiolitis
• Pulmonary hypertension
89
Pulmonary Involvement in Collagen Vascular Diseases
• Systemic sclerosis (scleroderma)
– Diffuse interstitial fibrosis with pleural involvement
90
Pulmonary Involvement in Collagen Vascular Diseases
| • Systemic lupus erythematosus
– Patchy, transient parenchymal infiltrates
• Occasionally severe lupus pneumonitis – Pleurisy
– Pleural effusions
91
Pulmonary Involvement in Collagen Vascular Diseases
• Pulmonary involvement in these diseases has a variable prognosis
• determined by: – Extent
– Histologic pattern of involvement
92
Tumors
Bronchogenic Carcinomas Bronchioloalveolar Carcinoma Bronchial Carcinoid Metastatic Carcinoma
93
Bronchogenic Carcinoma
* ~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
Etiology and Pathogenesis
* Tobacco smoking
| * Industrial hazards • Air pollution
• Genetic Factors
• Pulmonary scarring
95
Etiology and Pathogenesis: Smoking Related Carcinomas
* 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
Etiology and Pathogenesis
| • About 90% of lung cancers arise active smokers or those who quit recently
* 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
Etiology and Pathogenesis
• Not everyone who smokes or is exposed to cigarette smoke develops lung cancer
– 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
Histologic Classification
* Squamous cell carcinoma
| * Adenocarcinoma
• Small cell carcinoma
• Large cell carcinoma
99
Squamous Cell Carcinoma
| • Most common in men
• 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
Squamous Cell Carcinomas
* Large lesions can undergo central necrosis – Cavitation
* Preneoplastic lesions antedate the development of cancer
– Squamous metaplasia, with or without dysplasia
– Carcinoma in situ
101
Adenocarcinoma
| • Most common type in women and nonsmokers
• 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
Adenocarcinoma: Precursor Lesions
* 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
Small Cell Carcinoma ****
| • Pale gray, centrally located masses
• 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
Large Cell Carcinoma
* 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
Lung Cancer, Clinical Course
• Silent insidious
• 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
Lung Cancer: Prognosis
• 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
Bronchial Carcinoma
| • Overall 5 year survival rate for all stages combined is ~14%
* 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
Bronchial Carcinoid
| • Neuroendocrine tumor ****
• 1 – 5% of lung tumors
• Locallypenetrating,welldemarcated ****
• Occasionallycapableofmetastasis *****
•
109
Bronchial Carcinoid
• Clinical manifestations:
– Intralumenal growth
– Capacity to metastasize
– Elaboration of vasoactive amines – Carcinoid syndrome:
• Intermittent attacks of diarrhea, flushing, and cyanosis *****
110
Metastatic Tumors
* Lung is a frequent site for metastatic tumors
| * Spread via blood or lymphatics. ***
• Contiguous spread may also occur
111
Normal Lung
• 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
Pleural Effusion
* Common manifestation of both primary and secondary pleural disease
* May be
– Inflammatory
– Noninflammatory
113
Pleural Effusion
• Occurs in the following settings
– Increased hydrostatic pressure
– Increased vascular permeability
– Decreased osmotic pressure
– Increased intrapleural negative pressure (as in atelectasis
– Decreased lymphatic drainage
114
Inflammatory Pleural Effusions
• 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
Inflammatory Pleural Effusions
| • Purulent pleural exudate (empyema)
– results from bacterial or mycotic seeding of the pleural space
* 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
Inflammatory Pleural Effusion
• Hemorrhagic pleuritis
– Sanguineous inflammatory exudates
– Infrequent
– Typically found in hemorrhagic diatheses, rickettsial diseases, and neoplastic involvement
– Must be differentiated from hemothorax
117
Noninflammatory Pleural Effusions
• Hydrothorax
– Collection of serous fluid in the pleural cavity
– Most common cause is cardiac failure
• Hemothorax
– Collection of blood in the pleural fluid
– Typically caused by vascular trauma or rupture of aortic aneurysm
118
Noninflammatory Pleural Effusions
• Chylothorax
– An accumulation of milky fluid, usually from lymphatics
– Contains finely emulsified fats
– Most often caused by thoracic duct trauma or obstruction
