Exam 2: Respiratory System Diseases Flashcards
Respiratory Diseases
Acute Upper Respiratory Tract Infections
Infectious Rhinitis
Sinusitis
Pharyngitis/Tonsilitis
Respiratory Diseases
Vascular
Embolism/Infarction
Pulmonary hypertension
Goodpasture Syndrome
Pulmonary Edema
Respiratory Diseases
Obstructive/Restrictive Diseases
Emphysema
Asthma
Cystic Fibrosis
Pneumoconiosis
Hypersensitivity
Penumonitis
Sarcoidosis
Respiratory Diseases
Pleural Disease
Pleural Effusion
Pneumothorax
Non-specific Lung Diseases
Clearance
Cough
Mucociliary Escalator
Non-specific Lung Diseases
Secretions
Tracheobroncial (mucus)
Alveolar (surfactant)
Cellular components
Non-specific Lung Diseases
Cellular Defenses
Nonphagocytic (epithelium)
Phagocytic (alveolar macrophages)
Non-specific Lung Diseases
Biochemical Defenses
Proteinase inhibitors
Antioxidants
Specific Lung Diseases: Immunological
Antibody mediated
B-lymphocyte-dependent
Secretory immunoglobulin (IgA)
Serum immunoglobulins
Specific Lung Diseases: Immunological
Antigen presentation to lymphocytes
Macrophages and monocytes
dendritic cells
epithelial cells
Specific Lung Diseases: Immunological
Cell mediated immunologic responses
T-lymphocyte dependent
Cytokine mediated
direct cellular cytotoxity
Specific Lung Diseases: Immunological
Non-lymphocyte cellular immune responses
Mast cell/eosinophil dependent
usually respond to secretory immunoglobulin or cytokines
Acute Upper Respiratory Tract Infections
Clinical symptoms of Infectious Rhinitis (The Common Cold)
Nasal congestion with watery discharge
sneezing
scratchy, dry, sore throat
Acute Upper Respiratory Tract Infections
Pathogens of Infectious Rhinitis (The Common Cold)
Rhinoviruses
Others are less common (influenza, cornoaviruses, adenviruses, enteroviruses)
Acute Upper Respiratory Tract Infections
Treatment for Infectious Rhinitis (The Common Cold)
Anti-viral if available
mainly support for symptoms
Acute Upper Respiratory Tract Infections
Pathogensis of Infectious Rhinitis (The Common Cold)
Infection initiates immune response
immune mediators cause edema
* swellng and fluid leakage
* congestion and discharge
Acute Upper Respiratory Tract Infections
Potential complications of Infectious Rhinitis (The Common Cold)
Bacterial infections due to swelling, fluid accumulation
Middle ear infection (otitis media)
Sinus infection (sinusitis)
Acute Upper Respiratory Tract Infections
Sinusitis
Most commonly occurs after rhinitis
usually bacterial or viral infection
impairment of sinus drainage
Acute Upper Respiratory Tract Infections
What causes impairment of sinus drainage during Sinusitis?
Mucosal edema due to inflammation
Obstruction may be complete blockage
May lead to acute sinusitis to become chronic - if not resloved
Acute Upper Respiratory Tract Infections
What happens if obstruction of sinus drainage is complete blockage?
will result in accumulation of infected mucus (suppurative exudate) -> empyema
Acute Upper Respiratory Tract Infections
Complications of Sinusitis
Infection of neighboring structures (eye, skull, brain)
Usually just discomfort
(Add Clarifier)
Acute Upper Respiratory Tract Infections
Pharyngitis/Tonsilitis
Frequent companions of upper respiratory tract viral infections
Most common with rhinoviruses, echoviruses, and adenoviruses
Bacterial infections can be secondary to viral or primary causes
Acute Upper Respiratory Tract Infections
Symptoms of Pharyngitis/Tonsilitis
Redness
Edema
Enlargment of tonsils/lymph nodes
Acute Upper Respiratory Tract Infections
Most serious consequences of Pharyngitis/Tonsilitis
Rheumatic fever
Glomerulonephritis
Acute Upper Respiratory Tract Infections
Most serious consequences of Pharyngitis/Tonsilitis: Rehumatic Fever
Acute multisystem inflammatory disease - streptococcus - myocarditis, valvular abnormalitis
Acute Upper Respiratory Tract Infections
Recurrent acute tonsillitis may be linked to…
Chronic enlargment - surgery
Lung Disease
Atelectasis
Collapse of previously inflated lung
neonatal - incomplete expansion
Lung Disease
Three types of Atelectasis
Resorption (blockage of airways)
Compression (accumulation in pleural sac)
Contraction (fibrosis restricts expansion)
Lung Disease
Consequences of Atelectasis
Lowers blood oxygen
Increases risk infection
Lung Disease
What types of atelectasis are reversible?
Resorption
Compression
Lung Disease of Vascular Origin
Pulmonary Embolism
Something blocks vessel in lung
Most frequently a clot (can be air bubble, fatty deposit, other debris)
Lung Disease of Vascular Origin
Consequences of Pulmonary Embolism
Depend on size of obstruction
signals to body control system to lower BP (decrease CO)
Lung collapse
Lung Disease of Vascular Origin
Pulmonary Embolism: Blockage causes
Ischemia downstream
Increased pressure upstream
Lung Disease of Vascular Origin
Approximately 10% of emboli result in…
Pulmonary infarct
Lung Disease of Vascular Origin
The larger the ____ , the ____ the vessel it will block
The larger the vessel blocked….
Embolus
larger
the more tissue affected
Lung Disease of Vascular Origin
Consequences of Pulmonary Embolism: Large Blockage
Large blockage will kill quickly
no pathological change in lung
increased pressure damages in heart (right side heart failure, Cor Pulmonale)
Lung Disease of Vascular Origin
Pulmonary Embolism: Lung may collapse due to…
Lack of surfactant
Reduced movement in response to pain
Lung Disease of Vascular Origin
Treatment of Pulmonary Embolism
Anticoagulant (heparin)
Thrmbolytic (risky)
Lung Disease of Vascular Origin
Pulmonary Hypertension
Heart not pumping enough out of left side so blod backs up into lungs
RA still pumping properly
Lung Disease of Vascular Origin
Pulmonary Hypertension: Vascular Changes
Medial Hypertrophy - muscular and elastic arteries in lungs
Intimal fibrosis
Plexiform lesion - advanced HTN, tuft of capillaries, dilated thin-walled arteries
Lung Disease of Vascular Origin
Pathogenesis of Pulmonary HTN
Chronic Obstructive or Interstitial Lung Diseases
Heart Disease
Reccurent Emboli
Autoimmune diseases
Obstructive sleep apnea
Idiopathic
Lung Disease of Vascular Origin
Pathogenesis of Pulmonary HTN: Chronic Obstructive or Interstitial Lung Diseases
Destroy albeolar capillaries
Increase pulmonary vascular resistance
therefore, increase pulmonary BP
Lung Disease of Vascular Origin
Pathogenesis of Pulmonary HTN: Heart Disease
Damage to left side translates back to lung arteries
Lung Disease of Vascular Origin
Pathogenesis of Pulmonary HTN: Autoimmune diseases
Most common in systemic sclerosis
Increase vascular resistance (decrease elasticity)
Lung Disease of Vascular Origin
____ % of pulmonary htn have genetic basis
80%
Lung Disease of Vascular Origin
Clinical Symptoms of Pulmonary HTN
Only detectable when advanced
Dyspnea and fatigue
Rarely, chest pain
End stage: severe respiratory distress, cyanosis
Lung Disease of Vascular Origin
Treatment of Pulmonary HTN
Secondary disease - treat primary
Autoimmune or refractory - vasodilators
Lung transplantation
Lung Disease of Vascular Origin
Goodpasture Syndrome
Pulmonary hemorrhage syndrome
Autoimmune disease
Kidney and lung injury
Inflammatory-mediated destruction of alveolar basement membranes
Lung Disease of Vascular Origin
Goodpasture Syndrome: Autoimmune Disease
Autoantibody against type IV collagen
Type IV collagen is in basement membrane (e.g. of vasculature)
Lung Disease of Vascular Origin
Goodpasture Syndrome when it only affects the kidneys…
Anti-glomerular basement membrane disease
Lung Disease of Vascular Origin
Goodpasture Syndrome when it affects kidneys and lung…
Goodpasture syndrome
Lung Disease of Vascular Origin
Goodpasture Syndrome: Inflammatory-mediated destruction of alveolar basement membranes
Epitopes recognized by antibodies are buried deep in the protein
Environmental exposure may be required to ‘expose’ epitopes
Genetic predisopsition linked to certain HLA subtypes
Lung Disease of Vascular Origin
Pathology of Goodpasture Syndrome: Symptoms
Hemoptysis; X-ray will show focal consolidations
Death is usually due to renal involvement
Lung Disease of Vascular Origin
Treatment of hemoptysis due to Goodpasture Syndrome
plasmapheresis to remove autoantibodies + immunosuppression
Lung Disease of Vascular Origin
Pathology of Goodpasture Syndrome: Lungs
Red-brown consolidation
described as heavy
Lung Disease of Vascular Origin
Histology of Goodpasture Syndrome
Intra-alveolar hemorrhage
Focal necrosis in alveolar walls
Macrophages accumulate heme
Lung Disease of Vascular Origin
Late stages of Goodpasture Syndrome
Septal fibrosis (thickened)
Type II Penumocyte hypertrophy
Blood in alveolar spaces
Lung Disease of Vascular Origin
Pulmonary Edema
Leakage of fluid into alveolar space
Lung Disease of Vascular Origin
Pulmonary Edema is caused by…
Hemodynamic disturbances
Increased capillary permeability
Combination of the two
Lung Disease of Vascular Origin
Pulmonary Edema: Hemodynamic Disturbances
Increased pressure (more common)
Decreased pressure (less common)
Lung Disease of Vascular Origin
Pulmonary Edema: Increased capillary permeability
Damage to microvasculature
Infections, gas inhalation, liquid aspiration
Drugs and chemicals
Shock, trauma, radiation, transfusion
Lung Disease of Vascular Origin
Hemodynamic Edema
Most commonly the result of left-side congestive heart failure
Increases pressure in LV - increased pressure in lungs - fluid forced out of capillaries
Lung Disease of Vascular Origin
Microvascular injury edema
Damage to the capillary bed
Leakage of fluids and proteins
Acute Respiratory Distress Syndrome (ARDS)
Lung Disease of Vascular Origin
Microvascular Injury Edema: Damage to capillary bed
Primary to vascular endothelial cells
or to alveolar squamous pneumocytes
Both cell types impt for maintaining barrier between blood+air space
Lung Disease of Vascular Origin
Microvascular Injury Edema: Leakage of fluids and proteins
Interstitial space - restrictive disease
Alveoli - pneumonia
Lung Disease of Vascular Origin
Microvascular Injury Edema: Acute Respiratory Distress syndrome is due to…
Due to sudden diffuse edema
Acute Respiratory Distress Syndrome (ARDS)
Severe Acute Lung Injury
Abrupt onset of hypoxemia
Bilateral pulmonary infiltrates
no cardiac failure
Acute Respiratory Distress Syndrome (ARDS)
Acute Respiratory Distress Syndrome (ARDS)
Severe Acute Lung Injury
Inflammatory disease producing Diffuse Alveolar Damage (DAD)
Acute Respiratory Distress Syndrome (ARDS)
Diffuse Alveolar Damage (DAD)
Increased pulmonary vascular permeability
Edema
Epithelial cell death
Acute Respiratory Distress Syndrome (ARDS)
What are some causes of Acute Respiratory Distress Syndrome (ARDS)?
Mechanical trauma
near drowning
sepsis
barbituate overdose
gastric aspiration
Acute Respiratory Distress Syndrome (ARDS)
Pathogenesis of Acute Respiratory Distress Syndrome (ARDS)
- stress activated macrophages
- Inflammatory mediators damage cells (endothelium, Penumocytes)
- Neutrophils invade and debris accumulates (hyalinization
- Healing starts when macrophages produce TGFB and PDGF (activate fibroblasts)
Acute Respiratory Distress Syndrome (ARDS)
Two types of Pneumocyte damage
Loss of Squamous (I) - increased permeability
Loss of Cuboidal (II) - decreased surfactant, increased risk of alveolar collapse
Acute Respiratory Distress Syndrome (ARDS)
Acute Respiratory Distress Syndrome (ARDS) Symptoms - Lungs
Heavy
Filled with Fluis (Wet)
Acute Respiratory Distress Syndrome (ARDS)
Acute Respiratory Distress Syndrome (ARDS) Symptoms - Clinical
Lungs become stiff due to loss of surfactant
Dyspena/Tachypnea
Cyanosis/hypoxemia
harder to inflate
Acute Respiratory Distress Syndrome (ARDS)
Treatment of Acute Respiratory Distress Syndrome (ARDS)
High concentrations of oxygen
mechanical ventilation
treat underlying cause (e.g. sepsis)
Infections
Pneumonia
Lung infection by bacteria, viruses, mycoplasms, or fungi
responsible for 1/6 of US deaths
Characterized by lymphatic infiltrates in alveoli
Produces pulmonary edema; can also result from pulmonary edema
Infections
Types of Pneumonia
Community-acquired
Hospital-acquired
Aspiration
Chronic
Infections
Community-acquired Pneumonia
Typical - bacterial
Atypical - viral, mycoplasmal
Infections
Hospital-acquired Pneumonia
Mechanical ventilation is a risk factor
Infections
Aspiration Penumonia
Markedly debilitated patients, stroke victims
Abnormal gag/swallowing reflex
Infections
Chronic Pneumonia
Localized lesion
Immunocompetent patient
Infections
Causes of Penumonia
Cough reflex suppression/inhibition
* coma, anesthesia, neuromuscular disorders
Mucociliary apparatus damage
* cigarette smoke, hot gases, viral, genetic
Accumulation of secretions
* cystic fibrosis, bronchial obstruction
Decreased macrophage activity
* alcohol, tobacco, anoxia, ocygen intoxication
Edema or congestion (mucus)
Infections
What is Aspiration Pneumonia? What causes the damage?
Necrotizing Pneumonia; often fatal
Chemical
Bacterial
Infections
Aspiration Pneumonia: Chemical damage
Low pH of gastric acid damages cells in the airways and alveoli
Tissues necrossi and inflammation
Infections
Aspiration Pneumonia: Bacterial Damage
Oral flora (more than one; more aerobes than anaerobes)
Inflammation
Infections
Aspiration Pneumonia: Microaspiration
Very common (esp. in patients with GERD)
May exacerbate exisiting conditions like asthma, interstitial fibrosis, and transplant rejection
Infections
Bacterial Pneumonia
same species, different patterns
depends on Tx, patient susceptibility
Bronchopneumonia
Lobar
Infections
Bacterial Pneumonia - Bronchopenumonia
opaque spots
patchy consolidation
areas of acute inflammation
Infections
Bacterial Pneumonia: Lobar
X-ray - whole lobe is opaque
Consolidation of lung (hepatization)
Presense of fibrin and infection fill alveoli
Infections
Clinical Course of Pneumonia
Rapid onset
* fever
* chills
* cough (mucous with signs of infections)
Fibrinosuppurative pleuritis
* Lung swelling - neutrophil infiltration, fibrin aggregation
* pleuritic pain and pleural friction rub
Infections
Stages of Acute Pneumonia
Stage 2: early red hepatization
* neutrophil infiltrate
* congestion of septal capillaries
Stage 3: gray hepatization
* alveolar exudate in air spaces
Stage 4: resolution
* fibromyxoid masses
* macrophages and fibroblasts
Infections
Viral Pneumonia: SARS
Severe Acute Respiratory Syndrome
Coronavirus from civets in China
Transmisison through respiratory secretions
Incubation period of 2-10 days
Virus infects pneumocytes
Infections
Initial symptoms of SARS
Malaise
Myalgia
Dry cough
Fever
Chills
Infections
COVID-19
Virus is SARS-CoV-2
Spreads through the air in close contact
Declared pandemic in March 2020
Infections
Complications of COVID-19
Pneumonia and trouble breathing
Organ failure in several organs
Heart problems
Acute respiratory distress syndrome
Blood clots
Acute kidney injury
Additional viral and bacterial infections
Infections
Histoplasosis
Infection with Histoplasma capsulatum
* dimorphic fungi
* initiates T cell mediated response to contain
Geographical distribution
* Warm moist soil containing bird/bat droppings (Caves)
* OH, central S valley, Appalachia
Infections
Histoplasmosis clinically:
Acute pulmonary infection
Chronic (granulomatous) infection
Disseminated miliary disease
Infections
Pathology of Histoplasmosis
Macrophage aggregates filled with yeast
Will colonize nearby lymph nodes
Eventually - granulomas with giant cells - May develop fibrosis and calcifications
Gross appearance - perihilar mass lesions (can look like lymphoma)
Obstructive and Restrictive Diseases
Inhalation
Intercostal muscles contract to draw ribs upwards
Diaphragm contracts and pulls down
increased volume draws air in
decrease pressure in lungs
Obstructive and Restrictive Diseases
Exhalation
Muscles relax and elastic fibers retract
decreaed volume expels air
Increase pressure relative to atmospheric pressure
Obstructive and Restrictive Diseases
Obstructive and Restrictive Diseases
Diffuse pulmonary diseases
Obstructive and Restrictive Diseases
Obstructive
partial or complete obstruction at any level
increased resistance to air flow
Obstructive and Restrictive Diseases
Restrictive
Reduced expansion of parenchyma
Decreased total lung capacity
Obstructive and Restrictive Diseases
How are Obstructive and Restrictive Diseases diagnosed?
Obstructive - decreased forced expiratory volume (cant expire as much)
Restrictive - decreased FRV and vital capacity
Obstructive Diseases
Emphysema
with chronic bronchitis, COPD
Permanent enlargement of smaller airspaces
* destruction of walls of smaller air spaces
* no fibrosis
Obstructive Diseases
Patterns of Emphysema
Disease location is the acinus
Associated with tobacco smoke inhalation
Major Symptom: Dyspnea
Obstructive Diseases
Pathology of Emphysema
Enlargment of airways
Destruction of walls
No fibrosis
Less wall tissue
Obstructive Diseases
Pathogensis of Emphysema
Destruction of walls
* direct damage from toxins
* inflammatory response
* proteases released from cells
* infection
Obstructive Diseases
Emphysema Pathogenesis: Inflammatory response
Macrophages/epithelial cells relase leukotrienes, IL-8, TNF
Chemotaxis, inflammation, structural changes (act as growth factors)
Obstructive Diseases
Emphysema Pathogenesis: Proteases released from cells
Deficiency in protease inhibitors
* genetic component to emphysema
* alpha-1 anti-trypsin inhibits release
Damage CT (including elastic fibers)
Obstructive Diseases
Emphysema Pathogenesis: Infection
Not a major role, but may exacerbate inflammatory damage
Obstructive Diseases
Asthma
Complex multigenic disorder
Increased airway responsiveness to stimuli
* may not provole a response in unaffected individuals (adenosine, exercise)
Obstructive Diseases
Characteristics of Asthma
Episodic bronchoconstriction
Bronchial wall inflammation
Increased mucus secretion
Obstructive Diseases
Types of Asthma
Atopic
* Classic hypersensitivity reaction (IgE)
Non-atopic
* Hyperirritability due to viral infection
Drug-induced
* Aspirin (and other NSAIDS) affects balance of cyclooxygenase activity
Occupational
* exposure to fumes, dust, gases, chemicals
Obstructive Diseases
Asthma: Chronic inflammatory airway disease
Recurrent episodes
* wheezing, breathlessness, chest tightness, cough
Bronchoconstriction
* widespread, but variable
Airflow limitation (partially reversible)
Obstructive Diseases
How does asthma alter airway structure?
Thicker mucosal layer with eosinophils inbetween goblet cells
thicker basement membrane
macrophages in lamina propria
thicker smooth muscle layer (SM proliferation)
increased glands
Obstructive Diseases
What is involved in initiation of Asthma?
B and T lymphocytes
IgE
Mast cells
Eosinophils
Obstructive Diseases
Cellular Response to Asthma: Mast Cells
Smooth muscle contraction
increased mucus secretion
vasodilation
* endothelial leakage
* local edema
Obstructive Diseases
Cellular Response to Asthma: Epithelial cells
Cytokine production
* includes leukotrienes and prostaglandins
Obstructive Diseases
Asthma: Damage to epithelium: What are the two eosinophil mediators?
Major Basic Protein (Proteoglycan 2 (PRG2))
Eosinophil Cationic Protein (ribonuclease 3)
Obstructive Diseases
Asthma: Eosinophil Mediators: Proteoglycan 2 (PRG2)
Major Basic Protein
Cellular toxin (bacteria and mammalian)
Possibly by disordering cell membranes
Obstructive Diseases
Asthma: Eosinophil Mediators: Ribonuclease 3
Eosinophil Cationic Protein
Binds to cell surface heparan sulfate proteoglycans (endocytosis)
Apoptosis through caspase-8
also necrosis
Obstructive Diseases
Cystic Fibrosis
Mutation in chloride channel results in viscous mucus that obstructs passageways
Obstructive Diseases
Consequences of Cystic Fibrosis
Chronic lung disease
* increased risk of nfections
* chronic bronchitis
pancreatic insufficiency
* steatorrhea (excess fecal fat)
* malnutrition
Hepatic cirrhosis
intestinal obstruction
male infertility
Obstructive Diseases
Cystic fibrosis conductance regulator (CFTR)
Chloride channel expressed by epithelial cells
irregular folding promotes degredation
impaired secretion of chloride ion impares secretion of sodium ion and water
Obstructive Diseases
What is the function of viscous mucus in Cystic Fibrosis?
Plugs Passageways
In lung, obstructrs air movement
In glandular tissue, obstructs secretion
In digestive tract, causes blockages
Restrictive Disorders
Fibrosisng Disorders: Penumoconioses
Caused by particles
recognized as foreign
cannot be eliminated
Restrictive Disorders
Examples of Penumoconioses
Coal workers penumoconiosis (CWP) (Black Lung)
Silicosis
Anthracosis (innocuous CWP)
Asbestosis
Restrictive Disorders
Coal Miner’s Penumoconiosis: Complicated CWP
Progressive, massive fibrosis (PMF)
* more advanced disease
* compromised lung function
Black pigment associated with fibrosis
Restrictive Disorders
Clinical Pneumoconiosis: CWP
Progressive Massive Fibrosis (<10% of cases)
Pulmonary dysfunction
Pulmonary hypertension
Cor pulmonale
Restrictive Disorders
Clinical Pneumoconiosis: Silicosis
Increased susceptibility to TB
2X risk of lung cancer
Restrictive Disorders
Clinical Pneumoconiosis: Asbestosis
Dyspnea
Increased risk of lung cancer, mesothelioma
Restrictive Disorders
Granulomatous Disorders: Hypersensitivity pneumonia
allergic alveolitis
inflammation in alveoli
* decreased diffusion capacity
* decreased lung compliance
* decreased total lung volume
diverse causes, same tissue response
Restrictive Disorders
Pathology of Allergic Alveolitis
Patchy infiltrates in the interstitium
Loose granulomas without necrosis
Cells: Lymphocytes, plasma cells, epitheloid macrophages
Restrictive Disorders
Clinical Hypersensitivity Alveolitis: Acute attacks
Result in inhalation of antigenic dust
fever
dyspnea
cough
leukocytosis (increased WBC in blood)
Restrictive Disorders
Clinical Hypersensitivity Alveolitis: Chronic Exposure
Progresisve respiratory failure
Dyspnea
Cyanosis
Decrease in lung capacity and compliance - measure of lung’s ability to expand
Restrictive Disorders
Sarcoidosis
Granulomatous restrictive disease
affects other organs as well
* lungs are common
* spleen and liver
* bone marrow
* skin lesions
* eyes and muscle
unknown etiology
Restrictive Disorders
Characteristics of Sarcoidosis
Non-necrotizing granulomas
Frequent giant cells
chronic - may become scar
Restrictive Disorders
Lung Changes in Sarcoidosis
Granulomas are found along lymphatics
Lesions in the lung may heal, so will be fibrotic/hyalinized - interstitial fibrosis
Lymph node involvement is common
Restrictive Disorders
Where are granulomas found in the lymphatics in Sarcoidosis?
Around bronchi and blood vessels
may also involve alveoli and the pleura
Restrictive Disorders
What involvement do the Lymph Nodes have in Sarcoidosis?
Hilar and mediastinal
may develop calcification
tonsils are frequently affected as well
Restrictive Disorders
What is the clinical course of Sarcoidosis?
Depends on location, size, number of granulomas
Lung: progressive fibrosis and cor pulmonale
Spontaneous remission/steroid therapy
Pleural Disorders
Pleural Disorders
usually secondary to other lung disorders
Pleural Disorders
Pleural Effusion
accumulation of pleural fluid
Pleural Disorders
What causes fluid accumulation in Pleural Effusion?
Increased hydrostatic pressure (congestive heart failure)
Increased vascular permeability (pneumonia)
Decreased osmotic pressure (renal disease)
Increased intrapleural negative pressure (atelectasis)
Decreased lymphatic drainage
Pleural Disorders
How is accumulated fluid removed in Pleural Effusion?
Resorbed (minimal amount)
Drained (chest tube)
Pleural Disorders
Penumothorax
Air or gas in the pleural space
Pleural Disorders
Spontaneous Pneumothorax
May be idiopathic (no known cause)
or: Rupture of an alveolus, abcess cavity
Pleural Disorders
Traumatic Pneumothorax
Injury to the chest wall that allows air in
Pleural Disorders
Tension Pneumothorax
Flap valve: allows air in (inspiration) but not out (expiration)
Accumulation of air can cuase compression of other structures, including the other lung
Pleural Disorders
Symptoms of Pneumothorax
Respiratory distress due to compression, collapse, atelectasis of lung
