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174 Cards in this Set

  • Front
  • Back
Where does oxygen exchange occur?
from the alveoli and the pumonary capillaries
Where does exchange of carbon dioxide and other metabolites occur?
from the pulmonary capillaries to the alveoli
Conducting System
except for the vocal cords which are covered by stratifited squamous epi, the entire resp. tract is lined by pseudostratified, tall, columnar, ciliatd epi cells, heavily admixed with mucus secreting goblet cells
Type I Alveoli
-95% of surface
-thin and flat
-participate in gas exchange
Type II Alveoli
-5% of surface
-produce surfactant
-multiply and differentiate into Type I if lung is injured
What is the function of the nose and trachea?
-warm and humidify air
-trap particles >10um
What is the function of the mucociliary blanket?
-dispse of particles 2-10um
-swallow and cough
What is the function of the alveolar macrophages?
-engulf particles <2um
-smaller particles are exhaled
Atelectasis (collapse)
-los of lung volume due to inadequate expansion of airspaces resulting in shunting of sub-optimally oxygenated blood from pulm. arterial system to veins
What are the signs and symptoms of atelectasis?
-surgery- postoperative pain
-preexisting lung diseases- asthma, pneumonia, etc.
What causes resorption atelectasis?
obstruction that prevents air from reaching distal airways and residual air is resorbed and lung tissue collapses
What are the causes of obstruction in the lung? (6)
1. mucous plug
2. foreign bodies
3. blood clot post operatively
4. tumor
5. enlarged lymph nodes
6. vascular aneurysms
What causes a mucous plug? (4)
1. post-op
2. bronchial asthma
3. bronchiectasis
4. chronic bronchitis
What are the 4 types of atelectasis based on underlying mechanism?
1. resorption
2. compression
3. microatelectasis
4. contraction
Compression Atelectasis
assoc. with accumulations of blook, fluid, or air within pleural space
How does fluid usually get into the lung?
secondary to pleural effusion secondary to CHF
How does air usually get into the lung?
Basal atelectasis
elevated diaphragm seen in patient who are bedridden, have ascites, before and after surgery
Contraction Atelectasis
localized/generalized fibrosis hampers expansion
(non-obstructive atelectasis)
loss of lung expansion caused by complex events most result in loss of surfactant
-neonatal and adult RDS
-interstitial inflamm.
Is atelectasis treatable?
most are treatable EXCEPT contraction atelectasis
What does treatment of atelectasis prevent?
-superimposed infection
Obstructive Lung Disease
Limitation of airflow due to partial or complete obstruction at any level
What are the forms of obstructive lung disease? (5)
1. asthma
2. emphysema
3. bronchitis
4. bronchiectasis
5. foreign body
What are the common causes of pulmonary congestion and edema? (3)
1. left-sided heart failure
2. decreased oncotic pressure
3. microvasuclar disease
What are the clinical symptoms for pulmonary congestion and edema?
SOB, dyspnea, wet rales
What is the pathology of pulmonary congestion and edema?
-capillary engorgement
-intra-alveolar precipitate
-hemosiderin-laden macrophages
-pneumonia complication
How is obstructive lung disease measured clinically?
pulmonary function tests
-FEV decreased
-FVC normal
-ratio FEV/FVC <0.7
episodic, reversible bronchospasm resulting from an exaggerated response to various stimuli
What are the symptoms of asthma and who has it?
-acute episodic dyspnea, cough and wheezing
-5% adults -7-10% children
Intrinsic Asthma
normal IgE levels
What are the nonimmune triggers for intrinsic asthma? (6)
1. aspirin
2. pulmonary infections
3. cold
4. exercise
5. psychological stressors
6. chemical stressors
Extrinsic Asthma
-elevated IgE levels buy may be other immunoglobulins
-hypersensitivity of the airways to a variety of inciting agents
What are the three types of extrinsic asthma?
1. atopic asthma- IgE related asthma to foreign Ag
2. occupational asthma- immune reaction related to pneumoconiosis Ags (organic and inorganic dusts in the environment)
3. bronchopulmonary aspergilosis- IgE mediated asthma to fungal elements
What is the pathogenesis of extrinsic asthma?
-inc. sensitivity to histamine and methacholine
-inflamm. in airways
-inc. Th2 cells and get eosinophils and mast cells through production of IL-4,5,13
-divided into early and late phases
Early Phase Asthma
mast cells release histamine which triggers increased inflammation through mucosal intercellular junctions
Leukotrienes C4, D4 and E4
increase mucin secretion
Prostaglandins D2, E2 and F2a
bronchoconstriciton and increased vascular permeability
bronchospasm and inc. vascular permeability
Platelet activating factor
aggregation of platelets
Mast cell tryptase
inhibits normal bronchodilatory peptide
What are the most important late phase cells?
What do eosinophils do?
-release MBP and ECP which are directly toxic to lung epi cells
-relase peroxidase which causes tissue destruction
-damage through oxidative stress
-cycle of amplified and sustained inflammatory stress w/o additional exposure to triggering Ag
Late phase asthma
cellular phase with recruitment of neutrophils, eosinophils, and basophils followed by lymphocytes
Leukotriene B4
chemotactic factors
augment Th2 response
What is chemotactic for eosinophils?
platelet activation factor
Tumor necrosis factor (TNFa)
upregulates adhesion molecules on vascular endo
What is the pathogenesis of intrinsic asthma?
mediated through nonspecific inflamm. triggered in response to viral infections and noxious pollutants
Respiratory Synctial Virus
promotes secretion of Th2 cells which promote eosinophil chemotaxis in infants around 1st year of life
What dominates asthma?
mucus plugging
What are the two histological finding of mucus?
1. curschman spirals- mucus and shed epi
2. charcot-leyden crystals- crystallized eosinophil proteins
What is the treatment for asthma
bronchdilators and corticosteroids- inhaled and systemic
Status Asthmaticus
severe asthma resistant to therapy
What does long term asthma cause?
hyperinflation of the affected lung with air trapping distal to the obstruction
Chronic Obstructive Pulmonary Disease
-affects 10% of US population and 4th leading cause of death
-defines both emphysema with chronic bronchitis
-chronic irreversible lung injury
-most common cause is smoking injury
permanent enlargement of airspaces distal to the terminal bronchioles with destrcution of the alveolar walls
Where is emphysema restricted to?
lung acinus (the terminal bronchioles icluding resp. bronchiole, alveolar duct and alveolus)
What are the three types of emphysema?
1. centriacinar
2. panacinar
3. distal acinar
Centriacinar Emphysema
central or proximal parts affected commonly cigarette smoking with apical lung portions more involved
Panacinar Emphysema
al parts of the acinus are affected commonly a1 antitrypsin deficiency with lower lungs more involved
What typically results from a1 antitrypsin deficiency?
panacinar emphysema
Distal Acinar Emphysema
distal parts affected commonly producing bullae distally in the subpleural lungs with spontaneous pneumothorax
What is the pathogenesis of emphysema?
current theory includes an imbalance between protease-antiprotease activity (a1 antitrypsin deficiency and smoking) and oxidant antioxidant activity (smoking)
What genotype gives the deficiency of the enzyme a1 antitrypsin?
PiZZ genotype
TNFa and IL-8 attracts _______
What do neutrophils express?
cellular elastic proteases normally sequestered with elastic tissue destruction
What is the clinical course of emphysema?
1. dyspnea with hyperventilation
2. weight loss
3. reduced FEV and normal FVC and reduced FEV1/FVC- prolonged expiration with less retention of CO2
4. barrel chest
What is the treatment for emphysema?
bronchodilators, steroids, and oxygen
How does death occur with emphysema?
pulmonary failure with respiratory acidosis, recurrent infection, hypoxia, coma, and right sided heart failure (cor pulmonale) due to pulm. HTN
Bronchitis is more common in _________ and ________
male smokers
city dwellers
-cough >3 months in at least 2 conseecutive years
What is the defining feature of bronchitis?
-mucus hypersecretion with large bronchial involvement
-also inflamm, fibrosis, and resultant narrowing of the bronchioles
Compensatory emphysema
compensatory dilatation of the alveoli in response to loss of lung (post surgery)
Senile emphysema
overdistended lung form age related alterations with no tissue destruction
Obstructive overinflation
air trapped within the lung by subtotal occlusion by tumor or foreign body
Mediastinal emphysema
entrance of air into connective tissue from violent coughing or emesis; whooping cough, respiratory injury
What is chronic bronchitis almost always associated with?
What do irritants produce in bronchitis?
1. hypersecretion of mucus
2. hypertrophy of mucus glands
3. metaplastic formation of mucin secreting goblet cells in the bronchiole surface epi
4. inflamm. with CD8 cells, macrophages, and neutrophils
What is the histopathology of bronchitis? (5)
1. Reid index
2. goblet cells
3. inflamm. infiltrate
4. squamous metaplasia
5. dysplasia of epi cells that may lead to bronchogenic carcinoma
Reid Index
ratio of the thickness of submucosal gland layer to that of the bronchial wall
What are the symptoms of bronchitis?
chronic cough with productive sputum, hypercapnia (retention of CO2) with cyanosis, hypoxemia
How do we treat bronchitis?
bronchodilators and steroids
How does death occur with bronchitis?
respiratory acidosis, hypoxemia, coma recurrent infection, and pulmonary hypertension leading to right sided heart failure (cor pulmonale)
small airway disease characterized by:
-goblet cell metaplasia
-SM hypertrophy
permanent dilation of bronchi and bronchioles caused by destruciton of muscle and elastic supporting tissue from chronic infections
What is bronchiectasis a secondary disease from?
persistent infection due to obstruction by tumor, foreign bodies, or mucus plugging
-cough with copious sputus
Bronchiectasis may be caused by ______ and _______ diseases.
Cystic Fibrosis
widespread bronchiectasis with resultant viscous mucus plugging obstruction, superimposed infection, and dilatation of the bronchi
Immunoglobuling deficiency
states with chronic infections
Kartagener Syndrome
recessive disorder frequently assoc. with bronchiectasis and sterility in males
-cilia abnormal
-organs may be reverse
What is the pathogensis of bronchiectasis?
-obstruction, chronic persistent infection
-normal clearance of mucus is hindered
-chronic infection destroys elastic tissue and fibrosis leads to dilatation of the bronchial walls
Necrotizing pneumonias associated with _______ or ______ may predispose to bronchiectasis.
S. aureus
Klebsiella sp.
What may lead to end stage bronchiectasis?
What are the symptoms of bronchiectasis?
-chronic cough with mucopurulent, fetid sputum
-hemoptysis in some cases
-clubbing of the fingers
What is the treatment for bronchiectasis?
-antibiotics for infection and treat underlying disease process
How does death occur from bronchiectasis?
hypoxemia, resp. acidosis, coma, pulm. HTN leading to rt. sided heart failure, embolic abscesses to the systemic circulation
Restrictive Lung Disease
characterized by reduced compliance (more pressure equired to expand the lung)
-changes affect alveoli and capillaries
-fibrosis producing stiff lungs
-can be acute or chronic
How are restrictive lung diseases diagnosed?
by decreased FVC, CT scan of thorax and open lung biopsy
What is the only acute restrictive lung disease?
What are the five chronic restrictive lung disease?
1. idiopathic pulmonary fibrosis (intersitial pneumonia or desquamative interstitial pnemonia)
2. sarcoidosis
3. hypersensitivity pneumonitis
4. asbestosis and silicosis
5. difuse alveolar hemorrhage syndromes
What is the pathogenesis of ARDS?
-direct injury to the lung alvioli or indirect injury in the setting of a systemic process
What is ARDS direct lung injury?
-aspiration of gastric contents
What is ARDS indirect lung injury?
-severe shock due to trauma (blood loss)
acute lung injury that represents a continuum of progressive resp. failure
-acute dyspnea
-dec. arterial oxygen
-develop bilateral pulm. infiltrates
-absence of lt. sided heart failure = non-cardiogenic pulm. edema
What is the histopatholgy of ARDS?
-inc. permeability into the alveolus
-widespread surfactant loss
-oxidation-antioxidation imbalance
-activated neutrophils
-hyaline membrane formation lining distended alveolar ducts
What intrinsic repair takes place with ARDS?
-pulm. macrophages phagocytize hyaline membranes
-type II pneumocytes differentiate into type I pneumocytes
What is the outcome of intrinsic ARDS repair?
results in marked distrotion of lung parenchyma leading to diffuse interstitial fibrosis with distorted airways (honeycomb lung)
__% develop ARDS after acute insult within __hours.
What is the mortality rate of ARDS?
What is associated with poor outcome in ARDS?
high levels of IL1 and procollagen peptide III in BALs
What is the treatment for ARDS?
pressor support, ventilation, steroids, and treatment of underlying cause
Chronic Interstitial Lung Disease
progressive fibrosis of pulm. parenchyma (honeycomb lung)
-15% non-infectious lung processes
How do we diagnos chronic interstitial lung disease?
dec. FVC with dec. FEV and ratio unchanged
-need to rule out occupational exposure
Idiopathic Pulmonary Fibrosis
unknown etiology with resultant hypoxia and cyanosis
-male predominance
-diagnosis of exclusion
-soluble mediators attract inflammatory cells and produce fibrosis
What is the sequence of events for idiopathic pulmonary fibrosis?
interstitial edema and accumulation of inflammatory cells leading to fibrosis and inflammation
Usual Interstitial Pneumonia
heterogenous appearance of normal lung admixed with fibrosed lung
Desquamative Interstitial Pneumonia
assoc. w/ smoking and hypersensitivity with resultant pulmonary fibrosis
What is the clincical course and survival for idiopathic pulmonary fibrosis?
-insidiousl, chronic onset of nonproducting cough, cyanosis, cor pulmonale, and peripheral edema
-mean survival 2-4yrs
What is the treatment for idiopathic pulmonary fibrosis?
UIP- non-responsive to steroids
DIP- usually responds to steroids
multisystemic disease primarily affecting the lungs characterized by noncaseating, tight granulomas histologically
-must rule out TB and occupational lung disease
What is the pathogenesis of sarcoidosis?
-immune regulated, genetically predisposed
-Th1 driven process to inc. T cells and monocytes w/in granuloma
-anergy to candida and polyclonal hypergammaglobulinema
-driven by unknown Ag
How do we diagnose sarcoidosis?
-chest x-ray
-eye and sken involvement
-black pop. and females more
-higher prevalence in non-smokers
-histology diagnosed
What is the histopathology of sarcoidosis?
-noncaseating granulomas with central monocytes and rim of T cells, giant cells, asteroid bodies, schaumann bodies
Asteroid Bodies
stellate inclusions within giant cells, not specific for sarcoid
Schaumann bodies
laminated concretions of calcium and proteins
Where and the granulomas found in sarcoidosis?
-bronchiole connective tessue
-pulmonary venules
In sarcoidosis, granulomas can be found in the ______ 75% of the time and in the ______ 40% of the time.
bone marrow
What is increased in a patient with sarcoidosis? (3)
1. vitamin D
2. calcium
3. angiotensin converting enzyme
Mikulicz Syndrome
combined eye and parotid involvement in sarcoidosis
What is the treatment for sarcoidosis?
What is the mortality rate from progressive pulmonary fibrosis?
What is the pathogenesis in hypersensitivity pneumonitis?
bronchoalveolar lavage and blood specimens show:
-inc. inflamm. chemokines
-inc. CD4 and CD8
-precipitating Ab. w/ complement activation
-noncaseating granulomas
Hypersensitivity Pneumonitis
-immunologically mediated inflammatory lung disease primarily affecting the alveoli (extrinsic allergic alveolitis)
-presents as restrictive process
-occupational exposure
organic and inorganic dust syndromes
What is the histopathology of hypersensitivity pneumonitis?
-predominance of lymphocytes with plasma cells and epitheloid histiocytes
-interstitial noncaseating granulomas in 2/3 of specimens
What is a necessity when diagnosing hypersensitivity pneumonitis?
clinical correlation with occupational exposure
What does a diagnosis of hypersensitivity pneumonitis depend on?
specific precipitating antibodies to environmental dust
-a type of pneumoconiosis where exposure occurs in shipyards and industrial areas where asbestos was used
What asbestos fibers cause disease?
blue, brown and white
Lung reacts to asbestos when the fibers reach the ______ and ______ and cause fibrous thickening in the lower lung.
air sacs
What is the clinical course for asbestos exposure?
dyspnea following exposure to inciting Ag dependent on temporal exposure to Ag w/ fever, cough and constitutional complaints
What are the symptoms for asbestos?
1. breathlessness w/ loss of elasticity
2. NO cough or chest pain
3. progressive dyspnea w/ weight loss
4. asbestosis predisposes to bronchogenic carcinomas and mesthelioma, a risk inc. by cigarette smoking
What are the most common forms of chrystalline silica?
1. quartz
2. tridymite
3. cristobalite
Where does silica exposure occur?
mining, quarrying, stone cutting, sand blasting, some foundries
What happens when silica is inhaled?
it enters the lungs and there become engulfed by macrophages in which are destroyed and liberate a fluid causing a localized fibrous nodule which will obliterate the air sacs
What are the symptoms of silicosis?
dry morning cough (initially), dyspnea with exercise, fever, weight loss, and bloody sputum
What is the one form of pneumoconiosis that predisposes TB?
Diffuse Alveolar Hemorrhage Syndrome
primary disease not related to pneumonia, coagulation problems, or venous congestion
What is the triad for diffuse alveolar hemorrhage syndrome?
1. hemoptysis
2. anemia
3. diffuse pulm. infiltrates
What are the five types of diffuse alveolar hemorrhage syndrome?
1. Goodpasture syndrome
2. idiopathic pulm. hemosiderosis
3. Wegner's granulomatosis
4. collagen vascular disorders
5. severe lung transplantation rejection
Idiopathic Pulm. Hemosiderosis
-pulm. manifestatins similar to Good pasture syndrome in the lung
-no circulating anti-BM Ab in serum
-usually milder presentation than Goodpasture syndrome with most spontaneously recovering
Goodpasture Syndrome
-rapid concentric glomerulonephritis
-hemorrhagic interstitial pneumonitis
-caused by Ab to the BM found in kidneys and lungs
-progressive with most dying from disease
What does Goodpasture syndrom immunofluorescence detect?
linear deposition of IgG, sometimes IgA and IgM in renal biopsy
Wegener's Granulomatosis
necrotizing granulomas attacking both pulm. arteries, bronchi, and rapid crescenteric glomeruonephritis
What is the triad seen with Wegener's Granulomatosis?
1. chronic sinusitis
2. pulm. symptoms
3. renal disease
What are the four collagen vascular disorders?
1. SLE
2. rheumatoid arthritis
3. scleroderma
4. dermatomyositis-polymositis
Caplan syndrome
accelerated rheumatoid arthritis and coal miner's lung pneumoconiosis
What are the two vascular disorders of the lung?
1. pulm. thromboembolism
2. pulm. HTN
Pulmonary Thromboembolism
causes 50,000 deaths/yr from hemorrhage or infarction
What is the transplant pathogenesis?
1. lung susceptible to rejection and inflamm. destruction
2. chronicfejection targets airways and vessels leading to bronchiolitis obliterans
3. immunosuppression has decreased this disease in modern transplants
Bronchiolitis Obliterans
progressive obliteration of bronchiolar lumina by fibrosis
Pulmonary Thromboembolism
more than 95% from deep leg veins of lower legs, especially popliteal veins
What are the risk factors for pulm. thromboembolism? (6)
1. prolonged bed rest
2. surgery on legs
3. severe trauma/burns
4. birth control pill and peripartum
5. factor V leiden hyperhomocysteinemia
6. disseminated cancer (Trousseau syndrome)
How does death occur from pulm. thromboembolism?
-perfusion of lung zones that are atelectatic
-dec. in CO causes differenc ein arterial-venous oxygen saturation
-rt. to lt. shunting of blood through a patent foramen ovale
Saddle embolus
large emboli that impact the bifurcation of large pulm. arteries causing rt. sided heart failure (cor pulmonale)
What happens to the remainder of lung after thromboembolism?
-wedge shaped w/ base at pleural surface producing coagulative necrosis of the lung parenchyma and hemorrhage
Patients who have one pulm. embolus have a __% chance of having another.
What is the treatment for a pulm. thromboembolism?
anticoagulation w/ heparin and warfarin, Greenfield filter placement in the IVC
What is the pathogenesis of pulmonary hypertension?
Unknown mechanism
1. vasospasm theory- Raynaud's phenomenon
2. inimal and medial thickening theory
What are the primary forms of pulmonary hypertension? (3)
1. plexiform pulmonary arteriopathy
2. thrombotic pulm. arteriopathy
3. pulm. venoocclusive disease
What are the secondary forms of pulmonary hypertension? (3)
1. Cardiac- septal defects, lt. to rt. shunts, atrial myxoma, mitral stenosis
2. inflamm.- scleroderma, etc.
3. lung parenchymal disease- COPD, interstitial lung disease
What is the clinical course of pulmonary hypertension?
progesses to hypoxemia, cor pulmonale, and sudden death
What is the treatment for pulmonary hypertension?
treat underlying disease if secondary, use oxygen and calcium channel blockers