Release of growth factors causes proliferation of endothelial cells, smooth muscle cells, and fibroblasts.
Hypoxic pulmonary vasoconstriction further increases pulmonary artery pressures.
The release of inflammatory mediators and immune complexes can damage bronchial mucous membranes and alveolocapillary membranes.
The infection is usually limited to one or two lobes.
They diminish the number of acute exacerbations, slow the rate of decline in quality of life, and reduce the rate of decline in FEV1.
This process results in luminal narrowing and abnormal vasoconstriction, called remodeling.
PAH may not be detected until it is quite severe.
The most important guardian cell of the lower respiratory tract is the alveolar macrophage.
Some microorganisms release toxins from their cell walls that can cause further lung damage.
Pneumolysin is a protein released by pneumococcal bacteria that is cytotoxic to virtually every cell in the lung.
The common cold, pharyngitis (sore throat), and laryngitis.
Advanced age, immunocompromised status, underlying lung disease (especially COPD), alcoholism, altered consciousness, impaired swallowing, smoking, endotracheal intubation, malnutrition, immobilization, underlying cardiac or liver disease, and residence in a nursing home.
9% to 27%.
Inhalation of microorganisms.
Blood flow through the lungs can be disrupted by a number of disorders that result in occlusion of the vessels, an increase in pulmonary vascular resistance, or destruction of the vascular bed.
Gas exchange is reduced with restriction in lung volumes.
The release of TNF-α and IL-1 from macrophages and chemokines and chemotactic signals from mast cells and fibroblasts contribute to widespread inflammation in the lung.
S. pneumoniae microorganisms initiate innate and adaptive immune responses.
Alveolar edema creates a medium for the multiplication of bacteria and aids in the spread of infection into adjacent portions of the lung.
Smoking cessation.
Idiopathic PAH is characterized by endothelial dysfunction with overproduction of vasoconstrictors and decreased production of vasodilators.
Pulmonary hypertension associated with lung respiratory disease or hypoxia, or both.
Many pathogens, such as the pneumococcus, can release a DNase that cleaves the NET and thus escape neutrophil defense.
Rapid lysis of pneumococcal bacteria results in the release of intracellular bacterial proteins that can be toxic.
During the resolution of infection, increasing numbers of macrophages appear in the alveolar spaces, neutrophils degenerate, and fibrin threads and remaining bacteria are digested by macrophages and removed by lymphatic vessels.
Oropharyngeal candidiasis, hoarseness, and risk of pneumonia.
It reduces airway inflammation and is proving to be effective in selected individuals with severe COPD.
Pneumonia.
Hospital-acquired pneumonia (HAP).
Treatment consists of rest, aspirin, humidity, and a cough suppressant, such as codeine.
Major disorders that result from pulmonary vascular diseases include pulmonary embolism, pulmonary hypertension, and cor pulmonale.
Other less common nonthrombotic emboli include tissue fragments, lipids (fats), a foreign body, or an air bubble.
A blood clot becomes an embolus when all or part of it breaks away from the site of formation and begins to travel in the bloodstream.
The workload of the right ventricle increases, leading to right ventricular hypertrophy and potentially failure (cor pulmonale).
Macrophages present infectious antigens to the adaptive immune system, activating T cells and B cells with the induction of cellular and humoral immunity.
The pathogenesis of pneumococcal pneumonia (Streptococcus pneumoniae) serves as a model for understanding other forms of bacterial pneumonia.
Inflammatory cytokines and cells are released that cause alveolar edema.
Pulmonary rehabilitation, improved nutrition, and breathing techniques.
Long-term oxygen therapy and ventilation, if indicated.
Under most circumstances.
As community-acquired (CAP), healthcare-associated (HCAP), hospital-acquired (HAP), or ventilator-associated (VAP).
Yes, purulent sputum may be produced with some viral infections.
It is rare in previously healthy adults except after viral infection, but is common in those with COPD.
An individual with PE usually presents with the sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety.
The cough reflex and mucociliary clearance.
Increased risk for thrombosis associated with hemodynamic stasis, hypercoagulability, and endothelial injury is known as Virchow’s triad.
Pulmonary emboli can result in embolus with infarction, embolus without infarction, massive occlusion, or multiple pulmonary emboli.
Intracellular signaling abnormalities result in vascular proliferation.
Neutrophils are critical phagocytes that kill microbes through the formation of phagolysosomes filled with degradative enzymes, antimicrobial proteins, and toxic oxygen free radicals.
The immune response includes complement activation and the production of antibodies, which are crucial for opsonizing the encapsulated bacterium.
The involved lobe undergoes consolidation, where alveoli fill with blood cells, fibrin, edematous fluid, and pneumococci, giving lung tissue a red appearance.
By the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as mild, moderate, severe, or very severe.
The very young, the very old, or individuals with impaired immunity or underlying disease.
Community-acquired pneumonia (CAP).
Aspiration of oropharyngeal secretions.
The sensitivity for the presence of a clot is high, especially in the thigh and pelvis.
When bacteria are spread to the lungs in the blood from infection elsewhere in the body or from intravenous drug use.
Individuals with a history of previous emboli are at risk for recurrent pulmonary emboli.
Chest x-ray findings are nonspecific in PE and often can be normal for the first 24 hours until atelectasis occurs in the lung.
A normal serum d-dimer level makes the presence of a PE highly unlikely.
A pulmonary angiogram is necessary in rare cases to confirm the diagnosis of PE.
Venous stasis is minimized by bed exercises, frequent position changes, early ambulation, and pneumatic calf compression.
Rapid administration of anticoagulation, usually unfractionated or low-molecular-weight heparin and factor Xa inhibitors, follows the initial management of PE.
Clinical examination has low sensitivity for DVT.
Familial PAH (FPAH) is caused by mutations in the gene encoding the bone morphogenetic protein receptor type II (BMPR2).
Pulmonary artery hypertension associated with left heart failure or valvular disease is caused by increased pulmonary venous pressure.
Combined changes in vasoconstriction and cellular proliferation cause resistance to pulmonary artery blood flow.
The first indication is often an abnormality seen on a chest radiograph (enlarged pulmonary arteries).
Alveolar macrophages recognize pathogens through their pattern-recognition receptors, such as Toll-like receptors.
The accumulation of exudate in the acinus leads to dyspnea and V/Q mismatching and hypoxemia.
The release of pneumolysin and other intracellular bacterial proteins can cause worsening in clinical symptoms sometimes seen immediately after antibiotic treatment.
Respiratory tract infections.
Mortality from pneumonia is highest in older adults.
Individuals with viral bronchitis usually have a non-productive cough that occurs in paroxysms and is aggravated by cold, dry, or dusty air.
Through the inhalation of microorganisms released into the air when an infected individual coughs, sneezes, or talks, or from aerosolized water.
Seed the lung with microorganisms, especially during endotracheal suctioning.
With large emboli, a pleural friction rub, pleural effusion, fever, and leukocytosis may be noted.
Risk factors for PE include conditions and disorders that promote blood clotting as a result of venous stasis, hypercoagulability, and endothelial injury to the cells that line the vessels.
The effect of the embolus depends on the extent of pulmonary blood flow obstruction, the size of the affected vessels, the nature of the embolus, and the secondary effects.
Hemodynamically, this results in increased pulmonary artery pressures and can lead to right heart failure.
If pulmonary infarction occurs, shrinking and scarring develop in the affected area of the lung.
The recognition of individuals at high risk for PE is crucial to assessing the clinical presentation.
A fibrinolytic agent may be infused through a pulmonary artery catheter.
The normal pulmonary artery pressure is 15 to 18 mmHg.
Diet drugs, amphetamines, and cocaine have been linked to an increased risk for PAH.
Yes, viral pneumonia can be a primary infection, such as influenza pneumonia.
Older adults are at higher risk of fatal outcomes from severe viral pneumonia.
Individuals may demonstrate symptoms and signs of underlying systemic disease or sepsis.
Eventually, death results in most individuals with PAH.
A neutrophil extracellular trap (NET) is a meshwork of proteins extruded by neutrophils that can capture any bacteria that have not yet been phagocytosed.
The affected tissues become gray because of fibrin deposition over the pleural surfaces and the presence of fibrin and neutrophils in the consolidated alveoli.
Inhaled anticholinergic agents and beta agonists.
Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites.
It occurs in individuals with recent hospitalization, residence in a nursing home or extended care facility, home infusion therapy, chronic dialysis, or home wound care.
Chest pain often develops from the effort of coughing.
Bacteria that form biofilms.
The consequences of altered pulmonary blood flow may be of no functional significance or can result in severe and life-threatening changes in ventilation-perfusion ratios.
PE most commonly results from embolization of a clot from deep venous thrombosis involving the lower leg.
Genetic risks include factor V Leiden mutation, antithrombin II deficiency, protein S deficiency, protein C deficiency, and prothrombin 20210 gene mutations.
There is a release of neurohumoral substances such as serotonin, histamine, catecholamines, and angiotensin II, and inflammatory mediators such as endothelin, leukotrienes, thromboxanes, and toxic oxygen free radicals.
If the thrombus is large enough, infarction of lung tissue, dysrhythmias, decreased cardiac output, shock, and death are possible.
In most cases, the clinical manifestations of PE are nonspecific.
Reversal of the underlying cause of the thrombus is important in preventing recurrent venous thromboembolism.
COPD is the most common lung disease associated with PAH.
Sloughing of destroyed bronchial epithelium occurs throughout the respiratory tract, preventing mucociliary clearance.
No, the cough in viral pneumonia may be nonproductive.
The specimen may be contaminated with pathogens from oral secretions.
Empirical antibiotics are chosen based on the likely causative microorganism.
Individuals with AIDS are highly susceptible to respiratory tract infections, including multidrug-resistant TB.
Once TB bacilli are inspired into the lung, they multiply and cause nonspecific pneumonitis (lung inflammation).
They release interferon.
They play a role in the pathogenesis of idiopathic PAH.
The symptoms are often masked by primary pulmonary or cardiovascular disease.
Airway epithelial cells can recognize some pathogens directly, such as Pseudomonas aeruginosa and Staphylococcus aureus.
The damage to bronchial mucous membranes and alveolocapillary membranes causes the acini and terminal bronchioles to fill with infectious debris and exudate.
Yes, if possible.
In chronic hypoxemia.
α1-Antitrypsin augmentation.
Overall 20% to 50% mortality.
Individuals with bacterial bronchitis have a productive cough, fever, and pain behind the sternum that is aggravated by coughing.
No, the lack of clinical indicators for DVT does not rule out the possibility of PE.
They are expelled or held in check by mechanisms of self-defense.
Massive occlusion causes profound shock, hypotension, tachypnea, tachycardia, severe pulmonary hypertension, and chest pain.
The ECG may show evidence of strain on the right side of the heart.
Single or multidetector spiral CT arteriography has replaced the radionucleotide ventilation-perfusion scan in most hospitals.
If the embolus does not cause infarction, the clot is dissolved by the fibrinolytic system and pulmonary function returns to normal.
Evaluation of risk factors and predisposing factors is an important aspect of diagnosis because the clinical manifestations of PE are nonspecific.
Calf pain and tenderness, along with calf asymmetry when documented with a tape measure, are some of the most important findings in DVT.
Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure greater than 25 mmHg at rest.
PAH affects up to 1 in 200 individuals infected with HIV.
Any condition that causes chronic hypoxemia can result in pulmonary hypertension.
Yes, some forms of viral pneumonia can progress to severe systemic illness with many complications and high morbidity and mortality.
Signs include inspiratory crackles, increased tactile fremitus, egophony, and whispered pectoriloquy.
Prevention measures include prevention of aspiration, respiratory isolation of immunocompromised individuals, vaccination for appropriate populations, and reduction of ventilator-associated pulmonary infections.
Viral pneumonia is usually treated with supportive therapy alone, unless a secondary bacterial infection is present.
The incidence of TB in the United States has reached its lowest level since 1953, but the rate of decline has begun to slow.
Lung volume reduction surgery or transplantation.
Pneumonia.
Nearly one third.
The nasopharynx and oropharynx.
Bacterial bronchitis is treated with rest, aspirin, humidity, and antibiotics.
Occasionally, syncope (fainting) or hemoptysis occurs in PE.
Recurrent small emboli may not be detected until progressive incapacitation, precordial pain, anxiety, dyspnea, and right ventricular enlargement are exhibited.
Arterial blood gas results commonly reveal hypoxemia with respiratory alkalosis.
Single or multidetector spiral CT arteriography is used for further evaluation of PE.
The measurement of elevated serum troponin I levels has been useful in stratifying the risk and severity of PE.
At-risk individuals may receive prophylactic anticoagulation with unfractionated heparin, low-molecular-weight heparin, warfarin, or fondaparinux.
Assessment for DVT may indicate the presence of a lower extremity source for the thromboembolism.
Viral pneumonia provides an ideal environment for bacterial growth and damages ciliated epithelial cells, which normally prevent pathogens from reaching the lower airways.
The influenza virus invades the goblet cells and bronchial mucous glands.
Common symptoms include the onset of cough, dyspnea, and fever.
The pathogen is identified by means of sputum characteristics and cultures or, if sputum is absent, blood cultures.
Resistant strains of Pneumococcus are becoming more prevalent.
AIDS caused a significant increase in TB cases during the mid-1990s.
TB microorganisms usually lodge in the lung periphery, usually in the upper lobe.
By transitioning into a stage of dormancy.
TB may remain dormant for life.
Fatigue, weight loss, lethargy, anorexia, a low-grade fever that usually occurs in the afternoon, and night sweats.
By a positive tuberculin skin test (TST; purified protein derivative [PPD]), sputum culture, immunoassays, and chest radiographs.
Characteristic changes such as nodules, calcifications, cavities, and hilar enlargement.
Administration for an 18-month timeframe of a combination of at least four drugs to which the microorganism is susceptible, including a review of drug effectiveness at 6 months.
Pneumonia caused by aspiration or by exposure to Klebsiella or Staphylococcus.
The process of abscess emptying and cavity formation.
Pulmonary embolism (PE) is occlusion or partial occlusion of the pulmonary artery or its branches by an embolus.
A chest x-ray, arterial blood gas, and electrocardiogram (ECG) are obtained immediately when PE is suspected.
The serum d-dimer level measures a product of thrombus degradation by the fibrinolytic system.
Magnetic resonance imaging (MRI) is used in some centers for PE evaluation.
The ideal treatment of PE is prevention through risk factor recognition and elimination of predisposing factors.
The management of PE begins with the administration of oxygen and hemodynamic stabilization with fluids, if needed.
Unfortunately, DVT is often asymptomatic.
Idiopathic PAH (IPAH) usually occurs in women between the ages of 20 and 40 years.
Recurrent pulmonary embolism may be subclinical.
Examples include cytomegalovirus pneumonia in immunocompromised individuals.
Diagnosis is made on the basis of history, physical examination, white blood cell count, chest x-ray, stains and cultures of blood, and cultures of respiratory secretions.
Most individuals have hypoxemia and a respiratory alkalosis.
Infections with opportunistic microorganisms may require multiple drugs, including antifungals.
TB is transmitted from person-to-person in airborne droplets.
Granulomas create a confined environment.
They die, forming cheeselike material called caseation necrosis.
They develop so gradually that they are not noticed until the disease is advanced.
They will have a positive TST even if they have never had TB.
Isolating individuals with active tuberculosis, limiting use of immunosuppressive medications, and treating underlying immunocompromising diseases.
The waxy coat of M. tuberculosis.
A circumscribed area of suppuration and destruction of lung parenchyma.
Necrosis of consolidated tissue may progress proximally until it communicates with a bronchus.
Fever, cough, chills, excessive sputum production, and pleural pain.
Acute infection or inflammation of the airways or bronchi.
This causes widespread vasoconstriction that further impedes blood flow to the lung.
Diagnostic algorithms guide the diagnosis and treatment of PE.
The placement of a filter in the inferior vena cava can prevent emboli from reaching the lungs.
A fibrinolytic agent, such as streptokinase, may be used if a massive life-threatening embolism occurs.
Associated PAH (APAH) is a leading cause of mortality in many connective tissue disorders.
Common bacteria include S. aureus and Streptococcus pneumoniae.
Bronchial walls become edematous and infiltrated with leukocytes.
Other symptoms include chills, malaise, and pleuritic chest pain.
Further diagnostic studies may include molecular testing of blood or urine, bronchoscopy, or lung biopsy.
Global TB incidence and prevalence have declined in most regions of the world in recent years.
Some TB bacilli migrate through the lymphatics and become lodged in the lymph nodes.
Interferon inhibits the replication of the microorganisms and stimulates more macrophages to attack the bacterium.
Infection with human immunodeficiency virus (HIV).
Dyspnea, chest pain, and hemoptysis.
Enzyme-linked immunospot and quantitative blood interferon-gamma assay.
Alcohol abuse, seizure disorders, general anesthesia, and swallowing disorders.
By radiography.
Absent blood flow to a lung segment causes a ventilation-perfusion mismatch (increased dead space) and a decrease in surfactant production.
The risk of recurrent venous thromboembolism is 30% over the next 10 years, and is much higher in those individuals who have irreversible risk factors for the disease.
A list of an individual’s predisposing factors for venous thromboembolism can be inserted into one of several clinical prediction models (e.g., Wells Prediction Rule model) to obtain a prediction score that helps determine risk probability.
Some individuals may require emergent percutaneous or surgical embolectomy.
Viral pneumonia is seasonal, usually mild and self-limiting, but it can set the stage for a secondary bacterial infection.
Yes, viral pneumonia can be a complication of another viral illness, such as chickenpox or measles.
New or atypical forms include swine influenza A (H1N1) virus, avian influenza A (H5N1) virus, and the coronavirus that causes severe acute respiratory syndrome (SARS).
An elevated white blood cell count usually indicates infection, although it may be low if the individual is debilitated, immunocompromised, or has an overwhelming infection.
Adequate hydration and good pulmonary hygiene are important.
Tuberculosis (TB) is an infection caused by Mycobacterium tuberculosis, an acid-fast bacillus that usually affects the lungs but may invade other body systems.
Host susceptibility to TB infection is influenced by host and parasite genetic polymorphisms, including those that affect macrophages, tumor necrosis factor, and interleukins.
The TB bacterium is successful as a pathogen because it can survive within macrophages, resist lysosomal killing, and multiply within the cell.
Collagenous scar tissue grows around the tubercle.
Symptoms can appear within weeks of exposure to the bacillus.
The tubercle bacillus.
The development of an effective TB vaccine.
Abscess communication with a bronchus.
The influenza virus is the most common viral cause of pneumonia.
Most cases of pneumonia are preceded by an upper respiratory tract infection, which is usually viral.
Chest radiographs show infiltrates that may involve a single lobe of the lung or may be more diffuse.
Bacterial pneumonia is treated with antibiotics.
Tuberculosis (TB) is the leading cause of death from a curable infectious disease worldwide.
In immunocompetent individuals, the microorganism usually is contained by the inflammatory and immune response systems, and latent TB infection (LTBI) develops with no clinical evidence of disease.
The bacterium terminates its own central metabolism, stops replication, and transitions into a stage of dormancy.
About 10 days.
Those of pneumonia (i.e., cough, fever, chills, malaise).
The first step is establishing adequate ventilation and oxygenation.
Antivirals may be needed in severe cases of viral pneumonia.
Non-Hispanic Asians, non-Hispanic blacks, and Hispanics have higher rates of new TB cases.
Phagocytes engulf the TB bacilli and begin the process by which the body’s defense mechanisms isolate the bacilli, preventing their spread.
They seal off the colonies of bacilli, forming a granulomatous lesion called a tubercle.
Latent TB infection is asymptomatic.
Neurologic deficits, meningitis symptoms, bone pain, and urinary symptoms.
Past, latent, or active forms of the disease.
The new immunoassays are often not available.
Opportunistic microorganisms, such as fungi and mycobacteria.
Bronchoscopy.
Neutrophils and macrophages migrate to the area of inflammation in the lung.
They can activate cytotoxic T cells (CD8).
Cancer, immunosuppressive medications, poor nutritional status, renal failure, and other debilitating diseases.
Extrapulmonary TB disease.
The need for yearly chest radiographs to detect active disease.
They are more sensitive and specific for the diagnosis of latent TB and are not confounded by previous BCG vaccination.
The individual’s health history, the likelihood of bacterial resistance to certain drugs, and the presence of active disease.
New drugs and drug combinations, including immune amplifiers.
Inflammation causes alveoli to fill with fluid, pus, and microorganisms.
Immunocompromised individuals.
The administration of appropriate antibiotics and chest physical therapy, including chest percussion and postural drainage.
Progressive active disease occurs and may spread through the blood and lymphatics to other organs.
A cough that produces purulent sputum develops slowly and becomes more frequent over several weeks or months.
Up to 6 weeks.
Combinations of antibiotics (isoniazid, rifampin, pyrazinamide, and ethambutol) to control active disease or prevent reactivation of latent TB infection.
It leaves a cavity that has a radiographic appearance similar to that of a lesion of tuberculosis.
Viruses.
