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Bronchitis

Bronchitis

Bronchitis is an obstructive pulmonary disease characterized by inflammation of the bronchi of the lungs. It is a common disease of habitual smokers and residents of polluted cities. Like many disorders, bronchitis can be acute (short-term), or chronic (long-lasting). Chronic bronchitis is defined clinically as a persistent cough that produces sputum for at least three months in two consecutive years.

Features

Signs and symptoms

The primary symptom of chronic bronchitis is a persistent cough that produces sputum. A patient may have only this symptom for many years before others develop. Eventually, the patient will experience shortness of breath (dyspnea) on exertion. As the disease progresses, other symptoms may appear, such as an inability to sufficiently expel carbon dioxide from the lungs (hypercapnia) and insufficient oxygenation of the blood (hypoxemia) leading to cyanosis. Severe chronic bronchitis will commonly lead to cor pulmonale and heart failure

Morphology

When the airways of a lung affected by chronic bronchitis are viewed under a microscope, several features are usually observed:
- an increase in the number of goblet cells with mucus blocking the airway
- clusters of pigmented alveolar macrophages
- the presence of inflammatory cells (e.g. neutrophils)
- scarring (fibrosis) of the walls of the bronchioles

Diagnosis

A physical examination will often reveal decreased intensity of breath sounds (rhonchi) and extended expiration. A common test when ordered when evaluating a patient for bronchitis is a sputum culture. In this test, a sample of sputum from a patient is stained and examined for the presence of bacteria that can cause disease. There are a variety of lab test results that indicate the presence of chronic bronchitis in a patient, namely:
- a chest x-ray that reveals hyperinflation and increased bronchovascular markings
- a pulmonary function test that shows an increase in the lung's residual volume and a decreased vital capacity
- arterial blood gases that show a decreased level of oxygen in the blood and an increased level of carbon dioxide
- a sputum culture that has pathogenic microorganisms and/or neutrophils in it Diagnosis of acute bronchitis is aided by finding an elevation in the level of the diaphragm on chest x-ray.

Pathophysiology

The initiating event in developing chronic bronchitis appears to be chronic irritation due to inhalation of certain substances (especially cigarette smoke). The earliest clinical feature of bronchitis is increased secretion of mucus by submucousal glands of the trachea and bronchi. Damage caused by irritation of the airways leads to inflammation and infiltration of the lung tissue by neutrophils. The neutrophils release substances that promote mucousal hypersecretion. As bronchitis persists to become chronic bronchitis, a substantial increase in the number of goblet cells in the small airways is seen. This leads to further increased mucous production that contributes to the obstruction of the airways. The role of infection in the pathogenesis of chronic bronchitis appears to be secondary. However, although infection is not responsible for initiating bronchitis, it may have an important role in maintaining it. Acute exacerbations of the long-standing bronchitis may result from infections.

Treatment

The single most important thing a patient can do to improve chronic bronchitis is to quit smoking. Oxygen therapy, bronchodilator drugs, and lung volume reduction surgery are also used to treat chronic bronchitis.

Prognosis

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are possible complications of chronic bronchitis. The prognosis for patients with severe chronic bronchitis is poor. The median survival time of patients with severe bronchitis is four years (Medical Diagnosis and Treatment).

Prevention

Chronic bronchitis is very preventable. The main action to reduce your risk is to eliminate exposure to cigarette smoke. Smokers in the early stages of chronic bronchitis can change and improve the course of the disease by quitting smoking.

History

Bronchitis was originally named and described by Charles Bedham in 1808. It was introduced by P. Frank in his work "Interpretationes Clinicae" in 1812.

External links

Section Online medical references
- [http://www.merck.com/mrkshared/mmanual/section6/chapter69/69a.jsp Acute bronchitis] Merck Manual of Diagnosis & Therapy
- [http://www.merck.com/mrkshared/mmanual_home2/sec04/ch041/ch041a.jsp Bronchitis] The Merck Manual - Second Home Edition
- [http://www.merck.com/mrkshared/mmanual_home2/sec04/ch045/ch045a.jsp Chronic Obstructive Pulmonary Disease] The Merck Manual - Second Home Edition
- [http://www.merck.com/mrkshared/mm_geriatrics/sec10/ch78.jsp Chronic Obstructive Pulmonary Disease] The Merck Manual of Geriatrics
- [http://www.lungsonline.com/bronchitis.html Bronchitis ] Lungs OnLine
- [http://familydoctor.org/677.xml Acute Bronchitis] FamilyDoctor.org (American Academy of Family Physicians)

References

- "Chronic bronchitis." Springhouse Handbook of Diagnostic Tests, 2nd ed. (1999). ISBN 0-87434-982-6
- "Chronic obstructive pulmonary disease." 2005 Current Medical Diagnosis and Treatment. ISBN 0-07-143692-8
- Kumar, Vinay, Abul Abbas, and Nelson Fausto. Robbins and Cotran Pathologic Basis of Disease, 7th ed. (2005). ISBN 0-7216-0187-1
- Skinner, Henry Alan. The Origin of Medical Terms. (1970). Category:Pulmonology

Lung Disease

In medicine, pulmonology (aka pneumology) is the specialty that deals with diseases of the lungs and the respiratory tract. It is called chest medicine and respiratory medicine in some countries and areas. Pulmonology is generally considered a branch of internal medicine, although it is closely related to intensive care medicine when dealing with patients requiring mechanical ventilation. Surgery of the respiratory tract is generally performed by specialists in cardiothoracic surgery (or thoracic surgery). Chest medicine is not a specialty in itself but is an inclusive term which pertains to the treatment of diseases of the chest and contains the fields of pulmonology, thoracic surgery, and intensive care medicine. Pulmonology is concerned with the diagnosis and treatment of lung diseases, as well as secondary prevention (tuberculosis). Physicans specializing in this area are called pulmonologists.

Diagnosis

In medicine, 50% of all diagnoses can be made by a thorough medical history, and lung diseases are no different. The pulmonologist will conduct a general review and focus on:
- hereditary diseases affecting the lungs (cystic fibrosis, alpha 1-antitrypsin deficiency)
- exposure to toxins (tobacco smoke, asbestos, exhaust fumes, coal mining fumes)
- exposure to infectious agents (certain types of birds, malt processing)
- an autoimmune diathesis that might predispose to certain conditions (pulmonary fibrosis, pulmonary hypertension) Physical diagnostics are as important as in the other fields of medicine.
- Inspection of the hands for signs of cyanosis or clubbing, chest wall, and respiratory rate.
- Palpation of the cervical lymph nodes, trachea and chest wall movement.
- Percussion of the lung fields for dullness or hyperresonance.
- Auscultation (with a stethoscope) of the lung fields for diminished or unusual breath sounds. As many heart diseases can give pulmonary signs, a thorough cardiac investigation is usually included. Other tools include: -
- Laboratory investigation of blood (blood tests). Sometimes arterial blood gas measurements are also required.
- Spirometry (the determination of lung volumes in time by breathing into a dedicated machine; response to bronchodilatators and diffusion of carbon monoxide)
- Bronchoscopy with bronchoalveolar lavage (BAL), biopsy and epithelial brushing
- Chest X-rays
- CT scanning (MRI scanning is rarely used)
- Scintigraphy and other methods of nuclear medicine
- Positron emission tomography (especially in lung cancer)

Treatment

Surgical treatment in generally performed by the (cardio)thoracic surgeon, generally after primary evaluation by a pulmonologist. Medication is the most important treatment of most diseases of pulmonology, either by inhalation (bronchodilators and steroids) or in oral form (antibiotics, leukotriene antagonists). Oxygen therapy is often necessary in severe respiratory disease (emphysema and pulmonary fibrosis). When this is insufficient, the patient might require mechanical ventilation.

Training

Pulmonologists are physicians who after receiving a medical degree MD or DO complete residency training in internal medicine (3 years) followed by at least 2 additional years of subspeciality fellowship training in pulmonology.

Diseases managed by the pulmonologist

- Asthma
- Chronic obstructive pulmonary disease: -
- Chronic bronchitis
- Emphysema
- Cystic fibrosis (adults)
- Lung cancer diagnosis
- Pneumoconiosis
- Pneumonia
- Pneumothorax
- Psittacosis
- Pulmonary embolism
- Pulmonary fibrosis
- Pulmonary hypertension
- Pulmonary sequestration
- Sarcoidosis
- Sleep apnea or restless legs syndrome

Scientific research

Pulmonologists are involved in both clinical and basic research of the respiratory system, ranging from the anatomy of the bronchial epithelium to the most effective treatment of pulmonary hypertension (a disease notoriously resistant to therapy). ja:呼吸器学

Bronchi

A bronchus (plural bronchi, adjective bronchial) is a caliber of airway in the respiratory tract that conducts air into the lungs. No gas exchange takes place in this part of the lungs.

Anatomy

The trachea (windpipe) divides into two main bronchi, the left and the right, at the level of the sternal angle. The right main bronchus is wider, shorter, and more vertical than the left main bronchus. The main bronchi subdivide into two and three secondary bronchi that each serve the left and right lungs, respectively. The lobar bronchi divide into tertiary bronchi. Each of the segmental bronchi supplies a bronchopulmonary segment. A bronchopulmonary segment is a division of a lung that is separated from the rest of the lung by a connective tissue septum. This property allows a bronchopulmonary segment to be surgically removed without affecting other segments. The segmental bronchi divide into many primary bronchioles which divide into terminal bronchioles, each of which then gives rise to several respiratory bronchioles, which go on to divide into 2 to 11 alveolar ducts. There are 5 or 6 alveolar sacs associated with each alveolar duct. The alveolus is the basic anatomical unit of gas exchange in the lung. There is hyaline cartilage present in the bronchi, present as irregular rings in the larger bronchi (and not as regular as in the trachea), and as small plates and islands in the smaller bronchi. Smooth muscle is present continuously around the bronchi.

Role in disease

Bronchitis is viral or bacterial infection of the bronchi. Asthma is hyperreactivity of the bronchi with an inflammatory component, often in response to allergens. Chronic bronchitis (COPD) is smoking- or coal dust-induced chronic inflammation of the bronchi that leads to obstruction of the airways.

References

- Moore, Keith L. and Arthur F. Dalley. Clinically Oriented Anatomy, 4th ed. (1999). ISBN 0-7817-5936-6 Category:Respiratory system Category:Thorax

Lung

The lung is the essential organ of respiration in air-breathing vertebrates. Its principal function is to transport oxygen from the atmosphere into the bloodstream, and excrete carbon dioxide from the bloodstream into the atmosphere. This it accomplishes with its mosaic of specialized cells that form millions of tiny, exceptionally thin-walled air sacs where gas exchange takes place. Lungs also have nonrespiratory functions. Medical terms related to the lung often begin with pulmo-, from the Latin pulmonarius ("of the lungs"), cognate with the Greek pleumon ("lung").

The respiratory function of the lung

Energy production in living organisms often uses oxygen and produces carbon dioxide. Hence, life necessitates an efficient means of oxygen delivery to cells and carbon dioxide excretion from cells. In smaller organisms, such as single-celled bacteria, this process of gas exchange can take place entirely by simple diffusion. In larger organisms this is not possible; only a small prportion of cells are situated close enough to the surface for oxygen from the atmosphere to enter them through diffusion. Two major adaptations made it possible for organisms to attain great multicellularity: an efficient circulatory system that conveyed gases to and from the deepest tissues in the body, and a large respiratory system that centralized the task of obtaining oxygen from the atmosphere and bringing it into the body, whence it could rapidly be distributed to all tissues via the circulatory system. In air-breathing vertebrates, respiration occurs in a series of steps. Air is brought into the animal via the airways — in reptiles, birds and mammals this often consists of the nose, the pharynx, the larynx, the trahea, the bronchi and bronchioles, and the terminal branches of the respiratory tree. The lungs of these animals are a rich lattice of alveoli, which provide an enormous surface area for gas exchange. A network of fine capillaries transports blood over the surface of alveoli. Oxygen from the air inside the alveoli diffuses into the bloodstream across the exceptionally thin alveolar membranes, and carbon dioxide moves from the blooood to the alveoli via the same process. The drawing and explosion of air is driven by muscular action; in early tetrapods, air was driven into the lungs by the pharyngeal muscles, whereas in reptiles, birds and mammals a more compliclated musculo-skeletal system is used. In the mammal, a large muscle, the diaphragm (in addition to the internal intercostal muscles), drive ventilation by periodically altering the intra-thoracidc volume and pressure; by increasing volume and decreasing pressure, air is sucked into the airways, and by reducing volume and increasing pressure, the reverse occurs. During normall breathing, expiration is passive and no muscles are contracted (the diaphragm relaxes).

Nonrespiratory functions of the lung

In addition to respiratory functions such as gas exchange and regulation of hydrogen ion concentration, the lungs also:
- influence the concentration of biologically active substances and drugs used in medicine in arterial blood
- filter out small blood cots formed in the systemic veins
- serve as a physical layer of soft, shock-absorbent protection for the heart, which the lungs flank and nearly enclose.

Mammalian lungs

The lungs of mammals have a spongy texture and are honeycombed with epithelium having a much larger surface area in total than the outer surface area of the lung itself. The lungs of humans are typical of this type of lung. The environment of the lung is very moist, which makes it a hospitable environment for bacteria. Many respiratory illnesses are the result of bacterial or viral infection of the lungs. Breathing is largely driven by the diaphragm below, a muscle that by contracting expands the cavity in which the lung is enclosed. The rib cage itself is also able to expand and contract to some degree. As a result, air is sucked into and pushed out of the lungs through the trachea and the bronchial tubes or bronchi; these branch out and end in alveoli which are tiny sacs surrounded by capillaries filled with blood. Here oxygen from the air diffuses into the blood, where it is carried by hemoglobin. The deoxygenated blood from the heart reaches the lungs via the pulmonary artery and, after having been oxygenated, returns via the pulmonary veins. pulmonary vein

Anatomy

pulmonary vein The lungs are located inside the thoracic cavity, protected by the bony structure of the rib cage and enclosed by a double-walled sac called pleura. The inner layer of the sac (visceral pleura) adheres tightly to the lungs and the outer layer (parietal pleura) is attached to the wall of the chest cavity. The two layers are separated by a thin space called the pleural cavity that is filled with pleural fluid; this allows the inner and outer layers to slide over each other, and prevents them from being separated easily. The left lung is smaller than the right one to give way for the heart. The lungs attach to the heart and trachea through structures that are called the "roots of the lungs." The roots of the lungs are the bronchi, pulmonary vessels, bronchial vessels, lymphatic vessels, and nerves. These structures enter and leave at the hilus of the lung. The lungs are divided into lobes by the horizontal and oblique fissures. The right lung has three lobes and the left lung has two. A unique feature of the left lung is the cardiac notch, which helps create the lingula (Latin for "tongue") of the left lung. The lungs are connected to the upper airway by the trachea and bronchi. The trachea runs down the neck and divides into left and right bronchi behind the sternal angle. The right main bronchus is shorter and runs more vertically than the left. For this reason, it is more common to aspirate foreign objects into the right lung. The bronchi enter the lung and branch out to form the bronchial tree. The bronchi divide into smaller bronchioles, which terminate into alveoli. An alveolus is composed of respiratory tissue and is the site of gas exchange in the lung. The blood supply to the lungs is from two sources: the pulmonary vessels and the bronchial vessels. The bronchial vessels support the nonrespiratory tissue and the pulmonary vessels provide support to the respiratory tissue. The pulmonary arteries carry deoxygenated blood that has returned to the heart from the venous system to the lungs to be reoxygenated. The pulmonary veins carry oxygenated blood back to the heart to go to the arterial system. The right and left pulmonary arteries arise from the pulmonary trunk and carry "venous" blood to their respective lungs. The pulmonary veins, two on each side, carry "arterial" blood to the left atrium of the heart. The bronchial arteries that supply the nonrespiratory tissue of the lung arise from different sources. The left bronchial arteries come off of the thoracic aorta, however, the right bronchial artery has a variable source.

Avian lungs

Birds have a complex but highly efficient crosscurrent exchange system in their lungs, accompanied by air sacs to control the flow of gas through it. See bird respiration for a detailed account of this system. The lungs of birds differ significantly from those of mammals. In addition to the lungs themselves, birds have posterior and anterior air sacs (typically nine) which control air flow through the lungs, but do not play a direct role in gas exchange. They have a flow-through respiration system. When a bird inhales, air flows in through the trachea to the posterior air sacs, while air currently within the lungs flows into the anterior air sacs. When the bird exhales, the fresh air now contained within the posterior air sacs is driven into the lungs, and the stale air now contained within the anterior air sacs is expelled through the trachea and into the atmosphere. Two complete cycles of inhalation and exhalation are, therefore, required for one breath of air to make its way through the avian respiratory system. Avian lungs do not have alveoli, as mammalian lungs do, but instead contain millions of tiny passages known as parabronchi, connected at either ends by the dorsobronchi and ventrobronchi. Air flows through the honeycombed walls of the parabronchi and into air capillaries, where oxygen and carbon dioxide are traded with cross-flowing blood capillaries by diffusion, a process of crosscurrent exchange. The purpose of this complex system of air sacs is to ensure that the airflow through the avian lung is always traveling in the same direction - posterior to anterior. This is in contrast to the mammalian system, in which the direction of airflow in the lung is tidal, reversing between inhalation and exhalation. By utilizing a unidirectional flow of air, avian lungs are able to extract a greater concentration of oxygen from inhaled air. Birds are thus equipped to fly at altitudes at which mammals would succumb to hypoxia.

Reptilian lungs

Reptilian lungs are typically ventilated by a combination of expansion and contraction of the ribs via axial muscles and buccal pumping. Crocodilians also rely on the hepatic piston method, in which the liver is pulled back by a muscle anchored to the pubic bone (part of the pelvis), which in turn pulls the bottom of the lungs backward, expanding them.

Amphibian lungs

The lungs of most frogs and other amphibians are simple balloon-like structures, with gas exchange limited to the outer surface area of the lung. This is not a very efficient arrangement, but amphibians have low metabolic demands and also frequently supplement their oxygen supply by diffusion across the moist outer skin of their bodies.

Arachnid lungs

Spiders have structures called "book lungs", which are not evolutionarily related to vertebrate lungs but serve a similar respiratory purpose.

Crustacean lungs

The Coconut crab uses structures called branchiostegal lungs to breathe air, and indeed will drown in water.

Origins

The lungs of vertebrates are closely related (i.e. homologous) to the gas bladders of fish (but not to their gills). The evolutionary origin of both are thought to be outpocketings of the upper intestines. This is reflected by the fact that the lungs of a fetus also develop from an outpocketing of the upper intestines (see ontogeny and phylogeny). The article on swim bladders contains further details about the origin of these two organs.

External links

- [http://www.leeds.ac.uk/chb/lectures/anatomy7.html Dr D.R. Johnson: Introductory anatomy, respiratory system]
- [http://sln.fi.edu/biosci/systems/respiration.html Franlink Institute Online: The Respiratory System]
- [http://www.lungsonline.com Lungs OnLine]
- [http://news.bbc.co.uk/2/hi/health/3951797.stm Lungs 'best in late afternoon'] category:Respiratory system Category:Thorax Category:Cardiovascular system ms:Paru-paru ja:肺

Chronic

: For chronic in the context of Cannabis see list of street names of drugs and Wiktionary: Cannabis slang. The word chronic comes from chronos, the ancient Greek god of time.

Medicine

In medicine, a chronic disease is a persistent and lasting condition. More accurately, the chronic disease has a chronic course. Chronicity is usually defined as lasting more than three months. A chronic course must be differentiated from a recurrent course, where the disease relapses repeatedly, the relapses being separated by periods of temporary remission. The chronic course is often part of the definition of a disease and, therefore, often included in its name, for example:
- Chronic obstructive pulmonary disease
- Chronic fatigue syndrome
- Chronic hepatitis
- Chronic leukemia

Music

- A 1992 album by Dr. Dre called The Chronic.
- A 1999 album by Dr. Dre called 2001 (originally to be called The Chronic 2001).

Sputum

Sputum is matter that is coughed up from the respiratory tract, such as mucus or phlegm, mixed with saliva and then expectorated from the mouth. It can also contain pus, blood, fibrin, bacterial products or other foreign matter. A sputum sample is the name given to the mucus that is coughed up from the lower airways. It is usually used for microbiological investigations of respiratory infections. The best sputum samples contain very little saliva, as this contaminates the sample with oral bacteria. When a sputum specimen is plated out, it is best to get the portion of the sample that most looks like pus onto the swab. If there is any blood in the sputum, this should also be on the swab. Microbiological sputum samples are usually used to look for infections by Branhamella catarrhalis, Streptococcus pneumoniae and Haemophilus influenzae. Other pathogens can also be found.

Sputum

Dyspnea

Dyspnea (Latin dyspnoea, Greek dyspnoia from dyspnoos - short of breath) or shortness of breath (SOB) is perceived difficulty breathing or pain on breathing. It is a common symptom of numerous medical disorders.

Causes

- disorders within the lungs
- pulmonary hypertension
- atelectasis
- disorders in the ribcage
- kyphosis
- disorders in adjacent organs
- disorders in the nervous system
- disorders due to drugs and toxic substances.
- SARS
- Broncho-obstructive conditions
- emphysema
- COPD
- asthma
- broken ribs
- lung cancer
- malignant hypertension
- obesity
- patent ductus arteriosus

Related terms

- tachypnea, too-rapid breathing.
- bradypnea, too-slow breathing.
- orthopnea, dyspnea occurring in a recumbent position
- paroxysmal nocturnal dyspnea, dyspnea occurring during sleep. Category:Pulmonology Category:Symptoms ja:呼吸困難

Hypercapnia

Hypercapnia (from the Greek hyper = "above" and kapnos = "smoke") is a condition where there is too much carbon dioxide (CO₂) in the body. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs. Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of CO₂ (usually due to volcanic or geothermal causes), or by rebreathing exhaled carbon dioxide. Symptoms of early hypercapnia (i.e. where PaCO₂ is elevated but not extremely so) include flushed skin, full pulse, extrasystoles, muscle twitches, hand flaps, and possibly a raised blood pressure. In severe hypercapnia (generally PaCO₂ greater than 10kPa or 75mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death. In rebreather diving, this effect is sometimes called shallow-water blackout. In closed circuit SCUBA (rebreather) diving, exhaled carbon dioxide must be removed from the breathing system, usually by a scrubber containing a solid chemical compound with a high affinity for CO₂. If not removed from the system, it may be re-inhaled, causing an increase in the inhaled concentration.

Carbon dioxide poisoning during diving

There are a variety of reasons for CO2 retention where carbon dioxide is not being expelled completely when the diver exhales:
- The diver is exhaling into a vessel with inadequate ventilation, such as a long snorkel, full face diving mask, or diving helmet, and then re-inhaling from that vessel.
- The scrubber in the rebreather the diver is failing to remove sufficient carbon dioxide from the loop.
- The diver is overexerted, producing excess CO₂ due to elevated metabolic activity.
- The density of the breathing gas is higher at depth, so the effort required to fully inhale and exhale has increased, making breathing more difficult and less efficient.
- The diver is deliberately hypoventilating, or "skip breathing," a technique which conserves breathing gas with open-circuit scuba but should not be done with a rebreather. (On top of the risk of burst lung from holding the breath while ascending.)

References

- [http://answers.google.com/answers/threadview?id=197162 CO2 Effects on Humans] category:diving medicine category:pulmonology

Hypoxemia

Hypoxemia or reduced oxygen in the blood, can be caused by: 1. Low partial pressure of atmospheric oxygen (e.g., high altitudes) 2. Inadequate pulmonary ventilation (e.g., chronic obstructive pulmonary disease) 3. Carbon monoxide poisoning 4. Reduced hemoglobin content in erythrocytes 5. Decreased hematocrit

Cyanosis

Cyanosis refers to the bluish coloration of the skin due to the presence of deoxygenated hemoglobin in blood vessels near the skin surface.

Types

It can occur in the fingers, including underneath the fingernails, as well as other extremities (called peripheral cyanosis), or in the lips and face (central cyanosis).

Central cyanosis

Central cyanosis suggests a circulatory or ventilatory problem that leads to poorer blood oxygenation in the lungs or greater oxygen extraction due to slowing down of blood circulation in the skin's blood vessels. Acute cyanosis can be a result of asphyxiation or choking, and is one of the surest signs that respiration is being blocked. The elementary principle behind cyanosis is that oxygenated hemoglobin is red, while deoxygenated hemoglobin is blue. Thus oxygen deficiency - hypoxia - leads to blue discoloration of the lips and other mucus membranes.

Peripheral cyanosis

Peripheral cyanosis suggests that there is poor circulation in the small vessels involved, such as when a person's hands are very cold. However, this condition can also be permanent even in normal temperatures; see acrocyanosis.

External links

- [http://www.emedicine.com/med/topic3002.htm eMedicine]
- [http://skin-care.health-cares.net/cyanosis.php Health-cares.net]
- [http://www.tmc.edu/thi/cyanosis.html Texas Heart Institute] Category:Sign (medicine)

Cor pulmonale

Cor pulmonale is a medical term used to describe a failure of the right side of the heart. It is caused by prolonged high blood pressure in the right ventricle of the heart, which in turn is most often caused by pulmonary hypertension - prolonged high blood pressure in the arteries or veins of the lungs. People with heart disease, or lung diseases such as cystic fibrosis, are at greater risk.

Pathophysiology

There are several mechanisms leading to pulmonary hypertension and cor pulmonale:
- Pulmonary vasoconstriction
- Anatomic changes in vascularisation
- Increased blood viscosity
- Primary pulmonary hypertension

Causes

- Acute:
- Massive pulmonary embolization
- Exacerbation of chronic cor pulmonale
- Chronic:
- COPD
- Loss of lung tissue following trauma or surgery

Treatment

Elimination of the cause is the most important intervention. In pulmonary embolism, thrombolysis (enzymatic dissolution of the blood clot) is advocated if there is dysfunction of the right ventricle. In COPD, long-term oxygen therapy may improve cor pulmonale. Cor pulmonale may lead to congestive heart failure (CHF), with worsening of respiration due to pulmonary edema, swelling of the legs due to peripheral edema and painful congestive hepatomegaly. This situation requires diuretics (to decrease strain on the heart), sometimes nitrates (to improve blood flow) and occasionally inotropes (to improve heart contractility). CHF is a negative prognostic indicator in cor pulmonale.

External links

- The Merck Manual of Diagnosis and Therapy: [http://www.merck.com/mrkshared/mmanual/section16/chapter203/203c.jsp Cor Pulmonale] Category:Cardiology Category:Pulmonology

Heart failure

Congestive heart failure (CHF) (also called congestive cardiac failure and heart failure) is the inability of the heart to pump a sufficient amount of blood throughout the body, or requiring elevated filling pressures in order to pump effectively. CHF is an abnormal cardiac condition that reflects impaired cardiac pumping and blood flow. The pooling of blood leads to congestion in body tissue. The term heart failure is frequently misused, especially when given as cause of death: it is not synonymous with "cessation of heartbeat" – for which see cardiac arrest. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure".

Classification

There are many different ways to categorize heart failure, including:
- the side of the heart involved, (left heart failure versus right heart failure)
- whether the abnormality is due to contraction or relaxation of the heart (systolic heart failure vs. diastolic heart failure) The NYHA functional class is a commonly used way to gauge the progression of CHF in a particular patient. This classification is used to determine how much CHF limits their lifestyle, and does not apply to a particular decompensated episode.

Symptoms and signs

Signs of decompensated heart failure include pulmonary edema (fluid accumulation in the lungs), peripheral edema (fluid build-up in dependent portions of the body). Other physical examination findings include rales heard on chest auscultation, an enlarged or pulsatile liver, and jugular venous distension. Symptoms of decompensated heart failure include dyspnea (shortness of breath) on exertion, orthopnea (dyspnea that increases upon lying down), fatigue and paroxysmal nocturnal dyspnea ("cardiac asthma", shortness of breath that occurs hours or minutes after lying down).

Treatment

Individuals with heart failure are sensitive to small shifts in their intravascular volume status (the amount of fluid in their circulatory system). Increasing the volume in their circulatory system can cause symptoms and signs of decompensated heart failure, while decreasing the volume in the circulatory system can cause hypotension. The treatment of CHF focuses on treating the symptoms and signs of CHF and preventing the progression of disease. If there is a reversible cause of the heart failure (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, or hypertension), that should be addressed as well.

Medication

Treating the signs and symptoms of CHF involves maintaining a euvolemic state (normal fluid level in the circulatory system). This is done with the judicious use of diuretic agents, vasodilator agents, and positive inotropes. Delaying the progression of heart failure involves the use of ACE inhibitors, beta blockers, and aldosterone inhibitors. These agents have been proven to improve survival in individuals with CHF. While the mechanism of improving is not entirely clear, it appears that these agents prevent remodelling of the heart and therefore prevent progression of dilatation of the left ventricle.

Devices and surgery

Patients with NYHA class III or IV, LVEF of 35% or less and a QRS interval of 120ms or more may benefit from bi-ventricular pacemaker (CRT) placement or surgical remodelling of the heart. These treatment modalities may make the patient symptomatically better, improving quality of life and in some trials have been proven to reduce mortality. In the recently completed COMPANION trial, cardiac resynchronization therapy (pacing the left ventricle as well as the right ventricle) has been shown to improve survival in individuals with NYHA class III or IV heart failure with a widened QRS complex on EKG.² The CARE-HF trial, showed that patients receiving a Medtronic bi-ventricular pacemaker (CRT) and optimal medical therapy benefit from a 36% reduction in all cause mortality, and a reduction in cardiovascular related hospitalization.³ Additionally, patients with NYHA class II, III or IV, LVEF of 35% (without a QRS requirement) may benefit from an Implantable Converter Defibrillator (ICD), a device that is proven to reduce all cause mortality (death) by 23% compared to placebo. This mortality benefit was observed in patients who were already optimally managed on drug therapy.⁴ Another current treatment involves the use of left ventricular assist devices (LVADs). LVADs are battery-operated mechanical pump-type devices that are surgically implanted on the upper part of the abdomen. They take blood from the left ventricle and pump it through the aorta. LVADs are becoming more common and are often used by patients who have to wait for heart transplants. Acorn Cardiovascular, based in St. Paul, Minnesota, recently created the CorCap Cardiac Support Device (CSD), also known as the "heart sock." It is a dacron mesh that is placed around the heart. The elastic CSD works by mechanically restoring the contractility of the expanded heart. The ultimate treatment is cardiac transplant surgery (heart transplant) or implantation of an artificial heart.

References

1. [http://www.acc.org/clinical/guidelines/failure/hf_index.htm ACC / AHA guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult] ([http://www.acc.org/clinical/guidelines/failure/pdfs/hf_fulltext.pdf PDF Copy]) 2. Bristow MR, Saxon LA, Boehmer J, et al for the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. [http://content.nejm.org/cgi/content/abstract/350/21/2140 N Engl J Med 2004; 350:2140-2150.] 3. Cleland JGF, Daubert J-C, Erdmann E, et al; the Cardiac Resynchronization -- Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005 March 7 [http://content.nejm.org/cgi/content/short/NEJMoa050496v1 N Engl J Med 2005; 10.1056/NEJMoa050496] 4. Bardy GH, Lee KL, Mark DB, et al for the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. [http://content.nejm.org/cgi/content/abstract/352/3/225 N Engl J Med 2005; 352:225-237] 5. Donatelle, Rebecca J. Health: The Basics. 6th ed. San Francisco: Pearson Education, Inc. 2005.

Goblet cells

Goblet cells are glandular epithelial cells that are specifically designed to secrete mucus. The term goblet refers to their cup-like shape. In a mucicarmine stains, goblet cells can be easily identified by the deep red granules found within their cell bodies. The nuclei of goblet cells tend to be displaced toward the basal end of the cell body, close to basement membrane.

Reference

For further information see
- [http://arbl.cvmbs.colostate.edu/hbooks/pathphys/misc_topics/goblets.html this paper on Goblet Cells] Category:Cell biology

Neutrophils

: neutrophil granulocyte

Bronchiole

The bronchioles are the first airway branches that no longer contain cartilage. They are branches of the bronchi, and are smaller than one millimetre in diameter. There are no glands or cartilage in any of the bronchioles, and the epithelial cells become more cuboidal in shape. Bronchioles divide until they become terminal bronchioles. After these the respiratory bronchioles have sporadic alveoli on their walls. Eventually the respiratory tract branches into alveolar ducts, then alveolar sacs. Bronchospasm, a life-threatening situation, occurs when the smooth muscular tissue of the bronchioles constricts, severely narrowing their diameter. Bronchospasm is commonly treated by oxygen therapy and bronchodilators. The medical condition of inflammation of the bronchioles is termed bronchiolitis. Diseases of the bronchioles include asthma, bronchiolitis obliterans, respiratory syncytial virus infection, and influenza. Category:Respiratory system

Expiration

In respiration, expiration is initiated by a decrease in volume and positive pressure exerted upon the intrapleural space upon diaphragm relaxation. The positive pressure generated, relative to atmospheric pressure, allows airflow from the alveoli to the mouth and outside air. Expiration has an complementary relationship to inspiration, the cycling between these two efforst define respiration. ---- Expiration (2003) is an independent feature film directed by Gavin Heffernan, and winner of the Grand Jury Prize and Best Film at the Canadian Filmmakers' Festival.

External links

- [http://www.grobys.de/Expiration/ Expiration - official website]
- [http://www.imdb.com/title/tt0382680/ Expiration at IMDb.com] Category:Canadian films

Sputum culture

A sputum culture is a test to detect and identify bacteria or fungi that are infecting the lungs or breathing passages. Sputum is a thick fluid produced in the lungs and in the airways leading to the lungs. A sample of sputum is placed in a container with substances that promote the growth of bacteria or fungi. If no bacteria or fungi grow, the culture is negative. If organisms that can cause infection (pathogenic organisms) grow, the culture is positive. The type of bacterium or fungus will be identified with a microscope or by chemical tests. If bacteria or fungi that can cause infection grow in the culture, other tests may be done to determine which antibiotic will be most effective in treating the infection. This is called susceptibility or sensitivity testing. This test is done on a sample of sputum that is usually collected by coughing. For people who cannot cough deeply enough to produce a sample, a suction tube or needle may be inserted in the airway to collect the sputum.

Chest X-ray

A chest X-ray is a radiological film obtained by X-ray taken of the thorax which is used to diagnose problems with that area. Examples of such problems include but are not limited to:
- tension pneumothorax
- rib fracture
- pneumonia Chest X-Rays are among the most common films taken, being diagnostic of so many important problems.

External links

- [http://www.med-ed.virginia.edu/courses/rad/cxr/index.html Introduction to chest radiology: a tutorial for learning to read a chest x-ray] Category:Radiology

Pulmonary function test

Spirometry (meaning the measuring of breath) is the most common of the Pulmonary Function Tests (PFTs), measuring lung function, specifically the measurement of the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled. Spirometry is an important tool used for assessing conditions such as asthma, cystic fibrosis, and COPD. Spirometric maneuvers include slow vital capacity (SVC), forced vital capacity (FVC), tidal volume (TV) and maximum voluntary ventilation (MVV). The measurement of forced vital capacity is the most commonly performed maneuver, sometimes in conjunction with slow vital capacity and/or tidal volume. A plethysmograph can be used to measure functional residual capacity (FRC). Results are usually given in both raw data (liters, liters per second) and percent predicted - the test result as a percent of the "predicted values" for the patients of similar characteristics (height, weight, age, sex, and sometimes race). The interpretation of the results can vary depending on the physician and the source of the predicted values, but generally speaking, results nearest to 100% predicted are the most normal, and generally results over 80% are often considered normal. However, review by a doctor is necessary for accurate diagnosis of any individual situation. The spirometry test is performed using a device called a spirometer, which comes in many different varieties. Many produce a graph called a Flow-Volume Loop, which graphically depicts the flow of air compared to the total volume inspired or expired. Flow is listed along the Y-Axis and volume along the X-Axis. Most spirometers also display a Volume-Time curve, showing volume (liters) along the Y-Axis and time (seconds) along the X-Axis (not shown). plethysmograph The basic FVC test varies slightly depending on the equipment used. Generally, the patient is asked to take the deepest breath they can, and then exhale into the sensor as hard as possible, for as long as possible. It is sometimes directly followed by a rapid inhalation (inspiration), in particular when assessing possible inspiratory obstruction or restriction. Sometimes, the test will be preceded by a period of quiet breathing in and out from the sensor (tidal volume), or the rapid breath in (forced inspiratory part) will come before the forced exhalation. During the test, soft nose clips may be used to prevent air escaping through the nose. Filter mouthpieces may be used to prevent the spread of germs, particularly for inspiratory maneuvers. The maneuver is highly dependant on patient cooperation and effort, and is normally repeated at least three times to ensure reproducibility. Since results are dependent on patient cooperation, FEV₁ and FVC can only be underestimated, never overestimated. Sometimes, to assess the reversibility of a particular condition, a bronchodilator is administered before performing another round of tests for comparison. This is commonly referred to as a reversibility test, or a post bronchodilation test (Post BD), and is an important part in diagnosing asthma versus COPD. The most commonly used guidelines for spirometric testing and interpretation are set by the [http://www.thoracic.org/ American Thoracic Society] (ATS) and the [http://ersnet.org/ers/ European Respiratory Society] (ERS). Spirometry can also be part of a bronchial challenge test, used to determine bronchial hyperresponsiveness to either rigorous exercise, inhalation of cold/dry air, or with a pharmaceutical agent such as metacholine or histamine. Due to the patient cooperation required, spirometry can only be used on children old enough to comprehend and follow the instructions given (typically about 4-5 years old), and only on patients that are able to understand and follow instructions - thus, this test is not suitable for patients that are unconscious, heavily sedated, or have limitations that would interfere with vigorous respiratory efforts. Other types of PFTs are available for infants and unconscious persons.

Explanation of Common Test Values in FVC Tests

- FVC: Forced Vital Capacity - This is the total amount of air that you can forcibly blow out after full inspiration, measured in liters.
- FEV₁: Forced Expiratory Volume in 1 Second - This is the amount of air that you can forcibly blow out in one second, measured in liters. Along with FVC it is considered one of the primary indicators of lung function.
- FEV₁ / FVC - This is the ratio of FEV 1 and FVC, which showing the amount of the FVC that can be expelled in one second. In healthy adults this should be approximately 80%.
- PEF: Peak Expiratory Flow - This is the speed of the air moving out of your lungs at the beginning of the expiration, measured in liters per second.
- FEF 25-75% or 25-50%: Forced Expiratory Flow 25-75% or 25-50% - This is the average flow (or speed) of air coming out of the lung during the middle portion of the expiration (also sometimes referred to as the MMEF, for maximal mid-expiratory flow).
- FIF 25-75% or 25-50%: Forced Inspiratory Flow 25%-75% or 25%-50% - This is similar to FEF 25%-75% or 25%-50% except the measurement is taken during inspiration.
- FET: Forced Expiratory Time - This measures the length of the expiration in seconds.

Technologies Used in Spirometers Over the Years

- Volumetric Spirometers
- Water bell
- Bellows wedge
- Flow measuring Spirometers
- Fleisch-pneumotach
- Lilly (screen) pneumotach
- Turbine
- Pitot tube
- Hot-wire anemometer
- Ultrasound

External links

- [http://www.spirxpert.com/ Detailed information on spirometric testing, interpretation and physiology]
- [http://medizin.li/spirometer/spirometer-history.html History of spirometers and lung function testing]
- [http://www.spirometrie.info/en/ General information on spirometry] category:pulmonology category:physiology

Diaphragm

A diaphragm is some sort of separating membrane. This gives rise to several meanings:
- diaphragm (acoustics), a thin, semi-rigid membrane attached to the central magnet that produces sound in a loudspeaker
- diaphragm (anatomy), a shelf of muscle extending across the bottom of the ribcage of mammals
- diaphragm (contraceptive), a small rubber dome placed in the vagina to wall off the cervix, thus preventing sperm from entering
- diaphragm (mechanics), a sheet of a semi-flexible material anchored at its periphery
- diaphragm (optics), an opening in the lightpath of a lens or objective that can regulate the amount of light that passes
- Diaphragm seal

Bronchi

A bronchus (plural bronchi, adjective bronchial) is a caliber of airway in the respiratory tract that conducts air into the lungs. No gas exchange takes place in this part of the lungs.

Anatomy

Role in disease

References

- Moore, Keith L. and Arthur F. Dalley. Clinically Oriented Anatomy, 4th ed. (1999). ISBN 0-7817-5936-6 Category:Respiratory system Category:Thorax

Inflammation

Inflammation is the first response of the immune system to infection or irritation and may be referred to as the innate cascade. Inflammation is characterized by the following quintet: redness (rubor), heat (calor), swelling (tumor), pain (dolor) and dysfunction of the organs involved (functio laesa). The first four characteristics have been known since ancient times and are attributed to Celsus; functio laesa was added to the definition of inflammation by Rudolf Virchow in 1858.

Characteristics

Inflammation has two main components - cellular and exudative. The exudative component involves the movement of fluid, usually containing many important proteins such as fibrin and immunoglobulins (antibodies). Blood vessels are dilated upstream of an infection (causing redness and heat) and constricted downstream while capillary permeability to the affected tissue is increased, resulting in a net loss of blood plasma into the tissue - giving rise to edema or swelling. The swelling distends the tissues, compresses nerve endings, and thus causes pain. The cellular component involves the movement of white blood cells from blood vessels into the inflamed tissue. The white blood cells or leucocytes take on an important role in inflammation; they extravasate from the capillaries into tissue, and act as phagocytes, picking up bacteria and cellular debris. They may also aid by walling off an infection and preventing its spread. If inflammation of the affected site persists, released cytokines IL-1 and TNF will activate endothelial cells to upregulate receptors VCAM-1, ICAM-1, E-selectin, and L-selectin for various immune cells. Receptor upregulation increases extravasation of neutrophils, monocytes, activated T-helper and T-cytotoxic, and memory T and B cells to the infected site. Neutrophils are characteristic of inflammation - they are the first cells to appear in an infected area, and any section of inflamed tissue viewed under a microscope will appear packed with them. They are easily identified by their multilobed nuclei and granular cytoplasm and perform many important functions, including phagocytosis and the release of extracellular chemical messengers.

Leukocytes and cytokines

Various leukocytes are involved in the initiation and maintenance of inflammation. These cells can be further stimulated to maintain inflammation through the action of adaptive cascade through lymphocytes: T cells, B cells, and antibodies. These inflammation cells are:
- Mast cells which release histamine and prostaglandin in response to activation of stretch receptors. This is especially important in cases of trauma.
- Macrophages which release TNF-α, IL-1 in response to activation of toll-like receptors.

Outcomes

The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred, and the injurious agent that is causing it. There are three possible results to inflammation:
- Resolution, the complete reconstitution of damaged tissue, does not usually occur in the body.
- Connective tissue scarring. Some 24 hours after inflammation in a wound first occurs, the wound healing response will commence. This response involves the formation of connective tissue to bridge the gap caused by injury, and the process of angiogenesis, the formation of new blood vessels, to provide nutrients to the newly formed tissue. Often healing can not occur completely and a scar will form; for example after laceration to the skin, a connective tissue scar results which does not contain any specialized structures such as hair or sweat glands.
- Ongoing or chronic inflammation. If the injurious agent continues, chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterized by a dominating presence of macrophages in the injured tissue, which extravasate via the same methods discussed above (ICAM-1 VCAM-1). These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. This is why chronic inflammation is almost always accompanied by tissue destruction. Finally, an abscess, or a collection of pus, can form in chronic inflammation.

Systemic inflammation

Sepsis

When inflammation overwhelms the whole organism, systemic inflammatory response syndrome (SIRS) is diagnosed. When it is due to infection, the term sepsis is applied. Vasodilation and organ dysfunction are serious problems that may lead to septic shock and death.

Low-grade

With the discovery of interleukins, another concept of systemic inflammation developed. Although the processes involved are identical, this form of inflammation is not confined to a particular tissue but involves the endothelium (lining of blood vessels) and many other organ systems. High levels of several inflammation-related markers such as IL-6, IL-8, and TNF-α are associated with obesity [http://jcem.endojournals.org/cgi/content/full/85/9/3338?ijkey=c94031a625120a7e59ea52e88137260e974cee3a][http://jcem.endojournals.org/cgi/content/full/86/12/5864?ijkey=838bb038c4e311324ab354c88ea16afe51d6e823]. These levels are reduced in association with increased levels of antiinflammatory molecules within four weeks after patients begin a very low calorie diet [http://www.fasebj.org/cgi/content/full/18/14/1657]. The role of systemic inflammation as a cause and/or result of insulin resistance and atherosclerosis is the subject of intense research. It has little direct bearing on clinical care.

Inflammation examples

Inflammation is usually indicated by adding the suffix "-itis", as shown below. However, some conditions such as asthma do not follow this convention.
- appendicitis: appendix
- arteritis: arteries
- arthritis: joint
- blepharitis: eyelids
- bronchiolitis: bronchioles
- bronchitis: bronchi
- bursitis: bursa
- cervicitis: cervix
- cholecystitis: gall bladder
- colitis: colon
- conjunctivitis: conjunctiva
- dermatitis: skin
- dermatomyositis: skin and muscles
- encephalitis: brain
- endocarditis: endocardium
- endometritis: lining of the uterus
- enteritis: small intestine
- enterocolitis: small intestine and large intestine
- epicondylitis: epicondyle
- epididymitis: epididymis
- fasciitis: fascia
- fibrositis: fibrous connective tissue
- gastritis: stomach
- gastroenteritis: stomach and small intestine
- gingivitis: gingiva
- ileitis: ileum
- iritis: iris
- laryngitis: larynx
- meningitis: meninges
- myelitis: spinal cord
- myocarditis: myocardium
- nephritis: kidney
- omphalitis: umbilical cord
- orchitis: testicles
- otitis: ear
- pancreatitis: pancreas
- parotitis: parotid gland
- pericarditis: pericardium
- pharyngitis: pharynx
- pleuritis: pleura
- phlebitis: veins
- pneumonitis: lungs (also pneumonia)
- proctitis: rectum
- rhinitis: nasal lining
- sinusitis: sinus of the skull
- synovitis: synovial membrane
- tendonitis: tendon
- tonsillitis: tonsils
- uveitis: uvea
- vaginitis: mucosa of vagina
- vasculitis: blood vessels or lymph vessels
- vulvovaginitis: vulva and vagina Category:Pathology Category:Animal physiology Category:Symptoms ms:Keradangan ja:炎症

Oxygen therapy

Oxygen therapy is the use of oxygen as a medical treatment. It is generally used in patients with lung disease, as part of cardiopulmonary resuscitation, and experimentally to improve wound healing (Belda et al 2005).

Reference

- Belda FJ, Aguilera L, Garcia de la Asuncion J, Alberti J, Vicente R, Ferrandiz L, Rodriguez R, Company R, Sessler DI, Aguilar G, Botello SG, Orti R; Spanish Reduccion de la Tasa de Infeccion Quirurgica Group. Supplemental perioperative oxygen and the risk of surgical wound infection: a randomized controlled trial. JAMA 2005;294:2035-42. PMID 16249417. Category:Medical treatments

Pulmonary hypertension

In medicine, pulmonary hypertension (PH) or pulmonary artery hypertension (PAH) is an increase in blood pressure in the pulmonary artery or lung vasculature. Depending on the cause, it can be a severe disease with a markedly decreased exercise tolerance and right-sided heart failure. It was first identified by Dr Ernst von Romberg in 1891.

Signs and symptoms

A history usually reveals gradual onset of shortness of breath, fatigue, angina pectoris, syncope (fainting) and peripheral edema. In order to establish the cause, the physician will generally conduct a thorough medical history and physical examination. A detailed family history is taken to determine whether the disease might be familial.

Diagnosis

Normal pulmonary arterial pressure in a person living at sea level has a mean value of 12-16mmHg. Definite pulmonary hypertension is present when mean pressures at rest exceed 25 mmHg. Although pulmonary arterial pressure can be estimated on the basis of echocardiography, pressure sampling with a Swan-Ganz catheter provides the most definite measurement. Diagnostic tests generally involve blood tests, electrocardiography, arterial blood gas measurements, X-rays of the chest (generally followed by high-resolution CT scanning). A biopsy of lung tissue, angiography with endoluminal biopsy of the pulmonary artery, or biopsy of any associated skin lesions, is often attempted to obtain tissue for histopathological investigation. Clinical improvement is often measured in a "six-minute walking test", i.e. the distance a patient can walk in six minutes.

Causes and mechanisms

Pulmonary hypertension can be primary (occurring without an obvious cause) or secondary (a result of other disease processes.)

Primary PH

Primary pulmonary hypertension (PPH) is considered a genetic disorder. Certain forms of PPH have been linked to mutations in the BMPR2 gene, which encodes a receptor for bone morphogenic proteins, as well as the 5-HT(2B) gene, which codes for a serotonin receptor. Recently, characteristic proteins of human herpesvirus 8 (also known for causing Kaposi sarcoma) were identified in vascular lesions of PPH patients. However, it is not understood what roles these genes and viral particles play in PPH. PPH has also been associated to the use of appetite suppressants (e.g. Fen-phen). While genetic susceptibility to adverse drug reactions is suspected, the cause of the disease is still largely unknown. PPH is very rare but often fatal. Patients usually have no symptoms until they reach their late twenties or early thirties. It is characterized by elevated pulmonary vascular resistance attributable to the abnormal thickening of the vessel wall and narrowing of the lumen of arterioles in the lungs.

Secondary PH

Secondary pulmonary hypertension (SPH) is often due to chronic obstructive pulmonary disease (COPD). Other factors that have been linked to secondary pulmonary hypertension are:
- congenital heart disease featuring left-right shunting
- Eisenmenger's syndrome is reversal of the shunt due to pulmonary hypertension
- pulmonary embolism
- pulmonary fibrosis
- mitral regurgitation
- systemic sclerosis (scleroderma)
- portal hypertension (the "hepatopulmonary syndrome")
- sarcoidosis
- airway restrictive diseases such as asthma, chronic bronchitis,
- AIDS
- sickle-cell disease
- hypothyroidism A common consequence of chronic pulmonary hypertension is cor pulmonale (right sided heart failure) believed to be caused by the increased load on the right ventricle and atrium of the heart. A chest radiograph (X-ray) will often reveal an enlarged right atrium and ventricle, and prominent pulmonary arteries. An ECG will often demonstrate right ventricular hypertrophy or strain. Oedema and fluid retention follow.

Classification

In 2003, the 3rd World Symposium on Pulmonary Hypertension was convened in Venice to modify classification based on the new understanding of disease mechanisms. The revised system developed by this group provides the current framework for understanding pulmonary hypertension. The system includes several improvements over the former 1998 Evian Classification system. The terms "primary" and "secondary" were discontinued because they had limited diagnostic value. In addition, new classifications were added, including primary veno-occclusive disease(PVOD). Risk factor descriptions were updated, and the classification of congenital systemic-to pulmonary shunts was revised. A new classification of genetic factors in PH was recommended, but not implemented because available data were judged to be inadequate. The Venice 2003 Revised Classification system can be summarized as follows:
- WHO Group I - Pulmonary arterial hypertension(PAH)
- WHO Group II - Pulmonary hypertension with left heart disease
- WHO Group III - Pulmonary hypertension associated with lung diseases and/or hypoxemia
- WHO Group IV - Pulmonary hypertension due to chronic throbotic and/or embolic disease
- WHO Group V - Miscellaneous These terms are currently in use, but they are not yet as commonly used as the old terms of PPH and SPH.

Epidemiology

Women are almost twice as likely to present with PPH than men. The annual incidence is about 1 in 1,000,000.

Treatment

Treatment is determined by the condition underlying the cause of the hypertension. For instance, long term oxygen therapy has been proven to be useful in patients with chronic obstructive pulmonary disease, and when the pulmonary hypertension is due to chronic thromboembolism, inferior vena caval filter insertion or pulmonary endarterectomy can be performed. In PPH, lifestyle changes, digoxin, diuretics, oral anticoagulants, oxygen therapy and vasodilators are the mainstays of treatment. Synthetic prostacyclin (an eicosanoid) per continuous infusion is commonly used in PAH. Prostacyclin is available in three forms: by catheter (Flolan®), subcutaneously (Remodulin®), and recently approved is an inhaled version , iloprost (Ventavis®). There are two oral medications, bosentan (marketed as Tracleer®), an endothelin receptor antagonist and sildenafil, better known for its effects on erectile dysfunction, was approved in 2005. Two new oral medications are in the final stages of approval: sitaxsentan and ambriesatan. Pulmonary thromboendarterectomy (PTE) is a surgical procedure that is used when pharmaceutical management fails. It is the surgical removal of thrombus (clot) and the lining of the pulmonary artery; it is a large and difficult procedure which is currently performed in San Diego, California. Case series show remarkable success in selected patients.

Prognosis

Several studies have reported a mean survival of 2-3 years from time of diagnosis with the cause of death usually being right ventricular failure (cor pulmonale).

References

# Romberg E von. Über Sklerose der Lungenarterie. Dsch Arch Klin Med 1891-1892;48:197-206. # Deng Z, Morse JH, Slager SL, Cuervo N, Moore KJ, Venetos G, Kalachikov S, Cayanis E, Fischer SG, Barst RJ, Hodge SE, Knowles JA. Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene. Am J Hum Genet 2000;67:737-44. PMID 10903931. # Blanpain C, Le Poul E, Parma J, Knoop C, Detheux M, Parmentier M, Vassart G, Abramowicz MJ. Serotonin 5-HT(2B) receptor loss of function mutation in a patient with fenfluramine-associated primary pulmonary hypertension. Cardiovasc Res 2003;60(3):518-28. PMID 14659797. # Cool CD, Rai PR, Yeager ME, Hernandez-Saavedra D, Serls AE, Bull TM, Geraci MW, Brown KK, Routes JM, Tuder RM, Voelkel NF. Expression of Human Herpesvirus 8 in Primary Pulmonary Hypertension. N Engl J Med 2003;349:1113-22. PMID 13679525. # Abenhaim L, Moride Y, Brenot F, Rich S, Benichou J, Kurz X, Higenbottam T, Oakley C, Wouters E, Aubier M, Simonneau G, Begaud B. Appetite-suppressant drugs and the risk of primary pulmonary hypertension. International Primary Pulmonary Hypertension Study Group. N Engl J Med 1996;335:609-16. PMID 8692238. # Gladwin MT, Sachdev V, Jison ML, Shizukuda Y, Plehn JF, Minter K, Brown B, Coles WA, Nichols JS, Ernst I, Hunter LA, Blackwelder WC, Schechter AN, Rodgers GP, Castro O, Ognibene FP. Pulmonary Hypertension as a Risk Factor for Death in Patients with Sickle Cell Disease. N Engl J Med 2004;350:886-95. PMID 14985486. # Curnock AL, Dweik RA, Higgins BH, Saadi HF, Arroliga AC. High prevalence of hypothyroidism in patients with primary pulmonary hypertension. Am J Med Sci. 1999;318:289-292. PMID 10555089. # Proceedings of the 3rd World Symposium on Pulmonary Arterial Hypertension. Venice, Italy, June 23-25, 2003. J Am Coll Cardiol. 2004 Jun 16;43(12 Suppl S):1S-90S. PMID 15194171.

External links

- [http://www.merck.com/mrkshared/mmanual/section16/chapter203/203c.jsp The Merck Manual of Diagnosis and Therapy: Cor Pulmonale]
- [http://www.phassociation.org/ The Pulmonary Hypertension Association]
- [http://www.phassociation.org/Learn/Consensus-Statements/index.asp Consensus Statements]
- [http://www.phassociation.org/Learn/What-is-PH/ What is Pulmonary hypertension?]
- [http://www.nhlbi.nih.gov/health/public/lung/other/pph_doc.htm Facts About Primary Pulmonary Hypertension] from the National Heart, Lung, and Blood Institute (NHLBI)
- [http://www.hopkins-lungs.org/programs/ph/ Pulmonary Hypertension] from the [http://www.hopkins-lungs.org/ Division of Pulmonary and Critical Care Medicine of the Johns Hopkins School of Medicine].
- [http://www.uchospitals.edu/specialties/heart/services/pulmonary-hypertension/medical-update.html Pulmonary Hypertension: Medical Update for Healthcare Professionals] from the [http://www.uchospitals.edu University of Chicago Hospitals]. Category:Cardiology Category:Pulmonology

Cor pulmonale

Pathophysiology

Causes

- Acute:
- Massive pulmonary embolization
- Exacerbation of chronic cor pulmonale
- Chronic:
- COPD
- Loss of lung tissue following trauma or surgery

Treatment

External links

- The Merck Manual of Diagnosis and Therapy: [http://www.merck.com/mrkshared/mmanual/section16/chapter203/203c.jsp Cor Pulmonale] Category:Cardiology Category:Pulmonology

Category:Drivers who have won both in Champ Cars and the IRL

These are drivers who have won races in both the Champ Car World Series and the Indy Racing League. Two of the drivers on this page, Castroneves and Luyendyk, have won two Indianapolis 500s, each winning their first as a Champ Car driver (Luyendyk in 1990, Castroneves in 2001), and the other as an IRL driver (Luyendyk in 1997, Castroneves in 2002). Category:Auto racing competitions

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Bronchitis

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Lung Disease

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Lung

The respiratory function of the lung

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Carbon dioxide poisoning during diving

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Cor pulmonale

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Heart failure

Classification

Symptoms and signs

Treatment

Medication

Devices and surgery

References

See also

Goblet cells

Reference

Neutrophils

Bronchiole

Expiration

External links

Sputum culture

Chest X-ray

External links

Pulmonary function test