These include the following :
- Peptic Ulcer
- Gastritis
- Gastric Carcinoma
- Hirschsprung's disease
- Celiac sprue
- Crohn's disease
- Ulcerative colitis
- Paralytic Ileus
- Whipple disease
- Meckel's diverticulum
Thursday, November 29, 2007
Coming Up....
I shall be dealing with the diseases of the gut in the next few posts.
These include the following :
These include the following :
Poliomyelitis in India
A problem statement of Poliomyelitis in India.
This map shows the incidence of Wild Poliovirus in India.
Dengue Fever
Causes:
Caused by dengue virus (Flaviviridae, Arbovirus). 4 serotypes of this virus have been reported.
Characteristics of dengue virus: Icosahedral, envelope, internal matrix protein, 1 glycoprotein spike, single-stranded RNA.
It lives only in humans.
Transmitted by mosquito bite (Aedes aegypti mosquito, also Aedes albopictus and Aedes polynesiensis mosquitoes), typically during daytime.
Pathogenesis:
Incubation period 5-8 days (range 3-15 days)
It usually manifests as dengue hemorrhagic fever.
Caused by cross-reacting antibody at second infection and/or virulent virus and leakage of plasma through endothelial gaps.
Risk factors:
Mosquito season, travel to tropics and urban epidemics.
Endemic in Africa, Central and South America, Caribbean and southeast Asia.
Caused by dengue virus (Flaviviridae, Arbovirus). 4 serotypes of this virus have been reported.
Characteristics of dengue virus: Icosahedral, envelope, internal matrix protein, 1 glycoprotein spike, single-stranded RNA.
It lives only in humans.
Transmitted by mosquito bite (Aedes aegypti mosquito, also Aedes albopictus and Aedes polynesiensis mosquitoes), typically during daytime.
Pathogenesis:
Incubation period 5-8 days (range 3-15 days)
It usually manifests as dengue hemorrhagic fever.
Caused by cross-reacting antibody at second infection and/or virulent virus and leakage of plasma through endothelial gaps.
Risk factors:
Mosquito season, travel to tropics and urban epidemics.
Endemic in Africa, Central and South America, Caribbean and southeast Asia.
Malaria : The Risk
Malaria incidence rates in different parts of the world.
Source : WHO World Malaria Report 2005
Tetanus
Introduction:
Tetanus is a medical condition that is characterized by a prolonged contraction of skeletal muscle fibers. The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the Gram-positive, obligate anaerobic bacterium Clostridium tetani. Infection generally occurs through wound contamination, and often involves a cut or deep puncture wound. As the infection progresses, muscle spasms in the jaw develop hence the common name, lockjaw. This is followed by difficulty swallowing and general muscle stiffness and spasms in other parts of the body. Infection can be prevented by proper immunization and by post-exposure prophylaxis.
Types:
Local tetanus: It is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. The contractions may persist for many weeks before gradually subsiding. Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus.
Cephalic tetanus :It is a rare form of the disease, occasionally occurring with otitis media (ear infections) in which C. tetani is present in the flora of the middle ear, or following injuries to the head. There is involvement of the cranial nerves, especially in the facial area.
Generalized tetanus: It is the most common type of tetanus, representing about 80% of cases. The generalized form usually presents with a descending pattern. The first sign is trismus or lockjaw, followed by stiffness of the neck, difficulty in swallowing, and rigidity of pectoral and calf muscles. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes. Spasms continue for 3–4 weeks and complete recovery may take months.
Neonatal tetanus: It is a form of generalized tetanus that occurs in newborn infants. It occurs in infants who have not acquired passive immunity because the mother has never been immunized. It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument. Neonatal tetanus is common in many developing countries and is responsible for 14% (215,000) of all neonatal deaths, but is very rare in developed countries.
Prophylaxis:
In pregnant women, a two dose regimen is recommended i.e 1 vaccine in the 4th month and the next after 1 month.
In India, all newborns are vaccinated against this disease along with Diphtheria and Pertussis (DPT vaccine) in the 6th, 10th and 14th months, followed by boosters in the 18th month, 5th and 10th years.
Tetanus is a medical condition that is characterized by a prolonged contraction of skeletal muscle fibers. The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the Gram-positive, obligate anaerobic bacterium Clostridium tetani. Infection generally occurs through wound contamination, and often involves a cut or deep puncture wound. As the infection progresses, muscle spasms in the jaw develop hence the common name, lockjaw. This is followed by difficulty swallowing and general muscle stiffness and spasms in other parts of the body. Infection can be prevented by proper immunization and by post-exposure prophylaxis.
Types:
Local tetanus: It is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. The contractions may persist for many weeks before gradually subsiding. Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus.
Cephalic tetanus :It is a rare form of the disease, occasionally occurring with otitis media (ear infections) in which C. tetani is present in the flora of the middle ear, or following injuries to the head. There is involvement of the cranial nerves, especially in the facial area.
Generalized tetanus: It is the most common type of tetanus, representing about 80% of cases. The generalized form usually presents with a descending pattern. The first sign is trismus or lockjaw, followed by stiffness of the neck, difficulty in swallowing, and rigidity of pectoral and calf muscles. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes. Spasms continue for 3–4 weeks and complete recovery may take months.
Neonatal tetanus: It is a form of generalized tetanus that occurs in newborn infants. It occurs in infants who have not acquired passive immunity because the mother has never been immunized. It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument. Neonatal tetanus is common in many developing countries and is responsible for 14% (215,000) of all neonatal deaths, but is very rare in developed countries.
Prophylaxis:
In pregnant women, a two dose regimen is recommended i.e 1 vaccine in the 4th month and the next after 1 month.
In India, all newborns are vaccinated against this disease along with Diphtheria and Pertussis (DPT vaccine) in the 6th, 10th and 14th months, followed by boosters in the 18th month, 5th and 10th years.
Peptic Ulcer Disease
Introduction:
2 types viz gastric and duodenal.
Gastric ulcers are now common than duodenal ulcers and in the small intestine, they are associated with Meckel's diverticulum.
Causes:
The major causes are H. pylori (duodenal + gastric) or NSAIDs (gastric), Zollinger-Ellison syndrome, CMV and HSV infection.
Pathogenesis:
H. pylori infection may be prerequisite for almost all duodenal ulcers in absence of NSAIDs or ZE and 80% non-NSAID-induced gastric ulcers, yet most H. pylori-infected individuals do not develop ulcersacid is necessary, reduced bicarbonate, increased acid.
Complications:
- bleeding
- perforation, especially duodenal
- diabetes associated with increased 30-day mortality in patients with bleeding or perforated peptic ulcer
- older age associated with increased 30-day mortality in patients with bleeding or perforated peptic ulcer
- 5% gastric outlet obstruction
- posterior penetration (severe back pain), pancreatitis
Treatment:
- clarithromycin 500 mg twice daily
- amoxicillin 1 g twice daily
- metronidazole 500 mg twice daily
Wednesday, November 28, 2007
Rabies
Introduction:
Rabies (Latin: rabies, "madness, rage, fury") is a viral zoonotic disease that causes acute encephalitis (inflammation of the brain) in mammals. In non-vaccinated humans, rabies is almost invariably fatal after neurological symptoms have developed, but prompt post-exposure vaccination may prevent the virus from progressing.
Transmission and symptoms:
Any mammal may become infected with the rabies virus and develop symptoms, including humans. Most animals can be infected by the virus and can transmit the disease to humans. Infected bats, monkeys, raccoons, foxes, skunks, cattle, wolves, dogs or cats provide the greatest risk to humans. Rabies may also spread through exposure to infected domestic farm animals, groundhogs, weasels and other wild carnivores. Squirrels, rodents and rabbits are seldom infected.
The virus is usually present in the nerves and saliva of a symptomatic rabid animal. The route of infection is usually, but not necessarily, by a bite. In many cases the affected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise uncharacteristic behaviour. Transmission may also occur via an aerosol through mucous membranes; transmission in this form may have happened in people exploring caves populated by rabid bats. Transmission between humans is extremely rare, although it can happen through transplant surgery (see below for recent cases), or, even more rarely, through bites or kisses.
After a typical human infection by bite, the virus directly or indirectly enters the peripheral nervous system. It then travels along the nerves towards the central nervous system. During this phase, the virus cannot be easily detected within the host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. Once the virus reaches the brain, it rapidly causes encephalitis and symptoms appear. It may also inflame the spinal cord producing myelitis.
The period between infection and the first flu-like symptoms is normally two to twelve weeks, but can be as long as two years. Soon after, the symptoms expand to slight or partial paralysis, cerebral dysfunction, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, hallucinations, progressing to delirium. The production of large quantities of saliva and tears coupled with an inability to speak or swallow are typical during the later stages of the disease; this can result in "hydrophobia", where the victim has difficulty swallowing, shows panic when presented with liquids to drink, and cannot quench his or her thirst. The disease itself was also once commonly known as hydrophobia, from these characteristic symptoms. Death almost invariably results two to ten days after the first symptoms. It is neurotrophic in nature.
Prevention:
Rabies can be prevented by vaccination, both in humans and other animals. Virtually every infection with rabies was a death sentence, until Louis Pasteur and Emile Roux developed the first rabies vaccination in 1885. This vaccine was first used on a human on July 6, 1885 – nine-year old boy Joseph Meister (1876–1940) had been mauled by a rabid dog.
Their vaccine consisted of a sample of the virus harvested from infected (and necessarily dead) rabbits, which was weakened by allowing it to dry for 5 to 10 days. Similar nerve tissue-derived vaccines are still used now in some countries, and while they are much cheaper than modern cell culture vaccines, they are not as effective and carry a certain risk of neurological complications.
The human diploid cell rabies vaccine (H.D.C.V.) was started in 1967. Human diploid cell rabies vaccines are made using the attenuated Pitman-Moore L503 strain of the virus. Human diploid cell rabies vaccines have been given to more than 1.5 million humans as of 2006. Newer and less expensive purified chicken embryo cell vaccine and purified Vero cell rabies vaccine are now available. The purified Vero cell rabies vaccine uses the attenuated Wistar strain of the rabies virus, and uses the Vero cell line as its host.
Some recent works have shown that during lethal rabies infection blood-brain barrier (BBB) does not open in order to allow anti-viral immune cells to enter the brain, the primary site of rabies virus replication. This aspect contributes to the pathogenicity of the virus and artificially increasing BBB permeability promotes viral clearance. Opening the BBB during rabies infection has been suggested as a possible novel approach to treat the disease.
Post-exposure prophylaxis:
Treatment after exposure, known as post-exposure prophylaxis or "P.E.P.", is highly successful in preventing the disease if administered promptly, within fourteen days after infection. The first step is immediately washing the wound with soap and water, which is very effective at reducing the number of viral particles. In the United States, patients receive one dose of immunoglobulin and five doses of rabies vaccine over a twenty-eight day period. One-half the dose of immunoglobulin is injected in the region of the bite, if possible, with the remainder injected intramuscularly away from the bite. This is much less painful compared with administering immunoglobulin through the abdominal wall with a large needle, which is how it was done in the past. The first dose of rabies vaccine is given as soon as possible after exposure, with additional doses on days three, seven, fourteen, and twenty-eight after the first. Patients that have previously received pre-exposure vaccination do not receive the immunoglobulin, only the post-exposure vaccinations. Since the widespread vaccination of domestic dogs and cats and the development of effective human vaccines and immunoglobulin treatments, the number of recorded deaths in the U.S. from rabies has dropped from one hundred or more annually in the early twentieth century, to 1–2 per year, mostly caused by bat bites, which may go unnoticed by the victim and hence untreated.
P.E.P. is effective in treating rabies because the virus must travel from the site of infection through the peripheral nervous system (nerves in the body) before infecting the central nervous system (brain and spinal cord) and glands to cause lethal damage. This travel along the nerves is usually slow enough that vaccine and immunoglobulin can be administered to protect the brain and glands from infection. The amount of time this travel requires is dependent on how far the infected area is from the brain: if the victim is bitten in the face, for example, the time between initial infection and infection of the brain is very short and P.E.P. may not be successful.
Pre-exposure prophylaxis:
Currently pre-exposure immunization has been used on domesticated and normal non-human populations. In many jurisdictions, domestic dogs, cats, and ferrets are required to be vaccinated. A pre-exposure vaccination is also available for humans, most commonly given to veterinarians and those traveling to regions where the disease is common, such as India. Most tourists do not need such a vaccination, just those doing substantial non-urban activities. However, should a vaccinated human be bitten by a carrier, failure to receive subsequent post-exposure treatment could be fatal, although post-exposure treatment for a vaccinated human is far less extensive than that which would normally be required by one with no pre-exposure vaccination.
In 1984 researchers at the Wistar Institute developed a recombinant vaccine called V-RG by inserting the glycoprotein gene from rabies into a vaccinia virus. The V-RG vaccine has since been commercialised by Merial under the trademark Raboral. It is harmless to humans and has been shown to be safe for various species of animals that might accidentally encounter it in the wild, including birds (gulls, hawks, and owls).
Rabies (Latin: rabies, "madness, rage, fury") is a viral zoonotic disease that causes acute encephalitis (inflammation of the brain) in mammals. In non-vaccinated humans, rabies is almost invariably fatal after neurological symptoms have developed, but prompt post-exposure vaccination may prevent the virus from progressing.
Transmission and symptoms:
Any mammal may become infected with the rabies virus and develop symptoms, including humans. Most animals can be infected by the virus and can transmit the disease to humans. Infected bats, monkeys, raccoons, foxes, skunks, cattle, wolves, dogs or cats provide the greatest risk to humans. Rabies may also spread through exposure to infected domestic farm animals, groundhogs, weasels and other wild carnivores. Squirrels, rodents and rabbits are seldom infected.
The virus is usually present in the nerves and saliva of a symptomatic rabid animal. The route of infection is usually, but not necessarily, by a bite. In many cases the affected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise uncharacteristic behaviour. Transmission may also occur via an aerosol through mucous membranes; transmission in this form may have happened in people exploring caves populated by rabid bats. Transmission between humans is extremely rare, although it can happen through transplant surgery (see below for recent cases), or, even more rarely, through bites or kisses.
After a typical human infection by bite, the virus directly or indirectly enters the peripheral nervous system. It then travels along the nerves towards the central nervous system. During this phase, the virus cannot be easily detected within the host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. Once the virus reaches the brain, it rapidly causes encephalitis and symptoms appear. It may also inflame the spinal cord producing myelitis.
The period between infection and the first flu-like symptoms is normally two to twelve weeks, but can be as long as two years. Soon after, the symptoms expand to slight or partial paralysis, cerebral dysfunction, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, hallucinations, progressing to delirium. The production of large quantities of saliva and tears coupled with an inability to speak or swallow are typical during the later stages of the disease; this can result in "hydrophobia", where the victim has difficulty swallowing, shows panic when presented with liquids to drink, and cannot quench his or her thirst. The disease itself was also once commonly known as hydrophobia, from these characteristic symptoms. Death almost invariably results two to ten days after the first symptoms. It is neurotrophic in nature.
Prevention:
Rabies can be prevented by vaccination, both in humans and other animals. Virtually every infection with rabies was a death sentence, until Louis Pasteur and Emile Roux developed the first rabies vaccination in 1885. This vaccine was first used on a human on July 6, 1885 – nine-year old boy Joseph Meister (1876–1940) had been mauled by a rabid dog.
Their vaccine consisted of a sample of the virus harvested from infected (and necessarily dead) rabbits, which was weakened by allowing it to dry for 5 to 10 days. Similar nerve tissue-derived vaccines are still used now in some countries, and while they are much cheaper than modern cell culture vaccines, they are not as effective and carry a certain risk of neurological complications.
The human diploid cell rabies vaccine (H.D.C.V.) was started in 1967. Human diploid cell rabies vaccines are made using the attenuated Pitman-Moore L503 strain of the virus. Human diploid cell rabies vaccines have been given to more than 1.5 million humans as of 2006. Newer and less expensive purified chicken embryo cell vaccine and purified Vero cell rabies vaccine are now available. The purified Vero cell rabies vaccine uses the attenuated Wistar strain of the rabies virus, and uses the Vero cell line as its host.
Some recent works have shown that during lethal rabies infection blood-brain barrier (BBB) does not open in order to allow anti-viral immune cells to enter the brain, the primary site of rabies virus replication. This aspect contributes to the pathogenicity of the virus and artificially increasing BBB permeability promotes viral clearance. Opening the BBB during rabies infection has been suggested as a possible novel approach to treat the disease.
Post-exposure prophylaxis:
Treatment after exposure, known as post-exposure prophylaxis or "P.E.P.", is highly successful in preventing the disease if administered promptly, within fourteen days after infection. The first step is immediately washing the wound with soap and water, which is very effective at reducing the number of viral particles. In the United States, patients receive one dose of immunoglobulin and five doses of rabies vaccine over a twenty-eight day period. One-half the dose of immunoglobulin is injected in the region of the bite, if possible, with the remainder injected intramuscularly away from the bite. This is much less painful compared with administering immunoglobulin through the abdominal wall with a large needle, which is how it was done in the past. The first dose of rabies vaccine is given as soon as possible after exposure, with additional doses on days three, seven, fourteen, and twenty-eight after the first. Patients that have previously received pre-exposure vaccination do not receive the immunoglobulin, only the post-exposure vaccinations. Since the widespread vaccination of domestic dogs and cats and the development of effective human vaccines and immunoglobulin treatments, the number of recorded deaths in the U.S. from rabies has dropped from one hundred or more annually in the early twentieth century, to 1–2 per year, mostly caused by bat bites, which may go unnoticed by the victim and hence untreated.
P.E.P. is effective in treating rabies because the virus must travel from the site of infection through the peripheral nervous system (nerves in the body) before infecting the central nervous system (brain and spinal cord) and glands to cause lethal damage. This travel along the nerves is usually slow enough that vaccine and immunoglobulin can be administered to protect the brain and glands from infection. The amount of time this travel requires is dependent on how far the infected area is from the brain: if the victim is bitten in the face, for example, the time between initial infection and infection of the brain is very short and P.E.P. may not be successful.
Pre-exposure prophylaxis:
Currently pre-exposure immunization has been used on domesticated and normal non-human populations. In many jurisdictions, domestic dogs, cats, and ferrets are required to be vaccinated. A pre-exposure vaccination is also available for humans, most commonly given to veterinarians and those traveling to regions where the disease is common, such as India. Most tourists do not need such a vaccination, just those doing substantial non-urban activities. However, should a vaccinated human be bitten by a carrier, failure to receive subsequent post-exposure treatment could be fatal, although post-exposure treatment for a vaccinated human is far less extensive than that which would normally be required by one with no pre-exposure vaccination.
In 1984 researchers at the Wistar Institute developed a recombinant vaccine called V-RG by inserting the glycoprotein gene from rabies into a vaccinia virus. The V-RG vaccine has since been commercialised by Merial under the trademark Raboral. It is harmless to humans and has been shown to be safe for various species of animals that might accidentally encounter it in the wild, including birds (gulls, hawks, and owls).
Tuesday, November 27, 2007
Mesothelioma
Introduction:
Mesothelioma is a form of cancer that is almost always caused by previous exposure to asbestos. In this disease, malignant cells develop in the mesothelium, a protective lining that covers most of the body's internal organs. Its most common site is the pleura (outer lining of the lungs and chest cavity), but it may also occur in the peritoneum (the lining of the abdominal cavity) or the pericardium (a sac that surrounds the heart).
Signs and symptoms:
Pleural
Treatment:
Screening:
Screening for asbestos-related disease not recommended for general population, but may be appropriate if history of significant asbestos exposureif history of significant exposure and exertional dyspnea, spirometry and chest x-ray recommended in addition to history and physicalif no evidence of abnormalities, consider high-resolution CT which may reveal pleural-based plaques, CT is more sensitive than chest x-ray for detecting lesions and mild fibrosispresence of plaques indicates significant asbestos exposureif patient has abnormal spirometry results, imaging abnormalities, or suspected asbestos-related conditions, consider full pulmonary function tests, including measurement of lung volumes and diffusion capacity.
Mesothelioma is a form of cancer that is almost always caused by previous exposure to asbestos. In this disease, malignant cells develop in the mesothelium, a protective lining that covers most of the body's internal organs. Its most common site is the pleura (outer lining of the lungs and chest cavity), but it may also occur in the peritoneum (the lining of the abdominal cavity) or the pericardium (a sac that surrounds the heart).
Signs and symptoms:
Pleural
- Chest wall pain
- Pleural effusion
- Shortness of breath
- Fatigue or anemia
- Wheezing, hoarseness, or cough
- Blood in the sputum (fluid) coughed up
Abdominal
- Abdominal pain
- Ascites
- Mass in the abdomen
- Weight loss
Pathophysiology:
Treatment:
- Surgical approach: palliative decortication for pain control and to improve pulmonary function, surgical resection and intrapleural chemotherapy
- Radiation therapy: post-operatively as a consolidative treatment.
- Chemotherapy: Drugs of choice are cisplatin and pemetrexed, gemcitabine and cisplatin.
Prognosis:
Often fatal, poor response to treatment.
Screening:
Screening for asbestos-related disease not recommended for general population, but may be appropriate if history of significant asbestos exposureif history of significant exposure and exertional dyspnea, spirometry and chest x-ray recommended in addition to history and physicalif no evidence of abnormalities, consider high-resolution CT which may reveal pleural-based plaques, CT is more sensitive than chest x-ray for detecting lesions and mild fibrosispresence of plaques indicates significant asbestos exposureif patient has abnormal spirometry results, imaging abnormalities, or suspected asbestos-related conditions, consider full pulmonary function tests, including measurement of lung volumes and diffusion capacity.
Asbestosis
Introduction:
Pneumoconiosis = restrictive interstitial lung disease.
Organs Involved are lung (bibasilar), respiratory bronchioles and alveolar ducts.
It is the third most common interstitial fibrotic lung disease.
Etiolopathogenesis :
Caused by light thin sharp asbestos fibers, which induce inflammation and fibrosis. History of asbestos exposure, even a very remote one, is considered and a potential risk factor.
Complications:
Higher incidence of bronchogenic carcinoma and mesothelioma are the main complications. Other complications include hyalinized fibrocalcific plaques, fibrinous pleuritis, peribronchial fibrosis, recurrent respiratory infections and pleural effusion.
Physical Findings:
Cardiac findings are late, after pulmonary hypertension sets in. It may end up in right heart failure.
Basilar inspiratory rales are the usual auscultatory findings.
Extremities may have clubbing.
Diagnosis:
Blood shows increased ESR, hypergammaglobulinemia.
Chest skiagram shows pleural thickening or calcification (lower lobe predominance)
Histopathology examination is done by bronchoscopy, open biopsy or video-assisted thorascopy. Asbestos bodies (ferruginous bodies):
These are complex of hemosiderin and glycoprotein within macrophage.
Diffuse interstitial cellular and fibrotic reaction is a constant finding.
Pneumoconiosis = restrictive interstitial lung disease.
Organs Involved are lung (bibasilar), respiratory bronchioles and alveolar ducts.
It is the third most common interstitial fibrotic lung disease.
Etiolopathogenesis :
Caused by light thin sharp asbestos fibers, which induce inflammation and fibrosis. History of asbestos exposure, even a very remote one, is considered and a potential risk factor.
Complications:
Higher incidence of bronchogenic carcinoma and mesothelioma are the main complications. Other complications include hyalinized fibrocalcific plaques, fibrinous pleuritis, peribronchial fibrosis, recurrent respiratory infections and pleural effusion.
Physical Findings:
Cardiac findings are late, after pulmonary hypertension sets in. It may end up in right heart failure.
Basilar inspiratory rales are the usual auscultatory findings.
Extremities may have clubbing.
Diagnosis:
Blood shows increased ESR, hypergammaglobulinemia.
Chest skiagram shows pleural thickening or calcification (lower lobe predominance)
Histopathology examination is done by bronchoscopy, open biopsy or video-assisted thorascopy. Asbestos bodies (ferruginous bodies):
These are complex of hemosiderin and glycoprotein within macrophage.
Diffuse interstitial cellular and fibrotic reaction is a constant finding.
Prognosis:
May progress without further exposure
May progress without further exposure
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