View Comments about my blog from EMEDPAK.com
http://www.emedpak.com/NewsDetails.aspx?id=139
Become an E-saver!
EMED(Electronic medicine) “ Combat & Prevent disease”
emed (Electronic medicine) “ Combat & Prevent disease”
“Emed becomes first health platform to provide online services to all the five end-users of health facilities, i.e. Doctors, Students, General Public, Paramedical and Nurses” VISION ”To be the No.1 international health organization in promoting health & awareness according to the contemporary needs” MISSION ”We counsel & guide the three end users of health facilities i.e. doctors, students & general public , Paramedical and Nurses by creating awareness among them related to prevention & growing health issues”
Health Tip of The Day
Blog Archive
Monday, July 5, 2010
Saturday, July 3, 2010
The Citizens-Police Liaison Committee commonly known as CPLC.
www.cplc.org.pk/
They are really devoted to thier PAKLAND -Pakistan!
www.cplc.org.pk/
They are really devoted to thier PAKLAND -Pakistan!
Paralysis is the complete loss of muscle function for one or more muscles. Paralysis can be accompanied by a loss of feeling (sensory loss) in the affected area, if there is sensory damage as well as motor.
1 Causes
2 Variations
3 Paralysis in the animal world
Causes
Paralysis is most often caused by damage in the nervous system, especially the spinal cord. Other major causes are stroke, trauma with nerve injury, poliomyelitis, amyotrophic lateral sclerosis (ALS), botulism, spina bifida, multiple sclerosis, and Guillain-Barré syndrome. Temporary paralysis occurs during REM sleep, and dysregulation of this system can lead to episodes of waking paralysis. Drugs that interfere with nerve function, such as curare, can also cause paralysis. There are many known causes for paralysis, and perhaps more yet to be discovered.
Pseudoparalysis (pseudo- meaning false, not genuine) is voluntary restriction or inhibition of motion because of pain, incoordination, or other cause, and is not due to actual muscular paralysis.[1] In an infant, it may be a symptom of congenital syphilis.[2]
Variations
Paralysis could be localized, or generalized, or it may follow a certain pattern. Most paralyses caused by nervous system damage (i.e. spinal cord injuries) are constant in nature; however, there are forms of periodic paralysis, including sleep paralysis, which are caused by other factors.
Paralysis in the animal world
Many animal species use paralyzing toxins to capture prey, evade predation, or both. A well-known example is the tetrodotoxin of fish species such as Takifugu rubripes, the famously lethal pufferfish of Japanese fugu. This toxin works by binding to sodium channels in nerve cells, preventing the cells' proper function. A non-lethal dose of this toxin results in temporary paralysis. This toxin is also present in many other species ranging from toads to nemerteans. Another interesting use of paralysis in the natural world is the behavior of some species of wasp. To complete the reproductive cycle, the female wasp paralyzes a prey item such as a grasshopper and places it in her nest. She then lays eggs in the paralyzed insect, which is devoured by the larvae when they hatch. Many snakes also exhibit powerful neurotoxins that can cause non-permanent paralysis or death.
Paralysis can be seen in breeds of dogs that are chondrodysplastic. These dogs have short legs, and may also have short muzzles. Their intervertebral disc material can calcify and become more brittle. In such cases, the disc may rupture, with disc material ending up in the spinal canal, or rupturing more laterally to press on spinal nerves. A minor rupture may only result in paresis, but a major rupture can cause enough damage to cut off your circulation. If no signs of pain can be elicited, surgery should be performed within 24 hours of the incident, to remove the disc material and relieve pressure on the spinal cord. After 24 hours, the chance of recovery declines rapidly, since with continued pressure, the spinal cord tissue deteriorates and dies.
Another type of paralysis is caused by a fibrocartilaginous embolism. This is a microscopic piece of disc material that breaks off and becomes lodged in a spinal artery. Nerves served by the artery will die when deprived of blood.
The German Shepherd is especially prone to developing degenerative myelopathy. This is a deterioration of nerves in the spinal cord, starting in the posterior part of the cord. Dogs so affected will become gradually weaker in the hind legs as nerves die off. Eventually their hind legs become useless. They often also exhibit fecal and urinary incontinence. As the disease progresses, the paresis and paralysis gradually move forward. This disease also affects other large breeds of dogs. It is suspected to be an autoimmune problem.
Cats with a heart murmur may develop blood clots that travel through arteries. If a clot is large enough to block one or both femoral arteries, there may be hind leg paralysis because the major source of blood flow to the hind leg is blocked.
1 Causes
2 Variations
3 Paralysis in the animal world
Causes
Paralysis is most often caused by damage in the nervous system, especially the spinal cord. Other major causes are stroke, trauma with nerve injury, poliomyelitis, amyotrophic lateral sclerosis (ALS), botulism, spina bifida, multiple sclerosis, and Guillain-Barré syndrome. Temporary paralysis occurs during REM sleep, and dysregulation of this system can lead to episodes of waking paralysis. Drugs that interfere with nerve function, such as curare, can also cause paralysis. There are many known causes for paralysis, and perhaps more yet to be discovered.
Pseudoparalysis (pseudo- meaning false, not genuine) is voluntary restriction or inhibition of motion because of pain, incoordination, or other cause, and is not due to actual muscular paralysis.[1] In an infant, it may be a symptom of congenital syphilis.[2]
Variations
Paralysis could be localized, or generalized, or it may follow a certain pattern. Most paralyses caused by nervous system damage (i.e. spinal cord injuries) are constant in nature; however, there are forms of periodic paralysis, including sleep paralysis, which are caused by other factors.
Paralysis in the animal world
Many animal species use paralyzing toxins to capture prey, evade predation, or both. A well-known example is the tetrodotoxin of fish species such as Takifugu rubripes, the famously lethal pufferfish of Japanese fugu. This toxin works by binding to sodium channels in nerve cells, preventing the cells' proper function. A non-lethal dose of this toxin results in temporary paralysis. This toxin is also present in many other species ranging from toads to nemerteans. Another interesting use of paralysis in the natural world is the behavior of some species of wasp. To complete the reproductive cycle, the female wasp paralyzes a prey item such as a grasshopper and places it in her nest. She then lays eggs in the paralyzed insect, which is devoured by the larvae when they hatch. Many snakes also exhibit powerful neurotoxins that can cause non-permanent paralysis or death.
Paralysis can be seen in breeds of dogs that are chondrodysplastic. These dogs have short legs, and may also have short muzzles. Their intervertebral disc material can calcify and become more brittle. In such cases, the disc may rupture, with disc material ending up in the spinal canal, or rupturing more laterally to press on spinal nerves. A minor rupture may only result in paresis, but a major rupture can cause enough damage to cut off your circulation. If no signs of pain can be elicited, surgery should be performed within 24 hours of the incident, to remove the disc material and relieve pressure on the spinal cord. After 24 hours, the chance of recovery declines rapidly, since with continued pressure, the spinal cord tissue deteriorates and dies.
Another type of paralysis is caused by a fibrocartilaginous embolism. This is a microscopic piece of disc material that breaks off and becomes lodged in a spinal artery. Nerves served by the artery will die when deprived of blood.
The German Shepherd is especially prone to developing degenerative myelopathy. This is a deterioration of nerves in the spinal cord, starting in the posterior part of the cord. Dogs so affected will become gradually weaker in the hind legs as nerves die off. Eventually their hind legs become useless. They often also exhibit fecal and urinary incontinence. As the disease progresses, the paresis and paralysis gradually move forward. This disease also affects other large breeds of dogs. It is suspected to be an autoimmune problem.
Cats with a heart murmur may develop blood clots that travel through arteries. If a clot is large enough to block one or both femoral arteries, there may be hind leg paralysis because the major source of blood flow to the hind leg is blocked.
Tuesday, June 29, 2010
Hepatitis
Classification and external resources
Alcoholic hepatitis evident by fatty change, cell necrosis, Mallory bodies
ICD-10 K75.9
ICD-9 573.3
DiseasesDB 20061
MeSH D006505
Signs and symptoms
Acute
Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]
Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]
A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral edema and bleeding). This may become life-threatening and occasionally requires a liver transplant.
Classification and external resources
Alcoholic hepatitis evident by fatty change, cell necrosis, Mallory bodies
ICD-10 K75.9
ICD-9 573.3
DiseasesDB 20061
MeSH D006505
Hepatitis (plural hepatitides) implies inflammation of the liver characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar (ἧπαρ), the root being hepat- (ἡπατ-), meaning liver, and suffix -itis, meaning "inflammation" (c. 1727)[1]. The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.Signs and symptoms
Acute
Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]
Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]
A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral edema and bleeding). This may become life-threatening and occasionally requires a liver transplant.
Chronic
Chronic hepatitis often leads nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]
Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the abdominal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).
Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.[4]
Causes
Acute
Viral hepatitis:
Hepatitis A through E
Herpes simplex
Cytomegalovirus
Epstein-Barr
Yellow fever
adenoviruses
Non viral infection
toxoplasma
Leptospira
Q fever[5]
rocky mountain spotted fever[6]
Alcohol
Toxins: Amanita toxin in mushrooms, carbon tetrachloride, asafetida
Drugs: Paracetamol, amoxycillin, antituberculosis medicines, minocycline and many others (see longer list below).
Ischemic hepatitis (circulatory insufficiency)
Pregnancy
Auto immune conditions, e.g., Systemic Lupus Erythematosus (SLE)
Metabolic diseases, e.g., Wilson's disease
Chronic
Viral hepatitis: Hepatitis B with or without hepatitis D, hepatitis C (neither hepatitis A nor hepatitis E causes chronic hepatitis)
Autoimmune
Autoimmune hepatitis
Alcohol
Drugs
methyldopa
nitrofurantoin
isoniazid
ketoconazole
Non-alcoholic steatohepatitis
Heredity
Wilson's disease
alpha 1-antitrypsin deficiency
Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis[3]
Chronic hepatitis often leads nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]
Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the abdominal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).
Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.[4]
Causes
Acute
Viral hepatitis:
Hepatitis A through E
Herpes simplex
Cytomegalovirus
Epstein-Barr
Yellow fever
adenoviruses
Non viral infection
toxoplasma
Leptospira
Q fever[5]
rocky mountain spotted fever[6]
Alcohol
Toxins: Amanita toxin in mushrooms, carbon tetrachloride, asafetida
Drugs: Paracetamol, amoxycillin, antituberculosis medicines, minocycline and many others (see longer list below).
Ischemic hepatitis (circulatory insufficiency)
Pregnancy
Auto immune conditions, e.g., Systemic Lupus Erythematosus (SLE)
Metabolic diseases, e.g., Wilson's disease
Chronic
Viral hepatitis: Hepatitis B with or without hepatitis D, hepatitis C (neither hepatitis A nor hepatitis E causes chronic hepatitis)
Autoimmune
Autoimmune hepatitis
Alcohol
Drugs
methyldopa
nitrofurantoin
isoniazid
ketoconazole
Non-alcoholic steatohepatitis
Heredity
Wilson's disease
alpha 1-antitrypsin deficiency
Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis[3]
Alcoholic hepatitis
Main article: Alcoholic hepatitis
Ethanol, mostly in alcoholic beverages, is a significant cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.
Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C.[citation needed] The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis.
[edit]
Drug induced
Main article: Hepatotoxicity
A large number of drugs can cause hepatitis:[7]
Agomelatine (antidepressant)
Allopurinol
Amitriptyline (antidepressant)
Amiodarone (antiarrhythmic)
Atomoxetine [8]
Azathioprine[9]
Halothane (a specific type of anesthetic gas)
Hormonal contraceptives
Ibuprofen and indomethacin (NSAIDs)
Isoniazid (INH), rifampicin, and pyrazinamide (tuberculosis-specific antibiotics)
Ketoconazole (antifungal)
Loratadine (antihistamine)
Methotrexate (immune suppressant)
Methyldopa (antihypertensive)
Minocycline (tetracycline antibiotic)
Nifedipine (antihypertensive)
Nitrofurantoin (antibiotic)
Paracetamol (acetaminophen in the United States) can cause hepatitis when taken in an overdose. The severity of liver damage may be limited by prompt administration of acetylcysteine.
Phenytoin and valproic acid (antiepileptics)
Troglitazone (antidiabetic, withdrawn in 2000 for causing hepatitis)
Zidovudine (antiretroviral i.e., against HIV)
Some herbs and nutritional supplements[10]
The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Hormonal contraception can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.
Other toxins
Other Toxins can cause hepatitis:
Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel (Amanita ocreata), and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).
White phosphorus, an industrial toxin and war chemical.
Carbon tetrachloride ("tetra", a dry cleaning agent), chloroform, and trichloroethylene, all chlorinated hydrocarbons, cause steatohepatitis (hepatitis with fatty liver).
Cylindrospermopsin, a toxin from the cyanobacterium Cylindrospermopsis raciborskii and other cyanobacteria.
Metabolic disorders
Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.
Non-alcoholic steatohepatitis (NASH) is effectively a consequence of metabolic syndrome.
Main article: Alcoholic hepatitis
Ethanol, mostly in alcoholic beverages, is a significant cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.
Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C.[citation needed] The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis.
[edit]
Drug induced
Main article: Hepatotoxicity
A large number of drugs can cause hepatitis:[7]
Agomelatine (antidepressant)
Allopurinol
Amitriptyline (antidepressant)
Amiodarone (antiarrhythmic)
Atomoxetine [8]
Azathioprine[9]
Halothane (a specific type of anesthetic gas)
Hormonal contraceptives
Ibuprofen and indomethacin (NSAIDs)
Isoniazid (INH), rifampicin, and pyrazinamide (tuberculosis-specific antibiotics)
Ketoconazole (antifungal)
Loratadine (antihistamine)
Methotrexate (immune suppressant)
Methyldopa (antihypertensive)
Minocycline (tetracycline antibiotic)
Nifedipine (antihypertensive)
Nitrofurantoin (antibiotic)
Paracetamol (acetaminophen in the United States) can cause hepatitis when taken in an overdose. The severity of liver damage may be limited by prompt administration of acetylcysteine.
Phenytoin and valproic acid (antiepileptics)
Troglitazone (antidiabetic, withdrawn in 2000 for causing hepatitis)
Zidovudine (antiretroviral i.e., against HIV)
Some herbs and nutritional supplements[10]
The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Hormonal contraception can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.
Other toxins
Other Toxins can cause hepatitis:
Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel (Amanita ocreata), and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).
White phosphorus, an industrial toxin and war chemical.
Carbon tetrachloride ("tetra", a dry cleaning agent), chloroform, and trichloroethylene, all chlorinated hydrocarbons, cause steatohepatitis (hepatitis with fatty liver).
Cylindrospermopsin, a toxin from the cyanobacterium Cylindrospermopsis raciborskii and other cyanobacteria.
Metabolic disorders
Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.
Non-alcoholic steatohepatitis (NASH) is effectively a consequence of metabolic syndrome.
Obstructive
"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding, it leads to destruction and inflammation of liver tissue.
"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding, it leads to destruction and inflammation of liver tissue.
Autoimmune
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes, possibly due to genetic predisposition or acute liver infection; causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.Alpha 1-antitrypsin deficiency
In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.
Non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is the occurrence of fatty liver in people who have no history of alcohol use. It is most commonly associated with obesity (80% of all obese people have fatty liver). It is more common in women. Severe NAFLD leads to inflammation, a state referred to as non-alcoholic steatohepatitis (NASH), which on biopsy of the liver resembles alcoholic hepatitis (with fat droplets and inflammatory cells, but usually no Mallory bodies).
The diagnosis depends on medical history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is medical imaging, including such ultrasound, computed tomography (CT), or magnetic resonance (MRI). However, imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow-up blood tests and a repeated liver biopsy are required.
NASH is becoming recognized as the most important cause of liver disease second only to hepatitis C in numbers of patients going on to cirrhosis.[citation needed]
Ischemic hepatitis
Main article: Ischemic hepatitis
Ischemic hepatitis is caused by decreased circulation to the liver cells. Usually this is due to decreased blood pressure (or shock), leading to the equivalent term "shock liver". Patients with ischemic hepatitis are usually very ill due to the underlying cause of shock. Rarely, ischemic hepatitis can be caused by local problems with the blood vessels that supply oxygen to the liver (such as thrombosis, or clotting of the hepatic artery which partially supplies blood to liver cells). Blood testing of a person with ischemic hepatitis will show very high levels of transaminase enzymes (AST and ALT), which may exceed 1000 U/L. The elevation in these blood tests is usually transient (lasting 7 to 10 days). It is rare that liver function will be affected by ischemic hepatitis.
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes, possibly due to genetic predisposition or acute liver infection; causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.Alpha 1-antitrypsin deficiency
In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.
Non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is the occurrence of fatty liver in people who have no history of alcohol use. It is most commonly associated with obesity (80% of all obese people have fatty liver). It is more common in women. Severe NAFLD leads to inflammation, a state referred to as non-alcoholic steatohepatitis (NASH), which on biopsy of the liver resembles alcoholic hepatitis (with fat droplets and inflammatory cells, but usually no Mallory bodies).
The diagnosis depends on medical history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is medical imaging, including such ultrasound, computed tomography (CT), or magnetic resonance (MRI). However, imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow-up blood tests and a repeated liver biopsy are required.
NASH is becoming recognized as the most important cause of liver disease second only to hepatitis C in numbers of patients going on to cirrhosis.[citation needed]
Ischemic hepatitis
Main article: Ischemic hepatitis
Ischemic hepatitis is caused by decreased circulation to the liver cells. Usually this is due to decreased blood pressure (or shock), leading to the equivalent term "shock liver". Patients with ischemic hepatitis are usually very ill due to the underlying cause of shock. Rarely, ischemic hepatitis can be caused by local problems with the blood vessels that supply oxygen to the liver (such as thrombosis, or clotting of the hepatic artery which partially supplies blood to liver cells). Blood testing of a person with ischemic hepatitis will show very high levels of transaminase enzymes (AST and ALT), which may exceed 1000 U/L. The elevation in these blood tests is usually transient (lasting 7 to 10 days). It is rare that liver function will be affected by ischemic hepatitis.
"Stay Healthy and live life with full Zeal and zest",EmedPak.com
EmedPakThe new millennium has brought a lot of new changes in our lives. World is now like a global village. Someone correctly quoted that now this is an era of paperless world. It pointed towards the extensive use of electronic media. Taking the example of medical world, it takes years for new edition of any book to come whereas same new information is available on electronic journals & it is recognized for references and bibliography in research work.
Keeping in view the rapidly growing interest of medical professionals and students lot of efforts were done in West. But, in Faisalabad, Pakistan, it was brainwave of Dr Khurram Sohail Raja, (Assistant Professor). Dr Zahid Masood Khan (Associate Professor), Dr Ahmad Bilal (Professor of Medicine & Best graduate), Dr Sajid Sheikh (Associate Professor & Best graduate), Dr Hina Ayesha (Associate Professor & Best graduate) who worked upon this idea.
The team named the project as " emed (Electronic Medicine) ". Prof Dr Mohammad Saeed (Head of Biochemistry Department, Punjab Medical College, Faisalabad, Pakistan), Prof Dr Irshad ul Haq (Principal, University of Faisalabad), Prof Dr Mrs Tasneem Cheema (Head of Physiology Department, Punjab Medical College, Faisalabad, Pakistan) & Dr Mohammad Aslam (Head of Forensic Medicine, University of Faisalabad, Pakistan) proudly stood with the emed team of their students.
Respected and dedicated Dr.Khuram Sohail Raja
Keeping in view the rapidly growing interest of medical professionals and students lot of efforts were done in West. But, in Faisalabad, Pakistan, it was brainwave of Dr Khurram Sohail Raja, (Assistant Professor). Dr Zahid Masood Khan (Associate Professor), Dr Ahmad Bilal (Professor of Medicine & Best graduate), Dr Sajid Sheikh (Associate Professor & Best graduate), Dr Hina Ayesha (Associate Professor & Best graduate) who worked upon this idea.
The team named the project as " emed (Electronic Medicine) ". Prof Dr Mohammad Saeed (Head of Biochemistry Department, Punjab Medical College, Faisalabad, Pakistan), Prof Dr Irshad ul Haq (Principal, University of Faisalabad), Prof Dr Mrs Tasneem Cheema (Head of Physiology Department, Punjab Medical College, Faisalabad, Pakistan) & Dr Mohammad Aslam (Head of Forensic Medicine, University of Faisalabad, Pakistan) proudly stood with the emed team of their students.
Respected and dedicated Dr.Khuram Sohail Raja
Subscribe to:
Posts (Atom)