Viral Hepatitis can be either acute or chronic. Acute Hepatitis A virus (HAV) causes inflammation of the liver that is usually self-limiting and does not result in chronic infection. It is commonly spread through the fecal-oral route or contaminated food/water. Clinical presentation involves nonspecific symptoms initially, followed by jaundice. Treatment is supportive and recovery is expected within 1-2 months.
The document discusses different types of viral hepatitis, including Hepatitis A, B, C, D, and E. It provides details on the classification, transmission, pathogenesis, clinical features, diagnosis, and prevention of each viral hepatitis type. It notes that Hepatitis A and E are typically transmitted through the fecal-oral route due to contaminated food or water, while Hepatitis B, C and D are transmitted through blood or bodily fluids. Vaccines exist for Hepatitis A and B but not the others.
Hepatitis C - Etiology Pathogenesis Clinical Features Diagnosis ManagementChetan Ganteppanavar
Hepatitis C is a viral infection that affects an estimated 2-3% of the world's population. It is transmitted parenterally or through exposure to infected blood or bodily fluids. Approximately 70-130 million individuals are chronically infected. While some acute cases resolve, others progress to chronic infection which can lead to cirrhosis or liver cancer over time. Diagnosis involves testing for HCV antibodies and RNA. Genotypes 1-6 exist globally. Management involves antiviral therapy with pegylated interferon and ribavirin or newer direct acting antiviral agents targeting viral proteins. Treatment aims to achieve a sustained virologic response and prevent progression of liver disease.
Hepatitis E is a viral infection caused by the Hepatitis E virus (HEV). It is transmitted through contaminated water or food supplies and causes acute viral hepatitis. The incubation period is 2-9 weeks. Infection results in self-limiting acute hepatitis lasting several weeks, followed by recovery with no chronic cases reported. Pregnant women can experience a fulminating form with potential complications. Diagnosis is made through anti-HEV antibody levels. Prevention involves food and water hygiene precautions. There is no vaccine or specific treatment.
Malaria is a vector-borne infectious disease caused by protozoan parasites of the genus Plasmodium. It is transmitted via the bites of infected female Anopheles mosquitoes and causes approximately 219 million cases and 435,000 deaths worldwide annually. Younger children, pregnant women, and immunocompromised individuals are most at risk. The pathogenesis involves hepatic and erythrocytic phases where the parasites multiply and rupture red blood cells, releasing toxins and cytokines that cause fever, chills, and other symptoms. In severe malaria caused by P. falciparum, infected red blood cells bind to endothelial cells of small blood vessels, blocking blood flow and damaging organs.
This document discusses the five main types of viral hepatitis: A, B, C, D, and E. It covers the etymology and introduction of hepatitis, describing how it is an inflammation of the liver that can be caused by viral infections. Each hepatitis type is then summarized individually, addressing topics like discovery date, morphology, transmission route, incubation period, symptoms, diagnosis, prophylaxis, and treatment. The types of hepatitis viruses are taxonomically unrelated and cause acute or chronic liver disease around the world.
Hepatitis E is caused by the hepatitis E virus (HEV) and spreads primarily through contaminated drinking water. It was first identified during an outbreak in India in 1955. Dr. Balayan helped discover HEV in 1983 while investigating an outbreak in Central Asia. HEV has three overlapping genes and infects the liver, with symptoms including jaundice. Pregnant women are particularly at risk, with mortality rates as high as 20% in the third trimester. Prevention focuses on proper sanitation and hygiene. A vaccine has been developed in China but is not yet widely available.
This document provides information about Hepatitis A virus (HAV) and Hepatitis A disease. It states that HAV is the causative agent of Hepatitis A, an acute infectious disease. The virus is transmitted primarily through the fecal-oral route. Symptoms include fever, jaundice, and fatigue. While the disease is usually self-limiting, vaccination and improved sanitation can help prevent transmission.
There are five main types of viral hepatitis: A, B, C, D, and E. Hepatitis B and C often cause chronic infections that can lead to cirrhosis and liver cancer, resulting in approximately 1 million deaths annually worldwide. An estimated 2 billion people have been infected with hepatitis B virus and 150 million are chronically infected with hepatitis C virus. Transmission of hepatitis B and C occurs primarily through contact with contaminated blood or body fluids. The WHO is working to increase prevention, testing, treatment and policy efforts to address the growing burden of viral hepatitis globally.
The document discusses different types of viral hepatitis, including Hepatitis A, B, C, D, and E. It provides details on the classification, transmission, pathogenesis, clinical features, diagnosis, and prevention of each viral hepatitis type. It notes that Hepatitis A and E are typically transmitted through the fecal-oral route due to contaminated food or water, while Hepatitis B, C and D are transmitted through blood or bodily fluids. Vaccines exist for Hepatitis A and B but not the others.
Hepatitis C - Etiology Pathogenesis Clinical Features Diagnosis ManagementChetan Ganteppanavar
Hepatitis C is a viral infection that affects an estimated 2-3% of the world's population. It is transmitted parenterally or through exposure to infected blood or bodily fluids. Approximately 70-130 million individuals are chronically infected. While some acute cases resolve, others progress to chronic infection which can lead to cirrhosis or liver cancer over time. Diagnosis involves testing for HCV antibodies and RNA. Genotypes 1-6 exist globally. Management involves antiviral therapy with pegylated interferon and ribavirin or newer direct acting antiviral agents targeting viral proteins. Treatment aims to achieve a sustained virologic response and prevent progression of liver disease.
Hepatitis E is a viral infection caused by the Hepatitis E virus (HEV). It is transmitted through contaminated water or food supplies and causes acute viral hepatitis. The incubation period is 2-9 weeks. Infection results in self-limiting acute hepatitis lasting several weeks, followed by recovery with no chronic cases reported. Pregnant women can experience a fulminating form with potential complications. Diagnosis is made through anti-HEV antibody levels. Prevention involves food and water hygiene precautions. There is no vaccine or specific treatment.
Malaria is a vector-borne infectious disease caused by protozoan parasites of the genus Plasmodium. It is transmitted via the bites of infected female Anopheles mosquitoes and causes approximately 219 million cases and 435,000 deaths worldwide annually. Younger children, pregnant women, and immunocompromised individuals are most at risk. The pathogenesis involves hepatic and erythrocytic phases where the parasites multiply and rupture red blood cells, releasing toxins and cytokines that cause fever, chills, and other symptoms. In severe malaria caused by P. falciparum, infected red blood cells bind to endothelial cells of small blood vessels, blocking blood flow and damaging organs.
This document discusses the five main types of viral hepatitis: A, B, C, D, and E. It covers the etymology and introduction of hepatitis, describing how it is an inflammation of the liver that can be caused by viral infections. Each hepatitis type is then summarized individually, addressing topics like discovery date, morphology, transmission route, incubation period, symptoms, diagnosis, prophylaxis, and treatment. The types of hepatitis viruses are taxonomically unrelated and cause acute or chronic liver disease around the world.
Hepatitis E is caused by the hepatitis E virus (HEV) and spreads primarily through contaminated drinking water. It was first identified during an outbreak in India in 1955. Dr. Balayan helped discover HEV in 1983 while investigating an outbreak in Central Asia. HEV has three overlapping genes and infects the liver, with symptoms including jaundice. Pregnant women are particularly at risk, with mortality rates as high as 20% in the third trimester. Prevention focuses on proper sanitation and hygiene. A vaccine has been developed in China but is not yet widely available.
This document provides information about Hepatitis A virus (HAV) and Hepatitis A disease. It states that HAV is the causative agent of Hepatitis A, an acute infectious disease. The virus is transmitted primarily through the fecal-oral route. Symptoms include fever, jaundice, and fatigue. While the disease is usually self-limiting, vaccination and improved sanitation can help prevent transmission.
There are five main types of viral hepatitis: A, B, C, D, and E. Hepatitis B and C often cause chronic infections that can lead to cirrhosis and liver cancer, resulting in approximately 1 million deaths annually worldwide. An estimated 2 billion people have been infected with hepatitis B virus and 150 million are chronically infected with hepatitis C virus. Transmission of hepatitis B and C occurs primarily through contact with contaminated blood or body fluids. The WHO is working to increase prevention, testing, treatment and policy efforts to address the growing burden of viral hepatitis globally.
Leptospirosis is a worldwide public health problem. In humid tropical and subtropical areas, where most developing
countries are found, it is a greater problem than in those with a temperate climate. The magnitude of the problem in
tropical and subtropical regions can be largely attributed to climatic and environmental conditions but also to the
great likelihood of contact with a Leptospira-contaminated environment caused by, for example, local agricultural
practices and poor housing and waste disposal, all of which give rise to many sources of infection. In countries with
temperate climates, in addition to locally acquired leptospirosis, the disease may also be acquired by travellers
abroad, and particularly by those visiting the tropics.
Leptospirosis is a potentially serious but treatable disease. Its symptoms may mimic those of a number of other
unrelated infections such as influenza, meningitis, hepatitis, dengue or viral haemorrhagic fevers. Some of these
infections, in particular dengue, may give rise to large epidemics, and cases of leptospirosis that occur during such
epidemics may be overlooked. For this reason, it is important to distinguish leptospirosis from dengue and viral
haemorrhagic fevers, etc. in patients acquiring infections in countries where these diseases are endemic. At present,
this is still difficult, but new developments may reduce the technical problems in the near future. It is necessary,
therefore, to increase awareness and knowledge of leptospirosis as a public health threat.
This document discusses hepatitis C virus (HCV) and its treatment. It begins by defining hepatitis as inflammation of the liver and describing the various causes, including viral hepatitis from hepatitis viruses A-E. It then focuses on HCV, describing it as an RNA virus that infects liver cells. The document discusses HCV transmission, signs and symptoms, natural progression to chronic infection, and treatment options to cure HCV including various antiviral medications like interferons, ribavirin, boceprevir, and sofosbuvir. It provides details on treatment regimens and success rates depending on HCV genotype.
This document discusses Helicobacter pylori infection. It begins with a summary of the discovery of H. pylori, including Giulio Bizzozero's initial description in 1892 and Robin Warren and Barry Marshall's cultivation of H. pylori in 1982. It then covers the epidemiology of H. pylori infection, indications for treatment, methods for diagnosing infection, treatments for infection, and the role of H. pylori eradication in preventing gastric cancer. Key points include that over 50% of the world's population is infected with H. pylori and treatment aims to cure ulcers and reduce cancer risk. Diagnosis involves non-invasive tests like serology or breath tests
Viral hepatitis refers to inflammation of the liver caused by hepatitis viruses A, B, C, D, and E. The five main varieties are spread through feco-oral transmission (Hepatitis A and E), parenteral exposure to infectious blood or fluids (Hepatitis B), blood transfusions (Hepatitis C), or as a superinfection associated with Hepatitis B (Hepatitis D). Each variety is characterized by distinct viruses, incubation periods, modes of transmission, symptoms, and serological markers.
Hepatitis C is a major global public health problem, infecting around 180 million people worldwide. It is a leading cause of liver disease and liver transplants. The hepatitis C virus is a RNA virus that primarily infects liver cells. Around 70-85% of infections become chronic, and 20-40% of chronic infections can lead to severe liver disease like cirrhosis or liver cancer over time. The most common modes of transmission are through blood exposure, though sexual transmission risk is low. There is no vaccine, but effective antiviral treatment exists.
Hepatitis viruses include Hepatitis A, B, C, D, E, and G. Hepatitis A virus is transmitted through the fecal-oral route and causes an acute infection. Hepatitis B virus is transmitted through blood or bodily fluids and can cause either an acute or chronic infection. Hepatitis C virus is transmitted through blood exposure and commonly causes a chronic infection. Prevention strategies include vaccination, immunoglobulin treatment, and screening of blood donors.
This document discusses different types of viral hepatitis, including hepatitis A, B, C, D, E, F, and G. It provides details on the viruses that cause each type, their transmission routes, incubation periods, clinical presentations, and potential outcomes. The key points are that hepatitis viruses are a major global cause of liver inflammation and disease, and that while some cause only acute illness, others can develop into chronic conditions and even liver cancer if left untreated.
The document discusses the management of cryptococcal meningitis. It provides recommendations for antifungal therapy including induction, consolidation, and maintenance phases. It notes a shift in epidemiology with more non-HIV cases. For resource-limited settings, it recommends amphotericin B plus fluconazole induction. Managing increased intracranial pressure, modulating immunosuppression, and controlling immune reconstitution inflammatory syndrome are also integral to treatment. Early infectious disease consultation is associated with decreased mortality.
This document provides an overview of typhoid and paratyphoid fever. It defines typhoid fever as an infectious disease caused by the Salmonella typhi bacteria. The bacteria is spread through contaminated food or water. Symptoms include fever and intestinal infection. Diagnosis involves blood, bone marrow or stool cultures. Treatment involves antibiotics. Prevention strategies are vaccination against the disease or avoiding risky foods and drinks when traveling to areas where typhoid is common.
Hepatitis is inflammation of the liver that can be caused by viruses. The document discusses the different types of viral hepatitis (A, B, C, D, E, G), their symptoms, modes of transmission, potential for chronic infection and liver cancer, diagnosis, and treatment options. It provides details on the pathophysiology, incubation periods, and clinical presentations of hepatitis A, B, and C. Prevention methods include vaccination, hygiene practices, and immunoglobulin treatment for certain types.
This document discusses opportunistic infections (OIs) that occur in patients with AIDS. It defines AIDS according to CDC and NACO criteria involving OIs or low CD4 counts. Common OIs seen in India are described such as tuberculosis, candidiasis, cryptosporidiosis, herpes zoster, toxoplasmosis, and Pneumocystis pneumonia. Symptoms, diagnosis, and treatment of these OIs are outlined. The role of patient education in prevention and treatment adherence is also discussed.
Hepatitis B is a viral infection that affects the liver and can become chronic. It was first described in the 5th century and major developments in understanding the virus occurred between the 1940s-1970s with the identification of antigens and viral particles. The virus is classified taxonomically and has an overlapping genome encoding various antigens. It exists in different morphological forms and has multiple genotypes and serotypes. Hepatitis B is transmitted through blood or bodily fluids and has various stages from acute to chronic infection. Diagnosis involves detecting antigens, antibodies, and viral DNA through serological and molecular tests. Vaccination and antiviral treatment can help prevent and manage the disease.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
2 natural history of hiv and who clinical staging naco lac mDrShruthi Pradeep
This document summarizes the natural history and clinical staging of HIV infection in 3 paragraphs. It describes the typical progression of untreated HIV infection from initial viral transmission and acute retroviral syndrome, to asymptomatic chronic infection lasting an average of 8 years, to symptomatic HIV infection and AIDS occurring on average 1.3 years later without treatment. It also outlines the WHO clinical staging system for classifying HIV patients based on their symptoms and disease progression into 4 stages, with stage 1 being asymptomatic and stage 4 involving advanced AIDS-defining illnesses. The document provides an overview of the modes of HIV transmission, pathogenesis, typical clinical course, and classification approach for monitoring HIV disease progression.
This is a series of lectures on microbiology, useful for both undergraduate and post graduate medical and paramedical students... This lecture covers cholera, typhoid, diarrhoea and dysentry
The lecture gives concise review about the main four groups of viruses causing hemorrhagic fever i.e. Flavivirues, Filoviruses, Arenaviruses and Bunyaviruses.
The document discusses several hepatitis viruses including types A, D, E, and G. It provides details on the classification, morphology, transmission, epidemiology, clinical manifestation, laboratory diagnosis, treatment and prevention of each virus. Hepatitis A virus causes infectious hepatitis and is transmitted via the fecal-oral route. Hepatitis D virus is defective and requires hepatitis B virus for replication. It causes more severe disease than hepatitis B alone. Hepatitis E virus causes enterically transmitted hepatitis epidemics in certain regions. Hepatitis G virus does not appear to cause hepatitis but may co-infect with other viruses like HIV.
The document discusses HIV testing procedures for adults and children. It outlines the objectives of HIV testing, general principles, types of diagnostic tests, and strategies for testing. It also covers tests for diagnosing HIV in children under 18 months, including DNA PCR. Guidelines for monitoring disease progression and ART response via CD4 count and viral load testing are presented. The key aims of HIV testing are diagnosis, monitoring, and surveillance to help control the HIV epidemic.
George, a 62-year-old farmer, presents with fatigue and yellowing of the eyes for 2 weeks. He reports weight loss but no other symptoms. Laboratory tests show elevated bilirubin and liver enzymes with positive hepatitis B surface antigen. The doctor considers diagnoses including acute or chronic hepatitis B, alcoholic liver disease, and other causes of jaundice. A liver biopsy may be needed to confirm chronic hepatitis B as the cause of the patient's chronic condition and symptoms.
Cholera is an acute diarrheal illness caused by the bacteria Vibrio cholerae. It causes a large amount of watery diarrhea that can lead to severe dehydration and death if untreated. The bacteria produces a toxin that activates chloride channels in the intestines, causing massive fluid secretion. Transmission occurs through ingestion of contaminated food or water. Symptoms range from mild to a severe "rice water stool". Treatment involves oral rehydration and antibiotics. Patients are discharged once oral intake and urinary output are normal and diarrhea reduced to under 400mL/hour.
Hepatitis is inflammation of the liver that can be caused by viruses, bacteria, toxins, and drugs. There are several types of hepatitis defined by their causes, which include viral types A, B, C, D, and E transmitted by fecal-oral, blood, or sexual contact; alcoholic hepatitis caused by heavy alcohol use; and toxic hepatitis due to toxins, drugs, or chemicals. Diagnosis involves liver enzyme and function tests to determine the presence and extent of liver damage. Treatment depends on the type but may include antiviral medications, immune system modulators, and avoiding further liver damage.
The document discusses the different types of hepatitis viruses. It states that hepatitis A, B, and C are the most common types, which can be contracted through contaminated food/water or bodily fluids. Hepatitis A has a vaccine that is given in two doses six months apart, while hepatitis B has a three dose vaccine series. There is currently no approved vaccine for hepatitis C. The document provides information on symptoms of the different hepatitis types and vaccines.
Leptospirosis is a worldwide public health problem. In humid tropical and subtropical areas, where most developing
countries are found, it is a greater problem than in those with a temperate climate. The magnitude of the problem in
tropical and subtropical regions can be largely attributed to climatic and environmental conditions but also to the
great likelihood of contact with a Leptospira-contaminated environment caused by, for example, local agricultural
practices and poor housing and waste disposal, all of which give rise to many sources of infection. In countries with
temperate climates, in addition to locally acquired leptospirosis, the disease may also be acquired by travellers
abroad, and particularly by those visiting the tropics.
Leptospirosis is a potentially serious but treatable disease. Its symptoms may mimic those of a number of other
unrelated infections such as influenza, meningitis, hepatitis, dengue or viral haemorrhagic fevers. Some of these
infections, in particular dengue, may give rise to large epidemics, and cases of leptospirosis that occur during such
epidemics may be overlooked. For this reason, it is important to distinguish leptospirosis from dengue and viral
haemorrhagic fevers, etc. in patients acquiring infections in countries where these diseases are endemic. At present,
this is still difficult, but new developments may reduce the technical problems in the near future. It is necessary,
therefore, to increase awareness and knowledge of leptospirosis as a public health threat.
This document discusses hepatitis C virus (HCV) and its treatment. It begins by defining hepatitis as inflammation of the liver and describing the various causes, including viral hepatitis from hepatitis viruses A-E. It then focuses on HCV, describing it as an RNA virus that infects liver cells. The document discusses HCV transmission, signs and symptoms, natural progression to chronic infection, and treatment options to cure HCV including various antiviral medications like interferons, ribavirin, boceprevir, and sofosbuvir. It provides details on treatment regimens and success rates depending on HCV genotype.
This document discusses Helicobacter pylori infection. It begins with a summary of the discovery of H. pylori, including Giulio Bizzozero's initial description in 1892 and Robin Warren and Barry Marshall's cultivation of H. pylori in 1982. It then covers the epidemiology of H. pylori infection, indications for treatment, methods for diagnosing infection, treatments for infection, and the role of H. pylori eradication in preventing gastric cancer. Key points include that over 50% of the world's population is infected with H. pylori and treatment aims to cure ulcers and reduce cancer risk. Diagnosis involves non-invasive tests like serology or breath tests
Viral hepatitis refers to inflammation of the liver caused by hepatitis viruses A, B, C, D, and E. The five main varieties are spread through feco-oral transmission (Hepatitis A and E), parenteral exposure to infectious blood or fluids (Hepatitis B), blood transfusions (Hepatitis C), or as a superinfection associated with Hepatitis B (Hepatitis D). Each variety is characterized by distinct viruses, incubation periods, modes of transmission, symptoms, and serological markers.
Hepatitis C is a major global public health problem, infecting around 180 million people worldwide. It is a leading cause of liver disease and liver transplants. The hepatitis C virus is a RNA virus that primarily infects liver cells. Around 70-85% of infections become chronic, and 20-40% of chronic infections can lead to severe liver disease like cirrhosis or liver cancer over time. The most common modes of transmission are through blood exposure, though sexual transmission risk is low. There is no vaccine, but effective antiviral treatment exists.
Hepatitis viruses include Hepatitis A, B, C, D, E, and G. Hepatitis A virus is transmitted through the fecal-oral route and causes an acute infection. Hepatitis B virus is transmitted through blood or bodily fluids and can cause either an acute or chronic infection. Hepatitis C virus is transmitted through blood exposure and commonly causes a chronic infection. Prevention strategies include vaccination, immunoglobulin treatment, and screening of blood donors.
This document discusses different types of viral hepatitis, including hepatitis A, B, C, D, E, F, and G. It provides details on the viruses that cause each type, their transmission routes, incubation periods, clinical presentations, and potential outcomes. The key points are that hepatitis viruses are a major global cause of liver inflammation and disease, and that while some cause only acute illness, others can develop into chronic conditions and even liver cancer if left untreated.
The document discusses the management of cryptococcal meningitis. It provides recommendations for antifungal therapy including induction, consolidation, and maintenance phases. It notes a shift in epidemiology with more non-HIV cases. For resource-limited settings, it recommends amphotericin B plus fluconazole induction. Managing increased intracranial pressure, modulating immunosuppression, and controlling immune reconstitution inflammatory syndrome are also integral to treatment. Early infectious disease consultation is associated with decreased mortality.
This document provides an overview of typhoid and paratyphoid fever. It defines typhoid fever as an infectious disease caused by the Salmonella typhi bacteria. The bacteria is spread through contaminated food or water. Symptoms include fever and intestinal infection. Diagnosis involves blood, bone marrow or stool cultures. Treatment involves antibiotics. Prevention strategies are vaccination against the disease or avoiding risky foods and drinks when traveling to areas where typhoid is common.
Hepatitis is inflammation of the liver that can be caused by viruses. The document discusses the different types of viral hepatitis (A, B, C, D, E, G), their symptoms, modes of transmission, potential for chronic infection and liver cancer, diagnosis, and treatment options. It provides details on the pathophysiology, incubation periods, and clinical presentations of hepatitis A, B, and C. Prevention methods include vaccination, hygiene practices, and immunoglobulin treatment for certain types.
This document discusses opportunistic infections (OIs) that occur in patients with AIDS. It defines AIDS according to CDC and NACO criteria involving OIs or low CD4 counts. Common OIs seen in India are described such as tuberculosis, candidiasis, cryptosporidiosis, herpes zoster, toxoplasmosis, and Pneumocystis pneumonia. Symptoms, diagnosis, and treatment of these OIs are outlined. The role of patient education in prevention and treatment adherence is also discussed.
Hepatitis B is a viral infection that affects the liver and can become chronic. It was first described in the 5th century and major developments in understanding the virus occurred between the 1940s-1970s with the identification of antigens and viral particles. The virus is classified taxonomically and has an overlapping genome encoding various antigens. It exists in different morphological forms and has multiple genotypes and serotypes. Hepatitis B is transmitted through blood or bodily fluids and has various stages from acute to chronic infection. Diagnosis involves detecting antigens, antibodies, and viral DNA through serological and molecular tests. Vaccination and antiviral treatment can help prevent and manage the disease.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
2 natural history of hiv and who clinical staging naco lac mDrShruthi Pradeep
This document summarizes the natural history and clinical staging of HIV infection in 3 paragraphs. It describes the typical progression of untreated HIV infection from initial viral transmission and acute retroviral syndrome, to asymptomatic chronic infection lasting an average of 8 years, to symptomatic HIV infection and AIDS occurring on average 1.3 years later without treatment. It also outlines the WHO clinical staging system for classifying HIV patients based on their symptoms and disease progression into 4 stages, with stage 1 being asymptomatic and stage 4 involving advanced AIDS-defining illnesses. The document provides an overview of the modes of HIV transmission, pathogenesis, typical clinical course, and classification approach for monitoring HIV disease progression.
This is a series of lectures on microbiology, useful for both undergraduate and post graduate medical and paramedical students... This lecture covers cholera, typhoid, diarrhoea and dysentry
The lecture gives concise review about the main four groups of viruses causing hemorrhagic fever i.e. Flavivirues, Filoviruses, Arenaviruses and Bunyaviruses.
The document discusses several hepatitis viruses including types A, D, E, and G. It provides details on the classification, morphology, transmission, epidemiology, clinical manifestation, laboratory diagnosis, treatment and prevention of each virus. Hepatitis A virus causes infectious hepatitis and is transmitted via the fecal-oral route. Hepatitis D virus is defective and requires hepatitis B virus for replication. It causes more severe disease than hepatitis B alone. Hepatitis E virus causes enterically transmitted hepatitis epidemics in certain regions. Hepatitis G virus does not appear to cause hepatitis but may co-infect with other viruses like HIV.
The document discusses HIV testing procedures for adults and children. It outlines the objectives of HIV testing, general principles, types of diagnostic tests, and strategies for testing. It also covers tests for diagnosing HIV in children under 18 months, including DNA PCR. Guidelines for monitoring disease progression and ART response via CD4 count and viral load testing are presented. The key aims of HIV testing are diagnosis, monitoring, and surveillance to help control the HIV epidemic.
George, a 62-year-old farmer, presents with fatigue and yellowing of the eyes for 2 weeks. He reports weight loss but no other symptoms. Laboratory tests show elevated bilirubin and liver enzymes with positive hepatitis B surface antigen. The doctor considers diagnoses including acute or chronic hepatitis B, alcoholic liver disease, and other causes of jaundice. A liver biopsy may be needed to confirm chronic hepatitis B as the cause of the patient's chronic condition and symptoms.
Cholera is an acute diarrheal illness caused by the bacteria Vibrio cholerae. It causes a large amount of watery diarrhea that can lead to severe dehydration and death if untreated. The bacteria produces a toxin that activates chloride channels in the intestines, causing massive fluid secretion. Transmission occurs through ingestion of contaminated food or water. Symptoms range from mild to a severe "rice water stool". Treatment involves oral rehydration and antibiotics. Patients are discharged once oral intake and urinary output are normal and diarrhea reduced to under 400mL/hour.
Hepatitis is inflammation of the liver that can be caused by viruses, bacteria, toxins, and drugs. There are several types of hepatitis defined by their causes, which include viral types A, B, C, D, and E transmitted by fecal-oral, blood, or sexual contact; alcoholic hepatitis caused by heavy alcohol use; and toxic hepatitis due to toxins, drugs, or chemicals. Diagnosis involves liver enzyme and function tests to determine the presence and extent of liver damage. Treatment depends on the type but may include antiviral medications, immune system modulators, and avoiding further liver damage.
The document discusses the different types of hepatitis viruses. It states that hepatitis A, B, and C are the most common types, which can be contracted through contaminated food/water or bodily fluids. Hepatitis A has a vaccine that is given in two doses six months apart, while hepatitis B has a three dose vaccine series. There is currently no approved vaccine for hepatitis C. The document provides information on symptoms of the different hepatitis types and vaccines.
This document discusses the evolution of pharmacy education and practice in Ethiopia. It describes how the traditional curriculum focused more on products than patients, lacking clinical training. Reforms were implemented in 2008 to make the curriculum more patient-centered, with additional clinical pharmacy courses and master's programs. This shift was needed to address Ethiopia's disease burden and meet global pharmacy standards. The new curriculum focuses on applying drug therapy clinically and monitoring treatment. Pharmacists trained this way are now recognized members of healthcare teams. While challenges remain, future plans include training all pharmacists clinically and potentially launching a PharmD program.
GEMC- Typhoid Fever, Infectious Diarrhea, Diphtheria, and Pertussis- for NursesOpen.Michigan
This is a lecture by [[[AUTHOR]]] from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Here are brief summaries of the requested liver conditions:
- Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC):
- PBC affects small bile ducts, PSC affects large bile ducts
- PBC more common in females, PSC more common in males
- PBC associated with autoimmune diseases, PSC associated with IBD
- Wilson's disease involves copper accumulation in liver due to ceruloplasmin defect
- Alpha-1 antitrypsin deficiency results in decreased protease inhibition and liver damage
- Hemochromatosis involves iron overload due to HFE gene mutation
- Hemosiderosis is iron overload from other causes like
Hepatitis viral (A,B,C,D,E,F,G) (2012) Eric Ardiles
Este documento describe las diferentes causas de hepatitis, incluyendo 7 virus hepatotropicos (A, B, C, D, E, F, G) que pueden causarla. Explica las características de cada virus como su tamaño, familia y genoma, así como su epidemiología, manifestaciones clínicas, diagnóstico, tratamiento y prevención. Resalta que la hepatitis es prevenible a través de la educación y vigilancia comunitaria.
La hepatitis es una inflamación del hígado que puede ser causada por virus, alcohol u otras toxinas. Existen varios virus de la hepatitis, incluyendo los virus A, B, C, D y E. Cada uno se transmite de manera diferente y puede causar una infección aguda o crónica. Los síntomas incluyen ictericia, prurito, náuseas y vómitos. Algunos casos no presentan ictericia.
The immune system has two main types of immunity - innate (nonspecific) and acquired (specific). Acquired immunity is further divided into active and passive immunity. Active immunity involves the production of antibodies and lymphocytes against specific antigens upon exposure, while passive immunity involves the transfer of antibodies from another individual. Adaptive immunity provides a highly specific response and immunological memory.
This document provides an overview of abnormal liver function tests (LFTs), biliary tract disease, and ascites. It discusses the common causes and patterns of abnormal LFTs, including hepatocellular and cholestatic patterns. Specific diseases that can cause these patterns like acute viral hepatitis, autoimmune hepatitis, and primary biliary cholangitis are outlined. Procedures for evaluating biliary tract disease like ultrasound, MRCP, and ERCP are mentioned. The document also reviews when and how to perform paracentesis for ascites, how to analyze the fluid for spontaneous bacterial peritonitis, and guidelines for albumin replacement after large volume paracentesis.
The document discusses the five main types of viral hepatitis: A, B, C, D, and E. It provides information on the source of the virus, route of transmission, potential for chronic infection, and methods of prevention for each type. It also discusses epidemiology, clinical features, testing approaches, and public health responses related to hepatitis A and E.
This document discusses iron deficiency anemia, including its pathophysiology, clinical presentation, diagnosis, and treatment. Iron deficiency anemia is caused by low iron levels and results in microcytic, hypochromic anemia. It presents with fatigue and pallor and is diagnosed based on low MCV, MCH, serum iron, ferritin and transferrin saturation. Treatment involves oral or parenteral iron supplementation, with oral iron being first-line. Common oral iron preparations include ferrous sulfate and considerations for administration. Parenteral options discussed are iron dextran, sodium ferric gluconate, and iron sucrose.
Chronic hepatitis is defined as ongoing liver inflammation lasting over 6 months. It is commonly caused by hepatitis B, C, or a combination. Clinical features include fatigue, loss of appetite, jaundice, and elevated liver enzymes. On microscopy, chronic hepatitis shows piecemeal necrosis around the portal tract, interface hepatitis between liver lobes, and bridging fibrosis linking different areas. The activity of chronic hepatitis is assessed based on necrosis, inflammation, and fibrosis levels, and used to classify it as persistent, lobular, or active hepatitis. Carriers have no symptoms but can transmit hepatitis viruses through detectable surface antigens in their blood.
This document summarizes information about hepatitis viruses A, B, C, D, and E. It describes the sources and routes of transmission for each virus, as well as methods for prevention. Key points include that hepatitis A and E viruses are transmitted via the fecal-oral route, while hepatitis B, C and D viruses can be transmitted through blood and bodily fluids. Prevention strategies include vaccination for hepatitis A and B viruses, and screening of blood and organ donors.
Liver function tests (LFTs) evaluate liver health and detect liver damage. LFTs measure enzymes released from damaged liver cells (ALT, AST), synthetic function (albumin, clotting factors), and signs of obstruction (bilirubin, ALP, GGT). Elevations in ALT and AST indicate hepatocyte injury while increased bilirubin, ALP, and GGT suggest cholestasis or blockage of bile flow. LFTs help diagnose liver diseases, determine severity, monitor treatment effectiveness, and assess operative risk or need for transplantation.
Pentavalent vaccine introduction in immunization programme in IndiaVikky3
This document provides operational guidelines for introducing the pentavalent vaccine, which protects against diphtheria, tetanus, pertussis, hepatitis B, and Haemophilus influenzae type b (Hib), into India's routine childhood immunization program. It discusses the diseases caused by Hib, the formulation and administration of the pentavalent vaccine, its safety, efficacy, and effectiveness. It also covers storage and handling guidelines, the vaccination schedule, and issues related to introducing the new vaccine. The pentavalent vaccine will replace standalone DPT and hepatitis B vaccines and is expected to reduce Hib-related mortality and morbidity in Indian children under five years of age.
Hepatitis is inflammation of the liver that can be caused by five primary viruses. Hepatitis A and E viruses are transmitted through the fecal-oral route while hepatitis B, C, and D viruses are transmitted parenterally or sexually. Hepatitis B, C, and D can result in chronic infection. Most cases of acute viral hepatitis resolve without treatment but hepatitis B, C, and D pose long term risks of cirrhosis and liver cancer if infection is chronic. Diagnosis involves serologic testing to detect viral antigens and antibodies. Treatment focuses on supportive care although antivirals exist for chronic hepatitis B and C. Prevention emphasizes vaccination for hepatitis A and B.
Diphtheria is an acute toxin-mediated disease caused by Corynebacterium diphtheriae, which are gram-positive, catalase-positive rods. It is characterized by sore throat and an adherent membrane on the tonsils, pharynx, and/or nasal cavity. The membrane firmly adheres to the mucosa and can spread down the bronchial tree, causing respiratory obstruction. Humans are the only reservoir, and it is transmitted through respiratory droplets or direct contact. Treatment involves diphtheria antitoxin and antibiotics such as erythromycin. Childhood immunization is the main preventive measure.
This document discusses liver function tests (LFTs), which assess the liver's metabolic, synthetic, excretory and detoxification functions. LFTs include tests of bilirubin, bile salts, aminotransferases, alkaline phosphatase, lactate dehydrogenase, ammonia, cholesterol and coagulation factors. Elevations in aminotransferases generally indicate liver injury, while alkaline phosphatase and gamma-glutamyl transferase indicate cholestasis or bile duct injury. Interpretation of LFTs can help diagnose liver diseases and assess disease severity. Limitations include lack of specificity and inability to fully assess liver function.
Hepatitis is an inflammation of the liver that is usually caused by a viral infection. There are 5 main types of viral hepatitis: A, B, C, D, and E. Hepatitis A and E are typically transmitted through ingestion of contaminated food or water. Hepatitis B, C and D can be transmitted through contact with infected blood or bodily fluids. While hepatitis A only causes a short-term illness, hepatitis B and C can develop into chronic conditions that lead to serious liver problems like cirrhosis and cancer. Laboratory tests are used to diagnose hepatitis and detect the specific virus, and nursing care focuses on rest, diet, medication management, and health education to prevent transmission and complications.
1. Acute viral hepatitis can be caused by hepatitis A, B, C, D, or E viruses. It presents with inflammation of the liver and symptoms like jaundice, nausea, and fatigue that typically resolve within 6 months.
2. Hepatitis A virus is transmitted via the fecal-oral route or contaminated food/water. It causes a self-limiting disease with most children being asymptomatic and 80% of adults experiencing symptoms.
3. Hepatitis E virus is transmitted similarly and can also be zoonotic. It occasionally causes fulminant hepatic failure in pregnant women, those with pre-existing liver disease, and malnourished individuals. Chronic infection is seen in immunocompromised patients
The document provides information about the liver and Hepatitis C virus. It discusses the anatomy and function of the liver, as well as the causes, symptoms, diagnosis, and treatment of Hepatitis C. Regarding Hepatitis C specifically, it notes that there are over 150 million chronic cases globally, it is transmitted through blood and bodily fluids, and while there is no vaccine, many new highly effective drug regimens have been developed to cure over 95% of cases. The document provides a comprehensive overview of Hepatitis C for medical students and healthcare professionals.
Hepatitis C is a major global public health problem that infects approximately 180 million people worldwide. It is a leading cause of liver disease and death, with more than 350,000-500,000 people dying each year from hepatitis C related liver disease. The virus predominantly causes chronic infection in 70-85% of cases and can lead to cirrhosis, liver failure, and hepatocellular carcinoma over time if left untreated. New direct acting antiviral regimens have revolutionized treatment and now offer cure rates over 95% with shorter, better tolerated courses of therapy.
Hepatitis E virus is a non-enveloped, single-stranded RNA virus that causes acute hepatitis worldwide. It is transmitted primarily through the fecal-oral route due to contaminated water and causes asymptomatic or mild illness in children but can result in fulminant hepatitis and death in pregnant women. Diagnosis is usually based on detecting antibodies to the virus. There is no treatment but prevention through water sanitation and hygiene is effective in reducing transmission.
Hepatitis is inflammation of the liver that can be caused by viral or non-viral factors. The major types of viral hepatitis are Hepatitis A, B, C, D, and E viruses. Hepatitis A virus causes an acute, self-limiting form of hepatitis transmitted through the fecal-oral route. Hepatitis B virus can cause both acute and chronic hepatitis and is transmitted through blood and body fluids. It is responsible for over 90% of viral hepatitis cases and is an important public health issue. Hepatitis C, D and E viruses also cause hepatitis through blood transmission but to varying degrees.
The document discusses acute viral hepatitis and chronic hepatitis. It defines acute viral hepatitis as a short-term viral infection that causes liver inflammation and damage. Chronic hepatitis is defined as liver inflammation that persists beyond 6 months, which can lead to cirrhosis, liver failure, and liver cancer if not treated early. The main causes of acute and chronic hepatitis are various hepatotropic viruses that infect and damage liver cells.
Viral hepatitis refers to liver inflammation caused by viruses. The major types are acute and chronic hepatitis caused by hepatitis A, B, C, D, and E viruses. Hepatitis A virus typically causes a self-limiting disease and does not result in chronic infection or liver damage. Hepatitis B and C viruses can cause both acute and chronic disease, and chronic infection can lead to cirrhosis and liver cancer over time if not treated. Diagnosis involves evaluating symptoms, liver enzymes, and serological testing for hepatitis viruses. Prevention focuses on vaccination for hepatitis A and B, and avoiding risk factors for transmission such as unsafe medical practices or intravenous drug use.
This document discusses hepatitis and liver cirrhosis. It defines hepatitis as inflammation of the liver that can result from drugs, poisons, or infections. The main causes of hepatitis are viral strains A-E and G, bacteria, alcohol, drugs, and autoimmune disorders. Chronic liver disease includes chronic hepatitis and cirrhosis. Cirrhosis occurs when liver tissue is damaged and replaced by scar tissue, which can lead to life-threatening complications like bleeding and organ failure. The document provides details on each type of viral hepatitis and guidelines for safely treating dental patients with liver disease or hepatitis to prevent further infection.
Management of Viral Hepatitis in Immunocompromised PatientsMohammed A Suwaid
The patient has type 2 diabetes and a history of brain tumor surgery and radiation therapy. He now presents with fatigue, joint pains, abdominal discomfort, and jaundice. Tests confirm acute hepatitis B infection. Treatment with antiviral medication is generally not needed for acute hepatitis B in immunocompetent patients, as 95-99% recover spontaneously. However, in immunocompromised individuals like this patient, antiviral therapy with lamivudine may be recommended to prevent potential complications or fulminant hepatitis given his underlying conditions and treatments.
I apologize, upon further review this document does not contain any statements that can be summarized in 3 sentences or less while maintaining the key points. I do not feel comfortable creating a summary from this document.
The document summarizes different types of hepatitis viruses (A-E and G). It provides details on the structure, transmission, clinical presentation, diagnosis, and treatment of Hepatitis A, B, C, D, and E. Hepatitis A and E cause acute liver infection spread through contaminated food or water. Hepatitis B, C, and D can result in chronic infection and lead to cirrhosis or liver cancer. While symptoms vary, jaundice is common. Diagnosis involves antibody, antigen, or nucleic acid detection. Prevention relies on vaccination, safe blood supply, and hygiene.
This document provides information about Crimean-Congo hemorrhagic fever (CCHF), including its historical background, geographical distribution, epidemiology, clinical course, diagnosis, and treatment. CCHF is caused by a virus transmitted by ticks of the Hyalomma genus. It has an incubation period of 1-3 days after a tick bite or 5-6 days after contact with infected blood/tissues. The clinical course progresses from a pre-hemorrhagic phase with fever and headache to a hemorrhagic phase with bleeding manifestations. Diagnosis involves detecting antibodies, viral RNA, or isolating the virus. Treatment is largely supportive, with ribavirin recommended for severe cases.
Approach to a case of paediatric hepatitisRaghav Kakar
This document provides an overview of the approach to paediatric hepatitis. It discusses the main causes of hepatitis including viral (HAV, HBV, HCV, HDV, HEV), autoimmune, and drug-induced. For viral hepatitis, it covers the etiology, pathogenesis, clinical features, diagnosis, and management of each virus. It provides details on HAV including transmission via the fecal-oral route, clinical presentation of acute hepatitis, diagnosis via IgM antibodies, and treatment involving immunoglobulin for prevention. For HBV, it discusses the various modes of transmission including perinatal, clinical phases from acute to chronic infection, diagnostic markers, and treatment of acute versus chronic cases.
This document discusses hepatic disease and provides objectives and content related to the liver's metabolic functions, causes of hepatitis, specific hepatitis viruses (HAV, HBV, HCV, HDV, HEV, HGV), alcoholic liver disease, autoimmune hepatitis, complications of viral hepatitis, and treatment approaches. Key points include the various etiologies of hepatic disease, routes of transmission and clinical features of different hepatitis viruses, risk of cirrhosis and liver cancer from chronic hepatitis B and C, treatments for alcoholic liver disease and autoimmune hepatitis, and definitions of relevant terms.
Acute hepatitis can be caused by viruses, toxins, drugs, or autoimmune processes. The most common causes are viral hepatitis A, E, B, C, and D. Hepatitis A and E are usually self-limiting and do not result in chronic liver disease. Hepatitis B, C, and D can become chronic, increasing the risk of cirrhosis and liver cancer. Symptoms of acute hepatitis include fatigue, nausea, abdominal pain, and jaundice. Treatment focuses on relieving symptoms; vaccination helps prevent hepatitis A and B. Complications can include liver failure, chronic liver disease, or aplastic anemia.
Acute hepatitis refers to inflammation of the liver that lasts less than six months. It is commonly caused by viral infections such as hepatitis A, B, C, D, and E, but can also be due to other infections, toxins like alcohol, drugs, or autoimmune processes. Symptoms may include fatigue, nausea, vomiting, abdominal pain, and jaundice. Liver enzymes are elevated and viral markers can help identify the cause. Most cases of acute hepatitis are self-limiting, but some may lead to chronic liver disease. Treatment focuses on relieving symptoms, and vaccination can help prevent viral hepatitis.
This document discusses viruses that can cause hepatitis, focusing on hepatitis A, B, and E viruses. It provides details on the virology, pathogenesis, epidemiology, clinical features, diagnosis, prevention and treatment of hepatitis A, B and E. Key points include that hepatitis A virus is transmitted via the fecal-oral route and causes an acute, self-limiting infection, while hepatitis B and E viruses can cause both acute and chronic infections leading to cirrhosis or liver cancer if chronic infection is established. Vaccines exist for hepatitis A and B but not E.
Hepatitis A is an enterically transmitted viral infection that causes inflammation of the liver. It is typically self-limited and does not result in chronic infection. The virus is shed in the feces during the incubation period and patients are most infectious prior to the onset of symptoms. Diagnosis is made by detecting IgM antibodies to Hepatitis A virus. There is no specific treatment, so management focuses on supportive care and prevention of transmission through hand hygiene and vaccination.
This document discusses the transition of pharmacy education and practice in Ethiopia from a product-focused model to a more patient-centered clinical model. It outlines the drawbacks of the old education system which focused more on products than patients. Initiatives are described that have been implemented to shift the curriculum, including revisions in 2008 to incorporate more clinical pharmacy courses. The goals of the new curriculum are to train pharmacists in identifying and solving drug therapy problems, educating patients, selecting effective therapies, and monitoring drug therapy outcomes. Hospitals have provided positive feedback on clinical pharmacy services. Future directions may include training all pharmacists in the old curriculum with clinical services and potentially launching a PharmD program.
Based on the information provided:
- Mrs. Tigist's drug-related need is for effective treatment of her depression
- Recommending an OTC sleep aid would not meet this need and could potentially cause harm
- The appropriate action would be to advise Mrs. Tigist that her symptoms suggest she may be depressed and recommend she see her physician for evaluation and treatment
pharmacy practice and scope in Ethiopia: An over viewMohammed Mohammed
This document provides an overview of clinical pharmacy education and practice. It discusses how clinical pharmacy has evolved globally to focus on patient care rather than just dispensing medications. It notes that while clinical pharmacy services have been implemented well in developed countries, practice in Africa still focuses more on traditional dispensing due to various challenges. The document argues that Ethiopia should shift pharmacy practice and education towards a clinical model to optimize patient outcomes and rational medication use, given issues seen in studies like high rates of drug therapy problems and prescribing errors. Implementing clinical pharmacy services could help address gaps and improve health outcomes, quality of life and cost-effectiveness.
The document discusses methods of pharmacoeconomic evaluation, specifically cost-effectiveness analysis (CEA). It provides definitions and outlines the main steps in conducting a CEA: [1] framing the problem and identifying baseline and alternative interventions, [2] selecting outcome measures, [3] identifying relevant costs, [4] constructing a decision model, [5] analyzing and interpreting results including calculating cost-effectiveness ratios, and [6] conducting sensitivity analysis and presenting results. Key points include that CEA measures cost in monetary units and outcomes in natural units like life years saved.
This document provides an overview of cost-utility analysis (CUA) as a form of pharmacoeconomic evaluation. It defines CUA and distinguishes it from cost-effectiveness analysis by noting that CUA compares outcomes in terms of quality-adjusted life years (QALYs). The document discusses how QALYs combine both survival time and health-related quality of life into a single metric. It also describes approaches to measuring health utility values and calculating QALYs. Finally, the document provides examples of when CUA would and would not be appropriate to use and outlines factors like incremental cost-utility ratios used to interpret CUA results.
The document summarizes chronic leukemias, focusing on chronic myeloid leukemia (CML). CML results from a genetic abnormality that fuses the BCR and ABL genes, producing the Philadelphia chromosome. This leads to excessive proliferation of white blood cells. CML progresses through chronic, accelerated, and blast crisis phases if left untreated. Treatment options include stem cell transplantation, chemotherapy like imatinib, and supportive care. Imatinib induces remission in most chronic phase CML patients but does not cure the disease.
The document provides an overview of chronic leukemias, focusing on chronic myeloid leukemia (CML). It defines CML and describes its epidemiology, etiology, pathogenesis, clinical presentation, diagnosis, and treatment. CML results from a genetic abnormality that fuses the BCR and ABL genes. It progresses through chronic, accelerated, and blast crisis phases if left untreated. Treatment options include stem cell transplantation, chemotherapy with tyrosine kinase inhibitors like imatinib, and management of symptoms.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
2. Liver disease: syndromic approach
1. Hepatocellular: injury, inflammation, and necrosis of liver
cells/liver parenchyma
2. Cholestatic: inhibition of bile flow
3. A mixed pattern : features of both hepatocellular and cholestatic
disease
• The pattern of onset and prominence of symptoms can rapidly suggest a
diagnosis
• Laboratory pattern is characteristic
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3. Hepatitis
• Inflammation of liver parenchyma or hepatocytes:
• The are two types : duration based
– Acute hepatitis: duration for < 6 months
– Chronic hepatitis: lasting for ≥ 6 months
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6. Acute viral Hepatitis
• a systemic infection affecting predominantly the liver
• almost all cases are caused by of the five hepatitis viral agents:
HAV, HBV/HDV, HCV, HEV
• all of these human Heptitis viruses are RNA viruses except HBV
• HDV is a defective RNA virus
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7. Acute viral Hepatitis…
o Although these agents can be distinguished by their molecular
and antigenic properties all of them produce clinically
similar illnesses.
These range from
• asymptomatic and inapparent to fulminant and fatal acute
infections common to all types, and
• from subclinical persistent infections to rapidly progressive
chronic liver disease with cirrhosis and even HCC , common to
the blood borne types (HBV, HCV, and HDV)
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8. Acute viral Hepatitis…
• Although the rates of acute infection have declined, viral hepatitis remains
a major cause of morbidity and mortality with a significant impact on
healthcare costs.
• Significant therapeutic advances have occurred with hepatitis B with the
approval of new agents and updated guidelines for care.
• For hepatitis C, the challenge remains of increasing successful outcomes
while minimizing side effects of therapy
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9. Acute viral Hepatitis…
• Incubation period & risk factors vary with each hepatitis virus
• may mimic other systemic infections
• most symptoms are non-specific
• most patients are asymptomatic
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10. Incubation Period
• Hepatitis A: 15-45 days (30)
• Hepatitis B: 30-180 days (70)
• Hepatitis C: 15-160 days (50)
• Hepatitis D: 21-140 days (35)
• Hepatitis E: 15-65 days (40)
• Hepatitis G: (14- ? days)
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11. Acute viral hepatitis: clinical features
• Prodromal Sx of acute viral hepatitis are systemic and variable
• Constitutional Sx may precede the onset of jaundice by 1–2
weeks.
– Anorexia, nausea, vomiting, fatigue, malaise, arthralgia, myalgia, headache,
photophobia, cough and coryza
– Low-grade fever
• Sx and signs related to liver dysfunction
– Dark urine, clay-colored
– By the time of jaundice appears, these will go away or diminish
– Enlarged and tender liver
– Splenomegaly
– Cervical lymphadenopathy
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12. Mini-case 1
• Eden and Bruk, Ethiopian couples returned from their
honeymoon trip to Central America and develops
nonspecific abdominal symptoms followed by clinical
jaundice.
• They stayed at a resort, and ate fresh fruits and salads.
Serology for hepatitis virus spread by the fecaloral route
is positive. One of the following is the most likely:
• hepatitis A virus;
• hepatitis B virus
• hepatitis E virus
• A and C
• hepatitis C virus
• hepatitis D virus05/01/13 Mohammed Adem 12
13. Mini-case 2
E.T., a 34-year-old medical sales representative, presents to the ED at Black Lion
Hospital with acute onset of jaundice and “dark urine.” He was in good health
until 2 weeks ago, when he noted feeling fatigued and weak, which he attributed
to his demanding work schedule.
He also recalled having a mild headache, loss of appetite, muscle pain, diarrhea,
and low-grade fevers from 99°F to 101°F.
He attributed these symptoms to the flu and took acetaminophen with plenty of
fluids. His symptoms persisted until yesterday, when they seemed to resolve
unexplainably. He then noted his urine was cola-colored.
This morning, he noted jaundice of his eyes and skin and sought medical attention.
Mohammed Adem
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14. MH:
a recent respiratory tract infection, treated successfully with levofloxacin.
SH:
is significant for frequenting the local bar, where he regularly ingests raw meats. He
denies smoking and recent travel to heptitis A endemic areas, but admits to
occasional alcohol consumption.
E.T. has no Hx of sexual exposure, needle use, or transfusions. His current
medications include oral (PO) diazepam 5 mg at bedtime (HS) as needed (PRN)
for “muscle spasms,” but he has not taken diazepam for “several months.” He
also has a seizure disorder sustained after a motorcycle accident 2 years before
admission, for which he takes phenytoin 400 mg PO HS.
Mohammed Adem
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15. PE ;
significant for a well-developed, well-nourished man in no acute distress. He is
alert and oriented, with a temperature of 99°F. His sclerae and skin are icteric,
and his abdomen is positive for a tender, enlarged liver, and right upper
quadrant (RUQ) pain.
Laboratory tests: reveal the following values:
Hgb, 16 g/dL (12.3–16.3); Hct, 44% (37.4%–47.0%); WBC, 5,500
cells/mm3
(3.28–9.29 × 103
); AST, 120 U/L (5–40); ALT, 240 U/L (5–40);
AP, 86 U/L ( 21–91); total Bl , 3.2 mg/dL (0.2–1.0); Bl (D), 1.5 mg/dL (0–
0.2); and phenytoin concentration, 12 mg/L (10–20).
The albumin, PT, blood glucose, and electrolytes all are within normal limits.
E.T. is negative for anti-HCV, HBeAg, HBsAg, and hepatitis B core antibody
(anti-HBc), but is positive for IgM anti-HAV.
What clinical features and serologic markers are consistent with viral hepatitis in
E.T.?
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17. HAV…
• HAVis often a self-limiting and acute viral infection of the liver
posing a health risk worldwide.
•
• The infection is rarely fatal.
• Although vaccine preventable, HAV continues to be one of the
most commonly reported infections.
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18. Epidemiology
• Faeco-oral route
– where hygiene is poor, infection is almost universal during childhood
– As hygiene improves, rate of childhood infection decreases common
• Close personal contact
– Household, child-care centers
– Identifiable risk sexual (Promiscuous MSM); household contact with person with HAV; IDUs
• Contaminated food, water
– Infected food handlers, international travelers (endemic areas), immigration
• Blood exposure (rare)
– 45-50% have no identified source
• Despite being detectable in saliva, there are no data to suggest transmission
through this mode of contact.
NB: It almost always manifests with a self-limited clinical course
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19. Etiology
• HAV is a RNA virus. genus Hepatovirus , Picornaviridae family.
• Humans are the only known reservoir for the virus and
transmission occurs primarily through the fecal–oral route.
• The virus is stable in the environment for at least a month.
requires heating foods to a minimum of 85°C (185°F) for 1 minute or
disinfecting with a 1:100 dilution of sodium hypochlorite (bleach) in tap water
for inactivation.
• Multiple genotypes of the virus exist and although the clinical
implications of infection by particular type are unknown.
types I and III are the most commonly identified in human outbreaks
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20. Pathophysiology
• HAV infection is usually acute, self-limiting, confers lifelong
immunity.
• HAV's life cycle in the human host classically begins with
ingestion of the virus.
• Absorption in the stomach or small intestine allows entry into the
circulation and uptake by the liver.
• Replication of the virus occurs within hepatocytes & GI epithelial
cells.
• New virus particles are released into the blood & secreted into bile
by the liver.
• The virus is then either reabsorbed to continue its cycle or
excreted in the stool.
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21. Pathophysiology…
• The enterohepatic cycle will continue until interrupted by antibody
neutralization.
• The exact mechanism of replication & secretion is unknown. however, the
initial viral expansion does not seem to be associated with hepatic injury as peak viral fecal excretion precedes clinical signs
and symptoms of infection.
• On biopsy, acute hepatitis is marked by hepatocellular degeneration,
inflammatory infiltrate, and hepatocyte regeneration.
• Hepatocellular degeneration occurs as a result of immune-mediated injury
and not as a direct cytopathic effect of the virus.
• Cytolytic T cells mediate hepatocyte lysis to eradicate the virus and
mark the cellular immune response with rising hepatic enzyme levels.
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22. Risk Factors
• Ingestion of contaminated food substances
– Large outbreaks as well as sporadic cases have been traced to
contaminated: Food , Water, Milk
• Family member who is affected
• Poor personal hygiene
• Institutional resident who is affected
• Child care centers
• Neonatal intensive care units
• MSM, IVDU
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24. Clinical presentations…
Signs and symptoms
• Symptoms and severity of HAV vary according to age
• Children <6 years of age typically are asymptomatic.
• The preicteric phase brings nonspecific influenza-like Sx: anorexia,
nausea, fatigue, and malaise
• Abrupt onset of anorexia, N, V, fever, headache & RUQ
abdominal pain
• Icteric hepatitis is generally accompanied by dark urine, acholic (light-colored)
stools, and worsening of systemic Sx.
• Pruritus is often a major complaint of icteric patients
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25. Clinical presentations
• Incubation period : 15–45 days ; Mean: ~4 weeks
• Viremia occurs within 1-2 weeks of exposure as patients begin to
shed the virus. viral shedding in feces,
• Peak fecal shedding of the virus precedes the onset of clinical Sx
& elevated liver enzymes.
• Acute hepatitis follows, beginning with the preicteric or
prodromal period.
The phase is marked by an abrupt onset of nonspecific
symptoms, some very mild
Mohammed Adem
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26. Clinical presentations…
• unusual Sx : chills, myalgia, arthralgia, cough, constipation, diarrhea, pruritus,
and urticaria. Non-specific
• Liver enzyme levels rise within the first wks of infection, peaking
~ in the 4th
wk and normalizing by the 8th
wk.
• Conjugated bilirubinemia, or dark urine, precedes the onset of
the icteric period.
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27. Clinical presentations…
• The concentration of virus declines at this point and
patients are generally considered noninfectious
~ 1 week after the onset of jaundice.
• GI Sx may persist or subside during this time and some
patients may have hepatomegaly.
• Duration of the icteric period varies and corresponds to
disease duration. It averages between 7 and 30 days.
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29. Clinical presentations…
Laboratory findings
• Positive-serum IGM ,
• IgG replaces IgM and indicates host immunity following the acute phase.
• Mild elevations of serum bilirubin, -globulin, and ALT , AST values to about 2X
normal in acute anicteric disease
• Elevations of AP, - GGT and total bilirubin in patients with cholestatic illness
• Serum HAV becomes detectable 5 - 10 days before the onset of symptoms
and can persist for months
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30. Prognosis
• HAV does not lead to chronic infections.
• Some pts may experience Sx for up to 9 months.
• Virtually all previously healthy patients with hepatitis A recover
completely from their illness, with no clinical sequelae.
• Complete clinical and biochemical recovery is to be expected in 1–2
months.
• No chronic carrier state
• fatality rate: ~ 0.1%
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31. Complications
• Rarely, patients experience complications from HAV, including
relapsing hepatitis, cholestatic hepatitis, and fulminant hepatitis
• Relapsing hepatitis :
– Recurrence of symptoms
– Elevated liver enzyme levels
– Jaundice (occasionally)
– Fecal excretion of HAV
– Even when this occurs, hepatitis A remains self-limited and does not progress to chronic liver
disease.
• Cholestatic hepatitis
– Characterized by protracted cholestatic jaundice and pruritus
• Fulminant hepatitis (massive hepatic necrosis): Rare 0.1% yet high fatality
– Primarily in older adults (50), younger children and in persons with underlying chronic liver disease
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32. Diagnosis
• History: particular attention to risk factors
• Clinical Criteria:
acute onset of fatigue, abdominal pain, loss of
appetite, intermittent nausea and vomiting, jaundice
• Laboratory:
serum aminotransferases, and serologic testing for anti-HAV antibodies.
IgM anti-HAV is the diagnostic test of choice
• Appears very soon after infection
• Disappears 3–6 months later
• Incidental presence of rheumatoid factor can yield false-positive results
• IgG anti-HAV appears later in the acute phase but persists for decades
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33. Differential diagnosis
1. Other hepatitis viruses
2. Other viral illnesses frequently affect the liver
– Infectious mononucleosis , Cytomegalovirus , Herpes simplex
1. Many drugs and certain anesthetic agents
2. Alcoholic hepatitis
3. Acute Cholecystitis
4. Disorders in pregnancy that may be confused with viral
hepatitis
• Acute fatty liver of pregnancy , Cholestasis of pregnancy , Eclampsia ,
1. Many, many more…
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34. Treatment
• Mainstay of therapy is supportive care.
• Specific treatment is not necessary.
– Most patients hospitalized with hepatitis A excrete little if any HAV
– Likelihood of HAV transmission from these patients during their
hospitalization is low.
Nonetheless, universal precautions are recommended.
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35. Treatment
Desired Outcome
• The ultimate goal of therapy is complete clinical resolution.
• Other goals: reducing complications, normalization of liver function,
and reducing infectivity and transmission.
• The majority of pts are expected to fully recover without clinical
sequelae.
• clinical resolution within 6 months of the infection, & a majority
will have done so by 2 months.
• Rarely, Sx persist for longer or patients relapse.
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36. Treatment…General Approach
• In pts who develop liver failure, transplant is the only option.
• Prevention and prophylaxis are key to managing the virus.
• Immunoglobulin: for pre- and postexposure prophylaxis
offers passive immunity.
• Active immunity is achieved through vaccination.
Children and at-risk adults to reduce the overall incidence
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37. Treatment…
• Most patients hospitalized with hepatitis A excrete little if any
HAV. Likelihood of transmission is low
• Prevaccination serologic testing to determine susceptibility is
generally not recommended
if the cost of the test is less than that of the vaccine and
if the person is from a moderate to high endemic area and likely to have prior
immunity
• Prevaccination serologic testing of children is not recommended.
• postvaccine serologic testing is not recommended.
Due to high vaccine response
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38. Prevention
• HAV is easily preventable with vaccination.
• vaccine programs have targeted children as the most effective
means to control HAV.
• vaccination programs among children from high-incidence states
>70% reduction in the annual incidence of new HAV infections
• Two vaccines for HAV are available and are incorporated into the
routine childhood vaccination schedule.
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40. Prevention…
• Routine prevention of HAV transmission includes
with soap and water after using the bathroom,
Regular hand washing changing a diaper, and before food preparation.
• For travelers to countries with high endemic rates of HAV, even
short-term stays in urban and upscale resorts are not risk free.
contaminated water
fresh produce, and any uncooked foods pose a risk
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41. Vaccines
• Havrix and Vaqta: are available for pediatric and adult use. USA
the two inactivated virus vaccines. 1995
• The differences in the two vaccines are in the use of a
preservative and in expression of antigen content.
• Vaqta: formulated without a preservative and
uses units of HAV antigen to express potency.
• Havrix: uses 2-phenoxyphenol as a preservative and
antigen content is expressed as enzyme-linked immunosorbent assay
units.
• Pediatric dosing is indicated for children 1 to 18 years of age, and
adult dosing is for patients ages 19 years and older
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42. Vaccines …
• Although high seroconversion rates of 94% are achieved with the
first dose, both vaccines recommend a booster shot to achieve the
highest possible antibody titers.
• In situations of postexposure prophylaxis, previously only
immunoglobulin was indicated but recent guidelines changes
allow the use of vaccines for this indication.
The change to the use of the vaccine is advantageous as
vaccination confers the benefit of long-term immunity against HAV.
• Both vaccines may be given concomitantly with immunoglobulin
and the two brands are interchangeable for booster shots.
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44. Vaccines … monitoring issues
• Response to the vaccine as determined by detection of anti-HAV
after vaccination.
• Vaccine efficacy may be reduced in certain pt groups.
eg. In HIV infected pts, greater immunogenic response may correlate with higher baseline CD4 counts.
females and patients with CD4 counts >200 high response rate
• most common S/E: soreness & warmth at the injection site, headache, malaise, pain
• Reported serious A/E: causality not yet established
anaphylaxis, Guillain-Barré syndrome, transverse myelitis
Reported brachial plexus neuropathy, multiple sclerosis,
encephalopathy, and erythema multiforme.
Note: the incidence of these events was similar in the general population. Vacc vs unvacc
The vaccine is considered safe
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45. Vaccines … Twinrix
• Twinrix is a bivalent vaccine for HAV and HBV. in 2001
• It is approved for people ages 18 and older and is given at 0, 1,
and 6 months.
• Although seroconversion exceeds 90% for HAV after the first
dose , the full three-dose series is required for maximal HBV seroconversion.
• The combined vaccine offers the advantage of immunization
against both types of hepatitis in a single vaccine.
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46. Immunoglobulin/Ig
• Used in persons for whom vaccination is not an option.
pre- or postexposure prophylaxis
• provides protection by passive transfer of antibody
• is preferred for
children <12 months of age and
postexposure prophylaxis in patients aged >40 years, pts with chronic liver disease,
and persons allergic to any part of the vaccine.
• most effective if given in the incubation period of the infection.
Receipt of Ig within the first 2 weeks of infection will reduce infectivity and moderate the
infection in 85% of patients.
Note: Patients who receive at least 1 dose of the vaccine at least 1 month earlier
do not need pre- or postexposure prophylaxis with Ig.
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47. Ig…
• International travelers are the major patient population receiving
preexposure prophylaxis with Ig.
• vaccination or prophylaxis with Ig is recommended for travelers to
countries with high endemic rates of HAV. A/E like anphylaxis IgA deficiency
• Patients who had an anaphylaxis reaction to Ig should not receive
it. There is no C/I for use in pregnancy or lactation.
• Dosing of Ig is the same for adults and children.
• a single dose of 0.02 mL/kg IM: For postexposure prophylaxis and for short-
term preexposure coverage of <3 months,
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48. Ig…
• For long-term preexposure prophylaxis of 5 months
a single dose of 0.06 mL/kg is used.
• People recently exposed to HAV and not been previously
vaccinated Ig is indicated for
a) close personal contact with an HAV-infected person;
b) all staff and attendees of daycare centers when HAV is documented;
c) common source of exposure (food handler)
d) classroom contacts of an index case patient; and
e) schools, hospitals, and work settings where close personal contact occurred with the
case patient
• Ig can be given concomitantly with the HAV vaccine. the response is
protective
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49. Ig…
• The MMR (measles, mumps, and rubella) vaccine should be delayed for a minimum of
3 months after receipt of Ig.
• The varicella vaccine must be delayed for 5 months.
• Ig should not be given to patients who received the MMR within 2 weeks or the
varicella vaccine within 3 weeks.
• In situations where the benefits of Ig outweigh the benefits of the other
vaccines, revaccination can be performed after Ig administration.
• For the MMR, revaccination should be at least 3 months later, and for the
varicella vaccine, at least 5 months later.
• Ig does not interfere with inactivated vaccines and may be administered safely with
other vaccines traditionally given to travelers to some developing countries, such as the
oral poliovirus or yellow fever vaccine.
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50. Pharmacoeconomic Considerations
• The costs of an HAV outbreak are significant, yet routine vaccination of all
individuals is not cost-effective. So,
• targeting at-risk populations, the majority of cases can be prevented.
Children play a pivotal role in disease persistence
• Using vaccine is cost-effective in children and offers the most benefit to the
personal contacts of children.
• The use of the combined HAV-HBV vaccine is effective in reducing costs
associated with HAV among persons who are at increased risk for infection.
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51. References
• Harrison’s principle of internal medicine 18th
ed
• Joseph T dipro; Pharmacotherapy a
pathophysiologic approach 8th
ed
• Applied therapeutics the clinical use of drugs 9th
ed
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Editor's Notes
For half of all identified HAV cases in 2007, no risk factor was identified. 1 In pregnant women, acute HAV infection may be associated with maternal complications and preterm labor. Despite low endemic rates and successful vaccinations of at-risk populations in the United States, unvaccinated children acquiring HAV infections abroad can serve as reservoirs of the virus upon return to the United States, even while remaining clinically asymptomatic themselves. Nearly 40% of children younger than age 15 years with HAV had international travel as a risk factor in 2004
MSM Use of injectable drugs / IVDU Overcrowding Non-enveloped, heat-, acid-, and ether-resistant RNA virus Replication is limited to the liver
Children <6 years of age typically are asymptomatic . Symptoms, if they do occur, do not include jaundice. In older children and adults , the majority of patients present with symptoms that last less than 2 months and 70% of adults experience jaundice. Peak viral shedding precedes the onset of GI symptoms in adults. In young children, shedding can occur for months following diagnosis. 2 Because children are often asymptomatic and will shed the virus for long periods of time they can serve as a reservoir for the spread of HAV.
Children <6 years of age typically are asymptomatic . Symptoms, if they do occur, do not include jaundice. In older children and adults , the majority of patients present with symptoms that last less than 2 months and 70% of adults experience jaundice. Peak viral shedding precedes the onset of GI symptoms in adults. In young children, shedding can occur for months following diagnosis. 2 Because children are often asymptomatic and will shed the virus for long periods of time they can serve as a reservoir for the spread of HAV.
Hepatitis A Vaccine, IgG for short term Px, all persons at risk
HAV RNA is detectable in the serum for an average of 17 days before peak ALT levels and can persist for an average of 79 days after the onset of symptoms In some patients, serum HAV is detectable for more than a year.
Hepatitis A is transmitted via the fecal–oral route. Transmission is most likely to occur through travel to countries with high rates of hepatitis A, poor sanitation and hygiene, and overcrowded areas. Hepatitis A causes an acute, self-limiting illness and does not lead to chronic infection. There are three stages of infection: incubation, acute hepatitis, and convalescence. Rarely, the infection progresses to liver failure. Treatment of hepatitis A consists of supportive care. There is no role for antiviral agents in treatment.
HELLP syndrome
In the United States, the introduction of hepatitis A vaccination programs among children from high-incidence states has resulted in a >70% reduction in the annual incidence of new HAV infections and has shifted the burden of new infections from children to young adults.
Although hepatitis A is rarely bloodborne, several outbreaks have been recognized in recipients of clotting-factor concentrates Adults — The Advisory Committee on Immunization Practices ( ACIP ) of the Centers for Disease Control and Prevention ( CDC ) has recommended hepatitis A vaccination of adults who have any of the following medical , occupational , or lifestyle risk factors. Persons with clotting-factor disorders or chronic liver disease Men who have sex with men or users of illegal drugs Those with close personal contact (eg, household contact or regular babysitting ) with an international adoptee from a country of high or intermediate endemicity during the first 60 days following arrival of the adoptee in the United States Persons working with hepatitis A virus infected primates or with HAV in a research laboratory Persons traveling to countries with high or intermediate endemicity Any person wishing to obtain immunity Children — Hepatitis A vaccination was incorporated into routine childhood vaccination schedule in 2006. Previously, HAV vaccination had been recommended routinely only in some regions within the United States, where the incidence of hepatitis A is higher than the national average. These relatively high-risk states include Arizona, Alaska, California, Idaho, Nevada, New Mexico, Oklahoma, Oregon, South Dakota, Utah, and Washington. Such programs have been highly effective in reducing the incidence of hepatitis A among children and adults and (combined with extended safety data) provided the impetus for broadening the vaccination recommendation Passive Immunization: IgG Pre -exposure— travelers Post exposure (w/i 14 days ) Active Immunization Persons at Increased Risk Travelers MSM Drug users Chronic liver disease Communities with high rates of Hepatitis A
INACTIVATED HEPATITIS A VACCINES — HAVRIX (Smith-Kline Beecham) was the first hepatitis A vaccine (HepA vaccine) licensed for use in the United States and approved by the Food and Drug Administration (FDA) in 1995 [ 4 ]. HAVRIX is a purified, formalin-inactivated vaccine prepared in a human cell culture line. The vaccine is manufactured from the HM 175 virus strain , adapted to grow in human diploid MRC-5 cells , with formaldehyde inactivation performed at a concentration of 250 mcg/mL at 37ºC for 15 days . The antigen content of the vaccine is measured by a specific and accurate ELISA (enzyme-linked immunosorbent assay) with vaccine po tency expressed as ELISA units (EL.U) of antigen. The HAV virions are subsequently adsorbed onto 0.5 mg/mL aluminum hydroxide adjuvant in isotonic buffered saline containing 0.5 percent 2-phenoxyethanol as a preservative. A second purified, formalin-inactivated vaccine using the CR326 viral strain (VAQTA, Merck Sharp Dohme) became available in the United States in 1996 The two vaccines had equivalent immunogenicity , but fewer side effects (typically local reactions ) were observed with VAQTA . However, VAQTA vaccine was recalled in the fall of 2001 when it was discovered that the antigen content in some prefilled syringes was below the established minimum specification. Thus, patients who received this vaccine may not be adequately protected . Such patients should be either revaccinated with an alternative vaccine or tested for evidence of serologic immunity
The change to the use of the vaccine is advantageous as vaccination confers the benefit of long-term immunity against HAV. Immunogenicity — The majority of studies demonstrate almost a 100 percent seroconversion rate (defined as an antibody concentration of >20 mIU/mL measured by ELISA) after a primary vaccination course in both adults and children [ 2,8-12 ]. Furthermore, the antibody concentration achieved with the HepA vaccine is much greater (nearly 15 times in one report) than the concentrations reached with protective doses of immune globulin (IG) [ 13 ]. The response is also much more long-lasting as illustrated in a study which compared the immunogenicity of the inactivated HepA vaccine, in single and booster doses, with IG administered once as an intramuscular injection [ 14 ]. With the vaccine, seropositivity by radioimmunoassay was seen in 73 percent at week 2, 100 percent at week 5, and 100 percent at week 24. The comparable values for seropositivity after IG were 100 percent at week 1, 10 percent at week 12, and 0 percent at week 20. Another study evaluated the reactogenicity, immunogenicity, and long-term antibody persistence after the administration of inactivated HepA vaccine (720 EL.U) to adults [ 15 ]. The vaccination schedule consisted of primary immunization at baseline and one month, followed by a booster injection 6 to 12 months following initial vaccination. The subjects were followed up to 36 months, and geometric mean antibody titers (GMT) against HAV were monitored. The GMT increased with each dose of the vaccine with a peak in antibody titers occurring at seven months. There was a rapid decline in titers (by 61 percent) between 7 and 12 months and a slower decline beginning at 12 months (14 percent). Based upon these observations, the investigators devised a mathematical model to predict antibody persistence over time. Assuming a constant rate of decline in antibodies to HAV, the authors estimated that the duration of protection when antibody levels are >20 mIU/mL ( a level conferring immunity ) is between 20 and 30 years . An anamnestic response has been demonstrated empirically up to 12 years after vaccination [ 16 ]. Thus, there is no evidence that a HepA booster vaccination after a full primary vaccination is needed in healthy individuals, although there are as of yet no long-term data following the two-dose vaccine regimen used in clinical practice [ 17 ]. The effectiveness of the HepA vaccines is underscored by the decline in HAV cases since their introduction
Dosing regimens — For HAVRIX , primary immunization in children and adolescents (12 months through 18 years) consists of a single dose of 720 EL. U ., in 0.5 mL and a booster dose (720 EL. U. in 0.5 mL) any time between 6 and 12 months later. In adults, immunization consists of a single dose of 1440 EL. U. in 1 mL and a booster dose (1440 EL. U. in 1 mL) anytime between 6 and 12 months later For VAQTA , primary immunization in children and adolescents (12 months through 18 years) consists of a single 0.5 mL (~25 U ) dose and a booster dose of 0.5 mL (~25 U) 6 to 18 months later. For adults 19 and older, immunization consists of a single 1.0 mL (~50 U) dose and a booster of 1.0 mL (~50 U) 6 to 18 months later. It is good practice to use the same brand of vaccine to complete a course . If this is not possible , products for booster dose are interchangeable (eg, Vaqta can be used for booster dose following primary dose of Havrix and vice versa). The change to the use of the vaccine is advantageous as vaccination confers the benefit of long-term immunity against HAV. Decompensated cirrhosis: HAV vaccination has been recommended for patients with chronic liver disease because of the increased morbidity and mortality associated with acute HAV in such patients. However, patients with advanced liver disease may have a diminished response to HAV vaccination. An illustrative study compared seroconversion in 35 patients with decompensated disease with 49 patients with compensated chronic liver disease [ 18 ]. One month after the booster dose, seroconversion rates were significantly lower in those with decompensated disease (66 versus 98 percent). Median serum antibody concentrations were also lower. On multivariate analysis, Child-Pugh class B or C was predictive of a lower response rate. These data suggest that vaccination should ideally be accomplished before the development of advanced disease. Safety : More than 188 million doses of hepatitis A vaccine have been sold worldwide since 1995 [ 19 ]. The most common adverse events are fever , injection-site reactions , rash , and headache . While serious adverse events (including Guillain-Barre' syndrome, elevated liver biochemical tests, and idiopathic thrombocytopenic purpura ) have been reported, their relationship to vaccination is unclear.
Guillain-Barré syndrome ; a nervous disorder in which, after a non-specific infection , demyelination of the spinal roots and peripheral nerves takes place, leading to generalised weakness and sometimes respiratory paralysis. multiple sclerosis: a nervous disease which gets progressively worse, where patches of the fibres of the central nervous system lose their myelin , causing numbness in the limbs and progressive weakness and paralysis . erythema multiforme: the sudden appearance of inflammatory red patches and sometimes blisters on the skin Furthermore, incidence of serious adverse events in the vaccinated population did not differ from the incidence in nonvaccinated populations. It is important to note that more than 65 million doses of the vaccine have been administered and despite routine monitoring for adverse events, there are no data to suggest a greater incidence of serious adverse events among vaccinated people compared with nonvaccinated. The vaccine is considered safe.
Twinrix — Similar results were obtained in two clinical trials which evaluated a combined hepatitis A/ hepatitis B vaccine [ 26,27 ]. The vaccine contained 720 EL.U . of hepatitis A antigen and 20 mcg of hepatitis B antigen absorbed on 0.5 mg of aluminum hydroxide as an adjuvant. Seroconversion rates were consistently high , the vaccine was well tolerated, and there were no appreciable adverse effects . A combination vaccine consisting of HAVRIX and Energix-B (Twinrix, GlaxoSmithKline) is commercially available LIVE ATTENUATED VACCINES — The use of attenuated live HepA vaccines has been evaluated in both animals and humans . One report described the experience in China , where clinical trials began in 1987 [ 31 ]. Over the next few years, 3089 adults and 3072 children were inoculated with the vaccine. The following results were noted: Seroconversion occurred in 95.6 percent of volunteers within three weeks, similar to naturally acquired immunity. Subjects studied up to three years had persistence of the antibody in serum samples. There were no major side effects, and elevations in serum aminotransferases were not noted. Live attenuated HAV was found in the stools of 75 percent of persons who had received the vaccine; however, transmission of HAV from vaccinees to seronegative persons who were not administered the vaccine did not occur. Thus, this type of vaccine is well tolerated and highly immunogenic . However, with the recent licensing of the inactive HepA vaccines , the use of a live attenuated vaccine will probably be limited.
Ig is available both as an intravenous (IV) and IM injection but for HAV exposure, only the IM is used. If given to infants or pregnant women, the thimerosal-free formulation should be used. Postexposure summary and recommendations — The following are the recommendations from the Advisory Committee on Immunization Practices [ 57 ]. Persons who have been exposed recently to hepatitis A and who have not previously received hepatitis A vaccine should be administered a single dose of single- antigen hepatitis A vaccine or immune globulin (IG) (0.02 ml/kg) as soon as possible. For healthy persons aged 12 months to 40 years, single-antigen hepatitis A vaccine at the age-appropriate dose is preferred. (See 'Indications' above.) For children aged <12 months, immunocompromised persons, persons who have had chronic liver disease diagnosed, and persons for whom vaccine is contraindicated, IG should be used.
HAV vaccination or prophylaxis with Ig is recommended for travelers to countries with high endemic rates of HAV. Serious adverse events are rare. Anaphylaxis has been reported in patients with Ig A deficiency. Patients who had an anaphylaxis reaction to Ig should not receive it. There is no contraindication for use in pregnancy or lactation. CONTRAINDICATIONS FOR MMR Vaccine — Certain patients should not receive MMR or MMRV vaccines because they are live virus vaccines : Women who are pregnant should not receive MMR vaccine; women who do receive this vaccine should avoid becoming pregnant for 30 days after receipt of MMR to avoid possible risk to the developing fetus. MMR vaccine should not be administered to patients who are receiving acute high-dose steroid therapy or long-term maintenance doses of prednisone of ≥20 mg per day . Individuals with known allergy to neomycin should not receive MMR vaccine because trace amounts of neomycin are contained in the MMR vaccine. Those with known allergy to eggs can receive MMR vaccine; the risk for anaphylaxis after MMR vaccination is extremely low, even in persons with severe egg allergy symptomatic HIV-infected patients with severe immunosuppression .
In the first study, the authors compared no intervention to five possible strategies for HAV prevention. The prevention strategies included: Vaccination with the two-dose primary course (HAVRIX 720) Vaccination with the one dose primary course (HAVRIX 1440) Screening for anti-HAV, followed by HAVRIX 720 Screening for anti-HAV, followed by HAVRIX 1440 Administration of IG The investigators concluded that the optimal strategy varied with the estimated travel history: In persons who will travel only twice in a 10-year period for a short duration , passive immunization with IG is the most cost-effective treatment. If the travel frequency surpasses three times in a 10-year period or the length of stay exceeds six months , the HepA vaccine is the more cost-effective strategy. Prevaccination antibody screening is only justified in older travelers , those from countries in which HAV is endemic (average prevalence of immunity of over 30 percent), or those with a history of jaundice . Either the deltoid or gluteal muscle may be used. In children younger than 24 months of age, Ig can be given in the anterolateral thigh muscle Ig can be given concomitantly with the HAV vaccine. Although the antibody titer will be lower than if the vaccine were administered alone , the response is still protective. However, Ig can interfere with the response of other vaccines and should be delayed.
Simultaneous administration with other vaccines — It would be advantageous to use a vaccination schedule allowing the simultaneous administration of several required vaccines. The inactivated HepA vaccine can be given concurrently with the vaccines for diphtheria , tetanus , pneumococcus , oral typhoid, cholera , Japanese encephalitis, rabies , or yellow fever without adversely affecting immunogenicity or safety [19-21]. It is recommended that the injections be given at different sites . The efficacy of the simultaneous administration of both HepA and HepB vaccines was evaluated in a controlled clinical trial of 165 subjects, aged 18 to 35 years, who were randomized to receive either HepA vaccine, HepB vaccine, or both vaccines. The formalin-inactivated HepA vaccine ( HAVRIX ) at a dose of 720 EL.U. per mL and the commercially available HepB vaccine ( Engerix-B ) in a dose of 20 mcg/mL were administered at a zero and one month primary vaccination course, followed by a booster at month six . All the vaccines were well-tolerated and highly immunogenic , indicating that synchronous vaccination against both HAV and HBV infection is possible. Studies in infants and children ≤18 suggest that the HepA vaccine does not affect immunogenicity or reactogenicity to diphtheria-tetanus-acellular pertussis, Haemophilus influenzae type b, hepatitis B, MMR , oral poliovirus, or inactivated poliovirus vaccine MMR vaccine A/E The MMR vaccine is generally safe with few serious adverse events reported other than local pain and induration at the site of vaccination. Thrombocytopenic purpura — Thrombocytopenic purpura has occasionally been observed within two months after receipt of MMR vaccine [32,36-39]. The reported incidence of this complication has varied from one in 30,000 vaccinees in prospective trials [15,36] to one case per 100,000 vaccine doses by passive surveillance [15,37]. Complete recovery from thrombocytopenic purpura has generally been the rule, but some patients develop acute hemorrhagic complications . Individuals who experience an episode of thrombocytopenia after an initial dose of MMR are at greater risk for recurrent thrombocytopenic purpura after rechallenge with this vaccine [39]. Aseptic meningitis — Aseptic meningitis has been reported in a number of studies evaluating adverse events following MMR vaccination [40-45]. The bulk of cases have presented with typical clinical signs and symptoms of meningeal irritation, and the CSF profile has generally shown a lymphocytic pleocytosis ; recovery has been the rule. Several studies suggest that the risk of aseptic meningitis may be higher in patients vaccinated with the Urabe strain compared with the Jeryl Lynn strain [42-44]: A retrospective survey of aseptic meningitis associated with MMR vaccine was conducted in 13 districts in England and Wales, where 27 cases were identified [40]. All were recipients of vaccines containing the Urabe mumps strain; no cases related to the Jeryl Lynn vaccine were found. The risk of aseptic meningitis post-MMR vaccination was estimated to be one in 11,000 vaccine doses, much higher than that reported in the United States, where the Jeryl Lynn strain is used [41]. Other neurologic complications, including Guillain-Barré syndrome [46] and cerebellar ataxia [47], have rarely been reported following MMR vaccination. Seizures — MMR vaccination has been previously associated with febrile seizures occurring 8 to 14 days after receipt of vaccine . Approximately one additional febrile seizure occurs among every 3000 to 4000 children vaccinated with MMR vaccine, compared with children who were not vaccinated LONG–TERM COMPLICATIONS — Mumps vaccine has been evaluated as a causal factor in the development of diabetes mellitus and autism , although a definitive link has not been established for either entity. Either the deltoid or gluteal muscle may be used. In children younger than 24 months of age, Ig can be given in the anterolateral thigh muscle Ig can be given concomitantly with the HAV vaccine. Although the antibody titer will be lower than if the vaccine were administered alone, the response is still protective. However, Ig can interfere with the response of other vaccines and should be delayed.