The document summarizes the natural history and pathogenesis of HPV. It discusses the worldwide burden of cervical cancer, phylogenetic classification of HPV, and the viral lifecycle within host cells. Persistent infection with high-risk HPV types is required for progression from normal cervical epithelium to pre-cancerous lesions and eventually invasive cervical cancer, with the contribution of additional genetic mutations and external cofactors over long periods of time.
The document discusses human papilloma virus (HPV) including the virus itself, associated diseases, transmission, epidemiology, clinical manifestations, carcinogenic properties, vaccination, and treatment options. HPV is a common virus that can cause genital warts and various cancers like cervical cancer. Vaccination provides high efficacy against HPV types known to cause cancer and genital warts. Treatment depends on the manifestation but may include cryotherapy, laser ablation, or topical medications.
HUMAN PAPILLOMA VIRUS INFECTION & CERVICAL CANCER ABHIJIT BANIK
This document discusses cervical cancer, including its causes, risk factors, symptoms, and treatment/prevention. It notes that cervical cancer is caused by high-risk strains of the human papillomavirus (HPV), especially HPV 16 and 18. HPV works by integrating into the host cell's genome and inactivating tumor suppressor proteins, leading to uncontrolled cell growth. Screening and prophylactic vaccines can prevent most cases of cervical cancer.
The document discusses HPV and its link to various cancers. It explains that HPV is a virus that can cause warts and some cancers like cervical cancer. Persistent high-risk HPV infections can lead to pre-cancerous lesions and some cancers over time if left undetected and untreated. The document also discusses HPV vaccines that can help prevent HPV infections and reduce the risk of HPV-related cancers.
HPV (human papillomavirus) is extremely common, with 80% of sexually active people contracting a strain at some point. It causes various cancers and genital warts. While most HPV infections clear on their own, persistent infections increase cancer risk. Vaccines target high-risk HPV strains responsible for 70% of cervical cancers. They provide sustained, high-level immunity for at least 4.5 years with minimal side effects. Screening and vaccination can significantly reduce HPV-related cancers globally.
This document discusses Human Papilloma Virus (HPV) and cervical cancer. It describes the different types of HPV and their association with cervical lesions and cancer. It provides information on HPV vaccination, including efficacy against cervical lesions, safety, and recommendations for vaccination of girls ages 9-13.
Human papillomavirus (HPV) is a common sexually transmitted infection with over 100 types. More than 60 types can cause skin warts while high risk types 16, 18, 45 and 31 cause most cervical cancers. Genital HPV infections are very common among sexually active individuals, with about 20 million people infected at any time. HPV is transmitted through direct skin-to-skin contact during sexual activity and infected birth canals. While warts can be removed, the virus itself cannot be cured as it may grow back, but vaccines exist to protect against high risk HPV types.
This document provides information about human papillomavirus (HPV) including:
- There are over 100 types of HPV that can infect humans. High risk types like HPV 16 and 18 can cause cancers while low risk types cause genital warts.
- HPV is transmitted through skin to skin contact and infects mucosal surfaces. Most infections clear on their own but persistent infections can lead to cancers.
- HPV is associated with cervical, anal, penile, and oropharyngeal cancers. It is also associated with genital warts.
- The viral life cycle and genes involved in pathogenesis are described. Integration of viral DNA into host DNA is important for cancer development.
- Screening methods
The document discusses human papilloma virus (HPV) including the virus itself, associated diseases, transmission, epidemiology, clinical manifestations, carcinogenic properties, vaccination, and treatment options. HPV is a common virus that can cause genital warts and various cancers like cervical cancer. Vaccination provides high efficacy against HPV types known to cause cancer and genital warts. Treatment depends on the manifestation but may include cryotherapy, laser ablation, or topical medications.
HUMAN PAPILLOMA VIRUS INFECTION & CERVICAL CANCER ABHIJIT BANIK
This document discusses cervical cancer, including its causes, risk factors, symptoms, and treatment/prevention. It notes that cervical cancer is caused by high-risk strains of the human papillomavirus (HPV), especially HPV 16 and 18. HPV works by integrating into the host cell's genome and inactivating tumor suppressor proteins, leading to uncontrolled cell growth. Screening and prophylactic vaccines can prevent most cases of cervical cancer.
The document discusses HPV and its link to various cancers. It explains that HPV is a virus that can cause warts and some cancers like cervical cancer. Persistent high-risk HPV infections can lead to pre-cancerous lesions and some cancers over time if left undetected and untreated. The document also discusses HPV vaccines that can help prevent HPV infections and reduce the risk of HPV-related cancers.
HPV (human papillomavirus) is extremely common, with 80% of sexually active people contracting a strain at some point. It causes various cancers and genital warts. While most HPV infections clear on their own, persistent infections increase cancer risk. Vaccines target high-risk HPV strains responsible for 70% of cervical cancers. They provide sustained, high-level immunity for at least 4.5 years with minimal side effects. Screening and vaccination can significantly reduce HPV-related cancers globally.
This document discusses Human Papilloma Virus (HPV) and cervical cancer. It describes the different types of HPV and their association with cervical lesions and cancer. It provides information on HPV vaccination, including efficacy against cervical lesions, safety, and recommendations for vaccination of girls ages 9-13.
Human papillomavirus (HPV) is a common sexually transmitted infection with over 100 types. More than 60 types can cause skin warts while high risk types 16, 18, 45 and 31 cause most cervical cancers. Genital HPV infections are very common among sexually active individuals, with about 20 million people infected at any time. HPV is transmitted through direct skin-to-skin contact during sexual activity and infected birth canals. While warts can be removed, the virus itself cannot be cured as it may grow back, but vaccines exist to protect against high risk HPV types.
This document provides information about human papillomavirus (HPV) including:
- There are over 100 types of HPV that can infect humans. High risk types like HPV 16 and 18 can cause cancers while low risk types cause genital warts.
- HPV is transmitted through skin to skin contact and infects mucosal surfaces. Most infections clear on their own but persistent infections can lead to cancers.
- HPV is associated with cervical, anal, penile, and oropharyngeal cancers. It is also associated with genital warts.
- The viral life cycle and genes involved in pathogenesis are described. Integration of viral DNA into host DNA is important for cancer development.
- Screening methods
- Human papillomavirus (HPV) is a non-enveloped double-stranded DNA virus that can cause various cancers and genital warts. There are over 100 HPV types, with high-risk HPV 16 and 18 causing most cervical and other cancers.
- The HPV vaccines Gardasil (HPV4) and Cervarix (HPV2) protect against HPV 16 and 18 and can prevent cancers caused by these high-risk types if administered before exposure. Vaccination is recommended for girls and boys at age 11-12.
- HPV positive oropharyngeal cancer makes up the majority of oropharyngeal cancers and is associated with improved survival compared to HPV negative orophary
The document discusses human papillomavirus (HPV) and its role in cervical cancer. It provides a history of HPV research and establishes a causal link between high-risk HPV types and cervical cancer through large epidemiological studies. The document also examines HPV genome structure and how the E6 and E7 oncoproteins interact with host cell proteins to promote oncogenesis and immortalization, ultimately leading to cervical cancer if a persistent infection occurs.
- HPV (human papillomavirus) is the most common sexually transmitted infection that can sometimes cause serious illnesses like genital warts and cervical cancer.
- HPV is transmitted through skin-to-skin contact and condoms do not fully prevent transmission.
- While HPV often clears on its own, persistent infections can cause abnormal cell growth.
- There is an effective vaccine that protects against the HPV types that cause 70% of cervical cancers and 90% of genital warts. The vaccine is recommended before sexual debut.
- Widespread HPV vaccination combined with screening programs has significantly reduced HPV infections and related cancers.
This document discusses human papillomavirus (HPV), including its structure, types, life cycle, and role in cervical cancer. Key points include:
- HPV is a small, non-enveloped virus with circular double-stranded DNA. Over 100 types exist, with about 30 causing genital infections.
- Types are classified as low, intermediate, or high risk based on cancer-causing potential. High-risk HPV 16 and 18 cause most cervical cancers.
- HPV spreads through sexual contact and can cause genital warts or remain asymptomatic. Persistent infection can lead to cervical pre-cancer.
- The virus infects epithelial cells and hijacks the host cell cycle to replicate.
The presentation covers all major aspects of the virus including oncogenicity, Structure, Pathogenesis. It also covers preventive measures and vaccines. This presentation is targeted to students at bachelors level for allied/optional microbiology paper
- Human papillomavirus (HPV) is a small non-enveloped DNA virus that infects squamous epithelia and mucous membranes, producing different types of warts or papillomas. Over 70 types of HPV exist.
- HPV replicates in basal epithelial cells and causes lesions depending on the virus type, such as common warts or genital warts. HPV types 16 and 18 can cause invasive cancers like cervical cancer.
- HPV is transmitted through direct skin or mucosa contact and shows tissue specificity. Diagnosis involves pathology, cytology, or nucleic acid tests to identify the HPV type. Prevention includes vaccines and Pap smears, while treatment consists of surgery.
This document discusses HPV (human papillomavirus), its relationship to cervical cancer, and cervical cancer screening guidelines. It describes the different types of HPV and their risks, how HPV is transmitted, how infections typically progress, and methods of detection. The document also outlines cervical cancer screening guidelines and provides an introduction to colposcopy, using images to illustrate cervical abnormalities.
Human papillomavirus (HPV) is a DNA virus that infects epithelial cells and can cause cervical cancer. There are over 100 strains of HPV, with about 30 having the potential to transform cells and cause cancer. HPV is the most common sexually transmitted infection in the US, transmitted through unprotected sex. While most HPV infections clear on their own, persistent infections can lead to precancerous lesions and cervical cancer over time if left untreated. Diagnosis is usually based on abnormal Pap test results, and vaccination prior to sexual activity provides 90-95% protection against the HPV strains most likely to cause cancer.
Human papillomavirus (HPV) is a small double-stranded DNA virus that infects epithelial cells. There are over 100 types of HPV, which are classified based on DNA sequences and show specificity for different tissue sites. HPV is transmitted through direct skin-to-skin contact and causes various lesions, including common warts, genital warts, and some cancers. HPV replicates in basal cells of the epithelium and production of new virus particles is coupled to epithelial cell differentiation. Persistent infection with high-risk HPV types can potentially lead to cervical cancer over many years through viral integration and changes to host cell genes. Diagnosis involves cytology, immunohistochemistry, and nucleic acid tests. Prevention strategies include HPV vaccines
The document discusses HPV vaccination, including:
1) Cervical cancer is a major disease burden in India, with India accounting for about 25% of cervical cancer deaths worldwide. HPV is the cause of nearly all cervical cancers.
2) HPV vaccination aims to prevent cervical cancer by vaccinating against HPV types 16 and 18, which cause about 70% of cervical cancers. Vaccination is recommended for girls and women between ages 9-45 before sexual debut or exposure to HPV.
3) Real-world effectiveness data from Australia's HPV vaccination program shows decreases in HPV vaccine-type infections and high-grade cervical abnormalities in young women following the program.
Cervical cancer is a major health problem, but HPV vaccination and screening can reduce rates. HPV is transmitted sexually and can cause cervical cancer. The vaccine protects against high-risk HPV types 16 and 18, which cause most cancers. Northern Ireland has high HPV vaccination rates. While the vaccine reduces cancer risk, screening is still needed since the vaccine does not protect against all HPV types and cannot help women already infected. In the future, screening may shift to HPV testing as prevalence decreases due to vaccination.
HPV stands for human papillomavirus. There are over 100 types of HPV that can cause diseases like genital warts or cell changes leading to cervical cancer. HPV is spread through skin-to-skin genital contact and people may not show symptoms while still being able to spread the virus. The HPV vaccine protects against four high-risk types and is approved for girls and women ages 9 to 26 in the US.
All the guidelines recommend co testing as the modality of choice for cervical cancer screening.
However, Cobas test was approved by FDA as primary screening modality in 2014.
A brief explanation of a very common skin condition called warts. The presentation explains the types, morphology, pathogenesis and treatment of viral warts. Information taken from renowned dermatology books to assist students to prepare for USMLE, MRCP and post graduate MCPS and FCPS exams. Very beneficial for medical students, dermatologists, nurses and doctors.
The document discusses HPV and its link to various cancers. It explains that HPV is a virus that can cause warts and some cancers like cervical cancer. Persistent high-risk HPV infections can lead to pre-cancerous lesions and some cancers over time if left undetected and untreated. The document also discusses HPV vaccines that can help prevent HPV infections and reduce the risk of HPV-related cancers.
HPV infection and HPV-associated cervical cancer are significant public health issues, with an estimated 11,000 new cervical cancer cases and 4,000 deaths annually in the US. Globally, nearly 500,000 new cervical cancer cases occur each year, mostly in developing countries. Two HPV vaccines (Gardasil and Cervarix) were approved to protect against HPV types that cause cervical cancer and genital warts. However, the long-term effectiveness and safety of the vaccines have yet to be established, as clinical trials only involved small populations followed for a short period of 5 years. Numerous adverse reactions including pain, swelling, fever, and even death have been reported following vaccination. Mandating the HPV vaccine also faces
This document discusses cervical intraepithelial neoplasia (CIN), a precancerous condition affecting the cervix. It provides a historical background of CIN and describes the grading system used (CIN 1-3). Risk factors for CIN include HPV infection and early sexual activity. CIN results from abnormal cell growth in the cervix due to HPV infection. Progression from CIN to invasive cancer depends on the grade, with higher grades having greater risk. Diagnosis involves Pap testing, colposcopy, and HPV testing.
This document discusses cervical cancer worldwide and in Saudi Arabia. It provides statistics on the prevalence, incidence, and mortality of cervical cancer globally and within regions. It notes that cervical cancer incidence is very low in Saudi Arabia at 1.9 per 100,000 women but is expected to increase to 309 new cases by 2025. Risk factors, screening and prevention, stages and treatments are summarized.
Hepatitis B is a viral infection that affects the liver and can be either acute or chronic. It is transmitted through bodily fluids and can cause both acute and chronic liver disease. While acute hepatitis B resolves in 95-99% of adult cases, chronic hepatitis B affects approximately 350 million people worldwide and increases the risk of cirrhosis and liver cancer. Treatment for chronic hepatitis B involves antiviral medications to suppress the virus and prevent further liver damage.
- Human papillomavirus (HPV) is a non-enveloped double-stranded DNA virus that can cause various cancers and genital warts. There are over 100 HPV types, with high-risk HPV 16 and 18 causing most cervical and other cancers.
- The HPV vaccines Gardasil (HPV4) and Cervarix (HPV2) protect against HPV 16 and 18 and can prevent cancers caused by these high-risk types if administered before exposure. Vaccination is recommended for girls and boys at age 11-12.
- HPV positive oropharyngeal cancer makes up the majority of oropharyngeal cancers and is associated with improved survival compared to HPV negative orophary
The document discusses human papillomavirus (HPV) and its role in cervical cancer. It provides a history of HPV research and establishes a causal link between high-risk HPV types and cervical cancer through large epidemiological studies. The document also examines HPV genome structure and how the E6 and E7 oncoproteins interact with host cell proteins to promote oncogenesis and immortalization, ultimately leading to cervical cancer if a persistent infection occurs.
- HPV (human papillomavirus) is the most common sexually transmitted infection that can sometimes cause serious illnesses like genital warts and cervical cancer.
- HPV is transmitted through skin-to-skin contact and condoms do not fully prevent transmission.
- While HPV often clears on its own, persistent infections can cause abnormal cell growth.
- There is an effective vaccine that protects against the HPV types that cause 70% of cervical cancers and 90% of genital warts. The vaccine is recommended before sexual debut.
- Widespread HPV vaccination combined with screening programs has significantly reduced HPV infections and related cancers.
This document discusses human papillomavirus (HPV), including its structure, types, life cycle, and role in cervical cancer. Key points include:
- HPV is a small, non-enveloped virus with circular double-stranded DNA. Over 100 types exist, with about 30 causing genital infections.
- Types are classified as low, intermediate, or high risk based on cancer-causing potential. High-risk HPV 16 and 18 cause most cervical cancers.
- HPV spreads through sexual contact and can cause genital warts or remain asymptomatic. Persistent infection can lead to cervical pre-cancer.
- The virus infects epithelial cells and hijacks the host cell cycle to replicate.
The presentation covers all major aspects of the virus including oncogenicity, Structure, Pathogenesis. It also covers preventive measures and vaccines. This presentation is targeted to students at bachelors level for allied/optional microbiology paper
- Human papillomavirus (HPV) is a small non-enveloped DNA virus that infects squamous epithelia and mucous membranes, producing different types of warts or papillomas. Over 70 types of HPV exist.
- HPV replicates in basal epithelial cells and causes lesions depending on the virus type, such as common warts or genital warts. HPV types 16 and 18 can cause invasive cancers like cervical cancer.
- HPV is transmitted through direct skin or mucosa contact and shows tissue specificity. Diagnosis involves pathology, cytology, or nucleic acid tests to identify the HPV type. Prevention includes vaccines and Pap smears, while treatment consists of surgery.
This document discusses HPV (human papillomavirus), its relationship to cervical cancer, and cervical cancer screening guidelines. It describes the different types of HPV and their risks, how HPV is transmitted, how infections typically progress, and methods of detection. The document also outlines cervical cancer screening guidelines and provides an introduction to colposcopy, using images to illustrate cervical abnormalities.
Human papillomavirus (HPV) is a DNA virus that infects epithelial cells and can cause cervical cancer. There are over 100 strains of HPV, with about 30 having the potential to transform cells and cause cancer. HPV is the most common sexually transmitted infection in the US, transmitted through unprotected sex. While most HPV infections clear on their own, persistent infections can lead to precancerous lesions and cervical cancer over time if left untreated. Diagnosis is usually based on abnormal Pap test results, and vaccination prior to sexual activity provides 90-95% protection against the HPV strains most likely to cause cancer.
Human papillomavirus (HPV) is a small double-stranded DNA virus that infects epithelial cells. There are over 100 types of HPV, which are classified based on DNA sequences and show specificity for different tissue sites. HPV is transmitted through direct skin-to-skin contact and causes various lesions, including common warts, genital warts, and some cancers. HPV replicates in basal cells of the epithelium and production of new virus particles is coupled to epithelial cell differentiation. Persistent infection with high-risk HPV types can potentially lead to cervical cancer over many years through viral integration and changes to host cell genes. Diagnosis involves cytology, immunohistochemistry, and nucleic acid tests. Prevention strategies include HPV vaccines
The document discusses HPV vaccination, including:
1) Cervical cancer is a major disease burden in India, with India accounting for about 25% of cervical cancer deaths worldwide. HPV is the cause of nearly all cervical cancers.
2) HPV vaccination aims to prevent cervical cancer by vaccinating against HPV types 16 and 18, which cause about 70% of cervical cancers. Vaccination is recommended for girls and women between ages 9-45 before sexual debut or exposure to HPV.
3) Real-world effectiveness data from Australia's HPV vaccination program shows decreases in HPV vaccine-type infections and high-grade cervical abnormalities in young women following the program.
Cervical cancer is a major health problem, but HPV vaccination and screening can reduce rates. HPV is transmitted sexually and can cause cervical cancer. The vaccine protects against high-risk HPV types 16 and 18, which cause most cancers. Northern Ireland has high HPV vaccination rates. While the vaccine reduces cancer risk, screening is still needed since the vaccine does not protect against all HPV types and cannot help women already infected. In the future, screening may shift to HPV testing as prevalence decreases due to vaccination.
HPV stands for human papillomavirus. There are over 100 types of HPV that can cause diseases like genital warts or cell changes leading to cervical cancer. HPV is spread through skin-to-skin genital contact and people may not show symptoms while still being able to spread the virus. The HPV vaccine protects against four high-risk types and is approved for girls and women ages 9 to 26 in the US.
All the guidelines recommend co testing as the modality of choice for cervical cancer screening.
However, Cobas test was approved by FDA as primary screening modality in 2014.
A brief explanation of a very common skin condition called warts. The presentation explains the types, morphology, pathogenesis and treatment of viral warts. Information taken from renowned dermatology books to assist students to prepare for USMLE, MRCP and post graduate MCPS and FCPS exams. Very beneficial for medical students, dermatologists, nurses and doctors.
The document discusses HPV and its link to various cancers. It explains that HPV is a virus that can cause warts and some cancers like cervical cancer. Persistent high-risk HPV infections can lead to pre-cancerous lesions and some cancers over time if left undetected and untreated. The document also discusses HPV vaccines that can help prevent HPV infections and reduce the risk of HPV-related cancers.
HPV infection and HPV-associated cervical cancer are significant public health issues, with an estimated 11,000 new cervical cancer cases and 4,000 deaths annually in the US. Globally, nearly 500,000 new cervical cancer cases occur each year, mostly in developing countries. Two HPV vaccines (Gardasil and Cervarix) were approved to protect against HPV types that cause cervical cancer and genital warts. However, the long-term effectiveness and safety of the vaccines have yet to be established, as clinical trials only involved small populations followed for a short period of 5 years. Numerous adverse reactions including pain, swelling, fever, and even death have been reported following vaccination. Mandating the HPV vaccine also faces
This document discusses cervical intraepithelial neoplasia (CIN), a precancerous condition affecting the cervix. It provides a historical background of CIN and describes the grading system used (CIN 1-3). Risk factors for CIN include HPV infection and early sexual activity. CIN results from abnormal cell growth in the cervix due to HPV infection. Progression from CIN to invasive cancer depends on the grade, with higher grades having greater risk. Diagnosis involves Pap testing, colposcopy, and HPV testing.
This document discusses cervical cancer worldwide and in Saudi Arabia. It provides statistics on the prevalence, incidence, and mortality of cervical cancer globally and within regions. It notes that cervical cancer incidence is very low in Saudi Arabia at 1.9 per 100,000 women but is expected to increase to 309 new cases by 2025. Risk factors, screening and prevention, stages and treatments are summarized.
Hepatitis B is a viral infection that affects the liver and can be either acute or chronic. It is transmitted through bodily fluids and can cause both acute and chronic liver disease. While acute hepatitis B resolves in 95-99% of adult cases, chronic hepatitis B affects approximately 350 million people worldwide and increases the risk of cirrhosis and liver cancer. Treatment for chronic hepatitis B involves antiviral medications to suppress the virus and prevent further liver damage.
This document discusses cervical cancer and HPV in India. It notes that India accounts for 27% of new cervical cancer cases and deaths worldwide despite having only 16% of the global population. It is estimated that over 365 women will die from cervical cancer daily in India by 2025. HPV is the main cause of cervical cancer and certain HPV types are also associated with other cancers. The document discusses HPV vaccines as the primary prevention for HPV-related diseases and recommends routine vaccination of girls aged 9-12 years along with catch-up vaccination up to age 26. It provides details on the available HPV vaccines and their efficacy, safety and recommended dosage schedules.
1. Vaginitis is usually characterized by vaginal discharge, vulvar itching, irritation, and odor. Common causes include trichomoniasis, bacterial vaginosis, and vulvovaginal candidiasis.
2. Trichomoniasis is caused by the protozoan Trichomonas vaginalis and is transmitted sexually. Symptoms in women include frothy gray or yellow-green discharge and pruritus. Diagnosis is made by visualizing motile trichomonads on a saline wet mount.
3. CDC-recommended treatment for trichomoniasis is metronidazole 2g orally in a single dose. It is important to treat
This document provides information on managing abnormal Pap smear results according to the Bethesda system. It discusses the categories of Pap smear results including within normal limits, benign cellular changes, and epithelial cell abnormalities. It describes what constitutes an adequate versus inadequate sample. Abnormal results can be due to issues with the sample, inflammation, infection, or dysplastic changes. Management depends on the specific result and may include treating any infections, repeating the Pap smear, or proceeding to colposcopy and/or biopsy. The document outlines recommendations for various abnormal results including low grade and high grade squamous intraepithelial lesions, atypical squamous cells, glandular abnormalities and more.
El virus del papiloma humano (VPH) es una infección de transmisión sexual muy común que puede causar verrugas genitales. La infección por VPH a menudo no presenta síntomas y se transmite principalmente a través del contacto sexual sin protección. Las verrugas genitales son el síntoma más característico cuando hay síntomas presentes. El diagnóstico y tratamiento dependen del tipo y gravedad de la infección.
This document discusses cervical intraepithelial neoplasia (CIN), which refers to precancerous changes that occur in the cells of the cervix. It describes the anatomy of the cervix and transformation zone. CIN is believed to originate from a single focus in the transformation zone. Human papillomavirus (HPV) infection plays an important role in the development of CIN and cervical cancer. The document outlines grading of CIN (CIN 1-3), diagnostic tools like Pap smears and colposcopy, and treatment options.
Este documento describe los herpesvirus, incluidos el herpes tipo 1 y 2. Los herpesvirus forman una familia de virus divididos en tres subfamilias. El herpes tipo 1 se caracteriza por periodos de latencia en los ganglios trigéminos y puede causar lesiones orales y oculares. El herpes tipo 2 se caracteriza por periodos de latencia en la región genital y se transmite sexualmente. También describe el virus de Epstein-Barr, la causa más común de mononucleosis infecciosa, que se transmite a través de la saliva.
This document discusses pre-cancerous lesions of the cervix. It begins by defining premalignant lesions and explaining the multi-step process of carcinogenesis. It then discusses specific pre-cancerous lesions including hyperplasia, metaplasia, dysplasia, and cervical intraepithelial neoplasia (CIN). High-risk HPV infection plays a key role in the development of these lesions. Screening methods like the Pap test and HPV testing can detect pre-cancerous lesions early. Colposcopy is used to examine the cervix in more detail when abnormalities are found. Biopsies of suspicious lesions allow diagnosis and treatment if needed to prevent progression to invasive cancer.
This document summarizes the anatomy, histology, and pathologies of the uterine cervix. It discusses the normal cervix epithelium and how cervical inflammation and infections can cause conditions like cervicitis. Precancerous lesions like cervical intraepithelial neoplasia are often caused by human papillomavirus infection and can progress to invasive cervical cancer if left undetected and untreated. Screening methods like the Pap test aim to detect these early lesions to prevent cervical cancer.
This document discusses human papillomavirus (HPV) and its role in cervical cancer. It covers topics such as the types of HPV, how persistent high-risk HPV infections can lead to precancerous lesions and cancer, and the mechanisms by which HPV's E6 and E7 proteins cause cancer development by inactivating tumor suppressor proteins. It also addresses HPV prevalence, HPV-associated cancers, cofactors that increase cancer risk, screening and prevention methods like the Pap test and HPV vaccines, as well as treatment options.
Etiopathogenesis and natural history of ca cervixNiranjan Chavan
CERVICAL CANCER , the 2nd most common cancer in India can be easily prevented with proper adequate screening and awareness.
Adequate sex education is necessary to inculcate safe sexual practices to prevent HPV infection.
Etiopathogenesis and natural history of ca cervixNiranjan Chavan
CERVICAL CANCER , the 2nd most common cancer in India can be easily prevented with proper adequate screening and awareness.
Adequate sex education is necessary to inculcate safe sexual practices to prevent HPV infection.
HPV is a double stranded DNA virus that can cause warts and cancers. It is categorized into low-risk HPVs that cause warts and high-risk HPVs linked to cancers like cervical cancer. HPV is commonly transmitted sexually and globally infects about 11.7% of people. Persistent infection with high-risk HPV types can lead to cancer through viral proteins that inactivate tumor suppressor genes. While most HPV infections clear naturally, vaccination is recommended to prevent infection and cancer.
Cervical cancer is the leading cause of cancer in women in Africa. Infection with human papillomavirus (HPV) is the main risk factor for cervical cancer. Persistent HPV infection can cause chronic inflammation in the cervix through activation of inflammatory pathways. This review discusses research from the University of Cape Town that shows how the HPV virus activates inflammatory pathways like the cyclooxygenase (COX)-prostaglandin pathway in cervical cancer. This pathway promotes tumor progression by enhancing angiogenesis, immune cell recruitment, and tissue remodeling. Factors like seminal fluid can also increase inflammation in the cervix and modulate cancer risk.
This document discusses HPV, its link to cervical cancer, and CERVAVAC, an indigenous HPV vaccine developed in India. It provides background on HPV, noting it is the most common STI and can cause several cancers including cervical cancer. It explains how HPV evades the immune system and its lifecycle in the cervix. It classifies HPV types as high-risk or low-risk and notes that high-risk HPV 16 and 18 cause over 70% of cervical cancer cases globally. It discusses cervical cancer signs, symptoms and prevention methods like education, screening via Pap tests, and vaccination. It provides an overview of CERVAVAC, India's first indigenous HPV vaccine, and its goal of being affordable and
The Natural History of Type-specific Human Papillomavirus Infections in Femal...Alberto Cuadrado
This study examined the natural history of type-specific HPV infections in female university students over 24 months. Key findings include:
- The incidence rates of acquiring high-risk or low-risk HPV infections were similar at around 14 and 12 cases per 1000 women-months, respectively.
- HPV-16, -51, and -84 had the highest rates of new acquisition at around 5, 3, and 4 cases per 1000 women-months, respectively.
- HPV-16 infections persisted the longest on average at 18 months, followed by HPV-31 and HPV-53 at around 14-15 months. HPV-6 and HPV-84 cleared fastest on average in under 10 months.
- After
Cervical cancer is caused by human papillomavirus (HPV) infection. HPV infection is very common and in most cases does not cause health problems, but some high-risk HPV types can cause cervical cancer over many years if left untreated. Screening through regular Pap tests can detect pre-cancerous changes early so they can be treated before they develop into invasive cancer. A new HPV vaccine protects against the types of HPV that cause most cervical cancers.
This document discusses human papilloma virus (HPV), specifically:
1. HPV is a non-enveloped double stranded DNA virus that infects epithelial cells. High-risk HPV types like HPV-16 and HPV-18 express oncogenic proteins E6 and E7 that can lead to cervical cancer.
2. HPV is very common and most sexually active individuals will be infected at some point. While the virus often clears within 1-2 years, persistent infection with high-risk types increases the risk of precancerous cervical lesions and cancer.
3. The E6 and E7 oncoproteins of high-risk HPV inactivate tumor suppressor proteins and induce telomerase
HSIL and LSIL refer to high grade squamous intraepithelial lesion and low grade squamous intraepithelial lesion, respectively. LSIL is associated with transient HPV infection and often resolves on its own, while HSIL is considered a true precancerous lesion with a higher risk of progression to cervical cancer. Cytologically, LSIL shows koilocytosis with raisinoid nuclei and mild abnormalities. HSIL displays more severe nuclear abnormalities like increased size and irregular contours, loss of cell polarity, and a higher mitotic rate. Distinguishing between LSIL and HSIL is important for determining the severity of cervical dysplasia and appropriate clinical management.
Cervical intraepithelial neoplasia (CIN) are premalignant lesions of the cervix caused by persistent HPV infection. CIN1 lesions often regress on their own while CIN2 and CIN3 lesions have a higher risk of progression to invasive cancer if left untreated. Diagnosis is made through cervical cytology, HPV testing, and colposcopy. Treatment options include ablative procedures like cryotherapy for low-grade lesions and excisional procedures like LEEP for high-grade lesions. Screening programs utilizing Pap smears or visual inspection techniques aim to detect and treat CIN early to prevent the development of invasive cervical cancer.
The document discusses human papillomavirus (HPV) and related diseases like cervical cancer. It notes that HPV types 16 and 18 cause over 70% of cervical cancers worldwide. Cervical cancer rates have declined in countries with organized cervical screening programs. HPV is transmitted sexually and often clears without symptoms, but can sometimes cause cervical lesions and genital warts.
CERVICAL CARCINOMA The Role of the Human Papilloma Virus and Prospects for Pr...Alberto Cuadrado
This document discusses cervical carcinoma and prospects for primary prevention. It summarizes that cervical cancer is the second most common cancer in women worldwide, caused over 99% of the time by human papillomavirus (HPV) infection. Screening methods like Pap smears have been effective in developed countries but are too expensive for low-resource areas. The document explores more affordable options like visual inspection with acetic acid (VIA) and prospects for an HPV vaccination to help developing countries prevent cervical cancer.
Human papilloma virus in oropharyngeal cancersAhmad Qudah
This document discusses human papillomavirus (HPV) and its link to oropharyngeal cancers. It defines HPV as a small, double-stranded DNA virus that can cause warts, cancers, and sexually transmitted diseases. Certain HPV types, such as 16 and 18, have a strong association with cancers like cervical cancer and oropharyngeal cancer. HPV is diagnosed through tests like Pap smears, biopsies, and PCR. While there is no treatment for HPV itself, vaccines are available to protect against the types of HPV that commonly cause cancer. The rates of oropharyngeal cancer, which can be caused by HPV, have been rising, particularly in men who have sex with men.
Dr. nisreen cervical cancer screening in park hayatTariq Mohammed
The document discusses cervical cancer prevalence, incidence, and mortality worldwide and in Saudi Arabia. It notes that cervical cancer is the second leading cause of cancer death in women globally, with over 500,000 new cases and 288,000 deaths annually. In Saudi Arabia specifically, the incidence is very low at 1.9 cases per 100,000 women, accounting for 152 new cases and 55 deaths annually. However, little is known about HPV prevalence and transmission patterns in the country. The challenges in addressing cervical cancer in Saudi Arabia include understanding HPV and abnormal cytology prevalence, sexual practices, implementing screening programs, determining vaccine cost-effectiveness, and ensuring quality screening and colposcopy.
This document discusses pathology of the female genital tract, focusing on cervicitis and carcinoma of the cervix. It describes the etiology, pathogenesis and progression of cervical carcinoma. Cervicitis is usually caused by bacterial or viral infections and presents with inflammation of the cervix. Cervical carcinoma is often associated with HPV infection and develops through premalignant stages of cervical intraepithelial neoplasia. Regular Pap smear screening can detect cervical lesions early and reduce mortality from cervical cancer. The document outlines screening guidelines and pathological features of various cervical lesions, cancers and their staging.
Similar to Natural history and pathogenesis of hpv (20)
This document summarizes stem cell research projects conducted by Dr. Mohammad Abbas at King Abdulaziz University. It outlines 5 research groups: 1) Isolation and characterization of bone marrow mesenchymal stem cells from osteoarthritis patients, 2) Effect of heat shock on bone marrow MSCs from OA patients, 3) Evaluation of ex-vivo cartilage regeneration using MSCs from OA patients, 4) Impact of MSCs impregnated with cartilage paste on repairing cartilage defects in rabbits, and 5) Impact of a hyaluronic acid scaffold impregnated with MSCs and cartilage paste on surgically induced arthritis in rabbits. Additional research includes studies on the effects of catecholamines and NSAIDs
This document outlines the establishment of a stem cell research chair at King Abdulaziz University from 2009-2015. It begins with the author attending a knee surgery course in 2009 where he learned about cartilage regeneration techniques. He then proposed creating a research chair to RACI in 2010, which involved a lengthy approval process. He built up a research team of professors and clinicians from various specialties. Research projects focused on isolating and characterizing mesenchymal stem cells, cartilage regeneration, and animal studies on rabbits. The chair fulfilled regulatory requirements like submitting annual reports and had an organizational structure to oversee the research groups.
Bone marrow mesenchymal stem cells (BM-MSCs) and cartilage fragments were evaluated for their ability to enhance cartilage formation in an ex-vivo osteochondral defect model. BM-MSCs alone, cartilage fragments alone, or a combination of BM-MSCs and cartilage fragments were seeded into osteochondral defects. The combination of BM-MSCs and cartilage fragments showed improved cartilage formation and defect filling compared to BM-MSCs or cartilage fragments alone, as seen on histological and biochemical analysis. The results suggest that a combination of BM-MSCs and cartilage fragments may provide a more effective approach for cartilage repair.
The document describes a study that used whole-exome sequencing to identify novel genetic variations associated with osteoarthritis (OA) patients. Several variations were found in genes involved in cartilage development, extracellular matrix organization, and inflammatory/immune responses. Two novel mutations were validated by Sanger sequencing, including a mutation in the SELP gene and another in the COL6A6 gene. The approach identified variations in genes impacting pathways relevant to OA pathogenesis.
This study investigated the effects of heat from an arthroscope on human bone marrow-derived mesenchymal stem cells (hBMMSCs). hBMMSCs were isolated from osteoarthritis patients and exposed to heat from an illuminated arthroscope for various time periods as single cell suspensions or cell pellets. Cell suspensions exposed to heat showed decreased viability over time, while cell pellets maintained or increased viability. Gene expression analysis found increased expression of heat shock and inflammatory genes in cell suspensions compared to pellets after heat exposure. The results suggest that transplanting hBMMSCs as cell pellets may better protect them from heat effects during arthroscopic procedures and thus support cartilage regeneration.
The international federation for cervical pathology and colposcopy courseTariq Mohammed
This document provides an agenda and speaker information for a 3-day international colposcopy workshop taking place in Jeddah, Saudi Arabia from January 12-14, 2014. The workshop will focus on cervical cancer prevention, advances in understanding HPV, and management of lower genital tract diseases. It will include lectures, hands-on training, and case reviews led by experts from Europe, Canada, and Saudi Arabia. The goal is to train participants and raise awareness of cervical cancer screening and prevention methods.
The international federation for cervical pathology and colposcopy courseTariq Mohammed
This document summarizes the stages of human development from dust, to sperm and egg, to embryo, to fetus, and finally to a child that reaches maturity. It notes that some people die early while others live to a very old age, having gone through the full cycle of knowledge and then forgetting. It also describes how the earth appears barren but grows diverse plants when watered, relating this to human development from simple beginnings. The summary conveys the key points about human origins and development and the cycle of life in a concise three sentences.
The international federation for cervical pathology and colposcopy courseTariq Mohammed
The document discusses how God created humans from dust, then a sperm-drop, then a clinging clot, and then a lump of flesh to show how He develops humans. It notes that God determines the term people will stay in the womb, then brings them out as children to reach maturity. It also mentions that some people die early while others live to a very old age. The document ends by describing how the earth appears barren but grows beautiful plants when watered.
This document discusses treatment approaches for early stage cervical cancer. It notes that for invasive cervical cancers measuring less than 2 cm, removal of the parametrium may be omitted. For some very small tumors, pelvic lymphadenectomy can also be omitted as the risk of lymph node metastasis is limited. It also discusses outcomes from vaginal trachelectomy and laparoscopic pelvic lymphadenectomy for early stage cancers. The document considers conservative treatment approaches for stage IA2-IB1 cancers less than 3 cm in size, including a proposed study design stratifying patients based on tumor diameter.
Adenocarcinoma in situ (AIS) is the only known precursor to cervical adenocarcinoma. Appropriate management of AIS can prevent invasive adenocarcinoma in many cases. Cytology has lower sensitivity for detecting AIS compared to HPV testing. The usual interval between detectable AIS and invasive adenocarcinoma is at least 5 years, allowing time for screening and intervention. Glandular neoplasms account for about 25% of annual cervical cancer diagnoses. Management of AIS typically involves conization, though hysterectomy is the standard treatment due to the high risk of residual disease with conization alone. HPV testing can help monitor women with AIS who wish to preserve fertility after
This document discusses vulvar and vaginal diseases. It begins with anatomical considerations of the vulva and describes various benign and infectious vulvar lesions. It then discusses non-neoplastic epithelial disorders of the vulva and classifications of vulvar dermatological disorders. The document provides details on various vulvar diseases including lichen sclerosus and pigmented lesions. It concludes with a brief section on vaginal intraepithelial neoplasia.
This document summarizes key findings about HPV natural history and HPV testing for cervical cancer screening. It was found that HPV infection is very common but rarely leads to cancer. While persistent HPV infection can cause cervical cancer after 10-15 years, many cofactors are also involved in cancer development. Studies showed that HPV becomes undetectable within 2 years for most women. HPV testing was found to detect more pre-cancer than pap smears but also detected more lesions that may regress. HPV testing allows longer screening intervals for HPV-negative women and better protection against cancer compared to pap smears alone. While HPV testing is more effective, implementing new screening strategies poses challenges where pap smear systems are already in place.
1) The document discusses the HPV vaccine and summarizes data from clinical trials of the Cervarix and Gardasil vaccines. It finds that Cervarix demonstrated 93.2% efficacy against CIN3+ lesions irrespective of HPV type, while Gardasil demonstrated 43.0% efficacy against the same endpoint.
2) Long-term follow up data of the Cervarix vaccine showed sustained high antibody levels and protection against CIN3+ lesions up to 9 years post-vaccination. Challenge studies found Cervarix elicited an anamnestic response.
3) Both vaccines were well tolerated and showed cross-protection against non-vaccine HPV types. However, Cervarix demonstrated higher long
4 prof james bently management guidelines 2014Tariq Mohammed
This document provides guidelines for colposcopy management from the IFCCP Jeddah Jan 2014 conference and the ASCCP Management Guidelines 2012 and SOGC SCC Colposcopy Guidelines 2012. It discusses recommendations and algorithms for evaluating and managing various abnormal cytology results and histological findings identified during colposcopy, including ASCUS, LSIL, ASC-H, HSIL, AGC, cervical intraepithelial neoplasia grades, and other conditions. Management may involve repeat testing, colposcopy, biopsy, excisional procedures, or return to routine screening depending on the abnormality, risk level, and other factors.
Genital HPV is very common, with a lifetime risk of 70% for HPV infection and 10% for genital warts. Spontaneously, genital warts resolve in 20-30% of cases within 3 months. Biopsy is usually not required for healthy women under 35 years old with typical genital warts. Treatment choices depend on factors like patient preference, provider experience, and pregnancy status. Combination therapies may be used. Even after treatment, the latent virus remains, with a 30% recurrence rate of warts and potential for transmission to partners.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
1. NATURAL
HISTORY
AND
PATHOGENESIS
OF
HPV.
HASSAN
M
LATIFAH
MD
FRCSC
GYNECOLOGIC
ONCOLOGY
KFSH&RC
-‐
JEDDAH
2. § Incidence
and
worldwide
burden
of
cervical
cancer.
§ Phylogenetic
tree
of
HPV.
§ Pathogenesis
and
natural
history.
§ Genomic
background.
§ HPV
infection
at
cellular
level.
§ Conditions
required
for
transition
into
cervical
cancer
.
§ Cofactor
interaction
with
HPV.
§ Summary.
3. Ferlay J, et al. GLOBOCAN 2002 Cancer Incidence, Mortality and Prevalence Worldwide. IARC CancerBase; Lyon; 2004.
The most frequent cancers in women: incidence and
mortality
Global data
Incidence Mortality
Age-standardized rate per 100,000
Breast
Cervix
Colon/
Rectum
Lung
Stomach
Ovary
Corpus
0 5 10 15 20 25 30 35 40
37.4
16.2
14.6
12.1
10.3
6.6
6.5
Breast
Lung
Cervix
Stomach
Colon/
Rectum
Liver
Ovary
0 2 4 6 8 10 12 14
13.2
10.3
9.0
7.9
7.6
5.7
4.0
Age-standardized rate per 100,000
4. Worldwide Cancer Burden*
471
379
154
193
142
101
75
132
117
55
65
39
0 100 200 300 400 500 600
579
91
292
125
175
91
114
34
16
66
47
61
100200300400500600
Breast
Cervix uteri
Colon/Rectum
Stomach
Lung
Ovary
Corpus uteri
Liver
Oesophagus
Non-Hodgkin lymphoma
Leukaemia
Pancreas
More developed Less developed
2,176,000 2,562,000
Thousands
Total
Women
5. PAPILLOMAVIRUS
INFECTIONS
OF
THE
HUMAN
GENITAL
TRACT
§ Over
100
HPV
types
have
been
identified
to
date,
of
which
over
40
infect
the
genital
tract.
§ HPVs
primarily
target
infections
of
the
basal
cells
in
the
stratified
squamous
epithelium
and
metaplastic
cells
within
squamocolumnar
junctions.
6. Muňoz N, et al. Int J Cancer 2004; 111:278–285.
HPV
types
in
cervical
cancer
worldwide
HPVgenotype
35
58
52
33
31
45
18
16 53.5
70.7
77.4
80.3
82.9
85.2
87.4
88.8
0 10 20 30 40 50 60 70 80 90 100
Cervical cancer cases attributed to
the most frequent HPV genotypes, %
53.5
17.2
6.7
2.9
2.6
2.3
2.2
1.4
Cumulative
percentage
8. Normal
epithelium
Basement
membrane
Basal
(stem)
cells
Parabasal
cells
Squamous
layer
Mature
squamous
layer
Infected
epithelium
Cervical
canal
HPV
Lifecycle
in
the
Cervix
Frazer
IH.
Nat
Rev
Immunol
2004;4:46–54
Infection
of
basal
cells
Viral
assembly
Shedding
of
virus-‐
laden
epithelial
cells
Episomal
viral
DNA
in
cell
nucleus
Viral
DNA
replication
Uptake
&
internalisation
of
HPV
occurs
within
2
hours
9.
10.
11. Co-factors: OC use,
parity, other STDs
Co-factors: smoking, host
(HLA, p53 polymorphism)
Persistent HPV
infection with
oncogenic types
Transient
HPV
infection
Sexual activity:
woman and her
male partners
Invasive
cervical
cancer
Low grade
lesions
High grade
lesions
Normal
cervical
epithelium
Viral
factors:
variants
and viral
load
Co-factors: nutrition
A Multifactorial Model of Cervical Cancer Etiology
Spence, et al. AJC 2005.
12. Natural
Course
of
Genital
HPV
Infection
First
Lesion
Immune
Response
Incubation
Active Growth
Sustained
clinical
remission
Persistent or
recurrent
disease
Infection
Seroconversion
Average time
9mo
Low risk HPVs clear more rapidly than high risk HPVs
HPV 16 infection lasts on average 12-18 months
13. Genomic
background
§ All
PV(s)
share
a
similar
genomic
organization
consisting
of
an
early
(E)
gene
region
,
a
late(L)
gene
region
and
a
regulatory
region.
§ The
5
early
proteins
(E1,E2,E5,E6and
E7)
are
required
for
viral
replication
and
/or
cellular
transformation.
14. Role
of
E6
and
E7.
§ Expression
of
the
E6
oncoprotein
allows
the
infected
cell
to
be
insensitive
to
antigrowth
signals
and
to
evade
apoptosis.
§ Expression
of
the
E7
oncoprotein
leads
to
insensitivity
to
antigrowth
signals
and
the
immortalization
of
keratinocytes.
15. § HPV
mediated
oncogenesis
requires
accumulation
of
additional
genetic
mutations
over
time
.
§ This
suggests
a
long
precancerous
state
in
most
cases
of
invasive
cancer
that
allows
the
accumulation
of
secondary
genetic
mutations
along
with
other
cofactors
such
as
smoking
,
carcinogens
and
hormonal.
16. Human
PV(s)
and
cervical
neoplasia.
§ 4
steps
in
the
development
of
cervical
cancer
:
1-‐Infection
of
the
metaplastic
epithelium
of
the
TZ
with
one
or
more
carcinogenic
HPV.
2-‐Viral
persistence
.
3-‐Progression
to
CIN3.
4-‐Invasion.
17. Anatomy
of
the
TZ
§ The
TZ
is
defined
as
that
area
lying
between
the
original
SCJ
and
the
colposcopic
new
SCJ
§ Cervical
Cancer
originates
within
the
TZ.
18. Squamous
metaplasia
:
a
pivotal
process
in
cervical
carcinogenesis
§ The
increase
in
E2
level
during
puberty
leads
to
eversion
of
the
endovervical
columnar
epithelium.
§ The
process
of
repair
results
in
replacement
with
squamous
metaplastic
epithelium.
19. § Potential
carcinogens
at
times
of
active
metaplasia
can
deviate
it
to
a
neoplastic
pathway.
§ The
lifetime
risk
for
development
of
cervical
cancer
is
increased
26
folds
if
age
at
first
intercourse
is
within
1
yr
of
menarche
.
22. HPV
Immunology
§ Unlike
Hepatitis,
HPV
is
stealthy
&
evades
the
immune
system
§ Natural
infection
with
HPV
does
not
reliably
protect
against
future
infection
or
reactivation
§ Antibodies
are
considered
an
important
mediator
of
vaccine-‐induced
protection
by
preventing
entry
of
the
virus
into
the
basal
cell
23. Turn off the alarm systems
Keep a low profile
Don’t cause trouble – no violence
HPV – a Lesson in How to Evade
the Forces of Law and Order
24. § Most
HPV
infections
are
transient
and
usually
cleared
within
several
months
to
2
yrs.
§ 90%
of
women
clear
a
specific
HPV
type
after
2
yrs
of
observation.
§ Only
persistent
high
risk
infection
of
the
cervical
epithelium
appears
to
trigger
neoplastic
progression.
§ HPV
type
is
the
strongest
factor
affecting
the
risk
of
viral
persistence
.
25. § Only
1
in
10
to
1
in
30
HPV
infections
are
associated
with
abnormal
cervical
cytology.
§ HPV
16
is
highly
carcinogenic
with
an
absolute
risk
of
CIN
3
approaching
40%
at
3-‐5
yrs.
§ Up
to
1/3
of
women
have
more
than
1
HPV
type
.
§ The
average
time
from
HPV
infection
to
CIN
3
is
7-‐15
yrs
,
peaking
at
25-‐30
yrs.
26. Transition
into
invasive
cancer
§ The
seed
:
High
risk
HPV.
§ The
soil
:
Immature
metaplastic
epithelium
of
the
TZ.
§ The
median
age
of
women
with
cervical
cancer
is
2-‐3
decades
later
than
for
CIN
3.
§ This
suggests
generally
a
long
average
transit
time
for
CIN
3
to
invasive
cancer.
27. Time to acquisition of HPV
infection among women free of
HPV infection at enrollment
630 college-age women
followed from 1996-01
Richardson, et al. CEBP 2003; 42:485-490.
McGill-Concordia
University
Student
Cohort:
0 10 20 30 40
Time since enrollment (months)
0
0.1
0.3
0.2
0.5
0.4
0.6
0.7
Probabilityof
incidentHPVinfection
0 10 20 30 40
Time since enrollment (months)
0
0.1
0.3
0.2
0.4
0.5
Probabilityoflow-riskHPV
0 10 20 30 40
Time since enrollment (months)
0
0.1
0.3
0.2
0.4
0.5
Probabilityof
incidenthigh-riskHPV Any types
Non-oncogenic
types
Oncogenic
types
28. Clearance of a New HPV Infection:
Ludwig-McGill and McGill-Concordia Cohorts
1.00
0.75
0.50
0.25
0.00
0 4 12 16 20 24 28 32 368
1.0
0.8
0.6
0.4
0.2
0.0
Time Since Diagnosis of Infection
ProportionRemainingPositive
ForAnyHPVType
0 12 24 36
40
Franco, et al. JID 1999; 180:1415-1423.
Richardson, et al. CEBP 2003; 42:485-490.
29. Cofactor
Interaction
with
HPV.
§ Cigarette
smoking
has
been
demonstrated
to
be
a
risk
factor
for
cervical
and
vulvar
carcinoma.
§ Nicotine,
cotinine,
hydrocarbons,
and
tars
are
found
in
cervical
secretions
of
smokers.
§ The
mutagenic
activity
of
these
products
in
cervical
cells,
similar
to
that
observed
in
lung
cells,
point
to
an
important
role
for
these
compounds
in
cervical
carcinogenesis.
International
Collaboration
of
Epidemiological
Studies
of
Cervical
Cancer.
Carcinoma
of
the
cervix
and
tobacco
smoking
:collaborative
reanalysis
of
individual
data
on
13
541
women
with
carcinoma
of
the
cervix
and
23
017
women
without
carcinoma
of
the
cervix
from
23
epidemiological
studies.
Int
J
Cancer
2006
30. Infection
by
Other
Microbial
Agents.
§ Disruption
of
epithelial
integrity
and
reparative
metaplasia
associated
with
acute
cervicitis
caused
by
Chlamydia
trachomatis,
NG,
HSV,
or
Trichomonas
vaginalis
may
increase
susceptibility
to
genital
HPV
infection.
§
Chlamydial
infection
in
HPV-‐positive
women
is
also
associated
with
development
of
high-‐grade
CIN
and
invasive
cancer
suggesting
a
possible
cofactor
role
.
Samoff
E,
et
al.
Association
of
Chlamydia
trachomatis
with
persistence
of
high-‐risk
human
papillomavirus
in
a
cohort
of
femal
eadolescents.
Am
J
Epidemiol2005:668–675
31. Sex
hormonal
influences
§ Condylomata
acuminata
increase
rapidly
in
size
and
number
in
pregnancy.
§ Epidemiologic
studies
have
shown
an
increased
risk
of
CIN
in
long-‐term
oral
contraceptive
pill
(OCP)
users.
§ Prospective
follow-‐up
of
high-‐risk
HPV-‐positive
women
does
not
demonstrate
an
increased
risk
of
CIN
3
among
OCP
users
.
§ There
has
been
no
demonstrable
clinical
value
to
ceasing
oral
contraceptives
in
the
management
of
HPV-‐associated
disease.
Castle
PE
et
al
Hormonal
contraceptive
use,
pregnancy
and
parity,
and
the
risk
of
cervical
intraepithelial
neoplasia
3
among
oncogenic
HPVDNA-‐positive
women
with
equivocal
or
mildly
abnormal
cytology.
Int
J
of
Cancer
2005;117:1007–1012.
32. Exogenous
and
endogenous
immunosuppression.
§ Renal
transplant
patients
have
16
times
higher
chance
of
developing
CIN
compared
to
general
population.
§ The
risk
of
CIN
and
Cx
Cancer
is
increased
in
HIV
positive
women
.
§ Hodgkin s
disease
,
leukemia
and
collagen
vascular
diseases
are
associated
with
an
increased
incidence
and
recalcitrancy
of
HPV
associated
disease.
33. Dietary
factors
§ Deficiencies
of
vitamin
A
or
beta
carotene
may
increase
the
risk
of
CIN
and
cervical
cancer
.
§ >
50
%
reduction
in
persistence
of
high
risk
HPV
DNA
has
been
shown
in
patients
with
higher
levels
of
Vit
A
byproducts
within
their
system
.
34. Summary
§ There
are
over
40
common
genital
HPV
types
that
are
primarily
sexually
transmitted.
§ The
vast
number
of
women
will
be
infected
with
one
or
more
HPV
types
in
their
sexual
lifetime.
§ Persistent
infection
with
HPV
types
can
cause
abnormal
cytology
(Pap
tests)
including
diagnoses
of
ASC,
AGC,
LSIL,
and
HSIL,
as
well
as
abnormal
histology
identified
following
biopsy
diagnosis
as
CIN
1
to
3,
AIS,
and
cancer.
35. § Only
a
small
subset
of
women
infected
with
high-‐risk
carcinogenic
HPV
will
develop
invasive
cervical
cancer.
§ Although
carcinogenic
HPV
is
a
necessary
cause
of
invasive
cervical
cancer,
a
number
of
cofactors
have
been
associated
with
HPV
persistence
and
HPV-‐related
disease
progression
including:
(1)
viral
factors
such
as
genotype
(eg,
HPV
16)
(2)
tobacco
and
long-‐term
oral
contraceptive
use
(3)
genetic
and
immunologic
host
factors
including
innate
immunity.