Summary

This document provides an overview of liver cancer, including risk factors, clinical manifestations, and diagnostic findings. It details the causes, symptoms, and potential complications of the disease. The document also touches upon preventive measures and available treatment options.

Full Transcript

🎄 Thursday Liver Cancer Primary liver cancer is uncommon in the U.S. but more frequent in areas like Asia and Africa. The most common type is hepatocellular carcinoma (HCC), responsible for 75% of all liver cancers globally. He...

🎄 Thursday Liver Cancer Primary liver cancer is uncommon in the U.S. but more frequent in areas like Asia and Africa. The most common type is hepatocellular carcinoma (HCC), responsible for 75% of all liver cancers globally. Hepatocellular Carcinoma (HCC) typically occurs in individuals with chronic liver disease, especially cirrhosis, and is often associated with hepatitis B or C infections or long-term alcohol abuse Results from long-term damage → chronic inflammation leads to cell death, repair, and regeneration cycles → increasing the risk of DNA mutations. The liver is a common site for cancer that originates from other organs (colon, breast, or lung). These cancers spread to the liver via the portal venous system or the lymphatic system Thursday 1 Risk Factors Chronic liver disease (especially cirrhosis). Chronic Hepatitis B and C infections. Exposure to chemical toxins (vinyl chloride, arsenic). polyvinyl chloride (PVC) a type of plastic used in a wide range of products, including pipes, wire coatings, and packaging materials When vinyl chloride is inhaled or absorbed through the skin, it is metabolized in the liver into reactive intermediates that can damage DNA in liver cells (hepatocytes). These DNA mutations can lead to uncontrolled cell growth Arsenic naturally occurring element that is found in water, soil, and air. It can exist in both organic and inorganic forms, but inorganic arsenic (found in contaminated drinking water, pesticides, and industrial processes) is more toxic Long-term exposure to arsenic, particularly through contaminated drinking water or occupational exposure (e.g., mining, smelting) is associated with cancer Arsenic causes oxidative stress and DNA damage in cells, including liver cells. It interferes with DNA repair mechanisms, leading to mutations and the initiation of cancer. Arsenic is also thought to act as a tumor promoter, meaning it promotes the growth of cancer cells that have already developed due to other risk factors. Thursday 2 Aflatoxin contamination in food (common in tropical regions) (a toxin produced by molds found in poorly stored grains and nuts, is a potent carcinogen that increases the risk of HCC) Cigarette smoking combined with alcohol use. Clinical Manifestations Early Symptoms: Pain: Continuous, dull pain in the right upper quadrant of the abdomen, epigastrium, or back. Weight loss, weakness, anorexia, and anemia are common. Jaundice may develop if the tumor obstructs the bile ducts, leading to yellowing of the skin and eyes. Advanced Symptoms: Ascites (fluid accumulation in the abdomen) develops if portal veins are obstructed by tumor nodules. Liver damage caused by cancer impairs the liver's ability to produce albumin, a protein that maintains oncotic (colloid osmotic) pressure in the blood vessels. Low albumin levels reduce the oncotic pressure, allowing more fluid to leak out of blood vessels into the abdomen Liver enlargement: The liver may feel enlarged and irregular upon palpation. Metastasis to other organs like the lungs, bone, or brain causes additional symptoms. Thursday 3 Metastasis Liver metastasis is more common than primary liver cancer, with metastases frequently originating from the digestive system, breast, or lungs. Malignant tumors spread to the liver through the portal system or lymphatic channels or lymphatic system. Diagnostic Findings Laboratory Findings: Elevated serum levels of: Bilirubin, alkaline phosphatase, AST, GGT, and lactic dehydrogenase. Bilirubin byproduct of the breakdown of red blood cells → processed by the liver and will be eliminated in the body. In HCC, liver function is often impaired due to tumor growth, liver cirrhosis, or bile duct obstruction, therefore Bilirubin level is high. (liver cannot process and excrete bilirubin) ALP (alkaline phosphatase) is an enzyme found in the liver, bones, and bile ducts. Helps breakdown proteins It is often elevated in HCC due to obstruction of bile flow or infiltration of the liver by the tumor as the tumor grows, it will compress the bile duct → blockage of bile → liver produces ALP in bile duct cells (cholangiocytes) → bile flow is obstructed, ALP leaks into the bloodstream instead of being excreted through bile, causing elevated ALP levels. AST (Aspartate Aminotransferase) is an enzyme that is released into the bloodstream when liver cells are damaged. HCC leads to destruction or death of liver cells (hepatocytes). When these cells die, they release AST into the bloodstream, causing elevated levels. AST is often elevated alongside alanine aminotransferase (ALT). GGT (Gamma-Glutamyl Transferase) is involved in the metabolism and transport of bile and is released when the bile ducts are obstructed or when liver cells are damaged. LDH (Lactic Dehydrogenase) is an enzyme involved in cellular energy production. It is found in many tissues, including the liver → As liver Thursday 4 tissue is infiltrated or destroyed by HCC, LDH is released into the bloodstream → elevated LDH Alpha-fetoprotein (AFP) is elevated in about 30-40% of patients with HCC. AFP levels over 200 ng/mL are considered highly suspicious for HCC. Tumors in the liver often produce AFP Carcinoembryonic antigen (CEA): Elevated in advanced cancers. CEA is a tumor marker typically elevated in advanced cancers, including colon cancer, breast cancer, and sometimes HCC. Imaging: X-rays, liver scans, CT, MRI, PET, and ultrasound to evaluate the extent of the cancer. Biopsy: Confirms diagnosis, but there are risks of tumor seeding and complications (e.g., hemorrhage). Tumor seeding refers to the spread of cancer cells to surrounding tissues or along a needle track during a biopsy or surgical procedure. In the context of a liver biopsy, tumor seeding happens when cancer cells from a tumor are accidentally dislodged and deposited into adjacent areas as the biopsy needle is inserted and withdrawn. Medical Management Surgical Resection: Thursday 5 The treatment of choice if the tumor is confined to one lobe and liver function is sufficient for recovery. Lobectomy: Removal of a lobe of the liver is the most common surgical approach. Liver Transplantation: Liver transplantation may be an option for patients with small, localized HCC and cirrhosis. It involves the removal of a diseased liver and replacing it with a healthy donor liver from either a cadaver donor or a live donor (often using the right lobe). The procedure aims to restore liver function and improve patient survival. Milan criteria - to limit transplantation to patients who are most likely to have better outcomes the patient must have a single tumor measuring less than 5 cm three or fewer lesions with none over 3 cm in size Orthotopic Liver Transplantation (OLT) involves the replacement of the liver in its natural location. The procedure includes reconstruction of the hepatic vasculature and bile ducts to restore normal blood flow and bile drainage. Living donor liver transplantation (LDLT) involves using a portion of the donor’s liver (usually the right lobe) to transplant into the recipient. Immunosuppressive Therapy: Post-transplant, the success of the transplant depends heavily on immunosuppressive therapy to prevent graft rejection. Immunosuppressant drugs include cyclosporine (Neoral), tacrolimus (Prograf), corticosteroids, mycophenolate mofetil (CellCept), sirolimus Thursday 6 (Rapamune). Immunosuppressive therapy aims to block the immune response to the transplanted liver, but must be balanced to minimize toxicity and avoid over-suppression of the immune system, which can lead to infections and complications. "Triple therapy" typically includes a corticosteroid, a calcineurin inhibitor (e.g., tacrolimus or cyclosporine), and an antiproliferative agent or a TOR inhibitor. Corticosteriod - to reduce inflammation and prevent the body’s immune system from attacking the newly transplanted liver Calcineurin Inhibitor (tacrolimus) - inhibiting the enzyme calcineurin, which is essential for the activation of T-cells (a type of immune cell). This reduces the immune system's ability to recognize the transplanted liver as foreign and attack it. Antiproliferative agent (mycophenolate mofetil) - further suppress the immune response and provide additional protection against rejection without needing to excessively increase the dose of calcineurin inhibitors Some centers also use induction therapy, involving perioperative immunosuppressive drugs to reduce acute rejection risks. Patient Selection and MELD Score: Patients with irreversible liver diseases are candidates for liver transplantation. Candidates undergo evaluation, including assessment using the Model for End-Stage Liver Disease (MELD) score, which incorporates bilirubin, INR, creatinine, and the cause of liver disease to prioritize patients for transplantation. MELD scores are used to allocate organs to the most severely ill patients. MELD score=3.78×ln⁡(bilirubin)+11.2×ln⁡(INR)+9.57×ln⁡(creatinine)+6.43 MELD Score Range and Interpretation: < 9: Lower severity of liver disease. 10-19: Moderate liver disease, lower risk of death. 20-29: Severe liver disease with a higher risk of death. Thursday 7 30-39: Very severe liver disease. ≥ 40: Extremely high risk of death within 3 months without a transplant. Complications of Liver Transplantation: Bleeding: Common due to coagulopathy, portal hypertension, and surgical complications. Infection: A leading cause of death post-transplant due to the immunosuppressive therapy that lowers the body's ability to fight infections. Rejection: A major concern, as the body may recognize the new liver as foreign and attack it. Immunosuppressants are critical to prevent this. Biliary complications: Can include leakage, obstruction, or infection of the bile ducts after the procedure. Ethical Considerations: Organ allocation is a critical ethical issue, given the limited number of available livers. Decisions about allocation often balance distributive justice (fair distribution of organs) with individual patient needs. History of alcohol or drug abuse can complicate decisions, as there are debates about whether patients with substance abuse histories should be given priority over others. Living donor liver transplantation adds another ethical dimension, as the donor must undergo major surgery with inherent risks, and coercion must be avoided in the decision to donate. Nonsurgical Treatments: Radiation Therapy: Limited use due to liver tissue sensitivity, but techniques like transarterial chemoembolization (TACE) and radiofrequency ablation (RFA) target tumors more directly. delivering chemotherapy directly to the tumor while blocking the blood supply to it. This combined approach helps to limit the tumor's growth and increase the concentration of chemotherapy at the tumor site while minimizing the systemic effects on the rest of the body. Thursday 8 Chemotherapy: Often palliative. Sorafenib (Nexavar) is used in patients with stable hepatic function, and TACE is a promising treatment. Percutaneous Biliary Drainage used to relieve bile duct obstructions and restore the normal flow of bile from the liver to the small intestin A guidewire is passed through the needle into the bile duct. A small tube (catheter) is then inserted over the guidewire into the bile duct. This catheter can: Drain bile externally into a collection bag outside the body (external drainage). Redirect bile internally into the small intestine by passing the blockage (internal drainage). Both (internal-external drainage) depending on the patient's condition. Hepatitis Thursday 9 Hepatitis refers to inflammation of the liver, a vital organ responsible for essential processes like detoxification, protein synthesis, and bile production for digestion. Causes: Viral infections: Hepatitis viruses (HAV, HBV, HCV, HDV, HEV) Bacterial infections: Rarely, bacteria can infect the liver Bacteria from the intestines travel to the liver via the bile ducts → Bacteria circulating in the blood can seed in the liver, causing abscesses → bacterial toxins and the body’s immune response to infection cause liver cell damage and inflammation. Medications and hepatotoxins: Overuse or side effects of medications (acetaminophen) or toxins like alcohol can damage liver cells. liver metabolizes acetaminophen into safe compounds, but excessive doses overwhelm this process → Toxic byproducts (NAPQI)(N-acetyl-p- benzoquinone imine) build up and directly damage liver cells, leading to acute liver failure if untreated Chronic alcohol consumption leads to the accumulation of fat in liver cells (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis) → Alcohol produces toxic metabolites (acetaldehyde), which damage cell structures and promote immune-mediated injury. Goals of treatment: Resting the inflamed liver - Minimizing the liver's metabolic demands allows healing. Increasing blood supply - Adequate blood flow ensures oxygen and nutrient delivery for regeneration. Thursday 10 Cellular regeneration - Treatment aims to restore the liver's normal structure and function. Preventing complications - Proper care prevents progression to chronic hepatitis, liver failure, or cirrhosis. Curability of Hepatitis Hepatitis A and C: Both can be completely cured Hepatitis A - Resolves on its own without specific treatment. Hepatitis C - Curable with direct-acting antiviral (DAA) medications. Hepatitis B - May resolve on its own but has a higher likelihood of chronic liver dysfunction, requiring monitoring or treatment. Hepatitis A Hepatitis A is a viral liver infection caused by the Hepatitis A Virus (HAV). Previously known as infectious hepatitis, it is highly contagious and typically transmitted through ingestion of contaminated food or water. Individuals at Increased Risk!! Crowded Conditions Examples include daycares, nursing homes, or shelters where close contact increases the risk of transmission. Exposure to Poor Sanitation Living in areas with inadequate sewage treatment or improper waste management increases susceptibility. Transmission Fecal-oral route - The most common mode of transmission, where fecal matter containing the virus contaminates food, water, or surfaces. Person-to-person contact - Close contact with an infected person, such as through shared utensils or improper hygiene. Parenteral transmission - Rare, but can occur through blood exposure, though hepatitis A is not typically bloodborne. Contaminated food and water: Thursday 11 Uncooked shellfish, fruits, and vegetables from contaminated sources are common culprits Poorly washed utensils can also harbor the virus. Incubation and Infectious Period Incubation Period: 15 to 50 days after exposure. Infectious Period: Starts 2–3 weeks before symptoms appear and lasts until 1 week after jaundice develops. Testing for Hepatitis A Anti-HAV Antibodies - Presence confirms hepatitis A infection Immunoglobulin M (IgM) - Indicates active or recent infection and inflammation; remains elevated for 4–6 weeks. Immunoglobulin G (IgG) - Signifies previous exposure or immunity Stages of Hepatitis A Preicteric Stage: The virus invades the liver and begins replicating within hepatocytes (liver cells) → triggers the immune system to respond, causing inflammation and mild liver dysfunction Begins about 2 weeks post-exposure, before jaundice Symptoms include Flu-like signs - Malaise, fatigue, headache, muscle pain. Gastrointestinal disturbances - Anorexia, nausea, vomiting, diarrhea. Lab findings - Elevated serum bilirubin and liver enzymes. Highly transmissible during this stage - individual may shed HAV in feces without realizing they are infected Icteric Stage: The immune response escalates, destroying infected hepatocytes, which leads to the release of bilirubin (a breakdown product of red blood cells) into the bloodstream → Liver inflammation reduces its ability to process and excrete bilirubin, causing it to accumulate in the body Thursday 12 Starts 1–2 weeks after the preicteric stage. Symptoms include Jaundice - Yellowing of the skin and eyes occurs because bilirubin builds up in tissues. Dark urine (tea-colored) and clay-colored stools Persistent fatigue and abdominal pain. Pruritus (itching) may develop due to bilirubin deposition in the skin. Posticteric Stage: immune system clears the infection, and liver cells begin regenerating. Occurs 6–8 weeks after exposure during recovery. Symptoms improve as: Jaundice resolves. Stool and urine return to normal color. Energy levels and liver enzyme values normalize. Complication Fulminant Hepatitis is a rare but life-threatening complication of Hepatitis A (and other types of viral hepatitis). It involves severe, acute liver failure that can progress rapidly, often within days or weeks of symptom onset Massive hepatocyte (liver cell) destruction. Marked impairment of liver function, including: Loss of detoxification. Failure to produce clotting factors. Imbalance in fluid and electrolytes. Jaundice: Yellowing of the skin and eyes due to bilirubin buildup. Encephalopathy: Confusion, lethargy, or even coma due to ammonia buildup in the brain. Bleeding: Easy bruising or bleeding due to reduced clotting factors. Ascites: Accumulation of fluid in the abdomen. Edema: Swelling in the limbs. Hepatorenal syndrome: Kidney failure secondary to liver failure. Thursday 13 Treatment: Liver Transplant Prevention of encephalopathy (lactulose for ammonia control). Prevention Strict handwashing Avoid contaminated food Cook shellfish thoroughly before eating. Wash raw produce with clean water. Avoid street food or any food prepared under unsanitary conditions. Stool and needle precaution Treatment of Municipal Water Supplies Serological Screening of Food Handlers Hepatitis A Vaccine Two doses are administered 6 months apart for long-lasting protection. Who Should Get Vaccinated: Children aged 1 year or older. Adults in high-risk groups (e.g., travelers, individuals with chronic liver disease, food handlers). Effectiveness: Provides immunity in more than 95% of recipients after the first dose. Immune Globulin (Post-Exposure Prophylaxis) For those exposed to HAV and not vaccinated, immune globulin can prevent infection. Provides passive immunity by introducing pre-formed antibodies against HAV. Must be administered within 2 weeks of exposure for effectiveness. Immune Globulin and Vaccine for Close Contacts Household members and sexual partners of infected individuals are at high risk of transmission. Thursday 14 Combination Approach - Immune globulin offers immediate protection, while the vaccine ensures long-term immunity. Preexposure Prophylaxis for Travelers Travelers to areas with poor sanitation are at high risk of encountering HAV- contaminated food or water. Preexposure immune globulin or vaccination should be given before travel to endemic regions. Management Hepatitis A is self-limiting, so treatment focuses on supportive care to relieve symptoms and aid recovery Acetaminophen (Paracetamol) - Use cautiously to avoid further liver damage. Avoid NSAIDs - These can exacerbate liver injury in severe cases. Ondansetron - To manage nausea and vomiting. Immune Globulin Administer to individuals exposed to HAV within the last 2 weeks who are unvaccinated. Provides passive immunity and reduces disease severity Vitamin Supplements: Vitamin K: If clotting factors are reduced due to liver dysfunction. B-complex and Vitamin C: To support general liver health and recovery. Dietary Recommendations High-Calorie, High-Carbohydrate Diet - To provide energy and prevent muscle breakdown. Small, Frequent Meals - Helps reduce nausea and improve tolerance to food. Avoid Alcohol and Hepatotoxins - Prevents further liver stress Hydration - Oral rehydration or IV fluids for severe vomiting or diarrhea. Look for abdominal swelling, confusion (indicative of encephalopathy), or severe jaundice. Implement contact precautions for patients with active symptoms, especially diarrhea. Thursday 15 Relieve itching caused by jaundice: Avoid hot showers or baths. Recommend loose, non-irritating clothing. Hepatitis B Hepatitis B is a nonseasonal viral infection caused by the Hepatitis B Virus (HBV) The virus targets liver cells (hepatocytes), causing inflammation that may lead to chronic liver disease or complications like cirrhosis or cancer. Risk Factors IV Drug Users - Sharing needles increases the risk of exposure to HBV-infected blood. Long-Term Hemodialysis Patients - Repeated blood access increases the risk of exposure to contaminated equipment. Health Care Personnel - Accidental needlestick injuries or exposure to body fluids place healthcare workers at risk. Transmission Hepatitis B spreads through contact with infected blood or body fluids Blood or body fluid contact Any exposure to infected blood or bodily fluids like semen, vaginal secretions, and sometimes saliva can spread HBV Infected blood products Before rigorous blood screening protocols, HBV was frequently spread through transfusions of infected blood or blood products. Infected saliva or semen - Transmitted during intimate contact. Though less common, saliva can carry HBV if contaminated with blood (e.g., from gum disease). Saliva alone is typically low-risk unless blood is present Sexual activity involving exposure to semen is a major adult transmission route. Contaminated needles - Includes shared drug paraphernalia or unsafe medical practices. Thursday 16 Sexual contact - Major route of adult transmission. Parenteral exposure Parenteral means transmission via routes other than the digestive system. needle-stick injuries in healthcare workers or procedures like tattoos and piercings using unsterilized equipment Perinatal period From infected mother to baby during childbirth. Hemodialysis - Contaminated dialysis equipment or improper protocols. Sharing personal items - Razors and toothbrushes may harbor infectious blood. Incubation Period The incubation period for HBV is 60 to 180 days, during which the virus replicates before symptoms appear. Testing HBV Antigen-Antibody Systems: used to detect HBV markers, which help in diagnosing infection, determining infectivity, and assessing immunity Hepatitis B Surface Antigen (HBsAg): Confirms active infection (acute or chronic). Indicates that the individual is infectious. Presence indicates active infectious state. Chronic Hepatitis or Carrier State: If HBsAg persists for more than 6 months, it signifies chronic HBV infection or a carrier state. Hepatitis B Early Antigen (HBeAg): Confirms high viral replication and high infectivity. Disappearance typically indicates reduced infectivity. Antibodies to HBsAg (Anti-HBs): Indicates recovery from HBV infection. Confirms immunity, either from natural infection or vaccination. Thursday 17 Marker Result Interpretation HBsAg P Active infection HBeAg P High infectivity Anti-HBs P Immunity (recovery or vaccination HBsAg >6 months P Chronic infection or carrier state Complications Fulminant Hepatitis Acute, severe liver failure resulting from massive hepatocyte (liver cell) necrosis. Chronic Liver Disease Long-term liver inflammation and damage due to persistent HBV infection. Cirrhosis Extensive scarring of the liver, causing irreversible damage and impaired liver function. Primary Hepatocellular Carcinoma A type of liver cancer associated with chronic HBV infection. Prevention Strict Handwashing Screening Blood Donors Testing Pregnant Individuals: Needle Precautions Avoiding Contact - Intimate or fluid contact should be avoided with HBsAg- positive individuals. Vaccination: Hepatitis B Vaccine - Administered in three doses, providing lifelong immunity in most individuals. Combination vaccines protect against both Hepatitis A and B. Hepatitis B Immune Globulin (HBIG): Post-exposure prophylaxis for: Sexual exposure. Thursday 18 Percutaneous exposure (needlestick injuries). Transmucosal exposure (splashes to mucous membranes). Management Acute Hepatitis B: Most cases resolve spontaneously; supportive care is essential. Focus on symptom relief and preventing liver damage. Chronic Hepatitis B: Antiviral therapy to suppress viral replication and prevent complications. Antiviral Medications: Tenofovir or Entecavir: First-line agents for chronic hepatitis B. Reduce viral load and prevent liver damage. Interferon Alpha Boosts the immune system to fight the virus but has significant side effects (flu-like symptoms, mood changes) Interferon can lead to bone marrow suppression, resulting in low white blood cell (leukopenia), platelet (thrombocytopenia), or red blood cell (anemia) counts. Regular blood work is essential to track these values. Immune Globulin: Provides passive immunity post-exposure. [Post-exposure prophylaxis in combination with the Hepatitis B vaccine for unvaccinated individuals exposed to HBV] Hepatoprotective Support: Vitamin supplements and avoidance of hepatotoxic substances (alcohol). High-Carbohydrate, Low-Fat Diet: Provides energy while reducing liver stress. Hydration: Prevents dehydration and supports metabolic functions. Thursday 19 Hepatitis C Hepatitis C Virus (HCV) infection is a viral liver disease that can occur year- round. It can affect any age group, though specific populations are at higher risk. HCV is a common cause of: Posttransfusion hepatitis (due to unscreened blood in earlier decades). Chronic liver conditions in IV drug users. Risk factors for HCV are similar to Hepatitis B (HBV), as it is primarily transmitted via parenteral exposure. Individuals at Increased Risk Parenteral Drug Users Sharing needles is a significant risk factor. Frequent Transfusion Recipients Particularly before routine blood screening for HCV began in the 1990s. Health Care Personnel At risk from needlestick injuries and exposure to infected blood. People Born Between 1945 and 1965 A cohort with a higher prevalence of undiagnosed HCV, possibly due to unscreened blood transfusions. Prisoners High prevalence due to shared needles or unsterile tattooing equipment. Transmission HCV is transmitted parenterally, primarily through blood contact: Sharing contaminated needles or syringes. Receiving unscreened blood or blood products. Exposure to infected blood through healthcare procedures or injuries. Sharing personal items contaminated with blood (razors). Rarely, through sexual contact or perinatal transmission. Incubation Period Thursday 20 The incubation period is 2 weeks to 6 months, during which the virus replicates silently before symptoms or detectable antibody responses appear. Testing for HCV Anti-HCV Antibody Detects chronic infection. May indicate past exposure or active infection. HCV RNA Testing Confirms active infection by measuring viral RNA levels. Liver Function Tests (ALT, AST): Elevated levels indicate liver inflammation or damage. Prevention Strict Handwashing: Reduces the risk of indirect contact with contaminated blood or surfaces. Needle Precautions: Avoid sharing needles; use sterile equipment in healthcare and personal settings. Screening Blood Donors: Routine HCV testing in blood donations has dramatically reduced transmission. Management Direct-Acting Antivirals (DAAs) Revolutionized HCV treatment with high cure rates (>95%) These are a newer generation of medications designed specifically to treat Hepatitis C by directly targeting the virus itself. HCV needs certain proteins to survive and multiply. DAAs block these proteins, stopping the virus from making copies of itself. Sofosbuvir + Ledipasvir: Effective for genotypes 1, 4, 5, 6. (Genotype 1 is the most common in the US, so this combination is often used there) Sofosbuvir + Velpatasvir: works for all genotypes Thursday 21 Glecaprevir + Pibrentasvir: Works well for most patients and sometimes as quickly as 8 weeks Treatment Duration: Typically 8–12 weeks, depending on liver condition and HCV genotype. Ribavirin (less commonly used): May be combined with DAAs for complex cases. Ribavirin is an older drug that helps fight the virus indirectly by boosting your immune system to attack the virus. Side effects: Anemia, fatigue. Hydration and Nutrition: Support liver health with a well-balanced, low-fat diet and adequate hydration. Avoidance of Alcohol and Drugs: Prevent further liver damage by eliminating hepatotoxins. Regular HCV RNA levels to assess treatment response. Liver biopsy or elastography (FibroScan) to evaluate fibrosis or cirrhosis Educate patients on: Avoiding sharing needles, razors, or toothbrushes. Practicing safe sex if blood exposure is possible. Proper disposal of contaminated sharps or materials. Implement contact precautions in healthcare settings when handling bodily fluids. 🥷 Check for SVR (sustained virologic response) 12 weeks after therapy completion to confirm cure. Hepatits D Hepatitis D Virus (HDV) is found predominantly in the Mediterranean, Middle East, and parts of South America and Africa Thursday 22 HDV is a satellite virus that requires the Hepatitis B Virus (HBV) for replication and infection (HDV only occurs in the presence of active HBV infection) Coinfection with HDV and HBV intensifies the severity of acute hepatitis symptoms and increases the risk of complications Transmission: Similar to HBV: Blood and body fluids (parenteral routes) Prevention: Preventing HBV with vaccination also prevents HDV, as HDV cannot replicate independently High-Risk Individuals Drug Users Sharing needles or drug paraphernalia increases the risk of HBV and HDV transmission. Hemodialysis Patients: Repeated blood exposure raises the risk of infection. Frequent Blood Transfusion Recipients: Particularly relevant in areas with inadequate screening for HBV/HDV. Transmission Same as HBV: Bloodborne: Sharing contaminated needles or equipment. Unsafe transfusions. Body Fluids: Sexual contact. Exposure through open wounds or mucous membranes. Perinatal (rare): From mother to child during childbirth. Incubation Period 2 to 26 weeks - Depending on the viral load and immune response. Thursday 23 Testing for HDV Hepatitis D Antigen (HDAg): Detected early in the infection. Anti-HDV Antibody: Detected in later stages, confirming ongoing or past HDV infection. Liver Function Tests: Elevated ALT, AST, and bilirubin levels indicate liver inflammation. Prevention HBV Vaccination Effective HBV vaccination prevents both HBV and HDV infections, as HDV cannot exist without HBV. Standard HBV Precautions Strict Handwashing: To minimize contamination risks. Needle Safety: Avoid sharing or reusing needles. Screening of Blood Donors: Routine blood testing reduces transmission risk. Safe Sexual Practices: Use of barriers like condoms to reduce exposure. Avoid High-Risk Behaviors Do not share personal items like razors or toothbrushes that may come into contact with blood. Management of Hepatitis D There is no specific antiviral treatment directly targeting HDV. The primary goal is to suppress HBV replication since HDV depends on HBV for its lifecycle. Interferon Alpha May reduce HDV replication. Prolonged therapy (12–18 months) is often required, with limited effectiveness. Side effects: Flu-like symptoms, fatigue, depression. Thursday 24 Hepatitis E Hepatitis E Virus (HEV) is a waterborne virus primarily transmitted through the fecal-oral route. It is prevalent in regions with poor sewage disposal or where communal bathing in contaminated water is common. The risk of infection is similar to Hepatitis A (HAV), as both are fecal-oral in transmission. HEV usually causes a mild, self-limiting illness, except in pregnant individuals, particularly during the third trimester, where it can lead to severe complications and a high mortality rate. Individuals at Increased Risk Travelers Those visiting countries with high HEV incidence, such as: India, Myanmar (Burma), Afghanistan, Algeria, and Mexico. Consumption of Contaminated Food or Water: Eating or drinking items contaminated with fecal matter containing HEV increases the risk. Transmission Similar to Hepatitis A (HAV): Fecal-Oral Route: Consumption of food or water contaminated with feces. Poor Sanitation: Common in areas with inadequate sewage disposal. Contaminated Rivers or Communal Bathing: Major source of transmission in endemic areas. Incubation Period The incubation period for HEV is 2 to 9 weeks, during which the virus replicates before symptoms appear. Testing IgM Anti-HEV Antibody: Thursday 25 Detects acute infection. IgG Anti-HEV Antibody: Indicates past exposure or immunity. Liver Function Tests (LFTs): Elevated ALT, AST, and bilirubin levels indicate liver inflammation. Complications High Mortality Rate in Pregnant Individuals: Can reach up to 20–25% in the third trimester due to fulminant hepatic failure. Fetal Demise: Severe maternal HEV infection may lead to miscarriage, stillbirth, or preterm delivery. Prevention Strict Handwashing Safe Drinking Water Proper Food Hygiene Avoid High-Risk Areas Treatment As with HAV, there is no specific antiviral therapy for HEV. Treatment focuses on relieving symptoms and supporting liver function. Rest: Encouraged to reduce the liver’s metabolic workload. Hydration: Oral or intravenous fluids to prevent dehydration, especially in cases of diarrhea or vomiting. Nutritional Support: Small, frequent meals rich in carbohydrates to maintain energy levels. Liver Function Tests: Regularly monitor ALT, AST, and bilirubin to assess liver inflammation. Signs of Complications: Close monitoring in pregnant individuals for signs of hepatic failure or worsening symptoms. Thursday 26 Advise patients to avoid alcohol, acetaminophen, or other drugs that may stress the liver. Thursday 27

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