Ion Channels and G Proteins
Discussion on Ion Channels and G Proteins
Discussion on Ion Channels and G Proteins
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Liver injury labs are as follows ammonia levels, INR, fibrinogen, glucose, and lactate. Other abs include Alanine transaminase (ALT): 0 to 55 units per liter (U/L) Aspartate transaminase (AST): 0 to 48 U/L. Alkaline phosphatase (ALP): 30 to 129 U/L. Gamma-glutamyltransferase (GGT): 8 to 61 U/L. Bilirubin: 0.1 to 1.2 milligrams per deciliter (mg/dL). Prothrombin time (PT): 10.9 to 12.5 seconds. Albumin: 3.5 to 5.0 grams per deciliter (g/dL). Total proteins: 6.3 to 7.9 g/dL. Once diagnosed liver injury the medications can be adjusted based on the lab results. Also discontinuing of any acetaminophen orders also any other nephrotoxic medications will also be recommended (2022). rising burden of liver disease is mainly a reflection of the three the most common causes: alcohol-related liver disease, non-alcoholic fatty liver disease and viral hepatitis, although autoimmune liver disease is also a significant contributor.4 The burden of liver disease in children differs from that in adults, as although non-alcoholic fatty liver disease (NAFLD) is seen in all ages, reflecting the rise in childhood obesity, disease associated with injecting drug use and alcohol are rarely encountered (Newsome et al., 2018). Acute hepatitis A virus (HAV) infection highly contagious. People who get hepatitis A may feel sick for a few weeks or several months but usually recover completely and do not have lasting liver damage. In rare cases, hepatitis A can cause liver failure and even death. This is more common in older people and in people with other serious health issues, such as chronic liver disease (2022).
Hepatitis A virus (HAV) is one of the well-known viruses that cause hepatitis all around the globe. Although this illness has decreased in developed countries due to extensive immunization, numerous developing and under-developed countries are struggling with this virus, HAV can be contained and prevented with vaccination. HAV can spread through oral fecal contact and through contaminated foods and water. Acute viral hepatitis is a systemic illness that mainly affects the liver. Hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis D virus (HDV), and hepatitis E virus (HEV) are the viruses that cause almost all instances of acute viral hepatitis, Hepatitis can be present with little or no symptoms, although it frequently results in jaundice, anorexia, and malaise. Hepatitis infection is divided into two types: acute and chronic. Acute hepatitis remains for less than six months, whereas chronic hepatitis stays for an extended period (Torre et al, 2021). In conclusion, vaccination is key to control the spreading of the virus not only for HAV but for all other hepatitis viruses. Immunization has to be considered an important step, and this system will enable the early detection of epidemiologic transitions and the implementation of preventative efforts before HAV infection becomes a public health issue.
References
Newsome, P. N., Cramb, R., Davison, S. M., Dillon, J. F., Foulerton, M., Godfrey, E. M., Hall, R., Harrower, U., Hudson, M., Langford, A., Mackie, A., Mitchell-Thain, R., Sennett, K., Sheron, N. C., Verne, J., Walmsley, M., & Yeoman, A. (2018, January). Guidelines on the management of abnormal liver blood tests. Gut. https://pmc.ncbi.nlm.nih.gov/articles/PMC5754852/
https://my.clevelandclinic.org/health/diagnostics/17662-liver-function-tests. Liver Function Tests. (2022, November 9).
Hepatitis A basics | hepatitis A | CDC. (2025a, January 31). https://www.cdc.gov/hepatitis-a/about/index.html
Gholizadeh, O., Akbarzadeh, S., Ghazanfari Hashemi, M., Gholami, M., Amini, P., Yekanipour, Z., Tabatabaie, R., Yasamineh, S., Hosseini, P., & Poortahmasebi, V. (2023). Hepatitis A: Viral Structure, Classification, Life Cycle, Clinical Symptoms, Diagnosis Error, and Vaccination. The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale, 2023, 4263309. https://doi.org/10.1155/2023/4263309
Torre P., Aglitti A., Masarone M., Persico M., (2021) Viral hepatitis: milestones, unresolved issues, and future goals. World Journal of Gastroenterology.;27(28):4603–4638. doi: 10.3748/wjg. v27.i28.4603
Liver injury labs are as follows ammonia levels, INR, fibrinogen, glucose, and lactate. Other abs include Alanine transaminase (ALT): 0 to 55 units per liter (U/L) Aspartate transaminase (AST): 0 to 48 U/L. Alkaline phosphatase (ALP): 30 to 129 U/L. Gamma-glutamyltransferase (GGT): 8 to 61 U/L. Bilirubin: 0.1 to 1.2 milligrams per deciliter (mg/dL). Prothrombin time (PT): 10.9 to 12.5 seconds. Albumin: 3.5 to 5.0 grams per deciliter (g/dL). Total proteins: 6.3 to 7.9 g/dL. Once diagnosed liver injury the medications can be adjusted based on the lab results. Also discontinuing of any acetaminophen orders also any other nephrotoxic medications will also be recommended (2022). rising burden of liver disease is mainly a reflection of the three the most common causes: alcohol-related liver disease, non-alcoholic fatty liver disease and viral hepatitis, although autoimmune liver disease is also a significant contributor.4 The burden of liver disease in children differs from that in adults, as although non-alcoholic fatty liver disease (NAFLD) is seen in all ages, reflecting the rise in childhood obesity, disease associated with injecting drug use and alcohol are rarely encountered (Newsome et al., 2018). Acute hepatitis A virus (HAV) infection highly contagious. People who get hepatitis A may feel sick for a few weeks or several months but usually recover completely and do not have lasting liver damage. In rare cases, hepatitis A can cause liver failure and even death. This is more common in older people and in people with other serious health issues, such as chronic liver disease (2022).
Hepatitis A virus (HAV) is one of the well-known viruses that cause hepatitis all around the globe. Although this illness has decreased in developed countries due to extensive immunization, numerous developing and under-developed countries are struggling with this virus, HAV can be contained and prevented with vaccination. HAV can spread through oral fecal contact and through contaminated foods and water. Acute viral hepatitis is a systemic illness that mainly affects the liver. Hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis D virus (HDV), and hepatitis E virus (HEV) are the viruses that cause almost all instances of acute viral hepatitis, Hepatitis can be present with little or no symptoms, although it frequently results in jaundice, anorexia, and malaise. Hepatitis infection is divided into two types: acute and chronic. Acute hepatitis remains for less than six months, whereas chronic hepatitis stays for an extended period (Torre et al, 2021). In conclusion, vaccination is key to control the spreading of the virus not only for HAV but for all other hepatitis viruses. Immunization has to be considered an important step, and this system will enable the early detection of epidemiologic transitions and the implementation of preventative efforts before HAV infection becomes a public health issue.
References
Newsome, P. N., Cramb, R., Davison, S. M., Dillon, J. F., Foulerton, M., Godfrey, E. M., Hall, R., Harrower, U., Hudson, M., Langford, A., Mackie, A., Mitchell-Thain, R., Sennett, K., Sheron, N. C., Verne, J., Walmsley, M., & Yeoman, A. (2018, January). Guidelines on the management of abnormal liver blood tests. Gut. https://pmc.ncbi.nlm.nih.gov/articles/PMC5754852/
https://my.clevelandclinic.org/health/diagnostics/17662-liver-function-tests. Liver Function Tests. (2022, November 9).
Hepatitis A basics | hepatitis A | CDC. (2025a, January 31). https://www.cdc.gov/hepatitis-a/about/index.html
Gholizadeh, O., Akbarzadeh, S., Ghazanfari Hashemi, M., Gholami, M., Amini, P., Yekanipour, Z., Tabatabaie, R., Yasamineh, S., Hosseini, P., & Poortahmasebi, V. (2023). Hepatitis A: Viral Structure, Classification, Life Cycle, Clinical Symptoms, Diagnosis Error, and Vaccination. The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale, 2023, 4263309. https://doi.org/10.1155/2023/4263309
Torre P., Aglitti A., Masarone M., Persico M., (2021) Viral hepatitis: milestones, unresolved issues, and future goals. World Journal of Gastroenterology.;27(28):4603–4638. doi: 10.3748/wjg. v27.i28.4603
Appropriate Blood Tests for Suspected Acute Liver Injury
The liver plays a crucial role in maintaining homeostasis, and when acute injury occurs, a thorough evaluation is necessary to determine the extent of damage and underlying cause. Blood tests are essential in assessing liver function, hepatocellular integrity, and potential viral infections. The primary tests ordered for suspected acute liver injury include liver function tests (LFTs), coagulation studies, and viral serologies. Liver function tests provide insight into hepatocyte integrity and bile excretion. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are key markers of hepatocellular damage, often rising significantly in acute injury. In cases of acute hepatitis A virus (HAV) infection, ALT levels can exceed 1000 U/L, with AST also elevated but typically lower than ALT. Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) assess biliary function, with ALP being mildly elevated in HAV cases. Additionally, total and direct bilirubin levels are crucial in evaluating bile processing and excretion, often presenting as hyperbilirubinemia in acute HAV, which correlates with jaundice. Albumin levels, while generally normal in acute liver injury, may decrease in severe hepatic dysfunction.
Coagulation studies, including prothrombin time (PT) and international normalized ratio (INR), assess the liver’s synthetic function. Since the liver produces clotting factors, significant hepatic impairment can prolong PT/INR, indicating a decline in liver function. In mild cases of HAV, coagulation parameters remain normal, but in severe cases, PT may be prolonged. To confirm HAV infection, viral serologies are essential. The presence of HAV IgM antibodies indicates a recent or active infection, differentiating it from past exposure or vaccination. HAV IgG antibodies, on the other hand, suggest immunity from prior infection or immunization. The hallmark laboratory findings in acute HAV include markedly elevated ALT and AST, mild increases in ALP, hyperbilirubinemia, and a positive HAV IgM test, confirming acute infection.
References
Jameson, J. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., & Loscalzo, J. (2022). Harrison’s Principles of Internal Medicine (21st ed.). McGraw-Hill Education.
Lee, W. M. (2020). Acute liver failure. The New England Journal of Medicine, 382(22), 2137-2145. https://doi.org/10.1056/NEJMra1917038
Schuppan, D., & Afdhal, N. H. (2021). Liver cirrhosis. The Lancet, 398(10308), 1359-1371. https://doi.org/10.1016/S0140-6736(21)01374-X
Recent milestones in the understanding of gastric acid secretion and treatment of acid-peptic disorders include the discovery of histamine H2-receptors and development of histamine H2-receptor antagonists, identification of H+K+-ATPase as the parietal cell proton pump and development of proton pump inhibitors, and identification of Helicobacter pylori as the major cause of duodenal ulcer and development of effective eradication regimens (Schubert et al. 2008). The stimuli for acid secretions are as follows, Acetylcholine, Gastrin and Histamine. When this acid secretion combines food can digest but also it can create different issues, for example, it can facilitate digestion of protein as well as the absorption of iron, calcium, and vitamin B12. When we take medication is these secretions are necessary for absorption of certain drugs however taking too much medicine or eating the wrong foods can lead to acid-related clinical conditions. Parietal cells secrete hydrochloric acid at a concentration of approximately 160 mmol/L or pH 0.8. Acid is thought to gain access to the lumen via channels in the mucus layer created by the relatively high intraglandular hydrostatic pressures generated during secretion, approximately 17 mm Hg (Johnsson et al, 2001). The acids facilitate the ingestion of protein and absorption of iron, calcium, and vitamin B-12 as well as prevent bacterial overgrowth and enteric infection. However, if the acid levels and pepsin increase a risk of ulcers can occur. The principal of acid secretion is histamine released from ECL cells (paracrine); gastrin, released from G cells (hormonal); and ACh, released from postganglionic enteric neurons (neurocrine) (Schubert et al. 2008).
Helicobacter pylori (H. pylori) attack the lining that protects your stomach. Many people have it and won’t have any issues with ulcers until the time is right for one to start causing issues. As the host starts showing symptoms of an ulcer, the H pylori make an enzyme called urease that makes the acid in the stomach less acidic while weakening the stomach lining, furthermore the host is at a greater risk of being hurt by acid and pepsin, strong digestive fluids. That can lead to sores or ulcers in your stomach or duodenum (2024). Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world’s population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma (Kusters et al., 2006). In conclusion H pylori is a bacteria that is found in all of us how it develops is how it is going to affect us, by taking simple precautions such as eating food that is cleaned thoroughly and cooked in a safe way and by drinking clean and potable water from a sanitary source that will not have bacteria. Lastly, good hand hygiene is the best way to effectively protect ourselves from these bacteria.
References
Schubert, Mitchell L. et al (2008). Control of Gastric Acid Secretion in Health and Disease
Gastroenterology, Volume 134, Issue 7, 1842 – 1860
Johansson, M. ∙ Synnerstad, I. ∙ Holm, L. (2001). Acid transport through channels in the mucous layer of rat stomach Gastroenterology; 119:1297-1304
Helicobacter pylori. Johns Hopkins Medicine. (2024, May 13). https://www.hopkinsmedicine.org/health/conditions-and-diseases/helicobacter-pylori
Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J. (2006, July). Pathogenesis of helicobacter pylori infection. Clinical microbiology reviews. https://pmc.ncbi.nlm.nih.gov/articles/PMC1539101/
Gastric Acid Secretion and Its Regulation
Gastric acid secretion is regulated by a complex interplay of neural, hormonal, and paracrine pathways. The primary stimuli include acetylcholine (ACh), gastrin, and histamine. Acetylcholine, released by the vagus nerve, directly stimulates parietal cells to secrete hydrochloric acid (HCl). Gastrin, produced by G cells in the antrum of the stomach, binds to CCK2 receptors on parietal cells and enterochromaffin-like (ECL) cells, prompting histamine release. Histamine, secreted by ECL cells, activates H2 receptors on parietal cells, enhancing acid production via the cyclic AMP pathway (Niv & Dickman, 2020). While gastric acidity is crucial for digestion and microbial defense, excessive acidity poses significant risks. Strong acidity can lead to mucosal injury, increasing the likelihood of gastritis, peptic ulcer disease (PUD), and gastroesophageal reflux disease (GERD). Chronic acid exposure can also contribute to Barrett’s esophagus, a precancerous condition. Furthermore, excessive acid can impair pancreatic enzyme function and nutrient absorption, exacerbating deficiencies in iron, calcium, and vitamin B12 (Feldman et al., 2022).
Pathophysiology of Helicobacter pylori
Helicobacter pylori (H. pylori) is a Gram-negative, spiral-shaped bacterium that colonizes the gastric mucosa, primarily in the antral region. It produces urease, an enzyme that hydrolyzes urea into ammonia and carbon dioxide, creating a local buffering environment that allows the bacteria to survive in the highly acidic stomach. Additionally, H. pylori adheres to gastric epithelial cells and induces an inflammatory response by releasing virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), leading to mucosal damage (Malfertheiner et al., 2021). The persistent inflammation can disrupt normal gastric physiology, increasing acid secretion in duodenal ulcers or leading to gastric atrophy and hypochlorhydria in chronic gastritis, increasing the risk for gastric cancer.
References
Feldman, M., Friedman, L. S., & Brandt, L. J. (2022). Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. Elsevier.
Malfertheiner, P., Megraud, F., Rokkas, T., Gisbert, J. P., Liou, J. M., Schulz, C., & Wauters, T. (2021). Management of Helicobacter pylori infection: The Maastricht VI/Florence consensus report. Gut, 70(12), 2114-2132.
Niv, Y., & Dickman, R. (2020). Gastric acid secretion and its clinical implications: The role of histamine and gastrin. World Journal of Gastroenterology, 26(45), 7287-7301.
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