Posted: March 30th, 2022

The pathophysiology and pharmacology of chronic hepatitis B and glaucoma

The pathophysiology and pharmacology of chronic hepatitis B and glaucoma:
Chronic hepatitis B and glaucoma are two conditions that can significantly impact patients’ quality of life if left untreated. This article will discuss the pathophysiology and treatment approaches for both chronic hepatitis B infection and glaucoma. Understanding the biological mechanisms underlying these diseases can help healthcare providers develop targeted treatment plans.
Pathophysiology of Chronic Hepatitis B
Hepatitis B is caused by the hepatitis B virus (HBV), which primarily infects liver cells (hepatocytes). The virus enters the body through contact with infected blood or bodily fluids and can cause both acute and chronic infections (World Health Organization, 2021).[1] In the majority of cases, acute HBV infection is cleared by the immune system within 6 months. However, in approximately 5-10% of infected individuals, the virus persists in the liver for more than 6 months, developing into chronic hepatitis B.[2]
The pathophysiology of chronic HBV infection involves an inadequate immune response that fails to fully clear the virus. HBV evades the immune system by integrating its genetic material into the host hepatocyte DNA. This allows the virus to persist even at low levels without being recognized as foreign. Over many years of chronic infection, the virus can cause significant liver damage through ongoing necroinflammation and fibrosis.[3] Repeated cycles of injury and healing lead to the formation of scar tissue, or cirrhosis. Cirrhosis greatly increases the risk of liver cancer and liver failure.
Chronic hepatitis B is also characterized by periods of viral replication and remission. During active replication phases, HBV DNA and hepatitis B e antigen (HBeAg) levels are elevated in the bloodstream. This correlates with higher liver enzyme levels and greater liver inflammation and damage. In remission phases, HBV DNA and HBeAg decrease or become undetectable as the immune system gains some control over the infection.[4] However, the virus still persists in the hepatocytes and can reactivate at any time.
Pharmacological Management of Chronic Hepatitis B
The goals of chronicocytes and can reactivate at any time.
Pharmacological Management of Chronic Hepatitis B
The goals of chronic hepatitis B treatment are to suppress HBV viral replication, prevent progression of liver disease, and reduce the risk of complications like cirrhosis and liver cancer. The current standard of care involves long-term use of oral complications like cirrhosis and liver cancer. The current standard of care involves long-term use of oral antiviral medications from one of two drug classes: nucleos(t)ide analogues (NAs) or pegylated interferon alfa.[5]
NAs work by inhibiting the reverse transcriptase enzyme needed for viral replication. Commonly prescribed NAs include tenofovir disoproxil fumarate (TDF), entecavir, and tenofovir alafenamide (TAF). TheseTDF), entecavir, and tenofovir alafenamide (TAF). These agents significantly reduce HBV DNA levels and can induce a sustained virologic response inTDF), entecavir, and tenofovir alafenamide (TAF). These agents significantly reduce HBV DNA levels and can induce a sustained virologic response inTDF), entecavir, and tenofovir alafenamide (TAF). These agents significantly reduce HBV DNA levels and can induce a sustained virologic response in many patients. However, lifelong therapy is usually required to maintain viral suppression, as resistance can develop if treatment isTDF), entecavir, and tenofovir alafenamide (TAF). These agents significantly reduce HBV DNA levels and can induce a sustained virologic response in many patients. However, lifelong therapy is usually required to maintain viral suppression, as resistance can develop if treatment is stopped too early.[6] Pegylated interferon alfa stimulates the immune system to fight HBVTDF), entecavir, and tenofovir alafenamide (TAF). These agents significantly reduce HBV DNA levels and can induce a sustained virologic response in many patients. However, lifelong therapy is usually required to maintain viral suppression, as resistance can develop if treatment is stopped too early.[6] Pegylated interferon alfa stimulates the immune system to fight HBV but requires weekly injections for 48 weeks and is associated with more side effects than oral NAs.[7] The of treatment depends on factors like viral load, disease stage, comorbidities, resistance profile, and tolerability. Close monitoring of treatment response and potential side effects is also important for optimal management.
Pathophysiologyability. Close monitoring of treatment response and potential side effects is also important for optimal management.
Pathophysiology of Glaucoma
Glaucoma refers to a group of eye conditions characterized by progressive damage to the optic nerve. The most common form is primary open-angle glaucoma (POAG), which develops due to increased resistance of fluid outflow from the eye.[8] This causes elevated intraocular pressure (IOP), which over time leads to mechanical compression and ischemia of the optic nerve fibers. Loss of these nerve fibers results in characteristic changes to the optic disc such as cupping. If untreated, glaucoma can cause permanent vision loss, starting with peripheral vision and potentially progressing to complete blindness.[9]
The exact pathophysiological mechanisms underlying increased outflow resistance and IOP elevation in POAG are still under investigation. Risk factors like older age, African or Latino descent, family history, and high eye pressure suggest both genetic and environmental components play a role.[10] Current theories point to abnormalities or decreased flow in the trabecular meshwork, which is the eye’s primary drainage structure. Dysfunction and blockage in this area impede normal fluid outflow and drainage from the eye.
Pharmacological Management of Glaucoma
The primary goal in glaucoma treatment is lowering and maintaining IOP levels to slow or halt further optic nerve damage. First-line options typically involve topical eye drop medications that work by one of three main mechanisms: prostaglandin analogs, beta blockers, or alpha agonists.[11] Prostaglandin analogs like latanoprost are often the most effective class for lowering IOP. They work by increasing outflow of aqueous humor through the uveoscleral pathway. Beta blockers like timolol function by decreasing aqueous humor production. Alpha agonists such as brimonidine reduce IOP by decreasing aqueous humor secretion and increasing outflow facility.
If target IOP goals are not achieved with topical medications alone, additional treatment modalities may be considered. These include oral carbonic anhydrase inhibitors, topical combination therapies, laser trabeculoplasty procedures to improve drainage, and incisional surgeries like trabeculectomy as a last resort.[12] Close lifelong monitoring by an ophthalmologist is important, as glaucoma is a chronic progressive disease requiring long-term IOP control strategies. Early detection and treatment can help prevent vision loss.
Conclusion
In summary, chronic hepatitis B and glaucoma are both conditions with significant health impacts that require ongoing clinical management. Understanding their distinct pathophysiological mechanisms and pharmacological treatment approaches can optimize patient care and outcomes. With proper diagnosis and multidisciplinary treatment adherence, the progression of liver disease from hepatitis B and vision loss from glaucoma may be delayed or prevented.
References
[1] World Health Organization. Hepatitis B. 2021. https://www.who.int/news-room/fact-sheets/detail/hepatitis-b. Accessed date: MM DD, YYYY.
[2] Lok AS, McMahon BJ. Chronic hepatitis B: update 2009. Hepatology. 2009;50(3):661-662. doi:10.1002/hep.23190
[3] Chen CJ, Yang HI, Iloeje UH. Hepatitis B virus DNA levels and outcomes in chronic hepatitis B. Hepatology. 2009;49(5 Suppl):S72-S77. doi:10.1002/hep.22884
[4] McMahon BJ. The influence of hepatitis B virus replication levels on disease progression. Hepatol Int. 2009;3(3):334-342. doi:10.1007/s12072-009-9139-3
[5] European Association for Study of Liver; Asociacion Latinoamericana para el Estudio del Higado. EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection. J Hepatol. 2017;67(2):370-398. doi:10.1016/j.jhep.2017.03.021
[6] Terrault NA, Bzowej NH, Chang KM, Hwang JP, Jonas MM, Murad MH. AASLD guidelines for treatment of chronic hepatitis B. Hepatology. 2016: 2024 – Do my homework – Help write my assignment online;63(1):261-283. doi:10.1002/hep.28156
[7] Lok AS, McMahon BJ. Chronic hepatitis B: update 2009. Hepatology. 2009;50(3):661-662. doi:10.1002/hep.23190
[8] Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014: 2024 – Essay Writing Service | Write My Essay For Me Without Delay;311(18):1901-1911. doi:10.1001/jama.2014: 2024 – Essay Writing Service | Write My Essay For Me Without Delay.3192
[9] Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2014: 2024 – Essay Writing Service | Write My Essay For Me Without Delay;121(11):2081-2090. doi:10.1016/j.ophtha.2014: 2024 – Essay Writing Service | Write My Essay For Me Without Delay.05.013
[10] Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363(9422):1711-1720. doi:10.1016/S0140-6736(04)16257-0
[11] Realini T. Medical management of glaucoma. Ophthalmol Clin North Am. 2005;18(1):43-50, vii. doi:10.1016/j.ohc.2004.09.005
[12] Realini T. Medical management of glaucoma. Ophthalmol Clin North Am. 2005;18(1):43-50, vii. doi:10.1016/j.ohc.2004.09.005

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(Pathophysiology and Pharmacology) CASE STUDY ASSIGNMENT #2 …

CASE STUDY ASSIGNMENT #2

Name:______________________________________ Date: _________________

Read the following case studies and answer the questions. Your responses should be in hand written (be neat and clear) or typed using separate pages.

(25 points for each case study X 3 = Total 75 points)

Case Study A

J.B., age 35 has had chronic hepatitis B for 9 years. The origin of his acute infection was never ascertained. (Chapter 17)

Ace my homework – Write my paper – Online assignment help tutors – Discussion Questions

Describe briefly the pathophysiology of acute hepatitis B infection.
Describe the signs of preicteric stage and icteric stage of acute hepatitis B infection.
What serum markers remain high when chronic hepatitis B is present.
Explain the circumstances under which J.B. could transmit the virus (including the various stages of the disease like preicteric, icteric and so on) as well as the mode of transmission
Explain how cirrhosis develops from chronic hepatis B.

Case Study B

Baby K., age 14 months, has vomiting and diarrhea and is crying continuously because of what appears to be severe abdominal pain. The suspected cause is gastroenteritis caused by Staphylococcus aureus from milk custard that had not been properly stored. (Chapter 17)

Ace my homework – Write my paper – Online assignment help tutors – Discussion Questions

Briefly describe how Staphylococcus aureus in the custard could cause vomiting and diarrhea.
Describe the fluid and electrolyte imbalances that can be expected in Baby K.
Describe the signs of dehydration that can be expected in a child.
Explain why water alone would not be adequate treatment for the child.

Case Study C

Mr. A., has been treated for chronic glaucoma for 6 years. He has lost her peripheral vision but does not feel seriously impaired. There is one incident in his history 2 years ago when he decided to discontinue his eye drops for a month because he was comfortable and there was no change in his vision. He developed some eye comfort and blurred vision. Examination confirmed elevated intraocular pressure (IOP) but little additional permanent damage. Since then an increased strength eye drop was ordered to control IOP. (Chapter 15)

Ace my homework – Write my paper – Online assignment help tutors – Discussion Questions

Describe the pathophysiologic change in chronic glaucoma.
Explain the reason for eye discomfort and blurred vision with increased IOP.
Why is there decreased peripheral vision?

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