Hepatitis C
Instructions
Mike is a 23-year-old white male admitted for severe depression. He has a history of bipolar disorder and is currently taking valproate (Depakote) 500 mg XR daily. His psychiatrist ordered LFT\’s to follow the valproate therapy. LFT\’s were abnormal: ALT 1178 u/L, AST 746 u/L. the patient was asymptomatic. He denies fever, abdominal pain, nausea, vomiting or jaundice.
He denies using other medication or alcohol but admits using illicit IV drugs starting about 8 weeks ago and continuing to present. He never had a blood transfusion. Aside from valproate (Depakote) he is presently taking clonazepam 1 mg prn and fluoxetine (Prozac) 40 mg qd.
Other blood work: Direct bili 1 mg/dL, alk phos 188 u/L, anti-HCV negative on hospital day 1, positive on day 3. HCV-RNA PCR positive. Hep A, B, and D markers negative.
Patient diagnosis: Acute Hepatitis C.
- What is the pathophysiology of Hepatitis C ?
- What impact would the medications have on his liver function?
Solution
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In the case study, the patient was diagnosed with hepatitis C, after a thorough examination. According to Basit et al. (2022), the hepatitis C virus (HCV) is a serious health problem affecting about 185 million people globally. The number of individuals taking anti HCV globally is expected to have increased, between 1990 and 2005, from 2.3% to 2.8% (Basit et al., 2022). Some of the effects of hepatitis C include portal hypertension, hepatic decompensation, cirrhosis, and encephalopathy among others. Hepatitis C virus is the most common blood-borne virus or pathogen and the number one cause of morbidity and mortality.
According to 1, The RNA of hepatitis C virus enters the liver cell (hepatocyte) through endocytosis mediated by at least 4 co-receptors molecules. After entering the cytoplasm, the RNA is uncoated and then translated to about 10 mature peptides, which are cleaved by host proteases, as well as, the virally encoded proteases called NS3-4a serine proteases (Basit et al., 2022).
The mature peptides proceed to settle on the endoplasmic reticulum to form a replication complex that consists of an important enzyme known as the NS5B RNA-dependent RNA polymerase. This particular enzyme is known to catalyze the positive RNA strand into its negative strand intermediate that in turn, serves as the template for the synthesis of a new positive stand (Basit et al., 2022). The new DNA strands make mature virions. The virions exit the cell through exocytosis.
The virus can be detected in plasma within days after exposure. Normally, viremia rises to the peak between the first 8 and 12 weeks of infection, after which, the level drops to undetectable levels. However, about 50% to 85% of it tends to persist (Basit et al., 2022). Persistent infections occur due to weak CD4+ and CD8+ T-cell responses that are likely to fail to control viral replication.
Hepatitis C virus does not appear to be cytopathic when chronic infection occurs. Several external factors such as HIV/HV, alcohol consumption, Genotype 3 infection, obesity, and insulin resistance are associated with increased fibrosis progression and cirrhosis (Basit et al., 2022). The severity of fibrosis is strongly related to a high risk of fibrosis progression and cirrhosis through facilitating genetic aberrations and promoting neoplastic clones.
In one way or the other, hepatitis C is related to liver damage. In the case study, medications taken by the patient might have contributed to liver damage. According to Andrade et al. (2019), drug-induced liver injury is a liver injury that results from various types of drugs or herbs. Over the years, it has been reported that intrinsic and idiosyncratic reactions are responsible for drug-induced liver damage.
Andrade et al. (2019) state that higher daily doses tend to cause serious hepatic problems such as liver failure and transportation and sometimes even death. Therefore, dosage plays a significant role in idiosyncratic liver injury. Several medications including NSAIDs, statins, antibiotics, and anti-seizure drugs, might contribute to liver damage Andrade et al. (2019). Long-term use of the medications may cause hepatocellular and/or cholestatic liver damage. Therefore, precautions should be taken when taking daily medication for a prolonged time.
References
Andrade, R. J., Chalasani, N., Björnsson, E. S., Suzuki, A., Kullak-Ublick, G. A., Watkins, P. B., & Aithal, G. P. (2019). Drug-induced liver injury. Nature Reviews Disease Primers, 5(1), 1-22. https://doi.org/10.12701/yujm.2019.00297
Basit, H., Tyagi, I., & Koirala, J. (2022). Continuing Education Activity, StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK430897/