Chronic Lymphocytic Leukemia Case Study

1221 Words 5 Pages
1. The three treatment options function synergistically to benefit the patient with prostate cancer. The ionizing radiation causes single and double stranded breaks to the neoplastic cells DNA, this halts replication and cell function until it can be repaired. Etoposide is a podophyllotoxin that inhibits topoisomerase II, the enzyme responsible for unwinding the DNA. If the DNA cannot unwind, the cell will be unable to replicate, transcribe mRNA, or repair itself. If the cell is unable to repair it will undergo apoptosis. The final treatment is flutamide, an anti-androgen, which inhibits the androgen receptor. The tumor is androgen positive which means testosterone stimulates the neoplasia to grow. Flutamide blocks the androgen receptors and …show more content…
The three treatments for the patient with chronic lymphocytic leukemia work synergistically to provide the maximum effect for treating the cancer. The first treatment with cyclophoaphamide damages the neoplastic cell’s DNA by forming intra-strand and inter-strand cross-links. These cross-bridges halt replication of the cells until the damage can be repaired. The second treatment, cytarabine, inhibits the enzyme DNA polymerase. This inhibition prevents the cell from converting monomers into DNA polymers, a crucial step in DNA repair. When the tumor cells discover the effects of cyclophoaphamide, they will attempt to repair the damage with variety of enzymes including DNA polymerase, which is now non-functional due to the cytarabine. Lastly, the third treatment takes advantage of the being B-cell antigen positive. Rituximab is an antibody against the B-cell antigen present on the tumor; when the antibody binds to the antigen it blocks it. The antigen then becomes non-functional; this could help limit the spread (metastasizing) of the cancer while the other two drugs work to kill the neoplastic …show more content…
For 10 years the patient was in stage 1 of diabetes mellitus and was treated with only an AMPK agonist, which simulated exercises effects and independently brought glucose into cells without insulin’s effects. Stage 1 is where the patient has insulin resistance/tolerance, but still functional beta cells, which produce increasing amounts of insulin to overcome tolerance. The patient has now moved to stage 2 of type II diabetes, which means she still has insulin resistance but now has beta cell dysfunction from being overworked. For this patient I would look to the second-degree treatment options of a sulfonylurea and GLP-1 receptor agonist. The sulfonylurea is an inhibitor of potassium channels in the beta cells, which mimics the rise in ATP and depolarizes the cell allowing calcium influx and then insulin release. This medication will help to bring function back to the dysfunctional beta cells of the pancreas and produce more insulin. The GLP-1 agonist mimics the effects of the distal hormone glucagon-like peptide 1, which is released by the body in response to sugar absorption. This protein targets distal effectors throughout the body to increase insulin biosynthesis and beta cell proliferation in the pancreas and increase insulin sensitivity in the liver. The GLP-1 agonist will produce these same effects without the ingestion of carbohydrates, and help to increase insulin production and insulin

Related Documents