AIDS

The human deficiency virus is the primary cause of AIDS, also known as acquired immune deficiency virus syndrome. It destroys the CMI by spontaneously canceling out or destroying the CD4+T helper cells. When a patient's immunity is compromised, he or she is more vulnerable to infections and some types of cancer. A healthy person does not experience this since the organisms responsible do not produce the infection.

AIDS is an advanced HIV disease. There is currently no known cure for it, and it is usually considered fatal. Nonetheless, it is commonly included in the formulation of anti-HIV drugs, which are administered on a long-term basis from time to time. The average period usually revolves around 6 months, 12 or 15 years. (Pathophysiology, 2014)

The infection of HIV, in all cases, goes through stages and steps before it eventually turns to what is termed as AIDS. The stages above include;

1. Seroconversion illness. The stage takes place between 1to 6 weeks after the virus invention. Its symptoms are similar to that of flu.

2. Asymptomatic infection. After a process known as seroconversion, the virus count levels are usually very low. The replication process is also lowered. The most dangerous thing about this stage is that there are no symptoms and an individual can live for years (Bruyere, n.d.).

3. The swelling up of the lymph nodes for more than three months, a stage referred to as Persistent generalized lymphadenopathy (Pathophysiology, 2014).

4. Symptomatic infection. This is a stage with a lot of symptoms. The symptoms are collectively known as AIDS-related complex and this is where infections take advantage.

5. Lastly, the AIDS stage. This stage is marked by severe immunodeficiency but there are still signs of life. The CD4T cell count is tremendously low, accompanied threatening infections and tumors (Pathophysiology, 2014).

A unique tiny group of human beings exists. They are considered unique because they develop AIDS at an increasingly low rate or in some rare cases never at all. They are referred to us as non progressors (Bruyere, n.d.).

Pharmacology of AIDS.

HIV Reverse Transcriptase Inhibitors. They are categorized into two, mainly nucleoside and non-nucleoside. Non-nucleoside RTIs function to inhibit HIV reverse transcriptase. They are able to do this because they produce conformational changes in the enzyme (Bruyere, n.d.) Nucleoside RTIs function by inhibiting the replication of the RNA enzyme.

Protease inhibitors. Just as the name suggests, they function by inhibiting proteases. One disadvantage of them is that they do not inhibit or affect viral activity in the cells that acts as hosts. Entry inhibitors (Bruyere, n.d. . They are into two groups, namely enfuvirtide and maraviroc. They function by preventing HIV penetration in the cells.

Intergrase inhibitors. The HIV once it enters the body tries to incorporate itself in the DNA of the host. The intergrase help by not allowing DNA strand transfer (Pathophysiology, 2014).

Lab values.

ACD4 count is usually done. They are the white blood cells that are responsible for fighting off various infections in the body (Bruyere, n.d.). A normal healthy human being has a CD4 count range of between 500 -1500; however this can drop to below 200 due to HIV at an advanced state.

Malignant Melanoma.

The process in which melanocytes become melanoma is known as melanoma genesis. (Bruyere, n.d.). It composes of genetic mutations, which causes alteration of cell proliferation and differentiation and susceptibility to UV light.

In some studies, show that multiple ways of melanoma pathogenesis in skin which is sun protected, form association with nevus of high count, together with ultraviolet radiation.

The frequency difference of BRAF mutations can also be traced to different patterns of the sun exposure. BRAF mutations tend to be more prevalent in intermittently UV exposed skin. KIT mutations characterized by chronically sun exposed skin. The mutation prevalence can also be associated with melanoma histologic subtype (Pathophysiology, 2014).

Melanoma development seems to be multifactorial, and it is usually related to several risks which may include, fair complexion, sensitivity to the sun and severe sunburns (Pathophysiology, 2014).

Pharmacology of Malignant Melanoma.

Immune gene therapy is widely used. This therapy used to treat Malignant Melanoma has been categorized into two specific groups, according to an active or passive principle of immunology. These two groups are even further divided, with active immune gene therapy divided into cell vaccines, vaccinations based on DNA and finally direct cytokine transfer in the treatment of tumor.

Passive immune gene therapy uses cells which are anti-tumor and vitro activated. It comprises of two main fields for the transfer of gene techniques. The first step is effector cells modification genetically and then pre effector cells amplification (Bruyere, n.d.).

Clinical researches started few years ago are still ongoing and they majorly focus on the safety of the treatment as opposed to efficacy. This gene based treatment for Malignant Melanoma is still not that developed and can be said to be in experimental stage. However, with developments in new technology and research methods, it will eventually become safe and highly reliable in few years to come.

Lab values.

Immuno-histochemical is usually done for complete diagnosis. All the S-100 plus homatropine methylbromide are usually positive in melanoma (Bruyere, n.d.).

Reference

Bruyere, H. 100 case studies in pathophysiology.

Pathophysiology. (2014).