Response to Student: HIV Disorder

Student1points out that HIV disorder constitutes ribonucleic acid, RNA. Like other RNA viruses, the disease is regarded as a retrovirus that has the capability to reverse replicating nine of RNA into deoxyribonucleic acid (Soto Ramírez, 2004). What is important to note is that the disorder does not replicate until when it is inside a living cell. It only enters into a cell when gp 120 in the viral envelope binds to specific CD4 receptor sites on the surface, as noted by student 1. Upon entering into the cells, HIV manifests through attacking the immune system, making it defenseless against other infections (Arcangelo et al., 2017). This condition is known as an immunodeficiency in patients.

However, student one does not highlight a struggle that exists between HIV replication and the immune reactions of the patient, via immune-mediated and cell-mediated reactions. Research indicates that the HIV viral burden mainly mediates CD4+ T-cell damage. The destruction begins in the thymus, bone marrow, peripheral lymphoid organs, and within the nervous system, such as microglia. The outcome of this destruction is a malfunction of T-cell production and ultimate immune suppression (Arcangelo et al., 2017). Later on, during illness, HIV spreads from lymphoid organs to other organs such as the spinal cord, kidney, brain, liver, and lung.

Whereas student 1 points that the effective medications of HIV disorder are those that can hinder its replication mechanism, it should also be noted that most often, such drugs work more effectively when they are combined with pharmacokinetic enhancers (Arcangelo et al., 2017). The student also adds that the behavioral characteristics of patients can affect how the pathophysiology of the disorder and the medications used on them. This is true because behavioral characteristics affect an individual’s ability to accept that they have the HIV condition and procedures aimed at managing it. For instance, when one fails to accept the existence of the disorder in their bodies, they rarely agree to take their medications, thus making it difficult to control the disease. In such incidences, the pathophysiology enters its advance stage, causing irreversible impacts on the immune system, thus allowing the entrance of opportunistic infections.

Response to Leslie Pendleton: Systemic Lupus Erythematosus

Leslie notes that SLE emerges as a result of excessive polyclonal production of autoantibodies and circulating immune complexes. The disorder is characterized by TH2 immune response, which presents significant interleukin 10, IL-10 production (Atta et al., 2004). In simple terms, Leslies should just state that the body’s immune system produces antibodies that act against itself, especially against the cell nucleus proteins (Arcangelo et al., 2017). The attacks of these antibodies are the ones resulting in SLE.

Leslie also notes that SLE can affect several organ systems, but most impacts are felt on the joints, skin, kidney, blood cells, and nervous systems. The disorder causes a maladaptive response of the body’s second defense mechanism, resulting in autoimmune inflammation response with an array of physiological reactions such as effects on the skin (Arcangelo et al., 2017). What is essential to add in this context is that the maladaptive responses of the infection of lupus, which is chronic inflammation, are associated with a type 3 hypersensitivity reaction with the likely involvement of type 2 hypersensitivity (Arcangelo et al., 2017).

Just as indicated by Leslie, genetics has been found to have a significant impact on SLE pathophysiology. For instance, Genome-wide association research has depicted that not less than 60 risk loci for the susceptibility of SLE across individuals, with the sharing of the genetic risk across ethnicities and borders. Leslie identifies hydroxychloroquine and glucocorticoid drugs for relieving SLE symptoms. It should also be noted that benlysta medications can be combined with other lupus drugs to treat SLE (Fanuourikis et al., 2019). Also, under extreme flares of SLE associated with diverse effects on organs such as the kidney, steroids are the most preferred since they act quickly in symptom management. What is important to note is that the drugs used to treat SLE all have side effects, but patients are advised to seek physician’s guidance if the effects become unbearable.