Psoriasis

Introduction of disease

Psoriasis is a skin disorder that hastens the life cycle of skin cells. This results in a fast accumulation of cells on the skin’s surface. The extra skin that develops is scaly and characterized by red patches that are both painful and itchy. Psoriasis is a chronic disease that appears and withdraws after a while. The worldwide prevalence for psoriasis is 2 percent but varies with regions (Takeshita et al., 2017). Asian and some African populations have a lower prevalence of the condition. However, in Caucasian and Scandinavian populations, the prevalence rate is about 11 percent (Takeshita et al., 2017).  There are four different clinical subtypes of the disease. These are plague psoriasis, nail psoriasis, inverse psoriasis, guttate psoriasis, and pustular psoriasis (Conrad & Gilliet, 2018).

Plaque psoriasis is the most prevalent type and is characterized by dry, raised, red skin lesions engulfed in silvery scale (Conrad & Gilliet, 2018). Nail psoriasis affects nails on toes and fingers, which may appear decolorized or with abnormal growth. The guttate psoriasis is activated by a bacterial infection and is identified for its small, water-drop-shaped, scaly lesions on the scalp, legs, hands, and truck (Takeshita et al., 2017).  Inverse psoriasis affects genitals, breasts, groin, and armpits (Takeshita et al., 2017).

Etiology and risk factors

The causes of psoriasis stem from a combination of genetics and triggers. The disease has a genetic element that is reinforced by patterns of familial varieties (Rendon & Schäkel, 2019). First and second-generation relatives of patients with psoriasis are more likely to develop the condition. Additionally, monozygotic twins are two or three times more likely than dizygotic twins to develop psoriasis. Rendon and Schäkel (2019) noted that pinpointing the exact factors of genetics that are responsible for initiating immune responses that lead to psoriasis has proven problematic to understand. The genetic elements associated with psoriasis are responsible for different biological differences such as inflammation, keratinocyte biology, and antigen presentation, among other immune functions (Conrad & Gilliet, 2018).

Several triggers can initiate psoriasis. However, the triggers are not universal and vary from one person to another. Stress has been associated with aggravating existing psoriasis or initiating the disease for the first time. Koebner [KEB-ner] phenomenon where an injured or traumatized skin lead to a disease may cause psoriasis (Rendon & Schäkel, 2019). Scratches, sunburns, and vaccinations may trigger a Koebner response. Additionally, certain medications such as antimalarial, Quinidine, indomethacin, and those with lithium may trigger psoriasis. Inderal, a high blood pressure medication, amplifies the condition in 25-30 percent of the patients (Conrad & Gilliet, 2018).

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Pathophysiological Processes

In a normal human being, the skin consists of several layers. The top layer is made up of several layers called keratinocytes. These cells undergo division at the basal layer of the epidermis and grow upwards towards the surface where they are finally shed as dead skin (Conrad & Gilliet, 2018).

The pathophysiology of psoriasis involves several steps that include epidermal hyper-proliferation, abnormal differentiation of keratinocytes, and inflammation of the skin. The hyper-proliferation stage is marked by increased synthesis of DNA and a markedly declining life cycle of the epidermis. Abnormal keratinocyte differentiation encompasses the amplified expression of certain keratins and delayed expression of other keratins that differentiate the skin. The release of DNA may cause some dendritic cells to move to the lymph nodes, where they discharge interleukins that stimulate T-cells. Inflammation results from the permeation of neutrophils into the superficial dermis and epidermis and permeation of T cells into the dermis with a prevalence of CD8+ cells (Conrad & Gilliet, 2018). This infiltration of neutrophils into the growing skin causes a red coloration. In psoriasis, the cell turnover rate may be tenfold than in healthy skin cells. 

Clinical manifestations and Complications

Regardless of the type of psoriasis, the major symptoms that characterize the condition include red, flaky, crusty patches that have easily-shed silvery scales covering them. The patches may also be itchy and have a burning sensation. Additionally, symptoms of psoriasis develop in flares that occur in different lengths of time with periods of remission in between. The remission period can last for 1-12 months. Periods of flares and remission are difficult to predict. According to the National Psoriasis Foundation (2019), symptoms can range from mild to severe. Mild psoriasis can occupy up to 3 percent of the body, while moderate psoriasis can cover 3-10 percent. On the other hand, severe psoriasis may take up to more than 10 percent of the patient’s body.

People with psoriasis develop other diseases such as obesity, psoriatic arthritis, type 2 diabetes, Parkinson’s disease, and cardiovascular diseases, among others. People with psoriasis may also develop low self-esteem and depression.

Diagnostics

The diagnosis of psoriasis is fairly straightforward. Doctors diagnose psoriasis through examination of the skin, scalp, and nails (Takeshita et al., 2017). They can also examine medical history.  Additionally, a skin biopsy may also be conducted to pinpoint the precise type of psoriasis and to cancel out other disorders (Takeshita et al., 2017). 

The lack of cure and the relapsing tendency of the illness means that psoriasis requires long term therapy. The selected therapy for psoriasis depends on comorbidities and severity. Mild to moderate psoriasis is treated using phototherapy, vitamin D analogs, and glucocorticoids (Takeshita et al., 2017).

People with psoriasis can also use emollients to keep their skin moisturized while taking treatment. This will help reduce irritation and itching and help reduce the number of lesions or plaques that develop.  

References

National Psoriasis Foundation. (2019). About Psoriasis. National Psoriasis Foundation – Home. https://www.psoriasis.org/about-psoriasis

Rendon, A., & Schäkel, K. (2019). Psoriasis Pathogenesis and Treatment. International Journal of Molecular Sciences, 20(6), 1475. https://doi.org/10.3390/ijms20061475

Takeshita, J., Grewal, S., Langan, S. M., Mehta, N. N., Ogdie, A., Van Voorhees, A. S., & Gelfand, J. M. (2017). Psoriasis and comorbid diseases: epidemiology. Journal of the American Academy of Dermatology, 76(3), 377-390.

Conrad, C., & Gilliet, M. (2018). Psoriasis: from pathogenesis to targeted therapies. Clinical reviews in allergy & immunology, 54(1), 102-113.