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A 63-year-old man comes to the dermatology clinic because of rapidly progressing skin redness which has covered most of his body. He has coronary artery disease with a 3-vessel CABG, hypertension, and psoriasis. His medications include a beta-blocker, aspirin, ACE-inhibitor, statin, and topical clobetasol. He has not had any recent changes to his medications. His temperature is 38.8°C (101.8°F), pulse is 115/min, respirations are 16/min, and blood pressure is 95/68 mm Hg. His O2 saturation is 97% on room air. He is in no acute distress, but he is shivering. On examination, his oropharynx is clear without mucous membrane involvement. His skin exam shows diffuse erythema with an overlying scale covering over 90% of his body surface area. Which of the following is the most likely diagnosis?
Content Reviewers:Rishi Desai, MD, MPH
It can be incredibly itchy and form silver plaques on the skin that can be embarrassing, and have both physical and psychological effects.
Afflicted reality TV star Kim Kardashian, and singer Cyndi Lauper have each spoken out on how psoriasis can have a significantly negative impact on the quality of life.
Normally, the skin is divided into three layers--the epidermis, dermis, and hypodermis.
The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle.
Just above the hypodermis is the dermis, which contains nerves, sweat glands, lymph and blood vessels.
Just above the dermis is the epidermis.
The epidermis itself has multiple cell layers that are composed of developing keratinocytes - which are named for the keratin protein that they’re filled with.
Keratin is a strong, fibrous protein that allows keratinocytes to protect themselves from getting destroyed when you rub your hands through the sand at the beach.
Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of small, cuboidal to low columnar stem cells that continually divide and produce new keratinocytes.
These new keratinocytes migrate upwards, forming the other layers of the epidermis.
As keratinocytes in the stratum basale begin to mature and lose the ability to divide, they migrate into the next layer, called the stratum spinosum which is about 8 to 10 cell layers thick.
The stratum spinosum also has dendritic cells lurking around, which are star-shaped immune cells constantly patrolling for invading microbes as part of the body’s immune defense system.
The next layer up is the stratum granulosum which is 3 to 5 cell layers thick.
Keratinocytes in this layer begin the process of keratinization, which is the process where the keratinocytes flatten out, and get rid of their intracellular structures and die, and in the process they create the epidermal skin barrier.
Keratinization leads to development of the stratum lucidum layer which is 2 to 3 cell layers thick of translucent, dead keratinocytes that have shed nuclei.
The stratum lucidum is only found in thick skin like on the palms and soles of the feet, because those are the areas that need extra protection.
The stratum lucidum is absent in thin skin, which covers the rest of the body, and the other layers are thinner.
Finally, there’s the stratum corneum, or the uppermost and thickest layer of the epidermis, which is like a wall of 20-30 layers.
As new keratinocytes push up into the stratum corneum, older dead cells are sloughed off forming skin flakes or dandruff. In this way, the thickness of the epithelium remains constant with a regulated turn-over of keratinocytes.
Normally, there are microbes that live on the surface of the skin, but when there’s a tiny break in the skin or cut, those microbes have the ability to enter into the skin layer.
At that point, the body notices these ‘foreign invaders’ and immune cells called dendritic cells capture foreign antigens, break them down into little fragments that they then present to T-cells.
Cytokines are small proteins used in cell signaling - such as IL-12, IL- 23, interferon-γ, tumor necrosis factor or TNF, and IL-17, which specifically has been linked to chronic inflammation.
This entire process of inflammation increases keratinocyte proliferation in the skin. This also recruits other immune cells, like neutrophils, to the site of infection.
Once the microbe is completely destroyed, the immunologic response slowly returns back to normal.
In psoriasis, this immunologic response is abnormal, and it leads to excessive inflammation.
You can think of it as an over-amplification of the skin’s natural immune process that goes a bit haywire.
The causes of psoriasis aren’t clear but there’s definitely a genetic component and environmental triggers, like trauma, stress, dietary factors, smoking, or a previous infection.
Regardless of how the process is triggered, once it’s underway it doesn’t shut off, resulting in chronic damage to the skin.
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