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Lichen planus



Integumentary system


Lichen planus


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6 pages

Lichen planus

8 flashcards

USMLE® Step 1 style questions USMLE

2 questions

A 37-year-old man comes to the office because of itching over his shins for the past few months. The itching is unrelenting and is now interfering with his sleep. He has used several over-the-counter ointments, which have not helped. Past medical history is noncontributory. He is sexually active with a female partner and uses condoms consistently. He has a previous history of IV drug use in his early 20s. Physical examination shows multiple, well-healed track marks on his arms. Examination findings of the shins are shown below.

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Complete blood count is within normal limits. Further testing reveals elevated serum aminotransferase levels. This patient’s condition is associated with which of the following organisms?

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With lichen planus, lichen means tree moss and planus refers to flat, and the reason it’s called that, is that lichen planus is a flat-topped skin rash that looks a bit like tree moss.

Lichen planus is an immune-mediated disorder, meaning that the immune system has started attacking its own skin, resulting in a skin rash.

Lichen planus can also affect mucous membrane.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis.

The epidermis forms the thin outermost layer of skin.

Underneath, is the thicker dermis layer that contains the nerves and blood vessels.

And finally, there’s the hypodermis which is made of fat and connective tissue that anchors the skin to the underlying muscle.

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with.

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 stem cells that continually divide and produce new keratinocytes.

These new keratinocytes then migrate upwards to form the other layers of the epidermis.

The stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin.

As keratinocytes in the stratum basale 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 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 die.

Keratinization leads to development of the stratum lucidum layer which is 2 to 3 cell layers thick of translucent, dead keratinocytes.

Finally, there’s the stratum corneum, or the uppermost and thickest layer of the epidermis, which is like a wall of 20-30 layers, where the glycolipid acts like the cement and the dead keratinized cells are the bricks.

Now, the part of skin connecting the stratum basale of the epidermis to the underlying dermis is called the dermo-epidermal junction.

In healthy people, this junction looks like smooth waves between the epidermis and the dermis. But, if you look closely at this junction, there are two parts.

The first part is the lower portion of the plasma membrane of the keratinocytes in the stratum basale, which contains glue-like substances called hemidesmosomes.

These hemidesmosomes adhere keratinocytes of the stratum basale to the second component of this junction, which is called the basal lamina.

The basal lamina contains a group of molecules that provide structural and biochemical support to the keratinocytes.

Typically, when a cell becomes infected with viruses or mutated by cancer, antigens from inside this cell will be presented on MHC I molecules, which are found on all nucleated cells in the body.

If this were to happen, then a specific cell of the immune system called cytotoxic T cell would use its receptor to bind to the MHC class I molecule, which would cause it to release its payload of perforin and granzymes.

Perforin would perforate the target cell by forming pores, and these pores would allow the granzymes to enter into the cell. Once inside, the granzymes would induce apoptosis, or programmed cell death.

In lichen planus, some healthy non-infected keratinocytes start presenting antigens on MHC I molecules, and it’s unclear why they do that.

This antigen presentation on MHC I molecules enables cytotoxic T cells to attack these keratinocytes and kill them.

In killing the keratinocytes, these cytotoxic T cells also release cytokines, which recruit more cytotoxic T cells to the scene. That leads to more damage to the keratinocytes, as well as the surrounding tissue in the basal lamina.

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Cutaneous and Mucosal Lichen Planus: A Comprehensive Review of Clinical Subtypes, Risk Factors, Diagnosis, and Prognosis" The Scientific World Journal (2014)
  6. "Lichen Planus" New England Journal of Medicine (2012)
  7. "Interventions for erosive lichen planus affecting mucosal sites" Cochrane Database of Systematic Reviews (2012)