Psoriasis

Last updated: November 01, 2022

Psoriasis

I&D 1

I&D 1

Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Sepsis
Neonatal sepsis
Abscesses
Type I hypersensitivity
Food allergy
Anaphylaxis
Asthma
Type II hypersensitivity
Pemphigus vulgaris
Type III hypersensitivity
Poststreptococcal glomerulonephritis
Type IV hypersensitivity
Graft-versus-host disease
Contact dermatitis
Transplant rejection
Common variable immunodeficiency
Selective immunoglobulin A deficiency
X-linked agammaglobulinemia
DiGeorge syndrome
Thymic aplasia
Severe combined immunodeficiency
Ataxia-telangiectasia
Wiskott-Aldrich syndrome
Adenosine deaminase deficiency
Hyper IgM syndrome
Leukocyte adhesion deficiency
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Glucocorticoids
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
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Klebsiella pneumoniae
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Bacteroides fragilis
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Brucella
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Mycobacterium tuberculosis (Tuberculosis)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Leptospira
Treponema pallidum (Syphilis)
Coxiella burnetii (Q fever)
Viral structure and functions
Varicella zoster virus
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Hepatitis C virus
West Nile virus
Norovirus
Coronaviruses
HIV (AIDS)
Ebola virus
Rubella virus
Skin histology
Skin anatomy and physiology
Vitiligo
Albinism
Folliculitis
Atopic dermatitis
Psoriasis
Urticaria
Stevens-Johnson syndrome
Cellulitis
Erysipelas
Impetigo
Pigmentation skin disorders: Pathology review
Papulosquamous and inflammatory skin disorders: Pathology review
Vesiculobullous and desquamating skin disorders: Pathology review
Fascia and spaces of the neck
Otitis externa
Otitis media
Benign hyperpigmented skin lesions: Clinical
Hypopigmentation skin disorders: Clinical
Alopecia: Clinical

Transcript

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Psoriasis is a non-contagious, chronic autoimmune disease that causes skin inflammation, and is linked to other autoimmune deficiencies such as psoriatic arthritis.

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.

There are two different types of T Cells, cytotoxic T Cells, which directly kill infected cells, and helper T cells, that help to facilitate the overall immune response.

So, if the dendritic cells present these fragments and the fragments are recognized by the T-cell, then the T-cell releases cytokines.

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.

Key Takeaways

Psoriasis is an autoimmune disorder that affects the skin, which leads to the excessive proliferation of keratinocytes that don't mature correctly. It is characterized by thick, scaly, and silvery patches on the skin, known as plaques. These plaques are often itchy and painful, and they can crack and bleed. Psoriasis typically appears on the scalp, elbows, knees, and lower back, but it can also affect the nails, genitals, and mouth. Psoriasis treatment can include topical creams and ointments; immunosuppressive therapies, and UV phototherapy. For some individuals, there can be significant feelings of depression or anxiety, and a need for psychological counseling.

Sources

  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. "Psoriasis" The Lancet (2015)
  6. "New developments in the management of psoriasis and psoriatic arthritis: a focus on apremilast" Drug Design, Development and Therapy (2013)
  7. "Psoriasis Pathogenesis and Treatment" International Journal of Molecular Sciences (2019)
  8. "Psoriasis and its management" BMJ (2006)