Disorders of the epidermis

Question 1

Hyperproliferative hyperkeratosis:

Answer 1

• Too much stratum corneum because it is being MADE TOO QUICKLY
• “Inflammatory, hyper-proliferative, scaly skin diseases with prominent immune system involvement”

Question 2

Retention Hyperkeratosis:

Answer 2

• Too much stratum corneum because it is being MADE IMPROPERLY (leading to clumping/poor sloughing,etc.)
• “A heterogeneous group of inherited skin diseases exhibiting hyperkeratosis caused by abnormal stratum corneum formation (non-inflammatory)”

Question 3

What are the 4 layers of the epidermis?

Answer 3

• the basal cell layer
• spinous layer
• granular cell layer
• stratum corneum

Question 4

Is the epidermis vascular or avascular?

Answer 4

Avascular (nutrients diffuse from capillaries in the papillary dermis)

Question 5

Label the layers of the epidermis

Answer 5

Question 6

Name the cells of the epidermis

Answer 6

• melanocytes
• keratinocytes
• Merkel cells
• Langerhans cells

Question 7

keratinocytes

Answer 7

most common cells of the epidermis, ultimately form the stratum corneum

Question 8

Melanocytes

Answer 8

cells of epidermis that produce melanin, which is the primary mediator of skin color.

Question 9

Langerhans cells

Answer 9

cells of epidermis that are important immune surveillance and antigen-presenting cells

Question 10

Merkel cells

Answer 10

neuroendocrine cells of the epidermis, poorly understood function (assoc. with mechanoreceptors)

Question 11

How long does it normally take for a keratinocyte to move from the basal layer to the stratum corneum?

Answer 11

• normally takes about 28 to 30 days
• under hyperproliferative conditions such as psoriasis, can be shortened to as little as 3 to 5 days

Question 12

What are some major differences between hyperproliferative and retention hyperkeratosis?

Answer 12

• hyperprolif - stratum corneum made TOO quickly, prominent immune system involvement
• retenion - stratum corneum made IMPROPERLY, NON-inflamm

Question 13

What are some examples of hyperproliferative hyperkeratosis?

Answer 13

psoriasis and eczema

Question 14

What are examples of retention hyperkeratosis?

Answer 14

the ichthyoses

Question 15

Comment on the following about psoriasis:

• prevalence
• genetics
• etiology

Answer 15

• common - about 2% of population
• strong genetic component
• evidence increasingly suggests it’s an immune disease with prominent cutaneous manifestations

Question 16

Describe what psoriasis looks like (color, type of lesion, distribution, etc)

Where is it commonly found?

Answer 16

• scaly, red, symmetrically distributed plaques
• most commonly found on trunk and extensor extremities (ex: elbows and knees) but also common on scalp and buttocks

Question 17

Describe the scales of psoriasis.

Answer 17

• thick, adherent, often silvery/micaceous

Question 18

psoriasis vulgaris

Answer 18

aka chronic stationery psoriasis, plaque-like psoriasis

• affects 80-90% people with psoriasis
• usu appears as raised areas of inflammed skin covered with silvery white scaly skin (plaques)

Question 19

Comment on the pathology of psoriasis

Answer 19

• Elongation of the rete ridges
• Mixed inflammatory infiltrate with prominent neutrophils
• Hyperkeratosis with parakeratosis
• Small neutrophil aggregates in epidermis and stratum corneum
• Numerous blood vessels

Question 20

What are the arrows pointing to? What’s the derm dx?

Answer 20

dx: psoriasis vulgaris

Question 21

What is a Munro microabcess?

Answer 21

collection of neutrophils in the stratum corneum

& from our friend Dr. Wiki “abscess in the papillary epithelium consisting of PMN infiltrate and associated with psoriasis and seborrheic dermatitis”

Question 22

What is parakeratosis? What does it indicate?

Answer 22

• retained keratinocyte nuclei in the stratum corneum
• sign of rapid cell cycling and improper terminal differentiation

Question 23

Acanthosis

Answer 23

uniform elongation of the rete ridges; a common histo feature in psoriasis

Question 24

Id the following

Answer 24

Spongiform pustules of Kogoj
(collection of neutrophils in the epidermis) in psoriasis vulgaris

Question 25

What are some of the ways psoriasis can present clinically?

Answer 25

• Guttate: small papules/plaques (often triggered by Group A strep exposure)
• Erythrodermic: universal redness/scaling
• Pustular: multiple pustules,“lakes of pus”
• Palmoplantar: hyperkeratotic palms/soles
• Inverse: spares common sites
• Vulgaris (“plaque type”): plaques on arms/legs/trunk/scalp of variable size/involvement

Question 26

What other changes are seen in psoriasis?

Answer 26

• nail changes
  
  • pitting
  • onycholysis (detachment of nail from nail bed, starting at distal and/or lateral attachment)
  • oil drop sign

Question 27

Describe the nail changes in this image

Answer 27

• oil drop sign
• onchylosis (detachment of nail from nail bed starting at distal and/or lateral attachment)

Question 28

What joints are affected in psoriatic arthiritis? What is distribution? Severity?

Answer 28

• often affects distal interphalangeal joints
• asymmetric in distribution (“small and asymmetric”)
• severity varies (advanced cases are called arithritis mutilans)

Question 29

What is psoriasis a risk factor for?

Answer 29

heart disease

Question 30

Comment on psoriasis and:

• trauma
• bone marrow txp

Answer 30

• trauma can induce psoriatic plaques (koebnerization)
• psoriasis can be transferred OR cured via bone marrow txp

Question 31

What are some preciptating/aggravating factors for psoriasis?

Answer 31

• Infection (especially Group A strep)
• Stress
• Drugs (especially lithium, beta-blockers)
• Trauma (koebnerization)
• Alcohol
• Smoking

Question 32

Comment on hyperproliferation in psoriasis. Specifically, what is happening in the epidermis? the dermis?

Answer 32

• epidermis:
  
  • increased # of proliferating cells
  • greatly shortened cell cycle
• dermis:
  
  • inflamm infiltrate
  • vascular prolif (can’t be the epidermis b/c the epidermis is avascular)
  • growth factors
  • interleukin, cytokines . . . oh hey, immune response

Question 33

What treatment can we offer patients with psoriasis?

Answer 33

Therapies are directed at either aborting the inflammatory response, slowing down the keratinocyte cell-cycling, or both.

• anti-inflammatory agents
  
  • topical steroids
  • UV light
  • methotrexate
  • cyclosporine
  • biologic agents
• differentiation modulators
  
  • retinoids (acitretin)
  • vitamin D derivatives (calcipotriol)
  • coal tar

Question 34

atopic dermatitis

Answer 34

• eczema (also a hyperproliferative hyperkeratosis caused by inflammation)
• chronic
• recurrent
• pruritic

Question 35

When does atopic dermatitis begin?

Answer 35

usually in childhood (90% before age of 5 yr)

Question 36

What is atopic dermatitis associtated with?

Answer 36

• may be associated asthma and allergic rhinitis (atopic triad)
• genetic basis (variable expression) and environmental influence

Question 37

atopic triad

Answer 37

Asthma, allergic rhinitis (Hayfever), and atopic dermatitis (eczema)

Question 38

Dx Atopic dermatitis

Answer 38

Must have a history of a pruritic dermatitis and 3 or more of the following:

1) Involvement of flexural folds, neck, or cheeks.
2) History of asthma or hay fever (or FHx if pt < age 4).
3) General dry skin for > 1 year.
4) Visible flexural eczema.
5) Early onset

Question 39

Etiology of atopic dermatitis

Answer 39

• central “defect” - inappropriate barrier fxn of skin –> inappropriate exposure of immune system to environmental antigens –> inappropriate immune system activation in susceptible individuals (NOT all pts with compromised skin barrier)
• Note: diff skin-homing T cell populations than psoriasis