Xerosis and Dermatitis 1 Flashcards Preview

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Flashcards in Xerosis and Dermatitis 1 Deck (32)
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1
Q

Xerosis (what is it? other name?)

A

AKA dry skin

  • The skin is lacking moisture and this results in cracks in the skin surface.
  • It is often characterized by a pattern of fine lines, scaling and itching
  • Dry skin is commonly seen in people with atopic dermatitis (eczema).
2
Q

Xerosis - Pathophysiology (4 GENERAL POINTS)

A

Dry skin due to abnormalities in the integrity of the barrier function of the stratum corneum

Too much involucrin (a protein) may be expressed early, increasing cell stiffness.

Impaired skin barrier = increase in transepidermal water loss (TEWL)

Immune Response

3
Q

Xerosis - Pathophysiology-what are the contributing abnormalities (5)

A

Multiple contributing abnormalities:
1. There is an overall reduction in the lipids in the stratum corneum
2. Ratio of ceramides, cholesterol and free fatty acids may be altered.
- Most skin barrier disorders are characterized by a decreased ceramide content which leads to a defect in the epidermal layer.
3. Abnormal filaggrin (protein that bind to keratin fibers in the epidermal cells) expression
- This results in corneocyte deformation (flattening of surface skin cells), which disrupts the
organization of the extracellular lipid (fat).
4. There may be a reduction in proliferation of keratinocytes.
- Keratinocyte subtypes change in dry skin with decrease in keratins K1, K10 and increase in K5, K14.
5. too much involucrin (protein) may be expressed early, increasing cell stiffness

4
Q

Xerosis - Risk & Aggravating Factors (4)

A
  1. Age and Disease - (Nearly everyone > 60 years has dry skin, Postmenopausal, Hypothyroidism, Malignancy, HIV, Chronic renal disease, Diabetes, Malnutrition and weight loss)
  2. Drugs - (Retinoids (oral especially), Diuretics)
  3. Environmental - (Low humidity: in desert climates or
    cool, windy conditions, Excessive air conditioning, Direct heat from a fire or fan heater, Excessive bathing, Contact with soap, detergents and solvents, Inappropriate topical agents such as alcohol, Frictional irritation from rough clothing or abrasives)
  4. Genetics -(There is often a family history of dry
    skin, Those with atopic dermatitis are more
    susceptible )
5
Q

Xerosis - Presentation

A
Xerosis presents as:
- dull surface
- rough
- scaly
- cracked
When the skin becomes inflamed and fissured, it is
classified as dermatitis
6
Q

Dermatitis (what is it? other name?)

A

AKA “skin-inflammation”
-Non-specific term that describes a skin reaction that exhibits
swelling, erythema, scaling, vesicles and/or crusts.
-This term refers to a group of inflammatory conditions that affect the epidermis layer

7
Q

Dermatitis - Inflammatory response acute vs chronic

A

Acute: refers to a rapidly evolving red rash which may be blistered and swollen
Chronic: refers to a longstanding irritable area. It is often darker than the surrounding skin, thickened (lichenified) and `s evident of scratching.

8
Q

What is the Immune response for dermatitis? (think of the skin diagram)

A
  • Immune activation by resident innate immune cells leads to type 2 inflammation, led by inflammatory cytokines IL-4, IL-13, and IL-31.
  • Type 2 inflammation mediates barrier disruption, promotes further inflammation, and increases itch, leading to acute skin lesions.
  • Chronic disease is characterized by intensification of the effect of type 2/Th2 cytokines as well as involvement of Th1 inflammation, resulting in lichenification of the skin
  • Innate immune cells and proteins are always present and read to mobilize to fight microbes
  • Th1 and Th2 is off balance
9
Q

Dermatitis - Presentation - Acute

A
  • Erythema due to dilatation of the small blood vessels
  • Edema due to leakage of fluid from blood vessels and accumulation in tissues (vesicles may form).
  • Breakage of blisters results in oozing or weeping (vesicles), and evaporation of this fluid
    causes crusting and scaling.
  • Itchy
10
Q

Dermatitis - Presentation - Chronic

A
  • Skin becomes dry, and cracked (fissures). With
    prolonged itching and scratching, it thickens and the
    normal skin markings become more prominent (lichenfication).
  • Scaling and hyperpigmentation may be present
  • Itchy
11
Q

Atopic Dermatitis (what is it? other name?)

A

AKA - Eczema “to boil over”

Can be acute or chronic

12
Q

Atopic Dermatitis Epidemiology

A
  • Onset typically occurs early in life, with 60% of cases presenting by 1 year and 90% presenting by 5 years of age.
  • Prevalence of AD in the adult population varies regionally but is estimated to be up to ~10%.
  • Most cases of pediatric AD do resolve, a significant proportion do not, and in fact a small percentage of patients may first develop symptoms in adulthood.
13
Q

Atopic Dermatitis - Pathophysiology and Contributing Factors

A
  • Pathophysiology of AD is complex and includes genetic, immune, and environmental factors contributing to chronic inflammation.
    Atopic dermatitis, allergic rhinitis/conjunctivitis and allergic bronchial asthma belong to the atopic syndrome, or atopic diathesis (atopic triad)
  • Impaired barrier function makes skin more susceptible to environment and external triggers leading to exaggerated immune response
14
Q

Atopic Dermatitis - Presentation

locations?

A

3 phases of AD:
Infantile (<2yr): scalp, cheeks, outer elbows, middle chest, knees, diaper area

Childhood (2yr-puberty): neck, inner elbows, behind knees, feet

Adult: hands and feet

there is mild, moderate and severe AD
Start prescription therapy if there is morbidity

15
Q

Secondary skin infections - AD

A
  • Skin microflora
     Frequently (and more correctly) called the skin microbiota or the skin microbiome
     i.e. microorganisms that are resident on our skin
  • Total microbial cell count in and on our bodies is similar to the number of human cells
     After the gut, there are more microorganisms on the
    skin than anywhere else in the body
     Majority are bacterial species; however fungi, viruses and mites are also found on the skin of normal healthy humans
  • The majority of microorganisms on our skin are commensals, as they infrequently cause ill health.
     Commensal microorganisms can prevent colonization of pathogenic microorganisms such as S. aureus
  • However, in some circumstances commensal microbes such as S. epidermidis have beneficial or pathogenic roles.
  • There are products on the market that affect the microbiome in a good way
16
Q

Contact Dermatitis - Epidemiology

what are the 2 types?

A

Contact dermatitis is divided into 2 categories: irritant contact dermatitis (ICD) (80% of patients) and allergic contact dermatitis (ACD) (20% of patients)

17
Q

Irritant Contact Dermatitis - Pathophysiology and Contributing Factors

A

ICD is caused by irritation of the skin:
- Nonallergic reaction resulting from activation of the innate immune system by the direct cytotoxic effect produced by exposure to any substance.
Occurs when chemicals or physical agents damage the surface of the skin faster than the skin is able to repair the damage. Irritants remove oils and moisture from the outer epidermal layer, allowing chemical
irritants to penetrate more deeply and cause further damage by triggering inflammation.
- “If you are exposed to something long enough, there is a potential it will irritate your skin e.g. washing your hands again, and again, and again…”

18
Q

Irritant Contact Dermatitis - offending agents

A
  • Cosmetics
  • Skin-care products
  • Water and soaps
  • Saliva (baby drooling)
  • Textile dyes in clothing
  • Plants
19
Q

Irritant Contact Dermatitis - Aggravating factors

A
  • Inflamed skin
  • Burn
  • Skin infection
  • Pressure or friction on the skin
  • Excessive perspiration
  • Extremes in temperature
  • Occlusion of skin
20
Q

Irritant Contact Dermatitis (ICD) - Diaper Dermatitis (What is it?)

A
  • Area-specific contact dermatitis that is usually due
    to an irritant (urine +/- feces)
  • Diaper dermatitis is a term used for younger patients,
    incontinence-associated dermatitis is used for older
    patients.
21
Q

Diaper Dermatitis - Epidemiology

A

Prevalence in infants ranges from 25–53% varying with population, and up to 75% in diaper-wearing
incontinent elderly nursing home patients.
- Infants: peak incidence 9-12 months

22
Q

Diaper Dermatitis - Contributing Factors

A

Diaper environment predisposes the skin to damage

  • Overly moist skin that is occluded with diapers or diaper covers
  • Exposure to chemical (in wipes, diapers, soaps)
  • Mechanical friction with diaper
23
Q

Diaper Dermatitis - Possible Remitting Factor

A

Breastfeeding may be protective

- Feces are less copious, less alkaline and less caustic

24
Q

Diaper Dermatitis - Presentation

A

From slight to severe
Slight : faint pinkness
Mild: area of pinkness and few raised bumps
Moderate: definite pinkness in large area with small definite redness and scattered raised bumps
Moderate to severe: intense redness, peeling raised bumps, few fluid containing bumps
Severe: intense redness over large area of multiple raised bumps with fluid containing bumps

Erythema increases
Papules and pustules in worse cases
Tend to refer from moderate to severe
Compound prescription may be helpful

25
Q

Diaper - Plastic vs fabric

A
Cloth
- May also contribute to dermatitis if not adequately washed and rinsed of harsh cleansing chemicals.
- Better for the
environment?
- Cheaper?
Plastic
- Modern disposable diapers minimize skin exposure to moisture by wicking away liquid from skin
- Bad for the environment
- Expensive?

just keep baby’s bottom dry and clean

26
Q

Allergic Contact Dermatitis - Pathophysiology

A

Delayed or T cell–driven hypersensitivity immune reaction mediated by lymphocytes that have been previously sensitized
The incubation period after initial sensitization is 5–21 days and 12–48 hours after subsequent re-exposure, but the reaction may continue to develop for several weeks.

may use patch testing

27
Q

Allergic Contact Dermatitis - Epidemiology

A

Younger individuals have a more reactive immune
system BUT older individuals (elderly) may have
impaired epidermal barrier function so they may be
more reactive and have lower rates of recovery from
epidermal damage.

ask what they were doing 5 days before, weeks before

28
Q

Allergic Contact Dermatitis - Common offending agents

A
  • Latex
  • Nickel
  • Fragrances
  • Aloe vera
  • Lanolin - wool derivative
  • Topical antihistamines
  • Topical benzocaine (anesthetic)
  • Rhus genus (poison ivy)
    …and the list will grow…
29
Q

Allergic Contact Dermatitis - Presentation

A
  • Itchy, looks like “eczema”
  • Vesicles and blisters may form. Edema may be present.
  • May be diffuse (i.e. use of body wash, rash presents all over body) or confined (i.e. one finger reaction to nickel in ring).
  • Repeated or continued exposure to allergens results
    in chronic disease (skin becomes thickened, lichenification and fissures develop).
30
Q

Stasis Dermatitis - what is it? epidemiology?

A
  • Fairly common in elderly
  • One-third of patients have a previous history of lower leg deep vein thrombophlebitis related to trauma, pregnancy, surgery or prolonged illness.
  • Fluid collecting in the tissues of the legs resulting in the activation of the immune response
31
Q

Stasis Dermatitis - Contributing Factors

A

Results from chronic venous insufficiency.

32
Q

Stasis Dermatitis - Presentation

A
Often bilateral:
Lower part of calf and shin
- Swelling and edema
- Painful
- Pruritic, therefore subject to scratching (which makes it worse)
- Ulceration is a common complication