Skin Lesions / Non-Infectious Diseases (Common Skin Conditions) Flashcards
What are the functions of the skin?
Basic function is act as a barrier
* Protects against UV light/radiation
* Protects against excessive heat loss or overheating (thermoregulator)
- DOESN’T conduct heat –> good thing
* Prevents physical damage to organs
Maintains fluid balance
* Protects against dehydration
* Prevent water loss (maintains integrity of the skin)
Prevents against infection
* Protects against pathogens and allergens
* Wound repair and regeneration
- Metabolic functions
- Synthesizes & storage of Vitamin D
What is our largest organ?
SKIN
Skin Anatomy
- Approximately 15% of total body weight in adults
Thinnest epidermal layer
* Eyelids (<0.1mm)
- b/c they’re moving a lot
Thickest epidermal layer
* Soles of the feet (approx. 1.5mm)
* Palms of the hands (approx. 1.5mm)
- b/c has to put up with a lot more
- sweat glands on them that regulate heat
Thickest dermis layer
* Back (30 – 40 times thicker than the epidermis)
* Approximately 1 cm thick
What are the 3 layers of skin?
- Epidermis
- Dermis
- Subcutaneous (Hypo-dermis)
What is the Epidermis & what is its function?
- Outermost layer of the skin
- Serves as a barrier, maintains fluid balance in the body and prevents infection
(see with dry skin)
(contains flattened cells that’re continuously knocked off)
What is the Dermis & what is its function?
- Layer of connective tissue containing blood vessels, nerves, hair follicles,
sweat & oil glands - Protects the body from mechanical injury, binds water and helps with thermal regulation
What is the Subcutaneous (Hypo-dermis) & what is its function?
- Provides the body with buoyancy and is a storehouse for energy within the fat layers
Epidermis dets
- Ranges in thickness from 0.4 to 1.5 mm (depending on location on the body)
- Cells continually RENEW every 4 to 6 weeks
- Composed mainly of keratinocytes & dendritic cells
- Consists of 4 main layers
- Outermost layer is the stratum corneum
What are the Epidermis layers?
- Stratum corneum
- Granular cell layer (stratum granulosum)
- Squamous cell layer (stratum spinosum)
- Basal cell layer (stratum basale)
Epidermis
Stratum corneum layer
- Comprised mostly of dead skin cells
- A surface film that adds to protection (up of sebum, sweat, broken down keratinocytes and ceramides)
(imp. for ppl. with scliasis/ecsema)
Epidermis
Granular cell layer (stratum granulosum)
- 1 to 3 cells thick
- Flattened cells
Epidermis
Squamous cell layer (stratum spinosum)
- 5 to 10 cells thick
- cells become keratinized (give cell colour - melan in it)
Epidermis
Basal cell layer (stratum basale)
- Controls the renewal of new cells
- Cells renew approximately 28 days and move upward to the SC
(from basal up to SC)
Epidermis
Keratinocytes:
- 80-85% of the cells in the epidermis are derived from keratinocytes
- MAIN CELL TYPE in the epidermis (other is dendritic cells)
- Keratinocytes in the squamous cell layer start synthesis of keratin & prevent water loss from the body
- Prevent dehydration and infection
(gives hair, nails, & skin the hardness)
Where are Keratinocytes (epidermis) produced?
- Produced in the squamous layer to stratum corneum (loose nuclei & flatten as they move through the layers)
What are the Epidermis cell types?
- Langerhans cells: (2 - 8%)
- Basal Cells
- Merkel cells: (6-10%)
- Melanocytes: (5%)
Langerhans cells:
(2 - 8%) in epidermis
* Detects, attacks, neutralizes & eliminates foreign bodies
- involved in T-cell
Basal Cells:
- Precursor to keratinocytes
in epidermis
Merkel cells:
(6-10%) in epidermis
* Stimulates sensory nerves such as touch * High concentration in fingertips
Melanocytes:
(5%) in epidermis
* Responsible for pigment production * Gives hair and skin color
What epidermis cells are in the squamous cell layer?
Langerhans cells
What epidermis cells are in the basal cell layer?
Basal Cells
Merkel cell
Melanocytes
What is the function of the dermis?
- Provides structural integrity
(not connected to many common skin conditions)
- protects body from injury
What is the main component of dermis?
- Main component is collagen & elastin fibers
- Collagen = stress resistant material
- Elastin fibers = maintain elasticity of the skin
What does the dermis consist of?
- Connective tissue
- Blood vessels
- Sweat glands (apocrine, eccrine glands)
- Nerves
- Hair follicles/roots
- Oil (Sebaceous glands)
What are the 3 types of sweat glands?
- Eccrine sweat glands
- Apocrine sweat glands
- Apoeccrine sweat glands
Eccrine sweat glands:
- Responsible for body cooling
- Found mainly on the palms, soles of the feet, face, head & body trunk
(produce NO odor)
Apocrine sweat glands:
- Larger than eccrine glands that begin functioning at
puberty (milky consistancy b/c contains some fat cells & when it hits bacteria) - Found mainly in the underarm, nipples & genital areas
Apoeccrine sweat glands:
- Structural features of eccrine & apocrine glands
- Found only in the underarm area of adults
(develop during puberty - odorless)
Where do Sebaceous glands reside?
Reside primarily in the dermis
Where is the highest # of sebaceous glands found?
on the face and scalp
What doe the cells within the sebaceous glands contain?
sebum (lipid droplets)
What does sebum consist of?
oils such as triglycerides, fatty acids & cholesterol
* Sebum lubricates the hair and skin to protect against friction & protects the skin from light
* Has antibacterial activity and some anti-inflammatory activity
What would happen if we had sebaceous glands on our feet?
we’d glide around
Where do hair follicles begin from?
Hair follicles begin in the dermis with the hair bulb and shaft extending out to the epidermis
- born with a specific # & doesn’t change (so when you’re older they’re decreasing & won’t get them back, therefore hair thins & gets lost)
What are hair follicles connected to?
connected to sebaceous glands that provide sebum to the hair
What are the 3 stages of hair growth?
- Anagen phase (active growing, lasts 2 to 6 years and
determines hair length) - Transitional or catagen phase (follicle degenerates, stops growing, lasts 2 to 3 weeks)
- Telogen or resting phase (shedding occurs, last 3 to 4 months)
How do you know if someone has a hair loss problem?
- hair falling out in clumps, haridresser will notice
- if more than usual check it out (usual is 75-100 a day and 300 is abnormal)
What is Pediatric Skin like?
- Contains fewer moisturizing factors (lipids, melanin)
- Skin is thinner & more permeable
- Pediatric skin is more prone to chemical irritation and infections (impaired barrier function)
- b/c not fully dev. yet
- Increased rate & amount of topical drug absorption (adjusting dosing is necessary)
** Young children are not small adults!
- NOT treated the same
(begins dev. after 1st year of life)
What is Aged Skin like?
- Epidermis tends to thin with age * Decreased moisture in skin as a
person ages - Skin strength and elasticity decreases (wrinkles)
- Fat layers thin (less insulation & padding)
- Longer healing time, increased risk of skin injury
(become thinner)
(sebum production tends to go down - don’t sweat as much (b/c not prod. as much oil) - leads to drier skin)
What is Psoriasis?
- Inflammatory and hyperplastic (increase in cell number/proliferation) disease of skin (LIFELONG condition)
- Characterized by erythema (redness), itching and elevated scaly plaques
- Chronic, relapsing condition (doesn’t spread)
- can get better/worse at times, but won’t ever go away - goes in remission sometimes)
- Course of disease often unpredictable
What is the epidemiology of Psoriasis?
- Affects 2 – 4% of males and females world-wide
- Affects males & females equally
- Higher prevalence at higher altitudes
- It is not contagious (thought to be an immune disorder)
- Life-long condition
(runs in family)
What is the age of onset for Psoriasis?
- Mean age: ~ 23–37 years
Current theory:
2 distinct peaks with possible genetic associations
* Early onset
* Late onset
What is the early onset for Psoriasis?
(16–22 years)
* More SEVERE and EXTENSIVE
* More likely to have affected first-degree family member
What is the late onset for Psoriasis?
(57–60 years)
* MILDER form
* Affected first-degree family members nearly absent
What is Psoriasis’ current theory?
- GENETICS
- Higher in identical twins than fraternal twins
(if you have it, it’s likely someone in your family does) - IMMUNE RESPONSE
** T-cell mediated AUTOIMMUNE disease - connected through genetics
- Activated T cells induce keratinocyte proliferation thereby reducing differentiation which promotes a build up of skin plaques on the epidermis (hyper-proliferation of keratinocytes)
- ENVIRONMENTAL
- CO-MORBILITIES
- Monitor for signs of CV disease, diabetes, blood pressure
Describe the Abnormal Keratinocyte Proliferation
- Activated T cells induce rapid proliferation of keratinocytes (hyper- proliferation)
- mature & head up to epidermis faster
- This results in faster maturation than normal (3-5 days vs. >30 days) = abnormal cell differentiation (i.e. cells don’t function properly)
- Both result in scales and flakes (plaques) seen in psoriasis
- Plaques contain ~30x more keratinocytes than healthy skin
What are external triggers of Psoriasis?
The following can make it worse but won’t give you it:
- Excessive alcohol consumption
- Smoking (may increase risk & severity)
- Stress (impacts the immune system)
- Cold, dry weather
- Infections (strep throat or skin infections)
- Obesity (may develop in the skin creases and fold)
- Injury to the skin (scrape, bug bite, severe sunburn)
- Drugs: lithium, NSAIDs (indomethacin), beta-blockers, antimalarial medications, fluoxetine
- Skin trauma (cuts, bruises, burns, bumps, vaccinations, tattoos) = “Koebner phenomenon”
What are the types of Psoriasis? Describe them
- Chronic plaque (psoriasis vulgaris)
- Guttate
* Triggered by bacterial infections
* Small drop-shaped scales on trunk, arms or legs (rash) - Flexural
* Smooth, well-defined patches
* Affects body folds & genitals - Erythrodermic
* Red rash that peels and itches - Pustular
* Appears as pus filled lesions in patches - Psoriatic arthritis
* Swollen, painful joints similar to arthritis - Scalp
* Red, itchy areas with silver- white scales on the scalp - Nail
* Affects finger & toe nails
* Pitting, abnormal growth & discoloration
What is Plaque Psoriasis?
- Vulgaris = common
- Most common form (80 - 90% of patients)
What is the appearance of Plaque Psoriasis?
- Red/pink (light skin) or purple (dark skin), scaly plaques at
least 0.5cm in diameter - Raised, well defined, flat topped plaques with sharp borders (SYMMETRICAL)
- Typically covered with silvery white (light skin) or gray (dark skin) SCALES that constantly shed
What is the location of Plaque Psoriasis?
- Trunk (lower back), genitals, face, palms, soles and nails
- Occurs on the extensor surfaces of forearms & shins (elbows, knees)
What is Atopic Dermatitis like in infants ((3 – 6 months of age)?
- Weeping patches, crusted plaques on the face, neck and extensor surfaces
What is Atopic Dermatitis like in childhood (before 5 years of age)?
- Dry, flaking, rough, cracked areas
- Irritation of the flexural skin (back of the knees) (or behind elbow)
- in specific areas
What is Atopic Dermatitis like in Adult?
- Dry, scaly areas
- Flexural areas, hands, face and upper trunk
What is the appearance of Atopic Dermatitis?
- Red to brownish-gray (light skin) or dark brown, purple or gray (dark skin)
- SLIGHTLY RAISED patches or small bumps
- but not as raised as psoriasis
What are the symptoms of Atopic Dermatitis?
- Itching that can be severe (seems to be worse at night)
** “ITCH-SCRATCH” cycle can lead to infection
- good identifying factor
- ask if it’s affecting their quality of life –> if they can’t sleep b/c of it etc.
- Dry skin (may be cracked or scaly)
(worst in winter b/c dry air)
(better in summer b/c UV light & warmier)
What is the location of Atopic Dermatitis?
- Hands, feet, ankles, wrist, neck, inside bend of the elbows & knees
What is the epidemiology for Atopic Dermatitis of children?
- 10 -20% of children can develop AD
- Up to 65% of cases in children first occur before the age of 1 YEAR
- Approximately 80% of cases in children occur by the age of 5 YEARS
(b/t 1-5 years)
- Approximately 40% of those affected as children will develop AD again later in life
What is the epidemiology for Atopic Dermatitis of adults?
- 1 –3% of adults develop AD
- Approximately 1/2 of those with AD develop asthma later in life & 2/3 develop allergic rhinitis
What are the current thoughts for Atopic Dermatitis?
Complex disease that may be caused by impaired barrier function, infective agents, genetics & the environment
(Immune) Abnormalities in skin barrier
* IMPAIRED IMMUNE DEFENSE which can lead to an increased level of allergens,
irritants and bacteria entering the skin (triggers inflammation)
* POSSIBLE GENETIC PREDISPOSITION (filaggrin, increased IgE)
- low filaggrin in skin, more prone to dry skin; possibly AD
- lowers as we age
Environmental factors
* May activate the immune system leading to cytokines that cause inflammation
What is the “Outside-In” Model for Atopic Dermatitis?
(outside of skin to inside of skin)
- This model focuses on the defects in skin barrier function leading to inflammation
SKIN BARRIER DYSFUNCTION LEADS TO:
* Increase in water loss in the epidermis (itching)
* Increased risk of irritants, allergens and pathogens entering the skin
* Increased risk of bacterial & viral infections (Staph aureus in 80 –100% of AD patients)
- FILAGGRIN DEFICIENCY CAUSED BY A GENETIC DEFECT MAY CAUSE:
- Decreased hydration of the skin
- Bacterial skin colonization (mainly Staph aureus)
- Increased risk of allergen penetration into the skin
What is the “Inside-OUT” Model for Atopic Dermatitis?
- Immune dysfunction leading to increased IgE and barrier dysfunction
IMMUNE ABNORMALITIES
* Higher levels of IgE
** Imbalanced T-cell activity
* May have specific IgE environmental allergens (dust mites, grass, pets, pollen)
* Inflammation occurs and weakens the skin barrier
(disregulation of immune system)
What are pre-disposing factors of Atopic Dermatitis?
all related to dry skin; don’t cause AD, but make it worse
DECREASED HUMIDITY (caused by hot/cold, dry air or central heating)
* Decreased surface filaggrin & dry skin leading to itching
ENVIRONMENTAL ALLERGENS
* Harsh soaps (modify pH of skin, irritate the skin, causing dryness & increased
water loss from the skin)
* Dust mites, pollens, molds, animal dander (may worsen symptoms)
HOUSE DUST MITES
* Penetrate skin and worsen skin barrier dysfunction
INFECTIONS
* Staph aureus infections can cause “flare-ups”
STRESS
* May aggravate the condition
FOOD
* Defects in the skin barrier may contribute to food allergens
* Eczema may be an early indication of food allergies OR food allergies may be caused by AD (not as definite)
What is acne?
Chronic inflammatory condition of the pilosebaceous unit
When does acne begin?
Usually begins pre-puberty when sebaceous gland activity
increases
What is acne caused by?
Generally caused by increased sebum production & plugging of the follicles
- as we age sebum prod. decreases, so may not get it as much
Microcomedone:
- Obstructed sebaceous follicle
Whiteheads:
- Closed, plugged pores
- First visible sign of acne (about 5 months to develop)
- Tendency to rupture
- Non-inflammatory acne
Blackheads:
- Open, plugged pores
- Dark color due to melanin not dirt
- Larger & more stable than a whitehead
- Non-inflammatory acne
Papules:
- Small red bumps
Pustules (pimples):
- Papules with PUS at the tips
- Raised white lesion filled with pus
- Inflammatory acne
Nodules:
- Most severe type of acne
- Large, solid, painful lumps beneath the surface of the skin
- Inflammatory acne
What is the appearance of acne?
- Dependent on the severity of the condition
- Mild (a few papules/pustules)
- Moderate (some inflammatory lesions)
- Severe (larger number of non-inflammatory and inflammatory lesions with a few nodular lesions)
What is the location of acne?
- Face, neck, shoulders, chest and back
- generally more severe & maybe treated diff.
What is the epidemiology of acne?
Highest incidence in adolescents * 50% -95% adolescents
* 20% -30% for ages 20 –40 years old
- b/c sweat glands & sebaceous glands increase
Genetic relationship has been observed
* Higher occurrence in identical twins
* Positive family history
Approximately 90% of males and 80% of females experience acne before 21 years of age
- b/c sebum prod. is a little later in females
What is the pathophysiology of acne?
INCREASED SEBUM PRODUCTION
* Increase in circulating androgens increase the size & activity of sebaceous
glands
* Androgens control sebaceous gland secretions
* Sebum continues to increase & become trapped
* The sebum then solidifies forming a closed comedon
CHANGES IN THE KERATINIZATION PROCESS
* Keratinocytes become sticky & plug the follicles
COLONIZATION OF THE BACTERIA *Cutibacterium acnes (C. acnes)
* Normally found on the skin increases in numbers with pooling of the sebum
* Hydrolyzes sebum triglycerides into free fatty acids that may lead to an increase in keratinization formation
*(or may see P. acnes –> can be in animals as well, whereas C. acnes is more common in humans)
RELEASE OF INFLAMMATORY MEDIATORS IN ACNE SITES
* T-cells are generated in response to P acnes resulting in inflammation
What is Chickenpox (Varicella)?
CONTAGIOUS disease
- can be past the air
Caused by varicella-zoster
Incubation = 2 weeks after initial exposure
More severe in adults than children
Spread by coughing, sneezing or direct contact with the blisters
(get as a child - won’t get it twice)
What is Shingles (Herpes Zoster)?
- Likely NOT contagious
- Caused by varicella-zoster
- Rash begins a few days after the pain/tingling feeling begins
- Very painful (particularly on the face)
- Lasts 2 to 4 weeks but the pain can continue for much longer than that
What is Shingles (Herpes Zoster)?
- Likely NOT contagious
- but can maybe be if you touch it & then rub it in for ex
- Caused by varicella-zoster
- Rash begins a few days after the pain/tingling feeling begins
- Very painful (particularly on the face)
- Lasts 2 to 4 weeks but the pain can continue for much longer than that
- up to a year of pain b/c it’s sitting on nerves & sometimes stress can bring it out
(reactivates later on)
(more worried >50 but young ppl can get it too)
What is the appearance of Chickenpox (Varicella)?
- Rash (red on light skin, purple or dark brown on darker skin) that forms small, fluid filled, itchy blisters that scab
What is the location of Chickenpox (Varicella)?
- Typically starts on the chest, back and face
What is the symptoms of Chickenpox (Varicella)?
- Fever, fatigue, sore throat, headaches (last 5 to 7 days)
What is the appearance of Shingles (Herpes Zoster)?
- Rash (red on light skin, purple or dark brown on darker skin) with small, fluid filled, itchy blisters
- Appears on one side of the body in a band-like pattern
What is the location of Shingles (Herpes Zoster)?
- More common on the chest, upper or lower back and on one side of the body (affects the nerves)
What is the epidemiology of Chickenpox?
- Occurs all over the world
- Common disease in children
- Ages 4 to 10 years of age
What is the epidemiology of Shingles?
- Can occur at any age but is more common in those 50 - 60 years of age or older
- 1/5 adults can get it
What is the pathophysiology of Chickenpox & Shingles?
- Exposure to the virus causes the production of immunoglobulin G, M and A
- Varicella is thought to spread from mucosal & epidermal lesions to sensory nerves & remains dormant
- spit etc.
- Immune system prevents the virus from causing further infections
- REACTIVATION LATER in life results in herpes zoster (shingles) but it is unknown why
(stress can disturb an area & get shingles)
What is Alopecia mean?
hair loss
Androgenetic alopecia:
- Hereditary with shortened growth stage, decreased hair
thickness and hair loss - common in both m & f
Telogen effluvium:
- Excessive hair shedding & thinning possibly due to hormonal
changes, stress, serious illness, extreme weight loss
(>300 hairs lost - normal is 75-100 daily)
Anagen effluvium:
- Sudden and severe hair loss over entire scalp due to
chemotherapy, radiation and some medications
(reversible)
Alopecia areata:
- Autoimmune inflammatory disorder with patchy hair loss
Traction alopecia:
- Loss caused by excessive pulling of the hair (tight buns, ponytails, braids & hair extensions
What is the pathophysiology of Alopecia Areata?
Thought to be an AUTOIMMUNE, INFLAMMATORY CONDITION that affects hair follicles and the nails
* Associated with pre-existing autoimmune disorders
* Defect in the immune system that results in increased T-cells
and antibodies
FAMILY HISTORY CONNECTION
ENVIRONMENTAL FACTORS (can make it worse)
* Physical or emotional stress
* Comorbidities (depression, anxiety, thyroid disease, psoriasis, rheumatoid arthritis)
* Infections that create stress on the body
* Hormonal changes
What is Hyperhidrosis?
- EXCESSIVE SWEATING that affects quality of life
- CHRONIC condition
What is Primary Hyperhidrosis?
- Unknown cause
- Underarm most common
- Hands, feet, scalp & groin are less common
What is Secondary Hyperhidrosis?
Caused by environmental triggers
* Excessive heat or humidity
* Medical conditions (infections, hyperthyroidism, obesity)
* Medications (some antipsychotics, antidepressants and morphine)
(may see it on bottoms of feet where we normally don’t see it)
What is the pathophysiology of primary Hyperhidrosis?
Likely involves hyperactivity or dysfunction of the autonomic
nervous system involving sympathetic & parasympathetic pathways
- May have a genetic component as well (more research to be done)
What is the pathophysiology of secondary Hyperhidrosis?
Likely caused by medical conditions or medications that may increase acetylcholine release
- May have a genetic component as well (more research to be done)
