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Applied Pathophysiology > Skin Lesions / Non-Infectious Diseases (Common Skin Conditions) > Flashcards

Skin Lesions / Non-Infectious Diseases (Common Skin Conditions) Flashcards

1
Q

What are the functions of the skin?

A

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
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2
Q

What is our largest organ?

A

SKIN

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3
Q

Skin Anatomy

A
  • 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

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4
Q

What are the 3 layers of skin?

A
  1. Epidermis
  2. Dermis
  3. Subcutaneous (Hypo-dermis)
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5
Q

What is the Epidermis & what is its function?

A
  • 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)

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6
Q

What is the Dermis & what is its function?

A
  • 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
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7
Q

What is the Subcutaneous (Hypo-dermis) & what is its function?

A
  • Provides the body with buoyancy and is a storehouse for energy within the fat layers
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8
Q

Epidermis dets

A
  • 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
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9
Q

What are the Epidermis layers?

A
  • Stratum corneum
  • Granular cell layer (stratum granulosum)
  • Squamous cell layer (stratum spinosum)
  • Basal cell layer (stratum basale)
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10
Q

Epidermis

Stratum corneum layer

A
  • 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)

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11
Q

Epidermis

Granular cell layer (stratum granulosum)

A
  • 1 to 3 cells thick
  • Flattened cells
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12
Q

Epidermis

Squamous cell layer (stratum spinosum)

A
  • 5 to 10 cells thick
  • cells become keratinized (give cell colour - melan in it)
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13
Q

Epidermis

Basal cell layer (stratum basale)

A
  • Controls the renewal of new cells
  • Cells renew approximately 28 days and move upward to the SC
    (from basal up to SC)
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14
Q

Epidermis

Keratinocytes:

A
  • 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)

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15
Q

Where are Keratinocytes (epidermis) produced?

A
  • Produced in the squamous layer to stratum corneum (loose nuclei & flatten as they move through the layers)
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16
Q

What are the Epidermis cell types?

A
  • Langerhans cells: (2 - 8%)
  • Basal Cells
  • Merkel cells: (6-10%)
  • Melanocytes: (5%)
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17
Q

Langerhans cells:

A

(2 - 8%) in epidermis
* Detects, attacks, neutralizes & eliminates foreign bodies
- involved in T-cell

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18
Q

Basal Cells:

A
  • Precursor to keratinocytes

in epidermis

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19
Q

Merkel cells:

A

(6-10%) in epidermis
* Stimulates sensory nerves such as touch * High concentration in fingertips

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20
Q

Melanocytes:

A

(5%) in epidermis
* Responsible for pigment production * Gives hair and skin color

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21
Q

What epidermis cells are in the squamous cell layer?

A

Langerhans cells

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22
Q

What epidermis cells are in the basal cell layer?

A

Basal Cells

Merkel cell

Melanocytes

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23
Q

What is the function of the dermis?

A
  • Provides structural integrity

(not connected to many common skin conditions)
- protects body from injury

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24
Q

What is the main component of dermis?

A
  • Main component is collagen & elastin fibers
  • Collagen = stress resistant material
  • Elastin fibers = maintain elasticity of the skin
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25
Q

What does the dermis consist of?

A
  • Connective tissue
  • Blood vessels
  • Sweat glands (apocrine, eccrine glands)
  • Nerves
  • Hair follicles/roots
  • Oil (Sebaceous glands)
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26
Q

What are the 3 types of sweat glands?

A
  • Eccrine sweat glands
  • Apocrine sweat glands
  • Apoeccrine sweat glands
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27
Q

Eccrine sweat glands:

A
  • Responsible for body cooling
  • Found mainly on the palms, soles of the feet, face, head & body trunk

(produce NO odor)

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28
Q

Apocrine sweat glands:

A
  • 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
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29
Q

Apoeccrine sweat glands:

A
  • Structural features of eccrine & apocrine glands
  • Found only in the underarm area of adults

(develop during puberty - odorless)

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30
Q

Where do Sebaceous glands reside?

A

Reside primarily in the dermis

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31
Q

Where is the highest # of sebaceous glands found?

A

on the face and scalp

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32
Q

What doe the cells within the sebaceous glands contain?

A

sebum (lipid droplets)

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33
Q

What does sebum consist of?

A

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

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34
Q

What would happen if we had sebaceous glands on our feet?

A

we’d glide around

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35
Q

Where do hair follicles begin from?

A

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)
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36
Q

What are hair follicles connected to?

A

connected to sebaceous glands that provide sebum to the hair

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37
Q

What are the 3 stages of hair growth?

A
  1. Anagen phase (active growing, lasts 2 to 6 years and
    determines hair length)
  2. Transitional or catagen phase (follicle degenerates, stops growing, lasts 2 to 3 weeks)
  3. Telogen or resting phase (shedding occurs, last 3 to 4 months)
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38
Q

How do you know if someone has a hair loss problem?

A
  • 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)
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39
Q

What is Pediatric Skin like?

A
  • 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)

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40
Q

What is Aged Skin like?

A
  • 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)

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41
Q

What is Psoriasis?

A
  • 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
42
Q

What is the epidemiology of Psoriasis?

A
  • 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)

43
Q

What is the age of onset for Psoriasis?

A
  • Mean age: ~ 23–37 years

Current theory:
2 distinct peaks with possible genetic associations
* Early onset
* Late onset

44
Q

What is the early onset for Psoriasis?

A

(16–22 years)
* More SEVERE and EXTENSIVE
* More likely to have affected first-degree family member

45
Q

What is the late onset for Psoriasis?

A

(57–60 years)
* MILDER form
* Affected first-degree family members nearly absent

46
Q

What is Psoriasis’ current theory?

A
  • 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
47
Q

Describe the Abnormal Keratinocyte Proliferation

A
  • 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
48
Q

What are external triggers of Psoriasis?

A

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”
49
Q

What are the types of Psoriasis? Describe them

A
  1. Chronic plaque (psoriasis vulgaris)
  2. Guttate
    * Triggered by bacterial infections
    * Small drop-shaped scales on trunk, arms or legs (rash)
  3. Flexural
    * Smooth, well-defined patches
    * Affects body folds & genitals
  4. Erythrodermic
    * Red rash that peels and itches
  5. Pustular
    * Appears as pus filled lesions in patches
  6. Psoriatic arthritis
    * Swollen, painful joints similar to arthritis
  7. Scalp
    * Red, itchy areas with silver- white scales on the scalp
  8. Nail
    * Affects finger & toe nails
    * Pitting, abnormal growth & discoloration
50
Q

What is Plaque Psoriasis?

A
  • Vulgaris = common
  • Most common form (80 - 90% of patients)
51
Q

What is the appearance of Plaque Psoriasis?

A
  • 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
52
Q

What is the location of Plaque Psoriasis?

A
  • Trunk (lower back), genitals, face, palms, soles and nails
  • Occurs on the extensor surfaces of forearms & shins (elbows, knees)
53
Q

What is Atopic Dermatitis like in infants ((3 – 6 months of age)?

A
  • Weeping patches, crusted plaques on the face, neck and extensor surfaces
54
Q

What is Atopic Dermatitis like in childhood (before 5 years of age)?

A
  • Dry, flaking, rough, cracked areas
  • Irritation of the flexural skin (back of the knees) (or behind elbow)
  • in specific areas
55
Q

What is Atopic Dermatitis like in Adult?

A
  • Dry, scaly areas
  • Flexural areas, hands, face and upper trunk
56
Q

What is the appearance of Atopic Dermatitis?

A
  • 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
57
Q

What are the symptoms of Atopic Dermatitis?

A
  • 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)

58
Q

What is the location of Atopic Dermatitis?

A
  • Hands, feet, ankles, wrist, neck, inside bend of the elbows & knees
59
Q

What is the epidemiology for Atopic Dermatitis of children?

A
  • 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
60
Q

What is the epidemiology for Atopic Dermatitis of adults?

A
  • 1 –3% of adults develop AD
  • Approximately 1/2 of those with AD develop asthma later in life & 2/3 develop allergic rhinitis
61
Q

What are the current thoughts for Atopic Dermatitis?

A

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

62
Q

What is the “Outside-In” Model for Atopic Dermatitis?

A

(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
63
Q

What is the “Inside-OUT” Model for Atopic Dermatitis?

A
  • 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)

64
Q

What are pre-disposing factors of Atopic Dermatitis?

A

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)

65
Q

What is acne?

A

Chronic inflammatory condition of the pilosebaceous unit

66
Q

When does acne begin?

A

Usually begins pre-puberty when sebaceous gland activity
increases

67
Q

What is acne caused by?

A

Generally caused by increased sebum production & plugging of the follicles
- as we age sebum prod. decreases, so may not get it as much

68
Q

Microcomedone:

A
  • Obstructed sebaceous follicle
69
Q

Whiteheads:

A
  • Closed, plugged pores
  • First visible sign of acne (about 5 months to develop)
  • Tendency to rupture
  • Non-inflammatory acne
70
Q

Blackheads:

A
  • Open, plugged pores
  • Dark color due to melanin not dirt
  • Larger & more stable than a whitehead
  • Non-inflammatory acne
71
Q

Papules:

A
  • Small red bumps
72
Q

Pustules (pimples):

A
  • Papules with PUS at the tips
  • Raised white lesion filled with pus
  • Inflammatory acne
73
Q

Nodules:

A
  • Most severe type of acne
  • Large, solid, painful lumps beneath the surface of the skin
  • Inflammatory acne
74
Q

What is the appearance of acne?

A
  • 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)
75
Q

What is the location of acne?

A
  • Face, neck, shoulders, chest and back
  • generally more severe & maybe treated diff.
76
Q

What is the epidemiology of acne?

A

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

77
Q

What is the pathophysiology of acne?

A

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

78
Q

What is Chickenpox (Varicella)?

A

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)

79
Q

What is Shingles (Herpes Zoster)?

A
  • 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
80
Q

What is Shingles (Herpes Zoster)?

A
  • 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)

81
Q

What is the appearance of Chickenpox (Varicella)?

A
  • Rash (red on light skin, purple or dark brown on darker skin) that forms small, fluid filled, itchy blisters that scab
82
Q

What is the location of Chickenpox (Varicella)?

A
  • Typically starts on the chest, back and face
83
Q

What is the symptoms of Chickenpox (Varicella)?

A
  • Fever, fatigue, sore throat, headaches (last 5 to 7 days)
84
Q

What is the appearance of Shingles (Herpes Zoster)?

A
  • 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
85
Q

What is the location of Shingles (Herpes Zoster)?

A
  • More common on the chest, upper or lower back and on one side of the body (affects the nerves)
86
Q

What is the epidemiology of Chickenpox?

A
  • Occurs all over the world
  • Common disease in children
  • Ages 4 to 10 years of age
87
Q

What is the epidemiology of Shingles?

A
  • Can occur at any age but is more common in those 50 - 60 years of age or older
  • 1/5 adults can get it
88
Q

What is the pathophysiology of Chickenpox & Shingles?

A
  • 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)

89
Q

What is Alopecia mean?

A

hair loss

90
Q

Androgenetic alopecia:

A
  • Hereditary with shortened growth stage, decreased hair
    thickness and hair loss
  • common in both m & f
91
Q

Telogen effluvium:

A
  • Excessive hair shedding & thinning possibly due to hormonal
    changes, stress, serious illness, extreme weight loss
    (>300 hairs lost - normal is 75-100 daily)
92
Q

Anagen effluvium:

A
  • Sudden and severe hair loss over entire scalp due to
    chemotherapy, radiation and some medications

(reversible)

93
Q

Alopecia areata:

A
  • Autoimmune inflammatory disorder with patchy hair loss
94
Q

Traction alopecia:

A
  • Loss caused by excessive pulling of the hair (tight buns, ponytails, braids & hair extensions
95
Q

What is the pathophysiology of Alopecia Areata?

A

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

96
Q

What is Hyperhidrosis?

A
  • EXCESSIVE SWEATING that affects quality of life
  • CHRONIC condition
97
Q

What is Primary Hyperhidrosis?

A
  • Unknown cause
  • Underarm most common
  • Hands, feet, scalp & groin are less common
98
Q

What is Secondary Hyperhidrosis?

A

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)

99
Q

What is the pathophysiology of primary Hyperhidrosis?

A

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)
100
Q

What is the pathophysiology of secondary Hyperhidrosis?

A

Likely caused by medical conditions or medications that may increase acetylcholine release

  • May have a genetic component as well (more research to be done)

Applied Pathophysiology (34 decks)

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