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

Question

What does the dermis consist of?

Answer 1

* Connective tissue * Blood vessels * Sweat glands (apocrine, eccrine glands) * Nerves * Hair follicles/roots * Oil (Sebaceous glands)

Answer 2

* Eccrine sweat glands * Apocrine sweat glands * Apoeccrine sweat glands

Answer 3

* Responsible for body cooling * Found mainly on the palms, soles of the feet, face, head & body trunk (produce NO odor)

Answer 4

* 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

Answer 5

* Structural features of eccrine & apocrine glands * Found only in the underarm area of adults (develop during puberty - odorless)

Answer 6

Reside primarily in the dermis

Answer 7

on the face and scalp

Answer 8

sebum (lipid droplets)

Answer 9

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

Answer 10

we'd glide around

Answer 11

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)

Answer 12

connected to sebaceous glands that provide sebum to the hair

Answer 13

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)

Answer 14

- 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)

Answer 15

* 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)

Answer 16

* 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)

Answer 17

* 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

Answer 18

* 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)

Answer 19

* Mean age: ~ 23–37 years Current theory: 2 distinct peaks with possible genetic associations * Early onset * Late onset

Answer 20

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

Answer 21

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

Answer 22

* 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

Answer 23

* 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

Answer 24

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”

Answer 25

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

Answer 26

* Vulgaris = common * Most common form (80 - 90% of patients)

Answer 27

* 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

Answer 28

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

Answer 29

* Weeping patches, crusted plaques on the face, neck and extensor surfaces

Answer 30

* Dry, flaking, rough, cracked areas * Irritation of the flexural skin (back of the knees) (or behind elbow) - in specific areas

Answer 31

* Dry, scaly areas * Flexural areas, hands, face and upper trunk

Answer 32

* 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

Answer 33

* 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)

Answer 34

* Hands, feet, ankles, wrist, neck, inside bend of the elbows & knees

Answer 35

* 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

Answer 36

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

Answer 37

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

Answer 38

(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

Answer 39

* 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)

Answer 40

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)

Answer 41

Chronic inflammatory condition of the pilosebaceous unit

Answer 42

Usually begins pre-puberty when sebaceous gland activity increases

Answer 43

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

Answer 44

* Obstructed sebaceous follicle

Answer 45

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

Answer 46

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

Answer 47

* Small red bumps

Answer 48

* Papules with PUS at the tips * Raised white lesion filled with pus * Inflammatory acne

Answer 49

* Most severe type of acne * Large, solid, painful lumps beneath the surface of the skin * Inflammatory acne

Answer 50

* 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)

Answer 51

* Face, neck, shoulders, chest and back - generally more severe & maybe treated diff.

Answer 52

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

Answer 53

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

Answer 54

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)

Answer 55

* 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

Answer 56

* 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)

Answer 57

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

Answer 58

* Typically starts on the chest, back and face

Answer 59

* Fever, fatigue, sore throat, headaches (last 5 to 7 days)

Answer 60

* 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

Answer 61

* More common on the chest, upper or lower back and on one side of the body (affects the nerves)

Answer 62

* Occurs all over the world * Common disease in children - Ages 4 to 10 years of age

Answer 63

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

Answer 64

* 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)

Answer 65

* Hereditary with shortened growth stage, decreased hair thickness and hair loss - common in both m & f

Answer 66

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

Answer 67

* Sudden and severe hair loss over entire scalp due to chemotherapy, radiation and some medications (reversible)

Answer 68

* Autoimmune inflammatory disorder with patchy hair loss

Answer 69

* Loss caused by excessive pulling of the hair (tight buns, ponytails, braids & hair extensions

Answer 70

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

Answer 71

* EXCESSIVE SWEATING that affects quality of life * CHRONIC condition

Answer 72

* Unknown cause * Underarm most common * Hands, feet, scalp & groin are less common

Answer 73

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)

Answer 74

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)

Answer 75

Likely caused by medical conditions or medications that may increase acetylcholine release * May have a genetic component as well (more research to be done)