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Flashcards in Lecture 1 Deck (95):
1

What is UVC light?

A light that is antibacterial (Bacterial light)

2

What is UVB light?

290 to 320 nm (short wavelength)
Can cause sunburn, skin carcinoma and premature aging of skin.
Produces vitamin D3 in the skin

3

What is UVA light?

320 to 400 NM (longer wavelength)
Produces tanning and drug related photosensitivity.
Able to penetrate further into the dermis than UVB radiation.
No erythema because it is 800 to 1000 times less energetic than UVB radiation.

4

What are the factors that affect tanning?

Time (10AM - 2PM have highest radiation)
Clouds (60-80% still gets through)
Reflection (Snow reflects 85-100% and water reflects 95%)
Location (equator)
Clothing
Thickness of epidermis and stratum corneum.
Pigmentation of the skin.

5

What are the skin types?

I - Always burns, never tans
II - Always burns easily, tans minimally.
III - Sometimes burns and tans gradually
IV - Burns minimally, always tans well
V - Rarely burns, tans profusely
VI - Never burns, deeply pigmented.

6

What is the tanning mechanism of UVA?

Immediate pigmentation: Oxidizes the melanin already in the epidermis. Pigment darkening starts 5-10 minutes after exposure. Lasts 24 to 48 hours.

Delayed pigmentation: UVAA stimulates the increase in the number of melanocytes and increased pigment in these cells. Takes about 48 to 72 hours to develop after exposure. Peaks at 7 to 10 days and lasts weeks to months.

7

What is the tanning mechanism of UVB?

Stimulate epithelial cell growth making skin thicker.
Growth of the skin spreads melanin through more layers of the skin.
This protects the skin by absorbing and scattering additional UV radiation.
UVA hyperpigmentation does not protect skin long term as much as UVB hyperpigmentation.

8

What should you take soon after you think you have a sun burn?

NSAIDs and antihistamines

9

If sun poisoning is expected what should you do?

Refer to the ER.

10

What happens when you have a sunburn?

UVB penetrates into the dermis and causes an inflammatory reaction. Histamine, cytokines and prostaglandins are released. Symptoms are mild erythema, tenderness and edema.

11

What is a severe sun burn?

AKA Sun Poisoning
Second degree burn with blisters.
Fever, chills, weakness and shock.

12

What is MED?

minimal erythemal dose
The minimum single dose of UV radiation that produces clearly marginated erythema in the irradiated site.
1 MED - pink
2 MED - bright erythema
4 MED - painful sunburn
8 MED - blistering burn

13

What is SPF?

Sun Protection Factor
= MED of protected skin/MED of unprotected skin

14

The higher the SPF..

The less likely to burn
the longer time that can be spent in the sun.

15

How much percentage of UVB rays does each one block:
SPF 15
SPF 30
SPF 50

SPF 15 blocks 93%
SPF 30 blocks 97%
SPF 50 blocks 98%

16

What is the best SPF to pick?

between 15 and 30

17

If you are of skin type 1 or 2 what SPF should you choose?

greater than 30
greater than 40 for Lupus
greater than 45 for photosensitizing drugs

18

If you are of skin type III or V what SPF should you choose?

SPF 15 to 24

19

When does skin start to burn?

The moment you are EXPOSED!!

20

Adding a higher SPF after 1 MED will not help much. T/F

True

21

How often should you re-apply very water-resistant sunscreen?

80 minutes

22

What are some drugs that cause photosensitivity?

Tetracycline
Coal tar products
Diuretics
Estrogens and progestins
NSAIDs
Sulfonylureas

23

What is substantivity?

Ability to stay on skin and remain effective.
Alcohols

24

How often should you re-apply water-resistant sunscreen?

40 minutes

25

How often should you re-apply sweat-resistant sunscreen?

30 minutes

26

What are the sunblock products?

Zinc oxide
Titanium dioxide
Red petrolatum

27

What is the mechanism of action for sunblocks?

A physical sunscreen.
Reflects or scatters 100% of all UV radiation from 290 to 760 nm

28

When should you use a sunblock?

When you cannot limit or control sun exposure.
Usually used on prominently exposed areas like nose and ears..

29

What are the side effects of sunblocks?

May occlude pores causing miliaria, folliculitis or acne.
May stain clothing.
Not easily removed with water, but melts in hot sun.
Protection decreases after 2 hours of direct sun contact.

30

What are the chemical classes of sunscreens?

Para-aminobenzoic acid (PABA)
Cinnamates
Salicylates
Benzophenones
Anthrainalates
Dibenzoylmethane

31

Which chemical classes are UVB protection only?

Para-aminobenzoic acid (PABA)
Cinnamates
Salicylates

32

Which chemical classes are UVA and UVB (broad spectrum) protection?

Benzophenones
Anthrainalates
Dibenzoylmethane

33

What is the generic name of PABA?

Octyl dimethyl PABA
Padimate O

34

What is the generic name of Cinnamates?

Octyl Methoxycinnamate
Ethyhexyl p-methoxycinnamate

35

What is the generic name of salicylates?

2-ethyhexyl salicylate
homosalate

36

What is the generic name of benzophenones?

Oxybenzone
Dioxybenzone

37

What is the generic name of anthranilates?

Menthyl anthraniliate

38

What is the generic name of dibenzoylmethane?

Avobenzone

39

What is the mechanism of action of all sunscreens?

Absorbs UVB radiation (does not bounce off)
All classes of sunscreens can absorb some UVB radiation.
All sunscreens are a combination of products.

40

What is important about PABA?

Binds to skin proteins ( so people may be allergic to it)
Most antigenic sunscreen
You should apply an hour before sun exposure.
The most effective at absorbing UVB rays.
May stain clothing.

41

What is important about cinnamates?

It does not adhere to skin well and depends on the vehicle for substantivity.
non-staining.

42

What is important about salicylates?

Weak sunscreen
Does not adhere to the skin well
Easily removed by water or perspiration.

43

What is important about benzophenones?

Poor substantivity
Can cause sensitization

44

What is important about anthranilates?

Absorbs UVA radiation up to 370 nm
Used only in combination products to give broad UV coverage.

45

What is important about dibenzoylmethanes?

Absorbs mostly in the UVA range. Least in the UVB.
Activity starts to decrease after 15 minutes of use.

46

What is the anatomy of the skin?

Epidermis (dead):
Stratum corneum
Stratum germinativum - new skin cells are produced.

Dermis:
Location of the capillaries, nerves, glands. Beginning of hair root. Able to reproduce because they receive O2 and nutrients.

Hypodermis:
Adipose Tissue
Areolar Tissue

47

What do the keratinocytes do?

Make keratin which is a waxy substance that waterproofs the skin, prevents evaporation.

48

What do melanocytes do?

Make the color. Important for sun protection..

49

Where is the highest concentration for sebaceous glands?

Faces, scalp, back, and neck.

50

What is sebum?

glycerides, wax esters, and cholesterol.
Retards water loss from the skin

51

What is acne vulgaris?

AKA zits
A common, self-limiting disease of the pilosebaceous units of the skin, typically located on the face, upper back, and chest.

52

What are the types of non-inflammatory acne?

Closed comedone
Open comedone

53

What is closed comedone?

Non-inflammatory acne
Does not contain pus
Has a white color to it (White head - not what is normally called a white head by normal people)

54

What is an open comedone?

non-inflammatory acne
Has a little black spot on it.
Open to the environment (oxidizes melanin, gives it a black color- blackhead)

55

What are the types of inflammatory acne?

They are all pimples(small, prominent, inflamed elevation of the skin) and can be categorized as:
Papule - an inflammatory comedo that resembles a small (

56

When do males typically develop acne?

12-18 and resolves by mid 20's

57

When do females typically develop acne?

15-17 years; persists in 30s and 40s in 30% of women

58

What is the pathosphysiology of acne?

Increased androgen production in both sexes.
Follicular Hyperkeratiniaztion
Sebum Prodcution

59

Increased androgen production leads to what three factors that correspond to acne development?

Follicular Hyperkertinzation (causes skin to stick together)
Increasaed sebum production (Increased gland size/number)
Proliferation of propionibacterium acnes (sebum is their food source)

60

How does acne form?

Skin cells stick together and are not shed. Channel is plugged by a combination of skin cells and sebum. Normal flow of sebum is blocked.

61

How does Propionibacterium acnes cause acne?

It produces lipase which breaks down glyceride form sebum into free fatty acids (inflammatory to the skin). Free fatty acids irritate the follicular walls. Have an antigenic effect.

62

What are exacerbating factors to acne?

High humidity or sweating (Swell the keartinocytes and causes more sticking)
Acne mechanica (Anything that occludes the skin or irritates it like a baseball cap)
Occupational acne (Excessive dirt, vaporized cooking oil, exposure to some industrial chemicals)
Acne Cosmetica (mild form of acne to comediogenic oils like lanolin, mineral oil, cocoa butter in cosmetics)
Severe and prolonged periods of stress or emotions.
Hormones
Acne medica mentosa (drug induced acne)
Genetics

63

What are medications that can cause acne medica mentosa?

Phenytoin
Isoniazid
Moisturizers
Phenobarbital
Lithium
Estrogen
Steriods
(Azathioprine, quinine and rifampin)

64

Acne can not be caused by...

Diet (Chocolate, Fried Foods, and Sugar)
Poor personal hygiene
Sex

65

What is Psoriasis?

Not excema
Chronic disease characterized by recurrent exacerbations and remissions of thickened, erythematous and scaling plaques.

66

Evidence suggests that psoriasis has a genetic basis that requires environmental triggers to activate the disease. T/F

True

67

Men have psoriasis more often than woman. T/F

False they get it equally

68

What is the cause of psoriasis?

Unknown but there are several hypotheses:
Defects in the epidermal cell cycle
Genetic disposition
Immunologic disorders

69

What is the pathophysiology of psoriasis?

There is a defect in the epidermal cell cycle.
Only takes 1.3 days to divide and 4 days to mature and shed(7 times faster than normal!!!)
T cells contribute to the hyperproliferation of the epidermis.
Grows abnormal, scab-like skin.

70

Psoriasis is genetic and immunologic. T/F

True

71

What is the pathophysiology of psoriasis as an immunologic disorder?

Keratinocytes encounter an antigen or undergo trauma. Inflammatory triggers result in recruitment of T lymphocytes to the site. Histocompatibility complex triggers release of T-cell cytokines, resulting in vasodilation and new capillary formation (angiogenesis). T cell cytokines also result on further inflammation. Arachidonic acid levels become elevated (rate limiting state to create prostaglandins and leukotrienes).

72

What are contribution factors for psoriasis?

Cold/dry climates
Stress
Infections (Especially after strep infections)
Trauma - Koebner response - lesions begin at previous clear sites on skin as a result of trauma

73

What medications may causes psoriasis?

Lithium and Beta Blockers

74

What is the descriptions of psoriasis vulgaris (plaque)?

Sharply demarcated erythemateous papules covered with thick silvery scales.
Salmon-pink lesion underneath with pinpoint bleeding (Ausptiz sign)
Lesions most common elbows, knees, sacrum, limbs, hands, and SCALP.
However lesions can occur anywhere.
Most common form of psoriasis. Pruritis may occur in 20% of patients. Mildly painful but can be highly itchy.

75

What is the descriptions of guttate psoriasis (eruptive)?

Sudden eruption of pinpoint (0.5 - 1.5 cm) dark-red lesions
Located on Trunk and limbs.
Frequently found in young adults. Frequently preceded by a strep infection.

76

What is the descriptions of inverse psoriasis?

Smooth patches of red, inflamed, skin.
Armpits, groin, under the breasts, around the genitals, in skin folds.
More common in overweight people.
Worsened by friction and sweating.

77

What is the descriptions of pustular psoriasis (Von Zumbusch)?

Generalized eruption of painful erythematous plaques with rows or clusters of yellow 2-3 cm pustules.
May be generalized or localized to the palms and soles of the feet.
Accompanied with fever and malaise.
May be resistant to treatment by must treat aggressively.

78

What is the descriptions of erythrodermic psoriasis?

Generalized erythema with little or no scaling that can lead to a generalized desquamation skin peeling off of body. Effects all body sites, covering 75% of body surface area. Most severe form which may lead to death. May occur secondary to injury or pustular may to this form.

79

What are the other types of psoriasis?

Nail Psoriasis -pitting, ridging discoloration, and onycholysis

Psoriasis arthritis - Asymmetric involvement in hands, feet, and knee joints. Skin lesions usually precede joint involvement. Lacks elevation of rheumatoid factors and autoantibodies seen in rheumatoid arthritis.

80

What is dermatitis?

A dermatological condition that presents as a rash, dry skin and itching.

81

What is dermatitis caused by?

Allergies - atopic dermatitis, eczema or contact dermatitis
Genetics
Stress

82

What is the atopic triad?

Asthma, Allergic rhinitis, and Atopic dermatitis.
Exaggerated skin and mucosal reactivity to environmental stimuli

83

What are the three peak occurrences of the atopic triad?

Infant (6 months)
Children (under 14 years)
Adults

84

What are the phases of an allergic response?

Sensitization phase - an initial exposure, the allergic substance binds to epidermal proteins to form an antigen. Antibodies and T-cells are formed to the antigen.
Elicitation Phase - Upon subsequent exposures, hypersensitivity reaction occurs.

85

What are the signs and symptoms of allergic dermatitis?

Red to brownish-gray colored patches that look like chapping.
Pruritis which may be severe especially at night.
Small, raised vesicles which may leak fluids and crust over when scratched.
Thickened, cracked or scaly skin.
Raw, sensitive skin from scratching.
Secondary bacterial infections are common (staph infection)

86

What is the location of atopic dermatitis?

Hands and feet are the most common sites in adults and face and scalp are most common in children.
Elbows, behind the knees, ankles, wrists, neck and upper chest.
Skin around eyes including eyelids.

87

What are exacerbating factors of atopic dermatitis?

Exposure to allergens - foods, soaps, detergents, fragrances and chemicals.
Long, hot baths or showers.
Dry skin
Stress
Sweating
Rapid changes in temperature or low humidity
Solvents, cleaners, soaps, and detergents.
Wool or man-made fabrics or clothing.

88

Atopic dermatitis, contact dermatitis, and eczema are all the same disease. T/F

True

89

What are the allergic constituents of plant dermatitis?

Urushiol

90

What is the etiology of plant dermatitis?

An initial exposure, the urushiol binds to epidermal proteins to form an antigen.
Upon secondary exposure a hypersensitivity reaction occurs.
Lasts for 14-20 days.

91

What is a diaper rash?

An acute, transient inflammatory skin condition in the diaper area caused by either moisture, occlusion, chafin, continued contact with urine or feces or both, or mechanical or chemical irritation.

92

What are the symptoms of a diaper rash?

Mild - Mild erythema
Moderate - Erythema with maceration and chaffin (skin is flaking off)
Severe - papules, vesicles, oozing, ulceration, and secondary infection.

93

What are the benefits of breast-feeding?

babies urinate less frequently
Urines is less alkaline so not as irritating

94

How does the retention of fluids in a diaper cause diaper dermatitis?

Soiled diapers will hydrate the stratum corneum and swell.
The keratin will block the sweat glands.
Vesicle formation and irritation will occur.

95

What are the complications of diaper dermatitis?

Fungal and bacterial infections are the most common complication.
Candida albicans
Staphylococcus aureus (bacterial)
Cutaneous infections are secondary to untreated or improperly treated diaper rash.