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PHAR 300 (Kim) > Drugs & Cosmetics > Flashcards

Drugs & Cosmetics Flashcards

1
Q

Melanocytes are

A

cells that synthesize and eject melanin (pigment)

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2
Q

Blood supply for skin situated

A

in the dermis ends at the base of the epidermis.

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3
Q

How the skin is given the colour?

A

Ejected melanin from melanocytes are taken up by surrounding keratinocytes, the epidermal cells.

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4
Q

Exposure to UV light stimulates

A

melanocytes production and insertion of melanin –> tan.

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5
Q

Psoriasis is

A

immune reaction that causes hyper-proliferation of keratinocyte at the surface of the skin.

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6
Q

UVA in skins

A

better able to penetrate the skin, getting to the base of the dermis.

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7
Q

UVB in skins

A

reaches the epidermis (surface of the skin)

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8
Q

What makes less vulnerable to injury due to UV light?

A

Melanin does protect to some extent (people with darker skin)

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9
Q

What makes more vulnerable to injury due to UV light>

A

light skin, particularly people with freckles.

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10
Q

Photoaging is

A

skin damage by sun.

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11
Q

3 different types of cancers due to sun damage:

A

Basal cell carcinoma
Melanoma (most lethal type)
Squamous cell carcinoma
Basal cell carcinoma + squamous cell carcinoma = commun skin cancer.

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12
Q

SPF (sun protective factor) mean

A

indicate how effective the application will be ( ex. if use SPF 15, you can stay outside 15 more minutes before get sun burn.

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13
Q

Problems occurring in acne:

A

Increase in keratin production (Duck occlusion)
Increase sebum production (block the duck)
Inflammation of sebaceous gland that can rupture
Growth of microorganisms in the duct (release inflammatory mediator)

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14
Q

Blackhead is due to

A

Abnormal keratinocytes (produce excess amount of keratin) + sebum blocking the duct = becoming oxidized and darkening colour.

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15
Q

What make change a blackhead to a whitehead (pimple)?

A

If the trapped sebum is closed over, you can get bacteria and leukocytes.

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16
Q

Whitehead is due to

A

comedo closed with bacterial growth and inflammation with rupture of the follicle (cause the bump)

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17
Q

Retinoid roles:

A

normalize follicular keratinization

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18
Q

tx for acne:

A 
retinoids
benzoyl peroxide
isotretinoin
sulfur
azelaic acid
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19
Q

Retinoid are

A

Vit A derivatives

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20
Q

Action of Vitamin A

A

Act as hormones, altering gene expression and play major role in cellular differentiation.

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21
Q

Conversion of Vit A:

A

Retinol–> retinaldehyde–> retinoid acid

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22
Q

Retinol enter into the cell by

A

binding to Retinoic binding protein (RBP) after enter unbind.

23
Q

Retinol to nucleus steps:

A

Bind to cellular retinol binding protein (CRBP)–> retinol convert to retinoic acid (RA)–> bind to 2e carrier: CRABP–> transport into nucleus. In the nucleus, RA bind to RXR and RAR –> RARE –> gene expression

24
Q

Two retinoic receptors:

A

RXR and RAR (dimer) (form heterodimer)

25
Q

How retinoic acid turns on gene expression?

A

Dimer RXR and RAR (retinoic receptor) activated and bind to the retinoic acid response element (RARE).

26
Q

Accutane is

A

(Isotretinoin) a systemic retinoid. (orally)

27
Q

Contra-indication:

A

Female who might possibly get pregnant or is pregnant.

TERATOGEN

28
Q

Anti-herpes drugs action:

A

Inhibit viral reproduction mechanism by inhibiting viral DNA polymerase–>cause chain termination.

29
Q

Antiviral drugs for herpes example:

A

AcycloGTP

30
Q

The cuticle is

A

outside layer of the hair (layer of death cells)

31
Q

The cortex is

A

central part of the hair (microfibril and macrofibril)

32
Q

microfibrils are made up of

A

protofibrils

33
Q

anagen is

A

the growth of the hair phase

34
Q

catagen is

A

transition phase

35
Q

telogen is

A

the resting phase

36
Q

the normal cycle of hair follicle:

A

Anagen–>catagen–>telogen–>hair ejected and falls out.

Cycle starts over.

37
Q

Growth and shedding(fall out) of hair peaking in:

A

summer

38
Q

During pregnancy, hair tend to:

A

increase (anagen) and shedding tend to decrease.

Pregnancy prevent the follicles from stopping their growth.

39
Q

After delivery, the hair tend to:

A

lots of hair to fall out bc extra hair follicles in growth phare are immediately go into shedding phase.

40
Q

Curliness of hair is based on the chemistry of hair. The structure:

A

Hydrogen bonds can form between two adjacent hair shaft, or disulfide bonds (stronger).

41
Q

Getting a ‘‘prem’’:

A
  1. breaking disulfide bonds with first chemical
  2. re-forming disulfide bonds with second chemical in curly structure position of hair
    = curly permanet hair!
42
Q

Male pattern baldness:

A

thick terminal hairs of the head are replaced by fine, vellus hairs.
Higher level of 5a reductase–> Increase DHT

43
Q

Why female do not loss all hair with predisposition of balness?

A

bc less androgen

44
Q

Product for baldness that do work:

A

Minoxidil

Finasteride (propecia)

45
Q

Minoxidil action:

A

increase size of the follicle

prolongs the growth phase of the hair (prevent transition into small follicles producing vellus hairs)

46
Q

Finasteride (propecia) action:

A

Blocks the production of Dihydrotestosterone (DHT)

47
Q

Finasteride contra-indication:

A

Pregnant women –> TERATOGEN for male fetuses

48
Q

Tetracyclines effect on teeth?

A

Discoloration

49
Q

Hydroxyapatite is

A

crystal structure in enamel (surface part of teeth)

50
Q

Fluoride effect:

A

enter the hydroxyapatite to change it and produce fluoroapatite.

51
Q

Fluoroapatite advantages

A

more resistant to acid in plaque

More resistant to substances released by bacteria

52
Q

Dental fluorosis is

A

white spot in theeth, harmless

53
Q

Gingivitis can be tx with

A

mouthwash (phenols as active ingredient)

PHAR 300 (Kim) (19 decks)

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