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PHAR 303 (toxicology) > Skin and Eye > Flashcards

Skin and Eye Flashcards

final exam

1
Q

why do we have skin?

A
  • mechanical support
  • neurosensory
  • environmental barrier
  • many physiological roles –
  • thermal regulation
  • metabolism
  • regulate blood flow, fur and hair, sweat
  • electrolyte regulation
  • immune function
  • hormone function
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2
Q

layers of the skin

A
  1. epidermis
  2. dermis
  3. hypodermis
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3
Q

what is found throughout the layers of the skin?

A
  • hair follicles
  • sweat glands
  • innervation
  • vascular supply
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4
Q

which cells make up the epidermis?

A
  • langerhans cells
  • melanocytes
  • merkel cells
  • keratinocytes
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5
Q

what is the top layer of the epidermis

A

stratum corneum

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6
Q

function of Langerhan cells

A

part of the immune system (take up and process antigens) – antigen presenting cells

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7
Q

function of melanocytes

A

make pigment and insert into keratinocytes

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8
Q

function of Merkel cells

A

respond to touch (mechanosensors)

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9
Q

what makes up the stratum corneum?

A
  • dead keratinocytes called corneocytes
  • held by desmosomes and lipids
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10
Q

lifetime +path of keratinocytes

A
  • last 4 weeks
  • keratinocytes make their way up to the top of epidermis
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11
Q

role of stratum corneum

A

barrier that conserves moisture

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12
Q

why does the biology of the epidermis matter for toxicology?

A

Thickness varies in different parts of the body (important for dermal absorption):
- palms of hands/soles of feet have thick stratum corneum to resist abrasion
- thinnest region is behind the ear (drugs readily absorbed)
- thin skin has many hair follicles
Children have thinner skin:
- vulnerable to damage and absorption of molecules

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13
Q

role/function of the dermis

A
  • thermoregulation
  • supply the avascular epidermis with nutrients
  • secrete substances that give support and elasticity of the skin.
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14
Q

what makes up the dermis? what do they do?

A

fibroblasts which are responsible for secreting collogen, elastin, and ground substances.
They are also import for wound healing.

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15
Q

how can toxins and toxicants pass through the skin?

A
  • intracellular (through tight sections between cells)
  • via glands or hair
  • transcellular (when lipophilic)
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16
Q

which type of compound can go through the skin?

A

small, lipophilic molecules (e.g. toluene, benzene, carbon tetrachloride)

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17
Q

what are reasons why the barrier (skin) can be impaired?

A
  • disease
  • abrasion
  • elevated water content
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18
Q

examples of solvents?

A

toluene and turpentine

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19
Q

where is toluene used?

A

paint thinner and permanent markers

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20
Q

properties of industrial solvents, what does this tell us?

A

small, lipophilic, so can be absorbed through skin

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21
Q

what are effects of some industrial solvents?

A
  • cause local irritation
  • dissolve the lipid barrier (damages skin and makes it more susceptible)
  • systemically absorbed (can have effect on nervous system)
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22
Q

how is nicotine from a patch absorbed? what are the pharmacokinetics?

A
  • Slowly and steadily absorbed through skin
  • Gets directly into blood stream (no first pass)
  • but, some first-pass effect in skin since has some P450s, and phase 2 enzymes.
23
Q

what is dermatitis?

A

inflammation of the skin

24
Q

what is contact dermitis?

A

inflammation of the skin through contact with toxicants

25
Q

what are the main types of contact dermititis?

A
  • irritant
  • allergic
26
Q

what is irritant dermatitis?

A
  • Inflammatory response
  • No single mechanism of action – many cytokines
  • Intensity related to dose
  • Great individual variability
27
Q

types of chronic irritation

A
  • chronic irritation
  • acute irritation
28
Q

what is chronic irritation? what causes it?

A
  • irritant dermatitis from repeated exposure
  • from mild irritants such as soaps, detergents, solvents
29
Q

what is acute irritation? what causes it?

A
  • also called 2nd-degree chemical burn
  • substantially disrupts the cornified layer
  • strong acids, alkalies, oxidizing & reducing agents
30
Q

what does wet cement cause? why?

A

acute irritation
- is very alkaline (pH 12-14)
- sand and small particles irritate the skin
- Can’t feel burn from basic substances right away

31
Q

what is allergic dermatitis? when does it occur?

A
  • delayed (T-cell mediated) hypersensitive reaction
  • occurs when a molecule (called hapten) generates an allergic reaction
32
Q

mechanism of allergic dermatitis

A
  • hapten penetrate the lipid barrier and become attached to carrier proteins
  • hapten + carrier protein = antigen
  • antigens are processed by Langerhans cells
  • Langerhans cells present antigen to T cells in lymph nodes
  • T cells become “activated” and proliferate
  • over a 1–3 week period, activated T cells are generated and enter the circulation
  • then, when there is a 2nd contact, activated T cells induce inflammatory reaction (limited to area of 2nd exposure)
33
Q

what causes allergic dermatitis?

A
  • plants such as poison oak, poison ivy, henna
  • metals such as nickel
  • rubber from things such as gloves
  • glue (e.g. band-aids)
  • drugs (e.g. polysporin/neosporin)
34
Q

differences between irritant and contact dermatitis

A

irritant:
- more common
- from local toxic effect
- affects everyone; no sensitization required
- reaction soon after
- repeated exposure is required
- lesion restricted to area of exposure
- burning

allergic:
- less common
- delayed type hypersensitivity reaction
- sensitization required
- delayed reaction (hrs to days)
- small amount of allergen is enough
- localized but may be more diffuse
- no burning

35
Q

Exposure from light comes from what?

A
  • sun
  • indoor tanning
  • UVA (deeper) and UVB (UVC doesn’t reach us)
36
Q

why is it that UVC doesn’t reach us?

A

has a lower wavelength, so More energy = more reactions, causing more intense effects = don’t penetrate through atmosphere or skin as deep

37
Q

when can phototoxicity occur? what type of reaction occurs? what can cause it?

A

when certain compounds react with sunlight and damage skin
- not an immunologic response
- meaning no prior exposure to the photosensitizing agent is required

  • can be due to tattoo ink, drugs (antibiotics, Chlorpromazine), and plants (carrot, citrus, legume)
38
Q

which compound in plants is the most common reason for phototoxicity?

A

furanocoumarins (i.e. psoralen)

39
Q

mechanism of furanocoumarins

A
  • activated by long-wavelength UVA light
  • interacts with DNA covalently, causing DNA damage
40
Q

what is a Photocarcinogen?

A

substance which causes cancer when an organism is exposed to it + light

41
Q

how do photocarcinogens get activated (by which mechanism)?

A
  • after illumination, compound transitions to an excited state
  • compound becomes more chemically reactive
  • light can also cleave photocarcinogens, resulting in free radicals
42
Q

what is phtoallergy?

A

Photocontact dermatitis occurs upon exposure to sunlight:
- compound absorbs UV light, converted to hapten, type IV hypersensitivity reaction

43
Q

what can cause a photoallergic response?

A
  • antibacterial soaps (hexachlorophene)
  • drugs (antihistamines such as diphenhydramine)
  • ingredients in cosmetics (musk, sandalwood oil, ..)
44
Q

what is Urticaria? what happens?

A
  • means hives
  • type I or “anaphylactic” reaction, mediated by release of IgE and release of histamine
  • causes increases the permeability of capillaries to white blood cells/proteins (to engage pathogens in infected tissues)
45
Q

symptoms of Urticaria

A
  • wheals (red bumps)
  • itching
  • hayfever
  • bronchial asthma
46
Q

what can cause urticaria?

A

-plants
-latex
-antibiotics

47
Q

How do we determine sensitization using animals and cells?

A
  • Guinea pig maximization test
  • Mouse local lymph node assay (LLNA)
  • in vitro cell culture (Keratinocytes, and Langerhans)
  • in vitro skin irritancy test (EpiSkin)
48
Q

which part of the eye is more susceptible to toxicant injury?

A

anterior part of the eye (which faces out to world) – includes the Cornea, conjunctive and eyelids

49
Q

what is the main effect of compounds that are toxic to the retina, optic nerve, and visual cortex?

A

visual impairment

50
Q

which compounds can lead to visual impairment?

A

lead, methanol, methyl mercury

51
Q

does the eye contain metabolizing enzymes?

A

yes, both phase 1 and 2

52
Q

what are some ways to test toxicity in the eye?

A
  • used to use rabbits
  • now use isolated chicken eye
  • bovine corneal opacity permeability (normal is not very opaque)
  • Short Time Exposure In Vitro Test
53
Q

explain the Short Time Exposure In Vitro Test to look at eye toxicity.

A

Method for Identifying
i) Chemicals Inducing Serious Eye Damage
ii) Chemicals Not Requiring Classification for Eye Irritation or Serious Eye Damage
Test consists of:
- monolayer of Statens Seruminstitut
Rabbit Cornea (SIRC) cells
- 96-well plate MTT assay

54
Q

what are some household hazards?

A
  • paint thinner, cement
  • plants, UV light, insecticides, weeds, bees
  • cleaning products, bleach, medicine, Neosporin, band aids, antibacterial soaps
  • latex, oven cleaner
  • cosmetics, houseplant, nickel

PHAR 303 (toxicology) (14 decks)

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