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PATH 300 > Skin Disorders > Flashcards

Skin Disorders Flashcards

1
Q

What is the largest organ in our body?

A

The skin is our largest organ.

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2
Q

What are the external and internal factors involved in skin disease?

A
  • External factors include allergens/irritants, sunshine, heat/cold, chemicals, infections, and trauma.
  • Internal factors include psychological factors, genetic factors, internal diseases, drugs, and infections.
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3
Q

What are the different types of cells in the skin and their functions?

A

The skin contains keratinocytes (which shed all the time), melanocytes (which make melanin), Langerhans cells (a variant of macrophages), dendritic cells, Merkel cells (which have a sensory function), and blood vessels in the dermis.

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4
Q

What is the function of the sebaceous and sweat glands in the skin?

A

The sebaceous gland secretes a lubricant that keeps the skin moist, and the sweat gland secretes sweat to regulate body temperature.

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5
Q

What is atopic dermatitis and what are its risk factors?

A

Atopic dermatitis is a common skin condition, especially in children. Its risk factors include genetic predisposition, environmental factors, immunologic mechanisms, and epidermal barrier dysfunction.

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6
Q

What is the main feature of atopic dermatitis?

A
  • The main feature of atopic dermatitis is a genetic defect in barrier function, leading to abnormal tight junctions, filaments, and secretions.
  • This results in barrier damage, more antigen-presenting cells, release of Th2 cells in lymph nodes, and cytokines that cause even more barrier damage.
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7
Q

What is dermatitis herpetiformis and how is it linked to celiac disease?

A

Dermatitis herpetiformis is a condition characterized by immune complex deposition in the skin, specifically IgA deposition at the dermo-epidermal junction. It is linked to celiac disease because IgA antibodies against gliadin (a gluten product) in the intestinal mucosa enter circulation and deposit in the skin, triggering an inflammatory response.

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8
Q

What is allergic contact dermatitis and what causes it?

A

Allergic contact dermatitis is a classical reaction to substances like poison ivy and nickel, as well as skin creams, perfumes, etc. It is a type IV hypersensitivity reaction and involves a cell-mediated immune reaction.

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9
Q

What is the role of desmosomes and Hemidesmososmes in the skin?

A

Desmosomes are the main component that holds the keratinocytes together. Hemidesmosomes at the bottom anchor the basal layer of the skin down, giving the skin its mechanical strength.

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10
Q

What is the immune function of the skin?

A
  • The skin’s immune function involves a barrier layer that keeps many pathogens out.
  • If pathogens do get in, normal and Langerhans cells monitor with their extensions.
  • Keratinocytes can release cytokines and migrate to lymph nodes.
  • T-cells can be stimulated by dendritic cells. Dendritic cells are antigen-presenting cells and can migrate to local lymph nodes in response to exposure to allergens.
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11
Q

What are the features of severe cases of atopic dermatitis?

A

Severe cases of atopic dermatitis involve thickening of the epidermis and dermis, infiltration of many T cells, immune activation with T cells and cytokines, and Th2 cells releasing IL-4 and IL-13. Therapy is directed against Th2 cytokines – IL-4 and IL-13.

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12
Q

how does allergic dermatitis occur?

A

Small molecules (haptens) bind to self-proteins forming antigens. Dendritic cells are activated, migrate to regional lymph nodes, stimulating effector T cell formation. Primed T cells migrate to skin. Subsequent exposure leads to T cells releasing cytokines and chemokines producing the allergic reaction and skin lesions.

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13
Q

What is the role of keratinocytes in the skin?

A

Keratinocytes are cells in the skin that shed all the time. They play a crucial role in providing a barrier to environmental damage by heat, UV radiation, water loss, pathogenic bacteria, fungi, parasites, and viruses.

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14
Q

What is the role of melanocytes in the skin?

A

Melanocytes are cells located at the base of the skin. They produce melanin, which is taken up by keratinocytes. The amount of melanin taken up by the keratinocytes determines the color of the skin.

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15
Q

What is the role of Langerhans cells in the skin?

A

Langerhans cells are a type of dendritic cell found in the skin’s epidermal layer. They are a variant of macrophages and play a role in the skin’s immune response.

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16
Q

What is the role of Merkel cells in the skin?

A

Merkel cells are found in the skin and hair follicles. They have a sensory function and are associated with nerve endings to perceive touch.

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17
Q

What is the role of blood vessels in the skin?

A

Blood vessels in the dermis provide nutrients and oxygen to the skin. They also help regulate body temperature by adjusting the flow of blood to the skin’s surface.

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18
Q

What is the role of sebaceous glands in the skin?

A

Sebaceous glands are found in the skin and secrete an oily substance called sebum. This helps to lubricate and waterproof the skin and hair.

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19
Q

What is the role of sweat glands in the skin?

A

Sweat glands are found in the skin and secrete sweat. This helps to cool the body when it overheats and also plays a role in excreting waste products.

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20
Q

What is the role of the skin’s immune function?

A

The skin’s immune function involves a barrier layer that keeps many pathogens out. If pathogens do get in, normal and Langerhans cells monitor with their extensions. Keratinocytes can release cytokines and migrate to lymph nodes. T-cells can be stimulated by dendritic cells. Dendritic cells are antigen-presenting cells and can migrate to local lymph nodes in response to exposure to allergens.

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21
Q

What is psoriasis and what is its prevalence?

A

Psoriasis is an autoimmune disease with a prevalence of 3%. It often occurs with other autoimmune diseases or arthritis.

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22
Q

What are the typical sites for psoriasis?

A

Typical sites for psoriasis include the scalp, knees, and elbows.

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23
Q

What triggers psoriasis?

A

Psoriasis is triggered by a combination of genetic and environmental factors. It involves all cell types in the epidermis and dermis, including T-cells, keratinocytes, IL-17, TNFa, etc., and involves both innate and acquired immunity.

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24
Q

What are the degrees of burns and how are they categorized?

A

Burns are categorized by the depth of injury into 1st to 4th degree. 1st degree burns affect just the epidermis and will heal. 2nd degree burns affect the dermis. 3rd degree burns affect the fat layer, and 4th degree burns affect the muscle.

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25
Q

What is acne and what events are involved in its development?

A

Acne is a chronic inflammatory disease in the pilosebaceous unit. It involves increased sebum production, increased keratinocyte proliferation, inflammation, and bacteria. It involves both innate and adaptive immunity.

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26
Q

What types of UV radiation penetrate the atmosphere and what are their effects?

A

UVC does not penetrate the atmosphere. UVB penetrates the epidermis and is responsible for sunburn and immunosuppression. UVA reaches the dermis. Both UVA and UVB cause premature aging and cancer.

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27
Q

What is vitiligo and what causes it?

A

Vitiligo is characterized by the autoimmune destruction of melanocytes in discrete patches. It is caused by circulating antibodies and autoreactive T cells in lesions.

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28
Q

What is the effect of tanning on the skin?

A

Tanning is a reaction to injury and leads to broken vessels, wrinkles, pigmented blotches, etc. It causes changes in the skin such as the formation of darker moles or patches and can also cause damage to blood vessels.

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29
Q

What is the role of the transcription factor GATA6 in acne?

A

The transcription factor GATA6 restrains the proliferation of keratinocytes and sebocytes. It is downregulated in acne.

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30
Q

How is severe acne treated?

A

Severe acne is treated with retinoic acid, which stimulates GATA6 expression.

31
Q

What is cystic acne and how is it treated?

A

Cystic acne is a severe form of acne that is treated with isotretinoin.

32
Q

What is the role of melanin in protecting the skin from sun damage?

A

Melanin, produced by melanocytes, blocks light from reaching deeper layers of the skin, providing a protective mechanism against sun damage.

33
Q

What are the effects of tanning on the skin?

A

Tanning, a reaction to injury, leads to broken vessels, wrinkles, pigmented blotches, etc. It can cause changes in the skin such as the formation of darker moles or patches and can also cause damage to blood vessels.

34
Q

What percentage of aging is due to sun damage?

A

90%

35
Q

How does UVB cause immunosuppression?

A

UVB radiation suppresses the immune system, reducing its ability to fight off infections and diseases. This immunosuppressive effect is one reason why exposure to sun helps with mild psoriasis.

36
Q

How does UV induce vitamin D synthesis

A

UV radiation from the sun triggers the conversion of a compound in the skin into vitamin D3, which is then converted into the active form of vitamin D in the body.

37
Q

What is the rule of 9s in estimating burn area?

A

The rule of 9s is a method used to estimate the area of a burn. Each body part has a percent surface area, which is used to assess the total body surface area affected by the burn.

38
Q

Which skin types are more susceptible to damage?

A

Darker skin types are more protected and less susceptible to damage.

39
Q

What are the three types of skin cancer?

A

The three types of skin cancer are basal-cell carcinoma, squamous-cell carcinoma, and melanoma

40
Q

What is the most common type of skin cancer?

A

The most common type of skin cancer is basal-cell carcinoma.

41
Q

What is a common site for metastasis in skin cancer?

A

brain

42
Q

What are the ABCD characteristics of melanoma?

A

The ABCD characteristics of melanoma refer to Asymmetry, Border irregularity, Color variation, and Diameter greater than 6mm.

43
Q

What has been a major breakthrough in skin cancer therapy?

A

Immune checkpoint inhibitors have been a major breakthrough in skin cancer therapy.

44
Q

How can skin cancer be prevented?

A

Skin cancer prevention methods include wearing hats, protective clothing, and applying sunblock.

45
Q

What is Athlete’s Foot and how is it treated?

A

Athlete’s Foot is a highly contagious fungal infection that lives on keratin. It is now easily treated.

46
Q

What causes warts and where are they commonly found?

A

Warts are caused by human papilloma viruses and cause epidermal hyperplasia. They are commonly found on the hands and feet.

47
Q

What happens if basal-cell carcinoma and squamous-cell carcinoma are not removed?

A

If not removed, basal-cell carcinoma and squamous-cell carcinoma can grow and potentially spread to other parts of the body, causing serious health problems.

48
Q

Why is melanoma considered lethal?

A

Melanoma is considered lethal because it can spread quickly to other parts of the body if not detected and treated early

49
Q

What are immune checkpoint inhibitors and how do they help in skin cancer therapy?

A

Immune checkpoint inhibitors are a type of cancer treatment that block proteins made by some types of immune system cells and cancer cells. These proteins help keep immune responses in check and can keep T cells from killing cancer cells. When these proteins are blocked, the “brakes” on the immune system are released and T cells are able to kill cancer cells more effectively.

50
Q

What is the role of keratin in Athlete’s Foot?

A

Athlete’s Foot is a fungal infection that lives on keratin, a protein found in the outer layer of skin, hair, and nails.

51
Q

What is epidermal hyperplasia in the context of warts?

A

Epidermal hyperplasia is the thickening of the outermost layer of the skin. In the context of warts, it is caused by the human papilloma viruses which stimulate the rapid growth and multiplication of keratinocytes, leading to the formation of warts.

52
Q

Skin diseases and their frequency vary depending on what?

A

geography and age

53
Q

barrier function of the skin?

A

keeps out pathogens and ideally allergens, continually being turned over, can be abnormal in disease

54
Q

what is dermatitis?

A

Inflammation of the skin

55
Q

what are risk factors of atopic dermatitis?

A
  • genetic predisposition
  • environmental
  • immunologic mechanisms
  • epidermal barrier dysfunction
56
Q

what is normal filaggrin function?

A

aggregates keratin filaments and creates natural moisturizing factor.

57
Q

what is the therapy for dermatitis herpetiformis?

A

gluten-free diet

58
Q

what is the difference between acute and chronic allergic dermatitis?

A

Acute: will go away (happens when touch something once)
Chronic: when exposed to something all the time

59
Q

what triggers psoriasis and what downstream effects does this cause?

A
  • Triggered by overexpression of antimicrobial peptide LL37 (released by keratinocytes), activating dendritic cells.
  • Cytokines from dendritic cells and macrophages activate Th17 cells triggering chronic inflammation.
60
Q

pathology of psoriasis

A
  • thick layer of epidermis
  • Greatly accelerated production of keratinocytes with epidermal hyperplasia (b/c of cytokines) and deep ridges
  • Increased extension, density, and permeability of dermal capillaries, meaning that they are easily traumatized
61
Q

how does cell turnover compare in normal vs people with psoriosis?

A

normal turnover is 50 days, but here is 5 days – 10x more

62
Q

when does the onset for psoriasis usually occur?

A

adult, but can occur in children

63
Q

in psoriasis, __% have changes in toenails and fingers

A

50%

64
Q

what is the effect of the release of IL-17 and IL-22 in psoriosis?

A

induce epidermal hyperproliferation.
- keratinocytes secrete more inflammatory cytokines
- neutrophils are recruited, and a vicious circle is maintained

65
Q

what is the treatment for mild and severe psoriasis cases?

A
  • Mild cases respond to the immunosuppressive effects of sunlight
  • Severe cases effectively treated with antibodies to IL-17 (gives rapid reversal in over 80% of people)
66
Q

who is more vulnerable to burns?

A

children

67
Q

what is the animal model for acne?

A

there is none, it is a complex disease with multiple components

68
Q

what are the events involved in acne?

A
  1. Increased sebum production, sebocytes stimulated by androgens, leptin, many other factors.
  2. Increased keratinocyte proliferation
  3. Inflammation (neurophiles, macrophages, T-cells, etc.)
  4. Bacteria: skin microbiome may be abnormal and general bacteria growth is promoted.
69
Q

what is the therapy for acne?

A

various drugs decrease sebum production, antibacterial drugs, can normalize pattern of keratinization.

70
Q

role of melanin in tanning

A

UV simulates the increase production, serving as a protective mechanism (blocks light from reaching deeper in the skin)

70
Q

what are the two types pf pigment, giving the variations in skin colour?

A

eumelanin (dark brown to black) and pheomelanin (yellow to red in colour)

71
Q

what is the therapy for viltigo?

A

Harmless, no cure, small areas may respond to phototherapy.

72
Q

what are changes seen in the skin due to aging from sun damage?

A
  • Cause dense abnormal elastic fibres.
  • Keratinocyte necrosis triggers inflammation.

PATH 300 (9 decks)

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