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Pathophys > Skin Diseases > Flashcards

Skin Diseases Flashcards

1
Q

What is a macule?

A

flat discolored lesion less than 1 cm in diameter

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2
Q

What is a patch?

A

flat discolored lesion greater than 1 cm in diameter

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3
Q

What is a papule?

A

firm elevated lesion less than 1 cm

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4
Q

What is a plaque?

A

firm elevated lesion greater than 1 cm

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5
Q

What is a vesicle?

A

elevated, fluid-filled lesion less than 1 cm

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6
Q

What is a bulla?

A

elevated, fluid-filled lesion greater than 1 cm

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7
Q

What is a pustule?

A

vesicle or bulla that contains pus (not clear fluid)

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8
Q

What is a nodule?

A

firm elevated lesion (equal in diameter and in thickness)

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9
Q

What is an ulcer?

A

crater in skin (goes to epidermis, can go down to dermis)

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10
Q

What is a fissure?

A

small linear crack in skin

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11
Q

What lesion is equal in diameter and in thickness?

A

nodule

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12
Q

What lesion goes to the dermis and, in some cases, can also go down to the dermis?

A

ulcer

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13
Q

What is another name for contact dermatitis?

A

spongiotic or inflammatory dermatitis

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14
Q

What type of inflammatory cells are moving into the affected area in contact dermatitis?

A

lymphocytes

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15
Q

What type of cells are separating in the epidermis in contact dermatitis?

A

keratinocytes

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16
Q

Separation in the epidermis in pts with contact dermatitis is caused by what?

A

edema

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17
Q

What can severe edema cause in pts with contact dermatitis?

A

separation from dermis and epidermis

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18
Q

What does contact dermatitis look like under a microscope?

A

looks like a sponge (spaces between cells in epidermis)

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19
Q

What is contact dermatitis caused by? Give two examples:

A

skin coming into contact with allergen
ex: poison ivy / latex allergy

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20
Q

Describe contact dermatitis lesions:

A

localized, erythematous papules/pustules/vesicles and sometimes pustules

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21
Q

What type of hypersensitivity is contact dermatitis?

A

type IV hypersensitivity

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22
Q

How do you treat contact dermatitis?

A

topical corticosteroids

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23
Q

What is another name for psoriasis?

A

psoriasiform dermatitis

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24
Q

Psoriasis is an inflammatory disorder with epidermal ______.

A

thickening

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25
Q

Psoriasis is associated with what other inflammatory condition?

A

psoriasis arthritis

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26
Q

What percent of the population does psoriasis affect?

A

1-2% of the population
(possible genetic origin)

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27
Q

When is psoriasis typically manifested?

A

teenage years

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28
Q

What is the acute phase of psoriasis characterized by?

A

erythematous plaques

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29
Q

What is the chronic phase of psoriasis characterized by?

A

white with silvery scales

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30
Q

In the chronic phase of psoriasis, what causes the silvery scales?

A

epidermal thickening

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31
Q

Where is psoriasis typically found on the body?

A

scalp, trunk, extensor surfaces of arms/legs

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32
Q

What is the theory behind the cause of psoriasis?

A
  • antigens stimulate an immune response
  • T cells are activated
  • increase of cytokines led to inflammation
  • causes epidermal hyperplasia

NEGATIVE FEEDBACK LOOP

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33
Q

What are rete ridges commonly seen in histopathological images of psoriasis?

A

where the epidermis dips down

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34
Q

What is epidermopoiesis?

A

epidermal proliferation

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35
Q

Pt’s with psoriasis have how many more keratinocytes than someone with normal skin?

A

30x more keratinocytes

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36
Q

How long does it take for normal skin to shed?

A

2-3 weeks

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37
Q

In normal skin turnover, the cells of the stratum corneum are dead and lack what?

A

lack a nucleus

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38
Q

In psoriatic skin turnover, the cells of the stratum corneum have _____.

A

have nuclei

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39
Q

How long does it take for dead skin cells to surface in pts with psoriasis?

A

2-3 days

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40
Q

What is it called when cells of the stratum corneum have nuclei?

A

parakeratosis

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41
Q

Why do pt’s with psoriasis present with silvery scales?

A

because cell turnover is so fast and the skin cells haven’t shed yet

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42
Q

In pts with psoriasis, the endothelial cells become thickened. What does this cause?

A

dilated capillaries in dermis

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43
Q

What are the treatments for psoriasis?

A
  • corticosteroids
  • immunosuppressives (methotrexate)
  • biologics
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44
Q

What are two biologics that are used to treat psoriasis?

A

Humira and Otezla

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45
Q

Urticaria is commonly known as what?

A

hives

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46
Q

What type of hypersensitivity is urticaria?

A

Type I hypersensitivity

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47
Q

What are two skin diseases that are histamine related?

A

urticaria and atopic dermatitis

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48
Q

What type of lesions present with urticaria?

A

erythematous papular lesions (sometimes macular lesions)

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49
Q

Urticaria causes histamine to be released, what does this cause?

A
  • vasodilation and increased capillary permeability
  • stimulates nerve endings
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50
Q

What is a result of increased capillary permeability in pts with urticaria?

A
  • pruritus (inc. cap. perm. stimulates nerve endings)
  • vascular leasions
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51
Q

Urticaria is primarily caused from:

A
  • ingested foods (shellfish / peanuts)
  • medications
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52
Q

What type of dermatitis is lichen planus?

A

interface type of dermatitis (between epidermis and dermis)

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53
Q

Describe the lesions of lichen planus:

A

violet/purple papular lesions

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54
Q

What type of reaction is lichen planus?

A

cell mediated immune reaction

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55
Q

What is a cell mediated immune reaction?

A

where damage to keratinocytes occurs

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56
Q

Lichen planus can be a result of some medications. Give an example of two of these medications:

A
  • Therapeutic gold (for arthritis)
  • Antimalarials (Plaquenil)
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57
Q

What type of cell infiltration occurs at the epidermis/dermis border of lichen planus?

A

lymphocytic infiltration

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58
Q

What are the white areas in lichen planus?

A

keratinocytes dying and leaving spaces at border

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59
Q

In lichen planus, what happens in the epidermis where keratinocytes used to be?

A

vacuolation (formation of vacuoles)

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60
Q

Cells with necrotic keratinocytes can be seen in histological images of what skin disease?

A

lichen planus

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61
Q

Necrotic keratinocytes are also called what?

A

colloid bodies

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62
Q

Atopic dermatitis is also known as what?

A

eczema

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63
Q

What type of hypersensitivity is atopic dermatitis?

A

type I hypersensitivity

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64
Q

Atopic dermatitis in adults becomes hard, what is this called?

A

kinofied

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65
Q

What two things will you see increased in blood work of a pt with atopic dermatitis?

A

increased eosinophils and IgE

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66
Q

What is a common trigger for eczema (atopic dermatitis)?

A

change in temperature/humidity

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67
Q

What are some treatments for eczema?

A
  • topical corticosteroids
  • sometimes histamines
  • biologics (dupixent)
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68
Q

What biologic treats atopic dermatitis?

A

dupixent

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69
Q

What type of dermatitis is bullous pemphigoid?

A

a type of vesiculobullous dermatitis

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70
Q

What type of disease is bullous pemphigoid?

A

autoimmune disease (produces Ab against Ag in basement membrane)

71
Q

Epidermal cells hold onto basement membranes via junctions. What are these junctions called?

A

hemidesmosomes

72
Q

What are within hemidesmosomes?

A

antigens

73
Q

What happens to the skin in bullous pemphigoid? (hint: two things)

A
  1. epidermis separates from dermis completely
  2. dermal cells separate from basement membrane
74
Q

Where do blisters occur in bullous pemphigoid?

A

oral mucosa, extremities, lower trunk

75
Q

What proves IgG is produced against basement membranes in bullous pemphigoid?

A

immunofluorescence

76
Q

What is the treatment for bullous pemphigoid?

A

Prednisone (corticosteroid)

77
Q

What causes scleroderma?

A

IDIOPATHIC (but probably autoimmune disease)

78
Q

What is scleroderma?

A

systemic disease of abnormal collagen deposition

79
Q

Where is collagen deposited in scleroderma?

A

in blood vessels

80
Q

What occurs as a result of collagen deposits in blood vessels in a pt with scleroderma?

A
  • decrease in blood vessel diameter
  • decrease blood flow to organs in body/skin
81
Q

What is fibrosis and what happens when skin becomes fibrotic?

A
  • fibrosis = excessive collagen in dermis
  • skin becomes tight = pts unable to move fingers
82
Q

In severe cases of scleroderma, what happens?

A

can affect pt’s mouth/eyes (won’t be able to move them)

83
Q

Leukocytoclastic vasculitis (LCV) is an inflammatory process of what?

A

blood vessels

84
Q

What is one manifestation of systemic disease in pts with leukocytoclastic vasculitis (LCV)?

A

skin

85
Q

What is a trigger that causes leuokocytoclastic vasculitis in pts?

A

infection or medication

86
Q

Describe the inflammatory process of leukocytoclastic vasculitis:

A
  • Ab binding to Ag forms immune complex
  • complex sits in blood vessel walls
  • cascade of complement system occurs
  • complement causes infiltration of inflammatory cells
87
Q

What is attacked first in leukocytoclasic vasculitis (LCV)?

A

venules

88
Q

What is the most permeable blood vessels we have?

A

venules

89
Q

What causes the reddish brown papular lesions in leuokocytoclasic vasculitis?

A

inflammatory cells & fibrin leak out and separates epidermis from dermis

90
Q

What is the treatment for leukocytoclastic vasculitis?

A

corticosteroids

91
Q

What is cellulitis?

A

bacterial infection of dermis and hypodermis

92
Q

What can cellulitis sometimes look like?

A

DVT

93
Q

Describe cellulitis:

A

deep reddish color, warm to tough, very painful

94
Q

What does erysipelas mean?

A

bacterial infection of upper demis

95
Q

What are furuncles?

A

boils (red elevated nodule)

96
Q

Furuncles are an infection of what?

A

hair follicle

97
Q

What is cellulitis caused by?

A

staph aureus or strep

98
Q

What is impetigo caused from?

A

staph aureus or group A strep

99
Q

Impetigo is common in who? Is it contagious?

A

in children, very contagious

100
Q

How does impetigo start out as?

A

little vesicles

101
Q

The brown crusted lesions in pts with impetigo are formed how?

A

from ruptured little vesicles (very itchy)

102
Q

How do you treat impetigo?

A

topical abx

103
Q

What is acute necrotizing fasciitis?

A

flesh eating disease

104
Q

Acute necrotizing fasciitis is primarily due to what?

A

group A strep, especially staph pyogenes

105
Q

How does acute necrotizing fasciitis usually start?

A

starts as minor trauma or simple infection

106
Q

T/F acute necrotizing fasciitis goes down to epidermis

A

FALSE: goes down to epidermis AND dermis

107
Q

Acute necrotizing fasciitis can go down to subcutaneous tissue and fascia around muscles. What does this cause?

A
  • fascia becomes edematous
  • blocks small blood vessels
  • cuts off blood supply = can cause tissues to die
108
Q

What can acute necrotizing fasciitis sometimes look like?

A

cellulitis

109
Q

What symptoms can a pt develop if they have acute necrotizing fasciitis?

A
  • fever
  • hypotension
  • tachycardia
    = can lead to toxic shock
110
Q

How do you treat necrotizing fasciitis?

A

find out what bacteria is toxic
- topical abx, fluids, decried necrotic tissue

111
Q

What might need to happen if debridement of necrotic tissue becomes too much?

A

amputation

112
Q

Why does necrotizing fasciitis get so severe so quickly?

A

because no one recognizes the symptoms of the flesh eating disease

113
Q

What is the mortality rate of necrotizing fasciitis?

A

20-30%

114
Q

What type of reaction is erythema nodosum and what does it involve?

A

panniculitis type of rxn = involves subcutaneous fat

115
Q

What type of hypersensitivity is erythema nodosum?

A

delayed-type of hypersensitivity

116
Q

What can trigger erythema nodosum?

A

stress, IBS, estrogen oral contraceptive

117
Q

Who is erythema nodosum most common in?

A

3x more common in women

118
Q

What becomes thick due to an inflammatory process in erythema nodosum?

A

septa between lobules of fat

119
Q

Where can you find lesions in pts with erythema nodosum?

A

anterior aspect of lower extremities

120
Q

Describe the lesions of erythema nodosum:

A

firm, painful reddish-brown nodules

121
Q

Where does herpes simplex virus remain latent?

A

in sensory ganglion of the trigeminal nerve

122
Q

Where is herpes simplex virus present?

A

saliva

123
Q

What is the biggest tigger for herpes simplex virus?

A

stress!! sometimes pts can feel it coming on (will feel pain and tingling before flare up)

124
Q

How do you treat herpes simplex?

A
  • acyclovir (zovirax)
  • docosanol (abreva - over the counter)
  • valacyclovir (valtrex)
125
Q

What is varrucae?

A

warts produced by HPV 1-4

126
Q

Where do plantar warts grow?

A

grows on plantar aspect of interior foot

127
Q

How do you treat verrucae?

A

topical meds, liquid nitrogen, surgery

128
Q

What is tinea capitis and who is it common in?

A

fungal infection of scalp (common in children)

129
Q

What happens to the scalp in tinea capitis?

A

hair loss and scalp becomes erythematous

130
Q

What type of lesions are seen on the scalp in tinea capitis?

A

scaling lesions

131
Q

What is tinea capitis caused by?

A
  • microsporum canis (found in dogs)
  • tricophyton tonsurans
132
Q

What is the treatment of tinea capitis?

A

oral anti fungal = Gris-peg (griseofulvin)

133
Q

What is another name for tinea corporis?

A

ringworm

134
Q

Describe the lesions of tinea corporis

A

erythematous papular lesions (sometimes vesicles)

135
Q

What fungal infection is characterized by a clear center that is very itchy?

A

tinea corporis

136
Q

What is the treatment for tinea corporis?

A

topicals = Nizoral (ketoconazole)

137
Q

What is another name for tinea pedis?

A

athlete’s foot

138
Q

What is tinea pedis caused by?

A

tricophytan

139
Q

Where is tinea pedis commonly found?

A

in warm/damp areas (communal pools/showers)

140
Q

What is the treatment for tinea pedis?

A

topicals = Tinactin (tolnaftate)

141
Q

What is another name for tinea unguium?

A

onchomycosis

142
Q

What is tinea unguium?

A

fungal infection of nails (common in warm climates)

143
Q

What is scabies caused by?

A

sarcoptes scabieuse mite
(female mite that infects humans)

144
Q

What do the light brown lines indicate in a pt with scabies?

A

burrows with vesicles

145
Q

Why does the skin itch and become inflamed in pt’s who have scabies?

A

feces, as larvae move through skin

146
Q

Where is scabies typically found and commonly spread?

A
  • found in warm/closed up body parts (elbow, waist, neck)
  • commonly spread in bed linens
147
Q

What is the treatment for scabies?

A

Gammallin (topical lindane)

148
Q

What is another name for pediculosis?

A

lice

149
Q

What is pediculus humanus corporis?

A

Body nits

150
Q

What is pediculus pubis?

A

pubic nits

151
Q

What is pediculus humanus capitis?

A

Scalp nits

152
Q

Where does lice feed in pt’s with pediculosis?

A

feed on blood in scalp

153
Q

What causes the scalp to become itchy in pediculosis?

A

saliva of lice reacts with skin = itching

154
Q

What is the treatment for lice?

A

Nix (topical permethrin)

155
Q

Acne is an inflammatory reaction against what?

A

folliculo sebaceous glands

156
Q

Describe acne lesions, where it is commonly found, and who does it affect most?

A
  • papular, pustules
  • found on face, neck, chest, back
  • affects teens (puberty)
157
Q

What percent of people ages 40-50 will have acne?

A

3-5%

158
Q

How does acne occur?

A

keratin plug in hair follicle (when ruptured, causes inflammatory reaction)

159
Q

The inflammatory reaction in acne is caused by what cells?

A

lymphocytes

160
Q

What is a commensal bacteria in pt’s with acne that increased when excess sebum is available?

A

propionibacterium acnes

161
Q

What is the most common skin CA?

A

basal cell

162
Q

Describe what basal cell CA looks like:

A

shiney, papule, center becomes ulcerated

163
Q

Where does basal CA metastasize to?

A

slowly into dermis

164
Q

What is the second most common form of skin CA?

A

squamous cell

165
Q

Describe squamous cell CA:

A

scaly, erythematous, raised lesions with irregular borders

166
Q

Where can malignant melanoma originate from?

A
  • melanocytes in epidermis
  • collection of melanocytes like a mole
167
Q

What is a nevus?

A

a mole

168
Q

What skin CA has the worst prognosis?

A

malignant melanoma

169
Q

What are 4 basic categories of melanoma?

A
  • superficial spreading
  • lentigo melanoma
  • sacral lentigimous
  • nodular melanoma
170
Q

What is melanotic melanoma?

A

cancer of melanocytes that don’t produce melanin

171
Q

What is the 5 year survival rate of melanoma? What has contributed to this?

A
  • 99% survival rate if diagnosed before metastasis
  • pt education and counseling
172
Q

What cancer is second to leukemia to # of young lives lost?

A

malignant melanoma

173
Q

What is the ABCDE method and what is it used for?

A

used for diagnosing malignant melanoma

A - asymmetry
B- border irregularity
C - color (multiple)
D - diameter (more than 6 mm)
E - evolution (how its changed over time)

Pathophys (6 decks)

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