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Pathophysiology > EXAM 1 Pathophysiology of Skin and the Integumentum > Flashcards

EXAM 1 Pathophysiology of Skin and the Integumentum Flashcards

1
Q

layers of skin

A
  • epidermis
  • basement membrane
  • dermis
  • subcutaneous
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2
Q

pilosebaceous unit

A
  • 2-4 hairs
  • Sebaceous gland, apocrine sweat gland
  • Arrector pili muscle
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3
Q
  • At junction of the papillary and reticular dermis (gives pink color of skin)
  • Perfuses the dermal papilla
A

Subpapillary plexus/upper horizontal network

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4
Q
  • Provides blood to the entire dermis
  • At the dermal-subcutaneous interface
  • Larger blood vessels
A

Lower horizontal plexus

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5
Q

_________ also in dermis, contribute to immune defense

A

Lymphatics also in dermis, contribute to immune defense

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6
Q

regular/linear wounds caused by a clean, sharp-edged object i.e. scalpel, piece of glass

A

incisions

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7
Q

are irregular tear-like wounds caused by blunt trauma

A

lacerations

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8
Q

superficial wounds to the epidermis and dermis caused by friction (scraped off) i.e. scrape, road rash

A

abrasions

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9
Q

occur when skin is forcibly torn off or detached from its normal point of attachment i.e. where nail torn off, elderly catching thin skin on something

A

avulsions

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10
Q

caused by an object puncturing the skin

A

puncture wounds

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11
Q

caused by an object puncturing the skin and deeper tissues i.e. bullet wound, shrapnel

A

penetrating wounds

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12
Q

occur when the skin is intact but trauma to underlying structures has occurred

A

closed skin wounds

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13
Q

caused by blood vessel damage causing blood to collect under the skin

A

menatomas

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14
Q

smallest for of hematoma to largest

A
  • petechiae
  • purpura
  • ecchymosis
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15
Q

Hematomas caused by external trauma

A

contusions

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16
Q

caused by a great amount of force applied to tissue, injuring the compressed tissues (may be open)

A

crush injury

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17
Q

result from healing of injured tissues, but depending on a number of factors (e.g., heredity, amount of injury, stresses on site of healing), can vary in the form

A

all scars

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18
Q

caused by the presence of a large amount of vasculature (newer)

A

hyperpigmented scars

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19
Q

caused by loss of vasculature (older)

A

hypopigmented scars

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20
Q

scars which continue to thicken due to excessive collagen formation but do not extend beyond the boundary of the original wound

A

hypertrophic scars

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21
Q

result from overgrowth of granulation tissue which is slowly replaced by mature scar; firm, rubbery lesions

A

keloids

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22
Q

sunken recess in the skin, caused when underlying structures are lost, such as fat or muscle; associated with acne, chickenpox, MRSA – deeper structures are affected

A

atrophic scars

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23
Q

parallel to the orientation of collagen fibers of the reticular dermis

A

Langer’s lines

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24
Q

Incisions and excisional biopsies heal best with less scarring when made ________ to the Langer’s lines

A

Incisions and excisional biopsies heal best with less scarring when made parallel to the Langer’s lines

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25
Q

Heat induced injury of the skin and subcutaneous tissues (thermal injury)

A

burns

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26
Q

Burn injury determined by:

A
  • Length of exposure
  • Temperature of heating agent
  • Surface area involved
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27
Q

these burns heal by epithelial regeneration

A

epidermal burns

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28
Q

these tissues heal by scar replacement (second intention), may result in contractures

A
  • dermal

- subcutaneous

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29
Q

burn only affecting epidermis with inflammation of superficial dermis

A

first degree burn

sun burn

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30
Q
  • burn affecting epidermis into dermis
  • -Partial thickness – upper dermis
  • -Full thickness – deeper dermis
  • Blister formation
  • -When fluid accumulates below BM
A

second degree burn

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31
Q
  • burn causing destruction of epidermis and some / all dermis
  • After epidermis, dermis, into subQ
A

third degree burn

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32
Q

burn:

  • Painful, red but no blister formation
  • Heals in 3 to 10 days and requires palliative (pain relieving) treatment only
A

first degree burns

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33
Q
  • burns that involve the epidermis and upper portion of dermis resulting in dermal capillaries leaking
A

second degree burn - partial thickness

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34
Q
  • Painful, red, with blister formation
  • Maintain intact blisters for as long as possible
  • Heal with supportive care in 1 to 2 weeks
A

second degree burn - partial thickness

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35
Q

interface between the dermis and epidermis

A

basal lamina/basement membrane

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36
Q

site of vesicle and blister formation, when the two layers become separated by fluid accumulation (serous, purulent, hemorrhagic)

A

beneath basement membrane

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37
Q

Involve the epidermis and dermis, but sensory nerves intact

A

second degree burn - full thickness

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38
Q
  • Mottled pink, red, or waxy white regions, painful
  • Blisters are flat and dry rather than bullous
  • 1+ months to heal with scar formation; may have residual decreased sensation; risk of contractures
  • Require hydration, supportive wound care, antibiotics
A

second degree burn - full thickness

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39
Q
  • 1+ months to heal with scar formation; may have residual decreased sensation; risk of contractures
  • Require hydration, supportive wound care, antibiotics
A

second degree burn - full thickness

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40
Q

Extend into the hypodermis, may involve muscle, bone, tendons

A

third degree burn

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41
Q
  • Vary in color from white to yellow to black

- Hard, leathery, painless as sensory nerves are destroyed

A

third degree burn

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42
Q
  • Require skin grafts as regenerative dermal elements have been destroyed
  • Admission, antibiotics (IV), hydration, analgesia
  • Disfiguring, extensive contractures likely
A

third degree burn

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43
Q

Effects of extensive burn injury to skin

A
  • Initiates an acute phase response –> Fever, leukocytosis, anorexia, hypermetabolism, acute phase protein changes, cortisol elevation
  • Risk of infection due to immune suppression, loss of epithelial barrier
  • Dehydration and protein loss (epithelial barrier)
  • Difficulty with temperature regulation (epithelial barrier loss)
  • Organ dysfunction due to blood flow disruption (CV, renal, respiratory, GI)
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44
Q

causes of epidermal and dermal infections

A
  • bacterias
  • viruses
  • fungi
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45
Q

Organisms grow within _____ and in ______ space of dermis

A

Organisms grow within epidermis and in interstitial space of dermis

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46
Q

effects of infectious skin disorders

A
  • Consume nutrients, proteins
  • May injure or destroy host tissue
  • Cause inflammation (cardinal signs)
  • May spread in skin (cellulitis) and along fascial planes (fasciitis)
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47
Q

classified as primary (starts as an infection, e.g., impetigo) or secondary (complication of another disorder, e.g., infected pressure ulcers)

A

bacterial infections

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48
Q

Characteristics of infection determined by:

A
  • organism
  • host immune incompetence
  • tissue health
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49
Q

Bacterial infections are characterized by the presence of:

A
  • Inflammatory signs

- crusting

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50
Q

In bacterial infections, these may be released, causing rash, skin injury

A

exotoxins or endotoxins

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51
Q

Where might bacterial infections occur

A

dermis only, localized, or widespread

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52
Q

examples of bacterial skin infections

A
  • Impetigo
  • epysipelas
  • folliculitis
  • carbuncles
  • paronychia
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53
Q

A bacterial infection of the dermis following the pattern of lymphatic drainage

A

cellulitis

54
Q

characteristics of cellulitis

A
  • Skin erythema / swelling that expands, often quickly
  • Tight, glossy appearance to skin
  • Tenderness or pain
  • Systemic signs of infection (APR) including fever, chills and muscle aches
55
Q
  • Infection progresses along fascial lines
  • Bacteria grow and release toxins which kill tissue
  • Signs similar to cellulitis but more extreme
A

necrotizing fasciitis

56
Q
  • Results in thrombosis of the subcutaneous vessels, gangrene of the underlying tissues, sepsis
  • Multiple pathogens including Streptococcus pyogenes (“flesh-eating bacteria“)
A

necrotizing fasciitis

57
Q

what kind of infections can infect cells of the epidermis and dermis

A

viruses

58
Q

Result in direct tissue injury, immune reactions, rarely neoplasm

A

viral infection

59
Q

Neoplasm most commonly associated with infections of the _____ ________

A

Neoplasm most commonly associated with infections of the mucosal epithelium

60
Q

examples of viral infections

A
  • Human papilloma virus (HPV, causes warts – verruca vulgaris)
  • Herpes simplex virus 1 and 2
  • Herpes zoster (varicella zoster virus – chicken pox, shingles)
61
Q

what are verrucae

A

warts

62
Q

what does verruca vulargis mean

A

common wart

63
Q

Common, benign and caused by human papilloma virus (HPV)

Over 50 types of HPV having different infectious characteristics

A

verruca vulgaris

64
Q

Cause overproliferation of stratum germinativum with thickening of the stratum corneum

A

verruca vulgaris

65
Q

Common skin warts do not cause ______.

A

Common skin warts do not cause neoplasm.

66
Q

most common cause of cold sores (fever blisters)

A

HSV 1

67
Q

most common cause of genital herpes

A

HSV 2

68
Q

what describes:
Painful, small vesicles resulting from tissue injury and exudate formation below basement membrane at site of infection, eventually lyse and form shallow, ulcers on erythematous base

A

herpes simplex virus

69
Q
  • Lie dormant in sensory dorsal root ganglia, resurface in same area (see Herpes Zoster), enhanced expression with immunosuppression (stress, disease, age, injury, surgery)
  • May continue to shed virus even without obvious lesions
A

herpes simplex virus

70
Q

Primary infection causes chicken pox

A

herpes zoster/varicella zoster

71
Q

Systemic infection with characteristic skin rash progressing like other herpes viruses, from erythematous vesicles to ulcerations

A

herpes zoster/varicella zoster

72
Q
  • Fever, itch (usually not particularly painful in primary infection), worse symptoms in adults
  • Like other herpes viruses, lies dormant in dorsal root sensory ganglia
A

herpes zoster/varicella zoster

73
Q

Recurrent expression of varicella zoster/herpes zoster results in

A

shingles

74
Q
  • Rash similar to chicken pox except painful with parasthesias, then itchy
  • Pain may become permanent (zoster neuropathy)
A

herpes zoster

75
Q
  • Always follows dermatomal distribution, does not cross midline
  • May cause blindness if trigeminal nerve’s ophthalmic branch is affected
A

herpes zoster

76
Q

where can fungi invade

A
  • skin (dermatophytosis)
  • nails (onychomycosis)
  • oral cavity (thrush)
77
Q

what population are fungal infections most common

A

immunocompromised

i.e. diabetes, young, old, malnourished

78
Q

What kind of climate do fungi prefer

A

Frequently prefer warm, moist, non-sun exposed skin

79
Q

Raw, beefy red painful lesions in oral cavity (covered with white removable material), intertriginous and other moist areas (e.g., diaper

A

fungal infection

80
Q

Dry, flaking areas with central clearing on other areas

Flaking, yellowing, thickening nails

A

fungal infection

81
Q

local area of inflammation which contains a core of necrotic tissue and many neutrophils (purulent exudate)

A

abscess

82
Q
  • Purulent exudate often surrounded with a fibrous capsule (chronic inflammatory reaction)
  • May be associated with signs of localized (cardinal signs) or generalized (APR, fever) inflammation
A

abscess

83
Q
  • Risk of cellulitis, necrotizing fasciitis, sepsis

- Only treatment is incision and drainage

A

abscess

84
Q

common location of abscesses

A

exocrine glands that are blocked

85
Q

Caused by vascular compromise, resulting in necrosis of skin and deeper tissues

A

hypoxic skin disorders

86
Q

Unrelieved pressure causes tissue hypoxia and death, mostly over bony prominences; painful ulcers

A

decubitus ulcers (pressure)

87
Q

Venous stasis results in tissue swelling, causes tissue hypoxia and death; usually proximal to the medial malleolus; not very painful

A

venous stasis ulcers (high venous pressure)

88
Q

Arterial occlusion causes tissue hypoxia and death; very painful

A

arterial occlusion ulcers (low arterial pressure)

89
Q

Caused by repeated trauma due to lack of pain perception; painless

A

neuropathic ulcers

90
Q

Inherited inability of melanocytes to produce melanin (melanocytes are present in epidermis)

A

albinism

91
Q
  • Potential differential expression; eyes, skin, hair may be affected
  • Increased risk for sun damage to tissues, cancer

-affects that area and doesn’t spread

A

albinism

92
Q

Autoimmune response against melanocytes, causes localized melanocyte loss and depigmentation

A

vitiligo

93
Q
  • Manifested by flat (patches), irregular lesions of pigment loss
  • May be associated with other autoimmune diseases

-can spread!

A

vitiligo

94
Q

immune responses against antigen which result in excessive reactions and pathology

type 1, 2, 3, or 4

A

hypersensitivity responses

95
Q
  • Autoimmune responses
  • Poorly controlled or directed anti-microbial responses
  • Responses to non-threatening environmental antigens (allergens)
A

hypersensitivity responses

96
Q

Typical of responses to environmental allergens (“ordinary” allergy)

A

type 1 hypersensitivity

97
Q

Mediated by IgE and mast cells

A

type 1 hypersensitivity

98
Q

Symptoms may be localized –> Swelling, itching, fluid transudate or exudate, mucus, urticaria, vasodilation and respiratory smooth muscle constriction

A

type 1 hypersensitivity

99
Q

Symptoms may be systemic –> Widespread urticaria, anaphylaxis

A

type 1 hypersensitivity

100
Q

Mediated by IgG binding to cells or tissue components

A

type 2 hypersensitivity

101
Q

Results in pathology by

  • Stimulation of phagocytosis and killing (via Fc receptor)
  • Complement and Fc receptor activation with cell and tissue injury
  • Ig binding to receptors and antagonizing their activation or continuously stimulating (agonist)
A

type 2 hypersensitivity

102
Q

Stimulating phagocytosis via opsonization

  • Autoimmune thrombocytopenic purpura
  • Autoimmune hemolytic anemia
A

type 2 hypersensitivity

103
Q

Complement and Fc receptor activation

  • Acute rheumatic fever
  • Goodpaster syndrome
  • Autoimmune vasculitis
  • Pemphigus vulgaris
A

type 2 hypersensitivity

104
Q

Antibody binding to receptors

  • Graves disease (agonist)
  • Myasthenia gravis (antagonist)
  • Insulin-resistant diabetes (antagonist)
  • Pernicious anemia (antagonist)
A

type 2 hypersensitivity

105
Q

Results from the formation and deposition of immune complexes (complexes of Ig and antigen), resulting in complement activation and Fc-mediated phagocyte killing

A

type 3 hypersensitivity

106
Q
  • Systemic lupus erythematosus
  • Post-streptococcal glomerulonephritis
  • Polyarthritis nodosa – usually happen after another disease
  • Reactive arthritis
  • Serum sickness
A

type 3 hypersensitivity

107
Q

Also called delayed-type hypersensitivity

A

type 4 hypersensitivity

108
Q

Two mechanisms contribute:

  • CD4+ T lymphocytes respond to tissue antigens by secreting cytokines that stimulate inflammation and activate phagocytes
  • CD8+ T lymphocytes cause direct cell toxicity and killing of antigen-bearing cells (T cell mediated cytolysis)
A

type 4 hypersensitivity

109
Q 
Type 1 diabetes mellitus
Multiple sclerosis
Rheumatoid arthritis
Peripheral neuropathies (Guillain-Barré)
Inflammatory bowel disease
Contact sensitivity / contact dermatitis
Poison ivy rash
Nickel sensitivity
Positive TB test
A

type 4 hypersensitivity

110
Q
  • Autoimmune reactions (lupus, psoriasis)
  • Hypersensitivity reactions (eczema, urticaria, contact dermatitis, viral xanthems, erythema multiforme, drug reactions)
A

inflammatory skin disorders

111
Q
  • Stimulation of epidermis (stratus germinativum) results in overproduction (e.g., psoriasis)
  • Localized acute inflammation with histamine release (e.g., urticaria) – type 1 hypersensitivity
A

mechanisms of inflammatory skin disorders

112
Q
  • Deposits of antigen-antibody (Ag-Ab) in skin or capillaries activates complement, resulting in inflammation and rash (e.g., lupus, viral xanthems, Stevens-Johnson syndrome, drug reactions) – type 3 hypersensitivity
  • Type 4 hypersensitivity reaction attracting macrophages and T lymphocytes (e.g., erythema multiforme, poison ivy rash, contact dermatitis)
A

mechanisms of inflammatory skin disorders

113
Q
  • A UV light–induced dysplastic lesion of the skin

- Dysplasia of the keratinocytes in the mid to upper layers of the epidermis

A

actinic keratosis

114
Q
  • Brown, red, or skin-colored, rough, sandpaper-like consistency, may produce so much keratin that a “cutaneous horn” forms
  • Common in sun exposed body areas (face, ears, scalp, forearms, backs of the hands), fair skinned persons, areas with lots of sunshine
A

actinic keratosis

115
Q

-May progress to squamous cell carcinoma

A

actinic keratosis

116
Q

Sharply demarcated, hyperkeratotic, variably pigmented, round, flat, “waxy” plaques with a velvety to granular surface (“stuck-on” appearance)

A

seborrheic keratosis

117
Q
  • Particularly numerous on sun exposed areas such as the trunk, extremities, head, and neck (sometimes found on areas not exposed to sun)
  • Do not progress to carcinoma
A

seborrheic keratosis

118
Q

Localized hyperplasia of melanocytes in skin or mucous membranes

A

Nevus (nevi), also lentigo, melanocytic nevus, “mole”

119
Q
  • Tan to brown, uniformly pigmented, small macules to papules with well-defined, rounded borders
  • May be congenital or acquired
A

Nevus (nevi), also lentigo, melanocytic nevus, “mole”

120
Q

Larger than most nondysplastic nevi (often >5 mm across), flat macules, slightly raised plaques with a “pebbly” surface, or target-like lesions with a darker raised center and irregular flat periphery, uniform or variable color

A

dysplastic nevi

121
Q

May be associated with increased neoplasia risk

A

dysplastic nevi

122
Q
  • Patient may have hundreds of dysplastic nevi

- Over 50% will develop melanoma by age 60

A

dysplastic nevus syndrome

123
Q
  • Derived from basal epidermal layers (stratum germinativum)
  • 75% of nonmelanoma skin cancers
  • Areas of sun exposure, usually in 60+ year old persons
A

basal cell carcinoma

124
Q
  • Slow growing, rarely metastasize, may invade locally

- Flesh-colored, with telangiectatic vessels seen within it, pearly smooth border, sometimes central ulceration

A

basal cell carcinoma

125
Q
  • Derived from higher, squamous layers of the epidermis, derived from actinic keratoses
  • Second most common nonmelanoma skin cancers
  • Areas of sun exposure, usually in 40+ year old persons
A

squamous cell carcinoma

126
Q
  • Up to 5% metastasize, grow more quickly
  • Lesions which have not invaded through the basement membrane are sharply defined, red, scaling plaques (“carcinoma in situ”)
A

squamous cell carcinoma

127
Q
  • Advanced, invasive lesions are nodular, show variable keratin production (hyperkeratotic scale), may ulcerate
  • Keratocanthoma is thought to be a variant of well-differentiated one of these
A

squamous cell carcinoma

128
Q
  • Derived from melanocytes (normally in epidermis)

- Occur in skin (most common) also on mucosal surfaces, esophagus, meninges, eye

A

melanoma

129
Q
  • Relatively common, highly metastatic skin cancer

- Does not require sun exposure (but sun increases risk)

A

melanoma

130
Q
  • The most consistent clinical signs are changes in the color, size, or shape of a pigmented lesion
  • Risk evaluated by “Breslow thickness” or “Clark level”, related to depth of penetration into the epidermis or dermis
A

melanoma

131
Q

what are Breslow thickness or Clark level associated with?

A

metastatic potential at time of diagnosis (and 5 year survival rate)

Pathophysiology (4 decks)

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