EXAM 1 Pathophysiology of Skin and the Integumentum Flashcards
layers of skin
- epidermis
- basement membrane
- dermis
- subcutaneous
pilosebaceous unit
- 2-4 hairs
- Sebaceous gland, apocrine sweat gland
- Arrector pili muscle
- At junction of the papillary and reticular dermis (gives pink color of skin)
- Perfuses the dermal papilla
Subpapillary plexus/upper horizontal network
- Provides blood to the entire dermis
- At the dermal-subcutaneous interface
- Larger blood vessels
Lower horizontal plexus
_________ also in dermis, contribute to immune defense
Lymphatics also in dermis, contribute to immune defense
regular/linear wounds caused by a clean, sharp-edged object i.e. scalpel, piece of glass
incisions
are irregular tear-like wounds caused by blunt trauma
lacerations
superficial wounds to the epidermis and dermis caused by friction (scraped off) i.e. scrape, road rash
abrasions
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
avulsions
caused by an object puncturing the skin
puncture wounds
caused by an object puncturing the skin and deeper tissues i.e. bullet wound, shrapnel
penetrating wounds
occur when the skin is intact but trauma to underlying structures has occurred
closed skin wounds
caused by blood vessel damage causing blood to collect under the skin
menatomas
smallest for of hematoma to largest
- petechiae
- purpura
- ecchymosis
Hematomas caused by external trauma
contusions
caused by a great amount of force applied to tissue, injuring the compressed tissues (may be open)
crush injury
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
all scars
caused by the presence of a large amount of vasculature (newer)
hyperpigmented scars
caused by loss of vasculature (older)
hypopigmented scars
scars which continue to thicken due to excessive collagen formation but do not extend beyond the boundary of the original wound
hypertrophic scars
result from overgrowth of granulation tissue which is slowly replaced by mature scar; firm, rubbery lesions
keloids
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
atrophic scars
parallel to the orientation of collagen fibers of the reticular dermis
Langer’s lines
Incisions and excisional biopsies heal best with less scarring when made ________ to the Langer’s lines
Incisions and excisional biopsies heal best with less scarring when made parallel to the Langer’s lines
Heat induced injury of the skin and subcutaneous tissues (thermal injury)
burns
Burn injury determined by:
- Length of exposure
- Temperature of heating agent
- Surface area involved
these burns heal by epithelial regeneration
epidermal burns
these tissues heal by scar replacement (second intention), may result in contractures
- dermal
- subcutaneous
burn only affecting epidermis with inflammation of superficial dermis
first degree burn
sun burn
- burn affecting epidermis into dermis
- -Partial thickness – upper dermis
- -Full thickness – deeper dermis
- Blister formation
- -When fluid accumulates below BM
second degree burn
- burn causing destruction of epidermis and some / all dermis
- After epidermis, dermis, into subQ
third degree burn
burn:
- Painful, red but no blister formation
- Heals in 3 to 10 days and requires palliative (pain relieving) treatment only
first degree burns
- burns that involve the epidermis and upper portion of dermis resulting in dermal capillaries leaking
second degree burn - partial thickness
- Painful, red, with blister formation
- Maintain intact blisters for as long as possible
- Heal with supportive care in 1 to 2 weeks
second degree burn - partial thickness
interface between the dermis and epidermis
basal lamina/basement membrane
site of vesicle and blister formation, when the two layers become separated by fluid accumulation (serous, purulent, hemorrhagic)
beneath basement membrane
Involve the epidermis and dermis, but sensory nerves intact
second degree burn - full thickness
- 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
second degree burn - full thickness
- 1+ months to heal with scar formation; may have residual decreased sensation; risk of contractures
- Require hydration, supportive wound care, antibiotics
second degree burn - full thickness
Extend into the hypodermis, may involve muscle, bone, tendons
third degree burn
- Vary in color from white to yellow to black
- Hard, leathery, painless as sensory nerves are destroyed
third degree burn
- Require skin grafts as regenerative dermal elements have been destroyed
- Admission, antibiotics (IV), hydration, analgesia
- Disfiguring, extensive contractures likely
third degree burn
Effects of extensive burn injury to skin
- 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)
causes of epidermal and dermal infections
- bacterias
- viruses
- fungi
Organisms grow within _____ and in ______ space of dermis
Organisms grow within epidermis and in interstitial space of dermis
effects of infectious skin disorders
- Consume nutrients, proteins
- May injure or destroy host tissue
- Cause inflammation (cardinal signs)
- May spread in skin (cellulitis) and along fascial planes (fasciitis)
classified as primary (starts as an infection, e.g., impetigo) or secondary (complication of another disorder, e.g., infected pressure ulcers)
bacterial infections
Characteristics of infection determined by:
- organism
- host immune incompetence
- tissue health
Bacterial infections are characterized by the presence of:
- Inflammatory signs
- crusting
In bacterial infections, these may be released, causing rash, skin injury
exotoxins or endotoxins
Where might bacterial infections occur
dermis only, localized, or widespread
examples of bacterial skin infections
- Impetigo
- epysipelas
- folliculitis
- carbuncles
- paronychia
A bacterial infection of the dermis following the pattern of lymphatic drainage
cellulitis
characteristics of cellulitis
- 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
- Infection progresses along fascial lines
- Bacteria grow and release toxins which kill tissue
- Signs similar to cellulitis but more extreme
necrotizing fasciitis
- Results in thrombosis of the subcutaneous vessels, gangrene of the underlying tissues, sepsis
- Multiple pathogens including Streptococcus pyogenes (“flesh-eating bacteria“)
necrotizing fasciitis
what kind of infections can infect cells of the epidermis and dermis
viruses
Result in direct tissue injury, immune reactions, rarely neoplasm
viral infection
Neoplasm most commonly associated with infections of the _____ ________
Neoplasm most commonly associated with infections of the mucosal epithelium
examples of viral infections
- Human papilloma virus (HPV, causes warts – verruca vulgaris)
- Herpes simplex virus 1 and 2
- Herpes zoster (varicella zoster virus – chicken pox, shingles)
what are verrucae
warts
what does verruca vulargis mean
common wart
Common, benign and caused by human papilloma virus (HPV)
Over 50 types of HPV having different infectious characteristics
verruca vulgaris
Cause overproliferation of stratum germinativum with thickening of the stratum corneum
verruca vulgaris
Common skin warts do not cause ______.
Common skin warts do not cause neoplasm.
most common cause of cold sores (fever blisters)
HSV 1
most common cause of genital herpes
HSV 2
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
herpes simplex virus
- 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
herpes simplex virus
Primary infection causes chicken pox
herpes zoster/varicella zoster
Systemic infection with characteristic skin rash progressing like other herpes viruses, from erythematous vesicles to ulcerations
herpes zoster/varicella zoster
- Fever, itch (usually not particularly painful in primary infection), worse symptoms in adults
- Like other herpes viruses, lies dormant in dorsal root sensory ganglia
herpes zoster/varicella zoster
Recurrent expression of varicella zoster/herpes zoster results in
shingles
- Rash similar to chicken pox except painful with parasthesias, then itchy
- Pain may become permanent (zoster neuropathy)
herpes zoster
- Always follows dermatomal distribution, does not cross midline
- May cause blindness if trigeminal nerve’s ophthalmic branch is affected
herpes zoster
where can fungi invade
- skin (dermatophytosis)
- nails (onychomycosis)
- oral cavity (thrush)
what population are fungal infections most common
immunocompromised
i.e. diabetes, young, old, malnourished
What kind of climate do fungi prefer
Frequently prefer warm, moist, non-sun exposed skin
Raw, beefy red painful lesions in oral cavity (covered with white removable material), intertriginous and other moist areas (e.g., diaper
fungal infection
Dry, flaking areas with central clearing on other areas
Flaking, yellowing, thickening nails
fungal infection
local area of inflammation which contains a core of necrotic tissue and many neutrophils (purulent exudate)
abscess
- 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
abscess
- Risk of cellulitis, necrotizing fasciitis, sepsis
- Only treatment is incision and drainage
abscess
common location of abscesses
exocrine glands that are blocked
Caused by vascular compromise, resulting in necrosis of skin and deeper tissues
hypoxic skin disorders
Unrelieved pressure causes tissue hypoxia and death, mostly over bony prominences; painful ulcers
decubitus ulcers (pressure)
Venous stasis results in tissue swelling, causes tissue hypoxia and death; usually proximal to the medial malleolus; not very painful
venous stasis ulcers (high venous pressure)
Arterial occlusion causes tissue hypoxia and death; very painful
arterial occlusion ulcers (low arterial pressure)
Caused by repeated trauma due to lack of pain perception; painless
neuropathic ulcers
Inherited inability of melanocytes to produce melanin (melanocytes are present in epidermis)
albinism
- Potential differential expression; eyes, skin, hair may be affected
- Increased risk for sun damage to tissues, cancer
-affects that area and doesn’t spread
albinism
Autoimmune response against melanocytes, causes localized melanocyte loss and depigmentation
vitiligo
- Manifested by flat (patches), irregular lesions of pigment loss
- May be associated with other autoimmune diseases
-can spread!
vitiligo
immune responses against antigen which result in excessive reactions and pathology
type 1, 2, 3, or 4
hypersensitivity responses
- Autoimmune responses
- Poorly controlled or directed anti-microbial responses
- Responses to non-threatening environmental antigens (allergens)
hypersensitivity responses
Typical of responses to environmental allergens (“ordinary” allergy)
type 1 hypersensitivity
Mediated by IgE and mast cells
type 1 hypersensitivity
Symptoms may be localized –> Swelling, itching, fluid transudate or exudate, mucus, urticaria, vasodilation and respiratory smooth muscle constriction
type 1 hypersensitivity
Symptoms may be systemic –> Widespread urticaria, anaphylaxis
type 1 hypersensitivity
Mediated by IgG binding to cells or tissue components
type 2 hypersensitivity
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)
type 2 hypersensitivity
Stimulating phagocytosis via opsonization
- Autoimmune thrombocytopenic purpura
- Autoimmune hemolytic anemia
type 2 hypersensitivity
Complement and Fc receptor activation
- Acute rheumatic fever
- Goodpaster syndrome
- Autoimmune vasculitis
- Pemphigus vulgaris
type 2 hypersensitivity
Antibody binding to receptors
- Graves disease (agonist)
- Myasthenia gravis (antagonist)
- Insulin-resistant diabetes (antagonist)
- Pernicious anemia (antagonist)
type 2 hypersensitivity
Results from the formation and deposition of immune complexes (complexes of Ig and antigen), resulting in complement activation and Fc-mediated phagocyte killing
type 3 hypersensitivity
- Systemic lupus erythematosus
- Post-streptococcal glomerulonephritis
- Polyarthritis nodosa – usually happen after another disease
- Reactive arthritis
- Serum sickness
type 3 hypersensitivity
Also called delayed-type hypersensitivity
type 4 hypersensitivity
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)
type 4 hypersensitivity
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
type 4 hypersensitivity
- Autoimmune reactions (lupus, psoriasis)
- Hypersensitivity reactions (eczema, urticaria, contact dermatitis, viral xanthems, erythema multiforme, drug reactions)
inflammatory skin disorders
- Stimulation of epidermis (stratus germinativum) results in overproduction (e.g., psoriasis)
- Localized acute inflammation with histamine release (e.g., urticaria) – type 1 hypersensitivity
mechanisms of inflammatory skin disorders
- 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)
mechanisms of inflammatory skin disorders
- A UV light–induced dysplastic lesion of the skin
- Dysplasia of the keratinocytes in the mid to upper layers of the epidermis
actinic keratosis
- 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
actinic keratosis
-May progress to squamous cell carcinoma
actinic keratosis
Sharply demarcated, hyperkeratotic, variably pigmented, round, flat, “waxy” plaques with a velvety to granular surface (“stuck-on” appearance)
seborrheic keratosis
- 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
seborrheic keratosis
Localized hyperplasia of melanocytes in skin or mucous membranes
Nevus (nevi), also lentigo, melanocytic nevus, “mole”
- Tan to brown, uniformly pigmented, small macules to papules with well-defined, rounded borders
- May be congenital or acquired
Nevus (nevi), also lentigo, melanocytic nevus, “mole”
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
dysplastic nevi
May be associated with increased neoplasia risk
dysplastic nevi
- Patient may have hundreds of dysplastic nevi
- Over 50% will develop melanoma by age 60
dysplastic nevus syndrome
- Derived from basal epidermal layers (stratum germinativum)
- 75% of nonmelanoma skin cancers
- Areas of sun exposure, usually in 60+ year old persons
basal cell carcinoma
- Slow growing, rarely metastasize, may invade locally
- Flesh-colored, with telangiectatic vessels seen within it, pearly smooth border, sometimes central ulceration
basal cell carcinoma
- 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
squamous cell carcinoma
- 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”)
squamous cell carcinoma
- 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
squamous cell carcinoma
- Derived from melanocytes (normally in epidermis)
- Occur in skin (most common) also on mucosal surfaces, esophagus, meninges, eye
melanoma
- Relatively common, highly metastatic skin cancer
- Does not require sun exposure (but sun increases risk)
melanoma
- 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
melanoma
what are Breslow thickness or Clark level associated with?
metastatic potential at time of diagnosis (and 5 year survival rate)
