NURS 6220 ADVANCED PATHO FINAL STUDY GUIDE
SESSION 7: INTEGUMENTARY SYSTEM
Describe normal skin and its function
a. Skin is an organ
b. Three layers
i. Epidermis- composed of keratinocytes and scattered melanocytes
1. Epidermis undergoes keratinization, second most
important protective mechanism
2. Epidermal cells produce keratins which are cytoskeletal
proteins that are highly resistant to mechanical and chemical
injury
a. The keratin layer represents the final stage of epidermal
cell differentiation
b. Varies in thickness on diff anatomic sites
c. Most prominent on the palms and soles
3. Keratinized epidermis provides limited protection against
sunlight by preventing the penetration of light through the
skin
a. Keratinocytes are the principal cells of the
epidermis
i. They are aided by melanocytes,
the pigment-producing cells
1. Located in basal layer
2. Produce a brown pigment packed
into membrane-bound cytoplasmic
1
, bodies(melanosomes) and transferred
through the cytoplasmic process into
keratinocytes
3. This transfer of pigment is was
causes browning of skin when
exposed to sunlight
b. Keratinocytes with melanin are more resistant to UV
light and protect the body against the sunlight more
efficiently than non pigmented keratinocytes
ii. Dermis-composed of connective tissue, blood vessels, nerves, and
hair follicles, and skin adnexal glands, sebaceous glands (oil
glands- connected to hair follicles and secrete sebum made of
fatty acids and waxy esters, lubricates skin, softens hair shaft,
and is slightly acidic helps deter pathogens), sweat gland,
iii. Subcutis/hypodermis- composed of fat tissue
*Describe various skin infections* (on Final Study Guide)
1. Bacterial Infections
a. Impetigo
i. Caused by streptococcus pyogenes or staph. Aureus
ii. Most often found on face of small children- the mouth and nose
iii. Characterized by superficial pustules that rupture, leaving
honey-colored scabs
1. “Pustule”= vesicle filled with pus
2. Yellow-honey looking crusting blisters containing pus
3. Skin lesions are itchy
iv. Highly contagious; but responds well to systemic antibiotic
therapy and can heal without scars
b. Folliculitis
i. Caused by staph aureus
ii. Common form of infection limited to hair follicles
2
, 1. Typically involves hairy areas such as the beard
2. More common in men than females
3. Bacteria produces a purulent exudate that fills lumen of
hair follicle
a. The infection extends into the perifollicular tissue, a
furuncle (boil) develops
b. The infection can spread to adjacent hair follicles and
the original abscess enlarges to include several hair
follicles and a larger boil evolves, called a carbuncle;
mostly located in neck
c. Acne Vulgaris
i. Pathogenesis not fully understood
ii. Heredity, hormones and general cleanliness play a role
1. Begins at puberty, probably from sex hormones particullarly
androgens
a. Androgens stimulate development of sebaceous
glands on the face, neck, chest and back
2. Pathogenesis- keratin plugs, sebum, bacterial overgrowth
a. Sex hormones stimulate the developement of
sebaceous glands on the face, neck, chest, and back
b. Secretion of sebum is increased, evidenced by
greasy skin
c. Sex hormones promote hyperkeratosis at the orifice of
hair follicles
i. This blocks the discharge of sebum
ii. The stagnant sebum is colonized by anaerobic
bacteria (propionibacterium acnes)
iii. This results in formation of comedones,
which occur in two forms
1. Open to the surface comedo (blackhead)
2. Closed comedo (whitehead)
3
, iv. Through the action of bacterial lipases, the fat of
the sebum is broken down to glycerin and free
fatty acids
1. Release into tissue causes inflammation
v. Entire obstructed follicle and surrounding
connective tissue are transformed into
pustules or larger abscesses
1. May persist and become confluent
(acne conglobata), transform into
dermal cysts, or heal with scarring
(keloid acne)
vi. Scratching, picking or pressing of these
lesions may predispose individual to
secondary infections
d. Treatment focuses on decreasing the keratinization
of follicles with retinoic acid or keratinolytic agents and
controlling the infection with local or systemic
antibiotics
e. OVERVIEW: Hyperkeratotic epidermal plug (keratin
plugs) prevent the discharge of sebum. The retained
sebum is colonized by bacteria. Bacterial action
expands the follicle and ultimately leads to rupture and
discharge of infected purulent sebum into the adjacent
dermis.
d. Fungal Infections
i. Dermatophytosis- fungal infections of the skin
ii. Fungal pathogens= dermatophytes ten to live in “dead tissues”
iii. Common sites: feet, head, nails, axillae, groin
1. Tinea pedis- athlete's foot= begins between the toes
and spread locally
2. Tinea unguium= chronic nail infection
3. Tinea corporis= circular or irregularly shaped patches on
the skin and have a pale center and spreading margins
4
SESSION 7: INTEGUMENTARY SYSTEM
Describe normal skin and its function
a. Skin is an organ
b. Three layers
i. Epidermis- composed of keratinocytes and scattered melanocytes
1. Epidermis undergoes keratinization, second most
important protective mechanism
2. Epidermal cells produce keratins which are cytoskeletal
proteins that are highly resistant to mechanical and chemical
injury
a. The keratin layer represents the final stage of epidermal
cell differentiation
b. Varies in thickness on diff anatomic sites
c. Most prominent on the palms and soles
3. Keratinized epidermis provides limited protection against
sunlight by preventing the penetration of light through the
skin
a. Keratinocytes are the principal cells of the
epidermis
i. They are aided by melanocytes,
the pigment-producing cells
1. Located in basal layer
2. Produce a brown pigment packed
into membrane-bound cytoplasmic
1
, bodies(melanosomes) and transferred
through the cytoplasmic process into
keratinocytes
3. This transfer of pigment is was
causes browning of skin when
exposed to sunlight
b. Keratinocytes with melanin are more resistant to UV
light and protect the body against the sunlight more
efficiently than non pigmented keratinocytes
ii. Dermis-composed of connective tissue, blood vessels, nerves, and
hair follicles, and skin adnexal glands, sebaceous glands (oil
glands- connected to hair follicles and secrete sebum made of
fatty acids and waxy esters, lubricates skin, softens hair shaft,
and is slightly acidic helps deter pathogens), sweat gland,
iii. Subcutis/hypodermis- composed of fat tissue
*Describe various skin infections* (on Final Study Guide)
1. Bacterial Infections
a. Impetigo
i. Caused by streptococcus pyogenes or staph. Aureus
ii. Most often found on face of small children- the mouth and nose
iii. Characterized by superficial pustules that rupture, leaving
honey-colored scabs
1. “Pustule”= vesicle filled with pus
2. Yellow-honey looking crusting blisters containing pus
3. Skin lesions are itchy
iv. Highly contagious; but responds well to systemic antibiotic
therapy and can heal without scars
b. Folliculitis
i. Caused by staph aureus
ii. Common form of infection limited to hair follicles
2
, 1. Typically involves hairy areas such as the beard
2. More common in men than females
3. Bacteria produces a purulent exudate that fills lumen of
hair follicle
a. The infection extends into the perifollicular tissue, a
furuncle (boil) develops
b. The infection can spread to adjacent hair follicles and
the original abscess enlarges to include several hair
follicles and a larger boil evolves, called a carbuncle;
mostly located in neck
c. Acne Vulgaris
i. Pathogenesis not fully understood
ii. Heredity, hormones and general cleanliness play a role
1. Begins at puberty, probably from sex hormones particullarly
androgens
a. Androgens stimulate development of sebaceous
glands on the face, neck, chest and back
2. Pathogenesis- keratin plugs, sebum, bacterial overgrowth
a. Sex hormones stimulate the developement of
sebaceous glands on the face, neck, chest, and back
b. Secretion of sebum is increased, evidenced by
greasy skin
c. Sex hormones promote hyperkeratosis at the orifice of
hair follicles
i. This blocks the discharge of sebum
ii. The stagnant sebum is colonized by anaerobic
bacteria (propionibacterium acnes)
iii. This results in formation of comedones,
which occur in two forms
1. Open to the surface comedo (blackhead)
2. Closed comedo (whitehead)
3
, iv. Through the action of bacterial lipases, the fat of
the sebum is broken down to glycerin and free
fatty acids
1. Release into tissue causes inflammation
v. Entire obstructed follicle and surrounding
connective tissue are transformed into
pustules or larger abscesses
1. May persist and become confluent
(acne conglobata), transform into
dermal cysts, or heal with scarring
(keloid acne)
vi. Scratching, picking or pressing of these
lesions may predispose individual to
secondary infections
d. Treatment focuses on decreasing the keratinization
of follicles with retinoic acid or keratinolytic agents and
controlling the infection with local or systemic
antibiotics
e. OVERVIEW: Hyperkeratotic epidermal plug (keratin
plugs) prevent the discharge of sebum. The retained
sebum is colonized by bacteria. Bacterial action
expands the follicle and ultimately leads to rupture and
discharge of infected purulent sebum into the adjacent
dermis.
d. Fungal Infections
i. Dermatophytosis- fungal infections of the skin
ii. Fungal pathogens= dermatophytes ten to live in “dead tissues”
iii. Common sites: feet, head, nails, axillae, groin
1. Tinea pedis- athlete's foot= begins between the toes
and spread locally
2. Tinea unguium= chronic nail infection
3. Tinea corporis= circular or irregularly shaped patches on
the skin and have a pale center and spreading margins
4
