NR283 Exam 2 Study Guide
(Chapters 8, 10, 12, & 13)
Chapter 8: Skin Disorders
1. Describe the layers of the skin
a. Epidermis: 5 layers that vary in thickness
-Keratin: waterproofing
-Melanin: skin pigment-determines skin color
-Albinism: lack of melatonin production
-Vitiligo: small area of hypopigmentation
-Melasma: patches of darker skin
b. Dermis: Connective tissue containing elastic & collagen fibers
-Flexibility & strength of skin
-Contains nerves & blood vessels
-Sensory receptors: pressure, touch, pain, heat, cold
2. What are appendages in the skin? What is the function of each?
a. Hair follicles: Stratum Basale-hair producing
-Arrector pili muscle associated with hair follicle
b. Sebaceous glands: Produce sebum
-secretion increases at puberty-influence of sex hormones
c. Sweat glands:
i. Eccrine: glands all over body and secrete sweat through pores onto the skin
in response to increased heat or emotional stress
ii. Apocrine: sweat glands in axillae, scalp, face, external genitalia and the
ducts of these glands open into the hair follicles.
3. What are the 5 functions of the skin?
-First line of defense (mechanical barrier)
-Prevents excessive fluid loss
-Sensory perception
-Synthesizes vitamin D
4. Describe the following skin lesions: (Table 8-1)
, a. Vesicle: or blister, thin wall, raised, fluid filled
b. Plaque: slightly elevated, flat, “scale” like lesion
c. Crust: dry rough surface or dried exudate or blood
d. Lichenification: thick dry rough surface (leather like)
e. Keloid: raised irregular and increasing mass of collagen, resulting from excessive
scar tissue formation
f. Fissure: crack in tissue
g. Ulcer: cavity in tissue
h. Erosion: shallow moist cavity in epidermis
i. Comedome: mass of sebum, keratin & debris blocking the opening of a hair
follicle
5. What is pruritus? Chemical irritation caused by insect bites, allergic responses,
infestations by parasites.
a. What can cause it? Release of histamine in hypersensitivity response
b. Why is it harmful to scratch a pruritic area? May break skin increasing risk for
infection
c. Describe treatments for pruritus: topical agents (reduce sensation)
antihistamines or glucocorticoids. Avoidance of allergens. Antibiotics with
infections. Surgery, laser therapy, electrodessication, cryosurgery (Precancerous
lesions).
6. What is the differences between contact dermatitis and allergic dermatitis?
Contact: exposure to allergen (metals, cosmetics, soaps, chemicals, plants) Occurs on
first exposure. Pruritic rash develops at site few hours later. Direct chemical or
mechanical irritationdoes not involve immune response, is inflammatory b/c of direct
exposure (remove irritant, reduce inflammation w/ glucocorticoids)
Allergic: result of type 1 hypersensitivity (ingestion of substances: shellfish, drugs,
fruits, nuts).
Pruritic lesions & hives part of anaphylaxis (check for swelling around mouth & airway).
Administer EpiPen or other first aid.
,7. What is atopic dermatitis (Eczema)? Inherited tendency. Chronic inflammation from
response to allergens (eosinophilia & increased serum IgE levels).
a. What are clinical manifestations? Children: Rash is erythematous w/ serous
exudate.
Occurs on face, chest & shoulders. Adults: rash is dry, scaly, pruritic on flexor
surfaces
b. How is it treated? Topical glucocorticoids & antihistamines
8. What is psoriasis? Chronic inflammatory skin disorder. Abnormal T cell activation-
excessive proliferation of keratinocytes. Increased cellular proliferation
a. What are the clinical manifestations? Lesions on face, scalp, elbows, knees.
Itching or burning sensations
b. What cells are abnormally activated? T cell
c. What medication are severe cases treated with? Glucocorticoids, tar
preparations, antimetabolites
9. What is scleroderma? Skin disorder may be systemic & affect viscera. Increased
collagen deposition
a. What happens to produce hard, shiny, tight, immovable areas of skin?
Inflammation & fibrosis w/ decreased capillary networks
b. Can this happen elsewhere in the body? May cause renal failure, intestinal
obstruction, respiratory failure by distortion of tissues
10. What is cellulitis? Bacterial skin infection of the dermis & subcutaneous tissue.
a. What organism usually causes it? Staphylococcus aureus & sometimes
Streptococcus
b. What are clinical manifestations? Red, swollen & painful areas. Red streaks
develop along lymph vessels proximal to infected area
11. What is a furuncle (boils)? Bacterial Infection
a. What are the clinical manifestations? Large amount of frequent drainage of
purulent exudate
b. Why do we not want to squeeze a boil? Can result in spread of infection to other
areas b/c you’re actually pushing the infection further down in the skin rather than
pushing it out
, c. What are carbuncles? Collection of furuncles that form a large infected mass
12. What is impetigo? Infection, with the appearance of lesions that are common on the
face.
Pruritus is common=scratching & further spread of infection
a. Is it contagious? VERY in neonates
i.How is it spread? Close physical contact or fomites
b. What is the causative organism? S. aureus
c. What is the treatment? Topical antibiotics (early stages). Systemic
administration if extensive
13. What is acute necrotizing fasciitis? “Fleshing eating” Mixture of aerobic & anaerobic
bacteria at site of infection
a. What is the causative agent? Gram-pos. group A beta-hemolytic Streptococcus
b. What event usually precipitates acute necrotizing fasciitis? Trauma or
infection in the skin & subcutaneous tissue of an extremity
c. Can it be deadly? YES. Bacteria secrete toxins that break down fascia &
connective tissue= MASSIVE TISSUE DESTRUCTION. Systemic toxicity
develops w/ fever, tachycardia, hypotension, confusion, ORGAN FAILURE.
d. How is it treated? Antimicrobial therapy, fluid replacement, excision of all
infected tissue
(amputation)
14. What is the most common type of herpes simplex virus? Type 1 (HSV-1)
a. What does it cause? Cold sores or fever blisters
15. Describe the clinical manifestations of herpes simplex virus?
a. What does the latent stage mean? Does not show signs (asymptomatic) but still
have virus remains in sensory nerve ganglia
16. How is it transmitted? Direct contact with fluid from lesions
17. What medication is it treated with? Laser, freezing w/ liquid nitrogen & topical
medications w/
ASA compounds
18. What virus causes verrucae (warts)? HPV
(Chapters 8, 10, 12, & 13)
Chapter 8: Skin Disorders
1. Describe the layers of the skin
a. Epidermis: 5 layers that vary in thickness
-Keratin: waterproofing
-Melanin: skin pigment-determines skin color
-Albinism: lack of melatonin production
-Vitiligo: small area of hypopigmentation
-Melasma: patches of darker skin
b. Dermis: Connective tissue containing elastic & collagen fibers
-Flexibility & strength of skin
-Contains nerves & blood vessels
-Sensory receptors: pressure, touch, pain, heat, cold
2. What are appendages in the skin? What is the function of each?
a. Hair follicles: Stratum Basale-hair producing
-Arrector pili muscle associated with hair follicle
b. Sebaceous glands: Produce sebum
-secretion increases at puberty-influence of sex hormones
c. Sweat glands:
i. Eccrine: glands all over body and secrete sweat through pores onto the skin
in response to increased heat or emotional stress
ii. Apocrine: sweat glands in axillae, scalp, face, external genitalia and the
ducts of these glands open into the hair follicles.
3. What are the 5 functions of the skin?
-First line of defense (mechanical barrier)
-Prevents excessive fluid loss
-Sensory perception
-Synthesizes vitamin D
4. Describe the following skin lesions: (Table 8-1)
, a. Vesicle: or blister, thin wall, raised, fluid filled
b. Plaque: slightly elevated, flat, “scale” like lesion
c. Crust: dry rough surface or dried exudate or blood
d. Lichenification: thick dry rough surface (leather like)
e. Keloid: raised irregular and increasing mass of collagen, resulting from excessive
scar tissue formation
f. Fissure: crack in tissue
g. Ulcer: cavity in tissue
h. Erosion: shallow moist cavity in epidermis
i. Comedome: mass of sebum, keratin & debris blocking the opening of a hair
follicle
5. What is pruritus? Chemical irritation caused by insect bites, allergic responses,
infestations by parasites.
a. What can cause it? Release of histamine in hypersensitivity response
b. Why is it harmful to scratch a pruritic area? May break skin increasing risk for
infection
c. Describe treatments for pruritus: topical agents (reduce sensation)
antihistamines or glucocorticoids. Avoidance of allergens. Antibiotics with
infections. Surgery, laser therapy, electrodessication, cryosurgery (Precancerous
lesions).
6. What is the differences between contact dermatitis and allergic dermatitis?
Contact: exposure to allergen (metals, cosmetics, soaps, chemicals, plants) Occurs on
first exposure. Pruritic rash develops at site few hours later. Direct chemical or
mechanical irritationdoes not involve immune response, is inflammatory b/c of direct
exposure (remove irritant, reduce inflammation w/ glucocorticoids)
Allergic: result of type 1 hypersensitivity (ingestion of substances: shellfish, drugs,
fruits, nuts).
Pruritic lesions & hives part of anaphylaxis (check for swelling around mouth & airway).
Administer EpiPen or other first aid.
,7. What is atopic dermatitis (Eczema)? Inherited tendency. Chronic inflammation from
response to allergens (eosinophilia & increased serum IgE levels).
a. What are clinical manifestations? Children: Rash is erythematous w/ serous
exudate.
Occurs on face, chest & shoulders. Adults: rash is dry, scaly, pruritic on flexor
surfaces
b. How is it treated? Topical glucocorticoids & antihistamines
8. What is psoriasis? Chronic inflammatory skin disorder. Abnormal T cell activation-
excessive proliferation of keratinocytes. Increased cellular proliferation
a. What are the clinical manifestations? Lesions on face, scalp, elbows, knees.
Itching or burning sensations
b. What cells are abnormally activated? T cell
c. What medication are severe cases treated with? Glucocorticoids, tar
preparations, antimetabolites
9. What is scleroderma? Skin disorder may be systemic & affect viscera. Increased
collagen deposition
a. What happens to produce hard, shiny, tight, immovable areas of skin?
Inflammation & fibrosis w/ decreased capillary networks
b. Can this happen elsewhere in the body? May cause renal failure, intestinal
obstruction, respiratory failure by distortion of tissues
10. What is cellulitis? Bacterial skin infection of the dermis & subcutaneous tissue.
a. What organism usually causes it? Staphylococcus aureus & sometimes
Streptococcus
b. What are clinical manifestations? Red, swollen & painful areas. Red streaks
develop along lymph vessels proximal to infected area
11. What is a furuncle (boils)? Bacterial Infection
a. What are the clinical manifestations? Large amount of frequent drainage of
purulent exudate
b. Why do we not want to squeeze a boil? Can result in spread of infection to other
areas b/c you’re actually pushing the infection further down in the skin rather than
pushing it out
, c. What are carbuncles? Collection of furuncles that form a large infected mass
12. What is impetigo? Infection, with the appearance of lesions that are common on the
face.
Pruritus is common=scratching & further spread of infection
a. Is it contagious? VERY in neonates
i.How is it spread? Close physical contact or fomites
b. What is the causative organism? S. aureus
c. What is the treatment? Topical antibiotics (early stages). Systemic
administration if extensive
13. What is acute necrotizing fasciitis? “Fleshing eating” Mixture of aerobic & anaerobic
bacteria at site of infection
a. What is the causative agent? Gram-pos. group A beta-hemolytic Streptococcus
b. What event usually precipitates acute necrotizing fasciitis? Trauma or
infection in the skin & subcutaneous tissue of an extremity
c. Can it be deadly? YES. Bacteria secrete toxins that break down fascia &
connective tissue= MASSIVE TISSUE DESTRUCTION. Systemic toxicity
develops w/ fever, tachycardia, hypotension, confusion, ORGAN FAILURE.
d. How is it treated? Antimicrobial therapy, fluid replacement, excision of all
infected tissue
(amputation)
14. What is the most common type of herpes simplex virus? Type 1 (HSV-1)
a. What does it cause? Cold sores or fever blisters
15. Describe the clinical manifestations of herpes simplex virus?
a. What does the latent stage mean? Does not show signs (asymptomatic) but still
have virus remains in sensory nerve ganglia
16. How is it transmitted? Direct contact with fluid from lesions
17. What medication is it treated with? Laser, freezing w/ liquid nitrogen & topical
medications w/
ASA compounds
18. What virus causes verrucae (warts)? HPV
