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Chapter 13

Total questions: 10

Worksheet time: 5mins

Name
Class
Date
1.

A patient with long-standing venous insufficiency presents with a chronic ulcer on the medial malleolus. The wound base is shallow, exudative, and surrounded by hyperpigmented skin. Which pathophysiologic process most directly caused the hyperpigmentation?

a)

Increased melanin synthesis in basal keratinocytes

b)

Collagen breakdown from protease activity

c)

Hemosiderin deposition from red blood cell extravasation

d)

Fibroblast apoptosis from oxidative stress

2.

A 63-year-old man presents with a pearly papule on the scalp. Histology shows nests of basaloid cells with peripheral palisading in the dermis. Which pathophysiologic mechanism explains why this tumor rarely metastasizes?

a)

Slow growth due to low mitotic index

b)

Effective immune surveillance of keratinocyte antigens

c)

Limited local invasion due to basement membrane adherence

d)

Apoptosis triggered by ultraviolet light exposure

3.

A 28-year-old woman with atopic dermatitis develops S. aureus superinfection. Her eczema is linked to a loss-of-function mutation in the filaggrin gene. How does this defect predispose to infection?

a)

Inhibits dendritic cell migration to lymph nodes

b)

Increases keratinocyte turnover rate

c)

Impairs skin barrier by disrupting keratin aggregation and lipid organization

d)

Stimulates sebaceous gland hyperactivity

4.

A 34-year-old construction worker presents with hyperkeratotic papules on the hands caused by HPV. Which structural change in infected keratinocytes facilitates viral replication?

a)

Loss of tight junction integrity

b)

Proliferation of the stratum spinosum with koilocytosis

c)

Reduced desmosome formation in basal cells

d)

Flattening of the stratum granulosum

5.

A 45-year-old man develops necrotizing fasciitis after a minor leg injury. The infection progresses rapidly despite antibiotic therapy. Which bacterial factor is most responsible for the extensive tissue destruction?

a)

Endotoxin-mediated cytokine release

b)

Capsule-mediated inhibition of phagocytosis

c)

Exotoxin-induced proteolysis of fascia and subcutaneous tissue

d)

Biofilm formation on damaged epidermis

6.

A 50-year-old man presents with erythematous, scaly plaques on extensor surfaces. Histology shows acanthosis, parakeratosis, and elongation of rete ridges. Which immune pathway drives the keratinocyte hyperproliferation in this condition?

a)

IgE-mediated mast cell degranulation

b)

Th17-mediated release of IL-17 and IL-22

c)

NK cell–mediated cytotoxicity

d)

Complement activation via C3b deposition

7.

A 67-year-old immobile patient develops a stage 3 pressure injury. Which pathophysiologic change initiates tissue breakdown in this condition?

a)

Neutrophil infiltration into dermal vessels

b)

Apoptosis of epidermal keratinocytes from UV exposure

c)

Ischemia from sustained capillary compression exceeding arteriolar pressure

d)

Basement membrane thickening from chronic inflammation

8.

A 59-year-old man with a history of multiple blistering sunburns develops a dark lesion on his back. Biopsy reveals malignant melanocytes invading the papillary dermis. Which factor most accurately predicts his prognosis?

a)

Presence of ulceration

b)

Diameter of the lesion

c)

Breslow depth of invasion in millimeters

d)

Degree of pigmentation

9.

A patient sustains a deep partial‑thickness burn over the forearm. Which immediate pathophysiologic change at the burn site is primarily responsible for rapid fluid loss?

a)

Keratinocyte apoptosis from thermal injury

b)

Melanocyte destruction from heat

c)

Increased capillary permeability from histamine and inflammatory mediator release

d)

Loss of desmosomal adhesion between epidermal cells

10.

A 40‑year‑old woman presents with sharply demarcated hypopigmented patches on her arms. Skin biopsy shows absence of melanocytes in affected areas. Which immune process most likely caused these findings?

a)

Antibody‑mediated complement activation

b)

Neutrophil‑derived reactive oxygen species injury

c)

Cytotoxic T‑lymphocyte–mediated apoptosis of melanocytes

d)

NK cell perforin‑granzyme release targeting keratinocytes