NSG 530 Exam 2 | Advanced Pathophysiology | Practice Examination Page 1
, NSG 530 EXAM 2
Advanced Pathophysiology
Wilkes University
100-Question Practice Examination
2026/2027 Edition
1. A patient with a deep abrasion develops diffuse warmth, tenderness, and expanding erythema
involving the dermis and subcutaneous tissue. Which process best explains this presentation?
A) Cellulitis caused by bacterial invasion of deeper skin layers
B) Impetigo limited to the superficial epidermis
C) Tinea confined to keratinized tissue
D) Urticaria caused by transient mast-cell degranulation
Correct Answer: A) Cellulitis caused by bacterial invasion of deeper skin layers
Rationale: Cellulitis is an acute bacterial infection of the deep dermis and subcutaneous tissue, often entering
through a break in the skin. Its diffuse warmth, tenderness, swelling, and spreading erythema distinguish it from
superficial impetigo, transient urticaria, and dermatophyte infection of keratinized tissue.
2. During review of a painful rapidly progressive soft-tissue infection, the clinician notes severe pain
out of proportion to the visible lesion and systemic toxicity. Which pathophysiologic process is most
concerning?
A) Localized folliculitis involving a single hair follicle
B) Necrotizing fasciitis with rapidly spreading fascial destruction
C) Herpes zoster limited to a single sensory nerve root
D) Contact dermatitis from delayed hypersensitivity
Correct Answer: B) Necrotizing fasciitis with rapidly spreading fascial destruction
Rationale: Necrotizing fasciitis spreads quickly along fascial planes and may cause severe pain before dramatic
skin findings appear. Toxin production, thrombosis, and tissue ischemia promote extensive necrosis and systemic
toxicity. Folliculitis, contact dermatitis, and uncomplicated zoster generally do not produce this rapidly destructive
pattern.
3. An older adult develops a unilateral band of painful vesicles along the right thorax several decades
after childhood chickenpox. What mechanism produced the eruption?
A) Reactivation of latent varicella-zoster virus in a sensory ganglion
B) New systemic infection with human papillomavirus
C) Immune-complex deposition in dermal vessels
D) Primary infection with herpes simplex virus type 1
NSG 530 Exam 2 | Advanced Pathophysiology | Practice Examination Page 2
, Correct Answer: A) Reactivation of latent varicella-zoster virus in a sensory ganglion
Rationale: Herpes zoster results when latent varicella-zoster virus reactivates in a sensory ganglion and travels
along the affected dermatome. The unilateral vesicular distribution and neuropathic pain are characteristic. HSV-1,
HPV, and immune-complex vasculitis have different tissue tropisms and clinical patterns.
4. A child has superficial vesicles that rupture and leave honey-colored crusts around the nose and
mouth. Which disorder best matches these findings?
A) Cellulitis
B) Melanoma
C) Impetigo
D) Tinea corporis
Correct Answer: C) Impetigo
Rationale: Impetigo is a highly contagious superficial bacterial infection characterized by fragile vesicles or
pustules that rupture and form honey-colored crusts. Cellulitis involves deeper tissues and causes diffuse
erythema. Tinea is fungal and annular, whereas melanoma is a neoplasm rather than an acute crusting infection.
5. Following prolonged immobility, a patient develops nonblanchable erythema over the sacrum. What
is the earliest key mechanism in pressure injury formation?
A) Excess melanin production in the epidermis
B) Sustained pressure that impairs capillary blood flow and causes tissue ischemia
C) Increased sebum secretion from sebaceous glands
D) Accelerated keratinocyte turnover from autoimmunity
Correct Answer: B) Sustained pressure that impairs capillary blood flow and causes tissue ischemia
Rationale: Pressure injuries begin when sustained external pressure exceeds capillary perfusion pressure,
reducing local blood flow and causing ischemia. Continued oxygen and nutrient deprivation leads to cell injury and
necrosis. Pigmentation, sebaceous activity, and immune-driven keratinocyte turnover do not explain pressure-
related tissue breakdown.
6. A second-degree thermal burn is described as partial-thickness. Which tissue involvement is
expected?
A) Epidermal destruction with extension into part of the dermis
B) Damage confined entirely to the stratum corneum
C) Full destruction of epidermis, dermis, and subcutaneous tissue
D) Selective injury only to sebaceous glands
Correct Answer: A) Epidermal destruction with extension into part of the dermis
Rationale: Partial-thickness burns destroy the epidermis and extend variably into the dermis, commonly producing
blistering and significant pain because sensory structures remain partly intact. Superficial burns are confined to the
epidermis, whereas full-thickness burns destroy the entire dermis and may extend deeper.
7. A large burn causes widespread capillary leak during the early phase of injury. Which physiologic
consequence is most likely during the first several hours?
A) Immediate sustained hypertension from plasma expansion
NSG 530 Exam 2 | Advanced Pathophysiology | Practice Examination Page 3
, NSG 530 EXAM 2
Advanced Pathophysiology
Wilkes University
100-Question Practice Examination
2026/2027 Edition
1. A patient with a deep abrasion develops diffuse warmth, tenderness, and expanding erythema
involving the dermis and subcutaneous tissue. Which process best explains this presentation?
A) Cellulitis caused by bacterial invasion of deeper skin layers
B) Impetigo limited to the superficial epidermis
C) Tinea confined to keratinized tissue
D) Urticaria caused by transient mast-cell degranulation
Correct Answer: A) Cellulitis caused by bacterial invasion of deeper skin layers
Rationale: Cellulitis is an acute bacterial infection of the deep dermis and subcutaneous tissue, often entering
through a break in the skin. Its diffuse warmth, tenderness, swelling, and spreading erythema distinguish it from
superficial impetigo, transient urticaria, and dermatophyte infection of keratinized tissue.
2. During review of a painful rapidly progressive soft-tissue infection, the clinician notes severe pain
out of proportion to the visible lesion and systemic toxicity. Which pathophysiologic process is most
concerning?
A) Localized folliculitis involving a single hair follicle
B) Necrotizing fasciitis with rapidly spreading fascial destruction
C) Herpes zoster limited to a single sensory nerve root
D) Contact dermatitis from delayed hypersensitivity
Correct Answer: B) Necrotizing fasciitis with rapidly spreading fascial destruction
Rationale: Necrotizing fasciitis spreads quickly along fascial planes and may cause severe pain before dramatic
skin findings appear. Toxin production, thrombosis, and tissue ischemia promote extensive necrosis and systemic
toxicity. Folliculitis, contact dermatitis, and uncomplicated zoster generally do not produce this rapidly destructive
pattern.
3. An older adult develops a unilateral band of painful vesicles along the right thorax several decades
after childhood chickenpox. What mechanism produced the eruption?
A) Reactivation of latent varicella-zoster virus in a sensory ganglion
B) New systemic infection with human papillomavirus
C) Immune-complex deposition in dermal vessels
D) Primary infection with herpes simplex virus type 1
NSG 530 Exam 2 | Advanced Pathophysiology | Practice Examination Page 2
, Correct Answer: A) Reactivation of latent varicella-zoster virus in a sensory ganglion
Rationale: Herpes zoster results when latent varicella-zoster virus reactivates in a sensory ganglion and travels
along the affected dermatome. The unilateral vesicular distribution and neuropathic pain are characteristic. HSV-1,
HPV, and immune-complex vasculitis have different tissue tropisms and clinical patterns.
4. A child has superficial vesicles that rupture and leave honey-colored crusts around the nose and
mouth. Which disorder best matches these findings?
A) Cellulitis
B) Melanoma
C) Impetigo
D) Tinea corporis
Correct Answer: C) Impetigo
Rationale: Impetigo is a highly contagious superficial bacterial infection characterized by fragile vesicles or
pustules that rupture and form honey-colored crusts. Cellulitis involves deeper tissues and causes diffuse
erythema. Tinea is fungal and annular, whereas melanoma is a neoplasm rather than an acute crusting infection.
5. Following prolonged immobility, a patient develops nonblanchable erythema over the sacrum. What
is the earliest key mechanism in pressure injury formation?
A) Excess melanin production in the epidermis
B) Sustained pressure that impairs capillary blood flow and causes tissue ischemia
C) Increased sebum secretion from sebaceous glands
D) Accelerated keratinocyte turnover from autoimmunity
Correct Answer: B) Sustained pressure that impairs capillary blood flow and causes tissue ischemia
Rationale: Pressure injuries begin when sustained external pressure exceeds capillary perfusion pressure,
reducing local blood flow and causing ischemia. Continued oxygen and nutrient deprivation leads to cell injury and
necrosis. Pigmentation, sebaceous activity, and immune-driven keratinocyte turnover do not explain pressure-
related tissue breakdown.
6. A second-degree thermal burn is described as partial-thickness. Which tissue involvement is
expected?
A) Epidermal destruction with extension into part of the dermis
B) Damage confined entirely to the stratum corneum
C) Full destruction of epidermis, dermis, and subcutaneous tissue
D) Selective injury only to sebaceous glands
Correct Answer: A) Epidermal destruction with extension into part of the dermis
Rationale: Partial-thickness burns destroy the epidermis and extend variably into the dermis, commonly producing
blistering and significant pain because sensory structures remain partly intact. Superficial burns are confined to the
epidermis, whereas full-thickness burns destroy the entire dermis and may extend deeper.
7. A large burn causes widespread capillary leak during the early phase of injury. Which physiologic
consequence is most likely during the first several hours?
A) Immediate sustained hypertension from plasma expansion
NSG 530 Exam 2 | Advanced Pathophysiology | Practice Examination Page 3
