NUR 632 Exam 1 Questions and Answers Latest Update 2025-2026
Pressure Injuries - Answers Develops over bony prominence's when constant pressure on
tissues distorts capillaries and occludes the blood flow and oxygen supply. If pressure
continues unrelieved, the endothelial cells lining the capillaries become disrupted with platelet
aggregation, forming microthrombi that block blood flow and cause anoxic necrosis of
surrounding tissue.
Stage 1 Pressure Ulcer - Answers Nonblanchable erythema of intact skin, usually over bony
prominence
Stage 2 Pressure Ulcer - Answers partial thickness skin loss involving epidermis, dermis, or both
presenting as a shallow open ulcer with a pink-red wound bed without slough.
Stage 3 Pressure Ulcer - Answers Full-thickness skin loss involving damage or necrosis of
subcutaneous tissue that may extend down to, but not through, underlying fascia. Adipose
tissue visible in ulcer, granulation tissue and rolled wound edges often present.
Stage 4 Pressure Ulcer - Answers Full-thickness tissue loss with exposed bone, muscle, or
tendon. Can include undermining and tunneling.
unstageable pressure ulcer - Answers A full-thickness wound in which the amount of necrotic
tissue, or eschar, in the wound bed makes it impossible to assess the depth of the wound or the
involvement of underlying structures
Deep tissue pressure injury - Answers persistent non-blanchable deep red, maroon, or purple
discoloration of intact skin.
Pressure ulcer pathology - Answers Bacteria colonize the dead tissue, and infection is usually
localized and self-limiting. Proteolytic enzymes from bacteria and macrophages dissolve
necrotic tissue and cause a foul-smelling discharge that resembles, but is not, pus. The necrotic
tissue initiates an inflammatory response with potential pain, fever, and leukocytosis.
Allergic Contact Dermatitis (ACD) - Answers is a common form of T-cell mediated or delayed
hypersensitivity (type IV). The response is a consequence of alterations in the skin barrier
function with reaction to irritants. Release of cytokines, chemokines, and cytotoxins from
keratinocytes; dendritic cells (Langerhans); and natural killer cells and neuronal responses. Such
as pruritis.
Allergens can form the sensitizing anitgen; contact eith poison ivy is a common example.
Skin Allergic Response - Answers When the allergen comes in contact with the skin, the allergen
is bound to a carrier protein, forming a hapten-specific sensitizing antigen, Langerhans cells
process the antigen and carry it to T-cells in the draining lymph nodes. T cells then become
, sensitized to the antigen, releasing cytokines and chemokines leading to leukocyte infiltration
and antigen specific inflammation.
Sensitization - Answers usually develops with first exposure to the antigen, and symptoms of
dermatitis occur with reexposure.
Manifestations of allergic contact dermatitis include erythema and swelling with pruritic
vesicular leasions in the area of allergens contact.
Irritant contact dermatitis - Answers is a non-specific, inflammatory dermatitis caused by
activation of the innate immune system by pro-inflammatory properties of chemicals. The
intensity relates to concentration of irritant, exposure time, disruption of barrier, and age.
Atopic Dermatitis (Eczema) - Answers is more common in infancy and childhood.
Stasis Dermatitis - Answers Usually occurs on the legs as a result of venous stasis and edema.
Pooling of venous traps leukocytes that may release proteolytic enzymes. Increased venous
pressure widens interendothelial pores with deposition of red blood cells, fibrin, and other
macromolecules, making them unavailable for repair and promoting inflammation.
Treatment includes elevating the legs as soon as possible, compression stockings, and
avoiding standing for a long time.
seborrheic dermatitis - Answers is a common inflammation of the skin involving the scalp,
eyebrows, eyelids, ear canals, nasolabial folds, axillae, chest, and back. (Cradle cap in infants).
Malassezia infections causes inflammation with stratum corneum hyperproliferation (scaling)
and incomplete corneocyte differentiation. Alterations in the stratum corneum barrier allows
water to more readily leave the skin.
Folliculitis - Answers is an inflammation of the hair follicle and can be infectious, caused by
bacteria, viruses, fungi, or a noninfectious caused by trauma. S. Aureus is a common causative
organism.
The infection develops from proliferation of the microorganism around the opening of a follicle
then spreads to the follicle. Inflammation is caused by the release of chemotatic factors and
enzymes from bacteria. The lesions appear as as pustules and papules with surrounding areas
of erythema.
Foruncles (boils) - Answers inflamations of the hair follicle. They can develop from a folliculitis
that spreads through the follicular wall into the surrounding dermis. The invading
Pressure Injuries - Answers Develops over bony prominence's when constant pressure on
tissues distorts capillaries and occludes the blood flow and oxygen supply. If pressure
continues unrelieved, the endothelial cells lining the capillaries become disrupted with platelet
aggregation, forming microthrombi that block blood flow and cause anoxic necrosis of
surrounding tissue.
Stage 1 Pressure Ulcer - Answers Nonblanchable erythema of intact skin, usually over bony
prominence
Stage 2 Pressure Ulcer - Answers partial thickness skin loss involving epidermis, dermis, or both
presenting as a shallow open ulcer with a pink-red wound bed without slough.
Stage 3 Pressure Ulcer - Answers Full-thickness skin loss involving damage or necrosis of
subcutaneous tissue that may extend down to, but not through, underlying fascia. Adipose
tissue visible in ulcer, granulation tissue and rolled wound edges often present.
Stage 4 Pressure Ulcer - Answers Full-thickness tissue loss with exposed bone, muscle, or
tendon. Can include undermining and tunneling.
unstageable pressure ulcer - Answers A full-thickness wound in which the amount of necrotic
tissue, or eschar, in the wound bed makes it impossible to assess the depth of the wound or the
involvement of underlying structures
Deep tissue pressure injury - Answers persistent non-blanchable deep red, maroon, or purple
discoloration of intact skin.
Pressure ulcer pathology - Answers Bacteria colonize the dead tissue, and infection is usually
localized and self-limiting. Proteolytic enzymes from bacteria and macrophages dissolve
necrotic tissue and cause a foul-smelling discharge that resembles, but is not, pus. The necrotic
tissue initiates an inflammatory response with potential pain, fever, and leukocytosis.
Allergic Contact Dermatitis (ACD) - Answers is a common form of T-cell mediated or delayed
hypersensitivity (type IV). The response is a consequence of alterations in the skin barrier
function with reaction to irritants. Release of cytokines, chemokines, and cytotoxins from
keratinocytes; dendritic cells (Langerhans); and natural killer cells and neuronal responses. Such
as pruritis.
Allergens can form the sensitizing anitgen; contact eith poison ivy is a common example.
Skin Allergic Response - Answers When the allergen comes in contact with the skin, the allergen
is bound to a carrier protein, forming a hapten-specific sensitizing antigen, Langerhans cells
process the antigen and carry it to T-cells in the draining lymph nodes. T cells then become
, sensitized to the antigen, releasing cytokines and chemokines leading to leukocyte infiltration
and antigen specific inflammation.
Sensitization - Answers usually develops with first exposure to the antigen, and symptoms of
dermatitis occur with reexposure.
Manifestations of allergic contact dermatitis include erythema and swelling with pruritic
vesicular leasions in the area of allergens contact.
Irritant contact dermatitis - Answers is a non-specific, inflammatory dermatitis caused by
activation of the innate immune system by pro-inflammatory properties of chemicals. The
intensity relates to concentration of irritant, exposure time, disruption of barrier, and age.
Atopic Dermatitis (Eczema) - Answers is more common in infancy and childhood.
Stasis Dermatitis - Answers Usually occurs on the legs as a result of venous stasis and edema.
Pooling of venous traps leukocytes that may release proteolytic enzymes. Increased venous
pressure widens interendothelial pores with deposition of red blood cells, fibrin, and other
macromolecules, making them unavailable for repair and promoting inflammation.
Treatment includes elevating the legs as soon as possible, compression stockings, and
avoiding standing for a long time.
seborrheic dermatitis - Answers is a common inflammation of the skin involving the scalp,
eyebrows, eyelids, ear canals, nasolabial folds, axillae, chest, and back. (Cradle cap in infants).
Malassezia infections causes inflammation with stratum corneum hyperproliferation (scaling)
and incomplete corneocyte differentiation. Alterations in the stratum corneum barrier allows
water to more readily leave the skin.
Folliculitis - Answers is an inflammation of the hair follicle and can be infectious, caused by
bacteria, viruses, fungi, or a noninfectious caused by trauma. S. Aureus is a common causative
organism.
The infection develops from proliferation of the microorganism around the opening of a follicle
then spreads to the follicle. Inflammation is caused by the release of chemotatic factors and
enzymes from bacteria. The lesions appear as as pustules and papules with surrounding areas
of erythema.
Foruncles (boils) - Answers inflamations of the hair follicle. They can develop from a folliculitis
that spreads through the follicular wall into the surrounding dermis. The invading
