NUR 632 EXAM 1 QUESTIONS AND
CORRECT ANSWERS. VERIFIED
2025/2026.
Pressure Injuries - ANS 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 - ANS Nonblanchable erythema of intact skin, usually over bony
prominence
Stage 2 Pressure Ulcer - ANS 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 - ANS 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 - ANS Full-thickness tissue loss with exposed bone, muscle, or tendon.
Can include undermining and tunneling.
1 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
,unstageable pressure ulcer - ANS 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 - ANS persistent non-blanchable deep red, maroon, or purple
discoloration of intact skin.
Pressure ulcer pathology - ANS 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) - ANS 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 - ANS 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 - ANS usually develops with first exposure to the antigen, and symptoms of
dermatitis occur with reexposure.
2 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
, Manifestations of allergic contact dermatitis include erythema and swelling with pruritic
vesicular leasions in the area of allergens contact.
Irritant contact dermatitis - ANS 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) - ANS is more common in infancy and childhood.
Stasis Dermatitis - ANS 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 - ANS 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 - ANS 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.
3 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
CORRECT ANSWERS. VERIFIED
2025/2026.
Pressure Injuries - ANS 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 - ANS Nonblanchable erythema of intact skin, usually over bony
prominence
Stage 2 Pressure Ulcer - ANS 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 - ANS 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 - ANS Full-thickness tissue loss with exposed bone, muscle, or tendon.
Can include undermining and tunneling.
1 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
,unstageable pressure ulcer - ANS 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 - ANS persistent non-blanchable deep red, maroon, or purple
discoloration of intact skin.
Pressure ulcer pathology - ANS 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) - ANS 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 - ANS 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 - ANS usually develops with first exposure to the antigen, and symptoms of
dermatitis occur with reexposure.
2 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
, Manifestations of allergic contact dermatitis include erythema and swelling with pruritic
vesicular leasions in the area of allergens contact.
Irritant contact dermatitis - ANS 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) - ANS is more common in infancy and childhood.
Stasis Dermatitis - ANS 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 - ANS 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 - ANS 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.
3 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
