Pathophysiology Quiz: Pressure Injuries
20 questions · exam conditions
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Pressure InjuriesQuestion 1 of 20

Shear stress is a particularly destructive force in the development of sacral and coccygeal pressure injuries. Which statement provides the most accurate description of the specific pathophysiological mechanism of shear?

Shear is a superficial force that abrades the epidermis, similar to a rug burn, creating an entry point for bacteria.
Shear traps a layer of moisture between the skin and the support surface, leading to maceration and chemical irritation.
Shear describes the perpendicular force of body weight compressing tissue directly against a bony prominence.
Shear causes deep, angular distortion of tissue layers and stretches and occludes the perforating blood vessels that supply the skin from below.
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Pathophysiology Quiz

Pathophysiology Quiz: Pressure Injuries

Practice Pressure Injuries in Pathophysiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Pressure Injuries, giving you a quick way to practice the rules, question types, and explanations that matter most for Pathophysiology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

Shear stress is a particularly destructive force in the development of sacral and coccygeal pressure injuries. Which statement provides the most accurate description of the specific pathophysiological mechanism of shear?

  1. Shear is a superficial force that abrades the epidermis, similar to a rug burn, creating an entry point for bacteria.
  2. Shear traps a layer of moisture between the skin and the support surface, leading to maceration and chemical irritation.
  3. Shear describes the perpendicular force of body weight compressing tissue directly against a bony prominence.
  4. Shear causes deep, angular distortion of tissue layers and stretches and occludes the perforating blood vessels that supply the skin from below. (correct answer)
Explanation: Shear is a force parallel to the skin surface. It occurs when tissue layers slide over one another, such as when the skeleton slides down in a raised bed while the skin stays put. This movement stretches and angulates the blood vessels that run perpendicularly from the deep fascia to the skin. This distortion can lead to vessel occlusion, thrombosis, and ischemic necrosis of the deep tissues, making shear a particularly potent cause of severe, deep pressure injuries.

Question 2

An unresponsive patient is brought to the emergency department after being found on their side on a concrete floor for an estimated 12 hours. The nurse assesses a large, intact, purple, boggy-feeling area over the greater trochanter.

Which pathophysiological interpretation of this clinical finding is most accurate?

  1. This represents Stage 1 pressure injury; the non-blanchable discoloration will resolve quickly with pressure relief and repositioning.
  2. The finding is a simple contusion from a fall, and the pressure component is minimal given the short duration.
  3. This is a classic presentation of a suspected deep tissue pressure injury, indicating extensive necrosis of underlying muscle and fat. (correct answer)
  4. The purple color indicates venous pooling, a form of reactive hyperemia that shows the microcirculation is still intact and responding.
Explanation: The presentation—a localized area of persistent, non-blanchable, deep-colored discoloration (purple/maroon) with a boggy or mushy feel and intact skin after a period of intense/prolonged pressure—is the classic sign of a suspected deep tissue pressure injury (DTPI). This indicates severe damage and necrosis have already occurred in the deep tissues next to the bone, even though the skin has not yet broken down. It is far more severe than a Stage 1 injury or a simple contusion.

Question 3

A patient's Braden Scale assessment yields a score of 10, with the lowest possible score (1) in the 'Mobility' subscale, indicating the patient is completely immobile. How does this specific deficit most directly contribute to the pathophysiology of pressure injury?

  1. It leads directly to disuse muscle atrophy, which reduces the natural padding over bony prominences.
  2. It impairs the patient's ability to maintain adequate oral intake, leading to nutritional deficiencies.
  3. It increases the risk of shear and friction injuries because the patient requires total assistance for all repositioning.
  4. It eliminates the body's ability to perform small, even unconscious, weight shifts that are essential for restoring capillary blood flow. (correct answer)
Explanation: When you encounter questions about pressure injury pathophysiology, focus on the fundamental mechanism: prolonged pressure that exceeds capillary perfusion pressure (typically 25-32 mmHg) leads to tissue ischemia and subsequent necrosis. Complete immobility creates the most direct pathway to pressure injury because it eliminates the body's natural protective mechanism of frequent, small positional adjustments. Even during sleep, healthy individuals make hundreds of unconscious micro-movements that briefly relieve pressure and allow capillary refill. When this ability is completely lost, sustained pressure over bony prominences creates a continuous state of tissue hypoxia, making pressure injury development almost inevitable. Option A incorrectly suggests muscle atrophy is the primary mechanism. While disuse atrophy does occur with immobility, it's a slower process that contributes to long-term risk rather than the immediate pathophysiology of pressure injury formation. Option B confuses immobility with dysphagia or other feeding difficulties. Physical immobility doesn't directly impair oral intake ability, and nutritional deficiency, while important for healing, isn't the most direct pathophysiological consequence of the mobility deficit described. Option C addresses shear and friction forces, which are indeed problematic during repositioning of immobile patients. However, these mechanical forces cause more superficial tissue damage, whereas the question asks about the most direct contribution of immobility itself. Remember: pressure injury pathophysiology always returns to the basic principle of sustained pressure interrupting blood flow. The most dangerous aspect of complete immobility is losing those constant, subtle position changes that maintain tissue perfusion.

Question 4

A 78-year-old patient is placed in a high Fowler's position (head of bed elevated 60 degrees) to ease breathing. After two hours, the nurse notes a reddened area over the patient's sacrum. The patient frequently slides down in the bed.

Which combination of mechanical forces is most responsible for the development of potential deep tissue injury in this patient's sacral region?

  1. Sustained perpendicular pressure from body weight combined with shear force from the gravitational sliding of skeletal structures against stationary skin. (correct answer)
  2. Intermittent high pressure from repositioning efforts combined with friction from the bed linens against the epidermis.
  3. Friction alone, caused by the patient's skin rubbing against the bed sheets during repositioning attempts.
  4. Moisture from diaphoresis combined with direct pressure, leading to maceration and superficial tissue breakdown.
Explanation: In a high Fowler's position, the patient's body is subject to two primary forces. Perpendicular pressure is exerted by the body weight on the sacrum. Simultaneously, gravity pulls the skeleton downward, while the skin over the sacrum tends to remain in place due to friction with the bed. This creates a shear force, which stretches and distorts underlying tissues and blood vessels, leading to deep tissue injury. Friction is more superficial, and while moisture is a factor, the combination of pressure and shear is the key mechanism for deep injury in this scenario.

Question 5

A patient with limited mobility is repositioned after being on their left side for 4 hours. The nurse observes an area of reactive hyperemia over the left trochanter. Two hours later, after pressure has been relieved, the area appears pale, but the patient complains of a new, burning pain.

Which pathophysiological mechanism best explains the development of new pain and potential for further tissue damage after pressure has been relieved?

  1. Persistent anoxia from irreversible capillary collapse that occurred during the prolonged pressure period.
  2. The formation of reactive oxygen species and an influx of neutrophils upon restoration of blood flow, causing reperfusion injury. (correct answer)
  3. Direct mechanical lysis of cell membranes caused by the initial compressive force, leading to delayed nerve ending exposure.
  4. Bacterial translocation from the gut to the ischemic tissue, initiating a systemic inflammatory response.
Explanation: This scenario describes reperfusion injury. During the ischemic period, cells build up metabolic byproducts. When blood flow is restored (reperfusion), the sudden reintroduction of oxygen leads to the formation of damaging reactive oxygen species (free radicals). This, along with the influx of inflammatory cells like neutrophils, causes further cellular damage, inflammation, and pain, which is a paradoxical injury occurring after the initial insult (pressure) is removed.

Question 6

The average capillary arteriolar pressure is approximately 32 mmHg. A patient resting on a standard hospital mattress experiences a localized interface pressure of 45 mmHg over their coccyx. Assuming this pressure is sustained, what is the most immediate physiological consequence in the affected tissue?

  1. A compensatory reactive hyperemia response is initiated to increase local blood flow and nutrient delivery.
  2. Blood flow through the local capillaries and post-capillary venules ceases, leading to ischemia and a deficit of oxygen and nutrients. (correct answer)
  3. Lymphatic drainage is significantly enhanced, leading to a rapid reduction in interstitial fluid and tissue dehydration.
  4. The high pressure forces fluid from the intravascular space into the interstitium, causing acute localized edema.
Explanation: When external pressure (45 mmHg) exceeds the pressure that keeps capillaries open (intracapillary pressure, ~32 mmHg), the vessels collapse. This physically obstructs blood flow, leading to immediate local ischemia. Oxygen and nutrients can no longer reach the cells, and metabolic waste products cannot be removed. Reactive hyperemia occurs after the pressure is relieved, not during. Lymphatic vessels are also compressed, impairing drainage. Fluid shifts are a later consequence of cell injury and inflammation.

Question 7

A patient with end-stage renal disease (ESRD) is noted to have developed a rapidly progressing pressure injury. The patient undergoes hemodialysis three times a week.

Beyond general immobility and malnutrition, which factor most specific to the pathophysiology of ESRD and its treatment contributes significantly to this patient's risk?

  1. Peripheral edema common in ESRD, which effectively cushions bony prominences against pressure.
  2. The high-protein diet prescribed for dialysis patients, which can lead to excessive nitrogenous waste.
  3. Accumulation of uremic toxins making tissue more fragile, coupled with episodes of hypotension during dialysis that impair perfusion. (correct answer)
  4. Increased skin turgor and hydration due to fluid retention between dialysis sessions, which strengthens the skin barrier.
Explanation: Patients with ESRD have multiple unique risk factors. Uremia (the buildup of toxins in the blood) is associated with pruritus, calciphylaxis, and overall tissue fragility. Furthermore, the process of hemodialysis itself often causes significant fluid shifts and transient hypotension, which can severely compromise perfusion to already at-risk tissues for several hours at a time, exacerbating the effects of pressure.

Question 8

An 82-year-old patient with severe COPD, peripheral vascular disease (PVD), and cachexia is admitted for an exacerbation, requiring continuous oxygen therapy. The patient is largely immobile due to profound dyspnea and fatigue.

Among this patient's multiple risk factors, which one most directly compromises the final step of oxygen delivery to tissues under pressure, thereby dramatically lowering the tissue's tolerance to ischemia?

  1. Cachexia, by reducing the amount of protective subcutaneous fat over bony prominences.
  2. Peripheral vascular disease, which chronically reduces baseline arterial inflow to the lower extremities.
  3. Immobility, which causes prolonged, unrelieved pressure on the sacrum and heels.
  4. Systemic hypoxemia from COPD, which lowers the arterial oxygen tension (PaO2) of the blood arriving at the compressed capillaries. (correct answer)
Explanation: This question tests your understanding of the oxygen delivery cascade and how different pathophysiological states affect tissue oxygenation under stress. When tissues are compressed, they become critically dependent on whatever oxygen remains available in the blood supply that still reaches them. The correct answer is D because systemic hypoxemia directly reduces the oxygen content of blood arriving at compressed tissues. Under normal circumstances, tissues can tolerate brief periods of reduced blood flow because the blood that does reach them still carries adequate oxygen. However, when arterial oxygen tension (PaO2) is already low due to COPD, even normally adequate blood flow delivers insufficient oxygen. This dramatically lowers the tissue's ischemic tolerance because there's no oxygen reserve to draw upon when perfusion is compromised by external pressure. Option A is wrong because while cachexia reduces protective padding over bony prominences, it doesn't directly affect the oxygen-carrying capacity of blood reaching those areas. Option B incorrectly identifies PVD as the primary factor - while PVD does reduce baseline perfusion, the question asks specifically about compromising oxygen delivery under pressure, which is more directly affected by oxygen content than flow rate. Option C focuses on the mechanical cause of pressure rather than the physiological factor that determines tissue tolerance to that pressure. Remember that tissue ischemia results from both inadequate perfusion AND inadequate oxygen content. When evaluating risk factors for pressure injuries, always consider which factors affect the supply side (blood flow and oxygen content) versus the demand side (tissue metabolism and external pressure).

Question 9

A patient in the ICU for septic shock has a mean arterial pressure of 60 mmHg and is being treated with a continuous infusion of norepinephrine to maintain perfusion to vital organs.

How does the use of norepinephrine in this context create a 'perfect storm' for the development of severe pressure injuries?

  1. Norepinephrine increases blood pressure by causing profound peripheral vasoconstriction, which severely compromises cutaneous blood flow to pressure points. (correct answer)
  2. Norepinephrine increases the metabolic rate of the skin, making it more vulnerable to ischemia when pressure is applied.
  3. The drug promotes fluid retention and peripheral edema, which impairs nutrient delivery by increasing the distance from capillaries to cells.
  4. The patient's underlying hypotension is the sole risk factor, and norepinephrine mitigates this by improving overall circulation.
Explanation: Septic shock itself compromises perfusion. Norepinephrine, a potent vasopressor, works by constricting peripheral blood vessels to shunt blood centrally and raise blood pressure. While this is life-saving for vital organs (brain, heart), it comes at the cost of dramatically reducing blood flow to the skin and subcutaneous tissues. When this iatrogenic peripheral ischemia is combined with the external compression from immobility, the result is an extremely high risk of rapid and severe tissue necrosis.

Question 10

An immobile 85-year-old patient is admitted with pneumonia, a fever of 39°C (102.2°F), and urinary incontinence.

How do fever and incontinence synergistically increase this patient's risk of sacral pressure injury?

  1. Fever causes peripheral vasodilation, which shunts blood away from bony prominences, while incontinence introduces urea, which is directly toxic to epidermal cells.
  2. The combination leads to rapid systemic dehydration, which reduces tissue perfusion and skin turgor globally.
  3. Fever increases the metabolic rate and oxygen demand of skin cells, while moisture from incontinence macerates the stratum corneum, reducing its protective function. (correct answer)
  4. Incontinence provides a growth medium for bacteria, and the fever creates an ideal temperature for rapid proliferation, leading to primary skin infection.
Explanation: This is a synergistic interaction. The fever raises the metabolic rate of the tissue, meaning the cells require more oxygen and nutrients to survive. At the same time, the excessive moisture from incontinence weakens the skin's barrier (stratum corneum) through maceration and increases the coefficient of friction. Therefore, the tissue is more vulnerable to breakdown (due to moisture) at the same time its metabolic needs are higher (due to fever), making it exceptionally susceptible to ischemic injury from pressure.

Question 11

Consider two independent risk factors for a bed-bound patient: severe iron-deficiency anemia with a hemoglobin of 6 g/dL, and moderate protein-energy malnutrition with a prealbumin of 14 mg/dL. Which factor poses a more immediate and critical threat to tissue viability under pressure, and why?

  1. Malnutrition, because the lack of protein substrate prevents the constant cellular turnover required to maintain skin integrity.
  2. Malnutrition, because low prealbumin directly causes interstitial edema, which impairs diffusion of nutrients.
  3. Severe anemia, because it drastically reduces the oxygen-carrying capacity of the blood, rendering even minimal perfusion insufficient to prevent anoxic cell death. (correct answer)
  4. Severe anemia, because it forces the heart to increase its rate, which shunts blood away from the periphery to reduce cardiac workload.
Explanation: Both are serious risk factors. However, severe anemia presents a more acute threat to tissue under pressure. Pressure reduces blood flow (perfusion). The purpose of perfusion is to deliver oxygen. If the blood that is getting through has a severely limited capacity to carry oxygen (due to low hemoglobin), the tissue will become critically hypoxic and die much more quickly than in a person with normal hemoglobin. While malnutrition weakens tissue over time, severe hypoxia causes cell death within minutes to hours.

Question 12

In the initial moments after a high-magnitude pressure is applied to soft tissue, such as when a patient is dropped onto a hard surface, cellular injury can begin almost instantly. Which mechanism of injury predominates in this initial phase, even before significant ischemia has developed?

  1. Accumulation of lactic acid and other metabolic wastes from anaerobic metabolism.
  2. Direct mechanical strain and deformation of cell membranes and cytoskeletons, disrupting cellular integrity and function. (correct answer)
  3. Apoptosis triggered by the release of pro-inflammatory cytokines from surrounding tissue.
  4. Endothelial cell swelling and damage within capillaries due to profound anoxia.
Explanation: While ischemia (lack of blood flow) is a major component of pressure injury, direct mechanical forces can cause damage independent of blood supply. Intense, short-duration pressure can physically deform cells, stretching membranes beyond their elastic limit and disrupting the internal cytoskeleton. This direct damage can lead to necrosis before the effects of ischemia, which take minutes to hours to manifest, become the primary driver of injury.

Question 13

Shear stress is a particularly destructive force in the development of sacral and coccygeal pressure injuries. Which statement provides the most accurate description of the specific pathophysiological mechanism of shear?

  1. Shear is a superficial force that abrades the epidermis, similar to a rug burn, creating an entry point for bacteria.
  2. Shear traps a layer of moisture between the skin and the support surface, leading to maceration and chemical irritation.
  3. Shear describes the perpendicular force of body weight compressing tissue directly against a bony prominence.
  4. Shear causes deep, angular distortion of tissue layers and stretches and occludes the perforating blood vessels that supply the skin from below. (correct answer)
Explanation: Shear is a force parallel to the skin surface. It occurs when tissue layers slide over one another, such as when the skeleton slides down in a raised bed while the skin stays put. This movement stretches and angulates the blood vessels that run perpendicularly from the deep fascia to the skin. This distortion can lead to vessel occlusion, thrombosis, and ischemic necrosis of the deep tissues, making shear a particularly potent cause of severe, deep pressure injuries.

Question 14

A nurse identifies a localized area of intact skin over a patient's heel that is deep red and does not blanch when pressure is applied. What is the key pathophysiological significance of the non-blanchable nature of this erythema?

  1. It indicates a normal, transient inflammatory response to pressure, characterized by robust vasodilation.
  2. It signifies that friction has removed the top layers of the epidermis, exposing the highly vascular dermis.
  3. It reflects damage to the microvasculature with leakage of red blood cells into the interstitium, signaling a Stage 1 pressure injury. (correct answer)
  4. It is a sign of subcutaneous fat necrosis caused by the pressure, which will resolve without intervention.
Explanation: Blanchable erythema is redness that turns white with pressure and then red again when pressure is released; it indicates that the microcirculation is still intact and is simply dilated (vasodilation). Non-blanchable erythema signifies that the capillaries have been damaged by ischemia and/or reperfusion injury, allowing red blood cells to leak into the surrounding tissue. The redness persists despite pressure because the extravasated blood is trapped in the interstitium. This is the hallmark of a Stage 1 pressure injury and indicates a more significant level of tissue injury.

Question 15

A clinician is assessing an older adult's risk for pressure injury. The patient's lab results show a serum albumin of 2.8 g/dL. The patient reports a poor appetite for the last several weeks.

While low serum albumin is a widely recognized risk marker, what is the more direct physiological reason for this patient's heightened risk for tissue breakdown?

  1. Low plasma oncotic pressure from hypoalbuminemia causes massive interstitial edema, which compresses capillaries.
  2. Inadequate protein and calorie intake impairs the synthesis of collagen, immune cells, and transport proteins necessary for tissue maintenance and repair. (correct answer)
  3. Albumin is the primary buffer in the blood, and low levels lead to systemic acidosis, which makes cells fragile.
  4. The patient's poor appetite is likely due to zinc deficiency, which is the primary cause of impaired wound healing.
Explanation: Low serum albumin is often a marker of chronic malnutrition and inflammation, not just an acute problem. The more fundamental issue is the lack of substrate (protein, calories, vitamins) from poor nutritional intake. This directly impairs the body's ability to build and repair tissue, specifically through reduced collagen synthesis, weakened immune response, and lack of other essential proteins. While low oncotic pressure can contribute to edema, it's the underlying nutritional deficit that is the more direct and causal factor for impaired tissue integrity.

Question 16

In the initial moments after a high-magnitude pressure is applied to soft tissue, such as when a patient is dropped onto a hard surface, cellular injury can begin almost instantly. Which mechanism of injury predominates in this initial phase, even before significant ischemia has developed?

  1. Accumulation of lactic acid and other metabolic wastes from anaerobic metabolism.
  2. Direct mechanical strain and deformation of cell membranes and cytoskeletons, disrupting cellular integrity and function. (correct answer)
  3. Apoptosis triggered by the release of pro-inflammatory cytokines from surrounding tissue.
  4. Endothelial cell swelling and damage within capillaries due to profound anoxia.
Explanation: While ischemia (lack of blood flow) is a major component of pressure injury, direct mechanical forces can cause damage independent of blood supply. Intense, short-duration pressure can physically deform cells, stretching membranes beyond their elastic limit and disrupting the internal cytoskeleton. This direct damage can lead to necrosis before the effects of ischemia, which take minutes to hours to manifest, become the primary driver of injury.

Question 17

The average capillary arteriolar pressure is approximately 32 mmHg. A patient resting on a standard hospital mattress experiences a localized interface pressure of 45 mmHg over their coccyx. Assuming this pressure is sustained, what is the most immediate physiological consequence in the affected tissue?

  1. A compensatory reactive hyperemia response is initiated to increase local blood flow and nutrient delivery.
  2. Blood flow through the local capillaries and post-capillary venules ceases, leading to ischemia and a deficit of oxygen and nutrients. (correct answer)
  3. Lymphatic drainage is significantly enhanced, leading to a rapid reduction in interstitial fluid and tissue dehydration.
  4. The high pressure forces fluid from the intravascular space into the interstitium, causing acute localized edema.
Explanation: When external pressure (45 mmHg) exceeds the pressure that keeps capillaries open (intracapillary pressure, ~32 mmHg), the vessels collapse. This physically obstructs blood flow, leading to immediate local ischemia. Oxygen and nutrients can no longer reach the cells, and metabolic waste products cannot be removed. Reactive hyperemia occurs after the pressure is relieved, not during. Lymphatic vessels are also compressed, impairing drainage. Fluid shifts are a later consequence of cell injury and inflammation.

Question 18

A patient with end-stage renal disease (ESRD) is noted to have developed a rapidly progressing pressure injury. The patient undergoes hemodialysis three times a week.

Beyond general immobility and malnutrition, which factor most specific to the pathophysiology of ESRD and its treatment contributes significantly to this patient's risk?

  1. Peripheral edema common in ESRD, which effectively cushions bony prominences against pressure.
  2. The high-protein diet prescribed for dialysis patients, which can lead to excessive nitrogenous waste.
  3. Accumulation of uremic toxins making tissue more fragile, coupled with episodes of hypotension during dialysis that impair perfusion. (correct answer)
  4. Increased skin turgor and hydration due to fluid retention between dialysis sessions, which strengthens the skin barrier.
Explanation: Patients with ESRD have multiple unique risk factors. Uremia (the buildup of toxins in the blood) is associated with pruritus, calciphylaxis, and overall tissue fragility. Furthermore, the process of hemodialysis itself often causes significant fluid shifts and transient hypotension, which can severely compromise perfusion to already at-risk tissues for several hours at a time, exacerbating the effects of pressure.

Question 19

A patient's Braden Scale assessment yields a score of 10, with the lowest possible score (1) in the 'Mobility' subscale, indicating the patient is completely immobile. How does this specific deficit most directly contribute to the pathophysiology of pressure injury?

  1. It leads directly to disuse muscle atrophy, which reduces the natural padding over bony prominences.
  2. It impairs the patient's ability to maintain adequate oral intake, leading to nutritional deficiencies.
  3. It increases the risk of shear and friction injuries because the patient requires total assistance for all repositioning.
  4. It eliminates the body's ability to perform small, even unconscious, weight shifts that are essential for restoring capillary blood flow. (correct answer)
Explanation: When you encounter questions about pressure injury pathophysiology, focus on the fundamental mechanism: prolonged pressure that exceeds capillary perfusion pressure (typically 25-32 mmHg) leads to tissue ischemia and subsequent necrosis. Complete immobility creates the most direct pathway to pressure injury because it eliminates the body's natural protective mechanism of frequent, small positional adjustments. Even during sleep, healthy individuals make hundreds of unconscious micro-movements that briefly relieve pressure and allow capillary refill. When this ability is completely lost, sustained pressure over bony prominences creates a continuous state of tissue hypoxia, making pressure injury development almost inevitable. Option A incorrectly suggests muscle atrophy is the primary mechanism. While disuse atrophy does occur with immobility, it's a slower process that contributes to long-term risk rather than the immediate pathophysiology of pressure injury formation. Option B confuses immobility with dysphagia or other feeding difficulties. Physical immobility doesn't directly impair oral intake ability, and nutritional deficiency, while important for healing, isn't the most direct pathophysiological consequence of the mobility deficit described. Option C addresses shear and friction forces, which are indeed problematic during repositioning of immobile patients. However, these mechanical forces cause more superficial tissue damage, whereas the question asks about the most direct contribution of immobility itself. Remember: pressure injury pathophysiology always returns to the basic principle of sustained pressure interrupting blood flow. The most dangerous aspect of complete immobility is losing those constant, subtle position changes that maintain tissue perfusion.

Question 20

Consider two independent risk factors for a bed-bound patient: severe iron-deficiency anemia with a hemoglobin of 6 g/dL, and moderate protein-energy malnutrition with a prealbumin of 14 mg/dL. Which factor poses a more immediate and critical threat to tissue viability under pressure, and why?

  1. Malnutrition, because the lack of protein substrate prevents the constant cellular turnover required to maintain skin integrity.
  2. Malnutrition, because low prealbumin directly causes interstitial edema, which impairs diffusion of nutrients.
  3. Severe anemia, because it drastically reduces the oxygen-carrying capacity of the blood, rendering even minimal perfusion insufficient to prevent anoxic cell death. (correct answer)
  4. Severe anemia, because it forces the heart to increase its rate, which shunts blood away from the periphery to reduce cardiac workload.
Explanation: Both are serious risk factors. However, severe anemia presents a more acute threat to tissue under pressure. Pressure reduces blood flow (perfusion). The purpose of perfusion is to deliver oxygen. If the blood that is getting through has a severely limited capacity to carry oxygen (due to low hemoglobin), the tissue will become critically hypoxic and die much more quickly than in a person with normal hemoglobin. While malnutrition weakens tissue over time, severe hypoxia causes cell death within minutes to hours.