Pathophysiology of Burn Injury Practice Questions
20 free Pathophysiology of Burn Injury practice questions for the NCLEX Exam. Tap an option to answer — you get instant feedback, the correct answer, and a detailed explanation for every question.
What is the primary reason for intravascular hypovolemia in the immediate period after a major thermal burn injury (>30% TBSA)?
- A Direct loss of urine caused by acute kidney failure after the burn
- B Capillary leak with plasma shifting into the interstitial space
- C External hemorrhage from areas of skin breakage at the burn site
- D Rapid conversion of circulating fluid into fat within the tissues
Correct answer: Capillary leak with plasma shifting into the interstitial space
Burn injury triggers increased capillary permeability and plasma leakage into interstitial space, causing intravascular volume loss and hemoconcentration.
Which cellular mechanism contributes to cellular swelling and edema formation after a burn injury?
- A Increased sodium-potassium ATPase activity driving ions out of the cell
- B Enhanced cell membrane integrity preventing any abnormal ion movement
- C Inhibited sodium-potassium ATPase causing intracellular sodium and water buildup
- D Active extrusion of water from cells maintaining a normal cell volume
Correct answer: Inhibited sodium-potassium ATPase causing intracellular sodium and water buildup
After burn injury, sodium-potassium ATPase dysfunction occurs, leading to intracellular sodium accumulation and water movement into cells, causing swelling and edema.
What type of shock is characteristic of burn injury in the early phase?
- A Pure cardiogenic shock from direct thermal injury to the heart muscle
- B Pure obstructive shock from compression of the great vessels
- C Mixed shock with hypovolemic, distributive, and cardiogenic components
- D Only neurogenic shock from loss of sympathetic vascular tone
Correct answer: Mixed shock with hypovolemic, distributive, and cardiogenic components
Burn shock is complex, involving elements of hypovolemia, distributive shock, and cardiogenic shock contributing to the overall shock state.
Which of the following is a hallmark hemodynamic change during the early post-burn period?
- A Elevated cardiac output with low systemic vascular resistance
- B Decreased cardiac output with increased systemic vascular resistance
- C Normal cardiac output with normal systemic vascular resistance
- D Increased cardiac output with increased systemic vascular resistance
Correct answer: Decreased cardiac output with increased systemic vascular resistance
Burn shock often presents with decreased cardiac output due to hypovolemia and increased systemic vascular resistance from vasoconstriction and inflammatory mediator release.
What role do inflammatory mediators and oxidative stress play in burn pathophysiology?
- A They act only locally at the wound and have no systemic consequences
- B They drive endothelial damage, capillary leak, and a systemic inflammatory response
- C They reduce capillary leak and actively improve overall vascular integrity
- D They are largely irrelevant to fluid shifting after a thermal injury
Correct answer: They drive endothelial damage, capillary leak, and a systemic inflammatory response
Thermal injury induces the release of inflammatory mediators and oxidative stress, causing endothelial damage, increased permeability, and systemic inflammation.
Why does hypoalbuminemia occur early in major burn injuries?
- A Because albumin production by the liver increases dramatically after injury
- B Plasma protein loss through injured capillaries plus dilution from fluid therapy
- C Because burn patients are always placed on strict low-protein diets afterward
- D Because circulating albumin is rapidly converted into glucose for energy
Correct answer: Plasma protein loss through injured capillaries plus dilution from fluid therapy
Burn injury leads to leakage of plasma proteins, including albumin, into the interstitial space, reducing oncotic pressure and contributing to hypoalbuminemia.
Which statement correctly describes the time course of edema formation in severe burns?
- A Edema develops only after 48 hours and then resolves spontaneously on its own
- B Edema is biphasic: a rapid early phase then a slower phase over 12-24 hours
- C Edema occurs strictly in the burned areas and never in unburned tissue
- D Edema is completely absent whenever adequate fluid resuscitation is given
Correct answer: Edema is biphasic: a rapid early phase then a slower phase over 12-24 hours
After severe burns, edema rapidly develops within minutes and then progresses more slowly over 12-24 hours, affecting both burned and unburned tissues due to a systemic response.
Which factor increases fluid requirements for resuscitation in a burn patient?
- A A small total body surface area burn of less than ten percent
- B Complete absence of any associated inhalation injury
- C Inhalation injury together with delayed initiation of fluid therapy
- D Young patient age with no significant underlying comorbidities
Correct answer: Inhalation injury together with delayed initiation of fluid therapy
Inhalation injury and delayed initiation of fluid therapy lead to more capillary leak, systemic inflammation, and higher fluid needs for resuscitation in burn patients.
In severe burn injury, why might hemoglobin and hematocrit readings be elevated in the first 12 hours?
- A Because red blood cell production from marrow increases immediately
- B Because intravascular fluid loss causes hemoconcentration of blood
- C Because the burn itself rapidly induces a true anemia of injury
- D Because circulating plasma volume increases dramatically early on
Correct answer: Because intravascular fluid loss causes hemoconcentration of blood
Massive fluid shift out of the vascular compartment during burn injury causes plasma volume depletion and hemoconcentration, elevating hemoglobin and hematocrit early post-injury.
What is the primary reason for decreased urine output in early burn shock?
- A A genuine increase in urine production by both kidneys after the burn
- B Immediate intrinsic renal failure occurring in essentially all burns
- C Reduced renal perfusion from hypovolemia and high vascular resistance
- D Excessively high fluid intake simply diluting the urine being produced
Correct answer: Reduced renal perfusion from hypovolemia and high vascular resistance
In burn shock, hypovolemia and vasoconstriction reduce renal blood flow, leading to oliguria despite preserved renal structure in the very early phase.
Which electrolyte disturbance is most likely immediately after a major burn injury?
- A Hypokalemia caused by a shift of potassium into the cells
- B Hyperkalemia from cell lysis releasing intracellular potassium
- C No appreciable change in the serum potassium concentration
- D Hypocalcemia driven solely by increased parathyroid hormone
Correct answer: Hyperkalemia from cell lysis releasing intracellular potassium
Deep burns cause cell damage and potassium release from intracellular space, leading to early hyperkalemia as an electrolyte disturbance.
Why is the extracellular sodium concentration often increased in early burn shock?
- A Because the kidneys avidly retain sodium during early burn shock
- B Because large amounts of sodium are lost through the urine output
- C Because sodium shifts out of cells while plasma volume falls, concentrating it
- D Because most circulating sodium becomes tightly bound to plasma proteins
Correct answer: Because sodium shifts out of cells while plasma volume falls, concentrating it
Burn injury leads to sodium shift, loss of plasma volume, and concentration of remaining sodium in the intravascular space, elevating extracellular sodium levels.
What happens to myocardial function in burn shock, even after adequate fluid resuscitation?
- A Myocardial contractility reliably normalizes immediately after fluids
- B Myocardial depression may persist with high SVR and low cardiac output
- C Myocardial function is essentially never affected by a major burn injury
- D Myocardial contractility increases markedly due to resulting hypervolemia
Correct answer: Myocardial depression may persist with high SVR and low cardiac output
Burn shock involves not only hypovolemia but also myocardial depression and increased afterload, so even with fluid resuscitation, cardiac output may remain depressed.
Which statement best describes capillary oncotic pressure in burn injury?
- A It increases due to a rise in circulating plasma proteins
- B It remains essentially unchanged throughout the early phase
- C It decreases as plasma proteins leak into the interstitial space
- D It becomes irrelevant to transcapillary fluid shifts after a burn
Correct answer: It decreases as plasma proteins leak into the interstitial space
Plasma protein loss lowers oncotic pressure in capillaries, promoting fluid movement into the interstitial space and worsening edema.
In the microcirculation after burn injury, which change contributes to fluid extravasation?
- A Tightening of the endothelial junctions sealing the capillaries
- B A generalized decrease in capillary permeability after injury
- C Loss of the endothelial glycocalyx with leakage of protein and plasma
- D An isolated increase in capillary hydrostatic pressure only
Correct answer: Loss of the endothelial glycocalyx with leakage of protein and plasma
Burn injury damages the endothelial glycocalyx and disrupts vascular integrity, leading to proteins and fluid leakage into tissues.
What characterizes the systemic vascular response in the early phase of major burn?
- A Pure vasodilation occurring uniformly across all vascular beds
- B Local vasoconstriction at the burn site with systemic vasodilation elsewhere
- C Only vasoconstriction occurring everywhere throughout the body
- D Only vasodilation occurring within the directly burned tissues
Correct answer: Local vasoconstriction at the burn site with systemic vasodilation elsewhere
Burn injury initiates local vasoconstriction at the burn site while systemic mediators cause vasodilation in non-burned tissues, contributing to distributive shock.
Why is fluid resuscitation so time-sensitive in the pathophysiology of burn shock?
- A Because delays let the zone of stasis convert to irreversible necrosis
- B Because resuscitation fluids should only be started after 48 hours
- C Because early fluid administration almost always worsens the outcome
- D Because the timing of resuscitation has no real effect on tissue survival
Correct answer: Because delays let the zone of stasis convert to irreversible necrosis
Prompt fluid resuscitation helps maintain tissue perfusion, prevents conversion of the zone of stasis to necrosis, and reduces the risk of irreversible organ damage due to prolonged hypoperfusion.
A patient with a large burn is noted to have increased systemic vascular resistance despite adequate fluids. What pathophysiologic process explains this?
- A Decreased release of vasoactive mediators following the burn injury
- B Widespread vasodilation occurring exclusively across all vascular beds
- C Sympathetic activation and mediator-induced endothelial dysfunction raising afterload
- D Persistent pure hypovolemia acting as the only contributing factor
Correct answer: Sympathetic activation and mediator-induced endothelial dysfunction raising afterload
Even with fluid restoration, burn injury-induced endothelial dysfunction and sympathetic activation can lead to increased systemic vascular resistance, contributing to persistent vasoconstriction.
What is the primary driver for the formation of massive edema in both burned and non‐burned tissue after major burns?
- A Pure lymphatic obstruction blocking drainage from the tissues
- B Excessive intravenous fluid infusion acting as the sole cause
- C Increased permeability, low oncotic pressure, and altered Starling forces together
- D Simple whole-body dehydration without any vascular changes
Correct answer: Increased permeability, low oncotic pressure, and altered Starling forces together
Edema in burn injury results from increased capillary leakage, reduced oncotic pressure, altered Starling forces, and interstitial negative pressure, affecting both burned and non-burned tissues.
Why does burn injury sometimes lead to multiple-organ dysfunction syndrome (MODS) even when initial fluid resuscitation is adequate?
- A Because only the local tissue damage at the burn site matters
- B Because systemic inflammation, endothelial injury, and hypoperfusion persist
- C Because adequate resuscitation reliably cures all of the organ damage
- D Because the internal organs are essentially unaffected by major burns
Correct answer: Because systemic inflammation, endothelial injury, and hypoperfusion persist
Burn injury triggers systemic inflammatory responses, endothelial dysfunction, and ongoing tissue damage that can progress to MODS despite adequate initial resuscitation.