Pathophysiology: Chapter 49: Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults

Question 1

What is the final outcome of impaired cellular metabolism?

a. Cellular alterations in the heart and brain
b. Buildup of cellular waste products
c. Cellular alterations in the vasculature structures and kidneys
d. Impairment of urine excretion

Answer 1

ANS: B
The common pathway in all types of shock is impairment of cellular metabolism as a
result of decreased delivery of oxygen and nutrients, which are frequently coupled with an
increased demand, the consumption of oxygen and nutrients, and a decreased removal of
cellular waste products. Of the options available, this selection is the only accurate
outcome.

Question 2

Which clinical manifestation of septic shock confirms an elevation in immune system
response?
a. Tachycardia 
b. Increased white blood cell count
c. Low respiratory rate 
d. Hypothermia

Answer 2

ANS: B
Clinical manifestations common in septic shock are fever, high heart rate, high respiratory
rate, or elevations in immune responses, such as increased white blood cells and
circulating blood glucose.

Question 3

The release of catecholamine by the adrenal glands compensate for which initial effects of
hypovolemic shock?
a. Interstitial fluid moves out of the vascular compartment.
b. Systemic vascular resistance is decreased.
c. Heart rate is increased.
d. Water excretion is increased.

Answer 3

ANS: C
Compensatory mechanisms (see Figure 48-3) initially offset hypovolemia. Heart rate and
systemic vascular resistance increase as a result of catecholamine release by the adrenal
glands, which boosts cardiac output and tissue perfusion pressures. Compelled by a
decrease in capillary hydrostatic pressures, interstitial fluid moves into the vascular
compartment. The liver and spleen add to blood volume by disgorging stored red blood
cells and plasma. In the kidneys, renin (through several intermediaries) stimulates
aldosterone release and the retention of sodium and therefore water, whereas antidiuretic
hormone (ADH), or vasopressin, from the posterior pituitary gland increases water
retention. Data on the compensation of ADH, however, show that as shock worsens, ADH
in plasma decreases.

Question 4

Hypovolemic shock begins to develop when intravascular volume has decreased by what
percentage?
a. 5 c. 15
b. 10 d. 20

Answer 4

ANS: C
Hypovolemic shock begins to develop when intravascular volume has decreased by
approximately 15%.

Question 5

What type of shock develops as a result of the overstimulation of the parasympathetic
nervous system or the understimulation of the sympathetic nervous system?
a. Septic c. Anaphylactic
b. Cardiogenic d. Vasogenic

Answer 5

ANS: D
Only vasogenic shock refers to a widespread and massive vasodilation resulting from an
imbalance between parasympathetic and sympathetic stimulation of vascular smooth
muscle.

Question 6

What is the clinical hallmark of neurogenic shock as a result of the overstimulation of the
parasympathetic nervous system?
a. Vasoconstriction c. Increased metabolism
b. Vasodilation d. Respiratory distress

Answer 6

ANS: B
Neurogenic shock refers to a widespread and massive vasodilation that results from an
imbalance between parasympathetic and sympathetic stimulation of vascular smooth
muscle. None of the other options are related to this condition.

Question 7

Which form of shock is often more severe than other forms because of its sudden, rapid
systemic vasodilation?
a. Septic c. Anaphylactic
b. Hypovolemic d. Neurogenic

Answer 7

ANS: C
Anaphylactic shock is often more severe than other types of shock because the
hypersensitivity reaction, which triggers vasodilation, has other pathophysiologic effects
that rapidly involve the entire body. This action is not associated with the other options.

Question 8

What type of shock is related to a decrease in systemic vascular resistance?

a. Septic c. Hypovolemic
b. Cardiogenic d. Heart failure

Answer 8

ANS: A
Clinical manifestations of only septic shock are persistent low arterial pressure, low
systemic vascular resistance from vasodilation, and an alteration in oxygen extraction by
all cells.

Question 9

For which type of shock would antihistamines and corticosteroids be prescribed?

a. Septic c. Hypovolemic
b. Anaphylactic d. Cardiogenic

Answer 9

ANS: B
Only anaphylactic shock responds to the administration of epinephrine to decrease mast
cell and basophil degranulation. Antihistamines and steroids are administered to stop the
inflammatory reaction.

Question 10

Which condition is best defined as a clinical syndrome involving a systemic response to
infection, which is manifested by two or more of the systemic inflammatory response
syndrome criteria?
a. Bacteremia c. Septicemia
b. Sepsis d. Septic shock

Answer 10

ANS: B
Of the options available, only sepsis is best defined as a systemic response to infection that
is manifested by two or more criteria of the systemic inflammatory response syndrome.

Question 11

In septic shock, which mediators are antiinflammatory?

a. Interleukin (IL)–4 (IL-4), IL-10, and IL-13
b. Tumor necrosis factor–alpha (TNF-) and granulocyte cell-stimulating factor
c. IL-1, IL-2, and IL-6
d. Prostaglandin, leukotrienes, and bradykinin

Answer 11

ANS: A
In septic shock, the only antiinflammatory mediators released include
lipopolysaccharide-binding protein; IL-1 receptor antagonist; soluble cluster of
differentiation 14 (CD-14); type 2 IL-1 receptor; leukotriene 4-receptor antagonist; IL-4,
IL-10, and IL-13; and soluble TNF.

Question 12

What mechanism causes organ injury in primary multiple organ dysfunction syndrome
(MODS)?
a. Impaired immune response 
b. Impaired glucose use
c. Impaired perfusion 
d. Impaired ventilation

Answer 12

ANS: C
In primary MODS, the organ injury is directly associated with a specific insult, most often
ischemia or impaired perfusion from an episode of shock or trauma, thermal injury,
soft-tissue necrosis, or invasive infection. None of the other options accurately identifies
the cause of MODS.

Question 13

In secondary multiple organ dysfunction syndrome (MODS), what stimulates the normal
endothelial cells to change to a proinflammatory state?
a. Interleukin (IL)–4 (IL-4) and IL-13
b. IL-1, IL-6, and tumor necrosis factor (TNF)
c. Interferon gamma (IFN-) and granulocyte cell-stimulating factor
d. Prostaglandin, leukotrienes, histamine, and bradykinin

Answer 13

ANS: B
Normal endothelial cells have little interaction with leukocytes except when stimulated by
TNF, IL-1, and IL-6. This selection is the only option that accurately describes what
stimulates the normal endothelial cells to change to a proinflammatory state.

Question 14

What stimulates the respiratory burst and production of highly toxic free radicals in the
multiple organ dysfunction syndrome (MODS)?
a. Neutrophils adhering to the endothelium
b. Activation of the complement cascade
c. Release of prostaglandins, thromboxanes, and leukotrienes
d. Activation of the fibrinolytic system

Answer 14

ANS: A
The accumulation of activated neutrophils in organs is thought to play a key role in the
pathogenetic development of MODS. When neutrophils adhere to the endothelium, they
undergo a respiratory burst (oxidative burst) and release oxygen radicals. The respiratory
burst occurs as the activated neutrophil experiences a sudden increase in oxidative
metabolism, producing large quantities of highly toxic oxygen free radicals. This selection
is the only option that accurately identifies the stimulant of the respiratory burst that
results in the production of toxic free radicals.

Question 15

In multiple organ dysfunction syndrome (MODS), the gut hypothesis attempts to explain
which phenomena?
a. Paralytic ileus
b. Translocation of bacteria
c. Maldistribution of blood flow
d. Massive diarrhea accompanying septic shock

Answer 15

ANS: B
The loss of intestinal barrier function leads to the systemic spread of bacteria and/or
endotoxin from the gut (systemic endotoxemia). This phenomenon is called translocation
of bacteria. The gut hypothesis provides a possible explanation for the fact that an
infectious focus is not always found in individuals with MODS. The gut hypothesis is not
related to any other option.

Question 16

Blistering of the skin within minutes occurs in which type of burn injury?

a. First degree
b. Superficial second degree
c. Deep second degree
d. Third degree

Answer 16

ANS: B
The hallmark of superficial partial-thickness injury is the appearance of thin-walled,
fluid-filled blisters that develop within only a few minutes after injury. Blistering that
occurs within minutes of the burn injury is not a defining characteristic of the other
options.

Question 17

Which form of shock occurs from an acute burn injury?

a. Hypovolemic c. Cardiogenic
b. Septic d. Vasogenic

Answer 17

ANS: A
Burn shock consists of a hypovolemic cardiovascular component and a cellular
component. Hypovolemia associated with burn shock results from massive fluid losses
from the circulating blood volume. The other forms of shock are not directly related to an
acute burn injury.

Question 18

Which fluid is most often used in fluid resuscitation after a major burn injury?

a. Saline c. Lactated Ringer solution
b. Albumin d. Dextrose in water

Answer 18

ANS: C
Lactated Ringer solution is used most often because it closely approximates extracellular
fluid, the repository of fluid leaving the circulatory system during this phase of extensive
edema formation (see Table 48-4). The other options are not most often used in fluid
resuscitation after major burns.

Question 19

What is the most reliable criterion of adequate fluid resuscitation after a major burn
injury?
a. Blood pressure c. Respiratory rate
b. Pulse rate d. Urine output

Answer 19

ANS: D
The most reliable criterion for adequate resuscitation of burn shock is urine output. None
of the remaining options are considered reliable.

Question 20

The endpoint of burn shock is defined as the time when the individual is able to do which
of the following?
a. Maintain adequate blood pressure for 4 hours.
b. Maintain adequate urine output for 2 hours.
c. Manage pain without narcotics.
d. Manage pain during dressing changes.

Answer 20

ANS: B
The endpoint of burn shock is defined as the state in which the individual is able to
maintain adequate urine output for 2 hours with the intravenous fluid administration rate
equal to the individual’s calculated maintenance rate (see Box 48-4). None of the
remaining options are defined as the endpoint of burn shock.

Question 21

Which condition does a burn injury create for an extended period?

a. Hypervolemia c. Hyponatremia
b. Hypermetabolism d. Hypotension

Answer 21

ANS: B
Of the options available, a burn injury induces a hypermetabolic state that persists until
wound closure.

Question 22

What effect does a fatal burn injury have on interleukins (ILs)?
a. Decreases levels of IL-2, which may decrease T helper 1 (Th1) lymphocytes.
b. Decreases levels of IL-4, which causes a shift in production from Th1 to Th2
lymphocytes.
c. Decreases levels of IL-6, which produces cytokines.
d. Decreases levels of IL-12, which stimulates the production of immunoglobulins.

Answer 22

ANS: A
A fatal burn injury has often shown decreased levels of IL-2, which may result in
decreased Th1 lymphocytes. This option is the only accurate description of the effect a
fatal burn injury has on ILs.

Question 23

Daily evaporative water loss after a burn injury is approximately how many times the
normal?
a. 5 c. 15
b. 10 d. 20

Answer 23

ANS: D
Moncrief and Mason attempted to determine the magnitude of such a loss and determined
that daily evaporative water loss was in the range of 20 times normal in the early phase of
injury, with gradual decreases as wound closure is achieved.

Question 24

What is the significance of a high level of interleukin 1 (IL-1) in a patient who has
experienced severe burns?
a. Prognosis is poor. 
b. Antibiotic therapy is required.
c. Urinary function is improved. 
d. They are less at risk for death.

Answer 24

ANS: D
The level of IL-1 inversely correlates with burn survival; low levels may be associated
with a higher mortality. This selection is the only option that accurately identifies the
significance of a high level of IL-1.

Question 25

What is the purpose of monitoring procalcitonin (PCT) levels in a patient after a burn?

a. To help evaluate the potential risk for respiratory complications
b. To justify the initiation of antibiotic therapy
c. To determine when discontinuing antibiotic use is feasible
d. To help in the selection of appropriate antibiotic therapy agents

Answer 25

ANS: C
Seeking to decrease the use of antibiotics in the patient who is critically ill and thus
prevent resistance to antibiotics is an important strategy in treating infection. Recent
research suggests that monitoring serial PCT levels, a precursor hormone to calcitonin,
may be used to shorten antibiotic use in the treatment of respiratory infections. PCT,
normally not discernible on assay, when elevated may indicate specific proinflammatory
response during a bacterial infection. PCT levels should not be used as an indicator to start
antibiotics; however, if monitored sequentially at the start of empiric antibiotics and then
dropped to low levels, then discontinuation may be clinically indicated.

Question 26

How many milliliters of fluid replacement per hour does a 70-kg adult with a 50% total
body surface area burn and a body surface area of 2 m require?
a. 150 c. 350
b. 275 d. 500

Answer 26

ANS: B
A 70-kg adult with a 50% total body surface area burn and a body surface area of 2 m
requires the following:
Basal = (1500 ml/day) (2 m2 body surface area) = 3000 ml/24 hr or 125 ml/hr
Evaporative = (25 + 50% total body surface burn)
(2m2 total body surface area) = (75) (2) = 150 ml/hr
Total maintenance fluids = 125 ml + 150 ml = 275 ml/hr