NSG530 Exam 2 V3 | NSG 530 Advanced
Pathophysiology | Wilkes University
1. Following a myocardial infarction, the process of ventricular remodeling is primarily driven
by which of the following?
A. Decrease in sympathetic nervous system activity
B. Rapid regeneration of cardiac muscle cells
C. Hypertrophy of myocytes and collagen deposition
D. Immediate restoration of normal chamber geometry
Answer: C
Rationale: Ventricular remodeling involves structural changes in the heart’s size, shape,
and function after an injury such as an MI. This process is mediated by the activation of the
RAAS and sympathetic nervous systems, leading to myocyte hypertrophy and fibrosis.
While compensatory initially, chronic remodeling can lead to heart failure and decreased
cardiac output.
2. Which clinical finding is most characteristic of neurogenic shock, distinguishing it from
other types of shock?
A. Tachycardia
B. Increased systemic vascular resistance
C. Bradycardia
,D. Cool, clammy skin
Answer: C
Rationale: Neurogenic shock results from the loss of sympathetic tone, which leads to
massive vasodilation and an unopposed parasympathetic response. Unlike other forms of
shock that present with compensatory tachycardia, neurogenic shock typically features
bradycardia. The skin also remains warm and dry due to the inability to vasoconstrict.
3. In the pathophysiology of Disseminated Intravascular Coagulation (DIC), what is the
primary cause of excessive bleeding?
A. Increased production of clotting factors
B. Inhibition of the fibrinolytic system
C. An overabundance of Vitamin K
D. Consumption of platelets and coagulation factors
Answer: D
Rationale: DIC is characterized by widespread systemic activation of coagulation which
results in the formation of numerous microthrombi. This widespread clotting consumes the
body’s available platelets and clotting factors faster than they can be replaced.
Consequently, the patient experiences severe bleeding despite the initial clotting trigger.
4. A patient with a Ventilation/Perfusion (V/Q) ratio of 0.0 (low V/Q) is most likely
experiencing which condition?
A. Alveolar shunting
, B. Pulmonary embolism
C. Physiological dead space
D. Pneumothorax
Answer: A
Rationale: A V/Q ratio of 0 indicates that there is perfusion but no ventilation, which is
referred to as a shunt. This occurs when blood flows through pulmonary capillaries
without participating in gas exchange, such as in atelectasis or pneumonia. In contrast, a
high V/Q ratio or dead space occurs when there is ventilation but no perfusion.
5. What is the primary hemodynamic alteration observed in the early (hyperdynamic) phase
of septic shock?
A. Increased systemic vascular resistance (SVR)
B. Decreased systemic vascular resistance (SVR)
C. Decreased cardiac output
D. Increased pulmonary capillary wedge pressure
Answer: B
Rationale: Septic shock is unique because the initial phase is often ‘warm shock,’
characterized by massive vasodilation and low SVR. To compensate for the low resistance,
cardiac output usually increases significantly. As the condition progresses, the patient may
move into a cold phase where cardiac output drops and tissue perfusion worsens.
Pathophysiology | Wilkes University
1. Following a myocardial infarction, the process of ventricular remodeling is primarily driven
by which of the following?
A. Decrease in sympathetic nervous system activity
B. Rapid regeneration of cardiac muscle cells
C. Hypertrophy of myocytes and collagen deposition
D. Immediate restoration of normal chamber geometry
Answer: C
Rationale: Ventricular remodeling involves structural changes in the heart’s size, shape,
and function after an injury such as an MI. This process is mediated by the activation of the
RAAS and sympathetic nervous systems, leading to myocyte hypertrophy and fibrosis.
While compensatory initially, chronic remodeling can lead to heart failure and decreased
cardiac output.
2. Which clinical finding is most characteristic of neurogenic shock, distinguishing it from
other types of shock?
A. Tachycardia
B. Increased systemic vascular resistance
C. Bradycardia
,D. Cool, clammy skin
Answer: C
Rationale: Neurogenic shock results from the loss of sympathetic tone, which leads to
massive vasodilation and an unopposed parasympathetic response. Unlike other forms of
shock that present with compensatory tachycardia, neurogenic shock typically features
bradycardia. The skin also remains warm and dry due to the inability to vasoconstrict.
3. In the pathophysiology of Disseminated Intravascular Coagulation (DIC), what is the
primary cause of excessive bleeding?
A. Increased production of clotting factors
B. Inhibition of the fibrinolytic system
C. An overabundance of Vitamin K
D. Consumption of platelets and coagulation factors
Answer: D
Rationale: DIC is characterized by widespread systemic activation of coagulation which
results in the formation of numerous microthrombi. This widespread clotting consumes the
body’s available platelets and clotting factors faster than they can be replaced.
Consequently, the patient experiences severe bleeding despite the initial clotting trigger.
4. A patient with a Ventilation/Perfusion (V/Q) ratio of 0.0 (low V/Q) is most likely
experiencing which condition?
A. Alveolar shunting
, B. Pulmonary embolism
C. Physiological dead space
D. Pneumothorax
Answer: A
Rationale: A V/Q ratio of 0 indicates that there is perfusion but no ventilation, which is
referred to as a shunt. This occurs when blood flows through pulmonary capillaries
without participating in gas exchange, such as in atelectasis or pneumonia. In contrast, a
high V/Q ratio or dead space occurs when there is ventilation but no perfusion.
5. What is the primary hemodynamic alteration observed in the early (hyperdynamic) phase
of septic shock?
A. Increased systemic vascular resistance (SVR)
B. Decreased systemic vascular resistance (SVR)
C. Decreased cardiac output
D. Increased pulmonary capillary wedge pressure
Answer: B
Rationale: Septic shock is unique because the initial phase is often ‘warm shock,’
characterized by massive vasodilation and low SVR. To compensate for the low resistance,
cardiac output usually increases significantly. As the condition progresses, the patient may
move into a cold phase where cardiac output drops and tissue perfusion worsens.
