Psychology Quiz: Stress Response
20 questions · exam conditions
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Stress ResponseQuestion 1 of 20

A new drug is developed that selectively blocks the action of corticotropin-releasing hormone (CRH) at its receptors in the anterior pituitary. If this drug were administered to an individual about to experience a public speaking stressor, which physiological outcome would be expected?

Rapid cardiovascular changes with blunted cortisol response.
Blunted cardiovascular and cortisol responses.
Normal cortisol with exaggerated catecholamine release.
Increased ACTH due to lack of CRH inhibition.
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Psychology Quiz

Psychology Quiz: Stress Response

Practice Stress Response in Psychology 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 Stress Response, giving you a quick way to practice the rules, question types, and explanations that matter most for Psychology.

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

A new drug is developed that selectively blocks the action of corticotropin-releasing hormone (CRH) at its receptors in the anterior pituitary. If this drug were administered to an individual about to experience a public speaking stressor, which physiological outcome would be expected?

  1. Rapid cardiovascular changes with blunted cortisol response. (correct answer)
  2. Blunted cardiovascular and cortisol responses.
  3. Normal cortisol with exaggerated catecholamine release.
  4. Increased ACTH due to lack of CRH inhibition.
Explanation: The rapid increase in heart rate and blood pressure is mediated by the fast-acting SAM system (epinephrine/norepinephrine), which is not directly dependent on the HPA axis cascade. The drug blocks CRH, which prevents the pituitary from releasing ACTH. Without ACTH, the adrenal cortex will not be stimulated to release cortisol. Therefore, the SAM response would be intact, but the HPA axis (cortisol) response would be blunted.

Question 2

During a demanding cognitive task, a subject's heart rate increases rapidly, their palms become sweaty, and they report feeling 'on edge'. About 20 minutes later, blood tests show elevated levels of a hormone that is increasing glucose availability through gluconeogenesis. This physiological sequence is best explained by:

  1. Initial HPA axis activation causing cortisol release, followed by SAM system activation.
  2. Simultaneous and synergistic activation of both the SAM system and the HPA axis.
  3. Initial SAM system activation, followed by a slower-acting HPA axis response. (correct answer)
  4. A primary parasympathetic withdrawal followed by a secondary HPA axis activation.
Explanation: The rapid heart rate, sweating, and feeling 'on edge' are classic signs of sympathetic nervous system (SAM) activation and the release of epinephrine/norepinephrine. The elevation of a glucose-mobilizing hormone (cortisol) 20 minutes later is characteristic of the slower, more delayed HPA axis response. This illustrates the two-wave nature of the physiological stress response, with the SAM system acting first and the HPA axis following.

Question 3

Research indicates that chronic, prolonged exposure to high levels of cortisol can lead to atrophy of the hippocampus. This structural change is most directly linked to which functional impairment often seen in individuals with chronic stress?

  1. An inability to initiate the 'fight-or-flight' response via the sympathetic nervous system.
  2. A dysregulation of the HPA axis negative feedback, leading to sustained cortisol release. (correct answer)
  3. An over-sensitization of the adrenal medulla, resulting in excessive epinephrine release.
  4. A complete shutdown of the adrenal cortex, causing a severe cortisol deficiency.
Explanation: The hippocampus is rich in glucocorticoid receptors and plays a key role in the negative feedback loop of the HPA axis. When hippocampal neurons are damaged or atrophy due to chronic cortisol exposure, their ability to inhibit CRH release from the hypothalamus is impaired. This creates a vicious cycle where the 'off-switch' for the stress response is broken, leading to further sustained cortisol release.

Question 4

The HPA axis response evolved to manage acute physical threats. In the context of modern chronic psychological stress (e.g., work pressure), which evolutionarily adaptive feature of cortisol becomes most maladaptive?

  1. Increased heart rate and blood pressure, which improves oxygen delivery for immediate action.
  2. Mobilization of energy reserves (glucose), which prepares the body for physical exertion.
  3. Suppression of non-essential functions like the immune system, which conserves energy. (correct answer)
  4. Heightened alertness and arousal, which improves vigilance against physical predators.
Explanation: While suppressing immunity, digestion, and reproduction is adaptive when facing a brief physical danger (conserving energy for fight or flight), it becomes highly maladaptive when the stressor is psychological and chronic. Sustained immunosuppression leads to increased vulnerability to illness, a hallmark of chronic stress, without conferring any benefit for dealing with a demanding job.

Question 5

When comparing the body's two primary stress response systems, which statement most accurately distinguishes the temporal characteristics of the sympatho-adreno-medullary (SAM) system and the hypothalamic-pituitary-adrenal (HPA) axis?

  1. Both systems have a rapid onset, but the HPA axis response has a much shorter duration.
  2. The HPA axis has a rapid onset via hormonal pathways, while the SAM system has a slower onset via neural pathways.
  3. The SAM system initiates a rapid, short-lived response, while the HPA axis initiates a slower, more sustained response. (correct answer)
  4. The SAM system's response lasts for hours due to epinephrine, while the HPA axis response lasts only for seconds.
Explanation: The SAM system is a fast-acting neural pathway that causes the adrenal medulla to release epinephrine and norepinephrine, leading to the immediate 'fight-or-flight' symptoms. The HPA axis is a slower hormonal cascade (CRH -> ACTH -> cortisol) that takes longer to activate but whose effects (e.g., changes in metabolism) are more sustained and prolonged.

Question 6

Under conditions of chronic stress, the negative feedback mechanism of the HPA axis can become less effective, leading to a prolonged stress response. What is the most widely accepted cellular mechanism underlying this feedback resistance?

  1. An increase in the production of enzymes that rapidly degrade cortisol in the bloodstream.
  2. A downregulation of glucocorticoid receptors in the hypothalamus and hippocampus. (correct answer)
  3. A competitive inhibition of ACTH receptors on the adrenal cortex by a stress-induced peptide.
  4. An upregulation and sensitization of CRH receptors in the anterior pituitary gland.
Explanation: Chronic exposure to high levels of cortisol leads to a compensatory downregulation (a decrease in the number and sensitivity) of glucocorticoid receptors in key brain areas like the hypothalamus and hippocampus. With fewer receptors to detect the cortisol signal, the negative feedback becomes less efficient, requiring higher levels of cortisol to shut off the stress response, thus perpetuating the cycle of HPA axis hyperactivity.

Question 7

A medical student endures a week of intense final exams with very little sleep. Towards the end of the week, they develop a cold. The increased susceptibility to infection is most directly attributable to which effect of a key HPA axis hormone?

  1. ACTH-induced suppression of lymphocyte production in the bone marrow.
  2. CRH-mediated inhibition of inflammatory responses in peripheral tissues.
  3. Cortisol's role in mobilizing glucose, which depletes energy reserves for immune cells.
  4. Cortisol's immunosuppressive effects, including the inhibition of cytokine production. (correct answer)
Explanation: Sustained stress from the exams leads to prolonged elevation of cortisol via the HPA axis. While beneficial for short-term energy mobilization, a primary function of cortisol is to suppress the immune system and inflammatory responses. It achieves this by inhibiting the production of cytokines and the proliferation of lymphocytes, thereby making the individual more vulnerable to opportunistic infections like the common cold.

Question 8

An individual with a specific phobia is exposed to their feared stimulus, initiating a classic stress response. Researchers measure the plasma concentrations of two key stress hormones over the next hour.

Based on the known physiology of the stress response, a graph of the hormone concentrations over time would most likely show which pattern? Refer to the information in the passage.

  1. Hormone A (cortisol) peaks within 1-2 minutes, while Hormone B (epinephrine) peaks around 20-30 minutes.
  2. Hormone A (epinephrine) peaks within 1-2 minutes, while Hormone B (cortisol) peaks around 20-30 minutes. (correct answer)
  3. Both Hormone A (cortisol) and Hormone B (epinephrine) peak simultaneously within the first 5 minutes.
  4. Both Hormone A (cortisol) and Hormone B (epinephrine) show a slow, gradual rise, peaking together after about 45 minutes.
Explanation: The stress response involves two major systems with different timelines. The sympathetic nervous system (SAM) acts first, causing the adrenal medulla to release epinephrine almost instantly (peaking in 1-2 minutes). This is the 'fast' response. The HPA axis is the 'slow' response; the hormonal cascade (CRH -> ACTH -> cortisol) takes time, with cortisol levels typically peaking in the blood around 20-30 minutes after the initial stressor.

Question 9

An individual has a rare genetic mutation causing their glucocorticoid receptors in the brain to be exceptionally sensitive. How would this individual's HPA axis response to a moderate stressor likely differ from that of an individual with typical receptor sensitivity?

  1. They would exhibit an exaggerated and prolonged cortisol release due to enhanced pituitary stimulation.
  2. They would show a normal initial cortisol release, but the response would be excessively prolonged.
  3. They would mount a smaller cortisol response that is terminated more quickly and efficiently. (correct answer)
  4. They would have chronically elevated baseline cortisol levels due to continuous HPA axis activation.
Explanation: Highly sensitive glucocorticoid receptors mean that the negative feedback system is more efficient. A smaller amount of cortisol is needed to activate these receptors in the hypothalamus and hippocampus to shut down the HPA axis. Therefore, when faced with a stressor, their cortisol response would be more constrained (smaller peak) and would be terminated more rapidly once cortisol levels begin to rise.

Question 10

A patient presents with symptoms of hypercortisolism (e.g., central obesity, hypertension). Imaging reveals a tumor on one of their adrenal glands that is autonomously producing cortisol. What would be the expected levels of endogenous ACTH and CRH in this individual?

  1. High ACTH and high CRH
  2. High ACTH and low CRH
  3. Low ACTH and high CRH
  4. Low ACTH and low CRH (correct answer)
Explanation: The adrenal tumor is producing high levels of cortisol independent of HPA axis control. This pathologically high level of cortisol will exert a powerful negative feedback effect on both the pituitary gland and the hypothalamus. This feedback will suppress the pituitary's release of ACTH and the hypothalamus's release of CRH, leading to low levels of both hormones.

Question 11

An individual is administered a novel medication that significantly increases the metabolic clearance rate of cortisol, effectively reducing its half-life in the bloodstream. If this individual is subjected to a continuous, low-level stressor, what compensatory change in the HPA axis is most likely to occur over time?

  1. An increase in the tonic (baseline) secretion of CRH and ACTH to maintain normal cortisol levels. (correct answer)
  2. A decrease in the baseline secretion of CRH and ACTH to match the lower cortisol levels.
  3. A desensitization of glucocorticoid receptors in the brain to prevent over-stimulation.
  4. A complete shutdown of the HPA axis as it can no longer maintain hormonal balance.
Explanation: When you encounter questions about hormonal feedback systems, think about the body's drive to maintain homeostasis through compensatory mechanisms. The HPA (hypothalamic-pituitary-adrenal) axis operates on negative feedback, where cortisol normally inhibits its own production by suppressing CRH and ACTH release. In this scenario, the medication accelerates cortisol clearance, meaning cortisol levels drop faster than normal despite ongoing stress. The hypothalamus and pituitary detect these lower cortisol levels and interpret this as insufficient stress response. To compensate, they increase baseline secretion of CRH and ACTH, driving the adrenal glands to produce more cortisol and restore adequate levels for the stressful situation. Option A correctly identifies this upregulation response - the system compensates by increasing upstream hormone production to maintain cortisol availability during stress. Option B suggests the opposite response, which would worsen the cortisol deficiency rather than correct it. This contradicts the body's homeostatic drive. Option C describes receptor desensitization, but with lower (not higher) cortisol levels, there's no risk of over-stimulation requiring this protective mechanism. Option D proposes complete system shutdown, which is biologically implausible. The HPA axis is essential for survival and would adapt rather than cease functioning entirely. Remember: In endocrine feedback questions, identify what's being detected (low cortisol) and predict the logical compensatory response (increase production upstream). The body almost always tries to restore balance, not give up or worsen the imbalance.

Question 12

Research indicates that chronic, prolonged exposure to high levels of cortisol can lead to atrophy of the hippocampus. This structural change is most directly linked to which functional impairment often seen in individuals with chronic stress?

  1. An inability to initiate the 'fight-or-flight' response via the sympathetic nervous system.
  2. A dysregulation of the HPA axis negative feedback, leading to sustained cortisol release. (correct answer)
  3. An over-sensitization of the adrenal medulla, resulting in excessive epinephrine release.
  4. A complete shutdown of the adrenal cortex, causing a severe cortisol deficiency.
Explanation: The hippocampus is rich in glucocorticoid receptors and plays a key role in the negative feedback loop of the HPA axis. When hippocampal neurons are damaged or atrophy due to chronic cortisol exposure, their ability to inhibit CRH release from the hypothalamus is impaired. This creates a vicious cycle where the 'off-switch' for the stress response is broken, leading to further sustained cortisol release.

Question 13

When comparing the body's two primary stress response systems, which statement most accurately distinguishes the temporal characteristics of the sympatho-adreno-medullary (SAM) system and the hypothalamic-pituitary-adrenal (HPA) axis?

  1. Both systems have a rapid onset, but the HPA axis response has a much shorter duration.
  2. The HPA axis has a rapid onset via hormonal pathways, while the SAM system has a slower onset via neural pathways.
  3. The SAM system initiates a rapid, short-lived response, while the HPA axis initiates a slower, more sustained response. (correct answer)
  4. The SAM system's response lasts for hours due to epinephrine, while the HPA axis response lasts only for seconds.
Explanation: The SAM system is a fast-acting neural pathway that causes the adrenal medulla to release epinephrine and norepinephrine, leading to the immediate 'fight-or-flight' symptoms. The HPA axis is a slower hormonal cascade (CRH -> ACTH -> cortisol) that takes longer to activate but whose effects (e.g., changes in metabolism) are more sustained and prolonged.

Question 14

A new drug is developed that selectively blocks the action of corticotropin-releasing hormone (CRH) at its receptors in the anterior pituitary. If this drug were administered to an individual about to experience a public speaking stressor, which physiological outcome would be expected?

  1. Rapid cardiovascular changes with blunted cortisol response. (correct answer)
  2. Blunted cardiovascular and cortisol responses.
  3. Normal cortisol with exaggerated catecholamine release.
  4. Increased ACTH due to lack of CRH inhibition.
Explanation: The rapid increase in heart rate and blood pressure is mediated by the fast-acting SAM system (epinephrine/norepinephrine), which is not directly dependent on the HPA axis cascade. The drug blocks CRH, which prevents the pituitary from releasing ACTH. Without ACTH, the adrenal cortex will not be stimulated to release cortisol. Therefore, the SAM response would be intact, but the HPA axis (cortisol) response would be blunted.

Question 15

A medical student endures a week of intense final exams with very little sleep. Towards the end of the week, they develop a cold. The increased susceptibility to infection is most directly attributable to which effect of a key HPA axis hormone?

  1. ACTH-induced suppression of lymphocyte production in the bone marrow.
  2. CRH-mediated inhibition of inflammatory responses in peripheral tissues.
  3. Cortisol's role in mobilizing glucose, which depletes energy reserves for immune cells.
  4. Cortisol's immunosuppressive effects, including the inhibition of cytokine production. (correct answer)
Explanation: Sustained stress from the exams leads to prolonged elevation of cortisol via the HPA axis. While beneficial for short-term energy mobilization, a primary function of cortisol is to suppress the immune system and inflammatory responses. It achieves this by inhibiting the production of cytokines and the proliferation of lymphocytes, thereby making the individual more vulnerable to opportunistic infections like the common cold.

Question 16

An individual has a rare genetic mutation causing their glucocorticoid receptors in the brain to be exceptionally sensitive. How would this individual's HPA axis response to a moderate stressor likely differ from that of an individual with typical receptor sensitivity?

  1. They would exhibit an exaggerated and prolonged cortisol release due to enhanced pituitary stimulation.
  2. They would show a normal initial cortisol release, but the response would be excessively prolonged.
  3. They would mount a smaller cortisol response that is terminated more quickly and efficiently. (correct answer)
  4. They would have chronically elevated baseline cortisol levels due to continuous HPA axis activation.
Explanation: Highly sensitive glucocorticoid receptors mean that the negative feedback system is more efficient. A smaller amount of cortisol is needed to activate these receptors in the hypothalamus and hippocampus to shut down the HPA axis. Therefore, when faced with a stressor, their cortisol response would be more constrained (smaller peak) and would be terminated more rapidly once cortisol levels begin to rise.

Question 17

A patient presents with symptoms of hypercortisolism (e.g., central obesity, hypertension). Imaging reveals a tumor on one of their adrenal glands that is autonomously producing cortisol. What would be the expected levels of endogenous ACTH and CRH in this individual?

  1. High ACTH and high CRH
  2. High ACTH and low CRH
  3. Low ACTH and high CRH
  4. Low ACTH and low CRH (correct answer)
Explanation: The adrenal tumor is producing high levels of cortisol independent of HPA axis control. This pathologically high level of cortisol will exert a powerful negative feedback effect on both the pituitary gland and the hypothalamus. This feedback will suppress the pituitary's release of ACTH and the hypothalamus's release of CRH, leading to low levels of both hormones.

Question 18

An individual is administered a novel medication that significantly increases the metabolic clearance rate of cortisol, effectively reducing its half-life in the bloodstream. If this individual is subjected to a continuous, low-level stressor, what compensatory change in the HPA axis is most likely to occur over time?

  1. An increase in the tonic (baseline) secretion of CRH and ACTH to maintain normal cortisol levels. (correct answer)
  2. A decrease in the baseline secretion of CRH and ACTH to match the lower cortisol levels.
  3. A desensitization of glucocorticoid receptors in the brain to prevent over-stimulation.
  4. A complete shutdown of the HPA axis as it can no longer maintain hormonal balance.
Explanation: When you encounter questions about hormonal feedback systems, think about the body's drive to maintain homeostasis through compensatory mechanisms. The HPA (hypothalamic-pituitary-adrenal) axis operates on negative feedback, where cortisol normally inhibits its own production by suppressing CRH and ACTH release. In this scenario, the medication accelerates cortisol clearance, meaning cortisol levels drop faster than normal despite ongoing stress. The hypothalamus and pituitary detect these lower cortisol levels and interpret this as insufficient stress response. To compensate, they increase baseline secretion of CRH and ACTH, driving the adrenal glands to produce more cortisol and restore adequate levels for the stressful situation. Option A correctly identifies this upregulation response - the system compensates by increasing upstream hormone production to maintain cortisol availability during stress. Option B suggests the opposite response, which would worsen the cortisol deficiency rather than correct it. This contradicts the body's homeostatic drive. Option C describes receptor desensitization, but with lower (not higher) cortisol levels, there's no risk of over-stimulation requiring this protective mechanism. Option D proposes complete system shutdown, which is biologically implausible. The HPA axis is essential for survival and would adapt rather than cease functioning entirely. Remember: In endocrine feedback questions, identify what's being detected (low cortisol) and predict the logical compensatory response (increase production upstream). The body almost always tries to restore balance, not give up or worsen the imbalance.

Question 19

During a demanding cognitive task, a subject's heart rate increases rapidly, their palms become sweaty, and they report feeling 'on edge'. About 20 minutes later, blood tests show elevated levels of a hormone that is increasing glucose availability through gluconeogenesis. This physiological sequence is best explained by:

  1. Initial HPA axis activation causing cortisol release, followed by SAM system activation.
  2. Simultaneous and synergistic activation of both the SAM system and the HPA axis.
  3. Initial SAM system activation, followed by a slower-acting HPA axis response. (correct answer)
  4. A primary parasympathetic withdrawal followed by a secondary HPA axis activation.
Explanation: The rapid heart rate, sweating, and feeling 'on edge' are classic signs of sympathetic nervous system (SAM) activation and the release of epinephrine/norepinephrine. The elevation of a glucose-mobilizing hormone (cortisol) 20 minutes later is characteristic of the slower, more delayed HPA axis response. This illustrates the two-wave nature of the physiological stress response, with the SAM system acting first and the HPA axis following.

Question 20

An individual with a specific phobia is exposed to their feared stimulus, initiating a classic stress response. Researchers measure the plasma concentrations of two key stress hormones over the next hour.

Based on the known physiology of the stress response, a graph of the hormone concentrations over time would most likely show which pattern? Refer to the information in the passage.

  1. Hormone A (cortisol) peaks within 1-2 minutes, while Hormone B (epinephrine) peaks around 20-30 minutes.
  2. Hormone A (epinephrine) peaks within 1-2 minutes, while Hormone B (cortisol) peaks around 20-30 minutes. (correct answer)
  3. Both Hormone A (cortisol) and Hormone B (epinephrine) peak simultaneously within the first 5 minutes.
  4. Both Hormone A (cortisol) and Hormone B (epinephrine) show a slow, gradual rise, peaking together after about 45 minutes.
Explanation: The stress response involves two major systems with different timelines. The sympathetic nervous system (SAM) acts first, causing the adrenal medulla to release epinephrine almost instantly (peaking in 1-2 minutes). This is the 'fast' response. The HPA axis is the 'slow' response; the hormonal cascade (CRH -> ACTH -> cortisol) takes time, with cortisol levels typically peaking in the blood around 20-30 minutes after the initial stressor.