Chapter 2: Homeostasis and Adaptive Responses to Stressors

Chapter 2: Homeostasis and Adaptive Responses to Stressors

Complete Chapter Questions With Answers

Sample Questions Are Posted Below

MULTIPLE CHOICE

1. Indicators that an individual is experiencing high stress include all the following except

ANS:  D

Pupils dilate during stress from the effects of catecholamines. Tachycardia, diaphoresis, and increased peripheral resistance are indicators of stress and also occur due to catecholamine release.

REF:   Pg. 18 | Pg. 21

2. Which is not normally secreted in response to stress?

ANS:  D

Insulin secretion is impaired during stress to promote energy from increased blood glucose. Norepinephrine is secreted during stress as a mediator of stress and adaptation. Cortisol is secreted during stress as a mediator of stress and adaptation and stimulates gluconeogenesis in the liver to supply the body with glucose. Epinephrine is secreted during stress as a mediator of stress and adaptation and increases glycogenolysis and the release of glucose from the liver.

REF:   Pg. 17

3. Selye’s three phases of the stress response include all the following except

ANS:  A

Allostasis is defined as the ability to successfully adapt to challenges. Allostasis may/may not occur in response to stress. Alarm, resistance, and exhaustion are the three phases of the stress response as described by Selye in the general adaptation syndrome.

REF:   Pgs. 13-14

4. Many of the responses to stress are attributed to activation of the sympathetic nervous system and are mediated by

ANS:  A

Norepinephrine is secreted in response to activation of the sympathetic nervous system during stress by the adrenal medulla. Cortisol is secreted by the adrenal cortex. Glucagon is secreted by the pancreas. ACTH is secreted by the pituitary gland.

REF:   Pg. 17

5. The effects of excessive cortisol production include

ANS:  A

Cortisol suppresses immune function and inflammation and stimulates appetite. Cortisol leads to hyperglycemia by stimulating gluconeogenesis in the liver.

REF:   Pgs. 21-22