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Flashcards in Stress Deck (48)
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1

Stage 3 of stress response

Exhaustion. Reserves of resources are depleted

2

How does stress arise?

When we deplete the resources we have to fight stress

3

What does cortisol binding to glucocorticoid receptors in the hippocampus cause?

Less CRH release from hypothalamus which leads to less ACTH release by the pituitary which leads to less cortisol release by the adrenal gland

4

What does the hypothalamus use to communicate with the pituitary gland in the HPA axis?

Corticotropin releasing hormone (CRH)

5

What NTs are released by the SAM system?

Epinephrine and norepinephrine

6

What do more connections in the amygdala cause?

Earlier activation with less input

7

Communicates from the pituitary to the adrenal gland

ACTH

8

What things contribute to someone experiencing stress?

Short term vs long term, social support, personality, attitude, and locus of control

9

What NTs are released by the HPA axis?

Glucocorticoids (cortisol)

10

What does more stress lead to in term of behavior?

Worse behavior which leads to a weakened immune system

11

Stress and the common cold

More stress = more likely to get cold but must be exposed to virus to get it

12

What changes are seen in neurons exposed to long term stress (cortisol) in the hippocampus and the amygdala?

Hippocampus = Less spines, inhibited neurogenesis
Amygdala = More connections

13

This system provides a slower and longer stress response

Hypothalamus pituitary adrenal axis (HPA)

14

What does prolonged stress do in the HPA axis?

Disrupts negative feedback

15

What neurons are the most susceptible to apoptosis when there is too much cortisol and why?

Hippocampal neurons bc they contain the most cortisol receptors

16

Caused by an existing stress-causing factor or stressor

Stress

17

Stress that continues after the stressor is gone

Anxiety

18

How does maternal care impact stress (epigenetics)

Offspring with more nurture had milder HPA axis responses, more cort control, a good number of cort receptors

19

What are the 3 stages of the general adaptation response to stress

1. alarm
2. resistance
3. exhaustion

20

This NT is helpful in small amounts but harmful in large amounts

Cortisol

21

Pathway goes from hypothalamus to pituitary to adrenal gland

Hypothalamus pituitary adrenal axis (HPA)

22

How is the HPA axis stopped from producing more cortisol?

Hippocampus has receptor sites for cortisol that act to inhibit excessive release of CRH

23

Glucocorticoid receptor gene and epigenetics

More GR protein = calm down faster, good when need to explore and find food
Less GR protein = more prolonged stress, good in environment with lots of predators

24

What does too much calcium cause?

The cell is so depolarized it cant get back to resting. Apoptosis

25

Illness producing substances

Antigens

26

What else does too much cortisol cause other than too much calcium entering cells?

Increases amount of NT release

27

Communicates from the hypothalamus to the pituitary

CRH

28

Pathway goes from nerve impulses to spinal cord to preganglionic sympathetic fibers to adrenal glands

Sympathetic adrenal medullary system (SAM)

29

What stress NTs are immunosuppressive?

Catecholamines and cortisol

30

What types of personalities are at a higher risk for stress?

Competitive (type A)

31

Increases energy by converting proteins to glucose, increasing fat availability, and increasing metabolism

HPA axis. Cortisol

32

What is used to communicate between the pituitary and adrenal gland in the HPA axis?

ACTH

33

This system provides a fast stress response

Sympathetic adrenal medullary system (SAM)

34

Illness producing organisms

Pathogens

35

What do studies for stress and depression share?

They are the same

36

How is the HPA axis activated?

1. sensory info about threat reaches amygdala
2. amygdala sends signals to hypothalamus via stira terminalis
3. paraventricular nucleus of the hypothalamus releases CRH
4. anterior pituitary releases ACTH
5. ACTH causes adrenal glands to release cortisol
6. cortisol reaches neurons in brain causing inc release of NTs
7. hippocampus has receptor sites for cortisol, acts to inhibit excessive release of CRH

37

Stage 2 of stress response

Resistance. Continue coping using resources to cope

38

Long term effects of cortisol on calcium and the cell

Increases the amount of calcium entering the cells which can be excitotoxic and cause neurons to go through apoptosis

39

What area of the hippocampus has its cells destroyed in the presence of too much cortisol?

Cells in CA1 of they hippocampus

40

Stress coping strategies

Good sleep, balanced diet, aerobic exercise, face to face social networking (oxytocin), cognitive restructuring

41

What does the amygdala stimulate in the HPA axis?

CRH release in the paraventricular nucleus of the hypothalamus

42

Increases output from heart and liberates glucose from muscles for additional energy (gets us ready to go and uses our energy)

SAM system. Epinephrine and norepinephrine

43

Increases cells and cell products that kill infected and malignant cells and protect the body against foreign substances and may increase neurogenesis

Acute stress

44

Stage 1 of stress response

Alarm. Fight/flight response

45

Where are glucocorticoid receptors in the HPA axis that are involved in negative feedback?

Hippocampus, hypothalamus, and pituitary. Hippocampus most important

46

Compromises the immune system, interferes with memory, appetite, sexual desire and performance, energy, mood, and makes you more vulnerable to disease

Chronic stress

47

What can stress cause in the heart?

Inc blood pressure that leads to greater risk for heart attack

48

What does prenatal stress cause in adulthood?

Increased volume in lateral amygdala