Homestasis and Stress Flashcards

(37 cards)

1
Q

Homeostasis is______

A

feature of a system ( human body) that regulates a specific parameter to maintain stable condition

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2
Q

Homeostasis is ___________ regulated.

A

highly

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3
Q

Allostasis is________

A

mechanisms that let an organism maintain long-term stability and viability by coordinating body-wide (brain controlled) responses via overriding homeostatic setpoints to meet predicted needs

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4
Q

4 keys points of Allostasis

A
  1. achieves long term stability through change
  2. a series of coordinated changes in multiple systems
  3. override homeostatic mechanisms
  4. is preemptive and predictive ( zebra being chase by a lion)
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5
Q

Allostatic state

A

a period when there is an override of homeostatic setpoints

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6
Q

Allostatic load

A

short term burden caused by allostatic states

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7
Q

Allostatic overlaod

A

long term, maladpative allostatic load that causes damage to system

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8
Q

A stressor is__________

A

a positive or negative experiences that changes homestasis

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9
Q

What is a stress response?

A

a response to changes in allostatic or homeostatic balance

or

response to stressor

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10
Q

What is stress?

A

anything that changes the allostatic or homeostatic balance of a living organism

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11
Q

Sella Turcica

A

Where pituitary gland is encased

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12
Q

What is the purpose of releasing hormones/factors released by hypothalamus

A

Releasing hormones tell pituitary to release hormones found in pituitary into blood

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13
Q

2 types of neurons found in the paraventricular nucleus (PVN) of hypothalamus

A
  1. medial parvocellular ( parvo=small) neurons -secrete releasing factors into smaller, special circurlation via media eminence
  2. magnocellular ( magno=large) neurons -secrete oxycotin and vasopressin directly into general circulation
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14
Q

HPA axis and stress hormone release

A
  1. medial parvocellular neurons make and secrete CRH/F
  2. CRH/F is released in capillary bed called median eminence and carried down to anterior pituitary via superior hypophyseal artery ( a special portal circulation)
  3. CRH/F binds to CRH/F receptors on corticotrophs, cell type found in anterior pituitary
  4. Corticotroph are activated/stimulated by CRH/F to release ACTH in general blood circulation
  5. ACTH travels in blood to effector organ, adrenal cortex
  6. ACTH binds on receptor in adrenal cortex and stimulates release of cortisol
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15
Q

Hormones released by Posterior Pituitary

A
  1. ADH/vasopressin

2. Oxytocin

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16
Q

Adenohypopsis

A

the anterior pituitary
adeno=gland
a lot of blood vessels

17
Q

Neurohypopsis

A

posterior pituitary
neuro=neurons
contain alot of neuronal axons

18
Q

Cortisol/corticorsterone

A

main stress hormone in humans/rodents

hormones differ by one hydroxyl group

19
Q

biosynthesis of steroid hormones

A

precursor of all steroids is cholesterol

aldosterone, progesterone, testoterone, estrogen, cortisol

20
Q

How is stress response terminated

A
  1. removal of stressor

2. Negative feedback along the Hypothalamus, Pituitary, Effector Organ Axis

21
Q

What evidence shows that hippocampus is invovlved in stress response?

A

There is a dense concentration of cortisol/corticosterone receptors in the hippocampus

22
Q

3 types of effects caused by stress response

A
  1. CRFergic central effects ( hypothalamus)
  2. Glucocorticoid peripheral effects ( increase GC receptors)
  3. SNS mediated peripheral effects
23
Q

Effect of Stress on Reproduction

A

A CRFergic central effect

Stress inhibits reproduction

24
Q

Effect of stress on SNS

A

A SNS peripheral effect

Stress activates SNS system

25
Effect of stress on GC control
A GC peripheral effect stress increase stress hormone release and results in 1. Increase metabolism ( protein production) 2. Decreased immune response (immuno-suppression)
26
Mechanism of glucocorticoid effect during stress response
1. Cortisol can freely enter cell vis passing through cell membrane 2. Cortisol binds to glucocorticoid receptor inside cell 3. Glucocorticoid receptors are normally held in cytsol of cell by chaperone proteins like heat shock protein so the receptors can’t enter into nucleus of cell 4. Glucocorticoid displaces the chaperone protein and enters into nucleus as a glucocorticoid-glucocorticoid receptor complex 5. G-GC complex binds to glucocorticoid responsive element in nucleus and this recruits transcription factors 6. Transcription factors are start transcription of genes with glucose responsive elements; mRNA is translated to protein 7. Newly produced protein increases cellular function
27
Rate of change and Stress Response
Stress response occurs at molecular, cellular, and behavioral levels slow change-protein synthesis faster change-SNS
28
Effect of cortisol on neuron activity
hippocampal neurons fire more frequency
29
Brain structures that inhibit stress response
Hippocampus | Pre-frontal cortex
30
Brain structures that increase stress response
Amygdala
31
What happens to key brain structures during chronic stress?
Amygdala hypertrophies and then atrophies Hippocampus and prefrontal cortex atrophy
32
Net effect of Hypothalamus-Pituitary-Adrenal Cortex Axis in Chronic Stress Brain remodeling?
Stress response is lengthened because negative feedback mechanism are decreased and pro-stress mechanism are increased
33
Hippocampus activity and stress response
Acute stress: Hippocampus is healthy and decreases effects of stress Chronic stress: hippocampus is damaged and there is an increase in negative effects of prolonged stress response
34
Stress and Learning/memory
Acute stress: increase stress, increase learning and memory chronic stress: increase stress, decrease learning and memory
35
Why is stress an vital physiological feature?
Acute Stress and stress response has evoluntionary benefit; stress hormones help us survive stressful situations!
36
Describe the epigenetic nature of early life stress on organism
Stress during early development has negative long-lasting effects on brain and behavior Stress is not only mediated by genetic effects but also environment
37
What did low/high grooming rodent study reveal about epigenetic affects of stress
rats who had low stress/high groom enviroment had more demethlyaltion of the promoter NR3C1, the glucocorticoid receptor responsible for increased glucocorticoid receptor expression ( a good thing!) than rats that had high stress/low groom environment