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BIOL1013 > Acute stress response > Flashcards

Acute stress response Flashcards

1
Q

What is the central point for the endocrine system?

A

Hypothalamic-pituitary axis

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2
Q

What does the hypothalamus regulate the balance between?

A

The sympathetic/ parasympathetic nervous system and the endocrine systems

Hence: the neuro-endocrine system

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3
Q

Name 4 hypothalamic inputs from the neural and circulatory queues?

What information does each have?

A
  1. Forebrain (Limbic Structures): information from conscious and autonomic systems
  2. Spinal cord and Brainstem Structures: information related to visceral and somatic function
  3. Circumventricular Organ: receives information on blood protein composition
  4. Receptors inside the Hypothalamus: information on temperature, osmolarity, etc.
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4
Q

Tell me about the hypothalamic output?

A

Hypothalamic output directly via endocrine system (tropic hormones- ADH/oxytocin) and/or indirectly modify the neural pathways of sympathetic/ parasympathetic via the Locus Ceruleus (Coeruleus)

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5
Q

Where does the locus ceruleus recieve inputs from?

A

Inputs from prefrontal cortex, (responding to activity levels), Especially visual and auditory sensation and general autonomic and environmental stimuli

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6
Q
A
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7
Q

This shows the sympathetic and parasympathetic thoraco-lumbar

A
  • 8 celiac ganglia, 14 adrenal, 17 dorsal liver, 13- mesenteric (splanchnic nerve)
  • Sympathetic chain – or vertebral ganglia
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8
Q

What happens if a stimulus is percieved as a threat?

A

If stimulus perceived as a threat, intense and prolonged noradrenergic discharge of the locus ceruleus

  1. strongly activates the sympathetic nervous system.
  2. Causes release of adrenaline (little noradrenaline) from the adrenal medulla.

also, activation of other sympathetic nervous outputs

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9
Q

What does acute- or hyperacute stress facilitate?

A

Facilitate immediate physiological reactions in preparation for violent muscular action.

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10
Q

What does Acute- or hyperacute stress increase?

A

Cardiac output (increased speed, strength, and conduction)

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11
Q

What does Acute- or hyperacute stress constrict and dilate?

A

Constricts

  • Constriction of most systemic blood vessels (paling), -increase in circulatory return

Dilates

  • Dilation of muscle vessels
  • Dilation of pupil (mydriasis)
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12
Q

What does Acute- or hyperacute stress increase and inhibit?

A

Increase

  • Increases ventilation

Inhibits

  • Inhibition intestinal action (digestion slows) not sphincters
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13
Q

What does Acute- or hyperacute stress relax?

A

bladder

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14
Q

What does Acute- or hyperacute stress increase and decrease?

A

Decrease

Auditory exclusion (loss of hearing)

Increase

Acceleration of instantaneous reflexes - Shaking

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15
Q

What are the three main catecholamines based on?

A

They are active amines based on tyrosine

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16
Q

Name the 3 main catecholamines?

A
  1. Dopamine
  2. Noradrenaline
  3. Adrenaline
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17
Q

Tell me about Dopamine?

A

Widespread CNS neurotransmitter

(also, a hormone released by hypothalamus inhibiting prolactin release)

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18
Q

Tell me about Noradrenaline?

A

Neurotransmitter inducing “attention, arousal and alertness”,

(stress hormone) some hormonal effect

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19
Q

Tell me about adrenaline ?

A

Stress hormone, produced and stored in chromaffin cell of

adrenal medulla (can act as a neurotransmitter)

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20
Q

What type of cells are chromaffin cells?

Where are these cells found?
What are chromaffin cells stained with?

A
  • Chromaffin cells are neuroendocrine cells found in the medulla of the adrenal gland (chromaffin-like cells seen in other ganglia of the sympathetic nervous system)
  • Stain chromaffin cells with chromium
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21
Q

What is the adrenal medulla?

A

A modified sympathetic ganglion but here (neural derived) cells released adrenaline (>80%)

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22
Q

Why does the adrenal medulla make adrenaline?

A

They make adrenaline because the presence of adrenal cortex (very high cortisol) causes formation of the adrenal medulla

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23
Q

What is regulated by ACTH?

A

Tyrosine hydroxylase (TH) and Dopamine Beta-hydroxylase (DBH) are regulated by ACTH

24
Q

What is cortisol levels regulated by?

A

Phenyl ethanolamine N-methyltransferase (PNMT) regulate cortisol levels

25
Q

What pathway can affect the production of catecholamines?

A

Hence hypothalamus-pituitary-adrenal cortex pathway can affect the production of catecholamines

26
Q

Chronic stress increases adrenaline production by the adrenal glands in acute situation.

  • What stimulates the synthesis of noradrenaline and how?
  • What increases the expression of PNMT in chromaffin cells?
A
  1. Adrenocorticotropic hormone (ACTH) stimulates synthesis of noradrenaline by enhancing the expression of tyrosine hydroxylase and dopamine-β-hydroxylase
  2. Cortisol, from the adrenal cortex increases the expression of PNMT in chromaffin cells, enhancing adrenaline synthesis
27
Q

What type of signalling do catecholamines use?

A

G-protein coupled signalling

28
Q

Sometimes the same hormone can have different effects on same cell type in different tissues.

Give an example and the effect it causes

A

Example: Smooth muscle

  • Smooth muscle in bowel wall relaxes
  • Smooth muscle in iris sphincter relaxes

but

  • Smooth muscle in bowel sphincters contract
  • Smooth muscle in blood vessels in gut/skin contracts

use different receptors and turn on different signals

29
Q

Give an example of a receptor that can alter the function of different smooth muscles?

A

Adrenergic (adrenaline/ noradrenaline) receptor

30
Q

Give examples of the adrenergic receptor and what they cause?

A

alpha-adrenergic receptors cause smooth muscle constriction in intestinal vessels

beta2-adrenergic receptors cause smooth muscle relaxation in intestinal wall

31
Q

Whats the adrenergic family tree?

A
32
Q

How are the alpha and beta adrenergic receptors initially seperated?

A

by their different relative responses to the different catecholamines

33
Q

Tell me the potency of alpha and beta receptors

A

Alpha: noradrenaline ≥ adrenaline > isoprenaline

Beta: isoprenaline> adrenaline >> noradrenaline > dopamine

34
Q

All adrenergic receptors use G protein pathways

A
35
Q

What enzyme does Alpha1 (aGa) effect?

What effects does it cause?

A
36
Q

What enzyme does Alpha2 (aGi) effect?

What effects does it cause?

A

aGi is inhibitory so stops the effects seen

37
Q

What enzyme does beta (aGs) effect?

What effects does it cause?

A
38
Q

What does the alpha1 receptor act via and therefore induce?

What does it act in?

What does it induce?

A

a1 adrenergic receptor

  • Act via Gq (alpha type subunit), activating PLC and inducing Ca 2+ release (IP3) and DAG- which together activate PKC
  • In vascular smooth muscle constriction (vessels in skin, GI tract)

a1 blockers (e.g. Phentolamine reduce hypertension

  • Induces glycogenolysis (liver)
39
Q

What does the alpha2 receptor act via and therefore inhibit?

Whats it present on?

What does it inhibit and activate?

A
  • Act through Gi (as their alpha type subunit- inhibits the action of adenyl cyclase and PLC)
  • Present on sphincters in GI tract - causing contraction.
  • Also present in a and b cells of pancreas
  • Inhibits insulin release
  • Activates glucagon release
40
Q

What does the beta receptor act through?

What does the beta1 and beta2 act on?

A

Act through classical Gs (as their alpha type subunit- activating adenyl cyclase)

Beta 1: cardiac muscle

Beta 2: Gut and bronchiole smooth muscle and in vessels of skeletal muscle, in skeletal muscle cells, in liver

41
Q

Tell me how Beta 1 effects cardiac muscle

A
  • Chronotrophic (faster beat)
  • Ionotrophic (increased force)
  • Dromotrophic (increased conduction)
42
Q

Tell me how beta 2 effects Gut and bronchiole smooth muscle and in vessels of skeletal muscle

A
  • Relaxes causing vasodilation
  • ease of breathing
  • relaxed gut wall
  • (phosphorylation SMMK- inactivates enzyme)
43
Q

How does beta 2 effect skeletal muscle cells?

A
  • increases glycogenolysis and glycolysis,
  • ready for increased muscle activity
  • (also causes tremble)
44
Q

How does beta 2 effect the liver?

A

increases glycogenolysis

45
Q

Beta adrenergic receptor

A
46
Q

How do antagonists (beta blockers) work?

A
  • binds to receptor but doesn’t activate
  • Used to slow heart, allows better filling and reduced cardiac “stress” but effects β1 and β2 receptor classes so has non – heart effects (gut and muscle)
  • Modern blockers are heart- i.e. b1 specific (e.g. Betaxolol) they reduce the effect of excitement/physical exertion on heart rate and force of contraction,
  • Used in hypertension, angina and arrhythmias
  • Also reduces tremor
47
Q

Give an example of a beta blocker?

A
48
Q

What does glucose increase and reduce and where?

A
  • Increases glycogenolysis in liver
  • Reduces glycolysis in liver: Expresses alpha1 and beta receptors
49
Q

What does PKA inhibit in order to stop glycolysis in the liver?

A

PKA inhibits hepatic PFK-2 (L)

50
Q
A
51
Q

Tell me what cocaine inhibits and stimulates

A

Inhibits

inhibits uptake of:

  • Serotonin
  • noradrenaline
  • dopamine

Stimulates

  • Increases alertness
  • euphoria
  • motor activity
52
Q

What does circulating adrenaline degrade and what does this remove?

A

Circulating adrenaline degraded, all cells contain monoamine oxidases, which remove the amine and convert these to inactive aldehydes

53
Q

What do some antidepressants increase?

A

The activity of catecholamines

54
Q

Tell me some effects of antidepressants

A
  1. Block reuptake of noradrenaline/ dopamine (and other monoamines like serotonin)

Reboxetine

  1. Reducing their breakdown by inhibiting monoamine oxidases (MAO)
55
Q

What was the first antidepressant marketed, what was the issue with this?

A

Iproniazid (MAO-A inhibitor) was the first antidepressant marketed.

“patients became inappropriately happy” its chemistry is based upon hydrazine (rocket fuel)

BIOL1013 (9 decks)

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