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HHP > stress > Flashcards

stress Flashcards

1
Q

what is stress

A

a general term for any condition that actually or potentially poses a serious challenge to the body’s ability to maintain homeostasis

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2
Q

what types of stress exist

A

1) PSYCHOLOGICAL STATES OF STRESS

2) PHYSICAL CONDITIONS THAT CAUSE STRESS

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3
Q

what are some PSYCHOLOGICAL STATES OF STRESS

A

pain
fear
anxiety

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4
Q

what are some PHYSICAL CONDITIONS THAT CAUSE STRESS

A
  • dehydration
  • haemorrhage (significant loss of blood in short time)
  • infection
  • extremes of temperature
  • v severely intense exercise
  • surgery (tissue trauma so induces a severe metabolic response)
  • factors above can lead to SHOCK (eg cardiogenic shock, septic shock)
  • SO all conditions w potential to cause severe consequences
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5
Q

what is homeostasis

How is the body’s physiological homeostasis monitored

A

loops designed to induce negative feedback and correct problems

this information is relayed/monitored via the central nervous system by the hypothalamus in the brainstem, mainly controlled by sympathetic pathways
Lower maintenance is by the endocrine system w secretion from the adrenal glands

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6
Q

where does the hypothalamus send signals to

A

1) nervous system via sympathetic division of ANS

2) to adrenal glands by the endocrine system

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7
Q

what are the 2 main directions of response

A
  • rapid short term ‘fight or flight’ via sympathetic ANS
  • short term response via release of hormones from adrenal medulla
  • long lasting body responses via endocrine system
  • long term response via release of hormones from adrenal cortex of the adrenal glands
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8
Q

what does the hypothalamus stimulate during the fight or flight response

A
  • neurones from anterior and posterior pituitary glands (just below hypothalamus) to
  • sympathetic portion of ANS via spinal cord
  • endocrine system via the adrenal glands
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9
Q

what happens at the adrenal glands once stimulated by the hypothalamus in the short term response

A
  • neurones to adrenal medulla in the adrenal cortex

- from here adrenaline or noradrenaline is released

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10
Q

what is the action of the sympathetic nervous system

A

1) nerve endings release noradrenaline
2) incs HR and SV thus CO
3) constriction of blood vessels increases blood pressure
4) blood diverted away from non-essential organs TO the brain, heart + skeletal muscle
5) increase in ventilation
6) sweating

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11
Q

what are non-essential organs in the sympathetic response

A

ie the gut

not needed in fight or flight

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12
Q

what is an increase in ventilation

A
  • more rapid breathing

- to cope with anticipated elevated metabolic demand

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13
Q

why is the adrenal medulla interesting

A

its an organ which is both nervous tissue and endocrine

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14
Q

what happens in the adrenal medulla

A
  • preganglionic neurones enter
  • synapse with other cells
  • which release catecholamines (adrenaline and noradrenaline)
    So preganglionic nerve endings stimulate release of catecholamines
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15
Q

what are the adrenal glands

A
  • 2 small glands
  • above each kidney
  • really 2 endocrine organs (act as these)
  • the right one = slightly lower bc of the liver
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16
Q

what is in the
a) inner / central region
b) outer region
of the adrenal glands

A

a) adrenal medulla - regulates a brief rapidly acting short duration stress response (activated in brief response systems)
b) adrenal cortex - activates in more longer lasting response, has different layers to it which release different hormones

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17
Q

how does the adrenal medulla release adrenaline out into circulation

A

1) sympathetic preganglionic neurone enters
2) neurotransmitter activates the postganglionic cell (ie a chromaffin cell)
3) which releases adrenaline into the blood

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18
Q

what is a post ganglionic chromaffin cell different to

A
  • post ganglionic neurones (release their neurotransmitter directly onto whatever it is innervating)
  • whereas chromaffins release into the circulation when stimulated by release of neurotransmitters
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19
Q

what % of the adrenal medulla cells secrete

a) adrenaline / epinephrine
b) noradrenaline / norepinephrine

A

a) 80-90%

b) 10-20%

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20
Q

where are adrenaline + noradrenaline (catecholamines) stored

A

secretory granules (released when stimulated by the preganglionic sympathetic neurons)

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21
Q

what is the action of adrenaline + noradrenaline

A

1) rapid, short term action
2) rapid release
3) quick action at target cells
4) SHORT half life
- so quick but brief response

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22
Q

what is the half life of adrenaline

A

10 seconds

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23
Q

what are the 2 receptors that catecholamines act on and their subtypes

A

1) alpha adrenal receptors (a1 + a2 (a = alpha))

2) beta adrenal receptors (b1, b2 + b3 (b = beta))

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24
Q 
where are 
a) b1
b) b2
c) b3 
expressed
A

a) predominantly heart
b) more widespread
c) rare, only in small parts of kidney

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25
Q

how does adrenaline have biological / metabolic effects (in addition to its receptor based action)

A

IT STIMULATES

1) an increase in glycogenolysis to increase blood glucose
2) increase in gluconeogenesis (concerting precursors in the liver) to increase blood glucose
3) increased mobilisation of free fatty acids, alternative energy source by breakdown of fats, triglycerides and lipids

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26
Q

what is

a) glycogenolysis
b) gluconeogenesis

A

a) breakdown of glycogen store in liver and skeletal muscle

b) forming glucose from other molecules ie precursors in the liver

27
Q

how does noradrenaline principally act

A
  • induces vasoconstriction
  • by acting on alpha 1 adrenoreceptors
  • MORE POTENT on affecting peripheral vasonconstriction therefore BP by increasing TPR
28
Q

how does adrenaline principally act

A
  • cause vasodilation in some areas - by acting on / stimulating beta 2 adrenoreceptors in skeletal muscle (drives rerouting of the blood supply away from areas it isnt needed in the short term + instead to brain, skeletal muscle etc)
  • so increases oxygen supply to the muscle
  • MORE POTENT on affecting the heart and metabolic activities
29
Q

what do both noradrenaline and adrenaline do

A
  • inhibit insulin release (insulin able to form an anabolic hormone)
  • stimulate conversion of glucagon to glucose to increase blood glucose
  • so ample levels of glucose available for use as an energy source
30
Q

how does release of these hormones into the circulation supports the sympathetic system in times of stress

A
  • correlation between familiar emotional stress at elevated levels of noradrenaline
  • unfamiliar stress = driving driving pain associated with higher levels of adrenaline
31
Q

what is a PHAEOCHROMOCYTOMA

A
  • benign adenoma of adrenal medulla thus chromaffin cells

- will mean pts have problems coping w the stress response

32
Q

what are the symptoms of PHAEOCHROMOCYTOMA

A

1) abnormal growth of these cells means inc’d products out of the adrenal medulla
2) hypertension (incd blood pressure) - severe + dangerous if left long enough
3) elevated heart rate - dangerous if left long
4) elevated circulating blood glucose
5) increased sweating

33
Q

how is PHAEOCHROMOCYTOMA dealt with

A

surgical removal

  • can be lived without if sympathetic nervous system is intact
  • as there are 2 adrenal glands
34
Q

list the 3 factors which control stroke volume in the heart

A

1) ventricular contractility
2) end diastolic volume
3) afterload

35
Q

describe starlings law of the heart

A

when the heart rate at which blood flows into the heart (venous return - amnt of blood flowing back to heart) changes, the heart automatically adjusts its output to match inflow

36
Q

describe what is meant by the term afterload

A
  • afterload = load arterial pressure places on the myocardium after the heart starts to contract
37
Q

how can afterload be changed

A

1) physical barrier like aortic stenosis
2) coaptation of the aorta
3) reduced flexibility of the elasticity of major elastic arteries (ie aorta) which have ability to show capacity and elasticity + cope w pulsatile flow so if elasticity reduced = more effectively a hard wall that’s being pumped against by the left ventricle therefore inc’ing afterload

38
Q

what hormone does the adrenal cortex release in long lasting response to stress and what is its half life

A

CORTISOL (secreted in bursts)

60-90 minutes

39
Q

what does CORTISOL do

A
  • stimulates emergency mobilisation of resources in the body beneficial to support + drive tissue repair (necessary in many physical stress situations)
  • stimulates energy mobilisation
  • imp in stress from cardiovascular perspective as has actions on releasing blood glucose and blood pressure
40
Q

what is the 1 day cycle of cortisol secretion in the circadian rhythm (a 24 hour pattern) driven by

A

1) input of daylight recognised in retina. This stimulates secretion (affected in its regularity in blind people)
2) peak secretion in morning
3) trough level in early evening
4) reflects secretion of corticotropin releasing hormone and adrenocorticotropic hormone (these 2 are releasing hormones which need to be present for secretion via this pathway to occur)
5) affected by light/dark sleep cycles and so jetlag

So cortisol release stimulated more on a morning and reduces on an evening

41
Q

where are
a) corticotropin releasing hormone (CRH)
b) adrenocorticotropic hormone (ACTH)
secreted from

what do they do

A

a) hypothallamus
b) anterior pituitary

control levels of cortisol

42
Q

how is cortisol secretion affected by jetlag

A

circadian rhythm of body clock is pushed out by travel through multiple time zones

So cortisol secretion is impaired when our sleep cycle is interrupted

43
Q

how does cortisol act on carbohydrate metabolism to increase blood glucose

A

1) increases gluconeogenesis
2) reduces use of glucose
3) spares glucose for brain (eg after fasting)

44
Q

how does cortisol act on fat metabolism to increase fatty acids

A

1) increase mobilisation of fatty acids from fat stores
2) increase triglyceride breakdown
3) increases use of above for energy so sparing glucose

45
Q

how does cortisol affect protein metabolism

A
  • incs protein catabolism

- produced amino acids used for repair and enzyme formation

46
Q

what cardiovascular effects does cortisol have

A

1) inc BP (due to increased vasoconstriction which enhances the sympathetic autonomic response)
2) inc HR (same as above)

47
Q

explain the ANTI-INFLAMMATORY RESPONSE / ACTIONS OF CORTISOL

A

1) reduces inflammatory response preventing damage of nearby tissue (used pharmaceutically as an anti-inflammatory)
2) reduces immune response to prevent autoimmune disease

48
Q

describe the process of cortisol secretion

A

1) stress or circadian rhythm act on hypothalamus
2) CRH secretion inc’d
3) CRH stimulates anterior pituitary to release ACTH
4) ACTH acts on adrenal cortex which incs cortisol secretion
5) increased cortisol has negative feedback action on anterior pituitary (dec ACTH) and hypothalamus (dec CRH)

49
Q

where does cortisol act once secreted

A

1) many tissue to dec glucose and amino acid uptake
2) on adipose tissue to inc lipolysis
3) on muscles and other tissue to inc protein breakdown and dec protein synthesis
4) on liver to inc gluconeogenesis
- act catabolically

50
Q

in what disease is there hypersecretion of cortisol and what does this mean

A
  • cushings disease
  • due to adrenal cortex tumour
  • or secondary release - hypersecretion of cortisol due to elevated ACTH due to adenoma in benign glandular tumour in anterior pituitary gland
51
Q

what are the symptoms of cushings disease

A
  • ‘moon face’ and ‘buffalo hump’ (alterations in where subcutaneuos fatty tissue is deposited)
  • hyperglycaemia (lead to adrenal diabetes / diabetes mellitus due to adrenal pathology hypertension)
  • incd BP
  • thin limbs (loss of protein from their skeletal muscles due to excessive cortisol mediated protein breakdown)
  • anti-inflammatory actions and dec’d immune response so inc’d risk of infection
52
Q

how is cushings disease treated

A
  • surgical removal of the tumour
  • abdominal surgery to get adrenal cortex tumour
  • OR neurosurgery to remove tumour of anterior pituitary
53
Q

in what disease is there insufficient levels of cortisol (HYPOsecretion) and why

A
  • addisons disease
  • damage to adrenal cortex where theres reduction of cortisol and aldosterone (also generated by the adrenal cortex)
  • OR secondary due to pituitary damage thus reduced levels of ACTH + reduced secretion of cortisol (in that instance assuming pituitary damage only affecting ACTH it wouldn’t lead to reduced aldosterone)
54
Q

what are the symptoms of addisons disease

A

1) low BP
2) hypoglycaemia (low blood sugar)
3) pts susceptible to debilitating effects of stress due to disruption of cortisol levels

55
Q

how is addisons disease treated

A
  • replacement of cortisol and aldosterone if necessary (primary)
  • so taking supplements
56
Q

so outline the short term stress response

A

1) increase HR + BP
2) glycogenolysis
3) bronchioles dilate
4) blood flow patterns change so more alert, decreased activity of digestive system, reduced urine
5) increased metabolic rate

57
Q

how does the short term stress response occur

A
  • via sympathetic nervous system
    1) nerve impulses from hypothalamus to spinal cord
    2) the out on preganglionic sympathetic fibres
    3) to adrenal medulla
    4) act on chromaffin cells which release catecholamines into blood
58
Q

so outline the long term stress response

A

MINERALCORTICOIDS

1) Na and H2O retention by kidneys
2) inc blood vol and BP

GLUCOCORTICOIDS

1) gluconeogenesis
2) proteins + fats also catabolised for energy
3) increased blood sugar
4) immune system suppressed

59
Q

how does the long term stress response occur

A

1) hypothalamus secretes CRH
2) CRH acts on corticotrope cells of anterior pituitary which secretes ACTH
3) ACTH to adrenal cortex
4) adrenal cortex releases mineralcorticoids (ie aldosterone) and glucocorticoids (ie cortisol)

60
Q

what is fainting / syncope

A
  • parasympathetic response
  • VASOVAGAL SYNCOPE
  • loss in BP due to transient fall in perfusion pressure to the brain
61
Q

what can trigger VASOVAGAL SYNCOPE

A

1) emotional stress
2) phlebotomy
3) sight of blood
4) acute pain

62
Q

describe the sequence of event leading to syncope

A

1) emotional stress acts in cortex
2) signal passed to hypothalamus (which incs AVP release)
3) signal from hypothalamus to medulla
- medulla drives dec’d sympathetic output SO TPR decs contributing to reduc in BP
- medulla also causes inc in vagal output w reduced HR so reduced CO and reduc venous return. (ACTS TO reduce atrial stretch which is relayed back to the hypothalamus)
4) reduced TPR, CO and venous return give decreased arterial pressure (MAP)
5) leads to reduced cerebral blood flow in the brain
6) therefore loss of consciousness

63
Q

in which times of stress do the
A) adrenaline
B) noradrenaline
Support the sympathies system

A

A) unfamiliar stress incs its release

B) familiar emotional stress incs it’s release

HHP (10 decks)

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