pathophysiology of stress Flashcards

1
Q

what are themajor physical manifestation of stress?

A
  • tachycardia/hypertenstion
  • acuter hypoinsulinemaia= hyperglycaemia
  • splenic contraction- r;eease of RBC
  • decrease GI axctivity
  • sweating
  • pupillary dilation
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2
Q

describe the physiological Method of action of acute stress- SNS?

A
  • perceptions via the sense or psycholopgical trhreat
  • Amygdala interpets the infromation
  • communicates to hypothalamus- stimulating the SNS
    • Release of Nadr (repceotrs in adrneegric tissue)
    • receptors in sweat gland Ach- muscarinic
  • eye, lung, heart GI, glucose rgulation
    • dilation, increase ccardiac contractility, vasconstrictionb
  • srimualtion of the adrenal medulla- secret cortisol
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3
Q

describe how acute stress causes activation of the adrenal medulla and the effects

A

preganglionic neuorne synapse directly onto meduall

will release - adrrenal (80% and Nadr (20%

cardiovcascular effects

  • B1 recepotrs- heart contracitllity
  • A1 receptors- vasoncontrticion
  • hypertension

increas glucos levles (hyperglycaemia

liver- glycogenesis and gluconeogenesis-

pancrease B cells- inhbiiton of insulin ecretion

adipose tisuse- inhbit gluocs uptak-0 GLUT4 recepeotrs

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4
Q

what would we see in blood results after stress?

A

blood sugar up

cortisol upo

Hba1c unchanged

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5
Q

explain how Cortisol is released

A
  • hypothalamus recievres sensory or psychlogicla stress
  • hypothalamus secreesh CRH—> anterior pituriaty screats ACTH
  • scitvaes cortex of the adrenal gland (zona fasciulata)
  • secrete cortiols (glucocortiocid)
    • acts on nuclear hormone receptors
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6
Q

what are cortiols effect son metabolism?

A

mobilisation of energy stores in times of stress

gluconeogensis in the liver stops glycogenesis

skelelal uslce- increase protein degration- AA for Gluconeeoengeis

adipose tisuse= lipolysis- gluconeoegenesi

Pancreas-e inhbit insulin release- hyperglycaemia

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7
Q

how do gluccorticoids (cortiosl) have immunosuprression effects? (inside cells)

A

gneomioc- GR receptors promites IkBa sysntheiss which prvents p/50/.p65 (trnascirption factors-

prevent production of cytopkine-s block inflamamtory genees ( needed by immune cells to activate)

non gneomic- GR complexes directly bind to p65 subunit prevents p50/p65 nuclear trnactipion

suppres immune cell actviation (T cells and b cells)- blockjing trancritipn factors and trnacrpito of cytokines

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8
Q

how do glucocorticoids like Cortisol limit the recuitment of WBC to inflammed or infected tissues?

A

suppress cytokine production

prveebitn leukocyte extrvasaion into tissues (mehcnaism unclear)

vasocontriction of smooth muscle cells ( increase in andgreneric receptos on smooht muscle and Angiotensin 2)

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9
Q
A
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