pathophysiology of stress Flashcards
what are themajor physical manifestation of stress?
- tachycardia/hypertenstion
- acuter hypoinsulinemaia= hyperglycaemia
- splenic contraction- r;eease of RBC
- decrease GI axctivity
- sweating
- pupillary dilation
describe the physiological Method of action of acute stress- SNS?
- 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
describe how acute stress causes activation of the adrenal medulla and the effects
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
what would we see in blood results after stress?
blood sugar up
cortisol upo
Hba1c unchanged
explain how Cortisol is released
- 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
what are cortiols effect son metabolism?
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
how do gluccorticoids (cortiosl) have immunosuprression effects? (inside cells)
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
how do glucocorticoids like Cortisol limit the recuitment of WBC to inflammed or infected tissues?
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)