Download Free Medical The General Adaptation Syndrome PowerPoint Presentation

The General Adaptation Syndrome PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on adrenal gland, which is titled "The General Adaptation Syndrome", to know about the general adaptation syndrome (GAS). This three-stage process was developed by Hans Selye and describes the pattern of responses that our body goes through after being prompted by a stressor. There are three stages in the general adaptation syndrome, i.e., alarm, resistance, and exhaustion.

Tags : adrenal gland, The General Adaptation Syndrome, GAS, Hans Selye, stressor, alarm, resistance, exhaustion

Published on : May 06, 2021 | Views : 3515 | Downloads : 2

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

The General Adaptation Syndrome Figure 18.21
Slide 2-

Flow-sheet of Stress Response “Stressors”: temperature sounds images smells tastes pressure O2/CO2 sexual “Cortex” PNS PNS “INPUT” Hypo Pit “OUTPUT” “Motor Targets” heart blood vessels lungs adrenal glands sweat glands kidneys tissue enzymes others Adrenals
Slide 3-

Allostasis: achieving stability through change. Coping with stress, habituation
Slide 4-

ppt slide no 4 content not found
Slide 5-

Triad of systems mediate response to stress
Slide 6-

Stimulation of the HPA-axis by cytokines
Slide 7-

ppt slide no 7 content not found
Slide 8-

ppt slide no 8 content not found
Slide 9-

ppt slide no 9 content not found
Slide 10-

ppt slide no 10 content not found
Slide 11-

Consequences of persistant stress and allostatic load:negative cortisol feedback dwindles (receptor downregulation?) + a subpopulation of CRF secreting cells begin to synthesize and secrete vasopressin as a co-existing releasing factor
Slide 12-

Control of ACTH secretion: - regulated by hypothalamic neurons secreting two releasing factors: CRH-41 (corticotropin releasing hormone) ± AVP (arginine vasopressin). - various pathways utilizing different transmitters (5-HT, serotonin; NA, noradrenaline; NO, nitric oxide) provide excitatory inputs that define the magnitude of the CRH /AVP neuronal response, thus the quantity of peptides delivered into the pituitary portal plexus
Slide 13-

ppt slide no 13 content not found
Slide 14-

Stress (immobilization) up-regulates vasopressin synthesizing genes in a population of hypothalamic CRF-synthesizing neurons, and increases AVP in CRF immunoreactive terminals in the median eminence from Bartanusz et al., Endocrinology 132: 895-902, 1993.
Slide 15-

Summary: Chronic stress changes induced in the hypothalamic CRF system Prolonged exposure of the hippocampus to elevated cortisol levels impairs inhibitory feedback to CRF cells Add: reductions in the impact of negative cortisol feedback, so CRF cells more active → more drive on HPA axis Add: re-activation of vasopressin genes in a subpopulation of CRF cells, so they now produce two (stimulatory) peptides for secretion into the portal plexus Add: upregulation of vasopressin V1b type receptors in anterior pituitary corticotrophs (double whammy → more ACTH→more drive on HPA axis) Add: additional drive to PVN from other sites e.g.amygdala
Slide 16-

ppt slide no 16 content not found
Slide 17-

Cushing’s Syndrome
Slide 18-

Cushing’s SyndromeDN Orth, NEJM 332:791-803, 1995 Figure 1. Physiologic and Pathophysiologic Features of the Hypothalamic–Pituitary–Adrenal Axis in Normal Subjects and Patients with Cushing's Syndrome (Top Panels) and the Effect of Dexamethasone (Bottom Panels). Stimulation of the hypothalamus by other central nervous system centers, such as the locus caeruleus, regulates the secretion of CRH; corticotropin stimulates adrenal secretion of cortisol; and cortisol inhibits the secretion of both CRH and corticotropin. Adrenal (i.e., corticotropin-independent) Cushing's syndrome is caused by adrenal tumors and corticotropin-independent bilateral micronodular and macronodular adrenal hyperplasia. Low doses of dexamethasone are shown by thin blue arrows, and high doses by thick blue arrows. Normal hormone secretion is shown by thin purple lines, suppressed secretion by dotted purple lines, and hypersecretion by thick purple lines.
Slide 19-

ppt slide no 19 content not found
Slide 20-

ppt slide no 20 content not found
Slide 21-

ppt slide no 21 content not found
Slide 22-

ppt slide no 22 content not found
Slide 23-

Neuron, Vol. 20, 1093–1102, June, 1998, Copyright ã1998 by Cell Press Corticotropin Releasing Factor Receptor 1–Deficient Mice Display Decreased Anxiety, Impaired Stress Response, and Aberrant Neuroendocrine Development Corticotropin releasing factor (CRF) is a major integrator of adaptive responses to stress. Two biochemically and pharmacologically distinct CRF receptor subtypes (CRFR1 and CRFR2) have been described. We have generated mice null for the CRFR1 gene to elucidate the specific developmental and physiological roles of CRF receptor mediated pathways. Behavioral analyses revealed that mice lacking CRFR1 displayed markedly reduced anxiety. Mutant mice also failed to exhibit the characteristic hormonal response to stress due to a disruption of the hypothalamic-pituitary-adrenal (HPA) axis. Homozygous mutant mice derived from crossing heterozygotes displayed low plasma corticosterone concentrations resulting from a marked agenesis of the zona fasciculata region of the adrenal gland. The offspring from homozygote crosses died within 48 hr after birth due to a pronounced lung dysplasia. The adrenal agenesis in mutant animals was attributed to insufficient adrenocorticotropic hormone (ACTH) production during the neonatal period and was rescued by ACTH replacement. These results suggest that CRFR1 plays an important role both in the development of a functional HPA axis and in mediating behavioral changes associated with anxiety.
Slide 24-

ppt slide no 24 content not found
Slide 25-

ppt slide no 25 content not found