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+February 3rd 2014 Stress   

Any extreme external or internal stimulus eg surgery, infections, strong emotions, exams Triggers set of body changes called General Adaptation Syndrome All co-ordinated directly or indirectly by the hypotalmus ( bossof endocrine system)

Phases of Stress 1) Phase 1: Alarm reaction (fight or flight response) o Immediate = NS CNS (sensory input –detect change)

Hypothalmus (RAS therefore increase alertnas)

SNS

Organs

adrenal medulla

(discussed previously) E + NE (Prolongs fight or flight response) o

Effects of SNS + endocrine: a) Increase blood glucose  SNS inhibits insulin release  E, NE converts glycogen to glucose (in liver) b) Increase HR, force of contraction c) Increase resp rate d) Decrease blood flow to skin + abdominal viscera  Therefore more available for skel. + card.m, + brain( O2 + glucose to working organs)

e) Decrease in digestion and urine production 2) Phase 2: Resistance Reaction  Long term  Endocrine  Permits recover from the effects of 1) (alarm phase) (tissue repair, etc) or response to longer term stress(e.g. starvation)  Hypothalamic hormones initiate 2): Hypthalmus Growth Hormone releasing hormone (GHRH)

Corticotrophin Releasing hormone (CRH)

ANT pit Adrenocorticotropic hormone (ACTH)

Growth Hormone (GH)

Adrenal Cortex

Cortisol (glucocorticoid)  



GH a) Stimulates growth (protein production), cell reproductions Cortisol a) Releases in 30 sec of a stress but response not for hours-steroid hormone-acts on nuclear receptors b) Inhibits insulin release Release of hormones causes: a) Increase blood glucose  Liver stim, to produce new glucose from fats and later from proteins  Little insulin (because of inhibition)- glucose not taken up well, esp by skelm (at rest) + adipose tissue. Therefore: i) Glucose spared for use by NS ii) Metabolism of non NS directed to use fats for energy (control: GH, cortisol) – if stress continues, cortisol inhibits GH release and then proteins also used iii) Overall: increase FA and AA  energy (except brain) b) Inhibition of : immune system, bone formation, formation of CT (delayed healing) c) Release of aldosterone +antidiuretic hormone (ADH)

 Reduces salt + water loss at kidney to maintain blood vol. Long term effects  Decrease weight, increase bp, increase hr, immune suppression (cortisol), decrease bone density, increase risk of type two diabetes (because increase blood glucose) 3) Phase 3: Exhaustion  Result from: a) Depletion of body resources ie lipid reserves b) Loss of potassium (aldosterone effect) c) Damage to organs (heart, lover, kidneys) 

Male Reproductive Hormones

After Puberty Hypothalamus:

Gonadotropin Releasing Hormone (GnRH)

Anterior or Pituitary

LH (luteinizing hormone)FSH ( Follicle stimulating hormones)

Testes

Testosterone (leydig cells)

Spermatogenesis (in seminiferous tubules)

Functions of Testosterone: 1) Development of organs of reproductive tract + secondary sex characteristics 2) Stimulates bone growth at epiphyseal plate (converted in bone to Estrogen to stop growth = closure of plate) 3) Promotes protein anabolism 4) Directly stimulates spermatogenesis

Female Reproductive Hormones (27.22) After puberty Hypothalamus:

Gonadotropin releasing hormone (GnRH)

Ant pit

LH

FSH

Ovaries

ovulation

follicles develop (primary secondary)

Estrogens...