Stress physiology

hormone of stress response that stimulates appetite

Glucacorticoids stimulate appetite (made rats more willing to run mazes for food). more specifically stimulates appetite for starch, sugary, and fatty foods

A hormone of stress that inhibits appetite

CRH (which is released by hypothalamus, stimulates pituitary to release ACTH, and lead to the release of glucocorticoids) turns on sympathetic, increases viligance and aruous during stress while also suppressing appetite

How CRH and Glucacorticoids work together

• CRH secreted and acts w/in few secs → takes a couple mintues for the ACTH cascade to releasae the clucacorticoids and for them to surge in blood stream

• CRH leaves blood stream fast

• Glucacortiocids take minutes to hrs to act, and long time to be cleared from blood stream

• not all ppl have the same baseline or timing based on genetic and enviormental factos

Stressed for days - appetite

up goes CRH and up Glucocoticoids, followed by decrease in CRH while glucacorticoids stay high for recovery and suppression of appetite because of how long CRH was int he system because of the prolonged stress

hypersecreation of glucacoicords

hyperphagic = bigger appetite and crave sweets → not happen to people who secrete more glucaordicods only during stress

Frequence intermittent stressors

CRH bursts but constanct elevated glucoricords = increase in appetite

dieting and stress

people who restrict during non-stressed are more likley to stress eat

glucocorticoids and storage

glucocorticoids increase storage of ingested food, trigger fat cells to make enzymes that break down circulating nutrients into storage, specifically abdominal fat which has more receptors → do this with only high levles of insulin, finds livery easily (glucose → up blood sugar up insulin resistance) → more at risk for metabolic and cadiovasuclar disease

recovery period

increase in glucocorticoids and insluin

peristalsis

directional contraction, controled muscle movement

small and large intestines

• small intestines add water

• large intestines take water out of

• takes 10/20% of energy on digestion

stress stops digestive processes

no saliva, stomach stops, no enzymes/digestive acids secreted, no pertasis, no absoption

why we deficate when scared

by large intestines stuff is dead weight, empty to run faster, sympathetic system stimulates muscles movement in large intestine, move fast through large intestines so water can no be absorbed

functional GI issues realted to stress

• IBS, colon contracts and stress increases this more → both cause less sensitivy to skin pain and more to visceral pain

• IBS does not happen when asleep → can not stress

• childhood trauma increases IBS → hyper active to stree not always seen and lots of things can casue IBS*

peptic ulcer, gastric ulcuer, upper, duodenm

peptic: in stomach boarding stomach

gastric: within stomach

upper: esophageal

duodenal: stomanch and intestine

helicobacter pulori

bacteria found in ppl w/ stoamch ulcers/inflammation , can exist because wrapped in bicarbonate, causes gastritis , comprises ability of cells lining duodenums to defend themselves against stomach acids

helicobacter + other

has to be the bacteria plus something else (15% duodenal ulcers form in ppl w/ out heli), can be lifesytle, genetics, aspirin, or stress

• duodenal ulceration more likely to occur in ppl who are anxious, stressed, or depressed

peptic ulcers

30-60% of peptic ulcers have psychosocial factors

→ stressed people smoke/drink more

acid rebound

hydrochloric acid that pours into stoamch

• stoamch muscles thick puls secrete bicarbonate to neutralize acid

stressful period, sysmpathetic stops acid sectretion, stops thickening of walls, stops mucus and bicarbinate secreation to conserve engery → end stressful peroid and defenses are down → repeat this cycle and ulcers form

infractions (small stokes)

stopping of blood flow to gut cause them because of lack of O2, develop leasions of necrotic tissue which are building blocks of ulcers

→ less blood flow, less acid is pushed away

—> cells running on O2 form free radicals but during peroids of stress and less blood flow to gut no scaverngers are able to take away free raticles → problem during recoerya nd kill stomach cells = ulcers

immune suppression: helicobacter

triggers immune system to defent against it → decrease in immune system, increase in bacteria

insufficient amount of prostaglandins

micro ulcers are not repaired by prostaglandins which are thought to increase blood flow to the gut wall to heal them → with stress prostaglandins synthesis is inhibited by glucocorioids

stomach contractions

stress causes stoamch to initiate slow contractions, which add to ulcer risk, possible causing little burst of ischema, or mechanical movement

growth hormone

• helps break down fat sotres into circulation

• triggers somatomedis which promote cell division

• 
  

thyroid hormone

promotes growth hormone, releases and makes bone more responsibve to somatomedins → insulune stimular

puberty

estrogen increase so do long bones and growth hormones, same as testosterone which also promotes muscle growth → testosterone given before puberity can stunt muscle growth

starvation during pregnancy

thrifty metabolish for fetus, more risk for metabolic syndrome

• 1st erm = heart disease, obesity, and unhealthy cholestrol

• 2nd/3rd term = diabetes risk

undernourished as fetus but after birth had plenty of food = highly efficient at storing nutrion and had access

• lower weight as baby = higher risk of metabolic syndrome, diabetes,a dn hypertesnion

FOAD

fetal origins of adult diseases

• tenencies share across generations → thristy metabolish in pregnatn women → sjare less w/ fetus → etc =shared enviorment

fetus moniter signals of stress

losts of glucocorticoid's = stressful world = secreting excessive amount og glucocotricoids

• rats have higher glucacoticords, basal elvers, and stress responses and longer recovery peroid

• decrease in number of gulcocortoids receptros in brain taht is involved with turining off stress repsonse by inhibitng CRH rlease → less glucocortoicd receptors the less sensity tot he hromone singanl = less effective reining in subsequence glucocortiofd secretion = elevated levels → can be manipulated by injecting glucalcoticoids

prenatal stress

glucocotic secreioon in adult hood → birth weight ( and pre mature birth = more) - higher basal glucocoroid lever = higher risk of metabolic syndrome

pregnant rats

babies less sexually active, less devloped genitals

• glucocorticoid's and tesosterone similar in stuructre = increase of glucoroticoids in fetus blocks receptors for testosterone = no effect

very stress = anxious child rat → freeze around bright light, defeicates lots, cant learn in novel settins

• prenatal stress programs amygddala into life long aniety → amygdala has more receptors for glucocoticoids (mediate anxiety) and less receptorts for brain chemicals that reduce anxiety

• fewere coonnections b/w neurons in learning and memory

*hard to recreate in humans*

maternal deprevation

causes similar consquces as prenate stress (more glucocorticoids), same with inatentive mothers

childhood stress

building blocks for adult diseases (IBS long lasting stress response/sensitivity)

• long gime in orphange = more glucocorticoids more abuse = more glucuorticords and smaller frontal cortex

stress dwarism

low growth hormone levels in circulation

→ growth hromone secreated by pituitary glands, which is regulated by hypothalamus

• hypothalamus controls release of growth hormone through secretion of a stimulatory hormone and a inhbibitory hormone → stress dwarism two much inhibitoray hormone released → overactive sympathetic, body also less receptive to what growth hormone is released, some have more glucacoticoids

= GI problems. nutriton not abosirbed from intestines as well

touch

stimulates growth

short term stress and growth

growth hormone decreses during a stress response but jumps during recovery → short term stress supports growth in some species

• growth hormone stimulates somatomedias to stimulate bone growth/cell divison and also break down fat sotres and flush them into circulation

• → glucocorticoids, epi, norepinephrine, glucagon

growth hormone and energy

• growth hormone has energy mobiliing effects because it helps break down nutrients → declinse during stress

• needs perfect balance, not always perfect → somatomedin actuin not all shut down, fowth hormone could still be used

  • growth blocked 2 early no energy benefits, too late growth takes place

stress and rituals

• stress rituals delay growth when comapired to same gene pool with no stress rituals → 6-15 had less growth

• 2-6 had no impact

• 2 or younger had increased growth → what doesent kill you makes your stronger

glucocorticoids give as treatment in pregnancy

when given in high levels as treatment or have tumor that produces = smaller head circumference, emotional and behavior propblems in childhood but unknown lifelong effects → used in rare cases

homeostasis

external/internal change → results in loss of homeostasis → organism attempts to compensate → fails = illnesss or disease, susceeds = wellness

allostasis

coordinate change to meet predicted or current demand, the brain orchestrates a body wide responses

HPA axis, release of glucocorticoids

hypohalamus → CRH (cortisol releasing hormone) → anterior pituitary → ACTH → adrenal cortex

types of stress

actue physical processes, chronic physical challenges, psychological and social disruptions

stressor

anything that throws your body out of allostatic balance and the stress response is your bodies attempt to restore

stress

moblization of energy, delivery, inhibition of digestion/growth/repairs, sex, immunity, limited pain, cognitive and sensory skills

glucocorticoids

steroids from adrenal, similiar to epinethran, backs up activity

sympathetic activation

brain → sympathetic activation → adrenal medulla and nerve ending → releaseing norepinephrine and epinephrine

hormones and neurotransmitters released

glucocorticoids, glucagon, prolactin, endorphines, vasopressen/antidieretic hormones, sex hormones, oxytocin

glucagon

released from pancreas, breaks down triglycerides/release glucose so body can use energy

prolactin

released from anterior pituitary + suppress reproduction

endorphins

released from anterior pituitary and hypothalamus , pain inhibition

vasopressens/anti direcetic hormone

released from anterior pituitary, increase bp and decreases urination

oxytocin in stress response

cardiac output

co = hr x sv, increase with SNS, decrease with PNS

mean arterial pressure

proprotional to co x perephrial resistances

go over cardiosystem basics

asthorsclesosis

plaque build up, more pressure throught smaller radius (positive feedback loop)= higher BP

diameter of arteriols

blood vessels constantly getting signlas of neurotranmitter (norepinephrine) → alpha recpetiors = constricted with epi, B2 receptors in skeletal = dilate with epi

stress response in realtion to HR and SV

HR and SV go up which means CO goes up as well

sitting down in oral exam

higher glucose in blood, not utiliing blood glucose/ building blocks, take out energy and put it back in storage over and over takes more power

runner short up hill sprints

using up glucose in blood, vasodilates to muscles, decreases glucose and blood pressure, no insulin resistance,

steps of developong stress related cardiovascular disease

1. hypertension, work harder to regulate blood flow → thicker muscle → more rigid → increase in bp to push blood through thick muscle → thicker muscle etc

2. heart wall thicker, left ventricular hypertropy

3. damage to branch points at arteries (bifricuation), split and becomes inflamed, clotting, build up of atherscleortic plaque

4. continued stress → athersocleorissi → claudication (too luttle o2 to legs and chest causing pain)

5. thrombus, plaque loose, lodge in smaller blood vessels, in brain = stroke

6. myocardial ishemia → vasoconstriction

7. length of heart shorter when inhaling → not with chonic stress → does not slow down w/ exhale

CRP

c-reactive protien, measues inflamaton, mugrates to damaged vessels and helps amplify cascade of inflammation

estrogen and cardio vascular

estrogen and progesterone protect against heart disease, and decrease the risk of osteroporisis

psychcological death

genetic factors/ preexisiting damage to cardio vascular system, risk factors,

carbohydrates

glucose, monochacories → glycogen from liver and skeltal muslces

fats/lipids

fatty acids and glyceral → triglycerides from fat cells (adipose) and muscle

protiens

amino acids, protiens from muscle

insulin

fat to fat cells, stunykates glycogen and protien sysnthesis, can secrete in preporation for food, stopped w/ emergency send glucocortioicds to block transport of nutirience into fat cells

reverse storage

glucocortoids, glycogen, epi, norepinephrine, → triglycerides breakdown = fatty acids and glycerol in blood, protien back to individual amino acids → amino acids to live to convert to glucose

catecholomines

dopamine, norepinephrine, epinephrin, produced in brain and adrenal glands

cateocolamines repidy support fuel mobilization

liver glucogen is broken down into blood, fats broken downa dn released into blood, glucocortoicds keep them circualting in the system

glucocortioids benifital adaptive

good - insullin resistance to non using muscle during phsical stress response

bad - psychological = increase in insulin resistance overall, pacreases keeps secreating insulin which leads to diabetes

diabetes

insulince resistance caused by diet and exercise, large amount of insuln to get uptake into cells