Chapter 10: Internal Regulation Flashcards
advantages of constant high body temperatures and the brain mechanisms that maintain temperatures
- works to maintain a set point
- 2/3 of total energy goes to maintaining a set point
- 37degrees gain advantage by being as warm as possible with muscle activity
- warmer=warmer muscles=faster
- depends on areas in or near hypothalamus
- POH/AH monitors body temperature by monitoring its own temperature
- primary area for controlling physiological mechanisms (sweating/shivering)
Homeostasis
- process of temperature regulation
- negative feedback loop
What happens when body gets too hot?
-beyond 40-41 degrees proteins start to break bonds and lose useful properties
advantage of moderate fevers and the physiological mechanisms that produce fever
- body’s defence against the illness
- intruders invade the body and trigger white blood cells/leukocytes that release cytokines that attack the intruders
- cytokines stimulate vagus nerve that sends signal to hypothalamus that increases prostaglandins that stimulate specific prostaglandin receptor in one nucleus of hypothalamus necessary for fever
- moderate fever increases chance of surviving bacterial infection
- above 39 degrees=more harm than good
- above 41 degrees= life threatening
concepts of osmotic and hypovolemic thirst and stimuli that give rise to each
- concentration of all solutes in mammal remains constant @ 0.15M (set point)
- eat salty foods Na+ ions spread through blood and extracellular fluid but do not cross membrane into cells
- increase concentration of solutes outside the cells results in osmotic pressure drawing water from in osmotic pressure drawing water from cells into ECF
- neurons detect own loss of H20 and trigger OSMOTIC THIRST to help restore normal state, kidneys also excrete more concentrated urine
Osmotic
-thirst from eating salty foods
Hypovolemic
-thrist from losing fluids by bleeding or sweating
Hypovolemic conditions
- bleeding, diarrhea, or sweating
- body reacts with hormones that constrict blood vessels (vasopressin and angiotensin II)
- kidneys release enzyme renin when blood volume drops while splits off part of angiotensin to form angiotensin I that is converted to angiotensin II
- angiotensin II also triggers thrist with receptors that detect BP in large veins
- thirst=different from osmotic because you need to replace salts in addition to fluids
- angiotensin II reaches brain stimulates neurons in areas adjoining 3rd ventricle, these neurons send axons to hypothalamus where they release angiotensin II as NT
Salt Appetite
- Na+ low
- adrenal gland produce hormone aldosterone causing kidneys, salivary glands, and sweat glands to retain salt
Role of aldosterone + angiotensin II
- change properties of taste receptors on tongue
- neurons in nucleus of tractus solitarius and other neurons in brain to increase Na+ intake
- must be combined to have large effect
- each on own is small effect
Digestive system functino
-break food into smaller molecules that cells can use
Mouth
-need to taste and chew food to feel satisfied
Stomach
-distension of stomach= signal to end a meal via vagus nerve and splanchic nerves
Stomach
-distension of stomach= signal to end a meal via vagus nerve and splanchnic nerves
Duodenum
-fat in duodenum releases hormone oleoylethanolamide (OEA) which stimulates vagus nerve sending message to hypothalamus that delays next meal
Hormone cholecystokinin CCK
1) limits meal size by constricting sphincter between stomach and duodenum causing stomach to fill up more quickly
2) stimulates vagus nerve to send signals to hypothalamus causing cells to release NT that is shorter version of CCK (short term effect)
Glucose
- excess in bloodstream
- liver converts to glycogen and/or fat storage
- regulated by insulin and glucagon
Insulin
- enables glucose to enter the cell
- high levels=decreased appetite
Glucagon
-stimulates liver to convert stored glycogen to glucose when supplies are low in blood
functions, neurotransmitters, and outputs of the hunger- and satiety-sensitive neurons in the arcuate nucleus of the hypothalamus
- hunger sensitive cells get input from taste pathway via axons that release NT ghrelin
- satiety short and long term go to arcuate nucleus
- > glucose in blood (short term) directly stimulates satiety cells in arcuate nucleus and leads to increase insulin that stimulates satiety cells
- > body fat (long term) releases leptin which provides input
- output from arcuate nucleus goes to paraventricular nucleus of hypothalamus that inhibits later hypothalamus
ghrelin
-ghrelin released during food deprivation and is only known hunger hormone
Paraventricular nucleus
- inhibits lateral nucleus
- axons from satiety cells in arcuate nucleus send excitatory messages to paraventricular nucleus and releases neuropeptide alpha MSH (limits food intake)
- input from hunger neurons are inhibitory to paraventricular nucleus (GABA, NPY, +AgRP)
- NTs block satiety actions of paraventricular nucleus
Lateral nucleus
-additional pathways to cells in lateral nucleus release orexin
Orexin
- roles in feeding
1) increase persistence in seeking food
2) responds to incentives/reinforcement in general
Lateral hypothalamus
controls
- insulin secretion
- alters taste responsiveness
- facilitates feeding in other ways
- > axons from lat hyp. to NTS alter taste sensation
- > axons from lat hyp go to many parts of cerebral cortex helping with ingestion and swallowing and cause cortical cells to increase response to taste, smell, or sight of food
- > lat hyp increases pituitary gland secretion of hormones that increase insulin secretion
- > lat hyp sends axons to spinal cord that control autonomic responses (digestive secretion)
- stimulation of lateral hypothalamus increases drive to eat
Ventromedial Hypothalamus (VMH)
- inhibits feeding
- damage=increase weight
evidence for genetic contributions to obesity
- mutated gene for elanocortin receptor
- variant of FTO gene
- single mutations=uncommon, small % of obesity cases
- prader-wili syndrome= increase ghrelin in blood (4-5x more)
syndromal obesity
due to medical condition
evidence for genetic, environmental, and neurochemical contributions to obesity
- weight depends on combo of genes and environment
- sedentary lifestyle
commonly use weight loss techniques
- dieting (not reliable alone)
- need change in lifestyle
- increase exercise with decrease eating
- decrease or eliminate soft drinks
- gastric bypass surgery-part of stomach removed or sewed off so food cannot enter
Weight loss drugs
- fenfluramine- increase release of serotonin and block reuptake
- phentermine- blocks reuptake of norepinephrine and dopamine, produce brain effects similar to post meal
Bulimia nervosa
- alternate between binge eating and strict dieting (may include self induced vomiting)
- 95% also have depression, anxiety or other emotional problem
- increase production of ghrelin (result of binge/purge NOT cause)
- eating tasty food activates same area as addictive drugs
- can be seen as an addiction
