Chapter 10: Internal Regulation

Question 1

advantages of constant high body temperatures and the brain mechanisms that maintain temperatures

Answer 1

• 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)

Question 2

Homeostasis

Answer 2

• process of temperature regulation

- negative feedback loop

Question 3

What happens when body gets too hot?

Answer 3

-beyond 40-41 degrees proteins start to break bonds and lose useful properties

Question 4

advantage of moderate fevers and the physiological mechanisms that produce fever

Answer 4

• 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

Question 5

concepts of osmotic and hypovolemic thirst and stimuli that give rise to each

Answer 5

• 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

Question 6

Osmotic

Answer 6

-thirst from eating salty foods

Question 7

Hypovolemic

Answer 7

-thrist from losing fluids by bleeding or sweating

Question 8

Hypovolemic conditions

Answer 8

• 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

Question 9

Salt Appetite

Answer 9

• Na+ low

- adrenal gland produce hormone aldosterone causing kidneys, salivary glands, and sweat glands to retain salt

Question 10

Role of aldosterone + angiotensin II

Answer 10

• 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

Question 11

Digestive system functino

Answer 11

-break food into smaller molecules that cells can use

Question 12

Mouth

Answer 12

-need to taste and chew food to feel satisfied

Question 13

Stomach

Answer 13

-distension of stomach= signal to end a meal via vagus nerve and splanchic nerves

Question 14

Stomach

Answer 14

-distension of stomach= signal to end a meal via vagus nerve and splanchnic nerves

Question 15

Duodenum

Answer 15

-fat in duodenum releases hormone oleoylethanolamide (OEA) which stimulates vagus nerve sending message to hypothalamus that delays next meal

Question 16

Hormone cholecystokinin CCK

Answer 16

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)

Question 17

Glucose

Answer 17

• excess in bloodstream
• liver converts to glycogen and/or fat storage
• regulated by insulin and glucagon

Question 18

Insulin

Answer 18

• enables glucose to enter the cell

- high levels=decreased appetite

Question 19

Glucagon

Answer 19

-stimulates liver to convert stored glycogen to glucose when supplies are low in blood

Question 20

functions, neurotransmitters, and outputs of the hunger- and satiety-sensitive neurons in the arcuate nucleus of the hypothalamus

Answer 20

• 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

Question 21

ghrelin

Answer 21

-ghrelin released during food deprivation and is only known hunger hormone

Question 22

Paraventricular nucleus

Answer 22

• 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

Question 23

Lateral nucleus

Answer 23

-additional pathways to cells in lateral nucleus release orexin

Question 24

Orexin

Answer 24

• roles in feeding
  1) increase persistence in seeking food
  2) responds to incentives/reinforcement in general

Question 25

Lateral hypothalamus

Answer 25

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

Question 26

Ventromedial Hypothalamus (VMH)

Answer 26

• inhibits feeding

- damage=increase weight

Question 27

evidence for genetic contributions to obesity

Answer 27

• 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)

Question 28

syndromal obesity

Answer 28

due to medical condition

Question 29

evidence for genetic, environmental, and neurochemical contributions to obesity

Answer 29

• weight depends on combo of genes and environment

- sedentary lifestyle

Question 30

commonly use weight loss techniques

Answer 30

• 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

Question 31

Weight loss drugs

Answer 31

• fenfluramine- increase release of serotonin and block reuptake
• phentermine- blocks reuptake of norepinephrine and dopamine, produce brain effects similar to post meal

Question 32

Bulimia nervosa

Answer 32

• 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