Chapter 9 - Quiz 4 Flashcards
8.1: Temperature Regulation: Homeostasis and Allostasis
Define homeostasis, use an example (2)
-biological processes that keep body variables within a fixed range
-example: temperature regulation is like a thermostat with a fixed temperature and when the house goes past that temperature either the A/C or furnace turn on
8.1 Temperature regulation: homeostasis and allostasis
Define set point
-a single value that a body works to maintain
-for example, the concentration of calcium in your blood
8.1 Temperature regulation: homeostasis and allostasis
Define negative feedback
-homeostatic processes that reduce discrepancies from the set point
-much of motivated behaviour can be described as negative feedback: something causes a disturbance and behavior proceeds until it relieves the disturbance
8.1 Temperature regulation: homeostasis and allostasis
Define allostasis and give an example (2)
-it describes the adaptive way the body anticipates needs depending on the situation, thus avoiding errors rather than correcting them
-example: our change in body temperature throughout the day
8.1 Temperature regulation: controlling body temperature
Define basal metabolism, by what is most of this produced? (2)
-energy used to maintain a constant body temperature while at rest
-largely through metabolism in brown adipose cells, they burn fuel like muscles cells but release it directly as heat
-most of our energy goes into our basal metabolism
8.1 Temperature regulation: controlling body temperature
Define ectothermic and give an example of an animal (2)
-they depend on external sources for body heat, they do not generate heat themselves
-amphibians, reptiles and most fish
-Poikilothermic
8.1 Temperature regulation: controlling body temperature
Define endothermic and define who is? (2)
-they can generate enough body heat to remain significantly above the temperature of the environment
-mammals and birds
-can usually keep core temperature constant
-small mammals radiate heat rapidly and need lots of fuel to keep their bodies warm because of their small surface area
8.1 Temperature regulation: controlling body temperature
What mechanisms do endothermic beings have for warm environments? How could a being do this? (2)
-to cool down, we have evaporation
-this looks like sweating, licking themselves or panting
8.1 Temperature regulation: controlling body temperature
How could an endothermic being warm up in a cold environment? (3)
-shivering
-decreased blood flow to the skin to prevent blood from cooling
-fluffing out fur to increase insulation (goosebumps)
8.1 Temperature regulation: the advantage of constant high body temperat
What is the primary advantage of maintaining a constant high body temperature?
-it keeps an animal ready for rapid, prolonged muscle activity even in cold weather
8.1 Temperature regulation: the advantage of constant high body temperat
Why did animals evolve a temperature of 37 C? Why not a different temperature?
-it is a trade off between the advantage of a high temperature for rapid movement and the disadvantage of high temperature for protein stability and energy expenditure
8.1 Controlling body temp: Brain mechanisms
Which areas of the brain is the primary area for controlling phsyiological mechanisms of temperature control? What physiological responses does it control? (2)
-the preoptic area/anterior hypothalamus or POA/AH
-controls sweating, shivering, changes in heart rate and metabolism and changes in blood flow to the skin
8.1 Controlling body temp: Brain mechanisms
What are the sources of input to the POA/AH?
-temperature in the skin, organs and hypothalamus, as well as prostagladins and histamines when someone is sick
8.1 Controlling body temp: Brain mechanisms
What would damage to the POA/AH result in?
-mammals can still regulate body temperature, but less efficiently
8.1 Controlling body temp: Fever
What does a fever mean for your set point in your body? How do we know it is an adaptation to fight illness based on other beings and based on humans? (3)
-it increases the set point
-animals and reptiles will use behavioural means (going somewhere warmer) to produce a fever when they’re sick
-as well, a moderate fever reduces bacterial growth and makes the immune system work more vigorously
9.2: Mechanisms of water regulation
What does your posterior pituatary release and what does it do? Why? (3)
-releases vasopressin AKA antidiuretic hormone
-raises blood pressure by constricting blood vessels causing you to decrease urination and increase thirst
-if you’re dehdyrated, this helps compensate for the decreased blood volume and allows the kidneys to reabsorb water from urine, making it more concentrated
9.2 Osmotic thirst
What are the two types of thirst?
-eating salty foods causes osmotic thirst and bleeding or sweating causes hypovolemic thirst
9.2 Osmotic thirst
Define osmotic pressure
-water will flow across a semipermeable membrane from the area of low solute concentration to high solute concentration
9.2 Osmotic thirst
How do certain neurons trigger thirst? Describe the process starting with eating something salty and define osmotic thirst (3)
-when you eat something salty, sodium ions spread through the blood and extracellular fluid but do not cross the membrane into cells
-this results in a higher concentration of solutes outside the cell than inside and the water flows out of the cells
-certain neurons detect their own loss of water and then trigger osmotic thirst, a drive for water that helps restore the normal state
9.2 Osmotic thirst
How does the brain detect osmotic pressure? Why in this area specifically? Name the structures involved (3)
-receptors around the third ventricle detect osmotic pressure and the sodium content of the blood
-this area specifically because the blood-brain barrier is weak here
-they are the OVLT (organum vasculosum laminae terminalis) and the subfornical organ SFO
-the OVLT also recieves input from receptors in the digestive tract, allowing it to anticipate osmotic need before the rest of the body
9.2 Osmotic thirst
Describe the parts of the subfornical organ that control drinking (2)
-the lateral preoptic area
-parts of hypothalamus
9.2 Osmotic thirst
What two areas control the rate at which the posterior pituitary releases vasopressin?
-supraoptic nucleus and the paraventricular nucleus (PVN)
9.2: Hypovolemic thirst and sodium-specific hunger
What does angiotensin II do? What does this help with? What is it reacting to? (3)
-constricts the blood vessels
-triggers hypovolemic thirst
-reacting to low volumes of body fluid
9.2: Hypovolemic thirst and sodium-specific hunger
Define hypovolemic thirst
-thirst based on low volume
-animal would want to drink salty water
9.2: Hypovolemic thirst and sodium-specific hunger
Define sodium-specific hunger
-an animal suddenly gets a strong preference for salty tastes because they are deficient in sodium
9.2: Hypovolemic thirst and sodium-specific hunger
Describe aldosterone. Why does it get produced, what does it do? (2)
-produced when body’s sodium reserves are low
-causes the kidney’s, salivary glands and sweat glands to retain salt
9.2: Hypovolemic thirst and sodium-specific hunger
Compare osmotic and hypovolemic thirst. Caused by? Best relieved by? Receptor location? (3)
Caused by:
Osmotic - high solute concentration outside of cell
Hypovolemic - low blood volume
Best relieved by:
Osmotic - pure water
Hypovolemic - water containing solutes, near 0.15 M
Receptor location:
Osmotic - OVLT, subfornical organ and digestive tract
Hypovolemic - kidneys and blood vessels
9.2: Summary
Describe how the subfornical organs initiate thirst in anticipation of future needs? How does it anticipate decreasing it? (2)
-increases thirst during a meal and shortly before bedtime
-decreases thirst after drinking, long before the ingested water reaches the cells that need it
9.3: Digestion and food selection
What is a main role of the small intestine?
-absorbs digested materials into the blood, which carry those chemicals to body cells
9.3: Digestion and food selection
What is the main role of the large intestine?
-absorbing water and minerals and lubricates the remaining materials to excrete them
9.3: Digestion and food selection: Consumption of dairy products
When do most mammals lose the intestinal enzyme lactase?
-around the age of weaning
-the ability for adults to digest milk depends on genes, which are more prevalent in some ethnic groups than others
9.3 Short and Long term Regulation for Feeding
What is a sham-feeding experiment? What do they show us?
-everything an animal swallows leaks out of a tube connected to the esophagus or stomach
-these animals eat and swallow almost continually without become satiated, indicating that taste contributes to satiety but is not sufficient
9.3 Short and Long Term Regulation of Feeding
What is the main signal to end a meal? What happens to people who have had their stomach removed? (2)
-distension of a stomach
-people who have had their stomach removed still report satiety, meaning its not all in the stomach
-the vagus nerve conveys information to the brain about stretching of the stomach walls
9.3 Short and Long Term Regulation of Feeding
What is the duodenum? What is its main job?What does it release? (3)
-part of the small intestine adjoining the stomach
-it is a major site for absorbing nutrients
-releases cholecystokinin (CCK) which limits meal size
9.3 Short and Long Term Regulation of Feeding
How does CCK limit meal size? (2)
-constricts the sphincter muscle between the stomach and the duodenum causing the stomach to hold its contents and fill quicker, making you feel fuller faster
-stimulates vagus nerve
9.3 Short and Long Term Regulation of Feeding: Glucose, Insulin Glucagon
Which two pancreatic hormones regulate the flow of glucose into cells?
-insulin and glucagon
9.3 Short and Long Term Regulation of Feeding: Glucose, Insulin Glucagon
Describe insulin. When is it released? What does it allow for? What is its effect? (3)
-released immediately before meal, and during and after meal
-enables glucose to enter the cells
-preventing blood glucose levels from rising too quickly
-brain cells are an exception as glucose can cross them without insulin
9.3 Short and Long Term Regulation of Feeding: Glucose, Insulin Glucagon
Describe glucagon. Why is it released? What does it do? How does it effect the blood glucose levels? (3)
-released once the blood glucose levels lower
-stimulates the liver to convert some of its stored glycogen back to glucose
-raises the blood glucose levels
9.3 Short and Long Term Regulation of Feeding: Glucose, Insulin Glucagon
Why do people with very low insulin levels eat so much? How about those with high insulin levels? (2)
-Those with very low levels, as in type 1 diabetes, cannot get glucose to enter their cells, and therefore, they are constantly hungry. They pass much of their nutrition in the urine and feces. -Those with constantly high levels deposit much of their glucose into fat and glycogen, so within a short time after a meal, the supply of blood glucose drops
9.3 Short and Long Term Regulation of Feeding: Leptin
What is the purpose of leptin? How does it work? (2)
-leptin accounts for longer-term weight control
-fat cells produce leptin and it signals to the brain that you have more fat and do not need to eat as much and can exercise more, the reverse is true
-you can have a mutation in the gene for leptin, causing you to be overweight
-leptin does not work as a weight loss drug
9.3: Brain mechanisms
What is the master area for controlling appetite?
-arcuate nucleus of the hypothalamus
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
What signals is the arcuate nucleus sensitive to?
-hunger and satiety
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
Describe ghrelin. What is it caused by? What does it act on to do what? (2)
-this is the way the arcuate nucleus is sensitive to certain signals
-the stomach releases this NT during a period of food deprivation and it trigger stomach contractions
-also acts on hypothalamus to increase appetite
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
Describe the three ways the satiety-sensitive cells of the acruate nucleus receive several types of input. (3)
-include if each is short or long term signal
-distension of intestines triggers release of CCK (short-term signal)
-blood glucose directly stimulates satiety cells and prompts pancrease to release insulin (short-term)
-body fat releases leptin (long-term)
-nicotine also stimulates the satiety neurons
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
How does the pathway work from arcuate nucleus to paraventricular nucleus to the lateral nucleus of the hypothalamus? How does this relate to hunger signals and feeding? (3)
-axons from two kinds of neurons in the arcuate nucleus send competing messages to the paraventricular nucleus
-the paraventricular nucleus inhibits the lateral nucleus of the hypothalamus
-hunger signals increase feeding because they decrease the inhibition from the paraventricular nucleus
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
What are the inhibitory transmitters in the pathway from the arcuate nucleus to the lateral hypothalamus?
-GABA, neuropeptide Y (NPY) and agouti-related peptide AgRP
-inhibiting an inhibitor causes next excitation
9.3: Brain mechanisms: The arcuate nucleus and paraventricular hypothala
What are the satiety transmitters used in the arcuate nucleus pathway?
-melanocortins and glutamate
-melacortins is most important for satiety
9.3: Brain mechanisms: The lateral hypothalamus
In what ways does the lateral hypothalamus facilitate feeding?
-it improves taste, enhances cortical responses to food, and increases secretions of insulin and digestive juices.
9.3 Brain Mechanisms: Medial Areas of the Hypothalamus
How does the ventromedial nucleus of the hypothalamus and the axons passing by it influence eating? What happens to animals with damage in this area? Why? (3)
-regulating stomach emptying time and insulin secretion
-animals with damage in this area eat more frequently than normal
-because they store much of each meal as fat and then fail to mobilize their stored fats for current use
9.3
What are the three types of genes relating to obesity? (3)
-syndromal obesity occurs if a gene leads to both obesity and other medical problems
-monogenic obesity results from a single gene that doesn’t impair other body functions
-common
