Week 8 - Internal Regulation: Temperature, Third, and Hunger Flashcards

1
Q

This term is used to define the process of maintaining a variable that is within a fixed range, or maintaining a set point. Who coined this term.

A

Homeostasis, coined by Walter Cannon.

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2
Q

Using indoor temperature as an example, describe the four components of a regulatory mechanism. Which of these four steps would fail without negative feedback?

A

(1) System Variable: variable to manipulate, which is the temperature of the room.
(2) Set point/set range: the optimal value the variable should be (what we want the variable to get to), which is room temperature.
(3) Detector: the mechanism that monitors the value of the variable, which would be the thermostat.
(4) Correctional mechanism: restores the variable’s value to the set point we want, which would be the thermostat increasing the temperature to room temp.

The correctional mechanism would fail without negative feedback because negative feedback is what turns off or stops the variable from changing any further once it has reached its set point. So in this case, without negative feedback, the correctional mechanism would continue to increase in temperature past room temp.

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3
Q

Define the terms basal metabolism. Where does metabolism occur and why does it contain more mitochondria than other cells of its type?

A

Basal Metabolism: energy used at rest, so energy used just to maintain our body temperature, uses more than 2x more than any physical activity we do.

It occurs within brown adipose tissue, which is fat that gets activated when we get cold so it can produce heat and maintain body temp in cold environments. Since so much energy is needed for metabolism in brown adipose tissue, it contains more mitochondria within it.

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4
Q

Define the terms endothermic and ectothermic regarding body temperature.

A

Endothermic: controlling one’s body temp using physiological mechanisms (eg. humans shivering to heat up or sweating to cool down)

Ectothermic: relying on external sources for heat and cooling (eg. reptiles)

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5
Q

Which two areas of the brain receive information from thermoreceptors in the skin, liver, skeletal muscles, and hypothalamus, as well as cold receptors and heat receptors?

Define homeostatic redundancy.

A

The anterior hypothalamus and the POA (preoptic area).

Homeostatic redundancy refers to the fact that if one system in the brain is not working, another system will take over as a means of survival.

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6
Q

Describe the process of how the POA and anterior hypothalamus work when we get an infection.

A

When we get an infection, the immune system tries to destroy the infection by increasing out body temperature (fever). The immune system sends information to the hypothalamus that we have an infection, so the hypothalamus will produce prostaglandins and histamines to get sent to the POA/AH to cause common symptoms of a cold, like shivering, swearing, increased metabolism, etc.

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7
Q

What does it mean when we say humans are homeomorphic? Why are homeomorphic?

A

We can go in different environments with varying temperatures, but our body has physiological mechanisms in place that work to maintain the same body temp, letting us adapt to any environment.

This is because of allostasis, which is similar to homeostasis, but while homeostasis is meant to maintain a set point or range, allostasis recognizes that sometimes this point/range will change depending on the environment. For example, we may put on weight in the winter and lose weight in the summer.

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8
Q

What is the term for a brain mechanism that causes the ceasing of hunger or third, produced by adequate and available supplies or nutrients/energy (or water/fluid)? Describe why it is an anticipatory mechanism as opposed to a correctional mechanism?

A

Satiety Mechanism. Instead of maintaining a set point/range, it monitors how much we eat or drink

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9
Q

What does eating too much salt lead to high blood pressure?

A

Osmotic thirst. When the osmoreceptors such as OVLT and SFO sense that there is too much salt in the extracellular fluid, they send information to the hypothalamus to release vasopressin (specifically from the supraoptic nucleus and the PVN). Vasopressin then does 2 things, one of which is getting released into the blood portal, constricting blood vessels, thereby increasing blood pressure. The other thing is that it will signal the kidneys to excrete any excess sodium in the form of urine while conserving whatever water it can.

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10
Q

What four hormones get changes during hypovolemic thirst and what do they do?

A

(1) decreased ANP
- usually prevents high blood pressure and inhibits drinking behaviour
- so it is decreased to raise blood pressure and encourage drinking behaviour
(2) increased vasopressin
- increases blood pressure and conserves bodily fluids
(3) increased Angiotension II
- constricts blood vessels to raise blood pressure
(4) increased Aldosterone
- conserves both sodium and water

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11
Q

What is insulin used for? Why is it important?

A

Insulin is a hormone produced by the pancreas released during the absorption/digestion phase. It enables glucose to send energy to the PNS. It rises before, during, and after a meal. Before eating, it prepares the body to send glucose to the PNS before hand. It is important because it determines how much glucose enters the cells of the PNS

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12
Q

True or false: We need insulin to attach to glucose receptors to give energy to the brain and the PNS muscles.

A

False. Insulin is not needed to send glucose to the brain, it has direct access. It is only needed to send glucose to the muscles.

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13
Q

What is glucagon used for? Why do we need it?

A

Glucagon is the hormone that is released from the pancreas when we are not eating (fasting). It tells the liver to convert some of the stored glycogen into glucose to supply our body with the energy it needs when we’re not getting an immediate source of energy. We need it for 3 reasons:

(1) converts glycogen into glucose, which gets sent to the CNS (brain) to give it energy
(2) takes fatty acids from triglycerides in the long term reservoir and sends it to the PNS (muscles)
(3) takes glycerol from triglycerides in long term reservoir and converts it to glucose (energy), which is then directly sent to the brain

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14
Q

Describe Diabetes Mellitus.

A

A person will eat and glucose will enter their system, but the individual has low levels of insulin. This means glucose is not being properly sent to the cells of the PNS. Instead it will leave through urine and feces, but the person will remain hungry as their cells are starving. If they are hungry, they will continue to eat but without gets satiated, thereby potentially leading to weight gain.

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15
Q

What are the 3 signals that may initiate a meal? Define Glucoprivation and Lipoprivation.

A

(1) signals from the environment

(2) signals from the stomach
- ghrelin gets released from stomach to signal brain that we need food

(3) metabolism signals, such as Glucoprivation and Lipoprivation.

Glucaprivation: not enough glucose being available to cells which causes hunger (hypoglycemia)

Lipoprivation: not enough fatty acids available to cells that cause hunger

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16
Q

What suppresses ghrelin?

A

The duodenum, which is the first part of the small intestine. Once food reaches our small intestine, there are receptors in the small intestine that tell us we have gotten our nutrients from our food and we don’t have to be hungry anymore

17
Q

What connects the liver and the small intestine? Which nerve connects the liver and the medulla oblongata?

A

The liver and small intestine are connected via the hepatic portal. The liver interacts with the medulla oblongata via the vagus nerve.

18
Q

What are the 3 ways in which you can change hunger signals?

A

(1) By cutting the vagus nerve –> abolishes hunger
- liver is not sending glucoprivation/lipoprivation signals to the medulla oblongata (signals that we don’t have enough carbs or fats), so one would not feel hungry

(2) by injecting 2DG into the hepatic portal vein –> increases hunger
- 2DG decreases glucose, thereby sending glucoprivation signals to the medulla oblongata, signalling us to want to eat

(3) by injecting a drug that increases or decreases glucose DIRECTLY into the brain itself (the medulla)
- the brain needs glucose too, so whether it detects glucoprivation or not, the drug can either increase or decrease hunger depending on what we do

19
Q

What areas do the 4 short term satiety signals occur in?

A

(1) stomach
- distention of stomach (sends info to brain via vagus nerve), thereby giving satiation
- gastric receptors in stomach detect presence of nutrients via the splanchnic nerve, thereby giving satiation

(2) Small intestine (duodenum)
- CCK hormone gets released in response to fats entering the duodenum
- CCK regulates hunger by (1) closing the sphincter muscle between the stomach and duodenum, causing the stomach to hold onto its contents, thereby controlling the rate of stomach emptying (feeling of fullness), and (2) by stimulating the vagus nerve to send information to the hypothalamus to release a hormone very similar to CCK

(3) liver
- when liver receives nutrients from intestines via hepatic portal vein, the PYY hormone increases
- the more we eat, the more PYY gets produced
- liver then sends info to brain (medulla) via vagus nerve to give satiety

(4) hypothalamus
- there are insulin receptors in hypothalamus that tell the brain there is enough nutrients

20
Q

How do we get long term satiety signals? What happens to leptin when we lose fat?

A

Via Leptin, which is a hormone that is released by our fat cells of adipose tissue. Since it is stored in our fat, when we lose fat, we lose leptin, which causes us to move less and eat more.

21
Q

What areas of the hypothalamus are responsible for inhibiting eating behaviour (satiety) and encouraging eating behaviour? What would lesioning these areas result in?

A

Ventromedial Hypothalamus –> satiety center
- lesioning this area would result in abolishment of satiety, one would not feel full and they would always be hungry

Lateral Hypothalamus –> hunger/eating center
- lesioning this area would result in abolishment of hunger, one would not feel hunger or want to eat

22
Q

What are the two areas in the hunger-satiety pathway?

A

(1) Arcuate Nucleus –> “master area” for appetite control
- has neurons for both hunger (ghrelin) and satiety (CCK, insulin)

(2) Paraventricular Nucleus (PVN) -> inhibits the lateral hypothalamus (which is the eating/hunger center) and receives both inhibitory and excitatory signals from the arcuate nucleus

23
Q

What would happen if the arcuate nucleus inhibited the PVN? What about if it excited the PVN?

A

Since the PVN inhibits the lateral hypothalamus (the eating/hunger center), inhibiting the PVN would mean the lateral hypothalamus doesn’t get inhibited, and therefore, eating behaviour would occur

If the arcuate nucleus excited the PVN, the lateral hypothalamus would be inhibited, and therefore, eating behaviour would not occur.

24
Q

What are the hunger chemicals that get produced in the hypothalamus? What are the satiety chemicals that get produced in the hypothalamus?

A

Hunger chemicals –> orexigens (appetite inducing chemicals)

  • NPY and AgRP in arcuate nucleus (inhibits PVN, excites LH, and inhibits satiety cells in AN)
  • MCH (in LH)

Satiety chemicals –> melanocortins (appetite suppressing chemicals)

  • a-MSH in arcuate nucleus (excites PVN to inhibit LH, inhibits hunger cells of AN)
  • leptin receptors inhibit NPY/AgRP neurons from binding in AN (thereby inhibiting hunger)
  • PYY in gastrointestinal tract also inhibits NPY/AgRP of AN