Chapter 9: Homeostasis Flashcards

1
Q

Describe the characteristics of homeostatic systems.

A

Homeostasis: the maintenance of a relatively constant internal physiological environment
- deviations from optimum states can lead to motivation: the physiological process that induces or sustains a particular behavior.

negative feedback: deviation from the desired value, called the set point/set zone, triggers a compensatory action of the system.

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2
Q

What is redundancy? Give an example.

A

Our bodies have multiple mechanisms for monitoring our stores, conserving remaining supplies, and shedding excesses. Our physiological systems are monitored by more than one system.

Example: lesions in the preoptic area of rats impaired physiological responses to cold, but not for behavior slike pressing a lever for a cooling or a heating fan.

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3
Q

glucose is

A

principal sugar used for energy

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4
Q

glycogen is

A

glucose stored in the liver and muscles for the short-term, a process regulated by insulin.

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5
Q

What is insulin and how does it work?

A

Insulin is a pancreatic hormone that lowers blood glucose, promotes energy storage, and facilitates glucose utilization by the cells.

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6
Q

Explain the insulin trigger phases.

A
  1. Cephalic phase: triggered by sights, smells, and tastes that we have learned to associate with food.
  2. Digestive phase: food entering the digestive tract that prompts an additional release of insulin.
  3. Absorptive phase: as digested food is absorbed into the bloodstream, specialized liver cells caused glucodetectors which detect the increase in circulatory glucose and signal the pancreas to release insulin.
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7
Q

Explain nutrient regulation, using the terms lipid, ketones, and basal metabolism.

A
  • For longer-term storage, lipid (fat molecules) are stored in adipose tissue.
  • Under prolonged food deprivation, fat can be converted into glucose and ketones, which can be used as fuel.
  • basal metabolism: energy used for heat production, maintenance of membrane potentials, and life-sustaining processes.
  • metabolism is under homeostatic control and can be adjusted, so dietary changes will not always produce changes in weight.
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8
Q

Describe the differences between the functions of the ventromedial hypothalamus and the lateral hypothalamus in controlling hunger.

A

The hypothalamus is critically important for regulating metabolic rate, food intake, and body weight,

The ventromedial hypothalamus acts as the satiety region of the brain. VMH-lesioned rats ate in excess and became obese.

The lateral hypothalamus acts as the hunger center of the brain. Rats with LH lesions ceased eating and rapidly lost weight.

Note: due to redundancy of homeostatic systems, VMH lesioned rats eventually stopped eating and LH lesioned rats kept alive with a feeding tube eventually resumed eating and drinking, suggesting that there are multiple systems in the brain that control set points.

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9
Q

Describe the role of grehlin, PYY, and GLP-1

A

Grehlin, PYY and GLP-1 are short-term energy response hormones in the gut.
Grehlin = peptide gut hormone that stimulates appetite. Acts on the hypothalamic system to increase hunger.
PYY and GLP-1 = peptide gut hormone that spikes to higher levels after eating a meal and provides an appetite supressing signal. GLP-1 in particular responds to fatty foods and is involved in the reward system.

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10
Q

Explain how PYY and ghrelin hormones act upon the accurate nucleus which contains the POMC and NPY neurons.

A

Grehlin, PYY and GLP-1 act primarily on appetite stimulating NPY neurons. High levels of grehlin stimulate NPY and increase appetite. High levels of PYY inhibit the same NPY cells to reduce appetite.

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11
Q

Explain how leptin affects appetite control in the hypothalamus.

A

If there are high levels of leptin circulating in the bloodstream, this will activate POMC satiety neurons and simultaneously inhibit NPY neurons. Overall, this suppresses hunger. Remember, this is an ongoing long-term process.

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12
Q

What is the dual-center hypothesis?

A

That the ventromedial hypothalamus and the lateral hympothalamus work in opposition to each other.

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13
Q

Explain the role of orexin and the experiment on rats.

A

Orexin is another hormone that appears to control feeding bheavior. Direct injection of orexin, produced by neurons in the hypothalamus, into the hypothalamus increased rats feeding by sixfold. The brain’s reward system is also intimately involved with feeding.

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14
Q

Explain some of the other systems that control hunger and satiety, including the nucleus of the solitary tract, endocannabinoids, and cholecystokinin (CCK).

A

The nucleus of the solitary tract resides in the brainstem and is responsible for receiving visceral and taste information via the cranial nerves.

Cholecystokinin (CCK) is a peptide hormone released by the gall bladder after ingestion of food that is high in protein/fat. It is an appetite-suppressant that goes to the brain via the vagus nerve.

The Endocannabinoid system is a major regulator of appetite and feeding. Can potentially stimulate hunger (think “munchies”).

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15
Q

Obesity strategies for treatment

A
  1. Appetite control - drugs to dampen the hypothalamic appetite controller.
  2. Increased metabolism - cause the body’s metabolic rate to increase and burn more calories. Drugs that mimic metabolism-elevating actions of thyroid hormones
  3. Inhibition of fat tissue: interefere with the formation of new fat tissue.
  4. Reduced absorption - an obesity medication Orlistat works by interefering with the digestion of fat.
  5. Reduced reward - use drugs to reduce the brain’s reward circuitry
  6. Anti-obesity surgery: liposuction (surgical removal of fat tissue) or bariatric procedures which bypass part of the stomach/intestines to reduce absorptive capacity
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16
Q

Name and describe two eating disorders.

A
  1. Anorexia nervosa: a disorder in which the patients have no appetite (anorexia) and it originates in the nervous system (nervosa)

Treatments include family-based treatment (FBT), which focuses on “refeeding” of the anorexic patient instead of identifying causal factors.

  1. Bulimia is a related disorder in which suffers also believe themselves to be fatter than they are, but who periodically gorge themselves, particularly on junk food.
17
Q

Describe the difference between sleep-onset insomnia and sleep-maintenance insomnia.

A

Sleep-onset insomnia is a difficulty in falling asleep and can be caused by situational factors, such as shift work or jet lag.

Sleep-maintenance insomnia is a difficulty in staying asleep and may be caused by drugs or neurological and psychiatric factors.
- especially evident in respiratory disorders.

18
Q

Sleep state misperception

A

occurs when people report they haven’t slept even when EEG indicates that they have.

19
Q

Describe sleep apnea.

A

Breathing may stop or slow down when muscles in the chest and diaphragm relax too much or from changes in the pacemaker respiratory neurons in the brain stem.
- sleep apnea may be accompanied by snoring.

20
Q

Sudden infant death syndrome (SIDS)

A

This is the sudden, unexpected death of an apparently healthy infant who stops breathing, usually during sleep.
- arises from sleep apnea due to immature respiratory pacemaker systems or arousal mechanisms

21
Q

How do sleeping pills work?

A

Most sleeping pills bind to GABA receptors throughout the brain.

Use of sleeping pills

  • produces marked changes in sleep patterns that persist for days after use
  • causes them to become ineffective over time
  • can lead to daytime drowsiness and memory gaps

Behavioral methods support healthy sleep; sleeping pills do not.