Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSY324 Biological Psychology > Week 8: Internal Regulation > Flashcards

Week 8: Internal Regulation Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Psychology flashcards Psychology 101 flashcards GRE® Psychology flashcards
1
Q

Homeostasis

A

An active process to maintain a variable within a fixed range, or to maintain a set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 features of regulatory system

A

1) System variable
2) Set point
3) Detector
4) Correctional mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

System variable

A

variable to manipulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Set point

A

optimal value of the variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Detector

A

monitors the value of the variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Correctional mechanism

A

restores the variable’s value to set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

negative feedback

A

regulatory process that reduces discrepancies
from the set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

basal metabolism

A

Energy used to maintain a constant body
temperature while at rest
■ 2/3 of total energy dedicated to maintaining basal metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Endothermic

A

Controlling temperature by the body’s physiological
mechanisms (e.g., humans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ectothermic

A

Controlling temperature by relying on external sources
of heat or cooling. (e.g., reptiles )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What part of the brain contributes to basic motivational behaviours?

A

Hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which 2 parts of the hypothalamus receive input from thermoreceptors?

A

Anterior hypothalamus and preoptic area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Evidence of “Homeostatic Redundancy”

A

POA: Lesions impair physiological response
Lateral H: Lesions impair behavioral response
(in rats)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Homeothermic

A

having physiological mechanisms in place to maintain constant body temperature, despite changing environments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Detectors in thermal system

A

Hypothalamus, spinal chord, brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Allostasis

A

“stability through change”
Adaptive processes that maintain homeostasis

Whereas homeostasis waits for errors and then corrects them, allostasis uses prior knowledge to prevent and minimize errors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Satiety mechanism

A

A brain mechanism that causes cessation of hunger (or thirst), produced by adequate and available supplies of nutrients/energy (or water/fluid)

– Instead of regulating the system variable (i.e.,
nutrients/energy or water/fluid), it monitors the
correctional mechanism (ingestion)
■ an anticipatory mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Regulation of water in the body is essential for:

A
  • rate of chemical reactions
  • Maintenance of blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two kinds of thirst:

A

Osmotic thirst
Hypovolemic thirst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Osmotic thirst

A

Too much sodium chloride (salt) in the extracellular fluid
(e.g., From eating a big bag of salty chips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hypovolemic thirst

A

Loss of volume of extracellular fluid (e.g., from
excessive sweating or bleeding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

osmotic pressure

A

Tendency of water to move from areas of
low solute concentration to areas of high solute
concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do osmoreceptors detect?

A

osmotic pressure and salt content in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are osmoreceptors located?

A

third ventricle (circumventricular areas of the brain)
- Organum vasculosum laminae terminalis (OVLT) (also
receives info from digestive tract)
– Subfornical organ (SFO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Vasopressin

A

an antidiuretic hormone released from the pituitary (therefore retain water)
– Vasopressin regulates the kidneys to reabsorb water from urine and excrete concentrated urine to rid the body of excess sodium while conserving water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What controls rate of vasopressin released from posterior pituitary?

A

Supraoptic nucleus and PVN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Satiety Mechanism Process (6 steps)

A
  1. Body loses water (body fluids)
  2. Detectors signal loss of water (detectors)
  3. Drinking occurs (correctional mechanism)
  4. Stomach fills with water, sends signal to brain (stomach)
  5. Satiety mechanism inhibits further drinking (satiety mechanism)
  6. Water is absorbed (stomach), body fluids back to normal (body fluids)
28
Q

Change in blood pressure is measured by:

A

baroreceptors of heart, blood vessels, and kidneys

29
Q

Digestion

A

the process by which food is broken down to provide energy

30
Q

Digestion pathway

A

■ Begins in mouth (enzymes for carbs)
■ Esophagus to stomach (hydrochloric acid and
enzymes for proteins)
■ Small intestine (enzymes for proteins, fats,
and carbs)
■ Absorbed into bloodstream
■ Big intestine absorbs water and minerals
(lubricated and expelled)

31
Q

2 phases of digestion:

A

Absorptive/digestive phase
fasting phase

32
Q

Absorptive/digestive phase

A

– Nutrients are absorbed from the digestive system
– Insulin is secreted from pancreas
– Glucose feeds cells
– Amino acids aid in protein synthesis
– Excess glucose stored in liver (as glycogen) and adipose tissue (triglycerides)
– Fat is stored in adipose tissue

33
Q

Fasting phase

A

– Nutrients not available from the digestive system
– Glucagon secreted from pancreas (short-term)
– Glucose derived from glycogen and triglycerides (fatty acids, glycerol) (long-term)

34
Q

Insulin

A

pancreatic hormone that enables glucose to enter the cell

35
Q

Rise and fall of insulin

A

■ Insulin levels rise as someone is getting ready for a meal and after a meal
– Cephalic phase (thought, sight, or smell of food)
– Digestive phase (while eating to transport glucose to cells of the PNS)
– Absorptive phase (glucodetectors of liver to send satiety signal to the brain)
■ Consequently, high levels of insulin generally decrease appetite (satiety mechanism - signals that food is on its way)
■ As insulin levels drop, glucose enters the cell more slowly and hunger increases

36
Q

Glucagon

A

hormone released by the pancreas when glucose levels fall
■ Glucagon stimulates the liver to convert some of its stored glycogen to glucose to replenish low supplies in the blood

37
Q

short-term reservoir

A

– Located in cells of the liver
– Stores glycogen
– Reservoir reserved for CNS
■ During short-term fasting your liver feeds the brain by converting glycogen into glucose (via glucagon) and releases it into the blood to nourish cells of the CNS.

38
Q

long-term reservoir

A

– Located in adipose tissue
– Stores triglycerides
– Triglycerides contain glycerol and fatty
acids
– Increase in triglycerides increases fat
cells
– Important during fasting
■ During log-term states of fasting, the
adipose tissue supplies the brain with
glucose and the rest of the body with fatty
acids

39
Q

Diabetes Mellitus

A

-> blood glucose increases, but insulin level is low -> glucose does not enter the cells, leaves in urine and feces; thus hunger remains high ->
blood glucose levels stay high but cells are starving -> hunger ->
eating

40
Q

What causes you to eat?

A
  1. signals from the environment
  2. signals from stomach
  3. Metabolic signals
41
Q

Eating signals from the environment

A
  • Sight/smell of food
  • Time of day
42
Q

Eating signals from the stomach

A

▪ Stomach releases the hormone ghrelin to signal the
brain
▪ Ghrelin increases with fasting
▪ Injection of ghrelin increases food intake
▪ Ghrelin is suppressed by duodenum

43
Q

Metabolic signals to eat

A

▪ Glucoprivation = decreased glucose available to cells that causes hunger (hypoglycemia)
▪ Lipoprivation = decreased fatty acids available to cells

Detectors for metabolic variables:
✓ brain monitors glucoprivation
✓ liver monitors both glucoprivation and lipoprivation

44
Q

What stops eating?

A

Satiety signals

45
Q

Short-term satiety signals

A
  1. Stomach
    – Distention (via vagus nerve to the brain)
    – Gastric receptors that detect presence of nutrients in the stomach ( via splanchnic nerve to brain)
  2. Intestinal factors (duodenum):
    – Chemoreceptors in the duodenum; send info to brain about amount and type of nutrient;
    – CCK hormone in the duodenum when distended; controls rate of stomach emptying
    – PYY increases in same proportion of calories that are ingested
  3. Liver receives nutrients from intestines and sends satiety signal to brain
  4. Insulin receptors in hypothalamus
46
Q

Long-term satiety signals

A

■ When fat reserves decrease, leptin levels decline, and you react by eating
more and becoming less active, to save energy.
■ When leptin levels return to normal, you eat less and become more active
■ Ob KO mouse: mutation of Ob gene that disrupts production of leptin

47
Q

Leptin

A

hormone released by fat cells of adipose tissue determine long-term satiety cues

48
Q

Brain mechanism in hunger and satiety:
Hindbrain - Medulla Oblongata

A

▪ Contains neural circuits that detect hunger and satiety
signals and controls some aspects of food intake
▪ Receive taste info from tongue; info from stomach,
duodenum, & liver; detectors for glucose
▪ hunger increases activity of neurons in the medulla
▪ lesions abolish glucoprivic feeding

49
Q

Brain mechanism in hunger and satiety:
Hypothalamus - Ventromedial hypothalamus

A

Inhibits eating (Satiety center)
■ Lesion leads to overeating (frequent eating of normal meals) and weight gain.
■ Eating normal sized meals, but frequently (increased insulin and glucoprivation)

50
Q

Brain mechanism in hunger and satiety:
Hypothalamus - Lateral hypothalamus

A

(a.k.a. Hunger/Eating center) controls
eating/drinking behavior
■ Lesion causes cessation of eating and drinking
■ Lesions cause under-eating, weight loss.
■ Communicates with taste pathway of solitary nucleus of medulla.
■ Communicates with cortex to facilitate ingestion, swallowing and perception of food.
■ Communicates with spinal cord for digestion of food.
■ Communicates with pituitary to secrete hormones which further increase insulin

51
Q

Important hunger-satiety pathway:

A

Arcuate Nucleus (AN) -> Paraventricular Nucleus (PVN) -> Lateral hypothalamus (LH)

52
Q

Hunger-satiety pathway: Arcuate Nucleus (AN)

A

“Master Area” for appetite control
■ has neurons sensitive for hunger (ghrelin) and satiety (cck, insulin)

53
Q

Hunger-satiety pathway: Paraventricular Nucleus (PVN)

A

Inhibits the lateral hypothalamus
■ Receives input from arcuate nucleus (excited or inhibited)
■ Important for satiety
■ Lesions cause increased meal size, especially increased intake of carbohydrates

54
Q

Hunger-satiety pathway: lateral hypothalamus

A

Hunger/Eating center: controls
eating/drinking behavior

55
Q

Hunger chemicals in the hypothalamus

A

■ Production of orexigens (appetite inducing chemicals)
■ In AN: neuropeptide Y (NPY) and agouti-related peptide (AgRP)
– Project to Lateral hypothalamus (+) and PVN (-)
– Inhibit satiety cells of the AN
■ In LH: melanin-concentrating hormone (MCH) & orexin
– Project to brain areas important for feedings (motivation, motor) and to the ANS
(metabolism)

56
Q

Satiety chemicals in the hypothalamus

A

■ Production of melanocortins (appetite suppressing chemicals)
■ In AN: Alpha-melanocyte-stimulating hormone (α-MSH)
– Stimulates PVN which inhibits LH
– Inhibit hunger cells of the AN
■ Leptin receptors inhibit NPY/AgRP neurons
– Excitatory effect on melanocortin
■ PYY in gastrointestinal tract inhibit NPY/AgRP of AN

57
Q

The Hunger system

A

✓Hunger-sensitive neurons (NPY/AgRP) of the AN are stimulated by Ghrelin from stomach and/or from glucose-sensitive cells of the medulla.

✓Hunger-sensitive neurons of AN inhibit satiety cells of AN (α-MSH) and inhibit project to PVN.

✓AN stimulate orexigens (MCH and Orexin) of the Lateral hypothalamus

✓Projections from LH innervate other brain regions to facilitate motivation and eating behaviors

58
Q

The Satiety system

A

✓Hunger-sensitive neurons in AN (NPY/ArGP) are inhibited by PYY and Leptin.

✓Satiety-sensitive neurons in AN (α-MSH) are stimulated by Leptin and insulin.

✓Satiety-sensitive neurons of AN project to PVN and excite satiety action of PVN

59
Q

Eating disorders

A

obesity
obesity: Etiology
Syndromal obesity: Prader-Willi syndrome
anorexia nervosa
bulimia nervosa

60
Q

Obesity

A

■ Definition: BMI > 30
■ 60% adults and 30% children
■ Increased health problems:
– CHD and Stroke
– Type II Diabetes
– Arthritis
– Cancer
– Cognitive impairment,
– Early mortality

61
Q

obesity: etiology

A

■ Epigenetic changes in DNA expression (Dutch famine and Obese parents)
– Children born after maternal bariatric gastrointestinal bypass surgery are less obese and exhibit improved cardiometabolic risk profiles carried into adulthood compared with siblings born before maternal surgery.
■ Genetic mutations
– Heredity Leptin Deficiency
– Recessive leptin gene mutation
■ Intrauterine environment
– Maternal diabetes
■ Lifestyle behaviors

62
Q

syndromal obesity: Prader-willi syndrome

A

■ Genetic disruption on chromosome 15 which affects
hypothalamic development and function
■ No satiety signals
■ High ghrelin levels, normal NPY/AgRP, normal leptin
receptors

63
Q

Anorexia nervosa

A

Excessive dieting and compulsive exercise due to
exaggerated concern with overweight

64
Q

bulimia nervosa

A

binging followed by purging

65
Q

benefits of Mediterranean/prudent diet

A

– Decreased risk of cancer, CVD,
Parkinson’s and Alzheimer’s disease
– Reduced risk of depression
– Lower Allostatic Load or Biological
Stress

PSY324 Biological Psychology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions