Brainscape's Knowledge GenomeTM

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


See full index

HUB paper 2 > When things go wrong part 1 > Flashcards

When things go wrong part 1 Flashcards

1
Q

Energy sources for body & brain

A

1 - glucose
2 - glycogen
3 - Lipids

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

Detection system

A
  • recognise deviation from set point
  • alter physiology or behaviour to correct imbalance
  • recognize when correction has been effective
    (Does not apply to the long-term regulation of energy stores& feeding)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Glucostatic Hypothesis

A
  • Brain monitors circulating blood glucose levels
  • when they fall below a critical level, we become hungry
  • after we eat & blood glucose levels return to normal - no longer hungry
    BUT –> diabetics have high levels of glucose, always hungry without insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lipostatic Hypothesis

A
  • Brain monitors body fat stores
  • If they fall below a critical level - makes us hungry
  • After we’ve eaten & replaced missing body fat, not hungry anymore
    BUT - get hungry ~ 4hrs after a meal - not lost any weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bottom-up modulation

A

Ascending modulatory influences determine the level of incentive salience directed to specific nutrients

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

CNS regulation of energy homeostasis

A

CNS integrates input from long-term energy stores (e.g. leptin) & short-term meal-related signals (nutrients & gut-derived satiety signals) to regulate food intake & EE that is able to maintain stable body fat stores over time

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

Functions of the hypothalamus

A 
1 - regulation of food intake
2 - autonomic regulatory center (influences HR, BP, respiratory rate, GI mobility, pupillary diameter)
3 - regulation of thirst & water balance
4 - regulation of body T
5 - regulation of sleep wake cycle
6 - emotional responses 
7 - hormonal control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which structures does the hypothalamus influence secretion from in regulatin energy balance & metabolism?

A

1 - Thyroid gland
2 - Adrenal gland
3 - Pancreatic islet cells

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

Orexigenic substance

A

any substance that stimulates feeding behaviour

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

Anorexigenic substance

A

Any substance that inhibits feeding behaviour

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

AgRP/NPY Neurons

A

AgRP/NPY neuons express ghrelin receptors - detect ghrelin to facilitate energy intake (hunger-related metabolic molecule)

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

POMC neurons

A

POMC neurons express leptin or insulin receptors - respond to anorexigenic substances: adipose-originated leptin or pancreas-derived insulin

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

T/F POMC neurons expressing leptin receptors co-produce insulin receptors

A

False - POMC neurons expressing leptin receptors do not co-produce insulin receptors (& vice versa) indicating existence of heterogeneous subtypes of POMC neurons in hypothalamus

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

Dominant melanocortin receptors

A

MC3/4R

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

Arcuate Nucleus function

A

Integrates info for blood glucose & body fat levels

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

What are the 2 subtypes of arcuate nucleus neurons?

A

NPY & AgRP expressing neurons

POMC & CART expressign neurons

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

What does activation of NPY/AgRP neurons result in?

A

Increases food intake & decreases EE

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

What does activation of POMC neurons result in?

A

Decreases food intake increases EE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Short-term vs Long-term regulation of food intake

A

Short term regulation:
Preventing overeating at each meal
Long term regulation:
maintenance of normal quantities of energy stores in the body

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

Types of rapid feedback signals during a meal to regulate the amount eaten

A
  1. intestinal stretch receptors

2. Peripheral anorexic hormonal signals

21
Q

Hormones released by lipid & carbohydrates

A

Lipid - CCK release

Carbohydrates - GLP-1, PYY, Insulin

22
Q

CCK, GLP-1 & PYY role

A

CCK: released in response to fat entering the duodenum; Stimulates POMC/CART neurons
–> reduces food intake
GLP-1: released in response to carbohydrates in intestine; Stimulates POMC/CART neurons
–> reduces food intake
PYY: stimulated by food intake & released from GI tract; Inhibits the NPY/AgRP neurons
–> reduces food intake

23
Q

Peripheral orexigenic signal

A

Ghrelin:

stimulates food intake; produced by stomach

24
Q

NPY acts on which receptors in POMC

A

NPY acts on POMC NPY Y1 receptors -> inhibits POMC neurons

25
Q

Adipokines

A 
1 - leptin
2 - Resistin
3 - Adiponectin
4 - Visfatin
5 - TNF & IL
26
Q

Action of leptin

A

Correlates with adipose tissue mass - increase concentration & resistance in obese individuals
Ineffective peripherally in humans

27
Q

Action of resistin

A

Induced in obesity –> leads to insulin resistance

28
Q

Action of Adiponectin

A

Insulin sensitizing & anti-inflammatory
Suppressed in obese paralleling insulin resistance
Increases EE & fatty acid metabolism

29
Q

Action of TNF & IL-6

A

Promotes low level inflammation in fat & throughout body

30
Q

How does Leptin disinhibit POMC neurons?

A
  • Decreases GABAergic tone on POMC - mediated by AgRP neurons
  • Inhibits AgRP neurons
  • Inhibits pre-synaptic GABAergic neurons
31
Q

Selective antagonist on D2 dopamine receptors

A

Raclopride

32
Q

D2 receptor function

A

Activate inhibitory G-proteins by inhibiting adenylate cyclase - cAMP formation

33
Q

Increased Raclopride binding in anteroventral striatum in recovered anorexics could be due to:

A
  • Reduction in intrasynaptic DA concentration
  • Elevation of density of D2/D3 receptors
  • Increased affinity of D2/D3 receptors in this region
34
Q

More evidence for role of DA in anorexia

A
  1. CSF DA metabolites reduced in malnourished AN patients & persists after recovery
  2. AN have impairment in visual discrimination learning - reflects defective DA signaling
  3. Anorexics have altered frequency of functional polymorphisms of DA D2 receptor genes - may effect receptor efficiency of receptor transcription & translation
35
Q

Antagonist of H1 receptors

A

[11C]doxepin

36
Q

When obese individuals restrict energy by dieting:

A
  • > increased sympathetic activity - mobilize fatty acids from adipose stores
  • > results drop in leptin production that exceeds loss of fat from storage deposits
  • > reduced leptin - leads decreased muscle & other thermogenic organ sympathetic activity - leads to decreased resting EE
  • > low leptin levels - disinhibit NPY/AgRP neurons & inhibits POMC/CART neurons - causing a strong drive to seek & ingest food
37
Q

Diet induced weight loss increases baseline levels of :

A

Ghrelin

38
Q

Surgically induced weight loss (gastric bypass) decreases:

A

ghrelin
+ prolonged suppression of ghrelin
weight loss possibly due in part to lack of appetite stimulation

39
Q

The leading theory for maintenance of body weight as a result of long-term matching of food intake to EE relates to the:

A

Amount of fat stored in adipose tissue

40
Q

A defect resulting in a lack of neuropeptide Y in the hypothalamus would likely result in:

A

Decrease in appetite

41
Q

Leptin decreases the reward value of food by:

A
  • Inhibition of the JAK-STAT pathway
  • Inhibiting dopaminergic neurons in the ventral tegmental area

X - not by activating the JAK-STAT pathway in the ventral tegmental area

42
Q

Peripheral anorexigenic substances act on the arcuate nucleus by:

A

Stimulating POMC/CART neurons & increasing EE

43
Q

Insulin sensitizing & anti-inflammatory molecule that increases fatty acid metabolism & increases EE.
levels decrease in obese individuals

A

Adiponectin

44
Q

Molecule thought to be one of the main contributors to insulin resistance in obese individuals

A

Resistin

45
Q

Released in proportion to perceived pleasantness of food

A

Dopamine

46
Q

This drug is responsible for increased anxiety, sedative effects & increased dysphoria in recovered ANs - response that is opposite to that experienced by healthy individuals

A

Amphetamine

47
Q

Brain region that shows persistent hypoperfusion in recovered ANs even after weight gain

A

Anterior Cingulate Cortex (ACC)

48
Q

Reduction in volumes of this brain region results in deficits in perceptual organization & conceptual reasoning in recovered ANs

A

Right parietal lobe

49
Q

Increased density of these receptors (that bind [11C]doxepin) is thought to increase the vulnerability of women to develop anorexia

A

Histamine H1 receptors

HUB paper 2 (6 decks)

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