Control of regulation Flashcards

1
Q

An individual perceives thirst when:

What is the more potent stimulus

A

Body fluid osmolality is increased.
Blood volume is reduced.
Blood pressure is reduced.

Plasma osmolality increased is the more potent stimulus – change of 2-3% induces strong desire to drink.
Decrease of 10-15% in blood volume or arterial pressure required to produce the same response.

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2
Q

When plasma ADH is low how much volume of urine?

A

large volume of urine is excreted (water diuresis)

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3
Q

When plasma ADH is high how much volume of urine?

A

a small volume of urine is excreted (anti diuresis).

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4
Q
Osmoreceptors for ADH release found where?
Adaptation of brain where they're found?
Physiological change?
Action?
Also regulate?
A

Found in the hypothalamus, OVLT (Organum vasculosum laminae terminalis) , and SFO (Subfornical organ).
Blood brain barrier selectively allows some things through the brain, so these areas aren’t completely protected by blood brain barrier
Sense changes in body fluid osmolality
Cells shrink or swell in response (expand when plasma more dilute, and vice versa).
Send signals to the ADH producing cells in the hypothalamus to alter ADH release.
Same regions seem to regulate thirst.

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5
Q

Maintaining water balance:
Increased plasma osmolality
Decreased plasma osmolality

A

Increased plasma osmolality
Invokes drinking and ADH release.
Increased ADH stimulates kidney to conserve water.

Decreased plasma osmolality
Thirst is suppressed and ADH release decreased
Absence of ADH the kidney excretes more water.

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6
Q

Sensation of thirst

What’s involved?

A

Thirst is decreased by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolality.
Receptors in mouth, pharynx, oesophagus seem to be involved.
Relief of thirst sensation via these receptors is short lived.
Thirst is only completely satisfied once plasma osmolality is decreased or blood volume or arterial pressure corrected.
Circuits involved? (don’t know about them much except renin angiotensin system)

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7
Q

Renin-Angiotensin-Aldosterone system related to thirst diagram (slide 11, lecture 12)

A

Ang II also stimulates thirst

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8
Q

Body weight homeostasis summary diagram

slide 15, lecture 12

A

-

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9
Q

Hypothalamus diagram depicting anatomy

slide 18, lecture 12

A

Arcuate nucleus= important

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10
Q

Arcuate Nucleus

A

Key brain area involved in the regulation of food intake.
Incomplete blood brain barrier, allows access to peripheral hormones.
Integrates peripheral and central feeding signals.
Two neuronal populations:
1) Stimulatory (NPY/Agrp neuron)
2) Inhibitory (POMC (Proopiomelanocortin) neuron)
Neuronal populations are separate populations, no overlap at all

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11
Q

Arcuate Nucleus mechanism diagram

slide 21, lecture 12

A

Things that you want to respond to to regulate appetite cross blood brain barrier
Bind to receptors on neurons, downstream effect= stimulate/ suppress food intake
Cell bodies and receptors of neurons are in arcuate nucleus but axons extend all the way in the brain/ also into paraventricular nucleus which causes other downstream effects (food intake change/ metabolic changes too)

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12
Q

Arcuate Nucleus mechanism diagram

slide 21, lecture 12

A

Things that you want to respond to to regulate appetite cross blood brain barrier
Bind to receptors on neurons, downstream effect= stimulate/ suppress food intake
Cell bodies and receptors of neurons are in arcuate nucleus but axons extend all the way in the brain/ also into paraventricular nucleus which causes other downstream effects (food intake change/ metabolic changes too)

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13
Q

Melanocortin system summary diagram

slide 22, lecture 12

A

Agrp= Agouti-related peptide
Alpha MSH= alpha melanocyte stimulating hormone
MC4R=Melanocortin 4 receptor

Stimulation of MC4R= inhibition of food intake
Agrp is released from a different neuronal population but goes to same neurones
Agrp= endogenous antagonist on that receptor, Hungry= increased by increased Agrp which blocks inhibitory signal
Absence of POMC= eat a lot

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14
Q

Human CNS mutations affecting appetite

Symptoms?

A

No NPY or Agrp mutations associated with appetite discovered in humans.
POMC deficiency and MC4-R mutations cause morbid obesity.
POMC deficiency= lose all the molecules that it makes (ACTH= no corticosteroid regulation so need glucocorticoid replacement immediately after birth), get ginger hair because MC4-R mutation makes ginger hair, no alpha-MSH= obese because food intake not regulated

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15
Q

Signals from other brain regions that regulate appetite

A

Higher centres.
Amygdala- emotion, memory.
Other parts of the hypothalamus, e.g. lateral hypothalamus
Vagus to brain stem to hypothalamus.

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16
Q

Adipostat mechanism

A

Circulating hormone produced by fat
Hypothalamus senses the concentration of hormone.
Hypothalamus then alters neuropeptides to increase or decrease food intake.
Perhaps a problem with the regulation of the adipostat mechanism leads to obesity ?

17
Q

Leptin how many aas

A

Codes for 167 amino acid hormone

18
Q
Leptin made by?
Movement?
Regulates?
When is it low?
When is it high?
A

Made by adipocytes in white adipose tissue.
Circulates in plasma.
Acts upon the hypothalamus decreasing appetite (intake) and increasing thermogenesis (expenditure).
Low when low body fat
High when high body fat
Replacement in the ob/ob mouse decreases weight.

19
Q

Three ways in which the leptin regulatory loop could lead to obesity

A

Absent leptin
Regulatory defect, when adipose tissue expands, more leptin isn’t produced
Leptin resistance, similar to brain

Most obese people have leptin resistance

20
Q

Action of leptin

A

Adipose tissue produces leptin→ hypothalamus→ food intake+ energy expenditure+ fat and glucose metabolism affected

21
Q

Leptin resistance

A

Leptin circulates in plasma in concentrations proportional to fat mass.
Fat humans have high leptin.
Obesity due to leptin resistance- hormone is present but doesn’t signal effectively.
Leptin is ineffective as a weight control drug

22
Q

Congenital leptin deficiency
Mutation?
Symptoms
Treatment?

A

Small number of cases identified.
Mutation in ob gene-
Severely hyperphagic and obese.
In these children leptin has been effective in reducing body weight.

23
Q

Why do you feel less hungry after a meal?

1) Stretch receptors
2) Nutriments in circulation
3) Brain directly estimates calorie intake
4) Hormone signal from the gut

A

1) only if you’re really full

So ans= 4

24
Q

Peptide YY structure

A

36aa

sometimes cleave off first 2aas to make PYY 3-36

25
Q

Action of PYY 3-36

A

directly modulates neurons in the arcuate nucleus:
Inhibits NPY release.
Stimulates POMC neurons.
Decreases appetite.

26
Q

Ghrelin action

A
Opposite to PYY:
directly modulates neurons in the arcuate nucleus:
Stimulates NPY/Agrp neurons.
Inhibits POMC neurons.
Increases appetite
27
Q

Comorbities associated with obesity

A
Depression
Stroke
Myocardial Infarction
Hypertension
Diabetes
Peripheral vascular disease
Gout
Osteoarthritis
Bowel cancer
Sleep apnoea