Unit 11 - Hypothalamus Flashcards

1
Q

hypothalamic nuclei

A

part of diencephalon

under corpus callosum

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

role of hypothalamus

A

integrates autonomic responses and endocrine function with behaviour

  • controls BP and electrolyte composition - drinking, salt, appetite, blood osmolality, vasomotor tone
  • regulates temp - metabolic thermogenesis, behaviour
  • controls energy/metabolism - feeding, digestion, metabolic rate
  • behavioural expression - reproduction, emotional expression, circadian rhythm
  • controls stress response - vasomotor tone, secretion of stress hormones

compares sensory info with biological set points

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

thermoregulation

how does our temp change

A

heat production - heat loss

temp set point

37°C - circadian rhythm 0.5-0.7°C change

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

how does temp measurement differ in various parts of the body

A

rectal > head > trunk > hand > feet

exercise increases temp up to 40°C

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

where are thermoreceptors found

A

skin

deep tissues

spinal cord

extrahypothalamic regions

hypothalamus (20%)

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

types of thermoreceptors

A

Aδ and C fibres

separate warm and cold receptors (TPRV, Transient Potential voltage, receptors)

cold (Aδ) > warm (C)

activated at temperatures that are not necessarily painful

>42°C or <17°C is painful

lower threshold

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

cold fibres

A

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

warm fibres

A

C

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

peripheral thermoreceptors

A

anterolateral system to somatosensory cortex - SPINOTHALAMIC TRACT

also projections to thermoregulatory centre in hypothalamus

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

where are central thermoreceptors located on

A

GABA neurons

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

anterolateral system =

A

spinothalamic tract

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

increased heat production causes activation of

what does this cause

A

preoptic area in anterior hypothalamus

promotes heat loss

vasodilation, sweating, increased respiration

anorexia

apathy

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

lesion of preoptic area in anterior hypothalamus

A

chronic hypERthermia - inability to lose heat

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

increased heat loss activates

A

neurons in posterior hypothalamus

promotes heat generation

shivering, hunger, voluntary activity, vasoconstriction (goose bumps), curling

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

lesion of posterior hypothalamus

A

no effects at room temp

in cold, no ability to conserve heat

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

overview of hypothalamic control of temperature

A

Under normal circumstances the anterior hypothalamus inhibits posterior hypothalamus

Inhibition prevented with lowering in body temp

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

thermoregulation

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

decrease in temp

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

increase in temp

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

temp regulation in an infant

A

neonate has very narrow temp zone

very little capacity for heat conservation

brown fat has a high rate of metabolism, thermogenic function - High thermogenic value so produces a lot of heat but can also get used up

BY 3 MONTHS

metabolic rate increases

rise in ratio of mass to SA

increase in body fat

maturation of shiver response

3 month old has less capacity to dissipate heat than neonate

head - 40% of heat production, 85% of heat loss

if head is covered or overwrapped, CNS temp can increase dangerously

resp affected - SIDS

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

fever and temp

A

pyrogens/toxins → cytokines → OVLT → preoptic area

IL-1B, IL-6, IFNβ, IFNγ, TNFα: receptors in OVLT

causes local release of PGs in preoptic area which alter set point

heat production mechanisms ⇒ fever

beneficial in certain instances e.g. leprosy, viral infections

antipyretic effect of COX2 inhibitors (COX makes PGs) e.g. aspirin

23
Q

factors that stimulate thirst

A

dryness of pharyngeal mucus membrane

gastric/oropharyngeal signals

psychological and social factors

hyperosmolality

reduced blood volume

24
Q

hypothalamic mechanisms involved in thirst

A

organum vasculosum of the lamina terminalis (OVLT)/medial preoptic hypothalamus

plasma osmolality, ECF volume

25
Medial preoptic nucleus of hypothalamus and OVLT
Close anatomically Often grouped together GABAergic and glutaminergic neurons - increases or decreases thirst response
26
plasma osmolality - receptors where do they project to what do they do
osmoreceptors in OVLT detect change \<1% Na2+ conc (monitoring blood flow over them) projections to supra-optic and paraventricular nuclei to ***_produce_*** ADH released by pituitary increases thirst response and promotes fluid intake also, increases water permeability in DCT of kidney - AQP-2, which allow water to be reabsorbed ⇒ reduction in osmolality
27
reduced or absent secretion of ADH
diabetes insipidus
28
where is ADH produced
supra optic and paraventricular nuclei
29
what does ADH also act as
NT - emotional response to thirst - prefrontal cortex
30
thirst and fluid balance (ECF vol) - where and how is pressure monitored
BARORECEPTORS aortic arch and carotid sinus decrease ECF vol (\>10%) → low BP ADH release Mechanoreceptor - sense stretch depending on EC fluid vol - if we lose fluid, we decrease stretch and neural signal sent to hypothalamus - goes to OVLT and PV nucleus to produce ADH
31
RAA system
Renin produced in response to decrease in EC fluid vol angiotensin II receptors in subfornical (SFO) organ and OVLT signal sent to preoptic, supra-optic and PV nuclei ADH release
32
overview of thirst and fluid balance
reduction must be greater than 10%
33
C
34
lateral nuclei of hypothalamus = destruction/stimulation rate of activity
feeding centre chronically active - if there is not inhibitory control, we would never be hungry destruction ⇒ lack of desire for food, emaciation stimulation ⇒ increased appetite
35
ventromedial nuclei = function destruction/stimulation
sense of fullness inhibits feeding centre (LN of hypo.) destruction ⇒ obesity due to inability to depress feeding behaviour stimulation ⇒ reduced appetite, aphagia
36
apart from VM nuclei and lateral nuclei of hypothalamus, what other nuclei play a part in hunger and feeding
Paraventricular dorsomedial arcuate
37
injection of substances to PV nuclei
leads to selective food intake NA - CHO e.g. chocolate Galanin - fat opiates - protein
38
NA ⇒
CHO
39
galanin ⇒
fat
40
opiates ⇒
protein
41
overview of hypothalamic control of feeding
42
short term control of food intake - 4 methods
1. GI distension 2. GI hormonal factors 3. Ghrelin - GI hormone 4. Insulin
43
GI distension
stretch inhibitory receptors activated and inhibit feeding centres + stimulate satiety centre
44
GI hormonal factors
CCK - release due to fat entering duodenum and inhibits feeding centre - travel In blood - directly inhibit feeding centre and activate satiety centre Peptide YY - released by G tract 1-2hrs post feeding, inhibits feeding centre - longer effect - not hungry straight after a meal Glucagon Like Peptide and Insulin - appetite suppressant
45
ghrelin
mainly released by stomach, levels rise in fasting and decrease after eating - stimulate feeding behaviour most GI hormones inhibit feeding centre
46
overview of influences on hunger/feeding
47
long term control of food intake what is produced what is its effect
adipose tissue produces leptin - decreases food intake, increases energy use SUPPRESSES APPETITE release appetite-suppressing neuropeptides α-melanocyte stimulating hormone (α-MSH) cocaine and amphetamine related transcript (CART) INHIBITS STIMULATION OF FOOD INTAKE inhibits release of appetite-stimulating neuropeptides neuropeptide Y Agouti-related peptide
48
other effects of leptin
increased CRH (decreases food intake) increases SNS (neural projections from hypothalamus to vasomotor areas - increase in metabolic rate and energy expenditure) decreased insulin secretion by pancreatic β cells, which decreases energy stores overall acts to signal that enough energy stored and intake of food is no longer required
49
leptin deficiency
obesity and hyperphagia - observed in humans with mutations in genes encoding leptin relative deficiency of leptin may predict future weight gain
50
D