Hypothalamus Flashcards

1
Q

where are the major control point of the ANS?

A

hypothalamus
medulla
pons

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2
Q

what does the hypothalamus integrate?

A

neural and hormonal responses

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3
Q

what is the role of the hypothalamic nuclei ?

A

involved in the body, behavior and autonomic nervous system to control tasks like hunger, temperature regulation, sexual behavior, circadian rhythms and hormone release

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4
Q

supraoptic and paraventricular nuclei in the hypothalamus are responsible for producing what two key hormones?

A
  • Arginine Vasopressin (AVP), also known as antidiuretic hormone (ADH)
  • Oxytocin
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5
Q

What is another name for the posterior pituitary gland? anterior?

A

Neurohypophysis
Adenohypophysis

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6
Q

Nuclei like the arcuate nucleus release hormones such as

A

Dopamine, which inhibits prolactin

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7
Q

How is the anterior pituitary different from the posterior pituitary in terms of communication with the hypothalamus?

A

The anterior pituitary requires a venous plexus (blood vessel system), while the posterior pituitary uses direct neural connections

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8
Q

Are the vascular connections between the hypothalamus and pituitary inside the blood-brain barrier?

A

No, they are outside the blood-brain barrier, allowing negative feedback from circulating hormones.

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9
Q

what are the releasing hormones and their targets for the anterior pituitary?

A

GHRH → Growth Hormone (GH)
GnRH → FSH and LH
CRH → ACTH
TRH → TSH

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10
Q

what are the hormones released from nerve endings that directly enter the blood stream from the posterior pituitary?

A
  • Oxytocin for breast milk ejection, uterine contractions
  • AVP/ADH for water retention in kidneys
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11
Q

what are the target sites for GH that is released from the anterior pituitary and what occurs?

A
  • Liver: Stimulates production of IGF-1 (Insulin-like Growth Factor-1)
  • Adipose tissue: lipolysis and reduces glucose uptake
  • Muscles: Increases glucose and amino acid uptake, protein synthesis
  • Bones: Stimulates growth, collagen production, and cell division
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12
Q

what are the two negative feedback pathways for GH release?

A

Both GH and IGF-1can inhibit the hypothalamus (reducing GHRH and increasing SST) and the anterior pituitary (reducing GH release)

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13
Q

how can cortical centers start hypothalamic activity?

A

You feel stressed → the prefrontal cortex activates the hypothalamus → triggers the Hypothalamic–Pituitary–Adrenal axis → releases cortisol

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14
Q

how is oxytocin regulated?

A

positive feedback loop, during labor uterine contractions cause oxytocin release → which causes more contractions → which releases more oxytocin

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15
Q

what does the hypothalamus release when it senses stress?

A

CRH (corticotropin-releasing hormone)

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16
Q

what does the release of CRH trigger?

A

the anterior pituitary to release ACTH (adrenocorticotropic hormone) and Beta-endorphins (natural painkillers)

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17
Q

What does ACTH signal the release of?

A

cortisol from the adrenal medulla

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18
Q

what is cortisol?

A

a glucocorticoid that causes a delayed increase (6 hours) in blood glucose to defend against hypoglycemia

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19
Q

what is the function of beta-endorphins?

A

reduce pain response and elevate mood

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20
Q

when are beta-endorphins and cortisol mainly released?

A

during catabolic states like stress, exercise, starvation, and hypoglycemia

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21
Q

what can happen if an insulin dose is too high for type I/II diabetics?

A

hypoglycemia will result and cause for the
increase in activity in the NTS and the hypothalamus

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22
Q

what portion of the brain is activated in heightened states of alertness?

A

locus ceruleus
** (key center for NE release)

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23
Q

what happens when stress activates the sympathetic nervous system?

A
  • positive chronotropism (increased heart rate)
  • positive inotropism (increased heart contractility)
  • redirection of blood flow to skeletal muscles, heart and brain
  • vasodilation in skeletal muscles through beta-2 adrenergic receptors
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24
Q

what can happen if stress causes the over activation of the vagus nerve (increased vagal activity)?

A

shut-down response (PNS)
- Lower heart rate
- Lower cardiac output
- Reduced blood flow to the brain → which can lead to fainting (syncope) or CNS ischemia

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25
Q

what can chronic opioid use be linked too?

A

impaired sexual dysfunction, hypogonadism, decreased libido, infertility and androgen deficiency

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26
Q

what does chronic opioid use inhibit the release of?

A

GnRH from the hypothalamus which will cause a ↓ GnRH → ↓ LH and FSH → ↓ testosterone and sperm production

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27
Q

what withdraw drug can be linked to endocrine dysfunction?

A

methadone

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28
Q

How does the hypothalamus regulate body temperature in response to cold and heat?

A

through reflexes:
- posterior hypothalamus responds to cold exposure by triggering reflexes like shivering
- anterior hypothalamus responds to heat by triggering sweating and vasodilation

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29
Q

What are the main ways the body produces and loses heat to maintain temperature balance?

A
  • Heat Production through exercise, digestion and absorption of food and cellular metabolism
  • Heat Loss through radiation, conduction, vaporization and excretion (very small amount)
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30
Q

Why is it important to regulate core body temperature?

A

it influences enzyme function

31
Q

Where is the body’s temperature “set point” regulated, and how does the body maintain it?

A

hypothalamus
- it receives temperature signals from the peripheral nervous system, compares them to an internal “set point” and send autonomic signals to either increase heat loss or heat conservation/production

32
Q

How does the body generate heat in response to cold exposure?

A
  • Shivering and increased muscle activity via ANS and thyroid hormones
  • Brown adipose tissue (BAT) produces heat directly
  • White adipose tissue (WAT) can convert to BAT
  • thyroid gland increases secretion of T3 and T4 which increases BMR
33
Q

what is browning?

A

when WAT converts to BAT by activation of beta-3 adrenergic receptors

34
Q

How does the body preserve heat during cold exposure?

A

Vasoconstriction of skin blood vessels mediated by alpha-1 adrenergic receptor activation by NE

35
Q

Why is heat considered a stronger (pre-potent) stimulus than cold?

A

it can cause protein denaturation

36
Q

how does the body cool down?

A

vasodilation, eccrine sweat gland activation (most effective), decreased TSH and increased respiration rate

37
Q

how does the body prevent dehydration during exposure to high temperatures?

A

the body releases AVP through activation of warm receptors in the skin and warm venous blood returning to the hypothalamus

38
Q

how is a fever produced during inflammatory responses?

A

exogenous pyrogens cause the immune system to release cytokines (IL-1B and IL-6) which trigger the brain to release PGE2 which activates the anterior hypothalamus ↑ cAMP and ↑ body temperature and ↑ in thermoregulatory set point

39
Q

how do fever-reducing medications like NSAIDs work?

A

block PGE₂ production by inhibiting COX-2

40
Q

what can happen if a fever persists for too long?

A

if the fever is too high or lasts too long, it can become dangerous and cause damage (like brain issues or dehydration)

41
Q

how does cortisol effect appetite?

A
  • Moderate stress = more hunger
  • Chronic or severe stress = less or irregular hunger
42
Q

what are the key players that increase appetite?

A

Ghrelin (hunger hormone)
- NPY (Neuropeptide Y)
- AgRP (Agouti-related peptide)
- MCH (Melanin-concentrating hormone)
- Orexin
- Endocannabinoids (same system marijuana activates)

43
Q

what is leptin?

A

molecule released by fat cells after a meal to inhibit feeding behavior
*(many humans are resistant to leptin)

44
Q

what happens when there is anorexigenic signals (appetite suppressant)?

A

leptin and insulin activate POMC neurons in the arcuate nucleus to produce POMC protein that splits into α-MSH and ACTH

45
Q

what is the function of ⍺-MSH?

A

bind to MC4R (melanocortin-4 receptor) and inhibit food intake and increase energy use

46
Q

what happens when there is orexigenic signals (appetite stimulant)?

A

ghrelin activates AgRP/NPY neurons to release AgRP and NPY which increase appetite

47
Q

how does your body know when you are finished with a meal?

A
  • high blood sugar, insulin, and CCK will signal via the vagus nerve to the brain and activate POMC neurons
  • CRH increases cortisol (stress)
  • gastric distension stimulates vagus
48
Q

what does increased plasma leptin activate?

A

TORC1 genes which:
- activates CART gene → suppresses appetite
- activates KISS1 gene → signals reproductive readiness

49
Q

what can low leptin in men and women cause?

A
  • reduce rate of sperm production
  • amenorrhea (loss of periods in women)
50
Q

what can high levels of leptin lead to?

A

inhibition of LH

51
Q

When your blood sugar drops (low plasma glucose), your body activates

A

orexigenic signals like ghrelin, galanin and orexins A and B

52
Q

what area does ghrelin stimulate?

A

lateral hypothalamus area (LHA)

53
Q

how does Neuropeptide Y (NPY) stimulate appetite?

A

released from the medial arcuate nucleus and inhibits the release of CRH through activation of GABA producing neurons

54
Q

how does Orexin A and B stimulate appetite?

A

activates the LHA via GPCR pathways (Gs)

55
Q

what occurs under chronic low level stress?

A

ghrelin stimulates the release of NPY and Agouti-related peptide
- NPY binds Y1 receptors to increase food intake and inhibit GABA release (more CRH)
- AgRP blocks MC4R pathway and inhibits POMC neurons

56
Q

why do humans stress eat?

A

stress increases cortisol which increases hunger for comfort foods that activate the brain reward pathway
* over time the brain can become resistant to insulin and leptin, so it keeps thinking you’re hungry

57
Q

why does ghrelin drop after gastric bypass surgery?

A

theory is food no longer touches certain parts of the stomach lining, which may be crucial for ghrelin production

58
Q

how do the ENS & NTS (Nucleus Tractus Solitarius) connections influence appetite?

A
  • chemoreceptors in the gut send signals like stomach distention to the NTS —> ARC of the hypothalamus
  • high blood sugar causes astrocytes around POMC neurons to shrink which ↓ appetite
59
Q

what are the appetite and drug therapies for Chemotherapy-Induced Nausea and Vomiting (CINV)?

A
  • 5-HT₃ (Serotonin) Receptor Antagonists
  • Anticholinergics
  • Antihistamines
60
Q

what are the two main drivers for sleep-wake cycles?

A
  • Circadian Rhythm (Endogenous Clock)
  • Sleep drive
61
Q

what pattern do the two key hormones in the sleep-wake cycle follow and what do they do?

A

melatonin and cortisol follow a diurnal pattern
- melatonin is released by the pineal gland around 9 pm to help induce sleepiness
- cortisol rises in the early morning 4-6 am and help you to wake up

62
Q

what is sleep hygiene?

A

set of behavioral and environmental recommendations to optimize sleep drive

63
Q

when trying to diagnose a patient with insomnia and they present with restless leg syndrome what should you check?

A

ferritin levels

64
Q

what are the non-pharmological approaches for treatment of insomnia?

A
  • Cognitive behavioral therapy for insomnia (CBT-I, first line therapy)
  • Sleep hygiene
  • Sleep deprivation
  • Meditation or relaxation techniques
65
Q

what are the two ways thirst is triggered?

A

hypertonicity (increased plasma osmolality, mainly due to high sodium) or hypovolemia (low blood volume)

66
Q

what happens after the body detects changes in osmolality or blood volume?

A

osmoreceptors (in the PVN and SON of the hypothalamus) and baroreceptors/angiotensin II (in blood vessels) send signals to the hypothalamus that activates the thirst response

67
Q

AVP acts through what three types of GPCRs (G-protein coupled receptors)?

A
  • V1A and V1B receptors use Gq → activate IP3 and DAG → increase calcium → cause vasoconstriction
  • V2 receptors use Gs → increase cAMP → enhance water reabsorption in the kidney collecting ducts
68
Q

where is the thirst response regulated?

A

lateral hypothalamus

69
Q

what is diabetes insipidus and how is it treated?

A

a condition where AVP is deficient, causing excessive urination and thirst
- A synthetic form of AVP (like desmopressin) can be used to treat it

70
Q

what pathway does oxytocin work through?

A

Oxytocin acts through a GPCR, specifically using the Gq pathway that increases intracellular calcium, which causes smooth muscle contraction

71
Q

explain the Let-Down Reflex

A

neuroendocrine reflex triggered by suckling at the nipple
- Touch receptors in the nipple send signals via sensory nerves to the hypothalamus which activates oxytocin release and causes myoepithelial cells in the breast to contract

72
Q

How does the limbic system influence the neuroendocrine system?

A

The amygdala activates the hypothalamus, increasing the release of hormones and neurotransmitters like serotonin, dopamine, and glutamate, which can affect appetite and stress responses

73
Q

What are the effects of the limbic system on the autonomic and somatic motor systems?

A

It increases blood pressure, heart rate, and alertness (via ANS), and speeds up movement away from threats by reducing reaction time (via somatic motor control).