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BMS200 > week 3, lecture 1 > Flashcards

week 3, lecture 1 Flashcards

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1
Q

what regions in the 3rd ventricle allow selective passage of signals from the blood into the hypothalamus called?

A

circumventricular organs via ventricular fluid

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2
Q

what signals can the hypothalamus sense from the bloodstream?

A

Can sense osmolarity, glucose, signal peptides (short loop feedback, appetite mediators)… many

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3
Q

what areas does the hypothalamus communicate with?

A

brainstem, limbic areas, and cortex

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4
Q

what are the 2 types of neurons in the hypothalamus

A

magnocellular and parvocellular neruons

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5
Q

where are magnocellular neurons located

A

supraoptic and paraventricular nuclei

SON & PVN

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6
Q

where are parvocellular neurons located

A

many different nuclei

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7
Q

which are large or small; magnocellular vs parvocellular

A

magno= make large quantities of neurohormones

parvocellular= small

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8
Q

what neurohormones are in the magnocellular neurons?

A

oxytocin and vasopressin

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9
Q

what neurohormones are in parvocellular neurons of the hypothalamus

A

CRH, TRH, GHRH, GHIH, DA, GnRH/LHRH, PRH

–> i.e. oxytocin and vasopressin are magnocellular and everything else is parvocellualr

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10
Q

what is the output of the magnocellular neurons

A

posterior pituitary – release neurohormones into systemic circulation

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11
Q

what is the output of the parvocellular neurons

A

median eminence (portal vein towards anterior pituitary), brainstem, spinal cord

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12
Q

what is the hypothalamic- pituitary system? where does the signals first go?

A

go to anterior pituitary

The hypothalamus secretes releasing or inhibiting hormones into 1st set of capillaries

These travel down to the anterior pituitary and modulate hormone secretion from those cells

Anterior pituitary hormones control several other endocrine glands
–Thyroid, adrenal gland, gonads, liver

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13
Q

magnocellular vs parvocellular for anterior or posterior pituitary

A

magno= posterior
parvo= anterior

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14
Q

slide 9 chart

A

xx

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15
Q

posterior pituitary composed of?

A

Composed of axon terminals of magnocellular neurons and arteries forming inferior hypophyseal artery

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16
Q

anterior pituiaary is composed of?

A

Composed of endocrine tissues
(responsible for producing ACTH, GH, TSH, etc.)

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17
Q

what inputs foes the anterior pituairaty get

A

eceives hypothalamic neurohormones via the secondary capillary plexus that receives blood from portal vein (hypothalamic parvocellular neurons release hormones into the primary capillary plexus within median eminence)

Superior hypophyseal artery –>primary capillary plexus –> portal vein–> secondary capillary plexus

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18
Q

where does anterior pituitary release hormones to?

A

Releases hormones into the hypophyseal veins (into systemic circulation via internal jugular vein)

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19
Q

where does hypothalamus receive input from

A

Receives input from: CNS, intestines, heart, liver, stomach

Contain specialized neurons that are able to detect different senses: glucose-sensing neurons, osmoreceptors

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20
Q

positive and negative feedback loops in hypothalamus

A

Various hormones and signals from periphery can regulate hypothalamus via positive and negative feedback loops

Negative loop: CRH stimulates ACTH release from anterior pituitary, ACTH inhibits hypothalamus from releasing more CRH

Positive loop: Oxytocin stimulates uterine contractions, fetal head descends and stretches the cervix, triggering hypothalamus to release more oxytocin

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21
Q

what is the majority of feedback loops in hypothalamus

A

negative feedback

i.e. homeostatic or nonhomeo

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22
Q

long loop of hypothlamus and pituitary

A

target endocrine gland –> hypothalamus or pituitary

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23
Q

short loop of hypothalamus and pituitary

A

anterior pituitary –> hypothlamus

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24
Q

slide 13 chart

A

xc

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25
where is growth hormone made and by what?
Produced by somatotrophs within the anterior pituitary
26
how is growth hormone released
Released in pulsatile bursts, major burst at night (nocturnal) during slow-wave sleep
27
how is growth hormone transported and what is its half life
Transported with majority bound to growth-hormone binding protein to act as reservoir and to prolong half-life (protects against degradation) Half-life is 6-20 minuteswhat
28
what does growth hormone stimulate
Stimulates insulin-like growth factor 1 (IGF-1) release from liver
29
what is growth hormones function
stimulation of postnatal longitudinal growth (anabolic and mitogenic effects)
30
production of growth hormone throughout life
Production increases after 1-2 years, peaks in puberty, begins to decline in adulthood and continues with aging
31
what is growth hormone secretion stimulated by
GHRH and ghrelin GHRH (hypothalamus) Hypoglycemia (promotes GHRH release) Arginine Catecholamines (also reduce GHIH/somatostatin) Dopamine Cortisol, thyroid hormones and androgens also influence GH by modifying the responsiveness to GHRH and GHIH Ghrelin (stomach, pancreas, kidney, liver, hypothalamus)
32
what is growth hormone inhibited by
somatostatin/GHIH and IGF1 Somatostatin / GHIH Hyperglycemia Increase in non-esterified fatty acids Insulin-like growth factor 1 (IGF-1) Directly inhibits somatotrophs Stimulates GHIH (which further inhibits somatotrophs) Somatostatin: Synthesized by many parts of the brain and organs (pancreas, stomach, others) Binds to (1) Galpha-i somatostatin receptor and promote tyrosine phosphatase activity (2) K+ channels resulting in hyperpolarized cell (stops release of GH)
33
how does somatostatin/GHIH inhibit growth hormone?
binds g alpha somatostatin receptor and promote tyrosine phosphatase activity or k+ channels and hyper polarizes to stop release of growth hormone
34
growth hormone secretion decreases with age how?
n the adult, GH levels are reduced as a result of smaller pulse width and amplitude rather than a decrease in the number of pulses.
35
what type of receptor fro growth hormone
class 1 cytokine receptor family Location: liver, bone, kidney, adipose tissue, muscle, brain, eye, heart and immune cells There are 2 bindings sites which allow the GH receptors to dimerize once GH binds Dimerization resulting in increased JAK activity which leads to phosphorylation of tyrosine residues These will allow the release of activators of transcription proteins, which will promote the expression of GH- regulated genes (genes that are influenced by growth hormone)
36
what happens when growth hormone binds receptors
dimerization increasing JAK activity and phosphorylation tyrosine residues to release transcription proteins
37
growth hormone functions
longitudinal bone growth, lipolysis, protein synthesis, IGF1 production, reduce glucose uptake, gluconeogenesis, influences immune system, mood
38
what is IGF-1 regulated by
Regulated by GH, PTH and reproductive hormones (in bone)
39
IGF-1 function
stimulates bone formation, protein synthesis, glucose uptake into muscles, neuronal survival, myelin synthesis, bone turn over, collagen synthesis, linear growth, mitogen (DNA, RNA and protein synthesis)
40
IGF-1 throughout lifetime
Low at birth, increases during childhood/puberty, begins to decline in 3rd decade
41
outcomes of too much growth hormone
acromegaly (post puberty) or gigantism (pre puberty/ growth plate fusion)
42
what is acromegaly from
somatotorope adenoma
43
acromegaly cause
due to somatotrope adenoma resulting in over secretion of GH
44
bone and soft tissue impacts from acromegaly
Bone: Acral bony overgrowth result in frontal bossing Increased hand and foot size Mandibular enlargement with prognathism Wide space between incisor teeth Soft tissue: Increased heel pad thickness, increased shoe size, coarse facial features, large fleshy nose
45
neoplastic complications of acromegaly
increased cell proliferation GH – increase JAK/STAT pathway--> proliferation BRCA1 – breast cancer Suppression of regulatory proteins! they typically stop inappropriate DNA and cell replication--> colon and pituitary cancers Mitogen
46
metabolic complications from acromegaly
Promote gluconeogenesis Reduction in insulin signaling pathway Insulin Resistance
47
neurologic complications of acromegaly
If the somatotrope adenoma (aka AP tumour) grows large enough, it can: Impinge on the optic nerve (at the optic chiasm--> bitemporal hemianopsia) Increase intracranial pressure (headaches, eventually impacting cortical function, selected cranial nerves)
48
neurologic complications of acromegaly
bitemporal hemianopsia 1/2 of outside eye cant see out of
49
acromegaly and cardiovascular impact
Cardiomyopathy with arrhythmia’s Left ventricular hypertrophy Decreased diastolic function Hypertension -->thickening of arteries bc of increased collagen synthesis Upper airway obstruction with sleep apnea (common) Central sleep dysfunction Soft tissue laryngeal airway obstruction --> increased connective tissue causing thickening of posterior tongue Diabetes
50
gigantism cause
If increased GH secretion occurs before epiphyseal long bone closure (in children or adolescents) this results in gigantism
51
gigantism features
same as acromegaly plus increased height
52
prolactin is synthesized by? where?
lactotrophs (15-20% of anterior pituitary);
53
what causes an increase in the amount of lactotrophs (to then make prolactin)
estrogen amount of lactotrophs increases in response to estrogen (i.e. pregnancy)
54
when does secretion of prolactin increase
Secretion increases during sleep and reduces during wake hours
55
function of prolactin
development of mammary glands and milk production
56
how is prolactin inhibited
dopamine Under tonic inhibition from the dopamine binding to D2 receptors on the lactotrophs; dopamine released from hypothalamus Somatostatin and GABA also exert inhibitory impact
57
what is prolactin stimulated by
Stimulated by suckling and increased estrogen Suckling results in reduction of dopamine release from hypothalamus GnRH, serotonergic and opioidergic pathways also promote release as do Prolactin Releasing Factors (TRH, oxytocin, vasoactive intestinal peptide)
58
where is prolactin receptor
mammary gland, ovary, brain
59
prolactin function
* Developmammaryglands * Milksynthesis * Maintenanceofmilksynthesis Milk synthesis is prevented during pregnancy by high progesterone levels * * InhibitGnRH
60
What is the primary hormone responsible for stimulating both the synthesis and secretion of GH from somatotrophs? A. Somatostatin B. Insulin C. Ghrelin D. Growth hormone-releasing hormone (GHRH)
D. Growth hormone-releasing hormone (GHRH)
61
Which family of receptors do growth hormone cell surface receptors belong to? A. G-protein couple receptors B. Class 1 cytokine receptors C. Tyrosine kinase receptors D. Steroid receptors
B. Class 1 cytokine receptors
62
What is the primary physiologic effect of growth hormone? A. Stimulation of brain function B. Suppression of immune response C. Promotion of adipocyte differentiation D. Stimulation of postnatal longitudinal growth
D. Stimulation of postnatal longitudinal growth
63
What is the primary physiologic role of prolactin in the mammary gland? A. Inhibition of mammary gland development B. Suppression of milk synthesis C. Stimulation of milk production D. Regulation of lactose metabolism
C. Stimulation of milk production

BMS200 (46 decks)

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