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BMS200 > week 3, lecture 1 > Flashcards

week 3, lecture 1 Flashcards

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
Q

where is growth hormone made and by what?

A

Produced by somatotrophs within the anterior pituitary

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26
Q

how is growth hormone released

A

Released in pulsatile bursts, major burst at night (nocturnal) during slow-wave sleep

27
Q

how is growth hormone transported and what is its half life

A

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
Q

what does growth hormone stimulate

A

Stimulates insulin-like growth factor 1 (IGF-1) release from liver

29
Q

what is growth hormones function

A

stimulation of postnatal longitudinal growth (anabolic and mitogenic effects)

30
Q

production of growth hormone throughout life

A

Production increases after 1-2 years, peaks in puberty, begins to decline in adulthood and continues with aging

31
Q

what is growth hormone secretion stimulated by

A

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
Q

what is growth hormone inhibited by

A

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
Q

how does somatostatin/GHIH inhibit growth hormone?

A

binds g alpha somatostatin receptor and promote tyrosine phosphatase activity

or

k+ channels and hyper polarizes to stop release of growth hormone

34
Q

growth hormone secretion decreases with age how?

A

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
Q

what type of receptor fro growth hormone

A

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
Q

what happens when growth hormone binds receptors

A

dimerization increasing JAK activity and phosphorylation tyrosine residues to release transcription proteins

37
Q

growth hormone functions

A

longitudinal bone growth, lipolysis, protein synthesis, IGF1 production, reduce glucose uptake, gluconeogenesis, influences immune system, mood

38
Q

what is IGF-1 regulated by

A

Regulated by GH, PTH and reproductive hormones (in bone)

39
Q

IGF-1 function

A

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
Q

IGF-1 throughout lifetime

A

Low at birth, increases during childhood/puberty, begins to decline in 3rd decade

41
Q

outcomes of too much growth hormone

A

acromegaly (post puberty) or gigantism (pre puberty/ growth plate fusion)

42
Q

what is acromegaly from

A

somatotorope adenoma

43
Q

acromegaly cause

A

due to somatotrope adenoma resulting in over secretion of GH

44
Q

bone and soft tissue impacts from acromegaly

A

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
Q

neoplastic complications of acromegaly

A

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
Q

metabolic complications from acromegaly

A

Promote gluconeogenesis

Reduction in insulin signaling pathway

Insulin Resistance

47
Q

neurologic complications of acromegaly

A

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
Q

neurologic complications of acromegaly

A

bitemporal hemianopsia

1/2 of outside eye cant see out of

49
Q

acromegaly and cardiovascular impact

A

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
Q

gigantism cause

A

If increased GH secretion occurs before epiphyseal long bone closure (in children or adolescents) this results in gigantism

51
Q

gigantism features

A

same as acromegaly plus increased height

52
Q

prolactin is synthesized by? where?

A

lactotrophs

(15-20% of anterior pituitary);

53
Q

what causes an increase in the amount of lactotrophs (to then make prolactin)

A

estrogen

amount of lactotrophs increases in response to estrogen (i.e. pregnancy)

54
Q

when does secretion of prolactin increase

A

Secretion increases during sleep and reduces during wake hours

55
Q

function of prolactin

A

development of mammary glands and milk production

56
Q

how is prolactin inhibited

A

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
Q

what is prolactin stimulated by

A

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
Q

where is prolactin receptor

A

mammary gland, ovary, brain

59
Q

prolactin function

A
  • Developmammaryglands
  • Milksynthesis
  • Maintenanceofmilksynthesis
    Milk synthesis is prevented during pregnancy by high progesterone levels
    *
  • InhibitGnRH
60
Q

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)

A

D. Growth hormone-releasing hormone (GHRH)

61
Q

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

A

B. Class 1 cytokine receptors

62
Q

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

A

D. Stimulation of postnatal longitudinal growth

63
Q

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

A

C. Stimulation of milk production

BMS200 (46 decks)

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