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Unit 2 Phys II > L14 Hypothalamus+Pituitary > Flashcards

L14 Hypothalamus+Pituitary Flashcards

1
Q

posterior pituitary releases

A

OT

AVP

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2
Q

Anterior pituitary releases

A 
ACTH
GH
TSH
Prl
LH
FSH
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3
Q

manage: water balance, parurition, lactation, regulates BP, cardiac function, diuresis

A

posterior pituitary hormons

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4
Q

manage: metabolism, growth and development, reproduction, lactation, response to stress

A

anterior pituitary hormones

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5
Q

cells of the hypothalamus which project their axons down the infundibular process and terminate in the posterior lobe, where they release their hormones into a capillary bed

A

magnocellular neurons

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6
Q

hypothalamus —> posterior pituitary link

A

magnocellular neurons

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7
Q

hypothalamus —> anterior pituitary link

A

parvicellular neurons

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8
Q

project axons to the median eminence where they secrete releasing hormones and flow down the pituitary stalk in the hypothalamohypohyseal portal vessels to the anterior pituitary

A

parvicellular neurons

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9
Q

magnocellular neurons project their axons down the ________ to the _______

A

infundibular process

posterior lobe capillary bed

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10
Q

parvicellular neurons project their neurons down the _______ where they _______ which _________

A

median eminence
secrete releasing hormones
flow through the hypothalamohypophysela portal vessels to the anterior pituitary

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11
Q

GH is released from

A

somatotrophs

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12
Q

GHRH causes release of

A

GH

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13
Q

TRH causes release of

A

TSH

increased prolactin synthesis

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14
Q

Somatostatin causes

A

decreased synthesiss of GH and TSH

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15
Q

synthesize prolactin

A

mammotrophs

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16
Q

GnRH causes release of

A

LH, FSH by increasing their synthesis

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17
Q

LH and FSH target

A

gonads

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18
Q

CRH causes release of

A

ACTH from corticotrophs

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19
Q

ACTH targets

A

adrenal glands

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20
Q

PRF causes release of

A

prolactin from lactorphs

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21
Q

dopamine inhibits

A

prolactin

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22
Q

ADH and oxytoxin are synthesized as

A

preprohormones in the hypothalamic magnocellular neurons supraoptic and paraventricular nuclei (SON and PVN)

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23
Q

nonapeptides

A

have 9 aminoacids

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24
Q

ADH and oxytoxin are secreted

A

with neurophysins and terminal glycoprotein into fenetstrated pituitiary capillaries

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25
disulfide bridge in ADH and oxytocin is formed by
Cysteine residues at positions 1 and 6
26
plasma half life of ADH and oxytocin
short, 8 mins
27
neurophysin which binds ADH
NP II
28
neurophysin which binds oxytocin
NP I
29
precursor hormone of ADH/oxytocin is cleaved into 3 things
1. ADH/oxytocin 2. NP 3. terminal glycoprotein
30
NP arrangement
tetramers which bind 5 ADH
31
oxytocin has a __________ regulation
positive feedback
32
signals for more oxytocin release are transmitted to
cholinergic synapses within PVN and SON
33
stimulation for oxytocin release
stretch of cervix uterine contraction suckling of lactating breast
34
the uterus is more sensitive to oxytocin because ________ which is mediated by _______
increased density of OT receptors (OTR) | progesterone and OT
35
other factor that increases uterine responsiveness
increased gap junction formation between smooth muscle cells
36
milk ejection is caused by
OT stimulating contraction of myoepitherlial cells
37
what besides suckling can cause milk ejection
sight, smell, sound of infant | **suckling not required**
38
suckling effects on the uterus
mediated by oxytocin | contractions promote uterine regression after birth
39
OT effect on the heart
causes ANP/BNP release from cardiomyocytes
40
ANP and OT are found in both atria and ventricles but are more prominent in
atria
41
BNP is found
mainly in ventricles
42
ANP stimulates
nitric oxide release from vascular endothelium | kidneys to dump more water, K+, NA+ (OT also has this effect)
43
OT acts on ________ in the heart
OT-natriuretic peptide-nitric oxide axis
44
responds to hypertension/hypervolemia by renal baroreceptors or aortic baroreceptor impulses by stimulating oxytocinergic neurons
nucleus tractus solitarius
45
oxytocinergic neurons, when stimulated
decrease corticotropin releasing factor | induces synthesis of OT in PVN and SON
46
cardiovascular effects of OT
``` vasodilation increased NO production (by ANP) negative chonotrope/inotrope bradycardia increase in glucose uptake ```
47
endocrine effects of ANP/OT at the kidney
decreased cortisol, aldosterone, renin
48
prediabetes studies show
that OT causes glucose uptake by GLUT4 mechanism not mediated by insulin receptor pathway
49
nitric oxide causes
dilation of the coronary resistance vessels
50
OT that acts on the heart can come from
Pituitary or local
51
AVP is released
in response to an increase in plasma osmolarity: Na+ and Cl- (ex: dehydration) in response to decrease in blood volume or blood pressure (baroreceptors fire less) stimulated by AVP magnocellular neurons
52
osmoreceptors are found
anterior hypothalamus outside of the blood brain barrier
53
AVP vs thirst?
AVP release occurs before stimulation of thirst
54
AVP acts on
V2 receptor in kidneys ---> increased aquaporins 1-4 --> increased water uptake V1 receptor --> vasoconstriction
55
firing of baroreceptors
is inhibitors to release of AVP
56
baroreceptors also stimulate
thirst center
57
senses decreases in blood pressure and causes the release of renin
macula densa
58
sensitizes the osmoreceptors leading to enhanced AVP release
angiotensin II (from RAAS)
59
which is more sensitive, AVP osmolarity system or AVP blood volume system
osmolarity | **super sensitive**
60
during puberty when GH levels increase, _______-
IGF1 levels increase in parallel
61
pattern of GH secretion
diurnal pattern low during day, sharp rise at onset of sleep, slowly drop off until waking levels fluctuate, released in pulastile bursts
62
GH production
GHRH acts on somatrophs as a preprohormone
63
GH secretion is stimulated by
androgens: estrogen and teststerone
64
GHRH binds
G protein --> adenulate cyclase, PKA | PKA--> CREB phosphorylation
65
phosphorylated CREB
increases transcription of the gene Pit-1: 1. activates transcription of GH gene 2. up regulates GHRH receptor on somtotroph
66
somatostatin binds
Gi --> decreased adneylate cyclase --> decreased GH synthesis
67
used to clinically evaluate GH status by suppressing somatostatin, allowing unopposed GH secretion
arginine
68
other thing used to evaluate GH status
insulin challenges, as hypoglycemia increases GH
69
GH indirect effects
stimulating production of hepatic IGF-1
70
direct effects of GH
1. anabolic in muscle - -> positive nitrogen balance 2. lipolytic - -> activates hormone sensitive lipase 3. stimulates hepatic gluconeogenesis 4. increases in free fatty acids reduce glucose uptake by peripheral tissues, saving glucose for brain
71
diabetogenic effect of GH
antagonizes action of insulin | oversecretion of GH --> diabetes
72
IGF binding proteins
IGF-BPs 1-6 suynthesized in the liver, mostly IGF-BP3
73
effects of IGF
1. increase lean body mass 2. increase organ size and function 3. increase linear growth of bone
74
GHRH suppression
``` by somatostatin by ultrashort feedback loop of GH (autocrine inhibition of somatotroph) plasma IGF: 1. suppresses somatotroph GH release 2. stimulates somatostatin ```
75
conditions associated with increased plasma GH levels
BOTH abundance of food and scarcity of food
76
fed state with protein
protein synthesis favored, growth favored no change in caloric storage increased GH, IGF, and insulin
77
fed state with carbs
hyperglycemia inhibits GH --> no growth no change in IGF increased insulin --> storage increased caloric storage with no change in protein synthesis or growth
78
fasted state
caloric mobilization (catabolic) and gluocse sparing are favored increased GH --> lipolysis, IGF-BP3 increased glucagon, cortisol --> IGF-BP3 decreased insulin availability of IGF1 limited as more of it bound to IGF-BP3 --> growth is diverted
79
panhypopituitarism
defieciency in more than one anterior pituitary hormone
80
Dwarfism: puberty, IQ, lifespan, body shape
GH deficiency before puberty normal IQ normal lifespan normal/pudgy (loss of GH lipolysis) bodies
81
Laron dwarf MOA
genetic defect in expression of GH receptor --> GH resistant, normal/high serum GH levels Do not produce IGFs/IGF-BPs (due to lack of GH)
82
African pigmy MOA
do not exhibit normal rise in IGFs with puberty delayed rise in IGFs with GH (but some response) partial defect in GH receptors normal serum GH levels
83
acromegaly: puberty, cause, GH/IGF levels, effects
after puberty, after closure of epiphyses --> apositional bone growth tumor of somatotrophs GH hypersecretion, IGF levels increased slow onset, diabetes, prognathism, gynecomastia/lactation (PRL)
84
treatment of acromegaly
surgery octreotide (somatostatin analogues) dopamine analogues GH-receptor antagonists if PRL co-secreted
85
octreotide
somatostatin analogues
86
prognathism
seen in acromegaly, protruding jaw
87
gigantism: puberty, cause, manifestation, cause of death
excess GH before pubetry --> increased linear growth due to ephiphyseal plate stimulation pituitary involvement, tumor, decreased secretion of other hormones hyperinsulinemia, glucose intolerance/diabetses cardiac hypertrophy

Unit 2 Phys II (11 decks)

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