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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
Q

disulfide bridge in ADH and oxytocin is formed by

A

Cysteine residues at positions 1 and 6

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26
Q

plasma half life of ADH and oxytocin

A

short, 8 mins

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27
Q

neurophysin which binds ADH

A

NP II

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28
Q

neurophysin which binds oxytocin

A

NP I

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29
Q

precursor hormone of ADH/oxytocin is cleaved into 3 things

A
  1. ADH/oxytocin
  2. NP
  3. terminal glycoprotein
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30
Q

NP arrangement

A

tetramers which bind 5 ADH

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31
Q

oxytocin has a __________ regulation

A

positive feedback

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32
Q

signals for more oxytocin release are transmitted to

A

cholinergic synapses within PVN and SON

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33
Q

stimulation for oxytocin release

A

stretch of cervix
uterine contraction
suckling of lactating breast

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34
Q

the uterus is more sensitive to oxytocin because ________ which is mediated by _______

A

increased density of OT receptors (OTR)

progesterone and OT

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35
Q

other factor that increases uterine responsiveness

A

increased gap junction formation between smooth muscle cells

36
Q

milk ejection is caused by

A

OT stimulating contraction of myoepitherlial cells

37
Q

what besides suckling can cause milk ejection

A

sight, smell, sound of infant

suckling not required

38
Q

suckling effects on the uterus

A

mediated by oxytocin

contractions promote uterine regression after birth

39
Q

OT effect on the heart

A

causes ANP/BNP release from cardiomyocytes

40
Q

ANP and OT are found in both atria and ventricles but are more prominent in

A

atria

41
Q

BNP is found

A

mainly in ventricles

42
Q

ANP stimulates

A

nitric oxide release from vascular endothelium

kidneys to dump more water, K+, NA+ (OT also has this effect)

43
Q

OT acts on ________ in the heart

A

OT-natriuretic peptide-nitric oxide axis

44
Q

responds to hypertension/hypervolemia by renal baroreceptors or aortic baroreceptor impulses by stimulating oxytocinergic neurons

A

nucleus tractus solitarius

45
Q

oxytocinergic neurons, when stimulated

A

decrease corticotropin releasing factor

induces synthesis of OT in PVN and SON

46
Q

cardiovascular effects of OT

A 
vasodilation
increased NO production (by ANP)
negative chonotrope/inotrope
bradycardia
increase in glucose uptake
47
Q

endocrine effects of ANP/OT at the kidney

A

decreased cortisol, aldosterone, renin

48
Q

prediabetes studies show

A

that OT causes glucose uptake by GLUT4 mechanism not mediated by insulin receptor pathway

49
Q

nitric oxide causes

A

dilation of the coronary resistance vessels

50
Q

OT that acts on the heart can come from

A

Pituitary or local

51
Q

AVP is released

A

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
Q

osmoreceptors are found

A

anterior hypothalamus outside of the blood brain barrier

53
Q

AVP vs thirst?

A

AVP release occurs before stimulation of thirst

54
Q

AVP acts on

A

V2 receptor in kidneys —> increased aquaporins 1-4 –> increased water uptake
V1 receptor –> vasoconstriction

55
Q

firing of baroreceptors

A

is inhibitors to release of AVP

56
Q

baroreceptors also stimulate

A

thirst center

57
Q

senses decreases in blood pressure and causes the release of renin

A

macula densa

58
Q

sensitizes the osmoreceptors leading to enhanced AVP release

A

angiotensin II (from RAAS)

59
Q

which is more sensitive, AVP osmolarity system or AVP blood volume system

A

osmolarity

super sensitive

60
Q

during puberty when GH levels increase, _______-

A

IGF1 levels increase in parallel

61
Q

pattern of GH secretion

A

diurnal pattern
low during day, sharp rise at onset of sleep, slowly drop off until waking
levels fluctuate, released in pulastile bursts

62
Q

GH production

A

GHRH acts on somatrophs as a preprohormone

63
Q

GH secretion is stimulated by

A

androgens: estrogen and teststerone

64
Q

GHRH binds

A

G protein –> adenulate cyclase, PKA

PKA–> CREB phosphorylation

65
Q

phosphorylated CREB

A

increases transcription of the gene Pit-1:

  1. activates transcription of GH gene
  2. up regulates GHRH receptor on somtotroph
66
Q

somatostatin binds

A

Gi –> decreased adneylate cyclase –> decreased GH synthesis

67
Q

used to clinically evaluate GH status by suppressing somatostatin, allowing unopposed GH secretion

A

arginine

68
Q

other thing used to evaluate GH status

A

insulin challenges, as hypoglycemia increases GH

69
Q

GH indirect effects

A

stimulating production of hepatic IGF-1

70
Q

direct effects of GH

A
  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
Q

diabetogenic effect of GH

A

antagonizes action of insulin

oversecretion of GH –> diabetes

72
Q

IGF binding proteins

A

IGF-BPs 1-6 suynthesized in the liver, mostly IGF-BP3

73
Q

effects of IGF

A
  1. increase lean body mass
  2. increase organ size and function
  3. increase linear growth of bone
74
Q

GHRH suppression

A 
by somatostatin
by ultrashort feedback loop of GH (autocrine inhibition of somatotroph)
plasma IGF:
1. suppresses somatotroph GH release
2. stimulates somatostatin
75
Q

conditions associated with increased plasma GH levels

A

BOTH abundance of food and scarcity of food

76
Q

fed state with protein

A

protein synthesis favored, growth favored
no change in caloric storage
increased GH, IGF, and insulin

77
Q

fed state with carbs

A

hyperglycemia inhibits GH –> no growth
no change in IGF
increased insulin –> storage
increased caloric storage with no change in protein synthesis or growth

78
Q

fasted state

A

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
Q

panhypopituitarism

A

defieciency in more than one anterior pituitary hormone

80
Q

Dwarfism: puberty, IQ, lifespan, body shape

A

GH deficiency before puberty
normal IQ
normal lifespan
normal/pudgy (loss of GH lipolysis) bodies

81
Q

Laron dwarf MOA

A

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
Q

African pigmy MOA

A

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
Q

acromegaly: puberty, cause, GH/IGF levels, effects

A

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
Q

treatment of acromegaly

A

surgery
octreotide (somatostatin analogues)
dopamine analogues
GH-receptor antagonists if PRL co-secreted

85
Q

octreotide

A

somatostatin analogues

86
Q

prognathism

A

seen in acromegaly, protruding jaw

87
Q

gigantism: puberty, cause, manifestation, cause of death

A

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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