Endo - Hypothalamus-Pituitary Flashcards

1
Q

things ant pituitary regulates

A
thyroid
adrenals
repro glands
somatic growth
lactation
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2
Q

things post pituitary regulates

A

water metabolism

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3
Q

ant pit aka

A

adenohypophysis

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4
Q

post pit aka

A

neurohypophysis

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5
Q

hypothalamus fxn

A

collect and integrate signals from diverse sources

relay to pituitary

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6
Q

pituitary tumor –> blindness how

A

optic chiasm right above pit

swelling/tumor in pit compress optic nerve –> loss of visual fields/acuity

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7
Q

pit embryology

A

floor of diencephalon grows downward (infundibulum)
secretes factors to induce upgrowth of oral ectoderm (–> Rathke’s pouch)
rathke’s pouch –> adenohypophysis and detaches from oral ectoderm
infandibulum –> neurohypophysis - stays connected by median eminence?

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8
Q

neurons of PP

A

cell bodies in hypothalamus:
suproptic nucleu (ADH)
paraventricular nuclei (oxytocin)
all are magnocellular

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9
Q

ADH fxns

A

maintain ECF osmolarity

maintain blood volume

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10
Q

ADH mech

A

open aquoporin channels in CD of kidneys –> reabsorb water

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11
Q

ADH stimulation mech

A
  1. up ECF osmolarity: sensed by osmoreceptors in hypo –> target V2 receptor in renal cells
  2. down blood vol or BP: sensed by baroreceptors in atria –> target V1 recepors in vascular SM
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12
Q

oxytocin fxns

A

uterine motility

milk release

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13
Q

oxytocin stim + action steps

A
  1. stretch vagina and cervix –> target uterine myometrium

2. suckling –> target myoepithelial cells aroound mammary glands

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14
Q

PP hormones

A

oxytocin

ADH

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15
Q

AP hormones

A
prolactin (PRL)
growth hormone (GH)
thyroid stimulating hormone (TSH)
adenocorticotropic hormone (ACTH)
follicle stimulating hormone (FSH)
lutenizing hormone (LH)
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16
Q

AP cell types (+hormones)

A
corticotroph (ACTH)
thyrotroph (TSH)
gonadotroph (LH, FSH)
somatotroph (GH)
lactotroph (PRL)
17
Q

hypo hormones to AP path

A

parvocellular neurons stim
secreted from terminals in median eminence
hormones into hypophyseal-portal system to AP

18
Q

PRL inhibition

A

tonically inhibited

dopamine binds to D2 receptors on lactotrophs

19
Q

things that cause hyperprolactinemia

A
drugs that block dopamine
lesions that interfere w/ portal blood flow
primary hyperthyroidism (high TRH)
lactotroph adenomas (prolactinomas)
20
Q

PRL actions

A

enhance breast development in pregnancy

induce milk production

21
Q

PRL during preg

A

estrogen stim proliferation of pit lactotroph cells

but lactation is inhibited by high est and progest

22
Q

PRL post partum

A

rapid decline of est and progest allows lactation to start

ovulation may be suppressed due to PRL suppressing gonadotropins

23
Q

GH direct effects

A

action on tissues

lipolysis in adipocytes

24
Q

GH indirect effects

A

anything done by IGF-1

liver/tissue release IGF-1 in response to GH

25
GH feedback loop
GHRH --> GH (AP) --> IGF GHRH inhibit GHRH release, IGF inhibit GH release IGF and GH --> SS
26
GH receptor
cytokine receptor intracellular domain or receptor has protein tyrosine kinase (JAK) Jak cascade protein phosphorylation --> STAT proteins go into nucleus and alter DNA transcription
27
GH effects
``` postnatal growth of bones* (proliferate cart @ epi plates) up lean body mass down fat cell size (lipolysis) up blood gluc up organ size/fxn ```
28
GH stimulating factors
``` down glucose down FAs fasting puberty hormones (est, test) exercise stress alpha-adrenergic agonists ```
29
GH inhibitory factors
``` up glucose up FAs obesity SS beta adrenergic agonists pregnancy ```
30
GH pulses
10 pulses daily peak 1 hr after stage 3 or 4 sleep most in puberty low in elderly/obese
31
GH deficiency (children)
dwarfism retarded skeletal growth poorly developed muscles excessive subcutaneous fat
32
GH deficiency (adults)
``` reduced well-being increased fat mass (central obesity) dyslipidemia up CV disease down bone density ```
33
GH excess (before puberty)
``` gigantism glucose intolerance and hyperinsulinism CV problems (hypertrophy) up infections usually from pit tumors ```
34
GH excess (adults)
acromegaly insidious onset overgrowth of bone/CT --> course features decreased subcutanous fat metabolic derangements (glucose intolerance/diabetes)