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ENRE > Hypothalamic-Pituitary Relationships > Flashcards

Hypothalamic-Pituitary Relationships Flashcards

1
Q

What connects the hypothalamus and the pituitary gland?

A

hypophysial stalk

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2
Q

What happens with cancers of the pituitary?

A

expand up hypophyseal stalk into brain and against optic nerves

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3
Q

Where are the cell bodies of the post pit neurons located?

A

supraoptic nucleus (SON) = ADH mostly

Paraventricular nucleus (PVN) = oxytocin mainly

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4
Q

How is the hypothalamus connected to the anterior pituitary?

A

both neural and hormonal

connected by hypothalamic-hypophysial portal vessels

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5
Q

What is distinct about the hormones released from the hypothalamus to the ant pit?

A

delivered directly and in high concentration via hypothalamic-hypophysial portal vessels

hormones do not appear in systemic circulation in high concentration

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6
Q

At what rate are hypothalamic hormones released?

A

in pulsatile manner and are entrained to circadian rhythms

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7
Q

What are the differences btw primary, secondary, and tertiary endocrine disorders?

A

primary = defect in peripheral endocrine gland

secondary = defect in pituitary gland

tertiary = defect in hypothalamus

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8
Q

What are the only 2 ant pit hormones secreted by the same cell type?

A

FSH and LH = secreted by gonadotrophs

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9
Q

What are the stimulating hypothalamic hormones?

A

TRH –> TSH

CRH –> ACTH

GnRH –> LH, FSH

GHRH –> GH

TRH –> prolactin

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10
Q

What are the inhibitory hapothalamic hormones?

A

Somatostatin –> inhibits GH secretion

PIF –> inhibits prolactin secretion

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11
Q

What is acromegaly?

A

prolonged, excessive secretion of GH in adult life

excessive growth of soft tissue, cartilage, and bone in face, hands, and feet

usually pituitary tumor

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12
Q

how does GH affect the liver?

A

stimulates IGF-1 transcription and secretion by the liver –> positive feedback back to the hypothalamus and negative feedback back to ant pit

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13
Q

How is GHRH regulated?

A

negative feedback

it inhibits its own secretion from the hypothalamus

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14
Q

What are the 3 causes of acromegaly?

A

primary GH excess = ant pit tumor

extrapituitary GH excess = tumor secreting GH outside of ant pit

GHRH excess = tumor secreting GHRH (outside hypothalamus?)

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15
Q

How do you diagnose acromegaly?

A

increased serum IGF-1 (measure first bc GH fluctuates thru day, IGF-1 remains constant)

failure to suppress GH after oral glucose tolerance test

pituitary mass seen on brain MRI

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16
Q

How is a pituitary tumor removed?

A

surgery via stranssphenoidal approach

if tumor > 1 cm –> radiation therapy considered

17
Q

What are the medications that can treat acromegaly by lowering GH blood levels or blocking effects of GH?

A

octreotide or lanreotide = somatostatin analog

pegvisomant = GH receptor agonist

bromocriptine/cabergoline: dopamine receptor agaonist; may decrease GH secretion (<25% effective)

18
Q

When is GH secreted?

A

in a pulsatile manner

highest at night

higher during pubertal growth than at any other age

19
Q

What is GH deficiency due to?

A

decreased secretion of GHRH (hypothalamic dysfunction)

decreased GH secretion

failure to generate somatomedins

GH or somatomedin resistance

20
Q

What is the most common cause of GH excess?

what occurs?

A

mostly due to GH-secreting pit adenoma

before puberty: gigantism

after puberty: acromegaly = increased periosteal bone and extremity growth, organ growth, insulin resistance and glucose intolerance

21
Q

What is the diabetogenic effect of GH?

A

increase in blood glucose –> insulin resistance –> decreased glucose uptake and utilization

increased lipolysis in adipose tissue

results in increased blood insulin levels

22
Q

How does GH affect protein synthesis?

A

increases protein syn and organ growth

incr uptake of AAs stim synthesis of DNA, RNA, and protein

mediated by somatomedins (IGF-1)

23
Q

What GH effects are mediated by somatomedins?

A

protein synthesis and organ groth

linear growth due to increased metabolism and proliferation in chondrocytes

24
Q

How does fasting affect GH levels?

A

fasting –> increased GH, decr somatostatin, decr insulin –> decreased protein synthesis and growth –> increased caloric mobilization

25
Q

How does high prolactin affect FSH and LH?

A

high prolactin –> inhibits GnRH from hypothalamus –> decreased FSH and LH

26
Q

How does dopamine affect prolactin?

A

decreases prolactin

27
Q

What is the most common type of functional pit adenoma?

A

FSH and LH secreting –> increased prolactin –> hypogonadism adn galactorrhea

28
Q

what are the 6 types of pituitary adenoma?

A

ACTH-secreting –> cushings

TSH-secreting

GH secreting

prolactinoma

ADH-secreting = diabetes insipidus

non-functioning adenoma

29
Q

What is Sheehan syndrome?

A

postpartum hypopituitarism due to necrosis of pituitary gland

pit gland becomes enlarged during pregnancy –> postpartum hemorrhage causes BP drop –> pit necrosis

pts commonly present w/ agalactorrhea/difficulties in lactation

other hormone abnormalities can happen too

30
Q

How is oxytocin made and regulated?

A

prepro-oxyphysin -(cleavage and packaging into vesicles)-> pro-oxyphysin –> goes down hypothalamic-hypophyseal tract –> oxytocin in post pit –> goes to breast and uterus

31
Q

How is ADH synthesized and secreted?

A

prepropressophysin –> propressophysin –> goes down tract to post pit –> ADH in NPII –> released –> goes to kidney and arterioles

32
Q

What are the triggers of ADH secretion?

A

decreased BP –> cardiac and aortic baroreceptors –> sensory neuron to hypothalamus

decreased arterial stretch –> atrial stretch receptors –> sensory neuron to hypothalamus

increased osmolarity –> hypothalamic osmoreceptors –> interneuron to hypothalamus

33
Q

What is the strongest stimuli to ADH?

A

most sensitive to plasma osmolarity changes

34
Q

How does ADH work in the renal collecting duct?

A

binds V2 receptor = Gs –> Adenylyl cyclase, cAMP –> PkA –> aquaporins added into apical membrane

35
Q

What is diabetes insipidus?

A

lack of ADH or lack of ADH effect on renal collecting duct

lose water = frequent dilute urination

36
Q

What can cause nephrogenic DI?

A

lithium

chronic disorders

*desmopressin tx doesn’t work

37
Q

How is the water deprivation test for DI performed?

A

allow fluids overnight before test and give breakfast w/ no fluids

weigh pt

no fluid for 8 hrs; every 1-2 hr, weigh pt, empties bladder and test urine and plasma osmolarity

if plasma osm > 300 mOsM, STOP

ENRE (21 decks)

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