Unit 6 - Introduction to Endocrinology Flashcards Preview

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Flashcards in Unit 6 - Introduction to Endocrinology Deck (27)
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1
Q

what does the fetal-placental unit secrete?

A

human chorionic gonadotrophin - peptide that stimulates corpus luteum to make estrogen and progesterone during early pregnancy

human plagental alctogen - peptide with GH and PRL-like actions

estrogens (mostly estriol) and progesterone

2
Q

how do steroid and peptide-amine hormones differ in:

  • storage pools
  • interaction with cell membrane
  • receptor
  • action
  • response time
A

steroid

  • no pools (made on demand)
  • diffusion thru cell membrane
  • in cytoplasm/nucleus
  • regulation of gene transcription (primarily)
  • hours to days (primarily)

peptide-amines

  • secretory vesicles
  • binding to receptor on cell membrane
  • on cell membrane
  • signal transduction cascade(s) affect variety of cell processes
  • seconds to minutes
3
Q

what is pseudohypoparathyroidism? what can they increase risk for?

A

key defect is abnormality in stimulatory alpha subunit of heterotrimeric G PRO

  • causes impairment of ability of PTH to regulate body Ca and P homeostasis
  • low serum [Ca++] and high serum [PO3] (as if parathyroid glands removed)
  • increased circulating [PTH], just can’t act on target tissue
  • increased risk of hypothyroidism and gonadal dysfunction
4
Q

in what kind of fashion are hypothalamic and pituitary hormones released? (example with GH) what does this mean for hormonal treatment?

A

normally in cyclical fashion

  • GH increases with strenuous exercise, and first few hours of deep sleep
  • so can’t give infusions all at once, but at different times with different amounts
5
Q

what does the hypothalamic-pituitary axis do?

A

exerts central control over multiple endocrine organs

  • pituitary gland (hypophysis) is highly vascularized and lies at base of brain in sella turcica
  • secretion is regulated by hypothalamus via vascular (for anterior) and neural (for posterior) connections
6
Q

how does the hypothalamus connect with the anterior pituitary?

A

adenohypophysis; receives venous blood carrying neuropeptides from hypothalamus and pituitary stalks to different cell types in gland
-axons from hypothalamic nuclei extend to median eminence to release hormones into hypophyseal portal circulation, which carry them directly to anterior pituitary to inhibit/stimulate release of different hormones (PRO or glycoPRO) into systemic blood

7
Q

how does the hypothalamus connect with the posterior pituitary?

A

neurohypophysis; axons from hypothalamic nuclei extend to posterior pituitary, where oxytocin (from paraventricular nucleus) and vasopressin (from supraoptic nucleus) are stored until released into systemic bloodstream

  • posterior pituitary gets arterial blood
  • these hormones are smaller molecular mass peptides associated with neurophysins
8
Q

what is release of anterior pituitary hormones controlled by?

A

hypothalamic releasing factors (except PRL) delivered via portal connection

  • GH is under inhibitory control by somatostatin
  • PRL is inhibited by dopamine
9
Q

what are the releasing factors made in hypothalamus, the target cell, and hormone released by anterior pituitary?

A
  • GHRH (inhibited by somatostatin) targets somatotrophs to release GH
  • TRH targets thyrotrophs to release TSH
  • CRH targets corticotrophs to release ACTH
  • GnRH targets gonadotrophs to release both FSH and LH
  • lactotrophs are constantly inhibited by dopamine and only are “active” during pregnancy to release prolactin
10
Q

what are the targets of posterior pituitary hormones?

A

(PAO)

  • AVP/ADH targets the collecting duct to increase water permeability
  • OT (oxytocin) targets the uterus and breast for milk let down
11
Q

what are the hormones and their target/effects of anterior pituitary?

A

(FLAT P|G)

  • FSH - ovarian follicular cells to make estrogens and progestins; sertoli cells to initiate spermatogenesis
  • LH - ovarian follicular cells to make estrogens and progestins; leydig cells to make testosterone
  • ACTH - fasciculata and reticularis cells of adrenal cortex to make corticosteroids
  • TSH - thyroid follicular cells to make thyroid hormone
  • PRL - mammary glands to initiate and maintain milk production, promote breast development in puberty and pregnancy, and inhibit ovulation
  • GH - multiple somatic tissues
12
Q

are somatotropes and corticotropes acidophilic or basophilic?

A

somatotropes: acidophilic (30% of secreting cells)
corticotropes: basophilic (20% of secreting cells)

13
Q

what is the kind of feedback of the endocrine system?

A

“closed-loop” can be simple or involve hierarchial control

  • senses if it should increase or decrease activity
  • “long-loop” feedback of hormones released from peripheral glands onto hypothalamic-pituitary axis
  • “short-loop” feedback of anterior pituitary hormones feeding back on hypothalamus
14
Q

what does it mean when cell types are “dynamic”?

A

their release depends on hormonal status

-lactotropes make and release PRL during pregnancy)

15
Q

what makes PRL unique from other AP hormones? what happens if stalk is severed? what is its feedback loop?

A

under tonic inhibitory control by dopamine

  • so instead of decreasing levels if pituitary stalk is severed, circulating PRL will increase
  • TRH also stimulates PRL release
  • short loop negative feedback by enhancing hypothalamic dopamine release
16
Q

what do dopamine receptor antagonists and agonists do to PRL?

A

antagonists (D2 antipsychotic agents) will increase PRL (b/c decreased dopamine)

agonists (bromocriptine) inhibit PRL, and is used if have pyerprolactinemia

17
Q

processing of posterior pituitary hormones

A

both made in cell bodies of hypothalamus
-prepropressophysin made in supraoptic nucleus
–cleaved and packaged into propressophysin
–cleaved to ADH in axon to posterior lobe of pituitary
-prepro-oxyphysin made in paraventricular nucleus
–cleaved and packaged into pro-oxyphysin
–cleaved to oxytocin in axon to posterior lobe of pituitary
both released with APs

18
Q

what does oxytocin do?

A
  • stimulates milk ejection/let-down in response to suckling
  • uterine contractions during parturition in response to dilation of cervix
  • secreted in response to sight, smell, sound of infant, and orgasm
19
Q

what’s the primary stimulation for ADH?

A

increased body fluid osmolarity

20
Q

how does ADH regulate body fluid osmolarity?

A

secretion increases if increased serum osmolarity

  • acts on specific cells/regions of kidney to promote water reabsorption involving a receptor V2
  • contraction of vascular smooth muscle by stimulating V1 to increase total peripheral resistance
21
Q

what is central diabetes insipidus?

A

failure of posterior pituitary to secrete ADH

  • produce large volumes of dilute urine
  • body fluids become concentrated
22
Q

what is hypopituitarism? treatment?

A

inability of pituitary gland to produce hormones, or insufficiency of hypothalamic-releasing hormones

  • multiple causes, and unspecific clinical symptoms
  • can be life-threatening and lead to increased mortality
  • patients with TBI or subarachnoid hemorrage are at high risk (may be more common reason than pituitary tumors)
  • treat with hormone replacement therapy
23
Q

what happens if you have corticotropin deficiency?

A

chronic: fatigue, pallor, anorexia, weight loss (hypoglycemia, hypotension, anemia, lymphocytosis, eosinophilia, hyponatremia)
acute: weakness, dizziness, nausea, vomiting, circulatory collapse, fever, shock
children: delayed puberty, failure to thrive

24
Q

what happens if you have thyrotropin deficiency?

A

tiredness, cold intolerance, constipation, hair loss, dry skin, hoarseness, cognitive slowing (weight gain, bradycardia, hypotension)
children: growth retardation

25
Q

what happens if you have gonadotropin deficiency?

A

women: amenorrhea, loss of libido, dyspareunia, infertility (osteoporosis)
men: loss of libido, impaired sexual function, mood impairment, loss of facial/scrotal/trunk hair (decreased muscle mass, osteoporosis, anemia)
children: delayed puberty

26
Q

what happens if you have growth hormone deficiency/

A

decreased muscle mass/strength, visceral obesity, fatigue, decreased quality of life, impaired attention and memory (dyslipidemia, premature atherosclerosis)
children: growth retardation

27
Q

what happens if you have ADH deficdiency?

A

polyuria, polydipsia, polyuria (decrease durine osmolality, hypernatremia)

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