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Anatomy > Endo 2 (Pituitary) > Flashcards

Endo 2 (Pituitary) Flashcards

1
Q

What are the areas of the pituitary?

A

Anterior

  • adenohypophysis (true gland since it’s epithelial tissue)
  • arises from an outgrowth of the ectoderm of the roof of the mouth

Posterior

-neurohypophysis (made up of neurons- terminal axons that start in hypothalamus called neurosecretory cells)

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2
Q

How do the anterior and posterior pituitary develop?

A
  • ectoderm: embryonic layer that gives rise to CNS/PNS and integument
  • mesenchyme: undifferentiated cells
  • ectoderm: gives rise to roof of mouth
  • pouches begin to form called neurohypophyseal bud and Rathke’s pouch (hypophyseal pouch)
  • these buds come together and form anterior and posterior pituitary
  • pars intermedia is tissue between them
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3
Q

Where is pituitary located?

A
  • tuberculum sellae
  • hypophyseal fossa
  • dorsal sella
  • together form the sella turcica where pituitary sits
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4
Q
A
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5
Q

Describe pituitary tumours

A
  • mainly occur in adenohypophysis (neural tissue in neurohypophysis is postmitotic)
  • can lead to compression of optic chiasm (can lead to diplopia)
  • can be functional that release hormones or non functional that just take up space
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6
Q

How can pituitary tumours be removed?

A
  • goes through nasal cavity and go through sphenoid bone to get to pituitary
  • transsphenoidal hypophysectomy
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7
Q

When is blood flow to pituitary compromised? What happens?

A
  • inferior and superior hypophyseal arteries are branches off of the internal carotid artery
  • entire systemic BP has dropped dramatically (during labour and delivery, car accident)
  • if it drops in superior/inferior hypophyseal artery there might not be enough pressure to push blood through to pituitary
  • panhypopituitarism
  • low pressure in capillaries so hard to keep enough pressure to keep blood moving to pituitary
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8
Q

Do posterior and anterior pituitary communicate?

A
  • no
  • derived from different tissues
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9
Q

What are the hormones of the posterior pituitary?

A
  • oxytocin
  • antidiuretic hormone
  • both hydrophilic so they act on cell surface receptors
  • peptide hormones, 9 amino acids in length
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10
Q

What does ADH do?

A
  • tells kidney to reabsorb water so you don’t lose it (prevents diuresis)
  • maintains hydration
  • also known as vasopressin- high concentrations can directly stimulate smooth muscle of BVs to cause vasoconstriction
  • released from supraoptic nucleus (right above optic chiasm) of the hypothalamus
  • puts water permeable pores in the collecting duct of the kidney to bring in as much water as possible
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11
Q

When is ADH stimulated to release or inhibited?

A
  • released in response to increased osmolarity of the blood (lots of salts and dissolved minerals in the blood but not a lot of water)
  • low BP and low blood volume (kidneys will reabsorb water to maintain some of that blood volume)
  • pain and certain drugs (pain- usually follows a cut or injuries where you might lose blood volume)
  • inhibited by adequate or over hydration of the body and alcohol
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12
Q

How does alcohol affect ADH?

A
  • alcohol inhibits release of ADH from hypothalamus
  • causes inappropriate dehydration because it does not stop diuresis so you urinate more
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13
Q

How is oxytocin released?

A
  • neurosecretory cell in paraventricular nucleus of the hypothalamus
  • oxytocin made in cell body of hypothalamus
  • neural signals stimulate release (stretch on cervix, suckling on breast) from the hypothalamus to the posterior pituitary
  • released into blood stream
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14
Q

What are hormones of the anterior pituitary?

A
  • TSH: released in response to TRH from hypothalamus
  • FSH: stimulates development of follicles in ovaries, promotes sperm production in response to GnRH from hypothalamus
  • LH: release casued by GnRH and leads to sex hormone production in the gonads
  • ACTH: released by CRH in hypothalamus and causes cortisol release

*above are tropic hormones- turn on some other gland*

  • hGH: somatotropin- turns up growth of body released in response to GHRH (inhibited by GHIH)
  • prolactin: release caused by PRH and inhibited by PIH (not a tropic hormone)
  • MSH: causes melanocytes to make melanin (not really sure why it’s here)
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15
Q

How is hGH released?

A
  • GHRH produced in hypothalamus and travels through portal system to get to anterior pituitary to cause hGH release
  • GHIH produced in hypothalamus also
  • net effect of GHIH and GHRH determines how much GH will be released in the end
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16
Q

How is GH regulated?

A
  • GHRH produced in hypothalamus causes GH to be produced in anterior pituitary
  • causes bone growth, muscle growth, tissue repair (stress in body causes GH release as an anticipatory response)
  • as GH levels rise it shuts release of GHRH
  • GHIH can also reduce amount of GH released
17
Q

When is GH level highest?

A
  • more sleep you get, more GH gets released in the night
  • lets tissues repair and grow
18
Q

How does GH communicate with liver? How is this regulated?

A
  • tells liver to release glycogen into glucose
  • low blood glucose levels also causes release of GHRH to talk to anterior pituitary to release GH
  • GH causes more rapid breakdown of glycogen into glucose which gets released into the blood
  • use stored glucose for tissue repair
  • blood glucose levels will start to rise
  • as blood glucose levels rise, it will turn off the release of GHRH in hypothalamus
  • GHIH stimulus is hyperglycemia so it will be released then to reduce GH release which reduces glycogen breakdown and lowers blood glucose levels
19
Q

What would be effect of having a GH secreting tumour on glucose levels?

A
  • GH promotes hyperglycemia so it will cause hyperglycemia
  • could develop diabetes mellitus
20
Q

How is GH involved in long bone growth?

A
  • long bones grow at epiphyseal plate until 20
  • GH tells cartilage to continue growing then this cartilage ossifies
  • at puberty, testosterone and estrogen stop how much the cartilage is growing so that ossification catches up and the growth plate disappears
  • when cartilage is gone can’t grow bone any further
21
Q

What arises from gigantism?

A
  • occurs before puberty
  • hyperglycemia, diabetic ulcers
  • if GH levels are still high after puberty, other areas of body respond to GH where there is still cartilage
  • dermis can become thick because of GH, cartilaginous areas continue to grow so get exaggerated features (face, hands, feet)- called acromegaly
  • internal organs keep growing
  • puts stress on lower back
22
Q

How are sex steroids regulated? What do they do?

A
  • GnRH produced in hypothalamus and released when sex steroids are low
  • GnRH travels through portal system to anterior pituitary
  • causes release of LH and FSH in anterior pituitary
  • go to gonads and promote production of follicles, sperm (FSH) and testosterone, estrogen, progesterone (LH)
  • sex steroids have multiple effects (lipophilic so works on nucleur receptors); increased sex drive (acting on hypothalamus), secondary sexual characteristics (body hair, muscle growth, fat development)
  • as sex steroid levels go up, negative feedback shuts off release from hypothalamus and anterior pituitary
23
Q

How does OC pill work?

A
  • OC contain estrogen/progesterone or progesterone
  • provides stimulus to hypothalamus/anterior pituitary that there are enough sex steroids so stop release of GnRH, FSH, LH
  • prevents follicles from developing so then you can’t ovulate an egg
24
Q

How is prolactin regulated? What are the stimuli?

A
  • released in response to PRH from hypothalamus
  • prolactin production in anterior pituitary which causes milk production
  • PIH (aka dopamine) from hypothalamus can inhibit
  • suckling stimulates PRH release and prolactin release
  • PIH stimulated by high levels of estrogen and progesterone
  • during pregnancy, placenta produces a lot of estrogen and progesterone which feeds back to hypothalamus to release PIH
  • estrogen and progesterone are needed during development to develop the duct work but then prolactin is needed to turn on the milk production
  • when placenta is delivered, you lose estrogen and progesterone so PIH doesn’t have a big signal so we have PRH which causes milk production
25
Q

What results from too much prolactin?

A
  • infertility/reduced fertility
  • in females, when prolactin is high it stops release of GnRH so you aren’t releasing LH and FSH (amenorrhea)
  • galactorrhea (males and females)
  • impotence in males is common since testosterone production is often inhibited (gynecomastia is not a common symptom of excess prolactin although you would think so)
26
Q

How does lactation initiate?

A
  • ducts are inactive
  • requires estrogen and progesterone as well as GH, prolactin, and insulin to develop the duct work
27
Q

Lable the diagram and describe the route of the transsphenoidal hypophysectomy

A
28
Q

Label the diagram

A
29
Q

What does the superior hypophyseal artery do?

A
  • starts near hypothalamus
  • creates vascular bed at base of hypothalamus that collects releasing hormones that the hypothalamus is creating and shuttles them down to the anterior pituitary

**anterior and posterior pituitary have separate blood supplies**

30
Q

What kind of blood system supplies the anterior pituitary?

A
  • from superior hypophyseal artery, blood enters into hypophyseal portal veins then is drained through anterior hypophyseal veins
  • portal system (two capillary beds connected)
  • high BP in artery dissipates in capillary bed and becomes less pressure entering the veins
  • if it goes into another capillary bed, the pressure drops even more
31
Q

What is the blood supply to the posterior pituitary?

A
  • inferior hypophyseal artery generates a capillary bed
  • neurons put hormones into this capillary bed
  • drained by posterior hypophyseal vein
32
Q

What results from too little prolactin?

A
  • poor or absent milk production in women who should be lactating (block the PIH/dopamine receptors with domperidone, this will cause more milk)
  • infertility/subfertility associated with hypoprolactinaemia in men and women
33
Q
A

-nonlactating mamillary gland

34
Q
A

-lactating mamillary gland

35
Q

What are the effects of dopamine agonists and antagonists on milk production?

A
  • dopamine agonist will inhibit milk production
  • dopamine antagonists cause galactorrhea

Anatomy (27 decks)

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