Endo 2 (Pituitary) Flashcards
(35 cards)
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)
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
3
Q
Where is pituitary located?
A
- tuberculum sellae
- hypophyseal fossa
- dorsal sella
- together form the sella turcica where pituitary sits
4
Q
A
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
6
Q
How can pituitary tumours be removed?
A
- goes through nasal cavity and go through sphenoid bone to get to pituitary
- transsphenoidal hypophysectomy
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
8
Q
Do posterior and anterior pituitary communicate?
A
- no
- derived from different tissues
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
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
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
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
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
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)
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
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
What results from too much prolactin?
- 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
How does lactation initiate?
- ducts are inactive
- requires estrogen and progesterone as well as GH, prolactin, and insulin to develop the duct work
27
Lable the diagram and describe the route of the transsphenoidal hypophysectomy
28
Label the diagram
29
What does the superior hypophyseal artery do?
- 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
What kind of blood system supplies the anterior pituitary?
- 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
What is the blood supply to the posterior pituitary?
- inferior hypophyseal artery generates a capillary bed
- neurons put hormones into this capillary bed
- drained by posterior hypophyseal vein
32
What results from too little prolactin?
- 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
-nonlactating mamillary gland
34
-lactating mamillary gland
35
What are the effects of dopamine agonists and antagonists on milk production?
- dopamine agonist will inhibit milk production
- dopamine antagonists cause galactorrhea
