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24 Cards in this Set

  • Front
  • Back
where's the pituitary?
you know where
you know where
what does the pituitary look like?
*posterior part is an extension of the brain (neurohypophysis)
*anterior part gets brain input from neurohormones through portal circulation
*posterior part is an extension of the brain (neurohypophysis)
*anterior part gets brain input from neurohormones through portal circulation
explain the 2 parts of the pit.:
*Anterior: “adenohypophysis” originates from Rathke’s pouch (pharyngeal epithelium); neurons from the hypothalamus secrete releasing factors directly into portal vein to regulate pituitary hormone synthesis and release

*Posterior: “neurohypophysis” originates from neural tissue (extension of hypothalamus); consists of axons of neurons from the supraoptic and paraventricular nuclei that deliver hormones to posterior lobe for release
Molecular Regulation of Pituitary Development (chart):
*initial factor: HesX-1; acts on stem cells to start anterior pituitary development
*CRH-->ACTH
*HesX-1--> PROP-1 --> PIT-1
*PROP-1 --> FSH/LH
*PROP-1 suppresses HesX-1

*Mutations in HesX-1 halt this process! Called "multiple pituitary hormone deficiency" You only see the posterior pituitary in these patients.
Molecular Regulation of Pituitary Development:
Transcriptional activators direct embryonic development of the anterior pituitary; inactivating mutations produce multiple pituitary hormone deficiencies (MPHD)
Expression of HESX1 gene is very early (stem cells); role in optic nerve and anterior pituitary development
PROP1 is also early, required for repression of HESX1 and is prerequisite for PIT1
PIT1 discovered as activator of GH promoter; expressed throughout life
stuff the pit makes:
Anterior Pituitary Cell Types:
*Somatotrophs- GH-secreting cells, make up ~50% of the cell mass

*Lactotrophs- PRL-secreting cells, make up ~10-25% of the cell mass; proliferation accounts for increase in pituitary size during pregnancy

*Thyrotrophs- TSH-secreting cells, make up <10% of cell mass

*Corticotrophs- ACTH-secreting cells, make up 15-20% of cell mass

*Gonadotrophs- LH and FSH-secreting cells, making up 10-15% of cell mass
Hypothalamic Releasing Hormones:
*Regulate Anterior Pituitary Hormones
*Regulate Anterior Pituitary Hormones
Anterior Pituitary Hormones 3 Major “Families”:
*GH/Prolactin
Single chain polypeptides
Internal disulfide bridges

*TSH/LH/FSH
Glycoproteins: share an alpha subunit
Unique beta subunits
HCG (made in placenta)

*POMC (pro-opiomelanocortin)
Hydrolyzed into ACTH, ß-endorphin, MSH
regulation of GH secretion:
releasing factor- GHRH
inhibitory factor- Somatostatin
target tissues- liver, muscle, fat, bone (mostly liver)
feedback- IGF-1 feedback to pit and hypothalamus
releasing factor- GHRH
inhibitory factor- Somatostatin
target tissues- liver, muscle, fat, bone (mostly liver)
feedback- IGF-1 feedback to pit and hypothalamus
Normal daily secretion of GH:
Normal lifetime secretion of GH:
Regulation of GH (more complex boney slide)
*stomach--> empty stomach--> ghrelin--> more GH (positive feedback)
*stomach--> empty stomach--> ghrelin--> more GH (positive feedback)
Actions of Growth Hormone:
IGF-1 has a role in all these tissues EXCEPT adipose tissue
Functions and Regulation of GH (text):
*Regulation:
Hypothalamic: GHRH, SMS; pulsatile overnight Peripheral: IGF-I (somatomedin), Ghrelin
Irregular/intermittent release during sleep

*Activation:
Hypoglycemia, starvation, exercise, stress, sleep

*Action: Direct (1) vs Indirect (2)
1. Metabolic: lipolysis, protein synthesis, insulin resistance
2. Growth: IGF-I

*Mechanism: GHBP/GH Receptor dimerization
interaction of GH with receptors:
ALP= Acid labile subunit
ALP= Acid labile subunit
Overview of prolactin secretion factors:
releasing factor- TRH
inhibitory factor- Dopamine (more potent than TRH!)
target tissues- breasts (milk production/release)
feedback- prolactin (decreases dopamine)
Prolactin Regulation and Action:
*Regulation:
-Tonic inhibition by dopamine (neurons in hypothalamus and posterior pituitary)
-Stimulated by pregnancy, breast feeding, TRH
-PRL increases DA (negative feedback)

*Action:
-Proliferation, branching mammary ducts during puberty
-Growth, development mammary alveoli in pregnancy
-Milk production: suckling (positive feedback)
talk about that posterior pituitary...
talk about that posterior pituitary...
*Extension of Hypothalamus
*Terminal nerve fibers from hypothalamic supraoptic and para-ventricular nuclei

*Transported by carrier protein (neurophysin) to nerve terminals in posterior pituitary and released from granules by exocytosis into circulation

*Vasopression (ADH): water, BP
*Oxytocin: milk letdown, uterine contraction
Vasopressin:
*9 amino acid peptide, AVP, synthesized primarily in supraoptic nuclei, transported/stored posterior pituitary

*Controlled by
-osmolality (osmoreceptors in hypothalamus)
-vascular volume/pressure (baroreceptors in heart)

*Receptors determine action:
1. V1 aka V1a (vessels: vaso-constriction)
2. V2 (renal tubule: water re-absorption, sic “anti- diuretic hormone”; also increases factor VIII)
3. V3 aka V1b (corticotrophs: increase ACTH secretion)
effect of plasma osmolality on ADH:
-makes you thirsty
effect of blood pressure on ADH:
-takes a huge loss of pressure to elicit ADH
-osmolality has a greater effect on ADH than pressure
-takes a huge loss of pressure to elicit ADH
-osmolality has a greater effect on ADH than pressure
Vasopressin (AVP) Mechanism of Action:
*classic G PRO coupled receptor.
*AQP2= aquaporin 2
*ADH uses AQP2 to move H2O from urine to plasma.
*classic G PRO coupled receptor.
*AQP2= aquaporin 2
*ADH uses AQP2 to move H2O from urine to plasma.
problems you can have or acquire related to Water Regulation (Diabetes Insipidus):
Central DI: you don't make ADH
nephrogenic DI: the problem is in the kidney