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Physio Endocrinlogy Quiz 1 > Hypothalamus and Pituitary > Flashcards

Hypothalamus and Pituitary Flashcards

1
Q

What is the embryonic origin of the anterior lobe of the pituitary?
What are the 2 subdivisions of the anterior lobe?
What is the embryonic origin of the posterior lobe of the pituitary?
What are the 3 subdivisions of the posterior lobe?

A
  • Anterior lobe: Pharyngeal ectoderm invaginates from roof of oral cavity (Rathke’s pouch) to develop adenohypophysis with two discrete divisions: the anterior and intermediate lobes—epithelial glandular tissue and produces specific hormones.
  • Posterior lobe: Outpocketing of diencephalon forms neurohypophysis which includes the median eminence, pituitary stalk, and the neural lobe. Neural lobe made up of nerve terminals and glial cells, called pituicytes.
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2
Q

What is the Neural Lobe of the posterior pituitary?

A

• Neural lobe made up of nerve terminals and glial cells, called pituicytes.

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3
Q

What are the boundaries of the hypothalamus: anteriorly, latteraly, posteriorly?
The hypothalamus extends dorsally to where?
What is the most dorsal nuclei of the hypothalamus?

A
  • bounded anteriorly by optic chiasm and supraoptic nuclei(SON)
  • laterally by optic tracts and medial forebrain bundles
  • posteriorly by mammillary bodies
  • extends dorsally to the roof of the third ventricle.
  • Paraventricular neurons (PVN) form most dorsal nuclei of hypothalamus.
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4
Q

What is the hypothalamic supraoptic-paraventricular-neurohypophysial tract (HNS)?

A
  • large neurons originating in SON and PVN.
  • Axons course posteriorly toward pituitary gland, through median eminence and infundibular stalk, and terminate near an expanded pars nervosa which serves as a storage organ.
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5
Q

What does the hypothalamic supraoptic-paraventricular-neurohypophysial tract (HNS) do?

A

• synthesis and release of hormones oxytocin and vasopressin

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6
Q

What is the Hypothalamic Hypophysiotropictract (HHS)?

A

• small neurons of medial basal hypothalamus near the third ventricle which terminate in external zone of median eminence and proximal portion of pituitary stalk adjacent to the primary capillary plexus of the hypophysial portal system. These neurons are the source of the releasing factors or hormones which regulate the secretion of specific adenohypophysial hormones.

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7
Q

What does vasopressin do (generally)? How does its function relate to oxytoxin’s function? What is arginine vasopressin versus lysine vasopressin? What is Deaminio-8-D-arginine vasopressin used for?

A

Vasopressin is a potent antidiuretic and pressor hormone, but it also has some intrinsic oxytoxic (uterine muscle contraction) and milk ejection activity, and conversely oxytocin exerts a slight antidiuretic and vasopressor effect. Arginine vasopressin is the form found in Homo sapiens and most other mammals; lysine vasopressin is found in the pig family. Deamino-8-D-arginine vasopressin (DDAVP) is a useful therapeutic synthetic analogue with potent and prolonged antidiuretic activity and greatly reduced blood pressure effects.

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8
Q

Where are OT and VP synthesized?

A
  • OT and AVP (Arginine) are synthesized in separate magnocellular neurons of the SON and PVN and each hormone is associated with a specific larger (~10 kD) “carrier” protein called neurophysin (NP).
  • Note: both OT and VP are synthesized in both SON and PVN
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9
Q

Are VP and OT bound to plasma proteins in the circulation?

A

• VP and OT are not bound to plasma proteins in the circulation.

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10
Q

What is Deamino-8-D-arginine vasopressin (DDAVP)?

A

• a useful therapeutic synthetic analogue with potent and prolonged antidiuretic activity and greatly reduced blood pressure effects

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11
Q

Vasopressin is a potent antidiuretic and pressor hormone, but it also has some intrinsic oxytoxic (uterine muscle contraction) and milk ejection activity, and conversely oxytocin exerts a slight antidiuretic and vasopressor effect.

What hormone and hormone related molecules are found in the terminals of vaspressin and oxytocin nerons, respectively?

A
  • Vasopressin (VP), VP-associated neurophysin, glycopeptide (39 amino acid long)
  • Oxytocin, OT-associated neurophysin
  • Note: these are all released into the blood stream
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12
Q

What are VP-neurophysin, glycopeptide, and OT-neurophysin?

A
  • Vasopressin production begins with a precursor that includes vasopressin, VP-neurophysin, and glycoprotein. The latter two are cleaved to form VP
  • The same with Oxytocin
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13
Q

What are the peripheral roles of vasopressin? What are the respective receptors?

A
  • ADH via V2 receptor
  • Pressor agent via V1a receptor (increases blood pressure)
  • Increases ACTH release via V1b receptor
  • Note there is also a fourth action (not covered in this class)
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14
Q

What are the ideal blood circulating levels of vasopressin to activate V2 (ADH) vs V1a (pressor) receptors?

A
  • plasma levels of 10-20 fmol/ml result in maximum antidiuresis (compared to 1-4 fmol/ml in the normally hydrated state)
  • > 50 fmol/m are associated with pressor effects
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15
Q

What is the pathway for ADH via V2 receptors?

A

• Vasopressin binds to G-protein receptors of basolateral side of cells. Gs activates Adenylyl Cyclases ==> cAMP ==> insertion of aquaporin ==> H2O travels through pores passively due to osmosis

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16
Q

What is the pathway for pressor agent via V1a receptor (increases blood pressure)

A
  • Contracts small arteries and arterioles
  • G protein ==> phospholipase C (PL-C) cleaves PIP2 ==> IP3 and DAG. IP3 ==> increase free cytoplasmic Ca++ and constricts smooth muscle vasculature
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17
Q

What stimulates AVP (arginine vasopressin) release?

A

• an increase in the osmolality of the blood sensed by “osmoreceptors” located in the anterior hypothalamus adjacent to the SON and PVN.

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18
Q

Thought question: what would happen if you infused hypertonic saline solution into the internal carotid artery or ventricle?

A
  • stimulates the release of AVP. Increased electrical activity of SON and PVN neurons, occurs as a result of a rise in osmotic pressure of the extracellular fluid.
  • Note: Direct electrical stimulation of the neurons also causes the release of hormone from the pars posterior pituitary.
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19
Q

What inhibits AVP/ADH release?

A
  • Atrial stretch receptors release ANP which inhibites ADH/AVP
  • Arterial baroreceptors in the carotid sinus and aortic arch
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20
Q

What feedback mechanisms are more long term vs short term ECFV?

A
  • atrial stretch receptors are important in the regulation of extracellular fluid volume
  • osmoreception is more important in regulating the minute-to-minute secretion of antidiuretic hormone.
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21
Q

What are the effects of chronic dehydration on posterior pit stores of AVP? What about overhydration?

A
  • Dehydration leads to depletion of hormone stores in the posterior pituitary.
  • Overhydration leads to to hypotonicity of blood and inhibits the release of vasopressin.
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22
Q

Does AVP also have effects within the brain? What are they?

A
  • AVP neurons extend to many other parts of the brain and spinal cord
  • vasopressin acts as a hormone as well as a central nervous system neurotransmitter and/or neuromodulator, coordinating diverse systems for an integrated physiological response. For example, AVP is a dypsogen
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23
Q

What is the pathway for increasing ACTH release via V1b receptor

A
  • small neurons, not part of the magnocellular system, but in the paraventricular nuclei, contain VP. Their axons terminate in the median eminence and stimulate anterior pituitary corticotropes
  • G protein receptor, cAMP stimulation to release ACTH synergistically with corticotropin-releasing hormone (CRH)
  • AVP dramatically enhances the action of CRH
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24
Q

What is the half-life of AVP in humans? In pregnant women?

A
  • About 3 minutes
  • Hormone needs to constantly be replaced
  • Prego women break down AVP faster
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25
Q

Explain the release and action of OT with regard to milk let down.

A
  • when mammary gland nipples are stimulated by an infant
  • reflex from nerves in the nipple, through spinal cord and midbrain, to OT neurons in the SON and PVN triggering oxytocin secretion from the posterior pituitary.
  • Myoepithelial cells in the mammary gland acini are stimulated to contract, whereupon milk is forcefully ejected from the mammary ducts.
  • Note: stress can inhibit OT
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26
Q

Explain OT release and action during parturition.

A

Reflex from dilating cervix and contracting uterus stimulaterelease of oxytocin
• oxytocin secretion reaches maximum at the time of parturition.
• Although the role of oxytocin in the initiation of labor has not been established, parturition is expedited if exogenous OT is administered

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27
Q

How does progesterone interact with oxytocin?

A
  • Progesterone blocks OT from activating OT receptors
  • Since progesterone production by the placenta decreases towards the end of pregnancy, the influence of OT to increase motility of the uterus at a certain point may no longer be suppressed.
  • Local progesterone levels may maintain a quiescent uterus.
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28
Q

How does cortisol affect parturition?

A

• Cortisol produced by the fetus may trigger termination of pregnancy by suppressing placental progesterone and increasing estrogen and prostaglandin secretion.

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29
Q

What is oxytocinase and how does it affect gestation and parturition?

A

• Although the sensitivity of the uterus to OT increases as parturition draws near, increased plasma “oxytocinase” activity during pregnancy may keep oxytocin below threshold levels.

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30
Q

How is OT related to female and male coitus and reproduction?

A
  • coitus results in OT release
  • Sperm transport may be facilitated by uterine and oviduct motility during the follicular phase when estrogen secretion predominates and when ovulation is imminent.
  • OT in the male increases the ejaculatory response during coitus by stimulating genital duct musculature.
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31
Q

What are some emotional effects of OT?

A

• OT is known as the “love hormone”.

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32
Q

Explain hypothalamic (central) diabetes insipidus and nephrogenic diabetes insipidus

A
  • Central is deficient in AVP/ADH production
  • Nephrogenic has either deficient V2 receptors or abnormal aquaporin 2
  • Both lead to excessive dilute urine
  • Opposite of SIADH
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33
Q

Explain Syndrome of Inappropriate Secretion of ADH (SIADH)

A
  • Excessive amounts of vasopressin
  • Severe hyponatremia
  • Often caused by ectopic secretion due to cancer
  • Opposite of diabetes insipidus
34
Q

What are the 6 key hypophysiotropic peptides?

A
  • 1) thyrotropin releasing hormone (TRH)
  • 2) luteinizing hormone releasing hormone (LHRH) also known as gonadotropin releasing hormone (GnRH)
  • 3) somatostatin (SS) the growth hormone release inhibiting hormone(GHRIH)
  • 4) corticotropin releasing hormone (CRH)
  • 5) urocortins 1, 2, and 3 (not sure what this is or why prolactin inhibiting hormone is not listed)
  • 6) growth hormone releasing hormone (GHRH).
35
Q

How does the destruction of the basal hypothalamus, interruption of the hypophysial portal circulation, or transplantation of the pituitary gland to a peripheral site affect anterior pituitary hormone release?

A
  • increased secretion of prolactin and decreased secretion of the other anterior pituitary hormones.
  • The hypothalamus exerts a net inhibitory effect on prolactin (PRL) secretion and a net stimulatory effect on the secretion of growth hormone (GH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH).
36
Q 
What do each of the hypophysiotropic hormones affect both major/minor and positive negative?... GnRH
GHRH
GHIH (somatostatin)
TRH
PIH (dopamine)
CRH
A
  • GnRH releases LH and FSH
  • GHRH releases GH
  • GHIH (somatostatin) inhibits both GH and TSH release (also inhibits pancreas and GI tract)
  • TRH releases both TSH and PRL
  • PIH (dopamine) inhibits PRL
  • CRH releases ACTH
  • Note: GHRH and CRH release one and only one hormone. PIH inhibits one hormone. Other releasing hormone affect more than hormone
37
Q

Where are the cell bodies of the small neurons that innervated the anterior pituitary? Where do their axons terminate?

A
  • Near the third ventricle in the medial basal hypothalamus.

* Their axons terminate in the external layer of the median eminence in close association with capillaries.

38
Q

What is the median eminence?

A
  • part of the inferior boundary for the hypothalamus atop the pituitary stalk
  • bounded on its posterolateral region by the cerebral peduncles and on its anterolateral region by the optic chiasm.
  • The median eminence is one of the seven areas of the brain devoid of a blood–brain barrier
  • It is sometimes considered one of the circumventricular organs
39
Q

What is the pars tuberalis?

A

• The pars tuberalis is part of the anterior lobe of the pituitary gland, and wraps the pituitary stalk in a highly vascularized sheath.

40
Q

What is the tuber cinereum?

A

• hollow eminence of gray matter situated between the mammillary bodies and the optic chiasm. The tuber cinereum is part of the hypothalamus.

41
Q

What are the mamillary bodies?

A

a pair of small round bodies, located on the undersurface of the brain that form part of the limbic system.
• located at the ends of the anterior arches of the fornix.
• consist of two groups of nuclei, the medial mammillary nuclei and the lateral mammillary nuclei.
• Neuroanatomists have often categorized the mammillary bodies as part of the hypothalamus.

42
Q

What is the infundibulum?

A
  • The pituitary stalk is the connection between the hypothalamus and the posterior pituitary.
  • The hypothalamichypophesial tract travels through this.
43
Q
  • The pituitary stalk is the connection between the hypothalamus and the posterior pituitary.
  • The hypothalamichypophesial tract travels through this.
A
  • the infundibulum of the hypothalamus and a rich capillary network supplied by the anterior hypophysial artery and drained by the hypophysial portal veins.
  • An epithelial component, the pars tuberalis of the adenohypophysis, covers the surface of the tuber cinereum and pituitary stalk.
44
Q

What are some of the general functions of the hypophysiotropic hormones?

A
  • stimulating hormone release
  • stimulate cell differentiation and growth, hormone synthesis
  • sometimes inhibit hormone secretion.
45
Q

Receptors. When the neuropeptides secreted into the hypophysial portal blood reach the anterior pituitary cells, they bind to specific plasma membrane receptors and activate adenylate cyclase/cyclic AMP/cyclic GMP and/or phosphatidylinositol /Ca++ mechanisms.

A

Receptors. When the neuropeptides secreted into the hypophysial portal blood reach the anterior pituitary cells, they bind to specific plasma membrane receptors and activate adenylate cyclase/cyclic AMP/cyclic GMP and/or phosphatidylinositol /Ca++ mechanisms.

46
Q

Are the secretion of hypophysiotropic hormones consistent throughout the day? How does this influence the number of hypophysioreceptors in the hypophysis?

A
  • pulsatile or episodic which appears to maintain an optimum number of their receptors on pituitary cells
  • continuous administration leads to down regulation of specific receptors.
  • (Receptor number is also influenced by other hormones acting directly on pituitary cells.)
47
Q

Hypophysiotropic neurons are regulated by both hormonal and neural stimuli, including sensory information emanating from the external and internal environment to the hypothalamus

A

Hypophysiotropic neurons are regulated by both hormonal and neural stimuli, including sensory information emanating from the external and internal environment to the hypothalamus

48
Q

Explain NEURAL CONTROL OF THE HYPOTHALAMUS

A
  • Releasing factor cell bodies are in the lateral hypothalamus. There are ascending and descending nerves that communicate with the medial forebrain bundle.
  • Afferents arise from the medial forebrain bundle, amygdala, and the hippocampus (limbic system)
  • The limbic complex provide pathways for brain stem and cortical impulses to reach the hypothalamus.
49
Q

Adrenocorticotropic activity appears to be regulated by limbic afferents. Stimulation of the amygdaloid nuclei results in ____ release while hippocampal structures tend to inhibit the ___ neurons.

A
  • ACTH

* CRH

50
Q

What are the “short loop” and “long loop” feeback loops for pituitary hormones?

A

The short loop is the pit hormones directly inhibiting the hypothalamus
The long loop is the pit hormones affecting their target organs and the products of their target organs inhibit the hypothalamus

51
Q

What are the hormone producing cells of the anterior pituitary?

A
  • Corticotrope (ACTH)
  • Somatotrope (GH)
  • Lactotrope (PRL)
  • Thyrotrope (TSH)
  • Gonadotrope (LH and FSH)
52
Q

What are the three structural classifications of Anterior Pituitary hormones?

A
  • Pro-opiomelanocortin (POMC) polypeptides
  • Glycoproteins
  • Somatomammotropic proteins
53
Q

What are the products of Pro-opiomelanocortin (POMC) polypeptides? Explain their relationship.

A
  • Adrenocorticotropin (ACTH, corticotropin) (main product)
  • melanocyte-stimulating hormones (α-MSH and β-MSH)
  • β- and γ-lipotropins
  • α-, β- and γ-endorphin
  • The original pro-opiomelanocortin is one peptide that is cleaved different ways into its various products by the corticotope cells
54
Q

What are the Glycoproteins of the anterior pituitary?

A
  • thyroid-stimulating hormone (thyrotropin, TSH)
  • luteinizing hormone (lutropin, LH, interstitial cell-stimulating hormone, ICSH
  • follicle stimulating hormone (follitropin,FSH)
  • Note: human chorionic gonadotropin (hCG), although a product of the trophoblastic cells of the placenta, is included with this group because of its structural and functional similarities.
55
Q

Explain the alpha and beta chain relationships of the anterior pituitary glycoprotein hormones (and hCG, too)

A
  • Their alpha chains are identical and highly conserved
  • Their beta chains provide specificity
  • Both chains are necessary
56
Q

What are the Somatomammotropic proteins of the anterior pituitary?

A
  • growth hormone (GH, somatotropin, STH)
  • prolactin (PRL)
  • somatomammotropin (placental lactogen) is also included with this family due to structural similarities
57
Q

What are the targets and actions of Adrenocorticotropic Hormone (ACTH)?

A
  • membrane receptors in the zona fasciculata and zona reticularis of the adrenal cortex
  • increased production-release of glucocorticoids (e.g., cortisol
58
Q

What is the mechanism of steroidogenesis caused by ACTH?

A
  • Steroidogenesis is stimulated through increased conversion of cholesterol to pregnenolone.
  • mediated by an increase in intracellular cyclic AMP.
59
Q

Does ACTH always mediate through cAMP?

A
  • ACTH also exercises trophic effects (growth-promoting activity, RNA increases, protein increases) on other target cells
  • this trophic activity is not mediated through changes in cyclic AMP.
60
Q

What are normal Plasma concentratios of ACTH and when is the diurnal peak and nadir?

A
  • < 50 pg/ml
  • diurnal variation peak between 6 A.M. and 8 A.M.
  • nadir in the evening between 6 P.M. and 11 P.M.
61
Q

ACTH is composed of 39 amino acid residues. Explain the functions of
Amino chains 1 through 10, 4 through 10, 5 through 24.
Amino chain 11 through 24

A
  • 1-24ACTH contains essentially all of the steroidogenic activity of the molecule.
  • 1-10ACTH, 4-10ACTH and 5-24ACTH have the capacity to stimulate maximum steroidogenic activity in target cells although very high concentrations are required.
  • 11-24ACTH is completely inactive but has the capacity to inhibit ACTH activity when given in large amounts.
  • Therefore4-10ACTH is the portion of ACTH required for activation of receptors, and 11-24ACTH is that portion of the hormone involved in binding to the receptors without being able itself to activate them.
62
Q

Explain production/release of ACTH is Regulated by

1) Negative feedback
2) Positive stimulation
3) neurogenic stimulation

A

(i) Negative (-) feedback of cortisol at pituitary and hypothalamus.
(ii) Positive (+) regulation from hypothalamus by corticotropin-releasing hormone (CRH). Also urocortins 1,2 and 3 that act through CRH type 1and or type 2 receptors- Urocortins are important in long-term stress and anxiety.
(iii) Neurogenic stimuli pain, anxiety, pyrogen, hypoglycemia, vasopressin. Stress causes dramatic increases in the plasma levels of ACTH.

63
Q

How is β-MSH is formed?

A

• β-MSH is formed by the intracellular breakdown of β-lipotropin and γ-lipotropin.

64
Q

What is production/release of MSH activity is regulated by?

A
  • The same factors influencing production/ release of ACTH (described above).
  • (ii) The positive (+) influence of MSH releasing factor (MRF) from the hypothalamus.
  • (iii) The negative (-) influence of MSH release-inhibiting factor (MIF) from the hypothalamus.
65
Q

What are the effects of β-endorphin?

A

• lowers body temperature, produces analgesia, and can induce a state of catatonia (suspended animation) for up to 5 hours.

66
Q

What are enkephalins?

A
  • Another group of opioid peptides are the enkephalins, i.e., metenkephalin and leuenkephalin.
  • The structure of metenkephalin is found within β-lipotropin, but both enkephalins are now known to be generated from precursors other than POMC.
67
Q

Endorphins (endogenous morphines). These peptides (opioid peptides) all appear to be fragments of β-lipotropin. They are products of neurons in the central nervous system, although anterior pituitary corticotropes may release β-endorphin into the general circulation.

β-endorphin (61-91LPH)

α-endorphin (61-76LPH)

γ-endorphin (61-77LPH)

Opiate receptors were first demonstrated in the limbic system, and endorphins seem to be the endogenous ligands for these receptors.  α- and β-endorphins when injected into the brain of an experimental animal have opposite effects on body temperature and arousal
A

Endorphins (endogenous morphines). These peptides (opioid peptides) all appear to be fragments of β-lipotropin. They are products of neurons in the central nervous system, although anterior pituitary corticotropes may release β-endorphin into the general circulation.

β-endorphin (61-91LPH)

α-endorphin (61-76LPH)

γ-endorphin (61-77LPH)

Opiate receptors were first demonstrated in the limbic system, and endorphins seem to be the endogenous ligands for these receptors.  α- and β-endorphins when injected into the brain of an experimental animal have opposite effects on body temperature and arousal
68
Q

Glycoprotein Hormones (TSH, LH, FSH, hCG)
Each glycoprotein hormone is comprised of two peptide chains, the α-chain and the β-chain held together by non-covalent bonds (H-bonds, π-π interactions).
Both chains are required for biological activity.
α-chains of LH, FSH and TSH are identical, and comprised of 89 amino acid residues. The α-chain of hCG has an identical sequence with 3 additional amino acid residues at the N-terminus.
The β-chain of each hormone has a unique structure and these β-chains are comprised of between 110 amino acid residues (FSH) and 145 amino acid residues (hCG).

αLH + βTSH = thyrotropic activity
αTSH + βLH = luteotrophic activity
The following conclusions were reached:

(i) The α-chain must fulfill some important function because this structure has been rigidly conserved for the different hormones. It is now known that the C-terminal region (α83-92) of this component is largely responsible for activating the hormone-receptor complex once binding has taken place.
(ii) The specificity conferred by the β-chain seems to be for receptor binding. Despite differences between the β-chains, some of them show considerable homology. This explains why hCG can promote testosterone production by combining with and activating LH receptors in Leydig cells.

A

Glycoprotein Hormones (TSH, LH, FSH, hCG)
Each glycoprotein hormone is comprised of two peptide chains, the α-chain and the β-chain held together by non-covalent bonds (H-bonds, π-π interactions).
Both chains are required for biological activity.
α-chains of LH, FSH and TSH are identical, and comprised of 89 amino acid residues. The α-chain of hCG has an identical sequence with 3 additional amino acid residues at the N-terminus.
The β-chain of each hormone has a unique structure and these β-chains are comprised of between 110 amino acid residues (FSH) and 145 amino acid residues (hCG).

αLH + βTSH = thyrotropic activity
αTSH + βLH = luteotrophic activity
The following conclusions were reached:

(i) The α-chain must fulfill some important function because this structure has been rigidly conserved for the different hormones. It is now known that the C-terminal region (α83-92) of this component is largely responsible for activating the hormone-receptor complex once binding has taken place.
(ii) The specificity conferred by the β-chain seems to be for receptor binding. Despite differences between the β-chains, some of them show considerable homology. This explains why hCG can promote testosterone production by combining with and activating LH receptors in Leydig cells.

69
Q

What is the Mechanism of Action of glycoprotein hormones?

A

• through interaction with cell membrane receptors, and subsequent activation of the adenylate cyclase or inositol phosphate pathways.

70
Q

What does FSH do?

What does LH do?

A
  • FSH promotes gametogenesis in the testis, and follicle growth and estrogen (E2) synthesis in the ovary.
  • LH induces testosterone production by Leydig cells, the interstitial cells of the testis, and in the ovary luteinization of mature follicles resulting in formation of corpora lutea and estrogen (E2) and progesterone (P) production.
71
Q

What are the positive controls of FSH and LH? What are the negative controls? (short answer)

A
  • Positive: GnRH
  • Positive: high E2
  • Negative: E2 and progesterone
  • Negative: testosterone
  • Negative: inhibin produced by the Sertoli cells
  • Negative: stress is generally negative
72
Q

What are the positive controls of FSH and LH? What are the negative controls? (complete answer)

A
  • Positive (+) effects of GnRH (LHRH, LRF, LHRF, gonadoliberin) from the hypothalamus. The concentration and duration of GnRH action is important here because high and sustained concentrations can actually inhibit the release of the gonadotropins.
  • (ii) Positive (+) feedback of high E2 concentrations at both hypothalamus and pituitary prior to ovulation.
  • (iii) Negative (-) feedback of E2 and progesterone at the level of both the hypothalamus and pituitary.
  • (iv) Negative (-) feedback of testosterone in the hypothalamus and pituitary.
  • (v) Negative (-) feedback of inhibin produced by the Sertoli cells of the seminiferous tubules in males and in the ovarian follicle. Human inhibin is a 130 amino acid polypeptide inhibiting FSH specifically.
  • (vi) Neurogenic stimuli from the CNS. e.g., stress is generally negative.
73
Q

Note: the total stores of FSH and LH is released over a 12 - 24 hour period. Daily production

A

Note: the total stores of FSH and LH is released over a 12 - 24 hour period. Daily production

74
Q

TSH acts on the thyroid gland to promote production/release of the thyroid hormones (T4 and T3). It also stimulates cellular growth and an increased activity of a large number of metabolic processes in the gland.

A

TSH acts on the thyroid gland to promote production/release of the thyroid hormones (T4 and T3). It also stimulates cellular growth and an increased activity of a large number of metabolic processes in the gland.

75
Q

What are the postive and negative controls of TSH?

A
  • Negative: T3
  • Positive: TSH-releasing hormone (TRH, thyroliberin)
  • Neurogenic stimuli from the external environment… like a street sign that says: release T3
76
Q

What does Human Chorionic Gonadotropin (hCG) do?

A
  • maintains the corpus luteum during early pregnancy.
  • It is produced in large quantities during the first trimester of pregnancy.
  • It maintains the production of progesterone and estrogen by the corpus luteum until the role of this production is taken over by the placenta itself.
77
Q

What does Prolactin (PRL) do?

A
  • main function of PRL in humans is the initiation of lactation
  • weak general somatotropic activity
  • It has no known specific function in males although it has recently been suggested that PRL potentiates the action of LH and testosterone in the male reproductive tract.
78
Q

What are normal plasma levels of PRL?

A
  • The mean plasma levels in prepubital children, men and non-pregnant women are normally below 10 ng/ml. PRL levels rise in plasma throughout pregnancy.
  • The plasma half-life of PRL is 20-30 minutes, liver and kidneys being important sites of degradation.
79
Q

What are the positive and negative controls of prolactin?

A
  • Negative: prolactin release-inhibiting factor (PIF, prolactostatin). This is currently thought to be dopamine.
  • Positive: TRH
  • Positive: estrogens
  • Neurogenic input: Suckling at the breast stimulates PRL secretion via sensory pathways impinging upon the hypothalamus, which probably turns off PIF (dopamine) activity.
  • Prolactin then stimulates milk formation over the next 4 hours, so that it will be available at the next feeding. Such things as surgical stress can also cause release of prolactin.
80
Q

Explain the generally inhibited nature of prolactin.

A
  • The major influence of hypothalamic secretion on prolactin is inhibitory.
  • Hence, if the influence of the hypothalamus on lactotrope cells is removed by transplanting the pituitary to another vascular site, there is increased secretion of the hormone.
  • For comparion, in such a transplanted pituitary, the production/release of all other pituitary hormones is drastically diminished.

Physio Endocrinlogy Quiz 1 (6 decks)

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