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HMS Homeostasis II > Anterior Pituitary Part II > Flashcards

Anterior Pituitary Part II Flashcards

1
Q

The glycoprotein anterior pituitary hormones

A

TSH, LH, and FSH

hCG is also related structurally, but not an anterior pituitary hormone

The α-subunit is identical for all the hormones and consists of 92 amino acids with two carbohydrate side chains. The β-subunit is unique to each of the hormones (although similar in structure) and is what allows them to exert different physiologic effects.

The subunits are synthesized from separate mRNAs (i.e., 2 genes), the hormone is glycosylated and subunits are assembled during processing in the Golgi and secretory granules.

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2
Q

TRH

A

Tripeptide released from the hypothalamus into the hypothalamic-hypophyseal portal system. Stimulates production of both TSH and prolactin from the anterior pituitary.

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3
Q

Regulators of TRH

A

T3 (Triiodothyronine) exerts strong negative feedback on TSH and TRH secretion.

Somatostatin and dopamine from the hypothalamus exert minor inhibitory effects.

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4
Q

Hypothalamic-pituitary-thyroid axis diagram

A
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5
Q

FSH

A

Acts on the gonads, mainly to support the development of the gamete. In women, FSH stimulates growth of the follicle which supports the oocyte. In men, it stimulates Sertoli cells to support spermatogenesis.

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6
Q

Gonadotropes are the only anterior pituitary cell that . . .

A

. . . secretes two hormones. LSH and FSH.

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7
Q

Regulation of FSH

A

Main hypothalamic regulator is gonadotropin-releasing hormone (GnRH) which stimulates both FSH and LH release. It is released in a pulsatile manner starting at puberty and has different effects depending on the frequency of pulses and the presence of other hormones.

FSH secretion is suppressed by inhibins, hormones that are released in proportion to gametogenesis. Sex hormones (estrogen and testosterone) also exert negative feedback on GnRH and FSH secretion.

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8
Q

Hypothalamic-pituitary-gonadal axis

A
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9
Q

LH

A

Acts on the gonads, mainly to support the secretion of sex hormones (estrogen, progesterone and testosterone). In females, promotes formation of the corpus luteum after ovulation. Prior to ovulation, LH (along with FSH) stimulates ovarian estrogen secretion and, in the corpus luteum, stimulates both estrogen and progesterone secretion. Finally, the LH levels surge in mid-cycle to cause ovulation.

In males, LH stimulates Leydig cells in the testes to produce testosterone.

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10
Q

Menstrual cycle summary

A
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11
Q

Regulation of LH

A

Main hypothalamic regulator is gonadotropin-releasing hormone (GnRH) which stimulates both FSH and LH release. It is released in a pulsatile manner starting at puberty and has different effects depending on the frequency of pulses and the presence of other hormones.

Unlike the other pituitary hormones, there is positive feedback on LH secretion at certain times during the female menstrual cycle. In brief, estradiol at very high levels can cause an INCREASE in LH secretion.

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12
Q

Estrogen and LH

A

Low estrogen causes inhibition of LH

High estrogen causes positive feedback of LH by a separate mechanism

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13
Q

Prolactin

A

Effects glandular tissue of the breast, where it stimulates breast development and milk production in women. Prolactin suppresses GnRH / LH / FSH secretion but the importance of this effect in healthy individuals is unclear.

Highly structurally related to GH and human placental lactogen.

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14
Q

Regulation of prolactin

A

The main hypothalamic regulator of growth hormone secretion is dopamine which inhibits prolactin release. It is the only anterior pituitary hormone with an inhibitory hypothalamic regulator.Prolactin itself increases dopamine secretion, thus exerting negative feedback on its own secretion.

Stimulated by sleep, sucking on the breast, estrogen, TRH, ADH, oxytocin, and others.

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15
Q

Hypothalamic-Prolactin axis

A
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16
Q

Summary of anterior pituitary hormones (table)

A
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17
Q

Typical visual deficit resulting from mass effect of pituitary tumor on optic chiasm

A

Bitemporal hemianopia

Starts as superotemporal visual field loss if optic chiasm is compressed from below

Starts as inferotemporal visual field loss if optic chiasm is compressed from above

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18
Q

Syndrome resulting from compression of the cavernous sinus

A

Symptomatic aspects come from the compression of oculomotor nerves (impairing ocular movement and causing double vision) and the facial nerve, which may cause ptosis.Pupillary dilation is also common.

Trigeminal nerve is less commonly affected. When they are, the symptom is mainly facial numbness or pain

The internal carotid also runs through this area, but it is not usually affected due to its thick walls. Inflammation in the area may lead to thrombus generation, in which the clinical presentation would be stroke.

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19
Q

Stretching of the dura in the context of pituitary adenoma

A

Stretching of the sellar diaphragm is sensed as headaches that are usually described as retro-orbital and dull.

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20
Q

Invasion of pituitary adenoma into the sphenoid sinus

A

Can present as epistaxis, CSF leakage, and/or meningitis.

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21
Q

Invasion of pituitary adenoma into the hypothalamus

A

Hypothalamic injury typically results in a syndrome characterized by disturbances of circadian rhythm, appetite, thirst, sleep, temperature and mood.

Diabetes insipidus that results from hypothalamic damage is especially difficult to treat since these patients may not perceive thirst.

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22
Q

Diabetes insipidus

A

Uncommon disorder that causes an imbalance of fluids in the body. This imbalance makes you very thirsty even if you’ve had something to drink (polydypsia). It also leads you to produce large amounts of urine (polyuria)

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23
Q

Causes of sellar and suprasellar masses

A

Quite a large and diverse differential. Certainly pituitary adenomas, but also cancers of any other local structure, cysts, sarcoidosis, bacterial abscess, TB, eosinophilic granulomatosis, lymphocytic histiophysitis, metastases, etc, etc.

Often the final diagnosis is only made after surgical resection.

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24
Q

How common are pituitary adenomas?

A

As high as 22.5% on autopsies, however the clinically significant number is more like 0.1% or less in prevalence.

10-15% of all cranial tumors.

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25
Q

Pituitary adenomas

A

Slow-growing, usually benign tumors. Divided into functioning (hormone-producing) and non-functioning (non-hormone-producing).

Non-functioning present due to mass effect syndromes in the sellar and suprasellar region or destruction of functional parts of the pituitary.

Functioning present with overactive hormone secretion syndromes.

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26
Q

Multiple Endocrine Neoplasia 1 (MEN-1)

A

Autosomal dominant condition caused by mutations in the MEN1 gene

Genetic syndrome that presents with frequent pituitary adenomas and other endocrine adenomas, including parathyroid, gastrointestinal neuroendocrine, insulinomas, carcinoids, gastric parietal cell (gastrin-secreting), and nonfunctioning neuroendocrine tumors. The bolded are most common.

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27
Q

Relative frequency of pituitary adenomas

A
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28
Q

Craniopharyngioma

A

Benign tumor that arises from remnants of Rathke’s pouch. Usually suprasellar with solid and cystic components and sometimes calcifications.

Commonly present in childhood, with a second peak around age 55-65.

Present similarly to non-functioning adenomas with headaches / visual symptoms or pituitary hypofunctioning. Poor growth is often a presenting symptom in childhood craniopharyngiomas. Higher indicence of hypothalamic injury due to location.

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29
Q

In pregnancy, there is growth of ___

A

In pregnancy, there is growth of lactotropes

and a marked increase in prolactin levels to prepare the breasts for lactation postpartum.

30
Q

Cushing syndrome

A

Excess cortisol secretion. Patients present with weight gain, hypertension, striae, acne, proximal myopathy, bruising, diabetes. Can be adrenal, pituitary, hypothalamic, or paraneoplastic in origin. Common paraneoplastic sources are lung cancer, carcinoids, and other neuroendocrine tumors.

31
Q

Diagnosing Cushing syndrome`

A
  1. Confirm that there is too much cortisol
    • Measure salivary cortisol late at night (11pm-midnight) (normally low)
    • Measure the morning cortisol in the blood after you give dexamethasone 1 mg the night before (normally low)
    • 24-hour urine collection for urinary free cortisol measurement
  2. Confirm that the etiology is ACTH excess by measuring an ACTH level
  3. Distinguish ectopic ACTH from pituitary ACTH excess
    • Dexamethasone suppression challenge (pituitary adenomas will often suppress ACTH levels in response to high doses of dexamethasone),
    • Inferior petrosal venous sampling (measurement of ACTH levels at different areas of the venous system)
    • Imaging
32
Q

Treating Cushing syndrome

A
  • Surgical resection of tumor
  • Pasireotide (somatostatin analog)
  • Inhibitors of adrenal steroidogenesis (metyrapone, ketoconazole and mitotane)
  • Antagonists of the cortisol receptor (mifepristone)
  • Surgical bilateral adrenalectomy (will cause Nelson syndrome)
33
Q

Nelson syndrome

A

Due to the loss of negative feedback from high levels of cortisol, tumor growth can accelerate leading to very high ACTH levels (with resulting skin pigmentation due to co-secretion of other peptides acting on the melanocytes) and mass effects.

Radiation is sometimes used to prevent or treat this phenomenon

34
Q

Hyperprolactinemia

A

Prolactinomas are the most common functioning pituitary adenoma and a common cause of hyperprolactinemia. Other causes include agents that act as dopamine antagonists, “stalk effect”, and primary hypothyroidism (due to TSH’s co-stimulation of prolactin production).

Symptoms include galactorrhea, hypogonadism (resulting from prolactin suppression of FSH/LH) which presents as reduced libido and erectile dysfunction in men and oligo- / amenorrhea in women, as well as infertility and osteopoenia due to lack of sex hormones.

35
Q

Stalk effect

A

Presence of a lesion that disrupts the flow of hypothalamic regulatory hormones from the hypothalamus to the anterior pituitary

Commonly leads to lack of dopamine reaching the pituitary, resulting in hyperprolactinemia

36
Q

Treatment of prolactinomas

A

Unlike most pituitary adenomas, prolactinomas are not usually treated with surgery. Instead, treatment takes advantage of endocrine regulation of lactotroph growth and production of prolactin. Treatments include:

Bromocriptine and Cabergoline (both oral dopamine receptor agonists)

If these fail, then surgery is attempted instead. Occasional invasive prolactinomas may need radiation therapy

37
Q

Bromocriptine side effects

A

Stem from systemic activity. Nausea and vomiting, presumably because the area postrema in the medulla, which stimulates nausea and lies outside the blood–brain barrier, possesses dopamine receptors.

Known to be relatively safe for pregnancy, and so this is the drug of choice for women trying to conceive.

38
Q

Cabergoline side effects

A

Has been associated with valvular heart disease at higher doses (those used to treat Parkinson’s).

The advantages of cabergoline include a weekly or bi-weekly dosing interval and less frequent gastrointestinal adverse effects.

39
Q

Excess of TSH, FSH, LH

A

Pituitary tumors secreting the glycoprotein hormones are very rare.

TSH-producing pituitary tumor: Present w/ hyperthyroidism (weight loss, heat intolerance, palpitations) and will have a high or high-normal TSH value

Male patients with LH / FSH secreting tumors: increase in testosterone / testicular size.

Female patients with LH / FSH secreting tumors: menstrual irregularities

Some pituitary tumors will only secrete the α-subunit of TSH/FSH/LH; these are hormonally silent.

40
Q

Syndrome of Inappropriate ADH (SIADH)

A

Leads to excess free water reabsorption at the kidneys, leading to hypo-osmolality / hyponatremia which can lead to subtle mental status changes, fatigue, nausea, forgetfulness, confusion and, in severe cases, seizures and death.

Unlike the anterior pituitary hormones, excess of posterior pituitary hormones is not due to pituitary adenomas. Instead, it is most commonly related to other cranial or pulmonary causes, or medication effects. How these cause SIADH is poorly understood.

41
Q

Diagnosing SIADH

A
  • Ruling out “mimics” – thyroid disease and adrenal insufficiency
  • Confirming an elevated urine sodium level / urine osmolality in the setting of dilute plasma
  • ADH cannot be easily measured for technical reasons, and it is therefore not part of the diagnostic work-up
42
Q

Treating SIADH

A
  • Fluid restriction
  • Increase solute intake (usually increasing protein or salt intake in the food or by adding sodium chloride tablets or oral urea)
  • In rare cases, use of a vasopressin receptor antagonist. Conivaptan (mixed V1a and V2 receptor antagonist) and tolvaptan (specific V2 receptor antagonist) are vasopressin receptor antagonists that are approved for SIADH-induced hyponatremia
  • Demeclocycline (a tetracycline antibiotic) and lithium are two other pharmacologic treatments that have been used to treat SIADH, but are now rarely used to lack of efficacy and side effect profile
43
Q

Conivaptan

A

A mixed V1a and V2 receptor antagonist approved for use in euvolemic and hypervolemic hyponatremia (including SIADH).

Available orally.

44
Q

Tolvaptan

A

A specific V2 receptor antagonist approved for use in heart failure and SIADH.

Available orally.

45
Q

Central adrenal insufficiency

A

ACTH deficiency leading to cortisol deficiency

46
Q

Central hypothyroidism

A

TSH deficiency leading to T3/T4 deficiency

47
Q

Hypogonadotropic hypogonadism

A

LH/FSH deficiency leading to estrogen/progesterone/testosterone and gamete deficiency

48
Q

Growth hormone deficiency

A

Children will have short stature and low growth velocity.

Adults may have no symptoms, or symptoms of lower muscle mass, increased fat distribution, fatigue, osteoporosis, and adverse changes to blood lipids

49
Q

Diagnosing ACTH deficiency

A
  • Measure cortisol at 8am (when the level should be high)
  • Administer synthetic ACTH (cosyntropin stimulation test) and measure the cortisol level 30-60 minutes later (should be high)
  • Insulin tolerance test - Administer insulin to achieve hypoglycemia (glucose level <50 mg/dL). This will lead to a stress response with secretion of ACTH and also growth hormone in healthy patients. This test is quite uncomfortable for the patient and requires close monitoring to avoid seizures or cardiovascular events, and is therefore not commonly done.
50
Q

Diagnosing growth hormone deficiency

A
  • IGF-1 levels: This is not a very sensitive test, as many individuals with GH deficiency may have IGF-1 levels that are within the normal range.
  • Insulin tolerance test: Administer insulin to achieve hypoglycemia (glucose level <50 mg/dL). This will lead to a stress response with secretion of ACTH and also growth hormone in healthy patients. This test is quite uncomfortable for the patient and requires close monitoring to avoid seizures or cardiovascular events, and is therefore not commonly done.
  • Arginine stimulation test, or arginine-GHRH stimulation test: These agents should stimulate the secretion of growth hormone; patients with GH deficiency show a failure to see a sufficient rise of growth hormone.
51
Q

Treating hypopituitarism

A
  • Hormone replacement therapy!!!
  • Except for growth hormone, the hormone provided is usually the hormone produced by the target organ, rather than the pituitary stimulatory hormone (since they are proteins and can’t be taken orally)
52
Q

Thyrotropin

A

Recombinant TSH. Not usually used to treat secondary hypothyroidism, but rather is commonly used in conjunction with radioactive iodine treatment of thyroid cancer. Thyrotropin is administered before radioactive iodine therapy to maximize uptake of radiolabeled 131I isotope into thyroid tissue in patients with thyroid cancer. This approach enables the administration of smaller quantities of radioisotope, maintaining maximum radiation exposure specifically to thyroid tissue with less radiation exposure to other tissues.

53
Q

Endocrine regulation for IVF

A

FSH is used to stimulate ovulation for in vitro fertilization.

Two US Food and Drug Administration (FDA)-approved formulations are available. Urofollitropin is purified FSH isolated from the urine of postmenopausal women, and follitropin is a recombinant form of FSH. Both agents effectively stimulate ovulation but may cause ovarian hyperstimulation syndrome.

54
Q

Treating GH deficiency

A

Usually treated with GH replacement, although it often is not treated at all in adults. Usually treated with somatotropin, aka recombinant GH.

Typical dosing schedules involve daily subcutaneous or intramuscular injection. Somatropin therapy is costly and thus approved for use in the United States only for specific indications. Confirmed GH deficiency or panhypopituitarism (at least three hormonal axes affected) is required for approval.

Recombinant IGF-1, aka mecasermin, is an effective treatment for patients with GH insensitivity (so-called Laron dwarfism). Mecasermin is also approved for use in patients with GH deficiency and antibodies against growth hormone.

55
Q

Panhypopituitarism

A

Loss of at least three normal pituitary hormonal axes

56
Q

Pituitary apoplexy

A

Refers to acute intrapituitary hemorrhage. Can occur in patients with a preexisting adenoma, in women suffering a post-partum hemorrhage (called Sheehan syndrome), or in other circumstances.

Symptoms are sudden and can be severe. Patients often have pituitary insufficiency.

Treatment often includes surgery to decompress the optic chiasm, although some patients can be observed if there are no symptoms. In most cases, hormone replacement therapy, especially with a glucocorticoid, needs to be initiated emergently.

57
Q

Empty sella

A
  • A partially or completely empty sella is often an incidental MRI finding
  • Pituitary function is usually normal but some may develop hypopituitarism insidiously.
  • Some cases may be due to a silent infarction of a prior mass, with subsequent involution leaving an empty sella behind. In other cases, the finding may be due to intracranial hypertension.
58
Q

Idiopathic / Congenital hypogonadotropic hypogonadism

A
  • group of genetic disorders leading to a deficiency in GnRH/FSH/LH, with patients presenting with symptoms of hypogonadism
  • The most famous syndrome is Kallman syndrome, where there is a deficiency in the migration of GnRH neurons from the olfactory placode to the hypothalamus. This leads to both anosmia (lack of smell) and hypogonadism. It is X-linked.
  • Treatment consists of replacement of sex steroids. If fertility is desired, hCG (acting on the LH receptor) and FSH can be administered.
59
Q

Steroid-induced ACTH deficiency

A

Due to negative feedback, exogenous steroids suppress CRH and ACTH production.

If the exogenous steroid therapy is prolonged, there will have been atrophy of the corticotropes and also of the adrenal cortex. Thus, there will be a delay in re-achieving normal levels of endogenous glucocorticoids. During this period of delay, the patient has central adrenal deficiency and can develop symptoms of adrenal insufficiency, including an adrenal crisis.

 To avoid serious effects, exogenous steroids should be weaned if the treatment duration is longer than 3 weeks. A very slow wean may be necessary in long courses - regeneration may take up to 18 months.

60
Q

Posterior pituitary hormone deficiency and resulting diabetes insipidus

A

ADH deficiency leads to diabetes insipidus (DI). The name refers to the production of large amounts of insipid (tasteless) urine (to distinguish it from diabetes mellitus).

Patients with DI have a deficiency in ADH secretion (cranial DI) or a resistance to the action of ADH (nephrogenic DI). In the absence of ADH, patients are unable to concentrate their urine, so they create large amounts of dilute urine. If for whatever reason the patient cannot concommitantly increase intake in water, hypernatremia may result.

61
Q

Diagnosing ADH deficiency

A
  • Confirmation of polyuria (>3 L/day of urine output)
  • Rule out other causes of polyuria:
    • Diabetes mellitus
    • Primary polydipsia
    • A water restriction test: Consists of measuring serial plasma and urine sodium / osmolality levels while the patient is not drinking any water. Urine should become more concentrated in a patient with proper ADH and renal function.
    • To distinguish cranial from nephrogenic diabetes insipidus, exogenous ADH can be administered
  • ADH itself cannot be measured for technical reasons
62
Q

Treatment of ADH deficiency / corticogenic diabetes insipidus

A
  • Exogenous ADH
  • Desmopressin (ddAVP) stimulates the V2 receptors in the renal collecting tubule. Can be administered orally or as a nasal spray, or even intravenously/subcutaneously/intramuscularly. Main side effect is hyponatremia due to impaired free water excretion.
63
Q

Treatment of nephrogenic diabetes insipidus

A
  • Diuretics such as amiloride or hydrochlorothiazide
  • The proposed mechanism by which these diuretics prevent excessive loss of free water is paradoxical: they induce a volume-contracted state, which promotes enhanced absorption of water in the proximal tubule and thereby decreases delivery of water to the site of ADH resistance, the collecting ducts
64
Q

Summary of pituitary hormone excess and deficiency syndromes

A
65
Q

In men, LH is primarily responsible for ___ while FSH is primarily responsible for ___.

A

In men, LH is primarily responsible for regulation of testosterone production while FSH is primarily responsible for production of spermatozoa.

66
Q

___ is what initiates a new menstrual cycle following menses.

A

The climb in FSH when its inhibitory endocrine regulators disappear is what initiates a new menstrual cycle following menses.

67
Q

Dr. Hamnvic’s menstrual cycle diagram

A
68
Q
A
69
Q

Pituitary stem cell lineages

A
70
Q

The two pituitary lines that you cannot live without

A

Thyrotropes and corticotropes

These are endocrine emergencies

71
Q

Counter-regulatory glucose hormones

A

Hormones that are stimulated by hypoglycemia and in turn activate glucose mobilization from energy stores

Includes growth hormone, glucagon, cortisol, and epinephrine.

72
Q

If you cut off someone’s pituitary, will they develop diabetes insipidus?

A

No!! Because the hypothalamus is where vasopressin is produced and it can still release it into the bloodstream via other axons or regrown axons.

Unless, however, there is also hypothalamic damage. Worst case scenario is hypothalamic damage and organum vasculosum of the lamina terminalis (OVLT)/supraoptic crest damage (loss of thirst).

HMS Homeostasis II (35 decks)

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