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Endo Repro Exam > Pituitary Gland and Hypothalamus > Flashcards

Pituitary Gland and Hypothalamus Flashcards

1
Q

hypothalamus - anatomy

A

*located in brain at the intersection of cortex, cerebellum, and brainstem

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2
Q

hypothalamus - functions

A

*maintains homeostasis by coordinating endocrine and nervous system to regulate:
1. thirst
2. reproduction
3. stress
4. autonomic function
5. energy/metabolism
6. appetite
7. temperature
8. blood pressure
9. circadian rhythm

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3
Q

hypothalamus - embryology

A

*derived from the diencephalon (from the forebrain/prosencephalon)

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4
Q

hormones produced by the hypothalamus

A
  1. releasing hormones:
    -TRH, GHRH, GnRH, CRH
    -target tissue = anterior pituitary
  2. inhibitor hormones:
    -dopamine (prolactin inhibiting factor)
    -somatostatin (growth hormone inhibiting factor)
    -target tissues = anterior pituitary (both) and GI tract (somatostatin)
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5
Q

pituitary gland - anatomy

A

*has anterior and posterior portions, with a thin intermediate lobe between
*located outside the dura, below the optic chiasm in the sella turcica; can be accessed through the back of the nose (sphenoid bone)
*pituitary stalk (infundibulum) passes through the dura, connects hypothalamus & pituitary gland

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6
Q

anterior pituitary gland - embryology

A

*aka adenohypophysis
*derived from Rathke’s pouch, ectoderm from the roof of the developing mouth (epithelial in origin)
*glandular tissue; can PRODUCE hormones

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7
Q

posterior pituitary gland - embyrology

A

*aka neurohypophysis
*derived from an evagination of diencephalon: neuroectoderm
*neural tissue; STORES hormones

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8
Q

clinical correlation of pituitary gland embyrology

A

*oral ectoderm (Rathke’s pouch) travels upward and diencephalon moves down to form the pituitary gland
*apoptosis occurs at base of Rathke’s pouch

note - persistence of Rathke’s pouch may result in craniopharyngioma

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9
Q

craniopharyngioma - overview

A

*most common supratentorial tumor of childhood
*occurs due to persistence of Rathke’s pouch during embryogenesis
*often contains calcifications
*can interfere with the pituitary’s ability to secrete hormones (hypopituitarism)

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10
Q

hypothalamic & pituitary circulation: hypophyseal portal system

A
  1. hypothalamus releases hormones into primary capillary plexus, which then travel to secondary capillary plexus in anterior pituitary
  2. long hypothalamic neurons trigger release of hormones (ADH and oxytocin) stored in the posterior pituitary into a capillary plexus
  3. lack of blood-brain barrier around neuroendocrine structures near ventricles allows for rapid hormone transport and tight regulation
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11
Q

vulnerability of anterior pituitary gland to hypotension

A

*anterior pituitary gland lacks direct arterial blood supply → increased risk of INFARCTION in the setting of hypotension

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12
Q

anterior pituitary - composition

A

composed of many cells:
*somatotrophs → produce GH
*lactotrophs → produce prolactin
*corticotrophs → produce ACTH
*gonadotrophs → produce FSH, LH
*thyrotrophs → produce TSH

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13
Q

hypopituitarism - overview

A

*refers to under-secretion of one or more pituitary hormones:
*the hormones most critical to sustain life are cortisol (regulated by ACTH) and thyroid hormones, T3/T4 (regulated by TSH)
*acute treatment = screen for and treat cortisol and thyroid hormone deficiency
*if present, could also treat ADH, gonadotropin, and growth hormone deficiencies, but these hormones are not essential for life

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14
Q

hypopituitarism - potential causes

A

*secretory or non-secretory pituitary adenoma, craniopharyngioma, brain injury, radiation
*Sheehan syndrome, empty sella syndrome, pituitary apoplex, medication-induced

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15
Q

Sheehan syndrome - overview

A

*ischemic infarct of the pituitary following postpartum hemorrhage
*susceptible from physiologic pregnancy-induced pituitary growth
*presentation: failure to lactate, amenorrhea, cold intolerance, hypotension, shock, hyponatremia

recall - a potential cause of hypopituitarism

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16
Q

empty sella syndrome (overview)

A

*radiologic finding in which the sella turcica looks empty (filled with CSF) from flattening or atrophy of the pituitary gland
*pituitary may secrete hormone per usual (no atrophy)
*often idiopathic, common in obese females, associated with idiopathic intracranial hypertension

recall - a potential cause of hypopituitarism

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17
Q

pituitary apoplexy - overview

A

*sudden hemorrhage of the pituitary gland, usually in the presence of pre-existing pituitary adenoma
*severe, sudden headache, vision changes (bitemporal hemianopsia, diplopia), hypotension, shock

recall - a potential cause of hypopituitarism

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18
Q

medication-induced hypopituitarism - overview

A

*monoclonal antibody checkpoint inhibitors used in oncology (ipilimumab, pembrolizumab)

recall - a potential cause of hypopituitarism

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19
Q

anterior pituitary hormone families

A

anterior pituitary hormones are peptide hormones with certain hormones sharing structural components:
1. LH, FSH, TSH hormones: heterodimeric glycosylated proteins with alpha and beta subunits
2. ACTH and MSH are derived from a common proopiomelanocortin (POMC) precursor
3. growth hormone and prolactin are structurally similar

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20
Q

anterior pituitary hormone families: FSH, LH, and TSH shared features

A

*the alpha subunit is shared/common (identical)
*the beta subunit determines hormone specificity

clinical correlation: high levels of hCG can stimulate TSH receptors and cause hyperthyroidism

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21
Q

prolactin - overview

A

*non-steroid hormone
*receptor = nonreceptor tyrosine kinase
*produced by anterior pituitary
*structurally homologous to growth hormone
*main function = promotes lactation
*cleared by the kidneys

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22
Q

prolactin - functions

A

*promotes LACTATION:
-promotes mammary gland tissues development, duct proliferation and branching, and initiation of mild production by alveolar cells
-maintains milk production in response to nursing

23
Q

prolactin - regulation

A

*prolactin secretion is continually inhibited by dopamine
*dopamine agonists → INHIBIT prolactin secretion
*dopamine antagonists/inhibitors → STIMULATE prolactin secretion

24
Q

factors that INCREASE prolactin secretion

A
  1. dopamine inhibition / dopamine antagonists
  2. infant crying, nursing, nipple stimulation, chest wall injury
  3. high estrogen levels in pregnancy; estrogen therapy
  4. TRH
25
Q

factors that INHIBIT prolactin secretion

A
  1. dopamine / dopamine agonists
  2. prolactin itself (increases dopamine)
  3. progesterone (blocks receptors at breast during pregnancy)
26
Q

hyperprolactinemia - causes

A
  1. physiologic causes: pregnancy; nipple stimulation, chest wall trauma
  2. pathologic causes: prolactinoma; non-functioning adenoma or other tumor pressing on pituitary stalk; hypothyroidism
  3. medication ADEs: risperidone, phenothiazines, haloperidol, estrogen
  4. renal dysfunction
  5. idiopathic
27
Q

top 3 causes of hyperprolactinemia

A
  1. pregnancy
  2. prolactinoma
  3. medication side effects (from dopamine antagonists: decreased dopamine → increased prolactin secretion)
28
Q

hyperprolactinemia - symptoms

A
  1. premenopausal female symptoms: galactorrhea, infertility, amenorrhea
  2. male symptoms: gynecomastia, infertility, reduced libido, erectile dysfunction

note - can also have visual impairment, if the problem impacts the optic chiasm (near pituitary gland)

29
Q

prolactinoma - overview

A

*a pituitary adenoma characterized by over-proliferation of lactotroph cells of the anterior pituitary gland
*similar presentation as other causes of hyperprolactinemia, PLUS: MASS EFFECT:
-bitemporal hemianopsia from compression of the optic chiasm
-cranial nerve palsies, if adenoma is large enough
*pituitary adenoma may co-secrete hormones

30
Q

hyperprolactinemia - indications for treatment

A

*amenorrhea: goals of treatment = restore fertility and estrogen levels; low estrogen is detrimental to bone health for men and women
*galactorrhea

31
Q

hyperprolactinemia - treatment

A

*dopamine agonists: cabergoline, bromocriptine
*effect: prolactin secretion is inhibited by dopamine

32
Q

hypoprolactinemia - overview

A

*low prolactin levels
*symptoms: lactation difficulty
*usually due to anterior pituitary dysfunction: mass, infarction
*screen for other hormone deficiencies
*treat underlying cause, if possible (e.g. mass)
*no commercially available prolactin hormone replacement currently

33
Q

posterior pituitary - overview

A

*an extension of axons of paraventricular and supraoptic nuclei that extend from the hypothalamus
*posterior pituitary stores oxytocin and antidiuretic hormone (produced by paraventricular and supraoptic nuclei) in vesicles until releasing these hormones in response to action potentials

34
Q

oxytocin - overview

A

*produced in paraventricular (SAD POX) and supraoptic nuclei of the hypothalamus
*carried by neurophysin I via axons to posterior pituitary, where it is released
*receptors in brain, breasts, uterus
*uses a POSITIVE feedback loop
*acts via G protein-coupled receptor (subunit q) using PLC, DAG, IP3, PKC signaling pathways

35
Q

oxytocin - functions

A

*causes uterine contractions during labor
*responsible for milk let-down reflex in response to suckling
*modulates fear, anxiety, social bonding, maternal-infant bonding, mood, and depression

36
Q

oxytocin - regulation

A

*stimulated by:
1. infant crying and feeding: causes milk let-down and ejection via contraction of myoepithelial cells
2. cervical/vaginal stretch: causes uterine myometrial contraction to facilitate labor
-pharmacologic implication: used to induce labor and control post-partum hemorrhage
*uses a POSITIVE feedback loop (oxytocin leads to more oxytocin)

note - prolactin stimulates milk production, while oxytocin stimulates milk letdown (ejection from breast)

37
Q

antidiuretic hormone - alternate names

A

*ADH
*vasopressin
*arginine vasopressin (AVP)

38
Q

antidiuretic hormone - overview

A

*made in supraoptic (SAD POX) and paraventricular nuclei in the hypothalamus
*carried by neurophysin II down axons to be stored in posterior pituitary, where it is released

39
Q

antidiuretic hormone - regulation

A

*secretion is stimulated by:
1. increased plasma osmolality (detected by osmoreceptors)
2. hypovolemia / decreased blood volume (detected by baroreceptors)
3. increased Ang II

40
Q

antidiuretic hormone - functions

A

*regulates blood pressure and serum osmolality
*serum osmolality regulation: increased ADH → increased water reabsorption from urine → decreased serum osmolality (increased urine osmolality) and increased blood volume

41
Q

antidiuretic hormone - mechanism of action

A

*ADH binds V2 receptors (GCPRs) on collecting ducts in kidney → activation of adenylyl cyclase → cAMP-mediated phosphorylation of aquaporin 2
*aquaporins (water channels) translocate to luminal membrane and facilitate water reabsorption in the collecting ducts

42
Q

AVP deficiency and AVP resistance (central and nephrogenic diabetes insipidus)

A

*causes: decreased ADH levels (central) or lack of response to ADH (nephrogenic)
*effect: inability to reabsorb water → excess loss of water in urine
*clinical findings: profound polyuria & polydipsia; dehydration/hypovolemia; mental status changes
*lab findings: hypernatremia, high serum osm, low urine osm, low urine specific gravity

43
Q

causes of AVP-deficiency (AVP-D, central diabetes insipidus)

A

*insufficient ADH production
*look for a history of: pituitary surgery, CNS tumor, head trauma, autoimmune diseases, other hormone deficits, Langerhan’s cell histiocytosis, rare genetic causes

44
Q

treatment of AVP-deficiency (AVP-D, central diabetes insipidus)

A

*replace the hormone: arginine vasopressin (DDAVP)
*rehydrate

45
Q

diagnosis of AVP-deficiency (AVP-D, central diabetes insipidus): water deprivation test

A

*no change or slight increase in urine Osm (don’t have any ADH, so they can’t concentrate their urine)

46
Q

diagnosis of AVP-deficiency (AVP-D, central diabetes insipidus): desmopressin (DDAVP) administration

A

*significant increase in urine Osm (giving synthetic ADH allows them to concentrate their urine, b/c this is what they are missing)

47
Q

causes of AVP-resistance (AVP-R, nephrogenic diabetes insipidus)

A

*insufficient renal response to ADH
*can be due to:
-V2 receptor mutation or AQP2 mutation
-obstructive uropathy
-hypercalcemia
-drug side effect (lithium, democlocycline)
-genetic causes

48
Q

treatment of AVP-resistance (AVP-R, nephrogenic diabetes insipidus)

A

*treat the underlying cause
*diuretics: HCTZ
*rehydrate

49
Q

diagnosis of of AVP-resistance (AVP-R, nephrogenic diabetes insipidus): water deprivation test

A

*minimal change in urine Osm

50
Q

diagnosis of of AVP-resistance (AVP-R, nephrogenic diabetes insipidus): desmopressin administration

A

*minimal change in urine Osm (b/c they cannot respond to the ADH, regardless of giving them DDAVP)

51
Q

primary polydipsia - overview

A

*excessive water intake
*causes: psychiatric illness, hypothalamic lesion
*serum Osm: low
*ADH level: low/normal
*water restriction test = increase in urine Osm
*treatment = water restriction

52
Q

syndrome of inappropriate ADH (SIADH) - overview

A

*too much ADH → too much water retention
*clinical findings:
-hyponatremia (mental status changes, seizures, nausea, vomiting)
-low urine output
-labs: low Na+, low plasma Osm, high urine Osm

53
Q

syndrome of inappropriate ADH (SIADH) - causes

A

*paraneoplastic syndrome (small cell lung cancer producing ADH)
*pulmonary disease (pneumonia, TB, COPD)
*CNS disease
*medications: SSRIs, carbamazepine, etc
*other endocrine disease (hypothyroidism, hypocortisolism)

54
Q

syndrome of inappropriate ADH (SIADH) - treatment

A

*fluid restriction in stable patients; find/treat the underlying cause
*if symptomatic, severe hyponatremia, use:
-hypertonic saline
-ADH antagonists (tolvaptan)
-demeclocycline
-loop diuretics
*go slowly to avoid osmotic demyelination syndrome!

Endo Repro Exam (56 decks)

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