this lecture began our introduction to diagnosis of endocrine disorders, courtesy of dr. marcus miller.
the hypothalamus is the endocrine organ that receives information from the CNS and in turn stimulates the pituitary to release hormones. it carries a set of hormones as well, including TRH, CRH, GnRH, GHRH, somatostatin, ADH, oxytocin, and dopamine. [quick note: somatostatin acts as a GHRH antagonist, and dopamine acts as a prolactin antagonist] the hypothalamus is connected via nerves as well as blood to the pituitary, which is divided into 3 lobes, anterior (makes up 80%), intermediate, and posterior. the posterior pituitary acts as a storage for ADH and oxytocin, and the intermediate lobe also contains hormones such as the melanocyte stimulating hormone. because of the pituitary's location in the sella turcica, pituitary adenomas might lead to bitemporal hemianopsia due to the upward growth and subsequent impingement on the optic chiasm.
the anterior pituitary's general function is to stimulate peripheral endocrine organs such as the thyroid and regulate growth and lactation. it does this by release of a variety of hormones, including growth hormone, LH / FSH, TSH, prolactin, and ACTH. ACTH is responsible for stimulating cortisol production from the adrenals. LH stimulates ovulation and progesterone production in females and prolactin has the opposite effect, while also stimulating lactation.
the posterior pituitary is made up of modified nerve fibers, axons, and glial cells extending from the supraoptic and paraventricular nuclei from the hypothalamus. as mentioned before, the axons of the posterior pituitary store two hormones made in the hypothalamus, ADH and oxytocin. ADH's main action is in the kidney, stimulating water reabsorption in the distal tubules, while oxytocin stimulates lactation and uterine contraction, among other things.
hypopituitarism means decreased output of pituitary hormones and can be due to a variety of causes-- oftentimes the cause for panhypopituitarism (equal reduction in all AP hormones) is iatrogenic-- either through radiation to the head or surgery that reduces blood flow. other causes might include destructive processes such as inflammation or infection, hemochromatosis, malignancy. hypopituitarism can also result in dwarfism, which comes in several varieties as well- if resulting from panhypopituitarism, body proportions will be normal, while a selective GH deficiency might result in abnormal proportions. achondroplastic dwarfism is a third type that is not related to hypopituitarism (and therefore is unresponsive to GH supplication).
some pituitary pathologies: pituitary apoplexy is a hemorrhage into a pre-existing adenoma, resulting in a sudden onset headache and diplopia. severe cases might also lead to ischemic necrosis and may even result in death. the most common cause of ischemic necrosis is sheehan's syndrome, although patients with this syndrome may have a range of outcomes, ranging from asymptomatic to death. sheehan's syndrome is a situation where the already hypoxic pituitary in pregnant women (due to an increase in pituitary size without increased vasculature) is further compromised by obstetric hemorrhage, leading to vasospasm and ischemic necrosis.
pituitary adenomas are the most common cause of hyperpituitarism, although a good portion of pituitary adenomas are non functional and can remain undetected. they can be macro (greater than 1cm) or micro (less than 1cm) and comprise 10% of all intracranial neoplasms. functional adenomas are generally composed of one cell type and secrete a single hormone. the most common functional adenomas are: prolactinoma, ACTH producing, gonadotropin producing, and growth hormone producing.
the most common type of adenoma produces prolactin and is composed of weakly staining acidophilic cells-- within which prolactin can be detected in the secretory granules. in females, the effects of a prolactinoma are what one would expect from increased prolactin levels: amenorrhea, diminished libido, ovarian cysts (due to inhibition of ovulation), galactorrhea. in males, prolactinomas might manifest asymptomatically, or decreased libido. prolactinomas might be diagnosed by high serum prolactin levels, and an MRI will confirm the presence of one as small as 2mm.
growth hormone producing adenomas are the second most common type. they are measured / diagnosed primarily by increased IGF-1 levels, from increased hepatic production due to GH stimulation. GH excess can lead to a variety of signs/symptoms, including diabetes, HTN, hyperglycemia, CHF, gonadal dysfunction, and muscle weakness. if the adenoma is functional before growth plate closure, the result is pituitary giantism, in which body size is increased and arms / legs are disproportionately long. if the adenoma is function after growth plate closure, the result is acromegaly, which has its own characteristics: enlarged hands, feet, face (nose broadens, teeth get further apart, jaw protrudes), and organomegaly. GH producing adenomas are diagnosed via IGF-1 levels as well as the GH suppression test, in which GH levels do not drop as they should in response to glucose administration.
empty sella syndrome describes any condition in which the sella turcica is enlarged but not filled with pituitary tissue. risk factors include pregnancy, obesity, and hypertension. ESS is caused by increased intracranial pressure which leads to CSF entering the sella turcica, compressing the pituitary against its walls. presentation might be asymptomatic, or may have papilledema. ESS might also be due to a surgical procedure or radiation which has enlarged the sella turcica.
excess ADH production may be related to posterior pituitary dysfunction and can result in dysfunction in the water balance in the body. syndrome of inappropriate ADH describes such a condition, which can also be caused by ectopic sites, generally from cancer cells. the signs and symptoms might be limited to reduced urine, and the diagnosis might be made by highly concentrated urine, decreased plasma osmolality, and hyponatremia.
diabetes insipidus is a condition which results from ADH deficiency; either from an underproduction from the hypothalamus (central) or dysfunctional ADH receptors in the kidney (nephrogenic). DI results in polyuria and polydipsia, with the polyuria generally exceeding the polydipsia. central might be caused by surgery/trauma, tumors, infection, sheehan's syndrome, while nephrogenic might be caused by chronic renal disease, lithium, among other things. a useful test for distinguishing central, nephrogenic DI, and psychogenic polydipsia is the water deprivation test. after depriving water, patients with psychogenic polydipsia will have increased osmolality while the other two conditions will not. after administration of ADH, psychogenic polydipsia and central DI will increase urine osmolality (increased reabsorption produces more concentrated urine), whereas nephrogenic will remain the same.
questions
hypothalamus and pituitary...
1. what is the relative prevalence of endocrine issues related to the hypothalamus, pituitary, and thyroid?
2. what are the hormones released by the hypothalamus?
3. what is the effect of these hormones on the pituitary?
4. where is the pituitary gland located?
5. what is the pituitary gland covered by?
6. how might a pituitary adenoma lead to loss of peripheral vision?
7. what are the divisions of the pituitary? which division predominates?
8. describe the general function of the posterior pituitary.
9. describe the function of the intermediate pituitary.
10. dopamine exerts inhibitory control over which other hormone?
anterior pituitary...
11. what are the hormones released by the anterior pituitary?
12. what is a better marker for checking growth hormone activity than a simple serum growth hormone level test?
13. describe the general function of the hormones released by the anterior pituitary.
14. what does ACTH do?
15. what does LH do in males and females?
16. what does prolactin do?
posterior pituitary...
17. describe the structure / content of the posterior pituitary.
18. what are the two hormones that are stored in the axons of the posterior pituitary?
19. what does ADH do?
20. what does oxytocin do?
hypopituitarism and dwarfism...
21. most cases of hypopituitarism are the result of...
22. what are some other potential causes of hypopituitarism?
23. what are the two types of pituitary dwarfism?
24. what is achondoplastic dwarfism?
acute pituitary pathologies...
25. what is pituitary apoplexy?
26. what are the symptoms of a pituitary apoplexy?
27. what are the complications of a severe case of pituitary apoplexy?
28. sheehan's syndrome is the most common cause of...
29. describe the pathophysiology of sheehan's syndrome.
pituitary adenoma...
30. pituitary adenomas are the most common cause of...
31. pituitary adenomas are usually...
32. what percentage of intracranial neoplasms are pituitary adenomas?
33. what age range is most common for pituitary adenomas?
34. functional adenomas are usually...
35. what is the difference between a macro and microadenoma?
36. are males more likely to present with a macro or microadenoma?
37. what are the most common types of functional adenomas?
prolactinoma...
38. most prolactinomas are composed of...
39. prolactin can be detected within...
40. what are the signs and symptoms of a prolactinoma in females?
41. what percentage of secondary amenorrhea cases are due to prolactinomas?
42. what are the signs / symptoms of a prolactinoma in males?
43. what are some labs and imaging techniques useful in diagnosing prolactinomas?
44. what is a naturopathic treatment option for prolactinoma?
growth hormone producing adenoma...
45. persistent oversecretion of GH stimulates...
46. what are the signs and symptoms of a GH producing adenoma?
47. how is a GH producing adenoma classified if it is functional before vs. after growth plate closure?
48. describe the body proportions of a patient with pituitary gigantism.
49. what are the signs and symptoms of a patient with acromegaly?
50. what are the lab tests used to diagnose GH producing adenomas?
51. how can a GH producing adenoma be differentiated from hyperglycemia?
corticotroph adenoma...
52. what is a corticotroph adenoma?
53. what is the difference between cushing's syndrome and cushing's disease?
empty sella syndrome...
54. what is the empty sella syndrome?
55. what are the risk factors for ESS?
56. what is the etiology of ESS?
57. what are the signs/symptoms of ESS?
58. what is secondary ESS?
syndrome of inappropriate ADH...
59. what is SIADH?
60. what are some etiological factors that might lead to SIADH?
61. what are the signs / symptoms of SIADH?
62. what are the lab results for SIADH?
diabetes insipidus...
63. what are the two causes of diabetes insipidus?
64. what are the signs and symptoms of DI?
65. what are some etiologies of central DI?
66. what is a drug that might cause nephrogenic DI?
67. what is a test that can distinguish between central DI, nephrogenic DI, and psychogenic polydipsia?
68. what is one possible treatment for DI?
answers
1. hypothalamus problems are much rarer than pituitary and thyroid.
2. TRH
CRH
GnRH
GHRH
somatostatin
dopamine
ADH
oxytocin
3. stimulates pituitary, except for somatostatin and dopamine.
4. the sella turcica.
5. dura mater, except for the a thin opening which conveys a stalk from the hypothalamus.
6. the upward growth of a pituitary tumor will impinge on the optic chiasm, which will block the optic pathways responsible for peripheral vision bilaterally.
7. anterior, intermediate, posterior lobes. anterior is 80%.
8. storage unit for oxytocin and ADH.
9. also contains hormones or precursor to hormones such as melanocyte stimulating hormone and a hormone that increases aldosterone production.
10. prolactin.
11. growth hormone
LH and FSH
TSH
prolactin
ACTH.
[G L/F T P A] [go left, pa]
12. IGF-1 levels.
13. stimulates peripheral endocrine organs and regulates growth and lactation.
14. stimulates cortisol production in the adrenals.
15. stimulates ovulation and progesterone production in females, stimulates testosterone production in males.
16. promotes lactation and suppresses ovulation and fertility.
17. a modified neural network consisting of modified glial cells, nerve fibers, and axonal processes extending from the supraoptic and paraventricular nuclei of the hypothalamus.
18. ADH and oxytocin.
19. stimulates water reabsorption in distal tubules of nephron.
20. regulates lactation and uterine contraction.
21. radiation or surgery which reduce blood flow to the brain.
22. destructive lesions
destructive processes
impingement from malignancy
infection
hemochromatosis
sarcoidosis
23. resulting either from deficiency of all AP hormones or just GH, in which body proportions remain normal and abnormal, respectively.
24. genetic dysfunction of fibroblasts that results in abnormal cartilaginous development.
25. sudden hemorrhage into an existing pituitary adenoma.
26. sudden onset headache and diplopia.
27. ischemic necrosis, death.
28. ischemic necrosis of the pituitary.
29. in pregnant women, the anterior pituitary enlarges without corresponding vasculature increase. this hypoxic state combined with an obstetric hemorrhage can cause vasospasm of the blood supply and ultimately ischemia and necrosis.
30. hyperpituitarism.
31. non functional, isolated lesions with no associated neoplasms.
32. 10%.
33. 30-60.
34. made of one cell type that produces one hormone.
35. greater than or less than 1 cm.
36. macro because of the greater chance of adenoma remaining undetected due to the lack of hormonal feedback as compared to women.
37. prolactinoma, ACTH cell adenoma, gonadotropin adenoma, growth hormone adenoma
[pro act gon grow] [functionally proactive: go and grow!]
38. weakly staining acidophilic cells.
39. secretory granules within cytoplasm of cells.
40. diminished menses or amenorrhea
diminished libido
infertility
ovarian cysts
galactorrhea
[prolact amen libido infertility cysts galact] [amen; all infertile cysts in the galaxy now have libidos]
41. roughly 25%.
42. asymptomatic, or decreased libido / sperm count.
43. serum prolactin and MRI.
44. botanicals that have phytoestrogenic or progesterone agonist effects.
45. hepatic secretion of IGF-1
46. hyperglycemia, DM, HTN, CHF, gonadal dysfunction, muscle weakness/arthritis. [sugar sugar blood blood nads muscles]
47. before: pituitary giant
after: acromegaly
48. bigger body size with disproportionately long arms and legs.
49. disproportionately large hands, feet, face
enlargement of heart, thyroid, liver, adrenals
jaw protrusion
spreading of teeth
broadening of nose
"spade like" hands
50. IGF-1 levels and the GH suppression test.
51. in the GH suppression test of a hyperglycemic patient, GH will be suppressed, but won't be in a patient with a GH producing adenoma.
52. an adenoma that produces ACTH, leading to adrenal hypersecretion of cortisol.
53. cushing's syndrome describes a state of hypercortisolism, of which cushing's disease is a specific type related to a corticotroph adenoma.
54. any condition that leads to an enlarged sella turcica not filled with pituitary tissue.
55. obese females
multiple pregnancies
hypertension
[fat fetus food]
56. increased intracranial pressure leads to CSF entering the sella turcica and compressing pituitary against wall.
57. asymptomatic, may see papilledema.
58. ESS due to surgical procedure or radiation that has enlarged the sella turcica.
59. excess secretion of ADH by ectopic sites.
60. cancer (lung, breast, prostate), head trauma, narcotics.
61. oliguria with no other signs.
62. highly concentrated urine, low plasma osmolality, hyponatremia.
63. deficiency of ADH either by hypothalamus underproduction or kidney unresponsiveness.
64. polyuria, polydipsia.
65. trauma
surgery
tumor
infection
sheehan's
66. lithium.
67. the water deprivation test.
68. oxytocin.
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