Glossary of Block VIII, Week IV
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- which hormone do the following cells in the anterior pituitary secrete?
- 1. GH
3. ACTH, MSH, POMC, endorphins, lipotrophin
5. FSH, LH
- two hormones secreted by the posterior pituitary?
- 1. ADH
- 5 clinical manifestations of pituitary enlargement?
- 1. bitemporal hemianopsia
3. increased intracranial pressure
5. parenchymal compression
- hyperfunction of the pituitary gland usually means?
- pituitary adenoma
- a nonfunctional neoplasm of the pituitary is most likely?
- pituitary carcinoma
- describe the genetics of a pituitary adenoma
- monoclonal (all arise from a single somatic cell)
- peak age of incidence of a pituitary adenoma?
- 30-50 yrs
- T/F: a pituitary tumor can be microscopically differentiated between benign or malignant.
Only way you know if it is malignant is if it metastasizes. (function/secretion has nothing to do with it)
- Most pituitary adenomas are isolated, however, 3% occur with what syndrome?
- MEN type I
- what is the difference between a microadenoma and a macroadenoma?
- microadenoma is <1 cm
macroademona is >1 cm
- what is pituitary apoplexy?
- acute hemorrhage into a rapidly enlarging pituitary mass
- what is the most common pituitary tumor?
- what is the second most common pituitary tumor?
- Growth hormone adenoma
- clinical presentation of a prolactinoma?
- amenorrhea, glactorrhea, loss of libido, infertility
(tumor accounts for 25% of all cases of amenorrhea)
- two cell types a prolactinoma may be composed of?
- acidophilic or chromophobic cells
- besides a prolactinoma, what are some other causes of prolactinemia? (6)
- 1. pregnancy (physiologic)
2. lactotroph hyperplasia
5. renal failure
- how does the "stalk effect" result in prolactinemia?
- mass in suprasellar compartment disturbs normal inhibitory influence of hypothalamus.
- how are prolactinomas treated?
- bromocriptine (DA agonist)
- clinical presentation of growth hormone adenomas?
- gigantism in children
acromegaly in adults
- oncogene expressed in growth hormone adenomas?
- an excess of GH is associated with what systemic findings? (7)
- 1. gonadal dysfunction
2. diabetes mellitus
3. general muscle weakness
7. increased risk of GI cancers
- treatment of growth hormone adenomas?
- surgical removal
- clinical presentation of corticotroph adenomas?
- adrenal hypersecretion of cortisol -> this is Cushings disease causing Cushing syndrome
- what is Nelson Syndrome?
- a large destructive corticotroph adenoma that develops when the adrenal glands are removed
- gonadotroph adenomas produce?
- LH and FSH - cause little clinical symptoms
- how does a null cell adenoma present?
- mass effect
(secretes no hormone product)
- how much of the anterior lobe of the pituitary must be destroyed in order for hypopituitarism to be clinically apparent?
- 7 causes of hypopituitarism?
- 1. tumors, metastatic malignancies
3. mass lesions
4. pituitary apoplexy
7. ischemic necrosis
- postpartum necrosis of the anterior pituitary is known as?
- Sheehan's sydrome
- Sheehan's syndrome is secondary to?
- vasospasm of vessels that supply the pituitary -> causes sudden infarction
- in Sheehan's syndrome: why is the posterior pituitary spared?
- blood supply comes directly from arterial branches
- size changes to the pituitary during pregnancy and connection to Sheehan's syndrome?
- doubles in size (may become anoxic during obstetric hemorrhage or shock)
- two presenting s/s of Sheehan's syndrome?
inability to nurse
- an enlarged empty sella turcica not filled with pituitary tissue is called?
- empty sella syndrome
- in what type of patients is PRIMARY empty sella syndrome seen in? pathophysiology?
- obese women with multiple pregnancies
(defect in diaphragma sella allows arachnoid matter and CSF to herniate into sella and compress pituitary)
- ADH deficiency causes what clinical syndrome?
- Diabetes Insipidus
- three classic s/s of DI?
- 5 possible etiologies of DI?
- 1. head trauma
5. may arise spontaneously
- ADH excess causes which syndrome?
- SIADH (Syndrome of Inappropriate ADH Secretion)
- what is the most common cause of SIADH?
- paraneoplastic (SCC of the lung)
- clinical presentation of SIADH?
- excessive resorption of free water causes:
1. cerebral edema
2. hyponatremia (with resultant neurologic dysfunction)
*blood volume normal, no peripheral edema
- excess oxytocin is associated with which syndrome?
- NOT associated with any clinical syndromes!
- a slow growing tumor that is derived from the remnants of Rathke's pouch is known as a?
- age of onset of cranipharyngiomas?
- occur during childhood and adolescence
(but 50% present clinically after age 20)
- prognosis of a craniopharyngioma?
- malignany rare, good overall survival
- what are the 3 layers of the adrenal cortex from out to in and what does each layer produce?
- 1. Glomerulosa - Aldosterone
2. Fasciculata - Cortisol
3. Reticularis - Estrogens and Androgens
- what does the medulla of the adrenal gland secrete?
- what are the four possible causes of Cushings syndrome (excess cortisol secretion)?
- 1. Exogenous glucocorticoids
2. hypothalamic-pituitary disease (increased ACTH)
3. adrenal adenoma, carcinoma, hyperplasia
4. ectopic ACTH secretion by non-endocrine neoplasm
- what is the MCC of Cushings syndrome?
- exogenous glucocorticoids
- what do the adrenal glands look like in exogenous glucocorticoid induced Cushings?
- atrophy of adrenal cortex
- Cushings DISEASE is most common in:
1. which sex?
2. which age group?
- 1. Females
2. 20-30 yrs
- what do the adrenal glands look like in hypothalamic-pituitary disease causing Cushings syndrome?
- nodular hyperplasia
- two MCC of Cushing syndrome caused by hypothalamic-pituitary disease?
- 1. pituitary adenoma (produces ACTH)
2. hypothalamic stimulation/hyperplasia
- which is more common: an adrenal adenoma or carcinoma?
(carcinomas are more rare and seen primarily in children)
- what does the adrenal gland look like in Cushing syndrome caused by a primary adrenal neoplasm?
- uninvolved adrenal gland atrophies because of decreased ACTH
- Ectopic ACTH often comes from a SCC of the lung. what do the adrenal glands look like as a result?
- see bilateral cortical hyperplasia
- effect of increased cortisol on the adrenal glands?
- adrenal cortical atrophy
- 2 diagnostic tests/clues for Cushing syndrome?
- 1. increased 24 hr. urine free cortisol level
2. loss of diurnal pattern of cortisol secretion
- what levels to we look at to determine the cause of the Cushings syndrome?
- if ACTH levels respond to dexamethasone - we know the lesion is where?
(ACTH levels decrease in response to HIGH dose dexamethasone)
- predict the results of the dexamethasone suppression test if the cause is ectopic ACTH.
- NO reponse to ANY dose of dexamethasone
- what will the ACTH levels be like in an adrenal tumor that causes Cushings syndrome?
(cortisol is high)
- result of dexamethasone suppression test when an adrenal tumor is causing the Cushings syndrome?
- NO response to low or high dose dexamethasone (cortisol excretion cannot be suppressed)
- which disorder of the adrenal glands is important to diagnose because it may be a cure for hypertension?
- primary hyperaldosteronism
- 80% of all cases of primary hyperaldosteronism are caused by?
- Conn syndrome
(aldosterone producing adrenal adenoma)
- clinical s/s of primary hyperaldosteronism?
- 1. HTN
5. visual disturbances
6. frank tetany
- what are the following levels in primary hyperaldosteronism?
4. serum renin
- 1. high
- what is the difference (in the lab values) between a patient with secondary vs. primary hyperaldosteronism?
- secondary presents just like primary BUT also has HIGH serum renin concentrations
(secondary hyperadosteronism is SECONDARY to activation of the RAAS system)
- 4 clinical scenarios in which secondary hyperaldosteronism is seen?
- 1. CHF
2. decreased renal perfusion
4. pregnancy (estrogen incr. plasma renin substrate)
- which side are aldosterone producing adenomas (Conn syndrome) MC found in?
- what does the effected adrenal gland look like in Conn syndrome?
- solitary lesion
adrenal gland not overly enlarged
- diffuse and focal hyperlasia of adrenal cells is called?
- bilateral idiopathic hyperplasia
- which type of adrenocortical neoplasm MC causes virilization?
(carcinoma or adenoma)
- what is the MCC of congenital adrenal hyperplasias?
- enzyme deficiency that blocks cortisol production
- 90% of cases of congenital adrenal hyperplasia result from ?
- defective conversion of progesterone to 11-deoxycorticosterone. (deficiency or absence of 21-hydroxylase)
- what do the adrenals look like in all cases of congenital adrenal hyperplasia?
- bilaterally hyperplastic
- what are the three syndromes caused by a 21-hydroxylase deficiency?
- 1. salt-wasting syndrome
2. simple virilizing androgenital syndrome w/o salt wasting
3. nonclassic or late onset adrenal virilism
- what is the MC 21-hydroxylase deficiency?
- nonclassic (late onset) adrenal virilism
- which syndrome is a TOTAL lack of 21-hydroxylase?
- salt wasting syndrome
* NO mineralcorticoids synthesized, no cortisol synthesis
- clinical presentation of salt-wasting syndrome?
- 1. salt-wasting
6. CV collapse
- why is virilization seen in salt-wasting syndrome?
- steroid genesis is channeled to the only remaining pathway - sex steroids.
- simple virilizing adrenogenital syndrome without salt-wasting is only a partial 21-hydroxylase deficiency. how does it present?
- 1. genital ambiguity
2. enough aldosterone for salt absorption
3. low cortisol
4. increased testosterone
- why is adrenal hyperplasia seen in simple virilizing adrenogenital syndrome without salt-wasting?
- cortisol is low (not high enough to suppress ACTH) -> therefore see resultant hyperplasia
- s/s of nonclassic (late onset) adrenal virilism?
- virtually asymptomatic
may see hirsutism
- Treatment for 21-hydroxylase deficiency?
- exogenous glucocorticoids
- 5 settings in which ACUTE adrenal cortical insufficiency occurs?
- 1. crisis secondary to increased stress
2. rapid w/d of steroids
3. massive adrenal hemorrhage
4. postsurgical patients with DIC
5. Waterhouse-Friederichsen syndrome
- what population is W-F syndrome MC seen in?
- pathogenesis of W-F syndrome?
- 1. bacterial infx. leads to massive adrenal hemorrhage
2. leads to hypotension, shock
3. leads to DIC with skin purpura
4. acute adrenocortical insufficiency due to hemorrhage
5. death within hours
- MC bacteria known to cause W-F syndrome?
- Neisseria meningitidis (septicemia)
- primary chronic adrenocortical insufficiency is also known as?
- Addison's disease
- how much of the adrenal cortex must be compromised in order for addison's disease to be clinically apparrent?
- Addison's disease is more common in:
1. which sex?
2. which race?
- 1. Female
- MCC of Addison's disease?
(used to be TB, also can be metastatic cancer)
- which HLA antibodies is Addison's associated with?
- HLA-B8 and DR-3
- what will be apparent on biopsy if TB is the cause of the Addison's disease?
- why is hyperpigmented skin seen in Addisons?
- ACTH precursor hormone stimulates melanocytes
*only see with primary adrenocortical insufficiency
- clinical s/s of addison's?
- weakness, fatigue
anorexia, N/V, weight loss, diarrhea
- what are the blood glucose levels of a patient with addisons?
- LOW (secondary to glucocorticoid deficiency)
- secondary adrenocortical deficiency is due to?
- a disorder in the hypothalamus or pituitary
- describe the levels of the following in secondary vs. primary adrenocortical deficiency
- 1. secondary - normal, primary - low
2. secodary - normal, primary - high
- ACTH levels in secondary adrenocortical insufficiency?
- what do the adrenals look like in secondary adrenocortical insufficiency?
- are most adrenocortical neoplasms benign or malignant?
- which adrenocortical neoplasm is rare and highly malignant?
- adrenocortical carcinoma
- are most adrenocortical adenomas functional or nonfunctional?
- how can you tell if an adrenocortical adenoma is functional or nonfunctional?
- functional - see atrophy of adjacent cortex
nonfunctional - cortex normal thickness
- is an adrenocortical carcinoma more likely to be functional or nonfunctional?
- clinical presentation of adrenocortical carcinoma?
- virilism and other hyperadrenalism manifestations
- adrenocortical carcinoma tends to invade and metastasize to?
- invades adrenal vein, vena cava, lymphatics
*mets to regional nodes
(bone mets are rare)
- prognosis of adrenocortical carcinoma?
- avg. 2 yr. survival
- are adrenal myelolipomas benign or malignant?
(can be quite large)
- what type of cells secrete catecholamines in the medulla?
- chromaffin cells
- what is the difference between NE and E in regards to their sites of action?
- NE - local neurotransmitter
E - secreted into vascular system
- neuroendocrine cells that lie outside of the adrenal system make up?
- the paraganglion system
- three locations of paraganglion system?
- *brachiometric (near major arteries and CNs)
*intravagal (along vagus)
*aorticosympathetic (along abdominal aorta)
- an uncommon tumor of the adrenal medulla that synthesizes catecholamines is called?
- significance of a pheochromocytoma diagnosis?
- surgically correctable form of HTN
- when a pheochromocytoma occurs in the extra-adrenal paraganglia it called a?
(increased risk of malignancy)
- 10% of pheochromocytomas are familial: they are seen in which diseases/syndromes? (4)
- 1. MEN type I
3. von Hippel-Lindau disease
4. Sturge-Weber syndrome
- in relation to sporadic pheochromocytomas:
1. age of onset?
2. predominant sex?
- 1. 40-60
- in relation to familial pheochromocytoma?
1. avg. age of onset?
2. predominant sex?
- 1. childhood
- is a bilateral pheochromocytoma most likely sporadic or familial?
- histo characteristic of pheochromocytoma?
- zellballen (nests of polygonal cells)
- how is the diagnosis of a malignant pheochromocytoma made?
- must be metastases
- lab tests used for diagnosis of pheochromocytoma?
- increased urinary excretion of free catecholamines and their metabolites (VMA)
- what is the rule of 10s for pheochromocytoma?
- 10% familial
- prognosis of an extra-adrenal paraganglioma?
- 10-40% malignant
tend to reoccur
10% metastasize widely, lead to death
- what is the most common extracranial solid tumor of childhood?
- inheritance pattern of neuroblastoma?
- MC site of origin of a neuroblastoma?
- adrenal medulla
- inheritance pattern of MEN syndromes?
- other name for MEN I?
- Wermer syndrome
- other name for MEN II?
- Sipple syndrome
- the "3 P's" seen in MEN I?
- Primary hyperParathyroidism
Pancreatic lesion (islet cell tumors)
Pituitary tumor (MC Prolactinoma)
- avg. age of onset of MEN I?
- where is the mutation in MEN I?
- on chromosome 11
- clinical presentation of MEN I?
- problems secondary to peptide hormones (ie. hypoglycemia, peptic ulcer)
- what is seen in 100% of MEN IIA patients?
- medullary carcinoma of thyroid (secretion of calcitonin)
- what is seen in 50% of MEN IIA patients?
- what is seen in 10-20% of MEN IIA patients?
- parathyroid hyperplasia
- where is the mutation in MEN IIA and what gene does it code for?
- chromosome 10
codes for RET protooncogene
- what are the two features that distinguish MEN IIA from IIB?
- IIB has:
1. a different mutation in the RET protooncogene
2. multiple neuromas
- a varaint of IIA exists that is caused by germ line mutations of RET protooncogene. it is called?
- Familial MEdullary Thyroid Cancer
(predisposition ot medullary thyroid carcinoma but not the other clinical manifestations)
- three types of tumors found in the pineal gland?
- 1. germinoma
- MC tumor of the pineal gland?
(arises from embryonic germ cells)
- regarding a pineoblastoma:
1. age group MC found in?
2. rate of growth?
- 1. young people
2. fast growth, invasive
3. 1-2 yr. survival
- regarding a pineocytoma:
1. age group MC found in?
2. rate of growth?
- 1. adult
2. slow growth, well circumscribed
3. avg. 7 yr. survival
1. failure to thrive
2. growth failure
3. pubertal failure
- 1. failure to achieve required body weight
2. failure to grow at proper rate (linear growth)
3. failure to reach puberty by a certain time
- failure to thrive is MC seen in infants. Is this mostly due to an organic or psychosocial problem?
- psychosocial problem (80%)
- define short stature
- <2 SD below the mean for age (cross-sectional definition)
- define growth failure
- 4cm/yr between the age of 4-13 yrs
- what are the 3 categories of linear growth failure?
- 1. constitutional growth failure
2. acquired growth failure
3. congenital growth failure
- describe constitutional growth delay
- consistent slow growth
*catch up at a later date to reach adult height*
family history for "late bloomers," see growth plates upon XRay.
- prognosis and treatment of constitutional growth delay
- prognosis good
no treatment needed
- what are the 5 etiologies of congenital growth failure?
- 1. Turner's syndrome
2. Intrauterine growth retardation
3. genetic short stature
4. bone dysplasias (dwarfism)
5. psycho-social dwarfism
- describe the growth pattern of general congenital growth failure.
- persistent short stature
*born off the growth curve, gets more "off" as they age
- treatment for congenital growth failure caused by Turner's syndrome?
- GH therapy
(estrogen has NO effect on ultimate height)
- treatment for intrauterine growth retardation?
- GH (controversial)
- describe genetic short stature as a form of linear growth failure
- consistent low rate of growth (usually in 1st percentile). short parent/s, normal sexual maturity. can be treated with GH (ethics?)
- describe psycho-social dwarfism as a form of linear growth failure
- psych state affects pituitary hormone release - low GH secretion. rapid growth observed with environment change
- treatment of psycho-social dwarfism?
- behavioral or family therapy
- describe the growth pattern of acquired growth failure
- normal growth, then an abrupt fall off of the growth curve
- what are the four etiologies of acquired growth disorders?
- 1. hypothyroidism
2. GI disease (Chrohn's, sprue, chronic infx., etc)
3. Cortisol excess
4. GH deficiency
- GH deficiency is rare. what may it be associated with?
- traumatic delivery
- what are some clinical "stigmata" of a GH deficiency?
- "doll" facies
- regarding insulin:
1. two molecules that counteract insulin ACUTELY
2. two molecules that counteract insulin as a DELAYED response
- 1. glucagon, catecholamines
2. Cortisol, GH
- lab tests that may be ordered upon initial clinical growth evaluation?
- ESR, CBC, UA, stool, TSH
*X-ray of hand&wrist for bone age
*karytotype for Turner's (in females)
- which pituitary tests are suggested to be done with delayed bone age?
- GH stim tests
- what is the normal age of onset of puberty in a male?
(mean and range)
- mean - 11 yrs
- describe the sequence of pubertal events in a male
- 1. testes size >2.5 cm,l thinning, rugation of scrotum
2. initial pubic hair
3. increased penile size
4. growth spurt
*growth spurt occurs last in males
- describe the 5 Tanner classifications in males
- I - pre-pubertal
II - increaseed testicle size, scrotal changes
III - increased penile size (length)
IV - increased penile size (thickness)
V - adult
- what is the normal age of onset of puberty in females?
(mean and range)
- mean: 11
- when should a female be evaluated clinically for pubertal delay?
- * ages 13-14 if no breast bud development
* age 16 if no menses
- three early signs of puberty in a female?
- breast bud or pubic hairs
growth spurt or increased pubic hair
- describe the Tanner classification of breast development in a female (stages I-V)
- I - pre-pubertal
II - breast bud elevation, little if any areola development
III - Slight enlargement of areola but no separate contour from chest wall
IV - areola and nipple form secondary mound
V - adult breast
- besides endocrine, what is another etiology of delayed puberty?
- chronic disease
(lung, cardiac, GI)
- two etiologies of delayed puberty that are causes of primary gonadal dysfunction?
- 1. Turner's syndrome
2. Klinefelter's syndrome (but MC presents as infertility)
- name some hypothalamic-pituitary reasons for delayed puberty
- 1. idiopathic (GnRF deficiency)
2. Kallman's syndrome
3. FSH, LH deficiency (due to destructive pituitary lesion)
4. pituitary tumor (non-destructive prolactinoma)
- two "other" causes of delayed puberty?
- 1. exercise (ballet, gymnastics)
- name two synthetically produced growth hormones
- 1. somatropin recombinant (Humatope)
2. somatrem (Protropin)
- name a GHRH analog
- sermorelin acetate (GEREF)
- name three dopamine agonists
- 1. bromocriptine (Parlodel)
2. pergolide (Permax)
3. cabergoline (Dostinex)
- what is octreotide
- a somatostatin analog used to treat excessive GH
- what are the following drugs used for?
hMG, uFSH, chorionic gonadotropin
- treat female infertility
- what is gondadorelin acetate (Lutrepulse) used to treat?
- reproductive disorders secondary to GnRH deficiency
- what is the "main function" of GH?
- go to liver to stimulate production of IGF-1
- which hormones are derived from POMC?
- 1. ACTH
2. a- and b- MSH
3. b- and g- lipotropin
- ACTH stimulates the adrenal cortex to release?
- 1. cortisol (corticosteroids)
2. mineralocorticoids (aldosterone)
3. weak androgens (mainly androsteinedione)
- what are the primary regulators of aldosterone production?
- angiotensin II and extracellular K+ in the zona glomerulosa
(although elevated ACTH transiently increases mineralocorticoid levels)
- what stimulates POMC and ACTH synthesis (hint - released from hypothalamus)
- cortisol exhibits diurnal regulation. when do its levels peak?
- around 8am
- ACTH levels in response to stress?
- ACTH levels increase, thereby increasing cortisol levels
- what is considered to be the primary "job" of cortisol?
- down regulate the immune system
(decrease IL-1, 2, 6 and TNF-a)
- describe the ACTH assay test in distinguishing primary from secondary adrenal insufficiency
- primary - high ACTH levels due to poor negative feedback
secondary - low ACTH due to pituitary or hypothal. disease
- what is the problem with the ACTH test?
- some ACTH secreted by tumors is not picked up by the assay but is still biologically active. (false low ACTH values)
- name a pharmacologic ACTH analog that is used to test the integrity of the HPA axis
- cosyntropin (cortrosyn)
- what does the glycoprotien hormone family have in common?
- all members have the same a-subunit but differ in their b-subunit
- MOA of TRH?
- G-protein coupled system that increases PLC activity, increasing IP3 and DAG formation, both of which increase PKC activity.
*increased PKC activity stimulates TSH synthesis*
- what are the two pathways that control thyroid hormone secretion?
- 1. G protein activity leading to increased PKA activity
2. G protein activity leading to icreased PKC activity
- describe the release of GH throughout the day
- released in a pulsatile manner
*maximal increase at night
*most constant prior to onset of deep sleep
- GH release is inhibited by?
- what happens upon simultaneous exposure of the pituitary to GHRH and somatostatin?
- somatostatin wins: GH release is inhibited
- besides somatostatin, what is another inhibitor of GH release?
- IGF-1 (neg. feedback, also directly inhibits GHRH release)
- in general, the effects of GH are the opposite of?
- the effects of insulin
- via which pathway does GH upregulate receptors to carry out eventual functions?
- jak-stat pathway
(leads to prolonged IGF-1 activity)
- two synthetically produced GH used to treat GH deficient children?
- somatropin recombinant (Humatope)
- what should we look out for when treating with exogenous GH?
(IGF-1 can cause diabetic state)
- when would a child be treated with GHRH instead of GH?
- when they respond to GHRH (if problem is hypothalamic in nature, not in the pituitary)
- what is the GHRH analog used to give to GH deficient kids?
- sermorelin acetate (GEREF)
- compare synthetic GHRH to synthetic GH
- synthetic GHRH is cheaper but appears to be less effective than synthetic GH
- treatment for acromegaly?
- bromocriptine (parlodel)
- what is the MCC of acromegaly?
- GH producing adenomas
- why is the use of dopamine paradoxical in the treatment of GH excess?
- normally DA stimulates GH release.
- treatment of choice for a GH producing adenoma?
- tumor removal via surgery or irradiation
- when would octreotide be used?
- for metastatic carcinoid and GH producing tumors
(octerotide = somatostatin analog)
- what is the difference between octreotide and sandostatin LAR or lanreotide?
- octreotide is short acting and must be administered 3x per day
others are long acting formulations (once/month)
- what stimulates PRL secretion?
- what is the connection between TRH and PRL release?
- TRH stimulates PRL release
(pts. with extreme hypothyroidism can have hyperprolactinemia)
- what is unique about the regulation of PRL release?
- * under constant inhibition by hypothalamus
* no feedback inhibition
- why is lactation inhibited during pregnancy?
- high estrogen and progesterone levels inhibit lactation (although PRL levels are high)
- how does hyperprolactinemia suppress menstruation and cause infertility?
- high PRL supresses hypothalamic-pituitary-gonadal axis
- symptoms of hyperprolactinemia in:
- 1. galactorrhea, amenorrhea, infertility
2. infertility, impotence, galactorrhea
- treatment for hyperprolactinemia? MOA?
(activates D2 primary receptors thus inhibiting PRL release)
- two other meds used to treat hyperprolactinemia?
- pergolide (cost effective)
cabergoline (4x more potent than bromocriptine)
- which hormone is produced in response to FSH by the testes and ovaries and decreases FSH levels?
- why must several blood samples taken at different times be used to look for LH and FSH levels?
- pulsatile secretion
- location of action and physiological effects of FSH?
- acts on granulosa cells in the ovary, stimulates follicle development and estrogen synthesis
- location of action and physiological effects of LH?
- acts on ovarian cells, stimulates ovulation and progesterone synthesis
- location of action and physiological effects of CG?
- produced by blastocyst - maintains the synthesis of progesterone and estrogen during pregnancy
- in males: location of action and physiological effects of LH
- acts on Leydig cells: de novo testosterone synthesis
- in males: location of action and physiological effects of FSH
- acts on Sertoli cells: stimulates spermatogenesis
- how close to ovulation does the LH surge occur?
- 36 hrs
- CG could be used in males to test for what endocrine disorder?
- CG tests leydig cell function in males
(administer, if decreased plasma testosterone levels follow -> have L. cell failure)
- A GnRH challenge test would be used differentiate what causes of hypogonadism?
- pituitary vs. hypothalamic
- which pharmacological formulation contains equal amounts of LH and FSH and is used to treat female infertilty?
- human menopausal gonadotrophins (hMG)
- which pharmacologic formulation contains only FSH?
- urofollitropin (uFSH)
- which pharmacologic preparation contains CG and is used to treat female infertility?
- chorionic gonadotropin (Pregnyl, Profasil)
- what is CG used for in males?
- treatment of cryptorchidism
- effects of long term GnRH treatment in males?
- biochemical castration
(decrease # of GnRH receptors in pituitary: subsequent reduction in LH stimulated testost. synthesis)
- for a prolactinoma, list the following:
4. repr. status
- 1. same
4. amenorrhea, galactorrhea, infertility
- in the case of thyroid hormone inhibition, list the following:
4. repr. status
- 1. normal
2. increased (due to decreased TH)
3. increased (via stim. effect of TRF)
4. infertile, galactorrhea
- drugs that can cause increased PRL secretion?
hormones (hi-dose estrogen, TRH)
- why do body builders want to take GH exogenously?
- increased lipolysis, therefore decreases body fat
*also see skeletal growth
- in acromegaly due to a GH secreting somatotroph lesion, describe levels of the following:
- 1. GHRF decreased
2. GH increased
3. IGF-1 increased
4. glc increased
5. FFA increased
- MOA of octreotide in treating a GH tumor?
- somatostatin analog - will suppress the tumor
- 5 possible causes of panhypopituitarism?
- 1. intra-pituitary tumor
2. extra-pituitary tumor
3. lymphocytic hypophysitis
4. infiltrative diseases (sarcoid, MM, amyloid)
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