Block VIII, Week IV

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which hormone do the following cells in the anterior pituitary secrete? 1. somatotrophs 2. lactrotrophs 3. corticotrophs 4. thyrotrophs 5. gonadotrophs: 1. GH
2. prolactin
3. ACTH, MSH, POMC, endorphins, lipotrophin
4. TSH
5. FSH, LH
two hormones secreted by the posterior pituitary?: 1. ADH
2. Oxytocin
5 clinical manifestations of pituitary enlargement?: 1. bitemporal hemianopsia
2. headache
3. increased intracranial pressure
4. vomiting
5. parenchymal compression
hyperfunction of the pituitary gland usually means?: pituitary adenoma
a nonfunctional neoplasm of the pituitary is most likely?: pituitary carcinoma
(rare)
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.: FALSE
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?: prolactinoma
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
3. drugs
4. estrogens
5. renal failure
6. hypothyroidism
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?: gsp
an excess of GH is associated with what systemic findings? (7): 1. gonadal dysfunction
2. diabetes mellitus
3. general muscle weakness
4. HTN
5. arthritis
6. CHF
7. increased risk of GI cancers
treatment of growth hormone adenomas?: surgical removal
-or-
drug therapy
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? *clinical presentation?: 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?: 75%
7 causes of hypopituitarism?: 1. tumors, metastatic malignancies
2. cysts
3. mass lesions
4. pituitary apoplexy
5. surgery
6. radiation
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?: amenorrhea
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?: polydipsia
polyuria
dilute urine
5 possible etiologies of DI?: 1. head trauma
2. tumors
3. inflammation
4. surgery
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?: cranipharyngioma
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?: catecholamines
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?: adenoma
(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?: ACTH
if ACTH levels respond to dexamethasone - we know the lesion is where?: pituitary
(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?: low
(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
2. hypokalemia
3. weakness
4. parasthesias
5. visual disturbances
6. frank tetany
what are the following levels in primary hyperaldosteronism? 1. aldosterone 2. sodium 3. potassium 4. serum renin: 1. high
2. high
3. low
4. low
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
3. hypoalbuminemia
4. pregnancy (estrogen incr. plasma renin substrate)
which side are aldosterone producing adenomas (Conn syndrome) MC found in?: Left
what does the effected adrenal gland look like in Conn syndrome?: solitary lesion
adrenal gland not overly enlarged
yellow "bubble"
diffuse and focal hyperlasia of adrenal cells is called?: bilateral idiopathic hyperplasia
which type of adrenocortical neoplasm MC causes virilization? (carcinoma or adenoma): carcinoma
(not adenoma)
what is the MCC of congenital adrenal hyperplasias? inheritence pattern?: enzyme deficiency that blocks cortisol production
*AR inheritence
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? *result?: salt wasting syndrome
* NO mineralcorticoids synthesized, no cortisol synthesis
clinical presentation of salt-wasting syndrome?: 1. salt-wasting
2. hyponatremia
3. hyperkalemia
4. acidosis
5. hypotension
6. CV collapse
7. virilization
8. DEATH
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?: children
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?: 90%
Addison's disease is more common in: 1. which sex? 2. which race?: 1. Female
2. White
MCC of Addison's disease?: autoimmune
(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?: granulomas
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. sodium 2. potassium: 1. secondary - normal, primary - low
2. secodary - normal, primary - high
ACTH levels in secondary adrenocortical insufficiency?: LOW
what do the adrenals look like in secondary adrenocortical insufficiency?: small
"leaf-like"
are most adrenocortical neoplasms benign or malignant?: malignant
which adrenocortical neoplasm is rare and highly malignant?: adrenocortical carcinoma
are most adrenocortical adenomas functional or nonfunctional?: 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?: functional
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?: benign
(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?: pheochromocytoma
significance of a pheochromocytoma diagnosis?: surgically correctable form of HTN
when a pheochromocytoma occurs in the extra-adrenal paraganglia it called a?: paraganglioma
(increased risk of malignancy)
10% of pheochromocytomas are familial: they are seen in which diseases/syndromes? (4): 1. MEN type I
2. neurofibromatosis
3. von Hippel-Lindau disease
4. Sturge-Weber syndrome
in relation to sporadic pheochromocytomas: 1. age of onset? 2. predominant sex?: 1. 40-60
2. female
in relation to familial pheochromocytoma? 1. avg. age of onset? 2. predominant sex?: 1. childhood
2. male
is a bilateral pheochromocytoma most likely sporadic or familial?: 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
10% children
10% extra-adrenal
10% bilateral
10% malignant
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?: neuroblastoma
inheritance pattern of neuroblastoma?: NONE
(sporadic)
MC site of origin of a neuroblastoma?: adrenal medulla
inheritance pattern of MEN syndromes?: AD
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?: 40-50
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?: pheochromocytomas
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
2. pineoblastoma
3. pineocytoma
MC tumor of the pineal gland?: germinoma
(arises from embryonic germ cells)
regarding a pineoblastoma: 1. age group MC found in? 2. rate of growth? 3. prognosis?: 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? 3. prognosis?: 1. adult
2. slow growth, well circumscribed
3. avg. 7 yr. survival
define: 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
(longitudinal definition)
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
pudgy
small genitalia
small hands
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
PRL
MR scan
Cortisol evaluation
what is the normal age of onset of puberty in a male? (mean and range): mean - 11 yrs
range: 9-13
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
range: 9-16
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
menarche
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)
5. hypothyroidism
two "other" causes of delayed puberty? (think mental/lifestyle): 1. exercise (ballet, gymnastics)
2. psychosocial
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): CRH
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?: somatostatin
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)
somatrem (Protropin)
what should we look out for when treating with exogenous GH?: DM
(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?: sleep
stress
hypoglycemia
exercise
estrogen
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. females 2. males: 1. galactorrhea, amenorrhea, infertility
2. infertility, impotence, galactorrhea
treatment for hyperprolactinemia? MOA?: bromocroptine
(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?: inhibin
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: 1. dopamine 2. TRF 3. PRL 4. repr. status: 1. same
2. same
3. increased
4. amenorrhea, galactorrhea, infertility
in the case of thyroid hormone inhibition, list the following: 1. dopamine 2. TRF 3. PRL 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?: psychotropics
antiemetics (metoclopramide)
antihypertensives
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 2. GH 3. IGF-1 4. glucose 5. FFA: 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)
5. hemorrhage

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