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246 Cards in this Set
- Front
- Back
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
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besides somatostatin, what is another inhibitor of GH release?
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IGF-1 (neg. feedback, also directly inhibits GHRH release)
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in general, the effects of GH are the opposite of?
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the effects of insulin
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via which pathway does GH upregulate receptors to carry out eventual functions?
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jak-stat pathway
(leads to prolonged IGF-1 activity) |
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two synthetically produced GH used to treat GH deficient children?
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somatropin recombinant (Humatope)
somatrem (Protropin) |
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what should we look out for when treating with exogenous GH?
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DM
(IGF-1 can cause diabetic state) |
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when would a child be treated with GHRH instead of GH?
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when they respond to GHRH (if problem is hypothalamic in nature, not in the pituitary)
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what is the GHRH analog used to give to GH deficient kids?
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sermorelin acetate (GEREF)
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compare synthetic GHRH to synthetic GH
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synthetic GHRH is cheaper but appears to be less effective than synthetic GH
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treatment for acromegaly?
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bromocriptine (parlodel)
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what is the MCC of acromegaly?
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GH producing adenomas
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why is the use of dopamine paradoxical in the treatment of GH excess?
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normally DA stimulates GH release.
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treatment of choice for a GH producing adenoma?
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tumor removal via surgery or irradiation
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when would octreotide be used?
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for metastatic carcinoid and GH producing tumors
(octerotide = somatostatin analog) |
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what is the difference between octreotide and sandostatin LAR or lanreotide?
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octreotide is short acting and must be administered 3x per day
others are long acting formulations (once/month) |
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what stimulates PRL secretion?
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sleep
stress hypoglycemia exercise estrogen |
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what is the connection between TRH and PRL release?
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TRH stimulates PRL release
(pts. with extreme hypothyroidism can have hyperprolactinemia) |
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what is unique about the regulation of PRL release?
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* under constant inhibition by hypothalamus
* no feedback inhibition |
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why is lactation inhibited during pregnancy?
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high estrogen and progesterone levels inhibit lactation (although PRL levels are high)
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how does hyperprolactinemia suppress menstruation and cause infertility?
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high PRL supresses hypothalamic-pituitary-gonadal axis
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symptoms of hyperprolactinemia in:
1. females 2. males |
1. galactorrhea, amenorrhea, infertility
2. infertility, impotence, galactorrhea |
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treatment for hyperprolactinemia? MOA?
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bromocroptine
(activates D2 primary receptors thus inhibiting PRL release) |
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two other meds used to treat hyperprolactinemia?
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pergolide (cost effective)
cabergoline (4x more potent than bromocriptine) |
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which hormone is produced in response to FSH by the testes and ovaries and decreases FSH levels?
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inhibin
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why must several blood samples taken at different times be used to look for LH and FSH levels?
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pulsatile secretion
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location of action and physiological effects of FSH?
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acts on granulosa cells in the ovary, stimulates follicle development and estrogen synthesis
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location of action and physiological effects of LH?
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acts on ovarian cells, stimulates ovulation and progesterone synthesis
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location of action and physiological effects of CG?
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produced by blastocyst - maintains the synthesis of progesterone and estrogen during pregnancy
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in males: location of action and physiological effects of LH
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acts on Leydig cells: de novo testosterone synthesis
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in males: location of action and physiological effects of FSH
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acts on Sertoli cells: stimulates spermatogenesis
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how close to ovulation does the LH surge occur?
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36 hrs
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CG could be used in males to test for what endocrine disorder?
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CG tests leydig cell function in males
(administer, if decreased plasma testosterone levels follow -> have L. cell failure) |
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A GnRH challenge test would be used differentiate what causes of hypogonadism?
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pituitary vs. hypothalamic
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which pharmacological formulation contains equal amounts of LH and FSH and is used to treat female infertilty?
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human menopausal gonadotrophins (hMG)
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which pharmacologic formulation contains only FSH?
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urofollitropin (uFSH)
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which pharmacologic preparation contains CG and is used to treat female infertility?
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chorionic gonadotropin (Pregnyl, Profasil)
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what is CG used for in males?
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treatment of cryptorchidism
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effects of long term GnRH treatment in males?
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biochemical castration
(decrease # of GnRH receptors in pituitary: subsequent reduction in LH stimulated testost. synthesis) |
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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 |
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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 |
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drugs that can cause increased PRL secretion?
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psychotropics
antiemetics (metoclopramide) antihypertensives hormones (hi-dose estrogen, TRH) |
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why do body builders want to take GH exogenously?
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increased lipolysis, therefore decreases body fat
*also see skeletal growth |
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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 |
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MOA of octreotide in treating a GH tumor?
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somatostatin analog - will suppress the tumor
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5 possible causes of panhypopituitarism?
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1. intra-pituitary tumor
2. extra-pituitary tumor 3. lymphocytic hypophysitis 4. infiltrative diseases (sarcoid, MM, amyloid) 5. hemorrhage |