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features of polypeptide/protein hormones

large >500kDa
circulate unbound
Serum T1/2 = minutes
receptors on cell surfaces
second messengers that alter activity of other molecules within cells

examples of polypeptide/protein hormones

LH, FSH, catecholamines, ACTH, TSH, prolactin, GH, GHRH, CRH, GnRH, AVP, PTH, VIP, glucagon, insulin, somatostatin, IGF-I

features of steroid/thyronine hormones

small <500kDa
circulate bound to proteins
serum T1/2 = hours
receptors are located in the cytoplasm and nucleus
have direct nuclear action

examples of steroid hormones

testosterone, E2 (estrogen), progesterone, T4, T3, cortisol, aldosterone, vitamin D, thyroxine

the endocrine organs are

pituitary gland
thyroid gland
parathyroid gland
adrenal glands

this endocrine organ is considered the control center of the other endocrine organs

the hypothalamus

describe the negative feedback system

high levels of a hormone DECREASE hormone synthesis and secretion
low levels STIMULATE

describe the positive feedback system

high levels of a hormone STIMULATE, low levels INHIBIT

what happens to cell receptors if excess hormones are present

the receptors are down-regulated
the decreases receptor availability decreases the target tissue response to the excess hormone

what happens if the circulating hormone is depleted

the receptors are up-regulated
the increased receptor availability increases the likelihood of target tissue response

in primary hyper/hypo-function...

the alteration is in the function of a hormone-secreting gland

in secondary hyper/hypo-function...

the alteration is in pituitary or hypothalamic function

ectopic hyper/hypo-function

a hormone is secreted from a tissue other than its usual source


benign enlargement of a cluster of cells


abnormal new growth of tissue: generally considered MALIGNANT


benign enlargement of the entire gland

the pituitary gland is

an extension of hypothalamic neurons

what do hypothalamic nuclei synthesize

ADH & Oxytocin

where are ADH and Oxytocin synthesized

in the hypothalamus

where are ADH and Oxytocin stored

in the posterior pituitary

ADH is also known as

AVP - arginine vasopressin

what is the neurohypophysis

the posterior pituitary

how does ADH maintain water balance

inhibits diuresis

where does ADH act

on renal tubules (increases permeability @ collecting ducts) to cause water reabsorption -> urinary concentration

what regulates ADH secretion

osmoreceptors in the hypothalamus (detects osmolality of blood)
atrial & carotid barorecptors (detects circulating blood volume)

what hormones stimulate ADH secretion

angiotensin II, epi, cortisol, estrogen, progesterone

what inhibits the secretion of ADH

alcohol EtOH

what drugs stimulate the secretion of ADH

hydrochlorothiazide(HCTZ), chlorpropamide, morhine, propanolol, barbituates, nicotine, oxytocin, carbamazapine(tegretol)

stimuli for the secretion of ADH

increasing temoerature

what is the thresh-hold for ADH release and thirst stimulation

plasma osmolality >285 osm/L
normal osmolality 275 - 300 osm/L

a differential diagnosis for a patient with polyuria should include

diabetes mellitus (DM)
Cushing's syndrome
glucocorticoid therapy (corticosteroid use)
psychogenic polydypsia
nocturnal polyuria of Parkinson's disease
lithium use
diabetes insipidus (DI)

pt presents with excess urine volume >2L/day w/low specific gravity (decreased osmolality)
intense polydipsia - fluid intake of 2-20L/day
may have hypernatremia, dehydration, hypotension, vascular collapse

diabetes insipidus

when ADH is not present or inactive where can water not be conserved

the distal collecting tubules

causes of central DI (diabetes insipidus) include

hypothalamic or pituitary surgery
trauma to pituitary stalk
infections (encephalitis, syphilis, TB)
tumors of the pituitary or metastases to the pituitary
pituitary infarction (postpartum hemorrhage - Sheehan's syndrome)
pituitary inflammation (autoimmune hypophysitis)

causes of nephrogenic DI include

medications; lithium, demeclocycline, methicilin, foscarnet, EtOH, caffiene
chronic renal disease
chronic hypercalcemia
sickle cell anemia

what should you suspect in patients with persistent urinary incontinence/bedwetting

partial DI
symptoms are less intense

what tests will aid in the diagnosis of diabetes insipidus

plasma and urine osmolality
water deprivation test
24 hour urine- volume, glucose creatinine,osmolality
serum- glucose, BUN, calcium, uric acid, sodium, potassium, creatinine, osmolality
history and physical

how do you preform the Vasopressin Challenge Test

1.measure urine volume 12hrs prior to admin of dDAVP
2.give dDVAP- IV, SubQ, or intranasally
3.measure urine volume 12hrs after dDVAP is given
4.measure serum sodium if signs of hyponattremia are present
5. MRI of pituitary and hypothalamus

if a patient has central DI and you administer the Vasopressin Challenge test, what will you see?

decreased thirst
decreased urin output
increased urine osmolality

if you measure serum vasopressin (ADH) in a patient you suspect has DI, and you find elevated levels, what is that indicative of

nephrogenic DI

this is complication of nephrogenic DI


treatment of central DI

refer to neurologist & endocrinologist
desmopressin acetate
-lowest dose possible
-many dosing routes: oral, IV, IM, SubQ, intranasal, metered-dose inhaler

pt presents with acute nephrogenic DI

treat with indomethacin
50mg q8hrs

what might a nephrologist do for a pt with nephrogenic DI

indomethacin combined with HCTZ, desmopressin, or amiloride (potassium sparing diuretic)

how do HCTZ and amiloride help in nephrogenic DI

they produce a hyperosmolar urine while decreasing urine output

treatment for chronic/mild DI

maintain adequate water intake

characteristics of SIADH

normal vascular volume with hyponatremia
inappropriate ADH secretion in the absence of ANY osmotic stimulus
-decreased plasma osmolaity
-inappropriate concentration of the urine

some causes of ADH are

tumors secreting ectopic ADH
medications/drug induced
lesions in the pathway of receptors

80% of lung tumors are associated with


medications/drugs that can induce SIADH

antineoplastic agents
MDMA (ecstacy)
Cytotoxic therapy

lesions in the pathway of receptors that can cause ADH

CNS disorders: stroke, subarachnoid hemorrage, meningitis, encephalitis, trauma, brain tumor
pulmonary disease: TB, bacterial pneumonia
pain, physical stress, postoperative state

pt presents with; fatigue, headache, nausea & anorexia which progress to nausea and vomiting and eventually neurogenic impairment due to hyponatremia


normal serum sodium is 135-145 mEq/L at what point must you urgently treat hyponatremia

<120 mEq/L

clinical presentations of SIADH include

low plasma osmolality/decreased osmolality <280mosml/kg
inappropriately high urine osmolality for plasma osmolality
urine sodium >20mEq/L (elevated)
hypouricemia & low BUN
normal plasma volume (euvolemia)

where does excess fluid go in patients with SIADH

2/3 into the cells (ICF)
1/3 into ECF

what determines the treatment od SIADH

the severity and duration of hyponatermia

hyponatermia occurs over time and pt is asymptomatic

correct slowly with water restriction over time

if your pt with SIADH is euvolemic treat by

water restriction (500-1000mL/day - so as not to dilute sodium)
insure adequate sodium intake
Demeclocycline- for pts that can't adhere to water restriction (inhibits the effects of ADH on distal renal tubules)

if your SIADH pt is hypovolemic treat by

provide isotonic fluids (NS or LR) - surpresses hypovolemic stimulus for ADH release

at what serum sodium level is symptomatic hyponatremia seen

<120 mEq/L

a pt presents with hyponatremia and CNS symptoms, how do you treat them

IV saline + furisemide (Lasix)
~ when serum sodium is <115 mEq/L use hypertonic saline 3%

what are the syndromes of increases oxytocin secretion

none have been defined

what does oxytocin do

stimulates uterine contraction at time of labor and delivery
stimulates smooth muscle contraction in the breast during suckling

what are the cell types of the anterior pituitary

somatotrophs (50%)-GH
corticotrophs (15%)-ACTH
lactotrophs (15-20%)-PRL
gonandotrophs (10%)-LH & FSH
thyrotrophs (5%)-TSH

are pituitary tumors usually malignant

no, they are rarely malignant and seldom metastasize

what are the effects of a pituitary tumor

excess hormone productio + sequela
loss of function of the remaining gland
space-occupying effects

GnRH (gonadotropin releasing hormone) acts on which anterior pituitary hormone(s)


GHRH (growth hormone releasing hormone) acts on which anterior pituitary hormone(s)


TRH (thyrotropin releasing hormone) acts on which anterior pituitary hormone(s)


VIP PHI-27 (vasoactive intestinal polypeptide) acts on which anterior pituitary hormone(s)


CRH (corticotropin releasing hormone) ADH (antidiuretic hormone-vasopressin) act on which anterior pituitary hormone(s)


somatostatin is a hypothalamic inhibitory hormone that acts on


Dopamine is a hypothalamic inhibitory hormone that acts on


GH is inhibited by


TSH is inhibited by


prolactin is inhibited by


a pituitary hormone is most likely to result in excess secretion of

prolactin (60%)

the second most likely hormone secreted in excess due to a pituitary tumor is

GH (20%)

the third most likely hormone secreted in excess due to a pituitary tumor is

ACTH (10%)

what keeps prolactin in check


what is the major function of the pituitary

support lactation in the postpartum period
concentrations of prolactin increase 10 fold during pregnancy and lactation

things other than pregnancy and nursing that can cause increased prolactin secretion

nipple piercing, breast augmentation, mastectomy
chronic chest wall stimulation
pituitary stalk lesion
pituitary tumors that secret prolactin
dopamine antagonists (phenothiazines)

prolactin is secreted continuously unless

it is actively inhibited by dopamine

decreased prolactin secretion is caused by

dopamine agonist (cabergoline, bromocriptine, pergoglide)

who are prolactinomas most common in


are prolactinomas usually micro-(<1cm) or macro- (>1cm) adenomas

most are micro <1cm in diameter

premenopausal women with prolactinomas may present with

visual field abnormalities

postmenopausal women with prolactinomas may present with

headaches and visual field disturbances are common
space occupying effects

men with prolactinomas may present with

erectile dysfunction, diminished libido, and occasionally gynecomastia

space occupying effects of pituitary tumors

CSF rhinorrhea (sella turcica or sphenoid sinus)
unilateral defects CN III, IV, VI and ophthalamic & maxillary branches of V (cavernous sinuses)
bi-temporal heminopsia (optic chiasm)
headaches and pituitary insufficiency

when do you order an MRI evaluation of the pituitary on a patient with hyperprolactinemia

when all other possible causes have been ruled out

first thing you treat in a patient with prolactinoma

the underlying problem
ie- if TSH is increased, fix that 1st... then continue on

what is the medical treatment of choice for prolactinomas

cabergoline and bromocriptine
dopamine agonist
80% of patients will experience normal prolactin levels with therapy

when would you utilize the surgical option of traanssphenoid surgery on a patient with a prolactinoma

tumors are unresponsive to medical therapy
tumors affect visual field
tumor exhibits apoplexy
pt is intolerant or refuses medical therapy

when should radiation therapy be utilized on a patient with a prolactinoma

pt has a macroadenoma that enlarges despite medical therapy

what is the risk of radiation therapy in the treatment of prolactinomas

10 - 15% of patients

what stimulates the release of IGF-1

GH stimulates the release of IGF-1 in the liver and other tissues

what increases the release of GH

sleep- associated w/GH peaks
trauma - stress to the body
acute illness- stress to the body

what decreses the release of GH

somatostatin - inhibitory peptide
hyperglycemia/ingestion of food
increased levels of IGF-a - affects feedback loop

GH increases the following

linear growth in children
overgrowth of bones in acral areas
soft tissue growth
fatty acid release from adipose tissue
insulin resistance at peripheral tissues to maintain blood glucose in normal range
muscle growth
increased BMR and increased lean body mass
increased hepatic gluconeogenesis
induces Na+ and water retention->swollen hands and feet

GH will decrease

glucose uptake at muscle cells
peripheral glucose utilization

in adults a GH producing pituitary adenoma will cause

acromegaly (almost always caused by an adenoma)

children with a GH producing adenoma will have

gigantism and tall stature (occurs before epiphyseal plate closes
most are macroadenomas
less than 1% are malignant

musculoskeletal signs of acromegaly include

increased stature
frontal bossing
spade like hands w/widened fingers
sweaty palms
large feet
osteoarthritis (abnormal joint loading)

other than the obvious musculoskeletal signs what are some other signs/symptoms of acromegaly

dilated cardiomyopathy->cardiomegaly-> cardiac failure
impaired glucose tolerance;diabetes mellitus (30%)
headaches, tiredness, excessive sweating
temporal hemainopsia

why do you not measure GH when trying to diagnose acromegaly

GH levels fluctuate, measure IGF-1

if you measure IGF-1 levels and they are abnormal, what do you do next

order fasting IGF & Prolactin

if your patients fasting IGF level is elevated, give 75 g of glucose, then measure GH

if GH is elevated ( >2mU/L) after 60 minutes acromegaly is confirmed
(glucose normally suppresses GH)

what is the imaging study of choice for diagnosing acromegaly

MRI with contrast for hypothalamic or pituitary tumor
(tumor is seen in 90% of pts)
a CT scan be used if MRI is contraindicated

what should be included in your differential diagnosis if there is elevated GH and IGF-1

recent exercise
eating immediately before IGF-1 assay is drawn
acute illness or agitation
diabetes mellitus

some complications of acromegaly are

hypopituitarism, hypertension, impaired fasting glucose, dibetes mellitus, cardiac enlargement, cardiac failure, carpal tunnel syndrome, arthritis

the treatment of choice for acromegaly

pituitary microsurgery
endoscopic transnasal, transsphenoidal resection
symptom remission in 70% of patients

is mediacl treatment alone sufficient in treating acromegaly

not usually options include:
dopamine agonist:cabergoline, bromocriptine (Parlodel)
somatostatin analogue:octreotide and lanreotide
GH recptor antagonist: Pegvisomant

what and when is stereotactic radiosurgery used

when pts with acromegaly fail surgical or medical therapy

describe Cushing's disease

ACTH hypersecretion by a benign pituitary adenoma
3X more frequent in women
excess ACTH from the pituitary -> increased cortisol release from zona fasiculata of the adrenal cortex

pt presents with: central obesity, facial plethora, hypertension, hirsutism, menstrual irregularity, muscle weakness, abdominal striae, thin skin w/easy bruising, and glucose intolerance (or diabetes)


diagnosis of Cushing's disease is done by what test

24 hour urinary free cortisol level + plasma ACTH level

if your patient's UFC is elevated and their ACTH is suppressed

an adrenal tumor is likely

if your patient's UFC is elevated and their ACTH is normal or elevated

Cushing's disease or ectopic ACTH
perform high dose dexamthasone suppression test

if one pituitary hormone os found to be deficient what should you do

measure levels of the other pituitary hormones

you may see isolated deficiencies in these pituitary hormones



global failure of the pituitary gland

invasion, injury, and infarction are

major causes of pituitary insufficiency

sheehan's syndrome

postpartum necrosis
failure to lactate as well as amenorrhea
s/s of hypothyroidism and/or glucocorticoid insufficiency
symptoms could be delayed up to 15 years

the main cause of pituitary insufficiency is

apoplexy (infarction)
acute hemorrhage in a preexisting adenoma

if patient presents with severe headache and visual field deficits

acute hypopituitarism
treat with glucocorticoids immediately
pt requires immediate surgery for decompression of the pituitary fossa

ordered gradual loss of pituitary hormone secretion


if there is an ACTH deficiency

adrenal glands fail to secret sufficient amounts of cortisol

a sudden deficiency in in cortisol will cause

may cause cardiovascular collapse

a chronic deficiency in cortisol may cause

weakness, fatigue, weight loss, hypotension

if there is a TSH deficiency

the thyroid gland fails to secret sufficient amounts of T4 and T3

weakness, fatigue, and weight change are vague symptoms associated with


a deficiency in gonadotropins (FSH & LH)

in childhood- failure to enter normal puberty
in adult females- breast atrophy, loss of pubic hair, infertility, amenorrhea
in adult males- testicula atrophy, decreased libido, loss of body hair, E.D., infertility

a GH deficiency or a defect in a GH receptor

in infants/children- growth retardation, short stature, fasting hypoglycemia
in adults- abd adiposity, reduced strength, decreased lean body mass, impaired psychosocial well-being, increased systolic BP, increased LDL

prolactin deficiency

usually asymptomatic in non-pregant women
loss of lactation in postpartum period

in hypopituitary labs if T4 is low what will TSH be

it will NOT be elevated in response

treatment of pituitary tumor

transsphenoidal resection

treatment for ACTH deficiency

3-7.5 mg of prednisone or 15-30 mg hydrocortisone /day
2/3 in AM and 1/3 in PM
increase dose in stress (acute illness, surgery, trauma)

treatment for TSH deficiency

synthroid (levothyroxine 0.025-0.3 mg daily

treatment for gonadotropin (LH & FSH)

estrogen/progesterone treatment in females
testosterone for males
males-hCG injections, clomiphene
females-clomiphene (induces ovulation)

treatment for GH deficiency

asymptomatic adults: No treatment
somatotropin(hGH) injections for adults
hGH injections for children

treatment excess prolactin causing hypogonadism

dopamine agonist
cabergoline, bromocriptine

what is the major secretory product of the thyroid

T4 - thyroxine

where is T3 mainly produced

90% in peripheral tissues from circulating T4

this hormone is physiologically active


T3's physiological effects

INCREASED: O2 consumption, metabolic rate, heat production, plasma levels of free fatty acids, protein synthesis & degradation, cholesterol excretion to bile, glucose absorption
DECREASED: plasma cholesterol
ACCELERATES: cellular oxidation of free fatty acids
ENHANCES: gluconeogenesis
UP-REGULATES: catecholamine receptors

is most thyroid hormone free or bound to protein

99% of circulating thyroid hormone is bound to protein
thyroxine-binding prealbumin

what hormone levels are measured to evaluate thyroid function

TSH & Free T4

the following tests are used to evaluate thyroid function

serum thyroid hormones
thyroid antibodies (autoimmunity)
RALU-123 & Scan

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