endocrine pituitary gland Flashcards
endocrine glands secrete
hormones directly into the surrounding ECF
exocrine glands secrete
products through ducts
examples of exocrine glands
salivary and sweat glands
examples of endocrine glands
pituitary, thyroid, parathyroid, pancreas, adrenal, ovaries, testes, placenta
endocrine glands control
growth, behavior, metabolism, reproduction
hormones are
chemical messengers that transport info from one set of cells to another (endocrine cells to target cells)
binding to a target cell receptor is the primary event that initiates
a response to a hormone
the hormone receptor has high
specificity and affinity for the correct hormone
the synthesis and secretion of hormones by endocrine glands are regulated by
neural control, biorhythms, and feedback mechanisms
neural control of hormone secretion
can suppress or stimulate secretion
stimuli: pain, smell, touch, stress, sight, taste
hormones under neural control include
catecholamines, ADH, cortisol
biorhythms are
genetically encoded or acquired
can be circadian, weekly, or seasonal and vary with stages of life
pituitary function
collects and integrates information from almost everywhere in body and uses it to control the secretion of hormones
the pituitary and hypothalamus don’t have a
blood brain barrier to allow for feedback products to have a potent effect on them
the anterior lobe of the pituitary
adenohypophysis
the posterior lobe of the pituitary
neurohypophysis
blood supply to the pituitary is via
the superior and inferior hypophyseal arteries
the anterior pituitary secretes which hormones
6 hormones:
growth hormone, adrenocorticotropic, thyroid stimulating, follicle stimulating hormone, luteinizing hormone, prolactin
Thyrotropin releasing hormone pathway
released by hypothalamus to anterior pituitary that will release thyroid stimulating hormone to the thyroid glands
primary peripheral feedback hormone: triiodothyronine
Corticotropin releasing hormone pathway
released by hypothalamus to anterior pituitary to release adrenocorticotropic hormone (ACTH) to adrenal cortex
primary feedback: cortisol
gonadotropin releasing hormone pathway
released from hypothalamus to anterior pituitary to release follicle stimulating and luteinizing hormones to the gonads
primary feedback: estrogen, progesterone, testosterone
what are the hormones of the anterior pituitary that can be releasing or inhibiting
prolactin, growth hormone
primary pituitary disorder
defect to the peripheral endocrine gland (target gland)
secondary pituitary disorder
defect to the pituitary gland (ex. tumor)
tertiary pituitary disorder
defect to the hypothalamus (not common)
anterior pituitary HYPOsecretion causes
nonfunctioning tumors, hypophysectomy, postpartum shock, irradiation, trauma, infiltrative disorders (sarcoidosis)
signs and symptoms with anterior pit HYPOsecretion
visual changes (optic nerve near pit and can be compressed), papilloedema, increased ICP
anterior pituitary HYPERsecretion caused by
caused by benign adenomas usually
3 most common hormones that are secreted with anterior pit HYPERsecretion
prolactin, ACTH, and GH
growth hormone increases during
during stress, hypoglycemia, exercise, and deep sleep
major target for GH is the
liver, stimulates production of insulin like growth factor type 1 which mediates many of the effects of GH
GH hypersecretion
caused by growth hormone secreting pituitary adenoma
in adults - acromegaly
gigantism
acromegaly
sustained hypersecretion of GH after adolescence
gigantism
hypersecretion of GH prior to puberty (before closure of growth plates)
common features of acromegaly
skeletal and soft tissue overgrowth visceromegaly osteoarthritis glucose intolerance skeletal muscle weakness extrasellar tumor extension peripheral neuropathy
comorbities with acromegaly
HTN, cardiomyopathy, ischemic heart disease, diabetes, osteoarthritis, skeletal muscle weakness, increased lung volumes, sleep apnea, increased liver, spleen, kidneys, heart
acromegaly treatment
restore normal GH levels microsurgical removal of the tumor with preservation of the gland transsphenoidal approach - small intracranial approach - large irradiation supressant drug therapy
airway management considerations for acromegaly
enlarged tongue, lips, epiglottis, nasal turbinates, overgrowth of mandible, vocal cord dysfunction/narrowing
prone to upper airway obstruction, difficult mask, impaired visualization of cords, subglottic narrowing, dyspnea/hoarseness
aline considerations for acromegaly
check collateral circulation because there may be hypertrophy of the carpal tunnel ligament which can impede ulnar artery flow
transsphenoidal approach considerations for acromegaly
HOB 15 degrees aline lumbar drain maybe monitor for VAE treat intraop HoTN with hydrocortisone 50-100 mg IV minimal blood loss
venous air embolism s/s
drop in etco2
bradycardia/heart block
millwheel heart sound (heard with precordial or doppler)
complications with transsphenoidal approach
cranial nerve damage, epistaxis, hyponatremia, cerebral spinal fluid leak, DI
diabetes insipidus results in
insufficient ADH
diabetes insipidus diagnosis and treatment
diagnosis: low urine osmolarity, high serum osmolarity, hypernatremia
treat: monitor urine and electrolytes, DDAVP, restrict Na+ intake, fluid replacement
patient education getting transsphenoidal
there will be packing in their nose and they will need to breathe through their mouth when they wake up from surgery
posterior pituitary secretes
ADH and oxytocin
ADH controls
renal water excretion and reabsorption and is a major regulator of serum osmolarity
Oxytocin stimulates
uterine contractions, breast milk ejection, induce labor, decrease postpartum bleeding
posterior pituitary hormones synthesis/pathway
So, oxytocin and ADH are synthesized in the hypothalamus and travel via neurons on the hypothalamic-hypophyseal tract to the posterior pituitary where they are stored in axon terminals, they then are released into the blood when hypothalamic neurons fire
3 types of vasopressin receptors
v1 - mediates vasoconstriction
v2 - mediates water reabsorption in the renal collecting ducts
v3 - found in CNS and stimulate modulation of corticotrophin secretion
what stimulates ADH release
increased plasma sodium, increased serum osmolality, decreased blood volume, smoking, pain, stress, nausea, vasovagal reaction, angII, PPV
neurogenic or central DI caused by
caused by inadequate release of ADH from head trauma, brain tumors, neurosurgery, infiltrating pituitary lesions
nephrogenic DI caused by
renal tubular resistance to ADH
nephrogenic DI may be associated with
hypokalemia, hyperkalemia, genetic mutations, hypercalcemia, medication induced nephrotoxicity
inhibitors of ADH action or release
ethanol, demeclocyline, phenytoin, chlorpromazine, lithium
symptoms of ADH deficiency
polyuria (hallmark sign), dilute urine, dehydration, hypernatremia, low urine osmolarity <300, urine specific gravity <1.010, urine volume >2mL/kg/hr, serum osmolarity >290, sodium >145
hyperreflexia, weakness, lethargy, seizures, coma
major mechanism for controlling DI in awake patients
thirst
mild DI or incomplete DI treatment
meds that augment or release ADH or increase receptor sensitivity
carbamazepine, clofibrate
severe DI or complete DI treatment (plasma osmolarity >290)
DDAVP 1-2 mcg IV/SQ q12 hours or 5-40 mcg intranasal spray BID
aqueous vasopressin 5-10 units IM/SQ q8-12 hours
DDAVP
selective V2 agonist
DOA: 8-12 hours
less vasopressor activity
dose: 5-40 mcg/kg nasally, 0.5-2 mcg/day BID SQ
increases vwb factor (give 30 minutes prior to surgery)
perioperative administration of vasopressin is not necessary for incomplete DI because
the stress of surgery increases ADH secretion
ADH can cause ____ due to ___ and caution is necessary in patients with CAD
hypertension; arterial vasoconstriction
if plasma osmolarity rises above 290 what should be administered
D5W (free water)
hypersecretion of ADH can lead to
SIADH (syndrome of inappropriate ADH)
SIADH
disorder characterized by high circulating levels of ADH relative to plasma osmolarity and serum sodium concentration
ADH secretion causes the kidneys to ___ in SIADH
continue to reabsorb water
the urine is ___ relative to plasma and urine output is ___ in SIADH
hypertonic; low
SIADH vs DI
SIADH - serum osmolarity, sodium, and urine volume are low, urine osmolarity is hypertonic, treat with fluid restriction and hypertonic saline
DI - serum osmolarity, sodium, and urine volume are high, urine osmolarity is hypotonic, treat with DDAVP or vasopressin
clinical features of SIADH
water intoxication dilutional hyponatremia brain edema (lethargy, HA, nausea, confusion, seizures, coma)
severity of symptoms of dilutional hyponatremia is related to
the degree of hyponatremia and the rate of decrease in serum sodium
what procedure can cause dilutional hyponatremia?
TURP
causes of inappropriate secretion of ADH
hypothyroidism, pulmonary infection, lung carcinoma*, head trauma, intracranial tumors, pituitary surgery, meds (carbamazepine, TCAs, chlorpropamide, cyclophosphamide, oxytocin, nicotine, clofibrate)
neoplasms, especially small cell carcinomas of the lung are a common cause of
SIADH
mild SIADH with no symptoms of hyponatremia treatment
water restriction of 800-`1000mL/day of NS
SIADH with acute,severe hyponatremia (plasma sodium <115-120) or acute neurological symptoms treatment
IV hypertonic saline w/ or w/o loop diuretic
what can happen if rapidly increase sodium levels
central pontine demyelination syndrome = acute loss of brain water and neurological damage
plasma concentration of sodium must be replaced slow at a rate not to exceed
1-2 mEq/L or 6-12 mEq/L in 24 hours
what is something we can easily prevent in patients with SIADH perioperatively
prevent nausea!
