Endocrine Pituitary Gland Flashcards
Endocrine glands
secrete hormones directly into the surrounding ECF
Exocrine glands
products are discharged through ducts
ex. salivary, sweat glands
What are the important endocrine glands?
pituitary gland thyroid gland parathyroid glands pancreas adrenal glands ovaries & testes placenta
The mediators of the endocrine system are
*hormones
Hormones are _________ that transport information (a message) from one set of cells (endocrine cells) to another (target cells)
chemical messengers***
____________ is the primary event that initiates a response to a hormone
binding to a target cell receptor
The hormone receptor has high
specificity and affinity for the correct hormone
The location of the receptor directs the
hormone to the correct target organ or target cell
Some hormones, such as ________, have wide spread target sites while others, such as _______, act on one target issue
insulin; TSH
The synthesis and secretion of hormones by endocrine glands are regulated by:
neural control
biorhythms
feedback mechanisms
Describe neural control
can suppress or stimulate hormone secretion
stimuli include pain, smell, touch, stress, sight, & taste
hormones under neural control include catecholamines, ADH, cortisol
Describe biorhythms
genetically encoded or acquired biorhythms
the intrinsic hormonal oscillations may be circadian, weekly, or seasonal
they may vary with stages of life
Feedback mechanisms include
negative feedback
positive feedback
The regulatory pathway of tropic hormones includes
hypothalamus–> pituitary gland–> target gland
the target gland hormone provides feedback to the pituitary gland and the hypothalamus
The anterior pituitary secretes these hormones
growth hormone adrenocorticotropic hormone thyroid-stimulating hormone follicle-stimulating hormone Luteinizing hormone prolactin
The blood supply to the pituitary is via the
superior and inferior hypophyseal arteries
The pituitary collects and integrates information from almost everywhere in the body
& uses this information to control the secretion of vital pituitary hormones
Pituitary hormone secretion is regulated by
feedback control from peripheral target organ hormones or other target products
The pituitary and hypothalamus have virtually no
blood brain barrier; this allows feedback products to have a potent effect on them
The pituitary located at the base of the brain and has two distinct portions:
the anterior lobe (adenohyophysis) and the posterior lobe (neurohypophysis)
Describe the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for thyrotropin-releasing hormone.
Anterior pituitary target cell type: Thyrotroph
Anterior pituitary hormone: Thyroid-stimulating hormone (TSH)
Hormone target site: thyroid glands
Primary peripheral feedback hormone: Triiodothyronine
Describe the the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for corticotropin-releasing hormone.
anterior pituitary target cell type: corticotroph
anterior pituitary hormone: adrenocorticotropic hormone
hormone target site: zona fasciculata & zona reticularis of adrenal cortex
primary peripheral feedback hormone: cortisol
Describe the the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for gonadotropin-releasing hormone.
anterior pituitary target cell type: gonadotroph
anterior pituitary hormone: follicle stimulating hormone luteinizing hormone
hormone target site: gonads (testes, ovaries)
primary peripheral feedback hormone: estrogen, progesterone, testosterone
Describe the the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for prolactin-releasing factor.
anterior pituitary target cell type: lactotroph
anterior pituitary hormone: prolactin
Hormone target site: breasts
primary peripheral feedback hormone: none
Describe the anterior pituitary target cell type for prolactin-inhibitory factor
lactotroph
there is no peripheral feedback hormone
Describe the the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for growth-hormone releasing hormone
anterior pituitary target cell type: somatroph
anterior pituitary hormone: growth hormone
hormone target site: all tissues
primary peripheral feedback hormone: growth hormone, insulin, growth factor-1
Describe the the anterior pituitary target cell type, the anterior pituitary hormone, the hormone target site, and the primary peripheral feedback hormone for growth hormone inhibitory factor (somatostatin).
anterior pituitary target cell type- somatroph
anterior pituitary hormone: growth hormone
hormone target site: all tissues
primary peripheral feedback hormone: growth hormone, insulin, growth factor 1
Pituitary disorders can be
primary disorder
secondary disorder
tertiary disorder
Describe what a primary pituitary disorder involves
defect to the peripheral endocrine gland
Describe a secondary pituitary disorder.
defect to the pituitary
Describe a tertiary disorder.
defect to the hypothalamus
Anterior pituitary hyposecretion is known as
panhypopituitarism- generalized pituitary hypofunction
Causes of anterior pituitary hyposecretion include:
nonfunctioning tumors compress and destroy normal pituitary tissue hypophysectomy postpartum shock irradiation trauma infiltrative disorders
Surgical removal of a tumor of the pituitary gland may require
thyroid hormone
glucocorticoids
vasopressin
Surgical removal of the tumor or the pituitary gland can be done to
decompress or remove the tumor
to control bleeding
Anterior pituitary hypersecretion is usually caused by
genign adenomas
The three most common tumors of the anterior pituitary produce
prolactin–> amenorrhea, infertility/decreased libido, impotence
ACTH–> Cushing’s disease
GH–> promotes growth of all tissues capable of growing
tumors that secrete thyrotropin or gonadotropin are very rare
Growth hormone secretion increases during
stress, hypoglycemia, exercise, and deep sleep
Growth hormone exerts its effects on
almost every part of the body
Pulsatile fluctuations of growth hormone releasing hormone and growth hormone inhibiting hormone regulate
synthesis throughout the day
A major target for growth hormone is
the liver- GH stimulates production of insulin-like growth factor type 1 (IGF-1) which mediates many of the effects of GH
_______________ undergo hypertrophy and hyperplasia due to GH and IGF-1
skeletal muscle, heart, skin, and visceral organs
Growth hormone hypersecretion is usually caused by a
growth hormone secreting pituitary adenoma
Growth hormone hypersecretion is known as _____ in adults
acromegaly
acromegaly is the sustained hypersecretion of GH after adolescence
Gigantism is the
hypersecretion of GH prior to puberty (before closure of the growth plates- may reach 8 to 9 feet tall)
Common features of acromegaly include
skeletal overgrowth, soft tissue overgrowth, visceromegaly, osteoarthritis, glucose intolerance, skeletal muscle weakness, extrasellar tumor extension, peripheral neuropathy, challenging intubations
Comorbidities of acromegaly include
hypertension, cardiomyopathy, ischemic heart disease, diabetes, osteoarthritis, skeletal muscle weakness/fatigue, increased lung volumes, sleep apnea (d/t all of the airway changes), increased liver, spleen, kidneys, & heart
Treatment for acromegaly includes
restore normal GH levels
preferred initial treatment is microsurgical removal of the tumor with preservation of the gland
for small tumors, a transsphenoidal approach- going through sinus cavities
for large tumors an intracranial approach
irradiation and/or suppressant drug therapy are adjunctive treatments or for non surgical candidates
Anesthetic considerations for the surgery patients with acromegaly include:
airway management
sleep apnea >60%
postoperative respiratory obstruction or failure
systemic hypertension, ischemic heart disease, and arrhythmias
skeletal muscle weakness
hyperglycemia
entrapment neuropathies
if adrenal or thyroid axis impairment- may need stress-level glucocorticoid therapy & thyroid replacement
Describe the airway management concerns for the patient with acromegaly.
enlarged tongue, lips, nasal turbinates, & epiglottis, overgrowth of the mandible, vocal cord dysfunction
lead to upper airway obstruction, difficult mask fit, impaired visualization of cords, subglottic narrowing, dyspnea/hoarseness–> larynx involved
Preoperative preparation for the patient with pituitary surgery includes
thorough H&P concentrate on symptoms associated with acromegaly
labs should include glucose, electrolytes, and hormone levels
images should be done to determine the extent of the tumor invasion
EKG- look for signs of left ventricular hypertrophy and arrhythmias
consider an echo if the patient has cardiac dysfunction
optimized cardiac function
check collateral circulation at the wrist prior to a-line insertion–> hypertrophy of carpal tunnel ligament may impede ulnar artery flow
Anesthetic considerations for the transsphenoidal approach include
head of bed is elevated 15 degrees
a-line is usually inserted
a lumbar drain may be placed
consider monitoring for venous air emboli
usually not significant blood loss
use of submucosal injection of epinephrine containing solutions or use of topical vasoconstrictors may result in hypertension
the anesthetic technique chose should allow for muscle relaxation, smooth extubation and rapid neurlogoical assessment
For the transphenoidal approach intraoperative hypotension may be due to
inadequate cortisol secretion- replace with hydrocortisone 50 to 100 mg IV
For the transsphenoidal approach, blood loss is
usually minimal, there is the potential for large amounts of blood loss if a large cavernous sinus is inadvertently entered
With the transsphenoidal approach, a venous air embolism is possible if
large tumor invading a large sinus and/or steep head up position
Surgical complications of transsphenoidal approach include
cranial nerve damage, epistaxis, hyponatremia, cerebral spinal fluid leaks
diabetes insipidus
Diabetes insipidus can occur
intra or postoperatively because of surgical trauma to the posterior pituitary- the trauma is reversible
results in insufficient ADH
Diagnosis of diabetes insipidus is through
measuring serum electrolytes, hyperosmolar plasma, and urine osmolariy
Treatment of diabetes insipidus involves
monitor urine output and electrolytes- can give DDAVP, restrict Na intake
The posterior pituitary secretes
antidiuretic hormone (ADH or arginine vasopressin) and oxytocin
ADH controls
renal water excretion and reabsorption and is a major regulator of serum osmolarity
Oxytocin powerfully stimulates
uterine contractions, stimulates myoepithelia cells of the breast for milk ejection during lactation, is used for inducing labor and decreasing postpartum bleeding
The posterior pituitary antidiuretic hormone has three types of vasopressin receptors:
V1- mediates vasoconstriction
V2- mediates water reabsorption in the renal collecting ducts
V3- found in the CNS and stimulate modulation of corticotrophin secretion
Stimuli for ADH release include
increased plasma sodium increased serum osmolality decreased blood volume smoking (nicotine) pain stress nausea vasovagal reaction angiotensin II positive pressure ventilation
Types of diabetes insipidus include
neurogenic or central- caused by inadequate release of ADH
nephrogenic- renal tubular resistance to ADH
Causes of neurogenic diabetes insipidus include
head trauma, brain tumors, neurosurgery, infiltrating pituitary lesions
Neurogenic diabetes insipidus may be associated with
hypokalemia, hyperkalemia, genetic mutations, hypercalcemia, and medication induced nephrotoxicity
Inhibitors of ADH action or release include
ethanol, demeclocycline, phenytoin, chloropromazine, lithium
Symptoms of ADH deficiency include
polyuria- Hallmark symptom
inability to produce a concentrated urine
dehydration
hypernatremia
low urine osmolarity- <300 mOsm/L
urine specific gravity <1.010
Urine volume >2 mL/kg/hr
Serum osmolarity >290 mOsm/L and sodium >145 mEq/L
neurological symptoms of hyperreflexia, weakness, lethargy, seizures, and coma
______ is the major mechanism for controlling DI in awake patients
thirst
Medical treatment of DI depends on
the degree of ADH deficiency
Mild DI or incomplete DI can be treated with
medications that augment or release of ADH or increase receptor sensitivity
such as chlorpropamide, carbamazepine, clofibrate
Significant DI-complete DI can be treated with
ADH preparations such as DDAVP
it is considered to be plasma osmolarity >290 mOsm/L
DDAVP is a
selective V2 agonist with a duration of action of 8 to 12 hours
can be administered orally, subcutaneously, IV, & nasally
DDAVP has less
vasopressor activity
enhances antidiuretic properties
Preoperative assessment for the patient with DI includes
careful assessment of plasma electrolytes, renal function, and plasma osmolarity
dehydration makes these patients very sensitive to the hypotensive effects of general anesthetics
intravascular volume should be replaced with isotonic fluids over 24 to 48 hours
Preoperative treatment of diabetes insipidus includes preoperative administration of vasopressin is
not necessary for incomplete DI because the stress of surgery increases ADH secretion
Complete DI preoperative treatment includes
desmopressin
vasopressin
caution is necessary in patients with CAD–> ADH substitutes like ADH cause hypertension due to arterial vasoconstriction
Labs to measure for the patient with DI in the intraoperative and immediate postoperative period include
plasma osmolarity, urine output, and serum sodium
________ fluids should be given during the intraoperative period for patients with ADH deficiency and if the plasma osmolarity rises above 290 mOsm/L, _______ should be administered
isotonic fluids
D5W
Hypersecretion of ADH is known as
syndrome of inappropriate ADH
SIADH is a disorder characterized by
high circulating levels of ADH relative to plasma osmolarity and serum sodium concentration
With SIADH, ADH secretion cause the
kidneys to continue to reabsorb water despite the presence of hyponatremia & plasma hypotonicity
expansion of ICF and ECF occurs as well as hemodilution and weight gain
In SIADH, urine is
hypertonic relative to plasma and urine output is usually low
Treatment for SIADH includes
fluid restriction
if patient is symptomatic or serum Na is <115-120 mEq/L consider hypertonic saline
Clinical features of SIADH include
water intoxication, dilutional hyponatremia, & brain edema
Brain edema results in
lethargy, headache, nausea, mental confusion, seizures, and coma
With dilutional hyponatremia, the severity of symptoms is
related to the degree of hyponatremia and the rate of decrease in serum sodium
Causes of SIADH include
hypothyroidism, pulmonary infection, lung carcinoma, head trauma, intracranial tumors, pituitary surgery, and medications
The most common cause of SIADH is
neoplasms particularly small-cell carcinomas of the lung
Preoperative evaluation of the patient with SIADH includes
careful volume status evaluation
perioperative fluid management- fluid restriction that involves the use of an isotonic solution
CVP can help with guiding volume replacement
frequent measures of urine output, urine osmolarity, plasma osmolarity, and serum sodium concentration
prevent nausea because it is potent for releasing ADH
For mild SIADH with no symptoms of hyponatremia, the treatment is
treat with water restriction of 800 to 1000 mL/day of NS
SIADH with acute, severe hyponatremia is defined as a plasma sodium concentration of
<115-120 mEq/L or acute neurological symptoms may require IV hypertonic saline with or without a loop diuretic
Serum sodium should be measured every
2 hours during treatment
To prevent acute loss of brain water and possible permanent neurological damage
known as central pontine demyelination syndrome, plasma concentration of Na must be replaced slowly at a rate not to exceed 1 to 2 mEq/L/hr or 6 to 12 mEq/L in 24 hours
