Endocrine Pituitary Gland Flashcards
endocrine gland
secretes hormone directly into the surrounding ECF
exocrine gland
products discharged through ducts
important endocrine glands (7)
- pituitary gland
- thyroid gland
- parathyroid glands
- pancreas
- adrenal glands
- ovaries and testes
- placenta
hormones
- mediators of the endocrine system
- chemical messengers that transport information (a message) from one set of cells (endocrine cells) to another (target cells)
what is the primary event that initiates a response to the hormone?
binding to a target cell receptor
hormone receptor
- high specificity and affinity for the correct hormone
- location of the receptor directs the hormone to the correct target organ or target cell
neural control of hormone secretion
- can suppress or stimulate hormone secretion
- stimuli include pain, smell, touch, stress, sight, and taste
- hormones under neural control include catecholamines, ADH, cortisol
biorhytm control of hormone secretion
- genetically encoded or acquired biorhythms
- intrinsic hormonal oscillations may be circadian, weekly, or seasonal
- may vary with stages of life
feedback mechanism control of hormone secretion
- negative feedback loop
- positive feedback loop
pituitary gland function
- collects and integrates information from almost everywhere in the body
- uses information to control secretion of pituitary hormones
pituitary gland hormone secretion regulation
-regulated by feedback control from peripheral target organ hormones or other target products
do the pituitary and hypothalamus have a BBB?
no!! allows feedback products to have a potent effect on them
location of pituitary gland
sella turcica at base of brain
two portions of pituitary gland
- anterior lobe (adenohypophysis)
- posterior lobe (neurohypophysis)
what provides blood supply to the pituitary gland?
superior and inferior hypophyseal arteries
6 hormones secreted by anterior pituitary
- growth hormone (somatostatin) (GH)
- adrenocorticotropic hormone (ACTH)
- thyroid stimulating hormone (TSH)
- follicle stimulating hormone (FSH)
- luteinizing hormone (LH)
- prolactin
thyroid hypothalamic and anterior pituitary hormone system
- hypothalamic hormone = thyrotropin releasing hormone
- ant pit target cell = thyrotroph
- ant pit hormone = TSH
- hormone target site = thyroid gland
- primary feedback hormone = triiodothyronine (T3)
cortisol hypothalamic and anterior pituitary hormone system
- hypothalamic hormone = corticotropin releasing hormone
- ant pit target cell = corticotroph
- ant pit hormone = ACTH
- hormone target site = zona fasciculata and zona reticularis of adrenal cortex
- primary feedback hormone = cortisol
gonad hypothalamic and anterior pituitary hormone system
- hypothalamic hormone = gonadotropin releasing hormone
- ant pit target cell = gonadotroph
- ant pit hormone = FSH, LH
- hormone target site = gonads (ovaries, testes)
- primary feedback hormone = estrogen, progesterone, testosterone
pituitary disorders classification
- primary disorder = defect to the peripheral endocrine gland
- secondary disorder = defect to pituitary
- tertiary disorder = defect to the hypothalamus
panhypopituitarism
generalized pituitary hypofunction
causes of panhypopituitarism
- nonfunctioning tumors compress/destroy normal pituitary tissue
- hypophysectomy
- postpartum shock
- irradiation
- trauma
- infiltrative disorders (sarcoidosis)
treatment of panhypopituitarism
- surgical removal of the tumor or the pituitary gland
- decompress or remove tumor
- may require hormone replacement post op (TH, glucocorticoids, vasopressin)
anterior pituitary hypersecretion
-usually caused by benign adenomas
three most common tumors that cause anterior pit hypersecretion
- prolactin = amenorrhea, infertility, decreased libido, impotence
- ACTH = cushings
- GH = promotes growth of ALL tissues capable of growing
When does GH secretion increase
- stress
- hypoglycemia
- exercise
- deep sleep
what is a major target of GH?
- liver
- GH stimulates production of insulin-like growth factor type 1 (IGF-1) which mediates many of the effects of GH
what other tissues/organs grow because of GH?
- skeletal muscle
- heart
- skin
- other visceral organs
GH Hypersecretion
- usually caused by GH secreting pituitary adenoma
- adults = acromegaly
- children before puberty = gigantism
acromegaly
sustained hypersecretion of GH after adolescence
gigantism
hypersecretion of GH prior to puberty, before closure of growth plates
may reach 8 to 9 feet tall
common features of acromegaly
- skeletal overgrowth (overgrowth of mandible)
- soft tissue overgrowth (narrow glottic opening, large tongue)
- visceromegaly
- osteoarthritis
- glucose intolerance
- skeletal muscle weakness
- extrasellar tumor extension
- peripheral neuropathy
comorbidities associated with acromegaly
- HTN
- cardiomyopathy
- ischemic heart disease
- DM
- osteoarthritis
- skeletal muscle weakness/fatigue
- increased lung volumes
- sleep apnea (due to airway changes)
- increased size of liver, spleen, kidneys and heart
treatment of acromegaly
- restore normal GH levels
- microsurgical removal of tumor with preservation of the gland (preferred)
- small tumor = transsphenoidal approach
- large tumor = intracranial
- irradiation and/or suppressant drug therapy are adjunctive treatments for non surgical conditions
airway considerations for acromegaly
- airway changes = large tongue, lips and epiglottis, overgrowth of mandible, vocal cord dysfunction and enlarged tongue, epiglottis and nasal turbinates
- upper airway obstruction
- difficult mask
- impaired visualization of cords
- subglottic narrowing
- dyspnea/hoarseness (larynx involved)
- subglottic stenosis common (may need smaller tube)
other anesthetic considerations for acromegaly
- many have sleep apnea
- patients often have postop respiratory obstruction or failure
- may have HTN, ischemic heart disease, and arrhythmias
- skeletal muscle weakness
- hyperglycemia (monitor BG carefully)
- may have thyroid axis impairment too –> may need stress steroids and thyroid replacement
- entrapment neuropathies common
preop prep for pituitary surgery
- thorough history and physical
- labs = glucose, lytes, hormone levels
- imaging to determine extent of tumor invasion
- EKG - signs of LV hypertrophy and arrhythmias
- consider ECHO if cardiac dysfunction present
- optimize CV function before surgery
- allen test before a line insertion
anesthetic considerations for transsphenoidal approach
- HOB elevated 15 degrees
- art line for BP monitoring
- lumbar drain may be placed
- consider monitoring for VAE
- usually not significant blood loss
- submucosal injection of EPI or topical vasoconstrictors may result in HTN
- anesthetic technique chosen should allow for muscle relaxation, smooth extubation, and rapid neuro assessment
- hypotension may be due to inadequate cortisol - replace with hydrocort 50-100 mg IV
complications of transsphenoidal approach
- CN damage
- epistaxis
- hyponatremia
- CSF leaks
- DI
Diabetes insipidus (DI)
- can occur intra or post op because of surgical trauma to post pit (trauma is reversible)
- results in insufficient ADH
- diagnosis made by measuring serum lytes, plasma osm, urine osm
- treatment = monitor UOP and lytes; DDAVP, restrict sodium intake
posterior pituitary hormones
- ADH (arginine vasopressin)
- oxytocin
ADH
controls renal water excretion and reabsorption
major regulator of serum osmolarity
oxytocin
stimulates uterine contractions, stimulates myoepithelia cells of breast for milk ejection during lactation, used for inducing labor and decreasing postpartum bleeding
three types of vasopressin receptors
- V1 - vasoconstriction
- V2 - water reabsorption in renal collecting ducts
- V3 - found in CNS and stimulates modulation of corticotrophin secretion
posterior pit stimuli for ADH release
- increased plasma sodium
- increased serum osm
- decreased blood volume
- smoking (nicotine)
- pain
- stress
- nausea
- vasovagal reaction
- ang II
- PPV
types of DI
- neurogenic or central = caused by inadequate release of ADH
- nephrogenic = renal tubular resistance to ADH
causes of neurogenic DI
- head trauma
- brain tumor
- neurosurgery
- infiltrating pituitary lesions
what can nephrogenic DI be associated with
- hypokalemia
- hyperkalemia
- genetic mutations
- hypercalcemia
- medication induced nephrotoxicity
inhibitors of ADH action or release
- ethanol
- demeclocycline
- phenytoin
- chlorpromazine
- lithium
ADH deficiency symptoms
- polyuria (hallmark sign)
- inability to produce concentrated urine
- dehydration
- hypernatremia
- low urine osm (<300 mOsm/L)
- urine spec gravity < 1.010
- urine vol > 2 mL/kg/hr
- serum osm > 290 mOsm/L
- sodium > 145 mEq/L
- neuro symptoms = hyperreflexia, weakness, lethargy, seizures, coma
medical treatment for mild or incomplete DI
- meds that augment the release of ADH or increase receptor sensitivity
- chloropropamide
- carbamazepine
- clofibrate
medical treatment for significant DI
-ADH preparations like DDAVP
DDAVP
- selective V2 agonist
- DOA = 8-12 hours
- less vasopressor activity
- enhanced antidiuretic properties
- admin - oral, subQ, IV
posterior pituitary pre op assessment considerations
- careful assessment of plasma lytes, renal function, and plasma osm
- dehydration = sensitive to hypotensive effects of anesthetics
- intravascular volume replacement (24-48 hours before) with isotonic fluids
preop treatment of incomplete DI
-DDAVP treatment not necessary because surgical stress stimulates ADH secretion
preop treatment of complete DI
- DDAVP (1-2 mcg IV or subQ)
- aqueous vasopressin (5-10 units IM or SubQ)
- caution needed for patients with CAD (because of hypertension caused by ADH)
what do you do if the plasma osm rises above 290?
give D5W
SIADH
- syndrome of inappropriate antidiuretic hormone; characterized by high circulating levels of ADH releative to plasma osm and serum sodium concentration
- increased ADH causes kidneys to continue to reabsorb water despite presence of hyponatremia and hypotonicity of plasma
- expansion of ICF and ECF occurs along with hemodilution and weight gain
- urine - hypertonic relative to plasma and UOP low
SIADH treatment
- fluid restriction
- if patient symptomatic or serum sodium is <115-120, consider hypertonic saline
clinical features of SIADH
- water intoxication
- dilution hyponatremia
- brain edema
s/s of brain edema
- lethargy
- HA
- nausea
- mental confusion
- seizures
- coma
causes of SIADH
- hypothyroidism
- pulmonary infection
- lung carcinoma
- head trauma
- intracranial tumors (neoplasms esp small cell carcinomas)
- pituitary surgery
- meds
meds that cause SIADH
- carbamazepine
- tricyclic antidepressants
- chloropropamide
- cyclophosphamide
- oxytocin
- nicotine
- clofibrate
treatment of SIADH
- mild = water restriction of 800-1000 mL/day
- acute/severe hyponatremia = sodium concentration of <115-120; hypertonic
- SLOWLY increase to prevent central pontine demyelination syndrome
- serum sodium measured Q2H during treatment
rate to increase sodium in SIADH
1-2 mEq/L/hr or 6-12 mEq/L in 24 hours
preop eval of patient with SIADH
- careful volume status eval
- fluid restriction that involves isotonic solution
- CVP/SVV/PPV can help guide vol replacement
- measure UOP, urine osm, plasma osm, and plasma sodium
- prevent nausea because this will increase release of ADH
