Week 13 - Endocrine Flashcards
Where is the Pituitary Gland and what does it do?
It is attached to the Hypothalamus via pituitary stalk (Infundibulum) and is located in the Sella Turcica of the sphenoid bone
“Master Gland” – secretes at least 8 hormones that regulate organ function
*Critical to survival
What hormones does the Anterior Pituitary Gland produce?
ACTH (Adrenocorticotropic Hormone)
TSH (Thyroid-Stimulating Hormone)
GH (Growth Hormone)
PRL (Prolactin)
LH (Luteinizing Hormone)
FSH (Follicle-Stimulating Hormone)
What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of ACTH (adrenocorticotropic hormone)?
Released via Corticotropin-releasing hormone
Inhibited via glucocorticoids (cortisol)
Target = Adrenal Gland
Effect = secretion of the adrenal cortex (especially glucocorticoids - cortisol), formation of cholesterol in adrenal cortex
*ACTH levels are high in the mornings and low in the evening
What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of TSH?
Released via thyrotropin-releasing hormone
Inhibited via T3 and T4
Target = Thyroid gland
Effect = secretion of thyroid hormones
*SNS stimulation and corticosteroids suppress secretion of TSH
What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of GH (growth hormone)?
Released via growth hormone-releasing hormone
Inhibited via somatostatin, growth hormone, insulin-like growth factor-1,
Target = Liver, adipose tissue
Effects = growth of all tissues, increased rates of protein synthesis (anabolic effect), promotes lipid and carbohydrate metabolism, sodium and water retention
*most striking and specific effect is stimulation of linear bone growth
What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of prolactin (PRL)?
Released during pregnancy
Inhibited via dopamine
Target = ovaries, mammary glands
Effects = milk production (growth and development of breast in preparation for breast feeding), lipid and carbohydrate metabolism
*little metabolic activity
What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of LH and FSH?
Released via gonadotropin-releasing hormone
Inhibited via estrogen, testosterone
Target = gonads
Effects = sex hormone production and pubertal maturation
What are the 3 ways hyperpituitarism presents?
- Hormonal Hypersecretion
- Local mass effects (including pituitary hypofunction due to compression of normal gland)
- Incidental discovery during cranial imaging for unrelated condition
- Almost always related to pituitary adenoma – 10% of brain neoplasms
- Very often asymptomatic
What does growth hormone sitmulate?
- Longitudinal growth of bones, bone density, stimulates chondrocyte formation and increases muscle mass
- Acts on liver to stimulate gluconeogenesis and promote fat breakdown
- Increased mobilization of free fatty acids (ketogenic effect)
*high in childhood, maximal at puberty and decreases with age
What causes gigantism and acromegaly? What are their characteristics?
Hypersecretion of growth hormone by the anterior pituitary
- Gigantism: during childhood when growth plates are not closed
- Acromegaly: in adults – causes increased size of soft tissue in nose, mouth, tongue, and lips – develop cardiac disease, HTN, ventricular hypertrophy, OSA/airway obstruction
-leads to increased production of insulin like growth factor (IFG-1) by the liver
What is Cushing’s Disease?
Unregulated hypersecretion of ACTH by Pituitary adenoma
Hypercortisolism
- systemic HTN is most common manifestation (secondary to LV hypertrophy – concentric remodeling of heart)
- glucose intolerance occurs ~>60% (DM occurs in 1/3 of patients)
- moon facies (high incidence of OSA - no association w/ more difficulty w/ intubation)
Difference between the anterior pituitary and posterior pituitary
Anterior Pituitary = glandular secretory organ responsible for producing many hormones
Posterior Pituitary = a collection of axon terminals that arise from supraoptic and paraventricular nuclei of the hypothalamus responsible for secreting Oxytocin and Vasopressin
What is the primary stimulus for ADH secretion?
Increased Plasma Osmolarity
*other factors include: left atrial distention, decreased circulating blood volume, decreased arterial pressure, exercise, and certain emotional states
What is the function of both ADH and Oxytocin?
ADH - controls water secretion and extracellular fluid osmolality (controversially more potent vasoconstrictor than angiotensin II)
Oxytocin - promotes milk letdown and uterine smooth muscle contraction
*one of the few hormones with a positive feedback loop
Diabetes Insipidus vs Syndrome of Inappropriate ADH (SIADH)
Diabetes Insipidus = absence of ADH secretion
- most commonly associated with pituitary surgery (commonly transient)
- symptoms: abrupt onset of polyuria, thirst, and polydipsia (excessive water loss, hypernatremia)
SIADH = inappropriately high levels of ADH
- most commonly associated with CNS injury, trauma, and cancer (especially lung CA)
- symptoms: hyponatremia and sequella related to it
What action does vasopressin have on V1, V2, and V3 receptors?
V1: Stimulates V1 receptors in the vasculature to promote vasoconstriction
V2: Acts on renal collecting ducts – increases permeability to water (increases reabsorption of water) = more concentrated urine
V3 receptors are found on anterior pituitary - coupled with second messenger system – have a role in secretion of ACTH
What is the physiologic function of Oxytocin? What are the adverse effects when administered?
Stimulate cervical dilation and uterine contractions during labor
Allow milk to be let down into the subareolar sinuses during lactation
AE: water retention and hyponatremia
-IV admin causes vasodilation and subsequent hypotension with reflex tachycardia
What is the role of Parathyroid hormone?
Plays chief role in bone remodeling and Calcium homeostasis — secreted by Chief cells in the Parathyroid in response to hypocalcemia and elevated phosphorous levels
- stimulates bone resorption which releases Ca++ into the blood stream
- causes Ca++ reabsorption into circulation and phosphate excretion via the kidney
- facilitates Vitamin D conversion to its activated form to increase GI absorption of Calcium
*Net result of interactions of PTH, Ca, Vit D, and Calcitonin is maintenance of normal plasma Ca++ concentration — helps maintain normal cell function, nerve transmission, membrane stability, bone integrity, coagulation and intracellular signaling
What are the types of Hyperparathyroidism?
Primary – Excess PTH production
- most often due to parathyroid gland hyperplasia or tumor (this increases bone resorption and extracellular Ca++)
- Clinical signs = hypercalcemia, hypophosphatemia, nephrolithiasis, osteoporosis, fatigue, weakness, difficulties w/ cognition
- Treatment = surgical excision of parathyroid glands or tumor
Secondary – Generally a complication of chronic renal failure, but can be due to any disease causing hypocalcemia
What are the anesthetic considerations with Hyperparathyroidism?
Thorough preop eval to focus on effects of hypercalcemia and the degree of CV and/or renal complications
- ECG may be warranted (show shortened PR and QT intervals, potential for cardiac arrhythmias, pt may be hypertensive and hypovolemic - severe hypercalcemia)
- Focus should be on emergence in terms of potential concerns — surgery on thyroid or parathyroid glands can result in damage to the recurrent laryngeal nerve, airway swelling and hematoma formation
What does the Recurrent Laryngeal Nerve innervate and when can injury occur and what does it cause?
- Sensory innervation below true cords and into upper trachea
- Motor innervation to all intrinsic laryngeal muscles except cricothyroid and external branch of superior laryngeal nerve
Injury can occur with intubation, neck surgery, stretching of neck
- Unilateral Injury causes cord on injured side to assume midline position = hoarseness
- Bilateral Injury causes both cords to close to midline (adducted) position = aphonia and airway obstruction occurs ***airway emergency
What is hypoparathyroidism associated with and what is a major concern with it?
Generally associated with other endocrine disorders and as a result of surgical removal of parathyroid glands
- hypocalcemia is a major concern with inadvertent removal of parathyroid glands
- tetany related to hypocalcemia results in painful muscle spasms of facial muscles and extremities. also laryngeal muscle spasm and upper airway obstruction are possible
- ECG changes include prolonged QT and possible heart block
What are the different types of Multiple Endocrine Neoplasia?
MEN-1: rare, autosomal dominant syndrome
- parathyroid hyperplasia
- pituitary adenoma
- pancreatic neuroendocrine tumor
MEN-2A: autosomal dominant with incomplete penetrance and variable expression
- parathyroid hyperplasia
- medullary thyroid cancer
- pheochromocytoma
What is the physiology of the Thyroid gland?
Acinar gland positioned in the neck, anterior to the trachea
Rich vascular supply from superior and inferior thyroid arteries
Innervation from ANS
Divided into right and left lobes by thyroid isthmus
*made up of multiple types of cells – follicular cells, endothelial cells, para-follicular or C cells, fibroblasts, lymphocytes and adipocytes
What is the role of thyroid hormones?
Play a major role in normal growth and development
Play a chief role in cellular energy metabolism – stimulate carbohydrate metabolism and facilitate mobilization of free fatty acids
Increase oxygen consumption in nearly all tissues, expect the brain
- Thyrotropin releasing hormone (TSH) is produced in the hypothalamus and released in response to decreased free circulating thyroid hormone
- Iodide is required for thyroid hormone synthesis – body readily absorbs necessary iodine from dietary sources
*Thyroid gland also secretes calcitonin - important for calcium ion use
What are the three reasons thyroid disease and dysfunction occur?
As a result of alterations in levels of thyroid hormones
Impaired metabolism of those hormones
Resistance to effects of thyroid hormones
What are the two types of hypothyroidism?
Primary - Disease at the level of the thyroid gland (destruction of actual thyroid gland) – increased TSH levels, low thyroid hormones
*autoimmune disease, surgical excision or radioactive iodine therapy (iatrogenic causes)
Secondary - Dysfunction outside the gland – low TSH and thyroid hormone
*most often dysfunction of hypothalamus or pituitary gland – decreased thyroid hormone released from thyroid gland
*Lithium, amiodarone, iron and other medications can cause iatrogenic causes of hypothyroidism
What are the signs and symptoms of hypothyroidism?
Generally vague and nonspecific:
- Fatigue
- Lethargy
- Joint pains
- Muscle aches
- Cold intolerance
- Constipation
- Change in voice (rough sounding)
- Bradycardia (low voltage on ECG)
- Symptoms of heart failure
*absence of thyroid gland hormones decreases minute oxygen consumption to approx 40% less than normal
What is Myxedema Coma?
Severe Hypothyroidism
- rare, may occur in postop period due to triggers such as exposure to cold temp, infection, excessive sedation and analgesic medications
- decreased mental status/coma, hypothermia, bradycardia, hyponatremia, HF, and respiratory failure
Treatment = ICU care +/- mechanical ventilation, supportive therapy, rewarming, hydration, urgent IV admin of Levothyroxine and Hydrocortisone
*High Mortality
What is used to treat hypothyroidism?
Thyroid replacement therapy:
T4 (Thyroxine) = hormone of choice for thyroid replacement
- consistent potency and duration of action
- absorbed in small intestine
- Levothyroxine sodium most common – 50-200 mcg/day
T3 (Liothyronine sodium) = salt of triiodothyronine is also used and available in tablet and injection – 50-75 mcg/day
*recombinant TSH
What is Hyperthyroidism and the different causes?
Excessive thyroid hormone due to an over producing/excessive function of thyroid gland – causes increased metabolism and autonomic nervous system disturbances
Graves Disease = Most common cause
- other conditions include: toxic nodular goiter, toxic adenomatous disease of thyroid, excessive admin of thyroid hormone, excessive iodine intake, thyroiditis and follicular carcinoma and TSH producing tumor of pituitary gland
- excess thyroid hormones can expand oxygen consumption as much as 100% more than normal
What is the treatment for hyperthyroidism?
Anti-thyroid medications
Radioiodine – therapy of choice for Graves’ hyperthyroidism
Surgery
- Thioureylene Class: Propylthiouracil (PTU), Methimazole, and Carbimazole — inhibits thyroid hormone synthesis
- PTU inhibits peripheral conversion of T4-T3
- Iodine = oldest available treatment for hyperthyroid
What is a Thyroid Storm?
Severe form of Hyperthyroidism
-can mimic MH in clinical environment (related to undiagnosed/untreated hyperthyroidism)
Symptoms = hyperpyrexia (+/- 41*C), tachycardia, arrhythmias, weakness, and delirium… MI can also occur
Treatment = requires ICU supportive care
- Beta blockers, multiple anti-thyroid meds, iodine, cooling measures
- anti-thyroid meds (PTU) must be given before iodine which blocks the release of thyroid hormones
What is Sick Euthyroid Syndrome?
Thyroid Disorder where patient appear euthyroid clinically but have evidence of dysfunction on lab testing