iii. CNS manifestations from hyperosmolarity iv. Hyponatremia often present despite normal total body sodium levels 1. Each 100 mg% of hyperglycemia

Transcription

1 Endocrine Review I. Pituitary a. Anatomy & physiology i. Pituitary divided into 2 parts 1. Anterior (adenohypophysis) a. Secretes ACTH, GH, FSH, LH, TSH and prolactin i. Most under control of the hypothalamus through releasing hormones ii. Negative feedback loops ultimately control level of release 2. Posterior (neurohypophysis) a. Secretes vasopressin (ADH) and oxytocin i. These hormones are actually made in the supraoptic and paraventricular neurons and transport down the axons to the pituitary b. Hypothalamic osmoreceptors are the principal determinants of ADH release ii. Pituitary hormone functions 1. ACTH causes synthesis & release of glucocorticoids from adrenal cortex 2. GH promotes tissue growth and protein synthesis 3. FSH & LH are needed for normal spermatogenesis and ovarian function 4. TSH - causes synthesis & release of thyroid hormones 5. Prolactin supports breast development during pregnancy a. Prolactin secretion is increased by dopamine receptor antagonists such as droperidol 6. ADH regulates extracellular osmolarity and blood volume 7. Oxytocin enhances uterine activity during labor and acts on areolar myoepithelial cells as part of the suckling reflex b. Acromegaly i. Secondary to GH secreting tumor of the pituitary ii. Occurs with GH secretion after closure of epiphyseal plates causing expansion of the flat bones iii. Gigantism occurs if GH secretion occurs before closing of epiphyseal plates iv. Clinical manifestations 1. Expansion of flat bones of hands, feet, skull 2. HTN

2 II. 3. Dyslipidemia 4. Cardiomyopathy 5. Increased BMR 6. Glucose intolerance v. Anesthetic implications 1. Prepare for difficult intubation. Patients have large head, jaw, tongue and nasal bones 2. Obstructive sleep apnea common 3. Cardiomyopathy common Pancreas a. Insulin manufactured and secreted by Islets of Langerhans i. Approximately 50 U/day made in the adult ii. Insulin effects 1. Increased glucose & potassium entry into cells 2. Decreased glycogenolysis, gluconeogenesis, ketogenesis, lipolysis & protein catabolism 3. Promotion of protein synthesis iii. Diabetes mellitus 1. Classification a. Type I absolute insulin deficiency i. Prone to ketoacidosis b. Type II relative insulin deficiency i. Prone to hyperosmolarity c. Type III -? (some refer to this as gestational, some a secondary to genetic defects 2. Diabetes is characterized by an impairment of carbohydrate metabolism a. Fasting glucose > 126 mg% b. GTT > 200 mg% 3. Acute complications a. Diabetic ketoacidosis i. Lack of insulin allows catabolism of free fatty acids into ketone bodies ii. Organic acid formation with wide anion gap iii. Most commonly caused by infection iv. Severe dehydration present 1. NS safest replacement fluid v. Acidosis usually corrected by volume replacement b. Hyperosmolar non-ketotic coma i. Sufficient insulin present to prevent ketosis ii. Hyperglycemic diuresis results in dehydration and hyperosmolarity

3 iii. CNS manifestations from hyperosmolarity iv. Hyponatremia often present despite normal total body sodium levels 1. Each 100 mg% of hyperglycemia lowers sodium by 1.6 meq/l v. Treatment centers around volume replacement with NS and insulin infusion c. Hypoglycemia i. Defined as glucose < 50 mg% ii. Secondary to excess exogenous insulin iii. Effects 1. Lightheadedness to seizures 2. Catecholamine discharge 4. Long-term complications a. Microvascular disease resulting in: i. Hypertension ii. Diastolic dysfunction & CHF iii. Peripheral & cerebral vascular disease iv. Autonomic neuropathy v. Renal failure vi. CAD 5. Anesthetic considerations a. HgbA 1 C levels can identify patients with poor control b. Hypertensive diabetic patients have a 50% incidence of autonomic neuropathy i. Unable to respond appropriately to changes in intravascular volume ii. Delayed gastric emptying c. Chronic hyperglycemia leads to glycosylation of tissue proteins and a limited-mobility joint syndrome i. Temporomandibular and cervical joint immobility may affect intubation d. Preoperative sulfonylureas and metformin should be discontinued for 24 hours prior to surgery e. Intraoperative glucose management to maintain glucose < 180 mg% i. Reduces incidence of wound infection, neurologic problems, and cardiac dysfunction. ii. Tight control improves fetal outcome

4 III. f. Patients receiving NPH insulin are at increased risk for allergic reactions to protamine Thyroid a. Physiology i. Dietary iodine is absorbed by the thyroid and bound to tyrosine ii. End result is formation of T 3 and T 4 1. These hormones are bound to protein and stored in the thyroid 2. T 4 is stored in greater quantity, but is less potent 3. Peripherally T 4 is converted to T 3 4. Control of thyroid hormone release is thorough the hypothalamic release of TRF and the subsequent anterior pituitary release of TSH 5. Thyroid hormone increased carbohydrate and fat metabolism and controls metabolic rate iii. Calcitonin is produced by the parafollicular C-cells in the thyroid 1. Not clear what effects are in human formerly thought to lower calcium levels b. Hyperthyroidism i. Production and release of excess thyroid hormone ii. Usually caused by Grave s disease, toxic goiter, thyroiditis, pituitary tumors, adenomas or exogenous overdose iii. Clinical manifestations: 1. Tremor and CNS excitation 2. Tachycardia, afib, CHF (high output) iv. Treatment 1. PTU inhibits hormone synthesis a. A thiourea like thiopental. Allergic cross reactions possible 2. KI inhibits hormone release 3. Beta-blockers mask effects of adrenergic over activity a. Also inhibit conversion of T 4 to T 3 4. Radioactive iodine destroys the gland 5. Surgical resection v. Anesthetic considerations 1. Postpone surgery until euthyroid state achieved if possible 2. Continue antithyroid meds preop 3. Avoid ketamine and adrenergic agents 4. Patients may experience thyroid storm a. Most common in postop period b. Characterized by fever, tachycardia mental status changes

5 IV. i. Easily confused with malignant hyperthermia ii. Not associated with muscle rigidity iii. Treated with beta-blockers, hydration and hydrocortisone c. Thyroid resection associated with laryngeal nerve damage, hematoma formation with airway compromise, hypoparathyroidism and pneumothorax c. Hypothyroidism i. Most commonly caused by autoimmune disease (Hashimoto), surgical resection, antithyroid meds, iodine deficiency or pituitary axis failure ii. Clinical manifestations: cold intolerance, weight gain, muscle fatigue, depression iii. Cardiac changes: decreased inotropy & chronotropy with peripheral vasoconstriction iv. Pleural, abdominal and pericardial effusions are common v. Extreme hypothyroidism is called myxedema and is associated with mental status changes, CHF & SIADH vi. Treatment consists of thyroid hormone replacement with corticosteroid coverage vii. Anesthetic considerations 1. Postpone surgery until euthyroid 2. Decreased MAC and drug sensitivity 3. Careful intraop monitoring of glucose, sodium and CBC (anemia) 4. Long-standing hypothyroidism may result in an enlarge tongue and airway management issues Parathyroids a. Normal physiology i. Parathyroid hormone is the principal regulator of calcium homeostasis ii. Parathyroid hormone increases serum calcium 1. Promotes bone resorption 2. Decreases renal calcium excretion 3. Enhances GI absorption iii. Calcium 1. 99% stored in bone 2. In blood, 60% ionized, 40% protein bound b. Hyperparathyroidism i. Causes 1. Primary adenoma, carcinoma, hyperplasia 2. Secondary renal failure, malabsorption 3. Ectopic production hepatoma, bronchogenic Ca ii. Signs & symptoms

6 1. All result from hypercalcemia a. Hypertension, arrhythmias, shortened QT interval b. Impaired renal concentrating ability with metabolic acidosis, nephrolithiasis c. Muscle weakness d. Mental status changes iii. Anesthetic considerations 1. Normalize serum calcium with saline/furosemide diuresis 2. Biphosphonates also effective 3. Plicamycin and glucocorticoids also lower calcium 4. Avoid acidosis as this increases ionized fraction of serum calcium c. Hypoparathyroidism i. Causes most commonly result of surgical resection of the parathyroid glands ii. Signs & symptoms result of hypocalcemia 1. Neuromuscular irritability 2. Muscle weakness, decreased cardiac contractility iii. Anesthetic considerations 1. Normalize serum calcium 2. Alkalosis may further decrease ionized fraction of calcium 3. Increased sensitivity to NMBAs 4. Avoid rapid infusion of citrate containing blood products V. Adrenal Glands a. Anatomy & physiology i. Adrenal gland divided into 2 parts 1. Cortex secretes mineralocorticoids, glucocorticoids, sex hormones a. Mineralocorticoids (aldosterone) causes retention of sodium in distal renal tubule i. Secondarily volume is expanded ii. Potassium and hydrogen are excreted iii. Aldosterone secretion is stimulated by the rennin-angiotensin system & hyperkalemia iv. Secreted by the zona glomerulosa 1. Superficial layer b. Glucocorticoids (cortisol) i. Increase plasma glucose by enhancing gluconeogenesis and inhibiting peripheral glucose uptake

7 ii. Increase vascular and bronchial smooth muscle effects of catecholamines iii. Mild mineralocorticoid activity iv. ACTH is the principal regulator of secretion v. Average secretion is about 20 mg/day, but can be increased to 300 mg/day vi. Secreted by the zona fasciulata 1. Middle cortical layer c. Sex hormones i. Mostly androgens ii. Secreted by the zona reticularis 1. Deep cortical layer 2. Medulla secretes epinephrine, norepinephrine & dopamine a. 80% epinephrine b. Major control mechanism is preganglionic fibers of the sympathetic nervous system c. Adrenal medulla is functionally a postganglionic sympathetic terminal 3. b. Adrenal diseases i. Mineralocorticoid excess

8 1. Commonly a primary disease (Conn s syndrome) 2. Secondary causes involve the rennin-angiotensin system, CHF, cirrhosis & nephrotic syndrome 3. Clinical manifestations a. Hypertension b. Hypervolemia c. Hypokalemia & alkalosis 4. Anesthetic considerations a. Preoperative correction of fluid and electrolyte balance b. Use of spironolactone a specific aldosterone competitive inhibitor ii. Mineralocorticoid deficiency 1. Clinical manifestations a. Hypotension b. Hypovolemia c. Hyperkalemia and acidosis 2. Anesthetic considerations a. Volume replacement and correction of electrolyte abnormalities b. Use of fludrocortisones synthetic aldosterone analogue iii. Glucocorticoid Excess 1. Causes a. Exogenously administered steroids most common b. Hyperfunction of adrenals adenoma, etc c. ACTH excess secondary cause (Cushing s disease) d. Clinical manifestations (Cushing s syndrome) i. Muscle wasting ii. Osteoporosis iii. Obesity iv. Glucose intolerance v. Hypertension vi. Changes in mental status e. Anesthetic Considerations i. Patients are usually volume overloaded ii. Hypokalemia & alkalosis and fluid balance should be corrected iii. Increased sensitivity to NMBAs iv. Patients receiving exogenous corticosteroids require stress coverage of the equivalent of 300 mgs/day of hydrocortisone

9 v. Pneumothorax a common complication of adrenal surgery iv. Glucocorticoid deficiency (Addison s disease) 1. Usually combined with mineralocortocoid deficiency 2. Clinical manifestations a. Same as mineralocorticoid deficiency b. Hypoglycemia also present c. Addisonian crisis acute deficiency resulting in i. Circulatory collapse ii. Fever iii. Mental status changes iv. Hypoglycemia 3. Anesthetic considerations a. Adequate steroid replacement therapy i. Replacement necessary for any patient receiving steroid therapy by any route for more than 2 weeks in the previous year ii. Replacement should be the equivalent of 300 mg/day of hydrocortisone iii. Patients often have poor dentition and loose teeth v. Catecholamine Excess 1. Pheochromocytoma accounts for 0.1% of cases of hypertension % of pheochromocytomas are malignant 3. Clinical manifestations a. Paroxysmal headache b. Hypertension c. Sweating d. Palpitations 4. Laboratory testing a. Urinary catecholamines and metabolites i. Metanephrine & nor-metanephrine ii. Vanillymandelic acid iii. Plasma free metanephrine levels may be best indicator 5. Treatment a. Phenoxybenzamine alpha-blocker b. Beta-blockade only after alpha-blockade established and only in patients with tachycardia or arrhythmias c. Patients are volume contracted and volume expansion after alpha-blockade is important 6. Anesthetic considerations a. Avoid

10 i. Succinylcholine fasciculations may precipitate catechol release ii. Ketamine and sympathomimmetic agents iii. Vagolytic drugs iv. Histamine releasing drugs such as atracurium, morphine, meperidine v. Droperidol has been associated with hypertensive crisis b. Patients are volume contracted if preop preparation is inadequate c. Preparation with both vasodilator and pressor therapy c. Carcinoid syndrome i. Tumors located in the gastrointestinal tract that release serotonin, kallikrein and histamine ii. Initially these substances are secreted into the portal vein and immediately destroyed by the liver 1. Systemic symptoms implies metastasis iii. Clinical manifestations 1. Flushing 2. Tachycardia 3. Bronchospasm 4. Labile hypertension 5. Profuse diarrhea 6. Right sided valvular lesions iv. Anesthetic considerations 1. Avoid agents and techniques that cause release of tumor contents a. Avoid histamine releasing drugs b. Hypotension can precipitate tumor release i. Volume therapy is mode of choice for treatment of hypotension