NA 731 Endocrine Pathophysiology PDF (Fall 2022)

# NA 731 Pathophysiology for Nurse Anesthesia II - Fall 2022 ## Endocrine Pathophysiology ### Part One: Thyroid & Parathyroid ### Part Two: - Pituitary - Adrenal - Pancreatic - Metabolic - Genetic endocrine disorders ## Thyroid Gland - Bilobed tissue in the neck surrounding trachea caudal to th...

# NA 731 Pathophysiology for Nurse Anesthesia II - Fall 2022 ## Endocrine Pathophysiology ### Part One: Thyroid & Parathyroid ### Part Two: - Pituitary - Adrenal - Pancreatic - Metabolic - Genetic endocrine disorders ## Thyroid Gland - Bilobed tissue in the neck surrounding trachea caudal to the larynx that is connected by a bridge of tissue called the thyroid isthmus - Maintains optimal metabolism for normal tissue function - Secretes: - Thyroxine (T4): prohormone synthesized from tyrosine; 80% of thyroid hormone production - Triiodothyronine (T3): 5X more active than T4; produced from tyrosine metabolism or from conversion from T4 - Hormone actions: increased O2 consumption in almost all tissues - CV signs are often the earliest signs of thyroid dysfunction - Will alter MAC requirement for volatile anesthesia - This was more relevant when Halothane was in use: halothane is metabolized @ 20% → hyperthyroidism is a hypermetabolic state → more Halothane is being metabolized → need to increase MAC - Sevoflurane is only metabolized @ 2%, so MAC requirements likely will not change much ## Hyperthyroidism - Caused by three pathologic processes: - Graves disease: leading cause; affects 0.4% of Americans → systemic autoimmune disease - Thyroid stimulating antibodies bind to TSH receptors in thyroid, stimulating growth, vascularity, and hypersecretion of T4 and T3 - Characterized by low TSH with elevated T4 and T3 in the presence of thyroid-stimulating antibodies - Toxic multinodular goiter: arises from long-term goiter → dysphagia can be an issue with increased size (tracheal compression) - Toxic adenoma: neoplasm, differentiated with CT | Signs & Symptoms of Hyperthyroidism | | -------------------------------------- | | **General** | Anxiety | | | Exophthalmos | | | Tachycardia | | | Palpitations | | | Increased CO and inotropy | | **HEENT** | Cardiomegaly | | | **Wasting** | | **CV** | **Weakness** | | **Neuro** | Tremors of hands | | | Hyperactive DTR | | **GI** | Diarrhea | | **Psych** | Emotionally unstable | | **Skin** | **Warm** | | | **Moist** | ### Treatment for Hyperthyroidism - Antithyroid drugs methimazole or propylthiouracil for first-line therapy - Interfere with the production of thyroid hormones - Iodide: in high concentrations this inhibits release of hormones from the thyroid gland - effects are short-lived - Usually reserved for preparation of hyperthyroid patients for surgery, managing thyroid storm, or treating severe thyrocardiac case - There is no need to delay surgery in a patient with otherwise well-controlled thyrotoxicosis to initiate iodide - Beta blockers can decrease cardiac symptoms - Ablative therapy with radioactive 1311 or surgery for those with failed Graves treatment as well as for those with a goiter or toxic adenoma - Total or subtotal thyroidectomy → tracheal compression, uni- or bilateral RLN damage, damage to motor branch of SLN, or damage to parathyroids are all possible outcomes ### Thyroid Storm - Life threatening exacerbation of hyperthyroidism often precipitated by trauma, infection, medical illness, or surgery - Often presents intraoperatively like MH: hyperpyrexia, tachycardia, and hypermetabolism - Can have normal thyroid levels - Occurs most often in the postop period - TX: rapid alleviation of thyrotoxicosis as well as supportive care - If shock is present - vasopressor (phenylephrine) is indicated - Beta-blocker/digoxin for atrial fibrillation rate control - Mortality rate is 20% | Thyroid Storm Treatment | Effect | | ------------------------ | ----- | | Glucose IV fluid | Treat dehydration | | Beta blockers | Decrease SNS flow | | Glucocorticoids | Decrease hormone release and slow conversion of T4 to T3 | | Antithyroid Drug | Block hormone synthesis | ## Hypothyroidism - AKA Myxedema → affects 0.5% - 0.8% of adults - 95% of all cases are due to decreased production of thyroid hormones despite adequate or increased TSH - Most common cause in the US is thyroid removal, second most common is idiopathic, likely autoimmune - Hashimoto thyroiditis: autoimmune disease with goiterous enlargement and hypothyroidism - S&S: Slow, insidious, progressive course → subclinical hypothyroidism is present in 20% of geriatric females ### Treatment for Hypothyroidism - Levothyroxine sodium: replaces T4 hormone - Evidence of efficacy: sodium and water diuresis and reduction of TSH level - With cardiomyopathy an improvement in cardiac function is observed (10-12 days to reach therapeutic levels) - Treatment can lead to angina, which complicates treatment - With hypothyroidism and angina, angiography is recommended | Signs & Symptoms of Hypothyroidism | | -------------------------------------- | | **General** | Fatigue | | | Dry hair | | | Large tongue | | | Hoarse voice | | | Periorbital edema | | **HEENT** | **Decreased CO** | | | Impaired baroreceptor fxn | | | **EKG changes** | | | Cardiomyopathy | | | Pericardial effusions | | **CV** | Slow speech | | | Slow motor function | | **Neuro** | Relaxation of DTR | | | **Constipation** | | **GI** | **Apathy** | | **Psych** | **Pale** | | **Skin** | **Cool** | ### Anesthetic Management of Hypothyroidism - Risks: - Airway compromise 2/2 swollen oral cavity, edematous vocal cords, or goiter - Aspiration 2/2 decreased gastric emptying - Hypodynamic cardiac system → worsened by surgical stress and/or cardiac depressant volatile anesthetics - Prone to bradycardia, so pancuronium is suggested - Hypoxia 2/2 decreased ventilatory response to carbon dioxide and/or oxygen - Controlled ventilation is recommended - Hypothermia: difficult to treat - Electrolyte imbalances: hyponatremia and hypoglycemia are common - Extremely sensitive to opioids and other sedatives - Exaggerated response to vasodilation that occurs with volatile anesthetics - Steroid coverage (stress dose) will be needed due to likely adrenal suppression - 100-200 mg hydrocortisone OR 40-80 methylprednisolone (Solu-medrol) ~5 min prior to induction ### Hypothyroidism: Myxedema coma - Rare, severe form or hypothyroidism - Symptoms: - Delirium - Hypoventilation - Hypothermia (80% of patients) - Cardinal feature - Mortality rate > 50% - Medical emergency - TX: L-thyroxine or L-triiodothyronine with hydration and temp correction with mechanical ventilation if needed ### Goiter and Thyroid Tumors - Swelling of thyroid gland commonly caused by poor intake of iodine, ingestion of dietary or pharmacologic goitrogen, or defect in biotransformation pathway - In most cases a euthyroid state is present, but surgery is indicated if medical therapy isn't effective - Can lead to caval obstruction, airway obstruction, cardiac compression in extremes of growth - Airway/ventilation changes can occur with position/postural changes - With spontaneous ventilation, larger airways are supported by negative intrathoracic pressure, however with loss of spontaneous ventilation, compensation ceases, and airway obstruction occurs - Preop history of dyspnea in upright or supine position is predictive of airway obstruction - May not observe airway obstruction or evidence of cardiac compression unless general anesthesia is induced - CT scan is necessary to assess extent of tumor ### Anesthetic Management of Goiter and Thyroid Tumors - Local if possible → general if necessary - Avoid sedatives/opioids - AFOI with armored tube is the safest plan for airway - Semi-Fowlers position - Airway exam prior to Extubation to ensure bilateral cord movement - CPB equipment on standby ### Thyroid Surgery Complications - Morbidity near 13% - RLN provides motor innervation to all laryngeal muscles except the cricothyroid and sensory innervation to below the cords - Branches from the vagus nerve, descends into the thorax, then ascends via the tracheoesophageal groove #### Right RLN: - Loops under innominate artery #### Left RLN: - Loops under aortic arch #### RLN injury: - Can be unilateral or bilateral and can be temporary or permanent - Unilateral: hoarseness usually only for 3-6 months, but can be permanent - Bilateral: absent vocal cord function, may require tracheostomy #### SLN injury: - Results in weakening of voice - Internal branch: sensory innervation to larynx; branches off at great horn, pierces thyrohyoid membrane - External branch: motor innervation to cricothyroid - Injury → monotone voice #### Hypoparathyroidism: - 2/2 damage to blood supply → hypocalcemia in first 24-48h postop - Stridor can occur, which can develop into a laryngospasm - Tracheal compression 2/2 hematoma - May require evacuation of hematoma, re-entry, or tracheostomy ## Parathyroid Glands - Four glands that secrete PTH which regulates calcium concentration - Secretion of PTH is inversely related to plasma calcium concentration - Functions: - Promotes mobilization of bone calcium - Enhances conversion of vitamin D to active form which increases Gl absorption of Ca2+ - Increase renal tubular absorption of calcium - Inhibits renal absorption of phosphate - Stimulates the production of cAMP, which can escape via urine → an assay for cAMP can indicate PTG activity ## Primary Hyperparathyroidism - Results from excessive secretion of PTH 2/2: benign PT adenoma, carcinoma of PT, or hyperplasia of the PT - Dx: hypercalcemia with serum Ca > 5.5mEq/L OR ionized Ca > 2.5 mEq/L - Most common cause of hypercalcemia in general population - Cancer is most common cause in hospitalized patients - Tx: Removal of PT glands → expect [Ca] to normalize in 3-4 days | Signs & Symptoms of Hyperparathyroidism | | -------------------------------------- | | **NM** | Skeletal muscle weakness | | **Renal** | Polyuria and polydipsia | | | Decreased GFR | | **Blood** | Anemia | | | Prolonged PR | | | Shortened QTi | | **Cardiac** | Hypertension | | **GI** | Vomiting | | | GI pain | | | Pathologic fractures | | **Skeletal** | Collapse of vertebral bodies | | **Nervous** | Somnolence | | | Decreased pain sensation | | | Psychosis | ### Parathyroidectomy postoperative concerns - Postoperative tetany 2/2 hypocalcemia - Exacerbated by hypomagnesemia, which can lead to refractory hypocalcemia - Transient hyperchloremic metabolic acidosis can occur 2/2 deteriorating renal function ### Anesthetic Management of Primary Hyperparathyroidism - No evidence that any medications or techniques are necessary in the patient with primary hyperparathyroidism - Maintenance of hydration and urine output are important - Take care with positioning and padding → weakened bones - Coexisting muscular weakness may suggest a reduced requirement for muscle relaxation, but hypercalcemia can antagonize the effects of NDMR - Monitor for EKG changes ## Secondary Hyperparathyroidism - Compensation for a pathology that leads to hypocalcemia - Seldom leads to hypercalcemia - Treatment directed towards normalizing serum phosphate in patients with renal disease by administering a phosphate binder, orally ## Hypoparathyroidism - Pathology - Secretion of PTH is absent - Secretion of PTH is deficient - Peripheral tissues are resistant to effects of PTH - Almost always iatrogenic, occurring with inadvertent removal of PT during thyroidectomy - Pseudohypoparathyroidism: congenital disorder with PTH release but no kidney response to the hormone - S&S: mental retardation, calcified basal ganglia, obesity, and short fingers and toes - DX: Hypocalcemia (serum < 4.5mEq/L OR ionized < 2mEq/L) with low or inappropriately normal PTH hormone and hyperphosphatemia - S&S: variable depending on the onset of hypocalcemia - Acute: manifests often as airway abnormalities → stridor - Chronic: cardiac electrophysiologic changes (prolonged QTi with normal QRS, PR), fatigue, lethargy, cataracts - TX: Calcium gluconate or calcium chloride - Correction of respiratory or metabolic alkalosis - Calcium/Vitamin D ### Anesthetic Management of Hypoparathyroidism - Prevent further decreases in calcium and treat adverse effects of hypocalcemia → focus on cardiac symptoms - Hyperventilation and admin of bicarb can decrease calcium - Blood products containing citrate will not typically decrease calcium concentrations - lonized calcium can decrease with blood transfusions are rapid (500mL every 5-10min) as seen in CPB or liver transplant ## Pituitary Gland: The Master Gland - Bilobed body located beneath the hypothalamus, approximately the size of a pea - Divided into anterior and posterior segments - Anterior: adenohypophysis → originated from upper Gl cells during development - Posterior: neurohypophysis → derived from neural tissue - Releases hormones which are known to control a substantial number of body processes, including regulation of homeostasis, growth, reproduction, lactation, thyroid hormone release/balance | Pituitary Hormones | Cell Type | Principal Action | | ------------------ | -------- | ---------------- | | **Anterior Pituitary** | | | | Human growth hormone (somatotropin) | Somatotropes | Accelerates body growth; insulin antagonism | | Prolactin | Lactotropes | Stim secretion of milk and maternal behavior; inhib ovulation | | Luteinizing hormone | Gonadotropes | Stim ovulation in females; stim testosterone secretion in males | | Follicle-stimulating hormone | Gonadotropes | Stim ovarian follicle growth in females; spermatogenesis in males | | Adrenocorticotrophic hormone | Corticotropes | Stim adrenal cortex section and growth; steroid production | | Thyroid-stimulating hormone | Thyrotropes | Stim thyroid secretion and growth | | b-Lipotropin | Corticotropes | Precursor of endorphins | | **Posterior Pituitary** | | | | Arginine vasopressin | Supraoptic nuclei | Promotes water retention and regulates plasma osmolarity | | Oxytocin | Paraventricular nuclei | Causes ejection of milk and uterine contraction | #### Anterior Pituitary - GH: most abundant hormone of the AP → stimulates growth of all tissues in body and causes intense metabolic effects - Excess secretion leads to giantism, but with excess secretion after closure of epiphyseal growth plates, acromegaly occurs - Increases rate of protein synthesis, increase mobilization of fatty acids, antagonism of insulin action, and Na/H2O retention - Causes of release: GH-releasing hormone, stress, sleep, hypoglycemia, fasting, estrogens, dopamine, a-adrenergic agonists - Inhibition of release: GH-inhibiting hormone, pregnancy, hyperglycemia, cortisol, obesity - Prolactin: stimulated release can occur with stress, but also with pregnancy and some drugs (metoclopramide, cimetidine, opioids, methyldopa) - ACTH: regulates cortisol and androgens → release stim by stress, hypoglycemia, trauma, low cortisol, a-agonists, b-antagonists - Cushing Syndrome - overproduction of ACTH - TSH: accelerates the formation of thyroid hormones #### Posterior Pituitary - Reservoir for AVP and oxytocin - AVP synthesized in supraoptic nuclei - Oxytocin synthesized in paraventricular nuclei - Destruction of neurons in or near the supraoptic and paraventricular nuclei of the hypothalamus from surgery on the pituitary, trauma, cerebral ischemia, or malignancy can decrease production/release of AVP → Diabetes insipidus - Opposite is SIADH → dilutional hyponatremia that occurs from head injury, tumors, meningitis, and certain infections - Very common in small cell lung cancer - Assess urine specific gravity ## Anterior Pituitary Disorders - Acromegaly: too much growth hormone - Most often an adenoma in the anterior pituitary - S&S - Skeletal overgrowth: prognathism - Soft tissue overgrowth: lips, tongue, epiglottis, vocal cords - Connective tissue overgrowth: RLN paralysis - Visceromegaly - Glucose intolerance/DM - Osteoarthritis - Osteoporosis - Hyperhidrosis - Skeletal muscle weakness - Peripheral neuropathies are common due to nerve entrapment → document neuropathies prior to induction - Especially carpal tunnel syndrome w/ ulnar nerve - Increased incidence of hypertension, ischemic heart disease - Will develop eccentric hypertrophy ### Treatment: - Preferred initial therapy is transsphenoidal resection of the pituitary - If adenoma extends beyond the sella turcica into other structures often surgery/radiation are not feasible and long-acting somatostatin is used ### Anesthetic Management of Acromegaly - Airway is of primary concern: - Facial distortion can make mask ventilation difficult - Tongue and epiglottis enlargement interfere with visualization of larynx - Preop history of dyspnea on exertion or presence of hoarseness/stridor suggest laryngeal involvement - Could have a narrower glottic opening due to overgrowth of cartilage → may require smaller tube than predicted - Turbinate enlargement can make nasopharyngeal placement of ETT or G tube more challenging - If difficult intubation is predicted, an awake fiberoptic approach should be considered - Due to tissue overgrowth, the ulnar artery could be compressed → radial artery catheterization could be detrimental - Glucose monitoring is a priority - NO evidence that hemodynamic instability or alterations to gas exchange occur with acromegaly (acromegaly in isolation) ## Posterior Pituitary Disorders ### Diabetes Insipidus: not enough ADH - Absence of vasopressin (ADH) due to - Destruction of posterior pituitary → neurogenic DI - Failure of renal tubules to respond to ADH → nephrogenic DI - Dx: polydipsia and high output of dilute urine despite increased osmolality - Transient type occurs following pituitary surgery secondary to trauma to the posterior pituitary - Tx: oral intake initially, then IV infusions of electrolytes and fluids - Neurogenic: desmopressin → available IC, PO, and intranasal - Nephrogenic: low-sodium, low-protein diet, diuretics, and NSAIDs - Anesthesia management: monitor UOP and electrolyte concentrations ### SIADH: too much ADH - Common causes include - Tumors - Hypothyroidism - Porphyria - Lung carcinoma - Inappropriate secretion of ADH occurs during/following major surgeries - Dx: increased urinary sodium and osmolality + decreased serum sodium and osmolality - Tx: fluid restriction, high solute intake, salt tablets - Diuretics - Vasopressin receptor antagonists - Demeclocycline - IV hypertonic saline for those resistant to treatment → can lead to brain cell damage, called central pontine myelinolysis - MAX correction: < 8 mEq/L within 24 hrs ## Adrenal Glands - Adrenal cortex secretes three major classes of corticosteroids - Mineralocorticoids - Glucocorticoids - Androgens - Precursor of all corticosteroids is cholesterol - Divided anatomically into three zones: - Zona glomerulosa - secretes mineralocorticoids - Zona fasciculata - secretes glucocorticoids - Zona reticularis - secretes androgens and estrogens #### Zona Glomerulosa: Mineralocorticoids - Primarily aldosterone - 95% - Increases ECF volume via the increase reabsorption of sodium and thus water - Also decreases potassium concentration - Secretion is stimulated via increased potassium concentration and function of the RAAS - Mineralocorticoid activity is not regulated by ACTH #### Zona Fasciculata: Glucocorticoids - Primarily cortisol - 95% - Functions: - Developmental changes: increase during pregnancy to maximize fetal development to survive extrauterine life - Gluconeogenesis: 10X effect; accelerated rate can cause adrenal diabetes - Protein catabolism: breakdown protein stores in all tissue other than liver for the purpose of gluconeogenesis - Fatty acid metabolism: adrenal dysfunction can lead to "buffalo hump" buildup of fat - Anti-inflammatory Effects: stabilized liposomal membranes and decreases WBC migration to areas of inflammation - Perioperative stress will increase ACTH and cortisol release → peaks with NMBA reversal and Extubation - A deep extubation or avoiding the ETT in the first place (regional anesthesia) can decrease this response, but not eliminate - Must accommodate patients who take exogenous steroids! They are unable to produce their own cortisol in times of stress. - Stress dose: 100-200 mg hydrocortisone ## Adrenal Gland Disorders ### Pheochromocytoma - Catecholamine-secreting tumor - Uncontrolled release can result in malignant hypertension, CVA, and MI - 80% are found in the adrenal medulla - Organ of Zuckerkandl (bifurcation of aorta) - Neck - Thorax - Account for 0.1% of hypertension in adults, but has high mortality risk, making identification and treatment imperative → therapy can cure HTN - 90% are of unknown cause (isolated) - 10% are familial → usually bilateral adrenal tumors that appear in the same location one generation after the next - 10% are pediatric - DX: 24h urine to measure for - Plasma-free metanephrine > 400 pg/mL - Metanephrine > 220 pg/mL | Symptoms of pheochromocytoma | | ----------------------------- | | **More common** | **Less common** | | Hypertension | abdominal pain, nausea, vomiting, and diarrhea | | Sweating | Pallor | | Headache | Hallucinations | | Anxiety and panic (approximately 30% of patients) | Agitation/apprehension | | | Tremor | ### Preoperative Management for Pheochromocytoma - Alpha blockade - Lowers blood pressure - Increases intravascular volume → majority of pheo patients are normovolemic to slightly hypovolemic - Prevents hypertensive episodes (during pheo "attacks") - Adrenergic receptor sensitization - Decrease myocardial dysfunction - Beta blockade - in select patients who have tachycardia - Atenolol, labetalol, metoprolol, and esmolol - NEVER GIVE NON-SELECTIVE BETA BLOCKER BEFORE ALPHA BLOCKER - Phenoxybenzamine - Most frequently used for pheochromocytoma - 12 hr PO dosing - D/C 24-48 hours before surgery to avoid vascular dysfunction (severe hypotension) following tumor resection - Can cause significant tachycardia - Prazosin or Doxazosin - Pure alpha-1 - Shorter acting and cause less tachycardia than phenoxybenzamine - Easier to titrate to desired endpoint than phenoxybenzamine - Metyrosine - MOA: inhibits tyrosine hydroxylase from producing more catecholamine by as much as 80% by inducing calcium channel blockade (Calcium is a trigger for tumor release of NE/Epi) - Side effects: sedation, extrapyramidal side effects are possible ### Intraoperative Management of Pheochromocytoma - Optimal preparation requires alpha blockade with or without beta blockade, as well as correction of hypovolemia - Avoid drugs or maneuvers that cause release of catecholamines - Reduce and prevent fear, stress, pain, shivering, hypoxia, and hypercarbia - Avoid drugs that cause histamine release: morphine, atracurium, mivacurium - Avoid drugs that cause histamine release: morphine, atracurium, mivacurium - Avoid drugs that cause histamine release: morphine, atracurium, mivacurium - Intraoperative BP control: stabilize blood pressure with very short acting agents - Art line and CVP are recommended, while a PA catheter or TEE are sometimes necessary to guide fluid therapy, volume shifts, and underlying cardiac dysfunction - Hypotension is common after ligation of pheochromocytoma: patient has become dependent on the extra catecholamines produced by the tumor AND they have been on long-acting alpha blockers - 70-80 mmHg is not uncommon - Can be less responsive to pressors - Prevention: preload with fluid before vein ligation - Hypertension is common during pneumoperitoneum → despite this effect, laparoscopy is still preferred over laparotomy - It is common for systolic pressure to surpass 200 mmHg during the intraoperative phase, even with proper preparation - Consider increasing the depth of the anesthetic before administering anti-hypertensives - Sodium nitroprusside is the agent of choice for HTN - Phentolamine: alpha blocker that is effective but associated with tachyphylaxis and tachycardia - Nitroglycerin: larger doses lead to tachycardia - Labetalol: preferred for tumors that predominantly secrete epi (15% of pheochromocytomas produce primarily epinephrine instead of norepinephrine) - Magnesium sulfate: decreases catecholamine release, direct vasodilator, reduces sensitivity of receptors to catecholamines - Refractory hypertension: combo of SNP, esmolol, diltiazem, and phentolamine - Arrhythmias are typically ventricular → beta blockers and/or lidocaine; amiodarone has been used for SVTs ### Postoperative Management of Pheochromocytoma - Hypoglycemia is possible - 50% of patients are hypertensive for several days after surgery with 20-30% permanently hypertensive - Hypotension is the most frequent cause of death in the period immediately after surgery - Will require large volumes of fluid since the peripheral vasculature will be unresponsive to the level of catecholamines - Vasopressors may be necessary - Steroid supplement may be required ## Cushing Syndrome: too much cortisol - ACTH-dependent: high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol - ACTH-independent: excessive production of cortisol by abnormal adrenocortical tissue not regulated by hormones - Symptoms - Sudden onset of weight gain that is typically central and accompanied by thickening of facial fat - Hypertension - Glucose intolerance - Skeletal muscle weakness → perhaps decrease NMBA dose - DX: cortisol concentration measured in 24hr urine - TX: transsphenoidal microadenomectomy or resection of anterior pituitary ## Conn Syndrome: too much aldosterone - Excess secretion of aldosterone from an adenoma not under physiologic control - Associated with pheochromocytoma, hyperparathyroidism, and acromegaly - S&S: Hypertension, headache, polyuria, nocturia, muscle cramps or weakness - DX: Spontaneous hypokalemia with systemic hypertension - Mimics licorice overdose: HTN, hypokalemia, suppression of RAAS - TX: Potassium supplementation and aldosterone antagonist like spironolactone - HTN treated with systemic drugs - K-sparing diuretic like triamterene - Surgical excision of a secreting tumor ### Anesthetic Management: - Preop correction of K and treatment of hypertension → hypokalemia can alter response to NMBAS - Avoid hyperventilation: will further decrease potassium - PA Cath/TEE if necessary to measure filling pressures → fluid replacement is key - Exogenous cortisol administration ## Addison's Disease - Primary adrenal insufficiency: adrenal glands do not produce glucocorticoid, mineralcorticoid, or androgen hormones - 90% of the time this is autoimmune - Secondary adrenal insufficiency: failure to produce CRH or ACTH due to hypothalamic-pituitary disease → associated with a decrease only in glucocorticoid production - DX: Baseline plasma cortisol < 20 mcg/dL and cortisol of < 20 mcg/dL after ACTH stimulation - TX: Exogenous steroids - Patients on chronic steroid therapy are unable to produce their own in times of stress: hence, a "stress dose" is necessary to combat surgical stress - A five-day course of steroids decreases cortisol production for five days following discontinuation → must consider this with short- and long-term steroid therapy ### Anesthetic Management: - Treat hemodynamic instability if present - 100mg hydrocortisone every 6h - Correct volume deficits, which can be substantial - No technique or medication is favored