Endocrine
Disorders of ADH secretion
* SIADH = Too much ADH * DI = Too little ADH
Hormones released from posterior pituitary gland (neurohypophysis):
- Antidiuretic hormone (Water retention) - Oxytocin (Uterine contraction + breastfeeding)
Oral Hypoglycemic Medications
- Biguanides (metformin) - Sulfonylureas (glyburide) - Meglitinides (reaglinide) - Thiozolidinedines (rosiglitazone) - alpha-glucosidase inhibitors (acarbose) - Glucagon-like peptide-1 receptor agonist (exenatide) - Dipeptidyl-peptidase-4 inhibitors - Amylin agonists (pramlintide) Metformin carries a risk of lactic acidosis; however, there are conflicting data on this risk. Most providers discontinue metformin at least 24 hours before surgery Sulfonylureas are contraindicated in patients with sulfa allergy Thiazolidinediones are contraindicated in patients with liver failure
T1DM is:
- Caused by beta cell destruction - Most commonly caused by an autoimmune response - Typically associated with a thin and wasting body habitus - Is more likely to be associated with diabetes ketoacidosis
Diabetes Mellitus Anesthetic Management
- Diabetic autonomic neuropathy impairs the patient's ability to mount a sympathetic response to hypovolemia and the cardio-depressant effects of anesthetic drugs - Orthostatic hypotension - Increased risk of aspiration - Increased risk of hypothermia - Reduced ROM of AO joint - The prayer sign suggests an increased risk of difficult intubation - Peripheral neuropathy - Hypoglycemia can be masked by general anesthesia or beta-blockers - Schedule surgery early in the day to prevent interruption of nutriion and hypoglycemic therapy
Anesthetic considerations for Acromegaly
- Distorted facial features (difficult mask ventilation due to a poor seal) - Large toungue, teeth and epiglottis (difficult laryngoscopy) - Subglottic narrowing and vocal cord enlargement (difficult ETT placement - use a smaller tube) - Turbinate enlargement (risk of epistaxis - avoid nasal intubation if possible) - OSA is common - Increased risk of HTN, CAD, and rhythm disturbances - Glucose intolerance - Skeletal muscle weakness - Entrapment neuropathies are common
Hyperthyroidism Anesthetic Considerations
- Do NOT proceed to elective surgery until the patient is euthyroid. Successful medical management may require upwards of 6-8 weeks. - Emergency surgery warrants administration of a beta-blocker, potassium iodide, and glucocorticoids. Additionally, PTU should be started at this time. - A goiter can cause tracheal deviation or tracheomalacia - On you exam, goiter = awake intubation. The next best response is a technique that maintains spontaneous ventilation - Avoid sympathomimetics, anticholinergics, ketamine, and pancuronium - Not that you can find it in the US, but you should know that thiopental reduces the peripheral conversion of T4 to T3 - Exophthalmos increases the risk of corneal abrasion - Titrate NMBs carefully - increased incidence of myasthenia gravis and myopathy - Hypoxia and hypercarbia stimulate the SNS - Careful with positioning. Increased bone turnover increases the risk of osteoporosis
DM Diagnostic Criteria
- Fasting plasma glucose > 126 mg/dL - Random glucose level > 200 mg/dL + classic symptoms - Two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test - Hemoglobin A1C > 6.5%
What are the diagnostic critiria for diabetes mellitus?
- Fasting plasma glucose > 126 mg/dL - Random glucose level > 200 mg/dL + classic symptoms - Two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test - Hemoglobin A1C > 6.5%
Hormones released from the anterior pituitary gland (adenohypophysis) include:
- Follicle-stimulating hormone (Germ cell maturation + ovarian follicle growth (females)) - Leutinizing hormone (Testosterone production (males) + Ovulation (females) - Adrenocorticotropic hormone (Adrenal hormone release) - Thyroid-stimulating hormone (Thyroid hormone release) - Prolactin (Lactation) - Growth hormone (Cell growth)
Glucocorticoids - Energy Mobilization
- Gluconeogenesis (amino acids are converteed to glucose by the liver)—- Increased blood sugar - Protein catabolism (mainly muscle breakdown)—- Increased amino acid availability to the liver for gluconeogenesis - Fatty acid mobilization—-Increased FFA oxidation—-Increased abilitty to use fat for energy instead of glucose
Goals of Insulin Therapy
- HbA1c < 7% - Before a meal - glucose is 70 - 130 mg/dL - After a meal - glucose is <180
Anesthetic Management - Drugs to avoid
- Histamine releasing drugs: morphine, meperidine, atracurium, thiopental, and succinylcholine (if possible) - Succinylcholine-induced fasciculations can cause hormone release fom the tumor - Exogenous catecholamines can potentiate hormone release - Sympathomimetic agents: ephedrine and ketamine
What are the clinical features of Conn's syndrome?
- Hypertension - Hypokalemia - Metabolic alkalosis
What are the two cardiovascular side effects of hypocalcemia?
- Hypotension - Prolonged QT Interval
Thyroid Storm
- In response to stressful events (such as perioperative stress), the thyroid gland can increase hormone output - This can occur in hyper- and -euthyroid patients - During the perioperative period, this complication is most likely to happen 6 - 18 hours after surgery
Secondary hyperparathyroidism
- Is caused by something that stimulates the parathyroid glands to increase PTH output (the glands themselves are normal) - The most common cause is chronic kidney disease - Renal osteodystrophy is the term for bone disease caused by increased PTH secondary to chronic kidney disease
Primary Hyperparathyroidism
- Is the most common cause of hypercalcmia - Parathyroid adenoma is the most common cause of primary hyperparathyroidism - Predicatbly, these patients present with increased PTH levels, hypercalcemia, and hypophosphatemia - The best treatment is surgical resection of the parathyroid glands - After the parathyroid gland is remove, the surgeon will typically ask for blood to be sent for STAT analysis of the PTH level - often after each gland is excised and every 5 minutes until the PTH value drops. A decline in the PTH level indicates successful removal
Diabetic Ketoacidosis (Gap Acidosis + Hyperglycemia)
- More common with type 1 DM - Usually caused by infection - Not enough insulin —- ketoacidosis, hyperosmolarity (from increased glucose), and dehydration - Patient is hyperglycemic (> 250 mg/dL), but cells are starved for fuel - Metabolic acidosis causes Kussmaul's respirations - Acetone causes fruity-smelling breath - Treatment = volume resuscitation, insulin, K+ after acidosis subsides
Hyperglycemic Hyperosmolar State
- More common with type 2 DM - Usually caused by insulin resistance or inadequate production - Enough insulin is produced to prevent ketosis but not hyperglycemia - Hyperglycemia (> 600 mg/dL) significantly increases serum osmolarity (> 330 mOsm/L) - Compared to DKA, HSS is associated with a greater elevation in glucose and osmolarity - Glycosuria leads to dehydration and hypovolemia - Mild metabolic acidosis may occur (usually > 7.3 and no anion gap) - Treatment = volume resuscitation, insulim, correct electrolytes
Hormones NOT affected by negative feedback
- Oxytocin is unique in that it is part of a positive feedback loop. Uterine contraction increases oxytocin release, which then stimulates more intense uterine contraction and additional oxytocin release - Prolactin output is under neural control, where increased dopamine decreases prolactin release. This explains why dopamine (DA) antagonists (metoclopramide) cause hyperprolactinemia
Diabetic ANS Dysfunction
- Painless myocardial ischemia (referred pain pathways are dysfunctional) - Reuced vagal tone—-tachycardia - Risk of dysrhythmias - Orthostatic hypotension - Impaired respiratory compensation to hypoxia and hypercarbia—-Increased sensitivity to anesthetic drugs - Delayed gastric emptying—-Increased risk of aspiration - Impaired thermoregulation—-Increase risk of hypothermia - Regional anesthesia may worsen neurologic defects in the patient with diabetic polyneuropathy - Diarrhea and constipation
List 4 ways the body responds to hypocalcemia
- Parathyroid gland releases PTH - Osteoclasts in bone release Ca+2 - Ca+2 is reabsorbed in the kidneys - Ca+2 absorption in the gut increases in the presence of Vitamin D
Cushing's Syndrome Anesthetic Implications
- Pay special attention to aseptic technique - Careful positioning to reduce skin and bone injury - Consider post-op steroid supplementation - Diabetes inspidus (transient) follwing pituitary resection
Other DM Anesthetic Management
- Peripheral neuropathy usually begins in a "stocking and glove" distribution (lower legs and hands) - Peripheral neuropathy is treated with NSAIDs, antidepressants, and anticonvulsants - Assess for renal dysfunction - Osmotic diuresis—-fluid and electrolyte abnormality - Lactate in LR can be converted to glucose and may contribute to hyperglycemia - Schedule surgery early to prevent interruption of nutrition and hypoglycemic therapy - Hyperglycemia worsens neurologic outcome after ischemic brain injury - General anesthesia and diabetic autonomic neuropathy can mask intraoperativehypoglycemia - Beta-blockers can blunt the increased SNS reponse that accompanies hypoglycemia. Additionally, these drugs diminish the hyperglycemic effcts of endogenous epinephrine
Pituitary gland
- Pituitary gland resides in the sella turcica, and it is connected to the hypothalamus by the pituitary stalk - The anterior pituitary is also called adenohypophysis The posterior pituitary gland is also called the neurohypophysis
Hypothyroidism Anesthetic Management
- Severe hypothyroidism (myxedema) is an indication to cancel surgery - Mild to moderate hypothyroidism is acceptable for elective surgeries - Airway obstruction is due to a large tongue, swollen vocal cords, and goiter - Again, if you are asked about airway management for the patient with a goiter, the correct response will be awake intubation. The next best answer is a technique that maintains spontaneous ventilation - Delayed gastric emptying —- Increased risk of aspiration - Hypodynamic circulation —- Decreased HR, SV, Contractility, CO and baroreceptor responsiveness (Increased risk of hypotension with anethesia). - Inhalation induction is faster - MAC is unchanged (just like hyperthyroidism) - Hemodynamic support is best provided with sympathomimetics that iprove myocardial performance (not phenylephrine) - Decreased adenal function is common. Hypotension unresponsive to catecholamies can be treated with corticosteroids - Slowed hepatic metabolism and renal excretion can prolong drug effects - Lethargic patients are very sensitive to the effects of anesthetic drugs - Muscle weakness—- Increased sensitivity to non-depolarizing NMBs - D5NS provides glucose and cobats hyponatremia due to impaired clearane of free water
Anesthetic Management - Drugs to give
- Somatostatin (octreotide or lanreotide) inhibits the release of vasoactive substances from carcinoid tumors. This improves hemodynamic stability - Antihistamines (H1 & H2: diphenhydramine + ranitidine or cimetidine) - 5-HT3 antagonists - Steroids - Phenylephrine or vasopressin for hypotension
Diabetes cassification
- T1DM is characterized by lack of insulin production - T2DM is characterized by a relative lack of insulin + insulin resistance
T3 & T4 Comparison
- T3 has a greater biological activity - T3 has higher potency - T3 has shorter half-life - T3 is less protein-bound - T3 has smaller concentration in the blood (bound + unbound fractions) - Active form - Half-life = 1 day -T4 is a prohormone - "Delivery vehicle" - Less potent - Half-life = 7 days - Released by the thyroid - More protein bound
Hypothalamic-Pituitary Axis
- The hypothalamus links the central nervous system to the endocrine system. It monitors hormone concentrations in the systemic circulation and instructs the pituitary gland to increase or decrease the release of hormones (usually through negative feedback) - The pituitary gland is divided into the anterior and posterior glands
Hypothalamus
- The hypothalamus links the central nervous system to the endocrine system. It monitors hormone concentrations in the systemic circulation and then influence hormone output from the pituitary gland. It's able to do this because the hypothalamus resides outside of the blood brain barrier (BBB) - If hormone concentration rises, the hypothalamus instructs the pituitary to decrease the output of that hormone - If hormone concentration falls, the hypothalamus instructs the putuitary gland to increase the output of that hormone. - The hypothalamus communicates with the posterior pituitary gland through a series of neural connections and it communicates with the anterior pituitary gland with a group of releasing and inhibiting hormones NB: Since ADH & oxytocin are synthesized in the hypothalamus, there is no need for the hypothalamus to produce releasing and inhibiting hormone for them
Hypoparathyroidism
- The most common cause of primary hypoparathyroidism is iatrogenic gland removal during thyroidectomy - Treatment of primary hypoparathyroidism consists of supplementation of Ca+2, vitamin D, and Mg+2
Cretinism
- This is a complication of neonatal hypothyroidism that leads to limited physical and mental development
Myxedema Coma
- This is a complication of severe hypothyroidism - Coma is a consequence (not a cause) of severely impaired thyroid function
Hypothyroidism Medical Management
- Thyroid hormone is replaced with synthetic T4 (levothyroxine) - The initial response to therapy is natriuresis and decreased TSH
Cushing's Syndrome Treatment
- Transsphenoidal resection of the pituitary gland - Pituitary radiation - Adrenalectomy (if adrenal tumor)
Systemic hormones affected by negetive feedback systems
- Triidothyronine (T3) regulates TRH release - Cortisol regulates CRH release - Testosterone, estrogen, and progesterone regulates LHRH release - Growth hormone and insulin growth factor-1 regulate GHRH and GHIH release
Normal Insulin Secretion
- Under normal conditions, the pancreas secrets ~ 1 U/hr into the portal circulation - After a meal, insulin output increases 5 - 10 fold - Total insulin output is ~ 40 U/day - Beta-2 and PNS stimulation increase insulin secretion - Alpha-2 stimulation inhibits insulin secretion
T2Dm is:
- Usually caused by obesity - Associated with a relative lack of insulin production and peripheral insulin resistance - Is more likely to be associated with hyperglycemic hyperosmolar syndrome
Adrenal Insufficiency (Addison's Disease)
1. Adrenal insufficiency is characterized by the destruction of all cortical zones. This manifests as decreased producion of mineralocorticoids, glucocorticoids, and androgens 2. Adrenal insufficiency is a chronic state, but it can deteriorate into an acute adrenal crisis if the patient faces additional stress (infection, illness, sepsis, or surgery) 3. Exogenous steroid supplementation suppresses ACTH release from the anterior pituitary gland. Patients on chronic seroid therapy may require "stress dose" steroids to help combat perioperative stress 4. By inhibiting 11-beta-hydroxylase, etomidate causes dose-dependent adrenocortical suppression
What are 3 causes of primary hyperaldosteronism?
1. Aldosteronoma 2. Pheochromocytoma 3. Primary hyperthyroidism
What are 5 anesthetic considerations for patient with Cushing's Syndrome undergoing a pituitary resection?
1. Attention to aseptic technique 2. Carefully position to reduce skin and bone injury 3. Consider pst-op steroid supplementation 4. Diabetes insipidus following resection 5. Considerations for hyperaldosteronism
Carcinoid Syndrome
1. Carcinoid syndrome is associated with the secretion of vasoactive substances from enterochromaffin cells. It's usually associated with tumors of the GI tract, but it can also arise from loactions outside the GI tract. 2. When significant liver dysfunction occurs, carcinoid hormones aren't cleared by the liver, so they enter the systemic circulation and cause the signs and symptoms characteristic of carcinoid syndrome 3. The most common signs are flushing and diarrhea. You can also see bronchoconstriction, vasodilation, and hypotension 4. Drugs to avoid in the patient with carcinoid syndrome include morphine, succinylcholine (if possible), exogenous catecholamines, ephedrine, and ketamine 5. Carcinoid crisis is life-threatening and can occur in patients with carcinoid syndrome. S/sx include tachycardia, labile BP, and abdominal pain. Treatment includes somatostatin, antihistamines, steroids, and 5-HT3 antagonists
What are the most relevant endogenous steroids?
1. Cortisol 2. Cortisone 3. Aldosterone
Steroids Comparative Pharmacology
1. Cortisol has equal glucocorticoid and mineralocorticoid effects 2. Prednisone is an analog of cortisol, making it a good choice to treat adrnocortical insufficiency (Addison's disease) 3. Aldosterone doe NOT have glucocorticoids effects 4. Dexamethasone, betamethasone, and triamcinolone do NOT have mineralocorticoid effects 5. Triamcinolone is commonly administered in the epidural space to treat lumbar disc disease. This drug is unique because it is associated with a higher incidence of skeletal muscle weakness. It's also more likely to cause sedtion (not euphoria) and anorexia (not increased appetite)
Cushing's Syndrome
1. Cushing's syndrome is caused by cortisol excess either from overproduction or exogenous administration. As a point of semantics, Cushing's disease is the result of excess ACTH. 2. Cortisol has glucocorticod, mineralocorticoid, and androgenic effects. Therefore, you should expect the patient with Cushing's syndrome to have signs and symptoms reflecting all of these. - Glucocorticoids efects include hyperglycemia, weight gain, an increase in the incidence of infection, and osteoporosis. - Mineralocorticoid effects include HTN, hypokalemia, and metaboloc alkalosis - Androgenic effects include hirsutism, hair thinning, acne, gynecomastia, and impotence 3. Anesthetic implications: - Consider post-op steroid supplementation - Carefully position to reduce skin and bone injury - Practice aseptic technique 4. Treatment options include transsphenoidal resection of the pituitary gland, pituitary radiation, or adenalectomy
Glucocorticoid potency (most to least potent)
1. Dexamethasone 2. Methylprednisone 3. Cortisol 4. Aldosterone
Diabetes Mellitus
1. Diabetes is often described as "starvation in a sea of food." Although glucose is present in the bloodstream, it is unable to enter many of the cells that require it. This shifts metabolism towards protein catabolism and lipid oxidation. Remember that the brain and the liver don't need insulin for glucose uptake. - T1DM is characterized by a lack of insulin production (beta cell destruction) - T2DM is characterized by a relative lack of insulin + insulin resistance 2. Metabolic syndrome describes a group of characteristics that are common to patients with DM or to those who are at higher risk of developing DM. Diadnostic criteria of metobolic syndrome include at least three of the following: - Fasting plasma glucose > 100 - 110 mg/dL - Abdominal obesity (waist > 40 inches in men and > 35 inches in women) - Serum triglyceride level > 150 mg/dL - Serum HDL < 40 mg/dL in men and < 50 mg/dL in women - Blood pressure > 130/85 mm Hg 3. Diabetic ketoacidosis - More common with type 1 diabetes mellitus - Usually caused by infection - Treatment includes volume resuscitation, insulin, and potassium after acidosis subsides 4. Hyperglycemic hyperosmolar state - More common with type 2 diabetes mellitus - Usually caused by insulin resistance or inadequate insulin production - Glucose is typically higher that diabetic ketoacidosis is mild (if present) - Treatment includes volume resuscitation, insulin, and electrolyte correction
List 2 drugs that counte the hypoglycemic effect of insulin
1. Epinephrine 2. Glucagon
What are 5 characteristics of metabolic syndrome?
1. Fasting plasma glucose > 110 mg/dL 2. Abdominal obestity (waist > 40 inches in men and > inches in women) 3. Serum triglyceride level > 150 mg/dL 4. Serum HDL < 40 mg/dL in men and < 50 mg/dL in women 5. Blood pressure > 130/85 mmHg
How does aldosterone affect renal function?
1. Increases Na+ and water reabsorption 2. Increases K+ and H+ excretion
Hyperthyroidism Anesthetic considerations
1. Medical management for hyperthyroidism includes; - Thionamides (propylthouracil) - Beta-blockers (propranolol) - Potassium iodide - Radioactive iodine 2. Surgical treatment for hyperthyroidism includes subtotal or total thyroidectomy. Complications include hypothyroidism, hemorrhage, tracheal compression, recurrent laryngeal nerve injury, and hypocalcemia 3. Do NOT proceed to elective surgery until the patient is euthyroid. Successful medical management may require upwards of 6-8 weeks. 4. If the patient ha a goiter, you should choose the most conservative airway management (e.g. awake intubation) 5. Titrate NMBs carefully in the patient with hyperthyroidism because there's an increased incidence of myasthenia gravis and myopathy 6. Hypocalcemia due to resection of the parathyroid glands most commonly occurs 24-48 hours after surgery. This can lead to laryngospasm, muscle spasm, hypotension, prolonged QT interval, and mental status changes. The treatment is IV calcium. 7. Chvostek's sign and Trousseau's sign indicate hypocalcemia 8. Under anesthesia, thyroid storm can mimic MH, pheochromocytoma, neuroleptic malignant syndrome, and light anesthesia 9. Remember the four B's when treating the patient with thyroid storm. The best agents for perioperative use are bolded: - Block synthesis (methimazole, carbimazole, PTU, potassium iodide) - Block release (radioactive iodine, potassium iodide) - Block T4 to T3 conversion (PTU, propranolol, glucocorticoids) - Block beta receptors (propranolo, esmolol) 10. Don't give aspirin to treat hyperpyrexia in a patient with thyroid storm because it can dislodge T4 from plasma proteins
The systemic effects of diabetes mellitus ca be predicted by the long-term effects of hyperglycemia in neural and vascular tissue
1. Microvascular - Neuropathy (sensory, motor, autonomic) - Retinopathy - Nephropathy 2. Macrovascular - Coronary artery disease - Peripheral vascular disease - Cerebrovascular disease 3. Other - Stiff joint syndrome - Poor wound healing - Cataracts - Glaucoma
Hypothyroidism Anesthetic Considerations
1. Mild to moderate hypothyroidism does not appear to increase perioperative risk, so it's ok to proceed with elective surgery. Severe hypothyroidism (myxedema) is an indication to cancel surgery 2. Patients are at risk for aiway obstruction due to a large tongue, swollen vocal cords, and goiter 3. As is the case with hyperthyroidism, MAC is not changed in patients with hypothyroidism 4. Hypodynamic circulation—-Decreased HR, SV, Contractility, Cardiac Output, and baroreceptor responsiveness (Increased risk of hypotension with anesthesia). Hemodynamic suppor is best provided with sympathomimetics that improve myocardial performance (no phenylephrine) 5. Decreased adrenal function is common. Hypotension unresponsive to catecholamines can be treated with corticosteroids 6. Patients may be more sensitive to the effects of neuromuscular blockers
List 3 classes of medications used to treat peripheral neuropathy
1. NSAIDS 2. Antidepressants 3. Anticonvulsants
List 4 CV changes in patients with diabetic autonomic neuropathy
1. Painless myocardial ischemia 2. Reduced vagal tone—-tachycardia 3. Risk of arrythmias 4. Orthostatic hypotension
Besides the presence of hyperglycemia, what is the classic triad of symptoms associated with diabetes mellitus?
1. Polyuria 2. Deydration 3. Polydipsia
Mineralocorticoid Excess (Conn's Syndrome)
1. Primary hyperaldosteronism (Conn's syndrome) is caused by excessive aldosterone relase from the adrenal gland. Etiologies include aldosteronoma, pheochromocytoma, and primary hyperthyroidism 2. Long term licorice inhestion causes a syndrome that highly resembles hyperaldesteronism 3. Anesthetic considerations for the patient with Conn's syndrome include hypertension and hypokalemia
SIADH, DI & Acromegaly
1. SIADH is caused by an excessive level of ADH in the blood. Too little ADH in the blood causes DI 2. The most common cause of SIADH is traumatic brain injury (TBI), and the most common cause of DI is pituitary surgery 3. A patient with SIADH will have low urine output, while a patient with DI will have high urine output 4. Treatment of SIADH includes fluid restriction, demeclocycline, and hypertonic saline (if the patient is severely hyponatremic) 5. Treatment of DI iludes DDAVP or vasopressin along with supportive measures 6. Acromegaly can complicate airwaymanagement. Considerations include: * Distorted facial features * Large tongue, teeth, and epiglottis (difficult laryngoscopy) * Subglottic narrowing and vocal cord enlargement (difficult ETT placement) * Turbinate enlargement (risk of epistaxis) 7. Comorbidities associated with acromegaly include glucose intolerance, OSA, CAD, skeletal muscle weakness, and entrapment neuropathies
Insulin
1. Since patients with T1DM don't produce insulin, their survival depends on an exogenous supply. Patients with T2DM may require insulin if lifestyle modification and oral hypoglycemic agents fail. One unit of insulin equals the amount of insulin required to decrease the serum glucose concentration in a fasting rabbit to 45 mg/dL. 2. Regular insulin is the only formulation that can be given IV 3. Side effects of insulin overdose include tachycardia, hypetension, diaphoresis. This can be difficult to diagnose under anesthesia, particularly if the patient is on a beta-blocker 4. Chronic NPH use (or fish allergy) may sensitize the patient to protamine. This may not become apparent until a large protamine dose is given (e.g., cardiac surgery)
List 5 signs and symptoms of carcinoid crisis
1. Tachycardia 2. Hyper- or hypotension 3. Intense flushing 4. Abdominal pain 5. Diarrhea
Adrenal physiology
1. The adrenal gland is divided into the cortex and the medulla 2. Cortex synthesizes and releases 3 classes of steroids: - Mineralocorticoids (Aldosterone) - Glucocorticoids (Cortisol) - Androgens (Sex hormones) 3. The medulla synthesizes and releases 2 catecholamines: - Epinephrine (80%) - Norepinephrine (20%) 4. Adolsterone - Stress increases cortisol production - Increased cortisol initiates gluconeogenesis, protein catabolism, and fatty acid mobilization - Cortisol mitigates the inflammatory cascade by reducing cytokine release - Cortisol improves myocardial performance, and it's required for the vasculature to respond to the vasoconstrictive effects of catecholamines
Pancreas Physiology
1. The pancreas produces two broad types of hormones - Exocrine hormones (from acini tissue) are secreted into the duodenum for digestion - Endocrine hormones (from islets of Langerhans) are secreted into the systemic circulation for metabolism 2. Know these endocrine hormones: - Glucagon is secreted from alpha cells. It increases blood glucose - Insulin is secreted from beta cells. It reduces blood glucose - Somatostatin is secreted from delta cells. It inhibits insulin and glucagon. It also inhibits spanchnic blood flow, gastric motility, and gallbladder contraction - Pancreatic polypeptide inhibits pancreatic exocrine secretion, gall bladder contraction, gastric acid secretion, and gastric motility 3. Glucose is the primary stimulator of insulin releas from the pancreatic beta cells. Therefore, anything that increases serum glucose will also increase insulin release 4. The brain requires a steady supply of glucose for optimal function. Cerebral function generally declines when serum glucose falls below 50 mg/dL 5. Glucagon (1-5 mg IV) increases myocardial contractility, heart rate, and AV conduction by decreasing the intracellular concentration of cAMP. This occurs independently of ANS function
List 3 treatments a patient with Cushing's disease might undergo
1. Transsphenoidal resection of the pituitary gland 2. Pituitary radiation 3. Adrenalectomy (if adrenal tumor)
Parathyroid Hormone
1. Two hormone act antagonistically to regulate the ionized Ca+2 level - calcitonin and PTH. hese hormone affect Ca+2 regulation in the bone, intestine and kidneys. - PTH is produce in the parathyroid gland (chie cells). It increases ionized Ca+2 and decreases serum phosphate. - Calcitonin is produced in the thyroid gland (C cells). It decreases ionized Ca+2 and increases serum phosphate 2. Primary hyperparathyroidism - Primary hyperparathyroidism is the most common cause of hypercalcemia - Parathyroid adenoma is the most common cause of primary hyperparathyroidism. The best treatment is surgical resection of the parathyroid glands 3. Secondary hyperparathyroidism - Secondary hyperparathyroidism is caused by something that stimulates the parathyroid glands to increase PTH output (the glands themselves are normal) - The most common cause is chronic kidney disease 4. Hypoparathyroidism cause hypocalcemia 5. The most common cause of primary hypoparathyroidism is iatrogenic gland removal during thyrodectomy. Treatment includes supplementation of Ca+2 vitamin D and Mg+2
Thyroid Hormone Physiology
1. You can think of thyroid hormone as an "on switch" that stimulates a wide array of metabolic functions. Most of these are easy to predict if you can remember: High Thyroid hormone—-High BMR—-High O2 consumption + High CO2 production 2. Thyroid hormone increases myocardial performance independent of ANS input - increased HR, increasedd contractility, increased lusitropy, and decreased SVR 3. Thyroid disorders do NOT affect MAC (Minimum alveolar concentration). Instead, they affect cardiac output, which impacs the speed of anesthetic onset. Hypothyroidism increases the speed of onset (rate of rise of FA/F1), while hyperthyroidism can reduce the speed of onset 4. Grave's disease is the most common cause of hyperthyroidism, and Hashimoto's thyroiditis is the most common cause of hypothyroidism
Cardiac surgery with sternotomy
100 mg IV
Whipple procedure
100 mg IV
Colonoscopy
25 mg IV
Inguinal repair
25 mg IV
Colon resection
50 mg IV
Total joint replacement
50 mg IV
A goal of insulin therapy is to keep hemoglobin A1c below:
7%
Which type of pancreatic cells releases glucagon? A. Alpha B. Beta C. PP D. Delta
A. Alpha
Which hormone is produced primarily in the supraoptic nuclei? A. Antidiuretic hormone B. Oxytocin C. Adrenocorticotropic hormone D. Thyroid stimulating hormone
A. Antidiuretic hormone Antidiuretic hormone and oxytocin are produced in the hypothalamas and and released by the posterior pituitary gland ADH is formed primarily in the supraoptic nuclei, where as oxytocin is formed primarily in the paraventicular nuclei. Each of these nuclei can synthesize about one-sixth as much of the second hormone as its primary hormone. The pituitary stalk transports both hormones to the posterior pituitary gland, where they're released into the systemic circulation
Factors that stimulate the pancreas to increase insulin release include: (Select 2) A. Beta-2 agonists B. Volatile anesthetics C. Glucagon D. Alpha-2 agonists
A. Beta-2 agonists C. Glucagon NB: Glucagon, Beta-2 agonists, Hyperglycemia
Which of the following is the MOST common etiology of Cushing's syndrome? A. Chronic glucocorticoid therapy B. Adrenal cortex adenoma C. Cortisol secreting extra-adrenal tumor D. Pituitary adenoma
A. Chronic glucocorticoid therapy NB: An over production of cortisol by the adrenal cortex is called Cushing's syndrome - Diagnosis: Low ACTH level and high cortisol level - Etiologies: Chronic glucocorticoid therapy (most common cause) and adrenal cortex adenoma Hypersecretion of corticotropin-releasing hormone by the hypothalamus is called Cushing's disease. - Diagnosis: High ACTH level and a high cortisol level - Etiologies: Pituitary adenoma Cortisol secreting extra-adrenal tumors can also cause hyperadrenalism
A patient with adrenal insufficiency and sepsis requires an emergency intubation in the intensive care unit. Which drug should be avoided? A. Etomidate B. Propofol C. Ketamine D. Thipental
A. Etomidate NB: Adrenal insufficiency is characterized by the destruction of all the cortical zones. This manifests as decreased production of mineralocorticoids, and adrogens By inhibiting 11-beta-hydroxylase, a single induction dose of etomidate causes adrenocortical suppression for >8 hours. This could potentially convert adrenal insufficiency to acute adrenal crisis. Ketamine is often an attractive option in this context, but be aware that its negative inotropic properties can be unmasked in this patient population
Drugs that antagonize the hypoglycemic effect of insulin include: (Select 2) A. Glucagon B. Phenelzine C. Epinephrine D. Aspirin
A. Glucagon C. Epinephrine NB: Drugs that counter the hypoglycemic effects of insulin include epnephrine and glucagon Drugs that extend or enhance the hypoglyemic effect of insulin include MAOIs (phenelzine), salicylates (aspirin), and tetracycline
Signs of Cushing's syndrome include: (Select 4) A. Hypertension B. Hypotension C. Hyperkalemia D. Hypokalemia E. Metabolic alklosis F. Metabolic acidosis G. Hyperglycemia E. Hypoglycemia
A. Hypertension D. Hypokalemia E. Metabolic alkalosis G. Hyperglycemia NB: Cushing's syndrome results when the anterior pituitary gland releases an excessive amount of ACTH. In turn, this increases cortisol release from te zona fasciculata of the adrenal cortex Remember that cortisol has glucocorticoid, mineralocorticoid, and adronegic effects. Therefore, you should expect Cushing's syndrome to affect each of these areas
Complications of Addison's disease include: (Select 2) A. Hyponatremia B. Hypokalemia C. Hypervolemia D. Hyperpigmentation
A. Hyponatremia D. Hyperpigmentation NB: Addison's disease decreases mineralocorticoid (aldosterone) production. - K+ retention—-hyperkalemia - Na+ and Cl- wasting —-severe hypovolemia - Decreased CO results in shork-like state - Death within 3 days to 2 weeks Addison's disease decreases glucocorticoid (cortisol) production - Unable to store glucose as glycogen. This leads to hypoglycemia between meals - Stress (surgery, sepsis, trauma) is poorly tolerated and may lead to demise Patients with Addison's disease have an elevated ACTH and this can stimulate melanocytes in the dermis and epidermis to increase melanin secretion
What is the cause of endemic goiter? A. Iodine insuficiency B. Decreased thyroglobulin C. Decreased thyroid stimulating hormone D. Increased triidothyroinine
A. Iodine insuficiency NB: Thyroid stimulating hormone is released from the anterior pituitary gland. It affects the thyroid gland in 2 key ways: - It tells the thyroid gland to produce T3 and T4 (this requires iodine) - It tells the follicular tissue to produce thyroglobulin colloid (this does not require iodine) Iodine is a substance that the thyroid requires to synthesize triiodothyronine (T3) and thyroxine (T4). When iodine is not available (dietary deficiency), the thyroid is unable to produce a sufficient quantity of T3 and T4 Under normal conditions, there is a negative feedback loop where T3 and T4 supress TSH release. In the patient with a hypoactive thyroid, there isn't enough thyroid hormone to suppress TSH, so TSH remains chronically elevated. This presents a problem. Remember we said SH stimulates the follicles to make thyroglobulin colloid nd that does not require iodine. Since TSH is chronically elevated, the follicles continue to produce thyroglobulin colloid, and this causes the thyroid gland to increase in size. This is the cause of endemic goiter
Which drugs should be avoided in the patient with carcinoid syndrome? (Select 3) A. Ketamine B. Norepinephrine C. Vasopressin D. Rocuronium E. Morphine F. Octreotide
A. Ketamine B. Norepinephrine E. Morphine NB: Carcinoid syndrome is associated with the secretion of vasoactive substances from enterochromaffin cells. It is usually associated with GI tract tumors, but it can also arise from locations outside of the GI tract as well. We tend to avoid drugs that can precipitate hormone release by the tumor, therefore avoid drugs that: - Releae histamine (morphine) - Stimulate the SNS (ketamine) - Augment hormone release (norepinephrine) Octreotide is a primary treatment for carcinoid syndrome, rocuronium doesn't release histamine, and vasopressin is an acceptable treatment for hypotension
Differential diagnosis of thyroid storm should include all of the following EXCEPT: A. Myxedema B. Malignant hyperthermia C. Pheochromocytoma D. Neuroleptic malignant syndrome
A. Myxedema NB: The clnica presentation shares many characteristics with neuroleptic syndrome, malignant hyperthermia, pheochromocytoma, and light anesthesia Myxedema coma occurs with severe hypothyrodism. S/sx include: - Alveolar hypoventilation and hypoxia - CHF - Pericardial effusion - Bradycardia - Hypothermia - Hyponatremia Anesthetic considerations include: - Large tongue may increase risk of difficult intubation - Decreased anesthetic requirement - Expand intravascular volume - Treat electrolyte imbalance (risk of water intoxication) - Provide active warming - Treat with IV levothyroxine
What are the initial treatments for hypotension in a patient with carcinoid syndrome? (Select 2) A. Octreotide B. Phenylephrine C. Ephedrine D. Epinephrine
A. Octreotide B. Phenylephrine NB: The initial treatments of hypotension in a patient with carcinoid syndrome include IV fluids, phenylephrine, and octreotide (somatostatin) Sympathomimetic agents (ephedrine and epinephrine) can increase the release of vasoactive substances from the carcinoid tumor. Having said this, these agens may be required if the patient doesn't respond to the initial treatments outlined above. If sympathomimetic drugs are administered, they should be used with caution
Clinical features of primary hyperparathyroidism include: (Select 2) A. Pathologic fractures B. Laryngospasm C. Myocardial depression D. Shortened QT Interval
A. Pathological fractures D. Shortened Q interval NB: Primary hyperparathyroidism is the most common cause of hypercalcemia. These patients also present with increased PTH levels and hypophosphatemia Hypercalcemia shortens the duration of the QT interval (phase 2 plateau). Bone resorption leads to osteopenia, which predisposes the patient to pathologic fractures Hypocalcemia (which can occur following parathyrodectomy) can cause laryngospasm. Myocardial depression can also occur.
Compared to type 1 diabetes mellitus, choose the statements that MOST accurately describe type 2 diabetes mellitus. (Select 2) A. Peripheral sensitivity to insulin is reduced B. It is more likely to cause hyperglycemic hyperosmolar syndrome C. Is usually associated with a thin body hiatus D. It is usually caused by an autoimmunine response
A. Peripheral sensitivity to insulin is reduced B. It is more likely to cause hyperglycemic hyperosmolar syndrome
What laboratory values are consistent with a diagnosis of hyperparathyroidism? (Select 2) A. Phosphate = 2.1 mg/dL B. Calcium = 12.8 g/d C. Sodium - 150 mEq/L D. Potassium = 2.9 mEq/L
A. Phosphate = 2.1 mg/dL B. Calcium = 12.8 g/d NB: Parathyroid hormone is produced by the chief cells in the parathyroid gland. Excess parathyroid hormone causes hyperglycemia and hypophosphatemia. It doesn't affect potassium or sodium levels Normal extracellular concentrations: - Total calcium = 8.5 - 10.5 mg/dL - Total phosphate = 2.5 - 4.5 mg/dL
Which hormones are released by the anterior pituitary gland? A. Prolactin B. Leutinizing hormone C. Antidiuretic hormone (ADH) D. Oxytocin E. Corticotropin-releasing hormone F. Growth hormone
A. Prolactin B. Leutinizing hormone F. Growth hormone NB: The posterior pituitary releases two hormones: ADH & Oxytocin - The anterior pituitary releases six hormones (FLAT PiG) * Follice-stimulating hormone * Leutinizing hormone * Adrenocorticotropin * Thyroid-stimulating hormone * Prolactin * Growth hormone
When compared to T4, which statements BEST desribe T3? (Select 2) A. Shorter half-ligh B. Higher concentration in blood C. More protein-bound D. Higher potency
A. Shorter half-life D. Higher potency
Where does propylthiouracil (PTU) exert its pharmacologic effect? A. Thyroid gland B. Adrenal gland C. Anterior pituitary gland D. Parathyroid gland
A. Thyroid gland NB: PTU is a thionamide that blocks the reaction between iodine and tyrosine. This inhibits T3 and T4 production and also interferes with the conversion of T4 to T3 Other thionamides include methimazole and carbimazole
Is mask ventilation more difficultin acromegaly? A. Yes B. No
A. Yes - due to distorted facial features (poor seal)
Cushing's Syndrome Etiology
ACTH-Dependent - Increased ACTH stimulates cortisol release - Causes: Pituitary adenoma, acute ectopic ACTH syndrome ACTH-Independent - Adrenocortical tumor - Cause: Tumor releases cortisol independent of ACTH
Organ physiologic effect and its stimulation
Adrenal medulla = Systemic vasoconstriction Atrium = Natriuresis Adrenal cortex = Sodium reabsorption Posterior pituitary gland = Synthesis and insertion NB: Adrenal cortex—-Increased aldosteone—-Na+ and water retention as well as K+ and H+ wasting Adrenal medulla—-Increased EPI and NE—-Systemic vasoconstriction Atrum (atrial stretch)—-Increased atrial natriuretic peptide release—-natriuresis Posterior pituitary—-Increased antidiuretic hormone—-aquaporin synthesis and insertion in the renal collecting ducts—-water reabsorption to restore osmolality
Glucocorticoid potency relative to cortisol
Aldosterone = 0x Methylprednisolone = 5x Fludrocortisone = 10x Dexamethasone = 25x
Mineralocorticoids (Aldosterone)
Aldosterone release is increased by: 1. RAAS activation 2. Hyperkalemia 3. Hyponatremia ACTH only has a minor influence on aldosterone release. This explains why decreased ACTH does not cause hypoaldosteronism
What steroid has the greatest mineralocorticoid effect?
Aldosterone. It's 3,000 times more potent than cortisol
Trousseau's sign
An upper extremity cuff is inflated above SBP for three minutes. Decreased blood flow accentuates neuromuscular irritability—-muscle spasms of the hand and forearm
How much cortisol does the body produce each day?
Average cortisol production is 15 - 30 mg/day, with a normal serum level of 12 mcg/dL
Glucosuria is likely to occur when serum glucose exceeds: A. 120 mg/dL B. 180 mg/dL C. 240 mg/dL D. 300 mg/dL
B. 180 mg/dL NB: Glucosuria is glucose in the urine. The kidney's capacity to reabsorb glucose is exceeded whn serum is >180 mg/dL An elevate glucose in the urine exerts an osmotic effect, so glucosuria leads to polyuria which later leads to hypovolemia. Hypovolemia activates the thirst reflex, which explains why these patients are frequently thirsty (polydypsia) Indeed, the classic s/sx of diabetes mellitus are polydipsia, polyuria, and dehydration
Which medication should be avoided in the patient with thyroid storm? A. Propranolol B. Amiodarone C. Hydrocortisone D. Propylthiouracil
B. Amiodarone NB: A 200 mg amiodarone pill is 35% iodine by weight, and this amount of iodine is 20 times the optimal daily intake. - It can cause hypothyroidism by reducing T4 synthesis - It can cause hyperthyroidism by inhibiting the conversion f T4 to t3 Patients experiencing thyroid storm require steroid supplementation, because steroid metabolism is increased by the hypermetabolic state
Which hormones are released by the posterior pituitary gland? (Select 2) A. Prolactin B. Antidiuretic hormone C. Growth hormone D. Oxytocin
B. Antidiuretic hormone D. Oxytocin
When compared to diabetic ketoacidosis, a hyperglycemic hyperosmolar state is: (Select 2) A. Associate with a lower serum glucose B. Associated with a higher serum osmolarity C. More common is patients with type 2 diabetes mellitus D. Lower blood pH
B. Associated with a higher serum osmolarity C. More common is patients with type 2 diabetes mellitus NB: DKA - More common with type 1 DM - Usually caused by infection - Not enough insulin—-Ketoacidosis, hyperosmolarity (from increased glucose), and dehydration - Patient is hyperglycemic (> 250 mg/dL), but cells are starved for fuel - Treatment = volume resuscitation, insulin, K+ after acidosis subsides HHS - More common with tyep 2 DM - Usually caused by insulin resistance or inadequate production - Enough insulin is produced to prevent ketosis by not hyperglycemia - Hyperglycemia (> 600 mg/dL) significantly increases serum osmolarity (>330 mOsm/L) - Compared to DKA, HSS is associated with a greater elevation in glucose and osmolarity - Mild metabolic acidosis may occur (usually > 7.3 and no anion gap) - Treatment = volume resuscitation, insulin, correct electrolytes
Which of the following conditions is commonly associated with this EKG tracing? A. Myxedema B. Conn's syndrome C. Addison's disease D. Acromegaly
B. Conn's syndrome NB: Primary hyperaldosteronism is called Conn's syndrome Remember that aldosterone: - Increases Na+ AND water retention - Wastes K+ and H+ This EKG has a U wave, and you know that this suggests hypokalemia. This patient may also present with muscle weakness
All of the following hormones bind to a G-protein coupled receptor EXCEPT: A. Epinephrine B. Cortisol C. Vasopressin D. Norepinephrine
B. Cortisol Cellular receptors tend to be located in 1 of 3 places: 1. On the cell surface, you'll find receptors that bind catecholamine, protein, or peptide hormones (vasopressin, epi, ne) 2. In the cytoplasm is where you'll find receptors for most steroid hormones (cortisol) 3. In the nucleus is where you'll find receptors for thyroid hormones
All of the following hormones are released by the adenohypophysis EXCEPT? A. Luteinizing hormone B. Cortisol C. Thyroid stimulating gland D. Growth hormone
B. Cortisol Cortisol is released by the zona fasciculata of the adrenal cortex. Remember the mnemonic "GFR" for adrenal hormone production Anterior pituitary gland = adenohypophysis
Anesthetic considerations for the patient with diabetes insipidus include: A. Sodium restriction B. DDAVP (Desmopressin) C. 3% sodium chloride D. Demeclocyclie
B. DDAVP (Desmopressin) NB: Diabetes insipidus is caused by either inadequate ADH production or renal tubules that don't respond to ADH. Either way, this causes a tremendous water loss from the body (up to 18L+/day) - The most common cause of DI is pituitary surgery - Treatment consists of DDAVP (selective V2 agonist) * SC = 0.5 - 2 mcg BID * Nasal = 5 - 40 mcg QD NB: The syndrome of inappropriate ADH (SIADH) is caused by too much ADH. This causes the body to retain too much water. Treatment includes fluid restriction, hypertonic saline, and demeclocycline.
A patient with untreated hyperthyroidism and atrial fibrillation presents for emergency surgery. What is the BEST intervention at this time? A. Amiodarone B. Esmolol C. Propylthiouracil D. Delay surgery until a euthyroid state is achieved
B. Esmolol NB: The hyperthyroid patient presenting for non-emergency surgery should be canceled and managed medically until a euthyroid state is achieved. This patient requires an emergent, so you don't have the luxury of canceling Esmolol is the best option in this question. It reduce the SNS response, and it's easily titratable. For completeness, it does not inhibit the conversion of T4 to T3 like propranolol Propylthiouracil inhibits the conversion of T4 to T3; however, this requires days to begin to take effect. You don't have this much time We said that this patient has atrial fibrillation (a common consequence of hyperthyroidism). Amiodarone one would treat this; however, it contains a significant amount of iodine by weight. An important side effect of this drug is that it can cause hyper- or hypo- thyroidism. As such, it has the potential to worsen this patient's condition
Which of the following are complications of Conn's syndrome? (Select 2) A. Hypernatremia B. Hypokalemia C. Hypertension D. Metabolic acidosis
B. Hypokalemia C. Hypertension NB: Conn's syndrom occurs when there is an over production of aldosterone - usually from an adrenal tumor Excess aldosterone causes: - Na+ retention with passive reabsorptin of water (hypervolemia + HN) - K+ secretion into the collecting ducts by principal cells (hypokalemia) - H+ secretion in the collecting ducts by intecalated cells (metabolic alkalosis) Remember hypokalemia moves the resting membrane away from the threshold potential. This means its more difficult to generate an action potential. This explains why the patient with hypokalemia commonly experiences muscle weakness
A patient becomes hypotensive during resection of carcinoid tumor. What is the BEST drug to administer at this time? A. Norepinephrine B. Octreotide C. Phenylephrine D. Ketamine
B. Octreotide NB: Carcinoid syndrome is associated with secretion of vasoactive substanses from enterochromafin cells. The tumor can release vasoactive substances that increase or decrease blood pressure. Somatostatin (octreotide or lanreotide) inhibits release of vasoactive sustances from carcinoid tumors. This makes it the drug of choice if tumor secretions is etiology of hemodynamic instability. A fluid bolus is also indicated in the context of this question. Vasopressor can have an unpredictable effect on blood pressure. If you must give one, then phenylephrine is the best choice
Which insulin preparation can be administered intravenously? A. Very rapid-acting B. Rapid-acting C. Intermediate-acting D. Long-acting
B. Rapid-acting NB: Ony regular insulin can be given IV (or IM), and regular insulin is the only rapid-acting insulin in commercial use
Choose the statements that BEST describe the anesthetic considerations for the patient with hyperthyroidism. (Select 3) A. MAC is increased B. There is a higher incidence of corneal abrasion C. There is increased sensitivity to muscle relaxants D. Patients with mild hyperthyroidism can be cleared for elective surgery E. There is an increased risk for pathologic fractures during positioning F. Beta blockers are contraindicated
B. There is a higher incidence of corneal abrasion C. There is increased sensitivity to muscle relaxants E. There is an increased risk for pathologic fractures during positioning NB: - An increased cardiac output slows FA/FI, and this may be falsely interpreted as a higher anesthetic requirement. Know that MAC is unchanged! - The patient with hyperthyroidism is at risk for thyrotoxicosis, so the patient should be euthyroid for an electinve procedure - SNS stimulation can precipitate thyrotoxicosis and thyroid storm - Avoid drugs that activate the SNS (ketamine, pancuronium, ephedrine) - Direct actig sympathomimetics are better than indirect acting drugs - Hypercarbia and hypoxia can activate the SNS - Beta blockers are indicated to depress the SNS - Exophthalmos is an infiltrative proces involving the eyelids and the retrobulbar fat. Lid retraction and periorbital swelling makes closing the eyes more difficult, and this increases the risk of corneal abrasion. - Position carefully. Patients are prone to osteoporosis and fractures - Closely titrate muscle relaxants because of a higher incidence of myopathy and propensity towards mysthenia gravis
Which pathologic changes are expected with acromegaly? (Select) A. Microglossia B. Turbine hypertrophy C. Subglotting narrowing D. Epiglottic atrophy
B. Turbine hypertrophy C. Subglotting narrowing NB: Acromegaly results from over secretion of growth hormone after adolescence. 99% of the cases are associated with pituitary adenoma. A difficult mask and intubation should be anticipated. Dyspnea, stridor, or hoarseness signify airway involvement. A larger tongue (macroglossia) and epiglottis may make laryngoscopy more difficult. Subglottic narrowing along with vocal cord enlargement should be expected with acromegaly and may necessitate a smalle endotracheal tube. urbinate enlargement requires care with nasal intubation. Obstructive sleep apnea is common
Cortisol
Both gluco- and mineralocorticoid effects
Methylprednisone
Both gluco- and mineralocorticoid effects
Prednisone
Both gluco- and mineralocorticoid effects
What is the significance of the prayer sign in the patient with diabetes mellitus?
Brittle diabetes frequently have stiff joint syndrome with reduced range of motion. This include the AO (atlanto-occipital) joint, which can make intubation difficult
Other drugs that cause Adrenocortical Suppression
By inhibiting 11-beta-hydroxylase, etomidate causes dose-dependent adrenocortical suppression - After a single induction dose, this effect lasts 5-8 hours (some sources say up to 24 hours) - In non-cardiac surgical patients, induction with etomidate (rather than propofol) was associated with increased 30-day mortality - The need for a stable induction must be balanced against the potential risk of adrenocortical suppression * Ketoconazole also inhibit cortisol synthesis
Which of the following statements is true of cortisol? A. It engages with receptors on the cell membrane B. It inhibits insulin release C. An excess causes muscle wasting D. Its mineralocorticoid activity increases serum glucose
C. An excess causes muscle wasting NB: Cortisol is a glucocorticoid. One of its primary roles is gluconeogenesis, which raises serum glucose. Hypeglycemia stimulates the pancreatic beta cells to secrete insulin Cortisol also posesses some mineralocorticoid properties (think aldosterone). This leads to: - Na+ retention with passive reabsorption of water - K+ secretion into the collecitng ducts by principal cells - H+ secretion in the collecting ducts by intercalated cells Cortisol acts on intracellular cytoplasm receptors and stimulates the production of mRNA. It does not interact with membrane bound receptors. This explains why it has a delayed onset of action.
Etiologies of Addison's disease include: (Select 3) A. Adrenocorticotropic hormone deficiency B. Corticotropin releasing hormone deficiency C. Autoimmune disease D. Adrenal tumor E. Tuberculosis F. Pituitary tumor
C. Autoimmune disease D. Adrenal tumor E. Tuberculosis NB: Hypoadrenalism (adrenal insufficiency) can be primary or secondary Primary adrenal insufficiency is called Addison's disease. It occurs when the adrenal cortex fails to produce cortisol (Increased ACTH level and Decreased cortisol lel) Causes include: - Autoimmune disease (most common cause in US) - Tuberculosis (most common cause worldwide) - Heparin induced thrombocytopenia (HIT) - Diabetes type 1 - Hashimoto's thyroiditis - HIV - Trauma - Adrenal tumor Secondary adrenal insufficiency occurs when the pituitary gland doesn't secrete enough ACTH (Decreased ACTH level and Decreased cortisol level) Causes include: - Iatrogenic (chronic glucocorticoid supplementation - Hypothalamic or pituitary dysfunction (tumor, infection, or ablation) NB: Remember that a single dose of etomidate reversibly inhibits 11-beta-hydroxylase and impairs cortisol and aldosterone synthesis for 8-24 hours. Don't give it to the patient with Addison's disease
Which endocrine disorder is MOST likely to occur in a postoperative patient recovering from transsphenoidal hypophysectomy? A. Addisonian crisis B. Hypothyroidism C. Diabetes insipidus D. Syndrome of inappropriate antidiuretic hormone secretion
C. Diabetes insipidus NB: oo little antidiuretic hormone in the blood causes diabetes insipidus (DI). You should be on the lookout for this complication in patients undergoing pituitary surgery, such as transsphenoidal hypophysectomy DI presents with polyuria, so consider hypovolemia and electrolyte imbalances. Treatment is supportive and includes DDAVP or vasopressin
Somatotropin: A. Increases bone length following epiphyseal closure B. Decreases fatty acid mobilization C. Facilitates tissue growth D. Increases protein catabolism
C. Facilitates tissue growth NB: Growth hormone is also called somatotropic hormone or somatotropin. - It facilitates growth of all of the tissues in the body - It increases linear bone growth before epiphyseal closure - It increases protein synthesis (anabolic effect) - It enhances fatty acid mobilization and utilization (ketogenic effect)
All of the following are anesthetic considerations for myxedema EXCEPT: A. Restrictive lung disease B. Low cardiac output C. Hypernatremia D. Impaired drug metabolism
C. Hypernatremia NB: Hypothyroidism, in its most severe form, is called myxedema. This affects all the organ systems in the body - Lack of thyroid hormone decreases heart rate, contractility, and cardiac output - Pleural and pericardial effusions are common - In the liver, decreased metabolism manifests as slowed biotransformation reactions - In appropriate secreton of ADH is common, so these patients retain free water. This contribute to dilutional hyponatremia (not hypernatremia). Edema is common finding
Which of the following stimulate growth hormone secretion? (Select 3) A. Corticoseroids B. Increased fatty acid levels C. Hypoglycemia D. Alpha adrenergic agonists E. Surgery F. Pregnancy
C. Hypoglycemia D. Alpha adrenergic agonists E. Surgery NB: Growth hormne secretion is increased by: - Growth hormone releasing hormone from the hypothalamus - Stress and anxiety (including surgery) - Physiologic sleep - Hypoglycema - Decreased free fatty acid levels - Fasting - Dopamine - Alpha-adrenergic agonists - Estrogen
The following are consequenses of excess thyroid hormone EXCEPT: A. Vasodilation B. Diarrhea C. Hypoventilation D. tremors
C. Hypoventilation NB: Thyroid hormones increase the metabolic activity of nearly all the cells i the body. You must remember: High Thyroid hormone —- High basal metabolic rate (BMR) —-High VO2 + High CO2 production Vasodilation results from increased oxygen consumption. This improves tissue blood flow and oxygen delivery Increased carbon dioxide production requires that the patient increase (not decrease) minute ventilation Thyroid hormone excess increases the sensitivity of neuronal synapses in the spinal cord, leading to tremors Intestinal hypermotility results in diarrhea (risk of fluid and electrolyte imbalance)
All of the following are indicated in the treatment of severe hypercalcemia EXCEPT: A. 0.9 percent sodium chloride B. Calcitonin C. Lacted ringers D. Furosemide
C. Lacted ringers NB: Hypercalcemia should be treated when the serum calcium levels exceeds 13 mg/dL or if the patient is symptomatic. Treatment includes: - Hydration with 0.9 percent NaCl—- Dilutes serum Ca+2 and increased GFR hastens diuresis - Loop diuretic—- Enhances Ca+2 excretion - Calcitonin or bisphophonates—- Inhibits osteoclast bone resorption Lacted ringers contain calcium and should be avoided
Long-term consumption of which food is associated with a syndrom that resembles hyperaldosteronism? A. Organ meats B. Grapefruit juice C. Licorice D. Aged cheese
C. Licorice (glycyrrhizic acid) NB: Organ meats are high in purines, whcih can lead to worsening of symptoms in patients with gout Patients on MAO-inhibitors may need to refrain from foods high in tyramine, such as some aged cheeses Grapefruit juice is a must-know enzyme inhibitor
Which airway management technique should be avoided in the patient with acromegaly? A. Mask ventilation B. iGel placement C. Nasal intubation D. Direct vision laryngoscopy
C. Nasal intubation NB: While all airway techniques in th answer choices may be more difficult in the patient with acromegaly, nasal intubation should be specifically avoided due to the risk of epistaxis Acromegaly can complicate airway management. Considerations include: - Distorted facial features (difficult mask ventilation due to poor seal) - Large tongue, teeth, and epiglottis (difficult laryngoscopy) - Subglottic narrowing and vocal cord enlargement (difficult ETT placement) - Turbinate enlargement (risk epistaxis)
What is the MOST common cause of primary hyperparathyroidism? A. Invasive ductal carcinoma B. Multiple myeloma C. Parathyroid adenoma D. Lung adenocarcinoma
C. Parathyroid adenoma NB: Parathyroid adenoma is the most common cause of primary hyperparathyroidism Chronic renal disease (renal osteodystrophy) i the most common cause of secondary hyperparathyroidism
Which beta-blocker inhibits the conversion of T4 to T3? A. Nadolol B. Metoprolol C. Propranolol D. Caverdilol
C. Propranolol Beta-blockers are indicated for thyroid storm because they reduce SNS stimulation. Propranolol has the additional benefit of inhibiting the conversion of T4 (inactive) to T3 (active)
Decreases ionized Ca+2
Calcitonin
Increases serum phosphate
Calcitonin
Produced by C cells
Calcitonin
Increases Ca+2 deposition in bone
Calcitonini
Carcinoid Crisis
Carcinoid crisis is life-threatening and can occur in patients with carcinoid syndrome. S/sx include: - Tachycardia - Hyper- or hypotension - Intense flushing - Abdominal pain - Diarrhea
Matching endocrine diseas to their pathophysiology
Conn's Syndrome = Excess aldosterone Addison's Disease = Inadequate cortisol Cushing's Disease = Exess cortisol
Endocrine system & Endocrine system
Consider the endocrine system as a wireless system that sends information to target cells via hormones circulating in the blood Consider the nervous system as a wired system that sends information to target cells via neurotransmitters (electrical pathway) NB: Just like neurotransmitters, endocrine hormones act as first messengers that bind to a receptor and instruct a specific cell type to carry out a function. These receptors can include ion channels, G-proteins, enzymes, and gene activation
Glucocorticoids (Cortisol)
Cortisol does not interact with membrane-bound receptors. Instead, it diffuses through the lipid bilayer the binds with intracellular steroid receptors. By activating or inhibiting DNA transcription, cortisol influences protein synthesis inside the target cell. These processes require time, which explains the relatively slow onset of steroids medications. Cortisol production is 15 - 30 mg/day, with a normal serum level of 12 mcg/dL Stress can increase cortisol production upwards of 100 mg/day, with a serum level up to 30-50 mcg/dL during and after major surgery.
What are the hemodynamic effects of cortisol?
Cortisol improves myocardial performance by increasing the number and sensivity of beta receptors on the myocardium. Cortisol is also required for the vasoconstrictive effects of catecholamines
Glucocorticoids - Hemodynamics
Cortisol improves myocardial preformance by increasing the number and sensitivity of beta receptors on the myocardium. Cortisol is also required for the vasculature to respond to the vasoconstrictive effects of catecholamines
Glucocorticoids - Anti-inflammatory Effects
Cortisol mitiigates the inflammatory cascade by stabilizing lysosomal membranes and reducing cytokine release - It decreases the number of eosinophils and lymphocytes in the blood - Cortisol does NOT reduce histamine release during an antigen-antibody response - This accomplished by epinephrine at the beta-2 receptor on mast cells and basophils
Diagnostic criteria for diabetes mellitus includes an A1c greater than: A. 1.5% B. 2.5% C. 4.5% D. 6.5%
D. 6.5% NB: Diagnostic criteria for diabetes mellitus includes: - Hemoglobin A1c > 6.5% - Fasting plasma glucose > 126 mg/dL - Two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test - Classic symptoms + random glucose of 200 mg/dL A hemodlobin A1c correlates with an average serum plasma glucose of 126 mg/dL
The following factors can mask the signs of intraoperative hypoglycemia EXCEPT: A. General anesthesia B. Propranolol C. Diabetic autonomic neuropathy D. Hydrochlorothiazide
D. Hydrochlorothiazide NB: Decreased serum glucose activates the SNS. Increased serum epinephrine stimulates gluconeogenesis and glycogenolysis in the liver to restore a normal serum glucose concentration. Intraoperative hypoglycemia can be difficult to diagnose. Anything that blunts the SNS response can potentially mask the signs of intraoperative hypoglycemia. Examples include general anesthesia, diabetic autonomic neuropathy, and beta-blockers (propranolol) Thiazide diuretics have a unique side effect in that they increase serum glucose (hydrochlorothiazide, metolazone, and indapamide
Which drug should be avoided in the patient with hyperthyroidism? A. Propranolol B. Propylthiourail C. Radioactive iodine D. Levothyroxine
D. Levothyroxine Treatment of hyperthyroidism consists of antithyroid medications, beta-blockers, and thyroidectomy Antithyroid medications include: - Propylthiouracil (PTU) - Carbimazole - Radioactive iodine Radioactive iodine arrests the overproduction of thyroid hormones over 2-4 month period. It should not be given during pregnancy or to nursing mothers, because it can ablate the offspring's thyroid gland Levothyroxine is synthetic T4
A diagnosis of Grave's disease is consisten with: A. Somolence B. Elevated TSH C. Decreased free T4 D. Protein catabolism
D. Protein catabolism NB: Grave's disease is most common cause of hyperthyroidism. As an autoimmune disorder, TSH-receptor antibodies cause the thyroid gland to produce excess T3 and T4. This leads to s/sx of thyroid over stimulation. Grave's disease is more common in women Lab values consistent with a diagnosis of Grave's disease inclde: - Increased Free T4 (not decreased) - Decreased TSH (not increased) Signs and symptoms include: - Insomnia - Protein catabolism and weight loss - Exophthalmos - Anxiety - Heat intolerance
What effect does alpha-2 stimulation have on insulin release?
Decreased insuli release
4 mg/day for 12 weeks
Don't give stress dose
50 mg/day for 2 weeks
Don't give stress dose
Hormone and it's site of synthesis
Epinephrine = Adrenal medulla Cortisol = Zona fasciculata Estrogen = Zona reticularis Aldosterone = Zona glomerulosa NB: GFR = SSS (Salt, Sugar, Sex)
Suppression of the Hypothalamic-Pituitary Axis
Exogenous steroid supplementation suppreses ACTH release from anteior pituitary gland. Some patients on chronic steroid therapy wont be able to increase cortisol release in response to perioperative stress.
Avoid etomidate in hyperthyroidism?
False
Avoid glucocorticoids in hyoerthyroidism?
False
Elective surgery should be postponed for moderate disease in hypothyroidism?
False
Increased resistance to nondepolarizing NMBs in hyperthyroidism?
False
Inhalation iduction is slower than normal in hypothyroidism
False
Elective surgery should be postponed for up to 2 weeks in patients with hyperthyroidism
False (6-8 weeks)
Administer levothyroxine in hyperthyroidism?
False (hypothyroidism)
10 mg/day for 6 weeks
Give a stress dose
30 mg/day for 4 weeks
Give a stress dose
5 mg/day for 4 weeks
Give a stress dose
Other uses for Glucagon
Glcagon (1-5 mg IV) increases myocardial contractility, heart rate, and AV conduction by increasing the intracellular concentration of cAMP. It does this by independently of the autonomic nervous system, which is useful in the folowing situations: - Beta-blocker overdose - CHF - Low cardiac output after MI or cardiopulmonary bypass - Improving MAP during anaphylaxis Glucagon is also administered during ERCP to relaxc the biliary sphincter Nausea and vomiting are key side effects of glucagon
Oral diabetic agent to it's drug class
Glipizide = Sulfonylurea Pioglitazone = Thiazolidinedione Metformin =Biguadine Exenatide = GLP-1 agonist
Cushing's Syndrome Clinical Features
Glucocorticoid Effects: - Hyperglycemia - Weight gain (central obesity, buffalo, moon face) - Increased risk of infection - Osteoporosis - Muscle weakness - Mood disorder Mineralocorticoid Effects - Hypertension - Hypokalemia - Metabolic alkalosis Androgenic Effects - Women become masculinized (hirsutism, hair thinning, acne, amenorrhea) - Men become feminized (gynecomastia, impotence)
Buffalo humb
Glucocorticoid effects
Central Obesity
Glucocorticoid effects
Hyperglycemia
Glucocorticoid effects
Increased risk of infection
Glucocorticoid effects
Moon face
Glucocorticoid effects
Osteoporosis
Glucocorticoid effects
Betamethasone
Glucocorticoid effects only
Triamcinolone
Glucocorticoid effects only
Dexamethasone
Glucocorticoids effects only
Insulin Release and the Target Cell
Glucose is the primary stimulator of insulin release from the pancreatic beta cells. Therefore, anything that increases serum glucose will also increase insulin release
Acromegaly
Growth hormone (somatotropin) facilitates the growth of all tissues in the body - Acromegaly results from over secretion of growth hormone after adolescence - Nearly all cases are caused by a pituitary adenoma - Increased GH output before puberty causes gigantism
Paracrine function
Hormone acts adjacent to the site of origin
Autocrine function
Hormone acts at the site of origin
Endocrine function
Hormone enters the blood and acts at distant site
Insulin ranking according to it's duration of action
Humalog = 1 Humulin R = 2 Humulin N = 3 Lantus = 4 NB: Humalog (rapid acting) = 3.5 hours Humulin R (short acting regular) = 4-12 hours Humulin N (intermediate acting NPH) = 10 - 20 hours Lantus (long acting) = 12 - 24 hours Of these formulations, only Humulin R can be given IM or IV. All of the others are administered subcutaneously
Hypertension
Hyperparathyroidism
Lethargy
Hyperparathyroidism
Osteopenia
Hyperparathyroidism
Pacreatitis
Hyperparathyroidism
Polyurea
Hyperparathyroidism
Psychosis
Hyperparathyroidism
Short QT interval
Hyperparathyroidism
Increased resistance to depolarizing NMBs
Hyperthyroidism
Postoperative Hypocalcema after thyroid surgery
Hypocalcemia due to resection of parathyroid glands (without reimplantation) most commonly occurs 24-48 hours after surgery. If it happen to occur sooner, it's typically no earlier than 6-12 hours after surgery. Therefore, laryngospasm in the immediate postoperative period is not due to hypocalcemia Most s/s of hypocalcemia are a result of increased nerve and muscle irritability - Muscle spasm—-tetany - Laryngospasm - Mental status changes - Hypotension - Prolonged QT interval - Paresthesias - Chvostek's sign - Trousseau's sign NB: Treatement = IV calcium. When compared to chloride, calcium gluconate provides less elemental calcium, however it carries lower risk of necrosis if IV infiltration occurs.
Abdominal cramping
Hypoparathyroidism
Long QT interval
Hypoparathyroidism
Muscle spasm
Hypoparathyroidism
Myocardial depression
Hypoparathyroidism
Seizures
Hypoparathyroidism
Tetany
Hypoparathyroidism
Aldosterone Physiologic Effects
In the kidney, aldosterone enhances the reabsorption of sodium and the excretion of potassium and hydrogen. This causes: - Fluid retention and expansion of the extracellular space - Decreased serum potassium concentration - Metabolic alkalosis Aldosterone regulates intravascular volume. It does NOT regulate sodim concentration or osmolarity. Here is why: - When sodium is reabsorbed into the peritubular capillaries, water follows in direct proportion. The sodium concentration does not change - Osmolarity (and therefore sodium concentration) is controlled by antidiuretic hormone (ADH) - ADH increases the reabsorption of water by NOT sodium. Therefore, increased water reabsorption dilutes sodium, and reduced water reabsorption concentrates sodium
What effect does beta-2 stimulation have on insulin release?
Increased insulin release
What effect does the PNS stimulation have on insulin release?
Increased insulin release
Insulin
Inhibits glicagon release
Somatostatin
Inhibits glucagon and insulin release
Hyperglycemia
Inhibits glucagon release
Beta antagonists
Inhibits insulin release
Hypoglycemia
Inhibits insulin release
Volatile agents
Inhibits insulin release
Pancreatic hormone vs Cell type
Insulin = Beta cells Glucagon = Alpha cells Somatostatin = Delta cells Pancreatic polypeptide = PP cells NB: The pancreas produces two types of hormones" 1. Exocrine hormones are secreted into the duodenum for digestion (produced by the acini tissue) 2. Endocrine hormones are secreted into the systemic circulation for metabolism (produced by the islets of Langerhans)
Glucagon
Is a catabolic hormone that promotes energy release from adipose and the liver. It is: - secreted by alpha cells - A physiologic antagonist to insulin - Eliminated by the kidneys and liver, and has a half-lif of 3 - 6 minutes
Insulin
Is an anabolic hormone that promotes energy storage. It's elimitaed by the kidneys and liver and has an elimiation t1/2 of 5 minutes When energy abounds (after a meal), insulin secretion increases and plays a significant role in capturing and storing that energy. Insulin accomplishes this by: - Increasing glucose permeability in skeletal muscle, liver, and fat - Converting carbohydrates to glycogen in the liver and skeletal muscle - Converting excess carbohydrates to fats. These fats can be oxidized if blood sugar becomes low - Promoting cellular uptake of amino acids, potassium, magnesium and phosphate - Encouraging protein synthesis and discouraging protein breakdown - Stimulating the Na/K-ATPase. As an aside, this decreases serum potassium and is why we give insulin and D50 for hyperkalemia
Cushing's Syndrome
Is the result of cortisol excess either from overproduction or exogenous administration. As a point of semantics, Cushing's disease is the result of excess ACTH. Recall that cortisol has glucocorticoid, mineralocorticoid, and androgenic effects, so you should expect the patient with Cushing's syndrome to have signs and symptoms reflecting all of these
What is carcinoid syndrome?
It's associated with the secretion of vasoactive substances from enterochromaffin cells. It's usually asociate with tumors of the GI tract, but it can also arise from locations outside of the GI tract
What herbal supplement can cause a syndrome that resembles hyperaldosteronism?
Licorice
How does cortisol production change in response to perioperative stress?
Major perioperative stress can increase cortisol production upwards of 100 mg/day, with a serum level up to 30 - 50 mcg/dL
Oral hypoglycemic agent and it's unique risk
Metformin = Lactic acidosis Glyburide = Cross sensitivity with sulfa allergy Rosiglitazone = Promotes edema NB: Metformin disrupts mitochondrial function, ultimately reducing the intracellular concentration of ATP. Recall that pyruvate is the final product of glycolysis, and in the setting of mitochondrial dysfunction, the cell will shift to anaerrobic metabolism and produces lactate Glyburide is a sulfonylurea. This class of agents can cause an immunologic response in patients with sulfa allergy. Rosiglitazone expands the ECV, which can lead to edema
Hypertension
Mineralocorticoid effects
Hypokalemia
Mineralocorticoid effects
Metabolic alkalosis
Mineralocorticoid effects
Aldosterone
Mineralocorticoid effects only
Clinical features of hyper- and hypoparathyroidism
NB: Anesthetic considerations are similar to those for thyroidectomy
Feedback loops
Negative feedback: The response is negative (opposite) the initiating stimulus, which returns the parameter to a set point to maintain stability (homeostasis) Positive feedback: Provides an unstable cycle in which the system responds in a way that increases the maginitude of the response. thi results in the amplification of the original signal instead of stabilization
Two major systems that maintain homeostasis
Nervous system & endocrine system NB: These systems work in concert to optimiz physiologic function
Biopsy
No dose needed
Tooth extraction
No dose needed
Pancreatic Polypeptide (PP)
PP inhibits pancreatic exocrine secretion, gallbladde contraction, gstric acid secretion, and gastric motility
Parathyroid Hormone and Calcitonin
PTH and calcitonin are two hormones that act antagonisticaly to regulate the ionized Ca+2 level (i.e. Ca+2 that is free and not bound to plasma proteins, such as albumin). These hormones affect Ca+2 regulation in the bone, intestine, and kidneys - PTH increases Ca+2 and decreases serum phosphate - Calcitonin decreases ionized Ca+2 and increases serum phosphate * Don't confuse calcitonin with calcitriol (the active form of vitamin D)
Decreases serum phosphate
Parathyroid hormone
Increased ionized Ca+2
Parathyroid hormone
Increases Ca+2 resorption from born
Parathyroid hormone
Increases Ca+2 resorption in the kidneys
Parathyroid hormone
Produced by chief cells
Parathyroid hormone
Airway
Patientswith diabetes mellitus are at risk for stiffjoint syndrome. This can lead to a reduced range of motion of the atlanto-occipital joint The hands may also be affected, where the patient can not approximate the palmer sides of the metaphalangeal joints. This is called the prayer sign, and it suggests an increased risk of difficult intubation (due to reduced ROM of the AO joint)
Which synthetic steroid is best suited to treat Addison's disease?
Prednisone. Of all the synthetic steroids, it most closely resembles cortisol
How does this cause a goiter?
Remember that we said TSH stimulates the follicles to make thyroglobulin colloid and that this does not require iodine. Since TSH is chronically elevated, the follicles continue to produce thyroglobulin colloid, and this causes the thyroid glnd to increase in size. hs is the cause of endemic goiter
Name a cause of secondary hyperaldosteronism
Renovascular hypertension
Somatostatin
Somatostatin, also known as growth hormone-inhibiting hormone, regulates hormone output from the islet cells - It's released by the pancreatic delta cells - It inhibits insulin AND glucagon - It also inhibits splanchnic blood flow, gastric motility, and gall bladder contraction
Trauma
Stimlates glucagon release
Hypoglycemia
Stimuates glucagon release
Beta agonists
Stimulate insulin release
Catecholamines
Stimulate insulin release
Beta agonists
Stimulates glucagon release
Sepsis
Stimulates glucagon release
Stress
Stimulates glucagon release
Cortisol
Stimulates insulin release
Glucagon
Stimulates insulin release
Growth hormone
Stimulates insulin release
Hyperglycemia
Stimulates insulin release
Hyperthyroidism Surgical Management
Surgical treatment for hyperthyroidism includes subtotal or total thyroidectomy. Complications include hypothyroidism (tracheal compression), recurrent laryngeal nerve injury, and hypocalcemia
The Importance of Iodine
TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize T3 and T4. When iodine is not available (dietary deficiency), the thyroid gland is unable to produce enough 3 and T4. Under normal conditions, there is a negative feedback loop where T3 and T4 supress TSH release. In the patient with a hypoactive thyroid, there isn't enough thyroid hormone to suppress TSH, so TSH remains chronically elevated. This presents a problem.
Chvostek's sign
Tapping on the angle of the jaw (facial nerve / masseter muscle)—-facial contraction on the ipsilateral side
Recurrent Lyryngeal Nerve injury during thyroid surgery
The RLN innervates all the intrinsic laryngeal muscles except for the cricothyroid muscle (innervated by the Superior Laryngeal Nerve (SLN). Injury to the RLN during thyroid surgery can cause airway obstruction. - Unilateral injury —- ipsilateral vocal cord is positioned midline on inspiration = horseness - Bilateral injury —-both cords are positioned midline on inspiration—- airway obstruction - Have the patient say the letter "E" or "moon" to assess for nerve injury - A NIM endotracheal tube provides the ability to assess RNL integrity intraoperatively. When the electrodes on the tube are positioned between the vocal cords, a current can be applied to assess RLN function - AT the end of the procedure, direct laryngoscopy can be used to assess vocal cord function as well as help identify glottic edema
Adrenal gland & hormone classes
The adrenal gland is composed of the cortex (outer region) and medulla (inner region). Adrenal cortex - Zona glomerulosa - mineralocorticoids (aldosterone) - Zona fasciculata - glucocorticoids (cortisol) - Zona reticularis - androgens (dehydroepiandrosterone) Adernal medulla - Catecholamines (epinephrine and norepinephrine)
Adrenal Cortex (indepth)
The cortex has 3 zones that synthesize and release: 1. Mineralocorticoids (aldosterone) 2. Glucocorticoids (cortisol) 3. Androgens (dehydroepiandrosterone) * These hormones are derived from a cholesterol precursor Mnemonic - The cortisol layers (outside to inside) spell GFR - Remember what each one releases with: "salt, sugar, sex"
The insulin receptor consists of two alpha and two beta subunits that are joined together by disulfide bonds. When insulin binds to the receptor, the beta subunits activate tyrosine kinase, which then activates insulin-receptor substrates (IRS). The insulin cascade turns on the GLUT4 transporter, which increases glucose uptake by skeletal muscle and fat
The liver and brain do not require insulin for glucose uptake. This is particularly important in the brain because it requires a steady supply of glucose for optimal function. Indeed, cerebral function generally declines when serum glucose falls below 50 mg/dL
Adrenal Medulla (indepth)
The medulla synthesizes and release two catecholamines: - Epinephrine (80% of catecholamine output) - Norepinephrine (20% of catecholamine output)
Metabolic Syndrome
The metabolic syndrome describes the group of characteristics that are common to patients with DM or to those who are at higher risk of developing DM. Diagnostic criteria include at least three of the following: - Fasting plasma glucose 100 - 110 mg/dL (depends on the reference) - Abdominal obesity (waist > 40 inches in men and > 35 inches in women) - Serum triglyceride level > 150 mg/dL - Serum HDL < 40 mg/dL in men and < 50 mg/dL in women - Blood pressure > 130/85 mm Hg
Carcinoid Syndrome Signs & Symptoms
The mist common signs are flushing anf diarrhea. Concurent cardiac disease is common and manifests as pulmonic stenosis and tricuspid regurgitation - Protect the RV by avoiding conditions that increase PVR: hypoxia, hypercarbia, acidosis, nitrous oxide, and light anesthesia
Thyroid anatomy
The thyroid gland consists of left and right lobe that are joined by the thyroid isthmus The thyroid gland resides: - Anterior to the trachea - Inferior to the cricoid cartilage - Superior to the suprasternal notch The RLN courses along the lateral border of each thyroid lobe. This explains why the RLN can be injured during thyroid or parathyroid surgery
Thyroid anatomy & physiology
The thyroid gland stores and secretes three hormones: - T4 = Thryroxine (a prohormone synthesized from tyrosine) - T3 = Triidothyronine (active thyroid hormone) - Calcitonin (reduces serum Ca2+ (calcium ions)) The thyroid requires iodine to synthesize T3 and T4. When iodine is not available (dietary deficiency), the thyroid gland cannot produce enough T3 and T4. The recurrent larngeal nerve (RLN) courses along the lateral border of each thyroid lobe. This is why the RLN is at risk for injury during thyroid or parathyroid surgery
Thyroid Storm
Thyroid storm is a medical emergency that occur in hyperthyroid AND euthyroid patients * It is generally brought on by stressful events: infection, surgery etc * It most commonly occurs 6-18 hours after surgery S/S * Fever >38.5 dedrees C * Tachycardia / tacharrhythmias (a-fib) * HTN * CHF * Shock * Confusion and agitation *N/V Under anesthesia, thyroid storm can mimic MH, pheochromocytoma, neuroleptic malignant syndrome, and light anesthesia Management - Block synthesis (methimazole, carbimazole, PTU, potassium iodidde) - Block release (radioactive iodine, potassium iodide) - Block beta receptors (propranolol, esmolol) Other treatments - Cardiopulmonary support - Glucocorticoids (blocks conversion of T4 to T3 and supports the stress response - hypermetabolism consumes endogenous steroids) - Active cooling measures (cold iVF, ice packs) - Acetaminophen for fever - Don't give aspirin, because it can dislodge T4 from plasma proteins—-High free fraction of T4—-makes a bad situation worse
Production and Release of Thyroid Hormones
Thyroid-stimlating hormone is released from the anterior pituitary gland. It affects the thyroid gland in two key ways: 1. It tells the thyroid gland to produce T3 and T4 (this requires iodine) 2. It tells the follicular tissue to produce thyroglobulin colloid (this does not require iodine)
Parathyroid Hormone
To best understand how parathyroid hormone (PTH) works, we need to understand it in the context of whole-body calcium hemostasis We obtain Ca+2 from our diet, and we eliminate it in the urine. Hormones control how much Ca+2 we absorb in the intestine and how much we eliminate through the kidney Our bones function as a Ca+2 resevior, where we store Ca+2 as hydroxyapatite. his means we can deposit or remove Ca+2 fro our bones as needed. To understand this process, we need to understand the roles of osteoclasts and osteoblasts. * Osteoblasts are bone cells that promote bone deposition. They add Ca+2 to the bone, which reduces the ionized Ca+2 concentration in the blood * Osteoclasts are bone cells that promote bone resorption. They remove Ca+2 from bone, which icreases the ionized Ca+2 concentration in the blood
A large tongue may increase airway difficulty in hypothyroidism
True
Assess for tracheal deviation in hyperthyroidism?
True
Avoid pancuronium in hyperthyroidism?
True
Hyperthyroidism leads to osteoposis?
True
Increased sensitivity to nondepolarizing NMBs in hypothyridism
True
Carcinoid Syndrome Pathophysiology
When hepatic function is normal, carcinoid hormones are cleared by th liver. When significant liver dysfunction occurs, these hormones aren't cleared by the liver, so they enter the systemic circulation and cause the signs and symptoms characteristic of carcinoid syndrome Carcinoid syndrome can also occur if: - Hepatic function is normal, bt the amount of hormone produced by the tumor exceeds the liver's ability to clear it - The tumor resides in a location where blood flow bypasse the liver, such as the lungs
Is OSA common in acromegaly?
Yes
Is glucose intolerance common in acromegaly?
Yes
Is laryngoscopy more difficult in acromegaly?
Yes - due to larger tongue, teeth and epiglottis
Is it more difficult to pass an EE through the vocal cords in acromegaly?
Yes - due to subglottic narrowing and vocal cord enlargement
Adrenal gland & hormone classes
Zona glomerulosa = Mineralocorticoids Adrenal medulla = Catecholamines Zona reticularis = Androgens Zona fasciculata = Glucocorticoids
Where is aldosterone produced?
Zona glomerulosa of adrenal cortex
