Endocrine Flashcards
Hormone function and types of hormones (3)
Function: Signals molecules or chemical messengers that transport information from one set of cells (endocrine) to another (target)
Types:
-Peptide/protein (insulin, GH, ADH, angiotensin, EPO)
-Amine/amino (catecholamines, thyroxine)
-Lipids (steroid, cortisone, aldosterone, estrogen)
Hormone receptors
Peptide/protein
-Receptor site on cell surface is activated and generates 2nd receptor (cAMP used by vaso, TSH, parathyroid hormone)
Lipid
-Attracts specific hormone, lipophilic, diffuse into the cell (thyroid and steroid hormones)
Hormone regulation (3 control mechanisms)
- Neural controls (pain, smell, taste)
- Biorhythms (circadian)
- Feedback
Endocrine system is involved in regulation of ____
Behavior, growth, metabolism, fluid status, development, reproduction
Endocrine vs autocrine vs paracrine
Hormone enters…
- Endocrine: blood, acts at distant site
- Autocrine: at site of origin
- Paracrine: adjacent to site of origin
Endocrine glands
Pituitary Thyroid Parathyroid Adrenal Pancreas Ovaries Testes Placenta
Body functions modified by the pituitary gland
Homeostatic
Developmental
Metabolic
Reproductive
Pituitary glad located ___ connected to ___
Located at base of brain
Connected to hypothalamus
Anterior vs posterior pituitary communication with hypothalamus
Anterior:
-Via vascular system
Posterior:
-Via neural pathways
Hypothalamus connection controls pituitary hormone secretion
-No BBB between the two so feedback/communication can occur
6 hormones secreted by anterior pituitary
Growth hormone (GH)
Adrenocorticotropic hormone (ACTH)
-Cortisol/androgenic hormone release from adrenal cortex
Thyroid-stimulating hormone (TSH)
Follicle-stimulating hormone (FSH)
-Ovarian follicle development, spermatogenesis
Luteinizing hormone (LH)
-Ovulation, corpus luteum development, testosterone production
Prolactin
-Mammary gland development, milk production
-Inhibits synthesis/secretions of LH, FSH
Causes of anterior pituitary hyposecretion
- Large nonfunctional pituitary tumors - compress and destroy normal cells
- Postpartum shock, irradiation, trauma, hypophysectomy
Panhypopituitarism
Lack of pituitary hormones
- More common than a decrease in a single ant pit hormone
- > decreased thyroid function d/t decreased TSH
- > Decreased glucocorticoid production (by adrenal cortex) d/t decreased ACTH
- > Depressed sexual development and function d/t decreased gonadotropic hormone secretion
Treatment of pituitary tumor
Surgical removal
- Transphenoidal (nasal)
- Need thyroid hormone replacement and steroids peri-op
- May get diabetes insipidus after removal (give vasopressin)
Anterior pituitary hypersecretion
Most commonly tumors secrete prolactin, ACTH, or GH
- Prolactin -> infertility, amenorrhea, decreased libido (treat with dopamine agonist-bromocriptine)
- ACTH -> Cushings
Growth hormone
Hypothalamus regulates GH activity (negative feedback)
- Increased secretion in childhood, more in adolescence, plateaus in adulthood and decreases in old age
- Increased by stress, hypoglycemia, exercise, and deep sleep
- Increases blood glucose levels (decreases sensitivity of cells to insulin by inhibiting glucose uptake into cells
GH hyposecretion vs hypersecretions
Hyposecretion
-Dwarfism, hypoglycemia
Hypersecretion
-Usually caused by GH secreting pituitary adenoma
-Acromegaly -> thick large bones, enlarged organs (cardiomyopathy, HTN, atherosclerosis, LVH), increased lung volumes (VQ mismatch, increased extrathoracic obstruction), coarse facial features
-Gigantism -> if GH is elevated before adolescence, grow to 8-9 feet
-Glucose intolerance, diabetes (GH antagonist to insulin)
-Treatment: Remove pituitary tumor
Anesthetic plan for GH hypersecretion pituiraty tumor removal
Examine airway
- Difficult mask fit and DL due to tissue overgrowth and macroglossia
- May need smaller ETT - vocal cord enlargement
- Extubate alert
- Pre-op glucose and lytes
Posterior pituitary hormones (2)
Antidiuretic hormone (vasopressin, ADH)
-Controls water excretion/reabsorption in kidney
-Regulates serum osmolarity
Oxytocin
-Stimulates milk ejection during lactation
-Uterine smooth muscle contraction
-Derivatives used to induce labor/decrease postpartum bleeding
ADH stimulation
When plasma osmolarity is 284mOsm/L
-Normal 285-290
10-20% decrease in plasma volume or BP
-Baroreceptors send signal via vagal/glossopharyngeal nerves to hypothalamus -> hypothalamus increases ADH synthesis and release
Pain, emotional stress, nausea, hemorrhage
Diabetes insipidus
=Low ADH neurogenic (or inability of renal ducts to respond nephrogenic)
- Polyuria, polydipsia
- > Dehydration, hypernatremia
- Hyperreflexia, weak, lethargic, seizures, coma
Diabetes insipidus anesthetic considerations and treatment
Assess fluid status, electrolytes
-Surgery increases ADH release so pre-op vasopressin isn’t usually necessary with partial DI
-Monitor plasma osm, UOP, serum Na q1h
-Give isotonic fluids until serum osm=290, then hypotonic
Treatment (complete DI)
-Meds that increase ADH release or increase receptor response to ADH
-Short term=vasopressin
-Long term=desmopressin
Syndrome of inappropriate anti-diuretic hormone (SIADH) (characteristics, anesthetic consideration, treatment)
=High ADH levels
-Water reabsorbed in tubules even when hypoosmolar
-Low UOP -> water intoxication, hyponatremia -> brain edema
Slow emergence
Treatment
-Mild, without s/s of hyponatremia: fluid restriction (800mL/day)
-More severe: hypertonic saline with Lasix
-Correct Na levels slowly
Thyroid gland
Function
-Secrete thyroid hormones to regulate cellular metabolism and calcium balance
Nerves in proximity
-Recurrent laryngeal nerve and external motor branch of superior laryngeal nerve
3 hormones secreted by the thyroid gland
T4 -Thyroxine -93% of hormone -less potent in blood -prehormone: converted to T3 at tissue sites T3 -Triiodothyonine -7% of hormone -more potent in blood Calcitonin -Regulates calcium short-term Dependent on iodine for production
Actions of thyroid hormone
Increased metabolic rate, O2 consumption, heat production
-Secondarily increased heart, lung, kidney function
T3 plays a role in growth and development
Graves disease or thyrotoxicosis
Hyperthyroidism
S/S: Goiter, ST, anxiety, tremor, heat intolerance, insomnia, weight loss, a fib, skeletal muscle weakness
Dx: decreased TSH, increased T4
Tx:
-Meds to inhibit hormone synthesis (methimazole, propylthiouracil, carbimazole)
-Prevent hormone release (potassium, sodium iodine)
-Mask adrenergic overactivity (propranolol, atenolol)
-Destroy thyroid cell function (radioactive iodine)
-Surgery: subtotal thyroidectomy
Anesthetic management for hyperthyroid
Untreated symptomatic patients should only go to OR if life threatening
-Continue antithyroid meds and BB through morning of surgery to decrease SNS
-Esmolol inhibits T4 to T3
Assess airway for tracheal deviation from thyroid enlargement
*No ketamine, atropine, pancuronium (SNS stimulation)
-Deep anesthesia before intubation
-May need more inhalational agents (increased CO, blood volume)
-Treat intraop hypotension with direct pressors (phenylephrine)
*ETT with NIM (electrodes on VCs) to assess recurrent laryngeal nerve
Thyroid storm
Life-threatening
Caused by acute stress in undiagnosed or untreated hyperthyroid patient
-May occur anytime periop, more likely 6-18 hours posto
-Different from MH: No muscle rigidity, elevated creatinine kinase, respiratory acidosis
S/Sx:
-Tachycardia, agitation, a fib, fever (>38.5)
Tx:
-IV hydration with glucose
-Cooling/Tylenol
-Beta blockers
-Potassium iodide (block T4 and T3 release)
-Correct electrolytes/acid base imbalance
Recurrent laryngeal nerve palsy
Postop thyroidectomy complication
- Decreased occurance with NIM use
- Unilateral-hoarseness
- Bilateral-aphonia, stridor -> reintubate
Thyrotoxicosis vs MH
Thyrotoxicosis -Elevated HR/BP, A fib, CHF -Hyperprexia (fever), acidosis MH -Unexplained sudden increase in ETCO2 -Elevated HR, trismus (lockjaw), rapid temp rise, mottling, cyanosis
Hypothyroidism (etiology, s/sx, dx, tx)
Hashimoto thyroiditis Etiology -Autoimmune mediated inflammation -Iodine deficiency -Extreme=myxedema S/Sx -Lethargy, hypotension, bradycardia, CHF, gastroparesis, hypothermia, hypoventilation, hyponatremia, poor mentation Dx: Primary -Decreased T4 and/or T3 -Increased TSH Secondary -Decreased T4, T3, TSH Tx -Replace T4: synthroid
Preop anesthetic considerations for hypothyroid
Careful airway evaluation due to enlarged thyroid gland, enlarged tongue, myxedematous infiltration of VCs
-Severe hypothyroid a/w multiple complications with anesthesia - myocardial and baroreceptor function may be depressed
Intraop management for hypothyroid
- No effect on MAC
- Respiratory depression after opioids may be increased: assess for large tongue, goiter hypoxia and hypercarbia (ventilatory response to hypoxia/hypercarbia may be depressed)
- Hypotension/myocardial depressed from inhalation agents may be increased, plasma volume reduced
- Ketamine good for induction
- Body temp closely for hypothermia
- May be sensitive to NDMRs if experiencing muscle weakness
- Slower GI emptying - aspiration risk (RSI?)
- Potential adrenal insufficiency - periop cortisol
Myxedemia
End stage untreated severe hypothyroidism
- Hypothermic, hypoventilation, hyponatremic
- Only do surgery if lifesaving
Parathyroid hormone
Released in response to low serum ionized calcium
- Or hyperphosphatemia or hypomagnesemia
- Provides negative feedback control of calcium
- Increases extracellular calcium, decreases extracellular phosphate
- Increases renal calcium absorption and phosphate excretion
Calcitonin
Hormone secreted from thyroid in response to elevated ionized calcium, has weak effect (opposite of PTH)
Parathyroid dysfunction
Affects bone, intestinal tract (Ca absorption), kidney (VitD formation, Ca reabsorption, phosphate excretion)
Hyperparathyroid -> hypercalcemia
-HTN, ventricular dysrhythmias, shortened QT, impaired renal concentration, muscle weakness, osteoporosis, mental status changes
-Calcifications in organs (pancreas, kidney, heart, stomach)
Treatment of severe hypercalcemia during surgery
> 13-16
Isotonic saline and loop diuretic (Lasix)
-Avoid hypoventilation - hyperventilation/alkalosis decreases active ionized calcium (decreases calcium and K)
Bilateral RLN injury during parathyroidectomy
Requires immediate reintubation
Insulin effects on cells
Bind to receptor (peptide hormone)
- Protein activation cascades start
- Glut 4 transporter translocated to plasma membrane, influx of glucose
- Glycolysis
- Fatty acid synthesis
DM Type 1 (% of all DM, cause, characterized, risks)
5-10% of all DM cases
- Autoimmune destruction of beta cells in the pancreas
- Total deficiency in insulin production
- At risk for DKA and rarely HHNC
DM 2 characteristic
Impaired insulin secretion, peripheral insulin resistance, excessive hepatic glucose production (environmental, genetic, lifestyle factors)
DM periop (impact on recovery, highest risk, concerns)
DM patients will spend 50% more time in the hospital recovering from surgery
- Undiagnosed DM=higher risk
- Concerns: End-organ complications, glucose-lower regimen
Autonomic neuropathy in DM patients
Impaired gastric emptying -Aspiration risk -Slow gastric emptying -Reflux esophagitis -H2 blocker or metoclopramide preop, RSI Dysfunction of cardiac vagus nerve -Orthostatic hypotension, tachycardia, dysrhythmias Higher morbidity/mortality
Oral hypoglycemic (biggest flag, risks, preop holding)
Metformin
- Risk for hypotension and renal hypoperfusion -> lactic acidosis
- Hold 48 hours prior to surgery (controversial)
- New guidelines: Hold for 24 hours if renal compromise or giving contrast during surgery
DM medication instructions preop for Type I vs II vs insulin pump
DM I
-Dependent on insulin, reduce dose
-1/2 insulin PM before, no insulin or decreased dose AM
DM II
-1/2 insulin PM, none AM of surgery
Insulin pump
-Talk with patients, know settings, check site
-Decrease rate in PM and basal rate intraop
-Caution with radiation, electrocautery
-Hold all oral hypoglycemics preop
-Hold all non-insulin injectable medications DOS
Blood sugar goal during anesthesia
Mildly hyperglycemic (s/sx of hypoglycemia are masked)
- 80-180
- Check q1h
Protamine and NPH
Protamine sulfate anaphylaxis can occur in patients taking NPH or protamine zinc insulin
Hypoglycemia treatment (& how much 15mL D50 raises glucose)
25-50mL D50 followed by D5 gtt
- 70kg pt: 15mL D50 increase blood glucose by 30mg/dL
- 1mL D50 increases BG by 2mg/dL
Mortality for DKA vs HHS
Higher for HHS, affects the elderly/DM II patients more after an acute illness
Goal plasma osmolarity for HHS treatment
Diagnosis=>330mOsm/L
Give fluids
-(1/2 NS) if >320mOsm/L until <320, then NS
-Careful when giving fluids, patients typically elderly and can get cerebral edema or CHF
Adrenal cortex hormones
Mineralcorticoids -Aldosterone -Regulate extracellular volume and potassium (Na reabsorption, K secretion) Glucocorticoids -Cortisol -ACTH stimulates synthesis -Maintains/regulates immune/circulatory function Androgen hormones -Dehydroepiandrosterone
Adrenal medulla
Inner part of adrenal gland
-Secretes norepi, dopamine, and epi (80% catecholamine output)
Adrenal cortex dysfunction (types, effects, treatment)
Increased aldosterone production
2 types
-Primary: from adrenal adenoma (Conn syndrome), no stimulus
-Secondary: from increased renin production
-> increased urinary sodium and potassium exchange -> hyperNa, hypoK (HTN, weakness)
Tx: Remove tumor
Adrenal cortex dysfunction anesthetic plan
Correct fluid/lyte (K) balance preop
Manage HTN: spironolactone (aldosterone antagonist)
Peripheral nerve stimulator for muscle relaxants, hypoK may enhance MR
-Avoid hyperventilation (decrease K more)
Cushings syndrome
Excess cortisol/glucocorticoid -Commonly caused by superphysiologic exogenous doses of glucocorticoids for arthritis, asthma, autoimmune d/o, allergies S/Sx: -Central obesity, thin extremities -HTN -Glucose intolerance -Increased intravascular fluid volume, hypokalemia -Moon face, buffalo hump
Anesthetic management for cushing syndrome
- Correct fluid/lyte imbalance preop
- Spironolactone
- Careful positioning (osteopenia)
- Conservative with MR if skeletal muscle weakness
- Thromboemboli more common
Addisons disease
Adrenocortical insufficiency, decreased cortisol
-Adrenal androgen, glucocorticoid, mineralocorticoid all deficient
S/Sx: Hyperpigmentation, s/s c/w cortisol deficiency, aldosterone deficiency
Hemodynamic instability
Adrenal medulla dysfunction
Pheochromocytoma
-Catecholamine secreting tumor
S/Sx:
-Paroxysmal headache, HTN, sweating, palpitations
-Unexpected intraop HTN/tachycardia can be indication of this (during manipulation of abdominal cavity)
Dx:
-Clonidine will decrease neurogenic catecholamines but not ones from pheochromocytoma
Preop plan for pheochromocytoma
1: Alpha blocker, volume replacement
-1-2 weeks preop
2: Beta blocker if necessary for reflex tachycardia
-Added after several days of a-blockade
-Don’t add first because can cause vasodilation which can worsen HTN
Goals
-BP<160/90 for >24hrs
-Orthostatic hypotension (not <80/45 standing)
-<1 PVC every 5 mins
-No ST segment changes/T wave inversions on ECG for 1 week
-Hct decrease 5%: suggests adequate intravascular volume expansion, satisfactory alpha-blockade
Intraop pheochromocytoma (equipment/monitoring, meds, what to avoid)
A line Large bore PIVs Deep intubation (LTA kit helpful) Foley CVP/Swan Anticipate labile CV Meds -1 Alpha blockers -2 Beta blockers -Nicardipine -Magnesium sulfate -Nitroprusside, nitroglycerine Avoid -Ephedrine -Ketamine -Hypoventilation (stimulate SNS) -Atracurium (histamine release) -Morphine (histamine release)
Pheochromocytoma after tumor removal
Hypotension -d/t hypovolemia, a-blockade, tolerance to endogenous catecholamines which are now gone Tx: -Fluids -Phenylephrine -Norepi
Multiple endocrine neoplasia (MEN)
Overactivity of 1 + endocrine glands
-Inherited genetic effect
MEN 1:
-Parathyroid tumors, pancreatic tumors, pituitary tumors
MEN 2a:
-Medullary thyroid cancers, pheochromocytoma, parathyroid tumors
MEN 2b:
-Medullary thyroid cancers, pheochromocytoma, mucosal neuromas*
*=most commonly occuring
Carcinoid syndrome S/Sx
Results from slow growing tumors -Vasoactice substances are secreted from enterochromaffin cells S/Sx depend on vasoactive substance involved) (serotonin -> vasoconstriction, kallikrein and histamine -> vasodilation) -Right-sided heart failure (serotonin) -Labile BP (kallikrein, histamine) -Cutaneous flushing (kallikrein) -Bronchospasm (kallikrein, histamine) -Diarrhea, abdominal pain (serotonin)
Carcinoid syndrome (Dx, Tx, preop)
Dx: Serotonin metabolites in urine, elevated plasma chromogranin A
Tx: Surgical removal or management or symptoms
Preop:
-H1 and H2 blockers
-Evaluate extraintestinal manifestations (AXR)
-Octreotide 2 weeks before surgery
Octreotide and somatostatin for carcinoid syndrome
Octreotide
-Serotonin antagonist
-Inhibits all bioactive substances
Somatostatin
-Antagonize and suppress release of tumor products
-Binds to tumor cell receptors -> decreased secretion
Carcinoid syndrome intraop
A line, large PIV, CVP
- Avoid causing release of vasoactive substances from the tumor
- Treat refractory hypotension with vasopressin
- Octreotide available
- Steroids, H2 blockers
- Avoid histamine releasing substances (morphine, atracurium, succs)
- Deep anesthesia (eliminate cardiac fluctuations from light anesthetic
Hypoparathyroidism anesthetic implications
-Hypocalcemia
-Risk of laryngospasm
-Respiratory distress due to edema, bleeding, or bilateral RLN injury (requires immediate reintubation)
-Avoid hyperventilation
Tx: IV CaCl
Islets of Langerhans cell types
Cells in pancreas
Alpha: secrete glucagon
Beta: secrete insulin
Islet of Langerhans alpha, beta, delta cells
Alpha: Produce glucagon
Beta: Produce insulin
Delta: Produce somatostatin
-Inhibits GI motility and secretion of stomach acid
Insulins anabolic action
Anabolic=simpler molecules->complex, builds up tissues
Glucose -> glycogen and triglycerides
And has anticatabolic effect (prevents tissue breakdown to glucose)
6 endocrine organs that provide the endocrine component of the stress response
Anterior and posterior pituitary
Hypothalamus
Adrenal cortex and medulla
Pancreas
Hormonal response to surgical stress
Increased -Cortisol, glucagon, GH, catecholamines Decreased -Insulin Both ->Decreased glucose clearance and increased gluconeogenesis
Dawn phenomenon vs somogyi effect
Dawn phenomenon
-GH, cortisol, glucagon secreted overnight, increased blood glucose
-Need insulin overnight to counteract this
Somogyi effect
-When too much insulin is given at HS and pt gets hypoglycemic overnight
Insulin transport to systemic circulation
Produced by pancreas
~60 units/day
-First goes to liver where 20-50% is metabolized/deactivated
-When passing through liver, hepatic glucose production is suppressed
Metformin MOA
Decreases hepatic glucose production
-Prevents conversion of lactate to glucose
Increases insulin sensitivity (GLUT 4 transport to cell membranes)
IV insulin half life
7.5 minutes
Will be gone in 35 mins
Best to do drip
