thyroid disease and their anesthetic considerations – Flashcards

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thyroid, size, location
thyroid, size, location
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highly vascular 5th-1st thoracic lobes are connected by an isthmus
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anatomy of thyroid
anatomy of thyroid
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-recurrent laryngeal, inferior laryngeal artery and inferior laryngeal vein branches off vagus, dips off into chest and back into gland. supplys all lryngeal muscles except the crycothyroid membran which is supplied by superior laryngeal nerve.
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what is the functional purpose of the thyroid
what is the functional purpose of the thyroid
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it essentially increase the metabolic rate, increases proteins synthesis, neural maturation, and increased sensbility to catacolimenes.
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what is elevated in hyperthyroidism?
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T4 (thyroxine), this is low in hypothyroid
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what is higher in hypothyroidism?
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TSH- this is the moste sensitive to mild hypothyroidism
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Hallmark signs of hyperthyriod and hypothyroid SVR, HR, EF, CO, Blood Volume
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HYPERTHYROID: decrease SVR, increased HR, increased EF, increased CO, increased blood volume HYPOTHYROID: increased SVR, decreased HR, decreased EF, decreased CO, decreased Blood volume
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Hyperthyroidism
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multinodule goiter from graves disease is common amiodorone is rich in iodine and can cause iodine incued thyrotixicosis
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why do you get bulging of the eyes in graves disease
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because with hyperthyroidism antibodie bind in retro-orbital area casing swelling the eyes
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signs of hyperthyroidism
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red swollen skin
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treatment of hyperthyroidism
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Thioura deritives: methimazole, propythiouracil, (inhibit iodine, so thyroid cannot make thyoid hormone)
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hyperthyroid systemic effects
hyperthyroid systemic effects
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Life threating Tachycardia - hyperpyrexia - CHF - dehydration - shock - full bounding pulse - hypertension - atrial fibrillation - sweating, tremor - vomiting and diarrhea - confusion - agitation delirium - coma - metabolic acidosis can cause cardiovascular collapse, want to normalize thyroid function before surgery, can take 6-8 weeks to attain euthyroidism.
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what is the drug of choice for induction for people with thyroid storm risk?
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Thiopental. avoid sympathetic nervous sytem stimulates: pavulon, ketamine, ephedrine. protect patients eyes, and this disorder does not increase MAC.
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treatment of thyroid storm?
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oxygen electrolyte imbalance inderal-esmolol-potassium iodine-cortisol
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Management of anesthesia for thyroid patients
Management of anesthesia for thyroid patients
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-Normalize thyroid function prior to surgery -Pre-medicate -Induction agent of choice (thiopental if available) -Avoid sympathetic stimulants -Atrial fibrillation is present in 10-20% of pt Assessment of fluid and electrolyte balance -Airway assessment -Substernal goiters - Tracheoesophageal compression
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thyroidectomy
thyroidectomy
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want to monitr CA++ for 24-72 hours after surgery
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hypothyroidism
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hashimots is the most common
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what is the differnce between primary and secondary hyothyroidsim
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primary is more comone
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hypthyroid s/s
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untreated in children can lead to mental retardation and stunted growth
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Myxedema coma
Myxedema coma
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from hypothyroidism. this is medical emergency with 50% mortality. rare, does not effect MAC, the temperature regulations of these patients may effect the MAC of anesthesia
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treatment of myxedema coma?
treatment of myxedema coma?
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may want to give hydrocortisone
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other complications of hypothyroidism
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Neurologic changes Renal changes decreased glomerular filtration rate - decreased creatinine clearance - decreased free-water excretion Miscellaneous changes Decreased factors VIII & IX - decreased cholesterol Concomitant adrenal insufficiency Ileus & gastroparesis SIADH
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anesthetic management of hypothyroidism
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sensitive to drugs, may need RSI, fluid, difficult weaning -Hypothermia -Anemia -Hypoglycemia -Adrenal insufficiency (hydrocortisone) -Induction with ketamine or other hypnotic -Consider RSI MAINTENANCE ANESTHESIA -Minimize use of volatile anesthetics -Decreased cardiac output (take longer to get off) -Controlled ventilation - Maintain muscle relaxation -Avoid hypothermia -Postoperative respiratory depression -Consider adrenal insufficiency in refractory hypotension and give hydrocortisone
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Parathyroid
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Calcium -GI absorption 0.5-1.0 g/day (duodenum/jejunum) -Body reservoir of 1000 grams -Total serum calcium 8.8-10.4 mg/dL -40-50% (ionized), 40% protein bound (nonionized), 10-20% chelated nonionized -Normal renal excretion of 300-400 mg/day (maximum of 500 mg/day)
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parathyroid hormone
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it is stimulated by high levels of phosphate and low levels of magnesium and low serum ca+
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hyperparathyroidsim
hyperparathyroidsim
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all are decreased. can be associated with adenomas -Serum calcium above 11-12 mg/dL Concentration >14 may be life threatening -Generalized weakness -Renal: calculi, polyuria, polydipsia -Cardiac: HTN, short QT, prolonged PR -Skeletal: pain & pathologic fractures -Hematologic: anemia -CNS: somnolence. Psychosis, decreased pain
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early signs of hyperparathyroidism
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sedation vomiting, hypotonia, myasthenia gravis resemblense, systemic hypertension
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hyperparathyroidism therapy
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Thiazides will increase CA+ reabsorption
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anesthetic considerations for hyperparathyoidism
anesthetic considerations for hyperparathyoidism
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- can treat with calcium channel blocker -hypophosphate may leave calcium unopposed so make sure phsophate is adequate
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hypoparathyroidism
hypoparathyroidism
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low calcium -Hypocalcemia -Ionized calcium < 4.5 mEq/L -Prolonged QT with normal PR -Hyperposphatemia Therapy Acutely: calcium infusion Chronically: Oral calcium - Vitamin D supplements chvosticks sign is with low calcium
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how much calcium is in calcium chloride and gluconate
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27mg/ml of calium in chloride 9mg/ml of calcium in gluconate
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anesthetic management of hypoparathyroidism
anesthetic management of hypoparathyroidism
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stridor, tetany, monitor muscle block
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adrenal gland
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Arterial blood supply -Abdominal aorta Renal arteries Phrenic arteries -Venous drainage Left gland: renal vein Right gland: inferior vena cava medulla is what secretes: NE, EPI, DOPA Glomerus: aldosterone
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Glucocorticoids
Glucocorticoids
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ACTH regulates their secreation, this is like cortisol reguate homeostais sympathetic response enhancement
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Mineralcorticoids
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regulates extracellular fluid volume through like aldosterone function. Aldosterone accounts for 95% of mineral corticoid activity, conserves sodium and maintains normal potassium levels
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What is the hallmark for Acute atoic ACTH syndrome?
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Hypokalemia and hypertension. this is because acth controls both minercorticoids and glucocorticoids aldosterone gets rid of K+ and holds onto NA thus retaining water
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clinical featurs of glucocorticoid excess? (eg. cushings)
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muscle weakness, crazy, renal stones, fat deposits, rotund belly, hypokalemia
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Cushings disease
Cushings disease
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A. 24 hour urine for free cortisol B. High dose decadron suppression test, distinguish between cushing and ectopic syndrome (the steriods will inhibit ACTH) -If A and B normal (cushing's is excluded) -If Cushing's is confirmed, then etiologic diagnosis needs to be done -? plasma ACTH concentration suggests a pituitary tumor -If tumor suspected, obtain MRI
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anesthetic management of cushings disease (increased acth)
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want short acting dilators, patients may need blood pressure support when tumro has been removed. GIVE STRESS DOSE STEROIDS for hypophysectomy or Adrenalectomy
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Glucocorticoid deficiency (addisons disease)
Glucocorticoid deficiency (addisons disease)
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Two types: primary and secondary Primary: addisones, bilateral adreal distruction cannot produce glucocorticoids 2nd: hypothalmus or decreased acthTwo types: primary and secondary
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clinical signs and symptoms of addisons
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-Hyperpigmentation -Postural and supine hypotension -Asthenia -Muscle weakness -Anorexia & malaise -Abdominal pain & vomiting -Diarrhea or constipation & wt. loss -Salt craving -Myalgias & arthralgias -Mental status changes Steroid treatment shuts down acth production, so the most common cause of insufficent hormone response, this is because of negative feedback, so the body will not ask for more steroids by activating adrenals. <5mg/day of prednisone do not display signs of adrenal insufiicency.
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******dignosis of addisons****** what is the triad for diagnosis? ON TEST!!!
******dignosis of addisons****** what is the triad for diagnosis? ON TEST!!!
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HYPONATREMIA-HYPERKALEMIA-HYPOGLYCEMIA GIVE STRESS DOSE STEROIDS
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secondary adrenocortical insufficiency
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acth is not released
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Mineralcorticoid Excess
Mineralcorticoid Excess
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there is a lot of sodium retention and loss of K
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Conn's disease
Conn's disease
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Primary aldosteronism hypertension-Hypokalemic want to replace potassium and give diuretic
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explain the renin angiotensin aldosterone system
explain the renin angiotensin aldosterone system
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When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.[2] Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin converting enzyme found in the lungs. Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure.
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anesthetic management of hyperaldosteronism (excess mineralcorticoids Conn's disease)
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Restrict sodium and adminster spirolactone possibly adminster potassium, stress dose cortisone infusion.
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mineralocorticoid deficiency (hypoaldosteronism)
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Low aldosterone will have low na high K Hypovolemia
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Pheochromocytoma
Pheochromocytoma
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-#1Norepinephrine alone or in combination with epi -Epinephrine -Hyperglycemia and glucosuria -Dopamine -Centrally = Inhibits prolactin secretion Peripherally: -Small amount = renal vasodilation -Moderate = vasodilation of mesenteric and coronary vessels and peripheral vasoconstriction
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*******Pheochromocytoma triad of symptoms**********
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measure urine catacholimines TRIAD ON TEST: HYPERTENSION, DIAPHORESIS, AND H/A
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clonidine test for pheo reveals?
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clonidine will not effect blood pressure if pheo is present
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hypertension response in pheychromocytoma
hypertension response in pheychromocytoma
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this can cause dilated cardiomyopathy and CHF
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what do you treat a pheochromocytoma with first?
what do you treat a pheochromocytoma with first?
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always use beta first, never want uninhibited alpha. if you used a beta blocker first then you may depress the heard and output and not be able to overcome the SVR
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what medications wuld you want to avoid giving to a pheo?
what medications wuld you want to avoid giving to a pheo?
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AVOID MORPHINE! Avoid morphine, because it causes histamine release causing vasodilation promting more catacholine release, tumor manipulation can cause bonkers
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induction considerations with pheochromocytoma
induction considerations with pheochromocytoma
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Morpine, atricurium avoid Droperidrol, metoprolcimde avoid Start off hyperglycemic, release insulin in the absenbce of alpha stimulation
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anesthetic maintance with pheo
anesthetic maintance with pheo
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Prepare for hypotension after tumor revmoval with phenylephrine
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Post operative considerations with pheochroma?
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1.Hypotension and tachycardia 2.Hypoglycemia 3.Hypertension
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