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187 Cards in this Set
- Front
- Back
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Where is the thyroid gland located?
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-Anterior/inferior to larynx at 2nd-4th tracheal ring
-Grows retrosternally |
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What does thyroid secrete & what is its function?
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-T3 & T4, & calcitonin
-Incr. metabolic rate & VO2 -Regultes cellular respiration, incr. CHO/protein & fat metabolism -Thyroid hormones affect skeletal maturation in fetus & brain development in infancy |
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Function of calictonin?
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-promotes deposition of Ca+ in bones thereby decr. Ca+ conc. in ECF
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Major regulators of cellular metabolic activity?
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-T3 & T4
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Thyriod gland is responsible for ____ secretion?
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T4 (thyroxine)
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Daily secretion of T4?
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80-100 mcg/day
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How is 80% of T3 produced?
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-extrathyroidal deiodination of T4
-20% is produced directly from thyroid secretion |
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Explain the production of thyroid hormone?
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-Dietary iodine (H2O &NaCl) is reduced to iodide in GI.
-Circulating iodide is taken up by thyroid -Binds to thyrosine residues & forms T4 &T3 -T4 &T3 bind to thyroglobulin protein & stored as colloid until needed |
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____ is responsible for maintaining uptake of iodide & release of thyroid hormone?
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TSH
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Which is more potent, T3 or T4?
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-T3 is more potent but is present is smaller amts.
-T3 is also less protein bound |
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Explain the release of thyroid hormone?
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-Hypothalamus releases TRH (thyrotropin releasing hormone)
-TRH stimulates secretion of TSH by ant. pituitary -TSH stimulates thyroid to synthesize & release T3 &T4 |
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Explain the negative feedback mech. for thyroid?
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-T3 & T4 are major determinants of TSH secretion
-T3 & T4 inhibit release of TSH & to a smaller degree TRH via negative feedback |
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Name 2 drugs that can affect thyroid function?
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Amiodarone & dopamine
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Which thyroid hormone (T3 or T4) incr. cellular respiration & myocardial contractility?
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T4
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Cardiovascular effects of thyroid hormone?
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-Incr. B-adrenergic receptors in # (tachycardia)
-Decr. cardiac a-adrenergic receptors (vasodilation=incr. blood flow=incr.heat & perph. edema). -tachycardia, AF, CHF,incr. SV, incr. CO, incr. pulse pressure, PVC's, S3 |
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Diagnosis for hyperthyroidism?
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-Low or normal TSH in presence of elevated T3 &T4
-1% of population; females > -Incr. uptake of oral radioactive iodine(131I) |
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Most common cause for hyperthyroidism & other causes?
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-Graves dz/goiter is most common (20-30y mostly females)
-Adenoma: 2nd most common -Thyoiditis: subacute-viral or Hashimotos -Iodine induced -Cancer (rare) -Preg. (3-6mos.post-partum) -Amiodarone(iodine rich): iodine induced thyrotoxicosis |
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Hot vs. cold thyroid tissue?
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-Hot: rarely malignant
-Cold: malignant or benign |
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s/s of hyperthyroidism?
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-Nervousness, inrc. sweating, heat intol., palpitations, dyspnea, fatigue, weakness, wt. loss/gain(incr.appetite), diarrhea, warm moist skin
-thyroid lg., tachycardia, AF,CHF,incr. SV,EF,CO,PP,PVC,S3,peripheral edema, neck vein engorgement,exopthalmos -incr. insulin production=decr.K+ -incr.Ca+ due to incr. osteoclastic bone resorption from high T3 & T4 -Incr. gluocose b/c incr. requirement by cells -Chronically hypovolemic & vasodilated |
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Treatment for hyperthyroidism?
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-PTU: decr. peripheral conversion of T4 to T3 & decr. synthesis of T3 &T4
-B-blockers: decr. SNS activity (HR<90) -Corticosterioids b/c decr. adrenal reserves & also decr. peripheral conversion of T4 to T3 (dexamethasone) -Acetominophen (tylenol) as antipyretic -Virous hydration -radioactive iodine -Iopanoic acid (decr. conversion) |
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When should anti-thyroid drugs be started & why?
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-Before iodide treatment b/c possibility of worsening thyrotoxicosis
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Which is preferred B-blocker for hyperthyroidism & why?
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-Propanolol
-Decr. perh. conversion of T4 to T3 |
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Why acetominophen & not salicylates to treat pyrexia w/ hyperthyroidism?
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-Salicylates displace thyroid hormone from serum binding sites & then you have more free thyroid hormone.
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Iodine in the treatment of hyperthyroidism?
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-Lg. dose iodine blocks hormone release & decr. vascularity & size of thyroid gland
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Preparation of hyperthyroid pt. prior to surgery?
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-Goal: euthyroid <6-8wks; Propanolol + K+ iodide
-Airway assessment:tracheal deviation, carotid displacement, RLN damage |
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Intraop hyperthyroidism management?
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-Goal: depth of anesthesia to prevent exaggerated SNS response to stim.
-Avoid ketamine, pancuronium, caution w/ epi in regional anesthesia -Post induction hypotension treat w/ direct acting phenylephrine:vasoconstrictionw/o incr. HR(decr. HR) -Decr. initial dose of NMB b/c high incidence of myasthenia gravis -Head 30degrees careful w/ venous air embolism -Decr. HR or BP due to carotid stim. -GETA or LMA allows realtime VC visualization |
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Thyroidcetomy w/ medtronic NIM EMG ETT?
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-Avoid NMB b/c EMG monitors larynegal nerves
-1 size larger ETT -Do not use in pts. w/ implanted electrial devices |
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Post-op complications thyroidectomy?
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-Airway obst. due to edema, tracheomalacia (tracheal collapse), hematoma, RLN injury
-Thyroid storm (6-24h post) -Hypoparathyroidism (hypoCa+ 12-72h post) |
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Laryngeal N. supply?
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-Sensory & motor supply is from Sup. laryneal & Recuurent laryngeal N.
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Superior laryngeal N.?
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-Provides motor supply to cricothyroid muscles & sensation above cords
-External:motor -Internal:sensory -From epiglottis to VC (above VC) |
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Recurrent laryngeal N?
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-all other motor innervation (not cricothyroid) & sensation below VC
-From below VC, trachea & larynx |
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Most common nerve injury after thyroid surgery?
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-Unilateral RLN damage:hoarseness(paralyzed cord in intermediate position)
-Often transient |
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Other nerve injuries after thyroidectomy?
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Bil. RLN damage:less common, aphonia, paralyzed cords that flap together during inspiration=total obst.=reintubation
-SLN damage/paralysis: hoarseness & loss of sensation above VC |
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Thyroid storm?
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-Hyperthermia, incr. HR, CHF, dehydration,shock
-6-12h post op -May mimic MH, pheochromocytoma, light anesthesia -Mortality rate 10-75% |
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1st sign of hypocalcemic tetany?
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-larngeal stridor=laryngospasm
-tx w/ CaCl or CaGlu or by decr. mg+.(decr. mg+=incr. PTH=incr. Ca+) |
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Hypoparathyoidism (low Ca+ due to thyroidectomy)?
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-Seen 24-48hr post
-symptoms of hypoCa+ develop: laryngospasm & prolonged QT |
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Management of thyroid storm?
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-Chilled IVF
-Na+ iodide -PTU -Hydrocortisone(adrenal insuff. due to shock) -Propanolol or esmolol -Digoxin(CHF w/ AF, rapid vent. response) -Cooling blankets & acetaminophen & meperidine to prevent shivering |
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Hypothyroidism?
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-Decr. T3 & T4
-Primary:incr. or norm. TSH w/ low prod. of T3 & T4 from thyroid -Secondary:Hypothalamic or pituitary problem |
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Causes of hypothyroidism?
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-Thyroidectomy, radioactive iodine tx, iodine deficiency, gland dysfunction, cretinism
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When do you postpone surgery in hypothyroid pt?
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-Severe hypothyroidism (myxedema coma)
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Pre-op & Intra-op management of hyperthyroid pts?
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-Opioids have inc. depressant effects(prone to drug induced resp. depression, fail to respond to hypoxia & hypercapnia w/ incr. RR)=decr. induction dose
-PIA has depressant effects(b/c low CO incr. induction) but no change in MAC -Ketamine is ideal (STP ok) -Delayed gastric empyting (give regaln or H2 blocker) -Treat low BP w/ direct acting b/c of blunted baroreceptors |
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Manifestations of hypothyroidism?
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-Lethargy, cold intol.,Decr. CO & HR, perph. vasoconstriction(cold ext. & low BP after induction),decr. plt. adhesiveness, anemia,
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Myxedema coma?
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-Severe hypothyroid
-s/s:impaired mentation, hypoventilation, hypothermia, decr. Na+, poss. bowel obst. -80% mortality |
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Causes of myxedema coma?
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cold exposure, infection, trauma, & CNS depressants
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Treatment for Myxedema coma?
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-T3 & T4 replacement
-Steroids for adrenal insuff. -Vent. support -IVF & warm environment |
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Parathyroids?
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-Posterior & lateral to thyroid
-4 lobes -Secrete parathhormone (PTH) |
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Parathyroid hormone is regulated by?
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-Serum iCa+ conc.
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Parathormone (PTH)
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-Regulate Ca+ & osteoclastic activity (breakdown of bone).
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How does PTH increase Ca+?
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-By directly promoting bone resorption(breakdown of bone to release Ca+ into blood)
-By directly limiting renal excretion of Ca+ -By decreasing serum Phos.(Decr. phos. reabsorption by renal tubules=incr. Ca+ reabsorption) -Indirectly by incr. GI absorption of active form of Vit. D(1,25DOH)which is converted in the kidneys |
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How is PTH countered by calcitonin?
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Calcitonin promotes deposition of Ca+ into bones & also by preventing new osteoclast formation, thereby decr. ECF Ca+ conc.
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How much of Ca+ is protein bound?
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-40% is protein bound
-90% of that is bound to albumin -90% of all Ca+ is found in bone -of the left over 10%, 60% is active (ionized)& the 40% is protein bound |
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Ca+ functions?
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-Muscle contraction, coagulation, neurotransmitter release
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Effect of acidosis & Ca+?
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Acidosis decr. protein binding= incr. iCa+
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Effects of alkalosis & Ca+?
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Alkalosis incr. protein binding = decr. iCa+
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Relationship of high mg+ & PTH?
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-High Mg+ = decr. PTH secretion & incr. calcitonin sceretion = incr. Ca+ bone uptake but decr. serum Ca+
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Relationship of low Mg+ & PTH?
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-Low Mg+ = stimulates PTH= incr. serum Ca+
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Vit. D deficiency & Ca+?
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-Vit. D deficiency = decr. PTH ability to convert to active form 1,25dOH & therby decr. GI absorption & decr. bone absorption
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Why do pts w/ CRF have high PTH?
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-Compensatory mech. for hypoCa+ caused by decreased Vit.D metabolism by kidneys & decr. Ca+ reabsorption by kidneys
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Causes of hyperparathyroidism?
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-Most common: Adenoma
-CA, hyperplasia |
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S/s of hyperparathyroidism?
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-HyperCa+ manifestations
-Nephrolithiasis(most common) -confusion, HTN, arrhythmias -Polyuria, polydipsia |
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EKG changes w/ hyperparathyroidism?
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-Decr. refractory, incr. vent. excitation, prolonged & rounded Twaves, short QT
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Pre-op management of hyperparathyroidism?
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-IVF, lasix, biphosphonates, calcitonin(decr. resorption of Ca)
-Regaln, H2 blockers for GI s/s of PUD & constipation -Glucorticoids -Incr. Phos.= decr. Ca+ reaborption in renal tubules |
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Intraop management of hyperparathyroidism?
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-Avoid hypoventilation (acidosis decr. protein binding=incr. iCa+)
-Predisposed to vertebral compression fx w/ laryngoscopy(b/c osteoclastic activity) -Check vocal cord fxn |
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Post-op management of hyperthyroidism?
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-Assess for RLN damage
-Check Ca+ q 12h -Treat hypoCa+ w/ CaGlu or if Mg+ is low tx w/Mg+ (decr. PTH & incr. calcitonin=incr. Ca+ into bone & out of serum) |
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Clinical features of hypoparathyroidism?
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-HypoCa+
-Neuronal irritability -Laryngospasm, stridor, tetany, Sz, skeletal musclespasm or cramps, -CHF, decr. BP, prolonged QT -Paraesthesia & fatigue |
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Acute onset of hypoCa+ s/s after thyroid sx ?
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-Stridor & apnea
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Causes of hypoparathyroidism?
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-Underproduction of PTH or resistance end organ to effects of PTH
-Most common:Inadvertent removal of parathyroids -RAI or iodine therapy, neck trauma, granulomatous dz or CA -Severe hypoMg+ acn supress PTH -Burns & pancreatitis can cause hypoCa+ by supression of PTH & sequestration of Ca+ |
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Medical treatment for hypoparathyroidism?
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-Vit. D to incr. intestinal absorption
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Relationship of low Mg+ & PTH?
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-Low Mg+ = stimulates PTH= incr. serum Ca+
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Intraop management for hypoparathyroidism?
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-Normalize Ca+
-Avoid cardiac depressants -Avoid hyperventilation(alkalosis incr. binding= decr. iCa+) -Caution w/ PRBCs due to citrate incr. binding (give slowly) -Avoid albumin -If phos. high treat w/ alumminum hydroxide, fluids & diurectics (b/c by decr. phos. = incr. Ca+ reabosortion at renal tubules) -Correct coagulopathy |
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Chvosteks sign?
Trousseaus sign? |
-Chvosteks: contracture of facial N. by tapping as it passes parotid gland
-Trousseaus: contracture of fingers & wrist after application of BP cuff above SBP x3min. |
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Adrenal cortex secretes?
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-Zona fasciculata & zona reticularis: Cortisol & androgens
-Zona glomerulosa: aldosterone |
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Adrenal medulla secretes?
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-Epi(80%) & NE (20%)
-Dopamine |
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Most potent endogenous glucorticoid?
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Cortisol
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Explain the prod. & release of cortisol?
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-Hypothalamus releases CRF(corticotropin releasing hormone)
-CRF stimulates ant. pituitary to produce ACTH from POMC & secrete ACTH (adrenocorticotropin hormone) -ACTH then stimulates adrenal cortex to release cortisol |
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Function of glucorticoids?
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-Enhance gluconeogenesis(formation of glucose from subst. other than CHO by liver), incr. blood glucose, & promote hepatic glycogen synthesis
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Secretion of ACTH & CRF is regulated by ?
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1. glucorticoids
2. Sleep/wake 3. stress |
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What is the most potent regulator of ACTH secretion
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-Cortisol(glucortiocoid).
-(-) feedback that maintains cortisol levels normal |
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When does ACTH get released?
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-Diurnal(daytime every day)
-Max activity soon after awakening -trauma, surgery, intense exercise |
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Negative feedback of cortisol?
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When cortisol levels are high, cortisol inhibits release of CRH & ACTH
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By how much & when does cortisol levels peak post-op & when does it decrease?
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-Incr. by 5-10x
-6hr. post op -peak levels decr. by 24h |
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What controls release of mineralcorticoid aldosterone?
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-Renin angiotensin
-Serum K+ |
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Function of aldosterone?
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-Regulates ECV & K+ homeostasis by reabsorbing Na+ & secreting K+
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Cushing Syndrome?
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-Glucorticoid excess
-Overproduction of cortisol by adrenal cortex or by exogenous glucorticoid therapy |
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How to diagnose cushing's?
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-Failure of decadron to suppress endogenous cortisol secretion
-Incr. plasma ACTH & incr. 17-hydroxycorticosteriod (cortisol in urine) |
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How to distinguish b/w pituitary tumor or adrenal tumor as cause for cushings?
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-Pituitary adenoma: decr. cortisol & decr. 17-hydroxycorticosteroid when given dexamethasone b/c tumor retains (-) feedback
-Adrenal tumors: do not retain (-) feedback so cortisol & 17-hydrocorticosteroid remain incr. |
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Cushing's manifestations?
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-Truncal obesity & thin extremities
-Osteopenia (due to lack of protein deposition in bones, impaired Ca+ absorption & decr. bone formation) -Hypergylcemia, HTN due to fluid retention -emotional changes, susceptibility to infection -Abd.striae,buffalo hump, moon face, hirtuism -Hypokalemia,metabolic alkalosis, Vol. overloaded |
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Causes for cushings?
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-Mostly due to adrenal hyperplasia 2ndary to ACTH produced by ant. pituitary
-If over 60y then most likely from adrenal CA or ectopic ACTH produced from non-endocrine tumor |
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Intra-op considerations w/ Cushing's?
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-Treat hypokalemia & vol. overload status w/ K+ & spirinolactone
-Careful positioning due to osteopenia -If undergoing adrenalectomy: intraop glucorticoid -Control HTN, DM & lytes |
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Addison's?
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-Lack of glucorticoid production due to adrenocortical insuff.
-Primary or secondary |
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Primary Addison's?
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-Insuff. production of hormones by adrenal glands
-Not apparent until >90% of adrenal cortex is destroyed -Hyperpigmentation(compensatory incr. in ACTH & B-lipoprotein which stimulate melanocyte prod.) -Mineralcorticoid deficiency** = decr. in urine Na+ conservation |
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Most common cause & other causes for primary Addison's?
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-Autoimmune is most common cause
-TB, Hashimotos thyroiditis(Schmidts syn.), bacterial, viral, fungal, HIV, CA |
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Secondary Addison's?
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-Insuff. ACTH secretion by ant. pituitary
-No hyperpigmentation & no mineralcorticoid deficiency= salt & water bal. maintained |
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Causes of secondary Addison's?
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-Tumor, infection, surgical ablation or radiation therapy of ant. pituitary
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Most frequent cause of Addison's?
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-Idiopathic adrenal insuff. secondary to autoimmune destruction of gland
-Glucorticoid & mineralcorticoid insuff. |
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Do patients that receive chronic steroid tx have adrenal insuff?
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-Generally do not have adrenal insuff.
-They have HPA suppression & may develop acute adrenal insuff as a result of perioperative stress |
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Addisonian crisis?
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-Insuff. cortisol or other glucorticoid in relation to stress
-Shock like state w/ hypotension, hypovolemia & lyte imbal. -s/s:abd. pain, severe V/D, decr. LOC |
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Causes of Addisonian crisis?
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-HPA axis supression due to exogenous corticosteroids
-Autoimmune adrenalitis -Adrenal hemorrhage -Adrenal TB -Septic shock |
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Treatment for Addisonian crisis?
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-Supportive
-IV cortisol -Isotonic D5NS |
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How can HPA suppression occur?
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-Topical, regional, inhaled & PO steroids
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S/s of Addison's?
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-Chronic fatigue, muscle weakness, anorexia, wt. loss, N/V/D
-Decrease BP, women have decr. in axillary & pubic hair growth |
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Hyperaldosteronism?
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-Mineralcorticoid excess
-Hypersecretion of aldosterone causes incr. renal tubular exchange of Na+ for K+ & H+ -Incr. renal Na+ reabsorption & ECV expansion -Hypokalemia & metabolic alkalosis |
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Causes of hyperaldosteronism?
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-Adenoma, hyperplasia, or CA of adrenal cortex-glomerulosa
-Altered fxn of renin-angiotensin sys. |
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S/s of hyperaldosteronism?
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-HTN, hypervolemia, incr. Na+
-low K+, muscle weakness(due to low K+) -Metabolic alkalosis |
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In what patients would you consider hyperaldosteronism?
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-non-edematous pts w/ HTN & persistent hypokalemia
-Not receiving K+ wasting diuretics |
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General treatment considerations for hyperaldosteronism?
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-Restore intravascular vol. & electrolyte conc.
-Restrict Na+ intake -Administer K+ -Treat HTN |
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Conn's syndrome?
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-Primary hyperaldosteronism
-Do not have edema |
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Secondary hyperaldosteronism?
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-due to incr. renin prod.
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Mineralcortiocoid insuff?
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-Hypoaldosteronism
-Pt. are unable to incr. aldosterone prod. in response to salt restriction or vol. contraction |
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Causes of hypoaldosteronism?
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-After unilateral adrenalectomy for removal of aldosterone secreting adenoma
-Protracted heparin therapy(heparin therapy inhibits aldosterone prod.) -Pts. w/ deficient renin prod. -Seen in mild RF & long standing DM |
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S/s of hypoaldosteronism?
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-Hypotension, hyperkalemia, metabolic acidosis(impaired Na+/K+ exchange= not excreting K+ & H+ & not reabsorbing Na+)
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What drug can exacerbate hypoaldosteronism & why?
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-NSAID's
-Inhibit PGE synthesis which further inhibits renin release |
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Treatment for hypoaldosteronism?
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-ACTH therapy for pts w/ low renin secretion, hypoaldosteronism & renal dsfxn
-Fludrocortisone -Pts w/ CHF or HTN may require lasix therapy instead of mineracorticoid or in combo. |
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Who should receive perioperative steroid replacement?
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-Pts who have received daily steroids for non adrenal illness (asthma, arthitis, autoimmune dz) for at least 1-2 wks in 6-12mos. prior to surgery
-No proven optimal regimen -Pts using steroids at time of sx should get usual AM dose & supplemented at level equivalent to daily regimen -Use min. dose to protect pt & avoid impaired wound healing. |
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Adrenal medulla?
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-Post ganglionic neuron
-Secretes catecholamines that function as hormones -Output is coordinated by higher cortical centers connected to brainstem, emotion, physiologic stimuli |
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Synthesis of NE & Epi?
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-Tyrosine-tyrosine hydroxylase-DOPA-dopadecarboxylase-dopamine-dopamine beta hydroxylase- NE-M-metyltransferase-Epi
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Rate limiting step in the production of NE?
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-Tyrosine hydroxylase
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Where are catecholamines stored in the adrenal medulla?
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-Chromaffin cells
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Catecholamine 1/2 life?
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10-30 sec
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Biotransformation of NE & Epi is done by?
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-COMT (Catechol-O-methyltransferase) in liver & kidney
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Major end products of catechol metabolism?
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-Metanephrine & VMA (vanillymandelic acid)
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Pheochromocytoma?
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-Tumors of adrenal medulla that produce, store & secrete catechol.
-Commonly arise on right -May be found outside adrenal medulla(along paravetebral sympathetic chain-thorax, bladder,neck) |
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Causes for pheochromocytoma?
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-Soliatry tumors
-Can be autosomal dominant -MEN type IIA or IIB(polygalndular syn.) -Assoc. w/ Von-Recklinghausen neurofibromatosis or Von Hippel-Lindau dz |
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Manifestations of pheochromocytoma?
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-paroxysmal HTN (HA)
-diaphoresis, HA, tachycardia/palpitations -cardiac dysrhythmias -orthostatic hypotension(decr. blood vol.) -CHF, cardiomyopathy, cardiomegaly, LVH & non-specific T-wave changes. |
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Common triad of symptoms for pheochromocytoma?
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1. diaphoresis
2. HA 3. tachycardia/palpitations |
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Anesthetic pre-op management for pheochromocytoma?
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-Prazosin: 10-14d before sx
-Phenoxybenzamine -Restoration of intravascular vol. -B-blockade -Goal: control HR, suppress arrythmias & prevent BP lability -Phentolamine (as drip) |
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Phenoxybenzamine?
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-nonselective alpha blocker (block a2=inrc. NE release & incr. HR & CO)
-slow onset,long acting -severe orthostatic hypotension -c/o nasal stuffiness |
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Prazosin?
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-Selective a1 blocker
-dilates both arteries & veins -less reflex tacycardia (b/c no presynpatic a2 action) -orthostatic hypoBP, vertigo, & fluid retention) |
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Phentolamine?
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-Imidazole derivative
-non-selective a-blocker -Quick onset & short lasting -incr. baroreceptor response to decr. BP causes incr. SNS activity -presynaptic a2=NE release & incr. HR & CO -May cause dysrhythmias & angina -Use as drip -also used for infiltrate |
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Intra-op management for pheochromocytoma?
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-TEE
-Control BP w/ SNP & nicardipine -control tachydysrhythmias w/ esmolol(best), propanolol, or labetolol -Anticipate hypotension w/ ligation of tumor's venous blood supply -Consider pressor (NE or pheylephrine) infusion |
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Function of insulin?
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-Incr. glu & K+ entry into cell,
-Incr. glycogen, protein & FA synthesis -Decr. glycogenolysis & decr. gluconeogenesis |
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What endocrine dzs can result in DM?
|
-Dz that produce a hormone that opposes action of insulin
-glucagonoma, Pheochromocytoma, Acromegaly, Cushings -Steroid therapy |
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What stimulates release of insulin?
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-Incr. glucose, AA
-ANS via vagal stim. -B-adrenergic stim. (B-agonist) -alpha blockade |
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Sulfonylureas?
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-Enhance insulin secretion by B-cells & may cause hypoglycemia
-Glipizide, Glyburide -Hold while pt. is NPO |
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Biguanides?
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-Enhance sensitivity of hepatic & peripheral tissues to insulin
-Metformin (d/c pre-op due to lactic acidosis) |
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Insulinomimetics?
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-Incr. insulin sensitivity
-Thiazolidinediones -Troglitazone, Avandia -Should be cont., do not predispose to hypoglycemia |
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Alpha-glycoside inhibitor?
|
-Inhibits glucose & CHO absorption
-Acarbose -Should be held b/c only work when taken w/ food |
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How do you test autonomic fxn?
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-Measure beat to beat variation in HR during breathing, valsalva, & orthostatic changes in DBP & HR
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Frequent complication of DM I?
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-Stiff joint syndrome
-Prayer's sign= diff. laryngoscopy |
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Evidence of cardiac autonomic neuropathy?
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-Resting tachycardia, orthostaic hypotension
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Evidence of vagal autonomic neuropathy?
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-gastroparesis
-other: intraoperative hypothermia |
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DM perioperative care?
|
-Maintain euglycemia (110mg/dL)
-Can administer 1/3-1/2 usual am dose -glucose containing IVF -Pt. may be dehydrated due to osmotic diuresis |
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Rapid acting insulins?
|
-Lispro (humalog)
-Regular or Humalin -15-30 onset; last 4-6h |
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Intermediate acting insulin?
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-LPH
-Lente 1-4h onset; 24 durtaion |
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Long acting insulin?
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-Ultralente
-4-6h onset; 36h duration |
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Combination insulin?
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-NPH/regular
-50/50 or 70/30 mix |
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Hyperosmolar Non-ketotic coma?
|
-Insulin still avail= no ketones
-Often elderly w/ HAL -Min.to mild DM w/ profound hyperglycemia >600mg/dL -Hypernatremia (b/c dehydrated) & hypokalemia -dehydration & hyperosmolarity =Sz, coma, DVT's |
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Treatment for hyperosmolar non-ketotic coma?
|
-Fluid resuscitation
-small doses of insulin -K+ supplementation |
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DKA?
|
-Metabolic acidosis w/ lactic acidosis
-Ketoacidosis may be caused by binge drinking -hyperglycemia (300-500mg/dL) -Dehydration(osmotic diuresis & vomiting) -Hypokalemia- -Skeletal muscle weakness (can impair ventilation) due to low phos. that occurs w/ correction of acidosis |
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Patho of DKA?
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-Insuff. insulin to block metabolism of FA
-Results in accummulation of acetoacetate & B-hydroxbutyrate |
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S/s of DKA?
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-Leukocytosis, abd. pain, ileus, elevated amylase,
-Tachypnea to compensate for acidosis -dehydration, hypoK+ |
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Treatment of DKA?
|
-Insulin
-Isotonic (NS) IVF (avoid LR) -KCL when UOP >0.5ml/kg/h -Glucose 5% when serum glucose <250mg/dL -NaHCO3 to correct pH <7.1 |
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Goal for decreasing blood glucose?
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-10%/hr or 75-100mg/dL/h
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Each 1ml of D50% will inrc. blood glucose by ____ in 70kg pt?
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-2mg/dL
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Hypoglycemia?
|
- <50mg/dL
-Causes reflex catechol. release -s/s of SNS stimulation -In DM pts its due to excess insulin relative to CHO intake or DM pt w/ renal dz=prolongs insulins action |
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Master gland?
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Pituitary
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Pituitary gland located?
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-Sella tursica of spehnoid bone at base of skull
-Aka: hypophysis -Connected to hypothalamus by pituitary or hypophysial stalk |
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Adenohypophysis secretes?
& what is their function? |
-LH: induces ovulation & stim. testes to prod. androgens
-FSH: dev. of ovaries & testes -GH: skeletal dev., incr. protein synthesis & decr. rate of CHO metabolism -TSH: synthesis & release of T3 &T4 -ACTH: releases cortisol & adrogens from adrenal cortex, effects only glucorticoids |
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Neurohypophysis? secretes?
|
-Neuronal tissue
-Oxytocin -ADH |
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Function of ADH?
|
-Incr. resorption of free H2O by incr. cell permeability to H2O at collecting tubules
-Results in incr. blood vol. in response to blood osmolarity -Conc. urine is formed -Constricts smooth muscle |
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ADH release is caused by?
|
-PPV, stress, histamine, beta stim. & hyperthermia
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Causes of post. pituitary dysfxn.?
|
-Head injury
-Radiation -Tumors |
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DI?
|
-Decr. or absent ADH secretion due to destruction of post. pituitary(neurogenic) or lack of response to ADH (nephrogenic)
-Lg. urine output w/o glycosuria -Urine osmolarity < serum osmolarity (urine diluted & blood conc.) -Serum Na+ >145mEq/L |
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Diagnosis for DI is confirmed by ?
|
-Urine osmolarity incr. after vasopressin is given to pt. that has been on fluid restriction
|
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If urine output does not incr. after vasopressin you must consider?
|
-Nephrogenic DI
|
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Treatment for DI?
|
-Neurogenic: DDAVP(synthetic ADH)
-Nephrogenic: Chlorpropamide (sulfonylurea) oral hypoglycemic that stimulates release of ADH & sensitizes tubules to ADH |
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SIADH?
|
-Incr. release of ADH =decr. urine output
|
|
|
Causes for SIADH?
|
-Tumors,hypothyroidism, porphyria, lung CA
|
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Manifestations of SIADH?
|
-Dilutional hyponatremia
-Decreased serum osmolarity -incr. urine osmolarity w/ decr. UOP |
|
|
Treatment of SIADH?
|
-Restriction of daily fluids to 800ml
-Emergency treatment: hypertonic saline solution w/ lasix |
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What can happen by correcting hyponatremia too quickly?
|
-central pontine myelinosis & brain damage
|
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Hyperpituitarism?
|
-Rare; usually due to pituitary adenoma
-Acromegaly from excess GH -Cushing's ffrom excess ACTH prod. -Galactorrhea from excess prolactin secretion -Excessive TSH secretion is rare |
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|
Manifestations of acromegaly?
|
-enlarged sella tursica, HA, visual field defects, papilledema
-skeletal muscle weakness & overgrowth(prognathism), coarse facial features, lg. hands & feet, incr. mandibular size -Peripheral neuropathy, OA, osteoporosis, soft tissue overgrowth(tongue,epiglottis, lips),Lg. vocal cords = hoarseness(thickening VC), RLN damage (due to stretching) & small subglottic area |
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Anesthetic considerations for acromegaly?
|
-smaller ETT, various size face mask, potential diff. DL
-Use CV stable dxs -Enlarged tongue & epiglottis -Polypoid masses may be present -check for hx of stridor or dyspnea |
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|
Transphenoid adenohypophysectomy?
|
-Resection of pituitary tumors which may cause excess prolactin w/ galactorrhea, GH, & ACTH release
-Use RAE ETT, HOB 30deg -Mouth pack may obst.airway -Steroids -Avoid low vol. b/c brain shrinks & moves tumor -Might have to produce Valsalva to bring tumor closer -Avoid N2O -High risk for DI(tx w/DDAVP & IVF) |
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Common finding assoc. w/ pituitary adenoma?
|
prolactin w/ galactorrhea,
|
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Carcinoid syndrome?
|
-s/s caused by secretion of serotonin, kallikrein, bradykinin, & histamine released from carcinoid or chromaffin tumors
|
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|
Location of carcinoid tumors?
|
-GI tract: asymptomatic b/c cleared by liver
-Outside GI tract (lungs & ovaries) or pts w/ poor hepatic fxn: symptomatic |
|
|
Carcinoid syn. & serotonin release?
|
-Vasoconstriction =HTN & coronary artery spasm
-Incr. GI motility & diarrhea -Hypoalbuminemia b/c decr. proetin synthesis -Formation of 5HIAA -Stimulates glycogenolysis & gluconeogenesis |
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|
Carcinoid syn. & histamine release?
|
-Vasodilation & flushing
-Dysrhythmias -Bronchoconstriction -H1: smooth muscle contraction -H2: smooth muscle relaxation |
|
|
Carcinoid syn. & kallikrein release?
|
-Vasodilation (hypotension & flushing)
-Bronchoconstriction -Activates plasma factors & subsequently prod. bradykinin |
|
|
Carcinoid syn. & bradykinin release?
|
-Primary kinin
-Low doses: vasodilation -Prod. pain w/ PGE -Extravascular smooth muscle contraction -Incr. vascular permeability -Incr. leukocyte chemotaxis |
|
|
S/s of Carcinoid syn.?
|
-Hyperglycemia
-Flushing, cyanosis -Wide BP swings(usually hypoBP), decr.CO,R. sided valvular heart lesions(tricuspid regurg or pulm. stenosis), venous telangiectasia, dysrhythmias(PAC's or SVTs), bronchospasm, diarrhea & abd. pain, hepatomegaly, decr. albumin, edema |
|
|
Lung metabolism of _____ prevents L. side heart involvement in carcinoid syn?
|
serotonin
|
|
|
How is diagnosis of carcinoid syn. made?
|
-confirmed by detection of serotonin metabolites in urine (5-hydroxyindolleacetic acid)
-or suggested by elevated levels of chromogranin |
|
|
Treatment for Carcinoid syn.?
|
-Chemo, radiation,
-octreotide(somatostain analogue), serotonin (methysergide), & histamine blockers -Sugical excision of tumor |
|
|
Intraop management of Carcinoid syn.?
|
-Avoid drugs which cause histamine release
-Octreotide at induction & throughout -Treat hypotension w/ vol. expansion IVF & octreotide |
