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thyroid hormone primary action
- -maintain energy homeostasis
- -stimulate cell metabolism and activity
Thyroid gland innervation
- -adrenergic fibers coming off the cervical ganglion
- -cholinergic fibers from the vagus nerve
- -autonomic innervation controls blood flow
How does adrenergic stimulation affect blood flow to the thyroid gland? What about cholinergic stimulation?
- Adrenergic increases blood flow
- Cholinergic decreases blood flow
thyroid functional anatomy
made up of follicles (acini), surrounded by a layer of follicular cells, and filled with colloid
colloid is made up of thyroglobulin (a large glycoprotein)
Where are thyroid hormones stored?
In the thyroglobulin molecule that is in the colloid (which is in the follicle of the thyroid gland)
How much thyroid hormone can the thyroid gland store?
Enough to supply the body its usual requirement for 2-3 months
T or F, iodine and thyroglobulin (which contains about 70 tyrosine AA) combine to form the thyroid hormones?
The other name for T4
Of the thyroid hormones, how much is T4 and how much is T3?
Normal total level of T4 (thyroxine)?
Normal free level of T4?
- total 5-12 mcg/dl
- free 1-2 ng/dl
Biologic half life of T4
Is the free portion of the thyroid hormones bound or unbound?
unbound to proteins
Normal T3 level?
- T3 level 80-200 ng/dl
- Half life 24 hours
How much iodine do we need? Why?
- 1 mg iodine / week
- -essential for the formation of thyroid hormones
T3's other name
Which is more potent- T3 or T4?
Do T3 and T4 have the same qualitative effects?
Explain how ingested iodine is involved in forming T3 and T4
- -Iodine that we ingest gets absorbed in the GI tract
- -Gets converted to an anion (iodide)
- -Actively transported to the thyroid
- -Converted back to iodine and hooked onto AA tyrosine to from T3 and T4
What percent of T3 and T4 are bound to specifically to TBG (thyroid binding globulin)? What percent are protein bound?
What effect does this have?
- 70% bound to TBG
- 99% protein bound
acts as a reservoir and delays elimination of thyroid hormones
Why do we need to check free T4 levels as opposed to total T4 levels?
Only the free T4 is active (pt may have a high amount of T4 bound to TBG, but this doesn't mean the pt is hyperthyroid as the bound portion is not available)
To properly evaluate thyroid function what 2 labs should we look at?
free T4 and TSH
Explain the hypothalamic-pituitary-thyroid axis
- -Hypothalamus makes and releases (TRH) thyrotropin releasing hormone
- -This stimulates TSH release from the anterior pituitary
- -This stimulates the thyroid to increase synthesis and release of T3 and T4
- -The free T3 and T4 inhibit TRH and TSH via negative feedback
Aside from high levels of T3 and T4, what else can inhibit thyroid hormone production (by inhibiting TSH)?
What effect do the thyroid hormones have on CHO metabolism?
- -stimulates all aspects of CHO metabolism
- -rapid glucose uptake (increase glycolysis, gluconeogenesis, absorption from the GI tract, and insulin secretion)
- -likely due to increase in cellular metabolic enzymes
What effect do the thyroid hormones have on fat metabolism?
- -stimulate fat metabolism
- -lipids are mobilized from adipose
- -fat stores decrease
- -FA concentration in the plasma increases FA oxidation by the cells
- -decreased cholesterol, phospholipids, and triglycerides
Why will hypothyroid pts have increased cholesterol levels?
Increased TH decreases the concentration of cholesterol in the plasma, since they lack TH, their cholesterol is high
How do the thyroid hormones affect vitamin requirements, BMR, and body weight?
- Vit requirent and BMR are increased
- Body weight is decreased
What effect do the thyroid hormones have on CV system?
- -increased blood flow
- -increased CO
- -increased HR
- -increased strength of contraction
- -increased end products of metabolism as well (increased CO2 causing VD)
How do the thyroid hormones affect MAP?
MAP is unchanged
How do the thyroid hormones affect respirations, GI motility, and CNS?
- -Increased respirations and GI motility
- -CNS excitation.
Why does thyroid hormone increase the rate of secretion of other hormones?
It increases metabolism and therefore increases the requirement for other hormones
How does thyroid hormone affect adipose tissue and muscle?
Catabolic to both. Leads to lipolysis and protein breakdown.
What is the most physiologically active form of thyroid hormone?
- free T4
- -represents only about 0.02% of the total T4 level
What is the best measure of thyroid hormone at the cellular level?
TSH normal values
What is the incidence of hypothyroidism in adults?
- -decreased production of thyroid hormone in the setting of increased or normal TSH
- -95% of all cases
- -usually from surgical removal or radiation
- -most common form of primary hypothyroidism
- -Autoimmune process destroys thyroid tissue
- -TSH can't exert it's effects on the thyroid (no thyroid hormone production)
- -due to hypothalamic or pituitary disease
- -5% of cases
Clinical manifestations of hypothyroidism
- -cold intolerance
- -slow and insidious onset
- -mental and physical slowing, lethargy, apathy
- -wt gain with decreased appetite (decreased BMR)
- -large tongue, brittle hair, thick skin
CV changes associated with hypothyroidism
- -Decreased SV, HR, and CO
- -impaired baroreflex
- -ventricular arrhythmias
- -increased peripheral vascular resistance, decreased blood volume
- -increased cholesterol and triglycerides
Why might someone with hypothyroidism be an aspiration risk?
Due to decreased GI function
Respiratory effects of hypothyroidism
- -decreased VLC and diffusion capacity
- -decreased ventilatory response to hypoxia and hypercarbia (careful with sedation)
Diagnosis of hypothyroidism
- *Increased TSH*
- Decreased T3 and T4
- Subclinical- increased TSH with normal T4 (few symptoms)
- Overt- marked decrease in T4 and TSH 90 mU/L
- peaks in 10-12 days
- half life 7.5 days (but varies if hypo or hyperthyroid due to changes in BMR)
What does a total T4 level of < 1 mcg/ dl mean?
Severe hypothyroidism, need to cancel elective surgery
Pre-anesthesia evaluation for hypothyroidism
- -airway! pt may have tracheal deviation from enlarged thyroid or edema of VC and oral cavity
- -? reflux due to delayed gastric emptying
Is a pt with subclinical hypothyroidism ok to proceed with elective surgery?
What Na+ abnormality may be seen with hypothyroidism
-hyponatremia (dilutional due to impaired free water excretion)
How are deep tendon reflexes affected with hypothyroidism?
DTR are prolonged, pt may have increased NMB activity
T or F, hypothyroidism causes MAC to be decreased?
F, CO is decreased, so it only appears that MAC is decreased
Is neo or ephedrine preferred when treating hypotension in a hypothyroid pt?
Ephedrine as neo will cause an increase in SVR and due to decreased CO the pt's heart might not be able to pump against the increased rx
- -extreme hypothyroidism
- -medical emergency, mortality > 50%
- -most common in elderly women with long h/o hypothyroidism
- -characterized by: delirium, unconsciousness, hypoventilation, hypothermia, bradycardia, hypotension, and severe dilution hyponatremia
Myxedema coma treatment
T3 and T4 (but remember they take a while to kick in)
- Grave's disease
- toxic adenoma
- toxic nodular goiter
Clinical manifestations of hyperthyroidism
- -hypermetabolic state
- -anxiety, restlessness
- -warm moist skin, flushed
- -heat intolerance
- -muscle weakness and wasting
- -wt loss despite increased caloric intake
What effect does thyroid hormone have on bones
Promotes bone deposition and growth
CV side effects of hyperthyroidism
- -Tachycardia, palpitations, and arrhythmias
- -Increased cardiac work
- -hyperdynamic circulation (increased CO and myocardial contractility)
- -leading cause of hyperthyroidism
- -0.4% of population
- -F:M= 7:1
- -usually ages 20-40
Grave's disease classic triad
- -exopthalamus (abnormal connective tissue deposits in orbit and extraoccular muscles)
- -dermopathy (edematous skin)
- -Increased T3 and T4
- -Decreased TSH
Medical hyperthyroidism treatment
- -1st line treatment- anti-thyroid drugs- methimazole and PTU (propylthiouricil), inhibit synthesis of thyroid hormones
- -Inorganic iodine- AKA Lugol's solution, (inhibits thyroid hormone release), immediate but short term effects
- -radioiodine treatment (destroys thyroid gland)
- -BB to relieve symptoms
Surgical hyperthyroidism treatment
- -subtotal or total thyroidectomy
- -pts must be euthyroid first
- -prompt control (stored hormones can't be released)
- -corrects thyrotoxicosis in 95% of pts
Complications of thyroidectomy
- -hemorrhage with tracheal compression
- -recurrent laryngeal nerve damage (hoarseness and dyspnea post-op)
- -inadvertent removal of parathyroids
- AKA thyrotoxic crisis
- -life threatening
- -associated with major surgery or severe illness
- -likely to occur 6-18-24 hours post-op
CM of thyrotoxic crisis
- -hyperthermia (105)
- -severe tachycardia
- -restlessness, agitation, tremor
- -LOC, hypotension, HF
Treatment of thyroid storm
- -K iodine (Lugol's solution)
- -PTU (not available IV)
- -peripheral cooling, IVF
- -glucocorticoids (hypermetabolic state may be linked to relative cortisol deficiency)
Differentiation between MH and thyroid storm
- -MH has muscle rigidity, increased CK levels, and acidosis
- -thyroid storm does not
Pre anesthesia evaluation of pts with hyperthyroidism
- -elective surgery deferred until pt is euthyroid
- -emergency cases require PTU, BB (esmolol), and cortisol
What medications might you want to avoid with hyperthyroidism
- -anticholinergics (increased HR)
- -ex: scop patch
-ketamine, pancuronium, epi, ephedrine
Where are the parathyroids located?
- Embedded within the thyroid
- 2 in the superior thyroid
- 2 in the inferior thyroid
- -number and location may vary
2 types of parathyroid cells
- -chief cells (majority)- produce and secrete parathyroid hormone
- -oxyphil cells- unknown action
What type of hormone is parathyroid hormone?
parathyroid hormone target organ
bones and kidneys
Major effects of parathyroid hormone
- -maintain Ca++ homeostasis according to plasma Ca++ levels
- -increases plasma Ca++ level and decreases plasma phosphorus level
- -bone resorption of Ca++ (moves Ca++ from the bone into the plasma)
- -increases kidneys reabsorption of Ca++ in the distal tubules
What factors increase PTH release?
What factors supress PTH release?
- Vitamin D
- Severe hypomagnesemia
Where is calcitonin released from?
Parafollicular cells of the thyroid
What does calcitonin do?
Decreases plasma Ca++ levels
Which is more important in terms of regulating plasma Ca++ levels- calcitonin or PTH?
How much Ca++ is in the body and where is the majority stored?
- 1100 g
- 99% in bones and teeth
Various forms of Ca++ in the body and percentages
- Ionized 50%
- Protein bound 41%
- Complexed to anions 9%
What form of Ca++ is physiologically active?
What form of Ca++ is able to diffuse thru a lipid membrane?
- The Ca++ complexed to anions
- -protein bound can't (too big)
- -ionized can't (due to its charge, but it can go thru Ca++ channels)
Total Ca++ normal value
9-10 mg /dl
Ionized Ca++ normal value
What effect do PTH and calcitonin have on phosphorus levels?
Decreases phos reabsorption (phos is excreted in the urine)
Role of vitamin D on calcium levels
- -enhances absorption of dietary Ca++ from the GI tract
- -helps to reabsorb Ca++ from the renal tubules
- -both help to increase plasma Ca++ levels
- -impaired production of PTH
- -may be associated with other endocrine disorders
- -usual cause is surgical removal of the parathyroids
- -congenital disorder where the kidneys don't respond to PTH
- -pts have MR, calcifications of basal ganglia, obesity, and structural abnormalities
- -chovstek and trousseaus sign
- -decreased myocardial contractility
- -1st degree AVB
- -CHF and hypotension
- -high Ca++ diet with vitamin D
- -decrease renal Ca++ clearance with thiazide diuretics
- -acute hypocalcemia treated with 10 ml of 10% calcium gluconate
Hypoparathyroidism- anesthesia implications
- -prevent further decreases in Ca++ levels
- -(avoid hyperventilation as alkalosis will further decrease Ca++ levels)
- -ACD PRBC preservative can bind to Ca++
- -avoid albumin as it will bind to Ca+
- -treat adverse effects of hypocalcemia
- -excess secretion of PTH
- -primary, secondary, or ectopic
- -hallmark is serum total Ca++ of >5.5 meq/L or ionized > 2.5 meq/L
- -90% due to benign parathyroid adenoma (also with hyperplasia, it's the most common presenting symptom of MEN type 1)
- -also due to carcinoma
- -excess PTH secretion
- -response of parathyroid to secrete excess PTH to counteract hypocalcemia from some other disease process (ex: renal disease)
- -hypercalcemia does not usually occur as hypersecretion is 2/2 hypocalcema
- -treatment is to control underlying disease
- -AKA pseudohyperparathyroidism
- -secretion of PTH by tissues other than the parathyroid
- -occurs in CA of lung, breast, or kidney
CM of hyperparathyroidism
- -high Ca++ and low Phos levels
- -s/sx r/t high ionized calcium
- -decreased neuromuscular excitability
- -muscle weakness, decreased muscle tone
- -confusion, coma
- -polyuria and polydipsia
- Temporizing: hydration with IV saline, loop diuretics to inhibit calcium reabsorption in L of H
- Definitive: surgical, removal of abnormal or diseased gland, Ca++ levels normalize within 3-4 days
Anesthesia implications of hyperparathyroidism
- -maintain adequate hydration and UO
- -careful with sedation and avoid ketamine 2/2 mental status changes and somnolence
- -consider possibility of co-existing renal disease with drug selection
- -assess if primary, secondary, or ectopic