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282 Cards in this Set
- Front
- Back
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Two causes of hyperthyroidism
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toxic goiter (Grave's disease)
thyrtoxicosis |
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Another name for Grave's Disease
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toxic goiter
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In hyperthyroidism, the thyroid gland increases to ____ normal size
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2-3x normal size
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In hyperthyroidism, the thyroid gland increases to 2-3x normal size, what happens to the output
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it results in excessive thyroid hormone output
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Hyperthyroidism - neuro symptoms
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Anxious, restless, emotionally unstable, fatigue, insomnia
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Hyperthyroidism - skin symptoms
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Skin feels warm, moist, face is flushed
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Hyperthyroidism - hair/nails symptoms
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hair fine, nails soft an fragile
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Hyperthyroidism - eye symptoms
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wide-eyed stare, retracted eyelids
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Hyperthyroidism - heat symptoms
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heat intolerance
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Hyperthyroidism - bone symptoms
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osteoporosis due to high bone turn over
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Hyperthyroidism - GI symptoms
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diarrhea, weight loss
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Hyperthyroidism - cardiac symptoms
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increased cardiac workload (high metabolic demand)
increased CO and contractility |
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Hyperthyroidism - cardiac rhythm symptoms
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atrial arrhythmias
1. tachycardia - most common 2. new onset a-fib |
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Hyperthyroidism - cardiac symptoms
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increased EF
increased CO increased contractility increased intravascular volume decreased SVR |
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READ ARTICLE
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READ ARTICLE
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How is hyperthyroidism usually detected
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routine lab screening
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Most people with hyperthyroidism usually have ___ symptoms
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few
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Hyperthyroidism lab results
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elevated T3 and T4
reduced TSH |
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Treatment for hyperthroidism usually does not occur until
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TSH drops below 0.1 mU/L
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What may occur if TSH drops below 0.1 mU/L
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a-fib and increased r/f stroke or embolic events
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What causes a goiter
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compensatory hypertrophy and hyperplasia of thyroid tissue due to a reduction in thyroid hormone output
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Causes of goiter
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1. iodine deficiency
2. some drugs 3. defect in synthesis of thyroid hormones (producing hypothyroidism) |
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Size of goiter determined by
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how long iodine deficiency has been allowed to continue
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Goiter pt - where would thyroid levels be
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normal because thyroid gland is large enough to compensate for how hormone output
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Treatment for goiter
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1. give thyroxine - improve in 3-6 months
2. surgery - remove part or all |
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Another name for Graves disease
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toxic goiter
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What is the leading cause of hyperthyroidism
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graves disease
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Graves disease typically occurs in what pt population at what age
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women between age 20-40
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Although not fully known, what is the etiology of graves disease
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autoimmune disease with thyroid stimulating antibodies that bind to the TSH receptors in the thyroid, activated the cAMP system and stimulating the thyroid growth and output - resulting in hypersecretion of T3 and T4
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Graves disease is caused by the hypersecretion of
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T3 and T4
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Graves disease triad
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1. exopthalmos
2. hyperthyroidism 3. dermopathy (lumpy reddish skin over legs and feet) |
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The texture of dermopathy found in graves disease is like
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the texture of an orange - only red
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In graves disease the throid becomes
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very enlarged
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In severe cases of graves disease, the enlarged thyroid can cause
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dysphagia, choking sensations, inspiratory stridor, SVC obstruction syndrome,
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In graves disease, the gland becomes
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nodular
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In graves disease, radioactive iodine uptake in the nodules is
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increased
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How do you differentiate graves nodules from other tumors
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CT
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The goal of treatment for graves disease is to
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get the thyroid levels down
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Two agents used in graves disease to lower thyroid levels
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propylthiouracil or methimazole (tapazole)
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Agents used to treat graves disease - propylthiouracil or methimazole (tapazole) work by
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interferes with the formation of the thyroid hormones
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Graves disease drug propylthiouracil also works by
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interfering with the conversion of T4 to T3 in the tissue
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How long does treatment for graves disease with propylthiouracil or methimazole (tapazole) take to reach euthyroid condition
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6-8 weeks
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For graves disease, iodide in high concentrations (excites or inhibits) the release of hormones from hyperfunctioning gland
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inhibits
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How quickly does it take for high concentration iodide treatment and how long does it last
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immediately, lasts for weeks
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For what two reasons would high concentrated iodide be the treatment choice for graves disease
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surgery is urgent or patient is in thyroid storm
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For graves disease, if high concentration iodide is given - thyroid hormone release is (increased or decreased) and storage of thyroid hormone is (increased or decreased)
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release is decreased, storage is increased
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For graves disease, since high concentration iodide treatment causes increased storage of thyroid hormone
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it will coupled with other therapies to prevent thyroid release
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For graves disease, beta adrenergic antagonists (do or do not) reduce thyroid hormone levels with the exception of which drug
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do not, propranolol
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For graves disease, beta adrenergic antagonists except propranolol are helpful in the treatment of
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sweating, anxiety and cardiovascular symptoms
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For graves disease, propranolol reduces the conversion of ___ to ___ and reduces _____
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T4 to T3, metabolic rate
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For graves disease, if pt is not responsive to drug therapy or if relapse occurs, what next?
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ablation therapy with radioactive iodine
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For graves disease treatment with radioactive iodine, what is the remission rate
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80-98%
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For graves disease, after treatment with radioactive iodine, many people develop
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hypothyroidism
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For graves disease treatment with radioactive iodine has replaced ____ as a treatment option
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thyhroidectomy
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For correcting hyperthroidism, a subtotal thyroidectomy is (very effective or not effective) for correcting hyperthyroidism
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very effective
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For correcting hyperthroidism, the major disadvantages of a subtotal thyroidectomy include
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1. hypothyroidism
2. hemorrhage with tracheal compression 3. recurrent layngeal nerve damage (flaccid paralysis) 4. damage to motor branch of superior laryngeal nerve 5. Inadvertent removal of parathyroid gland |
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Preparation of patient for subtotal thyroidectomy is very important and should include
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1. euthyroid for 6-8 weeks
2. potassium iodide should be given 7-14 days before surgery 3. beta blockers should be given |
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How long before subtotal thyroidectomy surgery should pt be euthyroid
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6-8 weeks
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How long before subtotal thyroidectomy surgery should receive potassium iodide
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7-14 days
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Why give potassium iodide 7-14 days before subtotal thyroidectomy surgery should
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reduce glands vascularity and hormone release
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Why give beta blockers before subtotal thyroidectomy surgery
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helps to reduce cardiovascular effects - especially tachycardia
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For hyperthyroidism in pregnant patients, drug therapy is (preferred or not preferred)
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preferred
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For hyperthyroidism in pregnant patients, do antithyroid drugs cross the placenta
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no
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For hyperthyroidism in pregnant patients, propanolol is associated with
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interuterine growth retardation
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For hyperthyroidism in pregnant patients, if mom does not respond to antithyroid drugs, then what
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subtotal thyroidectomy is really the only choice
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What is a very serious from of hyperthyroidism
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thyroid storm
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Thyroid storm defined
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life threatening exacerbation of hyperthyroidism precipitated by trauma, infection, illness or surgery
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Exacerbation of thyroid storm
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trauma, infection, illness or surgery
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How is thyroid storm diagnosed
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based on symptoms
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During thyroid storm, thyroid tests will be high or low
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may not be all that high
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Treatment for thyroid storm is
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urgent and aggressive
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During thyroid storm, symptoms occur ____ and are associated with _____
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quickly, triggering event
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Why is it thought that thyroid storm occurs
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sudden shift from normally high level of protein bound thyroid hormone to an unbound level - perhaps due to other agents that bind proteins
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Treatment for thyroid storm includes addressing what life threatening symptoms:
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1. severe dehydration, CV instability tachycardia
2. Extreme agitation, altered level of consciousness 3, excessive heat production |
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Specific treatment during thyroid storm for excessive heat production
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cooling blankets, ice packs, cool humidified oxygen
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Specific treatment during thyroid storm for dehydration
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iv fluids and glucose administration
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Specific treatment during thyroid storm for tachycardia
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propranolol, labetalol or esmolol
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Other specific treatments during thyroid storm
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dexamethasone or cortisol
antithyroid drugs vasopressors (direct acting) |
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Mortality rate for thyroid storm
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20%
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Are thyroid tumors usually benign or carcinogenic
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could be either
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What lab values are associated with thyroid tumors
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they are not - euthyroid
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If a thyroid tumor is large, what may happen
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airway may be compromised - Hashimoto's thyroiditis
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Primary hypothyroidism lab values
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low T3
low T4 high TSH |
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Most common cause for hypothyroidism
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reactive iodine or gland ablation
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2nd most common cause for hypothyroidism
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idiopathic - where antibodies destroy the TSH binding sites
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Hashimotoes thyroiditis occurs due to
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the autoimmune destruction of the receptors and lead to a large goiter
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Is Hashimotoes thyroiditis primary or secondary hypothyroidism
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primary hypothyroidism
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Secondary hypothyroidism is usually caused by a problem with what two things
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hypothalmus or pituitary gland
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In an adult, secondary hypothyroidism is (slow or fast)
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slow and progressive
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Neuro symptoms for hypothyroidism include
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fatigue, lethargy, apathy, listlessness, slowed speech, dull intellect
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CV symptoms for hypothyroidism include
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ventricular disrhythmias - PVCs, VT
bradycardia, increased SVR, cool skin, reduced contractility, reduced baroreceptor function, pericardial effusions are common |
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Other symptoms for hypothyroidism include
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cold intolerance, decreased sweating
wt gain dry thick skin, brittle hair large tongue, deep hoarse voice edema in periorbital area (under eyes) and legs hypercholesterolemia ileus development uterine bleeding |
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Respiratory symptoms for hypothyroidism include
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ventilatory response to hypoxia and hypercarbia reduced
pleural effusions common |
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Severe from of hypothyroidism
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myxedema coma
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Myxedema coma typically affects what pt population
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elderly women with hx of hypothyroidism
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Most common symptom noted in myxedema coma
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hypothermia - 80 deg F
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Mortality for myxedema coma
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50%
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Why does pt become hypothermic during myxedema coma
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defective hypothalmic regulation
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Myxedema coma symptoms
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1. hypothermia
2. delirium 3. hypoventilation 4. dilutional hyponatremia 5. bradycardia |
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Myxedema coma is considered a
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medical emergency
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Treatment of myxedema coma
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IV thyroxine or triiodothyroxine
correct electrolyte imbalances mechanical ventilation warming devices hydrocortison to treat adrenal suppression associated with condition |
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How big are parathyroid glands
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pea sized
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How many parathyroid glands are there
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4
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Where are parathyroid glands located
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upper and lower poles of the thyroid gland
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What two electolytes are controlled by the parathyroid gland
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calcium and phosphate
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What type of feedback mechanism is used with the parathyroid gland
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negative
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Parathyroid glands produce ___ which is a ____
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parathyroid hormone, polypeptide hormone
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Low calcium levels cause a (decreased or increased) release of parahormone
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increased
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Parathormone impacts calcium levels by
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1. impacting GI absorption
2. impacting renal tubule reabsorption 3. impacting bone uptake and release |
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Primary parathyroidism results from excessive parahormone secretion due to
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benign adenoma, carcinoma, or hyperplasia of the parathyroid glands
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Benign cases account for ___ of hyperparathyroid cases
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90%
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Hallmarks of hyperparathyroidisms are
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1. elevated total serum (bound) ca++
2. elevated ion ca++ |
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If Ca++ levels increase gradually, this typically means tumor
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is benign
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If Ca++ levels increase quickly, this typically means tumor
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is cancerous
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Most common early symptoms of hyperparathyroidism
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vomiting and dehydration
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Most common treatment of hyperparathyroidism
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iv fluids with loop diuretic (inhibits Na+ and Ca++ reabsorption in the loop)
drugs that bind Ca++ |
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Severe hypercalciumia treatment
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hemodialysis
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Most definitive tx for hyperparathyroidism/hypercalciumia
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parathyroidectomy
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What is seen in hyperparathyroidism because of the loss of Ca++
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bone disease - resulting in osteitis fibrosa cystica
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Hyperparathyroidism results in
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brittle bones
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What is implication for brittle bones caused by hyperparathyroidism
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positioning
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Hyperparathyroidism - signs and symptoms - neuromuscular
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skeletal muscle weakness
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Hyperparathyroidism - signs and symptoms - renal
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polyruia and polydipsia
decreased GFR kidney stones |
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Hyperparathyroidism - signs and symptoms - hematopoeitic
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anemia
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Hyperparathyroidism - signs and symptoms - cardiac
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prolonged PR interval
short QT interval systemic hypertension |
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Hyperparathyroidism - signs and symptoms - GI
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vomiting
abdominal pain peptic ulcer pancreatitis |
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Hyperparathyroidism - signs and symptoms - skeletal
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skeletal demineralization
collapse of vertebral bodies pathologic fractures |
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Hyperparathyroidism - signs and symptoms - nervous system
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somnolence
decreased pain sensation psychosis |
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Hyperparathyroidism - signs and symptoms - ocular
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calcifications (band keratopathy)
conjuncitvitis |
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What occurs when there is a disease process that reduces the serum ca++ levels - the parathyroid gland reacts by pumping out more parathyroid hormone
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secondary parathyroidism
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Give an example of secondary parathyroidism
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ESRD pt who cannot rid himself of phosphorus and cannot hydrolyze vitamin D (required for ca++ absorption in the gut) - resulting hypocalcemia causes hyperplasia of the parathyroid gland
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Where is calcitonin released and what does it antagonize
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released from thyroid gland and weakly antagonizes parathyroid hormone
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Calcitonin deposits ____ into the ___, decreasing ____ concentrations in the _____ fluid
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calcium, bones, calcium, extracellular
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What is the most common cause of hypoparathyroidism
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thyroidectomy (surgical removal)
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hypoparathyroidism causes a (positive or negative) chvostek's sign
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positive
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How do you check the chvostek's sign
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tapping over the area of the facial nerve by the mandibular angle
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hypoparathyroidism causes a (positive or negative) trousseau's sign
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positive
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How do you check the trousseau's sign
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apply tourniquet to for three minutes - should get carpopedal spasm
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Related to low ca++, inspiratory stridor reflects
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neuromuscular irritability
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Two parts of the adrenal gland
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adrenal cortex
adrenal medulla |
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Where is the adrenal gland
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on superior pole of the kidney
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The adrenal medulla is functionally related to the
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sympathetic nervous system
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The adrenal medulla secretes
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hormones epinephrine and norepinephrine (in response to sympathetic stimulation)
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The adrenal cortex has a separate set of hormones called the
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corticosteroids
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Corticosteroids are systhesized from
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cholesterol
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READ handouts
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READ handouts
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Three types of corticosteroids
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mineralcorticoids
glucocorticoids androgens |
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Three layers of the adrenal cortex
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zonus glomerulosa
zonus fasciculata zonus reticularis |
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Which layer of the adrenal cortex is outer most layer and is thin
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zonus glomerulosa
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Which layer of the adrenal cortex is the largest and sits in the middle
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zonus fasciculata
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which layer of the adrenal cortex is the inner layer
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zonus reticularis
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Which layer of the adrenal cortex contains an exzyme called aldosterone synthase
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zonus glomerulosa
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Which layer of the adrenal cortex is responsible for production of the mineralcorticoids - specifically aldosterone
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zonus glomerulosa
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Which layer of the adrenal cortex responds the most to K+ concentration and the concentration of circulating angiotensin II
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zonus glomerulosa
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Which layers of the adrenal cortex is regulated by ACTH
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zonus glomerulosa
zonus fasciculata |
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The zonus glomerulosa layer of the adrenal cortex is regulated by ACTH - which responds to what two hormones and leads to the production and release of what
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hypothalmic (corticotropin releasing hormone) and the anterior pituttary (ACTH) which leads to the production and release of glucocorticoids - specifically cortisol and corticosterone - also produces small amounts of androgens
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Which layer of the adrenal cortex secretes androgens (dihudroepi andosterone - DHEA)as well as estrogens
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zonus fasciculata
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Does the adrenal medulla lie (above or below) the cortex
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the medulla lies below the cortex
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Which layer of the adrenal cortex is regulated by K+ and (something I can't make out) renin per wiki
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zonus glomerulosa
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Associate the zona glomerulosa with the
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mineralcorticoids
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Associate the zona fasciculata with the
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glucocorticoids
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Associate the zona reticularis with the
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adrenal androgens and
catecholamines |
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review how aldosterone works
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review how aldosterone works
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If we were to lose adrenocortical production we would die within
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2 weeks
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the major mineralcorticoid is
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aldosterone
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Other than aldosterone, what else has mineralcorticoid activity
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cortisol
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4 stimuli that cause aldosterone release
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1. increased K+ ion concentration in extracellular fluid
2. increased levels of angiotensin II 3. increased Na+ concentration in plasma 4. increased ACTH from anterior pituitary |
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Anther name for hyperaldosteronism
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Conn's syndrome
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Hyperaldosteronism is usually due to
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a tumor that is secreting an aldosterone-like substance
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Hyperaldosteronism is more common in (men or women)
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women
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Hyperaldosteronism is usually associated with what four things
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1. pheochromocytoma
2. hyperparathyroidism 3. acromegaly 4. renin system elevated or out of whack |
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Symptoms for hyperaldosteronism
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1. headache - retain Na+ + H20 = HTN
2. hypertension 3. hypokalemia 4. metabolic alkalosis (r/t H+ K+ pump) 5. PVCs on EKG |
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Treatment for hyperaldosteronism
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1. supplement K+
2. give competitive aldosterone antagonist (spironolactone) 3. K+ sparing diuretics 4. may require adrenal gland removal 5. If renin system was the culprit - give ACE inhibitors |
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Glucocorticoids are important to
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sustain life
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Glucocorticoids are responsible for utilization of
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proteins, carbs and fats
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Glucocorticoids are responsible for
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management of stress and controlling immune response to infection
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___ % of Glucocorticoids in the form of cortisol AKA ____
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90%, hydrocortisone
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Name something cortisol controls, impacts, and inhibits
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1. controls mobilization of amino acids from muscle cells fro gluconeogenesis (production of glucose from amino acids)
2. impacts glucose production from fat and carbs 3. inhibits uptake of glucose into cells |
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People on steroids have an increased
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blood glucose level
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Cortisol increases __ then produces what
(I didn't know how else to make this one) |
appetite, imbalance of fat deposits resulting in buffalo humps or moon face
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Stress increases production of ___ hormone, which leads to a large release of ____
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ACTH from anterior pituitary, cortisol
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List stresses that increase production of ACTH - and cortisol
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1. trauma
2. infection 3. intense heat or cold 4. sympathetic drugs - epi or norepi 5. surgery 6. injection of painful substance 7. restraining 8. disease |
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Cortisol facilitates
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catecholamine synthesis
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Cortisol modulates
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beta receptor synthesis, regulation, coupling, and the responsiveness of catecholamines
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Cortisol contributes to
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normal vascular permeability, tone, and cardiac contractility
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If suppress adrenal (ACTH) there is no response to
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catecholamines
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Why is cortisol/steroids used for inflammation
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1. review stages of inflammation
2. stabilizes lysosome membranes 3. decrease permeability of capillaries 4. decreases wbc migration and phagocytosis 5. suppresses lymphocyte production 6. stops fever by reducing the release of interleukin I from wbcs, which impacts the hypothalamus and causes a rise in body temp |
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ACTH structure is very similar to
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melanocyte stimulating hormone, lipotropin and endorphin
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When ACTH is released from the anterior pituitary what are released
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melanocyte stimulating hormone, lipotropin and endorphin
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See page 397
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See page 397
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Decadron is used for
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swelling
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Decadron is (slow or fast) to react
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slow
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Decadron is (short or long) acting
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long
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Cushing's disease means
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too much cortisol
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The most common cause of Cushing's disease is
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a secreting tumor (benign or malignant)
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Cushing's disease is associated with
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oat cell carcinoma
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Symptoms for Cushing's Disease (highlighted ones)
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hyperglycemia
hypertension hypokalemia |
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Treatment of Cushing's disease
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1, transspenoidal
2. microadenomectomy 3. pituitary radiation and or bilateral adrenalectomy |
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Two types of adrenal insufficiency
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1. addison's disease
2. iatrogenic |
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With addison's disease the adrenal glands are not able to generate enough
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glucocorticoids, mineral corticoids or androgens
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Most common cause of addison's disease is
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autoimmune destruction of the adrenal glands
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The number 1 cause of iatrogenic adrenal insufficiency is
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hypothalmic pituitary axis dysfunction due to steroid administration
other causes - radiation or removal of pituitary |
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Addison's disease - treatment
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supplement with corticosteroids and mineralcorticoids
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Addison's disease - symptoms
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fatigue, weakness, anorexia, vomiting, cutaneous and mucosal hyperpigmentation, hypotension, hypovolemia, hyponatremia, hyperkalemia
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With prolonged steroid exposure, what happens to the adrenal gland
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atrophies
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When the adrenal gland atrophies, what happens to cortisol response
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little or no response when cortisol levels are required to meet demands
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Time, depth length, and severity of surgery increases the release of what
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ACTH
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Increased ACTH causes what to rise
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cortisol levels
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Do ACTH levels remain high after surgery
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yes, into the post operative period
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People who have long term steroid use may have
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suppressed natural ability of the hypothalmus/pituitary to respond to stressful conditions
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If pts are on long term steroids and they are suddenly stopped, adrenal insufficiency may occur within
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24 hours
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How long does it take for pt's adrenals to recover following long term steroid use
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6-12 months
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People below what dose of prednisone for any length of time do not demonstrate HPA axis suppression and do not require preoperative supplementation
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5mg/day
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If a person who has been taking less than 5mg/day of predisone - should they take their dose on the day of surgery
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yes, they should take their normal daily dose
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For patients who are taking long term steroids, what time of doses are better and why
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morning doses are better than nighttime doses because cortical secretion is diurnal (active during daytime)
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Pt taking what dose of prednisone (or equivalent) for more than two weeks in the past 12 months are considered to have adrenal suppression
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5mg
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Adults make how much cortisol daily without stress
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20mg
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If you have determined that the patient needs steroid coverage, give how much of what drug when
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100mg hydrocortisone Q8H the night before and the morning of surgery
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Acromegaly is typically caused by what
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excessive growth hormone in adults, usually an adenoma in the pituitary
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The skull x-ray in an acromegaly patient demonstrates
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large sella turcica
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Why would an acromegaly pt develop a headache or papilledema (optic disc swelling)
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adenoma produces pressure which causes increased cranial pressure
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Why does an acromegaly pt present a problem for anesthesia
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1. huge epiglottis and tongue
2. increased length of mandible 3. plypoid masses in the pharynx 4. hoarneness and abnormal vocal cord movement (due to stretching) 5. cricoarytenoid joints may be stretched and impair vocal cord impairment - gayle says review muscles 6. stridor, dyspnea |
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Why may a patient with acromegaly have peripheral neuropathy
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nerve trapping and growth of limbs
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What may be an anesthetic monitoring concern for a pt with acromegaly
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a-line (poor distal flow)
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What condition may a patient with acromegaly have
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diabetes
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Treatment for a patient with acromegaly is
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removal of tumor
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Release of hormones from what 2 endocrine glands is regulated exclusively by nerve activity
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posterior pituitary and adrenal medulla (catecholamines)
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Does the posterior pituitary make hormones
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no, it stores them
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What are stored in the posterior pituitary
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ADH and oxytocin
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Where are ADH and oxytocin made
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hypothalmus
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If the posterior pituitary is cut at the stalk - will the hormones continue to circulate
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yes, because the hypothalmus will continue to produce them
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ADH is made in the
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supraoptic nuclei
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oxytocin is made in the
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paraventricular nuclei
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Both the supraoptic nuclei and the paraventricular nuclei also make
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small amounts of the other hormone - supraoptic makes small amounts of oxytocin (mostly made in paraventricular nuclei) and paraventricular makes ADH (mostly made in supraoptic nuclei)
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ADH and oxytocin have similar
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structures and partial functional similarities
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Because ADH and oxytocin have similar structures and partial functional similarities, an OB patient can get
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ADH effects - fluid retention
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know how/where ADH works
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know how/where ADH works
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ADH increases the number of
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aquaporins
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When small amounts of ADH are released, the number of
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aquaporins increases in minutes
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When the ADH level decreases, how long des it take for the the number of aquaporins to decrease
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5-10 minutes
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What determines how much ADH is released
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osmoreceptors detect the osmolarity of the blood circulating through the arteries supplying the hypothalmus
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Minute concentrations of ADH produce
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potent effect in the kidney
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Larger doses of ADH have what ability
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vasoconstriction
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What is the difference between ADH and vasopressin
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they are the same but vasopressin has a much higher dose
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When blood volume decreases ___ % there is a profound release of ADH
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15-25%
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With a loss of blood volume, what triggers the release of ADH
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1. stretch receptors in the atria are excited by overfilling, when volume decreases, they are unexcited (release of ADH)
2. decreases stretch receptor stimulation of the baroreceptors of the carotid and aorta results in ADH release |
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review efferent and afferent limbs of baroreceptors
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review efferent and afferent limbs of baroreceptors
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What is diabetes insipidus
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too little ADH
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What is syndrome of inappropriate anti diuretic hormone
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too much ADH
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DI is the absence of vasopressin due to
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1. destruction of the posterior pituitary
2. failure of the renal tubules to respond to ADH (nephrogenic DI) |
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Manifestations of DI
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1. polydipsia
2. increased serum osmolarity 3. decreased urine osmolarity 4. high urine output |
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Why does SIADH occur
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1. result of tumors
2. hypothyroidism 3. porphyria 4. small cell carcinoma 5. phenomenon after general anestheia |
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Manifestations of SIADH
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1. decreased serum osmolarity
2. hyponatremia 3. increased urine osmolarity 4. symptoms r/t hyponatremia (review these) know sz threshold, etc |
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Symptoms of hyponatremia
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confusion, lethargy, seizures, coma, death
arrhythmias muscle cramps nausea, vomiting basically - too much intracellular water |
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Thyroid article - several effects of T3 on the heart
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1. decreased SVR
2. increased cardiac inotropy 3. increased cardiac chronotropy 4. increased oxygen consumption 5. widened pulse pressure 6. increased tissue thermogenesis |
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Thyroid article - 4 effects of T3 on the blood volume
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1. increases volume (due to decreased SVR and renin-angiotensin-aldosterone system and increased renal Na+ reabsorption
2. increases erythropoietin production |
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Thyroid article - is there much T4-T3 in cardiac cells
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minimal
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Thyroid article - T3 affects two myosin heavy chains alpha and beta
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In humans
1. alpha - 2. beta - myosin heavy chains activated by T3 (predominates) |
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Thyroid article - Ca++ ATPase pump and phospholamban is regulated by
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T3
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Thyroid article - release of Ca++ and its reuptake in the SR are critical determinants of
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systolic contractile function and diastolic relaxation
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Thyroid article - increased HR, contractility, cardiac output are independent of
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concentrations of catecholamines
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Thyroid article - increased HR at rest or during sleep above ___ is normal during hyperthyroidism
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90
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Thyroid article - #1 and #2 most common signs for hyperthyroidism
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1. goiter
2. resting tachycardia |
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Thyroid article - in hyperthyroidism cardiac outputs of ____ higher than normal
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50-300%
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Thyroid Article - giving beta adrenergic agonists to hyperthyroid patients
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will decrease HR but not alter systolic or diastolic contractile performance (thyroid hormone acts differently on cardiac muscle)
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Thyroid Article - most common disrhythmia noted with hyperthyroidism
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sinus tachycardia
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Thyroid Article - a-fib occurs in what percent of hyperthyroid pts
(just know it causes a-fib I guess?) |
5-15% (pts had underlying heart dz)
<1% new onset a-fib (overt hyperthyroidism) 13% pts with unexplained a-fib have evidence of hyperhyroidism |
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Thyroid Article - if pt has new onset a-fib, they should have what checked
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serum thyrotropin levels
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Thyroid Article - use of anticoagulant therapy with hyperthyroid a-fib pts is
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controversial
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Thyroid Article - of hyperthyroid pts who had a-fib, 62% reconverted to SR 8-10 weeks after becoming euthyroid
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see previous
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Thyroid Article - pts with hyperthyroidism develop "high output failure" - true of false
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false - because the ability of the heart to maintain increased CO at rest and with exercise is preserved
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Thyroid Article - pts over 50 cardiovascular complications are chief cause of death
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see previous
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Thyroid Article - treatment of hyperthyroidsim
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propranolol or atenolol - goal is to decrease HR to normal
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Thyroid Article - pts with subclinical hyperthyroidism are at risk for
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a-fib
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Thyroid Article - most common signs for hypothyroidism
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bradycardia
mild hypertension narrowed pulse pressure attenuated activity on the precordial examination |
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Thyroid Article - nonspecific findings for hypothyroidism
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high serum cholesterol
high serum CK pericardial effusions nonpitting edema |
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Thyroid Article - hypothyroidism - SVR may increase by as much as
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50%
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Thyroid Article - hypothyroidism - heart failure is
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rare
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Thyroid Article - hypothyroidism - ECG changes
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prolonged QT
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Thyroid Article - hypothyroidism - treatment
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thyroxine therapy
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Thyroid Article - hypothyroidism - how many older women have subclinical hypothyroidism
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7-10%
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Thyroid Article - hypothyroidism - great drug to give
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amiodarone - iodine rich antiarrhythmic (but can induce hyperthyroidism)
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