achilles
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C
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| cyra
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C
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| ssrpk
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Thyroid storm is an acute condition; propylthiouracil takes 3-4 weeks inorder to take full effect!
so i guess in this particular condition beta-blocker should be superior to all else!
i will go with b!
plz explain the answer!
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| cyra
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Beta blockers definitely are an integral component of management of thyroid storm but these provide symptomatic relief by adrenergic blockade.That said,correction of the hyperthyroid state is essential(and o is the first step) which is done by the use of thioamides i.e PTU or methimazole(PTU is preferred).While it may take a while for PTU to exert its full effect it has a quick onset of action(about an hour)..... (PTU inhibits conversion of T4 to T3 as well as blocking iodination of tyrosine and therefore the secretion of T4).There is a specific order in which these drugs are given in the management of thyroid storm making sure at the same time that the underlying condition(e.g an infection) that brought about this episode is treated concurrently.
1.The first step to correct the hyperthyroid state is the administration of a thionamide: propylthiouracil (PTU) or methimazole (MMI).
2.The next step is to block the synthesis of thyroid hormone, which is achieved via the administration of inorganic iodine(KI).This is begun at least 1 hour after the administration of thionamides. Otherwise, providing iodine substrate to an overactive thyroid would only worsen the crisis.
3.Treatment to reduce peripheral action of thyroid hormones is via administration of Beta blockers.Once the thyroid gland has been suppressed, the last step in correcting the hyperthyroidism is to reduce the peripheral conversion of T4 to T3. T3 is approximately 10 times more biologically active than T4. PTU, propranolol, and steroids (dexamethasone, in stress doses equivalent to 200-300 mg of cortisol) all reduce the conversion of thyroid hormone to its more active form.
An excellent overview of all this is at the following link:
http://www.acep.org/webportal/membercenter/period...
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| AAAAA
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Emergency Department Care:
Do not delay treatment once thyroid storm is suspected.
Patients with severe thyrotoxicosis must be placed on a cardiac monitor. The patient should be intubated if profoundly altered. Supplemental oxygen may be required. Aggressive fluid resuscitation may be indicated.
Fevers are treated with cooling measures and antipyretics. However, aspirin should be avoided to prevent decreased protein binding and subsequent increases in free T3 and T4 levels. Only in the setting of subacute thyroiditis is aspirin indicated.
Aggressive hydration of up to 3-5 L/d of crystalloid compensates for potentially profound GI and insensible losses.
Appropriate electrolyte replacement should be directed by laboratory values.
Atrial fibrillation due to thyroid storm may be refractory to rate control, and conversion to sinus rhythm may be impossible until after antithyroid therapy has been initiated.
Intravenous glucocorticoids are indicated if adrenal insufficiency is suspected. Large doses of dexamethasone (2 mg q6h) inhibit hormone production and decrease peripheral conversion from T4 to T3.
Antithyroid medications such as propylthiouracil (PTU) and methimazole (MMI) oppose synthesis of T4 by inhibiting the organification of tyrosine residues.
PTU also inhibits the conversion of T4 to active T3.
Clinical effects may be seen as soon as 1 hour after administration. Both agents are administered orally or via a nasogastric tube.
PTU and MMI inhibit the synthesis of new thyroid hormone but are ineffective in blocking the release of preformed thyroid hormone. Iodide administration serves this purpose well; however, it should be delayed until 1 hour after the loading dose of antithyroid medication to prevent the utilization of iodine in the synthesis of new thyroid hormone. Lithium may be used as an alternative in those with iodine allergy.
Beta-adrenergic blocking agents are the mainstays of symptomatic therapy for thyrotoxicosis. Propranolol has been used with the greatest success due to the additional benefit of inhibition of peripheral conversion of T4 to T3.
Consultations:
An intensivist should be consulted for admission to an ICU when thyroid storm is the presumptive diagnosis.
An endocrinologist or internist may be helpful in confirming the diagnosis and in assisting in patient management.
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| AAAAA
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1 hour !!!!!!!!!!!!!!!!!
Antithyroid medications such as propylthiouracil (PTU) and methimazole (MMI) oppose synthesis of T4 by inhibiting the organification of tyrosine residues.
PTU also inhibits the conversion of T4 to active T3.
Clinical effects may be seen as soon as 1 hour after administration. Both agents are administered orally or via a nasogastric tube.
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| AAAAA
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ssrpk wrote:
Thyroid storm is an acute condition; propylthiouracil takes 3-4 weeks inorder to take full effect!
so i guess in this particular condition beta-blocker should be superior to all else!
i will go with b!
plz explain the answer!
EXCUSE ME, PTU ONLY TAKES 1 HOUR TO TAKE INTO EFFECT !!!
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| AAAAA
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Medical Care: Management of thyroid storm is a multi-step process. Blocking the synthesis, secretion, and peripheral action of the thyroid hormone is the ideal therapy. Aggressive supportive therapy then is used to stabilize homeostasis and reverse multiorgan decompensation. Additional measures are taken to identify and treat the precipitating factor, followed by definitive treatment to avoid recurrence. Thyroid storm is a fulminating crisis that demands an intensive level of care, continuous monitoring, and vigilance.
Blocking Thyroid Hormone Synthesis
Antithyroid compounds propylthiouracil (PTU) and methimazole (MMI) are used to block the synthesis of the thyroid hormone.
PTU also blocks peripheral conversion of T4 to T3 and hence is preferred in thyroid storm over MMI. MMI is the common agent used in hyperthyroidism.
PTU and MMI block the incorporation of iodine into thyroglobulin within 1 hour of ingestion.
A history of hepatotoxicity or agranulocytosis from previous thioamide therapy precludes use of PTU and MMI.
Blocking Thyroid Hormone Secretion
After initiation of antithyroid therapy, hormone release can be inhibited by large doses of iodine, which reduce thyroidal iodine uptake. Lugol solution or saturated solution of potassium iodide can be used.
Iodine therapy should be administered after approximately 1 hour following administration of PTU or MMI; iodine used alone helps to increase thyroid hormone stores and may increase the thyrotoxic state.
The iodinated x-ray contrast agent, sodium ipodate, can be administered instead of iodine and also inhibits peripheral conversion of T4 to T3. Potassium iodide (KI) decreases thyroidal blood flow and hence is used preoperatively in thyrotoxicosis.
Patients intolerant to iodine can be treated with lithium, which also impairs thyroid hormone release. Patients unable to take PTU or MMI also can be treated with lithium, as use of iodine alone is debatable. Unlike iodine, lithium is not subject to the escape phenomenon; lithium blocks the release of thyroid hormone throughout its administration.
Plasmapheresis, plasma exchange, peritoneal dialysis exchange transfusion, and charcoal plasma perfusion are other techniques used to remove excess circulating hormone. Presently, these techniques are reserved for patients who do not respond to the initial line of management.
The intravenous preparation of sodium iodide (given as 1 g slow infusion q8-12h) has been taken off of the market.
Blocking Peripheral Action of Thyroid Hormone
Propranolol is the drug of choice to counter peripheral action of thyroid hormone. Propranolol blocks beta-adrenergic receptors and prevents conversion of T4 to T3. It produces dramatic improvement in clinical status and greatly ameliorates symptoms.
Propranolol produces the desired clinical response in thyroid storm only after large doses.
Intravenous administration of propranolol requires continuous monitoring of cardiac rhythm.
Presently, esmolol is the ultra-short-acting beta-blocking agent used successfully in thyrotoxicosis and thyroid storm.
Noncardioselective beta-blockers (eg, propranolol, esmolol) cannot be used in patients with congestive cardiac failure, bronchospasm, or history of asthma. Guanethidine or reserpine can be used instead in these cases.
Successful treatment with reserpine in cases of thyroid storm resistant to large doses of propranolol has been documented. However, guanethidine and reserpine cannot be used in the presence of cardiovascular collapse or shock.
Supportive Measures
Aggressive fluid and electrolyte therapy is needed for dehydration and hypotension. This excessive hypermetabolic state, with increased intestinal transit and tachypnea, leads to immense fluid loss. Fluid requirements may increase to 3-5 L/day. Therefore, invasive monitoring is advisable in elderly patients and in those with congestive cardiac failure.
Pressor agents can be used when hypotension persists following adequate fluid replacement.
Add glucose to IV fluids for nutritional support.
Multivitamins, especially vitamin B-1, are added to prevent Wernicke encephalopathy.
Hyperthermia is treated through central cooling and peripheral heat dissipation.
Acetaminophen is the drug of choice, as aspirin may displace thyroid hormone from binding sites and increase severity of thyroid storm.
Cooling blankets, ice packs, and alcohol sponges encourage dissipation of heat. Use of a cooled humidified oxygen tent is advised.
Use of glucocorticoids in thyroid storm is associated with improved survival rates. Initially, glucocorticoids were used to treat potential relative insufficiency due to accelerated production and degradation owing to the hypermetabolic state. However, the patient may have type 2 autoimmune deficiency, in which Graves disease coexists with absolute adrenal insufficiency.
Glucocorticoids reduce iodine uptake and antibody titers of thyroid-stimulating antibodies with stabilization of the vascular bed. In addition, dexamethasone and hydrocortisone have an inhibitory effect on conversion of T4 to T3. Therefore, a stress dose of glucocorticoid (eg, hydrocortisone, dexamethasone) now is routine.
Cardiac decompensation, although seen more frequently in elderly patients, may appear in younger patients and in patients without underlying cardiac disease.
Digitalization is required to control the ventricular rate in patients with atrial fibrillation.
Anticoagulation drugs may be needed for atrial fibrillation and can be administered in the absence of contraindications. Digoxin may be used in larger doses than those normally used in other conditions. Closely monitor digoxin levels to prevent toxicity. As the patient improves, reduce digoxin dose.
Congestive cardiac failure is seen as a result of impaired myocardial contractility and may require Swan-Ganz catheter monitoring.
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| AAAAA
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ssrpk wrote:
Thyroid storm is an acute condition; propylthiouracil takes 3-4 weeks inorder to take full effect!
so i guess in this particular condition beta-blocker should be superior to all else!
i will go with b!
plz explain the answer!
PTU and MMI block the incorporation of iodine into thyroglobulin within 1 hour of ingestion
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| AAAAA
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ssrpk wrote:
Thyroid storm is an acute condition; propylthiouracil takes 3-4 weeks inorder to take full effect!
so i guess in this particular condition beta-blocker should be superior to all else!
i will go with b!
plz explain the answer!
the correct answer is c !!!
PTU takes 1 hour to work NOT 3-4 weeks !!!!!!
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| MAZI
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THE CORRECT ANSWER IS C
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| MAZI
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THANK YOU FOR YOUR COMPLETE EXPLANATION
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