Thyroid Storm Flashcards

1
Q

Thyroid storm is a syndrome of:

pathogenesis is unknown but probably results from rapid increases:

event often triggers thyroid storm in previously:

C/S:

A

acute thyrotoxicosis that occurs in hyperthyroid cats

thyroid hormone levels
coupled with SNS activation

diagnosed or undiagnosed hyperthyroid cats
although the event may not be readily apparent

CNS disturbances, hyperthermia, acute or severe vomiting and diarrhea, abdominal pain, icterus, cardiac murmurs with or without arrhythmias, pleural effusion, pulmonary edema, tachypnea, hypertension, retinopathies, extreme muscle weakness and cervical ventroflexion, thromboembolic disease, and sudden death

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2
Q

Dx:

Tx:

Successful outcome depends on rapid recognition of the clinical syndrome and aggressive therapy

A

C/S and elevated serum thyroid hormones

reducing thyroid hormones
blocking peripheral actions of thyroid hormones
systemic support, and elimination of precipitating event

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3
Q

Thyroid storm in humans:

semantics:

Thyrotoxicosis describes any condition:

A

defines a multisystem disorder resulting from organ exposure to excessive amounts of thyroid hormone

life threatening, significant cause of mortality in humans

> circulating thyroid hormone, overactive thyroid gland, because of leakage from a damaged thyroid gland, or from an exogenous source

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4
Q

High Levels of Circulating Thyroid Hormones

Is there increased circulating thyroid hormones in patients with thyroid storm?:

.:. how is dx made:

A

High Levels of Circulating Thyroid Hormones

no difference between serum thyroid hormone levels in human patients and in more stable hyperthyroid patients
-so yes high but not higher than normal hyperT4

C/S

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5
Q

Rapid, Acute Increases in Circulating Thyroid Hormones

What is more important for development of thyroid storm?:

i.e. when is it more likely to occur and why?

A

magnitude of change in serum thyroid hormone levels

  1. after radioactive iodine therapy
  2. thyroid sx. damage thyroid gland cause release T4
  3. abrupt cessation of antithyroid medication
    = resulting in a rapid rise in serum thyroid hormone
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6
Q

Hyperactivity of the Sympathetic Nervous System

is SNS catecholamines increased?:

A

no, serum and urine catecholamine levels in humans are within normal limits during thyroid storm

but C/S are controlled by β-adrenergic blockade..

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7
Q

Increased Cellular Response to Thyroid Hormones

illness makes tissue more responsive to T4

A

Increased Cellular Response to Thyroid Hormones - why SNS catecholamine cause issue

also-implicated in cases of thyroid storm resulting from infection, sepsis, hypoxemia, hypovolemia, and lactic acidosis or ketoacidosis

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8
Q

Potential Precipitating Events for Feline Thyroid Storm
Humans:

Cats:

A

Radioactive iodine therapy
Thyroidal or parathyroidal surgery
Abrupt withdrawal of antithyroid medications
Stress
Nonthyroidal illness
Administration of iodinated contrast dyes
Administration of stable iodine compounds
Vigorous palpation of the thyroid

same

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9
Q

C/S 4 categories:

ddx / category:

A

(1) fever, (2) CNS (3) GI and hepatic (4) CV

Constitutional Signs
Hyperthermia
Dehydration

Cardiovascular Signs
Arrhythmias
Atrial fibrillation, ventricular tachycardia
Gallop rhythm
Sinus tachycardia
Congestive heart failure
Hypertension
Thromboembolic disease

Respiratory Signs
Tachypnea

Neuromuscular Signs
Behavior changes
Mental dullness/obtundation
Seizures
Muscle weakness
Cervical ventroflexion
Gastrointestinal and Hepatic Signs
Abdominal discomfort or pain
Vomiting
Diarrhea
Icterus

Ocular Signs
Hyphema
Retinal lesions
Retinal detachment

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10
Q

dx:

What about total T4 and free T4

A

> T4, C/S, precipitating

elevated total thyroxine (T4) level
or a total T4 level in the high-normal range + elevated free T4 level

total T4 level may be in the normal range in a hyperthyroid cat, but it is expected that in animals suffering from thyroid storm, the total T4 and free T4 levels will be above the normal range

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11
Q

Tx - 4 problematic areas:

A

(1) reduce production and/or secretion of T4
(2) to counteract the peripheral effects of T4
(3) to provide systemic support
(4) ID eliminate the precipitating factor

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12
Q
  1. < T4
    methimazole MoA:

prevent further secretion of formed hormone:
iodine compounds

DexSP MoA:

A

methimazole - inhibits iodine incorporation into tyrosyl residues of thyroglobulin
prevents the synthesis of active thyroid hormone

1/2 dose in renal failure

stable iodine compounds such as potassium iodide
must be given 1 hour after methimazole administration because a large load of iodine will initially stimulate thyroid hormone production

Potassium iodide 25 mg PO q8
lipid-soluble radiographic contrast i.e. iopanoic acid, may be given at 100 mg per cat PO q1
-additional advantages of blocking peripheral conversion of thyroxine (T4) to triiodothyronine (T3)

  1. 1 to 0.2 mg/kg PO or IV inhibit the release of thyroid hormone from the thyroid gland
    - and to block the peripheral conversion of T4 to T3
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13
Q
  1. Inhibition of Peripheral Effects of Thyroid Hormone

β-adrenergic receptors:

Peritoneal dialysis, plasmapheresis, and hemodialysis have been used in human medicine, as has cholestyramine, which binds to thyroid hormone in the GI tract

A

propranolol inhibits the peripheral conversion of T4 to T3, although this effect happens slowly .:. propranolol may be advantageous in severely thyrotoxic cats

vs atenolol or esmolol only for B1 effects

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14
Q
  1. Supportive:
A

fluids
vs CHF tx that
hyperthermia - tx that
hypertension

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15
Q
  1. Eradication of the Precipitating Factor
A

do full diagnostic work-up

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16
Q

what does iodine do in hyperT4?

A

stable iodine compounds such as potassium iodide
must be given 1 hour after methimazole administration because a large load of iodine will initially stimulate thyroid hormone production

hyperthyroid patients, iodine acutely inhibits hormonal secretion [1], but the responsible mechanisms are uncertain. This is the most acute effect of iodine on thyroid status, occurring within hours of the start of therapy.

A second effect involves inhibition of iodine organification in the thyroid gland, thereby diminishing thyroid hormone biosynthesis, a phenomenon called the Wolff-Chaikoff effect