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Flashcards in Hypothyroidism/Hyperthyroidism Deck (49)
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Cause of:

Primary hypothyroidism

Secondary hypOthyroidism

Tertiary HypOthyroidism

primary: low T4/T3 from thryoid

secondary: low TSH from pituitary

tertiary: low TRH from hypothalamus


The most common cause of primary hypothyroidism is 

chronic lymphocytic thyroiditis (also known as Hashimoto’s thyroiditis). 


Explain pathogenesis of Chronic lymphocytic thyroiditis

Sensitization of the host’s own lymphocytes to various thyroidal antigens including thyroglobulin, thyroid peroxidase, and the TSH receptor. 


What can we detect in pts serum to dx Chronic Lymphocytic Thyroiditis. 

is this a genetic or environmental condition?

Antibodies to one or more of these antigens can be detected in many patients.

 Environmental factors (viral or bacterial infection, or high iodine intake) and genetic factors (e.g. defects in suppressor T lymphocytes) may be responsible for initiating the autoimmune process.


what causes the glandular destruction seen in chronic lymphocitic thyroiditis?

Cytokine release and inflammation ultimately result in glandular destruction. 


Causes of primary hypOthyroidism

Chrnic lyphocytic thyroiditis


reversible automimmne thyroiditis

thyroid irradiation

infiltrative/infectious disease

thryoid dysgeneisis

iodine deficency or excess

drugs: antiT drugs or Lithium


Causes of secondary/tertiary Hypothyroidism

tumors, trauma, inflitrative disease, drugs (Dopaimne or Glucocorticoids)

inactivationg mutations in gens coding for various proteins in hypothalamic-pit-thyroid axis


Signs and symptoms of hypothyroidism

, including lack of facial expression, dry and pale skin, absence of hair on the lateral third of the eyebrow, and puffiness of the face and lips (due to accumulation of mucopolysaccharides in the dermis). The nose is broadened, the tongue is large, smooth, red, and clumsy, and there is drooping of the eyelids


Severe hypothyroidism, sometimes referred to as ________, can be life threatening. This scenario is characterized by multiorgan dysfunction, profound hypothermia, hypoventilation, and hypotension; central nervous system signs are evident on physical examination. 

myxedema coma


What is the first test we perform when we suspect individual has hypOthryoidism



What is the relationship between TSH and T4


log linear: small change in T4 shows BIG change in TSH


If TSH is abnormal, or there is a high clinical index of suspicion for a central disease process, a ____is ordered to further characterize the thyroid condition

free T4 


how TSH can be ‘normal’ in secondary hypothyroidism?

 With low free T4 and T3, the NORMAL response of the pituitary would be an increase in TSH. If TSH is NOT increased, it is considered “inappropriately normal”. The few remaining normal thyrotrophs are working as hard as they can to restore thyroid function, and the best they can do is maintain TSH within the reference range. However, it is not enough TSH to restore thyroid function.


TSH levels are elevated

Free T4 and T3 are LOW

see + thyroid peroxidase thyroglobulin antibodies

Primary hypothyroidism


See decreased or normal TSH

LOW T3 and T4

negative for thryoid peroxidase antibodies

Secondary/tertiary hypothryoidsm


You find your patient has CENTRAL hypothyroidism (low or normal TSH and low Free T4) 

what test/imaging should you get next?

order MRI of the pititary and hypothalamus


What is the treatement of Primary Hypothyroidism

Thyroid hormone is most often administered as T4 alone (levothyroxine


you start a pt on levothyroxine for primary hypothyroidism, when do you re-check their levels to judge effectiveness of treatement?

 Because the half-life is approximately 7 days, we generally wait at least 5-6 half-lives before retesting and adjusting the thyroid hormone dose to achieve a TSH level between approximately 0.5 and 4 mU/L. 


Why is Liothyronine not commonly prescribed to tx Primary hypothyroidism

Liothyronine (synthetic version of triiodothironine/T3) is also available, but not commonly used because T4 is converted to T3 in peripheral tissues, and T3 has a short half-life with a need for frequent dosing. 


Common causes of HyPERthyroidism

The most common causes of primary hyperthyroidism are Graves’ disease (diffuse toxic goiter), toxic multinodular goiter, solitary toxic (follicular) adenoma, and “thyroiditis” (destruction d/t inflammation)


How does thyroiditits cause HYPERthryoidism if its destruction of the thryoid gland?

 Hyperthyroidism results from release of preformed thyroid hormone in this setting. 


 Secondary hyperthyroidism is a very rare condition due to a

 TSH-secreting pituitary adenoma.


Graves’ disease is an autoimmune condition of unknown cause. It is more common in____ and has a strong familial predisposition. Proposed environmental triggers include:


 stress, tobacco use, infection, and iodine exposure


Proposed pathophysiology of Graves

pathophysiology of Graves’ disease involves a defect in suppressor T lymphocytes (Ts) that allows helper T lymphocytes (TH) to stimulate B lymphocytes (B) to synthesize thyroid autoantibodies. 


What is the driving cause for thyrotoxicosis in Graves?

 thyroid-stimulating immunoglobulin (TSI) is the driving force for thyrotoxicosis


Signs of HYPER thryoidism from Graves

1. Alertness, emotional lability, nervousness, irritability

2. Poor concentration

3. Muscular weakness, fatigability

4. Palpitations

5. Voracious appetite, weight loss

6. Increased frequency of bowel movements

7. Heat intolerance


Clincal signs of hyperthryoidism

1. Hyperkinesia, rapid speech 2. Proximal muscle weakness, fine tremor 3. Fine, moist skin; fine, abundant hair; onycholysis (separation of the nail from its bed); pretibial skin thickening 4. Lid lag, stare, chemosis, periorbital edema, proptosis 5. Accentuated first heart sound, tachycardia, atrial fib


Describe the dermatopathy associated with Graves

 Marked thickening of the skin is noted, usually over the pretibial area. Thickening occasionally extends downward over the ankle and the dorsal aspect of the foot but almost never above the knee. 



Proptosis is associated with what and how is it measured?

specifically with GRAVEs, not just  hyperhthyroidism and use a Hertel exophthalmometer is used to measure the amount of proptosis. 


How does proptosis affect vision and what imaging do we order to see it?

Orbital CT scan in a patient with severe ophthalmopathy and visual failure. Note the marked enlargement of extraocular muscles posteriorly, with compression of the optic nerve at the apex of the orbital cone. 


Suspect pt has hyperthroidism

1. Get ____ levels

-to confirm primary, get ____ levles

get THS levels (will be low)

then confirm with T4/T3 levels (will be elevated or normal)


Pt has low TSH and high T4/T3 levels, you know they have primary hyperthryoidism, what test can you do to confrim its Graves?

hyroid stimulating immunoglobulins (TSI) can be measured. They are not always positive in patients with Graves’ disease, but if positive are very specific for Graves’ disease. 


You are trying to determine the cause of your pts Primary Hyperthyroidism. The TSI game back negative but you know they could still have Graves. What test do you do next?

radioiodine uptake/scan study


How do you interpret radioactive uptake studies:

diffuse bilateral uptake

uptake on one side

patchy uptake all over

diffuse bilateral uptake: Graves

uptake on one side: solitary toxic nodule

patchy uptake all over: toxic multinodular


what is the preferred therapy in young pts with Hyperthyroidism?

. Drug therapy is preferred in young patients, patients with mild hyperthyroidism, and patients with small/minimally enlarged thyroid glands as it is reversible and Graves’ disease can go into remission in some cases.


MOA of Methimazole and its use

Use: hyperthyoidism

 Inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland


What drug is prefered for tx of Hyperthroidism


but in 1st trimester of preggers use Propylthiouricil


Adjunctive therapy for hyperthyroidism patients who are intolerant of methimazole and in pregnant patients. 



MOA of Propylthiouracil

 Inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland. It also partially inhibits the peripheral deiodination of T4 to T3. 


What pts should not use Proplythioruricil?

 relatively low incidence of side effects (rash, joint pain, headache etc). Reversible agranulocytosis can occur and there is a black box warning for hepatic failure. 


 treatment of patients with hyperthyroidism and are in the preoperative period in preparation for thyroidectomy, and in conjunction with anti-thyroid drugs and propranolol, in the treatment of thyrotoxic crisis. 



rotect the thyroid from radioactive iodine fallout following a nuclear accident



MOA of iodide

- In pharmacologic doses, the major action of iodides is to inhibit hormone release. In addition, iodides decrease the vascularity, size, and fragility of a hyperplastic gland, making the drugs valuable as preoperative preparation for surgery


Side effects of Iodide

 acute sensitivity reaction (IV or IP) including angioedema and laryngeal edema, serum sickness like effects. Mild iodism simulates a "head cold." 


Drug used to cause thyroid destruction of an overactive or enlarged thyroid and in thyroid cancer for thyroid ablation and treatment of metastatic disease. 



MOA of 131-I

131I is trapped by the thyroid, incorporated into the iodoamino acids and deposited in the colloid of the follicles. 131I has a t1/2 of 8 days and emits both gamma rays and beta particles. The beta particles destroy the parenchymal cells of the thyroid.


What side effect do we worry about when using 131-I?

high incidence of delayed hypothyroidism. 


When would we recommend a thyroidectomy in pt with hyperhthyroidism?

Thyroidectomy may be appropriate in patients with very large glands, multinodular goiters, nodules suspicious for malignancy, allergy/intolerance to antithyroid drugs, inadequate response to antithyroid drugs, or contraindication/refusal of radioactive iodine.