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Flashcards in Hyperthyroidism Deck (15)
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1
Q

Etiologies of hyperthyroidism

A
  • Graves disease
  • Toxic multinodular goiter (GOF mutations in TSH receptor-> autonomous T4/T3 producing cells)
  • Iodine-induced thyrotoxicosis: jod-basedow (iodine supplementation in iodine deficient goiters leads to hyperthyroidism b/c there’s increased machinery and now fuel to make the hormones)
  • Autonomous hyper functioning nodule
  • Subacute thyroiditis
  • Post-partum thyroiditis
  • Factitious thyrotoxicosis
  • TSH-mediated thyrotoxicosis
2
Q

Physiologic response to hyperthyroidism

A
  • There is increased heat production secondary to increased activity in Na/K ATPase, Ca ATPase, FA turnover, and beta adrenergic activity
  • Exaggerated response to b adrenergic due to increased number and sensitivity of beta-adrenergic receptors, despite normal circulating catecholamine levels
  • There is tachycardia and increased CO (B1), coupled w/ vasodilation (B2)
  • There is increased blood volume to compensate for global vasodilation
3
Q

Signs and Sx of hyperthyroidism

A
  • Nervousness, anxiety, heat intolerance, palpitations, SOB, weight loss, trouble sleeping and concentrating, frequent bowel movements
  • Tremors, muscle atrophy/weakness, tachycardia, sweating, restlessness, rapid speech
4
Q

Grave’s disease 1

A
  • Autoimmune hyperthyroidism, most common form
  • Due to genetic predisposition (HLA-DR3 and HLA-B8) plus an inciting event (viral, bacterial, environmental)
  • This leads to damage of the thyroid, causing an inflammation (IFNg->Th2) reaction to occur
  • The B cells produce Abs to various epitopes from the thyroid, including TPO and TSH receptor
5
Q

Grave’s disease 2

A
  • Anti-TPO Ab doesn’t participate in pathogenesis (used as a marker for immune dysfxn), but TSH receptor Ab is an agonist for the TSH receptor
  • This Ab is TSI (thyroid stimulating immunoglobulin), and leads to growth and excess secretion of thyroid hormone (preferential T3 secretion) from the gland
  • Leads to a diffusely enlarged gland: a globally smooth goiter
  • If there is a carotid bruit its pathognomonic for graves disease
6
Q

Infiltrative ophthalmopathy of grave’s

A
  • Usually parallels the thyrotoxicosis, but has its own progression
  • Abs are made against EOMs and orbital adipocytes produce cytokines (IL1, TNF, IFNg) causing a local immune response
  • This leads to proliferation of adipocytes and fibroblasts, causing enlargement of orbital contents which impairs venous outflow
  • May see proptosis, periorbital edema, hyperemia/congestion of vessels, conjunctivitis/chemosis
  • Pts have decreased range of movement of EOMS: they can’t look up + out b/c of the tension that puts on the medial and inf rectus muscles
  • Can Rx eye Sx w/ lubrication, GCCs, surgical decompression
7
Q

Dermopathy (pretibial myxedema) of graves

A
  • Mucopolysaccharide infiltrate of the skin over the tibia
  • Due to a localized immune reaction leading to IgG stimulation of fibroblasts
  • No effective Rx
8
Q

Lab values in graves disease

A
  • Markedly elevated T3/T4 levels (T3/T4 ratio > 20:1, extremely high compared to normal ratio of 1:20)
  • Very low TSH levels (<.01)
  • Positive anti-TPO
  • RAIU (radioactive iodine uptake) is increased diffusely
9
Q

General Rx for hyperthyroidism

A
  • Block the beta-adrenergic excess: BBs
  • Block the excess in thyroid hormone synthesis: thioamides
  • Destroy thyroid gland by surgical excision or RAI
10
Q

Thioamides

A
  • PTU or tapazole: both inhibit all steps of thyroid hormone synthesis catalyzed by TPO
  • PTU also inhibits conversion of T4->T3 in peripheral tissues (1 5’D)
  • 18mo Rx w/ gradual response due to large stores of T4/T3 that must be depleted
  • Side effects: skin rash, cholestatic hepatitis, agranulocytosis is rare but life threatening
  • If pt gets sore throat or fever tell them to stop taking the meds and go to ER
  • Both are contradicted in pregnancy
  • Remember after Rxing someone with these drugs to bring down T4/T3 levels, the TSH level will lag behind normalization of T3/T4 levels 4-8 wks before coming down to a normal range
11
Q

BBs

A
  • Propanolol is preferred since it blocks both B1 and B2

- Prevents many of the Sx involved w/ hyperthyroidism

12
Q

Iodine Rx and RAI

A
  • High levels of normal iodine can be used to suppress TSH/TSI interaction to inhibit release of T4/T3
  • Response is rapid, generally used for a few days in conjunction w/ thioamides before surgery or in acute situation
  • Cannot be used long term when pt is pregnant
  • I131 Rx: destroys thyroid gland using beta emissions, used very frequently on pts w/ graves disease, multi nodular toxic goiter, toxic adenomas
  • Makes the pt hypothyroid by 10 yrs in those w/ graves disease (other diseases may remain euthyroid)
  • Surgery can be done in graves, but is preferred in those w/ adenomas and toxic multi nodular goiters (TMNG)
  • Indications for surgery: very large goiter or resistant to RAIU, desires early pregnancy, pregnancy w/ allergy to ATD
13
Q

Subacute thyroiditis 1

A
  • Caused by inflammation of the thyroid 2-3 wks post viral syndrome (URI)
  • Thyroid is diffusely enlarged and very tender to palpation (pain my be referred to ears)
  • Systemic signs of viral illness: fever, increased ESR, myalgia, sore throat
  • Elevation of T3 and T4 (T3:T4 < 18:1), RAIU >1% (not overactive in any areas)
  • Tg in serum is markedly elevated (due to dumping of thyroid hormones/Tg)
14
Q

Subacute thyroiditis 2

A
  • Temporal pattern: hyperthyroid phase (w/ low TSH) for 4 wks, then hypothyroid phase (high TSH and variable RAIU) for 8 wks, then recovery phase after 12 wks (euthyroid)
  • Rx: symptomatic using GCCs, propanolol
  • Thioamides are contraindicated as thyrotoxicosis is secondary to dumping of thyroid hormone (not making more)
15
Q

Post-partum thyroiditis

A
  • Painless thyroiditis w/ unknown cause
  • Usually present 8 weeks after birth when immune system reactivates
  • Thyroid is diffusely but minimally enlarged, firm and non-tender
  • Low RAIU w/ same clinical course of subacute thyroiditis
  • T3:T4 <18:1, but there is + anti-TPO Ab
  • Give BB for Sx relief
  • Eventually all women will become hypothyroid (may recur esp during future pregnancies)