Hyperthyroidism Flashcards
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)
