Treatment of Thyroid Disorders Flashcards
Where in the body is T4 converted to T3 ?
In kidney and liver
Describe findings on a radionucleotide thyroid scan (123I- or 99mTcO4 -uptake) for Grave’s disease and subacute thyroiditis.
Refer to slides 3 on page 2 and 4 on page 3
In diffuse goitre (e.g. Grave’s), more of the iodine is taken up and accumulated.
In subacute thyroiditis, no intake of radioisotopes.
Describe the main features of subacute thyroiditis.
Inflammation of the thyroid (e.g. post-infectious or AI) causes it to stop working (may be transient)
Acutely, release of stored thyroid hormones causes hyperT
Chronically, gland becomes exhausted, causing hypoT
Identify the main modalities of treatment of thyroid disorders. What are the main cons of these ?
Radioactive iodine, anti-thyroid drugs and surgery
MAIN CON:
None interrupts AI process
Identify main pharmacological treatment options for Hyperthyroidism.
• Thioureylenes (thioamides) including:
- Carbimazole (prodrug, better taken up by follicular cells; once inside cell, forms active form methimazole)
- Methimazole
- Propylthiouracil
- Radioactive Iodine (131I)
- β-blocker (e.g. Propranolol)
- Calcium supplements
How do Thioamides (Carbimazole, methimazole, and propylthiouracil) treat hyperthyroidism ? How long does their effects last ?
- Decrease the synthesis of thyroid hormones.
- Inhibit thyroperoxidase so reducing the iodination of thyroglobulin (so suppresses T3/4). Acts over 3-4 weeks.
How does iodine treat hyperthyroidism ?
- Converted to iodide and transiently reduces thyroid hormone secretion and vascularity of the gland
- Damages cells. Emits short-range β radiation and affects only the follicle cells.
State dose and administration of radioiodine in hyperT treatment.
Radioiodine (131I) is given orally and is selectively taken up by the thyroid. Given as a single (high) dose and lasts about 2 months (Not during pregnancy/ lactation)
Identify a side effect of radioiodine. How can this be treated ?
Hypothyroidism will eventually occur which can be treated with replacement therapy.
How do Calcium supplements treat hyperthyroidism ?
Maintain normal bone density
How do beta blockers treat hyperthyroidism ?
Outweight positive chronotropic, inotropic, and effects on CO of thyroid hormones.
Describe the structure of thiomides which are essential for antithyroid activity.
The thiocarbamide group is essential for antithyroid activity
Define Myxedema.
Term historically used to refer to HypoT (more specifically extreme form of hypothyroidism compounded by some stressful state, such as infection, MI or stroke), but also term used to describe dermatological changes associated with hypoT and hyperT conditions.
Describe mechanism that cause myxedema.
Results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesioned and normal skin causing swelling/puffiness of the subcutaneous tissue.
Distinguish between myxedema in hypoT and hyperT.
HyperT- symptoms limited to Pretibial myxedema (only 1-5% of patients)
HypoT- symptoms more prevalent and also include:
●Skin thickening
●Coarse skin
●Change in facial appearance
State the changes in the following enzymes that occur in hypoT:
- T4
- T3
- TSH
- Any other biomarkers
HypoT:
- T4: low
- T3: possibly low too
- TSH: raised unless pituitary problem
- Possibly various anti-thyroid antibodies
Describe the protirelin test.
Protirelin is TRH agonist: will bind to TRH receptors in the thyrotrophs, should stimulate TSH release and thyroid gland to release T3 and T4. If increase in T3/4, probably pituitary rather than thyroid defect.
Identify the main causes of congenital hypothyroidism.
-Hypoplasia of the gland (agenesis/dysgenesis AKA incomplete maturation)
-Familial enzyme defects
(dyshormonogenesis, some enzymes involved are mutated, so don’t produce active form of thyroglobulin)
- Iodine deficiency (endemic cretinism) (born to women in areas where low iodine intake in diet)
- Intake of goitrogens during pregnancy
- Pituitary defects (cause lack of TSH)
- Idiopathic
What are the main clinical features of congenital hypoT ?
- May have few or no clinical manifestations of thyroid deficiency
- The longer the condition goes undetected, the lower the IQ
Identify the main causes of acquired hypothyroidism.
Iodine deficiency
Auto-immune thyroiditis (antibodies developing in blood to something you’ve been infected with, which end up attacking thyroid)
Thyroidectomy or RAI therapy (thyroid gland obliterated surgically or by radiation e.g. after tumor)
TSH or TRH deficiency (hypoT or pituitary defect e.g. adenoma in the thyroid)
Medications (iodide and cobalt)
Idiopathic
What is the most common cause of hypoT ?
Hashimoto’s Disease
Describe treatment for Hypothyroidism.
Levothyroxine (standard T4 replacement therapy for hypothyroidism)
Liothyronine (teatment of choice for myxedema coma)
Explain mechanism of action of Levothyroxine.
Synthetic analogue of thyroxine - has all the actions of endogenous thyroxine
Explain mechanism of action of Liothyronine.
Synthetic analogue of tri-iodothyronine - has all the actions of endogenous tri-iodothyronine
