Disease of Thyroid Hormone Flashcards
What is the feedback control loop system between the hypothalamus, pituitary, and the thyroid? (Drawing of all the control loops)
What is the main cause of primary hypothyroidism?
Explain the pathogenesis.
Most common cause: Hashimoto’s Thyroiditis
Autoimmune lymphocytic disease against thyroids
Potential antigens: Thyroglobulin, thyroid peroxidase, TSH receptor
What are other causes of primary hypothyroidism?
- Partial/total thyroidectomy
- Silent and postpartum thyroiditis (autoimmune reversible)
- Thyroid irradiation
- Infiltrative/infectious causes
- Thyroid dysgenesis
- Iodine deficiency
- Iodine excess: Wolff-Chaikoff effect
- Drugs: Antithyroid agents, lithium
What are the causes of secondary/tertiary hypothyroidism?
- Tumors
- Trauma
- Infiltrative
- Drugs – Dopamine, glucocorticoids
- Inactivating mutations of hypothalamic-pituitary-thyroid axis
What are signs and symptoms of hypothyroidism?
What is a particularly distinctive finding?
What is the exreme form?
All related to slowed metabolism
Particularly distinctive finding: Periorbital puffiness
Extreme form: Myxedema coma
What are the lab findings for primary hypothyroidism for hypothyroidism?
Why is TSH preferred over T4 for diagnostics?
When do you use T4?
Picked due to log-linear relation to thyroid hormones
Much more sensitive indicator (minor changes in hormone will result in major changes of TSH)
Pair with a T4 level if you suspect secondary/tertiary
T4 vs T3
Name
Potency
Oral bioavailability
Half-life
Dosing
When should you test to see if any changes?
Retest TSH in 5-6 half-lives (6 weeks with T4 replacement)
What is the process involved in Graves’ hyperthyroidism?
Autoimmune disease against the thyroid in particular TSH receptor (Extra-thyroid receptors in eyes: proptosis)
Desensitizes TSH for feedback control so thyroid over produces
What is the process involved in sub-acute hyperthyroidism?
Inflammatory disease damaging thyroid resulting in spilling out of contents
Transient hyperthyroidism
What is the symptomology of hyperthyroidism?
Alertness, emotional lability, nervousness, irritability
Poor concentration
Muscular weakness, fatigability
Palpitations
Voracious appetite, weight loss,
Increased bowel movements
Heat intolerances
What are the signs of hyperthyroidism?
- Hyperkinesia, rapid speech
- Proximal muscle weakness, fine tremor
- Fine, most skin; fine, abundant hair; onycholysis (nail separation from bed); pretibial skin thickening
- Lid lag, stare, chemosis, periorbital proptosis
- Accentuated first heart sound, tachycardia, A-fib, widened pulse pressure, dyspnea
What is the diagnostic tool of choice for hyperthyroidism?
How does each of these present:
Graves’
Follicular Adenoma
Plummer’s disease
Sub-acute thyroiditis
Radiotracer (Iodine) uptake and scan
Graves’ disease showing increased uptake (homogenous, diffuse)
Solitary toxic nodule (follicular adenoma): Localized uptake
Toxic multinodular goiter (Plummer’s disease): Several distinct, mildly overactive nodules
Sub-acute appears as blank (no new uptake)
Methimazole
Tx for?
Mechanism?
Adverse?
- Tx of hyperthyroidism
- Inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland
- Adverse effects: Low incidence; distinguishable is agranulocytosis
Propylthiouracil (PTU)
Tx for?
Mechanism?
Adverse?
- Tx: Adjunctive therapy for hyperthyroidism patients who are intolerant of methimazole and in pregnant patients
Multiple doses per day so less desirable
Thyroid storm: Due to T4 to T3 conversion inhibition - Mechanism: Blocks oxidation of iodine in thyroid gland and partially inhibits peripheral deiodination of T4 to T3
- Adverse effects: Same as methimazole, but more common
What diagnostic algorithm is used for hyperthyroidism?
Which test is typically not used?
What is the exception to this?
TSI only positive in Grave’s disease, not taken except for pregnant women (because they cannot have a thyroid uptake scan)
