Thyroid Disease Flashcards
T3 ratios
some from gland directly
- some from T4 (Type 1 and 2 deiodinase)
- reverse T3 via Type 3 deiodinase
Things that inhibit Types 1/2 deiodinase, get more rT3 Starvation Severe illness Severe stress Neonatal period Glucocorticoids Propranolol Amiodarone Radiocontrast dyes
Serum total T4
4-12 micrograms/dL
only 0.02% is free and active T4
99.98% is bound and inactive:
TBG, TBPA, albumin
t1/2 of T4: 7 d
Serum total T3
-t1/2 1 day
total T3: 80-180 ng/dL
free 0.02%: 1-4 pg/mL
bound: TBG, albumin
causes of increased total T4 and total T3
-hyperthyroidism/thyrotoxicosis
-increased binding proteins:
estrogen
-thryoid hormone resistance
causes of increased free T4 and free T3
hyperthyroidism/thyrotoxicosis
-thyroid hormone resistance
Causes of decreased total or free T4 and T3
Hypothyroidism
Decreased serum protein binding
Euthyroid sick syndrome (nonthyroidal illness)
Drugs
Liver or kidney disease (total T4, total T3)
TSH: when is it useful and when is it not reliable?
normal range: 0.4-4
- *best test to screen for thyroid dysfunction
- indicates an individual’s thyroid hormone “set point”
-Elevated in primary hypothyroidism:
Lack of negative feedback by thyroid hormone
Suppressed in primary hyperthyroidism:
Excess negative feedback by thyroid hormone
When can one not rely on a TSH?
Abnormal pituitary gland
Ex. panhypopituitarism, TSHoma, idiopathic central hypothyroidism
TSH action
stimulates iodine uptake into thyroid follicular cells and thyroid hormone production
- binds to receptor, NIS is activated
- ultimately leads to production of T4 and T3
Sx of hyperthyroidism
nervous weight loss increased appetitie fatigue tremor heat intolerance
Dx of hyperthyroidism or thyrotoxicosis
Overt:
low TSH
increased free T4
increased free T3 (not used)
Sublclinical
low TSH
normal T4
normal T3
Thyroxtoxicosis
High circulating levels of thryoid hormone
1. no overproduction
-high RELEASE of preformed/stored T4 and T3: no true hyperthyroidism
“thyroiditis”
2. overproduction of T4 and T3 “hyperthyroidism”
- TSH should be low (TSH stimulates thyroid to take up iodine and synthesize T4 and T3.
- if TSH is suppressed, there should be no uptake of iodine
- a normal or elevated iodine uptake in the setting of a low TSH is abnormal and indicates autonomous production of thyroid hormone: true hyperthyroid state
- if uptake is low (approp in the setting of a low TSH), then thyroid hormone excess is due to high release of preformed thyroid hormone
Diagnostic eval
**look at slide 21
Etiology of hyperthyroidism: high uptake
Thyrotropin receptor antibody:
Graves’ disease
Hashitoxicosis
Thyroid autonomy:
Toxic adenoma
Toxic multinodular goiter (MNG)
HCG:
Hydatidiform mole
Choriocarcinoma
TSH:
TSH-oma (pituitary tumor)
Thyroid hormone resistance
Low uptake “hyperthyroidism”
No need to get thyroid scan (dark)
Subacute thyroiditis:
*Granulomatous thyroiditis (viral); de Quervain’s
Chronic lymphocytic thyroiditis (Hashimoto’s):
Postpartum thyroiditis
- Radiation-induced thyroiditis
- Infectious thyroiditis
Drug-induced thyroiditis
Ectopic thyrotoxicosis:
Factitious
Struma ovarii
*pain
Grave’s dx
- low TSH, high free T3, T4
- can also check for auto-ab against the TSH receptor (Thyroid stimulating immunoglobulin)
- diffuse enlargement and diffuse increased uptake upon scan
What else might you see with Grave’s disease?
Grave’s ophthalmopathy (thyroid eye disease)
-inflammation, mononuclear cell infiltration, collagen and glycosaminoglycans between EOM, edematous changes and fluid behind eyes: protrudes the globes
-Pretibial myxedema
Treatment of Grave’s Disease
Medications
Antithyroid drugs (methimazole, propylthiouracil), methimazole preferred over PTU in most cases- Inhibit synthesis of thyroid hormone
Beta blockers- Reduce systemic hyperadrenergic symptoms and effects (primarily tremor, palpitations, etc.)
Radioactive Iodine (131I)
Surgery
Destructive thyroiditis
ex:
subacute/granulomatous thyroiditis
postpartum thyroiditis
When high T4 phase:
may need Beta blockers
In high TSH phase:
may need LT4 bridge (levothyroxine T4)
Dx of hypothyroidism
overt:
high TSH
low free T4
subclinical:
high TSH
normal free T4
(small decrease in free T4 = large increase in TSH)
Sx of hypothyroidism
mental slowness weight gain decreased appetite fatigue (in both hyper/hypo) muscle cramps cold intolerance
Primary hypothyroidism
Chronic autoimmune (Hashimoto’s) thyroiditis
Transient hypothyroidism:
Silent or postpartum thyroiditis
Subacute or granulomatous thyroiditis
Iatrogenic:
Thyroid surgery/thyroidectomy
Radioactive iodine
External neck irradiation
Iodine deficiency or excess
Drugs:
Antithyroid drugs, lithium, amiodarone, tyrosine kinase inhibitors, iron, cholestyramine, phenytoin, carbamazepine
Infiltrative diseases:
Hemochromatosis, sarcoidosis, amyloidosis, fibrous (Reidel’s) thyroiditis, scleroderma
Infections:
M. tuberculosis, P. carinii
Congenital
Central Hypothyroidism (secondary or tertiary)
- pituitary tumor
- trauma
- postpartum pituitary necrosis (Sheehan’s syndrome)
- hypophysitis
- Craniopharyngiomas
- radiation therapy
- infiltrative disease
- TSH or TRH resistance
Hashimoto’s thyroiditis
thyroid autoantibodies:
TPO (thryoid peroxidase)
Tg (thyroglobulin)
Rate of developing hypothyroidism
- pts with elevated TSH and positive thyroid ab develop hypothyroidism at rate of 5%/yr
- TPO ab alone: 2%/yr
When to treat and what is used
- with TSH greater than 10mIU/L (normal 0.4-4)
- Controversial to tx b/t 5-10
Treat w/ Levothyroxine– synthetic T4
Goal: 1-2.5 mU/L
Myxedema coma
-endocrine emergency
-severe/extreme form of hypothyroidism
-Decreased cardiac output, bradycardia, respiratory depression, edema, altered mental status, hypothermia, metabolic derangements
High mortality rate
