5 - Thyroid Flashcards
1
Q
Causes of primary hypothyroidism
A
- Autoimmune thyroiditis (Hashimoto’s)
- Congenital
- Iodine deficiency
- Infiltrative disease (viral, bacterial)
- Drugs (lithium, amiodarone, interferons, tyrosine kinase inhibitors)
2
Q
Describe hormone trends
A
- Primary hyperthyroidism = high T3 and T4, low TSH; primary = target organ (thyroid gland) is damaged
- Primary hypothyroidism = low T3 and T4, high TSH
- Secondary hyperthyroidism = high T3, T4, and TSH (dysfunction is at pituitary gland)
- Secondary hypothyroidism = low T3, T4, and TSH
3
Q
Describe the function of thyroid hormones
A
- Affect the function of virtually every organ system
- Important for normal growth & dev’t in children
- Maintain metabolic stability in adults
4
Q
Clinical manifestation (signs and sx) of thyroid disorders
A
- Hypothyroidism = weakness, fatigue, poor concentration/ memory, bradycardia, constipation, weight gain w/ poor appetite
- Hyperthyroidism = hyperactivity, irritability, dysphoria, tremor, tachycardia, diarrhea, goiter (enlarged thyroid gland -> swelling of neck)
5
Q
Describe the role of TSH, T4, and T3
A
- TSH releases T4 & T3 (T4»_space;> T3)
- Majority protein bound = inactive
- Biologically most active = free T3
- T4 converted to T3 in periphery by 5’-deiodinase
6
Q
Why isn’t T3 used as a drug? (levothyroxine = T4)
A
T4 is converted to T3 & we don’t want to lose the body’s ability to perform this conversion & T4 has longer t1/2 (almost like a pro-drug)
7
Q
How do autoimmune thyroid diseases occur? What is the tx?
A
- Infiltration of thyroid w/ sensitized T lymphocytes (WBC)
- Acute inflammation of thyroid -> damage to gland -> release of T3 & T4
- Initially pt is hyperthyroid (high T3 & T4) but may become hypothyroid (in weeks to months)
- Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis)
- Most common initial presentation = enlargement of thyroid gland (goiter)
- Tx = exogenous T4
8
Q
Describe a goiter
A
- Generalized (diffuse) enlargement
- Caused by continuous stimulation by TSH
- Hashimoto’s – goiter eventually disappears due to progressive destruction of thyroid
9
Q
Describe thyroid nodules
A
- Enlargement in 1 part of the gland (asymmetrical)
- Caused by benign/ malignant nodule
- Rarely associated w/ destruction of gland & hypothyroidism
10
Q
Describe Graves’ disease
A
- Common cause of primary hyperthyroidism in adults & children
- Autoimmune, familial disposition
- Thyroid stimulating antibodies (TSAb) or thyroid stimulating immunoglobulins (TSI) mimic TSH -> autoimmune stimulation
- Continuous stimulation => high T3/T4; increase thyroid size
- Specific to Graves’ disease = opthalmopathy (pathogenesis unclear) & dermopathy (deposition of mucopolysaccharide; shin most common)
11
Q
How are thyroid disorders classified?
A
- Hypothyroidism diagnosed when TSH is high & FT4 is less than population reference range
- Subclinical hypothyroidism
- Mild to moderate increased TSH, but total & FT4 normal
- If TSH very high (> 10) tx may be offered as these px may be at higher risk of CV complications
- TSH is the most reliable therapeutic endpoint for tx of hypothyroidism b/c most sensitive marker for monitoring
12
Q
Lab monitoring for L-thyroxine tx
A
- FT4 is measured instead of FT3 b/c FT3 can be affected by other sources, so FT4 is more reliable
- After initiating or changing dose, re-measure FT4 & TSH 1 month later; want to measure levels in the morning
13
Q
Factors that alter thyroxine & triiodothyronine binding in serum
A
- Increased TBG (T4-binding globulin) – estrogens, methadone, perphenazine, SERMs
- Decreased TBG – androgens, anabolic steroids, glucocorticoids
- Binding inhibitors – salicylates, furosemide, phenytoin, carbamazepine, NSAIDs, heparin
14
Q
Consequences of untreated hypothyroidism
A
- Increased CV mortality
- Impaired intellectual function, depression, slowed speech, memory loss in elderly
- Anovulation, impaired fertility, increased rate of spontaneous abortion
- Myxedema coma (hypothermia, hypotension, hypoventilation, hyponatremia, bradycardia) – medical emergency
15
Q
Dosing levothyroxine
A
- Healthy, young adults (< 50 y/o), children, older adults recently diagnosed w/ hypothyroidism, older adults recently treated for hyperthyroidism – initial 100-150 mcg/day titrated by 25 mcg q4-6weeks
- Adults > 50 y/o w/o cardiac disease, adults < 50 y/o w/ cardiac disease – 25-50 mcg/day titrated by 12.5-25 mcg q4-6weeks
- Adults > 50 y/o w/ cardiac disease – 12.5-25 mcg/day titrated by 12.5-25 mcg q4-6weeks
- Sx improvement in 2-3 weeks; maximal sx improvement in 4-6 weeks
16
Q
Drug interactions w/ levothyroxine
A
- TUMS, ranitidine, multivitamin – reduce absorption
- Metformin – decrease TSH secretion, increase levothyroxine requirements, & hypo/hyperthyroidism has effect on insulin sensitivity (hyper = increased sensitivity & vice versa)
- Carbamazepine – increases levothyroxine clearance
17
Q
Monitoring for hypothyroidism
A
- TSH (primary hypo) or FT4/FT3 (central hypo) – 6-8 weeks until TSH normal, then q1year
- Signs & sx of hypo – weekly by pt (improve in 2-3 weeks; skin change 3-6 months)
- If clinical manifestations not resolved or re-appear –> check TSH level; consider drug/meal interactions or malabsorption
18
Q
Hypothyroidism tx during pregnancy
A
- T4 requirements increase to maintain euthyroid state (onset 4-6 weeks gestation; increases until week 16-30 then remains constant until delivery)
- Newly pregnant & receiving LT4 -> increase dose by 25-30% in first trimester (if once daily, increase to 9 doses/week)
- TSH is most accurate indication of thyroid status
- Measure q4weeks in 1st half of pregnancy, then q1week in week 26-32
- Following delivery –> reduce LT4 dose, then check TSH 6 weeks postpartum
19
Q
Pt counseling tips for thyroid replacement therapy
A
- Levothyroxine should be taken in the AM on empty stomach; important to take same time each day
- Do not take antacids, iron preparations, calcium supplements w/in 4 h of thyroid medication (decreased absorption)
- Try not to change brands (less fluctuation in TFT if using the same brand – “interchangeability” province-dependent)
- Signs & sx to report = chest pain, rapid HR, palpitations, heat intolerance, excessive sweating, increased nervousness, agitation, lethargy
20
Q
Describe liothyronine/ cytomel (T3)
A
- Used in some px monotherapy or in combo w/ levothyroxine (T4) to control hypothyroidism
- Long-term benefit of combo therapy remains unknown
21
Q
Consequences of untreated hyperthyroidism
A
- CV –> A fib, angina, HTN, peripheral edema, heart failure
- Ocular –> double vision, corneal damage, vision loss
- Skeletal –> hypercalciuria, mild hypercalcemia, slight increased fracture risk
- Thyroid storm – medical emergency
22
Q
Hyperthyroidism tx. Describe SE, duration, and monitoring
A
- Antithyroid medications (propylthiouracil, methimazole)
- PTU & MMI inhibit thyroid peroxidase (TPO) –> block iodination of tyrosine
- PTU inhibits 5’ deiodinase –> block peripheral conversion of T4 to T3
- Radioactive iodine to destroy gland
- Used in Graves’ disease, not used in thyroiditis
- Surgery to remove gland
- Sx relief w/ beta blockers
- SE –> maculopapular rash (responds to antihistamines), arthralgia, transient fever, GI intolerance
- Low risk of permanent hypothyroidism in the long-term
- Risk of cross-sensitivity between PTU & MMI is 50%
- Response in 4-8 weeks; max response in 4-6 months
- Duration = ~1-2 years
- Monitor q4weeks until euthyroid (CBC, PT, TFT, INR); after remission monitor q6-12months
23
Q
Pt counseling tips for radioactive iodine
A
- Concentrates in gland & destroys thyroid tissue
- SE mild thyroidal tenderness/ dysphagia; permanent hypothyroidism
- Differ pregnancy 6-12 months post RAI; no breastfeeding (okay for future pregnancies)
- Most cost effective
- Have the potential to contaminate close contacts via saliva, urine, or radiation emitting from their neck => don’t kiss, exchange saliva, or share food/eating utensils for 5 days; wash dishes in dishwasher if available
- Avoid close contact w/ infants, young children (< 8 y) & pregnant women for 5 days (can be in the same room, stay 2 m away)
- Flush toilet twice after urinating & wash hands thoroughly
24
Q
Radioactive iodine & SSKI
A
- SSKI = saturated solutions of potassium iodide
- Don’t use SSKI pre-RAI b/c RAI needs to concentrate in thyroid
- MOA = saturates iodide transport system, decreases size & vascularity of gland
- Efficacy – reduced sx x 2-7 days (quick onset), reduce T3 & T4 in weeks
25
Q
Beta blockers for thyroid disorders
A
- Propranolol & nadolol partially block T4 -> T3 conversion (but this is a small effect on tx)
- Role = adjunctive therapy w/ ATD (anti-thyroid drugs), RAI, iodides, surgery, thyroid storm, Graves or toxic nodules for sx management
- SE = N/V, anxiety, insomnia, bradycardia
- Verapamil, diltiazem may be considered if BB’s aren’t tolerated or CI
26
Q
Euthyroid sick syndrome
A
- Abnormal thyroid function in px w/ nonthyroidal illness
- Natural human response to getting sick
- Common in ICU px w/ no thyroid problem
- Reduced conversion of T4 -> T3 by T4-5’-deiodinase
- Thyroid function shouldn’t be assessed in seriously ill px unless there is a strong suspicion of thyroid dysfunction
- Tx not recommended – studies showed tx doesn’t improve survival
27
Q
Thyroid function in non-thyroidal illness
A
- Sick – T3 drops first (ex: hospital inpatient)
- TSH drops but not to zero (transient central hypothyroidism, low TBGs)
- Sickest – T4 drops (low T4 = poor prognosis)
28
Q
Hypothyroidism in the elderly
A
- Elderly px may have fewer sx than younger adults
- Memory loss, confusion, weight gain, dry skin, sleepiness
- Specific signs in elderly = ataxia, non-joint pain/ muscle ache, falling
29
Q
When to treat thyroid disorders
A
- Overt hypothyroidism
- Subclinical hypothyroidism if symptomatic, presence of anti-thyroid antibodies, or CV disease
- TSH target range = 0.45 – 4.12 mIU/L
- Dose according to pt response (sx improvement) & TSH tests
- Few px require doses > 200 mcg/day
