Thyroid Disorders Flashcards
Essential Basics What is the Thyroid pathway in normal people?
Works via the hypothalamus, anterior pituitary, and the thyroid gland
- Hypothalamus releases TRH
- TRH stimulates the anterior pituitary which releases TSH
- TSH goes and stimualtes the release/production of T4/T3 in the thyroid gland
What are the common cuases of Erroneious results in a Euthyroid pt?
Lab error!
Severe or acute illness - can cause low or high TSH
Medication
- Low Serum T4/T3
- Can be caused by NSAIDS/Salicyclates
- glucocorticoids
- High serum t4/t3
- oral estrogens
- heparin
- Amiodarone (HINT HINT HINT)
- Significant component of iodine that can cause erroneous thyroid results. Always have to watch patients thyroid levels when they are on amiodarone.
Explain the Feedback loops in the picture.
1) Normal thyroid gland, pituitary releases TSH to the thyroid which turns on the thyroid gland and produces t4. T4 has negative feedback on anterior pituitary
2) Hyperthyroidism. Lots of T4 being produced. Tells the pituitary to turn off the secretion of TSH. Get a low TSH and elevated levels of thyroid
3) Hypothyroidism Primary - lots of TSH being secreted but the thyroid gland isn’t producing any thryoid hormone. Get high levels of TSH but low levels of t4
4) Secondary hypothyroidism - Low TSH and low TH. Hypothalamus most likely the problem. Not secreting TRH so the anterior pituitary is not producing any TSH. With no TSH, the thyroid will not produce thyroid hormone.
What is Goiter, what can it present with?
Goiter is the enlargemnet of the thyroid gland. this is usually slow onset, and people don’t notice because it is non tender.
- It may present with hashimotos thyroiditis
- graves disease
- idodine deficiency
- genetic thryroid enzyme defects
- medications (lithium, amiodarone, interferons)
Absent if deficienct pituitary TSH, surgical destruction of the thyroid, radiation or radioactive iodine.
what is endemic goiter?
endemic goiter
- It is common in regions with low-iodine diets
- 115 countries mostly in developing areas but also in Europe.
- Remedied by adding potassium iodide to commercial salt. But this can trigger a graves epidemic for about 4 years. So much thyroid hormone ready to go just waiting for iodine
- 115 countries mostly in developing areas but also in Europe.
- Can see hypothyroidism or hyperthyroidism but most are normal.
- Can be multinodular and very large
- Labs:
- T4, TSH are both normal
- TSH as expected in hyper or hypo thyroidism
- Thyroid RAI uptake can be elevated
- Serum thyroglobulin can be elevated
Hypothyroidism what is primary, secondary, and tertiary. What else can cause it?
-
Primary hypothyroidism is hashimotos disease *******
- see weight gain, constipation, hair texture brittle, and nails are brittle.
-
Autoimmune disorder in which antibodies attack the thyroid
- can cause goiter but not always
- can have hyperthyroid attack right before becoming permanently hypothyroid.
- Secondary - anterior pituitary
- Tertiary - hypothalamus
- Also can be caused by peripheral resistance to thyroid hormones.
- Mild hypothyroidism can go unrecognized
- Myxedema and cretinism are usually recognized
- puffiness from hypothyroid.
Hashimotos Thyroiditis: symptoms/physical findings, cc, dx?, labs? tx?
- Hashimotos thyroiditis is the most common thyroid disorder in the united states
- Caused by autoimmune
- Can be associated with other autoimmune
- IBD
- celiac
- myasthenia gravis - EOMs
- Adrenal insufficiency
- Can be associated with other autoimmune
- Can occur in pregnancy or postpartum thyroiditis
- Can have subclinical hypothyroidism
- usually 65 and older, normal T4, and elevated TSH. Treat based on symptoms
- May have elevated antithyroperoxidase and or antithyroglobulin antibody
- Want to test for these antibodies, may not be necessary if you already have the infomration from TSH though.
s/s
- If symptomatic
- neck swelling, and pressure
- enlarged, firm, and finely nodular thyroid
- may be unilateral
- Get a hyperthyroid storm and then become hypothyroid
- Most likely to progress to permanent hypo in smokers
- 11% remission rate.
- Chief complaint
- fatigue
- weakness
- weight gain
- increased need for sleep,
- depression
- constipation
- cold intolerance
- changes in menses –> can occur in many disorders.
physical finding
- NONE- possible
- dry skin
- thinnin hair
- thickened skin
- thin, brittle nails
- anhidrosis
- hyporeflexia
- goiter
- puffiness of face and eyelids
- Myxedema
- Pericardial, pleural, and peritoneal effusions
- cardiac enlargement
- puffy face and eyelids
- peripheral edema
- myxedma coma
dx/screening
-
TSH - most sensitive test and single best test for thyroid screening
- normal range is 0.4-4.0-5.5 mU/L
- FT4
- Serum t3 - not as good as a test for hypo.
- Other labs
- Elevated antibodies against thyroperoxidase and thyroglobulin in hashimotos
- increased cholesterol
- increased liver enzymes
- increased creatine kinase
- hyponatremia
- anemia
- Make sure to rule out other causes such
- amiodarone, severe illness and lab error. Also clinically rule out adrenal insufficiency.
tx
- Levothyroxine (thyroxine, T4) is the treatment of choice. (Synthroid, levothyroid, levoxyl)
- Increased levels seen in 1-2 weeks and near peak-levels seen in 3-4 weeks.
How do you start treatment?\
- starting dose of levothyroxine is 50-100 micrograma a day
- Average dose of 1.6 micrograms per body weight
- patients with CAD or older than 60 start at 25-50 micrograms
- Dose increases by 25 micrograms every 1-3 weeks until euthyroid
How do you monitor treatment?
- Educate your patient on probably life-long treatment
- Bioavailability of formulations
- pregnancy and estrogen therpay can require increased dose
- Periodic clinical and lab assessments q 4-6 weeks
- Keep TSH between .4 and 2.0 mU/L ideally
- Most patients will not require referral to an endocrinologist and can be easily and efficiently managed in a primary care office
- Pts usually response to treatment quickly and satisfactorily. Relapse should trigger reassessment
Painful Subacute Thyroiditis/de Qurvain’s, definiton, s/s, dx, tx
s/s & cause
Probably a viral cause (post-URI)
- A painful and tender enlarged thyroid - red inflammed thyroid
- dysphagia
- low grade fever
- elevated ESR
- hyper thyroid –> hypothyroid
- can return to euthyroid in 12 months
- Looks and is very uncomfortable
- Be ready because they WILL have a hyperthyroid attack.
treatment
- ASA for pain and inflammation
- propranalol for thyrotoxic symptoms
- iodinated contrast agent to decrease T3
- Ipodate sodium/iopanoic acid to decrease FT4
- binds with free t4 so its not active in the body.
What are some symptoms thyroid cancer can cause and what are the types of thyroid cancer?
Usually present as a palpable firm, non-tender nodule that is asymptomatic but a large thyroid cancer can cause neck pressure, dysphagia, and hoarseness. 3% metastasize to local lymph nodes, bone, and lungs.
- Cancer types
- papillary - MC
- follicular
- medullary
- anaplastic
- (Please feel my ass)
- Papillary is most common and is also least aggressive
- Has the lowest mortality
- presents with single nodes or out of multinodular goiter
- RAI positive
- Origin - radiation exposure
- Follicular
- presents with dyphagia, and hoarsseness
- RAI positive
- from gene mutation/translocation
- Medullary
- presents with flushing and persistent diarrhea
- RAI neg
- Familial, sporatic, gene mutation
- Anaplastic
- Least common
- Most aggressive
- highest mortality
- presents with rapidly enlarging mass within a multinodular goiter, pressure sensation, dysphagia, vocal cord paralysis
- RAI neg
- Gene mutation causes it.
HyperThyroidism, Causes?
Multiple causes
- grave’s disease - autoimmune
- toxic multinodular goiter/solitary adenoma
- subacute thyroiditis
- hashimotos thyroiditis
- rare causes
Graves Disease, Causes, s/s, physical, labs. dx. tx
- Causes
- Dietary idodine supplementation
- amiodarone
- certain chemotherapy agents
- Associated with other autoimmune d/o
- sjorgen syndrome
- pernicious anemia
- DM type 1
- Hypoparathyroidism
- celiac disease
s/s & cc
- Insomnia/decreased need for sleep
- heat intolerance
- diaphoresis
- pruritis
- fatigue
- muscle weakness/cramps
- weight loss
- frequent bowel movements
- menstural irregularities
- palpatations
- nervousness
- Physical
- tachycardia
- fine hair
- thin nails
- tremor
- hyperreflexia
- goiter (could have bruit)
- exophthalmos
- pretibial myxedema
- a fib
Labs
- Low TSH
- elevated T4
- Serum TSI (TSHrAb), antibodies against thyroperoxidase and thyroglobulin elevated in graves
- hypercalcemia
- elevated liver enzymes
- increased alkaline phosphatase
- anemia
- decreased neutrophils
Tx
- Propanolol 20-40mg Qid - symptomatic tx
- Thiourea drugs (suppression of thyroid hormone production and output)
- Methimazole
- Propylthiouracil
- drug of choice in pregnancy
- Generally these medications are managed by endocrine
- For mild thyrotoxicosis - do not permanently damage thyroid, high recurrence of hyperthyroidism
- Iodinated contrast agents (blocks conversion of T4 to T3)
- Iopanoic acid
- ipodate sodium
- For very symptomatically thyrotoxic, subacute thyroiditis, t4 overdose, t3 can fall 62% in 24 hours
- Radioactive iodine (destorys overactive thyroid tissue)
- Do not give in pregnancy
- exophtalmos is a contraindication
- lifetime risk of hyperparathyroidism
- No increased risk of malignancy, can be used with propanolol, thyroid function is necessary to uptake RAI.
What is subclinical hyperthyroid?
Low TSH with normal FT4, T3
Thyrotoxicosis/thyrotoxic crisis (storm) What happens? How do patients present?
Patients present with
- extreme hyperthyroidism
- marked agitation/delirium
- very high fever
- severe tachycardia
- vomiting
- diarrhea
- dehydratoin
- cardiac arrhythmia
- heart failure
- myocardial infartion
- 30% of acute psychiatric episodes have elevated T4 levelsw ithout thyroxicosis or decreased TSH
RAI uptake, Elevated vs not elevated?
See elevated RAI uptake in hyperthyroidism
- graves
- toxic multinodular goiter
- hyperfunctioning nodule
Not elevated or low in hypothyroidism
- hashimoto’s
- subacute thyroiditis
Big takeaways Hashimotos vs Graves
Hashimotos
- Hypothyroidism (hyper than hypo)
- thyroid antibodies
- bolus during destruction
Graves
- Hyperthyroidism
- TSH receptor antibodies
- these activate the gland to make more TH.
