Thyroid Flashcards
What is hypothyroidism and severe name?
- thyroid hormone deficiency
- hypofuncitoning
- (myxedema = severe)
What is hyperthyroidism and severe name?
- thyroid hormone excess
- hyperfunctioning
- (thyroid storm = severe)
Hypothalamic Pituitary Thyroid Axis (pathway)
- Neural inputs to hypothalamus to secrete TRH
- TRH then stimulates ant pituitary to release TSH
- TSH then stimulates thyroid gland to synthesize and release thyroid hormones T3 and T4
**This process is a negative feedback loop = high T3 and T4 block TSH and TRH secretion
** Other factors affecting TH regulation: acute/chronic illness, starvation, medication
Thyroid Gland Anatomy
- Largest endocrine gland
- Two lateral lobes connected by isthmus - highly vascular
- Laryngeal nerves pass under the thyroid (voice box can be damaged during surgery)
- Not palpable in healthy individual
What is the function of the follicle of the thyroid?
structural and functional unit of thyroid
Parathyroid glands (4)
- on post. Surface
- PTG secrete PTH
Function of colloid of thyroid
- protein filled center w. Thyroglobulin protein (used in production of T3 and T4)
Parafollicular Cells of thyroid
- C-cells release calcitonin → work in Ca regulation to decrease serum Ca
- opposite of PTH
Thyroid Hormones
- T3 = active form → has 3 iodines
- T4 = inactive form → has 4 iodines
T3 can be made into T4
True or False
False
T4 can be made into T3 (not other way around)
Half Life of T3 and T4
T4 has longer half life than T3 (7 days vs 1.5 days)
T/F: Almost all T4 and T3 in plasma is protein bound
True
- Thyroxine binding globulin (TBG) = 70%
- albumin = 15%
- Thyroid binding pre albumin (TBPA) = <15%
Does the thyroid gland produce more T4 or T3?
Thyroid gland produces more T4 than T3
Where is T4 converted to T3?
T4 is converted to T3 primarily in peripheral tissues
- 35-40% of secreted T4 converted to T3 via peripheral deiodination
- 45% of secreted T4 is converted to inactive reverse T3
T/F: Free T4 and Free T3 are the most reliable tests for assessing thyroid hormone concentrations?
True
Free T4 and Free T3 are the most reliable tests for assessing thyroid hormone concentrations → measures unbound fractions of T3 and T4 → most are protein bound = inactive
T/F: FT4 is the most accurate indicator of euthyroidism?
False
TSH is the most accurate indicator of euthyroidism
Functions of the following tests:
TSH
TT4/TT3
FT4/FT3
TPOAb/TPA
RAIU
Scan
- TSH gives how well the HPT axis is working
- TT4 and TT3 → how much bioavailable T3 and T4 in the blood
- FT4/FT3 → direct measure of free T4/T3
- TPOAb/TPA → thyroid peroxidase antibodies test
- RAIU (radioactive iodine uptake) → given iodine and looking at how much the thyroid takes up
- Scan → size, shape, tissue activity
normal TSH
normal TT4 and TT3
normal FT4 and FT3
euthyroid
normal TSH
normal/decr TT4 and decr TT3
normal FT4 and FT3
Euthyroid Sick Syndrome
elevated TSH
decreased TT4 and TT3
decreased FT4 and FT3
primary hypothyroidism
elevated TSH
normal TT4 and TT3
normal FT4 and FT3
subclinical hypothyroidism
- may not have symtoms yet
low TSH
increased TT4 and TT3
increased FT4 and FT3
primary hyperthyroidism
low TSH
normal TT4 and TT3
normal FT4 and FT3
subclinical hyperthyroidism
- asymptomatic
low TSH
decreased TT4 and TT3
decreased FT4 and FT3
secondary hyperthyroidism
- problem not with thyroid itself but upstream –> ant. pit or hyothalamus
↑ TBG binding capacity
increased TT4 and TT3, normal FT4, FT3, TSH → influenced by factors like estrogens, oral contraceptives, and genetic TBG increase.
↓ TBG binding capacity / displace T4
decreased TT4 and TT3 with normal FT4, FT3, TSH → influenced by factors like cirrhosis/hepatic failure, androgens, high-dose salicylates, glucocorticoids, and nephrotic syndrome.
↓ peripheral T4 to T3 conversion:
decreased TT3 with normal TT4, FT4, FT3,TSH, influenced by PTU, propranolol, and glucocorticoids.
↓ pituitary and peripheral T4 to T3 conversion
Causes increased TT4, decreased TT3, transiently increased TSH, and increased FT4, influenced by iodinated contrast media, amiodarone, and non-thyroidal illness.
↑ T4 clearance by enzyme induction / increased fecal loss:
Results in decreased TT4, decreased FT4, and normal or increased TSH, influenced by drugs like phenytoin, phenobarbital, carbamazepine, and cholestyramine.
↓ TSH secretion and ↑ TSH secretion
↓ TSH secretion → dopamine agonists
↑ TSH secretion → dopamine blockers
T/F
TFT’s should NOT be performed in hospitalized patients unless hyper/hypothyroidism is the suspected cause of the clinical presentation or significant comorbidity
True
Name some of the main symptoms of Hypothyroidism
Weak, tired, cold intolerance, HA, weight gain, muscle cramps, constipation, thin/brittle nails, thin of skin, thickening tongue, goiter, anemia, puffy face
T/F: Prevalence of hypothyroidism higher in men than women
False
Prevalence higher in women than men
Difference between primary and secondary hypothyroidism
Primary = issue with thyroid gland
Secondary = problem with hypothalamus or ant pit. –> TSH or TRH deficiency
Can you know if someone has primary or secondary hypothyroidism just based on their TSH level?
↑ = possible hypothyroidism (need FT4 to confirm)
↓ = need FT4 to distinguish between primary and secondary hypothyroidism
Causes of Hypothyroidism
1° WITH gland enlargement
Hashimoto thyroiditis = most common cause, Iodide deficiency (rare here bc iodine in salt), Congenital hypothyroidism → prick baby foot, Natural goitrogens (rutabaga, turnip, cabbage)
1° w/o gland enlargement
Idiopathic atrophy, surgery, destruction of thyroid, radioactive/x ray, congenital hypothy., thyroiditis
Hashimoto’s Thyroiditis
- what is it?
- with or without goiter?
- antibodies?
- what is Hashitoxicosis
- Chronic autoimmune thyroiditis; characterized by gradual thyroid failure
- With or without goiter
- 95% of pt with Hashimoto disease have + antibodies (TgAb and TPOAb)
- May have transient hyperthyroidism (Hashitoxicosis) → sudden T3/T4 release right at start
Drug Induced Hypothyroidism
(2 drugs we talked about)
- Amiodarone (can cause either hypo/hyper)
- Lithium (infects the MIT + DIT step)
what is Myxedema Coma?
Occurs due to prolonged and severe thyroid hypofunction = medical emergency = need treatment
Hypothyroidism in Pregnancy
- maternal and fetal risks - list them
- Associated with poor maternal outcomes: infertile, miscarriage, pre-eclampsia (BP cond.), incr risk of stillbirth & c-section
- Ass with poor fetal outcomes: abnormal growth, cognitive issues
- High HCG levels stimulate thyroid receptors = lower TSH
Main Symptoms of Hyperthyroidism
- heat intolerance, short and light periods, weight gain/loss, increased sweating, bulging eyes, nails thick, diarrhea, fast HR, muscle weakness, hyperpigmented eyelids, pretibial myxedema
How would you diagnose primary Hyperthyroidism? What tests are helpful?
- decreased TSH WITH increased FT4 (T3, T4, FT3 also increased)
- autoantibody test (graves)
- RAIU (graves)
Graves Disease cause
- high levels of thyroid Ab
- TSH receptor stimulation due to Ab (IgG) leads to T3 and T4 production
- ususally have other auto immune conditions too
- have elevated RAIU
Thyroid Storm
- life threatening emergency
- aka decompensated thyrotoxicosis
- often triggered by stressful events = trauma, surgery, infection
3 Treatments for Hyperthyroidism
- Thioamides
- Radioactive Iodine
- Surgery
Thyroid Nodules are benign and asymptomatic? T/F
true
Patients with thyroid nodules are either hypo/hyperthyroid: T/F
false
they are euthyroid
Cold Nodule = hyperfuncitoning? T/F
False
it is hypofunctioning = nodule isnt producing any TH
- could be cause for malignancy
Hot Nodule = Hyperfuncitoning
True
- excessive TH production
