Endo - 1-22 - Hyperthyroidism

Front 1

Thyrotoxicosis

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When tissues rae exposed to and respond to an excess of thyroid hormone.

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Hyperthyroidism

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Hyperfunc of the thyroid gland resulting in thyrotoxicosis.

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Hyperthyroxinemia

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Elev measurable thyroid levels in the blood.

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What is more common? Multinodal goiter or toxic adenoma?

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multinodal goiter

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Genetic mutation of thyroid hormone receptor

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Can have types that have a constitutively active adenylyl cyclase with resultant autonomy of the gland.

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Common causes of thyrotoxicosis associated with hyperthyroidism

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Graves' disease and intrnsic thyroid autonomy (either toxic adenoma due to benign tumor or toxic multinodal goiter due to foci of functional anatomy)

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Causes of thyrotoxicosis not associated with hyperthyroidism

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(these all seem to be transient and physiological - body responding the way it should)

Inflammation - e.g. silent thyroiditis or subacute thyroiditis
Both due to release of stored hormone

Extrathyroidal source of TH
Exogenous hormone due to ingestion of it in some way.

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Uncommon etiologies of thyrotoxicosis associated with hyperthyroidism

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Production of thyroid stimulators such as TSH hypersecretion (thyrotroph adenoma or reistance to T4) or trophoblastic tumor (chorionic gonadotropin)

Or intrinsic thyroid autonomy due to Thyroid CA or struma ovarii (a toxic adenoma in dermoid tumor of the ovary)

Or drug induced (iodine containing agents or radiographic contrast agents)

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Uncommon etiologies of thyrotoxicosis not associated with hyperthyroidism

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Drug-induced thyroiditis
Infarction of a thyroid adenoma
Radiation thyroiditis.

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Graves' thyroid

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Homogenously enlarged with a bruit.

Can burn out eventually to become small and atypical.

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Triad of Graves

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Diffuse thyroid hyperplasia, infiltrative ophthalmopathy (in both or one eye) and dermopathy.

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Graves disease pathogenesis

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Defect in suppressot T cells. B lymphocytes also involved.

Activation of TSH receptor occurs resulting in thyroid hormone release and diffuse thyroid enlargement.

So the Ab basically acts like TSH.

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How to dx Graves in a pregnant pt

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Can't do iodine nuclear scanning.

So you check for inhibition of TSH binding to its receptor by the TSH-binding inhibitory Igs. - this is an assay.

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Sx, signs, associated disorders with Graves

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Infiltrative ophthalmopathy, dermopathy, vitiligo, Hashimoto's thyroiditis, pernicious anemia, Graves' IgG titers, myasthenia gravis.

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Reasons for increased CO, HR, vasodilation, systolic BP, pulse pressure, palpitations.

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Increased mitochondria (size, number and surface area) number result in more heat production so the body tries to dissipate it this way.

Effects on myocardial cAMP

Increase in beta receptors

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Sx, signs of hyperthyroidism/thyrotoxicosis

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Irritability or psychosis
Insomnia
Heat intol
weight loss
musc weakness (proximal)
tremor
palpit, tachycard, afib
angina, chf (in the elderly)
lymphadenopathy, hepatosplenomegaly, lymphocytosis
smooth, warm, moist skin
osteoporosis
hypomenorrhea
onycholysis (concave recession of nail bed)

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Graves eye disease

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reversible

peri-orbital edema
lid lag (upper eyelid is raised too high - too much symp activity)
infiltration of EOMs.

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Pretibial myxedema

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Pretibial deposit where skin is inf with hyaluronic acid (just as in normal myxedema) but the skin in coarse and purplish.

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Lab findings in Grave's disease

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TSH is suppressed - this is key

Increased Total or free T4 or T3 or increased T3 resin uptake.

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Lab findings of thyrotoxicosis due to low TBG levels

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T4 levels are normal but T3 resin uptake is high.

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Medical therapy of hyperthyroidism

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Thiocarbiamides - Propylthiouracil and methimazole

Iodide/lithium inhibition of hormone release. (used to tx thyroid storm and reduces vascularity of the gland pre-op)

Beta blockers

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Propylthiouracil or methimazole drug toxicity

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Can be fatal.

Rsih, fever, hepatitis, agranulocytosis.

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Propanolol

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also blocks T4 conversion to T3

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Definitive therapy

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Radioiodine ablation or subtotal thyroidectomy

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Toxic multinodal goiter

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Goiter that was euthyroid for years but became autonomous to release thyroid hormone.

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TSH levels in toxic tMNG

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usually about 0

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Nuclear scan of toxic MNG

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Areas of autonomy and patchy areas of heterogenous uptake.

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Two types of MNGs

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More common - Gland is full of nodules of various sizes

Less common - One or a limited number of nodules with uniform structure and function

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Apathetic hyperthyroidism

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Associated with toxic multinodal goiters.

Lacks of usual signs of hyperthyroidism and may only have weight loss, loss of appetite, or atrial fib.

A thyroid hormone level on the high end of normal is ABNORMAL in old pts because their T4 and T3 should decrease with time.

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Treatment of toxic MNG

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beta blockers, anti-thyroid meds, iodine ablation (most often), surgery (least often).

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Toxic adenoma

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Always benign.

Hypersecretion by a thyroid tumor or nodule.

Probably a G-prot mutation making adenylyl cyclase overactive.

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Treatment of toxic adenoma

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Iodine ablation usually.

Anti-thyroid drugs are used but not helpful long-term.

Beta blockers for catecholamine sx.

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Thyrotoxicosis factitia

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Self-admin of thyroid hormone. This leads to low iodine uptake, below normal TSH level, high T4, high free hormone levels, and high reverse T3.

Thyroid would be small or undetectable as well.

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Excess TSH secretion - response to TRH stimulation test

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BLunted response to it.

And will fail to suppress TSH when treated with T3.

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Excess TSH secretion

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One example is a TSH-secreting adenoma. (Note - this is not toxic adenoma which is in the thyroid)

Prodces excessive amounts of alpha subunit of TSH (I think that basically the glycosylation is not happening?)

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Tx of excessive TSH secretion

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Pituitary surgery and radiation therapy for macroadenomas.

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Trophoblastic tumors

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Secondary to excessive bHCG in malor pregnancies (hydatidiform mole).

Human placental thyrotropin and molar thyrtropin are both thyroid stimulators.

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Subacute thyroiditis

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Often the node is tender.

Inflammatory process with leakage of hormone.

Low iodine uptake.

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Clinical features specific to Graves

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These are systemic effects of the Abs that don't affect the thyroid but other stuctures. This is why you only see them with Graves'.

Ophthalmopathy, dermopathy and acropachy (soft tissue growth and periosteal expansion)

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Silent thyroiditis

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No pain but there is leakage of hormone.

Reverts to hypothyroid state then euthyroid state most often.

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Struma ovarii

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Teratomatous tissue in ovary. Seen with T4 elevations.
VERY VERY RARE!!!