Thyroid Disorders B&B Flashcards
why does thyroiditis not fit into hypo- or hyper- thryoidism?
both occur, depending on the phase of the disease
initially, inflammation of the thyroid causes thyroid hormone to spill into the bloodstream, raising its levels
in response, however, the thyroid will begin to produce less (neg. feedback), and levels will fall
so both hyper- and hypo-thyroidism occur in thyroiditis
myxedema
aka thyroid dermopathy: non-pitting edema of the skin, usually from hypothyroidism
due to hyaluronic acid deposits in the dermis - osmotic agent, pulls water out and causes swelling, usually face/periorbital
[however, note pretibial myxedema over the shins is seen in Grave’s disease, which is hyperthyroidism]
myxedema, or thyroid dermopathy, is non-pitting edema of the skin due to _____ deposits
hyaluronic acid - osmotically active, draws water out and causes swelling
where would you see skin swelling in patients with hypo- vs hyper-thyroidism, respectively, and what causes this condition?
myxedema: non-pitting edema due to hyaluronic acid deposits (osmotic agent)
hypothyroidism: facial/periorbital swelling
Grave’s disease (hyperthyroidism): pretibial myxedema (over the shins, special form of myxedema)
myxedema coma
coma from hypothyroidism
recall myxedema = thyroid dermopathy, non-pitting edema due to hyaluronic acid deposits (osmotic agent)
levels of ______ commonly rise in patients with hypothyroid myopathy
creatine kinase (CK) - serum levels usually rise in hypothyroidism, due to low levels of thyroid hormone
hypothyroid myopathy presents with weakness, cramps, myalgias
how does hypothyroidism affect sodium levels and what is thought to be the cause of this?
hypothyroidism —> hyponatremia due to high levels of ADH (causes SIADH)
may lead to confusion
what kind of drugs are levothyroxine (Synthroid) and liothyronine (Cytomel) and which one is preferred?
levothyroxine (Synthroid): synthetic T4 (thyroxine)
liothyronine (Cytomel): synthetic T3 (triiodothyronine)
levothyroxine preferred because T3 is rapidly absorbed from GI (causes mild hyperthyroidism symptoms like tachycardia, tremor), and T4 is converted to T3 anyway
dose is titrated until TSH is normal
Patient is presenting with recent onset of lethargy, dyspnea on exertion, cold intolerance, weight gain with loss of appetite, and constipation. On exam, you note hyporeflexia, bilateral weakness, cool skin, brittle hair, and bradycardia. What are you thinking, and what is the best initial test to run?
hypothyroidism - metabolism slows down
best initial test for suspected thyroid disorder is TSH!
[hypothyroidism presents with HIGH TSH]
Patient is presenting with recent weight loss despite increased appetite, diarrhea, and hyperactivity. They went to the ED one week ago for an episode of atrial fibrillation. On exam, you note hyperreflexia, warm and moist skin, fine hair, and tachycardia. The patient notes they feel uncomfortably warm. What are you thinking and what test will you run first?
hyperthyroidism - metabolism speeds up
when patient presents with new onset of atrial fibrillation you must exclude hyperthyroidism
best initial test for suspected thyroid disorder is TSH!
[hyperthyroidism presents with LOW TSH]
what causes thyroid storm and how does it present?
life-threatening thyrotoxicosis in a patient with pre-existing hyperthyroid disease, precipitated by an acute event such as surgery/trauma/infection
massive catecholamine surge —> fever, delirium, tachycardia (arrhythmia may cause death), hyperglycemia, hypercalcemia (high bone turnover)
Patient is a 34yo F with PMH of hyperthyroid disease presenting to the ED with fever and delirium which developed following an upper respiratory infection. Tachycardia is noted upon admission and labs are significant for hyperglycemia and hypercalcemia. What are you MOST worried about?
patient is presenting with thyroid storm - MOST worried about death from arrhythmia
life-threatening thyrotoxicosis in a patient with pre-existing hyperthyroid disease, precipitated by an acute event such as surgery/trauma/infection —> massive catecholamine surge
what causes goiter?
goiter = enlarged thyroid
due to high TSH but inability to produce T3/T4 (bc of low iodine), or thyroid stimulating antibodies (Grave’s)
when you suspect a thyroid disorder what is the BEST initial test??
TSH!!
T3/T4 fluctuate, and TSH levels reflect how much thyroid hormone the tissues are actually seeing so it’s much more sensitive
what is the cause of central hyper- or hypo- thyroidism?
rare disorders of the pituitary or hypothalamus which cause thyroid disease
most often hypothalamic-pituitary tumors which either block TRH/TSH secretion (—> hypothyroidism) or secrete TSH (—> hyperthyroidism)
or due to pituitary resistance to thyroid hormone and thus lack of negative feedback (—> hyperthyroidism)
when is it useful to measure reverse T3 levels?
reverse T3: isomer of T3 also derived from T4, usually parallels T4 levels
except for in euthyroid sick syndrome - decreased TSH and T3/T4 in critically ill patients due to their disease, NOT central hypothyroidism… rT3 will RISE due to impaired clearance
low rT3 —> central hypothyroidism
high rT3 —> sick euthyroid syndrome
how can central hypothyroidism be distinguished from euthyroid sick syndrome?
central hypothyroidism: hypothalamic pituitary axis is cause of low TSH/T3/T4
euthyroid sick syndrome: critically ill patients with low TSH/T3/T4
measure reverse T3: isomer of T3 also derived from T4, will be low in central hypothyroidism but RISE in euthyroid sick syndrome due to impaired clearance
what causes Grave’s disease?
thyroid stimulating antibodies which act like TSH —> hyperthyroidism
(autoimmune disease)
what are the 2 unique exam findings of Grave’s disease and why do these occur?
- exophthalmos (bulging eyes) - proptosis (eye protrusion) + periorbital edema
- pretibial myxedema (shin swelling)
both caused by T-cell activation of fibroblasts, which contain TSH receptor —> stimulate causes secretion of hyaluronic acid (glycosaminoglycan), which is osmotic agent that draws out water and causes swelling
how is Grave’s disease diagnosed?
hyperthyroid labs + exophthalmos (bulging eyes, unique to Grave’s)
can also measure “thyroid stimulating immunoglobulins” (TSH receptor antibodies)
methimazole vs propylthiouracil (PTU)
both are thionamides
methimazole: inhibits thyroid peroxidase (TPO), blocking organification of iodine and coupling of MIT/DIT
propylthiouracil (PTU): inhibits TPO and also 5’-deiodinase, thus also blunting peripheral conversion of T4–>T3
what are the adverse effects (3) of thionamides such as methimazole and propylthiouracil (PTU)? which one is of most concern?
- skin rash (common)
- agranulocytosis - rare drop in WBC that presents as fever/infection after starting the drug, possible aplastic anemia - most concerning side effect
- hepatotoxicity
which hyperthyroid drug should NOT be used in pregnant women?
methimazole (inhibits TPO) - teratogen, associated with congenital malformations
however ionizing thyroid ablation is also not safe, so propylthiouracil (PTU) often used during early pregnancy
how are the following used in the treatment of thyroid storm?
a. propranolol
b. thionamides
c. SSKI (saturated solution of potassium iodide)
d. steroids
a. propranolol (beta blocker): treats tachycardia but also is weak inhibitor of 5’-deiodinase, blocking T4–>T3 conversion
b. thionamides: methimazole blocks TPO, PTU blocks TPO + 5’-deiodinase
c. SSKI (saturated solution of potassium iodide): iodide load shuts down T4 production via Wolff-Chaikoff effect
d. steroids: reduce T4–>T3 conversion, suppress autoimmune damage, treat possible concomitant adrenal insufficiency (cortisol depleted in thyroid storm)
toxic multinodular goiter
nodules in thyroid that function independently, but usually have mutated TSH receptor so do not respond to TSH
if only 1 nodule, it’s called toxic adenoma
tx: radioactive iodine or surgery
how can radioactive iodine be used to distinguish between toxic multinodular goiter and cancer?
toxic multinodular goiter: nodules in thyroid that function independently, do not respond to TSH but continually produce thyroid hormone
thyroid (“hot”) nodules will take up radioactive iodine to make thyroid hormone, while cancer “cold” nodule) will not
much higher doses of radioactive iodine can also be used for thyroid ablation
Jod-Basedow phenomenon
iodine-induced hyperthyroidism, occurs in regions of iodine deficiency - many of these patients probably have toxic adenomas already
can also occur when patients with toxic adenomas (in non-deficient regions) are given drugs with high iodine content, expectorants (contain potassium iodide), CT contrast dye, or amIODarone (class III anti-arrhythmic)
A patient on your floor being treated for a toxic adenoma of the thyroid developed a cold. They were given an expectorant for their symptoms. Soon after, they develop symptoms of hyperthyroidism, despite their condition being well-controlled before. What is going on?
Jod-Basedow phenomenon: iodine-induced hyperthyroidism, seen in patients with toxic adenomas (thyroid nodules) who are exposed to high levels of iodine
many expectorants contain potassium iodide
type I vs type II amiodarone-induced hyperthyroidism
amIODarone: class III antiarrhythmic, contains 2 iodine atoms
type I: occurs in patients with pre-existing thyroid disease, iodine input results in excess hormone production
type II: direct toxic effect of the drug causes destructive thyroiditis which leads to release of T4/T3 (without increased hormone synthesis), can occur in patients without pre-existing illness
[note amiodarone can also cause hypothyroidism via Wolff-Chaikoff effect]
where is “endemic goiter” most common?
aka iodine deficiency, constant elevation in TSH results in enlarged thyroid (goiter)
common in mountainous areas, where iodine is depleted from the environment via water run-off
what chemical used in psychiatry is a known goitrogen?
goitrogens: substance that inhibit thyroid hormone production
[most common is iodine via Wolff-Chaikoff effect]
lithium also has this effect (used in psychiatry)
name 2 foods that are known goitrogens?
goitrogens: substance that inhibit thyroid hormone production
[most common is iodine via Wolff-Chaikoff effect]
cassava and millet are foods that have this effect
explain how amiodarone can cause hypothryoidism, aside from the ways it can cause hyperthyroidism (type I and II)
amIODarone contains 2 iodine atoms (class III anti-arrhythmic)
excess iodine can induce Wolff-Chaikoff effect (suppression of thyroid hormone synthesis, protective measure) - normal patients “escape” in a few weeks, but patients with pre-existing subclinical thyroid disease may have “failure to escape”
amiodarone also mimics T4 —> competitively inhibits 5’-diodinase (converts T4 to T3)
most common cause of non-dietary hypothyroidism
Hashimoto’s thyroiditis (chronic autoimmune thyroiditis): lymphocytes attack thyroid gland, associated with HLA-DR5
what are the histological findings of Hashimoto’s thyroiditis? (3)
- massive lymphocytic infiltrate - may form germinal centers
- Hurthle cells - enlarged eosinophilic follicular cells
- anti-TPO or anti-thyroglobulin antibodies - uninvolved in pathology, but can be measured
what do the following findings indicate:
- symptoms of hypothyroidism
- thyroid biopsy shows germinal centers and Hurthle cells
- genetic analysis shows HLA-DR5
Hashimoto’s thyroiditis (chronic autoimmune thyroiditis): lymphocytes attack thyroid gland, most common non-dietary cause of hypothyroidism
Hurthle cells - enlarged eosinophilic follicular cells
patients with Hashimoto’s thyroiditis are at an increased risk for developing what kind of cancer?
Hashimoto’s thyroiditis (chronic autoimmune thyroiditis): lymphocytes attack thyroid gland, most common non-dietary cause of hypothyroidism
increased risk of non-Hodgkin B cell lymphoma (this makes sense given lymphocytes are involved in the pathology)
de Quervain’s thyroiditis
aka granulomatous or subacute thyroiditis: granulomatous inflammation of the thyroid, presents with tender / enlarged thyroid, occurs in young women
usually resolves in a few weeks
Pt is a 23yo F presenting with concerns about tenderness in her neck. Upon palpitation, you note an enlarged thyroid gland. Upon questioning, pt denies any symptoms of hypothyroidism. She is worried it’s cancer. What will you tell her?
most likely granulomatous or subacute or de Quervain’s thyroiditis: granulomatous inflammation of the thyroid, presents with tender / enlarged thyroid, occurs in young women
usually resolves in a few weeks
Riedel’s thyroiditis
“rock hard” thyroid due to fibroblast activation —> collagen deposition
associated with IgG4 plasma cells
often extends beyond thyroid to parathyroids (hypoparathyroidism), recurrent laryngeal nerve (hoarseness), and trachea (difficulty breathing)
Pt is presenting with difficulty breathing and hoarseness. Upon palpitation, you note a “rock hard” thyroid. Biopsy shows IgG4 plasma cells. What is your diagnosis?
Riedel’s thyroiditis: fibroblast activation —> collagen deposition, associated with IgG4 plasma cells
often extends beyond thyroid to parathyroids (hypoparathyroidism), recurrent laryngeal nerve (hoarseness), and trachea (difficulty breathing)
what causes “painless thyroiditis”?
aka lymphocytic thyroiditis: variant of Hashimoto’s - lymphocyte infiltration of thyroid gland, but self-limited and resolves in a few weeks
causes transient hyperthyroidism, sometimes followed by hypothyroidism
