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228 Cards in this Set

  • Front
  • Back
at what day in utero does formation of the thyroid start, and what happens?
day 24 - evagination of the tongue base - descends in the midline of the neck forming the thyroglossal duct
what happens to the thyroglossal duct?
involutes prior to birth
what is the thyroid gland like morphologically?
two lobes conneted by an isthmus
what % have a pyramidal lobe?
what things may be left along the course of descent of the thyroid gland (3)?
1) aberrant thyroid gland; 2) ectopic thyroid tissue; 3) thyroglossal duct cysts/sinus tracts
where may aberrant thyroid glands be (2)?
1) lingual; 2) subhyoid
what may happen to thyroglossal duct cysts/sinus tracts (2)?
1) infection; 2) rarely cancer
what other unusual thing can happen in development of the thyroid gland?
excessive descent --> substernal thyroid
what are lobes divided into, and what are these divisions composed of?
thyroid gland is divided into lobules composed of follicles, where hormones are produced and stored
besides T3 and T4, what hormone is produced in the thyroid, and where?
parafollicular or C cells synthesize and secrete the hormone calcitonin
what is the name of T3, and the name of T4?
T3 - triiodothyronine; T4 - thyroxine
by what process are T3 and T4 formed (what reaction on what molecule?
post-transcriptional iodination of thyroglobulin
at what specific location do iodination and coupling reactions occur?
luminal cell membrane of follicular cells
in what form is the hornome stored?
as colloid
in what form is most T3 and T4 in circulation?
bound to plasma proteins (TBG, transthyretin, albumin, pre-albumin) for transport
what type of receptors do T3 and T4 interact with, and what is the result?
they interact with nuclear receptors in peripheral tissues --> increase in basal metabolic rate
what is T3 and T4 formation controlled by, and where does it come from?
T3, T4 formation controlled by TSH released from anterior pituitary in response to trophic factors from the hypothalamus
how are TRH and TSH levels controlled?
negative feedback from T3, T4
what type of enlargement is a goiter, and what is it secondary to?
hyperplastic enlargement of the thyroid secondary to impaired T3, T4 synthesis
what does the impaired synthesis of T3, T4 lead to?
increased TSH levels, which cause hypertrophy and hyperplasia of follicular cells
what classes of goiters are there (2)?
1) diffuse non-toxic (simple) goiter; 2) multinodular goiter
what part of the gland does diffuse non-toxic goiter involve?
what are the two forms of diffuse non-toxic goiter, and which is more common (bold)?
1) endemic; 2) sporadic
when is simple goiter endemic?
when it is present in more than 10% of the population
what causes endemic goiter (2)?
1) low levels of iodine in soil, water, diet; 2) goitrogens in diet
what sex/age is most likely to get sporadic goiter?
young adult female
what causes it (2)?
1) ingestion of substances that interfere with hormone synthesis; 2) hereditary enzymatic defects
how are these defects inherited?
autosomal recessive
what is the goiter called, when it is hereditary?
dyshormogenetic goiter
in most cases, what is the cause of sporadic goiter?
in most cases, cause not apparent
what happens in multinodular goiter?
recurrent hyperplasia and involution
what does this lead to?
irregular enlargement with nodules and cysts
what happens secondary to rupture of cysts, follicles, and vesicles (3)?
1) hemorrhage; 2) scarring; 3) calcifications
what type of problems do goiters cause in the neck?
mass effect compressing neck structures
how do they relate to neoplasms?
they can mask or mimic neoplasms
how do most goiters affect hormone deficiency, and what is the term for this?
most are euthyroid - the increase in mass overcomes hormone deficiency
what problem happens in a minority of goiters related to hormone production and what is this called?
Plummer's syndrome - a minority develop hyperfunctioning nodule, resulting in toxic multinodular goiter
hwo does this syndrome differ from Graves disease?
this syndrome does not have the skin and eye changes of Graves disease
how often are goiters associated with hypothyroidism?
what is the most common cause?
hyperfunctioning of the gland
what else can cause it (2)?
1) ingestion of exogenous substances (Synthroid, iodide); 2) leakage of hormone from non-hyperactive gland
what various organ systems does thyrotoxicosis affect (6)?
1) cardiac; 2) neuromuscular; 3) dermatologic; 4) GI; 5) ocular; 6) skeletal
what are the cardiac effects (5)?
1) tachycardia; 2) palpitiations; 3) arrhythmias (A-fib); 4) cardiomegaly; 5) CHF
what neuromuscular problems are caused by thyrotoxicosis (list - one bold term we definitely must know, plus others)?
hyperreflexia, tremors, hyperactivity, anxiety, poor concentration, forgetfulness, insomnia, proximal muscle weakness, wasting
what dermatologic problems are caused by thyrotoxicosis (list - one bold term we definitely must know, plus others)?
heat intolerance, warm/moist/flushed skin with increased sweating, hyperpigmentation, acropathy (thick fingers and toes)
where is there hyperpigmentation?
over extensor surfaces
what problems are caused in the gastrointestinal system (3)?
1) increased gut motility; 2) increased appetite; 3) overeating
what happens to weight?
weight loss despite increased food intake
what causes ocular problems?
sympathetic overstimulation
what pocular problems are caused (3)?
1) wide, staring gaze; 2) lid lag
what problems are caused in the skeleton (2)?
1) osteoporosis; 2) increased fractures
what is the most common cause of thyrotoxicosis, and what % of cases does this account for?
diffuse toxic hyperplasia (Graves disease) - 85% of cases
what are other common causes (2)?
1) toxic multinodular goiter (Plummer's syndrome); 2) toxic adenoma
what are what are three uncommon causes we must know?
1) choriocarcinoma/hydatidiform mole (extrathyroidal uterine/ovarian neoplasms); 2) TSH-secreting pituitary adenoma (rare); 3) struma ovarii (ovarian teratoma with ectopic thyroid)
how can neonates get thyrotoxicosis?
associated with maternal graves disease
can thyroiditis and/or thyroid carcinoma cause thyrotoxicosis?
what does primary thyrotoxicosis mean?
abnormality of gland itself
what drugs can be used to treat thyrotoxicosis (4)?
1) beta blockers; 2) propylthiouracil; 3) methimazole; 4) iodide (paradoxically)
what other treatments can be used (2)?
1) radioiodine ablation; 2) surgery
what type of disorder is Graves disease?
what three things does it induce?
1) thyrotoxicosis with diffuse hyperplasia of gland; 2) ophthalmopathy; 3) sometimes dermopathy
why is the eye pushed forward (3)?
1) fatty infiltration; 2) deposition of hydrophilic mucopolysaccharides; 3) periorbital edema
why is there lid retraction?
swollen and fibrotic extraocular muscles
what does incomplete closure of the eye lead to (2)?
1) keratitis; 2) corneal ulceration
what can happen to the optic nerve?
what type of immune reaction is Graves disease mediated by?
T cell mediated autoimmune phenomenon - immune reaction against thyroid follicular antigens that are also found in retro-orbital space
what is the dermopathy termed, and where doesit generally occur?
usually occurs ove shins or feet, and is termed "pretibial myxedema"
why is pretibial myxedema a confusing term?
because myxedema is usually associated with hypothyroidism
what happens to the skin, and why?
becomes thickened and indurated because of thickening of the dermis by deposition of glycosaminoglycas and ilymphocyte infiltration
what problems are unique to Graves disease (3)?
1) diffuse hyperplasia; 2) ophthalmopathy; 3) dermopathy
what is the female to male ratio in Graves disease?
7 to 1
what HLA alleles is Graves disease associated with (2)?
1) B-8; 2) DR-3
what etiological agent is found in the serum of patients with Graves disease (name and what they are)?
TSI - thyroid stimulating immunoglobulin - they are IgG immunoglobulins that bind to TSH receptors, stimulate adenyl cyclase activity, and increase release of thyroid hormonses
what are the possible courses of symptoms (2)?
1) wax and wane; 2) lead to thyroid storm (medical emergency if untreated)
what are drugs used for thyrotoxicosis (2)?
1) propylthiouracil; 2) methimazole
what are other treatments (2)?
1) radioiodine; 2) surgery
what are the three classes of hypothyroidism?
1) primary (gland); 2) secondary (pituitary or hypothalamic); 3) tertiary/central (hypothalamic disease)
what happens if hypothyroidism is present in infancy?
what is this manifested by (5)?
1) short stature; 2) retardation; 3) coarse facial features; 4) protruding tongue; 5) umbilical hernia
what can be done about this?
preventable if treated early
what happens if thyroid deficiency occurs during early fetal development (3)?
1) deaf-mutism; 2) spasticity; 3) severe mental retardation
what can cause thyroid deficiency during early fetal development (3)?
1) thyroid agenesis; 2) severe iodine lack; 3) congenital biosynthetic defect
what is hypothyroidism termed in an older child or adult?
what is the most characteristic sign of myxedema?
cold intolerance
what happens to reflexes?
where is hair lost, particularly?
especially on the outer third of eyebrows
what type of edema is there and where?
peri-orbital, peripheral non-pitting edema
what color does skin turn, and why?
yellow, secondary to sluggish conversion of carotenes to vitamin A in the intestine
what can happen to the voice?
what can happen to the GI system?
what can happen to the heart?
what are other symptoms of myxedema (list)?
fatigue, depression, lethargy, weight gain, low body temperature
what can severe hypothyroidism cause?
myxedema coma
what is it characterized by (5)?
1) loss of consciousness, ; 2) hypothermai; 3) hypoventilation; 4) sever bradycardia; 5) pericardial effusion
what is it difficult to be distinguished from?
addisonian crisis
how may it be treated emergently?
administer synthroid and cortisone
what are the three classes of causes of hypothyroidism?
1) insufficient thyroid parenchyma; 2) niterference with thyroid hormone synthesis; 3) suprathyroidal
what are four causes of insufficient thyroid parenchyma?
1) developmental; 2) surgical ablation; 3) radiation injury; 4) Hashimoto thyroiditis
what are four causes of niterference with thyroid hormone synthesis?
1) thyroid hormone resistance syndrome; 2) congenital biosynthetic defects (dyshormonogenetic goiter); 3) drugs; 4) autoimmune disorders
how is thyroid hormone resistance syndrome inherited?
autosomal dominant
what drugs can cause interference with thyroid hormone synthesis (3 examples)?
1) lithium; 2) iodides; 3) p-aminosalicylic acids
what types of suprathyroidal causes are there (2)?
1) pituitary lesions reducing TSH secretion; 2) hypothalamic lesions that reduce TRH delivery
what is an example of a pituitary lesion that reduces TSH secretion?
Sheehan's syndrome
what is the most common cause of primary hypothyroidism, in iodine-sufficient areas of the world?
Hashimoto's thyroidits
what types of thyroiditis are there (5 main)?
1) chronic autoimmune/Hashimoto's; 2) subacute granulomatous/DeQuervain thyroiditis; 3) subacute lymphocytic (painless) thyroiditis; 4) palpation thyroiditis; 5) Reidel's thyroiditis
what is the female predominance of Hashimoto's thyroiditis?
20 to 1
what HLA alleles is Hashimoto's associated with (2)?
1) DR-5; 2) DR-3
what is the pathogenesis of Hashimoto's?
sensitization of CD4+ T-helper cells to thyroid antigens
what does this lead to (2) and what part of the thyroid is attacked?
1) uncontrolled attack on follicular epithelium by cytotoxic T cells; 2) T-helper cell participation in B cell formation of autoantibodies
what is the most important type of antibodies are present, and what do they do?
TSH receptor antibodies are present that block the receptor
what are other autoantibodies directed against (3)?
1) thyroglobulin; 2) thyroid peroxidase; 3) iodine transporter
what should be remembered about gland enlargement in Hashimoto's?
it is painless
what can form in Hashimoto's and what does this raise suspicion of?
nodules can form, raising suspicion of neoplasm
what particular cells are seen in histology in Hashimoto's, and what are they?
Hurthle cells (follicle cells with abundant granular cytoplasm)
what else are seen in histology (2)?
1) lymphoplasmacytic infiltrates; 2) lymphoid follicles with germinal centers
what happens to thyroid hormone levels in early stages of Hashimoto's, and why?
transient thyrotoxicosis - follicles destroyed with release of hormone
what happens later?
hormones fall and hypothyroidism develops
what are patients at an increased risk for developing (2)?
1) B cell lymphomas; 2) other autoimmune diseases
what does subacute (granulomatous, DeQuervain) thyroiditis often follow?
upper respiratory viral infections (mumps, influenza, cocksakie, measles, others)
what is the course of this disease?
inflammation followed by period (2-8 weeks) of hypothyroidism, then complete recovery
what is gland like?
tender and enlarged, with pain on swallowing that radiates to upper neck, ears
what other symptoms may be present?
constitutional - malaise, anorexia, myalgia, fever
what is seen on histology (2), and what do they resemble?
aggregates of giant cells and macrophages, resembling granulomas
what is the cause and time course of subacute lymphocytic (painless) thyroiditis?
idiopathic, self-limited
what may it present like (2)?
1) symptomless; 2) thyrotoxicosis
what may it progress to in a minority of cases?
who is subacute lymphocytic (painless) thyroiditis most common in?
post-partum females
is there a risk of recurrence?
yes, following subsequent pregnancies
what two things were said not to be commonly seen in subacute lymphocytic thyroiditis?
1) fibrosis; 2) Hurthle cell metaplasia
what is palpation thyroiditis like on histology?
similar to subacute granulomatous
what is the cause of palpation thyroiditis?
vigorous palpation of the thyroid gland with mechanical disruption of follicles
is there any abnormality in thyroid function in palpation thyroiditis?
what is Riedel's thyroiditis, and how common is it?
rare form of fibrosing thyroiditis
where does fibrosis occur?
destructive fibrosis extends from thyroid to structures of the neck
what is gland like?
hard, painless gland
what can this lead to (3)?
1) laryngeal nerve paralysis; 2) shortness of breath; 3) difficulty swallowing
what does this disease simulate?
what may Riedel's thyroiditis be associated with?
thyroiditis elsewhere in the body
what can cause other thyroiditides (3)?
1) fungi; 2) blood-borne bacteria; 3) pneumocystis carinii in immunocompromised patients
how common are thyroid nodules, and what type are most (2)?
very common - most are 1) non-neoplastic (goitorous); 2) benign neoplasms (follicular adenomas)
what types of nodules are more likely to be neoplastic (3)?
1) solitary nodules; 2) nodules in younger patient; 3) nodules in males
what type of nodules are more likely to be benign?
hot nodules - those that take up radioiodine
what is associated with an increased risk of thyroid canceR?
history of radiation
what is the first diagnostic test performed on a thyroid nodule?
fine needle aspiration (rapid, relatively non-invasive, inexpensive)
what is the most common neoplasm?
follicular adenoma
what is it like (number, benign/malignant, encapsulation)?
benign, solitary, encapsulated
what is it like on radionuclide scanning?
what problem may is cause, rarely?
rarely hyperfunctional - toxic adenomas independent of TSH
what % of carcinomas are thyroid cancers?
what chromosomal rearrangements are said to be behind papillary carcinomas (2)?
1) RAS; 2) NTR k1
what forms of thyroid cancer are there (5)?
1) papillary carcinoma; 2) follicular carcinoma; 3) Hurthle cell neoplasm; 4) medullary carcinomas; 5) anaplastic carcinomas
what activating mutations are behind papillary carcinomas (2)?
1) BRAF; 2) RAS
what nuclear changes are behind follicular carcinomas?
1) RAS mutations; 2) PAX8-PPAR-gamma-1 fusion
what mutations are behind medullary carcinomas?
RET mutations
what mutations are behind anaplastic carcinoma?
inactivating point mutations in p53 suppressor gene
what is the most common form of thyroid cancer, what % of cancers does it account for, and who does it occur in (age, situation)?
papillary carcinoma - 75 to 85% of cases - most common in ages 20 to 40 and in patients with previous radiation exposure
is it encapsulated?
can be either encapsulated or infiltrating
what does it appear like histologically (shape of papillae, and other feature of them)?
complex branching papillae with fibrovascular cores
what do nuclei look like (3 features)?
1) optically clear "Little Orphan Annie Eye" nuclei; 2) intranuclear inclusions; 3) nuclear grooves
what other structures are seen in paplillary carcinoma (name and composition)?
psammoma bodies (concentrically calcified structures)
where do papillary carcinomas metastasize to?
regional lymph nodes
what type of growth do most papillary carcinomas exhibit, and what is the overall 10 year survival?
most exhibit indolent growth, and the overall ten year survival is over 95% - but prognosis depends on age and state of the disease
what variant of papillary carcinoma occurs that is more aggressive, and who does it occur in?
tall cell variant occurs in older patients, and is very aggressive
who is the prognosis best in?
children and young adults
what is the general treatment?
total thyroidectomy followed by radioiodine therapy
what is the second most common form of thyroid carcinoma, and what % of cases does it account for?
follicluar carcinoma - 10 to 20% of cases
what do lesions look like, and what are they difficult to distinguish from?
well-differentiated, encapsulated lesions are difficult to distinguish from follicular adenomas
what is the histologic criteria for follicular carcinoma (2 things it must invade)?
1) invasion of capsule/surrounding parenchyma; 2) vascular invasion (vessels in or beyond capsule)
where does follicular carcinoma metastasize to?
hematogenously, to bone, lungs, and brain
what is the treatment for follicular carcinoma?
total thyroidectomy followed by radioiodine therapy
what do Hurthle cell carcinomas behave like?
the same as non-Hurthle cell follicular adenomas and carcinomas - they are diagnosed using the same criteria (capsular and vascular invasion) as well
what are Hurthle cells like (what cells do they come from, and what do they look like)?
follicular cells with abundant granular cytoplasm
what % of thyroid carcinomas are medullary carcinomas, and what are they derived from?
5% - they are derived from parafollicular cells or C cells
what do these cells secrete?
in what setting do 20% of the cases occur in (3)?
1) MEN IIA; 2) MEN IIB; 3) familial tumors without associated MEN syndrome - most cases, though, are sporadic
what else occurs in MEN IIA (3)?
1) parathyroid hyperplasia; 2) parathyroid adenomas; 3) pheochromocytoma
what else occurs in MEN IIB (4)?
1) parathyroid hyperplasia; 2) pheochromocytoma; 3) Marfanoid habitus; 4) mucocutaneous ganglioneuromas
what type of mutations are seen in MEN IIA and MEN IIB syndrome?
germline mutations in RET proto-oncogene
what mutations are seen in nonfamilial (sporadic) medullary carcinomas?
RET mutations
are sporadic cases more likely in younger or older patients?
sporadic - older patients; MEN II - younger
what are cells like histologically in medullary carcinoma (2 possible shapes, something seen inside)?
rounded or spindled, with stippled chromatin
are medullary tumors encapsulated?
what other feature is seen in medullary carcinomas, histologically, and what is it compsed of/derived from?
amyloid tumor stroma (calcitonin derived)
what happens to this stroma when polarized?
it is CongoRed positive with apple-green birefringence when polarized
in what way unique to thyroid cancer may medullary carcinoma present?
paraneoplastic syndrome
what may these tumors release (4)?
1) CEA; 2) somatostatin; 3) serotonin; 4) vasoactive intestinal peptide
what are calcitonon and calcium levels like?
although calcitonin is elevated, hypocalcemia is not a prominent feature
what can MEN associated cases be masked by?
clinical manifestations from associated parathyroid lesion or pheochromocytoma
what should relatives of patients with medullary thyroid carcinoma be screened for (2)?
1) elevated calcitonin levels due to C cell hyperplasia; 2) RET mutation
what is a major precursor to medullary carcinoma in MEN IIA, and what is indicated?
C cell hyperplasia - thyroidectomy is indicated
what can serve as a good tumor marker for medullary thyroid cancer?
which types of medullary CA are aggressive tumors (2) and what is the five year survival rate?
1) those associated with MEN IIB; 2) sporadic cases - these are both aggressive with a 5 year survival rate of 50%
what medullary carcinomas are often indolent?
familial medullary carcinomas that are not associated with MEN
where do medullary carcinomas metastasize?
through bloodstream (bone, liver, lung) or to lymph nodes
what is the treatment for medullary carcinoma?
surgical excision and not radioactive iodine, as C cells are neuroendocrine cells and do not have iodine transport
what % of thyroid carcinomas are anaplastic carcinomas?
what do they look like histologically?
undifferentiated neoplasms
who do they occur in, and what is the progression and prognosis?
occur in the elderly, are large locally invasive rapidly growing neck masses that are uniformally fatal with no effective therapy
what is survival after diagnosis?
less than one year
what features are seen in dedifferentiated tumors (2)?
1) loss of I131 uptake; 2) decreased synthesis of thyroglobulin
how common are sarcomas in the thyroid?
what other type of malignancies are common in patients with history of Hashimoto thyroiditis?
lymphomas - particularly non-Hodgkins B cell lymphomas