Thyroid Pathology Flashcards
1
Q
What are two conditions that can develop as a result of developmental issues and/or remnants of the thyroid?
A
- thyroglossal duct cyst and lingual thyroid
- the thyroid develops at the bast of the tongue and then travels along the thyroglossal duct to its final spot in the anterior neck
- thyroglossal duct cyst: cystic dilation of the thyroglossal duct remnant causes an anterior neck mass
- lingual thyroid: persistence of thyroid tissue at the base of the tongue that presents as a mass on the base of the tongue
2
Q
What are the major symptoms of hyperthyroidism? What is the most common cause of hyperthyroidism?
A
- (most common cause is Graves disease)
- most symptoms are related to the elevated basal metabolic rate (BMR; increased Na+-K+-ATPase) and elevated sensitivity to sympathetic activity (because of increased B1-receptors)
- weight loss despite appetite increase, heat intolerance, sweating, tachycardia, increased cardiac output, hyperreflexia, tremor, anxiety, staring gaze with lid lag, diarrhea, weakness
- hyperglycemia may develop as well (because T3/T4 increases gluconeogenesis and glycogenolysis)
3
Q
What is Graves disease? How do patients commonly present?
A
- Graves disease is the most common cause of hyperthyroidism
- an autoimmune disease with IgG antibodies that stimulate TSH-receptors on the thyroid, resulting in excess T3/T4 production (type II HSR)
- patients present with hyperthyroidism (increased BMR and sympathetic activity); diffuse goiter; exophthalmos/proptosis and pretibial myxedema
- classic triad: thyrotoxicosis, infiltrative ophthalmopathy, and localized infiltrative dermopathy
4
Q
Explain the findings of exophthalmos and pretibial myxedema in patients with Graves disease.
A
- fibroblasts in the eyes and in the shins actually contain TSH receptors
- the auto IgG antibody therefore stimulates these cells to secrete glycosaminoglycans (mainly hyaluronic acid) and other connective tissue components, which cause swelling and protrusion of the eye (proptosis) and shin with a dough-like consistency
- although ocular involvement occurs in all patients with hyperthyroidism (lid lag, stare), exophthalmos/proptosis (and inflammation) are unique to Graves disease
- note that myxedema is actually synonymous with HYPOthyroidism, because it is highly associated with hypothyroidism (less so with hyperthyroidism - only really occurs in Graves disease in the shins)
5
Q
What is a major complication of Graves disease and what do patients develop? How do we treat Graves disease?
A
- major complication is a “thyroid storm”: massive amounts of T3/T4 are produced as a result of raised catecholamine levels due to stress; patient develops severe arrhythmia (major sign is severe tachycardia), hyperthermia, vomiting, and hypovolemic shock
- treat Graves disease with beta-blockers (to block the excessive sympathetic activity) and thyroid ablation; PTU or Methimazole (these are thioamides that inhbit thyroid peroxidase)
6
Q
What is a multi-nodular goiter? What is it due to? How do patients present? Does it cause hypo- or hyperthyroidism?
A
- multi-nodular goiter is an enlarged thyroid gland with multiple nodules
- it develops most commonly due to iodine deficiency and reflects impaired synthesis of thyroid hormones
- patients present with a nodular mass in their neck; if large enough, the goiter can cause mass effect compression of airway, esophagus, SVC, etc.
- majority of these are non-toxic, but some can become toxic (meaning that they can secrete T3/T4 without TSH regulation; hyperthyroidism can occur in this setting)
7
Q
What do we see on histology in Graves disease? What is this pattern called? What will the lab results reveal?
A
- histo: hypertrophy and hyperplasia of follicles with an empty space between the follicular cells and the colloid; this pattern is known as “scalloping of the colloid”
- lab: T3/T4 will be elevated and TSH will be reduced, presence of TSHRs (TSH-receptor stimulating) antibodies
8
Q
What are the major symptoms of hypothyroidism? What is it also known as? What are the major causes?
A
- hypothyroidism results in weight gain despite decreased appetite, cold intolerance, hypoactivity/lethargy, constipation, hyporeflexia, proximal muscle myopathy and weakness (raised serum creatine kinase), mental sluggishness, bradycardia, dry brittle hair with loss of outer 1/3 eyebrow, and myxedema (largely in the face and periorbital regions to cause a “tragic facial expression”)
- AKA myxedema (the two were classically synonymous); “myxedema coma” is an acute decompensated hypothyroidism sparked by a precipitating event and is a medical emergency
- caused by iodine deficiency and thyroiditis (main one being Hashimoto’s)
9
Q
What is hypothyroidism in infants/young children known as? How do patients present?
A
- known as cretinism
- results in severe mental and physical retardation, coarse facial features, enlarged tongue, and umbilical hernia
- look for the 6 P’s: Pot-bellied, Pale, Puffy-face, Protruding umbilicus, Protuberant tongue, and Poor brain development
10
Q
What are the three main types of thyroiditis? How can we tell each apart on clinical examination?
A
- Hashimoto’s thryoiditis: non-tender thryoid
- subacute granulomatous thyroiditis: very tender thyroid
- Reidel fibrosing thyroiditis: non-tender, but fixed and very hard/rock-like
11
Q
What is Hashimoto’s thyroiditis? Which two things is it associated with? How do patients present?
A
- Hashimoto’s thyroiditis (AKA chronic lymphocytic thyroiditis) is the number one cause of hypothyroidism in areas with sufficiency iodine; it is autoimmune related (antibodies target and destroy TSH receptors and T-cell mediated damage; types II and IV HSRs)
- it is associated with HLA-DR5 and also with an increased risk of non-Hodgkin lymphoma
- patients classiclly present with an initial bout of hyperthryoidism (because the follicles rupture from the inflammation) followed by hypothyroidism and a moderately enlarged non-tender goiter
12
Q
What lab findings do we see in Hashimoto’s thyroiditis? What about on histology?
A
- lab: lowered T3/T4 levels, raised TSH levels; anti-TPO (thyroid peroxidase) antibodies, anti-thyroglobulin antibodies, TSH receptor blocking antibodies
- histo: chronic inflammation, germinal centers of lymphoid aggregate, Hurthle cells (follicular epithelial cells with pink cytoplasm)
13
Q
What is subacute granulomatous thyroiditis? What is it also known as? How do patients present?
A
- AKA de Quervain thyroiditis
- this is a self-limiting (no treatment needed) thyroiditis that often follows a viral URTI
- patients present with a very tender thyroid (this is the only major thyroiditis that presents with tenderness), jaw pain, and with transient initial hyperthyroidism (it does NOT progress to permanent hypothyroidism because of its self-limiting nature)
14
Q
What lab findings do we see in subacute granulomatous thyroiditis (de Quervain)? What about on histology?
A
- lab: raised ESR, normal or transiently high T3/T4, normal (or transiently low) TSH
- histo: granulomatous inflammation (granulomas/multi-nucleated giant cells)
15
Q
What is Riedel thyroiditis? How do patients present? What is a major differential diagnosis for this disease?
A
- Riedel thyroiditis is characterized by chronic inflammation and the thyroid being replaced by fibrous tissue
- patients present with a fixed, hard (rock- or wood-like), non-tender goiter, and hypothyroidism
- major DDx: anaplastic carcinoma because the fibrosis can rapidly extend to and involve local structures (this has a very poor prognosis, so we definitely want to rule it out!); it mainly occurs in older patients, while Riedel thyroiditis occurs mainly in younger patients
