Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HMS Homeostasis II > Thyroid Physiology and Pathophysiology > Flashcards

Thyroid Physiology and Pathophysiology Flashcards

1
Q

Thyroid and parathyroid anatomy

A

Note the position of the four parathyroid glands, the vagus and recurrent laryngeal nerves, and the common carotid artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The thyroid is encased in . . .

A

. . . pretracheal fascia and therefore moves superiorly with swallowing, a feature that is useful during physical examination of the gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Arterial and venous supply of the thyroid

A

Note the redundancy in both arterial and venous supply, and also the location of the pretracheal lymph nodes inferiorly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Histologic appearance of thyroid tissue

A

The basic histological and functional unit of the thyroid is the thyroid follicle, which consists of cuboidal thyroid follicular cells arranged in a hollow sphere around a core of proteinaceous extracellular material called colloid

Follicular cells are oriented with their basolateral surface facing the interstitium, which contains blood vessels, and their apical surface facing the colloid into which they secrete thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Thyroglobulin

A

A protein that serves as the scaffold for synthesizing thyroid hormones.

Produced by follicular cells within the thyroid and secreted into the colloid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thyroid C-cells

A

aka parafollicular cells

Scattered throughout the thyroid interstitium between the follicles. C-cells secrete the hormone calcitonin, which can decrease serum calcium but has no clear role in normal human physiology.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thyroid embryology

A

The fetal thyroid begins as a thickening of the pharyngeal floor. Forms a diverticulum that descends caudally through the anterior neck. During this migration, a track called the thyroglossal duct is formed connecting the pharyngeal floor to the thyroid bed. This duct must then involute.

Begins to be functional at ~11-12 weeks.

Thyroid C-cells have a distinct embryologic origin in the ultimobranchial glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Thyroid dysgenesis

A

Deviation from the normal anatomic development of the thyroid.

Most common cause of congenital hypothyroidism. Thyroid may fail to generate, be hypoplastic, or fail to migrate down from the pharynx.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thyroglossal duct cysts

A

Congenital. Results from failure of the thyroglossal duct to involute during embryologic thyroid development.

May present as midline neck masses or become infected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dietary iodine absorption

A

Absorbed from the small intestine, and once in the circulation iodine is taken up by thyroid follicular cells via a specific sodium-iodide symporter (NIS). Expression of NIS is induced by TSH.

Under normal circumstances the thyroid has far greater avidity for iodine than any other tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sites of NIS expression

A

Generally, dietary iodine goes to the thyroid, where NIS expression is highest.

However, multiple other tissues express lower levels of NIS, including the salivary and lacrimal glands. NIS is also highly expressed in the lactating breast, where it transmits iodine from the mother to the breastfeeding infant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dietary iodine deficiency

A

Common in many parts of the world and results in hypothyroidism.

Resulting increase in TSH (a trophic factor for the thyroid) causes thyroid hypertrophy, which manifests clinically as goiter (thyroid enlargement).

When iodine deficiency occurs in infancy, the resulting hypothyroidism causes mental retardation, a condition known as endemic cretinism

Widespread iodization of salt is a public health measure that has virtually eliminated endemic cretinism in much of the developed world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Wolff-Chaikoff syndrome

A

Ingestion of excessive amounts of iodine results in hypothyroidism because supranormal concentrations of iodine within the follicular cell inhibit both thyroid hormone synthesis and the release of pre-formed thyroid hormone.

If excess iodine exposure persists, the normal thyroid will “escape” from the Wolff-Chaikoff effect and resume producing and releasing thyroid hormone within 3-7 days, so little if any clinical hypothyroidism occurs. However, this may not occur in neonates or patients with preexisting thyroid dysfunction. These patients may develop persistent hypothyroidism due to iodine excess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thyroid hormone synthesis

A

Iodide enters the follicular cell through the basolateral NIS and exits into the colloid through the apical anion channel pendrin. Iodine is then added to tyrosine residues on thyroglobulin, and shuffled around until T3 and T4 are produced, still bound to thyroglobulin. All of this is catalyzed by thyroperoxidase. T3 and T4 can then be released by proteolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Production of diatomic iodine in the colloid

A

Diatomic iodine is transiently produced through a two-step reaction with hydrogen peroxide generated by thyroid peroxidase.

Thyroid peroxidase then catalyzes the reaction of elemental iodine with tyrosine residues on thyroglobulin, adding one iodine atom with the other serving as an iodide leaving group.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MIT and DIT

A

Mono- and di-iodothyronine. Also produced, but not secreted from the colloid space. Instead the iodine just gets recycled in another cycle of T3/T4 production,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T3/T4 delivery

A

These hormones cannot circulate alone and must be bound to a chaperone, usually thyroxine-binding globulin, but sometimes albumin or pre-albumin. Only a tiny fraction of each hormone, less than 1%, is free and biologically active at any given moment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Total and free thyroxine

A

When interpreting thyroid function tests it is important to remember that abnormal binding protein levels can cause abnormal serum measurements of total T4 and/or total T3 even when free thyroid hormone concentrations are normal.

This is frequently the case for individuals taking estrogen contraceptives. Because estrogen potently increases thyroid binding globulin levels, such women have elevated total T4, but normal free T4 and TSH (since only unbound T4 can inhibit TSH production).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TRH regulation

A
  • Suppressed by thyroxine
  • Suppressed by starvation and systemic illness
  • Importantly, not suppressed by prolactin, even though TRH also stimulates prolactin release.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

TRH and prolactin

A

TRH also stimulates prolactin production, however prolactin does not inhibit TRH. Commonly, primary hypothyroidism leads to high levels of TRH and thus hyperprolactinemia. Hyperprolactinemia may then suppress FSH and TSH, resulting in hypogonadism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TSH and thyroxine mobilization

A

TSH binds and activates the TSH receptor on the basolateral membrane of thyroid follicular cells.

Activation of the TSH receptor stimulates thyroid hormone synthesis and release by increasing the expression and function of nearly all elements of this pathway, including NIS, TPO, and thyroglobulin. TSH is also a trophic factor for the thyroid, with excessive stimulation of the TSH receptor leading to hypertrophy of the thyroid gland, and inadequate TSH receptor action causing thyroid atrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TSH secretion is regulated primarily by. . .

A

. . . circulating free T4 levels.

small changes in free T4 produce large compensatory changes in serum TSH.

For this reason, serum TSH is the most sensitive test for diagnosing primary thyroid dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

___ is the most sensitive test for diagnosing primary thyroid dysfunction

A

Serum TSH is the most sensitive test for diagnosing primary thyroid dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

___ is the primary active thyroid hormone

A

T3 is the primary active thyroid hormone because it binds TRs with 15-fold greater affinity than T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is the thyroxine receptor located?

A

In the nuclei of target cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Deiodinase 1 and 2

A

Convert T4 to T3. About 80% of circulating T3 is produced by deiodination of T4, while 20% of circulating T3 is secreted directly by the thyroid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Deiodinase 3

A

Inactivates both T4 and T3 into the inactive metabolites reverse T3 (rT3) and T2, respectively

Reverse T3 is occasionally measured clinically to assess for excessive inactivation of thyroid hormone as a cause of hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Effects of thyroxine on the cardiovascular system

A
  • Increased heart rate
  • Increased contractility
  • Increased relaxation (lusitropic effect)
  • Peripheral vasodilation
  • Increased renal sodium and water excretion
  • Net effect: Increased systolic blood pressure, decreased diastolic blood pressure, widened pulse pressure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hypothyroidism vs thyrotoxicosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Thyroid function and pregnancy

A

hCG weakly cross-reacts with the TSH receptor, resulting in increased total T4 production during pregnancy.

However, free T4 levels are only slightly increased due to a marked rise in TBG levels that is induced by increased circulating estradiol.

This slight increase in free T4 feeds back to mildly suppress TSH to slightly below the nonpregnant reference range. Thus, laboratory pattern of mild subclinical hyperthyroidism is normal in the first trimester of pregnancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

THBR and free T4 index

A

It can be hard to interpret thyroid hormone levels in the context of other severe or chronic diseases. In these cases, a thyroid hormone binding ratio test may be performed and these values may be used to calculate a T4 index, which is an estimate of the free T4 concentration that can be more helpful in these patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Euthyroid sick syndrome

A

Term used to describe a typical pattern of transient derangement of serum thyroid function tests found in up to 75% of hospitalized patients in the absence of true thyroid disease. The classic pattern of nonthyroidal illness is low T3, normal or low T4, and normal or low TSH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Serum thyroglobulin

A

Produced by follicular cells, as an indicator of the presence and activity of thyroid tissue

Think of it like ferritin for iron studies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Thyroid Radioiodine Uptake and Scanning

A

Administer an oral dose of radioactive iodine and the percent of radiation retained in the thyroid is measured after 4 or 24 hours.

Because iodine uptake depends on the amount of iodine already in the gland, normal ranges vary among geographic regions based on iodine sufficiency. Euthyroid individuals can have low uptake if they are iodine replete. It is important to take into account a patient’s serum TSH when performing and interpreting radioiodine imaging.

Images may be obtained with a detector camera to localize any functional thyroid tissue, including ectopic thyroid tissue.

35
Q

Thyroid Ultrasound

A

Ultrasound is a noninvasive tool that can quantify thyroid size and assess gland vascularity. It is the optimal modality to diagnose and monitor thyroid nodules, and when appropriate, to guide fine-needle aspiration of thyroid nodules.

36
Q

Hypothyroidism origin

A

Inadequate action of thyroid hormone at the tissue level. Most common thyroid disorder, at 5% global prevalence.

Can arise from a secretory defect in thyroid itself (primary hypothyroidism) or in the hypothalamus or pituitary (secondary or central hypothyroidism). A rare form of hypothyroidism is accelerated degradation of circulating thyroid hormone at a rate that exceeds the synthetic capacity of the normal thyroid gland (consumptive hypothyroidism)

37
Q

Diagnosing hypothyroidism

A

Serum TSH and free T4 should be measured when hypothyroidism is suspected. Serum TSH is elevated in all patients with primary hypothyroidism; in more severe cases, serum free T4 is low. Patients with TSH elevation but free T4 still within the normal range are said to have subclinical hypothyroidism.

38
Q

Causes of primary hypothyroidism

A
  • Hashimoto’s thyroiditis: Lymphocytic infiltration of the thyroid parenchyma and destruction of follicular thyroid cells. Autoantibodies to thyroperoxidase (TPO) and/or thyroglobulin are causative (Type II Hypersensitivity). Patients with autoimmune thyroiditis often have an enlarged thyroid that may feel firm and irregular. This is primarily due to edema and fibrosis
  • Medications (lithium, amiodarone, tyrosine kinase inhibitors, IFN-a)
  • Iodine deficiency
  • Post-partum thyroiditis
  • Transient post-viral thyroiditis
  • Congenital hypothyroidism
39
Q

Secondary hypothyroidism causes

A

Most often due to acquired lesions of the hypothalamus or pituitary, usually from damage caused by tumor, trauma, surgery, therapeutic irradiation, autoimmune hypophysitis, or infiltrative disease (such as histiocytosis or sarcoidosis).

Secondary hypothyroidism is usually accompanied by other pituitary hormone deficiencies, so other pituitary axes should be tested and pituitary imaging obtained when a diagnosis of secondary hypothyroidism is confirmed.

40
Q

Consumptive hypothyroidism

A

Accelerated degradation of circulating thyroid hormones by tumors (such as gastrointestinal stromal tumors and infantile hemangiomas) that express very high levels of type 3 deiodinase (D3)

Have elevated serum rT3 and DIT

41
Q

Causes of thyrotoxicosis

A
  • Divided into those caused by hyperthyroidism and those not
  • With hyperthyroidism: Graves disease, TSH-secreting pituitary adenomas, “autonomous” thyroid tissue (aka toxic thyroid nodules)
  • Without hyperthyroidism: Levothyroxine overdose, transient thyroiditis (damage to thyroid releasing pre-formed T3/T4 from the colloid)
42
Q

Thyroid storm

A

Most severe clinical form of thyrotoxicosis, presenting with extreme tachycardia, hypertension, fever, GI disturbance, and altered mental status.

Thyroid storm is an endocrinologic emergency and has a high mortality rate if not treated aggressively.

43
Q

Grave’s disease

A

Type II hypersensitivity. Autoantibodies bind and stimulate the TSH receptor, leading to thyroid gland hyperfunction and hypertrophy. Has some overlap with Hashimoto’s thyroiditis, as some patients also have TPO and thyroglobulin autoantibodies.

Present with a symmetric goiter and hyperthyroidism. Graves orbitopathy is due to periorbital or conjunctival swelling or erythema, proptosis, diplopia, eye pain, or even vision loss. Dermopathy is rare and presents with nonpitting edema and fibrosis, classically on the anterior tibia (pretibial myxedema).

44
Q

Fetal Grave’s disease

A

Rarely, Grave’s disease autoantibodies may be passed from mother to fetus by FcRn. This is life threatening, and can lead to tachycardia, poor growth, fetal goiter, or in severe cases heart failure (hydrops).

If present, these can be treated by administering antithyroid medication such as methimazole to the mother, who will pass it across the placenta to the fetus.

45
Q

Toxic thyroid nodule / Toxic multinodular goiter

A

Nodules that produce thyroid hormone even in the absence of TSH. Typically arise in the 4th or 5th decade of life, are almost always benign, and generally harbor somatic activating mutations in the TSH receptor.

A thyroid nodule is defined to be autonomous if it is shown by radioiodine imaging to take up iodine when serum TSH is low. Toxic multinodular goiter often in areas of iodine deficiency, when autonomy arises in one or more nodules within a pre-existing multinodular goiter.

46
Q

Toxic thyroid nodule / Toxic multinodular goiter treatment

A

Definitive therapy with either radioiodine ablation or surgical resection is often pursued, although antithyroid drugs can control the hyperthyroidism in patients who do not desire radioiodine ablation or surgery.

47
Q

Transient thyroiditis

A

Caused by thyroid damage from autoimmune, postpartum, postviral, and drug-induced thyroiditis. Because the normal thyroid contains a limited amount of preformed hormone, thyrotoxicosis due to transient thyroiditis is usually self-limited and generally lasts less than 8 weeks.

Postviral thyroiditis is often painful, drug-induced thyroiditis is usually painless, and autoimmune thyroiditis may be either painful or painless.

48
Q

Acute suppurative thyroiditis

A

Bacterial or fungal infection that typically presents with symptoms of inflammation and a painful thyroid mass rather than with thyroid dysfunction.

49
Q

TSH-secreting pituitary adenoma treatment

A

Treatment may include surgery or medical management with somatostatin analogs.

50
Q

Resistance to thyroid hormone

A

Rare, congenital, caused by dominant mutations in TR-beta. Therefore, TSH secretion remains normal or elevated despite supranormal T4 and T3 levels.

Goiter is present due to persistent TSH stimulation, and excessive thyroid hormone signaling in tissues expressing the normal TR-alpha receptor—such as the heart, brain, and GI tract—result in findings such as tachycardia, attention deficit, and poor growth

Other clinical findings derive from inadequate thyroid hormone action in TR-beta-expressing tissues, such as sensorineural deafness caused by abnormal cochlear development.

51
Q

Treating thyrotoxicosis

A
  • Underlying cause (obv)
  • Beta-blockers
  • Corticosteroids (especially for autoimmune and drug-induced thyroditis. Anti-inflammatory and decrease peripheral T4->T3 conversion)
  • Methimazole (blocks thyroid hormone synthesis by inhibiting TPO function)
  • Propylthiouracil (same as above, but shorter half life and more complications)
  • Iodine (by triggering the Wolff-Chaikoff effect)
  • Radiofrequency ablation with 131I and TSH
  • Near-total thyroidectomy (risky due to proximity to important structures)
52
Q

Thyroid nodules

A

A discrete mass within the thyroid gland that is distinct from the surrounding parenchyma. Occur in up to 2/3 of adults and have a 5-15% chance of harboring cancer.

Mostly derived from follicular cells. Follicular-derived thyroid cancers are divided histologically into papillary, follicular, and anaplastic types. Papillary and follicular thyroid cancers are usually well-differentiated and slow growing with excellent prognosis, while anaplastic are poorly-differentiated and aggressive.

53
Q

Papillary thyroid cancer

A
  • Most common
  • Dysplasia of thyroid tissue with a pattern of branching and budding papillae
  • Calcifications called psammoma bodies are often seen
  • Unique nuclear changes including nuclear crowding, enlargement, and clearing, as well as irregular shapes, nuclear grooves, or round pseudo-inclusions​
  • The above may be observed and a diagnosis made by fine needle aspirate of the nodule
  • Often metastasizes to cervical lymph nodes, but more rarely spreads to distant sites
54
Q

What is going on in this thyroid biopsy?

A

Nuclei showing pseudoinclusions, suggestive of papillary thyroid cancer

55
Q

What is going on in this thyroid biopsy?

A

Crowding, enlargement, and clearing of the nuclei and formation of papillary structure between cells. Nuclei have a ground glass appearance and irregular shapes.

Papillary thyroid cancer

56
Q

What is going on in this thyroid biopsy?

A

Psammoma bodies in papillary thyroid carcinoma

Psammoma bodies are distinctive calcifications

57
Q

Follicular thyroid cancer

A
  • Shows a “microfollicular” pattern of very small follicles
  • Same pattern is also seen in benign follicular adenomas, and FTC can be distinguished from adenomas only by the presence of invasion into surrounding tissue or blood vessels.
  • Surgical resection is required for diagnosis
  • FTC is slightly more aggressive than PTC
  • Can spread to bone and lung
58
Q

What is going on in this thyroid biopsy?

A

Follicular thyroid cancer

59
Q

Anaplastic thyroid cancer

A
  • Composed of undifferentiated cells with marked pleiomorphism, nuclear atypia, and high mitotic activity
  • Grow rapidly and show extensive local and lymphovascular invasion
  • Not amenable to the adjunctive treatments used for well-differentiated thyroid cancers (like somatostatin)
  • 5-year mortality is close to 100%
60
Q

Medullary thyroid cancer

A
  • Arises from C cells
  • Accounts for only 1-2% of thyroid cancers
  • Round or polyhedral cells that stain strongly for calcitonin
  • Frequently spreads to local lymph nodes and may also metastasize to distant sites
  • Measuring serum calcitonin is useful
  • Virtually all MTCs are caused by mutations in the RET oncogene
  • 25% of cases are caused by RET mutations inherited as an autosomal dominant syndrome of multiple endocrine neoplasia​
61
Q

What is going on in this thyroid biopsy?

A

Medullary thyroid cancer

62
Q

What is going on in this thyroid biopsy?

A

Anaplastic thyroid cancer

63
Q

Clinical presentation and diagnosis of thyroid cancer

A
  • Often present on physical exam or incidental radiologic finding
  • Thyroid ultrasound is the optimal way to confirm the presence of a thyroid nodule and assess for evidence of malignancy
  • Fine needle aspirate
  • Evaluation of cervical lymph nodes
  • Surgical resection
  • TSH and T4 measurement (Note: If a thyroid cancer produces T4, it is benign. No evaluation for cancer is needed, but the nodule must be confirmed to be autonomous by radiologic iodine uptake)
64
Q

Treating thyroid cancer

A
  • Surgery is the primary and most important therapy for all thyroid cancers
  • Post-surgical radioiodine ablation: Follicular-derived thyroid cancers are well differentiated, they usually retain the ability to concentrate iodine. After surgical resection, radioactive iodine ablation can be used to destroy remaining thyroid cancer cells
  • TSH suppression: Most differentiated thyroid cancers respond to the trophic effect of TSH. Therefore, keeping the TSH serum suppressed with slightly excessive doses of L-T4 can reduce tumor growth and improve outcome in advanced thyroid cancers.
  • Monitoring: Even when optimally treated, thyroid cancers may recur even years later, so long-term monitoring is essential. This entails thyroglobulin measurement and thyroid ultrasound
65
Q

MCT8

A

Channel for T3 and T4 release on the basolateral surface of follicular cells in the thyroid. Necessary for T3 and T4 egress.

66
Q

Relative Total T4, Free T4, TBG, and TSH levels in the cases of primary hypothyroidism, primary hyperthyroidism, high levels of estrogen, and a TSHoma. (Make a table)

A
67
Q

Hormones with associated blood binding proteins

A
68
Q

Painful subacute thyroiditis (aka Quervian’s thyroiditis)

A
  • Often, but not always, preceded by respiratory tract infection
  • Triphasic:
    • Phase one: hyperthyroidism due to destruction of thyroid tissue and release of colloid contents
    • Phase two: hypothyroidism due to hypoplastic thyroid which must regenerate
    • Phase three: If the thyroid can regenerate, euthyroidism may be restored. (Note that if the thyroid was destroyed in phase II, the patient will have permanent hypothyroidism)
69
Q

Amiodarone-induced thyrotoxicosis

A

Occurs in 20% of patients who take amiodarone. May even develop up to 1 year post-cessation of the drug.

Can occur by two mechanisms: 1) Excess iodine (from drug metabolism) promotes T4 synthesis and release, most often in patients with history of subclinical thyroid disease, 2) amiodarone-induced thyroiditis causes destruction of some thyroid tissue and T4 release from colloid.

Type 1 is treated with high dose antithyroid drugs and type 2 is treated with corticosteroids.

70
Q

NEJM medical management of hyperthyroidism table

A
71
Q

Patients with Hashimoto’s thyroiditis tend to have symmetrically enlarged thyroids that are firm and bumpy, but are painless. What causes these physical changes?

A

Although the gland is hypofunctioning due to inflammation, TSH is still inducing active proliferation as a trophic factor. There is also fibrosis and edema occuring due to chronic inflammation, accounting for the stiffness in the gland.

72
Q

The antibodies in Hashimoto’s thyroiditis are. . .

A

. . .not pathogenic in themselves. Rather they are a marker of cell-mediated pathogenicity. This is similar to anti-ds-DNA antibodies in SLE.

73
Q

How do you go about dosing levothyroxine given that everyone has different ‘physiological’ levels of the free hormone?

A

Just dose to TSH! The dosage of levothyroxine should be such that TSH returns to the reference range.

74
Q

Physical signs of Grave’s disease

A
  • Proptosis (eye bulge)
  • Lid lag (upper eyelid has high adrenergic tone due to hyperthyroidism. Have the patient follow your finger up, and when you bring your finger down you see white sclera above their iris)
75
Q

Corticosteroids in treating thyrotoxicosis

A

Corticosteroids inhibit the pheripheral conversion of T4 to T3

76
Q

Methimazole

A

TPO inhibitor

Primary treatment for thyrotoxicosis

77
Q

Cases where pregnancy can induce thyrotoxicosis

A

Cases that have abnormally high hCG levels. Women pregnant with twins may experience this transient thyrotoxicosis during early pregnancy.

78
Q

“Stare” vs “proptosis”

A

Proptosis is true retro-orbital edema leading to bulding of the eyes. This is only seen in Grave’s disease.

Stare refers to seeing the white sclera above the iris, and indicates increased adrenergic tone which may be seen in any etiology of thyrotoxicosis.

79
Q

What is going on in this thyroid biopsy?

A

This is a classic histologic picture of Grave’s disease.

Note that the follicular cells are now columnar and have highly euchromatic nuclei with “scalloping” of the border with the colloid.

80
Q

Micro- vs macro-follicular architecture on FNA of thyroid nodules

A

Micro-follicular: Small clusters of cells (3-10)

Macro-follicular: Large clusters of cells (>25)

81
Q

If a thyroid follicular thyroid nodule is in-place without penetrating its tumor capsule, it is a ____. If it does penetrate its capsule, it is a ____.

A

If a thyroid follicular thyroid nodule is in-place without penetrating its tumor capsule, it is a follicular adenoma. If it does penetrate its capsule, it is a follicular carcinoma.

82
Q

“Salt and pepper” chromatin

A

Buzz word for neuroendocrine origin of a tumor

For the thyroid this means C cells.

83
Q

10 year old boy presents for evaluation for attention deficit disorder. He has difficulty concentrating throughout the interview, appears slightly agitated, and has a mild tremor. He is tachycardic and reports 4-5 bowel movements per day. Mild hearing loss is also detected on physical exam, and checking his blood lab history you notice that he had abnormally high LDL cholesterol for years. The thyroid is diffusely enlarged, but is not firm or painful. What is the likely diagnosis?

A

This is a classic case of a congenital TRβ loss-of-function mutation. Patients present with effective hyperthyroidism in TRα-expressing tissues, and hypothyroidism in TRβ-expressing tissues.

Here, his general hyperthyroid presentation is due to his TRα hyperthyroidism. His hearing loss, high LDL, and goiter are due to his TRβ hypothyroidism (his TSH levels are very high because he has no T4-mediated inhibition since this is via the TRβ!)

TRβ is expressed in the cochlea, on the liver, on thyrotropes in the pituitary, and in the hypothalamus.

84
Q

A patient presents with a syndrome of hypothyroidism due to Hashimoto’s thyroiditis, complicated by a blood pressure of 140/100, hypercholesterolemia, moderate obesity, and a family history of cardiac disease. How should you proceed with treatment?

A

A case like this with high risk for worsening of cardiovascular disease indicates a gradual increase in levothyroxine dose with careful monitoring of blood pressure and cardiovascular status to ensure that you are not provoking cardiovascular disease.

HMS Homeostasis II (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions