Endocrine 2 Flashcards

1
Q

Ectopic thyroid tissue can be found along the path of the thyroid’s ________ during embryonic development. Where exactly is ectopic thyroid tissue most commonly found?

A

found along the path of descent during development. Most commonly found at the base of the tongue and is called the lingual thyroid.

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2
Q

The interaction of thyroid hormone with its _____ ______ ______ ______ results in the formation of a hormone-receptor complex that binds to _____ ______ ______ _____ in target genes, regulating their transcription.

A

Thyroid hormones bind to nuclear thyroid hormone receptors (intracellular), which then go and bind to thyroid hormone response elements that regulate transcription

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3
Q

What is thyrotoxicosis?

A

A hypermetabolic state caused by elevated levels of T3 and T4 (most commonly from hyperthyroidism)

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4
Q

What are eight clinical manifestations of hyperthyroidism?

A
  1. Soft, warm, flushed skin.
  2. Heat intolerance.
  3. Sweating.
  4. Weight loss despite increased appetite.
  5. GI issues: diarrhea, malabsorption, hypermobility.
  6. Cardiac issues: palpitations, tachycardia, aggravation of heart disease in elderly –> CHF.
  7. Neuro: tremors, nervousness, thyroid myopathy.
  8. Ocular manifestations
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5
Q

What is thyroid myopathy? How common is it?

A

Proximal muscle weakness as a result of hyperthyroidism. Develops in 50% of pts with hyperthyroidism.

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6
Q

Describe the ocular manifestations associated with hyperthyroidism.

A

Sympathetic overstimulation results in a wide, staring gaze and lid lag.

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7
Q

What is “thyroid storm?”

A

An abrupt onset of hyperthyroidism –> acute elevation of catecholamines during stress –> medical emergency due to cardiac issues (arrhythmias, etc). Happens most commonly in people with Graves disease.

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8
Q

How is the diagnosis of hyperthyroidism made clinically?

A

Clinical features and lab data like TSH levels. TSH levels will be low (negative feedback).

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9
Q

What are the three causes of hypothyroidism?

A
  1. Defective thyroid hormone synthesis (goitrous hypothyroidism).
  2. Inadequate thyroid parenchyma function (thyroiditis).
  3. Inadequate TSH or TRH from pituitary or hypothalamus, respectively.
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10
Q

What is cretinism? What are its features (6)?

A

Hypothyroidism at an early age. Common in places where iodine deficiency is endemic. Features are:

  1. Skeletal system derangements
  2. CNS derangements incl. mental retardation
  3. Short stature
  4. Coarse facial features
  5. Protruding tongue
  6. Umbilical hernia
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11
Q

Name the disease:
Generalized apathy and mental sluggishness in adulthood with cold intolerance. Obesity is a common manifestation. Constipation from decreased GI motility. Pericardial effusions common and enlarged heart and heart failure seen in late stage.

A

Myxedema (hypothyroidism in adulthood)

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12
Q

How is hypothyroidism diagnosed?

A

MOST SENSITIVE TEST: elevated TSH (no feedback) seen in primary hypothyroidism. Decreased serum T4 is seen regardless of cause.

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13
Q

Chronic lymphocytic thyroiditis is also called _________ disease. It is the most common cause of _________ hypothyroidism in places where iodine levels are sufficient.

A

also called Hashimoto disease. Most common cause of goitrous hypothyroidism (defective thyroid hormone synthesis)

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14
Q

What is the cause of chronic lymphocytic thyroiditis aka Hashimoto disease? In what population is it most common?

A

Autoimmune destruction of the thyroid gland. Most prevalent in females (10:1 over males) between 45 and 65 years old.

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15
Q

Lymphocytic thyroiditis aka Hashimoto disease is usually seen in older women but is a major cause of _______ ______ in children.

A

nonendemic goiter

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16
Q

Describe the pathogenesis of Hashimoto disease.

A

Breakdown of thyroid self-tolerance –> CD4+ helper cell sensitization –> 3 pathways: 1) differentiation into TH1 cells that activate macrophages and cause thyroid injury, 2) CD8+ killer cell stimulation causes thyroid injury, and 3) B cell activation to plasma cells that make anti-thyroid Abs.

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17
Q

Is there a genetic component to Hashimoto thyroiditis? Is there an environmental component?

A

Yeah genetic, it occurs often in first-degree relatives.

Yeah environmental - more prevalent in places with greater iodine intake.

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18
Q

Describe the morphological changes seen in Hashimoto disease (6).

A
  1. Enlarged thyroid
  2. Tan colored
  3. Nodular pattern
  4. T lymphocyte infiltration with lymphocyte follicles and germinal centers
  5. Atrophy of thyroid follicles
  6. Acidophilic metaplasia of follicular epithelial (HURTHLE of oxyphil) cells
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19
Q

In the development of Hashimoto disease, transient ________ with corresponding elevated T3 and T4 levels may precede hypothyroidism.

A

transient thyrotoxicosis (hypERthyroidism) may occur first

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20
Q

Patients with Hashimoto thyroiditis often have other ________ diseases and are at increased risk for the development of _____ _________ _________.

A

often have other autoimmune diseases and are at increased risk for development of B-cell non-Hodgkin lymphomas.

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21
Q

Goiterous hypothyroidism is characterized by ________ of the thyroid due to iodine deficiency (NO inflammation) –> increased TSH levels –> thyroid follicular cell hypertrophy.

A

enlargement

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22
Q

Most patients with thyroid goiters are euthyroid. What does that mean?

A

It means the thyroid still makes thyroid hormone.

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23
Q

Some goiters are hormonally active, causing _________.

A

thyrotoxicosis (increased metabolism due to increased thyroid hormones)

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24
Q

Describe the pathogenesis from a diffuse goiter to a multinodular goiter.

A

Diffuse, symmetric thyroid gland enlargement + increased dietary iodine or increased functional demand for thyroid hormone –> follicular epithelium involution –> colloid goiter. Chronic episodes of hyperplasia causes irregular enlargement –> multinodular goiter.

25
Q

In a diffuse goiter, the follicles are lined by crowded _______ cells, which may pile up and form projections.

A

columnar

26
Q

What are the three overarching clinical features of Grave’s disease?

A
  1. Thyrotoxicosis
  2. Opthalmopathy (exopthalmos and proptosis)
  3. Dermopathy - thickened dermis
27
Q

What causes Graves disease? What population does it affect most?

A

Abnormal Abs bind to TSH receptors –> abnormally high thyroid hormone synthesis. Affects women more than men, common age is 20-40 years old.

28
Q

What environmental factor increases the risk for developing Graves disease?

A

Smoking

29
Q

Describe the microscopic morphological changes seen in Graves disease (4)

A
  1. Diffuse, symmetrical hyperplasia.
  2. Follicles lined by tall columnar epithelial cells that project into the lumina.
  3. SCALLOPED appearance due to high rates of colloid resorption.
  4. T and B lymphocyte infiltration and germinal centers.
30
Q

Thyroid adenomas can appear as either hot or cold nodules. Explain the difference.

A

Cold nodules don’t take up radioactive iodine that well and 10% can become malignant. Hot nodules do take up iodine, and are almost NEVER malignant.

31
Q

Are most thyroid adenomas functional, causing thyrotoxicosis?

A

Nope

32
Q

How is a thyroid adenoma diagnosed? What is the prognosis?

A

Biopsy and histologic exam. Excellent prognosis, they don’t recur and don’t metastasize.

33
Q

Describe two morphological changes seen in a thyroid adenoma.

A
  1. The tumor bulges out from the thyroid and is ENCAPSULATED (hallmark of follicular adenomas), well-defined.
  2. No papillary changes (that is seen in a malignant neoplasm only).
34
Q

What is the most common thyroid cancer, accounting for up to 90% of sporadic thyroid cancer cases in the U.S.?

A

papillary thyroid carcinoma

35
Q

Papillary thyroid carcinomas are most frequent between the ages of _____ and ____ and the female:male ratio is _____.

A

20 and 50, 3:1 female:male

36
Q

Name the causes of papillary thyroid carcinomas (5).

A
  1. Activation of MAP KINASE PATHWAY.
  2. Somatic mutations: RET proto-oncogene
  3. Iodine excess
  4. Radiation
  5. Genetics
37
Q

Describe the morphological changes seen in papillary thyroid carcinoma (6).

A
  1. Solitary or multifocal
  2. Ranging from well circumscribed and encapsulated to infiltrative.
  3. Fibrosis, calcification, cystic growth.
  4. Nuclear features (Dx is based on this): finely dispersed chromatin is clear - described as ground glass or ORPHAN ANNIE EYE nuclei.
  5. Papillary architecture present with dense fibrovascular cores.
  6. PSAMONNA BODIES with concentric calcified structures - looks like a cut onion.
38
Q

What is the survival rate from papillary thyroid carcinoma?

A

Very high (85% rate for 20 year survival)

39
Q

What causes 85% of cases of primary hyperparathyroidism? What causes the rest of the cases?

A

A solid parathyroid adenoma. Hyperplasia (5-10%) and carcinomas (1%) account for the rest.

40
Q

What does secondary hyperparathyroidism do to the parathyroid glands and why does it occur?

A

Causes diffuse enlargement of all four glands. Occurs due to hypocalcemia seen in end stage renal disease, malabsorption syndrome or Vit D deficiency

41
Q

What does tertiary hyperparathyroidism do to the parathyroid glands and why does it occur?

A

Causes diffuse enlargement of all four glands. Occurs due to autonomous PTH secretion even after stimulus is removed.

42
Q

What are the clinical features of hyperparathyroidism (5)?

A
  1. Increased serum ionized calcium.
  2. Increased PTH –> hypophosphatemia due to decreased phosphate retention.
  3. Bone demineralization (increased osteoclast activity).
  4. Urinary, bile stones.
  5. Cardiac arrhythmias and mental symptoms from increased Ca2+
43
Q

What are the causes of hypercortisolism (5)?

A
  1. Exogenous administration or steroids (iatrogenic Cushing’s).
  2. Primary adrenocortical hyperplasia
  3. Adrenocortical neoplasia (adrenal Cushings)
  4. ACTH - secreting pituitary adenomas.
  5. Paraneoplastic ACTH secretion (paraneoplastic Cushings)
44
Q

What is the difference between Cushing SYNDROME and Cushing DISEASE?

A

Cushing syndrome is hypercortisolism no matter the cause. Cushing disease is when a pituitary adenoma secretes ACTH.

45
Q

What gross morphological changes are seen in adrenal hyperplasia (4)? What are the microscopic changes (3)?

A

Gross: Yellow, thick, multinodular, fatty.

Microscopic: Lipid vacuoles, mild nuclear pleomorphism, no mitotic activity or necrosis seen.

46
Q

What are the clinical features of Cushing syndrome (8)?

A
  1. Obesity of the face (moon face), neck (buffalo hump), trunk and abdomen but NOT extremities (they can be wasted).
  2. Atrophic, stretched skin –> striae.
  3. Osteoporosis
  4. Proximal muscle wasting
  5. Hypertension
  6. CHF
  7. Hyperinsulinemia
  8. Decreased secondary sex characteristics and sexual drive.
47
Q

What is Addison’s disease?

A

Adrenal hypofunction resultant from adrenal gland destuction, pituitary or hypothalamic dysfunction, or exogenous steroid use.

48
Q

Name two endogenous and two infectious causes of Addison’s disease. What percentage of cases Addison’s are these responsible for?

A

Endogenous: autoimmune adrenalitis (Ab attack on cells that make steroids), or metastatic cancers that destroy the adrenal cortex.

Infectious: TB, AIDS

These are responsible for >90% of cases of Addison’s

49
Q

What are the clinical features of Addisons disease (6)?

A
  1. Weakness
  2. Weight loss
  3. GI symptoms
  4. Hypotension
  5. Electrolyte imbalance
  6. Hyperpigmentation (from MSH release)
50
Q

What is a pheochromocytoma?

A

A neoplastic disorder of the adrenal medulla. Chromaffin cells secrete excess catecholamines –> sustained or episodic hypertension.

51
Q

Most pheochromocytomas are _______ but a minority are hereditary. Name the four hereditary causes.

A

sporadic

hereditary: VHL disease, multiple endocrine neoplasia (MEN) types 2A/2B, NF1, RET

52
Q

___% of pheochromocytomas are unilateral, ___% are bilateral, and ___% are extraadrenal (paraganglioma)

A

80% unilateral, 10%, 10%

53
Q

Are pheochromocytomas most often benign?

A

Yeah (90%)

54
Q

Describe the histology of a pheochromocytoma.

A

Highly variable, typically has circumscribed nests of neoplastic cells (Zellballen). Tumor cells range from polyhedral to fusiform, with granular, amphophilic, or basophilic cytoplasm and vesicular nuclei. Eosinophilic globules are usually seen in the cytoplasm

55
Q

What are the clinical features of a pheochromocytoma?

A
  1. Bouts of sudden (paroxysmal) hypertension
  2. Tachycardia
  3. Nervousness
  4. Angina and MI may occur without coronary artery disease
56
Q

How is a phaeochromocytoma diagnosed?

A

Increased urinary levels of catecholamine metabolites, particularly vanillylmandelic acid

57
Q

Orphan Annie eye nuclei.

A

Papillary thyroid carcinoma

58
Q

What is the most common cause of clinically silent hypercalcemia?

A

Primary hyperparathyroidism

59
Q

Name the disease: A chronic enlargement of the thyroid gland, not due to a neoplasm, occurring endemically in certain localities, especially regions where glaciation occurred and the soil is low in iodine, and sporadically elsewhere.

A

thyroid goiter