BMS 200 > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

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1
Q

What is one of the most common endocrine diseases?

A

Hashimoto’s thyroiditis

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2
Q

What immune cells infiltrate the thyroid in Hashimoto’s?

A

T and B lymphocytes.

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3
Q

Which autoantibodies are useful in diagnosing Hashimoto’s thyroiditis?

A

Anti-TPO antibodies and anti-thyroglobulin antibodies

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4
Q

What autoimmune diseases are associated with Hashimoto’s thyroiditis?

A

Type 1 diabetes, Addison’s disease, pernicious anemia, vitiligo.

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5
Q

What does the thyroid gland look like in Hashimoto’s pathology

A

Enlarged gland with massive leukocyte infiltration, prominent germinal centers, and atrophic follicles.

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6
Q

What are the general symptoms of Hashimoto’s thyroiditis?

A

Fatigue, cold intolerance, slowing of mental/physical performance, goitre.

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7
Q

What are the dermatological features of Hashimoto’s thyroiditis?

A

Macroglossia, hoarseness, facial puffiness, periorbital edema

Cool, rough skin, carotenemia

Non-pitting dermal thickening (myxedema)

Dry/coarse hair, loss of lateral 1/3 of eyebrows.

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8
Q

What neurological symptoms can occur in Hashimoto’s thyroiditis?

A

Paresthesias, muscle cramps, delayed deep tendon reflexes, carpal tunnel syndrome.

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9
Q

What cardiovascular findings may be seen in Hashimoto’s thyroiditis?

A

Bradycardia, mild hypotension, hypercholesterolemia

Severe disease: CHF, angina, pericardial effusions, enlarged heart (interstitial edema).

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10
Q

What are the respiratory features of Hashimoto’s thyroiditis?

A

Hypoventilation, decreased exercise capacity.

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11
Q

How does Hashimoto’s thyroiditis affect reproduction?

A

Women: Menorrhagia or amenorrhea

Men: Erectile dysfunction.

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12
Q

What GI symptoms may occur in Hashimoto’s thyroiditis?

A

Constipation, weight gain, poor appetite.

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13
Q

What is the typical facial appearance in Hashimoto’s thyroiditis?

A

Puffy face and eyes, thickened skin, sometimes preserved lateral eyebrows.

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14
Q

What are other names for subacute thyroiditis?

A

De Quervain’s thyroiditis, granulomatous thyroiditis, viral thyroiditis.

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15
Q

What are the key pathological features of subacute thyroiditis?

A

Patchy inflammatory infiltrate

Multinucleated giant cells (from macrophages)

Early neutrophilic, later lymphocytic infiltration

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16
Q

What symptom makes subacute thyroiditis distinct from other thyroiditis types?

A

Painful, tender thyroid with neck pain (often mistaken for pharyngitis).

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17
Q

What thyroid function changes occur in subacute thyroiditis?

A

Phases of thyrotoxicosis → hypothyroidism → resolution (sometimes permanent hypothyroidism).

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18
Q

Who typically develops silent thyroiditis?

A

Patients with underlying autoimmune thyroid disease.

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19
Q

What is the clinical course of silent thyroiditis?

A

Mild thyrotoxicosis (2–4 weeks)

Mild hypothyroidism (4–12 weeks)

Resolution (but some develop permanent hypothyroidism).

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20
Q

What are the features of the goitre in silent thyroiditis?

A

Painless goitre, no fever, no ESR elevation.

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21
Q

What postpartum population is at risk of silent thyroiditis?

A

Up to 5% of women, 3–6 months after pregnancy.

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22
Q

What antibody is associated with silent thyroiditis in pregnancy?

A

TPO antibodies

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23
Q

What is a goitre?

A

An enlarged thyroid gland (may occur in hypo- or hyperthyroid states).

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24
Q

Which conditions commonly cause noticeable goitre?

A

Hashimoto’s thyroiditis

Graves’ disease

Nodular thyroid disease

Iodine deficiency

Thyroid neoplasms

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25
Is iodine deficiency a common cause of goitre in North America?
No, but it remains common in some parts of the world.
26
What is a diffuse non-toxic goitre?
Diffuse enlargement of the thyroid with no nodules and no thyrotoxicosis.
27
What is the most common cause of diffuse non-toxic goitre worldwide?
Iodine deficiency
28
Can diffuse non-toxic goitre occur with adequate iodine intake?
Yes, cause is then idiopathic
29
What is the pathophysiology of iodine-deficiency goitre?
↓ iodination of thyroglobulin → ↓ thyroid hormone production → ↑ TSH → thyroid enlargement with colloid accumulation.
30
What are the typical thyroid function test results in simple goitre?
T4 decreased, TSH mildly increased or normal.
31
What complication can occur from a large simple goitre?
Compression of trachea or thoracic outlet.
32
What is the histology of multinodular goitre?
Variable nodules in size and type Cystic colloid-filled areas Hypercellular hyperplastic regions Fibrosis common
33
What is the likely pathogenesis of MNG?
Starts as simple goitre → localized nodules grow independently of TSH → some may become neoplastic.
34
Are patients with non-toxic goitres usually hypo-, hyper-, or euthyroid?
Usually euthyroid, but hypothyroidism can occur.
35
What are possible mass effects of non-toxic goitre?
Substernal goitre: compression worsens when arms raised Dysphagia (esophageal compression) Dyspnea (tracheal compression)
36
How does the thyroid adapt to iodine deficiency?
ncreases MIT:DIT ratio in thyroglobulin Increases secretion of T3 relative to T4 (since T3 is more active).
37
Why does goitre develop in iodine deficiency?
Low T3/T4 → ↑ TRH and ↑ TSH → thyroid hypertrophy/hyperplasia.
38
What is cretinism?
Mental and physical developmental delays due to thyroid hormone deficiency during critical growth periods (historical medical term, not derogatory).
39
What is myxedema coma?
A rare, life-threatening complication of long-term hypothyroidism with an added precipitating factor.
40
What are common precipitating factors for myxedema coma?
Infections (pneumonia, UTI, sepsis), burns, pulmonary disease, GI bleed, stroke, trauma, surgery, hypoglycemia, hypothermia, medications.
41
What is “myxedema” referring to in hypothyroidism?
Non-pitting edema in hypothyroid dermopathy
42
What causes hypotension in myxedema coma?
Loss of protective vasoconstriction → inability to maintain blood pressure
43
What cardiovascular findings are seen in myxedema coma?
Hypotension → shock Bradycardia (especially dangerous if with low BP) Dysrhythmias (heart block, torsades de pointes).
44
How does neurologic progression occur in myxedema coma?
Lethargy/apathy → depression → disorientation + ↓ reflexes → coma.
45
What rare neurologic complications can occur in myxedema coma?
Psychosis, seizures (rare).
46
What respiratory complications occur in myxedema coma?
Hypoventilation Obstructive sleep apnea
47
What electrolyte abnormality is common in myxedema coma?
Hyponatremia.
48
What mechanisms cause hyponatremia in myxedema coma?
↑ ADH, ↓ GFR → water retention without proportional sodium retention.
49
What is the most common cause of thyrotoxicosis and who is most affected?
Graves’ disease
50
What is the key immunologic mechanism in Graves’ disease?
TSH receptor–stimulating immunoglobulins (TSIs) activate the TSH receptor independent of negative feedback
51
What environmental triggers are associated with Graves’ disease?
Smoking, stress, sudden iodine increase
52
Why is ophthalmopathy unique to Graves’ disease?
Orbital tissues express TSH-R → autoimmune attack, fibroblast activation, GAG deposition → muscle swelling, proptosis
53
What causes toxic MNG and who is affected?
Autonomous nodules secreting thyroid hormone independent of TSH; common in elderly; 15–30% of thyrotoxicosis cases
54
What is toxic adenoma?
Single nodule with activating TSH-R mutation → mild thyrotoxicosis; no history of iodine deficiency or MNG.
55
What is thyroid storm and when does it occur?
Life-threatening hyperthyroid crisis triggered by acute illness
56
What are hallmark signs of thyroid storm?
Hyperthermia, diaphoresis, severe tachycardia/dysrhythmia, CNS dysfunction (agitation → coma), GI upset, possible hepatic failure.
57
What are major causes of congenital hypothyroidism?
Thyroid dysgenesis, maternal TSH-R antibodies, genetic defects in TH synthesis, central hypothyroidism.
58
What is the most common thyroid adenoma and what % of neoplasms are malignant?
Follicular adenoma (benign); malignancy incidence ~15/100,000/year.
59
What are features of papillary thyroid carcinoma?
Most common; nuclear changes; metastasis to bone/lung; usually excellent prognosis unless invasive
60
What is medullary thyroid carcinoma derived from and what lab is useful?
C-cells; elevated calcitonin.
61
What is prognosis of anaplastic carcinoma?
Extremely poor; most die within 6 months.
62
Which pathways/mutations are common in thyroid cancers?
RET-RAS-BRAF pathway (70% of papillary), RAS mutations, p53 in poorly differentiated, β-catenin (CTNNB1).
63
What environmental factor strongly increases thyroid cancer risk?
Radiation exposure, especially radioactive iodine in childhood.
64
What are the mechanisms of PTU?
Inhibits thyroid peroxidase (main) and peripheral T4→T3 conversion (minor).
65
What is methimazole’s mechanism and main safety concern?
Inhibits thyroid peroxidase; less hepatotoxic than PTU
66
What is levothyroxine used for?
Synthetic T4 replacement for hypothyroidism
67
When is radioactive iodine therapy used?
For Graves’ disease resistant to drugs and well-differentiated thyroid cancers
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