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Pathoma Endo > 15.3 - 15.6 Thyroid > Flashcards

15.3 - 15.6 Thyroid Flashcards

1
Q

Cystic dilation of thyroglossal duct remnant

A

Thyroglossal duct cyst

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2
Q

Normally, the thyroid develops WHERE before traveling along the thyroglossal duct to the anterior neck

A

Back of tongue

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3
Q

What normally happens to the thyroglossal duct after the thyroid travels down it?

A

normally involutes, but if it persists, it may undergo cystic dilation

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4
Q

Persistance of thyroid tissue at the base of tongue (presents as mass at base of tongue)

A

Lingual thyroid

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5
Q

How does hyperthyroidism lead to increased BMR?

A

increased synthesis of Na+-K+ ATPase

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6
Q

How does hyperthyroidism lead to increased SNS activity?

A

increased expression of beta1-adrenergic receptors

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7
Q

cholesterol levels in hyperthyroidism

A

low

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8
Q

serum glucose in hyperthyroidism

A

high due to increased gluconeogenesis and glycogenenolysis

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9
Q

What type of autoantibody stimulates TSH receptor in Graves dz?

A

IgG

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10
Q

What type of HSR is Graves disease?

A

Type II HSR

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11
Q

HSR that is anaphylactic and atopic - free antigen cross-links IgE on presensitized mass cells and basophils, triggering release of vasoactive amines (histamine) that act at post capillary venules. Rxn develops rapidly after antigen exposure because of preformed antibody

A

Type I HSR

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12
Q

HSR that is cytotoxic (antibody mediated) - IgM, IgG bind to fixed antigen on “enemy” cell, leading to cellular destruction through 3 mechanisms

  • opsonization leading to phagocytosis or complement activation
  • complement-mediated lysis
  • antibody-dependent cell-mediated cytotoxicity (ADCC), usually due to NK cells
A

Type II HSR

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13
Q

HSR that is immune-complex mediated - antigen-antibody (IgG) complexes activate complement which attracts PMNs, wh/ release lysosomal enzymes

A

Type III HSR

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14
Q

HSR that is delayed (T-cell-mediated) type - sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved)

A

Type IV HSR

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15
Q

How do you test for type I HSR?

A

skin test for specific IgE

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16
Q

How do you test for type II HSR?

A

direct and indirect Coombes

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17
Q

How do you test for type III HSR?

A

immunofluorescent staining

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18
Q

How do you test for type IV HSR?

A

patch test, PPD

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19
Q

Muscle mass in hyperthyroidism

A

Decreased –> weakness

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20
Q

in what demographic does graves classically occur

A

women 20-40

21
Q
  1. Hyperthyroidism
  2. Diffuse goiter
  3. Exophthalmos
  4. Pretibial myxedema
A

Graves

22
Q

Name two glycosaminoglycans

A
  1. Chondroitin sulfate

2. hyaluronic acid

23
Q

TSH activation stimulates TSH-bearing fibroblasts behind the orbit –> buildup, inflammation

A

exophthalmos in Graves

24
Q

Histology of Graves

A

Irregular follicles with scalloped colloid and chronic inflammation

25
Q

Labs of Graves

A

Decreased TSH
Increased total and free T4
Hypocholesterolemia
Increased serum glucose

26
Q

Treatment of Graves

A
  1. Beta blockers
  2. Thioamide
  3. Radioiodine ablation
27
Q

A potentially fatal complication of Graves due to elevated catecholamines and massive hormone excess, usually in response to stress (surgery or childbirth)

A

Thyroid storm

28
Q

Presentation of thyroid storm (3 features)

A
  1. Arrhythmia
  2. Hyperthermia
  3. Vomiting –> hypovolemic shock
29
Q

Treatment of thyroid storm

A
  1. Propylthiouracil (PTU)
  2. Beta-blockers
  3. Steroids
30
Q

Inhibits peroxidase mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion of T4 to T3

A

PTU mechanism of action

31
Q

Enlarged thyroid gland with multiple nodules due to relative iodine deficiency; usually nontoxic (euthyroid)

A

Multinodular goiter

32
Q

Rarely, multinodular goiter becomes TSH independent leading to T4 release and hyperthyroidism

A

Toxic goiter

33
Q

hypothyroidism in neonates and infants

A

cretinism

34
Q

5 features of cretinism

A
  1. mental retardation
  2. short stature w/ skeletal abnormalities
  3. Coarse facial features
  4. Enlarged tongue
  5. umbilical hernia
35
Q
  1. Maternal hypothyroidism during early pregnancy
  2. thyroid agenesis
  3. dyshormonogenetic goiter
  4. iodine deficiency
A

causes of cretinism

36
Q

due to a congenital defect in thyroid hormone production, usually involving thyroid peroxidase

A

Dyshormonogenetic goiter

37
Q

Accumulation of glycoaminoclycans in the skin and soft tissue –> deepening of voice and large tongue

A

Myxedema due to hypothyroidism

38
Q

4 causes of hypothyroidism

A
  1. iodine deficiency
  2. hashimoto
  3. drugs (lithium)
  4. surgical removal/radioablation of thyroid
39
Q

Autoimmune destruction of the thyroid gland associated with HLA-DR5

A

Hashimoto

40
Q

How might hashimoto initially present

A

hyperthyroidism due to follicle damage

41
Q

Labs in hashimoto (after progression to hypothyroidism)

A

High TSH
Low T4
Antithryoglobulin & antithyroidperoxidase antibodies

42
Q

Histology of Hashimoto

A

Chronic inflammation w/ germinal centers and Hurthle cells

43
Q

What are Hurthle cells?

A

eosinophilic metaplasia of cells that line the thyroid follicles

44
Q

Hashimoto increases risk for

A

B cell (marginal zone) lymphoma

45
Q

How does B-cell (marginal zone) lymphoma present

A

enlarging thyroid gland late in disease course

46
Q

granulomatous thyroiditis following viral infxn that presents as a TENDER thyroid w/ transient hyperthyroidism

A

De Quervain Thyroiditis

Subacute granulomatous thyroiditis

47
Q

De Quervain prognosis

A

self-limited; 15% may progress to hypothyroidism

48
Q

Chronic inflammation w/ extensive fibrosis of thyroid gland –> hypothyroidism w/ hard as wood NONTENDER thyroid –> may extend to involve local structures (airway)

A

Reidel fibrosing thyroiditis

49
Q

Anaplastic carcinoma and Reidel fibrosing thyroiditis have the same clinical features. How to differentiate?

A

Reidel fibrosing thyroiditis tends to hit younger patients (40s) and malignant cells are absent

Pathoma Endo (7 decks)

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