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Endo > 15.3 - 15.6 Thyroid > Flashcards

15.3 - 15.6 Thyroid Flashcards

(49 cards)

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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

21
Q
  1. Hyperthyroidism
  2. Diffuse goiter
  3. Exophthalmos
  4. Pretibial myxedema
22
Q

Name two glycosaminoglycans

Study These Flashcards
A
  1. Chondroitin sulfate

2. hyaluronic acid

23
Q

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

Study These Flashcards
A

exophthalmos in Graves

24
Q

Histology of Graves

Study These Flashcards
A

Irregular follicles with scalloped colloid and chronic inflammation

25
Labs of Graves
Decreased TSH Increased total and free T4 Hypocholesterolemia Increased serum glucose
26
Treatment of Graves
1. Beta blockers 2. Thioamide 3. Radioiodine ablation
27
A potentially fatal complication of Graves due to elevated catecholamines and massive hormone excess, usually in response to stress (surgery or childbirth)
Thyroid storm
28
Presentation of thyroid storm (3 features)
1. Arrhythmia 2. Hyperthermia 3. Vomiting --> hypovolemic shock
29
Treatment of thyroid storm
1. Propylthiouracil (PTU) 2. Beta-blockers 3. Steroids
30
Inhibits peroxidase mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion of T4 to T3
PTU mechanism of action
31
Enlarged thyroid gland with multiple nodules due to relative iodine deficiency; usually nontoxic (euthyroid)
Multinodular goiter
32
Rarely, multinodular goiter becomes TSH independent leading to T4 release and hyperthyroidism
Toxic goiter
33
hypothyroidism in neonates and infants
cretinism
34
5 features of cretinism
1. mental retardation 2. short stature w/ skeletal abnormalities 3. Coarse facial features 4. Enlarged tongue 5. umbilical hernia
35
1. Maternal hypothyroidism during early pregnancy 2. thyroid agenesis 3. dyshormonogenetic goiter 4. iodine deficiency
causes of cretinism
36
due to a congenital defect in thyroid hormone production, usually involving thyroid peroxidase
Dyshormonogenetic goiter
37
Accumulation of glycoaminoclycans in the skin and soft tissue --> deepening of voice and large tongue
Myxedema due to hypothyroidism
38
4 causes of hypothyroidism
1. iodine deficiency 2. hashimoto 3. drugs (lithium) 4. surgical removal/radioablation of thyroid
39
Autoimmune destruction of the thyroid gland associated with HLA-DR5
Hashimoto
40
How might hashimoto initially present
hyperthyroidism due to follicle damage
41
Labs in hashimoto (after progression to hypothyroidism)
High TSH Low T4 Antithryoglobulin & antithyroidperoxidase antibodies
42
Histology of Hashimoto
Chronic inflammation w/ germinal centers and Hurthle cells
43
What are Hurthle cells?
eosinophilic metaplasia of cells that line the thyroid follicles
44
Hashimoto increases risk for
B cell (marginal zone) lymphoma
45
How does B-cell (marginal zone) lymphoma present
enlarging thyroid gland late in disease course
46
granulomatous thyroiditis following viral infxn that presents as a TENDER thyroid w/ transient hyperthyroidism
De Quervain Thyroiditis | Subacute granulomatous thyroiditis
47
De Quervain prognosis
self-limited; 15% may progress to hypothyroidism
48
Chronic inflammation w/ extensive fibrosis of thyroid gland --> hypothyroidism w/ hard as wood NONTENDER thyroid --> may extend to involve local structures (airway)
Reidel fibrosing thyroiditis
49
Anaplastic carcinoma and Reidel fibrosing thyroiditis have the same clinical features. How to differentiate?
Reidel fibrosing thyroiditis tends to hit younger patients (40s) and malignant cells are absent

Endo (12 decks)

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