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Endo/Repro > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

Thyroid embyrological origin

A

Developed from endoderm & 2nd pharyngeal pouch

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2
Q

How does TRH affect TSH?

A

Increases TSH by binding membrane receptor → thyroid stimulating immunoglobulin (TSI) → thyroglobulin

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3
Q

Most sensitive measure of thyroid function

A

TSH

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4
Q

How is iodine metabolized?

A

Dietary iodine → I- & Na+ symporter → travels to colloid via Pendrin pathway → oxidation

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5
Q

T3 composition

A

2 iodine + thyroglobulin

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6
Q

Describe Wolff-Chaikoff effect

A

Excess iodine exposure → inhibition of thyroid hormone synthesis by blocking thyroglobulin iodination

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7
Q

What is thyrotoxicosis

A

Hypermetabolic state d/t ↑ free T3 and T4

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8
Q

Two causes of thyrotoxicosis

A

1° hyperthyroidism: ↑ TSH d/t thyroid dysfunction
2° hyperthyroidism: hypothalamic/pituitary cause ↑ TSH

Graves causes most cases

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9
Q

7 B’s of hyperthyroidism

A

-Brain maturation
-Bone growth (synergism with GH & IGF-1) → bone turnover
-β-adrenergic effects (↑ β1 in heart: ↑ CO, HR, SV, contractility)
-BMR ↑
-Blood sugar
-Break down lipids (lipolysis)
-Babies (surfactant synthesis)

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10
Q

Labs in hyperthyroidism

A

↑ T4, ↓ TSH, ↑ 123 I, hyperglycemia, hyperlipidemia, hypercalcemia

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11
Q

Cause and labs of exogenous hyperthyroidism

A

Levothyroxine misuse (synthetic T4)

↑ free thyroxine, ↓ TSH, ↓↓ thyroglobulin

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12
Q

Graves Disease presentation

A

Female 20-40 years
Enlarged thyroid/Smooth goiter
Exophthalmos
Dermopathy (pretibial myxedema)

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13
Q

Graves disease genetics

A

HLA-DR3 or polymorphism in inhibitory T cell receptor CTLA-4

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14
Q

Pathogenesis of Graves

A

TSI IgG autoantibodies bind to TSH receptor → ↑ Adenylyl cyclase → ↑ thyroid hormones

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15
Q

What causes exophthalmos in Graves?

A

T cell lymphocytes recruit cytokines (TNF-α, IFN-γ) which ↑ fibroblast secretion of hydrophilic GAG’s

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16
Q

Graves microscopy

A

Tall, crowded columnar follicular epithelial cells.
Pale colloid with scalloped margins.
Lymphoid infiltrates.

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17
Q

Precipitating factors of thyroid storm (thyrotoxic crisis)

A

Graves pts with ↑ catecholamine levels (surgery or acute infection)

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18
Q

Thyroid storm symptoms and 1 important complication

A

Fever, flushing, sweating.

Cardiac dysrhythmias and sudden death.

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19
Q

Toxic multinodular goiter (Plummer syndrome) pathogenesis

A

Thyrotoxicosis d/t autonomous nodules that function independent of TSH stimulation

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20
Q

Morphology of toxic multinodular goiter

A

Colloid-rich follicles lined by flattened, inactive epithelium

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21
Q

Types of hypothyroidism

A

Cretinism (children) & Myxedema (adults)

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22
Q

Cretinism (Congenital Hypothyroidism) presentation

A

Severe mental retardation in infancy/early childhood (no manifestations at birth because maternal T4 crosses placenta)

Short stature, umbilical hernia, protruding tongue.

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23
Q

Causes of cretinism

A

Iodine deficiency, maternal hypothyroidism (IgG crosses placenta)

24
Q

Causes of myxedema

A

Hashimoto thyroiditis.
Iodine deficiency.
Idiopathic.

Or secondary hypothyroidism d/t pituitary failure

25
Q

Clinical features of myxedema

A

Slow, dumb, cold intolerance, overweight, DIASTOLIC HTN (Na/H2O retention), ATHERSCLEROSIS, periorbital puffiness, delayed DTRs, menorrhagia

26
Q

Lab findings of myxedema

A

↓ T4, ↑ TSH, hyperlipidemia (↓ LDL receptor synthesis)

27
Q

Important complication of myxedema

A

Myxedema coma: SUDDEN FALL IN TEMP, ↓ HR/BP, confusion, coma

Infection, MI, illness → ↓ T3/T4

28
Q

Hashimoto thyroiditis presentation

A

Females 45-65 yo with diffuse goiter “enlarged rubbery” thyroid

Initially hyperthyroidism → later hypothyroidism

29
Q

Hashimoto thyroiditis pathogenesis

A

autoimmune destruction of thyroid via:
-CD8 T cells (type IV HS)
-anti TPO & anti thyroglobulin Ab (type II HS)

30
Q

Hashimoto thyroiditis increases risk for ___.

A

B cell lymphoma (Marginal zone)

31
Q

Hashimoto microscopy

A

-Lymphoplasmacytic infiltrate w/ germinal centers
-Atrophic follicles
-Hurthle cells: oncocytic metaplastic large cells with granular eosinophilic cypoplasm

32
Q

Cause of postpartum thyroiditis

A

Decreased immunity during pregnancy → slow evolution of autoimmune response to thyroid autoantigens

33
Q

Postpartum thyroiditis presentation

A

Painless diffuse thyromegaly within 1 year of pregnancy

34
Q

Pathogenesis of postpartum thyroiditis

A

Self-limiting.

Destruction → sudden release of stored thyroid hormone → transient hyperthyroidism (1-3 months) → hypothyroidism (4-8 months → recovery to euthyroid state

35
Q

Subacute (De Quervain or Granulomatous) thyroiditis presentation

A

Female 30-50 yo w/ enlarged, firm, TENDER thyroid

Fever, jaw pain, redness over skin

Rare complication of septicemia

36
Q

Pathogenesis of subacute thyroiditis

A

Follows a viral infection → transient hyperthyroidism → euthyroid → hypothyroid → euthyroid

37
Q

Reidel’s (invasive fibrous) thyroiditis presentation

A

Female 40-60 yo with rock-like painless goiter

38
Q

Reidel’s pathogenesis

A

Associated with inflammatory fibrosclerotic conditions (fibrosis, sclerosing cholangitis)

39
Q

Reidel’s gross pathology

A

Tan gray, WOODY, avascular

40
Q

Reidel’s microscopy

A

Fibrous tissue & inflammatory infiltrate (plasma cells (IgG4), lympocytes, macrophages, eosinophils)

41
Q

Euthyroid sick syndrome presentation

A

abnormal thyroid function tests in normally functioning thyroid in hospitalized pts

42
Q

Euthyroid sick syndrome pathogenesis

A

↓ thyroid hormones d/t cytokines (IL6)

altered deiodinase enzyme activity

43
Q

Lab findings in euthyroid sick syndrome

A

↓ T3, ↑ T4, ↑ REVERSE T3, ↓ TSH, ↓ thyroid binding globulin

44
Q

Typical features of thyroid malignancy

A

young, male, cold nodule, pain, voice change

45
Q

Radio iodine uptake

A

Hot nodule (↑ uptake): Graves/Nodular goiter

Cold nodule (↓ uptake): adenoma/carcinoma

46
Q

Follicular adenoma morphology

A

Solitary, well-circumscribed nodule

47
Q

Most follicular adenomas are __.

A

Cold (non-functional)

May become hot/toxic via autonomous TSH receptor pathway mutations

48
Q

Four types of thyroid carcinomas

A

Papillary, Follicular, Medullary, Anaplastic (undifferentiated)

49
Q

All thyroid carcinomas are derived from ___, except ___.

A

thyroid follicular epithelium

medullary carcinoma (derived from parafollicular C cells)

50
Q

List the genetics of each type of thyroid carcinoma

A

Papillary: activation of MAP kinase pathway by RET/PTC rearrangements or BRAF point mutations

Follicular: RAS point mutations,, P13K/AKT/PTEN mutations, or PAX8-PPARγ translocations

Medullary: MEN2A & 2B RET mutations

Anaplastic: TP53 mutations

51
Q

How to distinguish between follicular carcinoma or adenoma

A

Carcinoma: thyroid capsular/vascular invasion

Adenoma: no invasion

52
Q

How to distinguish between follicular or papillary carcinoma

A

Papillary carcinoma: Psammoma bodies (concentric calcified structures in cores of papilla) & Optically clear nuclei (Orphan Annie eyes)

53
Q

Spread of follicular vs papillary carcinoma

A

Follicular: hematogenous

Papillary: lymphatic

54
Q

Which thyroid malignancies are multifocal, which aren’t?

A

Papillary: multifocal

Follicular adenoma & carcinoma: solitary

55
Q

Medullary carcioma parafollicular C cells secrete ___.

A

Calcitonin (tumor marker) + CEA

56
Q

Microscopic finding of medullary carcinoma

A

Amyloid polygonal deposits (Congo red stain/IHC)

Endo/Repro (4 decks)

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