15.3 - 15.6 Thyroid Flashcards
Cystic dilation of thyroglossal duct remnant
Thyroglossal duct cyst
Normally, the thyroid develops WHERE before traveling along the thyroglossal duct to the anterior neck
Back of tongue
What normally happens to the thyroglossal duct after the thyroid travels down it?
normally involutes, but if it persists, it may undergo cystic dilation
Persistance of thyroid tissue at the base of tongue (presents as mass at base of tongue)
Lingual thyroid
How does hyperthyroidism lead to increased BMR?
increased synthesis of Na+-K+ ATPase
How does hyperthyroidism lead to increased SNS activity?
increased expression of beta1-adrenergic receptors
cholesterol levels in hyperthyroidism
low
serum glucose in hyperthyroidism
high due to increased gluconeogenesis and glycogenenolysis
What type of autoantibody stimulates TSH receptor in Graves dz?
IgG
What type of HSR is Graves disease?
Type II HSR
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
Type I HSR
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
Type II HSR
HSR that is immune-complex mediated - antigen-antibody (IgG) complexes activate complement which attracts PMNs, wh/ release lysosomal enzymes
Type III HSR
HSR that is delayed (T-cell-mediated) type - sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved)
Type IV HSR
How do you test for type I HSR?
skin test for specific IgE
How do you test for type II HSR?
direct and indirect Coombes
How do you test for type III HSR?
immunofluorescent staining
How do you test for type IV HSR?
patch test, PPD
Muscle mass in hyperthyroidism
Decreased –> weakness
in what demographic does graves classically occur
women 20-40
- Hyperthyroidism
- Diffuse goiter
- Exophthalmos
- Pretibial myxedema
Graves
Name two glycosaminoglycans
- Chondroitin sulfate
2. hyaluronic acid
TSH activation stimulates TSH-bearing fibroblasts behind the orbit –> buildup, inflammation
exophthalmos in Graves
Histology of Graves
Irregular follicles with scalloped colloid and chronic inflammation
Labs of Graves
Decreased TSH
Increased total and free T4
Hypocholesterolemia
Increased serum glucose
Treatment of Graves
- Beta blockers
- Thioamide
- Radioiodine ablation
A potentially fatal complication of Graves due to elevated catecholamines and massive hormone excess, usually in response to stress (surgery or childbirth)
Thyroid storm
Presentation of thyroid storm (3 features)
- Arrhythmia
- Hyperthermia
- Vomiting –> hypovolemic shock
Treatment of thyroid storm
- Propylthiouracil (PTU)
- Beta-blockers
- Steroids
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
Enlarged thyroid gland with multiple nodules due to relative iodine deficiency; usually nontoxic (euthyroid)
Multinodular goiter
Rarely, multinodular goiter becomes TSH independent leading to T4 release and hyperthyroidism
Toxic goiter
hypothyroidism in neonates and infants
cretinism
5 features of cretinism
- mental retardation
- short stature w/ skeletal abnormalities
- Coarse facial features
- Enlarged tongue
- umbilical hernia
- Maternal hypothyroidism during early pregnancy
- thyroid agenesis
- dyshormonogenetic goiter
- iodine deficiency
causes of cretinism
due to a congenital defect in thyroid hormone production, usually involving thyroid peroxidase
Dyshormonogenetic goiter
Accumulation of glycoaminoclycans in the skin and soft tissue –> deepening of voice and large tongue
Myxedema due to hypothyroidism
4 causes of hypothyroidism
- iodine deficiency
- hashimoto
- drugs (lithium)
- surgical removal/radioablation of thyroid
Autoimmune destruction of the thyroid gland associated with HLA-DR5
Hashimoto
How might hashimoto initially present
hyperthyroidism due to follicle damage
Labs in hashimoto (after progression to hypothyroidism)
High TSH
Low T4
Antithryoglobulin & antithyroidperoxidase antibodies
Histology of Hashimoto
Chronic inflammation w/ germinal centers and Hurthle cells
What are Hurthle cells?
eosinophilic metaplasia of cells that line the thyroid follicles
Hashimoto increases risk for
B cell (marginal zone) lymphoma
How does B-cell (marginal zone) lymphoma present
enlarging thyroid gland late in disease course
granulomatous thyroiditis following viral infxn that presents as a TENDER thyroid w/ transient hyperthyroidism
De Quervain Thyroiditis
Subacute granulomatous thyroiditis
De Quervain prognosis
self-limited; 15% may progress to hypothyroidism
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
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
