SM155 Thyroid Pathophysiology Flashcards
Hypothyroidism vs. hyperthyroidism: activity level, heart rate, temperature perception, reflexes, weight change, bowel symptoms, skin/hair, edema
Hypothyroidism: low activity/lethargy/weakness/fatigue, bradycardia, cold intolerance, diminished reflexes, weight gain, constipation, dry/cool skin and coarse/brittle hair, myxedema (facial/periorbital)
Hyper: high activity, tachycardia, heat intolerance, increased reflexes, weight loss, diarrhea, warm/moist skin and fine hair, pretibial myxedema
Lab findings (TSH and T4/T3): primary hypothyroidism
TSH: high T4/T3: low
Lab findings (TSH and T4/T3): primary hyperthyroidism
TSH: low T4/T3: high
Lab findings (TSH and T4/T3): secondary hypothyroidism
TSH: low T4/T3: low
Lab findings (TSH and T4/T3): secondary hyperthyroidism
TSH: high T4/T3: high
Grave’s disease: pathophysiology
Autoimmune etiology. Autoantibodies bind TSH receptors and stimulate the thyroid to produce more thyroid hormone
Grave’s disease: antibody and associated HLA subtype
TSI (thyroid stimulating immunoglobulin)
HLA DR3
Grave’s disease: clinical signs
Ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter, connective tissue deposition
Grave’s disease: thyroid storm
Stress-induced catecholamine surge that can lead to death by arrhythmia
Grave’s disease: beta-blockers
Lower HR, helps with trembling and irritability
Grave’s disease: thionamides (when do you use one over the other?). Dangerous side effect?
Methimazole and Propylthiouracil (PTU) both block TPO. PTU also blocks 5’-deiodinase.
Only use PTU during first trimester of pregnancy.
Agranulocytosis.
Other autoimmune disease associated with Grave’s
Vitiligo
Endocrine ophthalmopathy
Seen in Grave’s disease.
Includes chemises, proptosis.
Radiotherapy
131-I destroys thyroid follicular cells with beta-irradiation. Slow onset of effects (need to treat with thionamides in the meantime).
Postpartum thyroiditis (PPT): definition, at risk groups
Occurrence of hyperthyroidism (or hypothyroidism) during the postpartum period
At risk: DI (type I), other autoimmune disease
Subacute thyroiditis (de Quervain’s): course, path finding, clinical signs
Self-limited, follows flu-like illness
Granulomas
High ESR, jaw pain, tender thyroid
Course of thyroiditis
Often hyper- initially (lots of hormone is pre-made and then released upon damage) and hypo- later in the course
Toxic multinodular goiter: pathophysiology, Jod-Basedow phenomenon,
Focal patches of overactive follicular cells (working independently of TSH due to activating mutation to the TSH receptor) secrete more T4/T3
Jod-Basedow: thyrotoxicosis when an iodine deficient patient is given iodine
Iodine deficiency: clinical sign, severe manifestation
Goiter Cretinism (severe fetal deficiency)
Congenital hypothyroidism: clinical signs (5 P’s)
Pot-bellied, pale, puffy-faced, protruding umbilicus, protuberant tongue
Riedel’s thyroiditis: pathophysiology, clinical signs
Thyroid gets replaced by fibrous tissue
Fixed, hard (rock-like), painless goiter
Hashimoto’s thyroiditis: antibodies, HLA subtype, associated cancer, histology, clinical signs
TPO and antithyroglobulin antibodies HLA-DR5 non-Hodgkin's lymphoma Hurthle cells, lymphocytes, germinal centers Diffuse, non-tender thyroid