Chapter 24- Thyroid Flashcards
Effects of T3/T4 on the liver
- Increased cholesterol synthesis
- Increased cholesterol reabsorption from plasma
- Conversion of cholesterol to bile acids
- increased fat oxidation/synthesis
- Increased gluconeogenesis
What is the affect of T3/T4 on muscle
- Increased protein catabolism
- Increased glucose utilization
- Increased fat oxidation
Where is thyroglobulin synthesized and stored
Synthesized and stored in the colloid
What is the most common cause of hyperthyroidism
Primary hyperthyroidism
What type of condition does diffuse hyperplasia fall into
Aka Graves’ disease
-Hyperthyroidism
What type of condition does hyper functioning multinodular goiter fall into
Hyperthyroidism
What type of condition does hyperfunctioning thyroid adenoma fall into
Primary hyperthyroidism
What type of condition does pituitary adenoma fall under
Secondary hyperthyroidism
IN the cause of suspected hyperthyroidism, which condition is suspected when the TSH level is low
Primary hyperthyroidism
IN the cause of suspected hyperthyroidism, which condition is suspected when the TSH level is high
Secondary hyperthyroidism, so basically pituitary adenoma
What are the four components of thyroid storm
- Fever
- Cardiac manifestations
- GI symptoms
- Precipitating history (drugs, pregnancy)
During thyroid storm, what are the cardiac manifestations that can be seen
- Tachycardia
- CHF
During thyroid storm, what are the GI symptoms that can be seen
- Diarrhea
- Jaundice
During thyroid storm, what are the past history factors that can contribute
- Pregnancy/postpartum
- Hemithyroidectomy
- Drugs, such as amiodarone
What are the treatments for the manifestations seen in thyroid storm
- Beta blockers (for cardiac)
- NSAIDs (for the fever)
What is the Wolf-Chaikoff effect
High doses of iodide will decrease the amount of thyroid production
What is the most common cause of hyperthyroidism
Graves disease
What are the clinical manifestations of Graves disease
1- Hyperthyroidism with gland enlargement
2- Infiltrative ophthalmopathy
3- Pretibial myxedema
What are the histological findings in the case of thyroid gland enlargement
Resorption follicles, which are basically just the hyper collection of the thyroid products
What is the cause of ophthalmopathy in Graves
1) Lymphocytes invade the preorbital space
2) Fibroblasts have TSH receptor, so are stimulated by TSHR Abs
3) Extraocular muscles swell
4) Hyloranadate and proteoglycans accumulates (aka matrix accumulation)
5) Adipocytes expand and fill space behind eyes
What is pretibial myxedema and what is it indicative for
-Infiltrative dermopathy causing scaly indurated skin on the shin area
What are the serum laboratory findings of TSH, T3/T4, TSI in the case of Graves
- T3/T4 high
- TSH low
- TSI high (thyroid stimulating Ig)
What are the clinical presentations of congenital hypothyroidism
Aka cretinism, from lack of thyroid:
- Mental retardation
- Growth retardation
- Course facial features
- Umbilical hernias
What are the genetic components that can cause congenital hypothyroidism
- PAX8, FOXE1, TSH receptor mutations all cause defects in thyroid development
- THRB mutations cause thyroid hormone resistance syndrome
What are the clinical skin findings in the case of hypothyroidism
Skin is:
- Course (follicular keratosis)
- Cool
- Dry
- yellowish (carotenemia)
What is the most common cause of hypothyroidism
Hashimoto thyroiditis
What is the pathogenesis of Hashimoto thyroiditis
-Autoantibodies against thyroglobulin and thyroid peroxidase
What is the process of Hashimoto hyroiditis causing hypothyroidism
1) Immune mediated insult
2) Hyperactivity and enlargement
3) Follicular cell exhaustion
What are the histological changes seen in Hashimoto thyroiditis
- Lymphcytic infiltrate appearance with germinal centers
- Hurthle cell metaplasia, where there are strophic follicule cells with eosinophilic changes
Which antibodies are present in Hashimoto thyroiditis
- antithyroglobulin AB aka hTg-Ab (80-90%)
- Antiperoxidase antibody aka hTPO-Ab (90-100%)