Hypothyroidism: Poor production of thyroid hormone: Hashimoto’s thyroiditis
Primary- Thyroid cannot meet the demands of the pituitary gland.
Secondary- No stimulation of the thyroid by the pituitary gland.
Hyperthyroidism: excessive production of thyroid hormone. Graves’ disease
Congenital adrenal hyperplasia: Excessive production of androgen and low levels of aldosterone and cortisol. (Geneticially inherited disorder). Different forms of this disorder that affect males and females differently.
Causes: Adrenal gland enzyme deficit causes cortisol and aldosterone to not be produced. Causing male sex characteristics to be expressed prematurely in boys and found in girls.
Primary/Secondary Hyperaldosteronism
Primary Hyperaldosteronism: problem within the adrenal gland causing excessive production of aldosterone.
Secondary Hyperaldosteronism: problem found elsewhere causing excessive production of aldosterone.
Cushing’s syndrome: Abnormal production of ACTH (adrenocoticotropic hormone) which in turn causes elevated cortisol levels.
Diabetic ketoacidosis: increased levels of ketones due to a lack of glucose.
Causes: Insufficient insulin causing ketone production which end up in the urine. More common in type I vs. type 2 DM.
T3/T4 Review
Both are stimulated by TSH release from the Pituitary gland
T4 control basal metabolic rate
T4 becomes T3 within cells. (T3) Active form.
T3 radioimmunoassay- Check T3 levels
Hyperthyroidism- T3 increased, T4 normal- (in many cases)
Medications that increase levels of T4:
Methadone
Oral contraceptives
Estrogen
Cloffibrate
Medications that decrease levels of T4:
Lithium
Propranolol
Interferon alpha
Anabolic steroids
Methiamazole
Lymphocytic thyroiditis: Hyperthyroidism leading to hypothyroidism and then normal levels.
Causes: Lymphocytes permeate the thyroid gland causing hyperthyroidism initially.
Graves’ disease: most commonly linked to hyperthyroidism, and is an autoimmune disease. Exophthalmos may be noted (protruding eyeballs). Excessive production of thyroid hormones.
Type I diabetes (Juvenile onset diabetes)
Causes: Poor insulin production from the beta cells of the pancreas. Excessive levels of glucose in the blood stream that cannot be used due to the lack of insulin. Moreover, the patient continues to experience hunger, due to the cells not getting the fuel that they need. After 7-10 years the beta cells are completely destroyed in many cases.
Type II diabetes
The body does not respond appropriately to the insulin that is present. Insulin resistance is present in Type II diabetes. Results in hyperglycemia.
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