Back To CoursePathophysiology Textbook
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Jen has taught biology and related fields to students from Kindergarten to University. She has a Master's Degree in Physiology.
Stress and illness can make us annoyed and cranky. When we're not feeling well, the people we like, even need, most in life can get on our nerves. Because we're upset, we attack them. Attacking something we need as a result of stress and sickness happens on a much smaller scale, too, in autoimmune disorders.
An autoimmune disorder can result from chronic injury or infection. In these disorders, the body mistakes its own cells or parts of cells as pathogens and instructs the immune system to attack and destroy them. Graves' disease and Hashimoto's thyroiditis are two autoimmune disorders that occur when the immune system attacks the thyroid gland.
Before we get into the similarities and differences of these disorders, let's review what we know about the thyroid gland. The thyroid gland is a two-lobed, butterfly-shaped gland located on top of the larynx. Its primary hormones are iodine-based: triiodothyronine (T3) and thyroxine (T4).
These hormones have a range of functions, but their largest role is in regulation of metabolism, the means by which we process food into a usable form of energy for cells. Thyroid hormones also increase our nerves' sensitivity to catecholamines and therefore activate the sympathetic nervous system. Recall that this part of our nervous system is responsible for the 'fight or flight' response.
When thyroid hormones are low in the bloodstream, the brain's hypothalamus releases a biochemical called thyrotropin-releasing hormone, or TRH. TRH acts on the pituitary gland, causing it to make thyroid-stimulating hormone, or TSH. Finally, TSH binds to receptors on the thyroid gland, signaling it to release T3 and T4. An increase in the level of these hormones in the blood is picked up by the hypothalamus and the system is halted via negative feedback.
This system of hormones works a little like cruise control in a car works to maintain the speed set by the driver. When the car's speed drops below the desired speed, the car's speedometer computer sends a signal to the car's throttle, telling it that the car needs to increase its speed. The throttle opens wider to allow more fuel to reach the car's engine, and the car's speed increases. When the set speed is reached, the system shuts off. In both Graves' and Hashimoto's, though, the body's immune system 'throws a wrench' into this negative feedback system.
Graves' disease is the most common cause of hyperthyroidism, or overactive thyroid, in the U.S. In Graves', the body's hyperactive immune system produces an antibody that attaches to the TSH receptors on the thyroid gland. Because TSH isn't actually triggering the release of T3 and T4, the negative feedback system the body has in place doesn't work and the thyroid continually makes and releases thyroid hormones. Since the antibodies consistently trigger the thyroid cells to produce more T3 and T4, the body responds by increasing the thyroid's size, causing a classic thyroid symptom called goiter.
The other primary external symptom of Graves' is called exophthalmos, or protrusion of the eyes. Exophthalmos has two causes. The first is due to a prolonged 'fight or flight' response - the widening of the eyes by a retraction of the upper lids. The second is due to that overactive immune system: the fat and muscles around the eyes become swollen due to an increase in the number of lymphocytes present and other symptoms of inflammation, pushing the eyes forward.
Internally, excess thyroid hormones are also stressing the sympathetic nervous system, constantly preparing us for a threat that's not really there. Resting metabolic rate increases, causing weight loss. Resting heart rate jumps irregularly (arrhythmia) or increases to over 100 beats per minute (tachycardia). Heat intolerance and heavy perspiration are also symptoms.
Diagnosis of Graves' through blood tests relies largely on high-circulating levels of T3 and T4 and low TSH levels, as well as antibodies for TSH receptors. Occasionally, an iodine uptake test is used for confirmation. In this test, the patient consumes a low dose of radioactive iodine. Since thyroid cells actively take up iodine, the degree and location of overactive cells present in radiography as darkened areas of the thyroid.
Pharmaceutical treatment for Graves' consists of symptom relief through beta blockers, which dull sympathetic nervous system activity, and antithyroid medications that prevent the thyroid from making hormones, such as methimazole. In more severe cases, surgical removal of or destruction of the hyperactive cells through radioactive iodine is a treatment option.
Hashimoto's thyroiditis is the most common cause of hypothyroidism, or underactive thyroid. In Hashimoto's, the body's immune system makes antibodies that attack and destroy a part of the thyroid hormone system, usually either a player in the biochemical pathway that thyroid cells use to make thyroid hormones or the TSH receptors themselves. Ultimately, the immune system causes death of thyroid gland cells.
It might seem to be logical that Hashimoto's would cause a decrease in the size of the thyroid gland. Actually, as with Graves, goiter is a common early symptom of Hashimoto's. This is because lymphocytes are attracted to and attacking thyroid tissue, leading to inflammation and swelling.
Goiter in Hashimoto's tends to be much less consistent throughout the thyroid, as opposed to the fairly regular increase in size due to Graves'. Destruction of thyroid tissue also means an initial, transitory increase in thyroid hormones, as T3 and T4 leak from destroyed cells. As these stores are depleted, though, the body isn't able to make more, and TSH levels increase as the body tries to boost thyroid hormone levels.
Internally, a lack of thyroid hormones means a drop in metabolism and a decreased sensitivity of the 'fight or flight' response. Resting metabolic rate drops, causing weight gain and a feeling of sluggishness, achiness, and fatigue. Heart rate slows (bradycardia) and patients develop an intolerance to cold, see a drop in perspiration, and can experience memory loss and confusion.
Myxedema, or skin swelling, is considered to be the classic symptom of hypothyroidism. Naturally, laboratory tests show a very low level of circulating T3 and T4 and usually a high concentration of both thyroid antibodies and TSH. Biopsy of the thyroid gland shows damaged thyroid cells and a large presence of lymphocytes. Treatment of Hashimoto's is lifelong and consists primarily of T4 replacement through medications like levothyroxine.
To summarize, let's compare and contrast these two conditions' similarities and differences:
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Back To CoursePathophysiology Textbook
20 chapters | 274 lessons