In general, hyperthyroidism is a disorder referring to a sustained overproduction of thyroid hormone (Mandel, Larsen, & Davies, 2012). Hyperthyroidism is estimated to affect 1%-2% world population; with women preponderate 10 times higher than men according to studies from UK and USA (Stevens, 2000).
Hyperthyroidism affects multiple body systems. For example, increased basal metabolic rate causes increased appetite and heat intolerance and increased protein degradation, resulting in muscle wasting and weakness. This is not helpful for a mother with a new born as it indicates that she might not be able to life her infant when she needs to.
There are four mechanisms in the development of Graves’ disease. Bystander activation: any antigens can activate any T cells within thyroid gland through cytokine secretion, to initiate autoimmunity against thyroid gland (Mandel, Larsen, & Davies, 2012). Molecular mimicry: some bacteria and viruses have similar protein structure as human, antigenic similarity of those microorganisms activates intrathyroidal T cells to initiate autoimmunity (Mandel, Larsen, & Davies, 2012). Expression of Human Leukocyte Antigen (HLA) Class II antigen: a local insult of thyroid gland triggers thyroidal inflammation, which then leads to the secretion of HLA Class II antigen from thyroid epithelial cells. This overexpression of thyroid gland can initiate autoimmunity (Mandel, Larsen, & Davies, 2012). Cryptic antigens: some intrathyroidal antigens carry cryptic epitopes, which activate T cells if an epitope is sufficient in amount. Activated T cells will then initiate autoimmunity (Mandel, Larsen, & Davies, 2012).
Risk factors for Graves’ disease are genetic susceptibility (genome wide studies have confirmed 8 genes associated), infection (no specific infection has been identified; nonetheless, animal studies have shown viral infection induced Graves’ disease), stress (stress supresses immunity and overcompensation occurs after stress is released. Autoimmunity might occur via overcompensation), gender (women have two pairs of X-chromosome hence greater incidence than man), pregnancy (same mechanism as stress), iodine (lack of iodine causes overproduction of thyroid hormone and excessive iodine damage thyroid gland), and radiation exposure (Graves’ disease might occur after iodine radiotherapy) (Mandel, Larsen, & Davies, 2012).
Subacute thyroiditis is directly or indirectly caused by viral infection, often seen in upper respiratory illness (Mandel, Larsen, & Davies, 2012). Mumps, Coxsackie, Influenza, Echo, and Adenoviruses have been identified as potential threats (Mandel, Larsen, & Davies, 2012). Damage to the thyroid gland causes excessive leak of thyroid hormones. Unlike Graves’ disease, subacute thyroiditis does not increase synthesis of thyroid hormones.
In Graves’ disease, TSH-R Ab is the major circulating antibody against thyroid antigens (Mandel, Larsen, & Davies, 2012). It targets TSH receptor on thyroid follicular cell membrane. TSH-R Ab acts as TSH receptor agonist that increases the intake of iodine and thyroid hormone synthesis and release (Mandel, Larsen, & Davies, 2012). In subacute thyroiditis, APO-Ab is the major antibody leads to destruction of the thyroid gland (Mandel, Larsen, & Davies, 2012). The destruction causes increasing release of thyroid hormones.
List five common signs and symptoms of the identified condition; for each provide a link to the underlying pathophysiology
Thyroid hormones stimulate many metabolic activities in tissues, leading to an increased basal metabolic rate (Lazar, 2012). Intracellularly, thyroid hormones target mitochondria to produce ATP. They also targets DNA, there are two nuclear thyroid hormone receptor (TR) genes are found in human, alpha and beta TR genes (Lazar, 2012). TR genes are further categorised in four forms. Each tissue