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Pathophysiology of Hyperthyroidism

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  Pathophysiology of Hyperthyroidism Thyrotoxicosis  results from the effects of excess thyroid hormone on peripheral tissues. Hyperthyroidism , the more specific term, is used to describe a state of thyrotoxicosis that is due to the overproduction of thyroid hormone by the thyroid gland. 3 most common cause of hyperthyroidism : Graves disease a.k.a autoimmune hyperthyroidism ), Toxic multinodular goitre & a toxic adenoma Other causes : multinodular goiter, adenoma, thyroiditis, and exogenous thyroid hormone. 1.   Graves Disease (Diffuse Toxic Goitre) -   affects females 7x than males -   peak age of onset is btween 20  –  40 yrs -   risk factors : family history of autoimmune disease, HLA-B8 genotype, smoking, high iodine intake or use of iodine-containing medications (eg amiodarone). -   Characterised by a triad of features: a) hyperthyroidism b)   diffuse thyroid enlargement c)   ophtalmopathy - this autoimmune disease is unique because does not destroy tissue but it results in hyperfunctioning of the thyroid gland -    Autoantibodies stimulate the TSH receptor via the cAMP pathway just like TSH and leads to overproduction of thyroid hormone. -   stimulus for Graves disease is unknown but viral illness and stress appear to play a role Etiopathogenesis : 1. Genetic factor association HLA-DR3, CTLA-4 and PTPN22 2. Other factors emotional stress and smoking 3. Autoantibodies i) TSI : binds to TSH receptor and stimulates increased release of thyroid hormones ii) TGI : stimulates proliferation of follicular epithelium iii) TBII : it inhibits binding of TSH to its own receptor. Clinical feature : all clinical features of thyrotoxicosis and specific Graves disease sign&symptoms -> Exopthalmos  2. Toxic multinodular goitre a.k.a Plummer disease -   2 nd  most common cause, affect at 60 yrs of age -   commonly found in areas of iodine deficiency -   a portion of thyroid gland develop automaticity and begins to secrete thyroid hormone in the absence of TSH signal.   -   This automaticity is the result of a somatic mutation in the TSH receptor signaling pathway, causing the continuous activation of the TSH-receptor pathway   -   T4 and T3 levels are elevated, and TSH level is suppressed   Clinical feature : only the core symptom of thyrotoxicosis, no opthalmopathy 3. Toxic adenoma -   develops slowly in the fourth to sixth decades of life -   a benign neoplasm, nodules secrete thyroid hormones independently because this tissue contains mutated TSH receptors -   rarely cause symptoms before reaching 3cm in diameter. -   Same like toxic multinodular goitre, caused by somatic mutations of the TSH-receptor signaling pathway which leads to increased automaticity of the thyroid tissue, but difference is that, the automaticity develops in an otherwise normal thyroid gland. Clinical Features of Thyrotoxicosis General  Anxiety Diaphoresis Fatigue Hair loss Heat intolerance Insomnia Irritability Weight loss  Cardiovascular  Arrhythmias Sinus tachycardia Systolic hypertension  Dermatologic  Pretibial myxedema Thin skin Onycholysis  Gastrointestinal  Frequent bowel movements  Hematologic  Anemia, normocytic   Pulmonary  Pleural effusions  Musculoskeletal  Muscle aches Osteoporosis Weakness  Neurologic  Brisk reflexes Fine tremor   Ophthalmologic  Lid lag Thyroid stare  Reproductive  Menstrual irregularities The rate of metabolism increases with excess thyroid hormone as the result of increases in the rates of both the synthesis and the degradation of biologic molecules, including protein, lipids, and carbohydrates. During the thyrotoxic state, the rate of degradation increases more than the rate of synthesis, resulting in a net catabolic effect. The consequences include weight loss and muscle weakness despite increased appetite and adequate caloric intake. Cardiovascular manifestations are among the first clinical consequences of the thyrotoxic state. Excess sympathetic nervous system (SNS) stimulation together withincreased peripheral oxygen demand secondary to the increased metabolic rate leads to increased cardiac output. This increase in cardiac output is initially due to an increase in heart rate and contractility but later results from an increase in stroke volume. Total  peripheral resistance decreases in order to supply more oxygen to peripheral tissues. The increase in cardiac output with a concurrent decrease in total peripheral resistance leads to the wide pulse pressure characteristic of the thyrotoxic patient. The SNS is stimulated by unknown mechanisms in the thyrotoxic state, but it is  believed that thyroid hormone likely plays a permissive role in the SNS, insofar as there are no signs of direct upregulation of the SNS, and levels of epinephrine, norepinephrine, and their metabolites remain unchanged. This increased sympathetic tone  in the thyrotoxic state leads to increases in heart rate, respiratory rate, the thyroid stare, and lagging of the upper eyelid. Stimulation of the SNS results in nervousness, irritability, hyperactivity, and fatigue; psychosis has also been observed in the thyrotoxic state. Symptoms of thyrotoxicosis can also be attributed to altered tissue growth and maturation including integumentary effects such as smooth skin, onycholysis, and osteoporosis.     
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