Toxic multinodular goiter (TMNG), also known as multinodular toxic goiter (MNTG), is an active multinodular goiter associated with hyperthyroidism. It is a common cause of hyperthyroidism in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).Toxic multinodular goiter is the second most common cause of hyperthyroidism (after Graves disease) in the developed world, whereas iodine deficiency is the most common cause of hypothyroidism in developing-world countries where the population is iodine-deficient. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goiter (thyroid enlargement); within a goitre, nodules can develop. Risk factors for toxic multinodular goiter include individuals over 60 years of age and being female. Signs and symptoms
Symptoms of toxic multinodular goitre are similar to that of hyperthyroidism, including:
heat intolerance
muscle weakness/wasting
hyperactivity
fatigue
tremor
irritability
weight loss
osteoporosis
increased appetite
non-painful goitre (swelling of the thyroid gland)
tachycardia (high heart rate - above 100 beats per minute at rest in adults)
tracheal compression
exophthalmos

Causes
Sequence of events:
Iodine deficiency leading to decreased T4 production. Induction of thyroid cell hyperplasia due to low levels of T4. This accounts for the multinodular goitre appearance. Increased replication predisposes to a risk of mutation in the TSH receptor. If the mutated TSH receptor is constitutively active, it would then become toxic and produces excess T3/T4 leading to hyperthyroidism. Diagnosis
Treatments
Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery. Another treatment option is injection of ethanol into the nodules.
Bigeminy is a cardiac arrhythmia in which there is a single ectopic beat, or irregular heartbeat, following each regular heartbeat. Most often this is due to ectopic beats occurring so frequently that there is one after each sinus beat, or normal heartbeat. The two beats are figuratively similar to two twins (hence bi- + gemini). For example, in ventricular bigeminy, a sinus beat is shortly followed by a premature ventricular contraction (PVC), a pause, another normal beat, and then another PVC. In atrial bigeminy, the other "twin" is a premature atrial contraction (PAC). Cause
After any PVC there is a pause that can lead to the development of bigeminy. A PVC wavefront often encounters a refractory AV node that does not conduct the wavefront retrograde. Thus the atrium is not depolarized and the sinus node is not reset. Since the sinus P wave to PVC interval is less than the normal P–P interval, the interval between the PVC and the next P wave is prolonged to equal the normal time elapsed during two P–P intervals. This is called a "compensatory" pause. The pause after the PVC leads to a longer recovery time, which is associated with a higher likelihood of myocardium being in different stages of repolarization. This then allows for re-entrant circuits and sets up the ventricle for another PVC after the next sinus beat.