Thyroid disorder reference

The thyroid is one of the largest endocrine glands in the body. This gland is found in the neck inferior to (below) the thyroid cartilage (also known as the Adam's apple in men) and at approximately the same level as the cricoid cartilage. The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones.

The thyroid participates in these processes by producing thyroid hormones, principally thyroxine (T₄) and triiodothyronine (T₃). These hormones regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. Iodine is an essential component of both T₃ and T₄. The thyroid also produces the hormone calcitonin, which plays a role in calcium homeostasis.

The thyroid is controlled by the hypothalamus and pituitary. The gland gets its name from the Greek word for "shield", after the shape of the related thyroid cartilage. Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the most common problems of the thyroid gland.

Anatomy

The thyroid gland is a butterfly-shaped organ and is composed of two cone-like lobes or wings: lobus dexter (right lobe) and lobus sinister (left lobe), connected with the isthmus. The organ is situated on the anterior side of the neck, lying against and around the larynx and trachea, reaching posteriorly the oesophagus and carotid sheath. It starts cranially at the oblique line on the thyroid cartilage (just below the laryngeal prominence or Adam's apple) and extends inferiorly to the fourth to sixth tracheal ring^{[citation needed]}. It is difficult to demarcate the gland's upper and lower border with vertebral levels as it moves position in relation to these during swallowing.

The thyroid gland is covered by a fibrous sheath, the capsula glandulae thyroidea, composed of an internal and external layer. The external layer is anteriorly continuous with the lamina pretrachealis fasciae cervicalis and posteriorolaterally continuous with the carotid sheath. The gland is covered anteriorly with infrahyoid muscles and laterally with the sternocleidomastoid muscle. Posteriorly, the gland is fixed to the cricoid and tracheal cartilage and cricopharyngeus muscle by a thickening of the fascia to form the posterior suspensory ligament of Berry^[1][2]. In variable extent, Zuckerkandl's tubercle, a pyramidal extension of the thyroid lobe, is present at the most posterior side of the lobe^[3][4]. In this region the recurrent laryngeal nerve and the inferior thyroid artery pass next to or in the ligament and tubercle. Between the two layers of the capsule and on the posterior side of the lobes there are on each side two parathyroid glands.

The thyroid isthmus is variable in presence and size, and can encompass a cranially extending pyramid lobe (lobus pyramidalis or processus pyramidalis), remnant of the thyroglossal duct. The thyroid is one of the larger endocrine glands, weighing 2-3 grams in neonates and 18-60 grams in adults, and is increased in pregnancy^{[citation needed]}.

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and sometimes by the thyroid ima artery, branching directly from the aortic arch. The venous blood is drained via superior thyroid veins, draining in the internal jugular vein, and via inferior thyroid veins, draining via the plexus thyroideus impar in the left brachiocephalic vein. Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and parathracheal lymph nodes. The gland is supplied by sympathetic nerve input from the superior cervical ganglion and the cervicothoracic ganglion of the sympathetic trunk^{[citation needed]}, and by parasympathetic nerve input from the superior laryngeal nerve and the recurrent laryngeal nerve.

In the fetus, at 3-4 weeks of gestation, the thyroid gland appears as an epithelial proliferation in the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula linguae at a point latter indicated by the foramen cecum. Subsequently the thyroid descends in front of the pharyngeal gut as a bilobed diverticulum through the thyroglossal duct. Over the next few weeks, it migrates to the base of the neck. During migration, the thyroid remains connected to the tongue by a narrow canal, the thyroglossal duct. Follicles of the thyroid begin to make colloid in the 11th week and thyroxine by the 18th week.

Physiology

The primary function of the thyroid is production of the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin. Up to 80% of the T4 is converted to T3 by peripheral organs such as the liver, kidney and spleen. T3 is about ten times more active than T4.^[5]

Significance of iodine

In areas of the world where iodine (essential for the production of thyroxine, which contains four iodine atoms) is lacking in the diet, the thyroid gland can be considerably enlarged, resulting in the swollen necks of endemic goitre.

Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom. Among amphibians, for example, administering a thyroid-blocking agent such as propylthiouracil (PTU) can prevent tadpoles from metamorphosing into frogs; conversely, administering thyroxine will trigger metamorphosis.

In humans, children born with thyroid hormone deficiency will have physical growth and development problems, and brain development can also be severely impaired, in the condition referred to as cretinism. Newborn children in many developed countries are now routinely tested for thyroid hormone deficiency as part of newborn screening by analysis of a drop of blood. Children with thyroid hormone deficiency are treated by supplementation with synthetic thyroxine, which enables them to grow and develop normally.

Because of the thyroid's selective uptake and concentration of what is a fairly rare element, it is sensitive to the effects of various radioactive isotopes of iodine produced by nuclear fission. In the event of large accidental releases of such material into the environment, the uptake of radioactive iodine isotopes by the thyroid can, in theory, be blocked by saturating the uptake mechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. While biological researchers making compounds labelled with iodine isotopes do this, in the wider world such preventive measures are usually not stockpiled before an accident, nor are they distributed adequately afterward. One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.^[10]

The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic cretinism in most developed countries, and some governments have made the iodination of flour mandatory. Potassium iodide and Sodium iodide are the most active forms of supplemental iodine.

Coughing reference(whooping)

Main info:Whooping Cough: Highly communicable, vaccine-preventable disease that lasts for many weeks and is typically manifested in children .
An infectious condition caused by the bacteria Bordetella pertussis

Pertussis, also known as whooping cough, is a highly contagious disease caused by the bacterium Bordetella pertussis; it derived its name from the characteristic severe hacking cough followed by intake of breath that sounds like "whoop"; a similar, milder disease is caused by B. parapertussis.[1] Although many medical sources describe the whoop as "high-pitched", this is generally the case with infected babies and children only, not adults.[2]


Worldwide, there are 30–50 million pertussis cases and about 300,000 deaths per year. Despite generally high coverage with the DTP and DTaP vaccines, pertussis is one of the leading causes of vaccine-preventable deaths world-wide. Most deaths occur in young infants who are either unvaccinated or incompletely vaccinated; three doses of the vaccine are necessary for complete protection against pertussis. Ninety percent of all cases occur in the developing world. Children tend to catch it more than adults.

Characterization

After a two day incubation period, pertussis in infants and young children is characterized initially by mild respiratory infection symptoms such as cough, sneezing, and runny nose (catarrhal stage). After one to two weeks, the cough changes character, with an increase of coughing followed by an inspiratory "whooping" sound (paroxysmal stage). Coughing fits may be followed by vomiting due to the sheer violence of the fit. In severe cases, the vomiting induced by coughing fits can lead to malnutrition and dehydration. The fits that do occur on their own can also be triggered by yawning, stretching, laughing, or yelling. Coughing fits gradually diminish over one to two months during the convalescent stage. Other complications of the disease include pneumonia, encephalitis, pulmonary hypertension, and secondary bacterial superinfection.^[3]

Because neither vaccination nor infection confers long-term immunity, infection of adolescents and adults is also common^[4] Most adults and adolescents who become infected with Bordetella pertussis have been vaccinated or infected years previously. When there is residual immunity from previous infection or immunization, symptoms may be milder, such as a prolonged cough without the other classic symptoms of pertussis. Nevertheless, infected adults and adolescents can transmit the bacteria to susceptible individuals.

Transmission and Diagnosis

Adults and adolescents are the primary reservoir for pertussis. Pertussis is spread by contact with airborne discharges from the mucous membranes of infected people, who are most contagious during the catarrhal stage. Because the symptoms during the catarrhal stage are nonspecific, pertussis is usually not diagnosed until the appearance of the characteristic cough of the paroxysmal stage. Methods used in laboratory diagnosis include culturing of nasopharyngeal swabs on Bordet-Gengou medium, polymerase chain reaction (PCR), immunofluorescence (DFA), and serological methods. The bacteria can be recovered from the patient only during the first three weeks of illness, rendering culturing and DFA useless after this period, although PCR may have some limited usefulness for an additional three weeks. For most adults and adolescents, who often do not seek medical care until several weeks into their illness, serology is often used to determine whether antibody against pertussis toxin or another component of B. pertussis is present at high levels in the blood of the patient.

Treatment with an effective antibiotic (erythromycin or azithromycin) shortens the infectious period but does not generally alter the outcome of the disease; however, when treatment is initiated during the catarrhal stage, symptoms may be less severe. Three macrolides, erythromycin, azithromycin and clarithromycin are used in the U.S. for treatment of pertussis; trimethoprim-sulfamethoxazole is generally used when a macrolide is ineffective or is contraindicated. Close contacts who receive appropriate antibiotics (chemoprophylaxis) during the 7–21 day incubation period may be protected from developing symptomatic disease. Close contacts are defined as anyone coming into contact with the respiratory secretions of an infected person in the 21 days before or after the infected person's cough began.