"Graves’ Disease and Type 1 Diabetes" is a good example of a paper on symptoms. Our patient has low levels of TSH which means that the release of T3 and T4 is not activated by the normal negative feedback loop but instead the binding of TSI to the TSH receptor. Functions of TH in the body Regulation of the rate of metabolism by accelerating the rate of food utilization Influences the rate of growth and development of the fetal nervous system It plays a role inactivation of a number of genes. Increases protein synthesis as well as catabolism Accelerates growth rate in children It stimulates carbohydrate and fat metabolism For the case of our patient, there are increased levels of TH.
The signs developed emanates from hyperthyroidism. Decreased TSH and increased TSI implications This phenomenon results in increased levels of TH because of two main reasons. Firstly, TSI binds to the TSH receptors hence stimulating continuous production of TH. Secondly, the negative feedback loop does not work because the initiator of hyperthyroidism is TSI, which is not normally part of the regulation system. TH Hormone TH is a peptide hormone. After the secretion by the thyroid follicles, very small quantities of thyroid hormone are transported in an unbound form.
The bulk of the hormone is transported bound to the plasma proteins in circulation. These proteins have no specific role in the activation of the hormone. TH bind a nuclear receptor that activates a cascade of events that results in activation of nuclear transcription for a number of genes. The permissive effect is a relationship that exists some hormones with their target cells. The relationship between thyroid hormone and epinephrine is such that the increase in thyroid hormone translates to activation of the epinephrine receptors in the target cell hence epinephrine is able to bind and have its effect on the cell.
TH is therefore very important in stress response because its increase will facilitate an increase in epinephrine the hormone responsible for fight, flight, or flight. TSI and hyperthyroidism TSI binds to the receptors for TSH in the thyroid gland activating the release of TH. The deficiency of a feedback control mechanism results in increased TH in the body resulting in hyperthyroidism. TSI is an agonist to TSH.
This is because they produce the same effect; the release of TH. Propranolol alleviates the symptoms of fast heartbeat and trembling. It reduces the rate of contraction of muscles including the cardiac muscles. Thioamides being an inhibitor of TH synthesis will be beneficial to the patient because it will reduce the release of TH hence alleviating the symptoms that result from hyperthyroidism. The TH levels will reduce when treated with Radioactive iodine 1311 because it reduces the activity of the thyroid gland hence reduced TH levels. Case 4.B: Type 1 DiabetesCause of type 1 DM The exact cause is unknown but it is believed that the disease is an autoimmune disorder.
Here the body’ s immune system attacks its own cells. Blood glucose levels are regulated by insulin and glucagon. When the glucose levels get high, insulin lowers them down. When the levels are too low glucagon initiates a series of processes that results in increased sugar levels. The interplay between the two hormones ensures that sugar levels are maintained within the body. Insulin deficiency results in the inability of the body to regulate its sugar.
The main sugar that is transported and used in the body is glucose, therefore glucose remains in circulation. Insulin reduces the blood sugar by facilitating the entry of glucose into cells for conversion to glycogen for storage purposes. Ketones are organic compounds that are formed through oxidation of secondary alcohols. In the body, they are usually formed when fat is broken down to produce energy. They can also be released in situations when insulin is deficient in aiding the utilization of energy by the body. The breakdown of fat results in the production of ketones whose concentration rises in the blood while some spills through the urine. Ketone bodies have a higher efficiency than glucose per unit oxygen hence they increase the mitochondrial load.
In addition, ketosis results in an increase in the blood PH. Glucose was not taken up by cells hence it remained in circulation, part of it spilled through the urine. Increased urine output results from the concentration gradient that is created in the kidney tubules by the high sugar, which causes increased reabsorption hence so much of the water in the body, gets out through the urine. Polydipsia results when the body losses so much of its water with high glucose levels.
The resultant is a feeling of thirst. Other complications include; Infections on the feet, numbness, problems with eyesight, pain on the foot, seizures, and loss of consciousness. Case 4.C: Addison’ s diseaseCause of Addison Disease It is caused by damage to the outer layer of the adrenal cortex. This reduces the level of the hormones produced in this regionThe presence of adrenal antibodies is an indicator that there is some damage to the adrenal gland, hence the antibodies are released to fight the damaging agents.
Their increase shows that there is a high likelihood of having the disease. Primary adrenal insufficiency is synonymous to Addison’ s disease; it refers to the inability of the adrenal glands to produce the steroid hormones produced in this region. These are mainly mineralocorticoids as well as glucocorticoids hormones. The roles played by these hormones are compromised hence the effects. For example, cortisol plays a critical role in the regulation of blood sugar levels, increase in body fat, helps the body to cope with stress and also plays a role in helping the body fight infections.
On the other hand, aldosterone, the major mineralocorticoid plays a very important role in the regulation of the sodium and potassium levels in the blood as well as blood pressure and volume. Loss of these functionalities results in the accompanying symptoms such as loss of appetite, body weakness, low blood pressure, as well as increased heart rate. Hyperpigmentation in Addison disease is caused by the drop in cortisol levels that activates the pituitary to produce ACTH.
ACTH is derived from pro-opiomelanocortin (POMC) that is a precursor of MSH and beta-endorphin. The rise in ACTH translates to high levels of melanocyte-stimulating hormone (MSH) as well as beta-endorphin. The effect of MSH is that it stimulates the melanocytes hence the pigmentation on the skin. Elevated ACTH is meant to regulate the production of cortisol. A reduction in cortisol should activate ACTH that acts on the adrenal cortex hence facilitating the production of cortisol. Adrenal crisis comprises of symptoms that demonstrate high levels of adrenal insufficiency that result from reduced levels of cortisol production.
This occurs when Addison’ s disease becomes severe or remains untreated for a long period. Addison treatment is through the provision of glucocorticoid as well as mineralocorticoid pills throughout the period that the person lives. Case 4.D: Cushing’ s Syndrome Liver, fat, lymphocytes, among other cellsCortisol plays a critical role in the regulation of blood sugar levels, increase in body fat, helps the body to cope with stress and also plays a role in helping the body fight infectionsGlucocorticoids are hormones that play a very important role in inflammation.
They are steroids in nature and include cortisol that plays a very critical role in the regulation of inflammation. These features are caused by the impact of increased cortisol exposure over a long period. The resultant is tumorous features such as the buffalo hump. Delayed wound healing is associated with the role of heat shock proteins that are affected by cortisol. Glucocorticoids do impair wound healing as well resulting in surgical morbidity.