Samuel was struck by a car while crossing Assembly Street. He suffered a bilateral transection of the spinal cord at T11. Discuss the impact of this injury on the sensory and motor branches of the nervous system. A bilateral transection of the spinal cord at T11 would result in paraplegia which is the loss of motor function below the waist. There would be no motor or sensory function below the level of injury. This injury would impact the lower limbs but would not cause injury to the upper extremities. A bilateral transection at T11 will result in severe back and leg pain. Due to the spinal flexibility of T11 it is prevalent to see injury in this part of the thoracic spine. Both the small intestines and colon would be innervated by this injury. The vagus nerve would be innervated in the parasympathetic division (craniosacral region) and the thoracic splanchnic nerves would be innervated in the sympathetic division (thoracolumbar region). Injury to the small intestines or colon could result in bowl perforation. This could leak into the abdomen area causing infection. The areas of the sympathetic division that would be influenced by this injury are the adrenal glands, bladder, and genitals. Samuel’s ability to deal with physical and emotional stress will be damaged due to lack of epinephrine from the adrenal medulla. The postganglionic terminals of the sympathetic system release norepinephrine to induce contractions of the bladder base, smooth muscle, and relaxation of the bladder body. Injury to the bladder could cause urine back up which could harm the kidneys. Samuel is also unable to have an erection now due to the lack of blood flow to the genitals. For the parasympathetic division the bladder and genitals would be impacted by this injury. When the bladder is full, sensory activity causes an increase in parasympathetic tone and lowers sympathetic activity causing the muscles to relax and bladder to contract. This afferent activity will be altered due to Samuel’s bilateral transection at T11. This could lead result in a blockage to the urine flow. Damage to the genitals would interfere with the relaxation of smooth muscle cells causing the inability of an erection. This would lead to the inability to have sexual intercourse. Discuss the 4 A’s (primary hormones) known to directly affect body water. Include in your discussion the class of hormone, the structure from which it is secreted, how the hormone is regulated, and the symptoms if the hormone is deficient or it is secreted in excess. The 4 A’s (primary hormones) that directly influence body water are: anti diuretic hormone (ADH), aldosterone, atrial natriuretic peptide (ANP), and angiotensin II (Ang II). Anti-diuretic hormone (ADH) is a peptide secreted by the posterior pituitary gland that plays a role in the regulation of water in the body. It aids to avoid dehydration by averting the formation of urine. ADH is regulated by osmoreceptors in the hypothalamus. If salt concentrations are high (high osmolarity) then the osmoreceptors will be activated and ADH will be stimulated to reabsorb water in the kidneys. Therefore, it preserves water in the body and prevents urination. If salt concentrations are low (low osmolarity), then the osmoreceptors are inactivated and ADH is not released causing the formation of urine. If there is an ADH deficiency it is referred to as diabetes insipidus. This would produce symptoms such as increased urine output, extreme thirst,bedwetting, and nocturia. Diabetes insipidus is due to death of cells that produce ADH in the posterior pituitary gland. The opposite of this or Syndrome of inappropriate ADH secretion (SIADH) or the overproduction of ADH is caused by either ADH-secreting tumor or hypovolemia. The blood concentrations of sodium are very dilute due to excessive reabsorption of water. This syndrome would lead to symptoms as hyponatremia, elevated urine osmolality, excessive urine sodium excretion. Aldosterone is a steroid and primary mineral corticoid. It is an essential electrolyte and water regulating hormone secreted from the adrenal glands. Sodium and Potassium are the minerals associated with aldosterone. It works to release potassium in the kidneys for sodium reabsorption. There are two primary regulators of aldosterone. One of them including if there are increased levels of potassium in the blood this results in modification to membrane potential which interferes with cellular functions. This causes fatigue and depresses heart rate. This causes the secretion of aldosterone resulting in increased absorption of sodium and water resulting in increased blood pressure. The second primary regulator is an indirect effect that includes decreased blood volume or blood pressure can also initiate the release of aldosterone. This causes a release of the protein renin from the kidneys due to a lowered blood pressure. Renin produces a series of events that results in the presence of Angiotensin II. This is associated with a pathway known as the Renin-angiotensin-aldosterone system (RAAS). This system plays a pertinent role in maintaining proper blood pressure. When blood pressure decreases, this system is put to work. Angiotensin II excites the cell in the adrenal cortex to release aldosterone. Aldosterone then causes the reabsorption of sodium and water leading to increased blood pressure. Two other factors that impact aldosterone regulation are increased stress and increased blood pressure or blood volume. These two factors also lead to increased absorption of sodium and water which results in the increased blood pressure. If aldosterone is secreted less than normal it is known as Hypo-Aldosteronism or Addison’s Disease. This would cause low blood pressure, low sodium/high potassium concentrations, and dehydration. If there is hypersecretion of aldosterone this is known as Aldosteronism. This due to a tumor in the adrenal cortex. This would lead to hypokalemia and hypertension. ANP is an amino acid-based hormone produced by the heart and is antagonistic to aldosterone. It was initially isolated from the atria of the heart. The heart secretes ANP when the atria walls are stretched excessively. When the walls are stretched too much it signifies a blood volume overload in the heart. This peptide impacts the Renin-angiotensin-aldosterone system (RAAS) by antagonizing its effects. A primary target of ANP are the kidneys which decreases sodium reabsorption. This means there is less