University:
University of Phoenix
Course:
HSC 214 | Anatomy and Physiology I
Academic year:

2024
Views:

267

Pages:

15
Author:

Nikolas Werner

Symptoms of Clinical Action Decrease in insulin level in blood leads to hyperglycemia (increased blood sugar level), which leads to: Glucosuria: Presence of glucose in urine Polyuria: Frequent urination Polydipsia: Increased thirst Acidosis: Increase ketone bodies in the body If a person shows all the above symptoms, then the person is called diabetic. Deficiency Insulin deficiency leads to a decrease in plasma cholesterol and phospholipid concentration. The high insulin content in blood leads to hypoglycemia (low blood glucose level). Glucagon Glucagon is secreted from the alpha cells of the pancreas, which check the blood glucose concentration. Its function is just opposite of insulin. Function The major function of glucagon is carbohydrate/glucose metabolism. It causes the breakdown of liver glycogen by glycogenolysis. It also increases the glucose level in liver, which increases the rate of intake of amino acids to form glucose. Glucagon also activates the lipases and maintains the concentration of free fatty acids. Glucagon inhibits the storage of triglycerides in liver. Clinical Action Hyper secretion of glucagon leads to an increase in blood glucose, kidney, and increase in strength of heart rate. Regulation of Insulin & Glucagon The glucagon secretion is increased by blood sugar. The blood sugar increases in blood inhibits glucagon synthesis and increases glucagon secretion. An increase in blood amino acids and heavy exercise also decrease glucagon concentration. The hormone somatostatin inhibits the secretion of insulin & glucagon. Somatostatin It acts locally on pancreas cells of Langerhans to decrease the concentration of insulin & glucagon. In brain, it inhibits the role of growth hormone. Pancreatic Polypeptide It is secreted from the F-cells of the pancreas and is responsible for an alkaline medium in the duodenum by releasing HCO3 (carbonate ion). Note: Type I Diabetes mellitus: Insulin-dependent diabetes mellitus (IDDM) caused by the lack of insulin synthesis. Type II Diabetes mellitus: It is caused by the decreased sensitivity of the target tissues towards insulin. It is non-insulin-dependent diabetes mellitus (NIDDM). Adrenal Gland There are two adrenal glands present at the superior pole of each kidney. Each adrenal weighs about 4.8g in an adult human being. The adrenal gland is divisible into two major parts: Outer adrenal cortex constitutes 80% of the total adrenal. Inner medulla constitutes 20% of the total adrenal. The adrenal medulla functionally resembles the sympathetic nervous system and is responsible for the secretion of hormones adrenaline or epinephrine, and noradrenaline or norepinephrine. The hormones secreted from the cortex are of a separate group of hormones called corticosteroids, synthesized from steroidal cholesterol. About 80% of the total adrenal gland is adrenal cortex, which is meant for secretion of corticosteroid hormones. The cortex is divided into 3 different zones: Zona glomerulosa (10%) Zona fasciculata (75%) Zona reticularis (10%) Among all these zones, the action of ACTH is mostly on zona glomerulosa and zona fasciculata. Zona Glomerulosa About 10% of the total adrenal cortex is zona glomerulosa. It secretes hormones called mineralocorticoids. They help maintain electrolyte balance in extracellular fluid, mainly Na+ and K+. The major mineralocorticoid secreted from zona glomerulosa is aldosterone. The glomerulosa cells contain the enzyme aldosterone synthase, which produces aldosterone. Aldosterone secretion is controlled by angiotensin-II. RAA Pathway The liver always contains angiotensinogen, which acts as a substrate for the enzyme renin. In presence of renin, a deca-peptide (angiotensinogen) is cleaved from angiotensinogen and converted into angiotensin-I. Now, angiotensin-I is in the presence of the enzyme ACE (angiotensin-converting enzyme), and is converted into angiotensin-II. Diagram: Liver -> Angiotensinogen Renin -> Angiotensin-I ACE -> Angiotensin-II Role of Angiotensin-II Angiotensin-II is a vasoconstrictor, which means it helps in decreasing the diameter of blood vessels. Zona Fasciculata It promotes the secretion of aldosterone. It ultimately increases the synthesis of ATP. It increases the concentration of Na+ in body fluid by absorbing Na+ from nephric filtrate and removing excess potassium from the body. Zona Fasciculata It constitutes 75% of the adrenal cortex. The hormones secreted from this region are glucocorticoids and the major glucocorticoids are cortisol and corticosterone. The cortisol is released in maximum amount while the corticosterone effect is slightly mineralocorticoid during heavy physical work. The cortisol is secreted to maintain the normal blood glucose level during heavy physical exertion. It increases the glycogen being used from skeletal muscles and adipose tissues and increases the glucose concentration in blood. Clinical Action Excess secretion of cortisol leads to obesity. The person becomes impossible to maintain the glucose concentration between the meals, which is a symptom of Addison disease. Note: Hyper secretion of adrenal cortex hormones leads to Cushing Syndrome. Zona Reticularis This part of adrenal cortex is responsible for the secretion of DHEA (dihydroepiandrosterone). This compound is secreted also in increasing the liver plasma proteins. It also promotes gluconeogenesis. It also helps in breakdown of triglycerides to increase fatty acid concentration. It has anti-stress activity.

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