Endocrine Disorders

• ENDOCRINE DISORDERS Reported by: Group 5 Reedan Cnyl Gaviola | Rhoda Hatiya | Michelle Joy Lim | Michelle Angela Ligsay 2019
• TODAY'S PRESENTATION CONTENTS 1 REVIEW OF ENDOCRINE SYSTEM 2 INSULIN & DIABETES MELLITUS 3 4 PARATHYROID HORMONE AND CALCIUM 5 GROWTH HORMONE 6 ANTIDIURETIC HORMONE 7 THYROID DISORDERS 8 PITUITARY HORMONES ADRENAL GLANDS
• MAJOR ENDOCRINE GLANDS


  • Pituitary Gland
  • Two Adrenal Glands
  • Thyroid Gland
  • Parathyroid Gland
  • Endocrine Portion Of The Pancreas
  • Gonads
  • Pineal Gland
  • Thymus
• Hormones


  Chemical messengers that may be classified by action, source, or chemical structure
• Hormones


  • Insulin = decreases blood glucose levels
  • Glucagon = Increases blood glucose levels
• Hormones


  • After acting on specific receptors on or in the target cells, the hormones are metabolized or inactivated by the kidneys to prevent excessive amounts from accumulating in the body over a period of time
  • There is also something as "Negative Feedback" which is responsible in proper "level control" of hormones
• As levels of glucose increase, the secretion of insulin increases. When glucose levels decrease, insulin secretion decreases.
• ENDOCRINE DISORDERS


  • An excessive amount of hormone
  • A deficit amount of hormone
• Endocrine disorders


  • Frequently, endocrine disorders cause distinctive changes in the individual's physical appearance, which may be helpful in diagnosis
  • The most common cause of endocrine disorders is the development of a benign tumor, or adenoma
  • Adenomas may be secretory, causing excess hormone, or they may have a destructive effect on the gland, causing hormonal deficit
  • Some cases, there are individuals who have target cells that are resistant or insensitive to the hormone, this lack to response may be a result from genetic defect(s), an autoimmune response, or excessive demand on the target cells
  • Congenital defects in the glands, hyperplasia, or infection(s) in the glands, abnormal immune reactions, and vascular problems
• Radioimmunoassay (RIA)


  Methods used to check serum hormone levels
• Enzyme-multiplied immunoassay technique (EMIT)


  Methods used to check serum hormone levels
• Chemoluminescence


  Methods used to check serum hormone levels
• Blood glucose or blood calcium levels


  May reflect the activity of the respective hormones
• Scans, ultrasound, and magnetic resonance imaging (MRI) are also helpful for checking the location and type of lesion the may be present
• Biopsy is essential to eliminate the possibility of malignancy
• Treatment(s) depends on the cause of the problem. Hormone deficits may be treated with replacement therapy, for example, insulin to treat diabetes mellitus. Adenomas causing excessive secretions may be removed surgically or by radiation therapy.
• DIABETES MELLITUS is caused by a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by insulin resistance.
• Insulin resistance


  Lack of response by cells to insulin
• Insulin


  An anabolic hormone
• Lack of insulin results in abnormal carbohydrate metabolism
• Insulin is not required for glucose transport for brain cells or glucose absorption in digestive tract
• Exercising can utilize glucose without proportionate amounts of insulin
• Excessive exercise can deplete blood glucose and result in hypoglycemia
• Exercising is helpful in controlling blood glucose levels in the presence of an insulin deficit
• DIABETES MELLITUS: TYPE 1 AND TYPE 2


  • TYPE 1 DIABETES
  • TYPE 2 DIABETES
• Type 1 Diabetes


  Formerly insulin-dependent diabetes mellitus (IDDM), also called juvenile diabetes or type I, occurs more frequently in children and adolescents, but can develop at any age
• Type 1 Diabetes


  Insulin deficit results from destruction of the destruction of pancreatic beta cells in autoimmune reaction, insulin required = metabolic needs of the body based on dietary intake and metabolic activity, Hypoglycemia and ketoacidosis are more likely to occur
• Type 2 Diabetes


  Formerly referred to as noninsulin-dependent diabetes mellitus (NIDDM), type II or mature-onset diabetes, based on decrease effectiveness of insulin or a relative deficit of insulin, may involve decreased pancreatic beta cell reproduction of insulin, increased resistance by body cells to insulin, increased production of glucose by the liver, or combination, Type 2 Diabetes is a milder form of diabetes, usually developing gradually in older adults, the majority of whom are overweight, Gestational diabetes may develop during pregnancy and disappear following the delivery of the child
• GENERAL COMPARISON OF TYPE 1 AND 2 DIABETES

  • Age at onset: Children and young adults (Type 1), Older adults (Type 2)
  • Onset: Acute (Type 1), Insidious (Type 2)
  • Etiology: Autoimmune destruction (Type 1), Family History, Familial, lifestyle and environment factors (Type 2)
  • Body weight: Thin (Type 1), Obese (Type 2)
  • Plasma insulin level: Very low (Type 1), Decreased or normal (Type 2)
  • Treatment: Insulin replacement (Type 1), Diet and exercise or oral hypoglycemic agents or insulin replacement (Type 2)
  • Occurrence of hypoglycemia or ketoacidosis: Frequent (Type 1), Less common (Type 2)
• PATHOPHYSIOLOGY: Initial Stage


  1. Insulin deficit results in decreased transportation and use of glucose in many cells of the body

  2. Blood glucose level rise (hyperglycemia)

  3. Excess glucose spills into the urine (glucosuria) as the level of glucose in the filtrate exceeds the capacity of the renal tubular transport limits to reabsorb it

  4. Glucose in the urine exerts osmotic pressure in the filtrate, resulting in a large volume of urine to be excreted (polyuria), with the loss of fluid and electrolytes (e.g sodium) from the body tissues

  5. Fluid loss through the urine and high blood glucose levels draw water from the cells, resulting in dehydration

  6. Dehydration causes thirst (polydipsia)

  7. Lack of nutrients entering the cells stimulates appetite
• PATHOPHYSIOLOGY: Progressive Effects


  1. Lack of glucose in cells results in catabolism of fats and proteins, leading to excessive amounts of fatty acids and their metabolites, known as ketones or ketoacids, in the blood

  2. Some ketoacids are excreted in the urine (ketonuria). Some diabetic patients test their urine for ketones

  3. 10. However, as dehydration develops, the glomerular filtration rate in the kidney is decreased and excretion of acids becomes more limited, resulting in decomposed metabolic acidosis, which has life threatening potential
• SIGNS AND SYMPTOMS


  • weight gain or increased abdominal girth
  • fluid loss
  • polyuria (nocturia)
  • thirst and dry mouth
  • fatigue and lethargy
  • followed by weight loss
  • increased appetite
  • 3Ps: polyuria, polydipsia, polyphagia
• DIAGNOSTIC TESTS


  • FASTING BLOOD GLUCOSE LEVEL
  • GLUCOSE TOLERANCE TEST
  • GLYCOSYLATED HEMOGLOBIN TEST (HbA1c)
  • GLUCOMETER
• TREATMENT


  • Diet
  • Exercise
  • Oral medications
  • Insulin injections
• COMPLICATIONS


  • ACUTE COMPLICATIONS: Hypoglycemia, Diabetic Ketoacidosis, Hyperosmolar Hypergycemic Nonketotic Coma
  • CHRONIC COMPLICATIONS: Vascular Problems, Neuropathy, Infections, Cataracts, Maternal Diabetes
• Many factors can lead to fluctuations in serum glucose levels and subsequent changes in cell metabolism throughout the body. These changes may result from variations in diet or physical activity, the presence of infections or alcohol use.
• PARATHYROID HORMONE AND CALCIUM Reported by Rhoda Hatiya
• Hypoparathyroidism

  May be caused by a congenital lack of the four parathyroid glands, following surgery or radiation in the neck region or as a result of autoimmune disease, Hypoparathyroidism leads to hypocalcemia, or low serum calcium levels
• Hypocalcemia


  Affects nerve and muscle function in different ways, Low serum calcium levels results in weak cardiac muscle contraction
• TREATMENT


  • Diet
  • Exercise
  • Oral medications
  • Insulin injections