Individuals Experiencing Endocrine Disorders

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Individuals Experiencing Endocrine Disorders

  1. 1. Individuals Experiencing Endocrine Disorders NURS 2016
  2. 2. Glands That Control Endocrine Regulation <ul><li>Hypothalamus </li></ul><ul><li>Pineal </li></ul><ul><li>Pituitary </li></ul><ul><li>Thyroid </li></ul><ul><li>Parathyroid </li></ul><ul><li>Thymus </li></ul><ul><li>Adrenal </li></ul><ul><li>Islets of Langerhorn </li></ul><ul><li>Ovaries/Testes </li></ul>
  3. 3. Figure 42-2 The pituitary gland, the relationship of the brain to pituitary action, and the hormones secreted by the anterior pituitary and the posterior pituitary.
  4. 4. Thyroid Gland <ul><li>Produces thyroxin (T4) and triiodothyronine (T3) and calcitonin </li></ul><ul><li>Release of thyroid hormones (T3 and T4) controlled by thyroid stimulating hormone (TSH) secreted by pituitary </li></ul><ul><li>T3 and T4 control cellular metabolism </li></ul><ul><li>TSH normal is 0.6-5.2 mg/L </li></ul><ul><li>Goiter: enlarged thyroid gland </li></ul>
  5. 5. Hypothyroidism CM Mild Moderate Severe Bradycardia Hypothermic Extreme fatigue Hair loss Brittle nails Dry skin Numb fingers Menstral disturb. Weight gain Skin becomes thick Mask-like face Mental processes subdued Slowed speech
  6. 6. Hypothyroidism Treatment <ul><li>Medications: </li></ul><ul><ul><li>Levothyroxin </li></ul></ul><ul><ul><li>Single dose in AM </li></ul></ul><ul><ul><li>Not IV </li></ul></ul><ul><ul><li>Therapeutic effect is not immediate </li></ul></ul>
  7. 7. Hyperthyroidism <ul><li>AKA: Grave’s disease Excess secretion of thyroid hormones </li></ul><ul><li>Clinical Manifestations </li></ul>Mild Moderate Severe Nervousness Irritable Palpitations Tachycardia Amenorrehea Poor heat toler. Excess perspirations Flushed skin Exophthalmos Increased appetite Decreased weight Fatigue/weakness
  8. 8. Hyperthyroidism Treatment <ul><li>3 main Treatments: </li></ul><ul><li>2 Pharmacological & 1 surgical </li></ul><ul><li>Radioactive iodine treatment: destroys overactive thyroid cells </li></ul><ul><ul><li>70-85% patients cured with one dose </li></ul></ul><ul><ul><li>High incidence of hypothyroidism </li></ul></ul><ul><ul><li>Fear of radioactive component </li></ul></ul><ul><li>Anti thyroid meds Propacil,Tapazole </li></ul><ul><li>Surgical removal </li></ul>
  9. 9. Hyperthyroidism <ul><li>NCP </li></ul><ul><ul><li>Maintain nutritional status </li></ul></ul><ul><ul><li>Enhance coping measures </li></ul></ul><ul><ul><li>Improve self esteem </li></ul></ul><ul><ul><li>Maintain normal body temperature </li></ul></ul><ul><ul><li>Monitor for complications –recurrent hyperthyroidism, permanent hypothyroidism </li></ul></ul><ul><ul><li>Promote /teach self care </li></ul></ul>
  10. 10. Acute Pancreatitis <ul><li>Inflammation of the pancreas </li></ul><ul><li>Range from a relatively mild, self-limiting disorder to a rapidly fatal disease </li></ul><ul><li>Autodigestion </li></ul><ul><li>Causes </li></ul><ul><li>Mortality is high </li></ul>
  11. 11. Clinical Manifestations <ul><li>Severe abdominal pain </li></ul><ul><li>Acute illness </li></ul><ul><li>Abdominal guarding </li></ul><ul><li>Ecchymosis </li></ul><ul><li>Nausea & vomiting </li></ul><ul><li>Hypotension </li></ul><ul><li>Acute renal failure </li></ul><ul><li>Tachycardia </li></ul><ul><li>Respiratory distress </li></ul><ul><li>Abnormal blood gas value </li></ul><ul><li>Fever, </li></ul><ul><li>Jaundice </li></ul>
  12. 12. Assessment <ul><li>Presence & character of pain </li></ul><ul><li>Serum amylase & lipase are 3x higher </li></ul><ul><li>Nutritional fluid status & hx </li></ul><ul><li>History of GI problems </li></ul><ul><li>Respiratory status </li></ul><ul><li>Abdominal pain, tenderness & guarding </li></ul>
  13. 13. Nursing Diagnoses <ul><li>Pain & discomfort </li></ul><ul><li>Imbalanced nutrition </li></ul><ul><li>Ineffective breathing pattern </li></ul><ul><li>Impaired skin integrity </li></ul><ul><li>Goal </li></ul>
  14. 14. Nursing Interventions <ul><li>Relieving Pain & discomfort </li></ul><ul><ul><li>Administer Demerol as ordered </li></ul></ul><ul><li>Improving nutritional status </li></ul><ul><ul><li>NPO, NG tube, IV fluid </li></ul></ul><ul><li>Providing wound care </li></ul><ul><li>Improving respiratory function </li></ul><ul><li>Monitoring complications </li></ul><ul><ul><li>Fluid & electrolyte disturbance </li></ul></ul><ul><ul><li>Pancreatic Necrosis </li></ul></ul><ul><ul><li>Shock & multiple organ failure </li></ul></ul>
  15. 15. Chronic Pancreatitis <ul><li>Progressive anatomic & functional destruction of the pancreas </li></ul><ul><li>Mechanical obstruction of the pancreatic & common bile ducts and duodenum </li></ul><ul><li>Inflammation & destruction of the secreting cells of the pancreas </li></ul>
  16. 16. Clinical Manifestations <ul><li>Severe upper abdominal & back pain </li></ul><ul><li>Risk of addiction to opiates </li></ul><ul><li>Weight loss </li></ul><ul><li>Altered digestion </li></ul><ul><li>Calcification of the pancreas </li></ul><ul><li>Management…depends on cause </li></ul><ul><li>Treatment directed towards </li></ul><ul><ul><li>Prevent acute attack </li></ul></ul><ul><ul><li>Relieving pain </li></ul></ul><ul><ul><li>Managing endocrine and exocrine inefficiency </li></ul></ul>
  17. 17. Hepatic Encephalopathy <ul><li>Profound liver failure </li></ul><ul><li>Accumulation of ammonia and other toxins </li></ul><ul><li>Hepatic coma </li></ul><ul><li>Clinical Manifestations </li></ul><ul><li>Mental changes </li></ul><ul><li>Motor disturbances </li></ul><ul><li>Asterixis </li></ul><ul><li>Hand writing becomes difficult </li></ul><ul><li>Constructional apraxia </li></ul><ul><li>Reflexes disappear & extremeties become flaccid </li></ul>
  18. 18. Hepatic Encephalopathy <ul><li>Diagnosis: </li></ul><ul><ul><li>EEG shows slowing brain waves </li></ul></ul><ul><li>Treatment: </li></ul><ul><ul><li>Lactulose reduces serum ammonia (watch for watery stools) </li></ul></ul><ul><ul><li>Vital signs, hand writing monitoring, hydration </li></ul></ul><ul><ul><li>Principles of Management </li></ul></ul>
  19. 19. An Overview of Hepatitis <ul><li>Inflammation of the liver caused by a virus </li></ul><ul><li>Clinical Manifestations: </li></ul><ul><li>Jaundice </li></ul><ul><li>Liver tenderness </li></ul>
  20. 20. Hepatic Cirrhosis <ul><li>Chronic, progressive disease with widespred fibrosis and nodule formation </li></ul><ul><li>Normal flow of blood, bile, and hepatic metabolites is altered by fibrosis and changes in the hepatocytes, bile ductules, vascular channels, and reticular cells </li></ul>
  21. 21. Hepatic Encephalopathy, Hepatitis, & Cirrhosis <ul><li>Chronic disorders and nurses treat them as such </li></ul><ul><li>Treatment: </li></ul><ul><ul><li>control ascites, bleeding esophageal varices, infection </li></ul></ul><ul><ul><li>proper nutrition, support, rest, corticosteriods may maximize liver function </li></ul></ul><ul><ul><li>no alcohol </li></ul></ul><ul><ul><li>avoid infection </li></ul></ul>
  22. 22. Clinical Manifestations Hepatic Cirrhosis <ul><li>Intermittent jaundice </li></ul><ul><li>Fever </li></ul><ul><li>Anorexia </li></ul><ul><li>Muscle wasting </li></ul><ul><li>Diarrhea </li></ul><ul><li>Depleted platelet count </li></ul><ul><li>Fatigue </li></ul><ul><li>Advanced detoriation </li></ul><ul><ul><li>Ascites </li></ul></ul><ul><ul><li>Varcies </li></ul></ul><ul><ul><li>Encephalopathy </li></ul></ul><ul><ul><li>Liver atrophy </li></ul></ul>
  23. 23. Diabetes <ul><li>Diabetes Insipidus </li></ul><ul><li>Diabetes Mellitus </li></ul><ul><ul><li>type I (IDDM) </li></ul></ul><ul><ul><li>type II (NIDDM) </li></ul></ul><ul><li>Gestational Diabetes </li></ul><ul><li>Diabetic Ketoacidosis </li></ul><ul><li>Diabetic Coma </li></ul><ul><li>Diabetic Neuropathy </li></ul>
  24. 24. Diabetes Insipidus <ul><li>Due to decreased secretion of ADH (usually from pituitary surgery) </li></ul><ul><li>Polyuria (9L/day) </li></ul><ul><li>Watch for dehydration </li></ul><ul><li>Transient in nature </li></ul>
  25. 25. DiabetesInsipidus <ul><li>Medical management </li></ul><ul><ul><li>To replace ADH </li></ul></ul><ul><ul><li>To ensure adeq fluid replacement </li></ul></ul><ul><li>Pharmacological treatment </li></ul><ul><ul><li>Desmopressin - spray </li></ul></ul><ul><ul><li>IM form of ADH </li></ul></ul><ul><li>Nursing Management </li></ul><ul><ul><li>Support </li></ul></ul><ul><ul><li>Teaching </li></ul></ul><ul><ul><li>Medical bracelet </li></ul></ul>
  26. 26. Diabetes Mellitus <ul><li>Type I (Insulin Dependent Diabetes Mellitus) </li></ul><ul><li>Causes: </li></ul><ul><ul><li>Genetic component (however many type I diabetics have no known relatives with diabetes) </li></ul></ul><ul><ul><li>Viruses may destroy beta cells </li></ul></ul><ul><ul><li>Unknown in most cases </li></ul></ul>
  27. 27. Type I <ul><li>Islet of Langerhans (more specifically the beta cells within) cannot produce enough or any insulin to combat glucose levels within the body </li></ul><ul><li>Consequently, glucose levels rise </li></ul><ul><li>Stress can trigger increased glucose response </li></ul><ul><li>Individuals become dependent on exogenous insulin administration to survive </li></ul>
  28. 28. Type II <ul><li>Type II (Non-insulin Dependent Diabetes Mellitus) </li></ul><ul><li>Causes: </li></ul><ul><ul><li>no known genetic component </li></ul></ul><ul><ul><li>obesity </li></ul></ul>
  29. 29. Type II <ul><li>Beta cells are unable to respond to hyperglycemia </li></ul><ul><li>This causes the beta cells to become less efficient with time </li></ul><ul><li>This process is reversible with normalization of glucose levels </li></ul><ul><li>Some individuals have a resistance to insulin that may trigger NIDDM as well </li></ul>
  30. 30. Clinical Manifestations
  31. 31. Gestational Diabetes <ul><li>Usually develops in 2nd or 3rd trimester </li></ul><ul><li>After delivery, glucose tolerance in most clients returns to normal </li></ul><ul><li>However, type II diabetes develops in 40-60% of women with GDM within 5-15 years </li></ul><ul><li>Most GDM require insulin adminstration </li></ul>
  32. 32. Diabetic Ketoacidosis <ul><li>A little patho: </li></ul><ul><ul><li>hyperglycemia occurs due to glucose cannot be transported to cells because of lack of insulin </li></ul></ul><ul><ul><li>the liver starts to convert glycogen back to glucose and increases synthesis of glucose </li></ul></ul><ul><ul><li>unfortunately the complicates matters </li></ul></ul><ul><ul><li>fatty acids are mobilized from adipose tissue and the liver starts to produce ketones </li></ul></ul><ul><ul><li>ketones are excreted in the urine and accumulate in the blood </li></ul></ul><ul><ul><li>metabolic acidosis occurs from the increased acid due to rising ketones </li></ul></ul>
  33. 33. Diabetic Ketoacidosis <ul><li>A medical emergency </li></ul><ul><li>Sometimes brought on by stress, surgery, pregnancy, puberty, infection </li></ul><ul><li>#1 cause: diabetic not taking his/her insulin (fed up or non-compliance) </li></ul><ul><li>S & S: </li></ul><ul><ul><li>ketosis </li></ul></ul><ul><ul><li>dehydration </li></ul></ul><ul><ul><li>electrolyte and acid-base imbalance </li></ul></ul>
  34. 34. DK Management <ul><li>Medical Management </li></ul><ul><ul><li>Txmt for hyperglycemia </li></ul></ul><ul><ul><li>Correct dehydration, electrolyte loss, acidosis </li></ul></ul><ul><li>Nursing Management </li></ul><ul><ul><li>Monitor for s/s hypokalemia </li></ul></ul><ul><ul><li>Monitor lab work for electrolytes </li></ul></ul><ul><ul><li>Monitor urine output </li></ul></ul>
  35. 35. Diabetic Coma <ul><li>Bicarbonate buffering system fails to compensate for ketosis </li></ul><ul><li>Respirations increase in rate and depth (Kussmaul’s respirations) & breath has fruity or acetone odour </li></ul><ul><li>Renal system attempts to excrete ketones which leads to hemoconcentration </li></ul><ul><li>Hemoconcentration impedes blood circulation & leads to tissue anoxia & lactic acid production </li></ul><ul><li>The rise in lactic acid production further acidifies blood pH </li></ul><ul><li>Rising ketones eventually overwhelms the body’s defenses against the acid & the body succumbs to coma </li></ul>
  36. 36. Diabetic Neuropathy
  37. 37. Other chronic complications <ul><li>macrovascular complications: </li></ul><ul><ul><li>coronary artery disease </li></ul></ul><ul><ul><li>cerebrovascular disease </li></ul></ul><ul><ul><li>hyptertension </li></ul></ul><ul><ul><li>peripheral vascular disease </li></ul></ul><ul><li>infections </li></ul><ul><li>nephropathy </li></ul><ul><li>retinopathy </li></ul>
  38. 38. Diabetic Neuropathy Management <ul><li>Overall goal is to: </li></ul><ul><ul><li>regulate blood glucose levels </li></ul></ul><ul><ul><li>prevent acute and chronic complications </li></ul></ul><ul><li>Proper management consists of: </li></ul><ul><ul><li>physical activity </li></ul></ul><ul><ul><li>diet </li></ul></ul><ul><ul><li>perhaps medications </li></ul></ul><ul><li>Education is a key element in diabetes control </li></ul>
  39. 39. Medications <ul><li>Oral: </li></ul><ul><ul><li>First generation: </li></ul></ul><ul><ul><ul><li>Orinase, Tolinase </li></ul></ul></ul><ul><ul><li>Second generation: </li></ul></ul><ul><ul><ul><li>Glucotrol, Diabeta (Glyburide) </li></ul></ul></ul><ul><ul><li>Third generation: </li></ul></ul><ul><ul><ul><li>Metformin, Acarbose </li></ul></ul></ul>
  40. 40. Medications <ul><li>Insulin: </li></ul><ul><li>Short Acting: </li></ul><ul><ul><li>Humulog, Regular </li></ul></ul><ul><li>Intermediate Acting: </li></ul><ul><ul><li>NPH, Lente, 30/70 </li></ul></ul><ul><li>Long Acting: </li></ul><ul><ul><li>Ultralente </li></ul></ul>
  41. 41. Insulin Action

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