Endocrine and Hepatic Disorders

1. Endocrine and Hepatic Disorders Diana Blum MSN Metropolitan Community College Nursing 2150

2. Objectives Recall physiology of endocrine system Compare clinical manifestations associated with hypofunction and hyperfunction of the pituitary gland Explain interventions for the treatment of disorders of the pituitary glands. Identify teaching priorities for the patient taking hormone replacement therapy for pituitary glands. Prioritize nursing care for the patient immediately following a post-transphenoidal hypophsectory Describe disorders of the adrenal glands to include clinical manifestation and treatment modalities

3. Objectives Describe disorders of the posterior pituitary glands including assessment interventions. Identify clinical manifestations for thyroid and parathyroid disorders. Explore assessment findings and treatment modalities for thyroid and parathyroid disorders.

4. Objectives Identify metabolic functions of the liver and liver disease including cirrohsis and surgical management. Discuss liver function tests and clinical manifestations of liver dysfunction Discuss management of esophageal varies Compare and contrast the different types of hepatitis.

5. Endrocrine glands Pituitary gland Adrenal gland Thyroid gland Islets cells of the pancreas Parathyroid glands Gonads

6. Hormones and Target tissue Hormones-Natural chemicals that exert their effects of a specific tissue Target tissue-usually located at a distance from the endocrine gland with no direct connection between the endocrine gland and the target tissue. Endocrine glands are �ductless glands�

7. Neuroendorcrine Regulation The primary function of the endocrine glands is to regulation of overall body function. The body must maintain a homoeostatis to respond to environmental changes. Temperature regulation Serum sodium levels

8. Lock and Key As hormones travel through the body, they can only recognize their target tissue. Each receptor site type is specific to only one hormone. Only the correct hormone can connect to the correct receptor. Once the hormone binds to the site the target tissue will change the tissues activity.

9. Disorders of the endorcrine system are related to either excess or deficiency of a specific hormone or to a defect at its receptor site. Onset Slow or insidious Abrupt or life threatening

10. Principle hormones of the endocrine glands Hypothalamus corticotropin-releasing hormone Thyrotropin releasing hormone Gonadotropin releasing hormone Growth hormone releasing hormone Growth inhibiting hormone Prolactin inhibiting hormone Melanocyte inhibiting hormone

11. Anterior pituitary Thyroid stimulating hormone Adrenocorticotropic hormone Luteinizing hormone Follicile stimulating hormone Growth hormone Melanocyte stimulating hormone

12. Posterior pituitary Vasopressin Oxytocin Triiosothyronine (T3) Thyroxine (T4) Calcitonin

13. Parathyroid Parathyoid hormone

14. Adrenal Cortex Glucocorticoid Mineralacorticoids

15. Ovary Estrogen Progesterone

16. Testes testosterone

17. Pancreas Insulin Glucagon somatostatin

18. Negative Feedback Control Mechanism Hormone secretion is dependant on the need of the body for the final action of that hormone. When the body moves away from homeostatis a specific change or action is required or a response is needed to correct the change. Supply and demand

19. Example of negative feedback control Blood sugar increase to above 120, hormone insulin is secreted. Insulin increases glucose uptake by the cells, causing a decrease in the blood glucose. Main action-insulin decreased the elevated blood sugar.

20. Functions of the glands Hypothalamus Small area of nerve and glandular tissue located beneath the thalamus on each side of the third ventricle of the brain. Shares a small closed circulatory system with the anterior pituitary Known as the hypothalamic-hypophysial portal system Hormones can travel directly to the anterior pituitary

21. Functions of the gland Pituitary gland Located at the base of the brain in a valley of the sphenoid bone called the sella turcica. PEA SIZED The hypothalamus and the pituitary work together. The hormones of posterior Pituitary are produced in the hypothalamus and are sent through the portal system. The hormones are stored in the nerve endings of the posterior Pituitary and are released into the blood when needed.

22. Function of the glands The pituitary hormone is responsible for many hormones and subsequent target tissues and actions.

24. Function of the glands Gonads Male and female reproductive endocrine glands. Male gonads are the testes Female gonads are the ovaries These glands are present at birth but do not begin to function until puberty

25. Function of the glands Adrenal glands They are vascular and tent shaped organs on top of the kidneys Outer portion-cortex Inner portion-medulla Each area works independently

27. Adrenal cortex is 90% of the adrenal gland. Mineralocorticoids are produced in the cortex Adrenal steroids and corticosteriods are produced in the cortex

28. Mineralcorticoids Aldosterone-chief mineralocortoid Maintains extracellular fluid volme Promotes sodium and water reabsorption and potassium excretion Aldosterone secretion is controlled by renin angiotensin system, ACTH, and potassium

29. Glucocorticoids Cortisol is secreter from the adrenal cortex Cortisol affects Carbohydrate, protein, and fat metabolism Emotional stability Immune function

30. Function of the Glands Adrenal medulla Sympathetic nerve ganglion that has secretory cells. Releases catacholamines including epinephrine and norepinephrine. Not essential for life, however plays a role in stress response.

31. Function of the glands Thyroid gland Found in the anterior neck below the cricoid cartilage. Rich in blood supply Produce hormones t3 and t4

33. Function of the thyroid gland Fetal development Control metabolic rate of all cells Regulate fat, carbohydrate, and protein production Increase red blood cell production Produces calcitonin-lowers calcium and phosphorus levels by reducing bone breaksdown.

34. Function of the glands Parathyroid gland Consists of four small glands located on the back of the thyroid gland. Chief cell of this gland production and secretion of PTH Regulates calcium and phosphorus metabolism by acting on the bone, kidneys and intestinal tract. Serum calcium is the major controlling factor of PTH.

36. Function of the glands Pancreas Lies behind the stomach and has endocrine and exocrine function. The islets of langerhans perform the endocrine functions. The Islets have three cell types. Alpha-secrete glucagcon Beta-secrete insulin Delta- secrete somatostatin

37. Function of the glands-pancreas The exocrine function involves the secretion of digestive enyzmes through ducts that empty into the doudenum. The main endorcrine function is to regulate blood sugar.

38. Pancreas Glucagon is the hormone the increase blood sugars The liver is the main target tissue for glucagon and it causes glycogenolysis-conversion of glycogen to glucose. Gluconeogensis-conversion of amino acids to glucose. This enhances the transport of amino acids to the muscle.

39. Pancreas Insulin Anabolic hormone, promotes the movement and storage of carbohydrates, protein and fat. Insulin lowers the blood glucose levels by enhancing glucose movement across the cell membrane.

40. Disorders of the Anterior Pituitary Hypopituitarism Hyperpituitarism

41. Patho Adenohypophysis-controls growth, metabolic activity and sexual development. GH, PROLACTIN, TSH, AdrenoCorticoTropin (ACTH), FSH, LH, MSH Disorders arise when the anterior pituitary does not work effectively or when the hypothalamus is not work effectively. (Primary pituitary dysfunction vs. secondary pituitary dysfunction)

42. Hypopituitarism If a person has hypopitutarism, the patient will exhibit deficiencies in one or more hormones. In rare cases, panhypopituitarism is present. (Decreased hormone production from the anterior pituitary) Deficiencies in ACTH and TSH are the most life threatening as the correspond to vital hormones from the adrenal gland and thyroid gland. The other hormones from the gonads LH and FSH interfere with sexual reproduction.

43. GH deficiency changes tissue growth although it is indirect. In GH deficiencies in adults Accelerate bone destruction and osteoporosis In GH deficiencies in children Small stature, growth retardation

44. Causes of hypopituitarism Anorexia nervosa Benign or malignant tumors of pituitary Postpartum hemorrhage Sheehan�s syndrome Compression of the pituitary gland Post partum hemorrhage leads to infarction of the gland. Sheehan's syndrome the gland enlarges during pregnancy and when hypotension occurs with hemorrhage ischemia and necrosis occurs. Usually develops immediately after surgeryCompression of the pituitary gland Post partum hemorrhage leads to infarction of the gland. Sheehan's syndrome the gland enlarges during pregnancy and when hypotension occurs with hemorrhage ischemia and necrosis occurs. Usually develops immediately after surgery

45. Clinical Manifestations GH Decreased bone density Fractures Decreased muscle strength

46. Clinical Manifestations Gonatropins-women Amenorrhea Anovulation Low estrogen levels Breast atrophy Decreased libido

47. Clinical Manifestations Gonatropins-male Decreased facial hair Reduced muscle mass Impotence Decreased body hair Loss of bone density

48. Clinical Manifestations Thyroid stimulating hormone (TSH) Weight gain Intolerance to cold Menstrual abnormalities Slow cognition lethargy

49. Clinical Manifestations Andrenocorticotropin-ACTH Decreased serum cortisol levels Pale sallow skin Headache Hypoglycemia hyponatremia

50. Diagnositics Stimulation test Usually involve injecting agents that are known to stimulate secretion of specific pituitary hormones. Skill x ray CT scan MRI

51. Nursing Interventions for hypopituitarism Replacement of defiecient hormone Androgens Avoid in men with prostate cancer Women will be given a combination of estrogen and progesterone. Gonadatropin releasing hormone and human gonadatropin are used to stimulate ovulation

52. Hyperpituitarism Oversecretion usually caused by pituitary tumor of hyperplasia Rare Can cause gigantism or acromegaly.

53. Gigantism-onset of GH hypersecretion occurs before puberty

54. Agromegaly Andre the GIANT stood 7 feet tall and died at 46. He did not treat his disease. Excessive secretion of GH occurs after puberty

55. Clinical manifestations Facial feature abnormalities Proganthism Changes to vision Organmegaly Hypertension Dysphagia Deepened voice Proganthism-jaw bone protusion Dysphagia due to large tongueProganthism-jaw bone protusion Dysphagia due to large tongue

56. Diagnostics Laboratory blood draw to determine which hormone is excessively secreting. CT scan MRI Suppression test Suppression test. Medication given that induces suppression of the pituitary gland and can determine what normal negative feedback control mechanism are intact. Insulin for gh Cortisol in the form of dexamethasone to suppress ACTH. If production of cortisol continues then that patient may have Cushing diseaseSuppression test. Medication given that induces suppression of the pituitary gland and can determine what normal negative feedback control mechanism are intact. Insulin for gh Cortisol in the form of dexamethasone to suppress ACTH. If production of cortisol continues then that patient may have Cushing disease

57. Non surgical management Drug therapy Dopamine agonist Parlodel Dostinex Both of these drugs stimulate the production of dopamine and inhibit the release of GH and PRL

58. Somatostatin analogues Octreotide-inhibits GH release Somavert-growth hormone blocker

59. Radiation therapy Takes a long time to be effective Not immediate is acute situations Side effects Optic nerve damage

60. Surgical Management of Hyperpituitarism Preop Education, education education Operative Use of a microscope makes incision in upper lip graft taken from thigh to prevent leak in CSF Education regarding the procedure, nasal packing, not to bend after surgery, cough sneeze etc. These item will cause the muscle graft to open and cause and increase in cranial pressure.Education regarding the procedure, nasal packing, not to bend after surgery, cough sneeze etc. These item will cause the muscle graft to open and cause and increase in cranial pressure.

61. Postoperative- Vital signs and: Monitor neurologic status Monitor fluid balance (transient diabetes insipidus) Instruct client not to sneeze, cough, blow nose. Encourage deep breathing exercises Monitor pad for nasal drip Instruct patient to use dental floss and oral rinse. Brushing teeth is not permitted.ita

62. Disorders of the Posterior Pituitary Diabetes insipidus Syndrome of Inappropriate Antidiuretic hormone

63. Diabetes insipidus DI- a water metabolism problem caused by the antidiuretic hormone inablilty to synthesize or the inabiliyt of the kidneys to act in response to ADH. Characterized by excessive diuresis

64. Three types of DI Nephrogenic-inherited Primary-defect in the hypothalamus or pituitary gland Drug related-Lithium

65. Key features Hypotension Decreased pulse pressure Tachycardia Increased Hbg,hct and BUN Increased UOP Poor skin turgor Irritablilty Decreased coginition Hyperthermia Lethargy leading to coma Classic sign of hypvolemic shockClassic sign of hypvolemic shock

66. Nursing interventions Primary management is with medications. Lypressin DDAVP Pitressin Diabinese See page for doses, interventions and rationales. Make sure to teach and educate the patient that is it is imperative that medication be taken as prescribed. Teach proper posistion of medication (DDAVP) medication administered by nasal spray.See page for doses, interventions and rationales. Make sure to teach and educate the patient that is it is imperative that medication be taken as prescribed. Teach proper posistion of medication (DDAVP) medication administered by nasal spray.

67. SIADH Case study- 77 year old female is taken to the ER for a fall at home. Assesment reveals Awake, alert and oriented Complains of pain to right hip. She has a history of hypertension and asthma. EKG shows NSR CBC wbc 9.4 rbc 3.9 hgb 12.1 hct 39.0

68. BMP Glucose 92 BUN 18 Cr 1.1 NA 130 K 4.2 CO2 37 Cl 97 Pulse ox 94% on RA VS 98.6, 84, 18, 156/93

69. Ms. Mills undergoes a THA without complications. IV solution is D51/2NS at 100ml/hr MSO4 PCA basal 1mg/hr with demand of 1mg every 10 minutes

70. Post op day 1 Ms. Mills is lethargic and confused Nausea Up to chair times 1 IV solution in increased to 125ml/hr. Inspiratory and expiratory wheezes with treatments that are not effective, O2 sats are 88 % on 2 Liters Moved to ICU for observation of respiratory status.

71. What is Ms. Mills suffering from? Explain the pathophysiology Siadh- a group of sypmptoms that occur when the ADH is secreted in the absence of osmotic or physiologic stimuli. You will see serum osmolality increase Decreased plasma volume Hypotenstion In SIADH �ADH continues to release even when plasma is hyperosmolar. Water is then retained which causes dilutional hyponatremia and expansion of the extracellular fluid volume. The increase in the plasma volume increase the glomular filtration rate of the kidneys and inhibits the release renin and aldosterone. Therefore you have increased sodium loss in urine leading to more hyponatremia. Siadh- a group of sypmptoms that occur when the ADH is secreted in the absence of osmotic or physiologic stimuli. You will see serum osmolality increase Decreased plasma volume Hypotenstion In SIADH �ADH continues to release even when plasma is hyperosmolar. Water is then retained which causes dilutional hyponatremia and expansion of the extracellular fluid volume. The increase in the plasma volume increase the glomular filtration rate of the kidneys and inhibits the release renin and aldosterone. Therefore you have increased sodium loss in urine leading to more hyponatremia.

72. On admission to ICU Na 116 K 3.5 Cl 86 BUN 9 Cr .8 Glucose 126 Hgb 9.1 Hct 27 Serum Osmolality 243 Urine Osmolality 541 Normal serum osmolality is 280Normal serum osmolality is 280

73. A swan ganz catheter is inserted to measure fluid and electrolyte and cardiac status. What is the role of ADH on water regulation? What are the major effects on organs? ADH regulates the water balance in the body. It is synthsized by the hypothalamus and stored in the pituitary. When released into the circulation it acts on the kidneys by increasing the permeability. This decreases the urine volume and more water is reabsored back into the circulation. The urine will be more concentrated. The blood volume is increased. This is different than DI serum osmolality and urine osmo are increased. In SIADH serum and urine osmo are decreased Basically seen as water intoxication. It has effects on the brain by cerebral edema, cardiovascular hypotension,lethargy, hostility and change in level of consciousness.. Manifestations can be seizures, tachycardia, coma decrease in deep tendon reflexes.ADH regulates the water balance in the body. It is synthsized by the hypothalamus and stored in the pituitary. When released into the circulation it acts on the kidneys by increasing the permeability. This decreases the urine volume and more water is reabsored back into the circulation. The urine will be more concentrated. The blood volume is increased. This is different than DI serum osmolality and urine osmo are increased. In SIADH serum and urine osmo are decreased Basically seen as water intoxication. It has effects on the brain by cerebral edema, cardiovascular hypotension,lethargy, hostility and change in level of consciousness.. Manifestations can be seizures, tachycardia, coma decrease in deep tendon reflexes.

74. As the RN what would you expect the MD to change or modify for Ms. Mills medical management? Iv fluids were changed to 3% NACL at 150 ml. Hypertonic solution. Lasix 80ml given IV push. Reduce the volume of blood Ms Mills will receive Declomycin 250 mg four times daily. This is a tetracycline derivative that inteferes with the ADH antidiuretic action and puts the patient into a state of DI. This medication is nephotoxic and needs monitor along with close monitoring of lab values.Iv fluids were changed to 3% NACL at 150 ml. Hypertonic solution. Lasix 80ml given IV push. Reduce the volume of blood Ms Mills will receive Declomycin 250 mg four times daily. This is a tetracycline derivative that inteferes with the ADH antidiuretic action and puts the patient into a state of DI. This medication is nephotoxic and needs monitor along with close monitoring of lab values.

75. What is the purpose of the serum and urine osmolality tests? Indicative of SIADH and DIIndicative of SIADH and DI

76. Ms. Mills still remains confused but her respiratory status has improved. Twenty four hours later her lab shows Na 132 K 3.2 Cl 98 Serum osmolality 275 Urine osmolality 400

77. At this time her IV solution is changed to D5 NS at 50 ml/hr. She is weaned off the oxygen and is alert awake and oriented. Vitals show 99.2 100 20 130/78

78. What other orders would expect from the MD at this time? Fluid restriction, continue lasix, and declomycin. If stable a high salt diet. Fluid restriction, continue lasix, and declomycin. If stable a high salt diet.

79. Ms Mills was transferred to a rehab unit for physical therapy and eventually moved back home.

80. Discuss two other sodium disorders that must be differientaited from SIADH? Why are elderly more prone? What are factors that contributed to the development of SIADH in Ms. Mills DI- already discussed Cerebral salt washing Most of these are seen in traumatic brain injuries Elderly are more prone to medical complexities, polypharmacy and related to orthopedic injuries in the elderly. Ms. Mills age of 77 Pre op NA level of 130 not investigated Asthma HCTZ for hypertension Morphine PCA pump Acute asthmatic episodeDI- already discussed Cerebral salt washing Most of these are seen in traumatic brain injuries Elderly are more prone to medical complexities, polypharmacy and related to orthopedic injuries in the elderly. Ms. Mills age of 77 Pre op NA level of 130 not investigated Asthma HCTZ for hypertension Morphine PCA pump Acute asthmatic episode

81. Nursing diagnosis Fluid volume excess related to compromised regulatory mechanism and intravenous overload. Altered though process related to cerebral edema

82. Disorders of the Adrenal Gland Acute adrenal insufficiency or Addisonian insufficiency Life threatening Cortisol and aldosterone needs are greater than the supply Related to stress, trauma, severe infection Hallmark characteristics of an adrenal crisis are vascular collapse and severe hypotension. Unless intervention occurs immediately, sodium level fall potassium increases. Patient will become hypotensive because of loss of aldosterone. Hallmark characteristics of an adrenal crisis are vascular collapse and severe hypotension. Unless intervention occurs immediately, sodium level fall potassium increases. Patient will become hypotensive because of loss of aldosterone.

83. Causes of Primary Adrenal insufficiency Autoimmune disease Tuberculosis Fungal lesions AIDS Hemorrhage (Adrenal) Adrenalectomy Radiation Usually occurs with progressive destruction of the adrenal gland. Classic symptoms are weakness, fatigue, anorexia with nausea vomiting, and diarrhea. Can often be confused with gastroenteritis. Hypoglycemia, hyponatremia and hyperkalemia are contributing factors to this process. In primary insufficiency 90% of the gland is usually deteroirated in order to see clinical manifestations. Tuberculosis is a rare cause of Addisons disease but it is seen mostly in japan. Primary if the most serious due to the lack of checks and balances in the negative feedback systemUsually occurs with progressive destruction of the adrenal gland. Classic symptoms are weakness, fatigue, anorexia with nausea vomiting, and diarrhea. Can often be confused with gastroenteritis. Hypoglycemia, hyponatremia and hyperkalemia are contributing factors to this process. In primary insufficiency 90% of the gland is usually deteroirated in order to see clinical manifestations. Tuberculosis is a rare cause of Addisons disease but it is seen mostly in japan. Primary if the most serious due to the lack of checks and balances in the negative feedback system

84. Causes of Secondary Adrenal insufficiency Pituitary hormones Hypophysectomy High dose pituitary radiation Brain radiation This usually occurs when there is a glucocortioid deficiency and a result of hypothalamic-pituitary-adrenal axis. It is associated with reduced amounts of ACTH This usually occurs when there is a glucocortioid deficiency and a result of hypothalamic-pituitary-adrenal axis. It is associated with reduced amounts of ACTH

85. Management of Adrenal insufficiency Hormone replacement Hyperkalemia management Hypoglycemia management There are three main goals Replacement of fluid volume and correction of electolytes. Hyperkalemia responds to volume expansion and glucocortroid replacment. Decadron on solucortef Give D50 and insulin to shift potassium back into cells Administer kayexalate Give diuretics Monitor I/O Administer IV glucose if warranted Most important find disease process or underlying illness and treat.There are three main goals Replacement of fluid volume and correction of electolytes. Hyperkalemia responds to volume expansion and glucocortroid replacment. Decadron on solucortef Give D50 and insulin to shift potassium back into cells Administer kayexalate Give diuretics Monitor I/O Administer IV glucose if warranted Most important find disease process or underlying illness and treat.

86. Diagnostic and labs for AC Complete Metabolic panel UA CT, MRI, skull x ray ACTH stimulation test (rapid and long)

87. Long term management Hydrocortisone Corrects glucocorticoid deficiency Florinef maintains electrolyte balance Florinef is a mineralocorticoidFlorinef is a mineralocorticoid

88. Adrenal gland hyperfunction The adrenal gland may oversecrete one or more of the adrenal hormones AKA Cushing�s syndrome, Cushing disease or hyperaldosteronism (excessive mineralocorticoid production)

89. Patients with Cushing�s disease (hypercortisolism) exhibit Problems with nitrogen, carbohydrate and mineral metabolism. Slow turnover is of plasma fatty acids �Buffalo hump� High levels of corticosteroids decrease immunity by destroying lymphocytes. Increased androgen production causes hirutism Hirutism- increased hair growth and will see acne. Scant or infrequent menses.Hirutism- increased hair growth and will see acne. Scant or infrequent menses.

90. Causes of increased cortisol levels Endogenous (Cushing disease) Adrenal hyperplasia Adenoma Carcinomas Pg 1474 Exogenous (Cushing Syndrome) asthma Autoimmune disorders Organ transplants Cancer chemo Allergic responses fibrosis

91. Clinical Manifestations Moon face Buffalo hump Weight gain Hypertension Muscle atrophy Paper like skin Hyperpigmentation Increased risk for infection Elevated blood sugars

92. Diagnostics and labs Patient will have Inc. BS Dec. lymph count Inc. sodium Dec. calcium Dec. potassium How does this compare to Addison�s disease? Page 1472Page 1472

93. UA CT, MRI Overnight dexamethasone testing 3 day low dose testing. 8 day high dose testing

94. Management of Cushing�s Drug therapy Lysodren Elipten Radiation therapy Treats pituitary adenomas Surgery Removal of tumor or pituitary itself Lysodren is cytotoxic for adrenal tumors Others decrease cortisol productionLysodren is cytotoxic for adrenal tumors Others decrease cortisol production

95. Hyperaldosteronism (Conn�s) Increased secretion of aldosterone which results in mineralcorticoid excess Most often caused by adrenal adenoma (primary hyperaldosteronism) Elevated levels of angiotensin II are seen in secondary hyperaldosteronism

96. Clinical manifestations Hypokalemia and elevated BP Headache Fatigue Nocturia Polydipsia Polyuria paresthesias Nocturia urination at night Polydipsia increased fluid intake Increased urination Numbness and tinglingNocturia urination at night Polydipsia increased fluid intake Increased urination Numbness and tingling

97. Diagnostic and labs UA specific gravity BMP CT MRI

98. Management of hyperaldosteronism Surgery for early stage Drug therapy Medication to increase K+ Aldactone Potassium supplements Be cautious to watch for signs and symptoms of hyperkalemia.Aldactone Potassium supplements Be cautious to watch for signs and symptoms of hyperkalemia.

99. Pheochromocytoma Catecholamine producing tumor that arises in chromaffin cells. Occurs in a single lesion on adrenal gland Releases epinephrine and norepinephrine Cause is unknown occur more in women then men. Could be inherited

100. Clinical Manifestations Intermittent episodes hypertension (classic) Headache Sweating Palpitations Impeding doom Drugs may induce hypertensive crisis Tricyclic antidepressants Glucagon Narcan Cheeses Tyaramine allergiesTricyclic antidepressants Glucagon Narcan Cheeses Tyaramine allergies

101. Diagnostic and Lab 24 hour UA to test for VMA (vanillylmandelic acid) a production of catecholamine metabolism) Ct MRI

102. Management Surgery- one or both of the adrenal glands are removed. Monitor BP and treat if hypertensive crisis Hydrate

103. Hepatic Disorders Most common liver function tests are ALT GGT AST Globulins Ammonia Cholesterol See chart on 1290 Liver is divided in 4 lobes. Circulation to the liver is extemely important to its function. Liver functions to metabolize glucose, ammonia convesion, protein metabolism, fat, vitamin and iron storage, drug metabolism, bile formation and bilirubin excretion.Liver is divided in 4 lobes. Circulation to the liver is extemely important to its function. Liver functions to metabolize glucose, ammonia convesion, protein metabolism, fat, vitamin and iron storage, drug metabolism, bile formation and bilirubin excretion.

104. Jaundice Bilirubin concentration in the blood is abnormally elevated, all the tissues become yellow, green in color. Becomes clinically evident with serum bilirubin levels above 2.3mg/dl

105. Types of Jaundice Hemolytic jaundice- increased destruction of the red blood cells. Found in pts with hemolytic transfusion reactions, Hepatocellular jaundice- inability of damaged liver cells to clear normal amounts of bilirubin from the blood. Usually caused by hepatitis disease, yellow disease or Mononucleosis.

106. Patients with Hepatocellular jaundice may be mildly ill or severely ill. Patient presents with lack of appetite, nausea, fatigue, weakness, and weight loss.

107. Obstructive jaundice- extrahepatic obstruction caused by an occlusion to the bile duct from a gall stone, tumor, or inflammatory process. Hereditary hyperbilirubinemia- increased serum bilirubin levels resulting from inherited disorders. (Gilbert�s syndrome, Dubin-Johnson and Rotor�s syndrome).

108. Portal Hypertension Obstructed blood flow through the damaged liver results in increased pressure throughout the portal venous system. Associated with hepatic cirrohosis

109. Ascites The pathophysiology of ascites is not clear. As a result of liver damage, large amounts of albumin rich fluid accumulate in the peritoneal cavity. Clinical symptoms Increased abdominal girth Rapid weight gain Shortness of breath Adominal striae Distended veins over the abdominal wall.

110. Treatment for Ascites Dietary modifications Diuretics Bed rest Paracentesis Transjugular intrahepatic protosystemic shunt See page 1295 for detail of TIPs procedureSee page 1295 for detail of TIPs procedure

111. Esophageal varies Dilated vein that are found in the submucosa of the lover esophagus or extend into to the stomach. Clinical manifestations Bleeding Hemataemesis Melena Signs and symptoms of hypovolemic shock

112. Diagnostics and Medical Management Upper endoscopy Portal Hypertension measurements Laboratory tests Medical management Manage bleeding

113. Medical Management Balloon tamponade Sclerotherapy Pharmacological intervention Vasopressin with nitroglycerin Inderal Corgard Inderal and Corgaard are beta blockersInderal and Corgaard are beta blockers

114. Medical management Esophageal banding therapy-the varies are banded by using a modified endoscope loaded with elastic rubber band that is slipped over the varies. Transjugular intrahepatic portosystemic shunting- TIPS

115. Hepatic Encephalopathy A life threatening complications of liver disease occuring with profound liver failure and results in high levels of ammonia circulating in the blood. Clinical manifestations Minor mental changes ( early phases) Motor dysfunction Alterations in mood and sleep Asterixis( flapping tremor to hands)

116. Diagnositic and Medical Management EEG to determine level of brain waves Patient are usually referred for aliver transplant after their first episode of encephalopathy. Medical management Lactulose-reduce the amount of ammomina in body.

117. Hepatitis Numerous amounts of hepatitis Hep A Hep B Hep C Hep D Hep E Hep G

119. Medical management of Hepatitis Bed rest during acute stages Patient teaching Prevention

120. Hepatic Cirrhosis A chronic disease characterized by repacement of normal liver tissue with diffuse fibrosis that destroy the structure and function of the liver. Types of cirrhosis Alcoholic cirrhosis Postnecrotic cirrhosis Biliary cirrhosis Alcoholic- Post necrotic- from acute viral hepatitis Biliary- chronic biliary obstruction and infectionAlcoholic- Post necrotic- from acute viral hepatitis Biliary- chronic biliary obstruction and infection

121. Clinical manifestations Liver enlargement Portal obstruction and ascites Infection Peritonitis Varies Edema Vitamin Deficiency Mental deterioration

122. Discuss 3 nursing diagnosis for Cirrhosis Risk for injury Impaired skin integrity Activity intolerance Impaired nutritionRisk for injury Impaired skin integrity Activity intolerance Impaired nutrition

123. Liver transplant Known as a solid organ liver transplant (OLTX). Used as last resort to treat end stage liver disease Immunosuppression is required for lifetime Prograf, Imuran, OKT3, cyclosporine

124. Liver transplant surgery Can take from 5-10 hours due to the large amount of ligation to venous collateral vessels. Blood loss can be great

125. Post operative OLTX Straight to ICU with hemodynamic monitoring. Complications Bleeding Rejection Infection Few hospitals in United States are sites for OLTX, UNMC, UCLA, Univ of Pittsburgh, Duke are noted as the best in the nation.