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Finla presentation on pitutary&aderenal gland

  1. 1. DEBRE MARKOS UNIVERSITY COLLEGE OF HEALTH SCIENCE BY: GETNET DESSIE(BSc,MSc in Adult health nursing) DMU may,2018 Pituitary gland disorder
  2. 2. By the end of this lecture, students should be able to: • Discuss the anatomy ,and functions of pituitary • Describe pituitary gland dysfunction, and pathophysiology. • Describe clinical manifestations of pituitary tumours, assessment and diagnostic findings, and an overview of medical management. • Define diabetes insipidus, describe its manifestations, diagnostic evaluation, medical and nursing management. Objectives
  3. 3. • Introduction • Pituitary anatomy & Physiology • Pituitary tumors, • Hypopituitarism • common hormone producing tumors: – Acromegaly – Cushing disease outline
  4. 4. • Anatomic and Physiologic Overview • The pituitary gland, or hypophysis, is a round structure about 1.27 cm (½ inch) in diameter • located on the inferior aspect of the brain. Introduction
  5. 5.  The pituitary often referred to as master gland because together with the hypothalamus,, it orchestrates the complex regulatory functions of multiple endocrine glands  consists of anterior and posterior lobe..  Pituitary hormones are produced in Pulsatile manner. Anatomic and Physiologic Overview……..
  6. 6. Anatomic and Physiologic Overview……..
  7. 7. 9 Endocrine glands in the human head and neck and their hormones
  8. 8. • Growth • Blood pressure • Uterine contractions during childbirth • Breast milk production • Sex organ functions • Thyroid gland function • Water and osmolality regulation in the body • Temperature regulation Function of the Pituitary
  9. 9. Anatomic and Physiologic Overview……..
  10. 10. • Rule of "Too's“ • Too-mor (tumor) Too much Too little When things go wrong
  11. 11. • pituitary tumor is calld “pituitary adenoma” — adeno means gland, oma means tumor. • Most pituitary adenomas develop in the front two-thirds of the pituitary gland. • That area is called the adenohypophysis, or the anterior pituitary (American brain tumor association 2015) Pituitary Tumors
  12. 12. • Almost all pituitary tumors are benign (non- cancerous) • These tumors don’t spread to other parts of the body, like cancers can do • but their location and effects on hormone production by target organs can cause life- threatening effects. Pituitary Tumors
  13. 13. • About 10,000 pituitary tumors are diagnosed each year in the United States. • When examining people who have died or who have had imaging tests (like MRI scans) of their brain for other health problems, it is found that as many as 1 out of 4 people have a pituitary adenoma without knowing it. (American cancer society,2014) key statistics about pituitary tumors
  14. 14. • Pituitary tumors account for 12 -19% of all primary brain tumors, making them the third most common primary brain tumor in adults, following meningioma and the gliomas. • 20 – 25% of the general population have small, symptomless pituitary tumors or cysts. • 10% have an abnormality big enough to see on magnetic resonance imaging (MRI). (American brain tumor association 2015) key statistics about pituitary tumors….. ..
  15. 15. • Pituitary tumors can be found in every age group, but their incidence tends to increase with age • Women are more often than men. (American brain tumor association 2015) • On systemic review prevalence of pituitary adenomas of 16.7% (14.4% in autopsy studies and 22.5% in radiologic studies)(Shereen Ezzat,2004). key statistics about pituitary tumors….. ..
  16. 16. • Pituitary tumors can occur at any age (including in children), but they are most often found in older adults. • Almost all of these tumors are benign pituitary adenomas. (American cancer society,2014) key statistics about pituitary tumors….. ..
  17. 17. • based on size:Microadenoma versus macroadenoma 1.Microadenomas(smaller than 1 cm). • rarely damage the rest of the pituitary or nearby tissues. • they can cause symptoms if they make too much of a certain hormone. • Many people actually have small adenomas that are never detected because they never grow large enough or secrete enough hormones to cause a problem. Pituitary Tumors classification
  18. 18. 2.Macroadenomas are tumors 1 cm across or larger. • Affect a person’s health in 2 ways. • First, they can cause symptoms if they make too much of a certain hormone. • Second, they can cause symptoms by pressing on normal parts of the pituitary or on nearby nerves, such as the optic nerves. Pituitary Tumors classification …………
  19. 19.  25% of the pituitary adenomas.  Null cell adenomas,  oncocytomas,  silent corticotroph adenomas and  silent gonadotroph and  thyroph adenomas fall into this group. These tumors grow slowly and generally cause minimal symptoms. non-functioning pituitary tumors
  20. 20. • When they expand outside the sella turcica, they may press on the nearby optic nerves causing vision loss and headache. • Such tumors can also compress the pituitary gland cause hypopituitarism, this symptom is associated with general weakness and fatigue, a pale complexion, loss of sexual function and apathy. non-functioning pituitary tumors
  21. 21. • anything that changes a person’s chance of getting a disease. For example; • smoking is a risk factor for cancer of the lung and many other cancers. • Family history What are the risk factors for pituitary tumors?
  22. 22. Genetic syndromes • Multiple endocrine neoplasia, type I (MEN1): This is a hereditary condition in which people have a very high risk of developing tumors of 3 glands: the pituitary, parathyroid, and pancreas. Can be Transmit to children What are the risk factors for pituitary tumors?
  23. 23. • Multiple endocrine neoplasia, type IV (MEN4): MEN4 is caused by inherited changes in a gene called CDKN1B. • McCune-Albright syndrome: This syndrome is caused by changes in a gene called GNAS1,that aren’t inherited but occur before birth. • Carney complex: This is a rare syndrome in which people can have heart, skin, and adrenal problems. What are the risk factors for pituitary tumors?
  24. 24. • These benign tumors do not spread outside the skull. • They usually remain confined to the sella turcica • Sometimes they grow into the walls of the sella turcica and surrounding blood vessels, nerves, and coverings of the brain. • They don’t grow very large, but they can have a big impact on a person’s health. Pathophysiology of Pituitary Tumors
  25. 25. • There is very little room for tumors to grow in this part of the skull. • Therefore, if the tumor becomes larger than about a centimeter across, it may grow upward, • can compress and damage nearby parts of the brain and the nerves that arise from it. • This can lead to symptoms such as vision changes or headaches (Signs and symptoms of pituitary tumors). Pathophysiology of Pituitary Tumors
  26. 26.  excess hormone secretion  local effects of a tumor  the result of inadequate production of hormone by the remaining normal pituitary, i.e. hypopituitarism. Effects of tumor on pituitary gland
  27. 27. Three principal types of pituitary tumors represent an overgrowth of (1) eosinophilic cells, (2) basophilic cells, or (3) chromophobic cells (neither of two) Pituitary Tumors
  28. 28. Eosinophilic –If it is early in life result in gigantism. –If the disorder begins during adult , acromegaly. – However, enlargement involves all tissues and organs of the body. – Many of these patients suffer from severe headaches and visual disturbances because the tumors exert pressure on the optic nerves (Porth, 2005). Clinical Manifestations
  29. 29. –loss of color discrimination, –diplopia (double vision), or blindness in a portion of a field of vision. –Decalcification of the skeleton, muscular weakness, and endocrine disturbances, similar to those occurring in patients with hyperthyroidism. Clinical Manifestations of Eosinophilic ………..
  30. 30. – Basophilic tumors give rise to Cushing's syndrome with features largely attributable to hyperadrenalism, including – masculinization and – amenorrhea in females, – truncal obesity, – hypertension, osteoporosis, and polycythemia. Clinical Manifestations of Basophilic tumors
  31. 31. – Chromophobic tumors represent 90% of pituitary tumors. – These tumors usually produce no hormones but destroy the rest of the pituitary gland, causing hypopituitarism. – People with this disease are often obese and somnolent and exhibit fine, scanty hair; dray, soft skin; a pasty complexion; and small bones. Clinical Manifestations of Chromophobic tumors
  32. 32. –headaches, –loss of libido, –visual defects progressing to blindness. –polyuria, polyphagia, –a lowering of the basal metabolic rate, and a subnormal body temperature. Clinical Manifestations of Chromophobic tumors ……….
  33. 33. • careful history and physical examination, including assessment of visual acuity and visual fields. • Computed tomography (CT) and magnetic resonance imaging (MRI) • Serum levels of pituitary hormones plus hormones of target organs (eg, thyroid, adrenal) to assist in diagnosis if other information is inconclusive. Assessment and Diagnostic Findings
  34. 34. • bromocriptine To decrease GH levels. • Radiation :Stereotactic or conventional radiation therapy. • Surgical removal of the pituitary gland through a transsphenoidal approach is the usual treatment. • Hypophysectomy – is the treatment of choice in patients with Cushing’s syndrome Medical &Surgical Management of pituitary Tumors
  35. 35. Medical &Surgical Management of pituitary Tumors
  36. 36. • Pre op hypophysectomy Anxiety r/t fear of unknown brain involvement Nursing Management &Nursing Diagnosis
  37. 37. • Sensory-perceptual alteration r/t : visual field cuts  diplopia  secondary to pressure on optic nerve. • Alteration in comfort (headache) r/t tumor growth/edema Nursing Management &Nursing Diagnosis
  38. 38. • Knowledge deficit r/t no post-op teaching • Teach the person about pain control ambulation hormone replacement activity Nursing Management &Nursing Diagnosis
  39. 39. • Incisional disruption after transsphenoidal hypophysectomy – Avoid bending and straining X 2 months post transsphenoidal hypophysectomy, – Use stool softeners – Avoid coughing – Saline mouth rinses – No toothbrushes for 7-10 days Nursing Management &Nursing Diagnosis
  40. 40. • Assess for any clear rhinorrhea –Notify physician –HOB 30 degrees –Bed rest Prevent Post-op complications
  41. 41. • Periocular edema/ecchymosis • Headaches • Visual field cuts/diplopia • Post operative care • hormone deficiency: Have no enough ADH • Decrease ACTH will require cortisone replacement due to decrease glucocorticoid production. Post-op complications…………………
  42. 42. • Decrease in sex hormones can lead to infertility due to decreased production of ova & sperm Post-op complications…………………
  43. 43. • Results in excess production and secretion of one or more hormones such as GH, PRL, ACTH. • Prolactin and GH are the hormones most commonly over-produced by adenomas • Most common cause is a benign adenoma. 1.Too much
  44. 44. • It may be primary or secondary defect • Primary: the defect is in the gland itself which releases that particular hormone that is too much or too little. • Secondary: defect is somewhere outside of gland i.e. GHRH from hypothalamus »TRH from hypothalamus Anterior hyper pituitary Disorders
  45. 45. 1.Gigantism
  46. 46. Gigantism……………. .
  47. 47. Gigantism……………. .
  48. 48. Some General Facts • 3 people in 1 million have pituitary gigantism in the world • 100 cases to day in United States • 2 – 3 times higher mortality rate in comparison to general population • No racial predilection • Males and females affected equally • Not a genetic disorder ( American brain ca socity,2010)
  49. 49. Robert Pershing Wadlow • Robert Wadlow – “The Alton Giant” • Tallest man ever at 8’11”, suffered from the disorder • Born normal weight and size but 30 lbs at 6 months of age • Died at 22
  50. 50. The Alton Giant • No treatment in 1920’s for overactive pituitary • Maintained normal lifestyle, • participated as a boy scout, collected stamps and enjoyed photography • Shoes cost $100 (specially made) • Worked for international shoe company as an attraction, went on nationwide tour in U.S. in exchange for free shoes for life
  51. 51. Cause and pathophysiology • The main cause of too much growth hormone released is from a non-cancerous tumor of the pituitary gland. • is the result of GH hypersecretion before the closure of the epiphyseal plates (childhood). – Abnormally tall but body proportions are normal
  52. 52. Clinical presentation  Excessive growth  The child is large for their age  Delayed puberty  Double vision or difficulty with peripheral vision, Headaches  Increased sweating  Large hands and feet  Thickening of facial features
  53. 53. Diagnostic Procedures  CT or MRI of head  There will be high prolactin levels  Increased insulin growth factor levels
  54. 54. Treatment  Surgery to remove the tumor  Medication that will reduce how much growth hormone is released  Radiation Therapy
  55. 55. complication • Life span is generally reduced and disturbed due to : • osteoarthritis, cardiovascular diseases, benign tumor growth, diabetes, varying levels of obesity and sleep apnea, • Tumor in pituitary can cause chronic headache and visual impairment due to proximity of gland to optic chiasm
  56. 56. Nursing consideration • Gigantism and acromegaly generally have outward negative effects that can be treated medically, i.e. sleep disturbances, joint pain, cardiovascular issues, etc. • Teach the patient to protect these complications • gigantism very traumatic emotionally
  57. 57. • Acromegaly is over secretion of GH in adulthood at age of greater than 17 years – Continued growth of boney, connective tissue leads to disproportionate enlargement of tissue.. – Rare condition – develops between ages 30-50 2. Acromegaly
  58. 58. In Iceland national survey from 1955-2013: o 32 men with diseases o Average age 44.5 o 9 patient died o Symptoms for more than 3 years o 25 (48%) develop HTN o 63 % cured after surgery (Gudrun thuridu hoskuldsdottir et.al,2015 etal) General facts about Acromegaly
  59. 59. • Acromegaly most often occurs as a result of a benign pituitary tumor (adenoma). • The excessive secretion of GH results in an overgrowth of soft tissues and bones in the hands, feet, and face. • Because the problem develops after epiphyseal closure, the bones of the arms and legs do not grow longer. Etiology and Pathophysiology
  60. 60. • The changes can occur over a number of years and may go unnoticed by family and friends. • Patients experience enlargement of hands and feet with joint pain that can range from mild to crippling. • Carpal tunnel syndrome • Thickening and enlargement of the bony and soft tissues on the face, feet, and head occur Clinical manifestation
  61. 61. • speech difficulties, • the voice deepens because of hypertrophy of the vocal cords. • Sleep apnea may occur because of upper airway narrowing • The skin becomes thick, leathery, and oily. • peripheral neuropathy and proximal muscle weakness. • Visual disturbance Headaches • hyperglycemia, Clinical manifestation
  62. 62. Clinical manifestation Acromegaly………
  63. 63. • glucose intolerance and manifestations of diabetes mellitus may occur, including polydipsia and polyuria • increases free fatty acid levels in the blood Clinical manifestation Acromegaly………
  64. 64.  History & physical exam  plasma insulin-like growth factor 1 (IGF-1)  OGTT :Two baseline GH levels are obtained before ingestion of 75 or 100 g of oral glucose, and additional GH measurements are made at 30, 60, 90, and 120 minutes.  Normally, GH concentration falls during an OGTT.  In acromegaly GH levels do not fall, and in some cases GH concentration rises. Assessment and diagnosis
  65. 65. • Serum GH – Men: <4 ng/mL (<4.0 mcg/L) – Women: <18 ng/mL (<18 mcg/L) – Values >50 ng/mL (>50 mcg/L) suggest acromegaly. • MRI and CT scan to detect pituitary tumor diagnosis
  66. 66. Treatment • Surgery (hypophysectomy is the primary choice) • Radiotherapy • Drug treatment – when surgery is not feasible • Combinations of above
  67. 67. • Dopamine agonists: Dopamine agonists work on the surface of the tumor to inhibit GH release from the tumour (Parlodel). • Somatostatin: GH receptor antagonist decreases the action of GH on target tissues. (octreocide acetate) • Dopamine agonists are taken by mouth but in general are less effective than somatostatin analogues, which have to be injected. Drug treatment of Acromegaly
  68. 68. NURSING ASSESSMENT • Assess the patient for signs and symptoms of abnormal tissue growth and evaluate changes in physical size. • It is important to question patients about increases in hat, glove, and shoe sizes
  69. 69. NURSING IMPLEMENTATION • elevating the head of the patient’s at 30-degree angle to avoids pressure on the sella turcica and decreases headaches • Monitor the pupillary response, speech patterns • Perform mouth care every 4 hours to keep the surgical area clean and free of debris • Observe the patient for any signs of bleeding, since hemorrhage may be a complication, particularly when larger tumors are removed
  70. 70. NURSING IMPLEMENTATION • Instruct the patient to avoid vigorous coughing, sneezing, Valsalva maneuver to prevent CSF leakage. • Notify the surgeon, and send any clear nasal drainage to the laboratory to be tested for glucose. • A glucose level greater than 30 mg/dL (1.67 mmol/L) indicates CSF leakage from an open connection to the brain. • If this happens, the patient is at increased risk for meningitis. • Observe for sign of DI
  71. 71. SIADH: syndrome of Inappropriate Anti-Diuretic Hormone • Too much ADH produced or secreted. • SIADH commonly results from malignancies, CHF, & CVA - resulting in damage to the hypothalamus or pituitary which causes failure of the feedback loop that regulates ADH. • Client retains water causing dilutional hyponaetremia & decreased osmolality. Hyper – Posterior Pituitary
  72. 72. – in the Europe Hyponatremia is the most common electrolyte didturbance btween 2.5% and 30% pt withn SIDH – The most common causes of SIADH are malignancy, – pulmonary disorders, CNS disorders and medication; – (M J Hannon and C J Thompson,2010) Facts about SIADH
  73. 73. CAUSES OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE Malignant Tumors • Small cell lung cancer • Pancreatic cancer • Lymphoid cancers (Hodgkin’s lymphoma, non- Hodgkin’s lymphoma, • Lymphocytic leukemia) European endocrinology society, 2010 • Drug Therapy • carbamazepine (Tegretol) • chlorpropamide • General anesthesia agents • Opioids • oxytocin • Thiazide diuretics • SSRI antidepressants • Tricyclic antidepressants
  74. 74. CAUSES OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE • CNS Disorders • Head injury • subdural hematoma, • Subarachnoid hemorrhage • Stroke • Brain tumors • encephalitis,meningitis • Cerebral atrophy • Guillain-Barré syndrome Miscellaneous Conditions • Hypothyroidism • Lung infection (pneumonia, • tuberculosis, lung abscess) • Chronic obstructive • pulmonary disease • Positive pressure mechanical • ventilation • HIV • Adrenal insufficienc European endocrinology society, 2010
  75. 75. Pathophysiology of SIADH FIG. Pathophysiology of syndrome of inappropriate antidiuretic hormone (SIADH).
  76. 76. • low urine output and increased body weight • Lethargy & weakness • Confusion or changes in neurological status • Cerebral edema • Muscle cramps • Decreased urine output • Weight gain without edema • Hypertension (Note: b/c of the low Na, edema will not accompany the FVE) Signs and Symptoms
  77. 77. • simultaneous measurements of urine and serum osmolality(, serum osmolality less than 280 mOsm/kg • Urine osmolality disproportionately elevated in relation to the serum osmolality • Urine specific gravity elevated >1.025 • Plasma ADH elevated • Serum sodium low(serum sodium less than 134 mEq/L) Assessment and diagnosis
  78. 78. 1. Hypo-osmolality; plasma osmolality <280 mosmol/kg, or plasma sodium concentration <134 mmol/l 2. Inappropriate urinary concentration (Uosm >100 mosmol/kg) for hyponatraemia 3. Patient is clinically euvolaemic 4. Elevated urinary sodium (>40 mmol/l), with normal dietary salt and water intake 5. Exclusion of hypothyroidism, diuretics and glucocorticoid deficiency – particularly in patients with neurosurgical conditions diagnostic criteria for the diagnosis of SIADH. European endocrinology socity (2010)
  79. 79.  Treat underlying cause  Hypertonic or isotonic IV solution  Monitor for signs of fluid and electrolyte imbalance  Monitor for neurological effects  Monitor in and out, Weight  Restrict fluid intake  Lithium inhibits action of ADH Treatment of SIADH
  80. 80. • If symptoms are mild and serum sodium is greater than 125 mEq/L the only treatment may be a fluid restriction of 800 to 1000 mL/day. • Position the head of the bed flat or elevated no more than 10 degrees to enhance venous return to the heart and increase left atrial filling pressure reducing the release of ADH Nursing management
  81. 81. • Lasix may given only if the serum sodium is at least 125 mEq/L (125 mmol/L) • Because furosemide increases potassium, calcium, and magnesium losses, supplements is needed Nursing management
  82. 82. • Frequent turning, positioning, and range-of-motion exercise (if patient is bedridden) • Protect the patient from injury (LOC). • Implement seizure precautions. • Provide the patient with frequent oral care and distractions to decrease discomfort related to thirst from the fluid restrictions. Nursing management
  83. 83. • It is Hormone deficiency caused by the inadequate secretion of one or more of the hormones normally secreted by the pituitary, • It may be caused by compression of the normal tissue by a developing tumor, surgery, or radiotherapy. HYPOPITUITARISM-ANTERIOR LOBE
  84. 84. • Dwarfism, condition of being undersized, or less than 127 cm (50 in) in height. • Some dwarfs have been less than 64 cm (24 in) tall when fully grown. • The term midget is usually applied to physically well-proportioned dwarfs. • The term pygmy is applied to people whose shortness of stature is a racial trait and not caused by disease. Decreased GH in child: Dwarfism
  85. 85. • cause – Cretinism – Down syndrome, – Achondroplasia – spinal tuberculosis; and deficiency of the secretions of the pituitary gland or of the ovary. Decreased GH in child: Dwarfism
  86. 86. • GH binds to receptors on liver cells and they release insulin- like growth factor- 1 (IGF-1). • This hormone causes body cells to grow and stimulates protein synthesis within cartilage, bones, and muscle. • This hormone increases the growth rate of bones and muscles during childhood. • GH stimulates the rate at which amino acids enter cells and protein synthesis occurs. • GH stimulates fat and carbohydrate metabolism.
  87. 87. Amount of Growth Hormone
  88. 88. Hyposecretion (underproduction) of the Growth Hormone during growing years causes slow bone growth and the epiphyseal plates close before normal height is reached. DX,  clinically  serum GH level Treatment: hormonal replacement What Causes this Disorder?
  89. 89. • Complete lack of GH is not fatal in adults as would be the case with some hormones, • but it can have major detrimental effects that may cause disease some years earlier than might otherwise have been the case. Hypopituitarism (Adult)- GH
  90. 90. • Lack of GH causes changes in blood cholesterol concentrations • GH deficient adults have been shown to suffer from excessive tiredness, anxiety, depression and generally feeling unwell, as well as having feelings of social isolation and a tendency to be easily upset. Hypopituitarism (Adult)- GH……….
  91. 91. –Increased CV disease –Excessive tiredness –Anxiety –Depression –Reduced “quality of life” –Possible premature death Generally Lack of GH leads to:
  92. 92. Hypofunction – Posterior pituitary Normal urine production
  93. 93. • Diabetes insipidus (DI) literally means the passage of copious volumes of urine 'lacking taste', in contrast to the 'sweet tasting' urine typical of diabetes mellitus. • DI is characterized by the production of large volumes of dilute urine (more than 3 liters per day) and constant thirst. Diabetes Insipidus
  94. 94. • DI is usually insidious but can occur with damage to the hypothalamus or the pituitary (neurogenic DI) • May be a result of defect in renal tubules, do not respond to ADH (nephrogenic DI) • Decreased production or release of ADH results in massive water loss • Leads to hypovolemic & dehydration Diabetes Insipitus (DI)
  95. 95. 1.Primary/Idiopathic: account for approximately 50 % of the cases of diabetes insipidus. 2. Injury to the hypothalamus –pituitary area: may result from head trauma, neurosurgical procedures such as hypophysectomy. 3. Less common causes: neoplasms, histiocytosis, granulomas, vascular lesions, infections (encephalitis) causes of Diabetes Insipidus
  96. 96. TYPES &ETIOLOGY OF DIABETES INSIPIDUS
  97. 97. facts about Diabetes Insipidus  in USA, 3 cases per 100,000 population  No significant sex-related differences in central or nephrogenic DI exist, with male and female prevalence being equal.  no significant differences in prevalence among ethnic groups have been found.  With both central and nephrogenic DI, inherited causes account for approximately 1-2% of all cases.  An incidence of about 1 in 20 million births for nephrogenic DI caused by AQP2 mutations (Romesh Khardori,2013)
  98. 98. • different types of receptor for vasopressin. • The V1 receptor present in the endothelial cells leads to a pressor effect by the activation of Ca++ pathway whereas • V2R is the one responsible for water reabsorption by activating cyclic adenosine monophosphate (cAMP) in the kidneys and opening of the aquaporin pathophysiology of Diabetes Insipidus
  99. 99. • balance is normally achieved by three mechanisms: 1.adequate vasopressin secretion 2.thirst appreciation and drinking 3.vasopressin-responsive kidneys pathophysiology of Diabetes Insipidus
  100. 100. pathophysiology of Diabetes Insipidus
  101. 101. • The onset of central DI is usually acute and accompanied by excessive fluid loss. • if it is secondary two brain surgery central DI has a triphasic pattern: abrupt onset of polyuria, urine volume normalizes, central DI is permanent. The third phase occurs within 10 to 14 days postoperatively. Clinical Manifestations
  102. 102. • Polyuria: with urine volume f 3-15 L daily, Nocturia is almost always present, which may disturb sleep and cause mild day time fatigue or somnolence. • Thirst (polydipsia): A conscious patient with normal thirst mechanism and free access to water will maintain hydration. Clinical Manifestations
  103. 103. • If oral fluid intake cannot keep up with urinary losses, severe dehydration results especially in unconscious patients or infants. • In addition, the patient may show central nervous system (CNS) manifestation ranging from irritability and mental dullness to coma, related to increasing serum osmolality and hypernatremia. Clinical Manifestations
  104. 104.  Polyuria of more than 3 litres per 24 hours in adults (may be up to 20!)  Urine specific gravity low <1.005  urine osmolality of less than 100 mOsm/kg (100 mmol/kg).  Serum osmolality is elevated (usually greater than 295 mOsm/kg Diagnostic Tests
  105. 105. • plasma osmolality in untreated patients helps to distinguish the cause of polyuria. • In DI, the loss of free water leads to high osmolality (up to 310 mOsm/kg). • In psychogenic polydipsia excess fluid intake is primary and serum osmolality is low (255 -280 mOsm/kg ) Diagnostic Tests
  106. 106. • Used to differentiate causes of diabetes insipidus . • After The patient is deprived of water for 8 to 12 hours osmolality is measured ! • Five (5 U) of aqueous vasopressin or 2 μg of desmopression is injected SC. Urine osmolality after 1 hr .Patients with central DI exhibit a dramatic increase in urine osmolality, from 100 to 600 mOsm/kg, In nephrogenic DI not increase. Water deprivation test
  107. 107. Interpretations of Water deprivation test
  108. 108. • Another test to differentiate central DI from nephrogenic DI is to measure the level of ADH after an analog of ADH (e.g., desmopressin) is given. • If the cause is central DI, the kidneys will respond to the hormone by concentrating urine. • If the kidneys do not respond in this way, then the cause is nephrogenic. Diagnostic Tests
  109. 109. Medical management includes Rehydration IV fluids (hypotonic) Symptom management Hormonal therapy For nephrogenic DI: thiazide diuretics, mild salt depletion, prostaglandin inhibitors (i.e. ibuprophen) Management
  110. 110. • Aqueous vasopressin SC or IM in doses of 5-10 U. Since effect lasts 6 h or less, use in chronic treatment is limited. • Desmopresin (synthetic vasopressin) in a dose of 0.05-0.2ml applied to the upper respiratory mucous membrane twice daily by nasal cannula or nasal spray. • The effect lasts 12-24 h, can be given SC or IV • Has preparation of choice for both adults and children. Management
  111. 111. • Chlorpropamide :in patients who have partial ADH deficiency : 250-500 mg PO • Thiazide diuretics: Thiazides are only partially effective, decreasing the urine volume by 30%-50 %. • Restricting salt intake may be helpful. • Prostaglandin inhibitors such as indomethacin (1.5-3 mg/kg/d PO in divided doses) may be effective. • Treatment of underlying causes of DI Management
  112. 112. –Carbamazepine   –In vivo studies showed carbamazepine decreased the urinary volume and increased the urinary osmolality by increasing that aquaporin 2 expression in the inner medullary collecting duct –Indapamide : for mild form of CDI as it increases urinary osmolality and decrease serum osmolality (J. D. Cook, Y. H. Caplan.et.al,2013) Evidences on Treatment of DI
  113. 113. – Chlorpropamide  : It potentiates the antidiuretic action of circulating arginine vasopressin and leads to a reduction of urinary output by 15%. – But it has side effect .i.e.hypoglycemia, hyponatremia, hyperlipidemia, hyperuricemia, hypercalcemia,hypokalemia, metabolic alkalosis, and myopathy. (J. D. Cook, Y. H. Caplan.et.al,2013) Treatment
  114. 114. –Lithum-induced NDI can be managed to a large extent by simply increasing water intake. –Amiloride at doses 2.5–10 mg/dL decreases the lithium entry into principal cells (Chadi Saifan, Rabih Nasr,2013) Treatment
  115. 115. – Thiazides induce hypovolemia and increase the proximal tubular water reabsorption and thus reduce polyuria. – NSAIDS on the other hand can reduce the negative effect of intrarenal prostaglandins on urinary concentrating mechanism and help manage NDI. (Chadi Saifan, Rabih Nasr,2013) Treatment
  116. 116.  assess for signs of fluid and electrolyte imbalance  Monitor patient level of consciousness  Assess serum and urine values  Assess level of drayness Nursing assessment
  117. 117. • Fluid Volume Deficit • Risk for Injury r/t altered LOC • Sleep Pattern Disturbance r/t urinary frequency or anxiety • Altered Urinary Elimination r/t excess urinary output • Body Image disturbance related to frequent urination POSSIBLE NURSING DIAGNOSIS
  118. 118.  Monitor for signs of fluid and electrolyte imbalance  Monitor in and out  Daily weight  Monitor for excessive thirst or output  Assess serum and urine values (decreased SG, decreased urine osmolality, high serum osmolality are early indicators of the problem Nursing intervention
  119. 119. – almost all of the pituitary related problems are directly or indirectly relted with tumor – Most of the time tumors are asymptomatic – Pituitary disorders are due to either increase or decrease hormonal secration – Anterior pituitary disorders • Excess:giantizem,acromegaly,cushing diseases • Hyposecretion,dawarfizem in childrens – Postirior:excess;SIADH,if Hypo:DI summery
  120. 120. After completion of the lecture the student able to ; • Understand the normal anatomic and physiological over view of adrenal gland • Describe major adrenal gland disorder.i.e pheochromocytoma,cushing syndrome, and primary aldostrolizem • Discuses etiology of adrenal gland disorders • Explain the pathophysiology and clinical presentation of those disorders • Identify the appropriate medical and nursing management Disorder of The Adrenal gland
  121. 121. Anatomic and Physiologic Overview
  122. 122. Anatomic and Physiologic Overview
  123. 123. • The adrenal gland lies just above the kidneys • Divided into two main sub-organs Adrenal cortex –Secretes the steroid hormones • Glucocorticoid • Mineralocorticoid • Androgens Anatomic and Physiologic Overview
  124. 124. Adrenal medulla Stimulation of preganglionic sympathetic nerve fibers, which travel directly to the cells of the adrenal medulla, causes release of the catecholamine hormones epinephrine and norepinephrine Anatomic and Physiologic Overview
  125. 125. –The hypothalamus secretes corticotropin- releasing hormone (CRH), –stimulates the pituitary gland to secrete ACTH, which stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). –Increased levels of the adrenal hormone then inhibit the production or secretion of CRH and ACTH. Anatomic and Physiologic Overview
  126. 126. Anatomic and Physiologic Overview
  127. 127. • Glucocorticoids • Glucocorticoids are secreted from the adrenal cortex in response to the release of ACTH from the anterior lobe of the pituitary gland • The glucocorticoids are so named because they have an important influence on glucose metabolism: • increased hydrocortisone secretion results in elevated blood glucose levels. Major hormones secreted from adrenal gland
  128. 128. • Mineralocorticoids: aldosterone • Mineralocorticoids exert their major effects on electrolyte metabolism. • They act principally on the renal tubular and gastrointestinal epithelium to cause increased sodium ion absorption in exchange for excretion of potassium or hydrogen ions. • It is primarily secreted in response to the presence of angiotensin II in the bloodstream. Major hormones secreted from adrenal gland
  129. 129. • Adrenal Sex Hormones (Androgens) • exert effects similar to those of male sex hormones. • The adrenal gland may also secrete small amounts of some estrogens, or female sex hormones. • ACTH controls the secretion of adrenal androgens. Major hormones secreted from adrenal gland
  130. 130. Pheochromocytoma • Pheochromocytoma is a tumor that is usually benign and originates from the chromaffin cells of the adrenal medulla. • In 90% of patients the tumor arises in the medulla; • in the remaining patients, it occurs in the extra- adrenal chromaffin tissue located in or near the aorta, ovaries, spleen, or other organs. Specific Disorders of the Adrenal Glands
  131. 131. • It may occur at any age, but its peak incidence is between 40 and 50 years of age • It affects men and women equally. • Ten percent of the tumors are bilateral, and 10% are malignant. • Because of the high incidence in family members of affected people, the patient's family members should be alerted and screened for this tumor. Pheochromocytoma…………………………..
  132. 132. • Pheochromocytoma is the cause of high blood pressure in 0.1% of patients with hypertension (Bravo & Tagle, 2003). • Although it is uncommon, it is one form of hypertension that is usually cured by surgery • without detection and treatment, it is usually fatal. Pheochromocytoma…………………………..
  133. 133. Rule of Tens: Ten percent of pheochromocytomas are: –bilateral ,malignant ,extra-adrenal, familial ,in children –Pheochromocytomas occur in people of all races, although they are diagnosed less frequently in blacks. (Michael A Blake,2015) Pheochromocytoma…………………………..
  134. 134. Pheochromocytomas may occur in persons of any age, but the peak incidence is from the third to the fifth decades of life. Fifty percent of pheochromocytomas in children are solitary intra-adrenal lesions, 25% are present bilaterally, and 25% are extra-adrenal. (Michael A Blake,2015) Pheochromocytoma…………………………..
  135. 135. – Multiple endocrine neoplasia, type II (MEN II) is a disorder resulting in tumors in more than one part of the body's hormone-producing (endocrine) system i.e.thyroid, parathyroid, lips, tongue and gastrointestinal tract. – Von Hippel-Lindau disease can result in tumors at multiple sites, including the central nervous system, endocrine system, pancreas and kidneys. Etiology: Genetic factors
  136. 136. –Neurofibromatosis 1 (NF1) results in multiple tumors in the skin (neurofibromas), pigmented skin spots and tumors of the optic nerve. –Hereditary paraganglioma syndromes are inherited disorders that result in either pheochromocytomas or paragangliomas. Etiology
  137. 137. –Pheochromocytomas are chromaffin cell tumor that synthesize and release catecholamines. –Norepinephrine is usually the most abundant with smaller doses of epinephrine. –All sign and symptoms is related with excessive catecholamines secretion Pathophysiology of Pheochromocytoma
  138. 138. • The nature and severity of symptoms depend on the relative proportions of epinephrine and norepinephrine secretion. • The typical triad of symptoms is headache, diaphoresis, and palpitations in the patient with hypertension • 8% of patients are completely asymptomatic. Clinical Manifestations
  139. 139. • The hypertension may be intermittent or persistent. • However, only half of patients with pheochromocytoma have sustained or persistent hypertension. • If the hypertension is sustained, it may be difficult to distinguish from other causes of hypertension. Clinical Manifestations………..
  140. 140. • tremor, • headache, • flushing, and anxiety. • Hyperglycemia may result from conversion of liver and muscle glycogen to glucose due to epinephrine secretion; Clinical Manifestations………..
  141. 141. – characterized by acute, unpredictable attacks lasting seconds or several hours. – Symptoms usually begin abruptly and subside slowly. – During these attacks, the patient is extremely anxious, tremulous, and weak. – Blood pressures exceeding 250/150 mm Hg have been recorded. clinical picture in the paroxysmal form of pheochromocytoma
  142. 142. – polyuria, nausea, vomiting, diarrhea, abdominal pain, and a feeling of impending doom. – Associated with blood pressure :dysrhythmias, dissecting aneurysm, stroke, and acute renal failure. – Postural hypotension, (lightheadedness, dizziness on standing) occurs in 70% of patients with untreated pheochromocytoma. clinical picture in the paroxysmal form of pheochromocytoma
  143. 143. – Physical exertion, Anxiety or stress – Changes in body position, Bowel movement, Labor and delivery – Foods high in tyramine, a substance that affects blood pressure, also can trigger a spell. – Tyramine is common in foods that are fermented, aged, pickled, cured, overripe or spoiled. factors that exacerbate acute attack:
  144. 144. – These foods may include: Some cheeses, beers and wines, Dried or smoked meats ,Avocados, bananas and fava beans, Pickled fish – Certain medications:Decongestants,Monoamine oxidase inhibitors (MAOIs), such as phenelzine (Nardil), tranylcypromine (Parnate) and isocarboxazid (Marplan),Stimulants, such as amphetamines or cocaine factors that exacerbate acute attack………
  145. 145. Clinically: “five Hs”: hypertension, headache, hyperhidrosis ,hypermetabolism, and hyperglycemia. –The presence of these signs has a 93.8% specificity and a 90.9% sensitivity for pheochromocytoma (Brunner 11th ,edition,American ca society ,2014). Assessment and Diagnostic Findings
  146. 146. –urine and plasma levels of catecholamines and metanephrine (MN), –a catecholamine metabolite, are the most direct and conclusive tests for over activity of the adrenal medulla. –A negative test result virtually excludes pheochromocytoma. – However, increased levels of at least one catecholamine or MN can occur in 10% of patients with essential hypertension. Assessment and Diagnostic Findings…………….
  147. 147. –A 24-hour specimen of urine is collected for determination of free catecholamines, MN, and VMA; the use of combined tests increases the diagnostic accuracy of testing. –Levels can be as high as two times the normal limit. Assessment and Diagnostic Findings…………….
  148. 148. Reference interval : • Vanillyl mandelic acid (VMA) : 1.4-6.5 mg/24 hr (7-33 μmol/day) • Keep 24-hr urine collection at pH <3.0 with HCl acid as preservative. • Metanephrine 92-934 mcg/day Assessment and Diagnostic Findings…………….
  149. 149. • A number of medications and foods, such as coffee and tea (including decaffeinated varieties), bananas, chocolate, vanilla, and aspirin, may alter the results of these tests; • Urine collected over a 2- or 3-hour period after an attack of hypertension can be assayed for catecholamine content. • Avoid physical stress :Supine position and at rest for 30 minutes Assessment and Diagnostic Findings…………….
  150. 150. • amphetamines, nose drops or sprays, decongestant agents, bronchodilators) may increase • Normal plasma values of epinephrine are 100 pg/mL (590 pmol/L); norepinephrine less than 100 to 550 pg/mL (590 to 3240 pmol/L). Assessment and Diagnostic Findings…………….
  151. 151. • Values of epinephrine greater than 400 pg/mL (2180 pmol/L) or norepinephrine values greater than 2000 pg/mL (11,800 pmol/L) are considered diagnostic of pheochromocytoma. • Values that fall between normal levels and those diagnostic of pheochromocytoma indicate the need for further testing. Assessment and Diagnostic Findings…………….
  152. 152. A clonidine suppression test normally decrease –In pheochromocytoma, increased catecholamine levels result from the diffusion of excess catecholamines into the circulation, bypassing normal storage and release mechanisms. Assessment and Diagnostic Findings…………….
  153. 153. –Imaging studies, such as CT, MRI, and ultrasonography, –evaluating the function of other endocrine glands because of the association of pheochromocytoma in some patients with other endocrine tumors. Assessment and Diagnostic Findings…………….
  154. 154. • Alcohol withdrawal • Labile essential hypertension • Hyperventilation • Multiple pharmacologic agents: Monoamine oxidase inhibitors (MAOIs), decongestants, and sympathomimetics Illegal drug use • Migraine headache • Autonomic neuropathy Differentials diagnosis
  155. 155. Non pharmacological –During an episode or attack of hypertension, tachycardia :bed rest with the head of the bed elevated to promote an orthostatic decrease in blood pressure. Medical Management
  156. 156. • alpha-adrenergic blocking agents (eg, phentolamine [Regitine]) or • smooth muscle relaxants (eg, sodium nitroprusside [Nipride]) to lower the blood pressure quickly. • Phenoxybenzamine (Dibenzyline), a long- acting alpha-blocker, may be used after the blood pressure is stable to prepare the patient for surgery. Pharmacologic Therapy
  157. 157. –Calcium channel blockers such as nifedipine –They are also useful for prevention of cardiovascular complications, because they prevent catecholamine-induced coronary vasospasm and myocarditis –propranolol (Inderal) may be used in patients with cardiac dysrhythmias and in those not responsive to alpha-blockers. Pharmacologic Therapy
  158. 158. –Alpha-adrenergic and beta-adrenergic blocking agents must be used with caution, because patients with pheochromocytoma may have increased sensitivity to them. –preoperatively catecholamine synthesis inhibitors, such as alpha-methyl-p-tyrosine (metyrosine) May be used Pharmacologic Therapy
  159. 159. • The definitive treatment of pheochromocytoma is surgical removal of the tumor, usually with adrenalectomy. • Bilateral adrenalectomy may be necessary if tumors are present in both adrenal glands. Surgical Management
  160. 160. • Manipulation of the tumor during surgical excision may cause release of stored epinephrine and norepinephrine, with marked increases in blood pressure and changes in heart rate. • Therefore, use of sodium nitroprusside (Nipride) and alpha-adrenergic blocking agents may be required during and after surgery Surgical Management…….
  161. 161. • Corticosteroid replacement is required if bilateral adrenalectomy or for the first few days or weeks after removal of a single adrenal gland. • IV administration of corticosteroids (methylprednisolone sodium succinate begin on the evening before surgery and continue during the early postoperative period to prevent adrenal insufficiency. Surgical Management…….
  162. 162. • Oral preparations of corticosteroids (prednisone) are prescribed after the acute stress of surgery diminishes. • Hypotension and hypoglycemia may occur because of the sudden withdrawal of excessive amounts of catecholamines. • Therefore, careful attention is directed toward monitoring and treating these changes. Surgical Management…….
  163. 163. • Blood pressure is expected to return to normal with treatment; one third of patients continue to be hypertensive after surgery if  not all pheochromocytoma tissue was removed,  pheochromocytoma recurs, or  if the blood vessels were damaged by severe and prolonged hypertension. Surgical Management…….
  164. 164. –Several days after surgery, urine and plasma levels of catecholamines and their metabolites are measured to determine whether the surgery was successful. Surgical Management…….
  165. 165. Cardiac: CHF, MI, arrhythmias, orthostasis from volume contraction Metabolic: Increased metabolic rate, weight loss Endocrine: Hyperglycemia from suppression of insulin production by the excessive catecholamines Complications of Pheochromocytoma
  166. 166. Assessment vital signs • Blood pressure – Hypertension (before and during surgery) – Hypotension (after surgery) • Blood sugar • Hypoglycemia (after surgery) • Hyperglycemia (before and during surgery) Nursing processes
  167. 167. hemodynamic parameters  fluid and electrolyte status— including intake and urinary output and urine catecholamine levels.  Assess the patient for bleeding and infection Assess the patient for pain Nursing asst…….
  168. 168. • Anxiety related to potential seriousness and Sudden onset sign and symptoms of the problem. • Ineffective renal tissue perfusion related to adverse effects of high blood pressure in renal vascular system. • Risk for injury related to potential for hypertensive crisis. Possible Nursing DX
  169. 169. preoperative • Patient preparation includes control of blood pressure and blood volumes; usually this is carried out over 4 to 7 days. • Nifedipine and nicardipine may be used safely without causing undue hypotension. Nursing Management
  170. 170. –the nurse informs the patient about the importance of follow-up monitoring to ensure that pheochromocytoma does not recur undetected –Several IV lines are inserted for administration of fluids and medications. preoperative……..
  171. 171. –The patient is monitored for several days in the intensive care unit with special attention given to ECG changes, arterial pressures, fluid and electrolyte balance, and blood glucose levels. postoperative phase nursing care
  172. 172. • Teaching Patients Self-Care • After adrenalectomy, use of corticosteroids may be needed. • Therefore, the nurse instructs the patient about their purpose, the medication schedule, and the risks of skipping doses or stopping their administration abruptly. postoperative phase nursing care……..
  173. 173. • It is important to teach the patient and family how to measure the patient's blood pressure and when to notify the health care provider about changes in blood pressure. • provides verbal and written instructions about the procedure for collecting 24-hour urine specimens to monitor urine catecholamine levels. postoperative phase nursing care……..
  174. 174. • Continuing Care • A follow-up visit from a home care nurse may be indicated to assess the patient's postoperative recovery, surgical incision, and compliance with the medication schedule. • This may help reinforce previous teaching about management and monitoring. postoperative phase nursing care……..
  175. 175. • nurse also obtains BP measurements and assists the patient in preventing problems that comes from long- term use of corticosteroids. • Because of the risk for recurrence of hypertension, periodic checkups are required, for young patients and families history of pheochromocytoma. • The patient should have appointments to observe urine levels of catecholamine. postoperative phase nursing care……..
  176. 176. 1) Pheochromocytomas are causes of hypertension. 2) Diagnosis is usually made by increased 24 hour urine catecholamine metabolites. 3) Surgery is the treatment of choice but it considered as high risk due to hemodynamic instability. 4) Pre-operative treatment includes use of alpha blockers, beta blockers, and metyrasine. Key Points about Pheochromocytomas
  177. 177. • Addison's disease, or adrenocortical insufficiency, occurs when adrenal cortex function is inadequate to meet the patient's need for cortical hormones. • Inadequate secretion of ACTH from the pituitary gland also results in adrenal insufficiency because of decreased stimulation of the adrenal cortex. Adrenocortical Insufficiency (Addison's Disease)
  178. 178. • Autoimmune or idiopathic atrophy of the adrenal glands is responsible for 80% to 90% of cases • surgical removal of both adrenal glands and infection of the adrenal glands. • Tuberculosis and histoplasmosis are the most common infections that destroy adrenal gland tissue. Etiology &Pathophysiology
  179. 179. • Therapeutic use of corticosteroids is the most common cause of adrenocortical insufficiency • sudden cessation of exogenous adrenocortical hormonal therapy, which suppresses the body's normal response to stress and interferes with normal feedback mechanisms. Etiology &Pathophysiology
  180. 180. • primary cause (Addison’s disease) Adrenocortical insufficiency (hypofunction of the adrenal cortex) • secondary cause (lack of pituitary ACTH secretion). • In Addison’s disease, all adrenal corticosteroids (glucocorticoids,mineralocorticoids, and androgens) are reduced but in secondary adrenocortical insufficiency, corticosteroids and androgens are deficient others are almost not decrease. Etiology &Pathophysiology
  181. 181. • In Iceland from secondary data 26 weman,27 men from 100,000 has Addison diseases (Anderi snaer,2016) • In Germany between 100 and 129 per million and showed an annual increase of 6.7 % on average. The prevalence was lower in men (73-90 per million with an annual increase of 5.5 % on average) than in women (129-169 per million with an annual increase of 7.1 % on average) (Meyer G .et.al,2014) General fact about Addison's
  182. 182. General fact about Addison's
  183. 183. • dark pigmentation of the mucous membranes and the skin, especially of the knuckles, knees, and elbows; (1st sign) • muscle weakness; anorexia; gastrointestinal symptoms; fatigue; emaciation; • hypotension; and low blood glucose, low serum sodium, and high serum potassium levels. Clinical Manifestations
  184. 184. • Mental status changes such as depression, emotional lability, apathy, and confusion are present in 60% to 80% of patients. • In severe cases, the disturbance of sodium and potassium metabolism may be marked by depletion of sodium and water and severe, chronic dehydration. Clinical Manifestations
  185. 185. • Addisonian crisis :With disease progression and acute hypotension, addisonian crisis develops causes  dehydration resulting from preparation for diagnostic tests  surgery Clinical Manifestations…..
  186. 186. • characterized by cyanosis and the classic signs of circulatory shock: • pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure. Clinical Manifestations Addisonian crisis
  187. 187. • In addition, the patient may complain of headache, nausea, abdominal pain, and diarrhea and may show signs of confusion and restlessness. • Even slight overexertion, exposure to cold, acute infection, or a decrease in salt intake may lead to circulatory collapse, shock, and death if untreated. Clinical Manifestations Addisonian crisis…….
  188. 188. • clinical manifestations presented appear specific, but it may presented with nonspecific symptoms. • The diagnosis is confirmed Combined measurements of early-morning serum cortisol and plasma ACTH are performed to differentiate patients with primary adrenal insufficiency from those with secondary adrenal insufficiency Assessment and Diagnostic Findings
  189. 189. • Patients with primary insufficiency have a greatly increased plasma ACTH level (more than 22.0 pmol/L) and a serum cortisol concentration lower than the normal range (less than 165 nmol/L) or • Other findings hypoglycemia , hyponatremia, hyperkalemia, and leukocytosis. Assessment and Diagnostic Findings……….
  190. 190. • If the adrenal cortex is destroyed,ACTH administration fails to cause the normal increase in plasma cortisol and urinary 17 hydroxycorticosteroids. • If the problem is on pituitary, a normal response to repeated doses of exogenous ACTH is seen, but no response occurs after the administration of metyrapone, which stimulates endogenous ACTH. Assessment and Diagnostic Findings……….
  191. 191. • In acute case First Rx circulatory shock: 5% dextrose in normal saline. • monitoring vital signs, and placing the patient in a recumbent position with the legs elevated. • Hydrocortisone, IV, 200 mg stat, followed by 100 mg, IV, 6 hourly until condition is stable • Vasopressor amines may be required if hypotension persists. Medical Management
  192. 192. • Maintenance • Prednisolone, oral, 5 mg morning and 2.5 mg evening each day - Patients SHOULD NOT stop treatment if they become ill. Rather double the regular doses of corticosteroids where required. • Revert to hydrocortisone, IV for even minor surgical procedures including labor and delivery Pharmacologic mgt
  193. 193. • Antibiotics may be administered if infection has precipitated adrenal crisis • Oral intake may be initiated as soon as tolerated. • IV fluids are gradually decreased after oral fluid intake is adequate to prevent hypovolemia. • supplement dietary intake with added salt during gastrointestinal losses of fluids through vomiting and diarrhea. Medical Management…………………………
  194. 194. • Assess for symptoms of fluid imbalance • blood pressure and pulse rate as the patient moves from a lying to a standing position. • skin color and turgor for hypovolemia. • assessments weight changes, muscle weakness, and fatigue and • any illness or stress that may have precipitated the acute crisis Nursing Management
  195. 195. • Monitoring and Managing Addisonian Crisis • The patient at risk is monitored for signs and symptoms indicative of addisonian crisis. • The patient with addisonian crisis requires immediate treatment with IV administration of fluid, glucose, and electrolytes, especially sodium; replacement of missing steroid hormones; and vasopressors. Nursing Management…………….
  196. 196. • anticipates the patient's needs and takes measures to meet them to avoid exertion which exacerbate addisonian crisis . • Assess vital signs, weight, and fluid and electrolyte status which indicates patient's progress. • efforts are made to identify and reduce the factors that may have led to the crisis. Nursing Management…………….
  197. 197. • Restoring Fluid Balance • assesses the patient's for fluid imbalance , • instructing the patient to report increased thirst, which may indicate impending fluid imbalance. • Lying, sitting, and standing BP provide information about fluid status. • A decrease in systolic pressure (20 mm Hg or more) may indicate depletion of fluid volume Nursing Management…………….
  198. 198. • Improving Activity Tolerance • Until the patient's is stabilized, avoid unnecessary exertion to decrease hypotenesion • Efforts are made to detect signs of infection or the presence of other stressors. • Explaining all procedures to the patient and family reduces their anxiety. Nursing Management…………….
  199. 199. • During the acute crisis, the nurse maintains a quiet, non stressful environment and performs all activities (eg, bathing, turning) for the patient. • Explaining the rationale for minimizing stress during the acute crisis assists the patient to increase activity gradually. Nursing Management…………….
  200. 200. • Teaching Patients Self-Care • patient and family members receive explicit verbal and written instructions about replacement therapy,how to modify the medication dosage and increase salt intake in times of illness, very hot weather, and other stressful situations. • About diet and fluid intake to help maintain fluid and electrolyte balance. Nursing Management…………….
  201. 201. • Teach about preloaded, single-injection syringes of corticosteroid for use in emergencies. • Specific instructions about how and when to use the injection are also provided. • Precautions (wear a medical alert bracelet) to administer corticosteroids. • Inform about signs of excessive or insufficient hormone replacement. Nursing Management…………….
  202. 202. –If the patient requires surgery, careful administration of fluids and corticosteroids is necessary before, during, and after surgery to prevent addisonian crisis. Nursing Management…………….
  203. 203. • Continuing Care • In some patients they might have concurrent illnesses or incomplete recovery • home care to assess the patient's recovery, monitor hormone replacement, and evaluate stress in the home. • The nurse assesses the patient's and family's knowledge about medication and dietary modifications. Nursing Management…………….
  204. 204. • Cushing's is a disorder in which the adrenal glands are producing too much cortisol (hypercotisolism). • If the source of the problem is the pituitary gland, then the correct name is Cushing's Disease • if it originates anywhere else (adrenal tumors, long term steroid administration) then the correct name is Cushing's Syndrome. Cushing's Syndrome
  205. 205.  Men had a 3x greater incidence of the ectopic ACTH syndrome,  Women are 3-8x more likely than men to develop Cushing's disease, 4-5x more likely to have Cushing's syndrome  Age-related incidence: increasing rapidly after age 50 years  Cushing's disease occurs mainly in women aged 25 to 45 years (European endocrinology society report ,2011) Facts about Cushing syndrome
  206. 206. • 40 cases per million population . • 2-5% of patients are with poorly controlled diabetes and hypertension. • Female preponderance is generally assumed to be close to 3:1  Frederic Castinetti et.al.2012 Facts about Cushing syndrome
  207. 207. • Iatrogenic hypercortisolism resulting from medical intervention is most common cause of Cushing Syndrome.i.e. long term glucocorticoid treatment for asthma, arthritis, and other conditions. • Pituitary hyper secretion and pituitary tumors account for 70% of Cushing’s Disease. Etiology - Hypercortisolism
  208. 208. • Adrenal tumors account for 30%. • Ectopic secretion of ACTH by tumors located outside the pituitary gland are rare cause of the syndrome and associated with increased morbidity/mortality (American CA socity 2014). Etiology - Hypercortisolism
  209. 209. Etiology - Hypercortisolism Frederic Castinetti et.al.2012
  210. 210. • Regardless of the cause, the normal feedback mechanisms that control the function of the adrenal cortex become ineffective, and the usual diurnal pattern of cortisol is lost. • The signs and symptoms of Cushing's syndrome are primarily a result of oversecretion of glucocorticoids and androgens (sex hormones), although mineralocorticoid secretion also may be affected. pathogenesis
  211. 211. • moon face - particularly filling in of the temporal fossa • weight gain - central obesity • muscle wasting and proximal myopathy (patients have difficulty standing from a seated position without use of arms), muscle wasting, osteoporosis, truncal obesity Clinical manifestation
  212. 212. • “buffalo hump” ( cervical fat pad ) and supraclavicular fat pads contribute to the Cushingiod appearance • Symptoms of androgen excess (e.g. oligomenorrhea, hirsutism, and acne) • Poor wound healing: due to impaired immune function. • Growth retardation in children may be severe. Clinical manifestation
  213. 213. • Neurological: Psychosis, emotional labiality, loss of memory, depression • Integumentary: ecchymosis, purple striae on abdomen, poor wound healing, skin infections, thin skin, acne. Clinical manifestation
  214. 214. Clinical manifestation………………..
  215. 215. • CV: HTN • GI: peptic ulcers • Metabolic: hyppokalemia, hypernatremia, edema, moon face, weight gain. • Classic symptoms of Cushing’s: moon face, buffalo hump, purple straie, truncal obesity. Clinical manifestation………………..
  216. 216. Clinical manifestation………………..
  217. 217. Clinical manifestation………………..
  218. 218. • 24 hr urine cortisol levels • Serum sodium levels • Serum potassium levels • Serum glucose level • Serum ACTH in Cushing Disease • ACTH suppression test to identify cause • Dexamethasone supression test: cause pituitary or adrenal • Radiological exam to reveal pituitary or adrenal tumor Assessment and Diagnosis
  219. 219. • Plasema (ACTH) (corticotropin) level • Measures plasma level of ACTH. • Reference interval: • Morning: <120 pg/mL (<26 pmol/L) • Evening: <85 pg/mL (<19 pmol/L) • Patient should be NPO after midnight before morning • blood draw between 6-8 AM. Assessment and Diagnosis
  220. 220. ACTH measurement : may help to differentiate the cause of Cushing’s syndrome a. High normal or slightly elevated ACTH in Cushing’s diseases b. Markedly elevated ACTH in Ectopic ACTH production c. Extremely low ACTH level in automatically functioning adrenal tumor is the source of excess cortisol. • Pituitary secretion of ACTH is suppressed due to the excess cortisol Assessment and Diagnosis
  221. 221. ACTH stimulation with cosyntropin • Used to evaluate adrenal function. • After baseline cortisol sample is drawn, give cosyntropin (synthetic ACTH) by IV bolus. • Cortisol samples are drawn 30 and 60 min after bolus. • Plasma cortisol at 60 min should increase by >7 mcg/dL from baseline. Assessment and Diagnosis
  222. 222. • Overnight Dexamethasone suppression test • Dexamethasone (Decadron) 1 mg (low dose) or 4 mg (high dose) is given at 11 PM to suppress secretion of corticotropin- releasing hormone. Plasma cortisol sample is drawn at 8 AM. • Reference interval: Cortisol level <3 mcg/dL (<0.08 μmol/L) for low dose and <50% of baseline in high dose indicates normal adrenal response. • Ensure that patient has fasted, not take med increase ACTH Assessment and Diagnosis
  223. 223. Standard Dexamethasone Suppression Test
  224. 224. Response for standard Dexamethasone Suppression Test
  225. 225. • Cortisol (free) Measures free (unbound) cortisol. Preferred test to evaluate hypercortisolism. • Reference interval: 20-90 mcg/24 hr (55-248 nmol/day) • Instruct patient about 24-hr urine collection and avoidance of stressful situations and excessive physical exercise. Assessment and Diagnosis
  226. 226. •At least two first-line tests should be abnormal to establish the diagnosis of Cushing's syndrome • Late night salivary cortisol, urinary cortisol, and the low-dose dexamethasone suppression tests are first-line tests • Urinary and salivary cortisol measurements should be obtained at least twice 2008 Endocrine Society Clinical Guidelines to dx cushing syndrom
  227. 227. 1. Adrenal adenoma : complete surgical resection of the adenoma cures the disease , but • patients may need cortisol replacement post operatively for several months 2. Ectopic ACTH syndrome: can be cured by treating or removal of the tumor that is producing the ectopic ACTH. Medical and surgical management
  228. 228. 3. Cushing’s Disease a. Pituitary radiation : is effective in children but it cures fewer than 1/3 of adult patients b. Bilateral adrenalectomy cures Cushing’s syndrome. Has Disadvantages: • Patients will develop Addison’s disease • Nelson’s syndrome: in which pituitary adenomas undergo rapid growth, Medical and surgical management
  229. 229. 3.Transphenoidal surgery: if due to a pituitary tumor • Where surgery is contraindicated or fails to reduce cortisol levels, adrenalectomy and/or pituitary radiation may be necessary. • Adrenocortical Inhibitors: (metapyrone, aminogluthimide, effective short-term. • Diet: low calorie, carbohydrate & salt. High potassium. treatment
  230. 230. • Fluid volume excess • Risk for infection • Risk for injury • Activity intolerance • Anxiety • Knowledge deficit • Risk for impaired tissue integrity Priority Nursing Diagnoses
  231. 231. • Diet • Medications • Medic alert bracelet • Hormone levels and stress • Signs of excessive or deficient adrenal hormones Patient Teaching
  232. 232. • Post op care for cranial surgery (CSF leak, ICP etc.) • Hydrocortisone therapy, some on a long- term basis • If surgery results in hypopituitarism, long- term hormone replacement therapy will be required • Moods swings and depression may be a serious problem that may take months to treat Post op Care following Transphenoidal Surgery
  233. 233. • It is due to Excessive production of aldosterone causes a distinctive pattern of biochemical changes and a corresponding set of clinical manifestations • Causes functioning tumors of the adrenal gland Primary Aldosteronism
  234. 234. • Hypokalemia, decrease hydrogen ions (alkalosis), • increase in pH and serum bicarbonate concentration. • The serum sodium level is normal or elevated, depending on the amount of water reabsorbed with the sodium. • Hypertension is the most prominent and almost universal Pathophysiology and Clinical Manifestations
  235. 235. • muscle weakness, cramping, and fatigue (Hypokalemia), • kidneys fail to acidify or concentrate the urine. • Diluted polyuria. • Serum, by contrast, becomes abnormally concentrated (polydipsia) and arterial hypertension. Pathophysiology and Clinical Manifestations
  236. 236. • aldosterone action on nerve receptors, such as the carotid sinus, result in hypertension. • sign of hypocalcemia,due to alkalosis • Glucose intolerance may occur, because hypokalemia interferes with insulin secretion from the pancreas. Pathophysiology and Clinical Manifestations
  237. 237. • high serum aldosterone and low serum renin levels. • aldosterone excretion rate after salt loading • The renin–aldosterone suppresion test can differentiating the cause of primary aldosteronism. • Antihypertensive medication may be discontinued up to 2 weeks before testing. Assessment and Diagnostic Findings
  238. 238. • Used to assess for hyperaldosteronism. • Reference interval: • Upright posture: 7-30 ng/dL (0.19-0.83 nmol/L) • Supine position: 3-16 ng/dL (0.08-0.44 nmol/L) Aldostrone level
  239. 239. • Adrenalectomy. • Spironolactone may be prescribed to control hypertension. • Patient is risk for fluctuations in adrenocortical hormones and requires administration of corticosteroids, fluids, and other agents to maintain blood pressure and prevent acute complications. Medical Management
  240. 240. • If the adrenalectomy is bilateral, replacement of corticosteroids will be lifelong; • if one adrenal gland is removed, replacement therapy may be temporarily necessary because of suppression by high levels of adrenal hormones. • A normal serum glucose level is maintained with insulin, appropriate IV fluids, and dietary modifications. Medical Management
  241. 241. • frequent assessment of vital signs to detect early signs and symptoms of adrenal insufficiency and crisis or hemorrhage. • Explaining all treatments and procedures, providing comfort measures, and providing rest periods can reduce the patient's stress and anxiety level. Nursing Management
  242. 242. 1. Disease of the adrenal cortex a) Resulting from excess production of hormones • Cushing’s syndrome : excess cortisol production • Primary hyperaldosteronism : excess production of aldosteron • b) Inadequate production ;Addison’s diseases : inadequate production of cortisol and aldosteron Summery of Common Adrenal gland diseases
  243. 243. 2. Disease of the adrenal medulla • Pheochromocytoma: excess production of catecholamine • In general adrenal gland problem are associated with either excess or Inadequate production of catecholamine, and hormones. Summery of Common Adrenal gland diseases
  244. 244. • American Cancer Society. (2014). Cancer facts and figures. Atlanta: Author. • Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 11th edition. • Brunner & Suddarth’s Textbook of Medical-surgical Nursing. 2010, 12th Ed. • Medical-Surgical Nursing: Patient-Centered Collaborative Care, 2013, 7th edition References
  245. 245.  Lewis Direkson ,Heitkemper Bucher,medical surgical nursing assessment,9th edition  Sharon L. Lewis, Shannon Ruff Dirksen, Et Al .Medical-surgical Nursing: Assessment And Management Of Clinical Problems, 2014, Elsevier Inc. Ninth Edition  Wolters Kluwer,Incrideble medical surgical nursing practice,2012 References
  246. 246. • Kumar and klark’s.clinical medicine, 2009, Elsevier Limited. 7th edition. • Porth’s pathophysiology. Concepts of Altered Health States, 2014 ,9th edition. • Patricia Gonce Morton, critical care nursing A holistic approach, 2013, 10th edition. References

Notas del editor

  • The pituitary gland is connected to the hypothalamus by a stalk. It is divided into an anterior adenohypophysis, whose main part is the anterior lobe, and a posterior neurohypophysis, whose main part is the posterior lobe of the pituitary.

  • The posterior pituitary stores and releases hormones that
    are actually produced by the hypothalamus, whereas the anterior
    pituitary produces and secretes its own hormones.
  • Women are more often than men. This may be a result or the tumors’ interference with the menstrual cycle, which sometimes makes symptoms more obvious.

  • Oncocytomas:tumor on oncocytes:epithelial cells xzed by hign mithoconderia
    Silent corticotroph adenomas :adenomas showing positive staining for actc in immunohistochemical.
    null-cell adenoma a pituitary adenoma whose cells give negative results on tests for staining and hormone secretion; although classically they were considered to be composed of sparsely granulated or degranulated (nonfunctioning) cells, some contain functioning cells and may be associated with a hyperpituitary state such as acromegaly or Cushing's syndrome. These tumors are often discovered clinically only when they have grown large and are pressing on surrounding structures. Called also chromophobic adenoma.
  • It is caused by changes in the gene MEN1, and is passed on to about half of the children of an affected parent.
  • Cyclic dependent kinase inhibitor
    GNAS1:Guainin nucleotide binding protein,alpha stimulatingactivity polypeptide 1
  • (the tiny space in the skull that the pituitary gland sits in).
  • (the tiny space in the skull that the pituitary gland sits in).
  • i.e., cells with no affinity for either eosinophilic or basophilic stains).

  • Cells which has acido philic granules:
  • ACTH secreting tumore
  • Basophilic:adenemo whose cell stain pale blue with basic dyes
  • Bromocriptine:inhibit prolactin release,decrese GH in the blood,dopamine agonist
    Stereotactic radiation therapy, which requires use of a neurosurgery-type stereotactic frame, may be used to deliver external-beam radiation therapy precisely to the pituitary tumor with minimal effect on normal tissue
  • Bromocriptine:inhibit prolactin release,decrese GH in the blood,dopamine agonist
    Stereotactic radiation therapy, which requires use of a neurosurgery-type stereotactic frame, may be used to deliver external-beam radiation therapy precisely to the pituitary tumor with minimal effect on normal tissue
  • Visual field loss, also known as “visual field cut,” can be partial or complete. For example, it can range from a nearly complete loss of peripheral vision to a small area of partial loss.
  • 2.72 metere,or 8 fit:11 inch
  • Tour:go around different nationes
  • Cripple___disable
  • Enlargement of the tongue results in
    may occur due to pressure on the optic nerve
    kin tags are very common small, soft skin growths.Skin tags are harmless but can be annoying.Skin tags tend to occur on the eyelids, neck, armpits, groin folds, and under breasts.A person may have anywhere from one to hundreds of skin tags.
  • Because GH mobilizes stored fat for energy, it increases free fatty acid levels
  • The peripheral actions of GH are mediated IGF-1:However, GH is released in a pulsatile fashion, requiring several samples
  • Make sure that patient has been fasting. Emotional
    and physical stress may alter results. Indicate patient
    fasting status and recent activity level on the
    laboratory slip. Send blood sample to laboratory
    immediately.
  • With treatment, bone growth can be stopped and tissue hypertrophy reversed.
    However, sleep apnea and diabetic and
    cardiac complications may persist.
  • Complaints
    of persistent and severe generalized or supraorbital headache may indicate CSF leakage into the sinuses. A CSF leak
    usually resolves within 72 hours when treated with head elevation and bed rest. If the leak persists, daily spinal taps may be
    done to reduce pressure to below-normal levels.
  • syndrome of Inappropriate Anti-Diuretic Hormone
  • Water intoxication, cerebral edema, severe hyponatremia
    cause altered neurological status, which untreated may cause death
  • Cretinism, a result of a disease of the thyroid gland, is the cause of most dwarfism ,
    Hereditary hypothyroidism
    Achondroplasia:the problem is change cartilage to bone
    During early fetal development, much of your skeleton is made up of cartilage. Normally, most cartilage converts to bone. However, if you have achondroplasia, a lot of the cartilage doesn’t convert to bone. This is caused by mutations in the FGFR3 gene.
  • Fgfr3-----fibroblast growth factore receptore 3
  • 20 liter of water may be excreted
  • Insidiuos:growth gradually without notice but dangerious
  • (adh), the pituitary hormone that controls kidney urine flow and concentration, is the most common.
    can result in transitory DI, but in some cases it may be permanent and may also be accompanied by the loss of other pituitary hormones

    Histiocytosis Histiocytosis is a general name for a group of disorders or "syndromes" that involve an abnormal increase in the number of immune cells that are called histiocytes.There are three major classes of histiocytosis:Langerhans cell histiocytosis, which is also called histiocytosis XMalignant histiocytosis syndrome (now known as T-cell lymphoma)Non-Langerhans cell histiocytosis (also known as hemophagocytic syndrome)This article focuses only on Langerhans cell histiocytosis (histiocytosis X).CausesHistiocytosis X has typically been thought of as a cancer-like condition. But more recently, researchers have begun to think it may be an autoimmune disorder. In this type of disorder, a person's immune cells mistakenly attack the body, rather than help the body fight infections. The extra immune cells the body makes may form tumors, which can affect various parts of the body, including the bones, skull, and other areas.
  • Primary polydipsia. This condition — also known as dipsogenic diabetes insipidus or psychogenic polydipsia — can cause excretion of large volumes of dilute urine. Rather than a problem with ADH production or damage, the underlying cause is intake of excessive fluids
  • AQP2:aquaporin 2
  • .vr__vasoperesion
    V1:has pressor effect. Increase blood pressure.vasoconstriction
  • The first phase of the triphasic pattern is a polyuric one that lasts 4-5 days, caused by inhibition of antidiuretic hormone (ADH). An immediate increase in urine volume and a concomitant fall in urinary osmolality occur. The second phase is an antidiuretic one that lasts 5-6 days, resulting from the release of stored hormone; urinary osmolality rises. The third phase can be permanent DI, when stores of ADH are exhausted and the cells that produce ADH are absent or unable to produce more.
  • psychogenic polydipsia :dray mouth due to phrnothiazin, Seizure,cardiac arres….due to hyponatremia
    Kideney fail to deal with fluid overload
  • Dehydration is continued until
    • Orthostatic hypotension and postural tachycardia appear,
    • 5% or more of the initial body weight has been lost, or
    • The urinary concentration does not increase by more than 30 mOsm/L in
    sequentially voided specimens for 3 hrs.
  • Chlorpropamide (an oral hypogycemic agent) may increase endogenous ADH
    Thiazide diuretics: have paradoxical effect on decreasing urine output in patients with DI. They are the preferred drugs for treating nephrogenic DI.

  • Indapamide:Antihypertensive :Diuretic, Thiazide-Related
  • Chlorpropamide:sulfonyl urea….oha
  • Amiloride is a potassium-sparing diureti
  • Chromaffin cells, also pheochromocytes, are neuroendocrine cells found mostly in the medulla of the adrenal glands (located above the kidneys) in mammals.
  • The two major disorders of the adrenal medulla are both tumors: pheochromocytoma ,neuroblastoma, a malignant tumor.
    ,neuroblastoma:ca of immature nerve cells
  • Von Hippel-Lindau tumore suppressor is aprotin coded by VHL gen.so if there is mutation on this gen tumore of multiple organ
  • A paraganglioma is a rare neuroendocrine neoplasm that may develop at various body sites (including the head, neck, thorax and abdomen). About 97% are benign and cured by surgical removal; the remaining 3% are malignant because they are able to produce distant metastases. "Paraganglioma" is now the most-widely accepted term for these lesions, that have been also described as: glomus tumor, chemodectoma, perithelioma, fibroangioma, and sympathetic nevi
  • Tyramine
    • Synthesized by bacteria and intestinal flora.
    • Found in foods like aged cheese, yeast products and salted
    fish.
    Mechanism of action
    • Release stored catecholamines.
    Tyramine:Cause serious drug interaction in patients taking MAO
    inhibitors….because released nor epinephrine is not
    metabolized by MAO……cause hypertensive crisis.
  • Metanephrine is a metabolite of epinephrine created by action of catechol-O-methyl transferase on epinephrine
  • Vanillyl mandelic acid (VMA)
    Measures urinary excretion of catecholamine metabolite. Levels are increased in pheochromocytoma.
  • Epinephrine <20 mcg/day
    Norepinephrine 15-80 mcg/day
  • 1- Clonidine
    Mechanisms
    • Stimulates the presynaptic alpha - 2 receptors leading to decrease of the norepinephrine release from the nerve endings
    → Inhibit motor stimulant.
  • CT, MRI….may also be carried out to localize the pheochromocytoma and to determine whether more than one tumor is present
  • Polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndromeAcute intermittent porphyriaCardiogenic pulmonary edemaRenovascular hypertensionSubarachnoid hemorrhageLead toxicity
  • Treatment with daily administration of corticosteroids for 2 to 4 weeks may suppress function of the adrenal cortex; therefore, adrenal insufficiency should be considered in any patient who has been treated with corticosteroids.

  • ACTH deficiency may be caused by supression of the hypothalamic-pituitary axis because of the
    administration of exogenous corticosteroids.
  • Melanocyte stimulation
  • pmol. (metrology) Symbol for the picomole, an SI unit of amount of substance equal to 10−12 moles.
  • Because of the need for lifelong hormonal replacement to prevent addisonian crises, the
  • The development of edema or weight gain may signify too high a dose of hormone; postural hypotension and weight loss frequently signify too low a dose
  • Mc cune alberight:disorders of bone,skin,endo
  • Susceptibility to bruising: is probably caused by enhanced capillary fragility.
  • Central obesity is caused by the effect of excess cortisol on fat distribution. Fat
    accumulation in the face, neck and trunk, while thelimns remain thin. The “moon face” ,
    “buffalo hump” ( cervical fat pad ) and supraclavicular fat pads contribute to the
    Cushingiod appearance
  • Hypertension : result from the vascular effects of cortisol and sodium retention
  • Diurnal levels correspond with variation of cortisol levels. Levels are higher in morning, lower in evening. ACTH is
    unstable; use prechilled blood tube and place on ice and send to laboratory immediately.
  • Diurnal levels correspond with variation of cortisol levels. Levels are higher in morning, lower in evening. ACTH is
    unstable; use prechilled blood tube and place on ice and send to laboratory immediately.
  • Administer test with continuous infusion method. Monitor site and rate of IV infusion.
    ACTH (cosyntropin) stimulation test
        
    The ACTH stimulation test measures how well the adrenal glands respond to adrenocorticotropic hormone (ACTH). ACTH is a hormone produced in the pituitary gland that stimulates the adrenal glands to release a hormone called cortisol. The man-made form of ACTH is called cosyntropin.

    Ensure sample collection at appropriate times.
  • Observe venipuncture site for bleeding and hematoma formation. Do not test acutely ill patients or those under stress.
    Stress-stimulated ACTH may override suppression. Screen patient for drugs such as estrogen and corticosteroids that may give false-positive results. Ensure accurate timing of medication and sample collection.
  • Some drugs (e.g., reserpine, diuretics, phenothiazines, insulin, amphetamines) may alter results.
  • Hypokalemic alkalosis may decrease the ionized serum calcium level
  • These tests include intravenous or oral
    salt loading, captopril and fludrocortisone suppression
    tes
  • Usually morning blood sample is preferred. Inform
    patient that the required position, supine or sitting/
    standing, must be maintained for 2 hr before the
    specimen is drawn.
  • Hypokalemia resolves for all patients after surgery, but hypertension may persist.
  • Hypokalemia resolves for all patients after surgery, but hypertension may persist.

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