1. The anterior pituitary produces what hormones
    • Growth hormone (GH)
    • Thyrotrotropic hormone (TSH)
    • Adrenocorticotropic Hormone (ACTH)
    • Melanocyte stimulating hormone (MSH)

    • Somatotropin
    • Prolactin
    • Luteotropic hormone
    • Follicle stimulating hormone
    • interstitial cell stimulating hormone
  2. The posterior pituitary produces what hormones
    Antidiuretic Hormone (ADH)-Reabsorption of water in kidneys

    Oxytocin-initiates breast milk and uterine contractions
  3. The tyroid produces
    • Triiodithyronine (T3)-controls body metabolism and influence physical and mental
    • Thyroxine (T4)-growth, nervous system activity, protein,fat, carb metabolism, reproduction
    • Calcitonin-lowers serum calcium levels, inhibits bone reabsorption
  4. The parathyroid produces
    Parathormone (PTH)-regulates calcium and phosphorus metabolism
  5. The Pancreas produces
    • Endocrine function insulin
    • Glucagon
    • Digestive enzymes
  6. The Adrenal Cortex produces
    • Glucocorticoids (cortisone, cortisol)
    • mineral corticoids (aldosterone)
    • sex hormones (androgens)
  7. The Adrenal medulla produces
    Catechaloamines (Epinephrine, norephinephrine)
  8. Growth Hormone (GH)
    • Comes from the Anterior Pituitary
    • Acts directly on bones and other tissues to stimulate growth
  9. Thyrotrotropic hormone (TSH)
    • comes from the Anterior Pituitary
    • stimulates the thyroid gland
  10. Adrenocorticotropic Hormone (ACTH)
    • comes from the Anterior Pituitary
    • stimulates the adrenal cortex
  11. Melanocyte stimulating hormone (MSH)
    • comes from the Anterior Pituitary
    • stimulates darking of the skin
  12. Antidiuretic Hormone (ADH)
    facilitates reabsorption of H2O in the kidneys
  13. Triiodithyronine (T3)
    Control body metabolism and influence physical and mental
  14. Thyroxide (T4)
    growth, nervous system activity, protein, fat, carbohydrate metabolism, reproduction
  15. Calcitonin
    lowers serum calcium levels, inhibits bone reabsorption
  16. Parathormone (PTH)
    regulates calcium and phosphorus metabolism
  17. Insulin
    enables glucose to freely enter cells, helps muscles and tissue oxidation of glucose, promotes stoarge of glycogen
  18. Glucagon
    increases gluconeogenesis in the liver
  19. Glucocorticoids (cortisone and cortisol)
    decreases protein synthesis, regulate serrum glucose by increasing rate of gluconeogenesis, suppress the inflammatory and immune responce, increase fat mobiliaztion, support adaptation during stressful situations
  20. Mineralocorticoids (Aldosterone)
    Facilitate reabsorption of NA+ and elimination of K+
  21. Androgens
    responsible for development of secondary sex characteristics
  22. Effect of Epinephrine and where produced?
    initiates stress response

    Adrenal Medulla
  23. Cause of Norepinephrine and where is it produced?
    causes vasoconstriction

    Adrenal Medulla
  24. Estrogen and where produced?
    Responsible for secondary sex characteristics, mammary duct system growth of graafian follicle in women

  25. Why do hormonal alterations occur?
    • Decrease in the # of receptors
    • imparied receptor function
    • andtibodies against receptors (autoimmune)
    • abnormal receptor number
  26. Hypofunction of endocrine
    • absence or impaired development of gland
    • gland destroyed
    • decline in function
  27. Hyperfunction of endocrine
    • excessive stimulation
    • hyperplasia
    • hormone producing hormone
  28. Primary hormone alteration
    defect in target gland responsible for producing the hormone
  29. secondary hormone alteration
    • target gland normal
    • deficient RH and SH from pituitary system
  30. Tertiary hormone alteration
    results from hypothalamic dysfunction
  31. Alterations of the Hypothalamic-Pituitary System
    interruption of the physical connections between the hypothalamus and the pituitary gland can cause disease
  32. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
    A syndrome characterized by high levels of ADH in the absence of normal physiologic stimuli for its release
  33. The most common causes of SIADH
    Ectopic secretion of ADH by tumor cell
  34. Who is at risk for SIADH
    pituitary surgery, post-op clients, positive pressure ventilation, medications, disease and injury to the CNS
  35. Pathophysiology of SIADH
    water intoxication due to water retention that leads to hyponatremia, hypoosmolarity, urine inappropriately concentrated w/ respect to serum osmolarity
  36. osmolarity
    • concentration of the blood
    • Normal 270-295
  37. Normal sodium levels
  38. Nomal Hematocrit
  39. Normal BUN
  40. Clinical manifestations of SIADH
    • decreased serum osmolality
    • decreased sodium level
    • increased urine osmolality
    • decreased hematocrit
    • decreased BUN
  41. Diabetes Insipidus "Tasteless diabetes"
    • insufficiency of ADH, leading to polyuria and polydipsia
    • hx of head injury, pituitary tmor, craniotomy
  42. Types of Diabetes Insipidus
    • Neurogenic (central)
    • Nephrogenic
  43. Neurogenic Diabetes Insipidus
    • insufficient ADH
    • may follow head injury or surgery near the lesion area
  44. Nephrogenic Diabetes Insipidus
    • End organ failure
    • insensitivity of the renal tubule to ADH
    • drugs and disorders damage the renal tubule
  45. Pathophysiology of Diabetes Insipidus
    • Partial or total inabilty to concentrate urine. Insufficient ADH secretion causes secretion of large volumes of dilute urine, leading to an increase in plasma osmolatity
    • urine out put 3 to >12 L/day
    • Specific Gravity 1.00-1.005
    • Dehydration can develop rapidly
  46. Specific Gravity
    • measure of concentration of urine
    • Normal 1.010 - 1.020
  47. Nursing Care for Diabetes Insipidus
    • Monitor fluids
    • Replace Fluids
    • Check neuro states
    • Check vital signs
    • check muccous membranes
  48. Clinical Manifestations of Diabetes Insipidus
    • Polyuria, nocturia, thirst, polydipsia
    • increase plasma osmolality
    • decrease urine spenific gravity
    • decreased urine osmolality
    • hypovolemia, tachycardia, decreased b/p
  49. Microadenoma
    pituitary tumors < 10 mm
  50. Macroadenoma
    pituitary tumors >10 mm
  51. Acromegaly
    occurs in adults who are exposed to continuously excessive levels of GH

    • slow progression, increased amounts of GH can't stimulate further lone bone growth, the result is connective tissue and bony proliferation
    • Diabetes mellitus may occur when the pancreas is unable to secrete enough insulin to offset the effects of GH
  52. The most common cause of Acromegaly
    GH secreting pituitary adenoma
  53. Clinical manifestations of Acromegaly
    enlaged tongue, interstitial edema, large sebaceous and sweat glands, coarse hair, enlarged bones of face, hands, feet, soft tissue overgrowth, HTN, heart failure
  54. Gigantism
    occurs in childern and adolescents, excessive secretion of GH by adenomas. Epiphyses not fused, excessive skeletal growth occures
  55. Dwarfism
    low GH in children can lead to
  56. Hyperthyroidism (Thyrotoxicosis)
    condition that results from increased levels of thyroid hormone. could be due to graves disease, adenomas, carcinomas, pituitary issue
  57. Most common cause of hyperthyroidism
    Graves disease
  58. Clinical Manifestations of Hyperthyroidism (Thyrotoxicosis)
    • result of increased circulating thyroid hormones
    • increased T3, T4, decreased TSH
    • clubing fingers, Tremors, increaed diarrhea, Menstrual changes (amenorrhea), intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, increase systolic BP, breast enlargement, weight loss, muscle wasting, nervousness, increased appetite
  59. Graves Disease
    • more common in women, Familial tendency, autoimmune disease
    • Thyroid autoantibodies are found in more than 95% of clients
  60. The hyperfunction of the thyroid gland leads to
    suppression of TSH and TRH, increased iodine uptake, increaed thyroid gland metabolism, lead to enlargment of the gland
  61. Goiter
    • enlarged thyroid gland
    • can be seen ini both hypo and hyperthyroidism
  62. Myxedema
    subcutaneous swelling legs and hands
  63. Ocular Manifestations of Grave's Disease
    Exophthalmos (Bulging eyes), Edema of the orbital contents, protrusion of the globe can occur which can lead to visual disturbances, irritation, pain
  64. Thyroid Storm
    • excerbation of hyperthyoidism
    • worsened thyrotoxic state that can be fatal if not treated
    • death can occur w/i 48hrs
    • most frequently occurs in undiagnosed, partially treated and stressed individuals
  65. Whos at risk for Thyroid Storm?
    infections, cardiopulmonary disorders, emotional distress, poor preparation for thyroid surgery
  66. Systoms of Thyroid storm
    Hyperthermia, tachycardia, high-output heart failure, agitation, NVD
  67. Hypothyroidism
    most common throid disorder due to deficient productoin of thyroid hormone by the throid gland
  68. Primary Hypothyrodism
    • loss of functional throid tissue
    • leads to decreased production of TH
    • that leads to increased production od TSH
    • that may lead to goiter
  69. Secondary Hypothyrodism
    • due to problem w/ pituitary gland and insufficient TSH
    • pituitary tumors
    • Decreased TSH, decreased TH
  70. Subacute thyroiditis
    nonbacterial inflammation preceded by a virus
  71. Autoimmune Thyroiditis
    • destruction of thyroid tissue
    • ex-Hashimoto disease
  72. Clinical Manifestations of Hypothyroidism
    hair loss, apathy, lethargy, dry skin (coarse & Scaly), muscle aches and weakness, constipation, intolerance to cold, receding hairline, facial & eyelid edema, Dull-blank expression, extreme fatigue, thick tongue, slow speech, anorexia, brittle nails and hair, menstrual disturbances

    late: subnormal temp, bradycardia, weight gain, decresed LOC, thickened skin, cardiac complications
  73. Myxedema in Hypothroidism result from
    • alteration in the composition of the dermis and other tissues
    • protein-mucopolysaccharide complex binds w/ water
  74. Myxedema Coma
    • excerbation of Hypothroidism
    • decreased LOC, hypothermia, hypoventilation, hypoglycemia,
  75. Congenital Hypothyroidism
    occurs in infants as a result of absent thyroid tissue and hereditary defects in thyroid hormone synthesis
  76. Cretinism
    due to untreated congenital hypothyroidism
  77. Thyroid Carcinoma
    • most common cause is exposure to ionizing radiation during childhood. Small thyroid nodule or metastatic tumor in lungs, brain, bone
    • s/s due to pressure on surrounding tissue
  78. Cushing Syndrome
    • manifestation of hypercortisolism from any cause
    • Cushing disease
    • Benign or Malignant adrenal tumor
    • Ectopic Cushing
    • Iatrogenic Cushing
  79. Cushing diseases is due to
    excessive anterior pituitary secretion of ACTH. Most individuals have a pituitary microadenoma which secretes ACTH
  80. Ectopic Cushing's
    non-pituitary ACTH secreting tumor small cell carcinoma of the lung
  81. Iatrogenic Cushing's
    longterm use of pharmacologic glucocorticoids
  82. Clinical Manifestations of Cushing's Syndrome
    personality changes, moon face, increase susceptibility to infection, gynecomastia, fat deposits on back, osteoporosis, hyperglycemia, CNS irritability, NA and Fluid retension, Thin extremities, GI distress (Increase acid), amenorrhea, hirsutism, thin skin, purple striae, bruises and petechiae
  83. Hirsutism
    excess facial hair
  84. In Cushing's Syndrome weight gain due to
    • adipose accumulation in trunk, face, cervical areas, sodium and water retention,
    • "Moon face, truncal obesity, buffalo hump"
  85. In Cushing's Syndrome glucose intolerance due to
    insulin resistance and increased gluconeogenesis
  86. In Cushing's Syndrome protein wasting due to
    catabolism effects of cortisone on peripheral tissues, collagen loss leads to thin skin, easy bruising, capillaries more visible
  87. In Cushing's Syndrome hyperpigmentation due to
    high levels of ACTH, stimulates increased MSH
  88. In Cushing's Syndrome elevated blood pressure due to
    NA+ retention
  89. In Cushing's Syndrome susceptible to infection due to
    suppression of immune system
  90. In Cushing's Syndrome irritability and depression due to
    cortisol effect
  91. In Cushing's Syndrome hair growth, acne, oligomenorrhea in females due to
    increased androgen levels
  92. In Cushing's Syndrome high risk for gastric ulcers due to
    increased gastric acid secretions
  93. In Cushing's Syndrome high risk for osteoporosis due to
    destruction of bone proteins and aalteration in Ca+ metabolism
  94. An example of Primary Adrenal Cortical Insufficiency
    Addison disease
  95. Addison Disease
    • autoimmune destruction of the adrenal glands is the most common cause
    • 90% of tissue destroyed before symptoms
    • characterized by elevated serum ACTH levels with inadequate corticosteroid synthesis and output
    • add hormones
  96. Clincal Manifestations of Addison Disease
    bronze skin pigmentation of skin, change in distrubution of body hair, GI disturbances, weakness, hypoglycemia, postural hypotension, weight loss
  97. Clinical Manifestations of Adrenal Crisis
    • profound fatigue
    • dehydration
    • vascular collapse
    • renal shut down
    • decreased serum NA
    • increased K
  98. Clincal Manifestations of Mineralcorticoid effect in Addison Disease
    • urinary loss of NA(Hyponatremia, loss of ECF), Cl, H2O
    • decreased excretion of K+ (hyperkalemaia)
  99. Clincal Manifestations of Glucocorticoid effects in Addison Disease
    • Hypoglycemia
    • Lethargy
    • Weakness
    • GI Symptoms
    • Weight loss
  100. Secondary Adrenal Cortical Insufficiency
    low ACTH levels cause inadequate adrenal stimulation, adrenal atrophy, and corticosteroidogenesis

    due to Exogenous steroids use (cannt be abruptly stoped due to "shutting off" of adrenal gland
  101. Acute Adrenal Crisis
    • precipitated by illness, stress, abrupt discontinuing of steroids

    can cause N/V, muscular weakness, hypotension, dehydration, vascular collapse

    care focused on dehydration
  102. 5 S's of Acute Adrenal Crisis
    • S=salt (replace)
    • S=sugar (replace)
    • S=Steroids (replace)
    • S= support
    • S= search for cause
  103. Hypersecretions of Adrenal Androgens and Estrogens are due to
    adrenal tumors, cushing syndroms, defects in steroid synthesis
  104. Feminization
    • hypersection of estrogen (excess)
    • development of female charcteristics
  105. Virilization
    • hypersecretion of androgens (excess)
    • development of male charcteristics
  106. Pheochromocytoma
    • A catecholamine producing tumor derived from the chromaffin cells of the adrenal medulla that contain sympathetic nevre cells
    • most common 40-60 yrs, men and women affected equaly
  107. CLinical Manifestations of Pheochromocytoma
    hypertension, headaches, diaphoresis, tachycardia, palpitations, hypermetabolism, glucose intolerance, warmth, heat intolerance
  108. Pheochromocytoma cause an excess productin of...
  109. Hyperparathyroidism
    increased PTH levels results in increase serum Ca levels
  110. Primary Hyperparathyroidism
    greater than normal secreations of PTH by one or more of the parathyroid glands, cause unknown, maybe due to adenoma, carcinoma, inheritance
  111. Secondary Hyperparathyroidism
    caused by increased PTH secondary to a chronic disease state. the most common cause is renal failure. Vitamin D metabolism is impaired in renal failure results hypocalcemia. The chronic renal failure induced hypocalcemia serves as a stimulus for increased PTH secretions
  112. Hypoparathyroidism
    • abnormally lof PTH levels
    • most common cause by damage to parathyroid glands during surgery ,
    • a lack of PTH causes a depressed serum calcium level and an increased serum phosphate level due to increased renal reabsoprtion of phosphate
  113. Clinical Manifestations of hypocalcemia
    • muscle spasm (Chvostek's)
    • hyperflexion (Trousseau's)
    • Dry Skin
    • Hair loss
    • done deformities
  114. To Diagnosis Diabetes Mallitus
    • 1. more than one fasting plasma glucose level >or = 126 mg/dl
    • 2. plasma glucose value in the 2 hr sample of OGTT > 200 mg/dl
    • 3. Casual plasma glucose level > or = 200mg/dl with symptoms
    • 4. HgbA1C= normal <7%
  115. HgbA1C
    shows overal status of a person BS for the past few months
  116. Classifications of Diabetes Mellitus
    • Type 1
    • Type 1.5
    • type 2
    • Gestational
  117. 1A Immune Mediated Diabetes Mellitus
    • environmental-genetic factors result in Bcell destruction
    • autoantibbodies detected of pancreas and B cells
    • 95%
    • peakage 11-13 years
  118. 1B Idiopathic Diabetes Mellitus
    • cause unknown
    • no evidence of autoimmunity
  119. Clincal Manistations of Type 1
    Polyuria, polydipsia, polyphagia, weight loss, fatigue, increase frequency of infection, rapid onset, insulin dependent, familial tendency, peak incidence from 10-15 years
  120. In Type 1 Diabetes Mellitus hyperglycemia due to
    lack of insulin
  121. In Type 1 Diabetes Mellitus polydipsia is due
    to elevated glucose levels pull water from cells which results in intracellular dehydration
  122. In Type 1 Diabetes Mellitus polyuria is due to
    the effects of hyperglycemia as an osmotic diuretic renal threshold for glucose excreded
  123. In Type 1 Diabetes Mellitus Polyphagia is due to
    depletion of cellular stores of CHO, fats, proteins, resulting in cellular starvation
  124. In Type 1 Diabetes Mellitus weight loss is due to
    fluid loss w/ osmotic diuresis, loss of body tissue
  125. In Type 1 Diabetes Mellitus fatigue is due to
    metabolic changes
  126. Pathophysiology of Type 2 Diabetes
    • 1. Peripheral insulin resistance
    • 2. Deranged secrections of insulin by pancreatic cells
    • 3. increased glucose production by the liver
  127. The biggest risk factor for type 2 diabetes
    obesity, diabesity, visceral fat
  128. Syndrome X (Metabolic Syndrome, Insulin Resistance syndrome)
    • 1. hyperglycemia
    • 2. hypertension
    • 3. hyperlipidemia
    • High triglycerides (>150
    • 4. Abdominal obsesity
  129. Normal FSBS
  130. Normal Triglycerieds
    • women <50
    • men<40
  131. Total Cholesterol
  132. Abdomainal girth
    • women <35
    • men <40
  133. Clinical Manifestations of Type 2 Diabetes
    genital pruritus, visual changes, parethesias, fatigue
  134. Impaired fasting Glucose (Borderline/Previsional Diabetics)
    Fasting glucose >100 and <126 mg/dl
  135. Impaired Glucose Tolerance (IGT)
    2 hour postload glucose level greater than or equal to 140 but less that 200 mg/dl
  136. Gestational Diabetes mellitus (GND)
    glucose intolerance first recognized during pregnacy, most likely in the third trimester. Following pregnancy glucose may normalize remaini impaired or progress to Diabetes Mellitus.
  137. Hypoglycemia
    • lowered plasma glucose 45-60 mg/dl
    • occcurs more frequently in individuals treated w/ insulin
  138. Symptoms of hypoglycemia
    tachycardia, diaphoresis, pallor, tremors, dizziness, headahcem visual changes

    • Adrengic-pallor, sweating, tachycardia, sweating, palpitations, hunger, restlesness, anxiety, tremors, clammy skin
    • Neurogenic- Fatigue, irritabilty, headache, visual changes, dizziness, convulsions
  139. Diabetic Ketoacidosis
    • most commonly occurs in Type 1 diabetics
    • develops when ther is an absolute or relative deficiency of insulini and an increase in insulin counterregulatory hormones. Hepatic glucose production increases. peripheral glucose usage decreases, fat mobiliaztion increase and ketogenesis is simulated
  140. Counterregulatory Hormones
    catecholamines, cortisol, glucagon, growth hormone

    are realses during a stress responce
  141. Precipitating Factors of DKA
    type 1, illness, infection, trama, surgery, mi, stress evernt
  142. Metabolic Components of DKA
    • Hyperglycemia (BG 300-750)
    • Ketosis (Ketones come from fat metabolism)
    • Metabolc Acidosis (ketones acid) ,low bicarb <15, low pH <7.3
  143. Clinical Manifestations of DKA
    polyuria, polydipsia, N/V, Fatigue, hypotension, tachycardia, stupor leads to coma, abdominal pain, fruity breath, kussmauls respirations
  144. Kussmauls Respirations
    • Hyperventilation
    • rapid , deep
  145. why is a person woth DKA at risk for dehydration?
    fluid loss from osmotic diuresis due to hyperglycemia
  146. What metabolic changes are seen in DKA
    K+ normal or elevated (Met Acid= high K+), shift of H20 and K+ from EC due to hyperosmolarity of ECF due to hyperglycemia, NA normal or decreased
  147. Hyperglycemia Hyperosmolar Nonacidotic diabetes (HHNKS)
    • more commonly seen w/ type 2 diabetes, levels of free fatty acid are in HHNKS are consistently lower than in DKA and is charcterized by a lack of ketosis
    • insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly
  148. factors contributing to development of HHNKS
    • Glucose levels>600-2000 mg/dl
    • Hyperosmolarity >350 mOsm/l
  149. HHNKS presentation
    • 1.Major stress event
    • 2. increased cortisol, glucagon, catecholamines
    • 3. hyperglycemia
    • 4. inadequate insulin secretion
    • 5. Hyperglycemia
    • 6. Osmotic Diuresis, Electrolye imblance
    • 7.Extreme dehydration and intracellular dehydration
    • 8. Nonketotic COMA, Death
  150. Clinical Manifestations of HHNKS
    • dehyration
    • neurological signs-changes in LOC, seizures, visual loss, may mimic strock
    • excessive thirst
    • electrolye loss
    • Potassium phosohorus sodium relacement needed, also rapid fluid replacement
  151. Peripheral Neuropathies
    • thickened vessel walls
    • caused by ischemia, segmental demyelinization
  152. Somatic Neuropathies
    • affects nerves that control sensations and muscle in the body
    • loss feeling, touch, sensation
    • burning pain
  153. Autonomic Neuropathies
    affects involuntary nerves controlling many body systems i.e bladder, GI sytem
  154. Diabetic Retionpathy
    retinal ischemia resulting from blood vessel changes and red blood cell aggregation
  155. Diabetic Nephropathy
    the glomeruli are injured by protein denaturation by high glucose levels and adverse effects of intraglomerular hypertension. Glomerular enlargement and glomerular basement membrane thickening result in diffuse intercapittary glomerulonecrosis. Proeinuria is a consistent sign of renal damage
  156. Macrovasular Disease
    • arise from development of atherosclerosis
    • damage to endothelial later of arteries

    coronary artery disease, Cerebrovascular diease, Peripheral vascular disease(see discolorarion, necrosis)
  157. Diabetic Foot Ulcer
    • common problem
    • due to sensory impairment and motor weakess
  158. Why is diabetic at high risk for infection
    • impaired vision
    • impaired touch
    • pathogens multiply
    • decreased blood supply
    • WBC function impairment
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