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Endocrine Disorders

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  • Sir Hindi ko po madownload... im reli interested to your topic and i learned a lot from your review lecture... Endocrinology is reli hard for me to understand but you simplified explainations and helped me understand. Kindly email this topic to me pls...pls... pls... jonaks1982@yahoo.com thanks a lot and more power to you SIR!!!!
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  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Factitious- artificial; self-induced; not naturally occurring.
  • Cachexia: a general weight loss and wasting occurring in the course of a chronic disease or emotional disturbance.
  • Transcript

    • 1. MAJOR DISORDERS OF THE ENDOCRINE SYSTEM Nio C. Noveno, RN, MAN
    • 2.  
    • 3. HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM
      • If the client is healthy,
      • the concentration of hormones
      • is maintained at a constant level.
      • When the hormone concentration rises,
      • further production of that hormone is inhibited.
      • When the hormone concentration falls,
      • the rate of production of that hormone increases.
    • 4. HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM
    • 5. DISORDERS OF THE ENDOCRINE SYSTEM
      • Primary
      • Problem in the target gland; autonomous
      • Secondary
      • Problem in the pituitary
      • Tertiary
      • Problem in the hypothalamus
    • 6. ANTERIOR PITUITARY DISORDERS
    • 7.  
    • 8.  
    • 9. HYPERPITUITARISM
      • May be due to overactivity of gland
      • or the result of an adenoma
      • Characterized by:
      • Excessive serum concentration
      • of pituitary hormones (GH, ACTH, PRL)
      • Morphologic and functional changes
      • in the anterior pituitary
    • 10. GROWTH HORMONE HYPERSECRETION
      • Gigantism
      • Prior to closure
      • of the epiphyses;
      • proportional growth
      • Acromegaly
      • After closure
      • of the epiphyses;
      • disproportional
      • growth
    • 11. HYPERPITUITARISM: CLINICAL MANIFESTATIONS
      • A rthritis
      C hest: barrel-shaped R ough facial features O dd sensations: hands and feet M uscle weakness & fatigue E nlargement of organs G rowth of coarse hair A menorrhea; breast milk production L oss of vision; headaches I mpotence; increased perspiration S noring
    • 12. HYPERPITUITARISM: CLINICAL MANIFESTATIONS
    • 13. HYPERPITUITARISM: MANAGEMENT
      • Medication
      • Bromocriptine-
      • Cabergoline
      • (dopamine agonists)
      • GH hypersecretion
      • and prolactinoma
      • Ocreotide
      • (somatostatin)
      • GH hypersecretion
      • Radiation
      • Indicated for larger
      • tumors
      • Surgery
      • Trans-sphenoidal
      • hypophysectomy
    • 14. TRANS-SPHENOIDAL HYPOPHYSECTOMY
      • Post-surgery nursing care
      • Semi- to high- Fowler’s position
      • Protect from infection and stressful situations
      • Hormone replacement
      • Constant neurologic checks
      • MIOW to check for DI
      • WOF CSF leak
      • Encourage deep-breathing, but not coughing
      • Institute measures to prevent constipation
        • [straining increases ICP]
    • 15. HYPOPITUITARISM
      • Deficiency of one or more
      • anterior pituitary hormones
      • Causes
      • Infections / Inflammatory disorders
      • Autoimmune diseases
      • Congenital absence
      • Tumor
      • Surgery / Radiation therapy
    • 16. HYPOPITUITARISM
      • Simmonds' disease
      • [Panhypopituitarism]
      • Complete absence
      • of pituitary hormones
      • Cachexia:
      • most prominent feature
      • Follows destruction
      • of the pituitary
      • by surgery, infection,
      • injury, or a tumor
      Sheehan’s syndrome [Post-partum pituitary necrosis] A complication of delivery Results from severe blood loss and hypovolemia  Pituitary ischemia
    • 17. HYPOPITUITARISM: CLINICAL MANIFESTATIONS
      • Hypo -thermia, -glycemia, -tension
      Loss of vision, strength, libido, & secondary sexual characteristics
    • 18. HYPOPITUITARISM: MANAGEMENT
      • Medication
      • Hormonal substitution
      • [maybe for life]
      • Corticosteroids
      • Levothyroxine
      • Androgen / Estrogen
      • Growth hormone
      • Radiation
      • Indicated for larger
      • tumors
      • Surgery
      • Trans-sphenoidal
      • hypophysectomy
    • 19. POSTERIOR PITUITARY DISORDERS
    • 20.  
    • 21.  
    • 22. DIABETES INSIPIDUS
      • Characterized by massive polyuria
      • due to either lack of ADH or renal insensitivity
      • Central DI
      • Due to a deficiency in ADH production
      • Nephrogenic DI
      • Due to a defect in the kidney tubules
      • that interferes with water absorption
      • Polyuria is unresponsive to ADH,
      • which is secreted normally.
    • 23. DIABETES INSIPIDUS: DIAGNOSTICS
      • Fluid deprivation test
      • Administration of desmopressin
      • 24-hour urine collection
        • for volume, glucose, and creatinine
      • Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium
    • 24. DIABETES INSIPIDUS: MANAGEMENT
      • Central DI :
      • Desmopressin, Lypressin [intranasal]
      • Vasopressin tannate in oil [IM]
      • Nephrogenic DI :
      • Indomethacin-
      • -hydrochlorothiazide
      • -desmopressin
      • -amiloride
      • Clofibrate, chlorpropamide
    • 25. SYNDROME OF INAPPROPRIATE ADH
      • Disorder due to excessive ADH release
      • Clinical Manifestations
      • Persistent excretion of concentrated urine
      • Signs of fluid overload
      • Hyponatremia
      • LOC changes
      • No edema
    • 26. SIADH: DIAGNOSTICS
      • Low serum sodium [<135 mEq/L]
      • Low serum osmolality
      • High urine osmolality [>100 mOsmol/kg]
      • High urine sodium excretion [>20 mmol/L]
      • Normal renal function: low BUN [<10 mg/dL]
    • 27. SIADH: MANAGEMENT
      • Maintain fluid balance
      • MIOW
      • Fluid restriction
      • Loop diuretic
      • [If with evidence of fluid overload]
      • Lithium or demeclocycline
      • [Chronic treatment]
      • Maintain Na balance
      • Increased Na intake
      • Emergency treatment of 3% NaCl, followed by furosemide
      • [If serum Na <120, or if patient is seizing]
      • Excessively rapid correction of hyponatremia may cause central pontine myelinolysis!
    • 28. THYROID DISORDERS
    • 29.  
    • 30.  
    • 31. THYROID FUNCTION TESTS
      • Serum TSH
      • Single best screening test [high sensitivity]
      • 0.38 – 6.15 mcU/mL
      • If TSH is normal, fT 4 should be normal.
      • Screening required beginning 35 years,
      • then q 5 years thereafter
      • Also used for monitoring thyroid hormone
      • replacement therapy
    • 32. THYROID FUNCTION TESTS
      • Serum fT 4
      • A direct measurement of free thyroxine,
      • the only metabolic fraction of T 4
      • 0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)
      • Used to confirm an abnormal TSH
    • 33. THYROID FUNCTION TESTS
      • Total serum T 3 and T 4
      • T 3 70 to 220 ng/dL (1.15 to 3.10 nmol/L)
      • T 4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L)
      • T 3 levels appear to be a more accurate
      • indicator of hyperthyroidism.
    • 34. THYROID FUNCTION TESTS
      • T 3 resin uptake test
      • Indirect measurement of unsaturated
      • thyroid-binding globulin (TBG)
      • 25 – 35% uptake
      • Thyroid antibodies
      • 5 – 10% of the population
      • Grave’s: 80%
      • Hashimoto’s: 100%
    • 35. THYROID FUNCTION TESTS
      • Thyroid scan / Radioscan / Scintiscan
      • Utilizes a gamma camera and radioisotopes
      • 123 I, thallium, americium,
      • technetium-99m [ 99m Tc] pertechnetate
      • Results
      • Hot areas: increased activity
      • Cold areas: decreased activity
    • 36. THYROID FUNCTION TESTS
      • Radioactive iodine uptake (RAIU)
      • Measures the proportion of administered tracer
      • dose of ¹²³I present in the thyroid gland
      • at a specific time after administration
      • Results
      • Hyper: high uptake
      • Hypo: low uptake
    • 37. THYROID FUNCTION TESTS
      • Fine-needle aspiration biopsy
      • Sampling of thyroid tissue to detect malignancy
      • Initial test for evaluation of thyroid masses
      • Results
      • Negative [benign]
      • Positive [malignant]
      • Indeterminate [suspicious]
      • Inadequate [non-diagnostic]
    • 38. THYROID FUNCTION TESTS
      • Nursing Implications
      • Determine whether the patient has taken medications or agents that contain iodine [antiseptics, multivitamins, cough syrup, amiodarone] because these may alter the test results.
      • Assess for allergy to iodine or shellfish.
      • For scans, tell patient that radiation is only minimal.
    • 39. HYPERTHYROIDISM
      • Increased basal metabolic rate (BMR)
      • Causes
      • Grave’s disease (autoimmune)
      • Initial manifestation of thyroiditis
      • TSH-screening pituitary tumor
      • Toxic adenoma
      • Factitious thyrotoxicosis
      • Amiodarone therapy
    • 40. HYPERTHYROIDISM: CLINICAL MANIFESTATIONS
      • G I hypermotility
      R apid weight loss A pprehension V olume deficit; voracious appetite E xophthalmos; erratic menses S ystolic BP elevated; sweating [tremors, tachycardia, palpitations]  in secondary disease  in primary disease TSH
    • 41. HYPERTHYROIDISM: CLINICAL MANIFESTATIONS
    • 42. THYROID STORM / THYROTOXIC CRISIS
      • Marked delirium
      • Severe tachycardia
      • Vomiting
      • Diarrhea
      • Dehydration
      • High fever
      Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery, RAI Increased systemic adrenergic activity: Severe hypermetabolism
    • 43. HYPERTHYROIDISM: MANAGEMENT
      • Anti-thyroid drugs
      • Propylthiouracil (PTU); methimazole
      • Blocks thyroid hormone (TH) synthesis
      • Used for pregnant women and patients
      • who have refused surgery or RAI treatment
      • During pregnancy, PTU is DOC.
      • 1% of infants born to mothers on anti-
      • thyroid therapy will be hypothyroid.
      • WOF agranulocytosis.
    • 44. HYPERTHYROIDISM: MANAGEMENT
      • RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s)
      • Adjunct to other anti-thyroid drugs
      • in preparation for thyroidectomy
      • Treatment for thyrotoxic crisis
      • Inhibit release and synthesis of TH
      • Decrease vascularity of the thyroid gland
      • Decrease thyroidal uptake of RAI
    • 45. HYPERTHYROIDISM: MANAGEMENT
      • Medications to relieve the symptoms
      • related to the increased metabolic rate:
      • Digitalis, propranolol (Inderal), phenobarbital
      • Well-balanced, high-calorie diet
      • with vitamin and mineral supplements
      • Subtotal or total thyroidectomy
    • 46. RAI THERAPY : NURSING IMPLICATIONS
      • NPO post-midnight prior to administration
      • [Food may delay absorption]
      • After initial dose:
      • Urine and saliva slightly radioactive x 24H
      • Vomitus highly radioactive x 6-8H
      • Institute full radiation precautions.
      • Instruct the patient to use appropriate disposal methods when coughing and expectorating.
    • 47. K OR NA IODIDE, SSKI (LUGOL’S) : NURSING IMPLICATIONS
      • Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste.
      • Give iodides through a straw to avoid teeth discoloration.
      • Force fluids to prevent fluid volume deficit.
      • Warn patient that sudden withdrawal may precipitate a thyrotoxic crisis.
      • Store in a light-resistant container.
    • 48. HYPOTHYROIDISM
      • A state of low serum TH levels
      • or cellular resistance to TH
      A utoimmune D evelopmental D ietary I odine deficiency O ncologic D rugs I atrogenic N on-thyroidal E ndocrine
    • 49. HYPOTHYROIDISM
      • Causes
      • Chronic autoimmune [Hashimoto’s] thyroiditis
      • Hypothalamic failure to produce TRH
      • Pituitary failure to produce TSH
      • Inborn errors of TH synthesis
      • Thyroidectomy / Radiation therapy
      • Anti-thyroid therapy
      • Iodine deficiency
    • 50. HYPOTHYROIDISM
      • Classified according to the time of life in which it occurs
      • Cretinism
      • In infants and young children
      • Lymphocytic thyroiditis
      • Appears after 6 years of age
      • and peaks during adolescence; self-limiting
      • Hypothyroidism without myxedema
      • Mild thyroid failure in older children and adults
      • Hypothyroidism with myxedema
      • Severe thyroid failure in older individuals
    • 51. HYPOTHYROIDISM: CLINICAL MANIFESTATIONS
      • D ry, brittle hair; dry, coarse skin
      E dema (periorbital) R educed BMR [bradycardia, bradypnea] A pathy; anorexia; anemia I ncreased weight; intolerance to cold L ethargy; loss of libido E nlarged tongue D rooling  in secondary disease  in primary disease TSH
    • 52. MYXEDEMA COMA
      • Hypotension
      • Bradycardia
      • Hypothermia
      • Hyponatremia
      • Hypoglycemia
      • Respiratory failure
      • Coma
      Precipitating Factors Acute illness Rapid withdrawal of thyroid medication Anesthesia / Surgery Hypothermia Opioid use
    • 53. HYPOTHYROIDISM: MANAGEMENT
      • Prevention
      • Prophylactic iodine supplements to decrease
      • the incidence of iodine-deficient goiter
      • Symptomatic cases
      • Hormonal replacement
      • Levothyroxine (Synthroid)
      • Liothyronine (Cytomel)
      • Liotrix (Thyrolar)
      • Dosage increased q 2-3 weeks
      • especially in elderly patients
    • 54. HYPOTHYROIDISM: MANAGEMENT
      • Tell patient to WOF:
      • Chest pain, palpitations, sweating,
      • nervousness, and other S/S of overdosage
      • Instruct the patient to take TH at the same time
      • each day to maintain constant hormone levels.
      • Suggest a morning dosage to prevent insomnia.
      • Monitor apical pulse and BP.
      • If pulse >100 bpm, withhold drug.
    • 55. HYPOTHYROIDISM: NURSING INTERVENTIONS
      • Diet : high-bulk, low-calorie
      • Encourage activity
      • Maintain warm environment
      • Administer cathartics
      • and stool softeners
      • To prevent
      • myxedema coma ,
      • tell patient to continue
      • course of thyroid
      • medication even if
      • symptoms subside.
      Maintain patent airway Administer medications: Synthroid, glucose, corticosteroids IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness
    • 56. PARATHYROID DISORDERS
    • 57.  
    • 58.  
    • 59. HYPERPARATHYROIDISM
      • Primary
      • Single adenoma
      • Genetic disorders
      • Multiple endocrine neoplasias
      • Secondary
      • Rickets
      • Vitamin D deficiency
      • Chronic renal failure
      • Phenytoin or laxative abuse
    • 60. HYPERPARATHYROIDISM: CLINICAL MANIFESTATIONS
      • C onstipation
      A pathy L ordosis C ardiac dysrhythmias U pset GIT L ow energylevels I ncreased BP  PO 4  PTH Calcium Alkaline phospatase
    • 61. HYPERPARATHYROIDISM: MANAGEMENT
      • Surgery to remove adenoma
      • Force fluids; limit dietary calcium intake
      • For life-threatening hypercalcemia:
      • Furosemide
      • Bisphosphonates
      • [Etidroanate (Didrodinel), pamidronate]
      • Calcitonin (Cibacalcin, Miacalcin)
      • Plicamycin (Mithracin) + glucocorticoid
      • Mithramycin
    • 62. HYPOPARATHYROIDISM
      • Causes
      • Congenital absence
      • or malfunction of the parathyroids
      • Autoimmune destruction
      • Removal or injury to one or more
      • parathyroids during neck surgery
      • Massive thyroid radiation therapy
      • Ischemic parathyroid infarction during surgery
    • 63. HYPOPARATHYROIDISM: CLINICAL MANIFESTATIONS
      • D yspnea; dysrhythmias
      E xtremities: tingling F otophobia I ncreased bone density C hvostek sign; cramps I rritability T rousseau sign; tetany  PO 4  PTH Calcium Alkaline phospatase
    • 64. HYPERTHYROIDISM: MANAGEMENT
      • IV Ca chloride or gluconate [emergency treatment]
      • DOC post-thyroidectomy
      • Oral Ca salts (Ca carbonate or gluconate)
      • Vitamin D supplementation
      • Increase intestinal Ca absorption
      • Dihydrotachysterol, ergocalciferol
    • 65. T rousseau’s & Chvostek’s E levated serum PO 4 ; low Ca 2+ T ingling A lkalosis; Arrhythmias N arrowing of airway I rritability C ramps
    • 66. HYPOPARATHYROIDISM
      • Parathormone injections [in acute attacks]
      • WOF allergies
      • Diet: High-calcium [spinach], low-phosphate [milk, cheese, egg yolks]
      • Al(OH) 2 , Gelusil, Amphogel p.c.
      • Pentobarbital (Nembutal)
      • [calm environment]
    • 67. T C AKE ARE ETANY RACHEOSTOMY ALCIUM GLUCONATE ALCIUM 8.6 – 10.6 mg / dL
    • 68. PHEOCHROMOCYTOMA
    • 69. ADRENAL GLANDS
    • 70. ADRENAL MEDULLA
      • Release cathecholamines
        • Epinephrine
        • Norephinephrine
      • Released during “fight or flight” situations (sympathetic effect)
    • 71. PHEOCHROMOCYTOMA
      • Adrenal tumor
      • Increased Epi and NEpi
      • Heredity
    • 72. PHEOCHROMOCYTOMA
      • H eadache
      • A nxiety
      • N ausea
      • E ye disturbances
      • S evere hypertension
    • 73. PHEOCHROMOCYTOMA BP HR Diaphoresis BMR VMA Glucose
    • 74. PHEOCHROMOCYTOMA
      • Adrenalectomy
      • Steroid treatment
      • Antihypertensive and antidysrhythmic
      • nitroprusside (Nipride)
      • propranolol (Inderal)
      • phentolamine (Regitine)
    • 75. PHEOCHROMOCYTOMA
      • MBP / MIO
      • Fluid replacements
      • Decrease environmental stimulation
      • Maintenance doses of steroids
      • Follow-up check up
      • 24-hour urine specimens
      • [VMA and catecholamine studies]
      • Avoid : coffee, chocolate, beer, wine, citrus fruit, bananas, and vanilla 24h before test
    • 76. ADDISON'S DISEASE
    • 77. ADRENAL CORTEX HORMONES
      • Glucocorticoids
        • Cortisol, corticosterone
        • Increase blood glucose levels by increasing rate of gluconeogenesis
        • Increase protein catabolism
        • Increase mobilization of fatty acids
        • Promote sodium and water retention
        • Anti-inflammatory effect
        • Aid the body in coping with stress
    • 78. ADRENAL CORTEX HORMONES
      • Mineralocorticoids
        • Aldosterone, Corticosterone, Deoxycorticosterone
        • Regulate fluid and electrolyte balance
        • Stimulate reabsorption of sodium, chloride and water
        • Stimulate potassium excretion
      • Under the control of Renin-Angiotensin-Aldosterone system (RAAS)
    • 79.  
    • 80. ADRENAL CORTEX HORMONES
      • Sex hormones
        • Androgens, Estrogens
        • Influences the development of sexual characteristics
    • 81.  
    • 82. ADDISON'S DISEASE
      • Hyposecretion of adrenocortical hormones
      • Destruction of the cortex
      • Idiopathic atrophy
    • 83. ADDISON'S DISEASE
      • W eakness
      • E xcess stress
      • A / N / V / D
      • K & ACTH elevation; Low Na, BP, cortisol, glucose
    • 84.  
    • 85. ADDISON'S DISEASE
      • Replacement of hormones
      • Hydrocortisone; Fludrocortisone
      • PNSS (0.9 NaCl)
      • Dextrose
      • Diet :
      • High-CHO & CHON
      • Low potassium, high sodium
    • 86. ADDISON'S DISEASE
      • VS, weight, and serum glucose level
      • 24-hour urine specimens
      • [LOW 17- hydroxycorticosteroids & 17-ketosteroids]
      • Electrolyte levels:  K;  Na
      • Bronze-skin
      • Changes in energy or activity
    • 87. ADDISON’S DISEASE
    • 88. ADDISON'S DISEASE
      • MVS [4x / day]
      • Infection, Addisonian crisis, dehydration
      • MIOW / MBP / MBG
      • Give steroids with milk or an antacid
      • Avoid : Contacts & Stress
    • 89. CUSHING'S SYNDROME
    • 90. CUSHING'S DISEASE
      • A drenal hyperplasia / tumor
      • C ushing’s disease
      • T umor-secreting ACTH
      • H ypothalamic
    • 91.
      • B uffalo hump
      • U nusual behavior (depression, personality changes, fatigability)
      • F acial features (moonface, hirsutism in women)
      • F at (truncal obesity)
      • A CTH and cortisol in blood elevated;
      • L oss of muscle mass
      • O verextended skin (abdominal striae with easy bruisability)
    • 92.
      • H ypertension, hyperglycemia, hypernatremia
      • U rinary cortisol elevated
      • M enstrual irregularities
      • P orosity of bones (osteoporosis)
    • 93. CUSHING’S SYNDROME
    • 94. CUSHING'S SYNDROME
      • Remove exogenous steroids
      • Hypophysectomy or irradiation
      • Adrenalectomy
    • 95. CUSHING'S SYNDROME
      • Cyproheptadine (Periactin)
      • Metyrapone
      • Mitotane (Lysodren)
      • Aminoglutethamide (Cytadren)
      • Potassium supplements
      • High-CHON; Low Na
    • 96. CUSHING'S SYNDROME
      • MVS, MIOW, MBP, MBG
      • Electrolyte levels: Na & K
      • Urine specimens
      • [LOW 17- hydroxycorticosteroids & 17-ketosteroids]
      • Physical appearance
      • Changes in coping & sexuality
      • [verbalization]
      • Stress reduction
    • 97. DIABETES MELLITUS
    • 98. DIABETES MELLITUS
      • Insulin resistance [GDM, age]
      • Failure in production
      • Blockage of insulin supply
      • Autoimmune response
      • Excess body fat
      • Heredity
    • 99. DIABETES MELLITUS
      • Type I [juvenile ]/IDDM
      • Type II [adult- onset type]/ NIDDM
        • gradual onset
      • diet and exercise obesity
      • Pancreatectomy, Cushing's syndrome, drugs
    • 100. DIABETES MELLITUS
      • Low insulin leads to :
      • Hyperglycemia
      • Glucosuria
      • Polyuria
      • Gluconeogenesis
    • 101. DIABETES MELLITUS
      • Complications
      • Microvascular
      • Retinopathy & Renal failure
      • Macrovascular
      • CV and PVD
      • Peripheral neuropathy
    • 102. P olyuria olydipsia olyphagia ruritus aresthesia oor healing oor eyesight
    • 103. Normal Impaired DM FBS <110mg/dl 110-125mg/dl ≥ 126mg/dl 2H OGTT <140mg/dl ≥ 140; <200mg/dl ≥ 200 mg/dl
    • 104. DIABETES MELLITUS
      • Diet
      • complex CHO [50% to 60%]
      • water-soluble fiber
      • oat, bran, peas, beans, pectin-rich FV
      • CHON [12% to 20%]
      • 60 and 85 g
      • CHOO [<30%]
      • 70 to 90 g/day / MUFA
    • 105. DIABETES MELLITUS
      • Insulin dose adjustments depend on :
        • physical and emotional stresses
        • specific type of insulin
        • condition and needs of the client
    • 106. Insulin Onset Peak Duration Ultra rapid acting insulin analog (humalog) 10-15 min 1 H 3 H SAI (humulin regular) ½ - 1 H 2-4 H 4-6 (8) H IAI (humulin lente, Humulin NPH) 3-4 H 4-12 H 16-20 H LAI (Protamine zinc, humulin ultralente) 6-8 H 12-16 H 20-30 H Premixed insulin (NPH-regular [80-20, 70-30, 50-50]) ½-1 H 2-12 H 18-24 hrs Insulin glargine (Lantus ) Slower than NPH No Peak 24 H
    • 107. DIABETES MELLITUS
      • Somogyi effect
      • Epinephrine & Glucagon
      • Glycogenolysis
      • [iatrogenically-induced hyperglycemia]
      • Lowering insulin dosage at night
      • MBG
    • 108. DIABETES MELLITUS
      • Insulin pump
      • Basal doses of regular insulin delivered every few minutes bolus doses delivered pc
      • Appropriate amount of insulin for 24 hours plus priming is drawn into syringe
      • The administration set is primed and needle inserted aseptically, usually into abdomen
    • 109. DIABETES MELLITUS
      • Client teaching points:
      • Proper insulin preparation using aseptic technique
      • When to remove the pump (e.g., before showering or sexual relations)
      • MBG at home
    • 110. INSULIN ADMINISTRATION
      • Increases the hypoglycemic effects of insulin
      • Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs
      Increases blood glucose levels Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives Increase the need for increased insulin dose Illness, infection, and stress
    • 111. ORAL HYPOGLYCEMIC AGENTS
      • Sulfonylureas
      • Promotes increase insulin secretion from pancreatic beta cells through direct stimulation
      • First Generation Agents :
      • Acetohexamide
      • Tolbutamide (Orinase)
      • Tolzamide (Tolinase)
      • Chlorpropamide (Diabenese)
      • Second Generation Agents :
      • Glipizide (Minidiab, Glucotrol)
      • Glyburide (DiaBeta, Glynase, Micronase)
      • Glimepiride (Amaryl)
    • 112. ORAL HYPOGLYCEMICS
      • Biguanides
      • Reduces hepatic production of glucose by inhibiting glycogenolysis
        • Decrease the intestinal absorption of glucose and improving lipid profile
      • Agents :
      • Phenformin
      • Metformin (Glucophage, Glucophage XR)
      • Buformin
    • 113. ORAL HYPOGLYCEMICS
      • Alpha-glucosidase inhibitors
        • Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas
        • Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially
        • Agents :
      • Acarbose (Precose, Gluconase, Glucobay)
      • Miglitol (Glyset)
    • 114. ORAL HYPOGLYCEMICS
      • Thiazolidinediones
      • Enhances insulin action at the cell and post-receptor site and decreasing insulin resistance
      • Agents :
      • Pioglitazone (Actos)
      • Rosiglitazone (Avandia)
      • Rosiglitazone + Metformin (Avandamet)
    • 115. DIABETES MELLITUS
      • Other therapies include:
      • pancreas islet cell grafts
      • pancreas transplants
      • implantable insulin pumps
      • cyclosporin [Sandimmune, Neoral]
    • 116. DIABETES MELLITUS
      • MBG [done pc and hs ] + HbA1C
      • MBP + weight
        • Renal function + MIO
        • Eye examination
    • 117. GLYCOSYLATED HEMOGLOBIN (HBA 1C )
      • Reflects effectiveness of treatment
        • < 7.5% (good control)
        • 7.6% - 8.9% (fair control)
        • > 9% (poor control)
    • 118. DIABETES MELLITUS
      • diet & weight
      • ketonuria
      • note infection
      • legs / feet / toenails check
      • [keep in between toes dry]
      • acceptance & understanding
    • 119. DIABETES MELLITUS
      • Administer insulin
      • sterile technique
      • rotating injection sites
      • dosage / types / strengths / peak
      • CHO source
        • Avoid : tight shoes; smoking; heat
    • 120. DIABETES MELLITUS
      • hypoglycemia
      • Headache
      • Nervousness
      • Diaphoresis
      • Rapid, thready pulse
      • Slurred speech
    • 121. THE CLIENT IS TIRED!
      • T
      • I rritability
      • R estlessness
      • E
      • D iaphoresis
      • Hypoglycemia: <50 mg/dL
      • Causes:
      • Overtreated hyperglycemia
      • Increased exercise
      • β -blockers
      • Gastric paresis
      • Alcohol intake
      • Erratic insulin absorption
      achycardia xcessive hunger xcitability remors
    • 122.
      • Mild :
      • S hakiness
      • T remors
      • E xcessive hunger
      • P aresthesias
      • P allor
      • D iaphoresis
      • Rx :
      • 10-15 gm carbohydrate
        • 2 oz. (1 small tube of) cake icing
        • 4 oz. orange juice
        • 6 oz. regular soda
        • 6-8 oz 2% skim milk
        • (4 to) 10 pieces of hard candy
    • 123.
      • Moderate :
      • D rowsiness
      • I mpaired judgment
      • D ouble or blurred vision
      • H eadache
      • I nability to concentrate
      • M ood swings
      • I rritability
      • S lurred speech
      • Rx :
      • 20-30 gm carbohydrate
      • Glucagon 1 mg SQ/IM
    • 124.
      • Severe :
      • S eizures
      • U nconsciousness
      • D isorientation
      • Rx :
      • 25 gm D 50 dextrose IV
      • Glucagon 1 mg IM/IV
    • 125. DIABETES MELLITUS
      • diabetic coma
      • Restlessness
      • Hot, dry, flushed skin
      • Thirst
      • Rapid pulse
      • Nausea
      • Fruity odor to breath
    • 126.
      • K etoacidosis
      • U rinary changes
      • S unken eyeballs
      • S kin is warm & flushed
      • M embranes are dry
      • A rrhythmias
      • U pset GI system
      • L ow BP
      • S aline solution
      • Rx :
      • Regular insulin drip
        • 0.9% or 0.45% NSS
        • 1:1 [100U:100cc]
      • Nursing care:
      • Check glucose
        • 250-300 mg/dL [q30-60mins]
        • 250 mg/dL
          • DC the drip
    • 127.
      • NON
      • K etosis is absent
      • E lectrolyte imbalance [K + decrease]
      • T hirst
      • O btundation
      • T reat with regular insulin drip
      • I nitiate diet
      • C orrect hyperglycemia
    • 128.
      • N ormal creatinine?
      • E rythrocyte sedimentation rate [ESR: 0-20 mm/hr]
      • P oor glycemic control
      • H emodialysis
      • R estrict: Na + , CHON, K + , weight
      • O utput & input (MIO)
      • N o symptoms
    • 129.
      • R educed O 2 in the eye
      • E levated sugar & BP
      • T ension is high in the retina
      • I ncreased lens opacity
      • N O eyesight
      • A nnual eye exam [every 6-12 months]
    • 130. MAJOR DISORDERS OF THE ENDOCRINE SYSTEM THANK YOU! Nio C. Noveno, RN, MAN