The endocrine system consists of glands that regulate metabolic processes through hormone secretion. Disorders can result from overactivity or underactivity of hormones. Common endocrine disorders include pituitary disorders like hyperpituitarism and hypopituitarism, thyroid disorders like hypothyroidism and hyperthyroidism, and parathyroid disorders like hypoparathyroidism. Symptoms depend on the hormone affected and include fatigue, weight changes, mood issues, and metabolic abnormalities. Treatment involves hormone replacement, medications, surgery, or lifestyle modifications. Nursing care focuses on monitoring for complications, providing support and education, and maintaining fluid and electrolyte balance.

1. ENDOCRINESYSTEM AND MAJOR DISORDERSBy: MISS SHENELL A. DELFIN, RN

2. FUNCTION:Endocrine system consist of a series of glands “ductless” that function individually or conjointly to integrate and control innumerable metabolic activities in the body.These glands automatically regulate various body processes by releasing chemical messengers called hormones.OVERACTIVITY OR UNDERACTIVITY of any one of them affects the whole system.

3. FUNCTION:Control and coordination of the processes which are wide spread in the body such as:Response to stress or injury

4. Growth and development

5. Reproduction

6. Fluids and electrolytes

7. Acid base-balance

8. Energy metabolism

9. ENDOCRINE GLANDS

11. ENDOCRINE GLANDS

12. ENDOCRINE GLANDS

15. ENDOCRINE GLANDS

17. ENDOCRINE GLANDS

19. ENDOCRINE GLANDS

20. HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISMCHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS, ADRENAL MEDULLA HORMONES)

21. NEGATIVE FEEDBACK MECHANISMDECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE (e.g. Thyroid gland release of Thyroxine)RETURN OF THE NORMAL CONCENTRATION OF HORMONE

22. NEGATIVE FEEDBACK MECHANISMINCREASED HORMONE CONCENTRATION IN THE BLOOD(e.g. Thyroxine)PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)DECREASED PRODUCTION & SECRETION OF TARGET ORGANOF THEHORMONE (e.g. Thyroid gland release of Thyroxine)RETURN OF THE NORMAL CONCENTRATION OF HORMONE

23. Endocrine DisordersIf you can remember what each hormone does in the body, it will be easier to remember what results from imbalances of that hormone. Most symptoms of hormone HYPERACTIVITY are the opposite of symptoms of that hormones HYPOACTIVITY.

24. ANTERIOR PITUITARY DISTURBANCESHYPOPITUITARISMHYPERPITUITARISM

25. PITUITARY ANTERIOR LOBE

26. HyperpituitarismMay be due to overactivity of glandor the result of an adenomaCharacterized by:Excessive serum concentrationof pituitary hormones (GH, ACTH, PRL)Morphologic and functional changesin the anterior pituitary

27. Growth Hormone HypersecretionGIGANTISM

28. Manifestations of acromegaly. Progressive alterations in facial appearance include enlargement of the cheekbones and jaw along with thickening of soft-tissue structures such as the nose, lips, cheeks, and the flesh above the brows. (Courtesy of Clinical Pathological Conference, American Journal of Medicine.)

29. Hyperpituitarism:Clinical ManifestationsArthritisChest: barrel-shapedRough facial featuresOdd sensations: hands and feetMuscle weakness & fatigueEnlargement of organsGrowth of coarse hairAmenorrhea; breast milk productionLoss of vision; headachesImpotence; increased perspiration Snoring

30. Hyperpituitarism:Clinical Manifestations

31. HypopituitarismDeficiency of one or moreanterior pituitary hormonesCausesInfections / Inflammatory disordersAutoimmune diseasesCongenital absenceTumorSurgery / Radiation therapy

32. Hypopituitarism:Clinical ManifestationsHypo-thermia, -glycemia, -tensionLoss of vision, strength, libido, & secondary sexual characteristics

33. DWARFISM

34. MANAGEMENTHYPOPITUITARISMSURGICAL REMOVAL / IRRADIATIONREPLACEMENT THERAPYTHYROID HORMONESSTEROIDSSEX & GROWTH HORMONESGONADOTROPINS (restore fertility)HYPERPITUITARISMSURGICAL REMOVAL / IRRADIATIONMONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS

35. Trans-sphenoidal hypophysectomy

36. POSTERIOR PITUITARY DISTURBANCESDIABETES INSIPIDUSSYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

37. FUNCTION:WHEN THERE IS A OF SERUM OSMOLALITY, THE NORMAL BODY RESPONSE IS TO THE SECRETION OF ADH.WHEN THE NORMAL FEEDBACK MECHANISM FOR ADH IS SUSTAINED, THERE IS EXCESSIVE WATER RETENTION IN THE BODYWHEN THERE IS OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS

40. DIABETES INSIPIDUSCHARACTERIZED BY A DEFICIENCY OF ADH. WHEN IT OCCURS, IT IS MOST OFTEN ASSOCIATED WITH :NEUROLOGICAL CONDITIONS, SURGERY, TUMORS, HEAD INJURY, OR INFLAMMATORY PROBLEMS

41. DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSINS/SX:POLYURIA 15-29L/ DAYPOLYDIPSIASG OF URINE IS <1.010S/SX OF DHNSHOCK

42. DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSINMANAGEMENTHORMONAL REPLACEMENT – FOR LIFEVASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAYNON-HORMONAL THERAPYCHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY TO DECREASEDVASOPRESSININCREASE FLUIDSMONITOR I&O + WEIGHT (MIOW)MAINTAIN FLUID & ELECTROLYTE BALANCE

43. SYNDROME OF INAPPROPRIATE ADH(SIADH)ELEVATED ADHS/SX:DECREASED SERUM SODIUMCX IN LOC TO UNCONSCIOUSNESSSEIZURESWATER INTOXICATIONN/VMENTAL CONFUSIONPersistent excretion of concentrated urineSigns of fluid overloadHyponatremia

44. SYNDROME OF INAPPROPRIATE ADHMANAGEMENT:WATER INTAKE RESTRICTIONADMINISTER AS ORDERED:NaClDiureticsDemeclocycline (declamycin) – a tetracycline analogue that interferes with the action of ADH on the collecting tubules

45. THYROID DISORDERS

47. Hypothyroidism underactive state of the thyroid gland hyposecretion of thyroid hormone most common in women, middle-age primary function is to control the level of cellular metabolism by secreting thyroxin (T4) and triiodothyronine (T3)DX: decreased T3, T4 Elevated TSH, cholesterol

48. HypothyroidismA state of low serum TH levelsor cellular resistance to THIodine deficiencyOncologicAutoimmuneDrugsDevelopmentalIatrogenicDietaryNon-thyroidalEndocrine

49. Pathophysiology inadequate secretion of thyroid hormone  general slowing of all physical and mental process

50.  metabolic rate

51.  oxidation of nutrients for energy

52.  heat production

53. Complications :Cretinism– severe physical and mental retardation resulting from severe deficiency of thyroid function in infancy or childhood (congenital hypothyroidism) requires lifetime hormone replacementMyxedema– occur from prolonged severe disease accelerated devt. of coronary artery disease coma – rapid dev’t. of impaired consciousness and suppression of vital functions

54. MYXEDEMA COMA- a condition resulting from persistent low thyroid production.

55. Med. Mgt. – thyroid replacement therapyLevothyroxine(Synthyroid) ,liothyronine Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR

56. Nsg. Interventions provide a warm environment, conducive to rest

57. avoid use of all sedatives

58. assist client in choosing calorie,  cholesterol diet

59.  fluid and fiber to relieve constipation

60.  physical activity and sensory stimulation gradually as condition improves

61. monitor cardiovascular response to increased hormone levels carefully

62. provide info. about prescribed medications (name, dosage, side effects) and importance of lifelong medical supervision

63. Hyperthyroidism over-secretion of the thyroid gland also called thyrotoxicosis or graves disease, tissues are stimulated by excessive thyroid hormone a recurrent syndrome, may appear after emotional stress or infection occurs mostly in women 20-50 yrs oldCauses : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause

64. Hyperthyroidism (cont.)DX: > elevated T3, T4 valuesT4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/Labnormal findings in the thyroid scanGoiter – enlargement of the thyroid gland due to  stimulation of the thyroid gland by TSHSimple goiter – enlarged thyroid glanddue to iodine deficiency, intake of goitrogenic foods  cabbage, turnips, soybeans

65. may be hereditaryGrave’s Disease disorder char. by one or more of the ff: diffuse goiter hyperthyroidism infiltrative opthalmopathy  exophthalmos seen in females under age 40

66. result from stimulation of the thyroid gland by thyroid-stimulating immunoglobulins (TSI) cause is unknown, may be hereditary, gender-related, often occurs after severe emotional stress or infection

68. Complications : cardiovascular disease (HPN, Angina, CHF) Exophthalmos – abnormal protrusion of the eyeballs caused by abnormal deposits of fat and fluid in the retroocular tissue Corneal abrasion Thyroid storm or crisis  life-threatening hypermetabolism and excessive adrenergic response (HR, RR, BP)

69. Thyroid Storm or Crisis a medical emergency pts. develop severe manifestation of hyperthyroidism  temp., tachycardia, dysrhythmias worsening tremors, restlessness delirious or psychotic state or coma abdominal pain  BP and RRPrecipitated by a major stressor: infection trauma or surgery (thyroidectomy) inadequate treatment

70. Do you take this woman as your wife…. In sickness and in health…TAKE ME! TAKE ME!!

72. Assessment Findings: Thyroid stormAnxiety

73. Flushed, smooth skin

74. Heat intolerance

75. Mood swings

76. Diaphoresis

77. Tachycardia

78. Palpitations

79. Dyspnea

80. Delirium, coma

81. Heart failureMed. Mgt.Medications Propylthiouracil (PTU) – antithyroid drug - blocks thyroid hormone production - can cause agranulocytosis - monitor pt. CBCMethimazole (Tapazole) – blocks TH prod. Iodine preparations –  the size and vascularity of the thyroid gland; inhibit release of thyroid hormones 1.) Lugol’s solution can be given with milk or fruit juice should be taken with a straw – may stain the teeth complications : brassy taste in the mouth, sore teeth and gums2.) Saturated solution of potassium iodide (SSKI)

82. Med. Mgt.Medications Propanolal (Inderal) and other adrenergic blockers relieve the adrenergic effects of excess thyroid hormone (sweating, palpitations, tremors)Radioactive iodine – limits the secretion of the hormone by damaging or destroying thyroid tissueSurgical intervention (performed only when pt. is in aeuthyroid state) subtotal thyroidectomy (large goiter)

83. total thyroidectomy (if carcinoma is present)Nsg. Interventions:Provide calm, restful envt. physical comfort, cool envt. temp., bathe frequently w/ cool waterprovide adequate rest, avoid muscle fatigue stressors in the envt.— noise and lightsrelaxation techniquesProvide adequate nutrients calorie,  protein, balanced diet (4,000-5,000 cal/day) fluid intakeRestrict stimulants (tea, coffee, alcohol)small, frequent feedings if hypermotility is presentDaily wt.

84. Nsg. Interventions:Provide emotional supportProvide eye careeye drops, dark glasses, patch eyes if necessaryelevate head of bed for sleeprestrict dietary sodiumassess adequacy of lid closureBe alert for complications

85. Post-op care after Thyroidectomy O2 therapy, suction secretions

86. Monitor for signs of bleeding and excessive edema

87. elevate head of bed 30o, support head and neck – to avoid tension on suturescheck dressing frequently, check behind the neck for bleeding assess for signs of resp. distress, hoarseness (laryngeal edema or damage) keep tracheostomy set in patient’s room for emergency use

88. Post-op Complications: be alert for the possibility of:1. Tetany(due to hypocalcemia caused by accidental removal of parathyroid glands)assess for numbness, tingling or muscle twitching

89. Chvostek’s sign and Trousseau’s sign

90. Ca+ gluconate IV2. HemorrhageWOF: hypotension, tachycardia, other signs of hypovolemia

91. WOF: irregular breathing, swelling, choking---possible hemorrhage and tracheal compression

92. WOF: early signs of hemorrhage: repeated clearing of the throat, difficulty swallowingPost-op Complications: be alert for the possibility of:3. Thyroid storm - life-threatening - sudden  release of thyroid hormone - fever, tachycardia, increasing restlessness and agitation, delirium

95. PARATHYROID GLAND DISORDERS

98. Promotes resorption of calcium from bone to maintain normal serum calcium levelsCALCIUM DEPOSITED IN THE BONEMobilization of calcium and phosphorous from boneRenal: increases calcium reabsorption and phosphate excretionCALCIUM STAYS IN THE BONEEXCRETION OF CALCIUM Hypoparathyroidism is characterized by decrease in the PTH levelPARATHYROID HORMONETINGLING OF FINGERS

99. CHVOSTEKS/ TROUSSEAU’S

100. FATIGUE, WEAKNESS

101. CARDIAC ARRHYTHMIAS

102. SEIZURE

103. BRONCHOSPASMFunction of calcium: maintains N muscle and neuromuscular responses.

104. Necessary component for blood coagulation mechanismsPromotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).HYPOCALCEMIA

105. TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCYTROUSSEAU'SSIGNCHVOSTEK'SSIGN

106. PARATHYROID DISORDERSDIAGNOSTIC TESTS:HEMATOLOGICALSERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASEURINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE

107. HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT:Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK, pcSEIZURE precLISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDECaGLUCONATE @ BEDSIDE

108. T ETANYAKERACHEOSTOMYC ALCIUM GLUCONATEAREALCIUM 8.6 – 10.6 mg / dL

109. HYPERCALCEMIA, LACK OF RESORPTION OF CALCIUM INTO THE BONE( BONE CYST AND PATHOLOGIC FRACTURE)Promotes resorption of calcium from bone to maintain normal serum calcium levelsTUBULAR CALCIUM DEPOSIT- KIDNEY STONES, AZOTEMIA, HPN BY RF, RENAL FAILURECALCIUM RELEASED INTO THE BLOOD LEADS TO BONE DAMAGEMobilization of calcium and phosphorous from boneRenal: increases calcium reabsorption and phosphate excretionHyperparathyroidism is characterized by excesssive secretion of PTHPARATHYROID HORMONEFunction of calcium: maintains N muscle and neuromuscular responses.

110. Necessary component for blood coagulation mechanismsMUSCLE WEAKNESSPERSONALITY CHANGESCARDIAC ARRHYTHMIASPromotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).ANOREXIAN/VCONSTIPATIONPEPTIC ULCER DSE

111. HYPERPARATHYROIDISMINCREASED PTH PRODUCTIONHYPERCALCEMIAHYPOPHOSPHATEMIAPRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLANDSECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:CHRONIC RENAL DSEMALABSORPTION SYNDROMEOSTEOMALACIA

112. HYPERPARATHYROIDISMMANAGEMENT:TX OF CHOICE : SURGICAL REMOVAL OF HYPERPLASTIC TISSUEIV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)LOW CaSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY

113. DISORDERS OF THE PANCREAS

114. DIABETES MELLITUS(TYPE I, TYPE II)

116. TWO TYPES OF DIABETES

117. Diabetes Mellitus is a chronic disorder of carbohydrate, protein, and fat metabolism resulting from insulin deficiency or abnormality in the use of insulinPredisposing factors: exact cause of diabetes mellitus remain unknown

118. genetic / hereditary predisposition

119. viruses

120. pancreatitis

121. pancreatic tumor

122. autoimmune disorder

123. obesity (overweight people require more insulin to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)

124. TypesInsulin – Dependent Diabetes Mellitus (IDDM) or Type I destruction of beta cells of the pancreas  little or no insulin production requires daily insulin admin.

125. may occur at any age, usually appears below age 15Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II probably caused by:

126. disturbance in insulin reception in the cells

127.  number of insulin receptors

128. loss of beta cell responsiveness to glucose leading to slow or  insulin release by the pancreas occurs over age 40 but can occur in children

129. common in overweight or obese

130. w/ some circulating insulin present, often do not require insulin

133. P olyuriaolydipsiaolyphagiaruritusaresthesiaoor healingoor eyesight

135. DIAGNOSTIC TEST FOR DMFasting Blood Sugar (FBS)NPO for 12 hours

136. Normal value= 80-120 mg/dl

137. 140 mg/dl or more – diagnostic of DMPostprandial blood sugarBlood is withdrawn 2 hrs. after a meal

138. N value = < 120mg/dl

139. 200 mg/dl or more is diagnostic of DM3. Oral Glucose Tolerance Test (OGTT)NPO 12 hrs, no smoking, coffee or tea, minimize activity, minimize stress

140. obtain FBS, administer 100 gm. Glucose by mouth diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs.

141. N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs.

142. Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucoseDiagnostic Tests for DM4. Glycosylated hemoglobinProvides information about blood glucose level during the previous 3 months

143. bec. glucose in the bloodstream attaches to some of the hemoglobin and stay attached during the 120-day lifespan of the RBCD-I-A-B-E-T-E-SD- DIET: 50-60% CHO, 20-30% FATS, 10-20% CHONI- INSULIN– TYPE 1A- ANTIDIABETIC AGENTS– TYPE 2B- BLOOD SUGAR MONITORINGE- EXERCISET- TRANSPLANT OF PANCREASE- ENSURE ADEQUATE FOOD INTAKES- SCRUPULOUS FOOT CARE

145. Management of HypoglycemiaGive simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugarGive Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouthAs soon as pt. regains consciousness, he should be given carbohydrate by mouthIf pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V.

147. Oral Antidiabetic Agents

148. Oral Antidiabetic Agents

149. DIABETES MILLETUSINSULIN THERAPYDISPENSED IN “U”/ml : eg 100, 80REFRIGERATEGIVEN @ ROOM TEMPGENTLY ROTATED, NOT SHAKENROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND

151. DIABETES MILLETUSINSULIN THERAPY:SITE OF INJECTION:ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS

154. B. Teach pt. on correct administration of insulin and other hypoglycemic agents.insulin in current use may be stored at room temp., all others in ref. or cool areaavoid injecting cold insulin  lead to tissue reactionroll insulin vial to mix, do not shake, remove air bubbles from syringepress (do not rub) the site after injection (rubbing may alter the rate of absorption of insulin)avoid smoking for 30 mins. after injection (cigarette smoking absorption)Rotate sitesFailure to rotate sites may lead to Lipodystrophy

155. Lipodystrophy – localized disturbance of fat metabolism

156. Ex. Lipohypertrophy – thickening of subcutaneous tissue at injection site, feel lumpy or hard, spongy result to  absorption of insulin making it difficult to control the pt.’s blood glucose

157. Teach pt. to estabilish and maintain a pattern of regular exerciseBenefits of exercise : promotes use of CHO & enhances action of insulin blood glucose levels need for insulin the no. of functioning receptor sites for insulinperform exercise after meals to ensure an adequate level of blood glucose

158. carry a rapid-acting source of glucose during exercise

159. excessive or unplanned exercise may trigger hypoglycemia

160. take insulin and food before active exercise

161. ACUTE COMPLICATIONS OF DIABETES MILLETUSDIABETIC KETO-ACIDOSIS (DKA)INSULIN SHOCKHYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA

163. Diabetic Ketoacidosis (DKA) ComaS/Sx:polyuria, thirstnausea, vomiting, abdominal pain –-- due to acidosisweakness, headache, fatigue --- due to acidosis and F/E imbalancedim visiondehydration, hypovolemic shock (PR, BP, dry skin, wt. loss)hyperpnea (Kussmaul’s breathing)acetone breath (fruity odor)lethargy  COMABlood glucose level > 250-350 mg/100 ml.

167. Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC)can occur when the action of insulin is severely inhibitedseen in pts. w/ NIDDM, elderly persons w/ NIDDMPrecipitating factors:infection, renal failure, MI, CVA, GI hemorrhage, pancreatitis, CHF, TPN, surgery, dialysis, steroidsS/Sx:polyuriaoliguria (renal insufficiency)

168. lethargy

169. temp, PR, BP, signs of severe fluid deficit

170. Confusion, seizure, coma

171. Blood glucose level > 600 mg/100 ml.HHONKS/SX:S/SX OF DKA WITHOUT:KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA

172. Interventions for DKA and Hyperosmolar ComaRegular insulin IV push or IV drip 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24 hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr)

173. Long-term Complications of DMVascular Changes) Macroangiopathy – hardening and damage of the walls of large arteriesCoronary Artery DiseaseCVA (Stroke)Peripheral vascular disease – foot ulcers and gangreneb. ) Microangiopathy – destruction of small blood vesselsRetinopathy – damage to retinal capillaries; hemorrhage, blindnessNephropathy – damage microcirculation of kidneys; CRF2. Neuropathy Damage to the neurons caused by vascular insufficiency and  blood glucoseSensory and motor impairmentNumbness, tingling, pain in extremities Painless neuropathyImpotence!!

177. DISORDERS OF THE ADRENAL GLANDS

178. ADRENAL GLANDSTIMULATED BY ACTHADRENAL MEDULLA- SECRETES CATECOLAMINE, (EPINEPHRINE, & NOREPINEPHRINE).ADRENAL CORTEX- MAIN BODY; RESP FOR SECRETION OF GLUCO,MINERALO, SEX HORMONES (ANDRO & ESTRO)FUNCTION IS TO CONTROL THE (-) FEEDBACK MECHANISMS REGULATING HORMONE RELEASE

180. ADRENAL CORTEX DISORERSADRENAL INSUFFICIENCY ( ADDISON’S DSE)CUSHING’S SYNDROME

181. ADRENAL INSUFFICIENCYADDISON’S DISEASEINCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS

183. Addison's DiseaseReplacement of hormones Hydrocortisone; FludrocortisonePNSS (0.9 NaCl)Dextrose Diet:High-CHO & CHONLow potassium, high sodium

184. Addison’s disease

185. Addison's DiseaseMVS [4x / day]Infection, Addisonian crisis, dehydrationMIOW / MBP / MBGGive steroids with milk or an antacidAvoid: Contacts & Stress

186. CUSHING’S SYNDROMECAUSE:SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOREXCESSIVE GLUCORTICOID ADMINISTRATION

187. CUSHING’S SYNDROMES/SX:TRUNCAL OBESITYBUFFALO HUMPMOON-FACEWT GAINSODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

188. CUSHING’S SYNDROMEPURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:OLIGOMENORRHEA HIRSUTISM GYNECOMASTIAHYPERTENSION FROM S. Na

190. CUSHING’S SYNDROMETREATMENT & NURSING CARE:PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSEDPROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMYTreat HPN

191. ALDOSTERONISMHYPERSECRETION OF ALDOSTERONECONN’S SYNDROME

192. CONN’S SYNDROMEPRIMARY ALDOSTERONISMCAUSE:ADRENAL ADENOMAS/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPNMANAGEMENT:SURGERYALDACTONE – ALDOSTERONE ANTAGONIST

194. ADRENAL MEDULLAHORMONES : EPINEPHRINE NOREPINEPHRINE EFFECTS

195. PHEOCHROMOCYTOMATUMOR OF ADRENAL MEDULLA SECRETES INCREASED AMOUNT OF CATECHOLAMINESA small tumor in the adrenal gland that secretes large amounts of epinephrine and norepinephrine.S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC ACID

196. VMA IN 24H URINEEND PRODUCT OF CATECHOLAMINE METABOLISMDRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:COFFEE & TEABANANAVANILLACHOCOLATES

197. PHEOCHROMOCYTOMAMANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINENURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUCOSE & ACETONE

199. RECAP:ANTERIOR PITUITARY:GIGANTISM,

200. ACROMEGALLY,

201. DWARFISMPOSTERIOR PITUITARY:DIABETES INSIPIDUS,

202. SIADHLOCATION: BASE OF THE BRAIN

203. RECAPADRENAL GLAND:ADDISON’S DSE

204. CUSHING SYNDROME

205. ALADOSTERONISMADRENAL MEDULLA:PHEOCHROMOCYTOMALOCATION: ON TOP OF THE KIDNEY

206. RECAPPANCREAS:DMLOCATION: POSTERIOR TO LIVERPARATHYROID:HYPORATHYROIDISM

207. HYPERPARATHYROIDISMLOCATION: NEAR THYROID

208. RECAPTHYROID:HYPOTHYROIDISM

209. CRETINISM

210. MYXEDEMA

211. HYPERTHYROIDISM (GRAVE’S DSE)LOCATION: ANTERIOR PART OF NECK

212. QUESTION NO. 1A CLIENT IS FOUND TO BE COMATOSE & HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50 MG/DL. WHAT NURSING ACTION IS IMPLEMENTED FIRST?INFUSE 1L OF D5W OVER A 12 HR PERIOD.ADMIN. 50% GLUCOSE IVCHECK THE CLIENT’S URINE FOR THE PRESENCE OF SUGAR AND ACETONEENCOURAGE THE CLIENT TO DRINK ORANGE JUICE W/ ADDED SUGAR

213. QUESTION NO.2WHAT IS THE PRIMARY ACTION OF INSULIN IN THE BODY?ENHANCES THE TRANSPORT OF GLUCOSE ACROSS THE CELL WALLSAIDS IN THE PROCESS OF GLUCONEOGENESISSTIMULATES THE PANCREATIC BETA CELLSDECREASE THE INTESTINAL ABSORPTION OF GLUCOSE

214. QUESTION NO.3POSTOPERATIVE THYROIDECTOMY NURSING CARE INCLUDES WHICH MEASURES?HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF HOARSENESS IS PRESENTPROVIDE LOW-CALCIUM DIET TO PREVENT HYPERCALCEMIACHECK THE DRESSING AT THE BACK OF THE NECK FOR BLEEDINGAPPLY SOFT CERVICAL COLLAR TO RESTRICT MOVEMENT

215. Any Questions???