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ENDOCRINE SYSTEM AND MAJOR DISORDERS By: MISS SHENELL  A. DELFIN, RN
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.
FUNCTION: Control and coordination of the processes which are wide spread in the body such as: ,[object Object]
Growth and development
Reproduction
Fluids and electrolytes
Acid base-balance
Energy metabolism,[object Object]
ENDOCRINE GLANDS
ENDOCRINE GLANDS
ENDOCRINE GLANDS
ENDOCRINE GLANDS
ENDOCRINE GLANDS
ENDOCRINE GLANDS
HORMONE REGULATION NEGATIVE FEEDBACK MECHANISM CHANGING 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)
NEGATIVE FEEDBACK MECHANISM DECREASED 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
NEGATIVE FEEDBACK MECHANISM INCREASED HORMONE CONCENTRATION IN THE BLOOD(e.g.        Thyroxine) PITUITARY GLAND IS INHIBITED TO RELEASE 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
Endocrine Disorders If 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.
ANTERIOR PITUITARY  DISTURBANCES HYPOPITUITARISM HYPERPITUITARISM
PITUITARY ANTERIOR LOBE
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
Growth Hormone Hypersecretion GIGANTISM
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.)
Hyperpituitarism:Clinical Manifestations Arthritis Chest: barrel-shaped Rough facial features Odd sensations: hands and feet Muscle weakness & fatigue Enlargement of organs Growth of coarse hair Amenorrhea; breast milk production Loss of vision; headaches Impotence; increased perspiration  Snoring
Hyperpituitarism:Clinical Manifestations
Hypopituitarism Deficiency of one or more anterior pituitary hormones Causes Infections / Inflammatory disorders Autoimmune diseases Congenital absence Tumor Surgery / Radiation therapy
Hypopituitarism:Clinical Manifestations Hypo-thermia, -glycemia, -tension Loss of vision, strength, libido, & secondary sexual  characteristics
DWARFISM
MANAGEMENT HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY THYROID HORMONES STEROIDS SEX & GROWTH HORMONES GONADOTROPINS (restore fertility) HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS
Trans-sphenoidal hypophysectomy
POSTERIOR PITUITARY DISTURBANCES DIABETES INSIPIDUS SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
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 BODY WHEN THERE IS     OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS
DIABETES INSIPIDUS CHARACTERIZED BY A DEFICIENCY OF ADH.  WHEN IT OCCURS, IT IS MOST OFTEN ASSOCIATED WITH : NEUROLOGICAL CONDITIONS,  SURGERY,  TUMORS,  HEAD INJURY,  OR INFLAMMATORY PROBLEMS
DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN S/SX: POLYURIA  	15-29L/ DAY POLYDIPSIA SG OF URINE IS      <1.010 S/SX OF DHN SHOCK
DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN MANAGEMENT HORMONAL REPLACEMENT – FOR LIFE VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY NON-HORMONAL THERAPY CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY TO DECREASEDVASOPRESSIN INCREASE FLUIDS MONITOR I&O + WEIGHT (MIOW) MAINTAIN FLUID & ELECTROLYTE BALANCE
SYNDROME OF INAPPROPRIATE ADH(SIADH) ELEVATED ADH S/SX: DECREASED SERUM SODIUM CX IN LOC TO UNCONSCIOUSNESS SEIZURES WATER INTOXICATION N/V MENTAL CONFUSION Persistent excretion of concentrated urine Signs of fluid overload Hyponatremia
SYNDROME OF INAPPROPRIATE ADH MANAGEMENT: WATER INTAKE RESTRICTION ADMINISTER AS ORDERED: NaCl Diuretics Demeclocycline (declamycin) – a tetracycline analogue that interferes with the action of ADH on the collecting tubules
THYROID DISORDERS
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
Hypothyroidism A state of low serum TH levels or cellular resistance to TH Iodine deficiency Oncologic Autoimmune Drugs Developmental Iatrogenic Dietary Non-thyroidal Endocrine
Pathophysiology ,[object Object]
  metabolic rate
  oxidation of nutrients for energy
  heat production,[object Object]
Complications : ,[object Object], requires lifetime hormone replacement ,[object Object], accelerated devt. of  coronary artery disease  coma – rapid dev’t. of impaired consciousness and               suppression of vital functions
MYXEDEMA COMA-  a condition resulting from persistent low thyroid production.
Med. Mgt. – thyroid replacement therapy Levothyroxine(Synthyroid) ,liothyronine  Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR
Nsg. Interventions ,[object Object]
  avoid use of all sedatives
  assist client in choosing calorie,  cholesterol 	diet
   fluid and fiber to relieve constipation
   physical activity and sensory stimulation 	gradually as condition improves
  monitor cardiovascular response to increased 	hormone levels carefully
  provide info. about prescribed medications (name, 	dosage, side effects) and importance of lifelong 	medical supervision,[object Object]
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 old Causes : adenoma, goiter,  viral inflammation, auto-immune glandular stimulation, grave’s disease  - most common cause
Hyperthyroidism (cont.) DX: > elevated T3, T4 values T4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L ,[object Object],Goiter – enlargement of the thyroid gland  ,[object Object],Simple goiter – enlarged thyroid gland ,[object Object]
may be hereditary,[object Object]
 result from stimulation of the thyroid gland by    thyroid-stimulating immunoglobulins (TSI) ,[object Object],    often occurs after severe emotional stress or     infection
Complications :  cardiovascular disease (HPN, Angina, CHF)  Exophthalmos – abnormal protrusion of the eyeballs ,[object Object],  the retroocular tissue  Corneal abrasion  Thyroid storm or crisis  life-threatening     hypermetabolism and excessive adrenergic    response (HR, RR, BP)
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 RR Precipitated by a major stressor:   infection  trauma or surgery (thyroidectomy)  inadequate treatment
Do you take this woman as your wife…. In sickness and in health… TAKE ME! TAKE ME!!
Assessment Findings: Thyroid storm ,[object Object]
Flushed, smooth skin
Heat intolerance
Mood swings
Diaphoresis
Tachycardia
Palpitations
Dyspnea
Delirium, coma
Heart failure,[object Object]
Med. Mgt. ,[object Object],Propanolal (Inderal) and other adrenergic blockers ,[object Object],  hormone  (sweating, palpitations, tremors) ,[object Object],             hormone by damaging or destroying thyroid tissue ,[object Object],euthyroid state) ,[object Object]
 total thyroidectomy (if carcinoma is present),[object Object]
Nsg. Interventions: Provide emotional support Provide eye care eye drops, dark glasses, patch eyes if necessary elevate head of bed for sleep restrict dietary sodium assess adequacy of lid closure Be alert for complications
Post-op care after Thyroidectomy ,[object Object]
 Monitor for signs of bleeding and excessive edema
 elevate head of bed 30o, support head and neck – to    avoid tension on sutures ,[object Object],    bleeding ,[object Object],    (laryngeal edema or damage) ,[object Object],    use
Post-op Complications: be alert for the possibility of: 1. Tetany(due to hypocalcemia caused by accidental removal of parathyroid glands) ,[object Object]
 Chvostek’s sign and Trousseau’s sign
 Ca+ gluconate IV2. Hemorrhage ,[object Object]
WOF: irregular breathing, swelling, choking---possible hemorrhage and tracheal compression
WOF: early signs of hemorrhage: repeated clearing of the throat, difficulty swallowing,[object Object]
PARATHYROID GLAND DISORDERS
Promotes resorption of calcium from bone to maintain normal serum calcium levels CALCIUM DEPOSITED IN THE BONE Mobilization of calcium and phosphorous from bone Renal: increases calcium reabsorption and phosphate excretion CALCIUM STAYS IN THE BONE EXCRETION  OF CALCIUM  Hypoparathyroidism is characterized by decrease in the PTH level PARATHYROID HORMONE ,[object Object]
CHVOSTEKS/ TROUSSEAU’S
FATIGUE, WEAKNESS
CARDIAC ARRHYTHMIAS
SEIZURE
BRONCHOSPASMFunction of calcium: ,[object Object]
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
TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY TROUSSEAU'SSIGN CHVOSTEK'SSIGN
PARATHYROID DISORDERS DIAGNOSTIC TESTS: HEMATOLOGICAL SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE PHOSPHATASE URINARY STUDIES URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE
HYPOPARATHYROIDISM XRAY: INCREASED BONE DENSITY MANAGEMENT: Ca SUPPLEMENT VIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK, pc SEIZURE prec LISTEN FOR STRIDOR OR HOARSENESS TRACHEOSTOMY SET @ BEDSIDE CaGLUCONATE @ BEDSIDE
T  ETANY AKE RACHEOSTOMY C  ALCIUM GLUCONATE ARE ALCIUM 8.6 – 10.6 mg / dL
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 levels TUBULAR CALCIUM DEPOSIT- KIDNEY STONES, AZOTEMIA, HPN BY RF, RENAL FAILURE CALCIUM RELEASED INTO THE BLOOD LEADS TO BONE DAMAGE Mobilization of calcium and phosphorous from bone Renal: increases calcium reabsorption and phosphate excretion Hyperparathyroidism is characterized by excesssive secretion of PTH PARATHYROID HORMONE Function of calcium: ,[object Object]
Necessary component for blood coagulation mechanismsMUSCLE WEAKNESS PERSONALITY CHANGES CARDIAC ARRHYTHMIAS Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form). ANOREXIA N/V CONSTIPATION PEPTIC ULCER DSE
HYPERPARATHYROIDISM INCREASED  PTH  PRODUCTION HYPERCALCEMIA HYPOPHOSPHATEMIA PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM: CHRONIC RENAL DSE MALABSORPTION SYNDROME OSTEOMALACIA
HYPERPARATHYROIDISM MANAGEMENT: TX OF CHOICE : SURGICAL REMOVAL OF HYPERPLASTIC TISSUE IV PNSS 5L/ DAY WITH DIURETICS CRANBERRY JUICE (ACID-ASH) LOW Ca STRAIN URINE FOR STONES CARE FOR PARATHYROIDECTOMY
DISORDERS OF THE PANCREAS
DIABETES MELLITUS (TYPE I, TYPE II)
TWO TYPES OF DIABETES
Diabetes Mellitus  is a chronic disorder of carbohydrate, protein, and    fat metabolism resulting from insulin deficiency or    abnormality in the use of insulin Predisposing factors: ,[object Object]
 genetic / hereditary predisposition
 viruses
 pancreatitis
 pancreatic tumor
 autoimmune disorder
 obesity (overweight people require more insulin        to metabolize the food they eat or the number of     insulin receptor sites in cells is decreased)
Types Insulin – Dependent Diabetes Mellitus (IDDM) or Type I ,[object Object],    insulin production ,[object Object]
 may occur at any age, usually appears below age 15Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II ,[object Object]
 disturbance in insulin reception in the cells
 number of insulin receptors
 loss of beta cell responsiveness to glucose leading to   slow or  insulin release by the pancreas ,[object Object]
 common in overweight or obese
 w/ some circulating insulin present, often do not require    insulin
P  olyuria olydipsia olyphagia ruritus aresthesia oor healing oor eyesight
DIAGNOSTIC TEST FOR DM Fasting Blood Sugar (FBS) ,[object Object]
Normal value= 80-120 mg/dl
 140 mg/dl or more – diagnostic of DMPostprandial blood sugar ,[object Object]
N value = < 120mg/dl
200 mg/dl or more is diagnostic of DM,[object Object]
obtain FBS, administer 100 gm. Glucose by mouth diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs.
N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs.
Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucose,[object Object]
bec. glucose in the bloodstream attaches to some of the hemoglobin and stay attached during the 120-day lifespan of the RBC,[object Object]
Management of Hypoglycemia Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth As soon as pt. regains consciousness, he should be given carbohydrate by mouth If 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.
Oral Antidiabetic Agents
Oral Antidiabetic Agents
DIABETES MILLETUS INSULIN THERAPY DISPENSED IN “U”/ml : eg 100, 80 REFRIGERATE GIVEN @ ROOM TEMP GENTLY ROTATED, NOT SHAKEN ROUTE : SQ ; IM OR IV  SYRINGE: 5/8 INCH ; SAME BRAND

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Endocrine System Disorders and Their Treatments

  • 1. ENDOCRINE SYSTEM AND MAJOR DISORDERS By: 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.
  • 8.
  • 10.
  • 13.
  • 14.
  • 16.
  • 18.
  • 20. HORMONE REGULATION NEGATIVE FEEDBACK MECHANISM CHANGING 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 MECHANISM DECREASED 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 MECHANISM INCREASED HORMONE CONCENTRATION IN THE BLOOD(e.g. Thyroxine) PITUITARY GLAND IS INHIBITED TO RELEASE 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 Disorders If 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 DISTURBANCES HYPOPITUITARISM HYPERPITUITARISM
  • 26. 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
  • 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 Manifestations Arthritis Chest: barrel-shaped Rough facial features Odd sensations: hands and feet Muscle weakness & fatigue Enlargement of organs Growth of coarse hair Amenorrhea; breast milk production Loss of vision; headaches Impotence; increased perspiration Snoring
  • 31. Hypopituitarism Deficiency of one or more anterior pituitary hormones Causes Infections / Inflammatory disorders Autoimmune diseases Congenital absence Tumor Surgery / Radiation therapy
  • 32. Hypopituitarism:Clinical Manifestations Hypo-thermia, -glycemia, -tension Loss of vision, strength, libido, & secondary sexual characteristics
  • 34. MANAGEMENT HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY THYROID HORMONES STEROIDS SEX & GROWTH HORMONES GONADOTROPINS (restore fertility) HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS
  • 36. POSTERIOR PITUITARY DISTURBANCES DIABETES INSIPIDUS SYNDROME 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 BODY WHEN THERE IS OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS
  • 38.
  • 39.
  • 40. DIABETES INSIPIDUS CHARACTERIZED 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 VASOPRESSIN S/SX: POLYURIA 15-29L/ DAY POLYDIPSIA SG OF URINE IS <1.010 S/SX OF DHN SHOCK
  • 42. DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN MANAGEMENT HORMONAL REPLACEMENT – FOR LIFE VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY NON-HORMONAL THERAPY CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY TO DECREASEDVASOPRESSIN INCREASE FLUIDS MONITOR I&O + WEIGHT (MIOW) MAINTAIN FLUID & ELECTROLYTE BALANCE
  • 43. SYNDROME OF INAPPROPRIATE ADH(SIADH) ELEVATED ADH S/SX: DECREASED SERUM SODIUM CX IN LOC TO UNCONSCIOUSNESS SEIZURES WATER INTOXICATION N/V MENTAL CONFUSION Persistent excretion of concentrated urine Signs of fluid overload Hyponatremia
  • 44. SYNDROME OF INAPPROPRIATE ADH MANAGEMENT: WATER INTAKE RESTRICTION ADMINISTER AS ORDERED: NaCl Diuretics Demeclocycline (declamycin) – a tetracycline analogue that interferes with the action of ADH on the collecting tubules
  • 46.
  • 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. Hypothyroidism A state of low serum TH levels or cellular resistance to TH Iodine deficiency Oncologic Autoimmune Drugs Developmental Iatrogenic Dietary Non-thyroidal Endocrine
  • 49.
  • 51.  oxidation of nutrients for energy
  • 52.
  • 53.
  • 54. MYXEDEMA COMA- a condition resulting from persistent low thyroid production.
  • 55. Med. Mgt. – thyroid replacement therapy Levothyroxine(Synthyroid) ,liothyronine Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR
  • 56.
  • 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.
  • 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 old Causes : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause
  • 64.
  • 65.
  • 66.
  • 67.
  • 68.
  • 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 RR Precipitated 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!!
  • 71.
  • 72.
  • 81.
  • 82.
  • 83.
  • 84. Nsg. Interventions: Provide emotional support Provide eye care eye drops, dark glasses, patch eyes if necessary elevate head of bed for sleep restrict dietary sodium assess adequacy of lid closure Be alert for complications
  • 85.
  • 86. Monitor for signs of bleeding and excessive edema
  • 87.
  • 88.
  • 89. Chvostek’s sign and Trousseau’s sign
  • 90.
  • 91. WOF: irregular breathing, swelling, choking---possible hemorrhage and tracheal compression
  • 92.
  • 93.
  • 94.
  • 96.
  • 97.
  • 98.
  • 103.
  • 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 DEFICIENCY TROUSSEAU'SSIGN CHVOSTEK'SSIGN
  • 106. PARATHYROID DISORDERS DIAGNOSTIC TESTS: HEMATOLOGICAL SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE PHOSPHATASE URINARY STUDIES URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE
  • 107. HYPOPARATHYROIDISM XRAY: INCREASED BONE DENSITY MANAGEMENT: Ca SUPPLEMENT VIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK, pc SEIZURE prec LISTEN FOR STRIDOR OR HOARSENESS TRACHEOSTOMY SET @ BEDSIDE CaGLUCONATE @ BEDSIDE
  • 108. T ETANY AKE RACHEOSTOMY C ALCIUM GLUCONATE ARE ALCIUM 8.6 – 10.6 mg / dL
  • 109.
  • 110. Necessary component for blood coagulation mechanismsMUSCLE WEAKNESS PERSONALITY CHANGES CARDIAC ARRHYTHMIAS Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form). ANOREXIA N/V CONSTIPATION PEPTIC ULCER DSE
  • 111. HYPERPARATHYROIDISM INCREASED PTH PRODUCTION HYPERCALCEMIA HYPOPHOSPHATEMIA PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM: CHRONIC RENAL DSE MALABSORPTION SYNDROME OSTEOMALACIA
  • 112. HYPERPARATHYROIDISM MANAGEMENT: TX OF CHOICE : SURGICAL REMOVAL OF HYPERPLASTIC TISSUE IV PNSS 5L/ DAY WITH DIURETICS CRANBERRY JUICE (ACID-ASH) LOW Ca STRAIN URINE FOR STONES CARE FOR PARATHYROIDECTOMY
  • 113. DISORDERS OF THE PANCREAS
  • 114. DIABETES MELLITUS (TYPE I, TYPE II)
  • 115.
  • 116. TWO TYPES OF DIABETES
  • 117.
  • 118. genetic / hereditary predisposition
  • 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.
  • 125.
  • 126. disturbance in insulin reception in the cells
  • 127.  number of insulin receptors
  • 128.
  • 129. common in overweight or obese
  • 130. w/ some circulating insulin present, often do not require insulin
  • 131.
  • 132.
  • 133. P olyuria olydipsia olyphagia ruritus aresthesia oor healing oor eyesight
  • 134.
  • 135.
  • 137.
  • 138. N value = < 120mg/dl
  • 139.
  • 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.
  • 143.
  • 144.
  • 145. Management of Hypoglycemia Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth As soon as pt. regains consciousness, he should be given carbohydrate by mouth If 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.
  • 146.
  • 149. DIABETES MILLETUS INSULIN THERAPY DISPENSED IN “U”/ml : eg 100, 80 REFRIGERATE GIVEN @ ROOM TEMP GENTLY ROTATED, NOT SHAKEN ROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND
  • 150.
  • 151. DIABETES MILLETUS INSULIN THERAPY: SITE OF INJECTION: ABDOMEN ANTERIOR THIGH ARM UPPER BACK BUTTOCKS
  • 152.
  • 153.
  • 154.
  • 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.
  • 158. carry a rapid-acting source of glucose during exercise
  • 159. excessive or unplanned exercise may trigger hypoglycemia
  • 160.
  • 161. ACUTE COMPLICATIONS OF DIABETES MILLETUS DIABETIC KETO-ACIDOSIS (DKA) INSULIN SHOCK HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA
  • 162.
  • 163. Diabetic Ketoacidosis (DKA) Coma S/Sx: polyuria, thirst nausea, vomiting, abdominal pain –-- due to acidosis weakness, headache, fatigue --- due to acidosis and F/E imbalance dim vision dehydration, hypovolemic shock (PR, BP, dry skin, wt. loss) hyperpnea (Kussmaul’s breathing) acetone breath (fruity odor) lethargy  COMA Blood glucose level > 250-350 mg/100 ml.
  • 164.
  • 165.
  • 166.
  • 167.
  • 169. temp, PR, BP, signs of severe fluid deficit
  • 171.
  • 172. Interventions for DKA and Hyperosmolar Coma Regular 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 DM Vascular Changes ) Macroangiopathy – hardening and damage of the walls of large arteries Coronary Artery Disease CVA (Stroke) Peripheral vascular disease – foot ulcers and gangrene b. ) Microangiopathy – destruction of small blood vessels Retinopathy – damage to retinal capillaries; hemorrhage, blindness Nephropathy – damage microcirculation of kidneys; CRF 2. Neuropathy Damage to the neurons caused by vascular insufficiency and  blood glucose Sensory and motor impairment Numbness, tingling, pain in extremities Painless neuropathy Impotence!!
  • 174.
  • 175.
  • 176.
  • 177. DISORDERS OF THE ADRENAL GLANDS
  • 178. ADRENAL GLAND STIMULATED BY ACTH ADRENAL 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
  • 179.
  • 180. ADRENAL CORTEX DISORERS ADRENAL INSUFFICIENCY ( ADDISON’S DSE) CUSHING’S SYNDROME
  • 181. ADRENAL INSUFFICIENCYADDISON’S DISEASE INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS
  • 182.
  • 183. Addison's Disease Replacement of hormones Hydrocortisone; Fludrocortisone PNSS (0.9 NaCl) Dextrose Diet: High-CHO & CHON Low potassium, high sodium
  • 185. Addison's Disease MVS [4x / day] Infection, Addisonian crisis, dehydration MIOW / MBP / MBG Give steroids with milk or an antacid Avoid: Contacts & Stress
  • 186. CUSHING’S SYNDROME CAUSE: SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOR EXCESSIVE GLUCORTICOID ADMINISTRATION
  • 187. CUSHING’S SYNDROME S/SX: TRUNCAL OBESITY BUFFALO HUMP MOON-FACE WT GAIN SODIUM RETENTION THINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM
  • 188. CUSHING’S SYNDROME PURPLE STRIAE – FROM THINNING OF SKIN ECHYMOSIS FROM SLIGHT TRAUMA ANDROGENIC EFFECTS: OLIGOMENORRHEA HIRSUTISM GYNECOMASTIA HYPERTENSION FROM S. Na
  • 189.
  • 190. CUSHING’S SYNDROME TREATMENT & NURSING CARE: PSYCHOLOGICAL SUPPORT PREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY Treat HPN
  • 191. ALDOSTERONISM HYPERSECRETION OF ALDOSTERONE CONN’S SYNDROME
  • 192. CONN’S SYNDROME PRIMARY ALDOSTERONISM CAUSE: ADRENAL ADENOMA S/SX: HYPOKALEMIA FATIGUE HYPERNATREMIA, HPN MANAGEMENT: SURGERY ALDACTONE – ALDOSTERONE ANTAGONIST
  • 193.
  • 194. ADRENAL MEDULLA HORMONES : EPINEPHRINE NOREPINEPHRINE EFFECTS
  • 195. PHEOCHROMOCYTOMA TUMOR OF ADRENAL MEDULLA SECRETES INCREASED AMOUNT OF CATECHOLAMINES A small tumor in the adrenal gland that secretes large amounts of epinephrine and norepinephrine. S/SX: HPN HYPERGLYCEMIA CARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC ACID
  • 196. VMA IN 24H URINE END PRODUCT OF CATECHOLAMINE METABOLISM DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST: COFFEE & TEA BANANA VANILLA CHOCOLATES
  • 197. PHEOCHROMOCYTOMA MANAGEMENT: SURGERY MEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE NURSING CARE: MONITOR BP IN SUPINE & STANDING MONITOR URINE FOR GLUCOSE & ACETONE
  • 198.
  • 199.
  • 201.
  • 203.
  • 205.
  • 206.
  • 208.
  • 212. QUESTION NO. 1 A 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 IV CHECK THE CLIENT’S URINE FOR THE PRESENCE OF SUGAR AND ACETONE ENCOURAGE THE CLIENT TO DRINK ORANGE JUICE W/ ADDED SUGAR
  • 213. QUESTION NO.2 WHAT IS THE PRIMARY ACTION OF INSULIN IN THE BODY? ENHANCES THE TRANSPORT OF GLUCOSE ACROSS THE CELL WALLS AIDS IN THE PROCESS OF GLUCONEOGENESIS STIMULATES THE PANCREATIC BETA CELLS DECREASE THE INTESTINAL ABSORPTION OF GLUCOSE
  • 214. QUESTION NO.3 POSTOPERATIVE THYROIDECTOMY NURSING CARE INCLUDES WHICH MEASURES? HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF HOARSENESS IS PRESENT PROVIDE LOW-CALCIUM DIET TO PREVENT HYPERCALCEMIA CHECK THE DRESSING AT THE BACK OF THE NECK FOR BLEEDING APPLY SOFT CERVICAL COLLAR TO RESTRICT MOVEMENT