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Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
Endocrine New Edition
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Endocrine New Edition

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  • Hi Shenell, I like your ppt on this very complex topic. It's quite detailed. Would you please send me a copy of it? Here's my email address:
    jsptuburan2013@yahoo.com
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  • Hi Shenell, I like you ppt about Endocrine. May I have a copy of this from you? Here's my email address, jsptuburan2013@yahoo.com
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  • It's wonderful presentation. May I please download? Thanks. My email elsolt05@rambler.ru
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  • 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. 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
  • 10.
  • 11. ENDOCRINE GLANDS
  • 12. ENDOCRINE GLANDS
  • 13.
  • 14.
  • 15. ENDOCRINE GLANDS
  • 16.
  • 17. ENDOCRINE GLANDS
  • 18.
  • 19. ENDOCRINE GLANDS
  • 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
  • 25. PITUITARY ANTERIOR LOBE
  • 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
  • 27. Growth Hormone Hypersecretion
    GIGANTISM
  • 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
  • 30. Hyperpituitarism:Clinical Manifestations
  • 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
  • 33. DWARFISM
  • 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
  • 35. Trans-sphenoidal hypophysectomy
  • 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
  • 45. THYROID DISORDERS
  • 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. 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 replacement
    • Myxedema– 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 therapy
    Levothyroxine(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 old
    Causes : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause
  • 64. Hyperthyroidism (cont.)
    DX: > elevated T3, T4 values
    T4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L
    • abnormal findings in the thyroid scan
    Goiter – enlargement of the thyroid gland
    • due to  stimulation of the thyroid gland by TSH
    Simple goiter – enlarged thyroid gland
    • due to iodine deficiency, intake of goitrogenic foods  cabbage, turnips, soybeans
    • 65. may be hereditary
  • Grave’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
  • 67.
  • 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 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. Assessment Findings: Thyroid storm
  • Med. Mgt.
    • Medications
    Propylthiouracil (PTU) – antithyroid drug
    - blocks thyroid hormone production
    - can cause agranulocytosis
    - monitor pt. CBC
    Methimazole (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 gums
    2.) 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 tissue
    • Surgical intervention (performed only when pt. is in a
    euthyroid 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 water
    provide adequate rest, avoid muscle fatigue
     stressors in the envt.— noise and lights
    relaxation techniques
    Provide adequate nutrients
     calorie,  protein, balanced diet (4,000-5,000 cal/day)
     fluid intake
    Restrict stimulants (tea, coffee, alcohol)
    small, frequent feedings if hypermotility is present
    Daily wt.
  • 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. 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 sutures
    • check 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 IV
    2. Hemorrhage
    • WOF: 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 swallowing
  • Post-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
  • 93.
  • 94.
  • 95. PARATHYROID GLAND DISORDERS
  • 96.
  • 97.
  • 98. 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
    Function of calcium:
    • maintains N muscle and neuromuscular responses.
    • 104. Necessary component for blood coagulation mechanisms
    Promotes 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. 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:
    • maintains N muscle and neuromuscular responses.
    • 110. Necessary component for blood coagulation mechanisms
    MUSCLE 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. 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:
    • 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. Types
    Insulin – 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 15
    Non 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
  • 131.
  • 132.
  • 133. P
    olyuria
    olydipsia
    olyphagia
    ruritus
    aresthesia
    oor healing
    oor eyesight
  • 134.
  • 135. DIAGNOSTIC TEST FOR DM
    Fasting Blood Sugar (FBS)
    • NPO for 12 hours
    • 136. Normal value= 80-120 mg/dl
    • 137. 140 mg/dl or more – diagnostic of DM
    Postprandial blood sugar
    • Blood is withdrawn 2 hrs. after a meal
    • 138. N value = < 120mg/dl
    • 139. 200 mg/dl or more is diagnostic of DM
  • 3. 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 glucose
  • Diagnostic Tests for DM
    4. Glycosylated hemoglobin
    • Provides 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 RBC
  • D-I-A-B-E-T-E-S
    D- DIET: 50-60% CHO, 20-30% FATS, 10-20% CHON
    I- INSULIN– TYPE 1
    A- ANTIDIABETIC AGENTS– TYPE 2
    B- BLOOD SUGAR MONITORING
    E- EXERCISE
    T- TRANSPLANT OF PANCREAS
    E- ENSURE ADEQUATE FOOD INTAKE
    S- SCRUPULOUS FOOT CARE
  • 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.
  • 147. Oral Antidiabetic Agents
  • 148. Oral Antidiabetic Agents
  • 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. 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 area
    avoid injecting cold insulin  lead to tissue reaction
    roll insulin vial to mix, do not shake, remove air bubbles from syringe
    press (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 sites
    • Failure 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 exercise
    Benefits of exercise :
    promotes use of CHO & enhances action of insulin
     blood glucose levels
     need for insulin
     the no. of functioning receptor sites for insulin
    • perform 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 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. Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC)
    can occur when the action of insulin is severely inhibited
    seen in pts. w/ NIDDM, elderly persons w/ NIDDM
    Precipitating factors:
    infection, renal failure, MI, CVA, GI hemorrhage, pancreatitis, CHF, TPN, surgery, dialysis, steroids
    S/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.
  • HHONK
    S/SX:
    S/SX OF DKA WITHOUT:
    KAUSMAUL’S BREATHING
    ACETONE BREATH
    METABOLIC ACIDOSIS
    KETONURIA
  • 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
  • 184. Addison’s disease
  • 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. RECAP:
    ANTERIOR PITUITARY:
    POSTERIOR PITUITARY:
    • DIABETES INSIPIDUS,
    • 202. SIADH
    LOCATION: BASE OF THE BRAIN
  • 203. RECAP
    ADRENAL GLAND:
    ADRENAL MEDULLA:
    • PHEOCHROMOCYTOMA
    LOCATION: ON TOP OF THE KIDNEY
  • 206. RECAP
    PANCREAS:
    • DM
    LOCATION: POSTERIOR TO LIVER
    PARATHYROID:
    • HYPORATHYROIDISM
    • 207. HYPERPARATHYROIDISM
    LOCATION: NEAR THYROID
  • 208. RECAP
    THYROID:
    LOCATION: ANTERIOR PART OF NECK
  • 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
  • 215. Any Questions???

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