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Endocrine Ppt

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Endocrine Ppt

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Endocrine Ppt

  1. 1. METABOLISM ENDOCRINE SYSTEM
  2. 2. ENDOCRINE GLANDS <ul><li>Development of mammary glands & lactation </li></ul>PROLACTIN/ LTH <ul><li>Growth of body tissues & bones </li></ul>GH/ SOMATOTROPIN <ul><li>Growth, maturation & function of sex organs </li></ul>FSH,LH <ul><li>Adrenal cortex to release hormones </li></ul>ACTH LOBE <ul><li>Thyroid to release hormones </li></ul>TSH <ul><li>PITUITARY </li></ul><ul><li>ANTERIOR </li></ul>FUNCTIONS HORMONES ENDOCRINE GLAND
  3. 3. ENDOCRINE GLANDS <ul><li>Affects skin pigmentation </li></ul>MSH <ul><li>INTERME- </li></ul><ul><li>DIATE LOBE </li></ul><ul><li>Stimulate uterine contractions </li></ul><ul><li>release of milk </li></ul>OXYTOCIN <ul><li>Regulates water metabolism </li></ul>ADH <ul><li>PITUITARY </li></ul><ul><li>POSTERIOR </li></ul><ul><li>LOBE </li></ul>FUNCTION HORMONE ENDOCRINE GLAND
  4. 4. ENDOCRINE GLANDS <ul><li>Slightly significant </li></ul>SEX HORMONES <ul><li>Glycogenolysis; </li></ul><ul><li>Gluconeogenesis </li></ul><ul><li>Na & water reabsorption </li></ul><ul><li>Antiinflammatory </li></ul><ul><li>Stress hormone </li></ul>CORTISOL <ul><li>Fluid & electrolyte balance; </li></ul><ul><li>Na reabsorption; </li></ul><ul><li>K excretion </li></ul>ALDOSTERONE ADRENAL CORTEX FUNCTION HORMONES ENDOCRINE GLAND
  5. 5. ENDOCRINE GLANDS <ul><li>Increase heart rate & BP </li></ul><ul><li>Bronchodilation, </li></ul><ul><li>Glycogenolysis </li></ul><ul><li>Stress hormone </li></ul>EPINEPHRINE NOR- EPINEPHRINE ADRENAL MEDULLA FUNCTION HORMONE ENDOCRINE GLAND
  6. 7. ENDOCRINE GLANDS <ul><li>Increase serum calcium by promoting bone decalcification </li></ul>PTH PARA- THYROID <ul><li>Decrease serum Ca by increasing bone deposition </li></ul>THYRO- CALCITONIN <ul><li>Regulate metabolic rate </li></ul><ul><li>P,C,F metabolism </li></ul><ul><li>Regulate physical & mental growth & development </li></ul>T3 & T4’ THYROID FUNCTION HORMONE ENDOCRINE GLAND
  7. 8. ENDOCRINE GLANDS <ul><li>Increase blood glucose by: </li></ul><ul><li>Gluconeogenesis </li></ul><ul><li>Glycogenolysis </li></ul>GLUCAGON <ul><li>ALPHA </li></ul><ul><li>CELLS </li></ul><ul><li>Decrease blood glucose by: </li></ul><ul><li>Glucose diffusion across cell membrane; </li></ul><ul><li>Converts glucose to glycogen </li></ul>INSULIN <ul><li>PANCREAS </li></ul><ul><li>BETA </li></ul><ul><li>CELLS </li></ul>FUNCTION HORMONE ENDOCRINE GLAND
  8. 9. ENDOCRINE GLANDS <ul><li>Development of secondary sex charac in male </li></ul><ul><li>Maturation of sex organs </li></ul><ul><li>Sexual functioning </li></ul>TESTOS- TERONE TESTES <ul><li>Development of secondary sex charac in female </li></ul><ul><li>Maturation of sex organs </li></ul><ul><li>Sexual functioning </li></ul><ul><li>Maintenance of pregnancy </li></ul>ESTROGEN & PROGES- TERONE OVARIES FUNCTION HORMONES ENDOCRINE GLAND
  9. 10. HORMONE REGULATION <ul><li>NEGATIVE FEEDBACK MECHANISM </li></ul><ul><li>CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE) </li></ul><ul><li>RHYTHMIC PATTERNS OF SECRETION </li></ul><ul><li>(e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES) </li></ul><ul><li>AUTONOMIC & C.N.S. CONTROL </li></ul><ul><li>(PITUITARY-HYPOTHALAMIC AXIS, </li></ul><ul><li>ADRENAL MEDULLA HORMONES) </li></ul>
  10. 11. NEGATIVE FEEDBACK MECHANISM <ul><li>DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine ) </li></ul><ul><li>PITUITARY GLAND </li></ul><ul><li>RELEASE OF STIMULATING HORMONE (e.g. TSH) </li></ul><ul><li>STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE </li></ul><ul><li>(e.g. Thyroid gland release of Thyroxine) </li></ul><ul><li>RETURN OF THE NORMAL CONCENTRATION OF HORMONE </li></ul>
  11. 12. NEGATIVE FEEDBACK MECHANISM <ul><li>INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine ) </li></ul><ul><li>PITUITARY GLAND IS INHIBITED TO </li></ul><ul><li>RELEASE STIMULATING HORMONE (e.g. TSH) </li></ul><ul><li>DECREASED PRODUCTION & SECRETION </li></ul><ul><li>OF TARGET ORGAN OF THE HORMONE </li></ul><ul><li>(e.g. Thyroid gland release of Thyroxine) </li></ul><ul><li>RETURN OF THE NORMAL CONCENTRATION OF HORMONE </li></ul>
  12. 13. CASE STUDY <ul><li>Katie, an elderly, came in because of palpitations. </li></ul><ul><li>VS revealed: 37.9 o , 120, 25, 140/ 90 </li></ul><ul><li>She expressed hyperactivty, sweating, increased appetite & weight loss </li></ul>
  13. 14. CASE STUDY <ul><li>She claimed history of goiter since her 30’s but no follow-up was done. </li></ul><ul><li>What are your nursing plans? </li></ul>
  14. 15. PLANNING <ul><li>HEALTH PROMOTION </li></ul><ul><ul><li>IODIZED SALT </li></ul></ul><ul><ul><li>CONTROLLING WEIGHT </li></ul></ul><ul><li>HEALTH MAINTENANCE & RESTORATION </li></ul><ul><ul><li>STEROID THERAPY </li></ul></ul>
  15. 16. STEROID THERAPY <ul><li>STEROID LEVELS </li></ul><ul><li>PITUITARY GLAND IS INHIBITED TO REALEASE ACTH </li></ul>ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA ADRENAL ATROPHY
  16. 17. STEROID THERAPY <ul><li>PHARMACOLOGIC CONSIDERATIONS: </li></ul><ul><li>PEPTIC ULCER IN SHORT TERM, HIGH DOSE STEROID TX </li></ul><ul><li>ADMINISTER DRUG: HIGHER DOSE IN THE MORNING, TAPERING TO LOWER ONES IN THE AFTERNOON </li></ul><ul><li>LAST DOSE @ MEAL TIME TO AVOID INSOMNIA </li></ul><ul><li>PALLIATIVE EFFECT </li></ul>
  17. 18. STEROID THERAPY <ul><li>ASSESSMENT: </li></ul><ul><li>BASELINE STEROID LEVEL IS ASSESSED BEFORE PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED </li></ul><ul><li>STEROID WITHDRAWAL (LOW STRESS TOLERANCE) </li></ul><ul><ul><li>EXHAUSTION </li></ul></ul><ul><ul><li>WEAKNESS </li></ul></ul><ul><ul><li>LETHARGY </li></ul></ul>
  18. 19. STEROID THERAPY <ul><li>ASSESSMENT: </li></ul><ul><li>ACUTE ADRENAL CRISIS </li></ul><ul><ul><li>RESTLESSNESS </li></ul></ul><ul><ul><li>WEAKNESS </li></ul></ul><ul><ul><li>HEADACHE </li></ul></ul><ul><ul><li>DHN </li></ul></ul><ul><ul><li>N/V </li></ul></ul><ul><ul><li>FALLING BP TO SHOCK </li></ul></ul><ul><li>PSYCHOLOGICAL CXS </li></ul><ul><ul><li>MOOD ELEVATION, </li></ul></ul><ul><ul><li>FRANK EUPHORIA </li></ul></ul><ul><ul><li>THEN, DEPRESSION </li></ul></ul>
  19. 20. STEROID THERAPY <ul><li>IMPORTANT FACTS: </li></ul><ul><li>MAJOR UNTOWARD EFFECTS: </li></ul><ul><ul><li>MASKS INFECTION </li></ul></ul><ul><ul><li>DEFENSE AGAINST INFECTION FROM LYMPHOPENIA </li></ul></ul><ul><ul><li>SLOW WOUND HEALING FROM ITS ANTIINFLAMMATORY EFFECT </li></ul></ul><ul><ul><li>P.U.D . ACTIVATION/ REACTIVATION </li></ul></ul><ul><ul><li>SERUM SODIUM </li></ul></ul><ul><ul><li>SERUM POTASSIUM </li></ul></ul>
  20. 21. STEROID THERAPY <ul><li>IMPORTANT FACTS: </li></ul><ul><li>MINOR UNTOWARD EFFECTS: </li></ul><ul><ul><li>PIGMENTATION </li></ul></ul><ul><ul><li>ACNE </li></ul></ul><ul><ul><li>FACIAL HAIR </li></ul></ul><ul><ul><li>MOON-FACIE </li></ul></ul>
  21. 22. STEROID THERAPY <ul><li>IMPORTANT FACTS: </li></ul><ul><li>PROBLEMS OF LONG TERM THERAPY: </li></ul><ul><ul><li>GROWTH RETARDATION </li></ul></ul><ul><ul><li>OBESITY </li></ul></ul><ul><ul><li>GASTRITIS TO P.U.D. </li></ul></ul><ul><ul><li>OSTEOPOROSIS </li></ul></ul><ul><ul><li>HPN </li></ul></ul><ul><ul><li>RENAL CALCULI </li></ul></ul><ul><ul><li>ADRENAL ATROPHY </li></ul></ul>
  22. 23. STEROID THERAPY <ul><li>STEROID LEVELS </li></ul><ul><li>PITUITARY GLAND IS INHIBITED TO REALEASE ACTH </li></ul>ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA ADRENAL ATROPHY
  23. 24. STEROID THERAPY <ul><li>IMPLEMENTATION </li></ul><ul><li>DECREASE Na IN THE DIET </li></ul><ul><li>CALORIC RESTRICTION </li></ul><ul><li>FOODS HIGH IN POTASSIUM </li></ul><ul><li>GIVE MEDS WITH ANTACIDS OR WITH FOOD </li></ul><ul><li>TEST STOOLS OR EMESIS FOR BLOOD </li></ul><ul><li>REPORT ANY EVIDENCE OF GI BLEEDING </li></ul><ul><li>LYMPHOPENIC PRECAUTION </li></ul>
  24. 25. ANTERIOR PITUITARY DISTURBANCES <ul><li>HYPOPITUITARISM </li></ul><ul><li>HYPERPITUITARISM </li></ul>
  25. 26. HYPOPITUITARISM ANTERIOR LOBE <ul><li>PANHYPOPITUITARISM </li></ul><ul><li>(SIMMOND’S DSE) </li></ul><ul><ul><li>DECREASED SECRETION OF ALL ANTERIOR LOBE HORMONES </li></ul></ul>
  26. 27. HYPERPITUITARISM ANTERIOR LOBE <ul><li>EOSINOPHILIC TUMOR </li></ul><ul><ul><li>INCREASED GROWTH HORMONE AND PROLACTIN </li></ul></ul><ul><li>BASOPHILIC TUMOR </li></ul><ul><ul><li>INCREASED TSH, FSH, LH, MSH, </li></ul></ul><ul><ul><li>INCREASED ACTH (CUSHING’S DSE) </li></ul></ul><ul><li>CHROMOPHOBE TUMOR </li></ul><ul><ul><li>INCREASED ACTH & GROWTH HORMONE </li></ul></ul>
  27. 28. PITUITARY ANTERIOR LOBE <ul><li>Decreased milk production </li></ul><ul><li>Underdevelopment of mammary glands </li></ul>PROLACTIN <ul><li>Exaggerated fxn of sex organs </li></ul><ul><li>Atrophy & infertility </li></ul>FSH <ul><li>Grave’s dse </li></ul><ul><li>Atrophy & depressed thyroid fxn </li></ul>TSH <ul><li>Cushing’s dse </li></ul><ul><li>Atrophy of adrenal cortex </li></ul>ACTH <ul><li>Gigantism – young </li></ul><ul><li>Acromegaly - adult </li></ul><ul><li>Dwarfism – young </li></ul><ul><li>Cachexia - adult </li></ul>GH HYPER FXN HYPO FXN HORMONE
  28. 29. MANAGEMENT <ul><li>HYPOPITUITARISM </li></ul><ul><ul><li>SURGICAL REMOVAL / IRRADIATION </li></ul></ul><ul><ul><li>REPLACEMENT THERAPY </li></ul></ul><ul><ul><ul><li>THYROID HORMONES </li></ul></ul></ul><ul><ul><ul><li>STEROIDS </li></ul></ul></ul><ul><ul><ul><li>SEX HORMONES </li></ul></ul></ul><ul><ul><ul><li>GONADOTROPINS (restore fertility) </li></ul></ul></ul><ul><li>HYPERPITUITARISM </li></ul><ul><ul><li>SURGICAL REMOVAL / IRRADIATION </li></ul></ul><ul><ul><li>MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS </li></ul></ul>
  29. 30. POSTERIOR PITUITARY DISTURBANCES <ul><li>DIABETES INSIPIDUS </li></ul><ul><li>SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE </li></ul>
  30. 31. DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN <ul><li>CAUSE: </li></ul><ul><li>TUMOR </li></ul><ul><li>TRAUMA </li></ul><ul><li>VASCULAR DSE </li></ul><ul><li>INFLAMMATION </li></ul><ul><li>PITUITARY SURGERY </li></ul><ul><li>S/SX: </li></ul><ul><li>POLYURIA </li></ul><ul><li>15-29L/ DAY </li></ul><ul><li>POLYDIPSIA </li></ul><ul><li>SG OF URINE IS </li></ul><ul><li><1.010 </li></ul><ul><li>S/SX OF DHN </li></ul><ul><li>SHOCK </li></ul>
  31. 32. DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN <ul><li>MANAGEMENT </li></ul><ul><li>HORMONAL REPLACEMENT – FOR LIFE </li></ul><ul><ul><li>VASOPRESSIN (PITRESSIN TANNATE IN OIL ) – IM OR NASAL SPRAY </li></ul></ul><ul><li>NON-HORMONAL THERAPY </li></ul><ul><ul><li>CHLORPROPRAMID E – INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN </li></ul></ul><ul><li>SALT & P RESTRICTED DIET, INCREASE FLUIDS </li></ul><ul><li>MONITOR I&O </li></ul><ul><li>MAINTAIN FLUID & ELECTROLYTE BALANCE </li></ul>
  32. 33. SYNDROME OF INAPPROPRIATE ADH <ul><li>ELEVATED ADH </li></ul><ul><li>CAUSES: </li></ul><ul><li>BRONCHOGENIC CA </li></ul><ul><li>NONENDOCRINE TUMORS </li></ul><ul><li>S/SX: </li></ul><ul><li>DECREASED SERUM SODIUM </li></ul><ul><ul><li>CX IN LOC TO UNCONSCIOUSNESS </li></ul></ul><ul><ul><li>SEIZURES </li></ul></ul><ul><li>WATER INTOXICATION </li></ul><ul><ul><li>N/V </li></ul></ul><ul><ul><li>MENTAL CONFUSION </li></ul></ul>
  33. 34. SYNDROME OF INAPPROPRIATE ADH <ul><li>MANAGEMENT: </li></ul><ul><li>WATER INTAKE RESTRICTION </li></ul><ul><li>ADMINISTER AS ORDERED : </li></ul><ul><ul><li>NaCl </li></ul></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><li>Demeclocycline (declamycin) – a tetracycline analogue that interferes with the action of ADH on the collecting tubules </li></ul></ul>
  34. 35. Mission possible
  35. 36. THYROID GLAND <ul><li>STIMULATED BY THYROID STIMULATING HORMONE (TSH) </li></ul><ul><li>NEEDS IODINE TO SYNTHESIZE HORMONE </li></ul><ul><li>SECRETES: </li></ul><ul><ul><li>THYROXINE (T4) </li></ul></ul><ul><ul><li>TRIIODOTHYRONINE (T3) </li></ul></ul>
  36. 37. THYROID DISTURBANCES <ul><li>DIAGNOSTIC TESTS : </li></ul><ul><li>B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN TIME </li></ul><ul><li>PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITH THYROID DAMAGE </li></ul><ul><li>SERUM THYROXINE (T4), SERUM TRIIODOTHYRONINE (T3), SERUM TSH </li></ul><ul><li>BLOOD SERUM CHOLESTEROL </li></ul><ul><li>RADIOACTIVE IODINE TESTS: </li></ul><ul><ul><li>T3 RED CELL UPTAKE </li></ul></ul><ul><ul><li>RADIOACTIVE IODINE UPTAKE (I131 </li></ul></ul><ul><ul><li>THYROID SCAN </li></ul></ul>
  37. 38. THYROID DISTURBANCES GRAVE’S DSE or Exophthalmic goiter <ul><li>CRETINISM- infants, young children </li></ul><ul><li>HYPOTHYROIDISM WITHOUT MYXEDEMA - atrophy/ destruction of thyroid gland </li></ul><ul><li>MYXEDEMA –adults </li></ul>HYPERTHYROIDISM HYPOTHYROIDISM
  38. 39. EFFECTS <ul><li>Increase heat </li></ul><ul><li>Deranged C metabolism, glycosuria </li></ul><ul><li>Increase use of F & P as fuel </li></ul><ul><li>Reduction in HEAT PRODUCTION </li></ul><ul><li>Failure of MENTAL & PHYSICAL GROWTH </li></ul><ul><li>increased storage of C, P & F </li></ul><ul><li>Abnormal collection of WATER </li></ul>HYPERTHYROIDISM HYPOTHYROIDISM
  39. 40. <ul><li>DECREASED </li></ul><ul><li>INCREASED </li></ul><ul><li>WARM, MOIST, FLUSHED </li></ul><ul><li>SOFT, SILKY </li></ul><ul><li>SERUM </li></ul><ul><li>CHOLESTEROL: </li></ul><ul><li>INCREASED </li></ul><ul><li>BMR: </li></ul><ul><li>DECREASED </li></ul><ul><li>SKIN: </li></ul><ul><li>THICK, PUFFY, DRY </li></ul><ul><li>HAIR: </li></ul><ul><li>DRY, BRITTLE </li></ul>HYPERTHYROIDISM HYPOTHYROIDISM
  40. 41. <ul><li>HYPERACTIVE </li></ul><ul><li>LABILE MOOD </li></ul><ul><li>HYPERSENSITIVE </li></ul><ul><li>TENSED </li></ul><ul><li>DECREASED </li></ul><ul><li>INCREASED </li></ul><ul><li>NERVOUS SYSTEM: </li></ul><ul><li>APATHETIC </li></ul><ul><li>LETHARGIC </li></ul><ul><li>MAYBE HYPERIRRITABLE </li></ul><ul><li>SLOW CEREBRATION </li></ul><ul><li>WEIGHT: </li></ul><ul><li>INCREASED </li></ul><ul><li>APPETITE: </li></ul><ul><li>DECREASED </li></ul>HYPERTHYROIDISM HYPOTHYROIDISM
  41. 42. MANAGEMENT <ul><li>MEDICAL: </li></ul><ul><li>REST </li></ul><ul><li>ANTITHYROID DRUGS: </li></ul><ul><li>LUGOL’S SOLUTION </li></ul><ul><li>THIOUREA DERIVATIVES </li></ul><ul><li>RADIOACTIVE IODINE </li></ul><ul><li>BETA-BLOCKERS </li></ul><ul><li>SURGICAL: </li></ul><ul><li>SUBTOTAL THYROIDECTOMY </li></ul><ul><li>MEDICAL: </li></ul><ul><li>HORMONE REPLACEMENT </li></ul><ul><li>DESSICATED THYROID </li></ul><ul><li>THYROGLOBULIN </li></ul><ul><li>Na LEVOTHYROXINE </li></ul><ul><li>Na LYOTHYRONINE </li></ul>HYPERTHYROIDISM HYPOTHYROIDISM
  42. 43. ANTITHYROID MEDICATIONS <ul><li>LUGOL’S SOLUTION </li></ul><ul><li>(POTASSIUM IODIDE) </li></ul><ul><ul><li>DECREASE THYROID VASCULARITY </li></ul></ul><ul><ul><li>INHIBIT IODINE RELEASE </li></ul></ul><ul><ul><li>DILUTED IN MILK / JUICE </li></ul></ul><ul><ul><li>STAINS THE TEETH- USE STRAW </li></ul></ul><ul><li>THIOUREA & DERIVATIVES </li></ul><ul><ul><li>(PTU,METHIMAZOLE) </li></ul></ul><ul><ul><li>BLOCK THYROID HORMONE RELEASE </li></ul></ul><ul><ul><li>TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA </li></ul></ul><ul><li>RADIOACTIVE IODINE </li></ul><ul><ul><li>PATIENT IS ISOLATED FOR 3 DAYS </li></ul></ul><ul><li>BETA BLOCKERS </li></ul><ul><ul><li>PROPANOLOL </li></ul></ul>
  43. 44. SUBTOTAL THYROIDECTOMY <ul><li>REMAINING TISSUE PROVIDES ENOUGH HORMONES FOR NORMAL FXN </li></ul><ul><li>PRE OP NURSING CARE: </li></ul><ul><li>PATIENT EDUCATION ON POST OP: </li></ul><ul><ul><li>LITTLE HOARSENESS </li></ul></ul><ul><ul><li>DIFFICULTY OF SWALLOWING </li></ul></ul><ul><li>POST OP NURSING CARE: </li></ul><ul><li>SEMIFOWLER’S </li></ul><ul><li>AVOID HYPEREXTENSION OF THE NECK </li></ul><ul><li>BE ASKED TO SPEAK @ 40 MIN INTERVAL – ASSESS RECURRENT NERVE INJURY </li></ul><ul><li>WATCH OUT FOR COMPLICATIONS. </li></ul>
  44. 45. SUBTOTAL THYROIDECTOMY <ul><li>COMPLICATIONS: </li></ul><ul><li>RECURRENT LARYNGEAL NERVE INJURY </li></ul><ul><ul><li>HOARSENESS </li></ul></ul><ul><li>HEMORRHAGE </li></ul><ul><ul><li>12-24 HRS POST OP </li></ul></ul><ul><ul><li>OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS </li></ul></ul><ul><ul><li>TRACHEOSTOMY SET @ BEDSIDE </li></ul></ul><ul><li>TETANY </li></ul><ul><li>RESPIRATORY OBSTRUCTION </li></ul><ul><li>THYROID STORM </li></ul>
  45. 46. TETANY <ul><li>DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVED </li></ul><ul><li>S/SX: </li></ul><ul><li>1 ST – TINGLING TOES & FINGERS </li></ul><ul><li>2 ND – CHEVOSTEK’S SIGN (TAPPING THE FACIAL MUSCLES) </li></ul><ul><li>3 RD – TROUSSEAU’S SIGN (CARPO-PEDAL SPASM WITH OCCLUSION OF CIRCULATION WITH A BP CUFF) </li></ul><ul><li>MANAGEMENT: </li></ul><ul><li>CALCIUM REPLACEMENT: CaGluconate IV </li></ul>
  46. 47. THYROID STORM / CRISIS <ul><li>S/SX: </li></ul><ul><li>HYPERTHERMIA </li></ul><ul><li>> 41C </li></ul><ul><li>TACHYCARDIA </li></ul><ul><li>APPREHENSION </li></ul><ul><li>RESTLESSNESS </li></ul><ul><li>IRRITABILITY </li></ul><ul><li>DELIRIUM </li></ul><ul><li>COMA </li></ul><ul><li>MANAGEMENT: </li></ul><ul><li>DECREASE TEMP </li></ul><ul><li>ANTITHYROID DRUGS </li></ul><ul><li>GLUCOSE </li></ul><ul><li>DIGITALIS </li></ul><ul><li>STEROIDS TO DECREASE ACTH </li></ul>
  47. 48. THYROID STORM / CRISIS <ul><li>INCREASED AMOUNT OF THYROID HORMONES </li></ul><ul><li>POST OP </li></ul><ul><li>AFTER RADIOACTIVE IODINE ADMINISTRATION </li></ul><ul><li>TOO SHORT PERIOD OF PRE OP TX </li></ul><ul><li>CAUSES: </li></ul><ul><li>EMOTIONAL STRESS </li></ul><ul><li>PHYSICAL STRESS </li></ul>
  48. 49. VARIANTS OF HYPERTHYROIDISM <ul><li>GRAVE’S DSE </li></ul><ul><li>THYROIDITIS </li></ul><ul><li>GOITER </li></ul>
  49. 50. GRAVE’S DISEASE <ul><li>CAUSE: </li></ul><ul><li>UNKNOWN </li></ul><ul><li>AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR </li></ul><ul><li>S/SX: TRIAD OF SYMPTOMS: </li></ul><ul><li>HYPERTHYROIDISM </li></ul><ul><li>OPHTHALMOPATHY </li></ul><ul><li>DERMOPATHY </li></ul>
  50. 51. OPHTHALMOPATHY <ul><li>EXOPHTHALMOS – ACCUMULATION OF FLUID IN THE FAT PADS BEHIND HE EYEBAL </li></ul><ul><li>LID LAG – PROMINENT PALPEBRAL FISSURE WHEN THE PATIENT LOOKS DOWN </li></ul><ul><li>THYROID STARE </li></ul><ul><li>(DARYMPLE’S SIGN) – INFREQUENT EYE BLINKING </li></ul>
  51. 52. DERMOPATHY <ul><li>PRETIBIAL MYXEDEMA </li></ul><ul><li>@ THE DORSUM OF THE LEG </li></ul><ul><li>RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN </li></ul><ul><li>CLUBBING OF FINGERS & TOES </li></ul><ul><li>OSTEOARTHROPATHY </li></ul>
  52. 53. THYROIDITIS <ul><li>CLASSIFICATION: </li></ul><ul><li>SUBACUTE, NONSUPPURATIVE </li></ul><ul><ul><li>UNKNOWN CAUSE </li></ul></ul><ul><ul><li>ASSOC. WITH VIRAL URT INFECTIONS </li></ul></ul><ul><li>CHRONIC, HASHIMOTO’S </li></ul><ul><ul><li>IMMUNOLOGICAL FACTORS </li></ul></ul><ul><ul><li>PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID </li></ul></ul>
  53. 54. GOITER <ul><li>ENLARGEMENT OF THE THYROID GLAND. </li></ul><ul><li>TYPES: </li></ul><ul><li>TOXIC NODULAR </li></ul><ul><li>NONTOXIC </li></ul>
  54. 55. TOXIC NODULAR GOITER <ul><li>COMMON IN ELDERLY </li></ul><ul><li>FROM LONG STANDING SIMPLE GOITER </li></ul><ul><li>NODULES </li></ul><ul><ul><li>FUNCTIONING TISSUE </li></ul></ul><ul><ul><li>SECRETES THYROXINE AUTONOMOUSLY FROM TSH </li></ul></ul>
  55. 56. NON-TOXIC GOITER <ul><li>(SIMPLE/ COLLOID/ EUTHYROID) </li></ul><ul><li>CAUSE : </li></ul><ul><li>IODINE DEFICIENCY </li></ul><ul><li>INTAKE OF GOITROGENIC SUBSTANCES/ DRUGS: </li></ul><ul><ul><li>CASSAVA, </li></ul></ul><ul><ul><li>CABBAGE, </li></ul></ul><ul><ul><li>CAULIFLOWER, </li></ul></ul><ul><ul><li>CARROTS </li></ul></ul><ul><ul><li>RADDISH </li></ul></ul><ul><ul><li>TURNIPS </li></ul></ul><ul><ul><li>RED SKIN OF PEANUTS </li></ul></ul><ul><ul><li>IODINE </li></ul></ul><ul><ul><li>COBALT </li></ul></ul><ul><ul><li>LITHIUM </li></ul></ul>
  56. 57. NON-TOXIC GOITER <ul><li>IMPAIRED THYROID HORMONE SYNTHESIS </li></ul><ul><li>SERUM THYROXINE </li></ul><ul><li>PITUITARY SECRETE TSH </li></ul><ul><li>THYROID GLAND ENLARGES </li></ul><ul><li>TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE </li></ul>IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCES
  57. 58. NON-TOXIC GOITER <ul><li>COMMON IN WOMEN: </li></ul><ul><li>ADOLESCENT </li></ul><ul><li>PREGNANT </li></ul><ul><li>LACTATING </li></ul><ul><li>MENOPAUSE </li></ul><ul><li>TREATMENT: </li></ul><ul><li>IODIZED OIL IM </li></ul><ul><li>IODINE TABLETS </li></ul><ul><li>SALT FORTIFICATION WITH IODINE </li></ul><ul><li>EDUCATE ABOUT INTAKE OF : </li></ul><ul><ul><li>SEAWEEDS </li></ul></ul><ul><ul><li>SHELLFISH </li></ul></ul><ul><ul><li>FISH- TAMBAN, HITO, DALAG </li></ul></ul>
  58. 59. MYXEDEMA COMA <ul><li>MEDICAL EMERGENCY </li></ul><ul><li>OCCURS IN SEVERE & UNTREATED MYXEDEMA </li></ul><ul><li>HIGH MORTALTY RATE </li></ul><ul><li>S/SX: </li></ul><ul><li>INTENSIFIED HYPOTHYROIDISM </li></ul><ul><li>NEUROLOGIC IMPAIRMENT COMA </li></ul>
  59. 60. MYXEDEMA COMA <ul><li>PRECIPITATING FACTORS: </li></ul><ul><li>FAILURE TO TAKE MEDS </li></ul><ul><li>INFECTION </li></ul><ul><li>TRAUMA </li></ul><ul><li>EXPOSURE TO COLD </li></ul><ul><li>USE OF SEDATIVES, NARCOTICS, ANESTHETICS </li></ul>
  60. 61. MYXEDEMA COMA <ul><li>MANAGEMENT: </li></ul><ul><li>IV THYROID HORMONES </li></ul><ul><li>CORRECTION OF HYPOTHERMIA </li></ul><ul><li>MAINTAIN VITAL FXNS </li></ul><ul><li>TREAT PRECIPITATING CAUSES </li></ul>
  61. 63. PARATHYROID GLAND <ul><li>4 GLANDS </li></ul><ul><li>SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph LEVELS </li></ul><ul><li>REGULATE CALCIUM & PHOSPHORUS METABOLISM </li></ul><ul><li>ORGANS AFFECTED: </li></ul><ul><li>BONES - RESORPTION </li></ul><ul><li>KIDNEYS </li></ul><ul><ul><li>Ca REABSORPTION </li></ul></ul><ul><ul><li>Ph EXCRETION </li></ul></ul><ul><li>GIT – ENHANCES Ca ABSORPTION </li></ul>
  62. 64. PARATHYROID DISORDERS <ul><li>DIAGNOSTIC TESTS: </li></ul><ul><li>HEMATOLOGICAL </li></ul><ul><ul><li>SERUM CALCIUM </li></ul></ul><ul><ul><li>SERUM PHOSPHORUS </li></ul></ul><ul><ul><li>SERUM ALKALINE PHOSPHATASE </li></ul></ul><ul><li>URINARY STUDIES </li></ul><ul><ul><li>URINARY CALCIUM </li></ul></ul><ul><ul><li>URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE </li></ul></ul>
  63. 65. HYPOPARATHYROIDISM <ul><li>DECREASED PTH PRODUCTION </li></ul><ul><li>HYPOCALCEMIA </li></ul><ul><li>CALCIUM IS: </li></ul><ul><ul><li>DEPOSITED IN THE BONE </li></ul></ul><ul><ul><li>EXCRETED </li></ul></ul><ul><li>CAUSE: </li></ul><ul><li>HEREDITARY </li></ul><ul><li>IDIOPATHIC </li></ul><ul><li>SURGICAL </li></ul>
  64. 66. HYPOPARATHYROIDISM <ul><li>S/SX: </li></ul><ul><li>ACUTE HYPOCALCEMIA </li></ul><ul><ul><li>TINGLING OF THE FINGERS </li></ul></ul><ul><ul><li>CHEVOSTEK’S, TROUSSEAU’S </li></ul></ul><ul><li>CHRONIC HYPOCALCEMIA </li></ul><ul><ul><li>FATIGUE, WEAKNESS </li></ul></ul><ul><ul><li>PERSONALITY CHANGES </li></ul></ul><ul><ul><li>LOSS OF TOOTH ENAMEL, DRY SCALY SKIN </li></ul></ul><ul><ul><li>CARDIAC ARRHYTHMIA </li></ul></ul><ul><ul><li>CATARACT </li></ul></ul>
  65. 67. HYPOPARATHYROIDISM <ul><li>XRAY: INCREASED BONE DENSITY </li></ul><ul><li>MANAGEMENT: </li></ul><ul><li>Ca SUPPLEMENT </li></ul><ul><li>VIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK, pc </li></ul><ul><li>SEIZURE prec </li></ul><ul><li>LISTEN FOR STRIDOR OR HOARSENESS </li></ul><ul><li>TRACHEOSTOMY SET @ BEDSIDE </li></ul><ul><li>CaGLUCONATE @ BEDSIDE </li></ul>
  66. 68. HYPERPARATHYROIDISM <ul><li>INCREASED PTH PRODUCTION </li></ul><ul><li>HYPERCALCEMIA </li></ul><ul><li>HYPOPHOSPHATEMIA </li></ul><ul><li>PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND </li></ul><ul><li>SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM: </li></ul><ul><ul><li>CHRONIC RENAL DSE </li></ul></ul><ul><ul><li>RICKETS </li></ul></ul><ul><ul><li>MALABSORPTION SYNDROME </li></ul></ul><ul><ul><li>OSTEOMALACIA </li></ul></ul>
  67. 69. HYPERPARATHYROIDISM <ul><li>S/SX: </li></ul><ul><li>BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRUCTURES </li></ul><ul><li>TUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIA </li></ul><ul><li>MUSCLE WEAKNESS </li></ul><ul><li>PERSONALITY CX, DEPRESSION </li></ul><ul><li>CARDIAC ARRHYTHMIAS, HPN </li></ul><ul><li>XRAY: BONE DEMINERALIZATION </li></ul>
  68. 70. HYPERPARATHYROIDISM <ul><li>MANAGEMENT: </li></ul><ul><li>TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE </li></ul><ul><li>IV PNSS 5L/ DAY WITH DIURETICS </li></ul><ul><li>CRANBERRY JUICE (ACID-ASH) </li></ul><ul><li>LOW Ca, HIGH Ph DIET </li></ul><ul><li>NO MILK, CAULIFLOWER & MOLASSES </li></ul><ul><li>STRAIN URINE FOR STONES </li></ul><ul><li>CARE FOR PARATHYROIDECTOMY </li></ul>
  69. 71. ADRENAL GLAND <ul><li>STIMULATED BY ACTH </li></ul><ul><li>HORMONE PRECURSOR: </li></ul><ul><ul><li>CHOLESTEROL </li></ul></ul><ul><li>SECRETES: </li></ul><ul><ul><li>CORTISOL </li></ul></ul><ul><ul><li>ALDOSTERONE </li></ul></ul><ul><ul><li>SEX HORMONES : ANDROGEN, ESTROGEN </li></ul></ul>
  70. 72. ADRENAL GLAND <ul><li>Physiologically insignificant </li></ul><ul><li>Becomes useful during menopause in women </li></ul>SEX HORMONE <ul><li>increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS </li></ul><ul><li>Blocks inflammation </li></ul><ul><li>Counteracts effect of histamine </li></ul>GLUCO- CORTICOIDS <ul><li>Renal : Na & Cl reabsorption; K excretion </li></ul><ul><li>GI : Na absorption </li></ul>ALDOSTERONE FUNCTION HORMONE
  71. 73. SYMPTOMATOLOGY <ul><li>ALDOSTERONE DEFICIENCY </li></ul><ul><li>DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON </li></ul><ul><li>HYPOTENSION TO SHOCK </li></ul><ul><li>INCREASED K </li></ul><ul><li>METABOLIC ACIDOSIS </li></ul>
  72. 74. SYMPTOMATOLOGY <ul><li>CORTISOL DEFICIENCY </li></ul><ul><li>ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY </li></ul><ul><li>HYPOGLYCEMIA </li></ul><ul><li>HYPOTENSION </li></ul><ul><li>INCREASED K, WEAK PULSE </li></ul><ul><li>PIGMENTATION </li></ul><ul><li>IMPAIRED STRESS TOLERANCE </li></ul>
  73. 75. SYMPTOMATOLOGY <ul><li>SEX HORMONE DEFICIENCY </li></ul><ul><li>LOSS OF BODY HAIR </li></ul><ul><li>LOSS OF LIBIDO OR IMPOTENCE </li></ul><ul><li>MENSTRUAL & FERTILITY DISORDER </li></ul>
  74. 76. ADRENAL CORTEX DISORERS <ul><li>ADRENAL INSUFFICIENCY </li></ul><ul><li>ADRENAL CRISIS </li></ul><ul><li>CUSHING’S SYNDROME </li></ul><ul><li>ALDOSTERONISM </li></ul>
  75. 77. ADRENAL INSUFFICIENCY ADDISON’S DISEASE <ul><li>INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS </li></ul>
  76. 78. ADRENAL CRISIS <ul><li>ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES </li></ul><ul><li>POSSIBLE COMPLICATION OF ADDISON’S DISEASE </li></ul>
  77. 79. ADRENAL CRISIS <ul><li>PRECIPITATING CAUSES: </li></ul><ul><li>ABDOMINAL DISCOMFORT </li></ul><ul><li>INFECTION </li></ul><ul><li>TRAUMA </li></ul><ul><li>HIGH TEMP </li></ul><ul><li>EMOTIONAL UPSET </li></ul><ul><li>ANTICOAGULANT DRUGS </li></ul>
  78. 80. ADRENAL CRISIS <ul><li>S/SX: </li></ul><ul><li>HYPOTENSION </li></ul><ul><li>FLUID LOSS </li></ul><ul><li>HYPONATREMIA </li></ul>
  79. 81. ADRENAL CRISIS <ul><li>LAB: </li></ul><ul><li>SERUM ELEC: DECREASED Na </li></ul><ul><li> INCREASED K </li></ul><ul><li>S. BUN : </li></ul><ul><li>S. GLUCOSE: </li></ul><ul><li>ADRENAL HORMONE ASSAY : HYDROXYCORTICOID & 17 KETOSTEROID IN 24-HR URINE DET . </li></ul>
  80. 82. ADRENAL CRISIS <ul><li>GOALS OF CARE: </li></ul><ul><li>TO REVERSE SHOCK </li></ul><ul><li>RESTORE BLOOD CIRCULATION </li></ul><ul><li>REPLENISH NEEDED STEROID </li></ul>
  81. 83. ADRENAL CRISIS <ul><li>TREATMENT: </li></ul><ul><li>D5NSS </li></ul><ul><li>ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE </li></ul><ul><li>NEOSYNEPHRINE - SHOCK </li></ul><ul><li>HIGH SALT DIET </li></ul><ul><li>ANTIBIOTICS </li></ul>
  82. 84. CUSHING’S SYNDROME <ul><li>CAUSE: </li></ul><ul><li>SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM </li></ul><ul><li> ACTH BY PITUITARY TUMOR </li></ul><ul><li>EXCESSIVE GLUCORTICOID ADMINISTRATION </li></ul>
  83. 85. CUSHING’S SYNDROME <ul><li>S/SX: </li></ul><ul><li>TRUNCAL OBESITY </li></ul><ul><li>BUFFALO HUMP </li></ul><ul><li>MOON-FACIE </li></ul><ul><li>WT GAIN </li></ul><ul><li>SODIUM RETENTION </li></ul><ul><li>THINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM </li></ul>
  84. 86. CUSHING’S SYNDROME <ul><li>PURPLE STRIAE – FROM THINNING OF SKIN </li></ul><ul><li>ECHYMOSIS FROM SLIGHT TRAUMA </li></ul><ul><li>ANDROGENIC EFFECTS: </li></ul><ul><li>OLIGOMENORRHEA </li></ul><ul><li>HIRSUTISM </li></ul><ul><li>GYNECOMASTIA </li></ul><ul><li>HYPERTENSION FROM S. Na </li></ul>
  85. 87. CUSHING’S SYNDROME <ul><li>TREATMENT & NURSING CARE: </li></ul><ul><li>PSYCHOLOGICAL SUPPORT </li></ul><ul><li>PREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED </li></ul><ul><li>PROMOTE SAFETY </li></ul><ul><li>SURGERY – SUB/TOTAL ADRENALECTOMY </li></ul>
  86. 88. ALDOSTERONISM <ul><li>HYPERSECRETION OF ALDOSTERONE </li></ul><ul><li>PRIMARY – CONN’S SYNDROME </li></ul><ul><li>SECONDARY </li></ul>
  87. 89. CONN’S SYNDROME <ul><li>PRIMARY ALDOSTERONISM </li></ul><ul><li>CAUSE: </li></ul><ul><li>ADRENAL ADENOMA </li></ul><ul><li>S/SX: </li></ul><ul><li>HYPOKALEMIA </li></ul><ul><li>FATIGUE </li></ul><ul><li>HYPERNATREMIA, HPN, TETANY </li></ul><ul><li>MANAGEMENT : </li></ul><ul><li>SURGERY </li></ul><ul><li>ALDACTONE – ALDOSTERONE ANTAGONIST </li></ul>
  88. 90. SECONDARY ALDOSTERONISM <ul><li>THE PROBLEM IS OUTSIDE THE ADRENAL GLAND: </li></ul><ul><li>e.g. RENIN – ANGIOTENSIN SYSTEM </li></ul>
  89. 91. ADRENAL MEDULLA <ul><li>HORMONES : EPINEPHRINE </li></ul><ul><li>NOREPINEPHRINE </li></ul><ul><li>EFFECTS </li></ul>
  90. 92. PHEOCHROMOCYTOMA <ul><li>TUMOR OF ADRENAL MEDULLA </li></ul><ul><li>SECRETES INCREASED AMOUNT OF CATECHOLAMINES </li></ul><ul><li>S/SX: </li></ul><ul><li>HPN </li></ul><ul><li>HYPERGLYCEMIA </li></ul><ul><li>CARDIAC ARRHYTHMIA & CHF </li></ul><ul><li>DIAGNOSTIC TEST : </li></ul><ul><li>VMA IN 24H URINE </li></ul>
  91. 93. VMA IN 24H URINE <ul><li>END PRODUCT OF CATECHOLAMINE METABOLISM </li></ul><ul><li>DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST: </li></ul><ul><ul><li>COFFEE & TEA </li></ul></ul><ul><ul><li>BANANA </li></ul></ul><ul><ul><li>VANILLA </li></ul></ul><ul><ul><li>CHOCOLATES </li></ul></ul>
  92. 94. PHEOCHROMOCYTOMA <ul><li>MANAGEMENT: </li></ul><ul><li>SURGERY </li></ul><ul><li>MEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE </li></ul><ul><li>NURSING CARE: </li></ul><ul><li>MONITOR BP IN SUPINE & STANDING </li></ul><ul><li>MONITOR URINE FOR GLUC & ACETONE </li></ul>
  93. 95. PANCREAS <ul><li>HORMONES: </li></ul><ul><li>INSULIN BY BETA CELLS </li></ul><ul><li>GLUCAGON BY ALPHA CELLS </li></ul>
  94. 96. DIABETES MILLETUS <ul><li>CAUSE: </li></ul><ul><li>INSUFFICIENCY OF INSULIN </li></ul><ul><li>LACK OF INSULIN </li></ul><ul><li>EFFECT: </li></ul><ul><li>HYPERGLYCEMIA </li></ul>
  95. 97. DIABETES MILLETUS PATHOPHYSIOLOGY REDUCED /NO INSULIN HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS OSMOTIC DEHYDRATION
  96. 98. DIABETES MILLETUS <ul><li>S/SX: </li></ul><ul><li>3 – P’s </li></ul><ul><li>WEIGHT LOSS </li></ul><ul><li>STAGES: </li></ul><ul><li>PREDIABETES </li></ul><ul><li>SUSPECTED </li></ul><ul><li>CHEMICAL </li></ul><ul><li>CLINICAL / OVERT </li></ul>
  97. 99. DIABETES MILLETUS <ul><li>PREDIABETES / POTENTIAL: </li></ul>CONCEPTION EVIDENCE OF GLUCOSE METABOLISM ALTERATION
  98. 100. DIABETES MILLETUS <ul><li>SUSPECTED/ SUBCLINICAL/ LATENT: </li></ul>PREDIABETES NO STRESS STRESS NORMAL GLUCOSE METABOLISM OVERT DIABETES
  99. 101. DIABETES MILLETUS <ul><li>CHEMEICAL: </li></ul>SUBCLINICAL GTT IS ABNORMAL NO STRESS STRESS ASYMPTOMATIC SYMPTOMATIC
  100. 102. DIABETES MILLETUS <ul><li>CLINICAL / OVERT: </li></ul>CHEMICAL PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS SYMPTOMATIC
  101. 103. DIABETES MILLETUS <ul><li>TYPES: </li></ul><ul><li>TYPE I </li></ul><ul><ul><li>JUVENILE ONSET </li></ul></ul><ul><ul><li>BEFORE 15 YO </li></ul></ul><ul><ul><li>LEAN/ NORMAL WEIGHT </li></ul></ul><ul><ul><li>ABSOLUTE INSULIN DEFICIENCY </li></ul></ul><ul><ul><li>INSULIN -DEPENDENT </li></ul></ul><ul><ul><li>PRONE TO DKA </li></ul></ul><ul><li>TYPE II – </li></ul><ul><ul><li>MATURITY ONSET </li></ul></ul><ul><ul><li>AFTER AGE 40 </li></ul></ul><ul><ul><li>OBESE </li></ul></ul><ul><ul><li>REDUCED INSULIN RECEPTOR </li></ul></ul><ul><ul><li>NONINSULIN DEPENDENT </li></ul></ul><ul><ul><li>PRONE TO HHONK </li></ul></ul>
  102. 104. DIABETES MILLETUS <ul><li>DIAGNOSTIC EXAMS: </li></ul><ul><li>FBS </li></ul><ul><li>2 HR- POSTPRANDIAL </li></ul><ul><li>OGTT </li></ul><ul><li>GLYCOSYLATED HGB </li></ul><ul><li>DEXTROSTRIP </li></ul><ul><li>URINE TESTS: </li></ul><ul><ul><li>BENEDICT’S </li></ul></ul><ul><ul><li>CLINITEST TAB </li></ul></ul><ul><ul><li>ACETONE TEST </li></ul></ul>
  103. 105. 2 HR POSTPRANDIAL BLOOD SUGAR <ul><li>INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST </li></ul><ul><li>TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD </li></ul>
  104. 106. OGTT <ul><li>CONFIRMATORY, WHEN OTHER BLOOD TESTS ARE BORDERLINE </li></ul><ul><li>3 DAYS OF NORMAL ACITIVITY & 150MG OF CARB DIET </li></ul><ul><li>NPO 10-12HRS BEFORE THE TEST </li></ul><ul><li>BASELINE BLOOD SUGAR TAKEN </li></ul><ul><li>GLUCOSE LOAD IS GIVEN, P.O. OR IV </li></ul><ul><li>BLOOD & URINE SPECS TAKEN 30 MIN, 1HR, 2HRS, 3 HRS, AFTER GLUCOSE LOADING </li></ul>
  105. 107. GLYCOSYLATED HEMOGLOBIN <ul><li>MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS </li></ul><ul><li>USEFUL TO CHECK: </li></ul><ul><ul><li>COMPLIANCE WITH THERAPY </li></ul></ul><ul><ul><li>HISTORY OF SUBCLINICAL OR CHEMICAL DIABETES </li></ul></ul>
  106. 108. DIABETES MILLETUS <ul><li>PLANNING & IMPLEMENTATION: </li></ul><ul><li>CLIENT’S ACTIVITY </li></ul><ul><li>DIET : C,F,P – 50, 30, 20 LOW SATURATED FATS, HIGH FIBER </li></ul><ul><li>DRUGS: </li></ul><ul><ul><li>ORAL HYPOGLYCEMICS </li></ul></ul><ul><ul><ul><li>BIGUANIDE </li></ul></ul></ul><ul><ul><ul><li>SULFONYLUREAS </li></ul></ul></ul><ul><ul><ul><li>CONTRAINDICATED - PREGNANCY </li></ul></ul></ul><ul><ul><li>INSULIN </li></ul></ul>
  107. 109. DIABETES MILLETUS <ul><li>INSULIN THERAPY </li></ul><ul><li>DISPENSED IN “U”/ml : eg 100, 80 </li></ul><ul><li>REFRIGERATE </li></ul><ul><li>GIVEN @ ROOM TEMP </li></ul><ul><li>GENTLY ROTATED, NOT SHAKEN </li></ul><ul><li>ROUTE : SQ (MTC); IM OR IV </li></ul><ul><li>SYRINGE: 5/8 INCH ; SAME BRAND </li></ul>
  108. 110. DIABETES MILLETUS <ul><li>INSULIN THERAPY: </li></ul><ul><li>SITE OF INJECTION: </li></ul><ul><ul><li>ABDOMEN </li></ul></ul><ul><ul><li>ANTERIOR THIGH </li></ul></ul><ul><ul><li>ARM </li></ul></ul><ul><ul><li>UPPER BACK </li></ul></ul><ul><ul><li>BUTTOCKS </li></ul></ul>
  109. 111. DIABETES MILLETUS <ul><li>INSULIN THERAPY REACTIONS: </li></ul><ul><li>LOCAL: </li></ul><ul><ul><li>STNGING </li></ul></ul><ul><ul><li>INDURATION </li></ul></ul><ul><ul><li>ITCHING </li></ul></ul><ul><li>LIPODYSTROPHY </li></ul><ul><li>GENERALIZED: </li></ul><ul><ul><li>HIVES </li></ul></ul><ul><ul><li>URTICARIA </li></ul></ul><ul><ul><li>ANTIHISTAMINES 30 MIN B4 </li></ul></ul><ul><ul><li>DESENSITIZATION </li></ul></ul>
  110. 112. LIPODYSTROPHY <ul><li>CAUSE: </li></ul><ul><li>FAULTY TECHNIQUE </li></ul><ul><li>TRAUMA </li></ul><ul><li>INJECTION OF REFRIGERATED INSULIN </li></ul><ul><li>MANAGEMENT: </li></ul><ul><li>ROTATING SITES: 1 AREA IS NOT USED MORE THAN ONCE EVERY 3 WKS </li></ul>
  111. 113. INSULIN THERAPY & HORMONAL ACTIVITY <ul><li>GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING: </li></ul><ul><ul><li>PHYSICAL TRAUMA </li></ul></ul><ul><ul><li>STRESS </li></ul></ul><ul><ul><li>INFECTION </li></ul></ul><ul><ul><li>ANXIETY </li></ul></ul><ul><ul><li>ANGER </li></ul></ul><ul><ul><li>FEAR </li></ul></ul><ul><ul><li>CHANGE IN LIFESTYLE </li></ul></ul><ul><li>INCREASE IN INSULIN DOSE IS NEEDED </li></ul>
  112. 114. SURPRISE!!!
  113. 115. ACUTE COMPLICATIONS OF DIABETES MILLETUS <ul><li>DIABETIC KETO-ACIDOSIS (DKA) </li></ul><ul><li>INSULIN SHOCK </li></ul><ul><li>HYPERGLYCEMIC, HYPEROSMOLAR, </li></ul><ul><li>NONKETOTIC (HHONK) COMA </li></ul><ul><li>SOMOGYI EFFECT </li></ul>
  114. 116. D.K.A. PATHOPHYSIOLOGY NO INSULIN MARKED HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS OSMOTIC DEHYDRATION KETOACIDOSIS
  115. 117. D.K.A. <ul><li>S/SX: </li></ul><ul><li>S/SX OF DM + </li></ul><ul><li>KETONURIA </li></ul><ul><li>METABOLIC ACIDOSIS </li></ul><ul><li>KUSSMAUL’S RESPIRATION </li></ul><ul><li>ACETONE BREATH </li></ul><ul><li>DHN </li></ul><ul><li>FLUSHED FACE </li></ul><ul><li>TACHYCARDIA </li></ul><ul><li>CIRCULATORY COLLAPSE COMA DEATH </li></ul>
  116. 118. D.K.A. <ul><li>MANAGEMENT: </li></ul><ul><li>ADEQUATE VENTILATION </li></ul><ul><li>FLUID REPLACEMENT </li></ul><ul><li>INSULIN – RAPID ACTING </li></ul><ul><li>ECG – ELEC IMB </li></ul>
  117. 119. INSULIN SHOCK <ul><li>LOW BLOOD SUGAR </li></ul><ul><li>CAUSE: </li></ul><ul><li>OVERDOSE OF EXOGENOUS INSULIN </li></ul><ul><li>EATING LESS </li></ul><ul><li>OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE </li></ul>
  118. 120. INSULIN SHOCK <ul><li>S/SX: </li></ul><ul><li>PARASYMPATHETIC </li></ul><ul><ul><li>HUNGER </li></ul></ul><ul><ul><li>NAUSEA </li></ul></ul><ul><ul><li>HYPORTENSION </li></ul></ul><ul><ul><li>BRADYCARDIA </li></ul></ul><ul><li>CEREBRAL </li></ul><ul><ul><li>LETHARGY, </li></ul></ul><ul><ul><li>YAWNING </li></ul></ul><ul><ul><li>SENSORIUM CX </li></ul></ul><ul><li>SYMPATHETIC </li></ul><ul><ul><li>IRRITABILITY </li></ul></ul><ul><ul><li>SWEATING </li></ul></ul><ul><ul><li>TREMBLING </li></ul></ul><ul><ul><li>TACHYCARDIA </li></ul></ul><ul><ul><li>PALLOR </li></ul></ul>
  119. 121. INSULIN SHOCK <ul><li>CLINICAL FINDING : </li></ul><ul><li>BLOOD GLUCOSE BELOW 55-60 mg% </li></ul><ul><li>TREATMENT: </li></ul><ul><li>GLUCOSE PO ( SUGAR, ORANGE JUICE OR CANDY) or IV </li></ul><ul><li>ADMINISTRATION OF GLUCAGON IM, IV OR SQ </li></ul>
  120. 122. HHONK PATHOPHYSIOLOGY Very insufficient INSULIN MARKED HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS Without KETOSIS SEVERE OSMOTIC DEHYDRATION
  121. 123. HHONK <ul><li>S/SX: </li></ul><ul><li>S/SX OF DKA WITHOUT: </li></ul><ul><ul><li>KAUSMAUL’S BREATHING </li></ul></ul><ul><ul><li>ACETONE BREATH </li></ul></ul><ul><ul><li>METABOLIC ACIDOSIS </li></ul></ul><ul><ul><li>KETONURIA </li></ul></ul>
  122. 124. LACTIC ACIDOSIS SEVERE TISSUE ANOXIA LACTIC ACID PRODUCTION AGGRAVATION OF EXISTING METABOLIC ACIDOSIS
  123. 125. SOMOGYI EFFECT TOO MUCH INSULIN HYPOGLYCEMIA GLUCAGON IS RELEASED LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS REBOUND HYPERGLYCEMIA + KETOSIS
  124. 126. CHRONIC COMPLICATIONS OF DIABETES MILLETUS <ul><li>DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM </li></ul><ul><ul><li>UNDERNOURISHMENT </li></ul></ul><ul><ul><li>ATHEROSCLEROSIS </li></ul></ul><ul><li>NEUROPATHY FROM: </li></ul><ul><ul><li>VASCULAR INSUFFICIENCY </li></ul></ul><ul><ul><li>VIT B DEFICIENCY </li></ul></ul><ul><ul><li>HYPERGLYCEMIA </li></ul></ul><ul><li>EYE COMPLICATIONS FROM ANOXIA </li></ul><ul><ul><li>CATARACT </li></ul></ul><ul><ul><li>DIABETIC RETINOPATHY </li></ul></ul><ul><ul><li>RETINAL DETACHMENT </li></ul></ul>
  125. 127. CHRONIC COMPLICATIONS OF DIABETES MILLETUS <ul><li>NEPHROPATHY </li></ul><ul><ul><li>DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY </li></ul></ul><ul><li>HEART DISEASE </li></ul><ul><ul><li>MI FROM ATHEROSCLEROSIS </li></ul></ul><ul><li>SKIN CHANGES </li></ul><ul><ul><li>DIABETIC DERMOPATHY – HYPERPIGMENTED & SCALY PRETIBIAL AREAS </li></ul></ul><ul><li>LIVER CHANGES </li></ul><ul><ul><li>ENLARGEMENT & FATTY INFILTRATION </li></ul></ul>
  126. 128. <ul><li>Ms A, 45 y.o., has a simple goiter. She’s being seen by the community health nurse for teaching & follow-up regarding nutritional deficiencies related to her goiter. Ms A’s problem is almost associated with what nutritional deficiency? </li></ul><ul><li>Calcium </li></ul><ul><li>Iodine </li></ul><ul><li>Iron </li></ul><ul><li>Sodium </li></ul>
  127. 129. GOD BLESS

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