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    Psycho endocrinology.drjma Psycho endocrinology.drjma Presentation Transcript

    • PSYCHOENDOCRINOLOGY Dr. James M. Alo, RN,MAN,MAP.PHD
    • ENDOCRINE GLANDSENDOCRINE HORMONES FUNCTIONSGLANDPITUITARY TSH Thyroid to release hormones ANTERIOR LOBE ACTH Adrenal cortex to release hormones FSH,LH Growth, maturation & function of sex organs GH/ Growth of body tissues & bones SOMATOTROPIN PROLACTIN/ Development of mammary glands & LTH lactation
    • ENDOCRINE GLANDSENDOCRINE HORMONE FUNCTIONGLANDPITUITARY ADH Regulates water metabolism POSTERIOR LOBE OXYTOCIN Stimulate uterine contractions release of milk INTERME- MSH Affects skin pigmentation DIATE LOBE
    • ENDOCRINE GLANDSENDOCRINE HORMONES FUNCTIONGLANDADRENAL ALDOSTERONE Fluid & electrolyte balance; Na reabsorption;CORTEX K excretion CORTISOL Glycogenolysis; Gluconeogenesis Na & water reabsorption Antiinflammatory Stress hormone SEX Slightly significant HORMONES
    • ENDOCRINE GLANDSENDOCRINE HORMONE FUNCTIONGLANDADRENAL EPINEPHRINE Increase heart rate & BP Bronchodilation,MEDULLA NOR- Glycogenolysis EPINEPHRINE Stress hormone
    • ENDOCRINE GLANDSENDOCRINE HORMONE FUNCTIONGLANDTHYROID T3 & T4’ Regulate metabolic rate P,C,F metabolism Regulate physical & mental growth & development THYRO- Decrease serum Ca by increasing bone deposition CALCITONINPARA- PTH Increase serum calcium by promoting bone decalcification THYROID
    • ENDOCRINE GLANDSENDOCRINE HORMONE FUNCTIONGLANDPANCREAS INSULIN Decrease blood glucose by: Glucose diffusion across cell BETA membrane; CELLS Converts glucose to glycogen ALPHA GLUCAGON Increase blood glucose by: Gluconeogenesis CELLS Glycogenolysis
    • ENDOCRINE GLANDSENDOCRINE HORMONES FUNCTIONGLANDOVARIES ESTROGEN & Development of secondary sex charac in female PROGES- Maturation of sex organs TERONE Sexual functioning Maintenance of pregnancyTESTES TESTOS- Development of secondary sex charac in male TERONE Maturation of sex organs Sexual functioning
    • HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISMCHANGING OF BLOOD LEVELS OFCERTAIN 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 MECHANISMDECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLANDRELEASE 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 MECHANISMINCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE (e.g. Thyroid gland release of Thyroxine) RETURN OF THE NORMAL CONCENTRATION OF HORMONE
    • CASE STUDYKatie, an elderly, came in because ofpalpitations.VS revealed: 37.9o , 120, 25, 140/ 90She expressed hyperactivty, sweating,increased appetite & weight loss
    • CASE STUDYShe claimed history of goiter since her30’s but no follow-up was done.What are your nursing plans?
    • PLANNINGHEALTH PROMOTIONl IODIZED SALTl CONTROLLING WEIGHTHEALTH MAINTENANCE &RESTORATIONl STEROID THERAPY
    • STEROID THERAPY STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH ENDOGENOUS CORTISOL PRODUCTION & ADRENAL ATROPHYRELEASE BY ADRENAL MEDULLA
    • STEROID THERAPYPHARMACOLOGIC CONSIDERATIONS: PEPTIC ULCER IN SHORT TERM, HIGH DOSE STEROID TX ADMINISTER DRUG: HIGHER DOSE IN THE MORNING, TAPERING TO LOWER ONES IN THE AFTERNOON LAST DOSE @ MEAL TIME TO AVOID INSOMNIA PALLIATIVE EFFECT
    • STEROID THERAPYASSESSMENT: BASELINE STEROID LEVEL IS ASSESSED BEFORE PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED STEROID WITHDRAWAL (LOW STRESS TOLERANCE) l EXHAUSTION l WEAKNESS l LETHARGY
    • STEROID THERAPYASSESSMENT: ACUTE ADRENAL CRISIS l RESTLESSNESS l WEAKNESS l HEADACHE l DHN l N/V l FALLING BP TO SHOCK PSYCHOLOGICAL CXS l MOOD ELEVATION, l FRANK EUPHORIA l THEN, DEPRESSION
    • STEROID THERAPYIMPORTANT FACTS: MAJOR UNTOWARD EFFECTS: l MASKS INFECTION l DEFENSE AGAINST INFECTION FROM LYMPHOPENIA l SLOW WOUND HEALING FROM ITS ANTIINFLAMMATORY EFFECT l P.U.D. ACTIVATION/ REACTIVATION l SERUM SODIUM l SERUM POTASSIUM
    • STEROID THERAPYIMPORTANT FACTS: MINOR UNTOWARD EFFECTS: l PIGMENTATION l ACNE l FACIAL HAIR l MOON-FACIE
    • STEROID THERAPYIMPORTANT FACTS: PROBLEMS OF LONG TERM THERAPY: l GROWTH RETARDATION l OBESITY l GASTRITIS TO P.U.D. l OSTEOPOROSIS l HPN l RENAL CALCULI l ADRENAL ATROPHY
    • STEROID THERAPY STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH ENDOGENOUS CORTISOL PRODUCTION & ADRENAL ATROPHYRELEASE BY ADRENAL MEDULLA
    • STEROID THERAPYIMPLEMENTATION DECREASE Na IN THE DIET CALORIC RESTRICTION FOODS HIGH IN POTASSIUM GIVE MEDS WITH ANTACIDS OR WITH FOOD TEST STOOLS OR EMESIS FOR BLOOD REPORT ANY EVIDENCE OF GI BLEEDING LYMPHOPENIC PRECAUTION
    • ANTERIOR PITUITARY DISTURBANCESHYPOPITUITARISMHYPERPITUITARISM
    • HYPOPITUITARISM ANTERIOR LOBEPANHYPOPITUITARISM (SIMMOND’S DSE)l DECREASED SECRETION OF ALL ANTERIOR LOBE HORMONES
    • HYPERPITUITARISM ANTERIOR LOBEEOSINOPHILIC TUMORl INCREASED GROWTH HORMONE AND PROLACTINBASOPHILIC TUMORl INCREASED TSH, FSH, LH, MSH,l INCREASED ACTH (CUSHING’S DSE)CHROMOPHOBE TUMORl INCREASED ACTH & GROWTH HORMONE
    • PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXNGH Dwarfism – young Gigantism – young Cachexia - adult Acromegaly - adultACTH Atrophy of adrenal Cushing’s dse cortexTSH Atrophy & Grave’s dse depressed thyroid fxnFSH Atrophy & infertility Exaggerated fxn of sex organsPROLACTIN Underdevelopment Decreased milk of mammary glands production
    • MANAGEMENTHYPOPITUITARISMl SURGICAL REMOVAL / IRRADIATIONl REPLACEMENT THERAPY l THYROID HORMONES l STEROIDS l SEX HORMONES l GONADOTROPINS (restore fertility)HYPERPITUITARISMl SURGICAL REMOVAL / IRRADIATIONl MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS
    • POSTERIOR PITUITARY DISTURBANCESDIABETES INSIPIDUSSYNDROME OF INAPPROPRIATEANTIDIURETIC HORMONE
    • DIABETES INSIPIDUSABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSINCAUSE: S/SX: TUMOR POLYURIA TRAUMA 15-29L/ DAY VASCULAR DSE POLYDIPSIA INFLAMMATION SG OF URINE IS PITUITARY <1.010 SURGERY S/SX OF DHN SHOCK
    • DIABETES INSIPIDUSABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSINMANAGEMENT HORMONAL REPLACEMENT – FOR LIFE l VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY NON-HORMONAL THERAPY l CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN SALT & P RESTRICTED DIET, INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE BALANCE
    • SYNDROME OF INAPPROPRIATE ADH ELEVATED ADHCAUSES: BRONCHOGENIC CA NONENDOCRINE TUMORSS/SX: DECREASED SERUM SODIUM l CX IN LOC TO UNCONSCIOUSNESS l SEIZURES WATER INTOXICATION l N/V l MENTAL CONFUSION
    • SYNDROME OF INAPPROPRIATE ADHMANAGEMENT: WATER INTAKE RESTRICTION ADMINISTER AS ORDERED: l NaCl l Diuretics l Demeclocycline (declamycin) – a tetracycline analogue that interferes with the action of ADH on the collecting tubules
    • Mission possible
    • THYROID GLANDSTIMULATED BY THYROID STIMULATINGHORMONE (TSH)NEEDS IODINE TO SYNTHESIZE HORMONESECRETES:l THYROXINE (T4)l TRIIODOTHYRONINE (T3)
    • THYROID DISTURBANCESDIAGNOSTIC TESTS: B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN TIME PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITH THYROID DAMAGE SERUM THYROXINE (T4), SERUM TRIIODOTHYRONINE (T3), SERUM TSH BLOOD SERUM CHOLESTEROL RADIOACTIVE IODINE TESTS: l T3 RED CELL UPTAKE l RADIOACTIVE IODINE UPTAKE (I131 l THYROID SCAN
    • THYROID DISTURBANCESHYPOTHYROIDISM HYPERTHYROIDISM CRETINISM- infants, GRAVE’S DSE oryoung children Exophthalmic goiter HYPOTHYROIDISMWITHOUT MYXEDEMA-atrophy/ destruction ofthyroid gland MYXEDEMA –adults
    • EFFECTSHYPOTHYROIDISM HYPERTHYROIDISM Reduction in HEAT Increase heatPRODUCTION Failure of MENTAL &PHYSICAL GROWTH increased storage of Deranged CC, P & F metabolism, glycosuria Abnormal collection Increase use of F &of WATER P as fuel
    • HYPOTHYROIDISM HYPERTHYROIDISMSERUMCHOLESTEROL:INCREASED DECREASEDBMR:DECREASED INCREASEDSKIN:THICK, PUFFY, DRY WARM, MOIST, FLUSHEDHAIR: SOFT, SILKYDRY, BRITTLE
    • HYPOTHYROIDISM HYPERTHYROIDISMNERVOUS SYSTEM: APATHETIC HYPERACTIVE LETHARGIC LABILE MOOD MAYBE HYPERSENSITIVEHYPERIRRITABLE TENSED SLOW CEREBRATIONWEIGHT:INCREASED DECREASEDAPPETITE:DECREASED INCREASED
    • MANAGEMENTHYPOTHYROIDISM HYPERTHYROIDISMMEDICAL: MEDICAL:HORMONE RESTREPLACEMENT ANTITHYROIDDESSICATED THYROID DRUGS:THYROGLOBULIN LUGOL’S SOLUTIONNa LEVOTHYROXINE THIOUREA DERIVATIVESNa LYOTHYRONINE RADIOACTIVE IODINE BETA-BLOCKERS SURGICAL: SUBTOTAL THYROIDECTOMY
    • ANTITHYROID MEDICATIONS LUGOL’S SOLUTION (POTASSIUM IODIDE) l DECREASE THYROID VASCULARITY l INHIBIT IODINE RELEASE l DILUTED IN MILK / JUICE l STAINS THE TEETH- USE STRAW THIOUREA & DERIVATIVES (PTU,METHIMAZOLE) l BLOCK THYROID HORMONE RELEASE l TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA RADIOACTIVE IODINE l PATIENT IS ISOLATED FOR 3 DAYS BETA BLOCKERS l PROPANOLOL
    • SUBTOTAL THYROIDECTOMYREMAINING TISSUE PROVIDES ENOUGH HORMONES FOR NORMAL FXNPRE OP NURSING CARE: PATIENT EDUCATION ON POST OP: l LITTLE HOARSENESS l DIFFICULTY OF SWALLOWINGPOST OP NURSING CARE: SEMIFOWLER’S AVOID HYPEREXTENSION OF THE NECK BE ASKED TO SPEAK @ 40 MIN INTERVAL – ASSESS RECURRENT NERVE INJURY WATCH OUT FOR COMPLICATIONS.
    • SUBTOTAL THYROIDECTOMYCOMPLICATIONS: RECURRENT LARYNGEAL NERVE INJURY l HOARSENESS HEMORRHAGE l 12-24 HRS POST OP l OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS l TRACHEOSTOMY SET @ BEDSIDE TETANY RESPIRATORY OBSTRUCTION THYROID STORM
    • TETANYDEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVEDS/SX: 1ST – TINGLING TOES & FINGERS 2ND – CHEVOSTEK’S SIGN (TAPPING THE FACIAL MUSCLES) 3RD – TROUSSEAU’S SIGN (CARPO-PEDAL SPASM WITH OCCLUSION OF CIRCULATION WITH A BP CUFF)MANAGEMENT: CALCIUM REPLACEMENT: CaGluconate IV
    • THYROID STORM / CRISISS/SX: MANAGEMENT: HYPERTHERMIA DECREASE TEMP > 41C ANTITHYROID TACHYCARDIA DRUGS APPREHENSION GLUCOSE RESTLESSNESS DIGITALIS IRRITABILITY STEROIDS TO DELIRIUM DECREASE ACTH COMA
    • THYROID STORM / CRISISINCREASED AMOUNT OF THYROID HORMONES POST OP AFTER RADIOACTIVE IODINE ADMINISTRATION TOO SHORT PERIOD OF PRE OP TXCAUSES: EMOTIONAL STRESS PHYSICAL STRESS
    • VARIANTS OF HYPERTHYROIDISMGRAVE’S DSETHYROIDITISGOITER
    • GRAVE’S DISEASECAUSE: UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATORS/SX: TRIAD OF SYMPTOMS: HYPERTHYROIDISM OPHTHALMOPATHY DERMOPATHY
    • OPHTHALMOPATHYEXOPHTHALMOS – ACCUMULATION OFFLUID IN THE FAT PADS BEHIND HE EYEBALLID LAG – PROMINENT PALPEBRAL FISSUREWHEN THE PATIENT LOOKS DOWNTHYROID STARE(DARYMPLE’S SIGN) – INFREQUENT EYEBLINKING
    • DERMOPATHYPRETIBIAL MYXEDEMA@ THE DORSUM OF THE LEGRAISED, THICKENED, PRURITIC,HYPERPIGMENTED SKINCLUBBING OF FINGERS & TOESOSTEOARTHROPATHY
    • THYROIDITISCLASSIFICATION: SUBACUTE, NONSUPPURATIVE l UNKNOWN CAUSE l ASSOC. WITH VIRAL URT INFECTIONS CHRONIC, HASHIMOTO’S l IMMUNOLOGICAL FACTORS l PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID
    • GOITER ENLARGEMENT OF THE THYROID GLAND.TYPES: TOXIC NODULAR NONTOXIC
    • TOXIC NODULAR GOITERCOMMON IN ELDERLYFROM LONG STANDING SIMPLEGOITERNODULESl FUNCTIONING TISSUEl SECRETES THYROXINE AUTONOMOUSLY FROM TSH
    • NON-TOXIC GOITER(SIMPLE/ COLLOID/ EUTHYROID)CAUSE : IODINE DEFICIENCY INTAKE OF GOITROGENIC SUBSTANCES/ DRUGS: l CASSAVA, l CABBAGE, l CAULIFLOWER, l CARROTS l RADDISH l TURNIPS l RED SKIN OF PEANUTS l IODINE l COBALT l LITHIUM
    • NON-TOXIC GOITER IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCESIMPAIRED THYROID HORMONE SYNTHESIS SERUM THYROXINE PITUITARY SECRETE TSH THYROID GLAND ENLARGES TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE
    • NON-TOXIC GOITER TREATMENT: IODIZED OIL IMCOMMON IN IODINE TABLETS WOMEN: SALT ADOLESCENT FORTIFICATION PREGNANT WITH IODINE LACTATING EDUCATE ABOUT MENOPAUSE INTAKE OF: l SEAWEEDS l SHELLFISH l FISH- TAMBAN, HITO, DALAG
    • MYXEDEMA COMA MEDICAL EMERGENCY OCCURS IN SEVERE & UNTREATED MYXEDEMA HIGH MORTALTY RATES/SX: INTENSIFIED HYPOTHYROIDISM NEUROLOGIC IMPAIRMENT COMA
    • MYXEDEMA COMAPRECIPITATING FACTORS: FAILURE TO TAKE MEDS INFECTION TRAUMA EXPOSURE TO COLD USE OF SEDATIVES, NARCOTICS, ANESTHETICS
    • MYXEDEMA COMAMANAGEMENT: IV THYROID HORMONES CORRECTION OF HYPOTHERMIA MAINTAIN VITAL FXNS TREAT PRECIPITATING CAUSES
    • PARATHYROID GLAND 4 GLANDS SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph LEVELS REGULATE CALCIUM & PHOSPHORUS METABOLISMORGANS AFFECTED: BONES - RESORPTION KIDNEYS l Ca REABSORPTION l Ph EXCRETION GIT – ENHANCES Ca ABSORPTION
    • PARATHYROID DISORDERSDIAGNOSTIC TESTS: HEMATOLOGICAL l SERUM CALCIUM l SERUM PHOSPHORUS l SERUM ALKALINE PHOSPHATASE URINARY STUDIES l URINARY CALCIUM l URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE
    • HYPOPARATHYROIDISM DECREASED PTH PRODUCTION HYPOCALCEMIA CALCIUM IS: l DEPOSITED IN THE BONE l EXCRETEDCAUSE: HEREDITARY IDIOPATHIC SURGICAL
    • HYPOPARATHYROIDISMS/SX: ACUTE HYPOCALCEMIA l TINGLING OF THE FINGERS l CHEVOSTEK’S, TROUSSEAU’S CHRONIC HYPOCALCEMIA l FATIGUE, WEAKNESS l PERSONALITY CHANGES l LOSS OF TOOTH ENAMEL, DRY SCALY SKIN l CARDIAC ARRHYTHMIA l CATARACT
    • HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT: 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
    • HYPERPARATHYROIDISM INCREASED PTH PRODUCTION HYPERCALCEMIA HYPOPHOSPHATEMIA PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM: l CHRONIC RENAL DSE l RICKETS l MALABSORPTION SYNDROME l OSTEOMALACIA
    • HYPERPARATHYROIDISMS/SX: BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRUCTURES TUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIA MUSCLE WEAKNESS PERSONALITY CX, DEPRESSION CARDIAC ARRHYTHMIAS, HPNXRAY: BONE DEMINERALIZATION
    • HYPERPARATHYROIDISMMANAGEMENT: TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE IV PNSS 5L/ DAY WITH DIURETICS CRANBERRY JUICE (ACID-ASH) LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSES STRAIN URINE FOR STONES CARE FOR PARATHYROIDECTOMY
    • ADRENAL GLANDSTIMULATED BY ACTHHORMONE PRECURSOR:l CHOLESTEROLSECRETES:l CORTISOLl ALDOSTERONEl SEX HORMONES : ANDROGEN, ESTROGEN
    • ADRENAL GLANDHORMONE FUNCTIONALDOSTERONE Renal : Na & Cl reabsorption; K excretion GI : Na absorptionGLUCO- increase serum glucose by CORTICOIDS gluconeogenesis & glycogenolysis esp during STRESS Blocks inflammation Counteracts effect of histamineSEX HORMONE Physiologically insignificant Becomes useful during menopause in women
    • SYMPTOMATOLOGYALDOSTERONE DEFICIENCY DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON HYPOTENSION TO SHOCK INCREASED K METABOLIC ACIDOSIS
    • SYMPTOMATOLOGYCORTISOL DEFICIENCY ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY HYPOGLYCEMIA HYPOTENSION INCREASED K, WEAK PULSE PIGMENTATION IMPAIRED STRESS TOLERANCE
    • SYMPTOMATOLOGYSEX HORMONE DEFICIENCY LOSS OF BODY HAIR LOSS OF LIBIDO OR IMPOTENCE MENSTRUAL & FERTILITY DISORDER
    • ADRENAL CORTEX DISORERSADRENAL INSUFFICIENCYADRENAL CRISISCUSHING’S SYNDROMEALDOSTERONISM
    • ADRENAL INSUFFICIENCY ADDISON’S DISEASEINCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS
    • ADRENAL CRISISACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIESPOSSIBLE COMPLICATION OF ADDISON’S DISEASE
    • ADRENAL CRISISPRECIPITATING CAUSES: ABDOMINAL DISCOMFORT INFECTION TRAUMA HIGH TEMP EMOTIONAL UPSET ANTICOAGULANT DRUGS
    • ADRENAL CRISISS/SX: HYPOTENSION FLUID LOSS HYPONATREMIA
    • ADRENAL CRISISLAB: SERUM ELEC: DECREASED Na INCREASED K S. BUN : S. GLUCOSE: ADRENAL HORMONE ASSAY : HYDROXYCORTICOID & 17 KETOSTEROID IN 24- HR URINE DET.
    • ADRENAL CRISISGOALS OF CARE: TO REVERSE SHOCK RESTORE BLOOD CIRCULATION REPLENISH NEEDED STEROID
    • ADRENAL CRISISTREATMENT: D5NSS ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE NEOSYNEPHRINE - SHOCK HIGH SALT DIET ANTIBIOTICS
    • CUSHING’S SYNDROMECAUSE: SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOR EXCESSIVE GLUCORTICOID ADMINISTRATION
    • CUSHING’S SYNDROMES/SX: TRUNCAL OBESITY BUFFALO HUMP MOON-FACIE WT GAIN SODIUM RETENTION THINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM
    • CUSHING’S SYNDROMEPURPLE STRIAE – FROM THINNINGOF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS: OLIGOMENORRHEA HIRSUTISM GYNECOMASTIAHYPERTENSION FROM S. Na
    • CUSHING’S SYNDROMETREATMENT & NURSING CARE: PSYCHOLOGICAL SUPPORT PREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY
    • ALDOSTERONISMHYPERSECRETION OF ALDOSTERONE PRIMARY – CONN’S SYNDROME SECONDARY
    • CONN’S SYNDROME PRIMARY ALDOSTERONISMCAUSE: ADRENAL ADENOMAS/SX: HYPOKALEMIA FATIGUE HYPERNATREMIA, HPN, TETANYMANAGEMENT: SURGERY ALDACTONE – ALDOSTERONE ANTAGONIST
    • SECONDARY ALDOSTERONISM THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:e.g. RENIN – ANGIOTENSIN SYSTEM
    • ADRENAL MEDULLAHORMONES : EPINEPHRINE NOREPINEPHRINEEFFECTS
    • PHEOCHROMOCYTOMA TUMOR OF ADRENAL MEDULLA SECRETES INCREASED AMOUNT OF CATECHOLAMINESS/SX: HPN HYPERGLYCEMIA CARDIAC ARRHYTHMIA & CHFDIAGNOSTIC TEST : VMA IN 24H URINE
    • VMA IN 24H URINEEND PRODUCT OF CATECHOLAMINEMETABOLISMDRUGS & FOOD TO BE WITHHELD24H B4 THE TEST:l COFFEE & TEAl BANANAl VANILLAl CHOCOLATES
    • PHEOCHROMOCYTOMAMANAGEMENT: SURGERY MEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINENURSING CARE: MONITOR BP IN SUPINE & STANDING MONITOR URINE FOR GLUC & ACETONE
    • PANCREASHORMONES: INSULIN BY BETA CELLS GLUCAGON BY ALPHA CELLS
    • DIABETES MILLETUSCAUSE: INSUFFICIENCY OF INSULIN LACK OF INSULINEFFECT: HYPERGLYCEMIA
    • DIABETES MILLETUS PATHOPHYSIOLOGY REDUCED /NO INSULIN OSMOTICDEHYDRATION HYPERGLYCEMIA GLUCOSURIA LIPOLYSIS CELLULAR HUNGER OSMOTIC DIURESIS WEIGHT LOSS POLYPHAGIA POLYURIA POLYDIPSIA
    • DIABETES MILLETUSS/SX: 3 – P’s WEIGHT LOSSSTAGES: PREDIABETES SUSPECTED CHEMICAL CLINICAL / OVERT
    • DIABETES MILLETUSPREDIABETES / POTENTIAL: CONCEPTION EVIDENCE OF GLUCOSE METABOLISM ALTERATION
    • DIABETES MILLETUSSUSPECTED/ SUBCLINICAL/ LATENT: PREDIABETES NO STRESS STRESS NORMAL GLUCOSE OVERT DIABETES METABOLISM
    • DIABETES MILLETUSCHEMEICAL: SUBCLINICAL GTT IS ABNORMAL NO STRESS STRESSASYMPTOMATIC SYMPTOMATIC
    • DIABETES MILLETUSCLINICAL / OVERT: CHEMICAL PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS SYMPTOMATIC
    • DIABETES MILLETUSTYPES: TYPE I TYPE II – l JUVENILE ONSET l MATURITY ONSET l BEFORE 15 YO l AFTER AGE 40 l LEAN/ NORMAL l OBESE WEIGHT l REDUCED INSULIN l ABSOLUTE INSULIN RECEPTOR DEFICIENCY l NONINSULIN l INSULIN -DEPENDENT DEPENDENT l PRONE TO DKA l PRONE TO HHONK
    • DIABETES MILLETUSDIAGNOSTIC DEXTROSTRIP EXAMS: URINE TESTS: FBS l BENEDICT’S 2 HR- l CLINITEST TAB POSTPRANDIAL l ACETONE TEST OGTT GLYCOSYLATED HGB
    • 2 HR POSTPRANDIAL BLOOD SUGARINTAKE OF 100GM GLUCOSE, 2 HRSBEFORE THE TESTTEST FOR ABILITY TO DISPOSEGLUCOSE LOAD
    • OGTTCONFIRMATORY, WHEN OTHER BLOOD TESTSARE BORDERLINE3 DAYS OF NORMAL ACITIVITY & 150MGOF CARB DIETNPO 10-12HRS BEFORE THE TESTBASELINE BLOOD SUGAR TAKENGLUCOSE LOAD IS GIVEN, P.O. OR IVBLOOD & URINE SPECS TAKEN 30 MIN, 1HR,2HRS, 3 HRS, AFTER GLUCOSE LOADING
    • GLYCOSYLATED HEMOGLOBINMEASURES GLUCOSE METABOLISMFOR THE PAST 3 MONTHSUSEFUL TO CHECK:l COMPLIANCE WITH THERAPYl HISTORY OF SUBCLINICAL OR CHEMICAL DIABETES
    • DIABETES MILLETUSPLANNING & IMPLEMENTATION: CLIENT’S ACTIVITY DIET : C,F,P – 50, 30, 20 LOW SATURATED FATS, HIGH FIBER DRUGS: l ORAL HYPOGLYCEMICS l BIGUANIDE l SULFONYLUREAS l CONTRAINDICATED - PREGNANCY l INSULIN
    • DIABETES MILLETUSINSULIN THERAPY DISPENSED IN “U”/ml : eg 100, 80 REFRIGERATE GIVEN @ ROOM TEMP GENTLY ROTATED, NOT SHAKEN ROUTE : SQ (MTC); IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND
    • DIABETES MILLETUSINSULIN THERAPY: SITE OF INJECTION: l ABDOMEN l ANTERIOR THIGH l ARM l UPPER BACK l BUTTOCKS
    • DIABETES MILLETUSINSULIN THERAPY REACTIONS: LOCAL: GENERALIZED: l STNGING l HIVES l INDURATION l URTICARIA l ITCHING l ANTIHISTAMINES LIPODYSTROPHY 30 MIN B4 l DESENSITIZATION
    • LIPODYSTROPHYCAUSE: FAULTY TECHNIQUE TRAUMA INJECTION OF REFRIGERATED INSULINMANAGEMENT: ROTATING SITES: 1 AREA IS NOT USED MORE THAN ONCE EVERY 3 WKS
    • INSULIN THERAPY &HORMONAL ACTIVITYGLUCORTICOIDS & EPINEPHRINECAUSES HYPERGLYCEMIA DURING:l PHYSICAL TRAUMAl STRESSl INFECTIONl ANXIETYl ANGERl FEARl CHANGE IN LIFESTYLEINCREASE IN INSULIN DOSE IS NEEDED
    • SURPRISE!!!
    • ACUTE COMPLICATIONS OF DIABETES MILLETUSDIABETIC KETO-ACIDOSIS (DKA)INSULIN SHOCKHYPERGLYCEMIC, HYPEROSMOLAR,NONKETOTIC (HHONK) COMASOMOGYI EFFECT
    • D.K.A. PATHOPHYSIOLOGY NO INSULIN OSMOTICDEHYDRATION MARKED HYPERGLYCEMIA GLUCOSURIA LIPOLYSIS CELLULAR HUNGER OSMOTIC DIURESIS WEIGHT LOSS KETOACIDOSIS POLYPHAGIA POLYURIA POLYDIPSIA
    • D.K.A.S/SX: S/SX OF DM + KETONURIA METABOLIC ACIDOSIS KUSSMAUL’S RESPIRATION ACETONE BREATH DHN FLUSHED FACE TACHYCARDIA CIRCULATORY COLLAPSE COMA DEATH
    • D.K.A.MANAGEMENT: ADEQUATE VENTILATION FLUID REPLACEMENT INSULIN – RAPID ACTING ECG – ELEC IMB
    • INSULIN SHOCKLOW BLOOD SUGARCAUSE: OVERDOSE OF EXOGENOUS INSULIN EATING LESS OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE
    • INSULIN SHOCKS/SX: PARASYMPATHETIC SYMPATHETIC l HUNGER l IRRITABILITY l NAUSEA l SWEATING l HYPORTENSION l TREMBLING l BRADYCARDIA l TACHYCARDIA CEREBRAL l PALLOR l LETHARGY, l YAWNING l SENSORIUM CX
    • INSULIN SHOCKCLINICAL FINDING : BLOOD GLUCOSE BELOW 55-60 mg%TREATMENT: GLUCOSE PO ( SUGAR, ORANGE JUICE OR CANDY) or IV ADMINISTRATION OF GLUCAGON IM, IV OR SQ
    • HHONK PATHOPHYSIOLOGY Very insufficient INSULIN SEVERE OSMOTICDEHYDRATION MARKED HYPERGLYCEMIA LIPOLYSIS GLUCOSURIA Without CELLULAR KETOSIS HUNGER OSMOTIC DIURESIS WEIGHT LOSS POLYPHAGIA POLYURIA POLYDIPSIA
    • HHONKS/SX: S/SX OF DKA WITHOUT: l KAUSMAUL’S BREATHING l ACETONE BREATH l METABOLIC ACIDOSIS l KETONURIA
    • LACTIC ACIDOSIS SEVERE TISSUE ANOXIA LACTIC ACID PRODUCTION AGGRAVATION OF EXISTING METABOLIC ACIDOSIS
    • SOMOGYI EFFECT TOO MUCH INSULIN HYPOGLYCEMIAGLUCAGON IS RELEASED REBOUND HYPERGLYCEMIA + LIPOLYSIS KETOSIS GLUCONEOGENESIS GLYCOGENOLYSIS
    • CHRONIC COMPLICATIONS OF DIABETES MILLETUS DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM l UNDERNOURISHMENT l ATHEROSCLEROSIS NEUROPATHY FROM: l VASCULAR INSUFFICIENCY l VIT B DEFICIENCY l HYPERGLYCEMIA EYE COMPLICATIONS FROM ANOXIA l CATARACT l DIABETIC RETINOPATHY l RETINAL DETACHMENT
    • CHRONIC COMPLICATIONS OF DIABETES MILLETUS NEPHROPATHY l DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY HEART DISEASE l MI FROM ATHEROSCLEROSIS SKIN CHANGES l DIABETIC DERMOPATHY – HYPERPIGMENTED & SCALY PRETIBIAL AREAS LIVER CHANGES l ENLARGEMENT & FATTY INFILTRATION
    • 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?a. Calciumb. Iodinec. Irond. Sodium