Psycho endocrinology.drjma

PSYCHOENDOCRINOLOGY

Dr. James M. Alo, RN,MAN,MAP.PHD

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONES FUNCTIONS

PITUITARYANTERIOR

TSH Thyroid to releasehormones

LOBE ACTH Adrenal cortex to releasehormones

FSH,LH Growth, maturation &function of sex organs

GH/SOMATOTROPIN

Growth of body tissues &bones

PROLACTIN/LTH

Development ofmammary glands &lactation

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONE FUNCTION

PITUITARYPOSTERIORLOBE

ADH Regulates water metabolism

OXYTOCIN Stimulate uterine contractionsrelease of milk

INTERME-DIATE LOBE

MSH Affects skin pigmentation

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONES FUNCTION

ADRENALCORTEX

ALDOSTERONE Fluid & electrolyte balance;Na reabsorption;K excretion

CORTISOL Glycogenolysis;GluconeogenesisNa & water reabsorptionAntiinflammatoryStress hormone

SEXHORMONES

Slightly significant

ENDOCRINE GLANDS

ENDOCRINEGLAND

HORMONE FUNCTION

ADRENALMEDULLA

EPINEPHRINENOR-EPINEPHRINE

Increase heart rate & BPBronchodilation,GlycogenolysisStress hormone

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONE FUNCTION

THYROID T3 & T4’ Regulate metabolic rateP,C,F metabolismRegulate physical & mental

growth & development

THYRO-CALCITONIN

Decrease serum Ca byincreasing bone deposition

PARA-THYROID

PTH Increase serum calcium bypromoting bone decalcification

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONE FUNCTION

PANCREASBETACELLS

INSULIN Decrease blood glucose by:Glucose diffusion across cell

membrane;Converts glucose to

glycogen

ALPHACELLS

GLUCAGON Increase blood glucose by:GluconeogenesisGlycogenolysis

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONES FUNCTION

OVARIES ESTROGEN &PROGES-

TERONE

Development of secondary sexcharac in female

Maturation of sex organsSexual functioningMaintenance of pregnancy

TESTES TESTOS-TERONE

Development of secondary sexcharac in male

Maturation of sex organsSexual functioning

HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM

CHANGING 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 FEEDBACKMECHANISM

DECREASED HORMONE CONCENTRATIONIN THE BLOOD (e.g. Thyroxine)

PITUITARY GLANDRELEASE OF STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TOPRODUCE & RELEASE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMALCONCENTRATION OF HORMONE

NEGATIVE FEEDBACKMECHANISM

INCREASED HORMONE CONCENTRATIONIN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)

DECREASED PRODUCTION & SECRETIONOF TARGET ORGAN OF THE HORMONE(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMALCONCENTRATION OF HORMONE

CASE STUDYKatie, an elderly, came in because ofpalpitations.

VS revealed: 37.9o , 120, 25, 140/ 90

She expressed hyperactivty, sweating,increased appetite & weight loss

CASE STUDY

She claimed history of goiter since her30’s but no follow-up was done.

What are your nursing plans?

PLANNINGHEALTH PROMOTIONl IODIZED SALTl CONTROLLING WEIGHT

HEALTH MAINTENANCE &RESTORATIONl STEROID THERAPY

STEROID THERAPY

STEROID LEVELS

PITUITARY GLAND IS INHIBITED TOREALEASE ACTH

ENDOGENOUS CORTISOLPRODUCTION &

RELEASE BY ADRENAL MEDULLAADRENAL ATROPHY

STEROID THERAPYPHARMACOLOGIC CONSIDERATIONS:

PEPTIC ULCER IN SHORT TERM, HIGHDOSE STEROID TX

ADMINISTER DRUG: HIGHER DOSE INTHE MORNING, TAPERING TO LOWER ONES INTHE AFTERNOON

LAST DOSE @ MEAL TIME TO AVOIDINSOMNIA

PALLIATIVE EFFECT

STEROID THERAPYASSESSMENT:

BASELINE STEROID LEVEL ISASSESSED BEFORE PROLONGED THERAPY ISSTARTED TO DETERMINE THE DOSE REQUIRED

STEROID WITHDRAWAL (LOW STRESSTOLERANCE)l EXHAUSTIONl WEAKNESSl LETHARGY

STEROID THERAPYASSESSMENT:

ACUTE ADRENAL CRISISl RESTLESSNESSl WEAKNESSl HEADACHEl DHNl N/Vl FALLING BP TO SHOCK

PSYCHOLOGICAL CXSl MOOD ELEVATION,l FRANK EUPHORIAl THEN, DEPRESSION

STEROID THERAPYIMPORTANT FACTS:

MAJOR UNTOWARD EFFECTS:l MASKS INFECTIONl DEFENSE AGAINST INFECTION FROM

LYMPHOPENIAl SLOW WOUND HEALING FROM ITS

ANTIINFLAMMATORY EFFECTl P.U.D. ACTIVATION/ REACTIVATIONl SERUM SODIUMl SERUM POTASSIUM

STEROID THERAPYIMPORTANT FACTS:

MINOR UNTOWARD EFFECTS:l PIGMENTATIONl ACNEl FACIAL HAIRl MOON-FACIE

STEROID THERAPYIMPORTANT FACTS:

PROBLEMS OF LONG TERM THERAPY:l GROWTH RETARDATIONl OBESITYl GASTRITIS TO P.U.D.l OSTEOPOROSISl HPNl RENAL CALCULIl ADRENAL ATROPHY

STEROID THERAPY

STEROID LEVELS

PITUITARY GLAND IS INHIBITED TOREALEASE ACTH

ENDOGENOUS CORTISOLPRODUCTION &

RELEASE BY ADRENAL MEDULLAADRENAL ATROPHY

STEROID THERAPYIMPLEMENTATION

DECREASE Na IN THE DIETCALORIC RESTRICTIONFOODS HIGH IN POTASSIUMGIVE MEDS WITH ANTACIDS OR WITHFOODTEST STOOLS OR EMESIS FOR BLOODREPORT ANY EVIDENCE OF GI BLEEDINGLYMPHOPENIC PRECAUTION

ANTERIOR PITUITARYDISTURBANCES

HYPOPITUITARISM

HYPERPITUITARISM

HYPOPITUITARISMANTERIOR LOBE

PANHYPOPITUITARISM(SIMMOND’S DSE)

l DECREASED SECRETION OF ALLANTERIOR LOBE HORMONES

HYPERPITUITARISMANTERIOR LOBE

EOSINOPHILIC 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 FXN

GH Dwarfism – youngCachexia - adult

Gigantism – youngAcromegaly - adult

ACTH Atrophy of adrenalcortex

Cushing’s dse

TSH Atrophy &depressed thyroid fxn

Grave’s dse

FSH Atrophy & infertility Exaggerated fxn ofsex organs

PROLACTIN Underdevelopmentof mammary glands

Decreased milkproduction

MANAGEMENTHYPOPITUITARISMl SURGICAL REMOVAL / IRRADIATIONl REPLACEMENT THERAPY

l THYROID HORMONESl STEROIDSl SEX HORMONESl GONADOTROPINS (restore fertility)

HYPERPITUITARISMl SURGICAL REMOVAL / IRRADIATIONl MONITOR FOR HYPERGLYCEMIA &

CARDIOVASCULAR PROBLEMS

POSTERIOR PITUITARYDISTURBANCES

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATEANTIDIURETIC HORMONE

DIABETES INSIPIDUSABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

CAUSE:TUMORTRAUMAVASCULAR DSEINFLAMMATIONPITUITARYSURGERY

S/SX:POLYURIA15-29L/ DAYPOLYDIPSIASG OF URINE IS<1.010S/SX OF DHNSHOCK

DIABETES INSIPIDUSABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

MANAGEMENTHORMONAL REPLACEMENT – FOR LIFEl VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR

NASAL SPRAY

NON-HORMONAL THERAPYl CHLORPROPRAMIDE – INCREASE RESPONSE OF THE

BODY TO DECREASED VASOPRESSIN

SALT & P RESTRICTED DIET, INCREASEFLUIDSMONITOR I&OMAINTAIN FLUID & ELECTROLYTEBALANCE

SYNDROME OFINAPPROPRIATE ADHELEVATED ADH

CAUSES:BRONCHOGENIC CANONENDOCRINE TUMORS

S/SX:DECREASED SERUM SODIUMl CX IN LOC TO UNCONSCIOUSNESSl SEIZURES

WATER INTOXICATIONl N/Vl MENTAL CONFUSION

SYNDROME OFINAPPROPRIATE ADH

MANAGEMENT:WATER INTAKE RESTRICTIONADMINISTER AS ORDERED:l NaCll Diureticsl Demeclocycline (declamycin) – a

tetracycline analogue that interferes withthe action of ADH on the collecting tubules

Mission possible

THYROID GLAND

STIMULATED BY THYROID STIMULATINGHORMONE (TSH)NEEDS IODINE TO SYNTHESIZE HORMONE

SECRETES:l THYROXINE (T4)l TRIIODOTHYRONINE (T3)

THYROID DISTURBANCESDIAGNOSTIC TESTS:

B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVENTIME

PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITHTHYROID DAMAGE

SERUM THYROXINE (T4), SERUMTRIIODOTHYRONINE (T3), SERUM TSHBLOOD SERUM CHOLESTEROLRADIOACTIVE IODINE TESTS:l T3 RED CELL UPTAKEl RADIOACTIVE IODINE UPTAKE (I131l THYROID SCAN

THYROID DISTURBANCESHYPOTHYROIDISM HYPERTHYROIDISM

CRETINISM- infants,young children

HYPOTHYROIDISMWITHOUT MYXEDEMA-atrophy/ destruction ofthyroid gland

MYXEDEMA –adults

GRAVE’S DSE orExophthalmic goiter

EFFECTSHYPOTHYROIDISM HYPERTHYROIDISM

Reduction in HEATPRODUCTION

Failure of MENTAL &PHYSICAL GROWTH

increased storage ofC, P & F

Abnormal collectionof WATER

Increase heat

Deranged Cmetabolism, glycosuria

Increase use of F &P as fuel

HYPOTHYROIDISM HYPERTHYROIDISM

SERUMCHOLESTEROL:INCREASED

BMR:DECREASED

SKIN:THICK, PUFFY, DRY

HAIR:DRY, BRITTLE

DECREASED

INCREASED

WARM, MOIST, FLUSHED

SOFT, SILKY

HYPOTHYROIDISM HYPERTHYROIDISM

NERVOUS SYSTEM:APATHETICLETHARGICMAYBE

HYPERIRRITABLESLOW CEREBRATION

WEIGHT:INCREASED

APPETITE:DECREASED

HYPERACTIVELABILE MOODHYPERSENSITIVETENSED

DECREASED

INCREASED

MANAGEMENTHYPOTHYROIDISM HYPERTHYROIDISMMEDICAL:HORMONEREPLACEMENT

DESSICATED THYROIDTHYROGLOBULINNa LEVOTHYROXINENa LYOTHYRONINE

MEDICAL:RESTANTITHYROID

DRUGS:LUGOL’S SOLUTIONTHIOUREA DERIVATIVESRADIOACTIVE IODINEBETA-BLOCKERS

SURGICAL:SUBTOTAL

THYROIDECTOMY

ANTITHYROID MEDICATIONSLUGOL’S SOLUTION

(POTASSIUM IODIDE)l DECREASE THYROID VASCULARITYl INHIBIT IODINE RELEASEl DILUTED IN MILK / JUICEl STAINS THE TEETH- USE STRAW

THIOUREA & DERIVATIVES(PTU,METHIMAZOLE)l BLOCK THYROID HORMONE RELEASEl TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA

RADIOACTIVE IODINEl PATIENT IS ISOLATED FOR 3 DAYS

BETA BLOCKERSl PROPANOLOL

SUBTOTAL THYROIDECTOMYREMAINING TISSUE PROVIDES ENOUGH HORMONES FOR

NORMAL FXN

PRE OP NURSING CARE:PATIENT EDUCATION ON POST OP:l LITTLE HOARSENESSl DIFFICULTY OF SWALLOWING

POST OP NURSING CARE:SEMIFOWLER’SAVOID HYPEREXTENSION OF THE NECKBE ASKED TO SPEAK @ 40 MIN INTERVAL –ASSESS RECURRENT NERVE INJURYWATCH OUT FOR COMPLICATIONS.

SUBTOTAL THYROIDECTOMYCOMPLICATIONS:

RECURRENT LARYNGEAL NERVE INJURYl HOARSENESS

HEMORRHAGEl 12-24 HRS POST OPl OBSERVE FOR IRREGULAR BREATHING, CHOKING

SIGNSl TRACHEOSTOMY SET @ BEDSIDE

TETANYRESPIRATORY OBSTRUCTIONTHYROID STORM

TETANYDEPENDS UPON THE NUMBER OF PARATHYROID GLANDS

REMOVED

S/SX:1ST – TINGLING TOES & FINGERS2ND – CHEVOSTEK’S SIGN (TAPPING THE FACIALMUSCLES)

3RD – TROUSSEAU’S SIGN (CARPO-PEDAL SPASMWITH OCCLUSION OF CIRCULATION WITH A BP CUFF)

MANAGEMENT:CALCIUM REPLACEMENT: CaGluconate IV

THYROID STORM / CRISISS/SX:

HYPERTHERMIA> 41C

TACHYCARDIAAPPREHENSIONRESTLESSNESSIRRITABILITYDELIRIUMCOMA

MANAGEMENT:DECREASE TEMPANTITHYROIDDRUGSGLUCOSEDIGITALISSTEROIDS TODECREASE ACTH

THYROID STORM / CRISISINCREASED AMOUNT OF THYROID HORMONES

POST OPAFTER RADIOACTIVE IODINEADMINISTRATIONTOO SHORT PERIOD OF PRE OP TX

CAUSES:EMOTIONAL STRESSPHYSICAL STRESS

VARIANTS OFHYPERTHYROIDISM

GRAVE’S DSE

THYROIDITIS

GOITER

GRAVE’S DISEASE

CAUSE:UNKNOWNAUTOIMMUNE WITH LONG-ACTINGTHYROID STIMULATOR

S/SX: TRIAD OF SYMPTOMS:HYPERTHYROIDISMOPHTHALMOPATHYDERMOPATHY

OPHTHALMOPATHY

EXOPHTHALMOS – ACCUMULATION OFFLUID IN THE FAT PADS BEHIND HE EYEBAL

LID LAG – PROMINENT PALPEBRAL FISSUREWHEN THE PATIENT LOOKS DOWN

THYROID STARE(DARYMPLE’S SIGN) – INFREQUENT EYEBLINKING

DERMOPATHYPRETIBIAL MYXEDEMA

@ THE DORSUM OF THE LEG

RAISED, THICKENED, PRURITIC,HYPERPIGMENTED SKIN

CLUBBING OF FINGERS & TOES

OSTEOARTHROPATHY

THYROIDITISCLASSIFICATION:

SUBACUTE, NONSUPPURATIVEl UNKNOWN CAUSEl ASSOC. WITH VIRAL URT INFECTIONS

CHRONIC, HASHIMOTO’Sl IMMUNOLOGICAL FACTORSl PRESENCE OF IMMUNOGLOBULINS &

ANTIBODIES DIRECTED AGAINST THETHYROID

GOITER

ENLARGEMENT OF THE THYROID GLAND.

TYPES:TOXIC NODULAR

NONTOXIC

TOXIC NODULARGOITER

COMMON IN ELDERLYFROM LONG STANDING SIMPLEGOITERNODULESl FUNCTIONING TISSUEl SECRETES THYROXINE

AUTONOMOUSLY FROM TSH

NON-TOXIC GOITER(SIMPLE/ COLLOID/ EUTHYROID)

CAUSE :IODINE DEFICIENCYINTAKE OF GOITROGENIC SUBSTANCES/DRUGS:l CASSAVA,l CABBAGE,l CAULIFLOWER,l CARROTSl RADDISHl TURNIPSl RED SKIN OF PEANUTSl IODINEl COBALTl LITHIUM

NON-TOXIC GOITER

IMPAIRED THYROID HORMONE SYNTHESIS

SERUM THYROXINE

PITUITARY SECRETE TSH

THYROID GLAND ENLARGESTO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE

IODINE DEFICIENCY ORINTAKE OF GOITROGENIC SUBSTANCES

NON-TOXIC GOITER

COMMON INWOMEN:ADOLESCENTPREGNANTLACTATINGMENOPAUSE

TREATMENT:IODIZED OIL IMIODINE TABLETSSALTFORTIFICATIONWITH IODINEEDUCATE ABOUTINTAKE OF:l SEAWEEDSl SHELLFISHl FISH- TAMBAN, HITO,

DALAG

MYXEDEMA COMA

MEDICAL EMERGENCYOCCURS IN SEVERE & UNTREATEDMYXEDEMAHIGH MORTALTY RATE

S/SX:INTENSIFIED HYPOTHYROIDISMNEUROLOGIC IMPAIRMENT COMA

MYXEDEMA COMA

PRECIPITATING FACTORS:

FAILURE TO TAKE MEDSINFECTIONTRAUMAEXPOSURE TO COLDUSE OF SEDATIVES, NARCOTICS,ANESTHETICS

MYXEDEMA COMA

MANAGEMENT:

IV THYROID HORMONESCORRECTION OF HYPOTHERMIAMAINTAIN VITAL FXNSTREAT PRECIPITATING CAUSES

PARATHYROID GLAND4 GLANDSSECRETES PARATHORMONE (PTH) INRESPONSE TO SERUM Ca & Ph LEVELSREGULATE CALCIUM & PHOSPHORUSMETABOLISM

ORGANS AFFECTED:BONES - RESORPTIONKIDNEYSl Ca REABSORPTIONl Ph EXCRETION

GIT – ENHANCES Ca ABSORPTION

PARATHYROID DISORDERSDIAGNOSTIC TESTS:

HEMATOLOGICALl SERUM CALCIUMl SERUM PHOSPHORUSl SERUM ALKALINE PHOSPHATASE

URINARY STUDIESl URINARY CALCIUMl URINARY PHOSPHATE - TUBULAR

REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISMDECREASED PTH PRODUCTIONHYPOCALCEMIACALCIUM IS:l DEPOSITED IN THE BONEl EXCRETED

CAUSE:HEREDITARYIDIOPATHICSURGICAL

HYPOPARATHYROIDISMS/SX:

ACUTE HYPOCALCEMIAl TINGLING OF THE FINGERSl CHEVOSTEK’S, TROUSSEAU’S

CHRONIC HYPOCALCEMIAl FATIGUE, WEAKNESSl PERSONALITY CHANGESl LOSS OF TOOTH ENAMEL, DRY SCALY SKINl CARDIAC ARRHYTHMIAl CATARACT

HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT:

Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER,JUICE OR MILK, pc

SEIZURE precLISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE

CaGLUCONATE @ BEDSIDE

HYPERPARATHYROIDISMINCREASED PTH PRODUCTIONHYPERCALCEMIAHYPOPHOSPHATEMIAPRIMARY – TUMOR OR HYPERPLASIA OF THEPARATHYROID GLAND

SECONDARY – COMPENSATORY OVERSECRETIONOF PTH IN RESPONSE TO HYPOCALCEMIA FROM:l CHRONIC RENAL DSEl RICKETSl MALABSORPTION SYNDROMEl OSTEOMALACIA

HYPERPARATHYROIDISMS/SX:

BONE PAIN : ESP @ THE BACK, PATHOLOGICFRUCTURESTUBULAR CALCIUM DEPOSITS - KIDNEYSTONES, RENAL COLIC, POLYURIA, POLYDIPSIAMUSCLE WEAKNESSPERSONALITY CX, DEPRESSIONCARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISMMANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OFHYERPLASTIC TISSUEIV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)LOW Ca, HIGH Ph DIETNO MILK, CAULIFLOWER & MOLASSESSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY

ADRENAL GLANDSTIMULATED BY ACTH

HORMONE PRECURSOR:l CHOLESTEROL

SECRETES:l CORTISOLl ALDOSTERONEl SEX HORMONES : ANDROGEN, ESTROGEN

ADRENAL GLANDHORMONE FUNCTION

ALDOSTERONE Renal : Na & Cl reabsorption; Kexcretion

GI : Na absorptionGLUCO-

CORTICOIDSincrease serum glucose by

gluconeogenesis & glycogenolysis espduring STRESS

Blocks inflammationCounteracts effect of histamine

SEX HORMONE Physiologically insignificantBecomes useful during menopause in

women

SYMPTOMATOLOGY

ALDOSTERONE DEFICIENCY

DECREASE IN PLASMA VOLUME LEADING TODEHYDRATONHYPOTENSION TO SHOCKINCREASED K

METABOLIC ACIDOSIS

SYMPTOMATOLOGY

CORTISOL DEFICIENCY

ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS,LETHARGYHYPOGLYCEMIAHYPOTENSIONINCREASED K, WEAK PULSEPIGMENTATIONIMPAIRED STRESS TOLERANCE

SYMPTOMATOLOGY

SEX HORMONE DEFICIENCY

LOSS OF BODY HAIRLOSS OF LIBIDO OR IMPOTENCEMENSTRUAL & FERTILITY DISORDER

ADRENAL CORTEXDISORERS

ADRENAL INSUFFICIENCY

ADRENAL CRISIS

CUSHING’S SYNDROME

ALDOSTERONISM

ADRENAL INSUFFICIENCYADDISON’S DISEASE

INCAPABILITY OF THE ADRENALCORTEX TO PRODUCEGLUCOCORTICOIDS IN RESPONSETO STRESS

ADRENAL CRISIS

ACUTE EPISODES FROM STRESSTHAT TAXES THE ADRENALCORTICAL FUNCTION BEYOND ITSCAPABILITIES

POSSIBLE COMPLICATION OFADDISON’S DISEASE

ADRENAL CRISIS

PRECIPITATING CAUSES:ABDOMINAL DISCOMFORTINFECTIONTRAUMAHIGH TEMPEMOTIONAL UPSETANTICOAGULANT DRUGS

ADRENAL CRISIS

S/SX:

HYPOTENSIONFLUID LOSSHYPONATREMIA

ADRENAL CRISISLAB:

SERUM ELEC: DECREASED NaINCREASED K

S. BUN :S. GLUCOSE:ADRENAL HORMONE ASSAY :HYDROXYCORTICOID & 17 KETOSTEROID IN 24-HR URINE DET.

ADRENAL CRISIS

GOALS OF CARE:TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

ADRENAL CRISIS

TREATMENT:D5NSSADRENAL CORTICAL HORMONEREPLACEMENT: INJECTABLENEOSYNEPHRINE - SHOCKHIGH SALT DIETANTIBIOTICS

CUSHING’S SYNDROME

CAUSE:SUSTAINED OVER-PRODUCTION OFGLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOIDADMINISTRATION

CUSHING’S SYNDROME

S/SX:TRUNCAL OBESITYBUFFALO HUMPMOON-FACIEWT GAINSODIUM RETENTIONTHINNING OF EXTREMITIES – FROMLOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHING’S SYNDROME

PURPLE STRIAE – FROM THINNINGOF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:

OLIGOMENORRHEAHIRSUTISMGYNECOMASTIA

HYPERTENSION FROM S. Na

CUSHING’S SYNDROME

TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM &IMMUNE RESPONSE ARE SUPPRESSED

PROMOTE SAFETYSURGERY – SUB/TOTAL ADRENALECTOMY

ALDOSTERONISMHYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME

SECONDARY

CONN’S SYNDROMEPRIMARY ALDOSTERONISM

CAUSE:ADRENAL ADENOMA

S/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPN, TETANY

MANAGEMENT:SURGERYALDACTONE – ALDOSTERONE ANTAGONIST

SECONDARYALDOSTERONISM

THE PROBLEM IS OUTSIDE THEADRENAL GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLA

HORMONES : EPINEPHRINENOREPINEPHRINE

EFFECTS

PHEOCHROMOCYTOMATUMOR OF ADRENAL MEDULLASECRETES INCREASED AMOUNT OF CATECHOLAMINES

S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF

DIAGNOSTIC TEST :VMA IN 24H URINE

VMA IN 24H URINE

END PRODUCT OF CATECHOLAMINEMETABOLISMDRUGS & FOOD TO BE WITHHELD24H B4 THE TEST:l COFFEE & TEAl BANANAl VANILLAl CHOCOLATES

PHEOCHROMOCYTOMA

MANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKINGAGENTS: PHENTOLAMINE

NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUC & ACETONE

PANCREAS

HORMONES:

INSULIN BY BETA CELLS

GLUCAGON BY ALPHA CELLS

DIABETES MILLETUS

CAUSE:INSUFFICIENCY OF INSULINLACK OF INSULIN

EFFECT:HYPERGLYCEMIA

DIABETES MILLETUSPATHOPHYSIOLOGY

REDUCED /NO INSULINREDUCED /NO INSULIN

HYPERGLYCEMIAHYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHT LOSS

OSMOTICDIURESISOSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULARCELLULARHUNGER

POLYPHAGIA

POLYDIPSIAPOLYDIPSIA

LIPOLYSIS

OSMOTICDEHYDRATION

DIABETES MILLETUS

S/SX:3 – P’sWEIGHT LOSS

STAGES:PREDIABETESSUSPECTEDCHEMICALCLINICAL / OVERT

DIABETES MILLETUS

PREDIABETES / POTENTIAL:

CONCEPTION

EVIDENCE OF GLUCOSE METABOLISMALTERATION

DIABETES MILLETUS

SUSPECTED/ SUBCLINICAL/ LATENT:

PREDIABETES

NO STRESS STRESS

NORMAL GLUCOSEMETABOLISM

OVERT DIABETES

DIABETES MILLETUSCHEMEICAL:

SUBCLINICAL

GTT IS ABNORMAL

NO STRESS STRESS

ASYMPTOMATIC SYMPTOMATIC

DIABETES MILLETUSCLINICAL / OVERT:

CHEMICAL

PERSISTENT INCREASED FBS

WITH OR WITHOUT STRESS

SYMPTOMATIC

DIABETES MILLETUSTYPES:

TYPE Il JUVENILE ONSETl BEFORE 15 YOl LEAN/ NORMAL

WEIGHTl ABSOLUTE INSULIN

DEFICIENCYl INSULIN -DEPENDENTl PRONE TO DKA

TYPE II –l MATURITY ONSETl AFTER AGE 40l OBESEl REDUCED INSULIN

RECEPTORl NONINSULIN

DEPENDENTl PRONE TO HHONK

DIABETES MILLETUS

DIAGNOSTICEXAMS:FBS2 HR-POSTPRANDIALOGTTGLYCOSYLATEDHGB

DEXTROSTRIPURINE TESTS:l BENEDICT’Sl CLINITEST TABl ACETONE TEST

2 HR POSTPRANDIALBLOOD SUGAR

INTAKE OF 100GM GLUCOSE, 2 HRSBEFORE THE TEST

TEST FOR ABILITY TO DISPOSEGLUCOSE LOAD

OGTTCONFIRMATORY, WHEN OTHER BLOOD TESTSARE BORDERLINE

3 DAYS OF NORMAL ACITIVITY & 150MGOF CARB DIETNPO 10-12HRS BEFORE THE TEST

BASELINE BLOOD SUGAR TAKENGLUCOSE LOAD IS GIVEN, P.O. OR IV

BLOOD & URINE SPECS TAKEN 30 MIN, 1HR,2HRS, 3 HRS, AFTER GLUCOSE LOADING

GLYCOSYLATEDHEMOGLOBIN

MEASURES GLUCOSE METABOLISMFOR THE PAST 3 MONTHS

USEFUL TO CHECK:l COMPLIANCE WITH THERAPYl HISTORY OF SUBCLINICAL OR

CHEMICAL DIABETES

DIABETES MILLETUSPLANNING & IMPLEMENTATION:

CLIENT’S ACTIVITYDIET : C,F,P – 50, 30, 20 LOW SATURATED FATS,HIGH FIBERDRUGS:l ORAL HYPOGLYCEMICS

l BIGUANIDEl SULFONYLUREASl CONTRAINDICATED - PREGNANCY

l INSULIN

DIABETES MILLETUS

INSULIN THERAPYDISPENSED IN “U”/ml : eg 100, 80REFRIGERATEGIVEN @ ROOM TEMPGENTLY ROTATED, NOT SHAKENROUTE : SQ (MTC); IM OR IVSYRINGE: 5/8 INCH ; SAME BRAND

DIABETES MILLETUS

INSULIN THERAPY:SITE OF INJECTION:l ABDOMENl ANTERIOR THIGHl ARMl UPPER BACKl BUTTOCKS

DIABETES MILLETUS

INSULIN THERAPYREACTIONS:LOCAL:l STNGINGl INDURATIONl ITCHING

LIPODYSTROPHY

GENERALIZED:l HIVESl URTICARIAl ANTIHISTAMINES

30 MIN B4l DESENSITIZATION

LIPODYSTROPHY

CAUSE:FAULTY TECHNIQUETRAUMAINJECTION OF REFRIGERATEDINSULIN

MANAGEMENT:ROTATING SITES: 1 AREA IS NOT USEDMORE THAN ONCE EVERY 3 WKS

INSULIN THERAPY &HORMONAL ACTIVITYGLUCORTICOIDS & EPINEPHRINECAUSES HYPERGLYCEMIA DURING:l PHYSICAL TRAUMAl STRESSl INFECTIONl ANXIETYl ANGERl FEARl CHANGE IN LIFESTYLE

INCREASE IN INSULIN DOSE IS NEEDED

SURPRISE!!!

ACUTE COMPLICATIONSOF DIABETES MILLETUS

DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR,NONKETOTIC (HHONK) COMA

SOMOGYI EFFECT

D.K.A.PATHOPHYSIOLOGY

NO INSULINNO INSULIN

MARKED HYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHTLOSS

OSMOTICDIURESISOSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULARCELLULARHUNGER

POLYPHAGIAPOLYPHAGIA

POLYDIPSIA

LIPOLYSISLIPOLYSIS

OSMOTICDEHYDRATION

KETOACIDOSISKETOACIDOSIS

D.K.A.S/SX:

S/SX OF DM +KETONURIAMETABOLIC ACIDOSISKUSSMAUL’S RESPIRATIONACETONE BREATHDHNFLUSHED FACETACHYCARDIACIRCULATORY COLLAPSE COMA DEATH

D.K.A.

MANAGEMENT:

ADEQUATE VENTILATIONFLUID REPLACEMENTINSULIN – RAPID ACTINGECG – ELEC IMB

INSULIN SHOCKLOW BLOOD SUGAR

CAUSE:OVERDOSE OF EXOGENOUS INSULIN

EATING LESS

OVEREXERTION WITHOUT ADDITIONALCALORIE INTAKE

INSULIN SHOCKS/SX:

PARASYMPATHETICl HUNGERl NAUSEAl HYPORTENSIONl BRADYCARDIA

CEREBRALl LETHARGY,l YAWNINGl SENSORIUM CX

SYMPATHETICl IRRITABILITYl SWEATINGl TREMBLINGl TACHYCARDIAl PALLOR

INSULIN SHOCK

CLINICAL FINDING :BLOOD GLUCOSE BELOW 55-60 mg%

TREATMENT:GLUCOSE PO ( SUGAR, ORANGE JUICEOR CANDY) or IVADMINISTRATION OF GLUCAGON IM, IVOR SQ

HHONKPATHOPHYSIOLOGY

Very insufficient INSULIN

MARKED HYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHTLOSS

WEIGHTLOSS

OSMOTICDIURESISOSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULARHUNGER

POLYPHAGIAPOLYPHAGIA

POLYDIPSIAPOLYDIPSIA

LIPOLYSISWithout

KETOSIS

SEVEREOSMOTIC

DEHYDRATION

HHONK

S/SX:S/SX OF DKA WITHOUT:l KAUSMAUL’S BREATHINGl ACETONE BREATHl METABOLIC ACIDOSISl KETONURIA

LACTIC ACIDOSIS

SEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTION

AGGRAVATION OF EXISTINGMETABOLIC ACIDOSIS

SOMOGYI EFFECTTOO MUCH INSULIN

HYPOGLYCEMIA

GLUCAGON IS RELEASED

LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS

REBOUNDHYPERGLYCEMIA

+KETOSIS

CHRONIC COMPLICATIONSOF DIABETES MILLETUS

DEGENERATIVE CHANGES IN THEVASCULAR SYSTEMl UNDERNOURISHMENTl ATHEROSCLEROSIS

NEUROPATHY FROM:l VASCULAR INSUFFICIENCYl VIT B DEFICIENCYl HYPERGLYCEMIA

EYE COMPLICATIONS FROM ANOXIAl CATARACTl DIABETIC RETINOPATHYl RETINAL DETACHMENT

CHRONIC COMPLICATIONSOF DIABETES MILLETUSNEPHROPATHYl DAMAGE & OBLITERATION OF CAPILLARIES

SUPPLYING THE KIDNEY

HEART DISEASEl MI FROM ATHEROSCLEROSIS

SKIN CHANGESl DIABETIC DERMOPATHY – HYPERPIGMENTED &

SCALY PRETIBIAL AREAS

LIVER CHANGESl ENLARGEMENT & FATTY INFILTRATION

Ms A, 45 y.o., has a simple goiter. She’sbeing seen by the community health nursefor teaching & follow-up regarding nutritionaldeficiencies related to her goiter. Ms A’sproblem is almost associated with whatnutritional deficiency?

a. Calciumb. Iodinec. Irond. Sodium