METABOLISM

ENDOCRINE

SYSTEM

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTIONS

PITUITARY

ANTERIOR

TSH Thyroid to release hormones

LOBE ACTH Adrenal cortex to release hormones

FSH,LH Growth, maturation & function of sex organs

GH/

SOMATOTROPIN

Growth of body tissues & bones

PROLACTIN/

LTH

Development of mammary glands & lactation

ENDOCRINE GLANDS

ENDOCRINE GLAND

HORMONE FUNCTION

PITUITARY

POSTERIOR

LOBE

ADH Regulates water metabolism

OXYTOCIN Stimulate uterine contractions

release of milk

INTERME-

DIATE LOBE

MSH Affects skin pigmentation

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTION

ADRENAL CORTEX

ALDOSTERONE Fluid & electrolyte balance;

Na reabsorption;

K excretion

CORTISOL Glycogenolysis;

Gluconeogenesis

Na & water reabsorption

Antiinflammatory

Stress hormone

SEX

HORMONES

Slightly significant

ENDOCRINE GLANDS

ENDOCRINE

GLAND

HORMONE FUNCTION

ADRENAL MEDULLA

EPINEPHRINE

NOR-

EPINEPHRINE

Increase heart rate & BP

Bronchodilation,

Glycogenolysis

Stress hormone

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONE FUNCTION

THYROID T3 & T4’ Regulate metabolic rate

P,C,F metabolism

Regulate physical & mental growth & development

THYRO-

CALCITONIN

Decrease serum Ca by increasing bone deposition

PARA-

THYROID

PTH Increase serum calcium by promoting bone decalcification

ENDOCRINE GLANDSENDOCRINE

GLAND

HORMONE FUNCTION

PANCREAS

BETA

CELLS

INSULIN Decrease blood glucose by:

Glucose diffusion across cell membrane;

Converts glucose to glycogen

ALPHA

CELLS

GLUCAGON Increase blood glucose by:

Gluconeogenesis

Glycogenolysis

ENDOCRINE GLANDS

ENDOCRINE

GLAND

HORMONES FUNCTION

OVARIES ESTROGEN &

PROGES-

TERONE

Development of secondary sex charac in female

Maturation of sex organs

Sexual functioning

Maintenance of pregnancy

TESTES TESTOS-

TERONE

Development of secondary sex charac in male

Maturation of sex organs

Sexual functioning

HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM

CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)

RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)

AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS,

ADRENAL MEDULLA HORMONES)

NEGATIVE FEEDBACK MECHANISM

DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

NEGATIVE FEEDBACK MECHANISM

INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND IS INHIBITED 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 of palpitations.

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

She expressed hyperactivty, sweating, increased appetite & weight loss

CASE STUDY

She claimed history of goiter since her 30’s but no follow-up was done.

What are your nursing plans?

PLANNINGHEALTH PROMOTION IODIZED SALTCONTROLLING WEIGHT

HEALTH MAINTENANCE & RESTORATIONSTEROID THERAPY

STEROID THERAPY

STEROID LEVELS

PITUITARY GLAND IS INHIBITED TO REALEASE ACTH

ENDOGENOUS CORTISOL

PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

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) EXHAUSTION WEAKNESS LETHARGY

STEROID THERAPYASSESSMENT:

ACUTE ADRENAL CRISIS RESTLESSNESS WEAKNESS HEADACHE DHN N/V FALLING BP TO SHOCK

PSYCHOLOGICAL CXS MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION

STEROID THERAPYIMPORTANT FACTS:

MAJOR UNTOWARD EFFECTS: MASKS INFECTION DEFENSE AGAINST INFECTION FROM

LYMPHOPENIASLOW WOUND HEALING FROM ITS

ANTIINFLAMMATORY EFFECTP.U.D. ACTIVATION/ REACTIVATION SERUM SODIUM SERUM POTASSIUM

STEROID THERAPYIMPORTANT FACTS:

MINOR UNTOWARD EFFECTS:PIGMENTATIONACNEFACIAL HAIRMOON-FACIE

STEROID THERAPYIMPORTANT FACTS:

PROBLEMS OF LONG TERM THERAPY:GROWTH RETARDATIONOBESITYGASTRITIS TO P.U.D.OSTEOPOROSISHPNRENAL CALCULIADRENAL ATROPHY

STEROID THERAPY

STEROID LEVELS

PITUITARY GLAND IS INHIBITED TO REALEASE ACTH

ENDOGENOUS CORTISOL

PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

STEROID THERAPYIMPLEMENTATION

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

ANTERIOR PITUITARY DISTURBANCES

HYPOPITUITARISM

HYPERPITUITARISM

HYPOPITUITARISMANTERIOR LOBE

PANHYPOPITUITARISM

(SIMMOND’S DSE)DECREASED SECRETION OF ALL

ANTERIOR LOBE HORMONES

HYPERPITUITARISMANTERIOR LOBE

EOSINOPHILIC TUMOR INCREASED GROWTH HORMONE AND

PROLACTIN

BASOPHILIC TUMOR INCREASED TSH, FSH, LH, MSH, INCREASED ACTH (CUSHING’S DSE)

CHROMOPHOBE TUMOR INCREASED ACTH & GROWTH

HORMONE

PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXN

GH Dwarfism – young

Cachexia - adult

Gigantism – young

Acromegaly - adult

ACTH Atrophy of adrenal cortex

Cushing’s dse

TSH Atrophy & depressed thyroid fxn

Grave’s dse

FSH Atrophy & infertility Exaggerated fxn of sex organs

PROLACTIN Underdevelopment of mammary glands

Decreased milk production

MANAGEMENT

HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY

THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)

HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA &

CARDIOVASCULAR PROBLEMS

POSTERIOR PITUITARY DISTURBANCES

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

CAUSE:

TUMOR

TRAUMA

VASCULAR DSE

INFLAMMATION

PITUITARY SURGERY

S/SX:

POLYURIA 15-29L/ DAY

POLYDIPSIA

SG OF URINE IS

<1.010

S/SX OF DHN

SHOCK

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

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

SPRAY

NON-HORMONAL THERAPY CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY

TO DECREASED VASOPRESSIN

SALT & P RESTRICTED DIET, INCREASE FLUIDSMONITOR I&OMAINTAIN FLUID & ELECTROLYTE BALANCE

SYNDROME OF INAPPROPRIATE ADH

ELEVATED ADH

CAUSES:BRONCHOGENIC CANONENDOCRINE TUMORS

S/SX:DECREASED SERUM SODIUM CX IN LOC TO UNCONSCIOUSNESS SEIZURES

WATER INTOXICATION N/V MENTAL CONFUSION

SYNDROME OF INAPPROPRIATE ADH

MANAGEMENT:WATER INTAKE RESTRICTION

ADMINISTER AS ORDERED:NaClDiureticsDemeclocycline (declamycin) – a

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

Mission possible

THYROID GLAND

STIMULATED BY THYROID STIMULATING

HORMONE (TSH)NEEDS IODINE TO SYNTHESIZE HORMONE

SECRETES:THYROXINE (T4)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 TSHBLOOD SERUM CHOLESTEROLRADIOACTIVE IODINE TESTS: T3 RED CELL UPTAKE RADIOACTIVE IODINE UPTAKE (I131 THYROID SCAN

THYROID DISTURBANCES

HYPOTHYROIDISM HYPERTHYROIDISM

CRETINISM- infants, young children

HYPOTHYROIDISM WITHOUT MYXEDEMA- atrophy/ destruction of thyroid gland

MYXEDEMA –adults

GRAVE’S DSE or Exophthalmic goiter

EFFECTS

HYPOTHYROIDISM HYPERTHYROIDISM

Reduction in HEAT PRODUCTION

Failure of MENTAL & PHYSICAL GROWTH

increased storage of C, P & F

Abnormal collection of WATER

Increase heat

Deranged C metabolism, glycosuria

Increase use of F & P as fuel

HYPOTHYROIDISM HYPERTHYROIDISM

SERUM

CHOLESTEROL:INCREASED

BMR:DECREASED

SKIN:THICK, PUFFY, DRY

HAIR:DRY, BRITTLE

DECREASED

INCREASED

WARM, MOIST, FLUSHED

SOFT, SILKY

HYPOTHYROIDISM HYPERTHYROIDISM

NERVOUS SYSTEM:APATHETIC

LETHARGIC

MAYBE HYPERIRRITABLE

SLOW CEREBRATION

WEIGHT:INCREASED

APPETITE:DECREASED

HYPERACTIVE

LABILE MOOD

HYPERSENSITIVE

TENSED

DECREASED

INCREASED

MANAGEMENTHYPOTHYROIDISM HYPERTHYROIDISM

MEDICAL:

HORMONE REPLACEMENT

DESSICATED THYROID

THYROGLOBULIN

Na LEVOTHYROXINE

Na LYOTHYRONINE

MEDICAL:

REST

ANTITHYROID DRUGS:

LUGOL’S SOLUTION

THIOUREA DERIVATIVES

RADIOACTIVE IODINE

BETA-BLOCKERS

SURGICAL:SUBTOTAL

THYROIDECTOMY

ANTITHYROID MEDICATIONSLUGOL’S SOLUTION

(POTASSIUM IODIDE) DECREASE THYROID VASCULARITY INHIBIT IODINE RELEASE DILUTED IN MILK / JUICE STAINS THE TEETH- USE STRAW

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

RADIOACTIVE IODINE PATIENT IS ISOLATED FOR 3 DAYS

BETA BLOCKERS PROPANOLOL

SUBTOTAL THYROIDECTOMYREMAINING TISSUE PROVIDES ENOUGH HORMONES FOR

NORMAL FXN

PRE OP NURSING CARE:PATIENT EDUCATION ON POST OP: LITTLE HOARSENESS 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 INJURY HOARSENESS

HEMORRHAGE 12-24 HRS POST OP OBSERVE FOR IRREGULAR BREATHING, CHOKING

SIGNS TRACHEOSTOMY SET @ BEDSIDE

TETANY

RESPIRATORY OBSTRUCTION

THYROID STORM

TETANYDEPENDS UPON THE NUMBER OF PARATHYROID GLANDS

REMOVED

S/SX:

1ST – TINGLING TOES & FINGERS2ND – 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:

HYPERTHERMIA > 41C

TACHYCARDIAAPPREHENSIONRESTLESSNESSIRRITABILITYDELIRIUMCOMA

MANAGEMENT:DECREASE TEMP

ANTITHYROID DRUGS

GLUCOSE

DIGITALIS

STEROIDS TO

DECREASE ACTH

THYROID STORM / CRISISINCREASED AMOUNT OF THYROID HORMONES

POST OP

AFTER RADIOACTIVE IODINE ADMINISTRATION

TOO SHORT PERIOD OF PRE OP TX

CAUSES:EMOTIONAL STRESS

PHYSICAL STRESS

VARIANTS OF HYPERTHYROIDISM

GRAVE’S DSE

THYROIDITIS

GOITER

GRAVE’S DISEASE

CAUSE:UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR

S/SX: TRIAD OF SYMPTOMS:HYPERTHYROIDISMOPHTHALMOPATHYDERMOPATHY

OPHTHALMOPATHY

EXOPHTHALMOS – ACCUMULATION OF FLUID IN THE FAT PADS BEHIND HE EYEBAL

LID LAG – PROMINENT PALPEBRAL FISSURE WHEN THE PATIENT LOOKS DOWN

THYROID STARE (DARYMPLE’S SIGN) – INFREQUENT EYE BLINKING

DERMOPATHYPRETIBIAL MYXEDEMA

@ THE DORSUM OF THE LEG

RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN

CLUBBING OF FINGERS & TOES

OSTEOARTHROPATHY

THYROIDITIS

CLASSIFICATION:

SUBACUTE, NONSUPPURATIVE UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS

CHRONIC, HASHIMOTO’S IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS &

ANTIBODIES DIRECTED AGAINST THE THYROID

GOITER

ENLARGEMENT OF THE THYROID GLAND.

TYPES:TOXIC NODULAR

NONTOXIC

TOXIC NODULAR GOITER

COMMON IN ELDERLY

FROM LONG STANDING SIMPLE GOITER

NODULES FUNCTIONING TISSUE SECRETES THYROXINE

AUTONOMOUSLY FROM TSH

NON-TOXIC GOITER(SIMPLE/ COLLOID/ EUTHYROID)

CAUSE :IODINE DEFICIENCYINTAKE OF GOITROGENIC SUBSTANCES/ DRUGS: CASSAVA, CABBAGE, CAULIFLOWER, CARROTS RADDISH TURNIPS RED SKIN OF PEANUTS IODINE COBALT LITHIUM

NON-TOXIC GOITER

IMPAIRED THYROID HORMONE SYNTHESIS

SERUM THYROXINE

PITUITARY SECRETE TSH

THYROID GLAND ENLARGES

TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE

IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCES

NON-TOXIC GOITER

COMMON IN WOMEN:ADOLESCENT

PREGNANT

LACTATING

MENOPAUSE

TREATMENT:IODIZED OIL IM

IODINE TABLETS

SALT FORTIFICATION WITH IODINE

EDUCATE ABOUT INTAKE OF: SEAWEEDS SHELLFISH FISH- TAMBAN, HITO,

DALAG

MYXEDEMA COMA

MEDICAL EMERGENCY

OCCURS IN SEVERE & UNTREATED MYXEDEMA

HIGH MORTALTY RATE

S/SX:INTENSIFIED HYPOTHYROIDISM

NEUROLOGIC IMPAIRMENT COMA

MYXEDEMA COMA

PRECIPITATING FACTORS:

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

MYXEDEMA COMA

MANAGEMENT:

IV THYROID HORMONES

CORRECTION OF HYPOTHERMIA

MAINTAIN VITAL FXNS

TREAT PRECIPITATING CAUSES

PARATHYROID GLAND4 GLANDS

SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph LEVELS

REGULATE CALCIUM & PHOSPHORUS METABOLISM

ORGANS AFFECTED:BONES - RESORPTION

KIDNEYS Ca REABSORPTION Ph EXCRETION

GIT – ENHANCES Ca ABSORPTION

PARATHYROID DISORDERS

DIAGNOSTIC TESTS:HEMATOLOGICALSERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE

URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR

REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISM

DECREASED PTH PRODUCTION

HYPOCALCEMIA

CALCIUM IS: DEPOSITED IN THE BONE EXCRETED

CAUSE:

HEREDITARY

IDIOPATHIC

SURGICAL

HYPOPARATHYROIDISM

S/SX:

ACUTE HYPOCALCEMIA TINGLING OF THE FINGERS CHEVOSTEK’S, TROUSSEAU’S

CHRONIC HYPOCALCEMIA FATIGUE, WEAKNESS PERSONALITY CHANGES LOSS OF TOOTH ENAMEL, DRY SCALY SKIN CARDIAC ARRHYTHMIA CATARACT

HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITY

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

SEIZURE prec

LISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE

CaGLUCONATE @ BEDSIDE

HYPERPARATHYROIDISMINCREASED 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 RICKETS MALABSORPTION SYNDROME OSTEOMALACIA

HYPERPARATHYROIDISMS/SX:

BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRUCTURESTUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIAMUSCLE WEAKNESSPERSONALITY CX, DEPRESSIONCARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISMMANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE

IV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)

LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSESSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY

ADRENAL GLAND

STIMULATED BY ACTH

HORMONE PRECURSOR: CHOLESTEROL

SECRETES: CORTISOL ALDOSTERONE SEX HORMONES : ANDROGEN, ESTROGEN

ADRENAL GLANDHORMONE FUNCTION

ALDOSTERONE Renal : Na & Cl reabsorption; K excretion

GI : Na absorption

GLUCO-

CORTICOIDS

increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS

Blocks inflammation

Counteracts effect of histamine

SEX HORMONE Physiologically insignificant

Becomes useful during menopause in women

SYMPTOMATOLOGY

ALDOSTERONE DEFICIENCY

DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON

HYPOTENSION TO SHOCK

INCREASED K

METABOLIC ACIDOSIS

SYMPTOMATOLOGY

CORTISOL DEFICIENCY

ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY

HYPOGLYCEMIA

HYPOTENSION

INCREASED K, WEAK PULSE

PIGMENTATION

IMPAIRED STRESS TOLERANCE

SYMPTOMATOLOGY

SEX HORMONE DEFICIENCY

LOSS OF BODY HAIR

LOSS OF LIBIDO OR IMPOTENCE

MENSTRUAL & FERTILITY DISORDER

ADRENAL CORTEX DISORERS

ADRENAL INSUFFICIENCY

ADRENAL CRISIS

CUSHING’S SYNDROME

ALDOSTERONISM

ADRENAL INSUFFICIENCYADDISON’S DISEASE

INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS

ADRENAL CRISIS

ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES

POSSIBLE COMPLICATION OF ADDISON’S DISEASE

ADRENAL CRISIS

PRECIPITATING CAUSES:

ABDOMINAL DISCOMFORT

INFECTION

TRAUMA

HIGH TEMP

EMOTIONAL UPSET

ANTICOAGULANT DRUGS

ADRENAL CRISIS

S/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 CRISIS

GOALS OF CARE:TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

ADRENAL CRISIS

TREATMENT:D5NSS

ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE

NEOSYNEPHRINE - SHOCK

HIGH SALT DIET

ANTIBIOTICS

CUSHING’S SYNDROME

CAUSE:SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID ADMINISTRATION

CUSHING’S SYNDROME

S/SX:TRUNCAL OBESITY

BUFFALO HUMP

MOON-FACIE

WT GAIN

SODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHING’S SYNDROME

PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:

OLIGOMENORRHEA

HIRSUTISMGYNECOMASTIA

HYPERTENSION FROM S. Na

CUSHING’S SYNDROME

TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED

PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY

ALDOSTERONISM

HYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME

SECONDARY

CONN’S SYNDROMEPRIMARY ALDOSTERONISM

CAUSE:ADRENAL ADENOMA

S/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPN, TETANY

MANAGEMENT:

SURGERYALDACTONE – ALDOSTERONE ANTAGONIST

SECONDARY ALDOSTERONISM

THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLA

HORMONES : EPINEPHRINE

NOREPINEPHRINE

EFFECTS

PHEOCHROMOCYTOMA

TUMOR 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 CATECHOLAMINE METABOLISM

DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:COFFEE & TEABANANAVANILLACHOCOLATES

PHEOCHROMOCYTOMA

MANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING AGENTS: 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 INSULIN

LACK OF INSULIN

EFFECT:

HYPERGLYCEMIA

DIABETES MILLETUS

PATHOPHYSIOLOGYREDUCED /NO INSULINREDUCED /NO INSULIN

HYPERGLYCEMIAHYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHT LOSSWEIGHT LOSS

OSMOTICDIURESISOSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULAR HUNGER

CELLULAR HUNGER

POLYPHAGIAPOLYPHAGIA

POLYDIPSIAPOLYDIPSIA

LIPOLYSISLIPOLYSIS

OSMOTICDEHYDRATION

OSMOTICDEHYDRATION

DIABETES MILLETUS

S/SX:

3 – P’s

WEIGHT LOSS

STAGES:

PREDIABETES

SUSPECTED

CHEMICAL

CLINICAL / OVERT

DIABETES MILLETUS

PREDIABETES / POTENTIAL:

CONCEPTIONCONCEPTION

EVIDENCE OF GLUCOSE METABOLISMALTERATION

EVIDENCE OF GLUCOSE METABOLISMALTERATION

DIABETES MILLETUS

SUSPECTED/ SUBCLINICAL/ LATENT:

PREDIABETESPREDIABETES

NO STRESS STRESSSTRESS

NORMAL GLUCOSEMETABOLISM

OVERT DIABETESOVERT DIABETES

DIABETES MILLETUSCHEMEICAL:

SUBCLINICALSUBCLINICAL

GTT IS ABNORMALGTT IS ABNORMAL

NO STRESSNO STRESS STRESSSTRESS

ASYMPTOMATICASYMPTOMATIC SYMPTOMATICSYMPTOMATIC

DIABETES MILLETUSCLINICAL / OVERT:

CHEMICALCHEMICAL

PERSISTENT INCREASED FBSPERSISTENT INCREASED FBS

WITH OR WITHOUT STRESSWITH OR WITHOUT STRESS

SYMPTOMATICSYMPTOMATIC

DIABETES MILLETUSTYPES:

TYPE I JUVENILE ONSET BEFORE 15 YO LEAN/ NORMAL

WEIGHT ABSOLUTE INSULIN

DEFICIENCY INSULIN -DEPENDENT PRONE TO DKA

TYPE II – MATURITY ONSET AFTER AGE 40 OBESE REDUCED INSULIN

RECEPTOR NONINSULIN

DEPENDENT PRONE TO HHONK

DIABETES MILLETUS

DIAGNOSTIC EXAMS:

FBS

2 HR- POSTPRANDIAL

OGTT

GLYCOSYLATED HGB

DEXTROSTRIP

URINE TESTS: BENEDICT’S CLINITEST TAB ACETONE TEST

2 HR POSTPRANDIAL BLOOD SUGAR

INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST

TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD

OGTT

CONFIRMATORY, WHEN OTHER BLOOD TESTS ARE BORDERLINE

3 DAYS OF NORMAL ACITIVITY & 150MG OF 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

GLYCOSYLATED HEMOGLOBIN

MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS

USEFUL TO CHECK:COMPLIANCE WITH THERAPYHISTORY OF SUBCLINICAL OR

CHEMICAL DIABETES

DIABETES MILLETUS

PLANNING & IMPLEMENTATION:CLIENT’S ACTIVITYDIET : C,F,P – 50, 30, 20 LOW SATURATED FATS, HIGH FIBER

DRUGS: ORAL HYPOGLYCEMICS

BIGUANIDE SULFONYLUREAS CONTRAINDICATED - PREGNANCY

INSULIN

DIABETES MILLETUS

INSULIN 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 MILLETUS

INSULIN THERAPY:

SITE OF INJECTION:ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS

DIABETES MILLETUS

INSULIN THERAPY REACTIONS:

LOCAL: STNGING INDURATION ITCHING

LIPODYSTROPHY

GENERALIZED: HIVES URTICARIA ANTIHISTAMINES

30 MIN B4 DESENSITIZATION

LIPODYSTROPHY

CAUSE:FAULTY TECHNIQUETRAUMAINJECTION OF REFRIGERATED INSULIN

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

INSULIN THERAPY & HORMONAL ACTIVITY

GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING: PHYSICAL TRAUMA STRESS INFECTION ANXIETY ANGER FEAR CHANGE IN LIFESTYLE

INCREASE IN INSULIN DOSE IS NEEDED

SURPRISE!!!

ACUTE COMPLICATIONS OF DIABETES MILLETUS

DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR,

NONKETOTIC (HHONK) COMA

SOMOGYI EFFECT

D.K.A.PATHOPHYSIOLOGY

NO INSULINNO INSULIN

MARKED HYPERGLYCEMIAMARKED HYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHT LOSS

WEIGHT LOSS

OSMOTICDIURESIS

OSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULAR HUNGER

CELLULAR HUNGER

POLYPHAGIAPOLYPHAGIA

POLYDIPSIAPOLYDIPSIA

LIPOLYSISLIPOLYSIS

OSMOTICDEHYDRATION

OSMOTICDEHYDRATION

KETOACIDOSISKETOACIDOSIS

D.K.A.

S/SX:S/SX OF DM +KETONURIAMETABOLIC ACIDOSISKUSSMAUL’S RESPIRATIONACETONE BREATHDHNFLUSHED FACETACHYCARDIA

CIRCULATORY COLLAPSE COMA DEATH

D.K.A.

MANAGEMENT:

ADEQUATE VENTILATION

FLUID REPLACEMENT

INSULIN – RAPID ACTING

ECG – ELEC IMB

INSULIN SHOCK

LOW BLOOD SUGAR

CAUSE:OVERDOSE OF EXOGENOUS INSULIN

EATING LESS

OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE

INSULIN SHOCKS/SX:

PARASYMPATHETIC HUNGER NAUSEA HYPORTENSION BRADYCARDIA

CEREBRAL LETHARGY, YAWNING SENSORIUM CX

SYMPATHETIC IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR

INSULIN SHOCK

CLINICAL FINDING : BLOOD GLUCOSE BELOW 55-60 mg%

TREATMENT:GLUCOSE PO ( SUGAR, ORANGE JUICE OR CANDY) or IV

ADMINISTRATION OF GLUCAGON IM, IV OR SQ

HHONKPATHOPHYSIOLOGY

Very insufficient INSULINVery insufficient INSULIN

MARKED HYPERGLYCEMIAMARKED HYPERGLYCEMIA

GLUCOSURIAGLUCOSURIA

WEIGHT LOSS

WEIGHT LOSS

OSMOTICDIURESISOSMOTICDIURESIS

POLYURIAPOLYURIA

CELLULAR HUNGER

CELLULAR HUNGER

POLYPHAGIAPOLYPHAGIA

POLYDIPSIAPOLYDIPSIA

LIPOLYSISWithoutKETOSIS

LIPOLYSISWithoutKETOSIS

SEVEREOSMOTIC

DEHYDRATION

SEVEREOSMOTIC

DEHYDRATION

HHONK

S/SX:

S/SX OF DKA WITHOUT:KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA

LACTIC ACIDOSIS

SEVERE TISSUE ANOXIASEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTIONLACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING

METABOLIC ACIDOSISAGGRAVATION OF EXISTING

METABOLIC ACIDOSIS

SOMOGYI EFFECTTOO MUCH INSULINTOO MUCH INSULIN

HYPOGLYCEMIAHYPOGLYCEMIA

GLUCAGON IS RELEASEDGLUCAGON IS RELEASED

LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS

LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS

REBOUNDHYPERGLYCEMIA

+KETOSIS

REBOUNDHYPERGLYCEMIA

+KETOSIS

CHRONIC COMPLICATIONS OF DIABETES MILLETUS

DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM UNDERNOURISHMENT ATHEROSCLEROSIS

NEUROPATHY FROM: VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA

EYE COMPLICATIONS FROM ANOXIA CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT

CHRONIC COMPLICATIONS OF DIABETES MILLETUS

NEPHROPATHY DAMAGE & OBLITERATION OF CAPILLARIES

SUPPLYING THE KIDNEY

HEART DISEASE MI FROM ATHEROSCLEROSIS

SKIN CHANGES DIABETIC DERMOPATHY – HYPERPIGMENTED &

SCALY PRETIBIAL AREAS

LIVER CHANGES 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. Calcium

b. Iodine

c. Iron

d. Sodium