Metabolism

METABOLISM

ENDOCRINE SYSTEM

Created by:

Nhelia S. Bañaga – Perez

Northeastern College

Santiago City, Philippines

Points to ponder • Affected in large part by structures in the nervous

system. • They may also influence the function of a large number

of other endocrine glands.• Affects the nervous system and in turn is mediated by

the nervous system.• Interacts with the immune system.• Other tissues produce hormone that are secreted into

body fluids and act on nearby cells and tissues. • Important in the regulation of the internal environment

of the body.

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 GLANDSENDOCRINE GLAND HORMONE FUNCTION

PITUITARY•POSTERIOR LOBE

ADH •Regulates water metabolism

OXYTOCIN •Stimulate uterine contractions •release of milk

• INTERME- DIATE LOBE

MSH •Affects skin pigmentation


HORMONES FUNCTION

ADRENAL CORTEX

ALDOSTERONE •Fluid & electrolyte balance; •Na reabsorption; •K excretion

CORTISOL •Glycogenolysis;•Gluconeogenesis•Na & water reabsorption•Antiinflammatory•Stress hormone

SEXHORMONES

•Slightly significant

ENDOCRINE GLANDS

ENDOCRINEGLAND

HORMONE FUNCTION

ADRENAL MEDULLA

EPINEPHRINENOR-EPINEPHRINE

•Increase heart rate & BP•Bronchodilation, •Glycogenolysis•Stress hormone


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 GLANDSENDOCRINEGLAND

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 GLANDSENDOCRINEGLAND

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 REGULATION

• NEGATIVE FEEDBACK MECHANISM

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

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

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

ADRENAL MEDULLA HORMONES)

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 STUDY

• Osang, an elderly, came in because of palpitations.

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

• She expressed hyperactivity, 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?

PLANNING• HEALTH PROMOTION– IODIZED SALT– CONTROLLING WEIGHT

• HEALTH MAINTENANCE & RESTORATION– STEROID THERAPY

STEROID THERAPY

STEROID LEVELS

PITUITARY GLAND IS INHIBITED TO RELEASE 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

LYMPHOPENIA– SLOW WOUND HEALING FROM ITS

ANTIINFLAMMATORY EFFECT– P.U.D. ACTIVATION/ REACTIVATION – SERUM SODIUM – SERUM POTASSIUM


• MINOR UNTOWARD EFFECTS:– PIGMENTATION– ACNE– FACIAL HAIR– MOON-FACIE


• PROBLEMS OF LONG TERM THERAPY:– GROWTH RETARDATION– OBESITY– GASTRITIS TO P.U.D.– OSTEOPOROSIS– HPN– RENAL CALCULI– ADRENAL 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 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 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

MANAGEMENT• HORMONAL 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 & Protein RESTRICTED DIET, INCREASE FLUIDS

• MONITOR I&O• MAINTAIN FLUID & ELECTROLYTE BALANCE

SYNDROME OF INAPPROPRIATE ADH

• ELEVATED ADH

CAUSES:• BRONCHOGENIC CA• NONENDOCRINE 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:– NaCl– Diuretics– Demeclocycline (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 TSH

• BLOOD SERUM CHOLESTEROL• RADIOACTIVE IODINE TESTS:

– T3 RED CELL UPTAKE– RADIOACTIVE IODINE UPTAKE (I131– THYROID SCAN

THYROID DISTURBANCESHYPOTHYROIDISM HYPERTHYROIDISM

•CRETINISM- infants, young children•HYPOTHYROIDISM WITHOUT MYXEDEMA- atrophy/ destruction of thyroid gland•MYXEDEMA –adults

GRAVE’S DSE or Exophthalmic goiter

EFFECTSHYPOTHYROIDISM 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 HYPERTHYROIDISMMEDICAL: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 MEDICATIONS• LUGOL’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’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– 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 & 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:• HYPERTHERMIA > 41C• TACHYCARDIA• APPREHENSION• RESTLESSNESS• IRRITABILITY• DELIRIUM• COMA

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:• HYPERTHYROIDISM• OPHTHALMOPATHY• DERMOPATHY

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

DERMOPATHY• PRETIBIAL 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 DEFICIENCY• INTAKE 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 MEDS• INFECTION• TRAUMA• EXPOSURE TO COLD• USE OF SEDATIVES, NARCOTICS, ANESTHETICS

MYXEDEMA COMA

MANAGEMENT:

• 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 – Ca REABSORPTION– Ph EXCRETION

• GIT – ENHANCES Ca ABSORPTION

PARATHYROID DISORDERS

DIAGNOSTIC TESTS:• HEMATOLOGICAL– SERUM CALCIUM– SERUM PHOSPHORUS– SERUM ALKALINE PHOSPHATASE

• URINARY STUDIES– URINARY CALCIUM– URINARY 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

HYPOPARATHYROIDISM

XRAY: INCREASED BONE DENSITY

MANAGEMENT:• Ca SUPPLEMENT• VIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR

MILK, pc

• SEIZURE prec• LISTEN FOR STRIDOR OR HOARSENESS• TRACHEOSTOMY SET @ BEDSIDE

• CaGLUCONATE @ BEDSIDE

HYPERPARATHYROIDISM• INCREASED PTH PRODUCTION• HYPERCALCEMIA• HYPOPHOSPHATEMIA• PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID

GLAND

• SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:– CHRONIC RENAL DSE– RICKETS– MALABSORPTION SYNDROME– 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, HPN

XRAY: 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 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 CRISIS

LAB:• 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


S/SX:• TRUNCAL OBESITY• BUFFALO HUMP• MOON-FACIE• WT GAIN• SODIUM RETENTION• THINNING OF EXTREMITIES – FROM LOSS OF

MUSCLE TISSUE DUE TO PROTEIN CATABOLISM


• PURPLE STRIAE – FROM THINNING OF SKIN• ECHYMOSIS FROM SLIGHT TRAUMA• ANDROGENIC EFFECTS:

OLIGOMENORRHEAHIRSUTISMGYNECOMASTIA

• HYPERTENSION FROM S. Na


TREATMENT & NURSING CARE:

• PSYCHOLOGICAL SUPPORT• PREVENT INFECTION – INFLAM & IMMUNE RESPONSE

ARE SUPPRESSED

• PROMOTE SAFETY • SURGERY – SUB/TOTAL ADRENALECTOMY

ALDOSTERONISM

HYPERSECRETION OF ALDOSTERONE

• PRIMARY – CONN’S SYNDROME

• SECONDARY

CONN’S SYNDROME• PRIMARY ALDOSTERONISMCAUSE:• ADRENAL ADENOMA

S/SX:• HYPOKALEMIA• FATIGUE• HYPERNATREMIA, HPN, TETANY

MANAGEMENT:• SURGERY• ALDACTONE – ALDOSTERONE ANTAGONIST

SECONDARY ALDOSTERONISM

• THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLA

HORMONES : EPINEPHRINENOREPINEPHRINE

EFFECTS

PHEOCHROMOCYTOMA• TUMOR OF ADRENAL MEDULLA• SECRETES INCREASED AMOUNT OF CATECHOLAMINES

S/SX:• HPN• HYPERGLYCEMIA• CARDIAC 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 & TEA– BANANA– VANILLA– CHOCOLATES

PHEOCHROMOCYTOMA

MANAGEMENT:• SURGERY• MEDICAL : ADRENERGIC BLOCKING AGENTS:

PHENTOLAMINE

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

PANCREAS

HORMONES:

• INSULIN BY BETA CELLS

• GLUCAGON BY ALPHA CELLS

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 DIET

• NPO 10-12HRS BEFORE THE TEST

• BASELINE BLOOD SUGAR TAKEN• GLUCOSE 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 THERAPY– HISTORY OF SUBCLINICAL OR CHEMICAL DIABETES

DIABETES MILLETUS

PLANNING & IMPLEMENTATION:• CLIENT’S ACTIVITY• DIET : 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:– ABDOMEN– ANTERIOR THIGH– ARM – UPPER BACK – BUTTOCKS

DIABETES MILLETUS

INSULIN THERAPY REACTIONS:

• LOCAL: – STNGING – INDURATION – ITCHING

• LIPODYSTROPHY

• GENERALIZED: – HIVES – URTICARIA– ANTIHISTAMINES 30

MIN B4– DESENSITIZATION

LIPODYSTROPHY

CAUSE:• FAULTY TECHNIQUE• TRAUMA• INJECTION OF REFRIGERATED INSULINMANAGEMENT:• 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 +• 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 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 BREATHING– ACETONE BREATH– METABOLIC ACIDOSIS– KETONURIA

LACTIC ACIDOSIS

SEVERE TISSUE ANOXIASEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTIONLACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING

METABOLIC ACIDOSISAGGRAVATION OF EXISTING

METABOLIC ACIDOSIS

SOMOGYI EFFECT

TOO 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. Calciumb. Iodinec. Iron d. Sodium

Health & Medicine

Metabolism