ENDOCRINE SYSTEM

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 GLAND

HORMONES TSH

FUNCTIONS
Thyroid to release hormones

PITUITARY ANTERIOR LOBE

ACTH FSH,LH GH/ SOMATOTROPIN PROLACTIN/ LTH

Adrenal cortex to release hormones Growth, maturation & function of sex organs Growth of body tissues & bones Development of mammary glands & lactation

ENDOCRINE GLAND

HORMONE ADH

FUNCTION
Regulates water metabolism

PITUITARY POSTERIOR LOBE

OXYTOCIN

Stimulate uterine contractions release of milk Affects skin pigmentation

INTERMEDIATE LOBE

MSH

ENDOCRINE GLAND

HORMONES
ALDOSTERONE

FUNCTION
Fluid & electrolyte balance; Na reabsorption; K excretion
Glycogenolysis; Gluconeogenesis Na & water reabsorption Antiinflammatory Stress hormone

ADRENAL CORTEX

CORTISOL

SEX HORMONES

Slightly significant

ENDOCRINE GLAND

HORMONE EPINEPHRINE NOREPINEPHRINE

FUNCTION
Increase heart rate & BP Bronchodilation, Glycogenolysis Stress hormone

ADRENAL MEDULLA

ENDOCRINE GLAND

HORMONE
T3 & T4

FUNCTION
Regulate metabolic rate P,C,F metabolism Regulate physical & mental growth & development

THYROID

THYROCALCITONIN

Decrease serum Ca by increasing bone deposition

Increase serum calcium by promoting bone decalcification

PARATHYROID

PTH

ENDOCRINE GLAND

HORMONE
INSULIN

FUNCTION
Decrease blood glucose by: Glucose diffusion across cell membrane; Converts glucose to glycogen Increase blood glucose by: Gluconeogenesis Glycogenolysis

PANCREAS BETA CELLS ALPHA CELLS

GLUCAGON

ENDOCRINE GLAND

HORMONES

FUNCTION
Development of secondary sex charac in female Maturation of sex organs Sexual functioning Maintenance of pregnancy Development of secondary sex charac in male Maturation of sex organs Sexual functioning

OVARIES

ESTROGEN & PROGESTERONE

TESTES

TESTOSTERONE

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)

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

RELEASE OF STIMULATING HORMONE (e.g. TSH)

PITUITARY GLAND

STIMULATION OF TARGET ORGANS TO

(e.g.
PRODUCE & RELEASE HORMONE Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

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

RELEASE STIMULATING HORMONE (e.g. TSH)

PITUITARY GLAND IS INHIBITED TO

DECREASED PRODUCTION & SECRETION

OF TARGET ORGAN OF THE HORMONE (e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

Osang, an elderly, came in because of palpitations. VS revealed: 37.9o , 120, 25, 140/ 90 She expressed hyperactivity, sweating, increased appetite & weight loss

She claimed history of goiter since her 30s but no follow-up was done. What are your nursing plans?

HEALTH PROMOTION
IODIZED SALT CONTROLLING WEIGHT

HEALTH MAINTENANCE & RESTORATION

STEROID THERAPY

STEROID LEVELS PITUITARY GLAND IS INHIBITED TO RELEASE ACTH

ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

PHARMACOLOGIC 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

ASSESSMENT: BASELINE STEROID LEVEL IS ASSESSED BEFORE

PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED

STEROID WITHDRAWAL (LOW STRESS

TOLERANCE) EXHAUSTION WEAKNESS LETHARGY

ASSESSMENT: ACUTE ADRENAL CRISIS

RESTLESSNESS WEAKNESS HEADACHE DHN N/V FALLING BP TO SHOCK

PSYCHOLOGICAL CXS
MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION

IMPORTANT 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

IMPORTANT FACTS:

MINOR UNTOWARD EFFECTS:

PIGMENTATION ACNE FACIAL HAIR MOON-FACIE

IMPORTANT FACTS:

PROBLEMS OF LONG TERM THERAPY:

GROWTH RETARDATION OBESITY GASTRITIS TO P.U.D. OSTEOPOROSIS HPN RENAL CALCULI ADRENAL ATROPHY

STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH

ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

IMPLEMENTATION

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

HYPOPITUITARISM HYPERPITUITARISM

PANHYPOPITUITARISM (SIMMONDS DSE)

DECREASED SECRETION OF ALL ANTERIOR LOBE HORMONES

EOSINOPHILIC TUMOR
INCREASED GROWTH HORMONE AND PROLACTIN

BASOPHILIC TUMOR
INCREASED TSH, FSH, LH, MSH, INCREASED ACTH (CUSHINGS DSE)

CHROMOPHOBE TUMOR
INCREASED ACTH & GROWTH HORMONE

HORMONE GH ACTH

HYPO FXN Dwarfism young Cachexia - adult Atrophy of adrenal cortex

HYPER FXN Gigantism young Acromegaly - adult Cushings dse

TSH
FSH PROLACTIN

Atrophy & depressed thyroid fxn Atrophy & infertility

Graves dse
Exaggerated fxn of sex organs

Underdevelopment of Decreased milk mammary glands production

HYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY
THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)

HYPERPITUITARISM
SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

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

MANAGEMENT HORMONAL REPLACEMENT FOR LIFE

NON-HORMONAL THERAPY

VASOPRESSIN (PITRESSIN TANNATE IN OIL) IM OR NASAL SPRAY CHLORPROPRAMIDE INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN

SALT & Protein RESTRICTED DIET, INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE BALANCE

ELEVATED ADH

CAUSES: BRONCHOGENIC CA NONENDOCRINE TUMORS S/SX: DECREASED SERUM SODIUM

WATER INTOXICATION
N/V MENTAL CONFUSION

CX IN LOC TO UNCONSCIOUSNESS SEIZURES

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

STIMULATED BY THYROID STIMULATING HORMONE (TSH) NEEDS IODINE TO SYNTHESIZE HORMONE SECRETES:
THYROXINE (T4) TRIIODOTHYRONINE (T3)

DIAGNOSTIC 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

HYPOTHYROIDISM
CRETINISM- infants, young children HYPOTHYROIDISM WITHOUT MYXEDEMAatrophy/ destruction of thyroid gland MYXEDEMA adults

HYPERTHYROIDISM
GRAVES DSE or Exophthalmic goiter

HYPOTHYROIDISM
Reduction in HEAT PRODUCTION Failure of MENTAL & PHYSICAL GROWTH increased storage of C, P&F Abnormal collection of WATER

HYPERTHYROIDISM
Increase heat

Deranged C metabolism, glycosuria Increase use of F & P as fuel

HYPOTHYROIDISM SERUM CHOLESTEROL:

INCREASED

HYPERTHYROIDISM

DECREASED

BMR:
DECREASED INCREASED
WARM, MOIST, FLUSHED SOFT, SILKY

SKIN:
THICK, PUFFY, DRY

HAIR:
DRY, BRITTLE

HYPOTHYROIDISM
NERVOUS SYSTEM:
APATHETIC LETHARGIC MAYBE HYPERIRRITABLE SLOW CEREBRATION

HYPERTHYROIDISM
HYPERACTIVE LABILE MOOD HYPERSENSITIVE TENSED

WEIGHT:
INCREASED DECREASED

APPETITE:
DECREASED INCREASED

HYPOTHYROIDISM MEDICAL: HORMONE REPLACEMENT

DESSICATED THYROID THYROGLOBULIN Na LEVOTHYROXINE Na LYOTHYRONINE

HYPERTHYROIDISM MEDICAL: REST ANTITHYROID DRUGS:

LUGOLS SOLUTION THIOUREA DERIVATIVES RADIOACTIVE IODINE BETA-BLOCKERS

SURGICAL:
SUBTOTAL THYROIDECTOMY

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

THIOUREA & DERIVATIVES

(PTU,METHIMAZOLE)

RADIOACTIVE IODINE
BETA BLOCKERS
PROPANOLOL

BLOCK THYROID HORMONE RELEASE TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA

PATIENT IS ISOLATED FOR 3 DAYS

REMAINING TISSUE PROVIDES ENOUGH HORMONES FOR NORMAL FXN

PRE OP NURSING CARE: PATIENT EDUCATION ON POST OP:

POST OP NURSING CARE:

LITTLE HOARSENESS DIFFICULTY OF SWALLOWING

SEMIFOWLERS AVOID HYPEREXTENSION OF THE NECK BE ASKED TO SPEAK @ 40 MIN INTERVAL ASSESS RECURRENT NERVE INJURY WATCH OUT FOR COMPLICATIONS.

COMPLICATIONS:

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

DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVED

S/SX: 1ST TINGLING TOES & FINGERS 2ND CHEVOSTEKS SIGN (TAPPING THE FACIAL
MUSCLES) 3RD TROUSSEAUS SIGN (CARPO-PEDAL SPASM WITH OCCLUSION OF CIRCULATION WITH A BP CUFF)

MANAGEMENT: CALCIUM REPLACEMENT: CaGluconate IV

S/SX:

MANAGEMENT:

HYPERTHERMIA > 41C TACHYCARDIA APPREHENSION RESTLESSNESS IRRITABILITY DELIRIUM COMA

DECREASE TEMP ANTITHYROID DRUGS GLUCOSE DIGITALIS STEROIDS TO DECREASE ACTH

INCREASED AMOUNT OF THYROID HORMONES

POST OP AFTER RADIOACTIVE IODINE ADMINISTRATION TOO SHORT PERIOD OF PRE OP TX CAUSES: EMOTIONAL STRESS PHYSICAL STRESS

GRAVES DSE
THYROIDITIS GOITER

CAUSE: UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR

S/SX: TRIAD OF SYMPTOMS: HYPERTHYROIDISM OPHTHALMOPATHY DERMOPATHY

EXOPHTHALMOS ACCUMULATION OF FLUID IN

THE FAT PADS BEHIND HE EYEBAL

LID LAG PROMINENT PALPEBRAL FISSURE WHEN

THE PATIENT LOOKS DOWN

THYROID STARE

(DARYMPLES SIGN) INFREQUENT EYE BLINKING

PRETIBIAL MYXEDEMA

@ THE DORSUM OF THE LEG

RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN CLUBBING OF FINGERS & TOES

OSTEOARTHROPATHY

CLASSIFICATION: SUBACUTE, NONSUPPURATIVE

UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS

CHRONIC, HASHIMOTOS
IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID

ENLARGEMENT OF THE THYROID GLAND.

TYPES:

TOXIC NODULAR
NONTOXIC

COMMON IN ELDERLY FROM LONG STANDING SIMPLE GOITER NODULES

FUNCTIONING TISSUE SECRETES THYROXINE AUTONOMOUSLY FROM TSH

(SIMPLE/ COLLOID/ EUTHYROID)

CAUSE :

IODINE DEFICIENCY INTAKE OF GOITROGENIC SUBSTANCES/ DRUGS:

CASSAVA, CABBAGE, CAULIFLOWER, CARROTS RADDISH TURNIPS RED SKIN OF PEANUTS IODINE COBALT LITHIUM

IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCES

IMPAIRED THYROID HORMONE SYNTHESIS SERUM THYROXINE

PITUITARY SECRETE

TSH

THYROID GLAND ENLARGES

TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE

TREATMENT: COMMON IN WOMEN:

ADOLESCENT PREGNANT LACTATING MENOPAUSE

IODIZED OIL IM IODINE TABLETS SALT FORTIFICATION WITH IODINE EDUCATE ABOUT INTAKE OF:
SEAWEEDS SHELLFISH FISH- TAMBAN, HITO, DALAG

MEDICAL EMERGENCY OCCURS IN SEVERE & UNTREATED MYXEDEMA HIGH MORTALTY RATE S/SX: INTENSIFIED HYPOTHYROIDISM NEUROLOGIC IMPAIRMENT COMA

PRECIPITATING FACTORS:

FAILURE TO TAKE MEDS INFECTION TRAUMA EXPOSURE TO COLD USE OF SEDATIVES, NARCOTICS, ANESTHETICS

MANAGEMENT:

IV THYROID HORMONES CORRECTION OF HYPOTHERMIA MAINTAIN VITAL FXNS TREAT PRECIPITATING CAUSES

4 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

DIAGNOSTIC TESTS: HEMATOLOGICAL

URINARY STUDIES

SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE PHOSPHATASE URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE

DECREASED PTH PRODUCTION HYPOCALCEMIA CALCIUM IS:

DEPOSITED IN THE BONE EXCRETED

CAUSE: HEREDITARY IDIOPATHIC SURGICAL

S/SX: ACUTE HYPOCALCEMIA

TINGLING OF THE FINGERS CHEVOSTEKS, TROUSSEAUS

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

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

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

S/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

MANAGEMENT:

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

STIMULATED BY ACTH HORMONE PRECURSOR:

CHOLESTEROL

SECRETES:
CORTISOL ALDOSTERONE SEX HORMONES : ANDROGEN, ESTROGEN

HORMONE
ALDOSTERONE

FUNCTION
Renal : Na & Cl reabsorption; K excretion GI : Na absorption increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS Blocks inflammation Counteracts effect of histamine

GLUCOCORTICOIDS

SEX HORMONE

Physiologically insignificant Becomes useful during menopause in women

ALDOSTERONE DEFICIENCY

DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON HYPOTENSION TO SHOCK INCREASED K METABOLIC ACIDOSIS

CORTISOL DEFICIENCY

ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY HYPOGLYCEMIA HYPOTENSION INCREASED K, WEAK PULSE PIGMENTATION IMPAIRED STRESS TOLERANCE

SEX HORMONE DEFICIENCY

LOSS OF BODY HAIR LOSS OF LIBIDO OR IMPOTENCE MENSTRUAL & FERTILITY DISORDER

ADRENAL INSUFFICIENCY
ADRENAL CRISIS CUSHINGS SYNDROME

ALDOSTERONISM

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

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

DISEASE

ADDISONS

PRECIPITATING CAUSES: ABDOMINAL DISCOMFORT INFECTION TRAUMA HIGH TEMP EMOTIONAL UPSET ANTICOAGULANT DRUGS

S/SX:

HYPOTENSION FLUID LOSS HYPONATREMIA

LAB:

SERUM ELEC: DECREASED Na

INCREASED K

S. BUN : S. GLUCOSE: ADRENAL HORMONE ASSAY :

HYDROXYCORTICOID & 17 KETOSTEROID IN 24HR URINE DET.

GOALS OF CARE:

TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

TREATMENT:

D5NSS ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE NEOSYNEPHRINE - SHOCK HIGH SALT DIET ANTIBIOTICS

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:
OLIGOMENORRHEA HIRSUTISM GYNECOMASTIA

HYPERTENSION FROM

S. Na

TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORT PREVENT INFECTION INFLAM & IMMUNE

RESPONSE ARE SUPPRESSED

PROMOTE SAFETY SURGERY SUB/TOTAL ADRENALECTOMY

HYPERSECRETION OF ALDOSTERONE

PRIMARY CONNS SYNDROME SECONDARY

PRIMARY ALDOSTERONISM CAUSE:

S/SX:

ADRENAL ADENOMA

HYPOKALEMIA FATIGUE HYPERNATREMIA, HPN, TETANY MANAGEMENT: SURGERY ALDACTONE ALDOSTERONE ANTAGONIST

THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:

e.g. RENIN ANGIOTENSIN SYSTEM

HORMONES : EPINEPHRINE NOREPINEPHRINE EFFECTS

TUMOR OF ADRENAL MEDULLA SECRETES INCREASED AMOUNT OF CATECHOLAMINES

S/SX: HPN HYPERGLYCEMIA CARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE

END PRODUCT OF CATECHOLAMINE METABOLISM DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:
COFFEE & TEA BANANA VANILLA CHOCOLATES

MANAGEMENT: SURGERY MEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE

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

HORMONES:

INSULIN BY BETA CELLS GLUCAGON BY ALPHA CELLS

INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD

CONFIRMATORY,
BORDERLINE

WHEN OTHER BLOOD TESTS ARE

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

MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS USEFUL TO CHECK:

COMPLIANCE WITH THERAPY HISTORY OF SUBCLINICAL OR CHEMICAL DIABETES

PLANNING & IMPLEMENTATION: CLIENTS ACTIVITY DIET : C,F,P 50, 30, 20 LOW SATURATED FATS,
HIGH FIBER

DRUGS:

ORAL HYPOGLYCEMICS

INSULIN

BIGUANIDE SULFONYLUREAS CONTRAINDICATED - PREGNANCY

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

INSULIN THERAPY: SITE OF INJECTION:

ABDOMEN ANTERIOR THIGH ARM UPPER BACK BUTTOCKS

INSULIN THERAPY REACTIONS: LOCAL:

STNGING INDURATION ITCHING

GENERALIZED:
HIVES URTICARIA ANTIHISTAMINES 30 MIN B4 DESENSITIZATION

LIPODYSTROPHY

CAUSE:

FAULTY TECHNIQUE TRAUMA INJECTION OF REFRIGERATED INSULIN MANAGEMENT: ROTATING SITES: 1 AREA IS NOT USED MORE
THAN ONCE EVERY 3 WKS

GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING:

PHYSICAL TRAUMA STRESS INFECTION ANXIETY ANGER FEAR CHANGE IN LIFESTYLE

INCREASE IN INSULIN DOSE IS NEEDED

SURPRISE!!!

DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA SOMOGYI EFFECT

NO INSULIN OSMOTIC DEHYDRATION

MARKED HYPERGLYCEMIA

GLUCOSURIA OSMOTIC DIURESIS

LIPOLYSIS
WEIGHT LOSS

CELLULAR HUNGER
POLYPHAGIA

KETOACIDOSIS

POLYURIA

POLYDIPSIA

S/SX:

S/SX OF DM + KETONURIA METABOLIC ACIDOSIS KUSSMAULS RESPIRATION ACETONE BREATH DHN FLUSHED FACE TACHYCARDIA CIRCULATORY COLLAPSE COMA

DEATH

MANAGEMENT:

ADEQUATE VENTILATION FLUID REPLACEMENT INSULIN RAPID ACTING ECG ELEC IMB

LOW BLOOD SUGAR

CAUSE:

OVERDOSE OF EXOGENOUS INSULIN EATING LESS OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE

S/SX: PARASYMPATHETIC

SYMPATHETIC
IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR

HUNGER NAUSEA HYPORTENSION BRADYCARDIA

CEREBRAL
LETHARGY, YAWNING SENSORIUM CX

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

Very insufficient INSULIN

SEVERE OSMOTIC DEHYDRATION

GLUCOSURIA OSMOTIC DIURESIS POLYURIA

MARKED HYPERGLYCEMIA

LIPOLYSIS Without KETOSIS

CELLULAR HUNGER

WEIGHT LOSS

POLYPHAGIA

POLYDIPSIA

S/SX: S/SX OF DKA WITHOUT:

KAUSMAULS BREATHING ACETONE BREATH METABOLIC ACIDOSIS KETONURIA

SEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING

METABOLIC ACIDOSIS

TOO MUCH INSULIN

HYPOGLYCEMIA

GLUCAGON IS RELEASED

LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS

REBOUND HYPERGLYCEMIA + KETOSIS

DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM

NEUROPATHY FROM:
VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT

UNDERNOURISHMENT ATHEROSCLEROSIS

EYE COMPLICATIONS FROM ANOXIA

NEPHROPATHY

HEART DISEASE SKIN CHANGES

DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY

MI FROM ATHEROSCLEROSIS
DIABETIC DERMOPATHY HYPERPIGMENTED & SCALY PRETIBIAL AREAS ENLARGEMENT & FATTY INFILTRATION

LIVER CHANGES

Ms A, 45 y.o., has a simple goiter. Shes being seen by the community health nurse for teaching & follow-up regarding nutritional deficiencies related to her goiter. Ms As problem is almost associated with what nutritional deficiency?
Calcium Iodine Iron Sodium

a. b.

c.
d.