METABOLISM

ENDOCRINE SYSTEM

ENDOCRINE GLAND

ENDOCRINE GLANDS
HORMONES FUNCTIONS
Thyroid to release hormones Adrenal cortex to release hormones Growth, maturation & function of sex organs

PITUITARY TSH ANTERIOR LOBE
ACTH FSH,LH

Growth of body tissues & GH/ bones SOMATOTROPIN

PROLACTIN/ LTH

Development of mammary glands & lactation

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE ADH FUNCTION
Regulates water metabolism

PITUITARY POSTERIOR LOBE

OXYTOCIN MSH INTERMEDIATE LOBE

Stimulate uterine contractions release of milk Affects skin pigmentation

Gluconeogenesis Na & water reabsorption Antiinflammatory Stress hormone Slightly significant ADRENAL CORTEX CORTISOL SEX HORMONES . Na reabsorption.ENDOCRINE GLAND ENDOCRINE GLANDS HORMONES FUNCTION ALDOSTERONE Fluid & electrolyte balance. K excretion Glycogenolysis.

Glycogenolysis Stress hormone ADRENAL MEDULLA .ENDOCRINE GLANDS ENDOCRINE GLAND HORMONE EPINEPHRINE NOREPINEPHRINE FUNCTION Increase heart rate & BP Bronchodilation.

.

C.F metabolism Regulate physical & mental growth & development Decrease serum Ca by increasing bone deposition Increase serum calcium by promoting bone decalcification THYROID THYROCALCITONIN PTH PARATHYROID .ENDOCRINE GLANDS ENDOCRINE GLAND HORMONE T3 & T4’ FUNCTION Regulate metabolic rate P.

ENDOCRINE GLANDS ENDOCRINE GLAND HORMONE FUNCTION Decrease blood glucose by: Glucose diffusion across cell membrane. Converts glucose to glycogen Increase blood glucose by: Gluconeogenesis Glycogenolysis PANCREAS INSULIN BETA CELLS ALPHA CELLS GLUCAGON .

ENDOCRINE GLANDS ENDOCRINE HORMONES GLAND FUNCTION OVARIES ESTROGEN & Development of secondary sex charac in female PROGESMaturation of sex organs TERONE Sexual functioning Maintenance of pregnancy TESTES TESTOSTERONE Development of secondary sex charac in male Maturation of sex organs Sexual functioning .

S. ADRENAL MEDULLA HORMONES) .g. CORTISOL.g CALCIUM & GLUCOSE) RHYTHMIC PATTERNS OF SECRETION (e. FEMALE REPRODUCTIVE HORMONES) AUTONOMIC & C.HORMONE REGULATION NEGATIVE FEEDBACK MECHANISM CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e. CONTROL (PITUITARY-HYPOTHALAMIC AXIS..N.

g. Thyroxine) PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g.g.DECREASED HORMONE CONCENTRATION IN THE BLOOD (e. Thyroid gland release of Thyroxine) RETURN OF THE NORMAL CONCENTRATION OF HORMONE . TSH) NEGATIVE FEEDBACK MECHANISM STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE (e.

TSH) NEGATIVE FEEDBACK MECHANISM DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE (e.g.g.INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLAND IS INHIBITED TO RELEASE STIMULATING HORMONE (e. Thyroid gland release of Thyroxine) RETURN OF THE NORMAL CONCENTRATION OF HORMONE .

120.9o . an elderly. came in because of palpitations. VS revealed: 37.CASE STUDY Katie. 25. sweating. 140/ 90 She expressed hyperactivty. 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 REALEASE ACTH ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA ADRENAL ATROPHY .

TAPERING TO LOWER ONES IN THE AFTERNOON LAST DOSE @ MEAL TIME TO AVOID INSOMNIA PALLIATIVE EFFECT .STEROID THERAPY PHARMACOLOGIC CONSIDERATIONS: PEPTIC ULCER IN SHORT TERM. HIGH DOSE STEROID TX ADMINISTER DRUG: HIGHER DOSE IN THE MORNING.

STEROID THERAPY ASSESSMENT: BASELINE STEROID LEVEL IS ASSESSED BEFORE PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED STEROID WITHDRAWAL (LOW STRESS TOLERANCE)  EXHAUSTION  WEAKNESS  LETHARGY .

 FRANK EUPHORIA  THEN.ASSESSMENT: ACUTE ADRENAL CRISIS RESTLESSNESS  WEAKNESS  HEADACHE  DHN  N/V  FALLING BP TO SHOCK  STEROID THERAPY PSYCHOLOGICAL CXS MOOD ELEVATION. DEPRESSION  .

  ANTIINFLAMMATORY EFFECT WOUND HEALING FROM ITS ACTIVATION/ REACTIVATION SERUM SODIUM SERUM POTASSIUM .STEROID THERAPY IMPORTANT FACTS: MAJOR UNTOWARD EFFECTS:  MASKS INFECTION  DEFENSE AGAINST INFECTION FROM LYMPHOPENIA  SLOW  P.U.D.

STEROID THERAPY IMPORTANT FACTS: MINOR UNTOWARD EFFECTS:  PIGMENTATION  ACNE  FACIAL HAIR  MOON-FACIE .

 OSTEOPOROSIS  HPN  RENAL CALCULI  ADRENAL ATROPHY .D.IMPORTANT FACTS: STEROID THERAPY PROBLEMS OF LONG TERM THERAPY:  GROWTH  OBESITY  GASTRITIS RETARDATION TO P.U.

STEROID THERAPY STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA ADRENAL ATROPHY .

STEROID THERAPY 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 .

ANTERIOR PITUITARY DISTURBANCES HYPOPITUITARISM HYPERPITUITARISM .

HYPOPITUITARISM ANTERIOR LOBE PANHYPOPITUITARISM (SIMMOND’S DSE)  DECREASED SECRETION OF ALL ANTERIOR LOBE HORMONES .

 INCREASED ACTH (CUSHING’S DSE) CHROMOPHOBE TUMOR  INCREASED ACTH & GROWTH HORMONE .HYPERPITUITARISM ANTERIOR LOBE EOSINOPHILIC TUMOR  INCREASED GROWTH HORMONE AND PROLACTIN BASOPHILIC TUMOR  INCREASED TSH. LH. FSH. MSH.

adult Cushing’s dse Grave’s dse Exaggerated fxn of sex organs Underdevelopment of Decreased milk mammary glands production .PITUITARY ANTERIOR LOBE HORMONE GH ACTH TSH FSH PROLACTIN HYPO FXN Dwarfism – young Cachexia .adult Atrophy of adrenal cortex Atrophy & depressed thyroid fxn Atrophy & infertility HYPER FXN Gigantism – young Acromegaly .

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 .

ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN DIABETES INSIPIDUS S/SX: POLYURIA 15-29L/ DAY CAUSE: TUMOR TRAUMA VASCULAR DSE INFLAMMATION PITUITARY SURGERY POLYDIPSIA SG OF URINE IS <1.010 S/SX OF DHN SHOCK .

INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE BALANCE .ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN DIABETES INSIPIDUS MANAGEMENT HORMONAL REPLACEMENT – FOR LIFE  VASOPRESSIN (PITRESSIN TANNATE IN OIL) NASAL SPRAY – IM OR NON-HORMONAL THERAPY  CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN SALT & P RESTRICTED DIET.

SYNDROME OF INAPPROPRIATE ADH ELEVATED ADH CAUSES: BRONCHOGENIC CA NONENDOCRINE TUMORS S/SX: DECREASED SERUM SODIUM   CX IN LOC TO UNCONSCIOUSNESS SEIZURES N/V MENTAL CONFUSION WATER INTOXICATION   .

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) .

AMT OF O2 USED BY A PERSON @ A GIVEN TIME PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITH THYROID DAMAGE SERUM THYROXINE (T4). SERUM TSH BLOOD SERUM CHOLESTEROL RADIOACTIVE IODINE TESTS:    T3 RED CELL UPTAKE RADIOACTIVE IODINE UPTAKE (I131 THYROID SCAN . SERUM TRIIODOTHYRONINE (T3).R..THYROID DISTURBANCES DIAGNOSTIC TESTS: B.M.

infants.THYROID DISTURBANCES HYPOTHYROIDISM HYPERTHYROIDISM CRETINISM. GRAVE’S DSE or young children Exophthalmic goiter HYPOTHYROIDISM WITHOUT MYXEDEMAatrophy/ destruction of thyroid gland MYXEDEMA –adults .

glycosuria Abnormal collection of Increase use of F & P WATER as fuel .EFFECTS HYPOTHYROIDISM HYPERTHYROIDISM Reduction in HEAT Increase heat PRODUCTION Failure of MENTAL & PHYSICAL GROWTH increased storage of Deranged C C. P & F metabolism.

MOIST. SILKY BMR: DECREASED SKIN: THICK. PUFFY.HYPOTHYROIDISM HYPERTHYROIDISM SERUM CHOLESTEROL: INCREASED DECREASED INCREASED WARM. FLUSHED SOFT. 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 MANAGEMENT DESSICATED THYROID THYROGLOBULIN Na LEVOTHYROXINE Na LYOTHYRONINE HYPERTHYROIDISM MEDICAL: REST ANTITHYROID DRUGS: LUGOL’S SOLUTION THIOUREA DERIVATIVES RADIOACTIVE IODINE BETA-BLOCKERS SURGICAL: SUBTOTAL THYROIDECTOMY .

METHIMAZOLE)   BLOCK THYROID HORMONE RELEASE TOXIC SIGNS: FEVER.USE STRAW THIOUREA & DERIVATIVES (PTU. LEUKOPENIA RADIOACTIVE IODINE  PATIENT IS ISOLATED FOR 3 DAYS PROPANOLOL BETA BLOCKERS  . SORETHROAT.ANTITHYROID MEDICATIONS LUGOL’S SOLUTION (POTASSIUM IODIDE)     DECREASE THYROID VASCULARITY INHIBIT IODINE RELEASE DILUTED IN MILK / JUICE STAINS THE TEETH.

SUBTOTAL THYROIDECTOMY
REMAINING 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 THYROIDECTOMY
COMPLICATIONS:
RECURRENT LARYNGEAL NERVE INJURY

HOARSENESS 12-24 HRS POST OP OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS TRACHEOSTOMY SET @ BEDSIDE

HEMORRHAGE
 

TETANY RESPIRATORY OBSTRUCTION THYROID STORM

TETANY
DEPENDS 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 / CRISIS S/SX: HYPERTHERMIA > 41C TACHYCARDIA APPREHENSION RESTLESSNESS IRRITABILITY DELIRIUM COMA MANAGEMENT: DECREASE TEMP ANTITHYROID DRUGS GLUCOSE DIGITALIS STEROIDS TO DECREASE ACTH .

THYROID STORM / CRISIS INCREASED 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 .

HASHIMOTO’S IMMUNOLOGICAL FACTORS  PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID  . NONSUPPURATIVE   UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS CHRONIC.THYROIDITIS CLASSIFICATION: SUBACUTE.

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 .

CAULIFLOWER.NON-TOXIC GOITER (SIMPLE/ COLLOID/ EUTHYROID) CAUSE : IODINE DEFICIENCY INTAKE OF GOITROGENIC SUBSTANCES/ DRUGS:           CASSAVA. CARROTS RADDISH TURNIPS RED SKIN OF PEANUTS IODINE COBALT LITHIUM . CABBAGE.

NON-TOXIC GOITER 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 .

TAMBAN. HITO. DALAG .NON-TOXIC GOITER TREATMENT: COMMON IN WOMEN: ADOLESCENT PREGNANT LACTATING MENOPAUSE IODIZED OIL IM IODINE TABLETS SALT FORTIFICATION WITH IODINE EDUCATE ABOUT INTAKE OF:    SEAWEEDS SHELLFISH FISH.

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

ANESTHETICS .MYXEDEMA COMA PRECIPITATING FACTORS: FAILURE TO TAKE MEDS INFECTION TRAUMA EXPOSURE TO COLD USE OF SEDATIVES. NARCOTICS.

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 METABOLISM ORGANS AFFECTED: BONES .RESORPTION KIDNEYS Ca REABSORPTION  Ph EXCRETION  GIT – ENHANCES Ca ABSORPTION .

TUBULAR REABSORPTION OF PHOSPHATE .PARATHYROID DISORDERS DIAGNOSTIC TESTS: HEMATOLOGICAL  SERUM CALCIUM  SERUM PHOSPHORUS  SERUM ALKALINE PHOSPHATASE URINARY STUDIES  URINARY CALCIUM  URINARY 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. WEAKNESS  PERSONALITY CHANGES  LOSS OF TOOTH ENAMEL. TROUSSEAU’S  CHRONIC HYPOCALCEMIA FATIGUE. DRY SCALY SKIN  CARDIAC ARRHYTHMIA  CATARACT  .

pc SEIZURE prec LISTEN FOR STRIDOR OR HOARSENESS TRACHEOSTOMY SET @ BEDSIDE CaGLUCONATE @ BEDSIDE . JUICE OR MILK.HYPOPARATHYROIDISM XRAY: INCREASED BONE DENSITY MANAGEMENT: Ca SUPPLEMENT VIT D SUPPLEMENT – LIQ FORM: WITH WATER.

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 .

RENAL COLIC.KIDNEY STONES. HPN XRAY: BONE DEMINERALIZATION . POLYURIA. DEPRESSION CARDIAC ARRHYTHMIAS.HYPERPARATHYROIDISM S/SX: BONE PAIN : ESP @ THE BACK. PATHOLOGIC FRUCTURES TUBULAR CALCIUM DEPOSITS . POLYDIPSIA MUSCLE WEAKNESS PERSONALITY CX.

CAULIFLOWER & MOLASSES STRAIN URINE FOR STONES CARE FOR PARATHYROIDECTOMY .HYPERPARATHYROIDISM 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.

ADRENAL GLAND STIMULATED BY ACTH HORMONE PRECURSOR:  CHOLESTEROL SECRETES: CORTISOL  ALDOSTERONE  SEX HORMONES : ANDROGEN. ESTROGEN  .

HORMONE ADRENAL GLAND 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 Physiologically insignificant Becomes useful during menopause in women ALDOSTERONE GLUCOCORTICOIDS SEX HORMONE .

SYMPTOMATOLOGY ALDOSTERONE DEFICIENCY DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON HYPOTENSION TO SHOCK INCREASED K METABOLIC ACIDOSIS .

SYMPTOMATOLOGY CORTISOL DEFICIENCY ANOREXIA. WT LOSS. LETHARGY HYPOGLYCEMIA HYPOTENSION INCREASED K. ABDOMINAL PAIN. N/V. 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 INSUFFICIENCY ADDISON’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 24HR URINE DET.

ADRENAL CRISIS GOALS OF CARE: TO REVERSE SHOCK RESTORE BLOOD CIRCULATION REPLENISH NEEDED STEROID .

SHOCK HIGH SALT DIET ANTIBIOTICS .ADRENAL CRISIS TREATMENT: D5NSS ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE NEOSYNEPHRINE .

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 RETENTION THINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM .

CUSHING’S SYNDROME PURPLE STRIAE – FROM THINNING OF SKIN ECHYMOSIS FROM SLIGHT TRAUMA ANDROGENIC EFFECTS: OLIGOMENORRHEA HIRSUTISM GYNECOMASTIA HYPERTENSION FROM S. Na .

CUSHING’S SYNDROME 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 .

HPN. TETANY MANAGEMENT: SURGERY ALDACTONE – ALDOSTERONE ANTAGONIST .CONN’S SYNDROME PRIMARY ALDOSTERONISM CAUSE: ADRENAL ADENOMA S/SX: HYPOKALEMIA FATIGUE HYPERNATREMIA.

SECONDARY ALDOSTERONISM THE PROBLEM IS OUTSIDE THE ADRENAL GLAND: e.g. RENIN – ANGIOTENSIN SYSTEM .

ADRENAL MEDULLA HORMONES : EPINEPHRINE NOREPINEPHRINE 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  BANANA  VANILLA  CHOCOLATES & TEA .

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 .

DIABETES MILLETUS CAUSE: INSUFFICIENCY OF INSULIN LACK OF INSULIN EFFECT: HYPERGLYCEMIA .

PATHOPHYSIOLOGY REDUCED /NO INSULIN REDUCED /NO INSULIN HYPERGLYCEMIA HYPERGLYCEMIA OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION GLUCOSURIA GLUCOSURIA OSMOTIC OSMOTIC DIURESIS DIURESIS POLYURIA POLYURIA DIABETES MILLETUS LIPOLYSIS LIPOLYSIS WEIGHT LOSS WEIGHT LOSS POLYDIPSIA POLYDIPSIA CELLULAR CELLULAR HUNGER HUNGER POLYPHAGIA POLYPHAGIA .

DIABETES MILLETUS S/SX: 3 – P’s WEIGHT LOSS STAGES: PREDIABETES SUSPECTED CHEMICAL CLINICAL / OVERT .

DIABETES MILLETUS
PREDIABETES / POTENTIAL:
CONCEPTION CONCEPTION

EVIDENCE OF GLUCOSE METABOLISM EVIDENCE OF GLUCOSE METABOLISM ALTERATION ALTERATION

DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETES PREDIABETES

NO STRESS

STRESS STRESS

NORMAL GLUCOSE METABOLISM

OVERT DIABETES OVERT DIABETES

DIABETES MILLETUS
CHEMEICAL:
SUBCLINICAL GTT IS ABNORMAL NO STRESS NO STRESS ASYMPTOMATIC ASYMPTOMATIC STRESS STRESS SYMPTOMATIC SYMPTOMATIC

DIABETES MILLETUS CLINICAL / OVERT: CHEMICAL CHEMICAL PERSISTENT INCREASED FBS PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS WITH OR WITHOUT STRESS SYMPTOMATIC .

DIABETES MILLETUS TYPES: TYPE I    TYPE II –        JUVENILE ONSET BEFORE 15 YO LEAN/ NORMAL WEIGHT ABSOLUTE INSULIN DEFICIENCY INSULIN -DEPENDENT PRONE TO DKA   MATURITY ONSET AFTER AGE 40 OBESE REDUCED INSULIN RECEPTOR NONINSULIN DEPENDENT PRONE TO HHONK .

DIABETES MILLETUS DIAGNOSTIC EXAMS: FBS 2 HRPOSTPRANDIAL OGTT GLYCOSYLATED HGB DEXTROSTRIP URINE TESTS: BENEDICT’S  CLINITEST TAB  ACETONE TEST  .

2 HRS BEFORE THE TEST TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD .2 HR POSTPRANDIAL BLOOD SUGAR INTAKE OF 100GM GLUCOSE.

P. 3 HRS. 2HRS.O. AFTER GLUCOSE LOADING . 1HR.OGTT CONFIRMATORY. OR IV BLOOD & URINE SPECS TAKEN 30 MIN. 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.

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  ARM  UPPER THIGH BACK  BUTTOCKS .

DIABETES MILLETUS INSULIN THERAPY REACTIONS: LOCAL: STNGING  INDURATION  ITCHING  GENERALIZED: HIVES  URTICARIA  ANTIHISTAMINES 30 MIN B4  DESENSITIZATION  LIPODYSTROPHY .

LIPODYSTROPHY CAUSE: FAULTY TECHNIQUE TRAUMA INJECTION 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!!! .

NONKETOTIC (HHONK) COMA SOMOGYI EFFECT . HYPEROSMOLAR.ACUTE COMPLICATIONS OF DIABETES MILLETUS DIABETIC KETO-ACIDOSIS (DKA) INSULIN SHOCK HYPERGLYCEMIC.

PATHOPHYSIOLOGY NO INSULIN NO INSULIN OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION MARKED HYPERGLYCEMIA MARKED HYPERGLYCEMIA GLUCOSURIA GLUCOSURIA OSMOTIC OSMOTIC DIURESIS DIURESIS POLYURIA POLYURIA LIPOLYSIS LIPOLYSIS CELLULAR CELLULAR HUNGER HUNGER POLYPHAGIA POLYPHAGIA WEIGHT WEIGHT LOSS LOSS KETOACIDOSIS KETOACIDOSIS POLYDIPSIA POLYDIPSIA .A.K.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.D. 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 SHOCK S/SX: PARASYMPATHETIC HUNGER  NAUSEA  HYPORTENSION  BRADYCARDIA  SYMPATHETIC IRRITABILITY  SWEATING  TREMBLING  TACHYCARDIA  PALLOR  CEREBRAL LETHARGY.  YAWNING  SENSORIUM CX  .

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 .

PATHOPHYSIOLOGY SEVERE SEVERE OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION GLUCOSURIA GLUCOSURIA OSMOTIC OSMOTIC DIURESIS DIURESIS POLYURIA POLYURIA Very insufficient INSULIN Very insufficient INSULIN MARKED HYPERGLYCEMIA MARKED HYPERGLYCEMIA LIPOLYSIS LIPOLYSIS Without Without KETOSIS KETOSIS HHONK CELLULAR CELLULAR HUNGER HUNGER WEIGHT WEIGHT LOSS LOSS POLYPHAGIA POLYPHAGIA POLYDIPSIA POLYDIPSIA .

HHONK S/SX: S/SX OF DKA WITHOUT:  KAUSMAUL’S BREATHING  ACETONE BREATH  METABOLIC ACIDOSIS  KETONURIA .

LACTIC ACIDOSIS SEVERE TISSUE ANOXIA SEVERE TISSUE ANOXIA LACTIC ACID PRODUCTION LACTIC ACID PRODUCTION AGGRAVATION OF EXISTING AGGRAVATION OF EXISTING METABOLIC ACIDOSIS METABOLIC ACIDOSIS .

SOMOGYI EFFECT TOO MUCH INSULIN HYPOGLYCEMIA GLUCAGON IS RELEASED LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS REBOUND REBOUND HYPERGLYCEMIA HYPERGLYCEMIA + + KETOSIS KETOSIS .

CHRONIC COMPLICATIONS OF DIABETES MILLETUS DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM   UNDERNOURISHMENT ATHEROSCLEROSIS VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT NEUROPATHY FROM:    EYE COMPLICATIONS FROM ANOXIA    .

CHRONIC COMPLICATIONS OF DIABETES MILLETUS NEPHROPATHY  DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY MI FROM ATHEROSCLEROSIS DIABETIC DERMOPATHY – HYPERPIGMENTED & SCALY PRETIBIAL AREAS ENLARGEMENT & FATTY INFILTRATION HEART DISEASE  SKIN CHANGES  LIVER CHANGES  .

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

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