Endocrine Ppt
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METABOLISM
ENDOCRINE
SYSTEM
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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
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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
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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
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ENDOCRINE GLANDS
ENDOCRINE
GLAND
HORMONE FUNCTION
ADRENAL MEDULLA
EPINEPHRINE
NOR-
EPINEPHRINE
Increase heart rate & BP
Bronchodilation,
Glycogenolysis
Stress hormone
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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
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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
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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
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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)
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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
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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
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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
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CASE STUDY
She claimed history of goiter since her 30’s but no follow-up was done.
What are your nursing plans?
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PLANNINGHEALTH PROMOTION IODIZED SALTCONTROLLING WEIGHT
HEALTH MAINTENANCE & RESTORATIONSTEROID THERAPY
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STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & RELEASE BY ADRENAL MEDULLA
ADRENAL ATROPHY
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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
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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
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STEROID THERAPYASSESSMENT:
ACUTE ADRENAL CRISIS RESTLESSNESS WEAKNESS HEADACHE DHN N/V FALLING BP TO SHOCK
PSYCHOLOGICAL CXS MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION
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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
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STEROID THERAPYIMPORTANT FACTS:
MINOR UNTOWARD EFFECTS:PIGMENTATIONACNEFACIAL HAIRMOON-FACIE
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STEROID THERAPYIMPORTANT FACTS:
PROBLEMS OF LONG TERM THERAPY:GROWTH RETARDATIONOBESITYGASTRITIS TO P.U.D.OSTEOPOROSISHPNRENAL CALCULIADRENAL ATROPHY
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STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & RELEASE BY ADRENAL MEDULLA
ADRENAL ATROPHY
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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
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ANTERIOR PITUITARY DISTURBANCES
HYPOPITUITARISM
HYPERPITUITARISM
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HYPOPITUITARISMANTERIOR LOBE
PANHYPOPITUITARISM
(SIMMOND’S DSE)DECREASED SECRETION OF ALL
ANTERIOR LOBE HORMONES
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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
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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
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MANAGEMENT
HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY
THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)
HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA &
CARDIOVASCULAR PROBLEMS
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POSTERIOR PITUITARY DISTURBANCES
DIABETES INSIPIDUS
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
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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
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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
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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
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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
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Mission possible
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THYROID GLAND
STIMULATED BY THYROID STIMULATING
HORMONE (TSH)NEEDS IODINE TO SYNTHESIZE HORMONE
SECRETES:THYROXINE (T4)TRIIODOTHYRONINE (T3)
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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
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THYROID DISTURBANCES
HYPOTHYROIDISM HYPERTHYROIDISM
CRETINISM- infants, young children
HYPOTHYROIDISM WITHOUT MYXEDEMA- atrophy/ destruction of thyroid gland
MYXEDEMA –adults
GRAVE’S DSE or Exophthalmic goiter
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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
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HYPOTHYROIDISM HYPERTHYROIDISM
SERUM
CHOLESTEROL:INCREASED
BMR:DECREASED
SKIN:THICK, PUFFY, DRY
HAIR:DRY, BRITTLE
DECREASED
INCREASED
WARM, MOIST, FLUSHED
SOFT, SILKY
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HYPOTHYROIDISM HYPERTHYROIDISM
NERVOUS SYSTEM:APATHETIC
LETHARGIC
MAYBE HYPERIRRITABLE
SLOW CEREBRATION
WEIGHT:INCREASED
APPETITE:DECREASED
HYPERACTIVE
LABILE MOOD
HYPERSENSITIVE
TENSED
DECREASED
INCREASED
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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
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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
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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.
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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
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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
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THYROID STORM / CRISISS/SX:
HYPERTHERMIA > 41C
TACHYCARDIAAPPREHENSIONRESTLESSNESSIRRITABILITYDELIRIUMCOMA
MANAGEMENT:DECREASE TEMP
ANTITHYROID DRUGS
GLUCOSE
DIGITALIS
STEROIDS TO
DECREASE ACTH
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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
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VARIANTS OF HYPERTHYROIDISM
GRAVE’S DSE
THYROIDITIS
GOITER
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GRAVE’S DISEASE
CAUSE:UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR
S/SX: TRIAD OF SYMPTOMS:HYPERTHYROIDISMOPHTHALMOPATHYDERMOPATHY
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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
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DERMOPATHYPRETIBIAL MYXEDEMA
@ THE DORSUM OF THE LEG
RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN
CLUBBING OF FINGERS & TOES
OSTEOARTHROPATHY
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THYROIDITIS
CLASSIFICATION:
SUBACUTE, NONSUPPURATIVE UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS
CHRONIC, HASHIMOTO’S IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS &
ANTIBODIES DIRECTED AGAINST THE THYROID
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GOITER
ENLARGEMENT OF THE THYROID GLAND.
TYPES:TOXIC NODULAR
NONTOXIC
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TOXIC NODULAR GOITER
COMMON IN ELDERLY
FROM LONG STANDING SIMPLE GOITER
NODULES FUNCTIONING TISSUE SECRETES THYROXINE
AUTONOMOUSLY FROM TSH
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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
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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
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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
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MYXEDEMA COMA
MEDICAL EMERGENCY
OCCURS IN SEVERE & UNTREATED MYXEDEMA
HIGH MORTALTY RATE
S/SX:INTENSIFIED HYPOTHYROIDISM
NEUROLOGIC IMPAIRMENT COMA
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MYXEDEMA COMA
PRECIPITATING FACTORS:
FAILURE TO TAKE MEDSINFECTIONTRAUMAEXPOSURE TO COLDUSE OF SEDATIVES, NARCOTICS, ANESTHETICS
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MYXEDEMA COMA
MANAGEMENT:
IV THYROID HORMONES
CORRECTION OF HYPOTHERMIA
MAINTAIN VITAL FXNS
TREAT PRECIPITATING CAUSES
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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
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PARATHYROID DISORDERS
DIAGNOSTIC TESTS:HEMATOLOGICALSERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE
URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
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HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION
HYPOCALCEMIA
CALCIUM IS: DEPOSITED IN THE BONE EXCRETED
CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL
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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
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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
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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
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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
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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
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ADRENAL GLAND
STIMULATED BY ACTH
HORMONE PRECURSOR: CHOLESTEROL
SECRETES: CORTISOL ALDOSTERONE SEX HORMONES : ANDROGEN, ESTROGEN
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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
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SYMPTOMATOLOGY
ALDOSTERONE DEFICIENCY
DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON
HYPOTENSION TO SHOCK
INCREASED K
METABOLIC ACIDOSIS
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SYMPTOMATOLOGY
CORTISOL DEFICIENCY
ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY
HYPOGLYCEMIA
HYPOTENSION
INCREASED K, WEAK PULSE
PIGMENTATION
IMPAIRED STRESS TOLERANCE
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SYMPTOMATOLOGY
SEX HORMONE DEFICIENCY
LOSS OF BODY HAIR
LOSS OF LIBIDO OR IMPOTENCE
MENSTRUAL & FERTILITY DISORDER
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ADRENAL CORTEX DISORERS
ADRENAL INSUFFICIENCY
ADRENAL CRISIS
CUSHING’S SYNDROME
ALDOSTERONISM
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ADRENAL INSUFFICIENCYADDISON’S DISEASE
INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS
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ADRENAL CRISIS
ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES
POSSIBLE COMPLICATION OF ADDISON’S DISEASE
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ADRENAL CRISIS
PRECIPITATING CAUSES:
ABDOMINAL DISCOMFORT
INFECTION
TRAUMA
HIGH TEMP
EMOTIONAL UPSET
ANTICOAGULANT DRUGS
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ADRENAL CRISIS
S/SX:
HYPOTENSION
FLUID LOSS
HYPONATREMIA
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ADRENAL CRISISLAB:
SERUM ELEC: DECREASED Na
INCREASED K
S. BUN :
S. GLUCOSE:
ADRENAL HORMONE ASSAY : HYDROXYCORTICOID & 17 KETOSTEROID IN 24-
HR URINE DET.
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ADRENAL CRISIS
GOALS OF CARE:TO REVERSE SHOCK
RESTORE BLOOD CIRCULATION
REPLENISH NEEDED STEROID
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ADRENAL CRISIS
TREATMENT:D5NSS
ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE
NEOSYNEPHRINE - SHOCK
HIGH SALT DIET
ANTIBIOTICS
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CUSHING’S SYNDROME
CAUSE:SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM
ACTH BY PITUITARY TUMOR
EXCESSIVE GLUCORTICOID ADMINISTRATION
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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
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CUSHING’S SYNDROME
PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISMGYNECOMASTIA
HYPERTENSION FROM S. Na
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CUSHING’S SYNDROME
TREATMENT & NURSING CARE:
PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED
PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY
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ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE
PRIMARY – CONN’S SYNDROME
SECONDARY
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CONN’S SYNDROMEPRIMARY ALDOSTERONISM
CAUSE:ADRENAL ADENOMA
S/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPN, TETANY
MANAGEMENT:
SURGERYALDACTONE – ALDOSTERONE ANTAGONIST
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SECONDARY ALDOSTERONISM
THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:
e.g. RENIN – ANGIOTENSIN SYSTEM
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ADRENAL MEDULLA
HORMONES : EPINEPHRINE
NOREPINEPHRINE
EFFECTS
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PHEOCHROMOCYTOMA
TUMOR OF ADRENAL MEDULLASECRETES INCREASED AMOUNT OF CATECHOLAMINES
S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF
DIAGNOSTIC TEST : VMA IN 24H URINE
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VMA IN 24H URINE
END PRODUCT OF CATECHOLAMINE METABOLISM
DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:COFFEE & TEABANANAVANILLACHOCOLATES
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PHEOCHROMOCYTOMA
MANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE
NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUC & ACETONE
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PANCREAS
HORMONES:
INSULIN BY BETA CELLS
GLUCAGON BY ALPHA CELLS
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DIABETES MILLETUS
CAUSE:
INSUFFICIENCY OF INSULIN
LACK OF INSULIN
EFFECT:
HYPERGLYCEMIA
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DIABETES MILLETUS
PATHOPHYSIOLOGYREDUCED /NO INSULINREDUCED /NO INSULIN
HYPERGLYCEMIAHYPERGLYCEMIA
GLUCOSURIAGLUCOSURIA
WEIGHT LOSSWEIGHT LOSS
OSMOTICDIURESISOSMOTICDIURESIS
POLYURIAPOLYURIA
CELLULAR HUNGER
CELLULAR HUNGER
POLYPHAGIAPOLYPHAGIA
POLYDIPSIAPOLYDIPSIA
LIPOLYSISLIPOLYSIS
OSMOTICDEHYDRATION
OSMOTICDEHYDRATION
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DIABETES MILLETUS
S/SX:
3 – P’s
WEIGHT LOSS
STAGES:
PREDIABETES
SUSPECTED
CHEMICAL
CLINICAL / OVERT
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DIABETES MILLETUS
PREDIABETES / POTENTIAL:
CONCEPTIONCONCEPTION
EVIDENCE OF GLUCOSE METABOLISMALTERATION
EVIDENCE OF GLUCOSE METABOLISMALTERATION
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DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETESPREDIABETES
NO STRESS STRESSSTRESS
NORMAL GLUCOSEMETABOLISM
OVERT DIABETESOVERT DIABETES
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DIABETES MILLETUSCHEMEICAL:
SUBCLINICALSUBCLINICAL
GTT IS ABNORMALGTT IS ABNORMAL
NO STRESSNO STRESS STRESSSTRESS
ASYMPTOMATICASYMPTOMATIC SYMPTOMATICSYMPTOMATIC
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DIABETES MILLETUSCLINICAL / OVERT:
CHEMICALCHEMICAL
PERSISTENT INCREASED FBSPERSISTENT INCREASED FBS
WITH OR WITHOUT STRESSWITH OR WITHOUT STRESS
SYMPTOMATICSYMPTOMATIC
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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
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DIABETES MILLETUS
DIAGNOSTIC EXAMS:
FBS
2 HR- POSTPRANDIAL
OGTT
GLYCOSYLATED HGB
DEXTROSTRIP
URINE TESTS: BENEDICT’S CLINITEST TAB ACETONE TEST
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2 HR POSTPRANDIAL BLOOD SUGAR
INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST
TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD
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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
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GLYCOSYLATED HEMOGLOBIN
MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS
USEFUL TO CHECK:COMPLIANCE WITH THERAPYHISTORY OF SUBCLINICAL OR
CHEMICAL DIABETES
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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
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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
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DIABETES MILLETUS
INSULIN THERAPY:
SITE OF INJECTION:ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS
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DIABETES MILLETUS
INSULIN THERAPY REACTIONS:
LOCAL: STNGING INDURATION ITCHING
LIPODYSTROPHY
GENERALIZED: HIVES URTICARIA ANTIHISTAMINES
30 MIN B4 DESENSITIZATION
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LIPODYSTROPHY
CAUSE:FAULTY TECHNIQUETRAUMAINJECTION OF REFRIGERATED INSULIN
MANAGEMENT:ROTATING SITES: 1 AREA IS NOT USED MORE THAN ONCE EVERY 3 WKS
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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
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SURPRISE!!!
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ACUTE COMPLICATIONS OF DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA)
INSULIN SHOCK
HYPERGLYCEMIC, HYPEROSMOLAR,
NONKETOTIC (HHONK) COMA
SOMOGYI EFFECT
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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
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D.K.A.
S/SX:S/SX OF DM +KETONURIAMETABOLIC ACIDOSISKUSSMAUL’S RESPIRATIONACETONE BREATHDHNFLUSHED FACETACHYCARDIA
CIRCULATORY COLLAPSE COMA DEATH
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D.K.A.
MANAGEMENT:
ADEQUATE VENTILATION
FLUID REPLACEMENT
INSULIN – RAPID ACTING
ECG – ELEC IMB
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INSULIN SHOCK
LOW BLOOD SUGAR
CAUSE:OVERDOSE OF EXOGENOUS INSULIN
EATING LESS
OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE
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INSULIN SHOCKS/SX:
PARASYMPATHETIC HUNGER NAUSEA HYPORTENSION BRADYCARDIA
CEREBRAL LETHARGY, YAWNING SENSORIUM CX
SYMPATHETIC IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR
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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
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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
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HHONK
S/SX:
S/SX OF DKA WITHOUT:KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA
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LACTIC ACIDOSIS
SEVERE TISSUE ANOXIASEVERE TISSUE ANOXIA
LACTIC ACID PRODUCTIONLACTIC ACID PRODUCTION
AGGRAVATION OF EXISTING
METABOLIC ACIDOSISAGGRAVATION OF EXISTING
METABOLIC ACIDOSIS
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SOMOGYI EFFECTTOO MUCH INSULINTOO MUCH INSULIN
HYPOGLYCEMIAHYPOGLYCEMIA
GLUCAGON IS RELEASEDGLUCAGON IS RELEASED
LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS
LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS
REBOUNDHYPERGLYCEMIA
+KETOSIS
REBOUNDHYPERGLYCEMIA
+KETOSIS
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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
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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
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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
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