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Endocrine Ppt
 

Endocrine Ppt

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Endocrine Ppt

Endocrine Ppt

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    Endocrine Ppt Endocrine Ppt Presentation Transcript

    • METABOLISM ENDOCRINE SYSTEM
    • ENDOCRINE GLANDS
      • Development of mammary glands & lactation
      PROLACTIN/ LTH
      • Growth of body tissues & bones
      GH/ SOMATOTROPIN
      • Growth, maturation & function of sex organs
      FSH,LH
      • Adrenal cortex to release hormones
      ACTH LOBE
      • Thyroid to release hormones
      TSH
      • PITUITARY
      • ANTERIOR
      FUNCTIONS HORMONES ENDOCRINE GLAND
    • ENDOCRINE GLANDS
      • Affects skin pigmentation
      MSH
      • INTERME-
      • DIATE LOBE
      • Stimulate uterine contractions
      • release of milk
      OXYTOCIN
      • Regulates water metabolism
      ADH
      • PITUITARY
      • POSTERIOR
      • LOBE
      FUNCTION HORMONE ENDOCRINE GLAND
    • ENDOCRINE GLANDS
      • Slightly significant
      SEX HORMONES
      • Glycogenolysis;
      • Gluconeogenesis
      • Na & water reabsorption
      • Antiinflammatory
      • Stress hormone
      CORTISOL
      • Fluid & electrolyte balance;
      • Na reabsorption;
      • K excretion
      ALDOSTERONE ADRENAL CORTEX FUNCTION HORMONES ENDOCRINE GLAND
    • ENDOCRINE GLANDS
      • Increase heart rate & BP
      • Bronchodilation,
      • Glycogenolysis
      • Stress hormone
      EPINEPHRINE NOR- EPINEPHRINE ADRENAL MEDULLA FUNCTION HORMONE ENDOCRINE GLAND
    •  
    • ENDOCRINE GLANDS
      • Increase serum calcium by promoting bone decalcification
      PTH PARA- THYROID
      • Decrease serum Ca by increasing bone deposition
      THYRO- CALCITONIN
      • Regulate metabolic rate
      • P,C,F metabolism
      • Regulate physical & mental growth & development
      T3 & T4’ THYROID FUNCTION HORMONE ENDOCRINE GLAND
    • ENDOCRINE GLANDS
      • Increase blood glucose by:
      • Gluconeogenesis
      • Glycogenolysis
      GLUCAGON
      • ALPHA
      • CELLS
      • Decrease blood glucose by:
      • Glucose diffusion across cell membrane;
      • Converts glucose to glycogen
      INSULIN
      • PANCREAS
      • BETA
      • CELLS
      FUNCTION HORMONE ENDOCRINE GLAND
    • ENDOCRINE GLANDS
      • Development of secondary sex charac in male
      • Maturation of sex organs
      • Sexual functioning
      TESTOS- TERONE TESTES
      • Development of secondary sex charac in female
      • Maturation of sex organs
      • Sexual functioning
      • Maintenance of pregnancy
      ESTROGEN & PROGES- TERONE OVARIES FUNCTION HORMONES ENDOCRINE GLAND
    • 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 TO
      • RELEASE 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
      • Katie, an elderly, came in because of palpitations.
      • VS revealed: 37.9 o , 120, 25, 140/ 90
      • She expressed hyperactivty, sweating, increased appetite & weight loss
    • CASE STUDY
      • She claimed history of goiter since her 30’s but no follow-up was done.
      • What are your nursing plans?
    • 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
    • STEROID THERAPY
      • 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
    • 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
    • STEROID THERAPY
      • ASSESSMENT:
      • ACUTE ADRENAL CRISIS
        • RESTLESSNESS
        • WEAKNESS
        • HEADACHE
        • DHN
        • N/V
        • FALLING BP TO SHOCK
      • PSYCHOLOGICAL CXS
        • MOOD ELEVATION,
        • FRANK EUPHORIA
        • THEN, DEPRESSION
    • STEROID THERAPY
      • 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
    • STEROID THERAPY
      • IMPORTANT FACTS:
      • MINOR UNTOWARD EFFECTS:
        • PIGMENTATION
        • ACNE
        • FACIAL HAIR
        • MOON-FACIE
    • STEROID THERAPY
      • IMPORTANT FACTS:
      • 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 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
    • HYPERPITUITARISM ANTERIOR 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 LOBE
      • Decreased milk production
      • Underdevelopment of mammary glands
      PROLACTIN
      • Exaggerated fxn of sex organs
      • Atrophy & infertility
      FSH
      • Grave’s dse
      • Atrophy & depressed thyroid fxn
      TSH
      • Cushing’s dse
      • Atrophy of adrenal cortex
      ACTH
      • Gigantism – young
      • Acromegaly - adult
      • Dwarfism – young
      • Cachexia - adult
      GH HYPER FXN HYPO FXN HORMONE
    • 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
        • CHLORPROPRAMID E – INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN
      • SALT & P 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 DISTURBANCES
      • 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
    • THYROID DISTURBANCES GRAVE’S DSE or Exophthalmic goiter
      • CRETINISM- infants, young children
      • HYPOTHYROIDISM WITHOUT MYXEDEMA - atrophy/ destruction of thyroid gland
      • MYXEDEMA –adults
      HYPERTHYROIDISM HYPOTHYROIDISM
    • EFFECTS
      • Increase heat
      • Deranged C metabolism, glycosuria
      • Increase use of F & P as fuel
      • Reduction in HEAT PRODUCTION
      • Failure of MENTAL & PHYSICAL GROWTH
      • increased storage of C, P & F
      • Abnormal collection of WATER
      HYPERTHYROIDISM HYPOTHYROIDISM
      • DECREASED
      • INCREASED
      • WARM, MOIST, FLUSHED
      • SOFT, SILKY
      • SERUM
      • CHOLESTEROL:
      • INCREASED
      • BMR:
      • DECREASED
      • SKIN:
      • THICK, PUFFY, DRY
      • HAIR:
      • DRY, BRITTLE
      HYPERTHYROIDISM HYPOTHYROIDISM
      • HYPERACTIVE
      • LABILE MOOD
      • HYPERSENSITIVE
      • TENSED
      • DECREASED
      • INCREASED
      • NERVOUS SYSTEM:
      • APATHETIC
      • LETHARGIC
      • MAYBE HYPERIRRITABLE
      • SLOW CEREBRATION
      • WEIGHT:
      • INCREASED
      • APPETITE:
      • DECREASED
      HYPERTHYROIDISM HYPOTHYROIDISM
    • MANAGEMENT
      • MEDICAL:
      • REST
      • ANTITHYROID DRUGS:
      • LUGOL’S SOLUTION
      • THIOUREA DERIVATIVES
      • RADIOACTIVE IODINE
      • BETA-BLOCKERS
      • SURGICAL:
      • SUBTOTAL THYROIDECTOMY
      • MEDICAL:
      • HORMONE REPLACEMENT
      • DESSICATED THYROID
      • THYROGLOBULIN
      • Na LEVOTHYROXINE
      • Na LYOTHYRONINE
      HYPERTHYROIDISM HYPOTHYROIDISM
    • 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 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
      • HEMORRHAGE
        • 12-24 HRS POST OP
        • OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS
        • TRACHEOSTOMY SET @ BEDSIDE
      • TETANY
      • RESPIRATORY OBSTRUCTION
      • THYROID STORM
    • TETANY
      • DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVED
      • S/SX:
      • 1 ST – TINGLING TOES & FINGERS
      • 2 ND – CHEVOSTEK’S SIGN (TAPPING THE FACIAL MUSCLES)
      • 3 RD – 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
    • 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 METABOLISM
      • ORGANS 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
    • HYPERPARATHYROIDISM
      • 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
    • 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, 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 GLAND
      • Physiologically insignificant
      • Becomes useful during menopause in women
      SEX HORMONE
      • increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS
      • Blocks inflammation
      • Counteracts effect of histamine
      GLUCO- CORTICOIDS
      • Renal : Na & Cl reabsorption; K excretion
      • GI : Na absorption
      ALDOSTERONE FUNCTION HORMONE
    • 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 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 24-HR URINE DET .
    • ADRENAL CRISIS
      • GOALS OF CARE:
      • TO REVERSE SHOCK
      • RESTORE BLOOD CIRCULATION
      • REPLENISH NEEDED STEROID
    • ADRENAL CRISIS
      • TREATMENT:
      • D5NSS
      • ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE
      • NEOSYNEPHRINE - SHOCK
      • HIGH SALT DIET
      • ANTIBIOTICS
    • CUSHING’S SYNDROME
      • CAUSE:
      • SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM
      • ACTH BY PITUITARY TUMOR
      • EXCESSIVE GLUCORTICOID ADMINISTRATION
    • CUSHING’S SYNDROME
      • S/SX:
      • TRUNCAL OBESITY
      • BUFFALO HUMP
      • MOON-FACIE
      • WT GAIN
      • SODIUM 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
    • CONN’S SYNDROME
      • PRIMARY ALDOSTERONISM
      • CAUSE:
      • 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 : 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 & 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
    • DIABETES MILLETUS
      • CAUSE:
      • INSUFFICIENCY OF INSULIN
      • LACK OF INSULIN
      • EFFECT:
      • HYPERGLYCEMIA
    • DIABETES MILLETUS PATHOPHYSIOLOGY REDUCED /NO INSULIN HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS OSMOTIC DEHYDRATION
    • DIABETES MILLETUS
      • S/SX:
      • 3 – P’s
      • WEIGHT LOSS
      • STAGES:
      • PREDIABETES
      • SUSPECTED
      • CHEMICAL
      • CLINICAL / OVERT
    • DIABETES MILLETUS
      • PREDIABETES / POTENTIAL:
      CONCEPTION EVIDENCE OF GLUCOSE METABOLISM ALTERATION
    • DIABETES MILLETUS
      • SUSPECTED/ SUBCLINICAL/ LATENT:
      PREDIABETES NO STRESS STRESS NORMAL GLUCOSE METABOLISM OVERT DIABETES
    • DIABETES MILLETUS
      • CHEMEICAL:
      SUBCLINICAL GTT IS ABNORMAL NO STRESS STRESS ASYMPTOMATIC SYMPTOMATIC
    • DIABETES MILLETUS
      • CLINICAL / OVERT:
      CHEMICAL PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS SYMPTOMATIC
    • DIABETES MILLETUS
      • TYPES:
      • TYPE I
        • JUVENILE ONSET
        • BEFORE 15 YO
        • LEAN/ NORMAL WEIGHT
        • ABSOLUTE INSULIN DEFICIENCY
        • INSULIN -DEPENDENT
        • PRONE TO DKA
      • TYPE II –
        • MATURITY ONSET
        • AFTER AGE 40
        • OBESE
        • REDUCED INSULIN RECEPTOR
        • NONINSULIN DEPENDENT
        • PRONE TO HHONK
    • DIABETES MILLETUS
      • DIAGNOSTIC EXAMS:
      • FBS
      • 2 HR- POSTPRANDIAL
      • OGTT
      • GLYCOSYLATED HGB
      • DEXTROSTRIP
      • URINE TESTS:
        • BENEDICT’S
        • CLINITEST TAB
        • ACETONE TEST
    • 2 HR POSTPRANDIAL BLOOD SUGAR
      • INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST
      • TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD
    • OGTT
      • CONFIRMATORY, WHEN OTHER BLOOD TESTS ARE BORDERLINE
      • 3 DAYS OF NORMAL ACITIVITY & 150MG OF CARB 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 INSULIN
      • MANAGEMENT:
      • ROTATING SITES: 1 AREA IS NOT USED MORE THAN ONCE EVERY 3 WKS
    • INSULIN THERAPY & HORMONAL ACTIVITY
      • GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING:
        • PHYSICAL TRAUMA
        • STRESS
        • INFECTION
        • ANXIETY
        • ANGER
        • FEAR
        • CHANGE IN LIFESTYLE
      • INCREASE IN INSULIN DOSE IS NEEDED
    • SURPRISE!!!
    • ACUTE COMPLICATIONS OF DIABETES MILLETUS
      • DIABETIC KETO-ACIDOSIS (DKA)
      • INSULIN SHOCK
      • HYPERGLYCEMIC, HYPEROSMOLAR,
      • NONKETOTIC (HHONK) COMA
      • SOMOGYI EFFECT
    • D.K.A. PATHOPHYSIOLOGY NO INSULIN MARKED HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS OSMOTIC DEHYDRATION KETOACIDOSIS
    • 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 SHOCK
      • S/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
    • HHONK PATHOPHYSIOLOGY Very insufficient INSULIN MARKED HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA CELLULAR HUNGER POLYPHAGIA POLYDIPSIA LIPOLYSIS Without KETOSIS SEVERE OSMOTIC DEHYDRATION
    • HHONK
      • S/SX:
      • S/SX OF DKA WITHOUT:
        • KAUSMAUL’S BREATHING
        • ACETONE BREATH
        • METABOLIC ACIDOSIS
        • KETONURIA
    • LACTIC ACIDOSIS SEVERE TISSUE ANOXIA LACTIC ACID PRODUCTION AGGRAVATION OF EXISTING METABOLIC ACIDOSIS
    • SOMOGYI EFFECT TOO MUCH INSULIN HYPOGLYCEMIA GLUCAGON IS RELEASED LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS REBOUND HYPERGLYCEMIA + 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?
      • Calcium
      • Iodine
      • Iron
      • Sodium
    • GOD BLESS