logging in or signing up ENDOCRINE SYSTEM.ppt--K mohster Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 499 Category: Others/ Misc License: All Rights Reserved Like it (0) Dislike it (0) Added: February 01, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript ENDOCRINE SYSTEM : ENDOCRINE SYSTEM Course Outline : Course Outline I. Overview of the anatomy and physiology of the endocrine system Course Outline : Course Outline II. Assessment 1. history of client 2. physical assessment a. radiological studies b. hematological studies c. metabolic studies / urinary studies d. hematological studies of steroids Course Outline : Course Outline III. Common Health Problems 1. Hypopituitarism a. hypogonadism b. dwarfism 2. Hyperpituitarism a. gigantism b. acromegaly 3. Diabetes insipidus Course Outline : Course Outline III. Common Health Problems 4. Hypothyroidism a. cretinism b. juvenile hypothyroidism c. myxedema 5. Hyperthyroidism 6. Hypoparathyroidism 7. Hyperparathyroidism Course Outline : Course Outline III. Common Health Problems 8. Addison’s disease 9. Cushing’s syndrome 10. Aldosteronism 11. Pheocromocytoma 12. Diabetes mellitus ANATOMY & PHYSIOLOGY : ANATOMY & PHYSIOLOGY ENDOCRINE GLANDS CONTINUOUSLY SECRETE PRODUCTS CALLED HORMONES HORMONES ARE CHEMICAL MESSENGERS THAT DELIVERS STIMULATORY OR INHIBITORY SIGNALS TO TARGET CELLS AS A RESULT OF FEEDBACK MECHANISM CLASSIFICATION: STEROID- ADRENAL CORTEX AND GONADS PEPTIDES (INSULIN) AMINE (EPINEPHRINE) Slide 13: PITUITARY GLAND ANTERIOR LOBE GROWTH HORMONE- STIIMULATES GROWTH OF BODY TISSUES AND BONES PROLACTIN – STIMULATES MAMMARY TISSUE GROWTH & LACTATION THYROTROPIC HORMONE (TSH) – STIMULATES THYROID GLAND GONADOTROPIC HORMONE (LH & FSH) – AFFECT GROWTH,MATURITY AND FUNCTIONING OF PRIMARY AND SECONDARY SEX ORGANS. TESTES AND OVARIES ADRENOCORTICOTROPIC HORMONE (ACTH) – STIMULATES STEROID PRODUCTION BY ADRENAL CORTEX MELANOCYTE-STIMULATING HORMONE (MSH)-MAY STIMULATE ADRENAL CORTEX, MAY AFFECT PIGMENTATION Slide 14: PITUITARY GLAND POSTERIOR LOBE ANTI-DIUIRETIC HORMONES (ADH,VASOPRESSIN)- PROMOTES REABSORPTION OF WATER BY THE DISTAL TUBULES AND COLLECTING DUCTS OF THE KIDNEY, OXYTOXIN – STIMULATES EJECTION OF MILK FR MAMMARY ALVEOLI INTO THE DUCTS STIMULATES UTERINE CONTRACTIONS MAY POSSIBLE BE INVOLVED IN THE TRANSPORT OF SPERM INTO THE REPRO TRACT OF THE FEMALE Slide 15: THYROID GLAND THYROXINE (T4) TRIIODOTHYRONINE (T3) INC METABOLIC ACTIVITY OF ALL CELLS STIMULATES FAT, PROTEIN AND CARBO METABOLISM THYROCALCITONIN LOWERS SERUM CALCIUM LEVELS AND ELEVATES PHOSPHATE LEVEL; OPPOSITE EFFECT FR THAT OF PTH Slide 16: PARATHYROID GLAND PARATHORMONE (PTH) INC. CALCIUM LEVELS AND DECREASES PHOSPHATE LEVELS INC. RESORPTION OF BONES Slide 17: ADRENAL CORTEX GLUCOCORTICOIDS (PRIMARILY CORTISOL)-SUGAR PROMOTES CARBO, PROTEIN AND FAT CATABOLISM INCREASES TISSUE RESPONSIVENESS TO OTHER HORMONES MINERALOCORTICOIDS (ALDOSTERONE) – SALT TENDS TO INC SODIUM RETENTION AND POTASSIUM EXCRETION ANDROGENS (MALE HORMONE)- SEX GOVERNS CERTAIN SEC SEX CHARACTERISTICS ALL CORTICOIDS ARE IMPORTANT FOR DEFENSE AGAINST STRESS OR INJURY Slide 18: ADRENAL MEDULLA EPINEPHRINE (ADRENALIN) – 80% NOREPINEPHRINE – 20% ELEVATES BLOOD PRESSURE CONVERTS GLYCOGEN TO GLUCOSE WHEN NEEDED BY MUSCLES FOR ENERGY INC. HEART RATE, CARDIAC CONTRACTILITY DILATES BRONCHIOLES Slide 19: OVARIES ESTROGENS PROGESTERONE STIMULATE DEVELOPMENT OF SECONDARY SEX CHARACTERISTICS EFFECT REPAIR OF THE ENDOMETRIUM AFTER MENSTRUATION Slide 20: TESTES TESTOSTERONE ESSENTIAL FOR NORMAL FUNCTIONING OF MALE REPRODUCTIVE ORGANS STIMULATES DEVELOPMENT OF SEC SEX CHARAC Slide 21: PANCREAS (ISLETS OF LANGERHANS) INSULIN – PROMOTES METABOLISM OF CARBO, PROTEIN AND FAT THUS DECREASING BLOOD GLUCOSE GLUCAGON – MOBILIZES GLYCOGEN STORES, THUS RAISING BLOOD GLUCOSE LEVELS SOMATOSTATIN – DECREASES SECRETION OF INSULIN, GLUCOAGONS, GROWTH HORMONE AND SEVERAL GI HORMONES (GASTRIN, SECRETIN) THYROID GLAND : THYROID GLAND ANTERIOR PART OF NECK THYROXINE (T4), TRIIODOTHYRONINE (T3), CONTROLS RATE OF CELLULAR METABOLISM THYROCALCITONIN -RELEASED WHEN THERE IS HIGH LEVEL OF PLASMA CALCIUM CALCIUM DEPOSITION - BONES. IODINE INGESTED REACTS WITH TYROSINE= THYROID HORMONES PARATHYROID GLANDS : PARATHYROID GLANDS FOUR SMALL GLANDS LOCATED BACK THYROID GLAND HORMONES: PARATHORMONE (PTH) INCREASES PLASMA CALCIUM, DEC PLASMA PHOSPHATE GIT: ABDORPTION OF CALCIUM RENAL: CONVERSION OF VIT D TO ITS ACTIVE FORM CALCIUM REABSORPTION AND PHOSPHATE EXCRETION Slide 26: FUNCTIONS OF CALCIUM: - NEUROMUSCULAR RESPONSE - BLOOD COAGULATION MECHANISMS CONTROL OF PTH: NEGATIVE FEEDBACK MECHANISM: WHEN SERUM CALCIUM ARE LOW, THERE IS INCREASED MOBILIZATION OF CALCIUM FR BONE, RESULTING IN AN INCREASE IN SERUM CALCIUM LEVELS ADRENAL GLAND : ADRENAL GLAND TWO SMALL STRUCTURES WHICH CAP THE TOP OF THE KIDNEYS. CORTEX: GLUCOCORTICOIDS (CORTISOL) GLUCONEOGENESIS MINERALOCORTICOIDS (ALDOSTERONE) SEX HORMONES- SEXUAL EFFECTS OF MASCULINIZATION MEDULLA: EPINEPHRINE (ADRENALINE) RESPOND TO FIGHT OR FLIGHT CONVERTS GLYCOGEN TO GLUCOSE BOOST O2 CARRYING CAPACITY OF BLOOD INCREASE CARDIAC OUTPUT NOREPINEPHRINE PANCREAS : PANCREAS POST OF STOMACH ENDOCRINE AND EXOCRINE FUNCTIONS ENDOCRINE – ISLETS OF LANGERHANS) ALPHA – GLUCAGON Converts glycogen to glucose BETA - INSULIN INFLUENCES CARBOHYDRATE, FAT AND PROTEIN METABOLISM TRANSPORT OF GLUCOSE INTO CELLS CONVERTS GLUCOSE TO GLYCOGEN- LIVER, MUSCLES REGULATES RATE OF CARBOHYDRATE BURNING CONVERTS FATTY ACIDS INTO FATS – STORED AS ADIPOSE TISSUES STIMULATING PROTEIN SYNTHESIS WITHIN THE TISSUE Slide 33: ENDOCRINE DISORDERS ANTERIOR PITUITARY GLAND DISORDERS: : ANTERIOR PITUITARY GLAND DISORDERS: GIGANTISM ACROMEGALY DWARFISM Slide 35: GIGANTISM AND ACROMEGALY ETIOLOGY: INCREASE SECRETION OF GROWTH HORMONE TUMORS OF ANTERIOR PITUITARY GLAND GIGANTISM – BEFORE EPIPHYSEAL CLOSURE. BONE GROWTH AND ALL OTHER TISSUES- WITH GIGANTIC BODY GROWTH ACROMEGALY – TRANSVERSE GROWTH. AFTER EPIPHYSEAL CLOSURE IN LONG BONES. ACROMEGALY : ACROMEGALY CLINICAL MANIFESTATIONS: - ENLARGED SUPRAORBITAL RIDGE - THICKENED TONGUE -PROJECTION OF THE JAW (PROGNATHISM) - ENLARGEMENT OF THE HANDS AND FEET - HYPERTROPHY OF THE SKIN - INCREASE IN SIZE OF THE NOSE - SEVERE HEADACHES, BITEMPORAL HEMIANOPIA- PRESSURE ON OPTIC NERVE Slide 39: ASSESSMENT: EXCESSIVE GROWTH OF ALL PARTS OF THE BODY THREE TIMES THE NORMAL HEIGHT FOR AGE MAY REACH OVER 80 INCHES Slide 40: DIAGNOSTIC: - INC SERUM GROWTH HORMONE LEVEL - X-RAYS, CT SCAN, MRI - PHYSICAL EXAMINATION COMPLICATIONS: - HEADACHE AND VISUAL FIELD DISTURBANCES - DM/GLUCOSE INTOLERANCE - GLUCONEOGENESIS, REDUCE GLUCOSE UPTAKE IN THE LIVER TREATMENT: - BROMOCRIPTINE - PITUITARY RADIATION - HYPOPHYSECTOMY HYPOPHYSECTOMY : HYPOPHYSECTOMY PITUITARY ADENECTOMY PARTIAL/COMPLETE REMOVAL PITUITARY GLAND SURGERY: CRANIOTOMY: TRANSFRONTAL TRANSPHENOIDAL : INNER ASPECT UPPER LIP; SELLA TURCICA ENTERED FLOOR OF NOSE PATCH – ABDOMEN OR THIGH COMPLICATION -HYPOPITUITARISM Slide 43: POST-OP: NASAL PACKING : 24 HRS ELEVATE HEAD – 30 DEGREES IV FLUIDS OBSERVE CSF LEAK (NOSE) ASSESS NASAL DRIP: CLEAR, POSITIVE FOR PROTEIN - MONITOR VS, I AND O, TEMP, WBC, NUCHAL RIGIDITY DEEP BREATHING, NO NOSE BLOWING, VALSALVA, BENDING FOR 2 MOS. ASSESS VISUAL ACUITY – HEMATOMA CORTICOSTEROIDS ARE STARTED POST OP FREQUENT ORAL HYGIENE – SOFT SWABS, NO TOOTHBRUSHING UNTIL INCISION HEALED PANHYPOPITUITARISM : PANHYPOPITUITARISM HYPOSECRETION ANT PITUITARY HORMONES ALL HORMONES ARE USUALLY AFFECTED CLINICAL MANIFEST- INADEQUATE HORMONE CAUSE: UNKNOWN, TUMOR HYPOPHYSECTOMY RADIATION DRUGS (BROMOCRIPTINE) HORMONE REPLACEMENT DWARFISM: : DWARFISM: DECREASE GROWTH HORMONE IN CHILDREN ASSESSMENT: RETARDED PHYSICAL GROWTH PREMATURE BODY AGING SLOW INTELLECTUAL DEVELOPMENT MANAGEMENT: REMOVAL OF CAUSE: TUMOR HUMAN GROWTH HORMONE INJECTION POSTERIOR LOBE- NEUROHYPOPHYSIS : POSTERIOR LOBE- NEUROHYPOPHYSIS ANTIDIURETIC, VASOPRESSIN – ADH- RENAL TUBULES OXYTOCIN- SMOOTH MUSCLE (UTERUS AND MAMMARY GLANDS POST PITUITARY GLAND DISORDERS: DIABETES INSIPIDUS SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE (SIADH) Slide 47: DIABETES INSIPIDUS DEC ADH ASSESSMENT: EXCESSIVE URINE OUTPUT SEVERE DEHYDRATION EXCESSIVE THIRST ANOREXIA, WEIGHT LOSS WEAKNESS CONSTIPATION DIAGNOSTIC FINDING: WATER DEPRIVATION TEST: LOW URINE SP GRAVITY, DEC SODIUM AND POTASSIUM HIGH SERUM OSMOLALITY, SODIUM AND POTASSIUM SIADH INCREASED ADH FEEDBACK MECH THAT REGULATES ADH DOES NOT FUNCTION PROPERLY ADH RELEASED EVEN WHEN PLASMA HYPO-OSMOLALITY IS PRESENT ASSESSMENT: ANOREXIA, N/V LETHARGY, HEADACHES CHANGE LEVEL OF CONSCIOUSNESS DEC DEEP TENDON REFLEXES TACHYCARDIA INC CIRC BLD VOL DEC URINARY OUTPUT DIAGNOSTIC TESTS: INC. URINE SP GRAVITY, SODIUM AND POTASSIUM LOW SERUM OSMOLALITY, SODIUM AND POTASSIUM NV 135 – 145 mEq/L Slide 48: NSG INTERVENTIONS RECORD I AND O MONITOR URINE SP GRAVITY, SKIN COND, WEIGHT, BP, PULSE, TEMP ADMINISTER: PITRESSIN- IM/IV WARM BEFORE ADMINISTRATION. EXTRAVASATION CAUSES IRRITATION DESMOPRESSIN ACETATE - NASALLY NSG INTERVENTIONS: RESTRICT WATER INTAKE (500 – 600 ML/24 HRS) DIURETCIS – EXCRETION OF WATER HYPERTONIC SALINE (3% NaCl) IV ADM DEMECLOCYCLINE (DECLOMYCIN) WEIGH DAILY I AND O MONITOR SERUM SODIUM LEVELS ASSESS LOC THYROID DISORDERS: : THYROID DISORDERS: HYPOTHYROIDISM MYXEDEMA COMA HYPERTHYROIDISM THYROID STORM CRETINISM Slide 56: MYXEDEMA/HYPOTHYROIDISM HYPOSECRETION OF THYROID HORMONE SLOWED PHYSICAL AND MENTAL FUNCTIONS PREDISPOSING FACTORS: INFLAMMATION OF THYROID IATROGENIC – THYROIDECTOMY, IRRADIATION, OVERTREATMENT WITH ANTITHYROIDS PITUITARY DEF IODINE DEF IDIOPATHIC ASSESSMENT: DEC ACTIVITY LEVEL SENSITIVITY TO COLD POTENTIAL ALT IN SKIN INTEGRITY DECREASED PERCEPTION OF STIMULI OBESITY, WEIGHT GAIN POTENTIAL FOR RESP DIFFICULTY CONSTIPATION ALOPECIA BRADYCARDIA DRY SKIN AND HAIR DEC ABILITY TO PERSPIRE GRAVES’ DIS (HYPERTHYROIDISM) HYPERSECRETION OF THYROID HORMONE ACCE PHYSICAL AND MENTAL FUNCTIONS PREDISPOSING FACTORS: THYROID-SECRETING TUMORS IATROGENIC- OVERTREATMENT FOR HYPOTHYROID PITUITARY HYPERACTIVITY SEVERE STRESS: PREGNANCY ASESSMENT: HYPERACTIVITY SENSITIVITY TO HEAT REST AND SLEEP DEPRIVATION INCREASED PERCEPTION OF STIMULI WEIGHT LOSS Slide 58: DIAGNOSTIC FINDINGS: DEC THYROID HORMONES DEC SERUM SODIUM ELEVATED SERUM TSH DEC I131 TREATMENT: HORMONE REPLACMENT: LEVOTHYROXINE LIOTHYRONINE THYROGLOBULIN DIET: LOW CALORIE, HIGH FIBER, HIGH PROTEIN DIARRHEA POTENTIAL FOR RESP DIFFICULTY TACHYCARDIA EXOPTHALMUS FREQ MOOD SWINGA NERVOUS, JITTERY FINE, SOFT HAIR MENSTRUAL CHANGES: OLIGOMENORRHEA AMENORRHEA DIAGNOSTIC TESTS: ELEVATED T3, T4 DEC TSH INC UPTAKE OF !131 THYROID SCAN - NODULES TREATMENT: ANTITHYROID DRUGS THIONAMIDES: (TAPAZOLE , PTU) IODINE: SSKI LUGOL’S SOL BETA BLOCKERS RADIOACTIVE IODINE (I131) ONE TREATMENT COMP: HYPOTHYROIDISM SURGERY SUBTOTAL THYROIDECTOMY TOTAL THYROIDECTOMY DIET: HIGH CAL, HIGH VIT. SMALL FREQUENT Slide 59: POST – OP: TRACHEOSTOMY SET BEDSIDE CALCIUM GLUCONATE IV BEDSIDE POSITION: SEMI-FOWLERS WITH HEAD ELEVATED AND SUPPORTED BY PILLOWS ASSESS DRESSING – HEMORRHAGE ASSESS COMPLAINTS OF PRESSURE OR FULLNESS INCISION SITE MONITOR VS ASSESS VOICE CHANGES OR RESPIRATORY DIFFICULTY (EDEMA) THYROID STORM (THYROTOXICOSIS) : THYROID STORM (THYROTOXICOSIS) LIFE-THREATENING, UNCONTROLLED HYPERTHYROIDISM ONSET-SPONTANEOUS TEMP – 41C- BEC BODY UNABLE TO RELEASE HEAT FROM INCREASED METABOLISM ASSESSMENT: EXTREME TEMP ELEVATION MARKED RESP DISTRESS TACHYCARDIA, APPREHENSION RESTLESSNESS – DELIRIUM, COMA, DEATH FR HEART FAILURE Slide 62: NSG INTERVENTIONS: COOL ROOM.HYPOTHERMIA BLANKET CHANGE LINEN FREQUENTLY – DIAPHORESIS MONITOR CARDIAC ARRHYTHMIAS EXOPTHALMOS: EYES DROPS/OINTMENT/PATCHES/MASK DARK COLORED GLASSES – CORNEAL IRRITATION MEDICAL MANAGEMENT: MEASURES TO DEC TEMP AND HEART RATE ANTITHYROID DRUGS O2 HYPOTHERMIA BLANKETS, ICE PACKS, TYLENOL HYDROCORTISONE Slide 63: NSG INTERVENTIONS: LIFETIME HORMONE REPLACEMENT: LEVOTHYROXINE (SYNTHROID) THYROGLOBULIN (PROLOID) DESSICATED THYROID LIOTHYRONINE (CYTOMEL) DIET: HIGH PROTEIN, LOW CALORIE, LOW CHOLESTEROL, HIGH ROUGHAGE, FLUIDS AVOID SEDATIVES, NARCOTICS PROVIDE EXTRA BLANKETS MONITOR OVERDOSE: TACHYCARDIA, RESTLESSNESS, NERVOUSNESS, INSOMNIA MYXEDEMA COMA : MYXEDEMA COMA SEVEREST FORM OF HYPOTHYROIDISM NOTED BY NONPITTING EDEMA CAUSE: INFECTION ASSESSMENT: PERIORBITAL EDEMA PUFFY HANDS AND FEET PROFOUND LETHARGY AND APATHY, HYPOGLYCEMIA SLOWED BODY METABOLISM HYPOVENTILATION - DEATH Slide 65: INTERVENTIONS: PATENT AIRWAY, IV FLUIDS, SYNTHROID, GLUCOSE IV MONITOR BP, MENTAL STATUS, ELECTROLYTES AND GLUCOSE, KEEP WARM CONGENITAL HYPOTHYROIDISM:CRETINISM : CONGENITAL HYPOTHYROIDISM:CRETINISM - DECREASE OR LACK PRODUCTION OF T3 AND T4 AT BIRTH - RESULT FR CONGENITAL LACK OF THYROID GLAND OR UNABLE TO PRODUCE HORMONES - MAY BECOME EVIDENT AT 3 TO 6 MONTHS - NEWBORN SCREENING ON ALL NEWBORNS - IF UNTREATED BEYOND AGE OF 2 – IRREVERSIBLE BRAIN DAMAGE OR MENTAL RETARDATION WILL OCCUR ETIOLOGY: - ANTITHYROID DRUGS DURING PREGNANCY - DEVELOPMENT ANOMALY OF THYROID GLAND ASSESSMENT: - SHORT THICK NECK AND ENLARGED TONGUE - SHORTER LEGS IN RELATION TO TRUNK - COGNITIVE IMPAIRMENT AS THE CHILD GROWS OLDER - DRY SCALY SKIN WITH LOW TEMP - BRADYCARDIA, GAIN IN BODY WEIGHT - HYPOTONIA, POOR FEEDING - CONSTIPATION, PROTRUDING ABDOMEN - LOW T3 AND T4 Slide 68: DIAGNOSTIC FINDINGS: DEC T3, T4 DEC TSH – HYPOTHALAMIC OR PITUITARY INSUFFICIENCY THYROID SCAN DEC X-RAY LONG BONES – DELAYED SKELETAL DEVELOPMENT TREATMENT: ORAL THYROID REPLACEMENT VIT D – TO PREVENT RICKETS NSG INTERVENTIONS: INSTRUCT CLIENT: THYROID REPLACEMENT – TAKE AT SAME TIME DAILY THYROXINE INSTRUCT FAMILY: PROGNOSIS IS EXCELLENT WITH REPLACEMENT THERAPY DISORDERS PARATHYROID GLAND : DISORDERS PARATHYROID GLAND HYPOPARATHYROIDISM HYPERPARATHYROIDISM Slide 70: HYPOPARATHYROIDISM DEC SEC OF PARATHYROID HORMONE ASSESSMENT: TETANY MUSCULAR IRRITABILITY (CRAMPS,SPASMS) CARPOPEDAL SPASM, CLONIC CONVULSIONS CHVOSTEK SIGN TROUSSEAU’S SIGN DYSPHAGIA PARESTHESIA, LARYNGEAL SPASM ANXIETY, DEPRESSION, IRRITABILITY TACHYCARDIA DIAGNOSTIC TESTS: SERUM CALCIUM SERUM PHOSPHOROUS X-RAY – BONE DENSE SULKOWITCH TEST FOR CALCIUM HYPERPARATHYROIDISM OVERSECRETION OF PARATHYROID HORMONE ASSESSMENT: FATIGUE, MUSCLE WEAKNESS CARDIAC DYSRHYTHMIAS EMOTIONAL IRRITABILITY RENAL CALCULI BACK AND JOINT PAIN, PATHOLOGICAL FRACTURES PANCREATITIS, PEPTIC ULCER DIAGNOSTIC TESTS: SERUM CALCIUM SERUM PHOSPHORUS X-RAY- BONE POROUS SULKOWITCH TEST FOR CALCIUM IN URINE Slide 71: Trousseau sign of latent tetany is a medical sign observed in patients with low calcium.[1] This sign may become positive before other gross manifestations of hypocalcemia such as hyperreflexia and tetany, but is generally believed to be more sensitive than the Chvostek sign for hypocalcemia. a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for "hand of the obstetrician") because is supposedly resembles the position of an obstetrician's hand in delivering a baby. Slide 72: The Chvostek sign (also Weiss sign) is one of the signs of tetany seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped at the angle of the jaw, the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcaemia (ie from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of nerves. Though classically described in hypocalcaemia, this sign may also be encountered in respiratory alkalosis, such as that seen in hyperventilation, which actually causes decreased serum Ca++ with a normal calcium level due to a shift of Ca++ from the blood to albumin which has become more negative in the alkalotic state. Slide 73: INTERVENTIONS: EMERGENCY TX: CALCIUM LACTATE IV SLOW RATE PATIENT TO REMAIN RECUMBENT FOR 30 MIN BEDSIDE: TACHEOSTOMY SET AND CALCIUM GLUCONATE ERGOCALCIFEROL (VIT D) ELEMENTAL CALCIUM AS LACTATE, GLUCONATE, OR CARBONATE OBSERVE FOR TETANY LOW-PHOSPHOROUS, HIGH-CALCIUM DIET INTERVENTIONS: RELIEVE PAIN PREVENT FORMATION OF RENAL CALCULI- INC FLUID INTAKE OFFER ACID-ASH JUICES (CRANBERRY AND PRUNE JUICE) (IMPROVES SOLUBILITY OF CALCIUM) ADMINISTER APPROPRIATE DIET PREVENT FRACTURES SAFETY PRECAUTIONS MONITOR POTASSIUM LEVELS (COUNTERACTS EFFECT OF CALCIUM ON CARDIAC MUSCLES) PROVIDE POSTPARATHYROIDECTOMY CARE (ESSENTIALLY SAME AS FOR THYROIDECTOMY) IV LASIX AND SALINE PROMOTE CALCIUM EXCRETION IV PHOSPHORUS IS USED ONLY FOR RAPID LOWERING OF CALCIUM LEVEL DIET: LOW CALCIUM, HIGH PHOSPHORUS SURGERY - PARATHYROIDECTOMY DISORDERS OF THE ADRENAL GLANDS : DISORDERS OF THE ADRENAL GLANDS ADRENAL CORTEX: ADDISONS DISEASE CUSHING’S SYNDROME CONN’S SYNDROME (HYPERALDOSTERONISM) ADRENAL MEDULLA: PHEOCHROMOCYTOMA Slide 77: ADDISON’S DISEASE HYPOSECRETION OF ADRENAL HORMONES PATHOPHYSIOLOGY: DEC Na + DEHYDRATION DEC BLD VOL + SHOCK INC K + MET ACIDOSIS + ARRHYTHMIAS DEC BLD SUGAR + INSULIN SHOCK ASSESSMENT: FATIGUE, WEAKNESS, DEHYDRATION, DEC BP, WEIGHT LOSS PATHOLOGICAL FRACTURES ETERNAL TAN DEC RESISTANCE TO STRESS, ALOPECIA LOSS OF SEC SEXUAL CHARACTERISTICS DIAGNOSTIC TESTS: ACTH STIMULATION TEST PLASMA CORTISOL AT 8 AM AND 4 PM NV – 7 TO 18 MG/DL AT AM AND 2 TO 10 MG/DL AT PM 17-HYDROXYCORTICOIDS IN 24 HR URINE NV – 2-10 MG/24 HRS TREATMENT: FLUID REPLACEMENT HYDROCORTISONE IV Q 6 HRS HORMONE REPLACEMENT FOR LIFE (BILATERAL ADRENALECTOMY) DIET: HIGH CARBO, SODIUM, AND PROTEIN, LOW POTASSIUM SMALL FREQUENT SALTY FOODS/TABLETS CUSHING SYNDROME HYPERSECRETION OF ADRENAL HORMONES ETIOLOGY: PITUITARY TUMOR STEROID THERAPY PATHOPHYSIOLOGY: INC NA + INC BLD VOL + INC BP DEC K + MET ALKALOSIS + SHOCK INC BLD SUGAR + KETOACIDOSIS ASSESSMENT: FATIGUE, WEAKNESS, OSTEOPOROSIS, MUSCLE WASTING, CRAMPS EDEMA, INC BP, PURPLE SKIN STRIATIONS ALOPECIA, DEPRESSION EMACIATION AMENORRHEA, HIRSUTISM, GYNECOMASTIA, DIAGNOSTIC TESTS: INCH ACTH DEC SERUM POTASSIUM, INC SODIUM AND GLUCOSE INC. 17-HYDROCORTICOSTEROIDS IN 24 HRS CT SCAN/MRI - TUMORS TREATMENT: POTASSIUM SUPPLEMENTS ADRENAL SUPPRESANTS ANTIDIABETIC MEDS, DIURETICS RADIATION THERAPY SURGERY HYPOPHYSECTOMY, ADRENALECTOMY DIET: HIGH K AND PROTEIN, LOW SODIUM, CARBO AND CALORIE ADDISONIAN CRISIS : ADDISONIAN CRISIS SEVERE EXACERBATION OF DISEASE PRECIPITATING FACTORS: STEROID WITHDRAWAL, SEPSIS, DRUGS (rifampicin, phenytoin, ketoconazole, opiates), ILLNESS, SURGERY, STRENUOUS ACTIVITY, ASSESSMENT: SUDDEN PENETRATING PAIN- BACK, ABDOMEN SEVERE HYPOTENSION, SHOCK, COMA, DEATH CUSHING’S SYNDROME : CUSHING’S SYNDROME INTERVENTIONS: : INTERVENTIONS: IV FLUIDS – 5% DEXTROSE IN SALINE IV GLUCOCORTICOIDS (SOLU-CORTEF) IV, MINERALOCORTICOID (FLUDROCORTISONE) BLOOD TRANSFUSIONS, SERUM ALBUMIN, VASOPRESSORS ANTIBIOTICS – INFECTION STRICT BED REST, ELIMINATE STRESS PRIMARY ALDOSTERONISM- CONN’S SYNDROME : PRIMARY ALDOSTERONISM- CONN’S SYNDROME EXCESSIVE SECRETION OF ALDOSTERONE FROM ADRENAL CORTEX SIGNS OF HYPOKALEMIA, HYPERNATREMIA ADRENALECTOMY PERFORMED – IF TUMOR BILATERAL – LIFELONG CORTICOSTEROIDS, FLUID, INSULIN (HYPERGLYCEMIA UNILATERAL – TEMPORARY SPIRONOLACTONE- IF UNABLE TO HAVE SURGERY ASSESSMENT: HYPERTENSION POLYURIA, POLYDIPSIA DEHYDRATION MUSCLE WEAKNESS, LEG CRAMPS, GENERALIZED FATIGU DIAGNOSTIC TESTS: SERUM SODIUM (HIGH) SERUM POTASSIUM (LOW) ALDOSTERONE (HIGH) NSG INTERVENTIONS: : NSG INTERVENTIONS: VS, B/P, I AND O, DAILY WEIGHTS SODIUM RESTRICTION MEDS FOR HYPERTENSION SPIRONOLACTONE, POTASSIUM SUPPLEMENTS DIET: LOW SODIUM, HIGH POTASSIUM, HIGH CALORIE, NO STIMULANTS ADRENAL GLAND DISORDERS : ADRENAL GLAND DISORDERS PHEOCHROMOCYTOMA : PHEOCHROMOCYTOMA SECRETES EXCESS EPINEPHRINE AND NOREPINEPHRINE MANIFESTATIONS: PERSISTENT HYPERTENSION PALPITATIONS, TACHYCARDIA HYPERGLYCEMIA, DIAPHORESIS NERVOUSNESS, APPREHENSION HEADACHE DIAGNOSTIC TESTS: 24-HOUR URINE FOR CATECHOLAMINES TOTAL PLASMA CATECHOLAMINE LEVELS CT SCAN, MRI, ULTRASOUND - TUMOR Slide 86: NSG INTERVENTIONS: -assess ECG changes, arterial pressures, blood glucose levels MEDICAL MANAGEMENT: -antihypertensives SURGICAL MANAGEMENT: -adrenalectomy -fluids, plasma and plasma substitutes to lessen hypotension-24 to 48 hours -corticosteroid replacement PANCREAS : PANCREAS Slide 90: 2/1/2011 90 ●Chronic, metabolic disease of the pancreas Insufficient secretion of insulin Disorder of carbohydrate, protein and fat metabolism DIABETES MELLITUS Slide 91: Types: Type 1: Insulin-dependent DM (IDDM) Absolute deficiency of insulin Antibodies Mumps, congenital rubella Type 2: Non-insulin-dependent DM (NIDDM) Relative deficiency of insulin Islet cell defect: dec insulin Reduction of receptor sites Heredity, obesity, Insulin resistance Type 3: gestational DM (GDM) No DM before pregnancy Type 4: Diabetes due to another condition: pancreatic disease Slide 92: Nsg Assessment: Type1 (abrupt) Type 2 (gradual) Hyperglycemia Polyuria Polydipsia Polyphagia Weight loss Weakness Skin (wounds) Urinary tract/vaginal infections Blurred visions Slide 93: Nursing Management: Maintain Normal sugar balance Monitor Blood glucose (self-monitoring) Premeal BG: Diabetics (target value): 90-130 mg/dl Nondiabetics (NV): < 110 mg/dl Peak Postmeal BG: Diabetics (target value): < 180 mg/dl Nondiabetics (NV): < 140 mg/dl Oral hypoglycemic Insulin Slide 94: Proper Diet: Food exchange list: (Dietitian) CHO:50-60%, Protein: 20-30%, Fats: 10-20%. Limit refined sugars, more complex carbo Regular Exercise: Regular: 4-7 days/week Elevate HR: 50% maximal rate Monitor BG before exercise Over 250 mg/dl (check ketone) Less than 100 mg/dl (snacks) Slide 95: Oral Hypoglycemic Agents: Sulfonylureas: Inc insulin secretion Chlorpropamide (Diabinese),Glipizide (Glucotrol), Glimepiride (Amaryl), Tolbutamide (orinase) Meglitinides: Inc insulin secretion Repaglinide (Prandin) Take 30 min before meals; Slide 96: Biguanides: Inc glucose uptake (muscles/adipose) Dec liver glucose release Metformin (Glucophage) Administered with meals Thiazolidinediones: Inc glucose uptake (muscles/adipose tissue) Dec liver glucose release Rosiglitazone (Avandia) Postmenopausal women may resume ovulation Alpha-Glucosidase Inhibitor: Slows CHO absorption Acarbose (Precose), Miglitol (Glyset): with meal Slide 97: INSULIN: Proper Storing: Room temp. : 28 days Refrigerate: not in use Prevent direct sunlight Slide 98: Proper Administration: Wash hands Rotate vials, no shaking Wipe top with alcohol swab Draw air equal to total dose 2 Insulin: adm w/n 5-15 min. Inject air: NR Insulin withdrawal: RN Slide 99: Type of administration: Syringe: U100/ml; 27-29 g; ½ inch long Slide 100: Prefilled pens (Novopen, Novolin) Fridge: 28 days, needle up Jet injector: high pressure Slide 101: Implantable Insulin pump Patch and Inhaled insulin Slide 102: Route: SQ : 45-90 degrees IV: regular Slide 103: Sites: Abdomen,arms, thighs,hips No aspiration Systemic rotation in one anatomical area: Do not use site in 2-3 wks 1 1/2 inches apart, NO to scar area Complications: lipohypertrophy/lipoatrophy Insulin : Insulin Slide 107: Fasting blood sugar (FBS)/Fasting Plasma glucose Fasting for at least 8 hrs (water permitted) NV: less than 100 mg/dl Pre-diabetes: 100-125 mg/dl DM: two separate results exceed 126 mg/dl Oral Glucose Tolerance test (OGTT) NPO for 8 hrs Fasting blood sample taken Drink 300 ml (75 g) glucose Bld drawn at 30 min intervals for 2 hrs To remain at rest; NO smoke/drink liquids DM: over 200 mg/dl at 2 hrs Slide 109: Random Blood Sugar: Bld drawn w/o fasting DM: 200 or over Glycosylated hemoglobin: Measures average blood glucose over 120 days At least twice a year No fasting Normal: 4 -6% Poor: over 8 % Urine for ketones: Impending ketoacidosis Done when BG exceeds 300 mg/dl Criteria for the diagnosis of DM : Criteria for the diagnosis of DM Fasting plasma glucose: equal or > 126 mg/dl OR Casual Plasma glucose: equal or > 200 mg/dl plus symptoms OR OGTT : 2-hr plasma glucose: equal or > 200 mg/dl Slide 111: Diabetic Ketoacidosis: Cause: Lack of insulin and ketosis Nursing Assessment: S. glucose: > 300 mg/dl Acidosis Kussmaul breathing (inc rate and depth) hyperkalemia sweet breath odor Ketonuria Anorexia, nausea, vomiting Slide 112: Hyperosmolar Hyperglycemic Nonketotic Coma(HHKS): Cause: insulin deficiency and profound dehydration Nursing Assessment: S. glucose: > 800 mg/dl Hyperglycemia and hyperosmolarity, Polyuria Dehydration. thirst Hypotension, tachycardia Flushed dry skin, decrease skin turgor Confusion, drowsiness Slide 113: Interventions: Regular insulin IV: IV fluids (0.9% NS) Flush insulin sol to entire tubing; discard the first 50 to 100 ml D5NS when BG reaches 250 to 300 mg/dl Cardiac monitoring, Foley catheter Slide 114: HYPOGLYCEMIA: BS < 60 mg/dl Cause: Too much insulin/hypo agent Little food Excessive activity Slide 115: Nsg Assessment: Mild: “DIRE” Diaphoresis, Increased Pulse Restless, Extra hungry Shaking, Pallor Dizziness, Yawning Interventions: “Rule of 15” Check BS 15 Grams of carbohydrate NOT better in 15 min, Check BS, Repeat Txt Next meal more than 30 min give snack of carbohydrate and protein (milk, cheese, cracker) Slide 116: 15 grams of CHO: 1/2 cup juice/regular soda 1 Tbsp honey/syrup/sugar 1 small tube glucose gel 3–4 glucose tablets 5 small sugar cubes 6–8 LifeSavers 8 oz skim (nonfat) milk Slide 117: Moderate Confusion Poor coordination Mood changes Slurred speech Interventions: Instant Glucose/Cake Frosting Gel Insert tube between gum/cheek NO response 15 min, give glucagon Next meal more than 30 min give snack of CHO,CHON Slide 118: Severe Unconsciousness Convulsions Intervention: Glucagon SQ,IM, IV May repeat in 15 min Hosp: D50%/50 IV Slide 119: Differentiate hyperglycemia from hypoglycemia Hot and dry, sugar is high; cold and clammy needs some candy Slide 120: Chronic Complications: Retinopathy and cataract Nephropathy Neuropathy Leg ulcers Arteriosclerosis and atherosclerosis Cardiac complications Vascular changes Causes: Basement membrane thickening Chronic ischemia- hypoxia DISORDERS OF THE PANCREAS : DISORDERS OF THE PANCREAS DIABETES MELLITUS TYPE 1 TYPE 11 GESTATIONAL DIABETES DIABETES MELLITUS : DIABETES MELLITUS COMPLEX, MULTISYSTEM DISEASE CHARACTERIZED BY THE ABSENCE OF OR SEVERE DECREASE IN THE SECRETION OR UTILIZATION OF INSULIN PATHOPHYSIOLOGY: PRIMARY FUNCTION INSULIN – DEC BLD GLUCOSE IF GLUCOSE NOT AVAILABLE: CELLS OXIDIZE FATS AND PROTEINS FATS – KETONE BODIES PROTEIN – CONVERTED TO GLUCOSE HORMONES THAT COUNTERACT INSULIN: GLUCAGON EPINEPHRINE CORTISOL GROWTH HORMONE CLASSIFICATIONS: TYPE 1- INSULIN DEPENDENT-DESTRUCTION BETA CELLS TYPE 2 - NON-INSULIN DEPENDENT- PARTIAL DEF/INSENSITIVITY TO INSULIN GESTATIONAL DIABETES Slide 130: TYPE 1 – INSULIN DEPENDENT DM - ABSENCE INSULIN PRODUCTION - ONSET – 10 TO 15 YRS - FAMILIAL TENDENCY – LEFETIME TYPE 2- NONINSULIN DEPENDENT - INSULIN DEFICIENCY: - DEFECT IN INSULIN PRODUCTION - EXCESSIVE DEMAND FOR INSULIN - ONSET – ADULT AFTER 40 - ASSOCIATED WITH OBESITY - FAMILY HISTORY - MAY REQUIRE INSULIN FOR CONTROL GESTATIONAL DM - DURING PREGNANCY- SECOND TRIMISTER - RETURNS TO NORMAL AFTER DELIVERY - INFANT – LARGE FOR GESTATIONAL AGE, MAY EXPERIENCE HYPOGLYCEMIA AFTER BIRTH Slide 131: ASSESSMENT: TYPE 1 AND 2: HYPERGLYCEMIA MANIFESTATIONS: - POLYURIA – INC. SERUM OSMOLARITY - POLYDIPSIA – INC LOSS OF FLUIDS - POLYPHAGIA - FATIGUE - INCREASED FREQUENCY OF INFECTIONS TYPE 1: - WEIGHT LOSS - BED-WETTING - ONSET: RAPID – DAYS TO WEEKS TYPE 2: - WEIGHT GAIN - VISUAL DISTURBANCES - ONSET: SLOW Slide 132: DIAGNOSTIC TESTS: - 2 OR MORE ABNORMAL TEST RESULTS: - FASTING BLOOD GLUCOSE LEVEL IS ABOVE 126 MG/DL - GLUCOSE TOLERANCE TEST: 2-HOUR GLUCOSE VALUES ARE GREATER THAN 200 MG/DL - RANDOM GLUCOSE: OVER 200 MG/DL WITH SYMPTOMS (3 P’S, WEIGHT LOSS) - GLYCOSYLATED HEMOGLOBIN- INCREASED. LESS THAN 7% IS CONSIDERED GOOD CONTROL Slide 133: TREATMENT: REGULAR PHYSICAL ACTIVITY PLANNED- 30-45 MIN 3-5X/WEEK, MOD AEROBIC DIET: CARBO: 50-60%, FAT: 20-30%, PROTEIN:10-20% PHARMACOLOGICAL INTERVENTION: INSULIN: ORAL HYPOGLYCEMIC AGENTS COMPLICATIONS OF POORLY CONTROLLED DM : COMPLICATIONS OF POORLY CONTROLLED DM DIABETIC KETOACIDOSIS HYPEROSMOLAR HYPERGLYCEMIA NONKETOTIC COMA Slide 135: DIABETES KETOACIDOSIS: - EXTREME HYPERGLYCEMIC STATE - KETONE BODIES- ACIDOSIS - TYPE 1 DM. - STRESS, INFECTION, SURGERY, LACK OF INSULIN - MANIFESTATIONS: - GLUCOSE:300-800 MG/DL - METABOLIC ACIDOSIS: Ph-6.8 – 7.3, Hco3- less than 15 mEq/L -EXCESSIVE WEAKNESS, INC. THIRST, - DEHYDRATION, FEVER (DUE TO DEHYDRATION) - N/V, DEC LEVEL OF CONSCIOUSNESS - FRUITY BREATH - KUSSMAUL RESP (DEEP RAPID RESP) MEDICAL MANAGEMENT: - NSS - RAPID ACTING INSULIN - WHEN BLD SUGAR 250 – 300, DEXTROSE IS ADDED TO IV SOL TO PREVENT HYPOGLYCEMIA - FLUSH 50 ML OF SOLUTION. INSULIN ADHERE TO PLASTIC OF IV SOLUTION SET - INFUSION PUMP Slide 136: HYPEROSMOLAR HYPERGLYCEMIA NONKETOTIC SYNDROME (HHNS) BLD GLUCOSE: 700-1200MG/DL DEHYDRATION: osmotic diuresis MANIFESTATIONS: DEHYDRATION, WARM, FLUSHED SKIN LETHARGY DECREASED LEVEL OF CONSCIOUSNESS TACHYCARDIA, DEC BP MEDICAL MANAGEMENT: SAME AS DKA CHRONIC COMPLICATIONS: : CHRONIC COMPLICATIONS: DIABETIC ANGIOPATHY- CHANGES IN THE VASCULAR SYSTEMCAD, CVA, PVD DIABETIC RETINOPATHY PROGRESSIVE IMPAIRMENT RETINAL CIRCULATION (RUPTURE)- HEMORRHAGE DIABETIC NEPHROPATHY- DECREASE IN KIDNEY FUNCTION DIABETIC NEUROPATHY- HIGH BLD SUGAR LEVELS CAUSE CHANGES WITHIN THE NEURONS. ULCERS FREQUENT INFECTIONS – GLYCOSURIA - UTI Slide 138: FOOT CARE: WASH WITH MILD SOAP AND WATER AND PAT DRY APPLY LANOLIN- PREVENT CRACKING/DRYING CUT TOENAILS STRAIGHT AVOID CONSTRICTING GARMENTS WEAR CLEAN, ABSORBENT SOCKS PROPERLY FITTING SHOES. BREAK NEW SHOES GRADUALLY INSPECT FEET DAILY AND NOTIFY MD FOR CUTS, BLISTERS DIAGNOSTIC TESTS : DIAGNOSTIC TESTS Slide 143: GROWTH HORMONE (GH) NPO AFTER MIDNIGHT MAINTAIN BEDREST UNTIL SERUM SAMPLE IS DRAWN NV: <5 ng/ml IN MEN; <10 ng/ml IN WOMEN URINE OSMOLARITY SERUM OSMOLARITY USED IN EVALUATING ADH DO SERUM AND URINE TESTS AT SAME TIME AND COMPARE RESULTS NORMALLY, URINE OSMOLARITY SHOULD BE HIGHER THAT SERUM URINE – 300 TO 900 mOsm/kg OF WATER SERUM – 285 TO 295 mOsm/kg OF WATER FLUID DEPRIVATION TEST : FLUID DEPRIVATION TEST WITHOLDING FLUIDS TO DETERMINE RESPONSE OF POSTERIOR PITUITARY GLAND IN RELEASING ADH PRE-PRO: FLUID WITHHELD 8 -1 2 HRS PLASMA AND URINE OSMOLALITY STUDIES START AND END OF TEST POST-PRO: FLUIDS RESUMED SLOWLY Slide 146: THYROXINE (T4) TRIIODOTHYRONINE (T3) THYROID-STIMULATING HORMONE (TSH) STIMULATION OF THE THYROID GLAND BY TSH WILL INITIATE THE RELEASE OF STORED THYROID HORMONE WHEN T3 AND T4 ARE LOW, TSH SECRETION INCREASES T3 AND T4 ARE USED TO CONFIRM ABNORMAL TSH PRE-PROCEDURE: NO IODINE (MEDS, FOODS) NV: T4 5-12 mcg/dl T3 70 – 220 ng/dl TSH – 0.2 – 5.4 mU/L Slide 147: NEONATAL THYROXINE (T4) POSITIVE TEST RESULT IS ASSOCIATED WITH HYPOTHYROIDISM PROCEDURE IS DONE BY MEANS OF A HEEL PUNCTURE ON INFANT LEVELS OF NEONATAL T4 ARE NOT INTERPRETED IN SAME TERMS AS SERUM T4 VALUES; NORMAL LEVELS VARY WITH AGE FROM 1 DAY TO 120 DAYS: 1-3 DAYS: 11-22 mcg/dl 1-2 WKS : 10-16 mcg/dl 1-4 MON: 8-16 mcg/dl THYROID SCAN/RADIOACTIVE IODINE UPTAKE (RAIU) : THYROID SCAN/RADIOACTIVE IODINE UPTAKE (RAIU) USE OF RADIOISOTOPE (113I) TO PROVIDE IMAGE OF THYROID GLAND PRE-PROCEDURE: NO IODINE 7 DAYS, PREGNANCY, BREASTFEEDING PATIENTS DISCONTINUING THYROID MEDS – 14 DAYS NO RADIOGRAPHIC EXAM WITH CONTRAST MEDIA PREVIOUS 3 MOS NPO AFTER MIDNIGHT RADIOISOTOPE – GIVEN BY RADIOLOGIST DAY OF EXAM POST-PROCEDURE: MAY RESUME FOODS AND FLUIDS NORMAL ABSORPTION: 24 HRS – 5 – 35% HIGH UPTAKE – HYPERTHYROIDISM LOW UPTAKE - HYPOTHYROIDISM FINE-NEEDLE ASPIRATION BIOPSY: : FINE-NEEDLE ASPIRATION BIOPSY: EXAMINATION OF THYROID TISSUE – MALIGNANCIES PRE-PRO: CONSENT POST-PRO: LIGHT PRESSURE TO SITE REASSURANCE Slide 151: ADRENAL MEDULLA URINARY VANILLYLMANDELIC ACID (VMA) DEPENDING ON HOW TEST IS MEASURES, THERE MAY BE DIETARY AND MEDICATION RESTRICTIONS. 24-HR URINE COLLECTION NV: < 8 mg IN 24 HRS. Increased with pheochromocytoma URINE CATHECHOLAMINES: (EPINEPHRINE,NOREPINEPHRINE,DOPAMINE,METANEPHRINE,NORMETANEPHRINE) SAME AS FOR VMA NO COFFEE, TEA, BANANAS, CHOCOLATE, VANILLA AND ASPIRIN – ALTERS RESULT ACTH STIMULATION TEST ACTH IS GIVEN AS IM OR IV BOLUS AND SAMPLES ARE DRAWN AT 30 AND 60 MIN TO EVALUATE ABILITY OF ADRENAL GLANDS TO SECRETE STEROIDS NV: INC. IN PLASMA CORTISOL LEVELS BY MORE THAN 7-10 mcg/dl ABOVE BASELINE Slide 152: ADRENAL CORTEX ACTH SUPPRESSION (DEXAMETHASONE SUPPRESSION TEST) AN OVERNIGHT TEST: A SMALL AMOUNT OF DEXAMETHASONE IS ADMINISTERED IN THE EVENING, AND SERUM AND URINE ARE EVALUATED IN THE MORNING; EXTENSIVE TEST MAY COVER 6 DAYS CUSHING’S SYNDROME IS RULED OUT IF SUPPRESSION IS NORMAL NV: NORMAL SUPP: 50% DEC IN CORTISONE PRODUCTION (CORTISOL LEVEL < 5 mcg/dl PLASMA CORTISOL LEVELS FOR DIURNAL VARIATIONS: Slide 153: ADRENAL CORTEX ACTH SUPPRESSION (DEXAMETHASONE SUPPRESSION TEST) AN OVERNIGHT TEST: A SMALL AMOUNT OF DEXAMETHASONE IS ADMINISTERED IN THE EVENING, AND SERUM AND URINE ARE EVALUATED IN THE MORNING; EXTENSIVE TEST MAY COVER 6 DAYS CUSHING’S SYNDROME IS RULED OUT IF SUPPRESSION IS NORMAL NV: NORMAL SUPP: 50% DEC IN CORTISONE PRODUCTION (CORTISOL LEVEL < 5 mcg/dl PLASMA CORTISOL LEVELS FOR DIURNAL VARIATIONS: ELEVATION IN PLASMA CORTISOL LEVELS OCCURS IN THE MORNING AND SIGNIFICANT DEC IN EVENING AND NIGHT – A DIURNAL VARIATION SECRETION HIGH IN EARLY MORNING, DECREASED IN EVENING 8 AM – 5-23 mcg/dl 4 PM – 3-13 mcg/dl 24-HOUR URINE FOR HYDROXYCORTICOSTEROIDS AND KETOSTEROIDS INCREASE IN URINE LEVELS INDICATES HYPERADRENAL FUNCTION MALE – 6-20 mg/24 HR F- 6-17 mg/24 HR CHILD UNDER 15 YRS < 5 mg/24 HRS Slide 154: PANCREAS – NV : 70 – 110 MG/DL ORAL GLUCOSE TOLERANCE TEST: PRE-PRO: 3 DAYS BEFORE: HIGH CARBO DIET FOR 3 DAYS NPO FOR 8-10 HRS BEFORE TEST BLOOD AND URINE SAMPLES TAKEN. GLUCOSE SOL GIVEN BLD AND URINE SAMPLES TAKEN: 30 MIN, 1 HR, 2 HRS POST-PRO: WATCH FOR HYPOGLYCEMIA/HYPERGLYCEMIA VALUE: 1 HR: < 200 mg/dl 2 HR: < 140 mg/dl 2-HR POSTPRANDIAL BLOOD SUGAR: MEASURING THE SERUM GLUCOSE 2 HRS AFTER A MEAL VALUE: 65 – 139 mg/dl FASTING BLOOD SUGAR: PRE-PROCEDURE: NPO – 8 HRS POST-PRO: MAY RESUME FOOD/FLUIDS VALUE: > 126 mg/dl IS DIAGNOSTIC FOR DM Slide 155: GLYCOSYLATED HEMOGLOBIN (HEMOGLOBIN A1C) AVERAGE BLD SUGAR PREVIOUS 120 DAYS FASTING NOT NECESSARY GOAL: WITH DM – 7.5% WITHOUT DM – 4-6% SERUM AMYLASE USED TO EVALUATE PANCREATIC CELL DAMAGE OTHER INTESTINAL INTESTINAL CONDITIONS CAUSE INCREASE VALUE: > 200 U/L URINARY AMYLASE IN PANCREATIC INJURY, MORE AMYLASE ENTERS BLOOD AND IS EXCRETED IN URINE MAY BE DONE ON A 2-HR OR A 24-HR URINE SPECIMEN VALUE: 2-HR SPECIMEN: 2-34 U 24-HR SPECIMEN: 24-408 U Slide 156: SERUM LIPASE APPEARS IN SERUM AFTER DAMAGE TO PANCREAS NORMAL VALUES VARY WITH METHOD ELEVATED IS ABNORMAL KETONE BODIES (ACETONE) KETONE BODIES OCCUR IN THE URINE BEFORE THERE IS A SIGNIFICANT INCREASE IN SERUM KETONES USE FRESHLY VOIDED URINE VALUE: NEGATIVE Slide 157: GLYCOSYLATED HEMOGLOBIN (HEMOGLOBIN A1C) AVERAGE BLD SUGAR PREVIOUS 120 DAYS FASTING NOT NECESSARY GOAL: WITH DM – 7.5% WITHOUT DM – 4-6% PHARMACOLOGY : PHARMACOLOGY ADH REPLACEMENT : ADH REPLACEMENT MEDS: DESMOPRESSIN (DDAVP): NASAL SPRAY, PO, IV SQ VASOPRESSIN (PITRESSIN): IM, SQ LYPRESSIN (DIAPID): NASAL SPRAY MONITOR DAILY WEIGHTS; CORRELATRE WITH I AND O VASOPRESSIN MORE LIKELY TO CAUSE ADVERSE CARDIOVASCULAR AND THROMBOEMBOLIC PROBLEMS SE: EXCESSIVE WATER RETNTION, HEADACHE, NAUSEA, FLUSHING ANTITHYROID : ANTITHYROID MEDS: PROPYLTHIOURACIL (PTU) PO METHIMAZOLE (TAPAZOLE ) PO MAY INCREASE ANTICOAGULATION EFFECT OF HEPARIN AND ORAL ANTICOAGULANTS MAY BE COMBINED WITH IODINE PREPARATIONS MONITOR CBC STORE TAPAZOLE IN LIGHT-SENSITIVE CONTAINER MAY BE USED BEFORE SURGERY OR TREATMENT WITH RADIOACTIVE IODINE S/E: AGRANULOCYTOSIS, ABDOMINAL DISCOMFORT, N/V,DIARRHEA, CROSSES PLACENTA Slide 161: MEDS: LUGOL’S SOLUTION: PO SATURATED SOLUTION OF POTASSIUM IODIDE (SSKI) ADMINISTER IN FLUID/JUICE TO DECREASE UNPLEASANT TASTE. Use straw-stains teeth MAY BE USED TO DECREASE VASCULARITY OF THYROID GLAND BEFORE SURGERY Milk- decreases absorption S/E: INHIBITS SYNTHESIS AND RELEASE OF THYROID HORMONE RADIOACTIVE IODIDE: : RADIOACTIVE IODIDE: CAUSES PARTIAL OR TOTAL DESTRUCTION OF THYROID GLAND THROUGH RADIATION MEDS: IODINE (123I OR 131l) PO INCREASE FLUIDS IMMEDIATELY AFTER TRETAMNET BECAUSE RADIOACTIVE ISOTOPE IS EXCRETED IN THE URINE THERAPEUTIC DOSE OF RADIOACTIVE IODINE IS LOW; NO RADIATION SAFETY PRECAUTIONS ARE REQUIRED CONTRAINDICATED IN PREGNANCY S/E: DISCOMFORT IN THYROID AREA; BONE MARROW DEPRESSION DESIRED EFFECT: PERMANENT HYPOTHYROIDISM THYROID REPLACEMENTS : THYROID REPLACEMENTS MED: LEVOTHYROXINE SODIUM (LEVOTHROID, LEVOXYL, SYNTHROID) PO, IM,IV LIOTHYRONINE (CYTOMEL) BE CAREFUL IN READING EXACT NAME ON LABEL OF MEDICATIONS; MICROGRAMS AND MILLIGRAMS ARE USED AS UNITS OF MEASURE GENERALLY TAKEN ONCE A DAY BEFORE BREAKFAST WITHIN 3-4 DAYS, BEGIN TO SEE IMPROVEMENT; MAXIMUM EFFECT IN 4-6 WEEKS LIFELONG TREATMENT S/E: OVERDOSE MAY RESULT IN SYMPTOMS OF HYPERTHYROIDISM: TACHYCARDIA, HEAT INTOLERANCE,NERVOUSNESS Slide 164: ADRENOCORTICAL HORM:CORTICOSTEROIDS, GLUCOCORTICOIDS ANTIINFLAMMATORY ACTION: SUPPRESS PRODUCTION OF LYMPHOCYTES STRESS EFFECT: RELEASE OF CORTICOSTEROIDS MEDS: CORTISONE ACETATE (CORTONE ACETATE); PO, IM HYDROCORTISONE (SOLU-CORTEF) IM,PO HYDROCORTISONE ACETATE (CORTAID,CORTICAINE) TOPICAL DEXAMETHASONE (DECADRON)PO,IV, IM, TOPICAL PREDNISONE (DELTASONE, METICORTEN)PO METHYLPREDNISOLONE;PO,IM,IV MINERALOCORTICOIDS : MINERALOCORTICOIDS FLUDROCORTISONE ACETATE (FLORINEF) GIVE PO DOSE WITH FOOD CHECK BP, ELECTROLYTES, I AND O, WEIGHT MAY DEC EFFECTS OF ORAL HYPOGLYCEMICS, INSULIN, DIURETICS, POTASSIUM SUPPLEMENTS INDICATIONS: ADRENAL INSUFFICIENCY ANTIHYPOGLYCEMIC AGENT : ANTIHYPOGLYCEMIC AGENT INCREASES PLASMA GLUCOSE LEVELS AND RELAXES SMOOTH MUSCLES MED: GLUCAGON: IM, IV, SQ WATCH FOR SYMPTOMS OF HYPOGLYCEMIA AND TREAT WITH FOOD FIRST, IF CONSCIOUS CLEINT USUALLY AWAKEN IN 5-20 MIN AFTER RECEIVING GLUCAGON IF CLIENT DOES NOT RESPOND, ANTICIPATE iv GLUCOSE TO BE GIVEN S/E: NON SIGNIFICANT ORAL HYPOGLYCEMIC AGENTS : ORAL HYPOGLYCEMIC AGENTS Slide 168: SULFONYLUREAS: STIMULATE PANCREAS TO MAKE MORE INSULIN MEDS: CHLORPROPAMIDE (DIABENESE)PO GLIPIZIDE (GLUCOTROL) PO GLYBURIDE (MICRONASE, DIABETA)PO GLIMEPIRIDE (AMARYL) PO TOLBUTAMIDE (ORINASE) PO TOLAZAMIDE (TOLINASE) PO TOLBUTAMIDE HAS SHORTEST DURATION OF ACTION; REQUIRES MULTIPLE DAILY DOSES GLYBURIDE HAS A LONG DURATION OF ACTION INTERACT WITH: CALCIUM CHANNEL BLOCKERS, ORAL CONTRACEPTIVES, GLUCOCORTICOIDS, PHENOTHIAZINES, THIAZIDES S/E: HYPOGLYCEMIA, JAUNDICE, GI DISTURBANCE, SKIN REACTIONS BIGUANIDE : BIGUANIDE DECREASE SUGAR PRODUCTION IN THE LIVER AND HELP THE MUSCLE USE INSULIN TO BREAK DOWN SUGAR MEDS: METFORMIN (GLUCOPHAGE) PO METFORMIN IS ADMINISTERED WITH MEALS METFORMIN HAS A BENEFICIAL EFFECT ON LOWERING LIPIDS WEIGHT GAIN MAY OCCUR S/E: DIZZINESS, NAUSEA, BACK PAIN, POSSIBLE METALLIC TASTE ALPHA-GLUCOSIDASE INHIBITOR : ALPHA-GLUCOSIDASE INHIBITOR SLOWS DOWN HOW THE BODY ABSORBS SUGAR AFTER EATING MEDS: ACARBOSE (PRECOSE) PO MIGLITOL (GLYSET) PO TAKE AT BEGINNING OF MEALS, NOT EFFECTIVE ON AN EMPTY STOMACH ACARBOSE IS CONTRAINDICATED IN CLIENTS WITH INFLAMMATORY BOWEL DISEASE FREQUENTLY GIVEN WITH SULFONYLUREAS TO INCREASE EFFECTIVENESS OF BOTH MEDICATIONS S/E: DIARRHEA, FLATULENCE, ABDOMINAL PAIN THIAZOLIDINEDIONES : THIAZOLIDINEDIONES ENHACE INSULIN UTILIZATION AT RECPTOR SITES MEDS: PIOGLITAZONE (ACTOS) PO ROSIGLITAZONE (AVANDIA) PO MAY AFFECT LIVER FUNCTION; MONITOR LFTs POSTMENOPAUSAL WOMEN MAY RESUME OVULATION; PREGNANCY MAY OCCUR S/E: WEIGHT GAIN, EDEMA MEGLITINIDES : MEGLITINIDES STIMULATE RELEASE OF INSULIN FROM BETA CELLS MEDS: NATGLINIDE (STARLIX) PO REPAGLINIDE (PRANDIN) PO RAPID ONSET AND SHORT DURATION TAKE 30 MIN BEFORE MEALS (OR RIGHT AT MEALTIME) DO NOT TAKE IF MEAL IS MISSED S/E: WEIGHT GAIN, HYPOGLYCEMIA INSULIN : INSULIN REDUCES BLOOD GLUCOSE BY INCREASING GLUCOSE TRANSPORT ACROSS CELL MEMBRANES ENHANCES CONVERSION OF GLUCOSE TO GLYCOGEN NSG INTERVENTIONS: ROTATE SITE TO PREVENT LIPOHYPERTROPHY (FIBROFATTY MASSES ) ONLY REG INSULIN – IV, ALL CAN BE GIVEN SQ Slide 174: TYPES OF INSULIN: ONSET PEAK DURATION RAPID ACTING - LISPRO – HUMALOG 10-15 MIN 1 HR 3 HRS - ASPART-NOVOLOG SHORT ACTING 30 – 60 MIN 2-3 HRS 4-6 HRS - HUMULIN R - NOVOLIN R - ACTRAPID HM INTERMEDIATE:NPH 3 – 4 HRS 4-12 HRS 16-24 HRS - HUMULIN N - LENTE - NOVOLIN L LONG ACTING - ULTRALENTE 6– 8 HRS 12-16 20-30 HRS - GLARDINE (LANTUS) SLOW PROLONGED ABSORPTION. CONSTANT CONC W/O PEAKS FOR 24 HRS COMBINATIONS:70% NPH-30% REGULAR - Mixtard 30 30-60 MIN 2-12 HRS 18-24 HRS - Humulin 70/30/Novolin 70/30 - Novomix 30 INSULIN ADMINISTRATION: : INSULIN ADMINISTRATION: - NO: DIRECT SUNLIGHT, FREEZER ROOM TEMPERATURE/COOL PLACE. DISCARD AFTER 30 DAYS INJECTION SITES: ABD, ARMS, THIGHS, HIPS 1 ½ INCHES APART. NO SAME SITE IN 2-3 WKS (LIPOHYPERTROPHY) NO INJECTION: SCAR, WEEPING ARE INSULIN SYRINGE- U 100 G 27 TO 29 ½ INCH LONG. 45 TO 90 DEGREES ANGLE DO NOT SHAKE: ROLL MIXING: RN NO MASSAGE, NO ASPIRATION PENS, JET INJECTORS, PUMPS,IMPLANTABLE INSULIN DELIVERY DRUG INTERACTION: ALCOHOL: HYPOGLYCEMIC EFFECT COMPLICATIONS OF INSULIN THERAPY : COMPLICATIONS OF INSULIN THERAPY HYPOGLYCEMIA- BELOW 50 MG/DL INSULIN LIPODYSTROPHY LIPOATROPHY- LOSS SUBCU FAT, DIMPLING LIPOHYPERTROPHY- FATTY MASSES INJECTION SITE. SOMOGYI PHENOMENON- HYPOGLYCEMIA IN THE EVENING WITH REBOUND HYPERGLYCEMIA IN THE MORNING. DAWN PHENOMENON- EARLY MORNING HYPERGLYCEMIA WITHOUT PREVIOUS HYPOGLYCEMIA . Tx: NPH AT 10 PM HYPOGLYCEMIA (INSULIN REACTION) : HYPOGLYCEMIA (INSULIN REACTION) - IS A CONDITION CHARACTERIZED BY A DECREASED SERUM GLUCOSE LEVEL, WHICH RESULTS IN DECREASED CEREBRAL FUNCTION RISK FACTORS: 1. POORLY CONTROLLED DM - TOO LITTLE FOOD -INCREASE IN EXERCISE W/O ADEQ FOOD - INC IN INSULIN INTAKE 2. EXCESSIVE ALCOHOL INTAKE 3. REFLEX ACTION OF INSULIN – (SOMOGYI EFFECT) MANIFESTATIONS: - LABILITY OF MOOD - CONFUSION - HEADACHE, LIGHTHEADEDNESS - TACHYCARDIA, HYPOTENSION - NERVOUSNESS, TREMORS, DIAPHORESIS - SEIZURE, COMA TREATMENT: - CONSCIOUS: MILK, ORANGE JUICE, HONEY, CANDY, GLUCOSE TABLETS - 50% DEXTROSE - UNCONSCIOUS: GLUCAGON IV ORAL HYPOGLYCEMIC AGENTS : ORAL HYPOGLYCEMIC AGENTS STIMULATES INSULIN RELEASE FROM FUNCTIONING BETA CELLS INCREASES INSULIN RECEPTOR SENSITIVITY NSG CONSIDERATIONS: TAKE BEFORE BREAKFAST AVOID ALCOHOL MONITOR SERUM GLUCOSE LEVELS TEACH: DIETARY CONTROL, SYMPTOMS OF HYPO AND HYPER GOOD SKIN CARE Slide 181: SULFONYLUREA-STIMULATE BETA CELLS TO PRODUCE INSULIN GLIMEPIRIDE (AMARYL) GLIPIZIDE (GLUCOTROL) GLYBURIDE (MICRONASE) BIGUANIDES:REDUCE ATE OF GLUCOSE PRODUCTION BY THE LIVER METFORMIN (GLUCOPHAGE) ALPHA GLUCOSIDASE INHIBITORS-SLOW ABSORPTION OF GLUCOSE ACARBOSE (PRECOSE) THIAZOLIDINEDIONES-IMPROVE INSULIN SENSITIVITY ROSIGLITAZONE (AVANDIA) PIOGLITAZONE (ACTOS) MIGLITINIDES-STIMULATE QUICK REL OF INSULIN BY BETA CELLS REPAGLINIDE (PRANDIN) You do not have the permission to view this presentation. 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ENDOCRINE SYSTEM.ppt--K mohster Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 499 Category: Others/ Misc License: All Rights Reserved Like it (0) Dislike it (0) Added: February 01, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript ENDOCRINE SYSTEM : ENDOCRINE SYSTEM Course Outline : Course Outline I. Overview of the anatomy and physiology of the endocrine system Course Outline : Course Outline II. Assessment 1. history of client 2. physical assessment a. radiological studies b. hematological studies c. metabolic studies / urinary studies d. hematological studies of steroids Course Outline : Course Outline III. Common Health Problems 1. Hypopituitarism a. hypogonadism b. dwarfism 2. Hyperpituitarism a. gigantism b. acromegaly 3. Diabetes insipidus Course Outline : Course Outline III. Common Health Problems 4. Hypothyroidism a. cretinism b. juvenile hypothyroidism c. myxedema 5. Hyperthyroidism 6. Hypoparathyroidism 7. Hyperparathyroidism Course Outline : Course Outline III. Common Health Problems 8. Addison’s disease 9. Cushing’s syndrome 10. Aldosteronism 11. Pheocromocytoma 12. Diabetes mellitus ANATOMY & PHYSIOLOGY : ANATOMY & PHYSIOLOGY ENDOCRINE GLANDS CONTINUOUSLY SECRETE PRODUCTS CALLED HORMONES HORMONES ARE CHEMICAL MESSENGERS THAT DELIVERS STIMULATORY OR INHIBITORY SIGNALS TO TARGET CELLS AS A RESULT OF FEEDBACK MECHANISM CLASSIFICATION: STEROID- ADRENAL CORTEX AND GONADS PEPTIDES (INSULIN) AMINE (EPINEPHRINE) Slide 13: PITUITARY GLAND ANTERIOR LOBE GROWTH HORMONE- STIIMULATES GROWTH OF BODY TISSUES AND BONES PROLACTIN – STIMULATES MAMMARY TISSUE GROWTH & LACTATION THYROTROPIC HORMONE (TSH) – STIMULATES THYROID GLAND GONADOTROPIC HORMONE (LH & FSH) – AFFECT GROWTH,MATURITY AND FUNCTIONING OF PRIMARY AND SECONDARY SEX ORGANS. TESTES AND OVARIES ADRENOCORTICOTROPIC HORMONE (ACTH) – STIMULATES STEROID PRODUCTION BY ADRENAL CORTEX MELANOCYTE-STIMULATING HORMONE (MSH)-MAY STIMULATE ADRENAL CORTEX, MAY AFFECT PIGMENTATION Slide 14: PITUITARY GLAND POSTERIOR LOBE ANTI-DIUIRETIC HORMONES (ADH,VASOPRESSIN)- PROMOTES REABSORPTION OF WATER BY THE DISTAL TUBULES AND COLLECTING DUCTS OF THE KIDNEY, OXYTOXIN – STIMULATES EJECTION OF MILK FR MAMMARY ALVEOLI INTO THE DUCTS STIMULATES UTERINE CONTRACTIONS MAY POSSIBLE BE INVOLVED IN THE TRANSPORT OF SPERM INTO THE REPRO TRACT OF THE FEMALE Slide 15: THYROID GLAND THYROXINE (T4) TRIIODOTHYRONINE (T3) INC METABOLIC ACTIVITY OF ALL CELLS STIMULATES FAT, PROTEIN AND CARBO METABOLISM THYROCALCITONIN LOWERS SERUM CALCIUM LEVELS AND ELEVATES PHOSPHATE LEVEL; OPPOSITE EFFECT FR THAT OF PTH Slide 16: PARATHYROID GLAND PARATHORMONE (PTH) INC. CALCIUM LEVELS AND DECREASES PHOSPHATE LEVELS INC. RESORPTION OF BONES Slide 17: ADRENAL CORTEX GLUCOCORTICOIDS (PRIMARILY CORTISOL)-SUGAR PROMOTES CARBO, PROTEIN AND FAT CATABOLISM INCREASES TISSUE RESPONSIVENESS TO OTHER HORMONES MINERALOCORTICOIDS (ALDOSTERONE) – SALT TENDS TO INC SODIUM RETENTION AND POTASSIUM EXCRETION ANDROGENS (MALE HORMONE)- SEX GOVERNS CERTAIN SEC SEX CHARACTERISTICS ALL CORTICOIDS ARE IMPORTANT FOR DEFENSE AGAINST STRESS OR INJURY Slide 18: ADRENAL MEDULLA EPINEPHRINE (ADRENALIN) – 80% NOREPINEPHRINE – 20% ELEVATES BLOOD PRESSURE CONVERTS GLYCOGEN TO GLUCOSE WHEN NEEDED BY MUSCLES FOR ENERGY INC. HEART RATE, CARDIAC CONTRACTILITY DILATES BRONCHIOLES Slide 19: OVARIES ESTROGENS PROGESTERONE STIMULATE DEVELOPMENT OF SECONDARY SEX CHARACTERISTICS EFFECT REPAIR OF THE ENDOMETRIUM AFTER MENSTRUATION Slide 20: TESTES TESTOSTERONE ESSENTIAL FOR NORMAL FUNCTIONING OF MALE REPRODUCTIVE ORGANS STIMULATES DEVELOPMENT OF SEC SEX CHARAC Slide 21: PANCREAS (ISLETS OF LANGERHANS) INSULIN – PROMOTES METABOLISM OF CARBO, PROTEIN AND FAT THUS DECREASING BLOOD GLUCOSE GLUCAGON – MOBILIZES GLYCOGEN STORES, THUS RAISING BLOOD GLUCOSE LEVELS SOMATOSTATIN – DECREASES SECRETION OF INSULIN, GLUCOAGONS, GROWTH HORMONE AND SEVERAL GI HORMONES (GASTRIN, SECRETIN) THYROID GLAND : THYROID GLAND ANTERIOR PART OF NECK THYROXINE (T4), TRIIODOTHYRONINE (T3), CONTROLS RATE OF CELLULAR METABOLISM THYROCALCITONIN -RELEASED WHEN THERE IS HIGH LEVEL OF PLASMA CALCIUM CALCIUM DEPOSITION - BONES. IODINE INGESTED REACTS WITH TYROSINE= THYROID HORMONES PARATHYROID GLANDS : PARATHYROID GLANDS FOUR SMALL GLANDS LOCATED BACK THYROID GLAND HORMONES: PARATHORMONE (PTH) INCREASES PLASMA CALCIUM, DEC PLASMA PHOSPHATE GIT: ABDORPTION OF CALCIUM RENAL: CONVERSION OF VIT D TO ITS ACTIVE FORM CALCIUM REABSORPTION AND PHOSPHATE EXCRETION Slide 26: FUNCTIONS OF CALCIUM: - NEUROMUSCULAR RESPONSE - BLOOD COAGULATION MECHANISMS CONTROL OF PTH: NEGATIVE FEEDBACK MECHANISM: WHEN SERUM CALCIUM ARE LOW, THERE IS INCREASED MOBILIZATION OF CALCIUM FR BONE, RESULTING IN AN INCREASE IN SERUM CALCIUM LEVELS ADRENAL GLAND : ADRENAL GLAND TWO SMALL STRUCTURES WHICH CAP THE TOP OF THE KIDNEYS. CORTEX: GLUCOCORTICOIDS (CORTISOL) GLUCONEOGENESIS MINERALOCORTICOIDS (ALDOSTERONE) SEX HORMONES- SEXUAL EFFECTS OF MASCULINIZATION MEDULLA: EPINEPHRINE (ADRENALINE) RESPOND TO FIGHT OR FLIGHT CONVERTS GLYCOGEN TO GLUCOSE BOOST O2 CARRYING CAPACITY OF BLOOD INCREASE CARDIAC OUTPUT NOREPINEPHRINE PANCREAS : PANCREAS POST OF STOMACH ENDOCRINE AND EXOCRINE FUNCTIONS ENDOCRINE – ISLETS OF LANGERHANS) ALPHA – GLUCAGON Converts glycogen to glucose BETA - INSULIN INFLUENCES CARBOHYDRATE, FAT AND PROTEIN METABOLISM TRANSPORT OF GLUCOSE INTO CELLS CONVERTS GLUCOSE TO GLYCOGEN- LIVER, MUSCLES REGULATES RATE OF CARBOHYDRATE BURNING CONVERTS FATTY ACIDS INTO FATS – STORED AS ADIPOSE TISSUES STIMULATING PROTEIN SYNTHESIS WITHIN THE TISSUE Slide 33: ENDOCRINE DISORDERS ANTERIOR PITUITARY GLAND DISORDERS: : ANTERIOR PITUITARY GLAND DISORDERS: GIGANTISM ACROMEGALY DWARFISM Slide 35: GIGANTISM AND ACROMEGALY ETIOLOGY: INCREASE SECRETION OF GROWTH HORMONE TUMORS OF ANTERIOR PITUITARY GLAND GIGANTISM – BEFORE EPIPHYSEAL CLOSURE. BONE GROWTH AND ALL OTHER TISSUES- WITH GIGANTIC BODY GROWTH ACROMEGALY – TRANSVERSE GROWTH. AFTER EPIPHYSEAL CLOSURE IN LONG BONES. ACROMEGALY : ACROMEGALY CLINICAL MANIFESTATIONS: - ENLARGED SUPRAORBITAL RIDGE - THICKENED TONGUE -PROJECTION OF THE JAW (PROGNATHISM) - ENLARGEMENT OF THE HANDS AND FEET - HYPERTROPHY OF THE SKIN - INCREASE IN SIZE OF THE NOSE - SEVERE HEADACHES, BITEMPORAL HEMIANOPIA- PRESSURE ON OPTIC NERVE Slide 39: ASSESSMENT: EXCESSIVE GROWTH OF ALL PARTS OF THE BODY THREE TIMES THE NORMAL HEIGHT FOR AGE MAY REACH OVER 80 INCHES Slide 40: DIAGNOSTIC: - INC SERUM GROWTH HORMONE LEVEL - X-RAYS, CT SCAN, MRI - PHYSICAL EXAMINATION COMPLICATIONS: - HEADACHE AND VISUAL FIELD DISTURBANCES - DM/GLUCOSE INTOLERANCE - GLUCONEOGENESIS, REDUCE GLUCOSE UPTAKE IN THE LIVER TREATMENT: - BROMOCRIPTINE - PITUITARY RADIATION - HYPOPHYSECTOMY HYPOPHYSECTOMY : HYPOPHYSECTOMY PITUITARY ADENECTOMY PARTIAL/COMPLETE REMOVAL PITUITARY GLAND SURGERY: CRANIOTOMY: TRANSFRONTAL TRANSPHENOIDAL : INNER ASPECT UPPER LIP; SELLA TURCICA ENTERED FLOOR OF NOSE PATCH – ABDOMEN OR THIGH COMPLICATION -HYPOPITUITARISM Slide 43: POST-OP: NASAL PACKING : 24 HRS ELEVATE HEAD – 30 DEGREES IV FLUIDS OBSERVE CSF LEAK (NOSE) ASSESS NASAL DRIP: CLEAR, POSITIVE FOR PROTEIN - MONITOR VS, I AND O, TEMP, WBC, NUCHAL RIGIDITY DEEP BREATHING, NO NOSE BLOWING, VALSALVA, BENDING FOR 2 MOS. ASSESS VISUAL ACUITY – HEMATOMA CORTICOSTEROIDS ARE STARTED POST OP FREQUENT ORAL HYGIENE – SOFT SWABS, NO TOOTHBRUSHING UNTIL INCISION HEALED PANHYPOPITUITARISM : PANHYPOPITUITARISM HYPOSECRETION ANT PITUITARY HORMONES ALL HORMONES ARE USUALLY AFFECTED CLINICAL MANIFEST- INADEQUATE HORMONE CAUSE: UNKNOWN, TUMOR HYPOPHYSECTOMY RADIATION DRUGS (BROMOCRIPTINE) HORMONE REPLACEMENT DWARFISM: : DWARFISM: DECREASE GROWTH HORMONE IN CHILDREN ASSESSMENT: RETARDED PHYSICAL GROWTH PREMATURE BODY AGING SLOW INTELLECTUAL DEVELOPMENT MANAGEMENT: REMOVAL OF CAUSE: TUMOR HUMAN GROWTH HORMONE INJECTION POSTERIOR LOBE- NEUROHYPOPHYSIS : POSTERIOR LOBE- NEUROHYPOPHYSIS ANTIDIURETIC, VASOPRESSIN – ADH- RENAL TUBULES OXYTOCIN- SMOOTH MUSCLE (UTERUS AND MAMMARY GLANDS POST PITUITARY GLAND DISORDERS: DIABETES INSIPIDUS SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE (SIADH) Slide 47: DIABETES INSIPIDUS DEC ADH ASSESSMENT: EXCESSIVE URINE OUTPUT SEVERE DEHYDRATION EXCESSIVE THIRST ANOREXIA, WEIGHT LOSS WEAKNESS CONSTIPATION DIAGNOSTIC FINDING: WATER DEPRIVATION TEST: LOW URINE SP GRAVITY, DEC SODIUM AND POTASSIUM HIGH SERUM OSMOLALITY, SODIUM AND POTASSIUM SIADH INCREASED ADH FEEDBACK MECH THAT REGULATES ADH DOES NOT FUNCTION PROPERLY ADH RELEASED EVEN WHEN PLASMA HYPO-OSMOLALITY IS PRESENT ASSESSMENT: ANOREXIA, N/V LETHARGY, HEADACHES CHANGE LEVEL OF CONSCIOUSNESS DEC DEEP TENDON REFLEXES TACHYCARDIA INC CIRC BLD VOL DEC URINARY OUTPUT DIAGNOSTIC TESTS: INC. URINE SP GRAVITY, SODIUM AND POTASSIUM LOW SERUM OSMOLALITY, SODIUM AND POTASSIUM NV 135 – 145 mEq/L Slide 48: NSG INTERVENTIONS RECORD I AND O MONITOR URINE SP GRAVITY, SKIN COND, WEIGHT, BP, PULSE, TEMP ADMINISTER: PITRESSIN- IM/IV WARM BEFORE ADMINISTRATION. EXTRAVASATION CAUSES IRRITATION DESMOPRESSIN ACETATE - NASALLY NSG INTERVENTIONS: RESTRICT WATER INTAKE (500 – 600 ML/24 HRS) DIURETCIS – EXCRETION OF WATER HYPERTONIC SALINE (3% NaCl) IV ADM DEMECLOCYCLINE (DECLOMYCIN) WEIGH DAILY I AND O MONITOR SERUM SODIUM LEVELS ASSESS LOC THYROID DISORDERS: : THYROID DISORDERS: HYPOTHYROIDISM MYXEDEMA COMA HYPERTHYROIDISM THYROID STORM CRETINISM Slide 56: MYXEDEMA/HYPOTHYROIDISM HYPOSECRETION OF THYROID HORMONE SLOWED PHYSICAL AND MENTAL FUNCTIONS PREDISPOSING FACTORS: INFLAMMATION OF THYROID IATROGENIC – THYROIDECTOMY, IRRADIATION, OVERTREATMENT WITH ANTITHYROIDS PITUITARY DEF IODINE DEF IDIOPATHIC ASSESSMENT: DEC ACTIVITY LEVEL SENSITIVITY TO COLD POTENTIAL ALT IN SKIN INTEGRITY DECREASED PERCEPTION OF STIMULI OBESITY, WEIGHT GAIN POTENTIAL FOR RESP DIFFICULTY CONSTIPATION ALOPECIA BRADYCARDIA DRY SKIN AND HAIR DEC ABILITY TO PERSPIRE GRAVES’ DIS (HYPERTHYROIDISM) HYPERSECRETION OF THYROID HORMONE ACCE PHYSICAL AND MENTAL FUNCTIONS PREDISPOSING FACTORS: THYROID-SECRETING TUMORS IATROGENIC- OVERTREATMENT FOR HYPOTHYROID PITUITARY HYPERACTIVITY SEVERE STRESS: PREGNANCY ASESSMENT: HYPERACTIVITY SENSITIVITY TO HEAT REST AND SLEEP DEPRIVATION INCREASED PERCEPTION OF STIMULI WEIGHT LOSS Slide 58: DIAGNOSTIC FINDINGS: DEC THYROID HORMONES DEC SERUM SODIUM ELEVATED SERUM TSH DEC I131 TREATMENT: HORMONE REPLACMENT: LEVOTHYROXINE LIOTHYRONINE THYROGLOBULIN DIET: LOW CALORIE, HIGH FIBER, HIGH PROTEIN DIARRHEA POTENTIAL FOR RESP DIFFICULTY TACHYCARDIA EXOPTHALMUS FREQ MOOD SWINGA NERVOUS, JITTERY FINE, SOFT HAIR MENSTRUAL CHANGES: OLIGOMENORRHEA AMENORRHEA DIAGNOSTIC TESTS: ELEVATED T3, T4 DEC TSH INC UPTAKE OF !131 THYROID SCAN - NODULES TREATMENT: ANTITHYROID DRUGS THIONAMIDES: (TAPAZOLE , PTU) IODINE: SSKI LUGOL’S SOL BETA BLOCKERS RADIOACTIVE IODINE (I131) ONE TREATMENT COMP: HYPOTHYROIDISM SURGERY SUBTOTAL THYROIDECTOMY TOTAL THYROIDECTOMY DIET: HIGH CAL, HIGH VIT. SMALL FREQUENT Slide 59: POST – OP: TRACHEOSTOMY SET BEDSIDE CALCIUM GLUCONATE IV BEDSIDE POSITION: SEMI-FOWLERS WITH HEAD ELEVATED AND SUPPORTED BY PILLOWS ASSESS DRESSING – HEMORRHAGE ASSESS COMPLAINTS OF PRESSURE OR FULLNESS INCISION SITE MONITOR VS ASSESS VOICE CHANGES OR RESPIRATORY DIFFICULTY (EDEMA) THYROID STORM (THYROTOXICOSIS) : THYROID STORM (THYROTOXICOSIS) LIFE-THREATENING, UNCONTROLLED HYPERTHYROIDISM ONSET-SPONTANEOUS TEMP – 41C- BEC BODY UNABLE TO RELEASE HEAT FROM INCREASED METABOLISM ASSESSMENT: EXTREME TEMP ELEVATION MARKED RESP DISTRESS TACHYCARDIA, APPREHENSION RESTLESSNESS – DELIRIUM, COMA, DEATH FR HEART FAILURE Slide 62: NSG INTERVENTIONS: COOL ROOM.HYPOTHERMIA BLANKET CHANGE LINEN FREQUENTLY – DIAPHORESIS MONITOR CARDIAC ARRHYTHMIAS EXOPTHALMOS: EYES DROPS/OINTMENT/PATCHES/MASK DARK COLORED GLASSES – CORNEAL IRRITATION MEDICAL MANAGEMENT: MEASURES TO DEC TEMP AND HEART RATE ANTITHYROID DRUGS O2 HYPOTHERMIA BLANKETS, ICE PACKS, TYLENOL HYDROCORTISONE Slide 63: NSG INTERVENTIONS: LIFETIME HORMONE REPLACEMENT: LEVOTHYROXINE (SYNTHROID) THYROGLOBULIN (PROLOID) DESSICATED THYROID LIOTHYRONINE (CYTOMEL) DIET: HIGH PROTEIN, LOW CALORIE, LOW CHOLESTEROL, HIGH ROUGHAGE, FLUIDS AVOID SEDATIVES, NARCOTICS PROVIDE EXTRA BLANKETS MONITOR OVERDOSE: TACHYCARDIA, RESTLESSNESS, NERVOUSNESS, INSOMNIA MYXEDEMA COMA : MYXEDEMA COMA SEVEREST FORM OF HYPOTHYROIDISM NOTED BY NONPITTING EDEMA CAUSE: INFECTION ASSESSMENT: PERIORBITAL EDEMA PUFFY HANDS AND FEET PROFOUND LETHARGY AND APATHY, HYPOGLYCEMIA SLOWED BODY METABOLISM HYPOVENTILATION - DEATH Slide 65: INTERVENTIONS: PATENT AIRWAY, IV FLUIDS, SYNTHROID, GLUCOSE IV MONITOR BP, MENTAL STATUS, ELECTROLYTES AND GLUCOSE, KEEP WARM CONGENITAL HYPOTHYROIDISM:CRETINISM : CONGENITAL HYPOTHYROIDISM:CRETINISM - DECREASE OR LACK PRODUCTION OF T3 AND T4 AT BIRTH - RESULT FR CONGENITAL LACK OF THYROID GLAND OR UNABLE TO PRODUCE HORMONES - MAY BECOME EVIDENT AT 3 TO 6 MONTHS - NEWBORN SCREENING ON ALL NEWBORNS - IF UNTREATED BEYOND AGE OF 2 – IRREVERSIBLE BRAIN DAMAGE OR MENTAL RETARDATION WILL OCCUR ETIOLOGY: - ANTITHYROID DRUGS DURING PREGNANCY - DEVELOPMENT ANOMALY OF THYROID GLAND ASSESSMENT: - SHORT THICK NECK AND ENLARGED TONGUE - SHORTER LEGS IN RELATION TO TRUNK - COGNITIVE IMPAIRMENT AS THE CHILD GROWS OLDER - DRY SCALY SKIN WITH LOW TEMP - BRADYCARDIA, GAIN IN BODY WEIGHT - HYPOTONIA, POOR FEEDING - CONSTIPATION, PROTRUDING ABDOMEN - LOW T3 AND T4 Slide 68: DIAGNOSTIC FINDINGS: DEC T3, T4 DEC TSH – HYPOTHALAMIC OR PITUITARY INSUFFICIENCY THYROID SCAN DEC X-RAY LONG BONES – DELAYED SKELETAL DEVELOPMENT TREATMENT: ORAL THYROID REPLACEMENT VIT D – TO PREVENT RICKETS NSG INTERVENTIONS: INSTRUCT CLIENT: THYROID REPLACEMENT – TAKE AT SAME TIME DAILY THYROXINE INSTRUCT FAMILY: PROGNOSIS IS EXCELLENT WITH REPLACEMENT THERAPY DISORDERS PARATHYROID GLAND : DISORDERS PARATHYROID GLAND HYPOPARATHYROIDISM HYPERPARATHYROIDISM Slide 70: HYPOPARATHYROIDISM DEC SEC OF PARATHYROID HORMONE ASSESSMENT: TETANY MUSCULAR IRRITABILITY (CRAMPS,SPASMS) CARPOPEDAL SPASM, CLONIC CONVULSIONS CHVOSTEK SIGN TROUSSEAU’S SIGN DYSPHAGIA PARESTHESIA, LARYNGEAL SPASM ANXIETY, DEPRESSION, IRRITABILITY TACHYCARDIA DIAGNOSTIC TESTS: SERUM CALCIUM SERUM PHOSPHOROUS X-RAY – BONE DENSE SULKOWITCH TEST FOR CALCIUM HYPERPARATHYROIDISM OVERSECRETION OF PARATHYROID HORMONE ASSESSMENT: FATIGUE, MUSCLE WEAKNESS CARDIAC DYSRHYTHMIAS EMOTIONAL IRRITABILITY RENAL CALCULI BACK AND JOINT PAIN, PATHOLOGICAL FRACTURES PANCREATITIS, PEPTIC ULCER DIAGNOSTIC TESTS: SERUM CALCIUM SERUM PHOSPHORUS X-RAY- BONE POROUS SULKOWITCH TEST FOR CALCIUM IN URINE Slide 71: Trousseau sign of latent tetany is a medical sign observed in patients with low calcium.[1] This sign may become positive before other gross manifestations of hypocalcemia such as hyperreflexia and tetany, but is generally believed to be more sensitive than the Chvostek sign for hypocalcemia. a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for "hand of the obstetrician") because is supposedly resembles the position of an obstetrician's hand in delivering a baby. Slide 72: The Chvostek sign (also Weiss sign) is one of the signs of tetany seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped at the angle of the jaw, the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcaemia (ie from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of nerves. Though classically described in hypocalcaemia, this sign may also be encountered in respiratory alkalosis, such as that seen in hyperventilation, which actually causes decreased serum Ca++ with a normal calcium level due to a shift of Ca++ from the blood to albumin which has become more negative in the alkalotic state. Slide 73: INTERVENTIONS: EMERGENCY TX: CALCIUM LACTATE IV SLOW RATE PATIENT TO REMAIN RECUMBENT FOR 30 MIN BEDSIDE: TACHEOSTOMY SET AND CALCIUM GLUCONATE ERGOCALCIFEROL (VIT D) ELEMENTAL CALCIUM AS LACTATE, GLUCONATE, OR CARBONATE OBSERVE FOR TETANY LOW-PHOSPHOROUS, HIGH-CALCIUM DIET INTERVENTIONS: RELIEVE PAIN PREVENT FORMATION OF RENAL CALCULI- INC FLUID INTAKE OFFER ACID-ASH JUICES (CRANBERRY AND PRUNE JUICE) (IMPROVES SOLUBILITY OF CALCIUM) ADMINISTER APPROPRIATE DIET PREVENT FRACTURES SAFETY PRECAUTIONS MONITOR POTASSIUM LEVELS (COUNTERACTS EFFECT OF CALCIUM ON CARDIAC MUSCLES) PROVIDE POSTPARATHYROIDECTOMY CARE (ESSENTIALLY SAME AS FOR THYROIDECTOMY) IV LASIX AND SALINE PROMOTE CALCIUM EXCRETION IV PHOSPHORUS IS USED ONLY FOR RAPID LOWERING OF CALCIUM LEVEL DIET: LOW CALCIUM, HIGH PHOSPHORUS SURGERY - PARATHYROIDECTOMY DISORDERS OF THE ADRENAL GLANDS : DISORDERS OF THE ADRENAL GLANDS ADRENAL CORTEX: ADDISONS DISEASE CUSHING’S SYNDROME CONN’S SYNDROME (HYPERALDOSTERONISM) ADRENAL MEDULLA: PHEOCHROMOCYTOMA Slide 77: ADDISON’S DISEASE HYPOSECRETION OF ADRENAL HORMONES PATHOPHYSIOLOGY: DEC Na + DEHYDRATION DEC BLD VOL + SHOCK INC K + MET ACIDOSIS + ARRHYTHMIAS DEC BLD SUGAR + INSULIN SHOCK ASSESSMENT: FATIGUE, WEAKNESS, DEHYDRATION, DEC BP, WEIGHT LOSS PATHOLOGICAL FRACTURES ETERNAL TAN DEC RESISTANCE TO STRESS, ALOPECIA LOSS OF SEC SEXUAL CHARACTERISTICS DIAGNOSTIC TESTS: ACTH STIMULATION TEST PLASMA CORTISOL AT 8 AM AND 4 PM NV – 7 TO 18 MG/DL AT AM AND 2 TO 10 MG/DL AT PM 17-HYDROXYCORTICOIDS IN 24 HR URINE NV – 2-10 MG/24 HRS TREATMENT: FLUID REPLACEMENT HYDROCORTISONE IV Q 6 HRS HORMONE REPLACEMENT FOR LIFE (BILATERAL ADRENALECTOMY) DIET: HIGH CARBO, SODIUM, AND PROTEIN, LOW POTASSIUM SMALL FREQUENT SALTY FOODS/TABLETS CUSHING SYNDROME HYPERSECRETION OF ADRENAL HORMONES ETIOLOGY: PITUITARY TUMOR STEROID THERAPY PATHOPHYSIOLOGY: INC NA + INC BLD VOL + INC BP DEC K + MET ALKALOSIS + SHOCK INC BLD SUGAR + KETOACIDOSIS ASSESSMENT: FATIGUE, WEAKNESS, OSTEOPOROSIS, MUSCLE WASTING, CRAMPS EDEMA, INC BP, PURPLE SKIN STRIATIONS ALOPECIA, DEPRESSION EMACIATION AMENORRHEA, HIRSUTISM, GYNECOMASTIA, DIAGNOSTIC TESTS: INCH ACTH DEC SERUM POTASSIUM, INC SODIUM AND GLUCOSE INC. 17-HYDROCORTICOSTEROIDS IN 24 HRS CT SCAN/MRI - TUMORS TREATMENT: POTASSIUM SUPPLEMENTS ADRENAL SUPPRESANTS ANTIDIABETIC MEDS, DIURETICS RADIATION THERAPY SURGERY HYPOPHYSECTOMY, ADRENALECTOMY DIET: HIGH K AND PROTEIN, LOW SODIUM, CARBO AND CALORIE ADDISONIAN CRISIS : ADDISONIAN CRISIS SEVERE EXACERBATION OF DISEASE PRECIPITATING FACTORS: STEROID WITHDRAWAL, SEPSIS, DRUGS (rifampicin, phenytoin, ketoconazole, opiates), ILLNESS, SURGERY, STRENUOUS ACTIVITY, ASSESSMENT: SUDDEN PENETRATING PAIN- BACK, ABDOMEN SEVERE HYPOTENSION, SHOCK, COMA, DEATH CUSHING’S SYNDROME : CUSHING’S SYNDROME INTERVENTIONS: : INTERVENTIONS: IV FLUIDS – 5% DEXTROSE IN SALINE IV GLUCOCORTICOIDS (SOLU-CORTEF) IV, MINERALOCORTICOID (FLUDROCORTISONE) BLOOD TRANSFUSIONS, SERUM ALBUMIN, VASOPRESSORS ANTIBIOTICS – INFECTION STRICT BED REST, ELIMINATE STRESS PRIMARY ALDOSTERONISM- CONN’S SYNDROME : PRIMARY ALDOSTERONISM- CONN’S SYNDROME EXCESSIVE SECRETION OF ALDOSTERONE FROM ADRENAL CORTEX SIGNS OF HYPOKALEMIA, HYPERNATREMIA ADRENALECTOMY PERFORMED – IF TUMOR BILATERAL – LIFELONG CORTICOSTEROIDS, FLUID, INSULIN (HYPERGLYCEMIA UNILATERAL – TEMPORARY SPIRONOLACTONE- IF UNABLE TO HAVE SURGERY ASSESSMENT: HYPERTENSION POLYURIA, POLYDIPSIA DEHYDRATION MUSCLE WEAKNESS, LEG CRAMPS, GENERALIZED FATIGU DIAGNOSTIC TESTS: SERUM SODIUM (HIGH) SERUM POTASSIUM (LOW) ALDOSTERONE (HIGH) NSG INTERVENTIONS: : NSG INTERVENTIONS: VS, B/P, I AND O, DAILY WEIGHTS SODIUM RESTRICTION MEDS FOR HYPERTENSION SPIRONOLACTONE, POTASSIUM SUPPLEMENTS DIET: LOW SODIUM, HIGH POTASSIUM, HIGH CALORIE, NO STIMULANTS ADRENAL GLAND DISORDERS : ADRENAL GLAND DISORDERS PHEOCHROMOCYTOMA : PHEOCHROMOCYTOMA SECRETES EXCESS EPINEPHRINE AND NOREPINEPHRINE MANIFESTATIONS: PERSISTENT HYPERTENSION PALPITATIONS, TACHYCARDIA HYPERGLYCEMIA, DIAPHORESIS NERVOUSNESS, APPREHENSION HEADACHE DIAGNOSTIC TESTS: 24-HOUR URINE FOR CATECHOLAMINES TOTAL PLASMA CATECHOLAMINE LEVELS CT SCAN, MRI, ULTRASOUND - TUMOR Slide 86: NSG INTERVENTIONS: -assess ECG changes, arterial pressures, blood glucose levels MEDICAL MANAGEMENT: -antihypertensives SURGICAL MANAGEMENT: -adrenalectomy -fluids, plasma and plasma substitutes to lessen hypotension-24 to 48 hours -corticosteroid replacement PANCREAS : PANCREAS Slide 90: 2/1/2011 90 ●Chronic, metabolic disease of the pancreas Insufficient secretion of insulin Disorder of carbohydrate, protein and fat metabolism DIABETES MELLITUS Slide 91: Types: Type 1: Insulin-dependent DM (IDDM) Absolute deficiency of insulin Antibodies Mumps, congenital rubella Type 2: Non-insulin-dependent DM (NIDDM) Relative deficiency of insulin Islet cell defect: dec insulin Reduction of receptor sites Heredity, obesity, Insulin resistance Type 3: gestational DM (GDM) No DM before pregnancy Type 4: Diabetes due to another condition: pancreatic disease Slide 92: Nsg Assessment: Type1 (abrupt) Type 2 (gradual) Hyperglycemia Polyuria Polydipsia Polyphagia Weight loss Weakness Skin (wounds) Urinary tract/vaginal infections Blurred visions Slide 93: Nursing Management: Maintain Normal sugar balance Monitor Blood glucose (self-monitoring) Premeal BG: Diabetics (target value): 90-130 mg/dl Nondiabetics (NV): < 110 mg/dl Peak Postmeal BG: Diabetics (target value): < 180 mg/dl Nondiabetics (NV): < 140 mg/dl Oral hypoglycemic Insulin Slide 94: Proper Diet: Food exchange list: (Dietitian) CHO:50-60%, Protein: 20-30%, Fats: 10-20%. Limit refined sugars, more complex carbo Regular Exercise: Regular: 4-7 days/week Elevate HR: 50% maximal rate Monitor BG before exercise Over 250 mg/dl (check ketone) Less than 100 mg/dl (snacks) Slide 95: Oral Hypoglycemic Agents: Sulfonylureas: Inc insulin secretion Chlorpropamide (Diabinese),Glipizide (Glucotrol), Glimepiride (Amaryl), Tolbutamide (orinase) Meglitinides: Inc insulin secretion Repaglinide (Prandin) Take 30 min before meals; Slide 96: Biguanides: Inc glucose uptake (muscles/adipose) Dec liver glucose release Metformin (Glucophage) Administered with meals Thiazolidinediones: Inc glucose uptake (muscles/adipose tissue) Dec liver glucose release Rosiglitazone (Avandia) Postmenopausal women may resume ovulation Alpha-Glucosidase Inhibitor: Slows CHO absorption Acarbose (Precose), Miglitol (Glyset): with meal Slide 97: INSULIN: Proper Storing: Room temp. : 28 days Refrigerate: not in use Prevent direct sunlight Slide 98: Proper Administration: Wash hands Rotate vials, no shaking Wipe top with alcohol swab Draw air equal to total dose 2 Insulin: adm w/n 5-15 min. Inject air: NR Insulin withdrawal: RN Slide 99: Type of administration: Syringe: U100/ml; 27-29 g; ½ inch long Slide 100: Prefilled pens (Novopen, Novolin) Fridge: 28 days, needle up Jet injector: high pressure Slide 101: Implantable Insulin pump Patch and Inhaled insulin Slide 102: Route: SQ : 45-90 degrees IV: regular Slide 103: Sites: Abdomen,arms, thighs,hips No aspiration Systemic rotation in one anatomical area: Do not use site in 2-3 wks 1 1/2 inches apart, NO to scar area Complications: lipohypertrophy/lipoatrophy Insulin : Insulin Slide 107: Fasting blood sugar (FBS)/Fasting Plasma glucose Fasting for at least 8 hrs (water permitted) NV: less than 100 mg/dl Pre-diabetes: 100-125 mg/dl DM: two separate results exceed 126 mg/dl Oral Glucose Tolerance test (OGTT) NPO for 8 hrs Fasting blood sample taken Drink 300 ml (75 g) glucose Bld drawn at 30 min intervals for 2 hrs To remain at rest; NO smoke/drink liquids DM: over 200 mg/dl at 2 hrs Slide 109: Random Blood Sugar: Bld drawn w/o fasting DM: 200 or over Glycosylated hemoglobin: Measures average blood glucose over 120 days At least twice a year No fasting Normal: 4 -6% Poor: over 8 % Urine for ketones: Impending ketoacidosis Done when BG exceeds 300 mg/dl Criteria for the diagnosis of DM : Criteria for the diagnosis of DM Fasting plasma glucose: equal or > 126 mg/dl OR Casual Plasma glucose: equal or > 200 mg/dl plus symptoms OR OGTT : 2-hr plasma glucose: equal or > 200 mg/dl Slide 111: Diabetic Ketoacidosis: Cause: Lack of insulin and ketosis Nursing Assessment: S. glucose: > 300 mg/dl Acidosis Kussmaul breathing (inc rate and depth) hyperkalemia sweet breath odor Ketonuria Anorexia, nausea, vomiting Slide 112: Hyperosmolar Hyperglycemic Nonketotic Coma(HHKS): Cause: insulin deficiency and profound dehydration Nursing Assessment: S. glucose: > 800 mg/dl Hyperglycemia and hyperosmolarity, Polyuria Dehydration. thirst Hypotension, tachycardia Flushed dry skin, decrease skin turgor Confusion, drowsiness Slide 113: Interventions: Regular insulin IV: IV fluids (0.9% NS) Flush insulin sol to entire tubing; discard the first 50 to 100 ml D5NS when BG reaches 250 to 300 mg/dl Cardiac monitoring, Foley catheter Slide 114: HYPOGLYCEMIA: BS < 60 mg/dl Cause: Too much insulin/hypo agent Little food Excessive activity Slide 115: Nsg Assessment: Mild: “DIRE” Diaphoresis, Increased Pulse Restless, Extra hungry Shaking, Pallor Dizziness, Yawning Interventions: “Rule of 15” Check BS 15 Grams of carbohydrate NOT better in 15 min, Check BS, Repeat Txt Next meal more than 30 min give snack of carbohydrate and protein (milk, cheese, cracker) Slide 116: 15 grams of CHO: 1/2 cup juice/regular soda 1 Tbsp honey/syrup/sugar 1 small tube glucose gel 3–4 glucose tablets 5 small sugar cubes 6–8 LifeSavers 8 oz skim (nonfat) milk Slide 117: Moderate Confusion Poor coordination Mood changes Slurred speech Interventions: Instant Glucose/Cake Frosting Gel Insert tube between gum/cheek NO response 15 min, give glucagon Next meal more than 30 min give snack of CHO,CHON Slide 118: Severe Unconsciousness Convulsions Intervention: Glucagon SQ,IM, IV May repeat in 15 min Hosp: D50%/50 IV Slide 119: Differentiate hyperglycemia from hypoglycemia Hot and dry, sugar is high; cold and clammy needs some candy Slide 120: Chronic Complications: Retinopathy and cataract Nephropathy Neuropathy Leg ulcers Arteriosclerosis and atherosclerosis Cardiac complications Vascular changes Causes: Basement membrane thickening Chronic ischemia- hypoxia DISORDERS OF THE PANCREAS : DISORDERS OF THE PANCREAS DIABETES MELLITUS TYPE 1 TYPE 11 GESTATIONAL DIABETES DIABETES MELLITUS : DIABETES MELLITUS COMPLEX, MULTISYSTEM DISEASE CHARACTERIZED BY THE ABSENCE OF OR SEVERE DECREASE IN THE SECRETION OR UTILIZATION OF INSULIN PATHOPHYSIOLOGY: PRIMARY FUNCTION INSULIN – DEC BLD GLUCOSE IF GLUCOSE NOT AVAILABLE: CELLS OXIDIZE FATS AND PROTEINS FATS – KETONE BODIES PROTEIN – CONVERTED TO GLUCOSE HORMONES THAT COUNTERACT INSULIN: GLUCAGON EPINEPHRINE CORTISOL GROWTH HORMONE CLASSIFICATIONS: TYPE 1- INSULIN DEPENDENT-DESTRUCTION BETA CELLS TYPE 2 - NON-INSULIN DEPENDENT- PARTIAL DEF/INSENSITIVITY TO INSULIN GESTATIONAL DIABETES Slide 130: TYPE 1 – INSULIN DEPENDENT DM - ABSENCE INSULIN PRODUCTION - ONSET – 10 TO 15 YRS - FAMILIAL TENDENCY – LEFETIME TYPE 2- NONINSULIN DEPENDENT - INSULIN DEFICIENCY: - DEFECT IN INSULIN PRODUCTION - EXCESSIVE DEMAND FOR INSULIN - ONSET – ADULT AFTER 40 - ASSOCIATED WITH OBESITY - FAMILY HISTORY - MAY REQUIRE INSULIN FOR CONTROL GESTATIONAL DM - DURING PREGNANCY- SECOND TRIMISTER - RETURNS TO NORMAL AFTER DELIVERY - INFANT – LARGE FOR GESTATIONAL AGE, MAY EXPERIENCE HYPOGLYCEMIA AFTER BIRTH Slide 131: ASSESSMENT: TYPE 1 AND 2: HYPERGLYCEMIA MANIFESTATIONS: - POLYURIA – INC. SERUM OSMOLARITY - POLYDIPSIA – INC LOSS OF FLUIDS - POLYPHAGIA - FATIGUE - INCREASED FREQUENCY OF INFECTIONS TYPE 1: - WEIGHT LOSS - BED-WETTING - ONSET: RAPID – DAYS TO WEEKS TYPE 2: - WEIGHT GAIN - VISUAL DISTURBANCES - ONSET: SLOW Slide 132: DIAGNOSTIC TESTS: - 2 OR MORE ABNORMAL TEST RESULTS: - FASTING BLOOD GLUCOSE LEVEL IS ABOVE 126 MG/DL - GLUCOSE TOLERANCE TEST: 2-HOUR GLUCOSE VALUES ARE GREATER THAN 200 MG/DL - RANDOM GLUCOSE: OVER 200 MG/DL WITH SYMPTOMS (3 P’S, WEIGHT LOSS) - GLYCOSYLATED HEMOGLOBIN- INCREASED. LESS THAN 7% IS CONSIDERED GOOD CONTROL Slide 133: TREATMENT: REGULAR PHYSICAL ACTIVITY PLANNED- 30-45 MIN 3-5X/WEEK, MOD AEROBIC DIET: CARBO: 50-60%, FAT: 20-30%, PROTEIN:10-20% PHARMACOLOGICAL INTERVENTION: INSULIN: ORAL HYPOGLYCEMIC AGENTS COMPLICATIONS OF POORLY CONTROLLED DM : COMPLICATIONS OF POORLY CONTROLLED DM DIABETIC KETOACIDOSIS HYPEROSMOLAR HYPERGLYCEMIA NONKETOTIC COMA Slide 135: DIABETES KETOACIDOSIS: - EXTREME HYPERGLYCEMIC STATE - KETONE BODIES- ACIDOSIS - TYPE 1 DM. - STRESS, INFECTION, SURGERY, LACK OF INSULIN - MANIFESTATIONS: - GLUCOSE:300-800 MG/DL - METABOLIC ACIDOSIS: Ph-6.8 – 7.3, Hco3- less than 15 mEq/L -EXCESSIVE WEAKNESS, INC. THIRST, - DEHYDRATION, FEVER (DUE TO DEHYDRATION) - N/V, DEC LEVEL OF CONSCIOUSNESS - FRUITY BREATH - KUSSMAUL RESP (DEEP RAPID RESP) MEDICAL MANAGEMENT: - NSS - RAPID ACTING INSULIN - WHEN BLD SUGAR 250 – 300, DEXTROSE IS ADDED TO IV SOL TO PREVENT HYPOGLYCEMIA - FLUSH 50 ML OF SOLUTION. INSULIN ADHERE TO PLASTIC OF IV SOLUTION SET - INFUSION PUMP Slide 136: HYPEROSMOLAR HYPERGLYCEMIA NONKETOTIC SYNDROME (HHNS) BLD GLUCOSE: 700-1200MG/DL DEHYDRATION: osmotic diuresis MANIFESTATIONS: DEHYDRATION, WARM, FLUSHED SKIN LETHARGY DECREASED LEVEL OF CONSCIOUSNESS TACHYCARDIA, DEC BP MEDICAL MANAGEMENT: SAME AS DKA CHRONIC COMPLICATIONS: : CHRONIC COMPLICATIONS: DIABETIC ANGIOPATHY- CHANGES IN THE VASCULAR SYSTEMCAD, CVA, PVD DIABETIC RETINOPATHY PROGRESSIVE IMPAIRMENT RETINAL CIRCULATION (RUPTURE)- HEMORRHAGE DIABETIC NEPHROPATHY- DECREASE IN KIDNEY FUNCTION DIABETIC NEUROPATHY- HIGH BLD SUGAR LEVELS CAUSE CHANGES WITHIN THE NEURONS. ULCERS FREQUENT INFECTIONS – GLYCOSURIA - UTI Slide 138: FOOT CARE: WASH WITH MILD SOAP AND WATER AND PAT DRY APPLY LANOLIN- PREVENT CRACKING/DRYING CUT TOENAILS STRAIGHT AVOID CONSTRICTING GARMENTS WEAR CLEAN, ABSORBENT SOCKS PROPERLY FITTING SHOES. BREAK NEW SHOES GRADUALLY INSPECT FEET DAILY AND NOTIFY MD FOR CUTS, BLISTERS DIAGNOSTIC TESTS : DIAGNOSTIC TESTS Slide 143: GROWTH HORMONE (GH) NPO AFTER MIDNIGHT MAINTAIN BEDREST UNTIL SERUM SAMPLE IS DRAWN NV: <5 ng/ml IN MEN; <10 ng/ml IN WOMEN URINE OSMOLARITY SERUM OSMOLARITY USED IN EVALUATING ADH DO SERUM AND URINE TESTS AT SAME TIME AND COMPARE RESULTS NORMALLY, URINE OSMOLARITY SHOULD BE HIGHER THAT SERUM URINE – 300 TO 900 mOsm/kg OF WATER SERUM – 285 TO 295 mOsm/kg OF WATER FLUID DEPRIVATION TEST : FLUID DEPRIVATION TEST WITHOLDING FLUIDS TO DETERMINE RESPONSE OF POSTERIOR PITUITARY GLAND IN RELEASING ADH PRE-PRO: FLUID WITHHELD 8 -1 2 HRS PLASMA AND URINE OSMOLALITY STUDIES START AND END OF TEST POST-PRO: FLUIDS RESUMED SLOWLY Slide 146: THYROXINE (T4) TRIIODOTHYRONINE (T3) THYROID-STIMULATING HORMONE (TSH) STIMULATION OF THE THYROID GLAND BY TSH WILL INITIATE THE RELEASE OF STORED THYROID HORMONE WHEN T3 AND T4 ARE LOW, TSH SECRETION INCREASES T3 AND T4 ARE USED TO CONFIRM ABNORMAL TSH PRE-PROCEDURE: NO IODINE (MEDS, FOODS) NV: T4 5-12 mcg/dl T3 70 – 220 ng/dl TSH – 0.2 – 5.4 mU/L Slide 147: NEONATAL THYROXINE (T4) POSITIVE TEST RESULT IS ASSOCIATED WITH HYPOTHYROIDISM PROCEDURE IS DONE BY MEANS OF A HEEL PUNCTURE ON INFANT LEVELS OF NEONATAL T4 ARE NOT INTERPRETED IN SAME TERMS AS SERUM T4 VALUES; NORMAL LEVELS VARY WITH AGE FROM 1 DAY TO 120 DAYS: 1-3 DAYS: 11-22 mcg/dl 1-2 WKS : 10-16 mcg/dl 1-4 MON: 8-16 mcg/dl THYROID SCAN/RADIOACTIVE IODINE UPTAKE (RAIU) : THYROID SCAN/RADIOACTIVE IODINE UPTAKE (RAIU) USE OF RADIOISOTOPE (113I) TO PROVIDE IMAGE OF THYROID GLAND PRE-PROCEDURE: NO IODINE 7 DAYS, PREGNANCY, BREASTFEEDING PATIENTS DISCONTINUING THYROID MEDS – 14 DAYS NO RADIOGRAPHIC EXAM WITH CONTRAST MEDIA PREVIOUS 3 MOS NPO AFTER MIDNIGHT RADIOISOTOPE – GIVEN BY RADIOLOGIST DAY OF EXAM POST-PROCEDURE: MAY RESUME FOODS AND FLUIDS NORMAL ABSORPTION: 24 HRS – 5 – 35% HIGH UPTAKE – HYPERTHYROIDISM LOW UPTAKE - HYPOTHYROIDISM FINE-NEEDLE ASPIRATION BIOPSY: : FINE-NEEDLE ASPIRATION BIOPSY: EXAMINATION OF THYROID TISSUE – MALIGNANCIES PRE-PRO: CONSENT POST-PRO: LIGHT PRESSURE TO SITE REASSURANCE Slide 151: ADRENAL MEDULLA URINARY VANILLYLMANDELIC ACID (VMA) DEPENDING ON HOW TEST IS MEASURES, THERE MAY BE DIETARY AND MEDICATION RESTRICTIONS. 24-HR URINE COLLECTION NV: < 8 mg IN 24 HRS. Increased with pheochromocytoma URINE CATHECHOLAMINES: (EPINEPHRINE,NOREPINEPHRINE,DOPAMINE,METANEPHRINE,NORMETANEPHRINE) SAME AS FOR VMA NO COFFEE, TEA, BANANAS, CHOCOLATE, VANILLA AND ASPIRIN – ALTERS RESULT ACTH STIMULATION TEST ACTH IS GIVEN AS IM OR IV BOLUS AND SAMPLES ARE DRAWN AT 30 AND 60 MIN TO EVALUATE ABILITY OF ADRENAL GLANDS TO SECRETE STEROIDS NV: INC. IN PLASMA CORTISOL LEVELS BY MORE THAN 7-10 mcg/dl ABOVE BASELINE Slide 152: ADRENAL CORTEX ACTH SUPPRESSION (DEXAMETHASONE SUPPRESSION TEST) AN OVERNIGHT TEST: A SMALL AMOUNT OF DEXAMETHASONE IS ADMINISTERED IN THE EVENING, AND SERUM AND URINE ARE EVALUATED IN THE MORNING; EXTENSIVE TEST MAY COVER 6 DAYS CUSHING’S SYNDROME IS RULED OUT IF SUPPRESSION IS NORMAL NV: NORMAL SUPP: 50% DEC IN CORTISONE PRODUCTION (CORTISOL LEVEL < 5 mcg/dl PLASMA CORTISOL LEVELS FOR DIURNAL VARIATIONS: Slide 153: ADRENAL CORTEX ACTH SUPPRESSION (DEXAMETHASONE SUPPRESSION TEST) AN OVERNIGHT TEST: A SMALL AMOUNT OF DEXAMETHASONE IS ADMINISTERED IN THE EVENING, AND SERUM AND URINE ARE EVALUATED IN THE MORNING; EXTENSIVE TEST MAY COVER 6 DAYS CUSHING’S SYNDROME IS RULED OUT IF SUPPRESSION IS NORMAL NV: NORMAL SUPP: 50% DEC IN CORTISONE PRODUCTION (CORTISOL LEVEL < 5 mcg/dl PLASMA CORTISOL LEVELS FOR DIURNAL VARIATIONS: ELEVATION IN PLASMA CORTISOL LEVELS OCCURS IN THE MORNING AND SIGNIFICANT DEC IN EVENING AND NIGHT – A DIURNAL VARIATION SECRETION HIGH IN EARLY MORNING, DECREASED IN EVENING 8 AM – 5-23 mcg/dl 4 PM – 3-13 mcg/dl 24-HOUR URINE FOR HYDROXYCORTICOSTEROIDS AND KETOSTEROIDS INCREASE IN URINE LEVELS INDICATES HYPERADRENAL FUNCTION MALE – 6-20 mg/24 HR F- 6-17 mg/24 HR CHILD UNDER 15 YRS < 5 mg/24 HRS Slide 154: PANCREAS – NV : 70 – 110 MG/DL ORAL GLUCOSE TOLERANCE TEST: PRE-PRO: 3 DAYS BEFORE: HIGH CARBO DIET FOR 3 DAYS NPO FOR 8-10 HRS BEFORE TEST BLOOD AND URINE SAMPLES TAKEN. GLUCOSE SOL GIVEN BLD AND URINE SAMPLES TAKEN: 30 MIN, 1 HR, 2 HRS POST-PRO: WATCH FOR HYPOGLYCEMIA/HYPERGLYCEMIA VALUE: 1 HR: < 200 mg/dl 2 HR: < 140 mg/dl 2-HR POSTPRANDIAL BLOOD SUGAR: MEASURING THE SERUM GLUCOSE 2 HRS AFTER A MEAL VALUE: 65 – 139 mg/dl FASTING BLOOD SUGAR: PRE-PROCEDURE: NPO – 8 HRS POST-PRO: MAY RESUME FOOD/FLUIDS VALUE: > 126 mg/dl IS DIAGNOSTIC FOR DM Slide 155: GLYCOSYLATED HEMOGLOBIN (HEMOGLOBIN A1C) AVERAGE BLD SUGAR PREVIOUS 120 DAYS FASTING NOT NECESSARY GOAL: WITH DM – 7.5% WITHOUT DM – 4-6% SERUM AMYLASE USED TO EVALUATE PANCREATIC CELL DAMAGE OTHER INTESTINAL INTESTINAL CONDITIONS CAUSE INCREASE VALUE: > 200 U/L URINARY AMYLASE IN PANCREATIC INJURY, MORE AMYLASE ENTERS BLOOD AND IS EXCRETED IN URINE MAY BE DONE ON A 2-HR OR A 24-HR URINE SPECIMEN VALUE: 2-HR SPECIMEN: 2-34 U 24-HR SPECIMEN: 24-408 U Slide 156: SERUM LIPASE APPEARS IN SERUM AFTER DAMAGE TO PANCREAS NORMAL VALUES VARY WITH METHOD ELEVATED IS ABNORMAL KETONE BODIES (ACETONE) KETONE BODIES OCCUR IN THE URINE BEFORE THERE IS A SIGNIFICANT INCREASE IN SERUM KETONES USE FRESHLY VOIDED URINE VALUE: NEGATIVE Slide 157: GLYCOSYLATED HEMOGLOBIN (HEMOGLOBIN A1C) AVERAGE BLD SUGAR PREVIOUS 120 DAYS FASTING NOT NECESSARY GOAL: WITH DM – 7.5% WITHOUT DM – 4-6% PHARMACOLOGY : PHARMACOLOGY ADH REPLACEMENT : ADH REPLACEMENT MEDS: DESMOPRESSIN (DDAVP): NASAL SPRAY, PO, IV SQ VASOPRESSIN (PITRESSIN): IM, SQ LYPRESSIN (DIAPID): NASAL SPRAY MONITOR DAILY WEIGHTS; CORRELATRE WITH I AND O VASOPRESSIN MORE LIKELY TO CAUSE ADVERSE CARDIOVASCULAR AND THROMBOEMBOLIC PROBLEMS SE: EXCESSIVE WATER RETNTION, HEADACHE, NAUSEA, FLUSHING ANTITHYROID : ANTITHYROID MEDS: PROPYLTHIOURACIL (PTU) PO METHIMAZOLE (TAPAZOLE ) PO MAY INCREASE ANTICOAGULATION EFFECT OF HEPARIN AND ORAL ANTICOAGULANTS MAY BE COMBINED WITH IODINE PREPARATIONS MONITOR CBC STORE TAPAZOLE IN LIGHT-SENSITIVE CONTAINER MAY BE USED BEFORE SURGERY OR TREATMENT WITH RADIOACTIVE IODINE S/E: AGRANULOCYTOSIS, ABDOMINAL DISCOMFORT, N/V,DIARRHEA, CROSSES PLACENTA Slide 161: MEDS: LUGOL’S SOLUTION: PO SATURATED SOLUTION OF POTASSIUM IODIDE (SSKI) ADMINISTER IN FLUID/JUICE TO DECREASE UNPLEASANT TASTE. Use straw-stains teeth MAY BE USED TO DECREASE VASCULARITY OF THYROID GLAND BEFORE SURGERY Milk- decreases absorption S/E: INHIBITS SYNTHESIS AND RELEASE OF THYROID HORMONE RADIOACTIVE IODIDE: : RADIOACTIVE IODIDE: CAUSES PARTIAL OR TOTAL DESTRUCTION OF THYROID GLAND THROUGH RADIATION MEDS: IODINE (123I OR 131l) PO INCREASE FLUIDS IMMEDIATELY AFTER TRETAMNET BECAUSE RADIOACTIVE ISOTOPE IS EXCRETED IN THE URINE THERAPEUTIC DOSE OF RADIOACTIVE IODINE IS LOW; NO RADIATION SAFETY PRECAUTIONS ARE REQUIRED CONTRAINDICATED IN PREGNANCY S/E: DISCOMFORT IN THYROID AREA; BONE MARROW DEPRESSION DESIRED EFFECT: PERMANENT HYPOTHYROIDISM THYROID REPLACEMENTS : THYROID REPLACEMENTS MED: LEVOTHYROXINE SODIUM (LEVOTHROID, LEVOXYL, SYNTHROID) PO, IM,IV LIOTHYRONINE (CYTOMEL) BE CAREFUL IN READING EXACT NAME ON LABEL OF MEDICATIONS; MICROGRAMS AND MILLIGRAMS ARE USED AS UNITS OF MEASURE GENERALLY TAKEN ONCE A DAY BEFORE BREAKFAST WITHIN 3-4 DAYS, BEGIN TO SEE IMPROVEMENT; MAXIMUM EFFECT IN 4-6 WEEKS LIFELONG TREATMENT S/E: OVERDOSE MAY RESULT IN SYMPTOMS OF HYPERTHYROIDISM: TACHYCARDIA, HEAT INTOLERANCE,NERVOUSNESS Slide 164: ADRENOCORTICAL HORM:CORTICOSTEROIDS, GLUCOCORTICOIDS ANTIINFLAMMATORY ACTION: SUPPRESS PRODUCTION OF LYMPHOCYTES STRESS EFFECT: RELEASE OF CORTICOSTEROIDS MEDS: CORTISONE ACETATE (CORTONE ACETATE); PO, IM HYDROCORTISONE (SOLU-CORTEF) IM,PO HYDROCORTISONE ACETATE (CORTAID,CORTICAINE) TOPICAL DEXAMETHASONE (DECADRON)PO,IV, IM, TOPICAL PREDNISONE (DELTASONE, METICORTEN)PO METHYLPREDNISOLONE;PO,IM,IV MINERALOCORTICOIDS : MINERALOCORTICOIDS FLUDROCORTISONE ACETATE (FLORINEF) GIVE PO DOSE WITH FOOD CHECK BP, ELECTROLYTES, I AND O, WEIGHT MAY DEC EFFECTS OF ORAL HYPOGLYCEMICS, INSULIN, DIURETICS, POTASSIUM SUPPLEMENTS INDICATIONS: ADRENAL INSUFFICIENCY ANTIHYPOGLYCEMIC AGENT : ANTIHYPOGLYCEMIC AGENT INCREASES PLASMA GLUCOSE LEVELS AND RELAXES SMOOTH MUSCLES MED: GLUCAGON: IM, IV, SQ WATCH FOR SYMPTOMS OF HYPOGLYCEMIA AND TREAT WITH FOOD FIRST, IF CONSCIOUS CLEINT USUALLY AWAKEN IN 5-20 MIN AFTER RECEIVING GLUCAGON IF CLIENT DOES NOT RESPOND, ANTICIPATE iv GLUCOSE TO BE GIVEN S/E: NON SIGNIFICANT ORAL HYPOGLYCEMIC AGENTS : ORAL HYPOGLYCEMIC AGENTS Slide 168: SULFONYLUREAS: STIMULATE PANCREAS TO MAKE MORE INSULIN MEDS: CHLORPROPAMIDE (DIABENESE)PO GLIPIZIDE (GLUCOTROL) PO GLYBURIDE (MICRONASE, DIABETA)PO GLIMEPIRIDE (AMARYL) PO TOLBUTAMIDE (ORINASE) PO TOLAZAMIDE (TOLINASE) PO TOLBUTAMIDE HAS SHORTEST DURATION OF ACTION; REQUIRES MULTIPLE DAILY DOSES GLYBURIDE HAS A LONG DURATION OF ACTION INTERACT WITH: CALCIUM CHANNEL BLOCKERS, ORAL CONTRACEPTIVES, GLUCOCORTICOIDS, PHENOTHIAZINES, THIAZIDES S/E: HYPOGLYCEMIA, JAUNDICE, GI DISTURBANCE, SKIN REACTIONS BIGUANIDE : BIGUANIDE DECREASE SUGAR PRODUCTION IN THE LIVER AND HELP THE MUSCLE USE INSULIN TO BREAK DOWN SUGAR MEDS: METFORMIN (GLUCOPHAGE) PO METFORMIN IS ADMINISTERED WITH MEALS METFORMIN HAS A BENEFICIAL EFFECT ON LOWERING LIPIDS WEIGHT GAIN MAY OCCUR S/E: DIZZINESS, NAUSEA, BACK PAIN, POSSIBLE METALLIC TASTE ALPHA-GLUCOSIDASE INHIBITOR : ALPHA-GLUCOSIDASE INHIBITOR SLOWS DOWN HOW THE BODY ABSORBS SUGAR AFTER EATING MEDS: ACARBOSE (PRECOSE) PO MIGLITOL (GLYSET) PO TAKE AT BEGINNING OF MEALS, NOT EFFECTIVE ON AN EMPTY STOMACH ACARBOSE IS CONTRAINDICATED IN CLIENTS WITH INFLAMMATORY BOWEL DISEASE FREQUENTLY GIVEN WITH SULFONYLUREAS TO INCREASE EFFECTIVENESS OF BOTH MEDICATIONS S/E: DIARRHEA, FLATULENCE, ABDOMINAL PAIN THIAZOLIDINEDIONES : THIAZOLIDINEDIONES ENHACE INSULIN UTILIZATION AT RECPTOR SITES MEDS: PIOGLITAZONE (ACTOS) PO ROSIGLITAZONE (AVANDIA) PO MAY AFFECT LIVER FUNCTION; MONITOR LFTs POSTMENOPAUSAL WOMEN MAY RESUME OVULATION; PREGNANCY MAY OCCUR S/E: WEIGHT GAIN, EDEMA MEGLITINIDES : MEGLITINIDES STIMULATE RELEASE OF INSULIN FROM BETA CELLS MEDS: NATGLINIDE (STARLIX) PO REPAGLINIDE (PRANDIN) PO RAPID ONSET AND SHORT DURATION TAKE 30 MIN BEFORE MEALS (OR RIGHT AT MEALTIME) DO NOT TAKE IF MEAL IS MISSED S/E: WEIGHT GAIN, HYPOGLYCEMIA INSULIN : INSULIN REDUCES BLOOD GLUCOSE BY INCREASING GLUCOSE TRANSPORT ACROSS CELL MEMBRANES ENHANCES CONVERSION OF GLUCOSE TO GLYCOGEN NSG INTERVENTIONS: ROTATE SITE TO PREVENT LIPOHYPERTROPHY (FIBROFATTY MASSES ) ONLY REG INSULIN – IV, ALL CAN BE GIVEN SQ Slide 174: TYPES OF INSULIN: ONSET PEAK DURATION RAPID ACTING - LISPRO – HUMALOG 10-15 MIN 1 HR 3 HRS - ASPART-NOVOLOG SHORT ACTING 30 – 60 MIN 2-3 HRS 4-6 HRS - HUMULIN R - NOVOLIN R - ACTRAPID HM INTERMEDIATE:NPH 3 – 4 HRS 4-12 HRS 16-24 HRS - HUMULIN N - LENTE - NOVOLIN L LONG ACTING - ULTRALENTE 6– 8 HRS 12-16 20-30 HRS - GLARDINE (LANTUS) SLOW PROLONGED ABSORPTION. CONSTANT CONC W/O PEAKS FOR 24 HRS COMBINATIONS:70% NPH-30% REGULAR - Mixtard 30 30-60 MIN 2-12 HRS 18-24 HRS - Humulin 70/30/Novolin 70/30 - Novomix 30 INSULIN ADMINISTRATION: : INSULIN ADMINISTRATION: - NO: DIRECT SUNLIGHT, FREEZER ROOM TEMPERATURE/COOL PLACE. DISCARD AFTER 30 DAYS INJECTION SITES: ABD, ARMS, THIGHS, HIPS 1 ½ INCHES APART. NO SAME SITE IN 2-3 WKS (LIPOHYPERTROPHY) NO INJECTION: SCAR, WEEPING ARE INSULIN SYRINGE- U 100 G 27 TO 29 ½ INCH LONG. 45 TO 90 DEGREES ANGLE DO NOT SHAKE: ROLL MIXING: RN NO MASSAGE, NO ASPIRATION PENS, JET INJECTORS, PUMPS,IMPLANTABLE INSULIN DELIVERY DRUG INTERACTION: ALCOHOL: HYPOGLYCEMIC EFFECT COMPLICATIONS OF INSULIN THERAPY : COMPLICATIONS OF INSULIN THERAPY HYPOGLYCEMIA- BELOW 50 MG/DL INSULIN LIPODYSTROPHY LIPOATROPHY- LOSS SUBCU FAT, DIMPLING LIPOHYPERTROPHY- FATTY MASSES INJECTION SITE. SOMOGYI PHENOMENON- HYPOGLYCEMIA IN THE EVENING WITH REBOUND HYPERGLYCEMIA IN THE MORNING. DAWN PHENOMENON- EARLY MORNING HYPERGLYCEMIA WITHOUT PREVIOUS HYPOGLYCEMIA . Tx: NPH AT 10 PM HYPOGLYCEMIA (INSULIN REACTION) : HYPOGLYCEMIA (INSULIN REACTION) - IS A CONDITION CHARACTERIZED BY A DECREASED SERUM GLUCOSE LEVEL, WHICH RESULTS IN DECREASED CEREBRAL FUNCTION RISK FACTORS: 1. POORLY CONTROLLED DM - TOO LITTLE FOOD -INCREASE IN EXERCISE W/O ADEQ FOOD - INC IN INSULIN INTAKE 2. EXCESSIVE ALCOHOL INTAKE 3. REFLEX ACTION OF INSULIN – (SOMOGYI EFFECT) MANIFESTATIONS: - LABILITY OF MOOD - CONFUSION - HEADACHE, LIGHTHEADEDNESS - TACHYCARDIA, HYPOTENSION - NERVOUSNESS, TREMORS, DIAPHORESIS - SEIZURE, COMA TREATMENT: - CONSCIOUS: MILK, ORANGE JUICE, HONEY, CANDY, GLUCOSE TABLETS - 50% DEXTROSE - UNCONSCIOUS: GLUCAGON IV ORAL HYPOGLYCEMIC AGENTS : ORAL HYPOGLYCEMIC AGENTS STIMULATES INSULIN RELEASE FROM FUNCTIONING BETA CELLS INCREASES INSULIN RECEPTOR SENSITIVITY NSG CONSIDERATIONS: TAKE BEFORE BREAKFAST AVOID ALCOHOL MONITOR SERUM GLUCOSE LEVELS TEACH: DIETARY CONTROL, SYMPTOMS OF HYPO AND HYPER GOOD SKIN CARE Slide 181: SULFONYLUREA-STIMULATE BETA CELLS TO PRODUCE INSULIN GLIMEPIRIDE (AMARYL) GLIPIZIDE (GLUCOTROL) GLYBURIDE (MICRONASE) BIGUANIDES:REDUCE ATE OF GLUCOSE PRODUCTION BY THE LIVER METFORMIN (GLUCOPHAGE) ALPHA GLUCOSIDASE INHIBITORS-SLOW ABSORPTION OF GLUCOSE ACARBOSE (PRECOSE) THIAZOLIDINEDIONES-IMPROVE INSULIN SENSITIVITY ROSIGLITAZONE (AVANDIA) PIOGLITAZONE (ACTOS) MIGLITINIDES-STIMULATE QUICK REL OF INSULIN BY BETA CELLS REPAGLINIDE (PRANDIN)