Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Endocrine Elisa A. Mancuso RNC-NIC, MS, FNS Professor of Nursing • Hormones – Regulate growth & activity of cells – Interact with receptors of “target tissues” – Regulate metabolism & stress response – Maintain fluid & electrolyte balance – Sexual reproduction • Feedback mechanism – ↑ Blood Level = ↓ Gland Secretion – ↓ Blood Level = ↑ Gland secretion Thyroid Gland • Takes up I & changes I to react with tyrosine • I + tyrosine → Thyroid hormones T4 + T3 • TSH secrets T4 & T3 – Dependent on blood levels – ↑ T4 or T3 = ↓ TSH – ↓ T4 or T3 = ↑ TSH Thyroid Hormones Thyroxin- T4 • Maintains metabolism in steady state – Temp Cardiac GI Neuro • Cellular metabolic activity → Rate of O2 use • Stimulates growth and development – Protein synthesis & Tissue Differentiation • Essential for brain development in first 2 years Triidothyronine- T3 • Rapid & Intermediate metabolic actions Thyrocalcitonin • Maintain serum Ca++ & PO4 levels – ↑↑ Ca++ in serum → Calcitonin is released – ↓↓ Ca++ serum and promote Ca+ bone deposit Hypothyroidism Most common pediatric endocrine disorder • Failure of Thyroid gland development (aplasia) – ↓↓ T3 and T4 – Initially provides enough T3 & T4 for 1st year. – Then unable to meet rapid body growth needs. • Anti-thyroid drugs or I deficiency during pregnancy • PKU-Phenylketonuria. • Genetic defect in synthesis of thyroxin. • Gunthrie Test (PKU) performed at 48 hours of life. • • Unable to convert phenylalanine (amino acid) to tyrosine. Congenital Hypothyroidism Cretinism- Infancy • Girls 3x more common • If not tested and untreated displays signs and symptoms in 3-6 weeks • Early DX best prognosis • Tx before 3 months and baby will grow and develop normally. • No treatment will lead to mental • retardation Clinical Signs “Very Good Baby” • Lethargic & “sleeps well” • ↓ BMR ↑ weight, cold & mottled • Anorexia & Poor feeding • Hypotonia • Constipation • Hoarse cry • Dry Skin Facial Features • • • • • Broad nose Wide fontanels and sutures Broad, flat nose Protruding tongue Short thick neck Disproportionate Body • Short arms & legs Acquired Hypothyroidism Juvenile • Lymphocytic thyroiditis- “Hashimoto’s” • Autoimmune Disease – Auto-antibodies bind to TSH receptor sites on thyroid gland – ↓ levels of T3 T4. – Atrophy of thyroid gland • Cause of antibody production unknown • Associated with goiter Sign and Symptoms • • • • • • • • • ↓↓ Growth Edema of face, eyes and hands ↓ Decreased BMR Increased weight gain ↓ V/S = ↓ Temp, ↓ HR and ↓ BP Lethargy ↑ sensitivity to cold Forgetfulness ↓ Decreased mental alertness Myxedema • Dry thicken skin • Fat accumulation – subcutaneous tissue • Brittle hair – coarse and sparse Diagnosis • Thyroid scan • TSH Radioimmunoassay • ↑TSH with ↓T3 and ↓ T4 Therapy Synthroid (l-thyroxine) 5-10 PO ug/kg/day • Individualized to pt’s TSH level • Initially low dose • Gradually ↑ (over 4-8 weeks) • Allow body time to adjust to changes – – • ↑ BMR & ↑ V/S Monitor V/S, HR, Temp & BP! Lifelong therapy – √ T3 & T4 q 6 months Nursing Interventions • Activity – Accept pt’s lethargy – Need ↑ time to do ADLs • Skin care – – – – Oils, lotions Frequent position changes Prevent chilling Encourage layering of clothes • Diet – – ↑Fiber ↑Protein ↑Vit D = ↑ Bone Growth ↓ Cals ↓ Fats ↓ Fluids = ↓ Edema Synthroid Toxicity Overdose of Medication • ↑Irritable & Nervousness • ↑ BMR & ↑ Temp ↑ HR ↑ BP • Wide pulse pressure • Diaphoresis, tremors, V & diarrhea • Therapy – √ serum T3 T4 – Hold med or ↓dose Hyperthyroidism Neonatal hyperthyroidism • Maternal Grave’s disease – Thyroid Stimulating immunoglobulins (TSI), autoantibodies passed through the placenta to fetus. – TSI binds to TSH receptors = excess thyroid hormone production • Excessive maternal I exposure • Neonatal thyroid hypertrophy to uptake • excess I Neonatal Graves Disease • • • • • • • Irritability Tachycardia Hypertension Voracious appetite with FTT (↓ Weight) Flushing Prominent eyes Goiter – Tracheal compression – ↑ Respiratory distress → asphyxia Grave’s Disease Autoimmune condition – Thyroid stimulating immunoglobulin rxn = ↑ T3 T4 – Hyperplasia of thyroid gland • Develops gradually over 6 -12 months • Suppression of TSH = No Feedback mechanism • Peak incidence is 11 and 15 years • Girls 5 times > boys • + Family history of thyroid disease Signs and Symptoms • Goiter • Exopthalmos – ↑↑ risk corneal abrasion • ↑↑ Appetite & ↓↓ weight – (-) N balance • ↑↑ VS @ rest – HR> 160 Palpitations – ↑ BP → CHF – ↑ Temp = Heat intolerance • Peripheral vasodilation – Flushed skin • • ↓↓ Attention span Emotional liability & cry easily Medications Propylthiouracil (PTU) 50 – 100mg/day ÷ bid • Interferes with I conversion to thyroxine • Prevents T3 and T4 synthesis • Takes 3 - 4 weeks, No effect on available T3 T4 • Side Effects – Skin rash-urticaria, – Agranulocytosis- S/S of infection = STOP med! • Monitor for overdose • ↓ VS ↑ Lethargy Sleepiness Methimazole (Tapazole) 0.2mg/kg q12H • Blocks formation of new T3 and T4. • Available T3 and T4 must be used up Medications Potassium Iodine SSKI (Lugol’s solution) – ↓ pituitary TSH = ↓ Thyroxin ↓ T3 T4 – ↓ glands vascularity – used a surgery ↓bleeding • Side Effects – – – – Swelling of salivary glands Metallic taste, burning of mouth & throat. Sore teeth & gums, skin rash √ serum K+ Surgery Sub Total Thyroidectomy • Removes majority of gland 5/6 (leave isthmus. • Gradually takes over body’s needs • Hormone replacement initially • Then gradually taper off Post-op complications • Hemorrhage – √ blood behind neck ↑VS • Respiratory distress• – Laryngeal edema √ stridor (trach at bedside) – Dysphasia Laryngeal nerve damage √ speech Thyroid Storm Life Threatening Crisis • Acute infection or Post-op – Manipulation of thyroid – ↑↑ release of thyroxin ↑↑ BMR • Abrupt onset – ↑↑ Temp 106 ↑↑ BP – ↑↑ Apical >200 Fatal arrhythmia's – Severe irritability/restlessness – Electrolyte imbalances – Vomiting – Delirium → coma → death Therapy Medications • Tylenol No ASA (↑T4 and T3 ) • MSO4 =↓ CNS & VS • Lugol’s Solution (SSKI) & PTU • • • • – ↓ vascularity and ↓ thyroxine Cortisone ↓ inflammation Propranol ↓ CO ↓↓ Temp via Hypothermia blanket O2 for ↑ BMR demands Nursing Interventions Environment • • • Open windows & Keep away from heat Frequent rest periods Consistent routine and ↓ stimulation • • • • Meet metabolic needs Small frequent meals ↑ Protein, ↑ Carb, ↑ Calories No Junk food! Diet Hypersecretion of Pituitary • Gigantism – 12 year old boy 6 ft 5 in – ↑↑ Growth via ↑↑ STH – ↑↑ muscles & viscera • ↑↑ ICP ↑↑ HA • Death @ age 30 – Cardiac unable to sustain CO • Therapy – Irradiation & Hypophsectomy Hyposecretion of Pituitary Dwarfism (Vertically challenged) – Lesion, trauma or idiopathic • ↓ STH ↓ GH • ↓Growth < 10% • Disproportionate growth – Hands & feet short & chubby – adult male @ 4ft • Therapy – Surgery & Hormone Replacement – STH, ACTH, TSH, FSH, LH, MSH, – Thyroxin, Synthroid – Reinforce Age appropriate behaviors Insulin Dependent Diabetes Mellitus Type I - IDDM Juvenile Onset • Genetic Predisposition or virus – causes an autoimmune process – destroys pancreatic insulin secreting B cells • ↓↓↓ Insulin Production – Glucose unable to enter the cells = Hyperglycemia – Glucose unavailable for cell metabolism = – cellular starvation IDDM • Fatty Acids – Fats break down → fatty acids → Ketones – Ketones used as source of energy & release H++ • Metabolic Acidosis (Ketoacidois) • Remaining ketones accumulate in tissues • Excreted via urine (ketonuria) • Exhaled via lungs (Acetone/fruity breath) • Gluconeogenesis – Proteins break down ▲ to glucose in liver – ↑ Glucose circulating in blood → hyperglycemia Clinical Signs • Polyphagia – ↑ appetite but unable to use glucose – Protein & lipid catabolism = body is starving!! – Muscle wasting with rapid weight loss = (–) N balance • Polyuria (enuresis is the 1st sign!!) – Glucose acts as a diuretic> Renal Threshold (180mg/100cc) – Excrete ↑ urine to remove glucose & ketones – ↑ Loss of electrolytes (Na+, Cl+, Ca+, Mg, PO4) • Polydipsia – ↑ Thirst due to polyuria – ↑ Intake > 2-3 Liters/day • Hyperglycemia – – ↑ serum glucose glucose adheres to vaginal wall = ↑ vaginal yeast infections Diagnosis • Fasting Blood Sugar (FBS) >120mg/dl – May miss 85% early chemical diabetes • Post-prandial->150mg/dl – Eat ↑↑ carbohydrate meal (75-100 gm) – √ BS p 2H • Glucose Tolerance Test (GTT) > 200 – FBS & Urine S & A – Drink Glucola (75 gm carb) – √ BS & urine S & A q ½ H (x 4) • Glycosylated Hemoglobin (GHB, HbA1c) – Reflects BS for last 3-4 months – WNL 5.5 – 8 Poorly controlled >11.5 – Ketoacidosis >15 Treatment Insulin • ↑↑ Uptake & utilization of glucose by muscle & fat cells. Inhibits release of glucose in liver • Rapid Acting- Regular, Humulin R or Lispro – Onset 30 mins Peak 2-4H Duration 6-8H • Intermediate- NPH, Lente – Onset 2H Peak 6-8H • Long Acting- Ultralente, PZI – Onset 4-8H Peak 16-24H • Insulin Glargine-Lantus (rDNA origin) – Steady concentration over 24H No peaks. – Cannot be mixed with other insulin's Duration 12-16H Duration 30-36H Insulin • Pediatric Dosages – Combination of Regular, NPH or Lantus 2 doses – AM (2/3 daily dose) ½ H a breakfast – PM (1/3 daily dose) ½ H a dinner • Administration – √ Brand √ Type – “clear to cloudy” 1st draw up Regular – SQ @ 90 angle – Rotate sites (Abd → Arms → Thighs) • Coverage – Based on BS (200-250 -2u R) – Additional regular insulin added to daily dose • Insulin Pump – Consistent coverage – No need for multiple daily injections – ↑ Independence & control – ↓ Ketoacidosis Diet Therapy Maintain adequate calories for growth spurt. Need food for metabolism with insulin • NCS = No Concentrated Sweets & ↓ fats • ADA exchange diet – 3 meals + 3 snacks/day – ↑ Flexibility c exchanges 75 kcal = 1point • Meal planning – Consider school, activities & sports – Pt. preferences • Exercise – ↑ food intake 10-15gm complex carbs – for q 30 mins activity Patient Teaching • Essential for optimal health – ↑ knowledge ↑compliance ↑control ↑health – Short sessions 15 -20 mins – Practice using equipment/supplies a D/C – Pathophysiology • S/S & Therapy • Long term sequella: – ↑ Infections, Retinopathy, Glomerulonecrosis, ↑ BP – Separate teaching for Pt & Family • Adolescents need to be empowered and independent Hypoglycemia (Insulin Shock) ↑ Insulin ↓ Food ↑ Exercise • Rapid Onset • Sympathetic NS activated (Cool & Clammy) • • • • Hungry, irritable, tremors, dizzy Diaphoresis, pale skin, flushed cheeks HA, blurred vision, slurred speech, ↑ HR, shallow respirations, seizures • Therapy √ BS q 15 mins • Mild: milk or OJ • Moderate: Simple sugar (Lifesaver) • Severe: Glucagon IM/IV Ketoacidosis (Diabetic Coma) ↑ Food ↑ Stress/Infection ↓Insulin • Gradual onset days – weeks • Kussmaul’s Respirations • Deep & rapid sighing breaths • Exhale = release ↑CO2, H+ = ↑ pH • Acetone Breath (fruity, sweet odor) • Metabolic Acidosis:↓ pH ↓ HCO3 ↓ PO2 • Hyperkalemia ↑ K+ • • K+ follows glucose from cells → blood • Muscle weakness & Cardiac arrhythmias Dehydration (Hot & Dry) • ↑ Temp, skin hot & dry, lethargic, mallar flush • ↓ Turgor & sunken eyeballs DKA Therapy • ICU & NPO – √ V/S & BS Continuously • C/R monitor √ arrhythmias • Pulse ox & ABG • √ Neuro for cerebral edema • Electrolytes (√ K+) – Rebound Hypokalemia » K+ follows glucose → cells •√ I & O – IV NaCl & Regular Insulin (0.1u/kg)IVPB – NaHCO3 IVPB for metabolic acidosis – Constantly assess Pt’s response to RX!