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EndocrineEndocrine Elisa A. Mancuso RNC-NIC, MS, FNS Professor of Nursing.

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Presentation on theme: "EndocrineEndocrine Elisa A. Mancuso RNC-NIC, MS, FNS Professor of Nursing."— Presentation transcript:

1 EndocrineEndocrine Elisa A. Mancuso RNC-NIC, MS, FNS Professor of Nursing

2 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

3 Thyroid Gland Takes up I & changes I to react with tyrosine I + tyrosine → T hyroid hormones T4 + T3 TSH secrets T4 & T3 –Dependent on blood levels – ↑ T4 or T3 = ↓ TSH – ↓ T4 or T3 = ↑ TSH

4 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

5 Hypothyroidism Most common pediatric endocrine disorder Failure of Thyroid gland development (aplasia) – ↓↓ T3 and T4 –Initially provides enough T3 & T4 for 1 st 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.

6 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

7 Clinical Signs “Very Good Baby” Lethargic & “sleeps well” ↓ BMR ↑ weight, cold & mottled Anorexia & Poor feeding Hypotonia Constipation Hoarse cry Dry Skin

8 Facial Features Broad nose Wide fontanels and sutures Broad, flat nose Protruding tongue Short thick neck Disproportionate Body Short arms & legs

9 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

10 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

11 Myxedema Dry thicken skin Fat accumulation –subcutaneous tissue Brittle hair – coarse and sparse Diagnosis Thyroid scan TSH Radioimmunoassay ↑ TSH with ↓ T3 and ↓ T4

12 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

13 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

14 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

15 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

16 Neonatal Graves Disease Irritability Tachycardia Hypertension Voracious appetite with FTT ( ↓ Weight) Flushing Prominent eyes Goiter –Tracheal compression –↑ R espiratory distress → asphyxia

17 Grave’s Disease Autoimmune condition –Thyroid stimulating immunoglobulin rxn = ↑ T3 T4 –Hyperplasia of thyroid gland Develops gradually over months Suppression of TSH = No Feedback mechanism Peak incidence is 11 and 15 years Girls 5 times > boys + Family history of thyroid disease

18 Signs and Symptoms Goiter Exopthalmos – ↑↑ risk corneal abrasion ↑↑ Appetite & ↓↓ weight –(-) N balance ↑↑ rest – HR> 160 Palpitations – ↑ BP → CHF – ↑ Temp = Heat intolerance Peripheral vasodilation –Flushed skin ↓↓ Attention span Emotional liability & cry easily

19 Medications Propylthiouracil (PTU) 50 – 100mg/day ÷ bid Interferes with I conversion to thyroxine Prevents T3 and T4 synthesis Takes 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

20 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+

21 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

22 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

23 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

24 Nursing Interventions Environment Open windows & Keep away from heat Frequent rest periods Consistent routine and ↓ stimulation Diet Meet metabolic needs Small frequent meals ↑ Protein, ↑ Carb, ↑ Calories No Junk food!

25 Hypersecretion of Pituitary Gigantism –12 year old boy 6 ft 5 in – ↑↑ Growth via ↑↑ STH – ↑↑ muscles & viscera ↑↑ ICP ↑↑ HA age 30 –Cardiac unable to sustain CO Therapy – Irradiation & Hypophsectomy

26 Hyposecretion of Pituitary Dwarfism (Vertically challenged) –Lesion, trauma or idiopathic ↓ STH ↓ GH ↓ Growth < 10% Disproportionate growth –Hands & feet short & chubby –adult 4ft Therapy –Surgery & Hormone Replacement – STH, ACTH, TSH, FSH, LH, MSH, – Thyroxin, Synthroid –Reinforce Age appropriate behaviors

27 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

28 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

29 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 1 st 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 –↑ I ntake > 2-3 Liters/day Hyperglycemia – ↑ serum glucose – glucose adheres to vaginal wall = ↑ vaginal yeast infections

30 Diagnosis Fasting Blood Sugar (FBS) >120mg/dl –May miss 85% early chemical diabetes Post-prandial->150mg/dl –Eat ↑↑ carbohydrate meal ( 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

31 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 minsPeak 2-4H Duration 6-8H Intermediate- NPH, Lente –Onset 2HPeak 6-8HDuration 12-16H Long Acting- Ultralente, PZI –Onset 4-8HPeak 16-24H Duration 30-36H Insulin Glargine-Lantus (rDNA origin) – Steady concentration over 24H No peaks. – Cannot be mixed with other insulin's

32 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” 1 st draw up Regular 90 angle –Rotate sites (Abd → Arms → Thighs) Coverage –Based on BS ( u R) –Additional regular insulin added to daily dose Insulin Pump –Consistent coverage – No need for multiple daily injections – ↑ Independence & control – ↓ Ketoacidosis

33 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

34 Patient Teaching Essential for optimal health – ↑ knowledge ↑ compliance ↑ control ↑ health –Short sessions mins –Practice using equipment/supplies a D/C –Pathophysiology S/S & Therapy Long term sequella: –↑ I nfections, Retinopathy, Glomerulonecrosis, ↑ BP –Separate teaching for Pt & Family Adolescents need to be empowered and independent

35 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

36 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

37 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!


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