EndocrineEndocrineEndocrineEndocrineElisa A. Mancuso RNC-NIC, MS, Elisa A. Mancuso RNC-NIC, MS,

FNSFNS

Professor of NursingProfessor 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 HormonesThyroxin- 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

HypothyroidismMost 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 HypothyroidismJuvenile

• 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

TherapySynthroid (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 ToxicityOverdose 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 DiseaseAutoimmune 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+

SurgerySub 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

Diet• Meet metabolic needs• Small frequent meals• ↑ Protein, ↑ Carb, ↑ Calories • No Junk food!

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 PituitaryDwarfism (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

TreatmentInsulin• ↑↑ 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 Duration 12-16H

• Long Acting- Ultralente, PZI– Onset 4-8H Peak 16-24H Duration 30-36H

• Insulin Glargine-Lantus (rDNA origin)– Steady concentration over 24H No peaks.– Cannot be mixed with other insulin's

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 TherapyMaintain 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!