Download Endocrine

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
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↑ T4 or T3 = ↓ TSH
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↓ T4 or T3 = ↑ TSH
Thyroid Hormones
Thyroxin- T4
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Maintains metabolism in steady state
– Temp
Cardiac
GI
Neuro
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Cellular metabolic activity → Rate of O2 use
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Stimulates growth and development
– Protein synthesis & Tissue Differentiation
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Essential for brain development in first 2 years
Triidothyronine- T3
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Rapid & Intermediate metabolic actions
Thyrocalcitonin
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Maintain serum Ca++ & PO4 levels
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↑↑ Ca++ in serum → Calcitonin is released
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↓↓ 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.
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• 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
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retardation
Clinical Signs
“Very Good Baby”
• Lethargic & “sleeps well”
• ↓ BMR ↑ weight, cold & mottled
• Anorexia & Poor feeding
• Hypotonia
• Constipation
• Hoarse cry
• Dry Skin
Facial Features
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Broad nose
Wide fontanels and sutures
Broad, flat nose
Protruding tongue
Short thick neck
Disproportionate Body
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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
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Associated with goiter
Sign and Symptoms
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↓↓ 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
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TSH Radioimmunoassay
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↑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
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↑ BMR & ↑ V/S
Monitor V/S, HR, Temp & BP!
Lifelong therapy
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√ T3 & T4 q 6 months
Nursing Interventions
• Activity
– Accept pt’s lethargy
– Need ↑ time to do ADLs
• Skin care
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Oils, lotions
Frequent position changes
Prevent chilling
Encourage layering of clothes
• Diet
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↑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
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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
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excess I
Neonatal Graves Disease
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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
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Girls 5 times > boys
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+ 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
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↓↓ Attention span
Emotional liability & cry easily
Medications
Propylthiouracil (PTU) 50 – 100mg/day ÷ bid
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Interferes with I conversion to thyroxine
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Prevents T3 and T4 synthesis
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Takes 3 - 4 weeks, No effect on available T3 T4
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Side Effects
– Skin rash-urticaria,
– Agranulocytosis- S/S of infection = STOP med!
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Monitor for overdose
• ↓ VS ↑ Lethargy Sleepiness
Methimazole (Tapazole) 0.2mg/kg q12H
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Blocks formation of new T3 and T4.
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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
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Side Effects
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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)
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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
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Vomiting
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Delirium → coma → death
Therapy
Medications
• Tylenol No ASA (↑T4 and T3 )
• MSO4 =↓ CNS & VS
• Lugol’s Solution (SSKI) & PTU
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↓ vascularity and ↓ thyroxine
Cortisone ↓ inflammation
Propranol ↓ CO
↓↓ Temp via Hypothermia blanket
O2 for ↑ BMR demands
Nursing Interventions
Environment
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Open windows & Keep away from heat
Frequent rest periods
Consistent routine and ↓ stimulation
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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
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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
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STH, ACTH, TSH, FSH, LH, MSH,
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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 =
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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
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↑ 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
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Ketoacidosis >15
Treatment
Insulin
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↑↑ Uptake & utilization of glucose by muscle & fat cells.
Inhibits release of glucose in liver
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Rapid Acting- Regular, Humulin R or Lispro
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Onset 30 mins
Peak 2-4H
Duration 6-8H
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Intermediate- NPH, Lente
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Onset 2H
Peak 6-8H
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Long Acting- Ultralente, PZI
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Onset 4-8H Peak 16-24H
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Insulin Glargine-Lantus (rDNA origin)
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Steady concentration over 24H No peaks.
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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)
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Coverage
– Based on BS (200-250 -2u R)
– Additional regular insulin added to daily dose
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Insulin Pump
– Consistent coverage
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No need for multiple daily injections
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↑ Independence & control
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↓ 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
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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)
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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)
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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+
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• 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
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NaHCO3 IVPB for metabolic acidosis
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Constantly assess Pt’s response to RX!