ENDOCRINE DISEASES AND CONDITIONS

DIABETES

Type I or Type II

Type I Type IIJuvenile diabetes Most common form of

diabetesUsually diagnosed in children and young adults

Millions diagnosed and many unaware they have it

Body will not produce insulin

Either the body does not produce enough insulin or the cells ignore the insulin

Only 5% of diabetics are a type I

Symptoms – Type I

Frequent urination

Unusual thirst

Extreme hunger

Unusual weight loss

Extreme fatigue and irritability

Symptoms – Type II

Any of the type I symptoms

Frequent infections

Blurred vision

Cuts and bruises that are slow to heal

Tingling or numbness in the hands or feet

Recurring skin, gum or bladder infections

Prevention

Type II can be prevented or delayed

Lead a healthy lifestyle

Change your diet

Increase your physical activity

Maintain a health weight

Myths

• Diabetes is not that serious of a disease

• If you are over weight you will eventually develop type II diabetes

• Eating too much sugar can cause diabetes

• People with diabetes must eat special foods

• People with diabetes cannot eat carbs or sugars

• It is ok to eat as much fruit as you want because it is healthy

Diabetic Ketoacidosis (DKA)

Insulin deficiency and excessive stress hormone

Typically in Type I but can be in Type II

Elevated glucose promotes osmotic diuresis and dehydration

• Stress hormones stimulate free fatty acids which cause a release of ketones

• Causes decreased myocardial contractility and cerebral function

• Usually brought on by infection and stress

Interventions

• Gradually return to normal metabolic balances

• FSBS and notify the MD of the results

• 2 large bore IV’s• NS at a rate of 1 liter per hour• O2 and maintain ABC’s• Insulin drip per protocol• Monitor patient every 5-15 minutes

until stable• Closely monitor intake and output• Cardiac monitor

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)

• Occurs in type II• Profound dehydration from elevated

glucose and osmotic diuresis• No ketones-not enough insulin to start

the process• Can be caused by infection, stroke or

sepsis• High mortality rates

Interventions

• FSBS and notify the MD of the results• May require intubation• 2 large bore IV’s• NS 1 liter over 1 hour• Insulin drip per protocol• Monitor the patient every 5-15

minutes until stable• Closely monitor the intake and output• Cardiac monitor

Hypoglycemia

• Serum glucose drops below 50• Below 35-the brain cannot adequately

extract oxygen• Results in hypoxia and eventually

coma• Any person with an altered level of

consciousness should be considered to have low glucose until proven otherwise

Interventions

• O2 and maintain ABC’s• FSBS and notify MD of results• If alert and oriented x3, give oral

glucose solutions (oj, milk, etc. )• Establish IV• ½ to 1 amp of 50% dextrose (D50) per

MD’s orders• Monitor the mental status closely• Monitor the FSBS every 15-30 minutes• Order a meal tray STAT• Cardiac Monitor

ADRENAL CRISIS Addison’s Disease (adrenal insufficiency) Adrenal cortex ceases to produce

glucocorticoid and mineralocorticoid hormones

Acute stressors, infection, hemorrhage, trauma, surgery, burns, pregnancy, or abrupt cessation for Addison’s disease

Life threatening because hormones are necessary for the maintenance of blood volume, BP, and glucose homeostasis

ADRENAL CRISIS

Suspect with patients who have septicemia with unexplained deterioration, major illness who have abdominal, flank, or chest pain, with dehydration, fever, hypotension, or shock, and adrenal hemorrhage

Death because of circulatory collapse and hyperkalemia- induced dysrhythmia

ADRENAL CRISIS- ASSESSMENT

Subjective data History of present illness

Rapid worsening of symptoms of adrenal insufficiency

Fever Nonspecific abdominal pain; may simulate acute abdomen

N&V

ADRENAL CRISIS- ASSESSMENT Medical history

Primary adrenal insufficiency Hyperpigmentation of skin Weakness, fatigue, lethargy Anorexia and weight loss Nausea, vomiting, diarrhea Salt craving Postural hypotension Allergies Medications

ADRENAL CRISISPhysical examinationAppears acutely illSigns of shock as a result of dehydration

Hypotension, but may have warm extremities

Tachycardia Tachypnea Orthostatic hypotension

ADRENAL CRISIS

Physical examination Fever Altered mental status, confusion Hyperpigmentation of skin Very soft heart sounds

ADRENAL CRISISDiagnostic proceduresCBC: anemia of chronic diseaseElectrolyte levels

Hyponatremia Hyperkalemia

Blood glucose level: hypoglycemiaBUN: elevated (azotemia secondary to dehydration)

UA

ADRENAL CRISIS

UA Blood cultures Plasma cortisol level ECG

Low voltage Flat or inverted T wave Prolonged QT, QRS, or PR intervals CXR CT of abdomen: if diagnosis not clear

ADRENAL CRISIS

Interventions O2, IV, monitor VS, with Orthostatic VS I&O Weight Monitor signs of adequate tissue perfusion:

capillary refill and skin temperature and moisture

ADRENAL CRISIS Medications

Dexamethasone Hydrocortisone Corticotropin Glucose Vasopressors

Monitor electrolytes Monitor cardiac function Prepare for admission Instruct about disease process

MYXEDEMA COMA Severe form of hypothyroidism Marked impairment of CNS and cardiovascular decompensation

Recognition of this illness is hampered by its insidious onset and rarity

Winter, elderly women with HX of hypothyroidism Precipitating factors include: serious infection (pneumonia and UTI), sedative or tranquilizer use, stroke, exposure to cold environment, and termination or thyroid hormone replacement

Death is common, but can survive if prompt adequate care

MYXEDEMA COMA History of present illness

Recent illness Progressive decline in intellectual status Apathy, self-neglect Emotional labiality Anorexia Recent weight gain

Medical history Hypothyroidism or thyroid surgery Allergies Medications: thyroid replacement hormone, recent use of tranquilizers and sedatives

MYXEDEMA COMAObjective dataPhysical exam

Decreased mental status Depressed mental acuteness Confusion or psychosis Pale, waxy, edematous face with periorbital edema

Dry, cold, pale skin

MYXEDEMA COMAObjective dataPhysical exam

Non-pitting extremity edema Thin eyebrows Deep, coarse voice Scar form prior thyroidectomy Vital Signs

Hypothermia, usually above 95 F Bradycardia with distant heart sounds Hypoventilation, Hypotension

MYXEDEMA COMA Diagnostic procedures

Electrolytes: hyponatremia ABG’s: hypoxia and hypercarbia Thyroid studies: low thyroxine (T4),

elevated thyrotropin (thyroid stimulating hormone [TSH])

MYXEDEMA COMA ECG

Low voltage Sinus bradycardia Prolonged QT interval CBC: anemia and decreased WBC BUN and creatinine: elevated Blood sugar: variable hypoglycemia CXR UA Obtain pretreatment plasma cortisol level

MYXEDEMA COMA

InterventionsMonitor airway, breathing, circulation, and other vital signs

O2 as orderedIV, IV fluids

Hypertonic salineCrystalloidsWhole blood

MYXEDEMA COMA

Interventions Meds as ordered

IV thyroid hormone Glucocorticoid Vasoconstrictors

Rewarm patient Use passive rewarming with blankets and increased room temperature

Avoid rapid rewarming Be prepared for seizures

THYROID STORM

Extreme and rare form of thyrotoxicosis High mortality Untreated or inadequately treated

hyperthyroidism, who experiences surgery, infection, trauma, or emotional upset; thyroid surgery; radioactive iodine administration

Cardiac decompensation with CHF (terminal event), CNS dysfunction, GI disorders

Life-threatening emergency

THYROID STORM- ASSESSMENT

History of present illness Fever N&V&D Abdominal pain Worsening of thyrotoxicosis symptoms Anxiety Restlessness, nervousness, irritability Generalized weakness Possible coma Precipitation event or intercurrent illness

THYROID STORM Medical history

Thyrotoxicosis Thyroid disease Easy fatigability Weight loss Sweating Body heat loss and heat intolerance

THYROID STORM Objective data

Physical exam Fever: temp may exceed 104 Tachycardia (120-200), systolic

hypertension Chest: crackles

THYROID STORM

Warm, moist, velvety skin; becomes dry as dehydration develops

Spider angiomasTremulousnessDelirium, agitation, confusion, comaThin silky hairEnlarged thyroid gland with thrill or bruit

THYROID STORM

Eye signsLid lagStareExophthalmosPeriorbital edema

Hepatic tenderness or jaundice

THYROID STORM Diagnostic procedures

Cardiac monitoring/ECG: sinus tachycardia wand atrial fibrillation/flutter

Thyroid function studies T4: elevated Triiodothyronine (T3): elevated resin

uptake TSH: decreased

Serum cholesterol level: decreased

THYROID STORM

Diagnostic procedures Electrolyte levels Serum glucose increased CBC: increased WBC with left shift BUN or creatinine level Hepatic studies: increased liver enzymes UA Cultures and radiographs and indicated

THYROID STORM

Interventions O2, airway,

breathing, circulation, VS

IV of D5 and isotonic solution

Cardiac monitoring

Meds as ordered Vasopressors Antipyretic D50 Propylthiouracil every 8 hours Glucocorticoids, hydrocortisone Iodine: lugol’s solution,

potassium iodide Digitalis, propranolol Antibiotics Vitamins and thiamine Sedatives

THYROID STORM

Use cooling blanket, cold packs

Prepare patient/significant others for patient’s admission

Explain procedures to patient/significant others

References

American Diabetic Association

Emergency Nursing Core Curriculum, ENA

Fundamentals of Nursing, Potter and Perry