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Individuals Experiencing Endocrine Disorders
 

Individuals Experiencing Endocrine Disorders

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    Individuals Experiencing Endocrine Disorders Individuals Experiencing Endocrine Disorders Presentation Transcript

    • Individuals Experiencing Endocrine Disorders NURS 2016
    • Glands That Control Endocrine Regulation
      • Hypothalamus
      • Pineal
      • Pituitary
      • Thyroid
      • Parathyroid
      • Thymus
      • Adrenal
      • Islets of Langerhorn
      • Ovaries/Testes
    • Figure 42-2 The pituitary gland, the relationship of the brain to pituitary action, and the hormones secreted by the anterior pituitary and the posterior pituitary.
    • Thyroid Gland
      • Produces thyroxin (T4) and triiodothyronine (T3) and calcitonin
      • Release of thyroid hormones (T3 and T4) controlled by thyroid stimulating hormone (TSH) secreted by pituitary
      • T3 and T4 control cellular metabolism
      • TSH normal is 0.6-5.2 mg/L
      • Goiter: enlarged thyroid gland
    • Hypothyroidism CM Mild Moderate Severe Bradycardia Hypothermic Extreme fatigue Hair loss Brittle nails Dry skin Numb fingers Menstral disturb. Weight gain Skin becomes thick Mask-like face Mental processes subdued Slowed speech
    • Hypothyroidism Treatment
      • Medications:
        • Levothyroxin
        • Single dose in AM
        • Not IV
        • Therapeutic effect is not immediate
    • Hyperthyroidism
      • AKA: Grave’s disease Excess secretion of thyroid hormones
      • Clinical Manifestations
      Mild Moderate Severe Nervousness Irritable Palpitations Tachycardia Amenorrehea Poor heat toler. Excess perspirations Flushed skin Exophthalmos Increased appetite Decreased weight Fatigue/weakness
    • Hyperthyroidism Treatment
      • 3 main Treatments:
      • 2 Pharmacological & 1 surgical
      • Radioactive iodine treatment: destroys overactive thyroid cells
        • 70-85% patients cured with one dose
        • High incidence of hypothyroidism
        • Fear of radioactive component
      • Anti thyroid meds Propacil,Tapazole
      • Surgical removal
    • Hyperthyroidism
      • NCP
        • Maintain nutritional status
        • Enhance coping measures
        • Improve self esteem
        • Maintain normal body temperature
        • Monitor for complications –recurrent hyperthyroidism, permanent hypothyroidism
        • Promote /teach self care
    • Acute Pancreatitis
      • Inflammation of the pancreas
      • Range from a relatively mild, self-limiting disorder to a rapidly fatal disease
      • Autodigestion
      • Causes
      • Mortality is high
    • Clinical Manifestations
      • Severe abdominal pain
      • Acute illness
      • Abdominal guarding
      • Ecchymosis
      • Nausea & vomiting
      • Hypotension
      • Acute renal failure
      • Tachycardia
      • Respiratory distress
      • Abnormal blood gas value
      • Fever,
      • Jaundice
    • Assessment
      • Presence & character of pain
      • Serum amylase & lipase are 3x higher
      • Nutritional fluid status & hx
      • History of GI problems
      • Respiratory status
      • Abdominal pain, tenderness & guarding
    • Nursing Diagnoses
      • Pain & discomfort
      • Imbalanced nutrition
      • Ineffective breathing pattern
      • Impaired skin integrity
      • Goal
    • Nursing Interventions
      • Relieving Pain & discomfort
        • Administer Demerol as ordered
      • Improving nutritional status
        • NPO, NG tube, IV fluid
      • Providing wound care
      • Improving respiratory function
      • Monitoring complications
        • Fluid & electrolyte disturbance
        • Pancreatic Necrosis
        • Shock & multiple organ failure
    • Chronic Pancreatitis
      • Progressive anatomic & functional destruction of the pancreas
      • Mechanical obstruction of the pancreatic & common bile ducts and duodenum
      • Inflammation & destruction of the secreting cells of the pancreas
    • Clinical Manifestations
      • Severe upper abdominal & back pain
      • Risk of addiction to opiates
      • Weight loss
      • Altered digestion
      • Calcification of the pancreas
      • Management…depends on cause
      • Treatment directed towards
        • Prevent acute attack
        • Relieving pain
        • Managing endocrine and exocrine inefficiency
    • Hepatic Encephalopathy
      • Profound liver failure
      • Accumulation of ammonia and other toxins
      • Hepatic coma
      • Clinical Manifestations
      • Mental changes
      • Motor disturbances
      • Asterixis
      • Hand writing becomes difficult
      • Constructional apraxia
      • Reflexes disappear & extremeties become flaccid
    • Hepatic Encephalopathy
      • Diagnosis:
        • EEG shows slowing brain waves
      • Treatment:
        • Lactulose reduces serum ammonia (watch for watery stools)
        • Vital signs, hand writing monitoring, hydration
        • Principles of Management
    • An Overview of Hepatitis
      • Inflammation of the liver caused by a virus
      • Clinical Manifestations:
      • Jaundice
      • Liver tenderness
    • Hepatic Cirrhosis
      • Chronic, progressive disease with widespred fibrosis and nodule formation
      • Normal flow of blood, bile, and hepatic metabolites is altered by fibrosis and changes in the hepatocytes, bile ductules, vascular channels, and reticular cells
    • Hepatic Encephalopathy, Hepatitis, & Cirrhosis
      • Chronic disorders and nurses treat them as such
      • Treatment:
        • control ascites, bleeding esophageal varices, infection
        • proper nutrition, support, rest, corticosteriods may maximize liver function
        • no alcohol
        • avoid infection
    • Clinical Manifestations Hepatic Cirrhosis
      • Intermittent jaundice
      • Fever
      • Anorexia
      • Muscle wasting
      • Diarrhea
      • Depleted platelet count
      • Fatigue
      • Advanced detoriation
        • Ascites
        • Varcies
        • Encephalopathy
        • Liver atrophy
    • Diabetes
      • Diabetes Insipidus
      • Diabetes Mellitus
        • type I (IDDM)
        • type II (NIDDM)
      • Gestational Diabetes
      • Diabetic Ketoacidosis
      • Diabetic Coma
      • Diabetic Neuropathy
    • Diabetes Insipidus
      • Due to decreased secretion of ADH (usually from pituitary surgery)
      • Polyuria (9L/day)
      • Watch for dehydration
      • Transient in nature
    • DiabetesInsipidus
      • Medical management
        • To replace ADH
        • To ensure adeq fluid replacement
      • Pharmacological treatment
        • Desmopressin - spray
        • IM form of ADH
      • Nursing Management
        • Support
        • Teaching
        • Medical bracelet
    • Diabetes Mellitus
      • Type I (Insulin Dependent Diabetes Mellitus)
      • Causes:
        • Genetic component (however many type I diabetics have no known relatives with diabetes)
        • Viruses may destroy beta cells
        • Unknown in most cases
    • Type I
      • Islet of Langerhans (more specifically the beta cells within) cannot produce enough or any insulin to combat glucose levels within the body
      • Consequently, glucose levels rise
      • Stress can trigger increased glucose response
      • Individuals become dependent on exogenous insulin administration to survive
    • Type II
      • Type II (Non-insulin Dependent Diabetes Mellitus)
      • Causes:
        • no known genetic component
        • obesity
    • Type II
      • Beta cells are unable to respond to hyperglycemia
      • This causes the beta cells to become less efficient with time
      • This process is reversible with normalization of glucose levels
      • Some individuals have a resistance to insulin that may trigger NIDDM as well
    • Clinical Manifestations
    • Gestational Diabetes
      • Usually develops in 2nd or 3rd trimester
      • After delivery, glucose tolerance in most clients returns to normal
      • However, type II diabetes develops in 40-60% of women with GDM within 5-15 years
      • Most GDM require insulin adminstration
    • Diabetic Ketoacidosis
      • A little patho:
        • hyperglycemia occurs due to glucose cannot be transported to cells because of lack of insulin
        • the liver starts to convert glycogen back to glucose and increases synthesis of glucose
        • unfortunately the complicates matters
        • fatty acids are mobilized from adipose tissue and the liver starts to produce ketones
        • ketones are excreted in the urine and accumulate in the blood
        • metabolic acidosis occurs from the increased acid due to rising ketones
    • Diabetic Ketoacidosis
      • A medical emergency
      • Sometimes brought on by stress, surgery, pregnancy, puberty, infection
      • #1 cause: diabetic not taking his/her insulin (fed up or non-compliance)
      • S & S:
        • ketosis
        • dehydration
        • electrolyte and acid-base imbalance
    • DK Management
      • Medical Management
        • Txmt for hyperglycemia
        • Correct dehydration, electrolyte loss, acidosis
      • Nursing Management
        • Monitor for s/s hypokalemia
        • Monitor lab work for electrolytes
        • Monitor urine output
    • Diabetic Coma
      • Bicarbonate buffering system fails to compensate for ketosis
      • Respirations increase in rate and depth (Kussmaul’s respirations) & breath has fruity or acetone odour
      • Renal system attempts to excrete ketones which leads to hemoconcentration
      • Hemoconcentration impedes blood circulation & leads to tissue anoxia & lactic acid production
      • The rise in lactic acid production further acidifies blood pH
      • Rising ketones eventually overwhelms the body’s defenses against the acid & the body succumbs to coma
    • Diabetic Neuropathy
    • Other chronic complications
      • macrovascular complications:
        • coronary artery disease
        • cerebrovascular disease
        • hyptertension
        • peripheral vascular disease
      • infections
      • nephropathy
      • retinopathy
    • Diabetic Neuropathy Management
      • Overall goal is to:
        • regulate blood glucose levels
        • prevent acute and chronic complications
      • Proper management consists of:
        • physical activity
        • diet
        • perhaps medications
      • Education is a key element in diabetes control
    • Medications
      • Oral:
        • First generation:
          • Orinase, Tolinase
        • Second generation:
          • Glucotrol, Diabeta (Glyburide)
        • Third generation:
          • Metformin, Acarbose
    • Medications
      • Insulin:
      • Short Acting:
        • Humulog, Regular
      • Intermediate Acting:
        • NPH, Lente, 30/70
      • Long Acting:
        • Ultralente
    • Insulin Action