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Hypo/Hyperthyroidism, Addison's Disease, Cushing's syndrome, Preschooler Growth and Development, End of Life, Cystic Fibrosis, COPD, Asthma/Exacerbation, Eating Disorders, Personality Disorders, OCD
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Hypothyroidism
Hypothyroidism: Reduced or absent hormone secretion from the thyroid gland that results in whole-body decreased metabolism from inadequate cellular regulation
Primary: Thyroid cannot produce adequate amounts of thyroid hormones
Secondary: Thyroid isn’t being stimulated by the pituitary gland to produce hormones
Hashimoto’s thyroiditis: Autoimmune disorder in which infection and inflammation of the thyroid gland causes the production of autoantibodies to thyroglobulin (Tg) or thyroid peroxidase (TPO),, which results in extensive tissue destruction and reduced secretion of thyroid hormones
Diagnosis: High TSH and low T4 (and T3)
Cause of Hypothyroidism
Primary Causes
Decreased Thyroid Tissue
Surgical or radiation-induced thyroid destruction
Autoimmune thyroid destruction
Congenital (poor thyroid development)
Cancer (thyroidal or metastatic)
Decreased Synthesis of Thyroid Hormone
Endemic iodine deficiency
Drugs:
Amiodarone
Guaifenesin
Lithium
Secondary Causes
Inadequate Production of Thyroid-Stimulating Hormone
Congenital pituitary defects
Pituitary tumors, trauma, infections, or infarcts
Hypothalamic tumors, trauma, infections, or infarcts
Risk Factors of Hypothyroidism
Females (especially African Americans)
Pregnancy (multiparous)
Radiation to upper chest or neck region
Thyroid surgery
Type 1 Diabetes
Family history of thyroid disease
Anti-thyroid hormone treatment for hyperthyroidism
30 years and older
BMI >25
Deficient iodine intake
Maternal/Fetal Risks of Hypothyroidism During Pregnancy
Risks to the pregnant client can range across all pregnancy trimesters
Repeated first-trimester pregnancy loss through spontaneous miscarriage
Increased risk of developing gestational diabetes
Preeclampsia
Placental abruption
Preterm labor
Postpartum hemorrhage
Increased risk of psychological manifestations in the postpartum period
Fetal Risks
Placenta dysfunction
Preterm birth
Rare potential for development of a goiter
Signs/Symptoms of Hypothyroidism (CV, Respiratory, GI, Metabolic, Reproductive, Psychosocial)
Bradycardia
Decreased activity intolerance
Diastolic hypertension
Pericardial effusion
Dyspnea
Hypoventilation
Pleural effusion
Abdominal distention/ascites
Constipation
Weight gain
Decreased basal metabolic rate
Decreased body temperature
Cold intolerance
Anovulation (absence of ovulation)
Decreased libido
Menstrual changes (amenorrhea or prolonged periods)
Impotence (men)
Apathy
Depression
Signs/Symptoms of Hypothyroidism (Integumentary, Neuromuscular, Physical)
Cool, pale/ash gray, dry, coarse, scaly skin
Decreased hair growth, with loss of eyebrows hair
Dry, coarse, brittle hair
Thick, brittle nails
Confusion
Decreased tendon reflexes
Hearing loss
Impaired memory
Inattentivemess
Lethargy or somnolence
Muscle aches and pain
Slowing of intellectual functions
Slowness or slurring of speech
Facial puffiness
Goiter (enlarged thyroid gland)
Hoarseness
Nonpitting edema of the hands and feet
Periorbital edema
Thick tongue
Weakness, fatigue
Treatment of Hypothyroidism
Lifelong thyroid hormone replacement
Take in the morning on an empty stomach with water 30 - 60 minutes before eating
Take at the same time each morning
Use the same drug manufacturer (have prescriber write “no substitutions” on the prescription)
Space iron, calcium, and magnesium 4 hours from ingestion (reduces absorption of levothyroxine)
Start on lowest dose and gradually increase if needed
Yearly thyroid hormone labs
Myxedema Coma
Myxedema Coma: A serious complication of untreated or poorly treated hypothyroidism with dangerously reduced cardiopulmonary and neurologic functioning, although few affected adults become comatose. Decompensated metabolic state.
Cellular energy is decreased, and metabolites that are compounds of proteins and sugars called glycosaminoglycans (GAGs) build up inside cells. GAG buildup increases mucus and water, forming cellular edema (myxedema)
Precipitating Factors:
Infection
Cold exposure
Stroke
Meds (amiodacrone, lithium)
Signs/Symptoms of Myxedema Coma
Enlarged and thicken tongue
Non-pitting edema (pretibial, top of feet/hands, elbows, and face)
Bradycardia (Decreased CO and perfusion)
Decreased gas exchange
Hypothermia
Hypotension
Greatly reduced level of consciousness and cognition
Constipation
Poor appetite
Infertility, heavy menstruation
Cool extremities and swelling of the limbs
Enlarged thyroid (goiter)
Thinning hair, hair loss
Loss of eyebrow hair
Puffy face
Carpal tunnel syndrome
Findings and Treatment of Myxedema Coma
Serum glucose levels: increased (hypoglycemia)
ABGs: hypoxemia, hypercapnia
ECG: prolonged QT, low voltage
Pericardial effusion
Treatment
Supportive (airway, rewarming)
Hydrocortisone
IV Levothyroxine (T4) and T3 supplementation
IV glucose
Monitor vital signs hourly (BP, temperature)
Monitor level of consciousness
Institute aspiration precaution
Hyperthyroidism
Hyperthyroidism: Excessive thyroid hormone secretion from the thyroid gland
Subclinical hyperthyroidism will decrease the serum level of TSH but not change the serum level of T4. Therefore, no subjective or objective manifestations of hyperthyroidism will exist.
In overt hyperthyroidism, there will be a decrease in the serum level of TSH, an increase in the serum level of T4, and the presence of subjective and objective findings.
Graves Disease: Autoimmune disorder in which the production of autoantibodies (thyroid-stimulating immunoglobulins) that attach to the thyrotropin (TRAb) receptor on the thyroid gland greatly increases thyroid hormone production
Non-hispanic white females between 30 - 50
Diagnosed: Low TSH and High T4/T3
Risk Factors for Hyperthyroidism
Autoimmune disorders
Grave’s Disease
Family history of thyroid disease
Pregnancy or recently postpartum
Adrenal insufficiency
Pernicious anemia (VItamin B12 deficiency)
Type I Diabetes Mellitus
Smoking
Over consumption of iodine containing foods
Low socioeconomic status
Toxic multinodular goiter (TMNG)
Excessive use of thyroid replacement hormones
Thyroiditis
Subacute thyroiditis: an enlarged thyroid that is inflamed and causes the client pain
Postpartum thyroiditis: an enlarged thyroid that develops after giving birth
Painless thyroiditis: likely an autoimmune condition of an enlarged thyroid without the level of pain of subacute thyroiditis
Signs/Symptoms of Hyperthyroidism
Chest pain
Dysrhythmias
Increased systolic blood pressure
Palpitations
Rapid, shallow respirations
Tachycardia
Increased appetite
Increased stools (diarrhea)
Weight loss
Fatigue
Heat intolerance
Increased basal metabolic rate
Amenorrhea
Erectile dysfunction
Gynecomastia
Anxiety
Mood swings
Hyperactivity
Restlessness
Diaphoresis
Fine, soft, silky body hair
Smooth, warm, moist skin
Thinning of scalp hair
Eyelid retraction, eyelid lag
Hyperactive deep tendon reflexes
Insomnia
Muscle weakness
Tremors
Goiter
Wide-eyed or startled appearance (exophthalmos)
Maternal/Fetal Risks for Hyperthyroidism During Pregnancy
Threats to the pregnant client can range across all pregnancy trimesters
Preeclampsia
Preterm labor
Thyroid storm
Fetal Risks
Preterm birth
Small for gestation age (SGA) measurement
Fetal demise
Congenital malformations
Fetal tachycardia
Fetal hyperthyroidism
Development of a fetal goiter
Both PTU and methimazole carry a risk of fetal congenital disabilities when taken in the first trimester. There are also risks associated with impairment to the fetal thyroid function and the potential for goiter formation since the placental transfer of these medications exists. PTU has a lower risk and, therefore, is recommended for the first 4 months of pregnancy or up to week 16. Pharmacological therapy should then be changed to methimazole for the remainder of the pregnancy.
Treatment for Hyperthyroidism
Methimazole (also decreases the immune response)
Suppresses synthesis of thyroid hormones
Monitor for symptoms of hypothyroidism
Propylthiouracil
Suppresses synthesis of thyroid hormones
Darkening of the urine, pale stools, and jaundice can indicate liver toxicity or failure
Beta blockers
For symptom control (relieves diaphoresis, tachycardia, anxiety, and palpitations)
Iodine (Saturated solution of potassium iodine [SSKI])
Control transport of iodine into the thyroid
Given 1 hour after other medications
Radioactive iodine is given 1 week after admin to decrease the risk for an exacerbation of hyperthyroidism
Radiation precautions: sit to urinate, close the lid and flush 2 – 3 times, avoid contact with pregnant women/infants/young children for 1 week, stay 6 feet away from people, don’t share drinks/food, don’t prepare food for others
Partial or Total Thyroidectomy
Complications include hemorrhage, respiratory distress, parathyroid gland injury (resulting in hypocalcemia), tetany, damage to the laryngeal nerves, and thyroid storm
Thyroid Storm
A life-threatening event that occurs in patients with uncontrolled hyperthyroidism, most often with Graves disease
Other Risk Factors
Trauma from injury, surgery, or burns
COVID-19
Diabetic ketoacidosis
Pregnancy
Infections
Drug reactions
Strong cardiovascular system connection
cardiovascular disease, hypertension, tachyarrhythmias, ischemic heart disease
Signs/Symptoms of Thyroid Storm
Thyrotoxicosis
Respiratory distress
Arrhythmias
Severe hypertension
High fever (104 - 106 F)
Tachycardia
Agitation
Delirium
Congestive heart failure
Loss of consciousness
Seizures
Death
Treatment of Thyroid Storm
Maintain a patent airway and adequate ventilation.
Give oral antithyroid drugs as prescribed: methimazole or propylthiouracil.
If antithyroid drugs cannot be used, a bile acid sequestrant such as chole-styramine may be ordered to help reduce thyroid levels.
Administer iodide solution, nonsalicylate antipyretic drugs, and glucocorticoids as prescribed.
Give oral propranolol as prescribed to control heart rate.
Monitor continually for cardiac dysrhythmias.
Monitor vital signs every 15 to 30 minutes.
Provide comfort measures, including a cooling blanket.
Correct dehydration with normal saline infusions per orders.
Apply cooling blanket or ice packs to reduce fever.
Anorexia nervosa
Persistent energy intake restriction leading to significantly low body weight in context of age, sex, developmental path, and physical health
Fear of gaining weight or becoming overweight
Disturbance in self-perceived weight or shape
Restricting type: The individual drastically restricts food intake and does not binge or purge.
Binge-eating/purging type: The individual engages in binge eating or purging behaviors (self-induced vomiting, laxative, diuretics, and/or enemas)
Characteristics
Patients are preoccupied with food and the rituals of eating, along with a voluntary refusal to eat.
This condition occurs most often in female patients from adolescence to young adulthood
Onset can be associated with a stressful life event, such as college.
Compared to patients who have restricting type, those who have binge-eating/purging type have higher rates of impulsivity and are more likely to abuse drugs and alcohol.
Signs/Symptoms for Anorexia Nervosa
Body weight that is less than 85% of expected normal weight
Patient perception that they are severely overweight and sees this image reflected in the mirror
High interest in food but not eating; terrified of gaining weight
Fine, downy hair (lanugo) on the face and back
Yellowed skin (elevated carotene levels)
Pale, cool extremities
Poor skin turgor
Muscle weakness
Decreased vital signs (low BP, low PR, low temp, irregular HR)
Fluid and electrolyte imbalances (dehydration)
hypomagnesium, hypophosphatemia, hypochloremia, hyponatremia, hypokalemia
metabolic alkalosis (vomiting) or metabolic acidosis (laxative use)
Amenorrhea
Purging type: dental erosions/caries, enlargement of the parotid glands
Constipation (dehydration) or diarrhea (laxative use)
Russell’s sign: self-induced vomiting causes calluses or scars on the hands
Decreased estrogen (females) and testosterone (males)
Bulimia Nervosa
An episodic, uncontrolled, compulsive, rapid ingestion of large amounts of food in a short time period, followed by purging behaviors to prevent weight gain.
Purging type: The client uses self-induced vomiting, laxatives, diuretics, and/or enemas to lose or maintain weight.
Nonpurging type: The client can compensate for binge eating through other means (excessive exercise and the misuse of laxatives, diuretics, and/or enemas).
Characteristics
Most patients who have bulimia nervosa maintain a weight within a normal range or slightly higher. BMI is 18.5 to 30
The average age of onset in female patients is late adolescence or early adulthood.
Between binges, patients typically restrict caloric intake and select low-calorie "diet" foods.
The dentist is often the first person to notice bulimia due to tooth enamel erosion
Signs/Symptoms of Bulimia Nervosa
Weight within a normal range or slightly higher. BMI is 18.5 to 30
Esophageal tears, gastric rupture
Can exhibit low self-esteem, impulsivity, and difficulty with interpersonal relationships
Need for an intense physical regimen
Purging type: dental erosions/caries, enlargement of the parotid glands
Diarrhea (laxative use)
Russell’s sign: self-induced vomiting causes calluses or scars on the hands
Hypokalemia
Loss of bone density
Menstrual irregularities
Cognitive Distortions with Eating Disorders
Overgeneralization: "Other people don't like me because I'm fat."
"All-or-nothing" thinking: "If I eat any dessert, I’Il gain 50 pounds."
Catastrophizing: "My life is over if I gain weight."
Personalization: "When I walk through the hospital hallway, I know everyone is looking at me."
Emotional reasoning: "I know I look bad because I feel bloated."
Distorted body image: “When I look in the mirror, I see myself as obese.”
Risk Factors for Eating Disorders
Involved in modeling, ballet, or athletics where weight is monitored and thinness is encouraged
History of obesity
Family history of eating disorders
Being a picky eater in childhood
Interpersonal relationships (overly controlling parents)
Feelings of ineffectiveness, helplessness, and depression
Distorted body image
Media influence and pressure from society to have the “perfect body”
Hypothalamic, neurotransmitter, hormonal, or biochemical imbalance
History of abuse
Early Manifestations of Eating Disorders
PRODROMAL MANIFESTATIONS
Increase or decrease in weight that is not related to a medical condition
Abnormal eating habits, like severe dieting
Ritualized mealtime behaviors, like counting calories
Lying about food intake
Preoccupation with weight and body image
Compulsive and/or excessive exercising
Interventions for Eating Disorders
Positive approach to support and promote self-esteem
Provide a highly structured environment
Set meal times, small frequent meals, liquid supplements, high fiber, vitamin supplement
Limit caffeine, high-fat, high-sodium foods
Rewards for completing meals or consuming certain number of calories
Allow patient to make choices where appropriate
Monitor bathroom use after meals
Monitor amount of exercise
Establish realistic goals (2-3 lbs/week)
Monitor vital signs, intake & output
Individual, group, family counseling
Nutrition education
Personality Disorders Clusters
Cluster A: Odd or eccentric thinking or behaviors or traits
Paranoid, Schizoid, Schizotypal
Cluster B: Dramatic, emotional or erratic/impulsive traits
Antisocial, borderline, histrionic, narcissistic
Cluster C: Anxious and fearful traits
Avoidant, dependent, obsessive-compulsive
Cluster A: Paranoid Personality Disorder
Paranoid: Characterized by distrust and suspiciousness toward others based on unfounded beliefs that others want to harm, exploit, or deceive the person
Cluster A: Schizoid Personality Disorder
Schizoid: Characterized by emotional detachment, disinterest in close relationships, and indifference to praise or criticism; often uncooperative
Cluster A: Schizotypal Personality Disorder
Schizotypal: Characterized by odd beliefs leading to interpersonal difficulties, an eccentric appearance, and magical thinking or perceptual distortions that are not clear delusions or hallucinations
Cluster B: Antisocial Personality Disorder
Antisocial: Characterized by disregard for others with exploitation, lack of empathy, repeated unlawful actions, deceit, failure to accept personal responsibility; evidence of conduct disorder before age 15; sense of entitlement; manipulative, impulsive, and seductive behaviors; non-adherence to traditional morals and values; verbally charming and engaging
Patient’s diagnosed with borderline personality disorder are at a higher risk for danger to others
Cluster B: Borderline Personality Disorder
Borderline: Characterized by instability of affect, identity, and relationships, as well as splitting behaviors, manipulation, impulsiveness, and fear of abandonment; often self-injurious and potentially suicidal; ideas of reference are common; often accompanied by impulsivity
Patient’s diagnosed with borderline personality disorder are at a higher risk for danger to self
Cluster B: Histrionic Personality Disorder
Histrionic: Characterized by emotional attention-seeking behavior, in which the person needs to be the center of attention; often seductive and flirtatious
Cluster B: Narcissistic Personality Disorder
Narcissistic: Characterized by arrogance, grandiose views of self-importance, the need for consistent admiration, and a lack of empathy for others that strains most relationships; often sensitive to criticism
Cluster C: Avoidant Personality Disorder
Avoidant: Characterized by social inhibition and avoidance of all situations that require interpersonal contact, despite wanting close relationships, due to extreme fear of rejection; have feelings of inadequacy and are anxious in social situations
Cluster C: Dependent Personality Disorder
Dependent: Characterized by extreme dependency in a close relationship with an urgent search to find a replacement when one relationship ends
Cluster C: Obsessive-Compulsive Personality Disorder
Obsessive-Compulsive: Characterized by indecisiveness and perfectionism with a focus on orderliness and control to the extent that the individual might not be able to accomplish a given task
Risk Factors for Personality Disorders
Comorbid substance use disorders
History of nonviolent and violent crimes
Prior childhood abuse/trauma
Emotionally reactive/detached caregivers
Genetic and biochemical influences
Cultural factors
General Characteristics with Personality Disorders
Inflexibility/maladaptive responses to stress
Compulsiveness and lack of social restraint
Inability to connect in social/professional relationships
Tending to provoke interpersonal conflicts
LIFESPAN CONSIDERATIONS
Children may exhibit difficulties in developing social relationships and school classwork.
Adolescents may report being bullied for having odd habits, behaviors, or ideas.
Adults may have trouble forming intimate relationships, maintaining or establishing careers, and fulfilling opportunities to mentor future generations.
Defense Mechanisms used by Patient’s with Personality Disorders
Repression: Unconsciously putting unacceptable ideas, thoughts, and emotions out of awareness
ADAPTIVE USE: A person preparing to give a speech unconsciously forgets about the time when they were young and kids laughed at them while on stage.
MALADAPTIVE USE: A person who has a fear of the dentist continually forgets to go to their dental appointments.
Suppression: Voluntarily denying unpleasant thoughts and feelings
ADAPTIVE USE: A student puts off thinking about a fight they had with a friend so they can focus on a test.
MALADAPTIVE USE: A person who has lost their job states they will worry about paying bills next week.
Regression: Sudden use of childlike or primitive behaviors that do not correlate with the person's current developmental level
ADAPTIVE USE: A young child temporarily wets the bed when they learn that their pet died
MALADAPTIVE USE: A person who has a disagreement with a co-worker begins throwing things at their office.
Undoing: Performing an act to make up for prior behavior (most commonly seen in children).
ADAPTIVE USE: An adolescent completes their chores without being prompted after having an argument with their parent.
MALADAPTIVE USE: An individual buys their significant other flowers and gifts after an incident of partner abuse.
Splitting: Demonstrating an inability to reconcile negative and positive attributes of self or others into a cohesive image (commonly associated with borderline personality disorder)
ADAPTIVE USE: n/a
MALADAPTIVE USE: A client tells a nurse that the nurse is the only one who cares about them, yet the following day, the client refuses to talk to that nurse.
Interventions for Personality Disorders
Structured milieu therapy
Safety: self-harm/suicide risk especially with borderline personality disorder; risk of harming others with antisocial personality disorder
Cluster A: emphasize pre-existing patient strengths and skills, develop resources to find and maintain personal relationships
Schizoid or schizotypal types tend to isolate themselves, nurses should respect that need.
Cluster B: develop skills to limit dramatic/emotional behaviors
Limit-setting and consistency are essential with patients who are manipulative (borderline and antisocial)
Histrionic types benefit from assertiveness training and modeling as well as psychotherapy
Cluster C: develop skills to manage feelings of anxiety
Dependent types benefit from assertiveness training and modeling as well as psychotherapy
Medications: Antidepressants, anxiolytic, antipsychotic, or mood stabilizers
Psychotherapy, group therapy, and case management
OCD
OCD: A mental health condition that is characterized by intrusive thoughts of unrealistic obsessions and tries to control these thoughts with compulsive behaviors, such as repetitive cleaning of a particular object or washing hands.
There are many who have OCD tendencies, but these thoughts and actions may not necessarily interfere with one’s everyday life.
When the ability to function normally is affected, one becomes maladaptive and in need of help.
Risk Factors for OCD
Female gender
Family history of OCD
Stressful life events
Comorbid mood or personality disorders (especially anxiety disorders)
Signs/Symptoms of OCD
Obsessions or compulsions are time-consuming and result in impaired social and occupational functioning
Common obsessions:
Fear of germs, dirt, or contamination
Fear of losing control over yourself
Fear of forgetting something important
Intrusive thoughts of aggression, harm, or inappropriate behavior
Desire to have things in a certain order or place
Common compulsions:
Excessive cleaning or handwashing
Ordering, numbering, counting, or arranging things in a particular way
Repeatedly checking things
Repeating mantras or prayers
Motor or verbal tics
Interventions for OCD
Assess anxiety level
Assess suicidality
Provide calm, quiet environment
Therapeutic communication strategies
Relaxation techniques
Allow time for client rituals
Psychotherapy
Medication (SSRIs: Fluvoxamine, paroxetine, fluoxetine, Buspirone for long-term management)
Support groups
Exercise
Hypothalamic-Pituitary Axis
An information system in the body in which the hypothalamus receives feedback from multiple areas of the central nervous system and hormone levels in the endocrine glands and sends a message to the pituitary gland to release or hold hormones.
The hormones involved include thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone, prolactin, and adrenocorticotropic hormone.
The hypothalamus and the pituitary gland regulate many body functions, such as body temperature (through TSH thyrotropin-releasing hormone), fluid balance (antidiuretic hormone or vasopressin), blood pressure (dopamine), appetite, stress (cortisol), sleep (melatonin via the pineal gland), and reproductive health (gonadotropin-releasing hormone).
Addison’s Disease
Addison’s disease is a disorder of the adrenal glands in which the glands are damaged and unable to produce adequate amounts of cortisol and aldosterone. An insufficient amount of these hormones diminishes the body’s ability to maintain metabolism, electrolyte balance, blood pressure, and blood glucose levels and also creates an inability to control inflammation
Causes of Addison’s Disease
Primary
Autoimmune dysfunction
Tuberculosis
Metastatic cancer
HIV-III (AIDS)
Hemorrhage
Gram-negative sepsis
Adrenalectomy (usually as treatment for Cushing’s syndrome)
Abdominal radiation therapy
Drugs (mitotane) and toxins
Secondary
Pituitary tumors
Postpartum pituitary necrosis
Hypophysectomy (removal of the pituitary gland)
High-dose pituitary or whole brain radiation
Cessation of long-term corticosteroid drug therapy
Signs/Symptoms of Addison’s Disease
Hypoglycemia (from decreased cortisol)
Peptic Ulcers (from decreased gastric acid)
Excessive BUN levels (from decreased glomerular filtration)
Anorexia and weight loss (from decreased glomerular filtration)
Fluid and Electrolyte Imbalances
Hyperkalemia, hypercalcemia, hyponatremia
Hypovolemia
Hypotension
Salt cravings
Metabolic acidosis (potassium retention promotes reabsorption of hydrogen ions)
Decreased body, axillary, and pubic hair in females (low adrenal androgen levels)
Hyperpigmentation
Vitiligo
Nausea, vomiting, abdominal pain
Joint/muscle pain
Muscle weakness
Fatigue
Menstrual changes (women) and impotence (men)
Addisonian Crisis (Acute Adrenal Insufficiency)
Medical emergency in which the need for cortisol and aldosterone is greater than the body’s supply. It often occurs in response to a stressful event (e.g. surgery, trauma, severe infections, adrenal hemorrhage, etc.) especially when the adrenal hormone output is already reduced.
Problems are the same as chronic adrenal insufficiency, but more severe and life-threatening symptoms can appear without warning
S/s: severe hypotension, hypoglycemia, hyperkalemia, abdominal pain, weakness, weight loss
Treatment:
Administer glucocorticoids, glucagon/glucose and insulin w/ dextrose (for hypoglycemia), loop/thiazide diuretics (for hyperkalemia)
Place in Trendelenburg to improve blood pressure
Emergency Management for Acute Adrenal Insufficiency
Hormone Replacement
Start rapid infusion of normal saline or dextrose 5% in normal saline.
Initial higher doses of hydrocortisone sodium or dexamethasone are administered as an IV bolus.
Administer additional hydrocortisone sodium by continuous IV infusion over the next 8 hours.
Give an additional dose of hydrocortisone intramuscularly concomitantly with hydration every 12 hours.
Initiate an IV H2 histamine blocker (e.g., cimetidine) for ulcer prevention.
Hyperkalemia Management
Administer insulin and dextrose intravenously to shift potassium into cells. Dosing is often based on renal function.
Give potassium binding and excreting resin.
Give loop or thiazide diuretics. Avoid potassium-sparing diuretics.
Cardiac cell membrane stabilization with IV calcium.
Initiate potassium restriction.
Monitor intake and output.
Monitor heart rate, rhythm, and ECG for signs and symptoms of hyperkalemia (slow heart rate; heart block; tall, peaked T waves; fibrillation; asystole.
Hypoglycemia Management
Administer IV glucose as per orders.
Prepare to administer glucagon as needed and as per orders.
Maintain IV access.
Monitor blood glucose level hourly.
Labs/Diagnostics for Addison’s Disease
Low sodium
High potassium
High calcium
High bicarbonate
Normal to low glucose (fasting)
High BUN
High cortisol (serum and saliva)
ACTH stimulation test (definitive test)
IV ACTH is given and plasma cortisol levels are taken at 30 & 60 mins
No cortisol response in primary Addison’s; increased cortisol response for secondary Addison’s
Primary Addison’s
Elevated eosinophils
Elevated ACTH
Nursing Interventions for Addison’s Disease
Daily weights and I&O
Orthostatic BP assessments
Preventing hypoglycemia
Assessing cardiac function (telemetry)
Vital signs every 1-4 hours
Monitor lab values to identify hemoconcentration
Hormone replacement therapy
Hydrocortisone IV or prednisone PO to correct glucocorticoid deficiency
Fludrocortisone (mineralocorticoid) may be needed to restore fluid and electrolyte balance
Cushing’s Syndrome
Cushing’s syndrome is a disorder in which excessive amounts of cortisol are excreted. This results in associated health problems such as hypertension, osteoporosis, metabolic syndrome, diabetes, and increased risk for infections.
Cushing’s disease is caused by endogenous factors: adrenal hyperplasia, adrenocortical tumor, pituitary tumor, lung/GI/pancreatic tumors (these secrete ACTH)
Cushing’s syndrome is caused by chronic therapeutic use of glucocorticoids for organ transplant, chemotherapy, autoimmune diseases, asthma, allergies, or chronic fibrosis
Signs/Symptoms of Cushing’s Syndrome/Disease
Increased total body fat with fat redistribution
Truncal obesity, “buffalo hump.” and “moon face”
Increased breakdown of tissue protein
Decreased muscle mass/strength, thin skin (striae on abdomen, thighs, and upper arms), and fragile capillaries
Bone density loss (osteoporosis)
Fragility fractures, decreased height/vertebral collapse, aseptic necrosis of the femur head, slow or poor healing of bone fractures
Increased risk for infection and decreased inflammatory response
Reduced number of circulating lymphocytes, inhibited macrophage activity, reduced antibody synthesis, and inhibited production of cytokines and inflammatory chemicals (e.g. histamine)
Increased androgen production
Acne, hirsutism, clitoral hypertrophy, thinning hair
Decreased estrogens and progesterones
Oligomenorrhea (scant or infrequent menses)
Hypertension, bounding pulses
Cardiac hypertrophy
Frequent dependent edema
Increased appetite
Peptic ulcers (increased HCl acid and decreased gastric mucus)
Bruising, petechiae
Impaired glucose intolerance (hyperglycemia)
Sleep disturbances
Labs/Diagnostics for Cushing’s Syndrome/Disease
Labs
High cortisol (serum, saliva, and urine)
ACTH levels (high, if pituitary is the cause; low, if adrenal dysfunction/medication is the cause)
Increased blood glucose levels
Decreased lymphocyte counts
Increased sodium levels
Decreased calcium and potassium levels
24-hour urine collection: high free cortisol levels
Dexamethasone suppression test: uses administration of dexamethasone at bedtime, then 8 a.m. blood draw for serum cortisol levels and another 24-hr urine collection to measure cortisol excretion
When cortisol levels are suppressed vey dexamethasone, Cushing’s disease is not present
Diagnostics
X-ray, MRI, CT can reveal tumors or lesions on pituitary gland, adrenal gland, GI tract, lung, and
pancreas
Treatment for Cushing’s Syndrome/Disease
Tapering or eliminating corticosteroids (for Cushing’s syndrome)
Drug therapy (ketoconazole, mitotane, hydrocortisone)
Fluid and sodium restrictions
Chemotherapy (for removal of tumors causing disease)
Hypophysectomy (removal of pituitary gland, if cause of disease)
Monitor for CSF leaks through sinus cavity (test fluid for glucose, look for “halo” appearance)
Provide glucocorticoid replacement therapy
Avoid brushing teeth for 2 weeks
Avoid anything that increases intracranial pressure (bending, straining, etc)
Adrenalectomy (removal of one or both adrenal glands)
Provide glucocorticoid and hormone replacement therapy
Patient will be in ICU for recovery