12.1 Endocrine Part 2 Flashcards
Endocrine System
- Regulates metabolism, growth, reproduction, aging, and responses to adverse conditions
- Feedback mechanisms are disrupted by stress, environmental temperature and nutritional status
Endocrine Disorders
Primary - Originate in target gland responsible for hormone production
Secondary - Target gland is normal but function is altered due to pituitary system releasing inappropriate amounts of stimulating hormones
Tertiary - Caused by hypothalamic dysfunction
Hypothalamus
- Hypothalamus receptors monitor hormone, nutrient, and ion levels
- When these receptors get stimulated, it regulates the secretion of releasing/inhibiting hormones produced in the anterior pituitary gland
- These hormones released in the pituitary control the autonomic nervous system and pituitary activity which controls thirst, hunger, body temperature, and other homeostatic systems.
Pituitary Gland (Master Gland)
- Located at the base of the brain
- Controls functions of many different glands and cells throughout the body
- It is also called “hypophysis”
Hypothalamic-Pituitary Axis (HPA)
- Controls endocrine glands and other physiological function
- The anterior pituitary synthesis and release of hormones is regulated by the hypothalamus
Organs and associated hormones
Hypothalamus - Releasing/Inhibiting Hormones
Anterior Pituitary - Tropic Hormones
Posterior Pituitary - ADH, Oxytocin
Thyroid - T4, T3, Calcitonin
Parathyroid - PTH (Parathyroid Hormone)
Pancreas - Glucagon/Insulin
Adrenal Cortex - Cortisol, Aldosterone, Androgens, Estrogens
Adrenal Medulla - Catecholamines
Reproductive - Estrogen, Progesterone, Testosterone
Target Cells and Target Organs
- These contain receptors that react to specific hormones
- Hormones in the blood are either unbound in the blood (free) or travel while attached to a transport carrier
- Peptide and proteins are usually unbound
- Thyroid hormones are carried by carrier proteins (they are also synthesized in the liver)
Anterior Pituitary Gland
RELEASES THE BELOW
- Follicle Stimulating Hormone (FSH)
- Luteinizing Hormone (LH)
- Prolactin
- Adrenocorticotropic Hormone (ACTH)
- Thyroid Stimulating Hormone (TSH)
- Growth Hormone (GH)
Posterior Pituitary Gland
- Releases ADH, Vasopressin, and Oxytocin. (ADH and Vasopressin are the same)
SIADH - Hyperactivity of posterior pituitary
DI (Diabetes Insipidus) - Hypoactivity of posterior pituitary
- Issues with pituitary gland are usually caused by benign tumors
Which Hormones Affect Which Organs
ADH (Vasopressin) - Kidneys
Oxytocin - Uterus and Breasts
Growth Hormone (GH) - Bones and Soft Tissue
ACTH - Adrenal Cortex
TSH (Thyroid Stimulating Hormone) - Thyroid
FSH and LH - Testes
Prolactin - Breasts
Adrenal Cortex - Adrenocorticosteroids Thyroid - Thyroid Hormones Testes - Testosterone Ovary - Estrogen Corpus Luteum - Progesterone
Hypopituitarism
- Deficiency of 1+ pituitary hormones
- Clinical manifestations vary depending on the hormone that is deficient
PANHYPOPITUITARISM - Deficiency of ALL PITUITARY HORMONES
Manifestations of Hypopituitarism
GH (Growth Hormone) - Causes lower bone density, fractures are common, decreased muscle strength and increased serum cholesterol
LH, FSH (Luteinizing Hormone and Follicle Stimulating Hormone)
- In women it causes amenorrhea (absence of menstruation), anovulation (eggs are not released during menstrual cycle), decreased estrogen levels, breast atrophy (smaller), loss of bone density, lower axillary (armpit) and pubic hair, and decreased libido
- In men it causes lower facial hair, ejaculation volume, muscle mass, bone density, body hair, libido, and impotence (erectile dysfunction)
TSH (Thyroid Stimulating Hormone) - Weight gain, intolerance to cold, menstrual abnormalities, slow cognition, lethargy, hirsutism
ACTH - Lower axillary and pubic hair in women, pale/sallow complexion, malaise, lethargy, anorexia, postural hypotension, headache, hypoglycemia, hyponatremia
ADH - Large urine output, lower specific gravity, hypovolemia, increased thirst, increased plasma osmolarity
Hyperpituitarism
- Over-secretion of hormones caused by tumors (pituitary adenomas, genetic mutations, hyperplasia)
Manifestations
- Nervous, rapid/irregular heartbeat, weight loss, fatigue, muscle weakness
TREATMENT
- Drug therapy to shrink the tumor
- Radiation therapy to treat tumor (mainly for people who cannot get surgery and don’t respond well to medications). This type of therapy can damage surrounding organs
- STEROTACTIC THERAPY (Gamma knife procedures) Deliver high dose of radiation to tumor.
- PATIENTS WHO UNDERGO RADIATION THERAPY NEED HORMONE REPLACEMENTS BECAUSE PITUITARY HORMONES SECRETION GRADUALLY DECLINES
Transsphenoidal Hypophysectomy (For Hyperpituitarism)
- Small incision through nose or upper lip to remove tumor. May require long-term pituitary hormone replacement after surgery. May also cause leakage of cerebrospinal fluid.
PREOP CARE - IV antibiotics
- Teaching Mouth Breathing (because of incision to lip and nose)
- Importance of hormone replacement therapy
POSTOP CARE - Monitor neurological signs of increased intracranial pressure
- Assess for nasal drainage (can mean CSF leak)
- Elevated HOB to 30 degrees to reduce headache
- Assess for meningitis, transient diabetes insipidus, hypopituitarism
- Hormone replacement therapy
- Avoid coughing after surgery and Valsalva Maneuver
- Avoid toothbrushing
Diabetes Insipidus
- Deficiency of ADH which affects water metabolism (reabsorption of water)
- Can either be caused by decreased ADH synthesis or kidneys do not respond to ADH
Neurogenic (Central) DI
- Caused by tumor, head trauma, genetic abnormalities
Nephrogenic DI
- Kidneys do not respond to ADH
- ADH is ineffective in the renal tubules
- Can be caused by genetic defects, or drug related (lithium)
- Can also be caused by extreme ingestion of water (ingesting too much water) which is usually because of damage to the part of the brain that affects thirst
Pathogenesis of DI
- Deficiency or decreased response to ADH causes fluid loss. This includes large amounts of diluted urine, dehydration, and increased sodium levels.
Manifestations of DI
- Polyuria with low specific gravity (chief sign)
- Polydipsia
- Increased sodium levels
FLUID DEFICIT
- Hypotension
- Tachycardia
- Poor Skin Turgor
- Weight Loss
- Hypovolemic Shock
Nursing Interventions for DI
- Assess fluid volume with I&O, Daily Weights, Urine Output, Serum/Urine Osmolarity
- ESPECIALLY IMPORTANT TO CHECK SODIUM LEVELS
Desmopressin (DDVAP)
- TREATS CENTRAL DI (Neurogenic) by replacing insufficient ADH being made in the posterior pituitary or hypothalamus
- IS NOT EFFECTIVE IN TREATING NEPHROGENIC DI (can be used to see which type a patient has. If the medication is not effective the patient most likely has nephrogenic DI)
- THIS IS USUALLY A LIFELONG THERAPY
EDUCATION
- Medication administration (IV, IM, SC, PO, Sublingual, Intranasal)
- Teach patient to check their daily weights and need for regular blood work
Side Effects
- Headache, nausea, vomiting
- HYPONATREMIA, SEIZURES
SIADH (Syndrome of Inappropriate ADH)
- Abnormal secretion of vasopressin (ADH) whether plasma osmolarity is low or normal
- Normal feedback mechanism is not properly functioning
- This causes fluid retention and dilutional hypernatremia
- FLUID OVERLAD IN IVF (DOES NOT CAUSE EDEMA)
Causes
- Head trauma, cerebrovascular disease, brain inflammation (Think head)
- Infection, Asthma, TB, Pulmonary Disease (Think Lungs)
- Cancer, Medication, Hereditary
Pathogenesis of SIADH
- Increased ADH leads to increased water reabsorption and dilutional hypernatremia
- Does not cause edema
- Causes decreased renin and aldosterone
Clinical Manifestations of SIADH
- All signs are due to hyponatremia
SODIUM LEVEL MANIFESTATIONS
130-140 - Increased BP, Thirst, Impaired Taste, Anorexia, Dyspnea on Exertion, Fatigue, Dulled Sensorium
120-130 - Vomiting and Abdominal Pain
115 - Confusion, Lethargy, Muscle Twitching, Convulsions (think brain, this is when it starts getting bad)
110-115 - Neurological Damage
SIADH Interventions
- Mild Hyponatremia - Fluid restriction (800-1000cc a day) to increase serum sodium and osmolarity
- Severe Hyponatremia - Hypertonic NaCl (3%) and fluid restriction (500cc a day)
General Interventions
- Daily weight
- Sodium levels
- Diuretics, Hypertonic Saline, Vasopressin Antagonist, Demeclocycline
- Monitor fluid overload (Most important is crackles in lungs)
- Neurological Assessments
Chronic Management
- Fluid restriction 800-1000 cc a day
- Maintain follow up appointments for blood work
- Diuretics, Electrolyte Replacement, Vasopressin Antagonist
Conivaptan (Vaprisol)
- ADH Antagonist
- ONLY IV
- Used for hyponatremic patients
- Make sure to monitor serum sodium to prevent hypernatremia
Tolvaptan (Samsca)
- Oral vasopressin antagonist
- Reduces hyponatremia in hypervolemic or euvolemic (normal fluid) patients
IMPORTANT WITH ALL MEDICATION TREATMENTS FOR THIS. MONITOR SODIUM BECAUSE RAPID RISE IN LEVELS CAN CAUSE BRAIN DAMAGE
Thyroid Gland
- Produces T3, T4 and Calcitonin
- Hypothalamus releases thyrotrophin-releasing hormone (TRH) which stimulates anterior pituitary gland to produce thyroid stimulating hormone (TSH)
- TSH stimulates thyroid to release t3, t4 and calcitonin
Thyroid Hormone
- Controls cellular metabolic activities in all major body organs
- Increases metabolism and protein synthesis
- T3 is more stronger and faster acting than T4
- Calcitonin is released in response to high calcium levels and increases calcium deposits in bone
Thyroid Diagnostic Tests
- Serum tests of TSH and thyroid antibodies
- Can also check for serum thyroglobulin which is the precursor to thyroid hormone. Thyroglobulin can be elevated in patients with thyroid cancer or large amounts of benign thyroid conditions.
Goiter
- Visible enlargement of thyroid gland
- Usually caused by iodine deficiency
- Decreased iodine causes decreased T3, T4, with increased TSH. This causes enlargement of the thyroid gland
Hyperthyroidism (Thyrotoxicosis) (Graves Disease)
- This is a hypermetabolic state
- Early signs are weight loss and nervousness
- Later Goiter (Enlarged Thyroid) and Exophthalmos (Bulging Eyes) can occur (important)
Other Signs (EVERYTHING SPEEDS UP)
- Tachycardia, Dysrhythmia, Elevated Systolic BP
- Fatigue, Insomnia, Tremors
- Heat Intolerance
- Menstrual Irregularities
- Increased Appetite
- Diarrhea
- Flush/Warm/Soft/Moist Skin
- Diaphoresis
- Angina
MOST IMPORTANT IS THAT IT CAN CAUSE “HIGH OUTPUT HEART FAILURE” WHICH IS CAUSED BY INCREASED METABOLIC DEMAND, NOT HEART DISEASE
Propylthiouracil (PTU)
- Blocks synthesis of Hormones (conversion of T4 to T3)
INTERVENTIONS
- Monitor cardiac parameters
- Observe for hypothyroidism
- Only given PO
- Watch for rash, n/v, agranulocytosis, systemic lupus erythematosus (SLE)
Methimazole (Tapazole)
- Inhibits synthesis of thyroid hormones
More toxic than PTU
Watch for rash
Sodium Iodide
- Suppresses release of thyroid hormone
- Given 1 hour after PTU or Methimazole
Watch for edema, hemorrhage, and GI upset
Potassium Iodide
- Suppresses release of thyroid hormone
- Discontinue if you notice a rash
- Watchout for toxic iodinism
Beta Blockers (-lol drugs)
- Monitor Cardiac Status
- Hold if bradycardia or decreased CO is noticed
- Use with caution in HF patients
Hyperthyroidism Medication Therapy
- MEDICATIONS DO NOT CURE THE DISEASE THEY ONLY PUT IT IN A STATE OF REMISSION
Thyrotoxic Crisis (Thyroid Storm)
- Life-threatening condition from heightened hyperthyroidism
Signs
- N/V
- Severe Tachycardia
- Heart Failure
- Delirium
- Hyperthermia
- Shock or Coma
INTERVENTIONS
- ABC’s (adequate airway, oxygen delivery, control of dysrhythmias)
- IV fluids
- Anti-thyroid drugs
- Calm, quiet environment to reduce stress
Thyroiditis
- Inflammation of thyroid gland
- Treated with drugs or surgery
Thyroidectomy
- Removal of thyroid
- Pre-op Goals - Reduce stress and avoid thyroid storm
- Pre-op Education - Avoid caffeine or other stimulants
- Post-op care - GREATEST CONCERN IS MAINTAINING AIRWAYS. SWELLING MAY CAUSE AIRWAY OBSTRUCTION. Monitor respirations and have emergency tracheotomy tray available.
- Patient should be in semi fowler position and discouraged from talking
- Patient may be at risk for hypocalcemia after surgery
Hypothyroidism
- Insufficient thyroid hormone
- Iodine deficiency is the most common cause in underserved areas
Primary Cause - Damaged Thyroid
Secondary Cause - Decreased TSH/TRH
DIAGNOSTIC
- TRH Stimulation Test
Primary Hypothyroidism - TSH levels are low and TRH administration produces little change in TSH levels
Secondary Hypothyroidism - TRH does not generate increase in TSH
Tertiary Hypothyroidism - Delayed increase in TSH after administration of TRH
Hypothyroidism Clinical Manifestations
- OPPOSITE OF HYPERTHYROIDISM (EVERYTHING SLOWS DOWN)
- Bradycardia
- Hypotension
- Weight gain
- Intolerance to Cold
- Fatigue/Lethargy
- Slow speech, hair loss, dry skin, brittle nails, muscle weakness, slow GI motility, decreased CO and contractility, dyspnea on exertion, increased cholesterol, increase bruising, anemia
Myxedema
- Causes non-pitting edema (especially around the eyes, hands, feet, and between shoulder blades)
- Voice gets husky due to edema in larynx and tongue
Myxedema Coma
- Caused by poorly treated hypothyroidism
- Heart muscles become flabby which results in decrease perfusion, respiratory failure, hypotension, hypoglycemia, hypothermia, high mortality.
Management of Hypothyroidism
- Stimulate or replace thyroid hormone
- Drug Therapy is life long
- Patients with diabetes need increased insulin once they reach normal thyroid state (euthyroid)
EDUCATION
- Importance of medication compliance
- Overdose of Medications Signs (orthopnea, dyspnea, tachycardia, palpations, nervous, insomnia)
Levothyroxine (Synthroid)
Synthetic T4 (drug of choice)
- Half life of 7 days
- Take 30-60 minutes before breakfast
- Lower doses for geriatric patients with cardiac issues
ADVERSE EFFECTS
- Tachycardia, tremors, angina
- THIS DRUG CAN INTENSIFY EFFECTS OF WARFARIN SO MONITOR APTT AND PT-INR
Thyroid Cancer
Papillary - Slow growing. Most common type (Usually affects young women)
Follicular - Most common in elderly patients. Spreads to bone and lungs
Medullary - Most common in 50+
Anaplastic - Rapid growing, aggressive tumor that directly invades surrounding tissue.
Parathyroid Glands
- 4 glands on posterior surface of thyroid
- Regulates calcium and phosphorous balance
- Increase PTH also increases calcium and lowers phosphorous
- PTH is released when the body senses low calcium levels
- PTH increases calcium by telling osteoclasts to breakdown bone and release calcium into the blood.
- PTH also increases absorption of calcium by activating vitamin D to promote absorption in kidneys.
Hyperparathyroidism
- Most common disorder. Over-secretion of parathyroid hormone causing hypercalcemia. This causes loss of bone density, gastric inflammation, kidney stones, bone tenderness, excessive urination.
MANIFESTATIONS (may have no symptoms)
- Apathy
- Fatigue/Muscle Weakness
- N/V and Constipation
- Hypertension and Cardiac Dysrhythmias
DIAGNOSTICS
- Elevated PTH, Elevated Serum Calcium, Decreased Serum Phosphate
- Can also check urine calcium levels
- MRI/CT can check for adenoma (cancer)
Categories of Hyperparathyroidism
Primary - Increased secretion of PTH. Usually cause by benign neoplasm or adenoma resulting from radiation to head or neck. Can be seen with hypercalcemia and hypophosphatemia
Secondary - Caused by low levels of calcium which induces release of too much PTH. Caused by vitamin D deficiency, renal failure, hyperphosphatemia
Tertiary - Hyperplasia of parathyroid causes automatic release of PTH despite serum calcium levels. Example is kidney transplant patient after period of dialysis for CRF.
Treatment for Hyperparathyroidism
- Primary/Secondary - Surgery (parathyroidectomy). Early post-op patients can have mild to severe tetany. For severe tetany, provide calcium gluconate. Patient may require lifelong calcium supplements.
- Non surgical treatment can include frequent ambulation, diet with high fluids, medications that lower calcium (biphosphates such as Fosamax), Estrogen and Progesterone, Oral Phosphates, and Calciminmetic Agents like Sensipar.
Hypercalcemic Crisis
- Extreme elevation of calcium
- Causes neurologic, cardiovascular, and renal symptoms (LIFE THREATENING)
TREATMENT - Rapid rehydration with IV isotonic fluids.
- Calcitonin and Corticosteroids are also given to reduce serum calcium by increasing deposition in the bone.
Hypoparathyroidism
- Due to abnormal development of parathyroid, destruction of parathyroid glands, vitamin D deficiency.
MANIFESTATIONS - Tetany, numbness, tingling in extremities, stiffness in hands and feet
- Bronchospasm, laryngeal spasm, EG changes
- CHVOSTEK SIGN AND TROUSSAEU SIGN DUE TO HYPOCALCEMIA
MANAGEMENT - Increase serum calcium with calcium gluconate IV
- Pentobarbital is given to decrease neuromuscular irritability
- Parathormone can be given but allergic reactions should be watched for
- Quiet environment
- High calcium and vitamin D diet with low phosphorous
Adrenal Glands
- Includes the cortex and medulla
- Produces hormones that help regulate metabolism, immune system, BP, and stress
- Cortex produces corticosteroids (cortisol, aldosterone, androgens)
- Medulla produces epinephrine and norepinephrine
Adrenal Cortex
- Stimulated by ACTH to release glucocorticoid hormones. This directly effects carbohydrate metabolism. It also has anti-inflammatory effects, growth suppression, and influences awareness and sleep habits. THE MOST POTENT GLUCOCORTICOID IS CORTISOL.
Cortisol
- Helps body respond to stress, maintain BP and cardiovascular function, slows immune system inflammatory response, maintains glucose in the blood, regulates metabolism of protein, carbs and fat.
Mineralocorticoid (Aldosterone)
- Most potent one is aldosterone
- Regulated by the renin-angiotensin system
- Causes sodium retention and potassium/hydrogen loss.
- Maintains blood pressure and water/salt balance.
- Deficient Aldosterone causes loss of sodium which causes a drop in blood volume and pressure.
Adrenal Medulla
- Secretes catecholamines epinephrine and norepinephrine
- Used in fight or flight response
- Promotes hyperglycemia
Hyperaldosteronism (CONNS DISEASE)
- Primary Hyperaldosteronism caused by single small adrenocorticoid adenoma
- Secondary hyperaldosteronism caused by non-adrenal causes such as renal artery stenosis, renin-secreting tumor, and CRF (Chronic Renal Failure)
MANIFESTATIONS
- Hypernatremia
- Hypertension (headaches)
- Hypokalemia (weakness, fatigue, dysrhythmias)
- Glucose Intolerance
- Metabolic Alkalosis
INTERVENTIONS
- Remove the tumor source
- Low sodium diet with potassium sparing diuretics
- Calcium Channel Blockers and Inspra (aldosterone receptor antagonist)
Nursing Care
- Assess VS with special attention to BP
- Potassium levels
Pheochromocytoma
- Catecholamine producing tumor in adrenal medulla
- Tumor releases epinephrine and norepinephrine
- Unknown cause but treated by removing tumor
- Hallmark sign is Hypertension
Phentolamine
- Alpha 1 and 2 adrenergic antagonist
- Decreases BP in patients with pheochromocytoma. Also prevents tissue necrosis with IV extravasation drugs that produce alpha-1 mediated vasoconstriction (norepinephrine and dopamine)
ADVERSE EFFECTS
- Orthostatic hypotension, reflex tachycardia, nasal congestion
- Given via IM or IV 1-2 hours before surgery
Cushing Syndrome
- Excessive anterior pituitary secretion of ACTH. Occurs with pituitary hormone and excessive production of cortisol. Most often caused by a tumor or can be caused by long time use of glucocorticoid therapy.
- Can cause increased sodium, glucose, and decreased potassium. High levels of cortisol leads to increased fat, breakdown of protein (catabolism), and altered metabolism of fat, glucose, calcium. It also inhibits inflammatory/immune responses.
Clinical Manifestations Cushing’s Syndrome
BUFFALO HUMP - Accumulation of fat between the shoulder blades
- Moon face
- Truncal obesity
- Hyperglycemia
- Hypertension
- Stretch Marks (Striae)
- Osteoporosis
- Poor wound healing
- Increased risk of infection
- Gastric ulcers
Cushing Syndrome Assessment
- Physical Assessment
- Lab tests such as cortisol levels in serum, saliva and urine.
- 24 hour urine test for free cortisol then dexamethasone suppression test if the results are borderline
- DIAGNOSTIC FOR Dexamethasone suppression test is elevated serum cortisol with absence of acute illness.
NURSING DIAGNOSIS
- Risk of injury/infection
- Self care deficit
- Impaired skin integrity
- Disturbed body image
Hypercortisolism Management
- Prevent fluid overload, drug therapy that suppresses cortisol production, restriction of fluids and sodium, as well as monitoring I&O, electrolytes, and EKG
Surgery
- Hypophysectomy
- Adrenalectomy
POST-OP CARE
- Observe for shock
- Prevent injury/infection
- Rapid changes in BP or HR should be notified to practitioner
- Strict I&O monitoring
- CORTICOSTEROID THERAPY NEEDS TO BE TAPERED OFF, NOT STOPPED ABRUPTLY
Addison’s Disease
- Adrenocortical Insufficiency.
- Autoimmune disease of inadequate cortisol and aldosterone
Primary causes - Damage to adrenal glands which causes lack of function where all 3 corticosteroids are reduced
Secondary causes - Pituitary disease or alteration in hypothalamus pituitary pathway results in lack of pituitary ACTH secretion. Corticosteroids and androgens are proficient but mineralocorticoids are sufficient.
Addison’s Disease Manifestations
- Decreased sodium, glucose and increased potassium, ACTH
- Muscle weakness, fatigue
- Anorexia
- GI symptoms
- Dark pigmentation of skin and mucosa
- Hypotension, low blood glucose, low sodium,
- High potassium
- Confusion
Addison’s Disease Diagnosis
- Disturbed body image
- Self care for weakness, fatigue, muscle wasting, altered sleep patterns
- Risk of injury from weakness
- Fluid volume deficit
- Risk of infection
- Knowledge deficit
Addisonian Crisis
- Insufficient cortisol during stress
- Caused by sepsis, trauma, stress, illness, adrenal hemorrhage, steroid withdrawal
SYMPTOMS
- N/V
- Muscle Weakness
- Hypotension
- Dehydration
- Vascular Collapse
Monitor fluid volume deficit, encourage foods high in sodium, administer hormone replacement therapy
Avoid stress and activity until stable due to activity intolerance
Educate on the importance of medications and avoiding stress
Corticosteroid Therapy Education
- Important to take medications at regular intervals
- MEDICATIONS MUST BE TAPERED OFF AND NOT STOPPED ABRUPTLY DUE TO RISK OF ADRENAL INSUFFIENCY (ADDISONS DISEASE)
- These medications are used for patients with adrenal insufficiency to replace corticosteroids
FLUDROCORTISONE IS THE ONLY MINERALCORTICOID REPLACEMENT AVAILABLE (ALDOSTERONE)
Hydrocortisone (Cortef)
- Synthetic Cortisol
- Suppresses inflammation and immune responses by inhibiting migration of leukocytes and phagocytes
ADVERSE EFFECTS
- Adrenal suppression and iatrogenic Cushing’s syndrome
Dexamethasone
- Synthetic steroid that mainly effects glucocorticoids not mineralocorticoids
- Used to diagnose crushing’s syndrome and treat allergic/inflammatory conditions
ADVERSE EFFECTS
- GI distress, headache, insomnia, restlessness, depression
Fludrocortisone (Florinef)
- Potent Mineralcorticoid replacement therapy
- Used for Addison’s disease, hyperaldosteronism, and adrenal hyperplasia
ADVERSE EFFECTS
- Hypertension, edema, cardiac enlargement, hypokalemia
