ENDOCRINE DISORDERS Flashcards
WHAT CONTROLS AND RELEASES THE
PITUITARY HORMONES
HYPOTHALAMUS
POSTERIOR PITUITARY GLAND (PPG) (SECRETES 3) (LEADS TO 2 D/O)
Oxytocin → stimulation of uterus during childbirth, milk ejection after birth
ADH (antidiuretic hormone) → increases water reabsorption in the kidneys (causes vasoconstriction)
PPG SECRETES: (3)
*ADH, vasopressin
* Oxytocin
- Hyper: (ADH)-SIADH*
- Hypo: (ADH)-DI*
-Tumors: 95% benign
ANTERIOR PITUITARY GLAND (APG) (6)
APG SECRETERS: (6)
FSH, LH, prolactin, ACTH, TSH, GH
Hyper: *Cushing syndrome *(ACTH), gigantism (children)(GH), acromegaly (Adult)(GH)
Hypo: dwarfism, panhypopituitarism(GH)
SURGERY AND COMPLICATIONS OF
POSTERIOR PITUITARY GLAND
POST-OP CARE= PREVENT Complications (5)
*Surgery: *
Hypophysectomy (transsphenoidal–endoscopic transnasal approach) *
(Upper gum to intro nasal/cranial area)
POST-OP CARE= PREVENT Complications:
*CSF leaking/infection
*Diabetes insipidus
*Hypopituitarism
*Visual disturbances
Diabetes insipidus (DI)
(DI): deficiency of ADH (vasopressin)
Hypo of ADH → cannot hold water (DI)
Excessive thirst and large volume of diluted urine (↑UO)
Very low Urine Specific Gravity (↓USG; less than 1.006)
Dehydration, hypernatremia, weight loss, hypotension, fatigue, HA
Priority: extreme Dehydration (d/t shock)
*↑ Output ↓Specific gravity ↑Na ↓Wt ↓Bp Fatigue, Headache
Replacement of ADH –
Desmopressin (DDAVP)-– effective result = ↓UO
TX FOR DI
Treatment → replacement of fluids/ADH → DESMOPRESSIN (DDAVP) → to evaluate treatment urine output ↓
Treatment: Increase fluids
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
(SIADH) → ↑↑ADH causing excessive fluid retention → fluid overload
Retain fluids–water intoxication/ dilutional hyponatremia / seizure
↓UO, ↑USG, Weight gain, hypertension, HA, N/V, anorexia, ↓ LOC, Often nonendocrine origin;
*bronchogenic carcinoma (malignant lung cells synthesize and release ADH) *
TX FOR SIADH
Treat UNDERLYING cause:
*PRIORITY: Restrict fluids and get rid of fluid (diuretics) hyponatremia ↑ r/o seizures→ seizure precautions
IV fluids (NS or 3% hypertonic saline) + diuretics;
effective result =↑UO
clinical manifestation for SIADH
↓UO, ↑USG
Weight gain, hypertension, HA, N/V, anorexia, ↓ LOC
can be caused by cancer that has spread within the lungs, tumors are releasing ADH → bronchogenic carcinoma (severe SOB, ↓wt, severe cough, Na 128)
THROID HORMONES AND WHAT IT CONTROLS
TSH, T3, T4 also produces calcitonin
Triiodothyronine (T3) → more potent
& more rapid-acting than T4
Thyroxine (T4) → measured with TSH to diagnose
- Iodine is contained in thyroid hormone
*Calcitonin is secreted in response to high plasma calcium level and increases calcium deposition in bone
THYROID HORMONES LAB VALUES
PRIMARY AND SECONDARY
Primary thyroid disease is the thyroid is the problem Secondary thyroid is R/T problems in the pituitary gland
Normal
TSH: 0.5 – 3.0 → > 4 = hypo
T4: 0.9 – 1.7 the higher the # = hyper
TSH (Pituitary produced)
T4 (thyroid produced)
Primary Hypothyroidism: TSH↑/T4↓
Neg feedback is ↑ TSH to try and stimulate the ↓ T4 Problem is in the thyroid
Secondary Hypothyroidism TSH↓/T4 ↓
Both levels are low b/c there is not enough TSH from pituitary to stimulate T4
Primary Hyperthyroidism TSH↓/T4↑
Problem is in Thyroid so T4 ↑ but pituitary gland is TSH ↓ not trying to stimulate
Secondary Hyperthyroidism TSH↑/T4↑
Pituitary gland is overproducing TSH so T4 is also high
THYROID DX TEST (6)
TSH the single best screen test/ monitoring thyroid replacement test
* Serum free T4* / T3 and T4
* Thyroid antibodies: antithyroid antibodies present
→hashimoto’s thyroiditis & Graves’ disease
Radioactive iodine uptake (RAIU):→ use* I 123*
→high uptake in hyperthyroidism (up to 90%)
NPO 6-8 hrs/LMP check –contraindicated in pregnancy
• Avoid contact with pregnant women or children
• Flush toilet 2-3 x after use
• Increase hydration
-use disposable utensils
-Instruct patient to *drink increased amount of fluids for 24 to 48* hours unless this is contraindicated. -Radionuclide will be eliminated in 6 to 24 hours. *Fine-needle biopsy (FNA) * *Thyroid scan*, radioscan, or scintiscan: -Thyroid scan used to look for nodules/ tumors * Serum thyroglobulin: to detect persistent or recurrent thyroid carcinoma/CANCER
What is Hypothyroidism
and what causes it ?
Deficiency of thyroid hormone ; *Slow metabolic rate *
Causes:
* Autoimmune thyroiditis*
(Hashimoto’s disease) – most common cause
Affects women 5X more frequently than men
Can also be caused by older age → atrophy of gland Previous tx for hyperthyroidism → iodine131/ thyroidectomy
Radiation to head/neck for cancers
Medications → lithium, iodine compounds, antithyroid meds
CLINICAL MANIFESTATION OF
HYPOTHYROIDISM
Early symptoms may be nonspecific
Fatigue; brittle & thick nails dry hair, skin; numbness and tingling of fingers (*paresthesias); amenorrhea or menorrhagia, cold intolerance, bradycardia; weight gain
subdued emotional and mental responses;
slow speech; tongue, hands, and feet may enlarge; constipation; hoarseness or husky voice,
personality and cognitive changes;
cardiac (↓CO, MI, ↑Chol &TRG) and
respiratory (low exercise tolerance, dyspnea) complications
COMPLICATIONS OF HYPOTHYROIDISM (2)
AND PRIORITY TREATMENTS
Myxedema coma/crisis- medical emergency;
-causes:
↓(LOW)T3
change of LOC to stupor, coma, & death D/T → ↓T3
↓body temp (hypothermia),↓BS (hypoglycemia),
↓Na (hyponatremia), ↓o2(hypoxia), ↓C.O (cardiac output), ↓basal HR, ↑BP, ↑CO2(hypercarbia)
-Increased risk for pts who are undiagnosed and
elderly who develop some type of infection or
increased stress, trauma.
TX. t3 therapy (t4 therapy slower effect but can work)
Cardiovascular collapse → hypothermia, hypotension, hypoventilation*
PRIORITY: maintain airway, O2
TX: IV thyroid hormone, IV fluids, glucose, steroids
MEDICAL MANAGEMENT FOR
HYPOTHYROIDISM (6//7)
Treatment:
Synthetic levothyroxine -replacement therapy
Start low-dose and MONITOR CLOSELY → need to restart body metabolism slowly to prevent MI (ISCHEMIA SYMPTOMS) and overstimulation of heart.
-Effective tx will show → ↑HR ↑RR ↑BP ↓Wt
Medication given in AM before breakfast on empty stomach
Monitor labs and ↑ dose every 4 – 6 week intervals as needed
Lifelong therapy
*↑Sensitivity to hypnotic & sedative agents;
→ reduce dosage
DIET FOR HYPOTHYROIDISM (5)
↑fiber ↑fluids (push fluids)
↓calorie ↓cholesterol ↓low fat
what is
HYPERTHYROIDISM ?
most common d/o?
What Lab values seen in a Diognostic test ?
overactive metabolism (release of thyroid hormone)
(Grave’s Disease) autoimmune D/O (most common)
-8x more women; 20-40 y/o mostly
↓ TSH and ↑ free thyroxine (free T 4), RAIU (I 123)
S/S of HYPERTHYROIDISM
or ‘THYROTOXICOSIS’
Palpitations, tremors. heat intolerance *
Brittle/thin nails Amenorrhea/no periods
Goiter *↓Wt * Possible dysrhythmias
Exophthalmos
Flushed skin/warm/moist Heart Failure
↑HR ↑BP ↑ Appetite & dietary intake ↑GI (diarrhea) ↓Cardiac Output d/t ↑HR
WHAT IS Exophthalmos ?
NURSING INTERVENTIONS FOR IT? (5)
fluid build-up behind eye pushes eye forward:
N.I: Artificial eye drops, dark glasses, reduce salt intake, ↑HOB, tape eyelids closed to sleep → will not return to normal 100%
WHAT IS Thyroid storm (Thyrotoxic crisis) ?
WHO. ARE AT RISK? Who are PRIORITY?
NURSING INTERVENTIONS?
Thyroid storm (Thyrotoxic crisis) –
-Excessive amounts hormones released leading to
→ Life-threatening MEDICAL emergency →
especially accompanied w/ FEVER →[PRIORITY]
(Thyroidectomy pts. at risk)→ from ↑stressors
N.I.
(Maintain patent airway, Reduce fever, Replace fluids)
Eliminate/manage stressor) → put pt. away from station
-Tracheostomy at bedside for thyroidectomy
WHAT are the TWO
Antithyroid medication tx? SE?
Antithyroid medications → Proylthiouracil (PTU)
Methimazole (Tapzole)
-Good results in 4 to 8 weeks (full effect in 2-3 mo)→ Agranulocytosis with Methimazole →
↓WBC (agranuloscytosis) → ↑ r/o infection: notify MD of any S.E. sore throat, diarrhea
What med class provides a symptomatic relief of thyrotoxicosis ?
Beta Blocker → Propranolol (Inderal) → used to lower and stabalize HR/BP, ↓ cardiac disfunctions
Medical Management of Hyperthyroidism?
Medications?
(Antithyroid Agents)-
*Propylthiouracil [PTU] - good results in 2-3 months
*Methimazole [Tapazole] - good results in 2-3 months
*Sodium or potassium iodine solutions - - delayed response 2- 3 months
*Saturated solution of K+ iodine (SSKI) [Lugol’s solution] - delayed response 2- 3 months
*Radioactive I131 PO therapy [one-time tx] - delayed response 2- 3 months
*Beta-blockers (propranolol): - symptomatic relief of thyrotoxicosis
*Dexamethasone (corticosteroid)- treat crisis and decreased thyroid hormone and vascularity of gland
- Reduce activities of thyroid hormone and ↓vascularity of thyroid glands; Used before surgery and to treat crisis
** possible SE of all hyperthyroid treatments is the development of hypothyroidism
Radioactive Iodine
I 131 PO therapy (5)
TREATMENT?
(Iodine goes straight to thyroid → Delayed response
→ 2 to 3 months)
* Avoid contact with pregnant women or children
* Flush toilet 2-3 x after use
* Increase hydration
*use disposable utensils
TX is Surgery: → subtotal/total thyroidectomy
Treatment or surgery may result in hypothyroidism -Need for lifelong thyroid hormone replacement-
tx w/ Levothyroxine d/t hypothyroid
Subtotal or Total
Thyroidectomy
-removal of part or all of your thyroid
Treatment of choice for thyroid cancer
Potential Risk of Thyroid storm d/t sudden release of hormones during surgery removal and ↑stress
**Administer iodine → ↓ vascularity & bring to euthyroid conditions (eu- means stable/normal)
preop teaching for Thyroidectomy (5)
Education:
↓ caffeine and stress stimulants
Leg exercises, head support, neck ROM
Thyroidectomy Postoperative Care (5)
(PREVENTING COMPLICATIONS)
-
Monitor respirations; potential airway impairment
-Oxygen, suction equipment, tracheostomy tray in
patient’s room
-Semi-Fowler’s position, support head with pillows
-Avoid neck flexion & tension on suture line - Monitor for Laryngeal nerve damage
assess voice for Hoarseness, but limit talking
(d/t edema to vocal cord)
* Persistent > 3-4 days* or worsening w/ stridor,
high-pitched voice, respiratory obstruction or
restlessness – Notify to HCP* - Monitor potential bleeding and
hematoma formation; →Check both anterior and posterior of dressing for bleeding →blood may pool on back of neck with dressing in front remaing dry
4.Potential hypocalcemia r/t injury or removal
of parathyroid glands; →monitor for hypocalcemia
(Tetany – numbness and tingling of face &
extremities, bronchospasm & laryngospasm)
→* Treat with IV calcium gluconate
-
Monitor thyroid storm → d/t rapid release of
thyroid hormone and added stress
Parathyroid Glands
-Four glands on the posterior thyroid gland
*Parathormone (parathyroid hormone/PTH)
PTH →regulates calcium and phosphorus balance
↑ PTH = ↑ calcium level in blood → ↑ Ca absorption→
↑ Calcium = ↓ Phosporus → from ↓PTH
Calcium involvement
Normal labs
Ca is involved with:
nerve & heart conduction,
muscle contractions,
Prothrombin synthesis (coagulation)
Peripheral vassal constriction (↑BP)
affecting GI system→ slows down intestine →↓peristalsis
Normal Ca → 8.5-10.5 mg/dL
GOAL → 9-10.5 mg/dL
Hyperparathyroidism
MANIFESTATION
↑serum calcium, osteoporosis, renal calculi, *nausea, vomiting, constipation (distention), hypertension, cardiac dysrhythmias
-apathy, fatigue, and muscle weakness
-increase Ca in blood is coming from breakdown of bones → leaving bones weaker Osteoporosis
Psycological mainisfestations:
Airway obstruction d/t extreme muscle weakness Severe neuro, CV, and renal failure
HYPERPARATHYROIDISM TX AND DIET
TX:
* Parathyroidectomy *
*Hydration therapy: *risk of renal calculi →renal failure *Furosemide (Lasix) [LOOP DIURETICS]– to excrete calcium from urine
* Encourage mobility reduce calcium excretion from bones
↑ Ambulation ↑ Fluids ↓ Dietary Calcium
- Diet: encourage fluid, avoid excess or restricted calcium
What is Hypercalcemic Crisis?
Treatment?
Ca > 13mg/dl→ severe compromise of multiple systems Airway obstruction d/t extreme respiratory muscle weakness , Severe neuro, CV, and renal failure
Tx: Rehydrate w/ large IV volume
Furosemide to get rid of serum Ca
Calcitonin = ↑ bone reabsorption of Ca Bisphosphonates inhibits bone reabsoprtion →
↑ Ca → Dialysis to remove Ca (↓Ca)
Fosamax (alondranate) →tx for osteoporosis d/t biphosphonate medication
Hypoparathyroidism & IT’S Clinical Manifestations (9)
Deficiency of parathormone usually d/t surgery— thyroidectomy, parathyroidectomy, or radical neck dissection.
results in hypocalcemia and hyperphosphatemia
Manifestations include :
Tetany, hypotension, bradycardia,
N/V/D, abdominal pain (cramps)*
- Chvostek’s sign*: tapping facial nerve causes twitching of mouth, nose, and eye
Trousseau’s sign: carpopedal spasm via BP cuff>3min
(both signs indicate hypocalcemia]
Management of Hypoparathyroidism
- GOAL of Calcium → 9-10.5 mg/dL
*Treat/replace with a Combination of
→Calcitrol, calcium, magnesium, and vit. D2 or D3
Calcium gluconate IV –given after thyroidectomy →
↓tetany and fix hypocalcemia
-May also use sedatives such as pentobarbital to decrease neuromuscular irritability and in case of seizure activity
-Limit environmental stimulation → ↓ noise, drafts, bright lights and no sudden movement for tetany
Osteoporosis
can develop with both hyper- and hypo- parathyroidism
Hyper because it is pulling calcium from bones and leaving them weak
Hypo because there isn’t enough to support the bones
Secondary Hyperparathyroidism
→ body attempts to fix the low calcium resulting from kidney damage and high levels of phosphorus d/t overstimulating parathyroid hormone →
kidneys make vit D → to absorb calcium
→ No kidneys, No vit D → no calcium absorption
Diet for Hypoparathyoidism
Diet: ↑ Calcium + ↓ Phosporus
Diet: Avoid milk, milk products, organ meat, egg yoke d/t high phosphorus
Spinach, chocolate, peanuts d/t high oxalate that binds with calcium and ↑ Ca loss through stool
↑ Vit D to help calcium be absorbed
High phosphorous needs to be brought down
- Amphojel →(phosphate binders) used in chronic kidney failure/disease to bind to phosphorous and eliminate through GI
How many parts are in the Adrenal Glands?
WHAT DO THEY DO ?
2 parts → medulla (inner) & cortex (outer)
*Adrenal medulla- fx as part of ANS
*Catecholamines→epinephrine and norepinephrine
→ neurotransmitters of SNS
*Adrenal Cortex is responsible for adrenocortical activity (ACTH)
(3 S’s: Sugar, Salt, Sex)
[GMA]
Glucocorticoids → (cortisol/stress hormone) →
Regulate metabolism, ↑ blood glucose; Critical in
physiologic stress response
Mineralocorticoids → (mainly aldosterone){RAAS) → works on kidney proximal tubules → ↑ Na reabsorption and ↓ K through excretion
Androgens → (sex hormones) → growth/development, sexual activity
Pheochromocytoma
Adrenal Medulla tumor/tumor within the kidneys
Triad of symptoms: headache, diaphoresis & flushing, palpitations in patients with hypertension
Triad of Symptoms = Five H’s, Adrenergic & hypermetabolism symptoms (flushing palpatations), & Paroxysmal form: “impending doom”
Five H’s – Hypertension, Hyperhidrosis, Headache, Hypermetabolism, Hyperglycemia
*Adrenergic & hypermetabolism symptoms (flushing palpatations) = chest pain, abdominal pain (N/V/constipation), mydriasis, heat intolerance, weight loss *
Paroxysmal form: “impending doom” - extreme high BP (250/150), anxiety, vertigo, dyspnea – life-threatening risk for cardiac dysrhythmia, stroke, acute renal failure
DIAGNOSTIC FOR Pheochromocytoma
Diagnostic: urine and blood test to measure
→ Plasma catecholamines and catecholamine metabolites (BP HORMONES)
(metanephrine (MN) and vanillylmandelic (VMA))
→ 24-hour urine collection is needed
Pheochromocytoma Treatment
Unilateral or Bilateral Adrenalectomy
Tx: Removal of adrenal gland (unilateral or bilateral)
Bilateral Adrenalectomy: life-long corticosteroids replacement
*Unilateral adrenalectomy: glucocorticoid replacement–up to 2 years
Adrenal Cortex is responsible for adrenocortical activity (ACTH)
Problem can also be if Pituitary gland is producing →
↑ACTH → ↑adrenal function
Tumors in other parts of body can also cause extra hormones → ↑ACTH
Cushing Syndrome (2)
due to *1.excessive adrenocortical activity (↑ACTH ) or *2.corticosteroid medications
-↑ACTH: ACTH-secreting pituitary adenoma (sitting on medulla cortex) -Adrenal tumors/ Ectopic ACTH production by tumors
CUSHING SYNDROME MANIFESTATION
Hyperglycemia, Hypernatremia,
Hypokalemia, Hypocalcemia *
↑weight gain, central type obesity w/ “buffalo hump”, thin extremities, moon-face, acne, *hirsutism (↑ abnormal facial hair),hypertension, PUD, ↑WBC, ↑chol, menstrual irregularity hyperpigmentation striae, osteoporosis, muscle wasting
D/T- Corticosteroid medication:
*r/o ↑ Osteoporosis (for pts w/ long term corticosteroid put on Ca)
*Diabetes-related symptoms → ↑slow wound healing, r/o infection
*↑Corticosteroids r/o peptic ulcers → put on PPI
DIAGNOSTIC TESTING FOR
CUSHING SYNDROME
Dexamethasone suppression test
1 mg dexamethasone PO at 11 pm→measure
cortisol level at 8 am the following morning →suppression of cortisol less than 5 mg/dL→
indicates the hypothalamic-pituitary-adrenal axis are properly functioning→ *Normal= A. Pituitary makes less ACTH →Adrenal Cortex make less cortisol (glucocorticoids)
**Cushing Syndrome= If A. Pituitary makes less ACTH → Adrenal Corterx still making cortisol (glucocorticoids)
same 24-hour urine collection and blood test as Pheochromocytoma; Urine cortisol levels are higher than the normal range of 80 to 120 mcg → in 24 hours indicate Cushing syndrome
Nursing Interventions for Cushing Syndrome
*Treatment depends on cause (surgery)
-If problem is pituitary gland then then removal of pituitary or adrenal glands if adrenal is problem
*If cause is Iatrogenic r/t illness by Tx or examination
-If problem is medication → taper off the medication or try to lower the dosage
Postoperative care for
Cushing Syndrome (5)
*↑ Risk of hemorrhage
* *High doses of corticosteroids administered IV during and several days after surgery →
↑ risk of infection and ↑ delayed wound healing
- Report any significant changes in vital signs
*-Monitor for acute adrenal insufficiency
→ Addisonian Crisis
DIET FOR CUSHING SYNDROME
*Diet: ↓Na ↑K ↑protein ↑Ca ↓calorie
*Banana, Orange
Hyperaldosteronism
*too much ↑↑ aldosterone (via Mineralocorticoids)
→ *↑ (Na/sodium) fluid retention→ (↑Na ↑Bp) with *excessive (↓↓K) potassium loss + (hydrogen ion excretion)↓H+
→Muscle weakness, Cardiac dysrhythmia
symptoms of Hyperaldosteronism (6)
*↑Na (HYPERNATREMIA)
*↑Bp (HYPERTENSION) w/ hypokalemic alkalosis
*↓ K (alkalosis) (HYPOKALEMIA)
*Muscle weakness
*Cardiac dysrhythmias
*No Edema
Treatment for Hyperaldosteronism
Tx:
*Spironolactone (potassium-sparing diuretic) → will help get rid of fluids without getting rid of potassium
-Calcium- channel blockers to ↓Bp
-Dexamethasone to ↓ hyperplasia (enlargement of organ) = Cushing Syndrome
Surgical Tx: Adrenalectomy
-removal of adrenal gland or to remove adenoma
Adrenocortical Insufficiency
/ Addison’s disease (2)
(1) *Lack of ANY of the adrenal cortex hormones [ACTH] →Lack of Glucocorticoids/Mineralocorticoids/Androgens
(2) *Iatrogenic: d/t adrenal suppression by exogenous
steroid use/ surgical removal of adrenal gland
When on long-term corticosteroids→ the adrenal gland suppresses its production → if you suddenly stop meds the body takes time to start back up → will cause Addison’s → meds have to be tapered off because the body needs time to wake up
MANIFESTATIONS OF
Adrenocortical Insufficiency/ Addison’s disease
*Hypoglycemia, Hyponatremia, Hyperkalemia,
Hypercalcemia, fatigue, muscle weakness,
GI disturbances (N/V/D/cramps due to high K)[DKA PTs] hyperpigmentation (bronze-colored skin pigmentation of skin and mucosa), hypotension (orthostatic), weight loss, mental changes (confusion), apathy, emotional liability
Addisonian Crisis/
Adrenal Crisis
Addisonian crisis:
*classic signs of circulatory shock (hypovolemic shock) cool & clammy→Hypoglycemia with dehydration
**Triggers: ↑stress (physical, psychological), infection, surgery; *Sudden withdrawal of corticosteroid hormone therapy; lack of cortisol →prevents the body from responding appropriately;
**Severe hypotension, ↑pulse, ↑respiration, severe headache *
Nursing Intervention for
Addisonian Crisis/
Adrenal Crisis
Diet?
PRIORITY: VAD [IVF] with immediate high dose of steroid & IV (D5NS), vasopressors
*Moniotor V/S (postural BP) + Sodium levels → fix levels
*Reduce stressors, ↓ stimulation, monitor v/s, electrolytes
Diet: ↑protein ↑ carbs adequate Na-
Treatment for Addisonian Crisis/
Adrenal Crisis
Hormone therapy: lifelong replacement
*Hydrocortisone replacement (Give in AM = stay active)
*Increase during periods of stress (fever, influenza, extraction of teeth and rigorous physical activity, such as playing tennis on a hot day or running a marathon)
-If vomiting or diarrhea occurs, notify the health care provider immediately → electrolyte replacement and parenteral administration of cortisol may be necessary
*Fludrocortisone (Florinef) → replacement of mineral corticosteroid→ once in the morning
* Monitor for signs and symptoms of corticosteroid deficiency and excess
Emergency kit: 100 mg of IM hydrocortisone → with written instructions
Corticosteroid Therapy
*Widely used drugs to treat →. Most important drug for anti-inflammation
adrenal insufficiency (ACTH LOW) d/t removal of tumor
suppress inflammation & autoimmune response,
control allergic reactions,
reduce transplant rejection
Patient teaching-
* Timing of doses: Should be taken in the morning with food to reduce gastric irritation
* Need to take as prescribed, tapering required to discontinue or reduce therapy
*Discharge instructions after bilateral adrenalectomy *
-Wear MedicAlert bracelet at all times
-Avoid exposure to extremes of temperature, infection, and stress
-Teach how to adjust medication and when to call health care provider
-Lifetime replacement therapy
