Endocrine lecture EXAM 3 Flashcards
Is the endocrine system positive or negative feedback
Negative feedback
Anterior pituitary hormone production (just the stuff for the lecture)
-ACTH )Adrenocorticotropic hormone
-TSH , Thyroid stimulating hormine
Thyroid hormone production
T3: Tri-iodothyronine
T4: Thyroxine
Calcitonin
Parathyroid hormone production
-PTH: Parathyroid hormone
Adrenal gland hormone production (For this lecture)
-Cortisol (Glucocorticoid)
-Aldosterone (Mineralcorticoid)
Endocrine pathway for hormones
-Hypothalamus -> Pituitary -> hormone site
Hypothalamus
-Primarily maintains homeostasis in the body
-Links the nervous system with the endocrine system via the pituitary gland
-Secretes inhibiting or releasing hormones which stim/inhibit the anterior pituitary
Adrenocorticotrophic hormone (ACTH)
-Stims the adrenal cortex, making cortisol
-If there isnt enough cortisol in circulation, ACTH levels will rise
Thyroid stimulating hormone (TSH)
Stimulates the thyroid gland to make t3 and t4
-Negative feedback system
-Iodine is needed too, for the production of TH
-Thyroid hormone controls metabolic activity
-TH is made in the follicular cells in the thalamus
Calcitonin
-Made in C cells
-Secreted when there is a high plasma calcium level, leading to a reduction in Ca in the blood
-Works opposite to PTH
-Moves the Ca back into the bone
Hypothyroidism
-Inadequate amounts of T3/T4
-Decreases the metabolic rate of all body systems
-Primary secondary and tertiary
Primary hypothyroidism
-Dysfunction of the thyroid gland
-Caused by:
-Autoimmune
-Surgical removal of part or the entire thyroid gland
-Radiation to thyroid gland
-Meds
-Thyroiditis, viral infection, iodine (too much too little), congenital
Hashimoto’s thyroiditis
Auto immune attack of the thyroid causing primary hypothyroidism
Meds causing hypothyroidism
-Amiodarone
-Lithium
-Interferon, Interleukin-2, Immunotherapy (Cancer drugs)
Secondary hypothyroidism
-Failure of ant pituitary to stimulate the thyroid gland by inadequate secretion of TSH (tumor or radiation)
Tertiary hypothyroidism
-Hypothalamus doesnt produce Thyroid release hormone (TRH)
Hypothyroidism S+S
-Everything slows down
-Fatigue (Most common)
-Forgetful
-Depression
-Thinning of hair
-Dry flaky skin and brittle nails
-Constipation
-Intolerance to cold (feel cold all the time)
-Abnormal menstraual cycles
-Weakness
-Bradycardia
-Hypotension
-Edema
-Accelerated atherosclerotic disease
Hypothyroidism diagnostics
-Radioisotope I-123: Uptake will be slow in hypothyroidism (Slow absorption=low thyroid)
-EKG: Sinus brady, cardiac dysrhythmias (Later sign)
What labs are decreased in hypothyroidism
T3/T4
TSH in SECONDARY hypothyroidism
What labs are increased in hypothyroidism
-TSH in primary
-Antibody test if there is a disease process involved
Hypothyroidism treatment
-Meds: Essentially TH
-Need to take meds for life
-Take in the morning on empty stomach with water (8 oz)
-NPO except water for 60 min after taking thyroid meds, no other meds at the time
-No supplements (Ca, vitamin D, Mg, minnerals, iron) for at least 4 hrs from levothyroxine
-Take at the same time every day
-Start dose low and titrate up based on blood work
-Can affect levels of digoxin, warfarin, and may need increased insulin (Increased blood sugar)
Hypothyroidism in elderly
-Only treat if symptomatic, with lowest dose possible
-Huge risk of A-fib, Tachycardia
Hypothyroidism meds (T4)
-Levothyroxine (Synthroid, Euthyrox, Euthyroid)
-Synthetic T4
Amour Thyroid
-Dried pig thyroid
-Contains T3+T4, hard to regulate serum levels as a result
Liothyronine
-T3, may be used with T4
-Short acting
What supplements cant you take with levothyroxine
-Ca
-Vitamin D
-Mg
-Minerals
-Iron
-For at least 4 hrs after
Inpatient mgmt of hypothyroidism
-Cardio changes: (Low BP/HR dysrhythmias), Chest pain edema
-Monitor weight
-Monitor mental status changes, Safety? (long time without treatment)
- Gradual activity with lots of rest periods
-Anti-embolism stockings
-Resp monitoring, Lung sounds, RR, ABG
-*Low cal high bulk diet, fluids (Gaining weight from disease)
-Monitor bowel movements
-Reassure pt, symptoms are reversible and they take time
-Med admin
-Activity intolerance
Hypothyroidism teaching
-Meds might take a couple weeks: Pt cannot adjust meds in the mean time to feel better
-Avoid certain supplements with meds
-Follow up with provider
-Diet and weight loss promotion and improve bowel function
-When to call provider
When to call provider hypothyroidism
-S+S pf hyperthyroidism (Too high of dose)
-Risk of thyrotoxicosis
A nurse is collecting data from a client who is suspected of having an endocrine disorder and is scheduled for diagnostic testing that involves the use of a contrast medium. The nurse would inform the physician if the client stated which of the following?
A. “My father had diabetes when he got older.”
B. “I have an allergy to shrimp and shellfish.”
C. “I take a multivitamin every day.”
D. “Years ago, I took a steroid for my asthma.”
B. “I have an allergy to shrimp and shellfish.”
Radioscope I-123
-Slow absorption=hypothyroidism
-Contraindicated in preg, iodine or shellfish allergy (Depending on the extent they can pre med)
- if had a recent radiology exam with iodine containing contrast, need to wait 8 weeks to preform this
-Low iodine diet for best results
Myxedema Coma
-Life threatening hypothyroidism coma
-Occurs if hypothyroidism isnt treated properly or a major stressor occurs
Myxedema coma: Cardinal signs
-Hypothermia
-Altered mental status
-Cardio depression (Hypotension and bradycardia)
-Also resp failure
-Hyponatremia
-Hypoglycemia
-Coma
Myxedema coma mgmt
-ABC first and foremost
-Monitor for MI and acute coronary syndrome
-ECG: Bradycardia
-Monitor mental status
-ABG (hypoxia, hypercapnia, respiratory acidosis)
-Monitor body temp, Blankets are fine, do NOT apply direct heat
-Fluid replacement, NS (I+O)
-IV bolus levothyroxine -> IV until stable then oral
-Monitor for hypoglycemia
-Monitor for sources of infection and stress which can cause this (UTI, stress, Sepsis)
Why dont you apply direct heat Myxedema coma
-Vasodilation causing vascular collapse
Hyperthyroidism
-Everything is fast
-Too much TH
-Increased metabolic rate and o2 consumption
Causes of hyperthyroidism
-Graves disease: Autoimmune disease caused by excessive stim of thyroid by circulating immunoglobulins
-Thyroid storm: Excessive output of TH
-Thyroiditis
-Toxic Nodular Goiter: Thyroid nodules cause excessive secretion of T3 and T4, more area more hormone
-Exogenous Hyperthyroidism
Graves disease
-Autoimmune causing hyperthyroidism
-Eyes popin out (Opthalmopathy)
Graves opthalmopathy
-Eyes poppin out
-Not equal, lids are retracted
-pt looks down, lid lags behind
-Needs to be referred to a specialist
-Affects cranial nerves 3/6
Main hyperthyroidism S+S
-Nervousness, jittery, anxious
-Tachycardia/palpitations
-Tremors
-Heat intolerance
-Excessive sweating
-Frequent stools
-Insomnia
Other S+S hyperthyroidism
-Increased appetite
-Weight loss
-Exophthalmos: edema in the extra-ocular muscles and fat tissue behind eye (Graves)
-Elevated systolic BP
-Cardiac dysrhythmias, A-fib
Labs decreased Hyperthyroidism
TSH
Labs increased hyperthyroidism
-T3/T4
-Thyroid stimulating immunoglobulins (TSI), For graves
-Thyrotropin receptor antibodies (TRAB) also graves
Nursing mgmt: Hyperthyroidism
-Report temp increase greater than 1 degree
-Monitor EKG for cardiac stuff
-Dont palpate the thyroid, makes more TH
-Minimize activity, lots o rest periods (Fast metabolism)
-Calm, cool environment, cool showers, reduce room temp
-High cal high protein meals and snacks
-I+O
-Eye protections for the bulgin eyes
-Prepare for surgery
-Dosing for the drugs
Methimazole (Tapazole)
-Treatment of choice for hyperthyroidism
-Thionamide
-Inhibits the synthesis of TH
-Does not remove hormone already present
-Need to monitor CBC for agranulocytosis (Severe WBC drop), Thrombocytopenia, and increased LFT for liver tox
Propylthiouracil (PTU)
-Thionamide
-Used of methimazole is not tolerated
-Liver tox (elevated LFT, dark urine, jaundice)
-Inhibits synthesis of TH
-Used in hyperthyroidism
Sodium or potassium Iodine (Lugol’s soln, SSKI)
-Inhibits release of TH
-Used short term before surgery in hyperthyroidism
Beta Blockers (Thyroid)
Used in hyperthyroidism for treating tachycardia palpitations
Only true hyperthyroidism treatment
-Radioactive I-131 therapy
-Surgery
Radioactive I-131 therapy
Used in hyperthyroidism to ablate the thyroid into not producing TH
-Will become hypothyroid after, and will require meds
-After the procedure you need to avoid preg women, children for a week
-Also need to use another toilet and wash clothes separate, dont share saliva
Surgery, thyroid
Can be subtotal or total thyroidectomy
-Need some or full thyroid hormone replacement
Post op thyroidectomy care
-ABC (Airway impairment, laryngeal spasm, swelling)
-Bleeding and hematoma formation, check the dressing
-Semi fowlers position, supporting the head and neck
-NPO until cleared by speech patho
-Assess voice, hoarseness, laryngeal nerve injury (Vocal cord paralysis )
Patient education: post op thyroidectomy
-Check S+S of hypocalcemia related to destruction of parathyroid gland
-Check Chvostek sign
-Check Trousseau sign
-Assess for c/o numbness/ tingling around mouth and distal extremities (LET PROVIDER KNOW)
-Muscle cramping or spasm
Trousseau Sign
-Puff Bp cuff up for 1-4 min
-Hand and fingers spasm, in palmar flexion= positive
-Shows early tetany, hypocalcemia if positive
-Italian hand
Chvostek sign
-Tappin the face below below and infront of the ear
-Face twitching occurs on one side of the mouth, nose and cheek is positive
Thyroid storm
-Thyrotoxicosis, Thyroid crisis
-Surge of TH in the blood which further increases metabolism
-Medical emergency, needs treatment
-High mortality rate
Thyroid storm causes
-Uncontrolled hyperthyroidism (Graves disease, infection, trauma, emotional stress, DKA, Dig toxicity, after RAI)
Thyroid storm findings
-Hyperthermia
-Hypertension
-Delirium
-Vomiting, ab pain
-Tachydysrhythmias
-Chest pain
-Dyspnea
-Palpitations
-Hyperthyroid symptoms but accelerated
Thyroid storm mgmt
-ABC (Airway and oxygenation)
-Treat hyperthermia with cooling blanket, icepacks , Tylenol
-Trach tray in room for emergency intubation
-Cont ECG monitoring
-IV hydration to prevent vascular collapse, I+O
-Give meds
Why cant you give aspirin with thyroid storm
It increases free T4 making the issue worse
Meds thyroid storm
-IV fluids
-Methimazole or PTU to prevent further synthesis or release of hormone
-Sodium Iodine to decrease the output of T4 from the thyroid gland, 1 hour after methimazole or PTU
-Admin Beta blockers to block symp nervous system effects
-Glucocorticoids if adrenal insufficiency is suspected or to treat the shock
What pharmacologic therapy does the nurse anticipate administering when the patient is experiencing thyroid storm? (Select all that apply.)
A. Acetaminophen
B. Iodine
C. PropylthiouracilPTU
D. Synthetic levothyroxine
E. Dexamethasone (Decadron)
A. Acetaminophen
B. Iodine
C. PropylthiouracilPTU
E. Dexamethasone (Decadron)
Ya just dont give TH during hyperthyroidism
Treatments for thyroid storm: a hypothermia mattress or blanket, ice packs, a cool environment, hydrocortisone, and acetaminophen (Tylenol); propylthiouracil (PTU) or methimazole to impede formation of thyroid hormone and block conversion of T4 to T3, the more active form of thyroid hormone; and iodine, to decrease output of T4 from the thyroid gland.
The nurse is assessing the endocrine system of a client. Which statement indicates to the nurse that the client is experiencing a condition that affects endocrine function? Select all that apply.
A. “I cannot stand to be in hot weather.”
B. “I do not have any energy to do what I normally do.”
C. “I do not know why my skin has gotten so dry lately.”
D. “It seems like the fat on my legs moved to my stomach.”
E. “I get up in the middle of the night to void only occasionally.”
A. “I cannot stand to be in hot weather.”
B. “I do not have any energy to do what I normally do.”
C. “I do not know why my skin has gotten so dry lately.”
D. “It seems like the fat on my legs moved to my stomach.”
E is normal
Parathyroid glands
- 4 glands on the posterior thyroid gland
-Only make parathyroid hormone to maintain Ca levels in blood
Parathyroid hormone (PTH)
-Causes bone to release calcium, raising blood levels
-Helps intestines absorb Ca from food
-Helps kidneys retain Ca instead of urinating it
-Works opposite to Calcitonin
Increased Phosphorus
Decreased Calcium, they have an inverse relationship
Hypoparathyroidism
-Parathyroid glands secrete too little PTH
-Low ca levels, low PTH levels, HIGH phosphorus levels
Hypoparathyroidism causes
-Destruction or injury to parathyroid glands during surgery
-Autoimmune
-Congenital
-Radiation to neck
-Vitamin D deficiency
Hypoparathyroidism manifestations
-Muscle twitching or spasm
-Laryngospasm/stridor/ wheezing
-Numbness and tingling around mouth fingers, hands , toes feet
-Confusion and seizures
-HF and arrhythmia (Heart needs Ca for contraction)
Severe hypocalcemia progression
Tetany, chovstek and trousseau signs -> CNS and neuromuscular irritability
Tetany
-Hypocalcemia
-General muscle hypertonia with tremor and spasmodic or uncoordinated contractions
Severe hypocalcemia signs
Tetany,
-Chvostek sign
-Trousseau sign
mgmt of hypoparathyroidism
-Restore Ca levels
-Supportive care for acute life threatening attack or tetany
-Cardiac monitoring
-Recombinant human PTH: Normalizes PTH level which will increase Ca in blood (only in emergent situation)
-Calcium gluconate IV, given in emergent situation
-Vitamin D for Ca absorption (Calcitriol)
-Mg replacement (If the cause is related to low magnesium)
-Quiet environment (No drafts, no bright lights, no sudden movement)
-Diet high in Ca and low in P
-Oral Calcium and Vitamin D for life
Hyperparathyroidism
-One or more of the parathyroid glands are overactive and PTH levels are high
-Elevated PTH -> hypercalcemia -> bone thinning and kidney stones
Hyperparathyroidism causes
-Adenoma (Benign tumor)
-Hyperplasia of the parathyroid glands (Not technically cancerous)
-Multiple endocrine neoplasia type 1
-Familial hypocalciuric hypercalcemia
Hyperparathyroidism manifestations
-Asymp/ vague if there is only a slight elevation
-At severe levels: Apathy, fatigue, muscle weakness, nausea, vomiting , constipation, hypertension, cardiac dysrhythmias
Hyperparathyroidism treatment
-Surgical removal of abnormal parathyroid tissue
-Hydration
-Biphosphonates (P is opposite of Ca)
-Cincalcet decreases the amount of PTH the parathyroid glands make and lowers levels in the blood
Hypercalcemic Crisis
-Occurs from hyperparathyroidism
-Occurs from an elevation of serum Calcium levels
-Elevated Calcium= CNS depression
-Neuro, cardio and kidney symptoms that can be lifethreatening-
-Risk of osteoporosis
Hypercalcemic crisis mgmt
-Rapid rehydration with large volumes of IV isotonic saline fluids (dilute the blood)
-Calcitonin and corticosteroids are admin in emergencies
-Bisphosphonates
-Goals are to reduce the serum calcium level by increasing calcium deposition back into the bone
Hypercalcemic crisis diagnostics
-Serum calcium, ionized calcium, PTH level, Vitamin D level, renal function
-Ultrasound of neck
-CT scan
-Bone mineral density
Vitamin D role
Calcium absorption
Adrenal cortex
-Outer layer of the adrenal gland
-Secretes
Mineralocorticoids
Glucocorticoids
Androgens/Estrogen
Mineralocorticoids
-Aldosterone
-Reabsorption of Na and excretion of K by the kidneys
-Adrenal cortex
Glucocorticoids
-Cortisol: suppression of the immune response, assist in the stress response, assist with BP maintenance and CV function, glucose , protein and fat metabolism
-Adrenal cortex
Adrenal medulla
-Inner portion
-Secretes Catecholamines: Epi and NE
-Causes vasoconstriction
Epinephrine
Fight or flight response (bronchial dilation, increased BP , increased glucose, increased HR)
-Causes vasodilation
Addison’s disease
-Destruction of the adrenal cortex , No hormone production (aldosterone and cortisol)
-Primary and secondary causes
Primary Addison’s disease
-At the site
-Auto immune disorder
-Infection
-Bilateral adrenalectomy
-Hemorrhage into the gland
-Neoplasms, radiation
Secondary Addison’s disease
-Pituitary tumor, hypophysectomy, hypopituitarism, immunotherapy, radiation
-**Abrupt cessation of long term steroid use **
Addison’s disease symptoms
-Fatigue/ muscle weakness (main symptom)
-Weight loss/appetite loss/ abdominal pain, N+V diarrhea
-Dehydration, decreased urine output, salt craving
-Confusion/ decreased coordination, anxiety, irritability
-Hypotension, orthostasis
-Dark bronze pigmentation of skin and mucosa, vitiligo
Addison’s disease labs
-Hypoglycemia (Loss of Glucocorticoids)
-Hyponatremia (Loss of aldosterone )
-Hyperkalemia (Loss of aldosterone)
-Hypercalcemia
-Increased WBC
-Increased renal function (Worse)
Addison’s disease test
-Serum ACTH
-AM cortisol levels
-1mg dexamethasone suppression test
-ACTH stimulation test
Most serious complication of addison’s
Adrenal Crisis
Adrenal Crisis
-Life threatening condition
-Rapid decline of cortisol and aldosterone
-Critical hypotension, hypoglycemia, hyponatremia, hyperkalemia
-Like regular addison’s but exadurated
-Essentially its an abnormality that leads to shock/death
Adrenal crisis: Decreased Cortisol
-Liver: Decreased hepatic glucose output –> Hypoglycemia –> Coma/death
-Stomach: Decreased digestive enzymes–> Vomiting, cramps, diarrhea –> Hypoglycemia/ hypotension –> shock –Coma and death
Adrenal crisis: Decreased aldosterone
-Kidney: Na+Water loss, K retention –> Hypoglycemia/hypotension –> shock –> coma/death
-Heart: Arrhythmia, and decreased CO –> hypotension –> shock –> coma/death
Causes of adrenal crisis
-Abrupt cessation of steroids **
-Infection/sepsis
-Stress: MI, surgery, anesthesia , volume loss, hypoglycemia
-Adrenal trauma –> hemorrhage
-Adrenal gland thrombosis
mgmt of adrenal crisis
-Immediate IV steroids (start with 100mg and taper)
-IV fluids, bolus of NS for fluids and salt wasting
-Hypoglycemia: D50 if needed (Also cause insulin)
- Treat hyperkalemia (Insulin/Kayexalate)
-Vasopressors for hypotension
-Add fludrocortisone when stable (BP/orthostasis)
-Antibiotics
-VTE prohylaxis
-Small frequent meals high in Na, protein, low K foods
Med mgmt of addison’s: Glucocorticoids
-Oral hydrocortisone/prednisone/cortisone
-Used in adrenocorticoid replacement therapy
-Physiological dose when stabilized (20 mg in am and 10 in afternoon)
-Double dose in periods of sick or stress
-Severe deficit give IM dose and go to hospital
-Give with food
Physiological dose, Addison’s
Mimics the normal hormonal pattern
-large dose in morning small in afternoon to mimic the boost of cortisol when you first wake up
Med mgmt of addison’s: Mineralocorticoid
-Fludrocortisone (Prevent dehydration and hypotension)
-Hypotension is a huge concern
-Observe for signs of cushing’s syndrome
-Increase dose in times of stress
Addison’s disease patient centered care
-Priorities physical care, prevent shock
-Monitor fluid electrolyte imbalances
-Admin IV fluids with saline to restore fluid volume
-Observe for dehydration check for orthostatic VS
-I+O, daily weight
-IV hydrocortisone
-Vasopressors (hypotension)
-Check ECG for arrhythmia (Bradycardia, heart block, peaked T waves) from potassium
-Monitor and treat hyperkalemia (Kayexalate, Insulin and dextrose, calcium
-Sodium bicar: for acidosis and to move K into the cell
-Monitor and treat hypoglycemia
-Calm safe environment
-Recumbent with legs elevated
Care of a pt with adrenal insufficiency: Risk for fluid volume deficit
-Monitor S+S of fluid volume deficit
-Encourage fluids and foods
-Select foods high in sodium
-Admin hormone replacement as prescribed, electrolyte replacement
Care of a pt with adrenal insufficiency: Activity intolerance and fatigue
-Avoid stress and activity until stable
-Preform all activities for pt when in crisis
-Maintain a quiet non stressful environment
-Measures to reduce anxiety
Care of a pt with adrenal insufficiency: Self care deficit
Weakness, fatigue, muscle wasting, altered sleep patterns
Care of a pt with adrenal insufficiency: Risk for infection
Teach to avoid sick people, crowds, S+S infection, increase hydrocortisone use when sick
-Avoid stress avoid infection
Adrenal insufficiency Discharge teaching
-Call 911 for Addison crisis, teach S+S
-Med adherence, do not stop hydrocortisone replacement, cannot stop on their own without doctor
-Avoid stress, strenuous activities in hot weather
-Avoid crowds, illness, and wash your hands
-Big dose of meds in morn smaller dose in afternoon
-Diet
-Increased meds when sick or stressed
-Need med alert bracelet with adrenal insufficiency
-Emergent IM steroid when in a crisis: need to teach injection
-Note and teach any illness or stressors that may cause a crisis
Adrenal insufficiency diet
High protein, high carb, enough sodium
People with adrenal insufficiency can stop taking meds without doctors permission
T/F?
False if they do this it can trigger an Addisonian crisis
Cushing syndrome Causes
-Long term use of steroids
-Excessive secretion of cortisol from adrenal cortex secondary to hyperplasia
-Pituitary secreting excess ACTH
-Ectopic production of ACTH from certain types of cancer
-Cancer mgmt and auto immune too
Cushing syndrome S+S: Physical observation
-Moon Face
-Buffalo hump (fat deposit on cervical spine area)
-Purple striae on abdomen breast upper arms (where fat is deposited)
-Truncal obesity, with skinny extremities
-Hirsutism
-Thining or balding hair (head)
-Acne thin skin, ecchymosis
-Menstrual irregularities
Cushing syndrome S+S: Bone
-Aseptic necrosis of femur
-Osteoporosis (effect of long term steroid as well)
-Compression fracture of spine and spontaneous Fx
Cushing syndrome S+S: Heart and vasculature
-HF
-Htn
-Decreased wound healing
-Decreased inflammatory response
Cushing syndrome S+S: Electrolyte balance, fluid and glucose
-Fluid retention
-Sodium retention
-Hyperglycemia (impaired glucose tolerance)
-Altered calcium metabolism
-Hypokalemia
-Metabolic alkalosis
Cushing syndrome S+S: Mental
Mood alterations/psychosis
Cushing syndrome S+S: Muscle
Muscle weakness/ myopathy
Thin extremities
Cushing syndrome S+S: GI
Peptic ulcer disease
Cushing syndrome S+S: sexual
Impotence
Cushing’s syndrome Labs: Increased
-Plasma cortisol levels (blood and urine)
-1 Mg dexamethasone supression test (shows a high cortisol level)
-ACTH levels salivary cortisol level (done at bed time and shows a high level of cortisol)
-24 urine (cortisol in urine)
-Glucose and Sodium are elevated
Cushing’s syndrome Labs: Decreased
-Potassium
-Calcium
-Leukocytes(Immune system is supressed)
mgmt of Cushing’s: Radiation or surgery
-Remove pituitary tumor, or adrenalectomy
-Mgmt of diabetes preop
-Post op symptoms of adrenal insufficiency within 12-24 hours after resection due to reduction in circulating hormone: need temp hydrocortisone
-Bilateral adrenalectomy: needs lifetime steroid replacement
Mgmt of Cushing’s: long term steroid use
Wean slowly and allow adrenal gland to function again (can take months)
mgmt of Cushing’s: adrenal enzyme inhibitors
-Inhibits cortisol production
-If syndrome is caused by ectopic ACTH secretion by a tumor which cannot be eradicated
-Metyrapone, Aminoglutethimide, Mitotane (adrenal cancer), Ketoconazole
Nursing mgmt of cushing syndrome
-I+O, daily weight
-Treat hypovolemia, assess
-Monitor for hypertension and hypokalemia
-Monitor for addisonian crisis
-Maintain safety (skin, trauma, patho)
-Ensure physical activity as tolerated
-Meticulous skin care
-Infection control/hand-washing
-Monitor for GI bleed (peptic ulcers)
-Hyperglycemia mgmt (Can become diabetic easily)
-PSych support, body image
Nursing mgmt of cushing post op, transsphenoidal
-HOB elevated
-Nasal packing
-Frequent mouth care
-Avoid increasing ICP, (Nose blowing/coughin)
-Monitor for CSF leak
-Monitor for adrenal insufficiency
-Fluid and electrolyte mgmt
-N+V diarrhea
Nursing mgmt of cushings hydrocortisone post op
-Daily weight
-VS
-Monitor lytes and glucose
-Monitor for infection
-Stress dose/ emergency IM dose
A nurse is providing care to a client with primary hyperparathyroidism. Which interventions would be included in the client’s care plan? Select all that apply.
A. Monitor gait, balance, and fatigue level with ambulation.
B. Monitor for fluid overload.
C. Monitor for signs and symptoms of diarrhea.
D. Encourage intake of dairy products, seafood, nuts, broccoli,
and spinach.
A. Monitor gait, balance, and fatigue level with ambulation.
B. Monitor for fluid overload.
Excessive calcium in the blood depresses the responsiveness of the peripheral nerves, accounting for fatigue and muscle weakness. A large volume of fluid is encouraged to keep the urine dilute.
Possible effects include nausea, vomiting, and constipation.
Client would be on a calcium-restricted diet.
Nursing care for a client in addisonian crisis should include which intervention?
A. Encouraging independence with activities of daily living (ADLs)
B. Allowing ambulation as tolerated
C. Offering extra blankets and raising the heat in the room to keep the client warm
D.Placing the client in a private room
D.Placing the client in a private room
The client in addisonian crisis has a reduced ability to cope with stress as a result of an inability to produce corticosteroids. A private room is easy to keep quiet, dimly lit, and temperature controlled. Also, visitors can be limited to reduce noise, promote rest, and decrease the risk of infection. The client should be kept on bed rest, receiving total assistance with ADLs to avoid stress as much as possible. Because extremes of temperature should be avoided, measures to raise the body temperature, such as extra blankets and turning up the heat, should be avoided.
