NURS 444 Week 9 Flashcards
Anterior Pituitary Gland
-Tropic hormones- controls hormones secreted by other glands (TSH, ACTH, FSH/LH)
- Growth hormone
- Prolactin
Posterior Pituitary gland
- Antidiuretic hormone
- Oxytocin
SIADH
abnormal or sustained secretion of ADH (antidiuretic hormone)
SIADH s&s
- fluid retention
- serum hypo- osmolality
- dilutional hyponatremia
- hypochloremia
- concentrated urine in presence of normal or increased intravascular volume or renal function
common causes of SIADH
most common is malignancy (small cell lung cancer?)
Low osmolality
high osmolality
low- low particles (electrolytes)
high- high particles
Clinical manifestations of SIADH
(dilutional hyponatremia)
> muscle cramping/ twitching
weakness/ fatigue
thirst
dyspnea on exertion
low UOP
increased weight
vomiting
abdominal cramps
seizures
lethargy
confusion
headache
comaa
SIADH diagnostic studies
urine and serum osmolality
- serum osmolality < 280 mOsm/kg
- specific gravity > 1.005
Serum sodium levels < 120 mEq/L
For mild symptoms and Na >125
restrict fluid intake to 800 - 1,000 mL/day
symptomatic and < 120 with symptoms
- IV hypertonic fluids (3% saline)- slow infusion
- loop diuretic (Lasix)- only when Na is 125
- fluid restriction of 500 mL/day
Nursing management of SIADH
monitor
- VS
- I&O
- daily weights
- LOC
- urine specific gravity
- signs of hyponatremia
Nursing management of SIADH cont.
- Restrict fluids as ordered (500-1000 mL/day)
- HOB flat or no more than 10 degrees
- protect from injury
- seizure precautions
- oral hygiene
Diabetes Insipidus
DEFICIENCY of production or secretion of ADH.
- decreased renal response to ADH
Classifications of DI
- Central DI: neurogenic DI.
- nephrogenic DI
- Primary DI (psychogenic DI)
Central DI (neurogenic DI)
most common
associated with a lesion of the hypothalamus, infundibular stem, or posterior pituitary. Interferes with ADH synthesis, transport, or release.
- Can also be caused by brain surgery, injury or infection
Nephrogenic DI
adequate ADH but decreased response in kidney.
- hypokalemia and hypercalcemia may lead to nephrogenic DI
-lithium causes drug-induced nephrogenic DI
Primary DI (psych)
less common
associated with excessive intake of water intake
DI
increased serum osmolality (hypernatremia)
DI clinical manifestations
< polydipsia and polyuria
< excretion of a lot of urine (5-20 L/day)
< generalized weakness
< nocturia
< weight loss
< constipation
< poor skin turgor
< hypotension
< tachycardia
< shock
< irritability
< mental dullness
< coma
DI labs
5-20 L/day urine output
- low specific gravity < 1.005
- low urine osmolality < 100 mOsm/ kg
- elevated serum osmolality > 295 mOsm/kg
Diagnostic studies for central DI
water restriction test
- obtain baseline weight, pulse, BP, plasma, osmolality, and urine specific gravity
- patient withholds fluids for 8-16 hours before test.
Primary DI association
associated more with overhydration and hypervolemia
DI management
early detection
maintenance of adequate hydration
patient teaching
Central DI management
- fluid and hormone replacement is the cornerstone for treatment!
+ hypotonic saline or D5W
+ desmopressin acetate (DDAVP)- analog of ADH
(given orally, iV, subcutaneuous, nasal spray)
+ aqueous vasopressin, vasopressin tannate, lysine vasopressin
+ Chlorpropamide (Diabenese)
+ Carbamazepine (Tegretol)
Management of neurogenic DI cont.
dietary measures- low sodium diet (no more than 3g/day)
- thiazide diuretics
- Indomethacin (Indocin)- when above not affective. Helps increase renal response to ADH
Adrenal Cortex hormones
- glucocorticoids
- mineralocorticoids
- androgen
Glucocorticoids
regulate metabolism, and increase blood glucose
critical to psychologic stress response
mineralocorticoids
regulate;
-sodium balance
-potassium balance
androgen
contributes to;
- growth and development in both genders
- sexual activity in adult women
Problems associated with adrenal cortex
Excess glucocorticoids- most common is administration of exogenous corticosteroids
85% of endogenous cases are due to an adrenocorticotropic hormone (ACTH)- secreting pituitary tumor
Cushing’s Disease (mainly in women 20s-40s)
Problems associated with adrenal cortex cont.
other causes;
-Adrenal tumors (more common in women 20-40)
- ectopic ACTH production in tumors outside hypothalamic- pituitary- adrenal axis
usually lung and pancreas tumors
more common in men
Cushing’s Syndrome causes
> prolonged use of steroids
ACTH-secreting pituitary disease (Cushing’s disease)
Carcinoma/ adenoma- cortisol-secreting in the adrenal cortex
excess secretion of ACTH of neoplasm outside the pituitary/adrenal glands (lung)
Clinical manifestations of excess corticosteroids
- weight gain (trunk, face, cervical spine)
- thinning of hair
- purplish-red striae on abd, breast, buttocks
- easy bruising
- hyperglycemia
- muscle wasting/ weakness in extremities
- delayed wound healing
- mood disturbances; irritability, anxiety
- insomnia
clinical manifestations of excess mineralocorticoid
hypertension
unexplained hypokalemia (low K)
clinical manifestations of excess androgen
menstrual disorders and hirsutism in women
gynocomastia and impotence in men
severe acene
Diagnostic studies for adrenal (excess) problems
^ 24-hour urine for free cortisol
^ low-dose dexamethasone suppression test used for borderline 24-hr urine cortisol
^ CT/ MRI of pituitary and adrenal glands
^ hypokalemia and alkalosis (ectopic ACTH syndrome and adrenal carcinoma)
^ plasma ACTH may be low, normal, or elevated
24-hour urine
Cortisol levels
levels above 80-120 mcg/day = Cushing syndrome
adrenal (excess) disorder GOAL
normalize hormone secretion
adrenal (excess) disorder TREATMENT depends on cause
- pituitary adenoma
- adrenal tumors or hyperplasia
- ectopic ACTH-secreting tumors: managed by treating primary neoplasm
DRUGS ARE INDICATED WHEN SURGERY IS CONTRAINDICATED OR AS ADJUNCT TO SURGERY. CAN BE TOXIC
What to do when Cushing’s syndrome develop from use of corticosteroids
- discontinue
- taper
- decrease dose
- convert to alternate-day regimen
tapering prevents potential life-threatening adrenal insufficiency
acute interventions for adrenal excess problems
assessment of s&s of hormone and drug toxicity
- complicating conditions;
cardiovascular disease
DM
`infection
Nursing management for excess adrenal hormones
- monitor: Vs, daily weight, glucose, infection
- monitor s&s
abnormal thromboembolic phenomena - pre-op and post-op care
TEACH
- wear medic alert bracelet
- avoid exposure to stress, extreme temps., infection
- lifetime corticosteroid replacement is required
Adrenocortical insufficiency
- primary cause: Addison’s disease.
- secondary cause: lack of pituitary ACTH secretion (rarely decrease in mineralocorticoids)
Addison’s disease
most common cause is autoimmune response
most common in white females
all three classes of corticosteroids are decreased
Clinical manifestations of adrenal insufficiency
disease usually advanced before diagnosis
** progressive weakness
** fatigue
** weight loss
** anorexia
** skin hyperpigmentation (typically in Addison’s)
- orthostatic hypotension
- hyponatremia
- hyperkalemia
- n&v
- diarrhea
- irritability, depression
Addisonian crisis
life-threatening
- insufficient adrenocortical hormones
- sudden, sharp decrease in hormones triggered by;
` stress
` withdrawal of hormone replacement
` after adrenal surgery
` following sudden pituitary gland destruction
Severe manifestations of glucocorticoid and mineralocorticoids
– hypotension
– tachycardia
– dehydration
– hyponatremia
– hyperkalemia
– hypglycemia
– fever
– weakness
– confusion
Adrenal insufficiency diagnostic studies
subnormal levels of cortisol
- levels fail to rise over basal levels with ACTH stimulation test;
latter indicates primary adrenal disease.
positive response to ACTH stimulation indicates functioning adrenal gland - other abnormal lab tests
- ECG
- CT or MRI
adrenal insufficiency treatment
+ hydrocortisone: both glucocorticoid and mineralocorticoid properties. Used as replacement commonly
+ glucocorticoids must be increased in times of stress
+ mineralocorticoid replacement with fludrocortisone (Florinef) with increased salt in diet
Addisonian crisis care
Tx directed at;
shock management
high-dose hydrocortisone replacement
Acute care for adrenal insufficiency
! frequent assessment
! Assess VS
! signs of electrolyte and fluid imbalance every 30 min to 4 hr for first 24 hr
! daily weights
! corticosteroid therapy DILIGENTLY
! protect against infection
! assist w/ daily hygiene
! protect from extremes: light, noise, temp.
Instructions for replacement of hormones
glucocorticoids given in divided doses
mineralocorticoids given once in the mornign; mimic circadian rhythm, decrease SE of corticosteroids