exam 2
hormones classification
amines and amino acids - epinephrine, thyroid hormones
peptides, polypeptides, proteins, glycoproteins - TRH, FSH, GH
steroids - corticosteroids
fatty acid derivatives - retinoids
function of the endocrine system
coordinating cellular interaction
metabolism/growth and development
fluid and electrolyte balance
acid-base balance
adaptation
reproduction
aging
response to adverse conditions
endocrine review of systems
any changes in:
energy level
tolerance to heat/cold
weight
thirst, frequency of urination
bowel function
body proportions: muscle mass, fat, fluid distribution
secondary sex characteristics, sex dysfunction
menstrual cycle
concentration, sleep patterns, mood
vision
joint pain
diagnostics for endocrine diagnosis
blood - hormones, autoantibodies, secondary effects, radioimmunoassay (antigen levels)
urine - hormone, metabolites, 24h collections
stimulation - confirms hypofunction by testing response
suppression - detects hyperfunction (failure of negative feedback)
imaging - radioactive scanning, MRI, CT, ultrasonography, positron emission tomography (PET), dual energy x-ray absorptiometry)
genetics - more routine. identification of specific genes rt endocrine disorders. detects gene mutation
diabetes insipidus (DI)
Hypo- ADH
deficiency or resistance of antidiuretic hormone aka ADH or vasopressin
decreased ADH =water loss
s/s:dilute polyuria and polydipsia
types of DI
Central DI: lack of vasopressin production or secretion
Nephrogenic DI: renal resistance to vasopressin
Dipsogenic DI/Primary DI: excessive water intake
Gestational DI: excess vasopressinase
all result in excessive hypotonic urine but tx varies
causes of central DI
trauma to hypothalamus, infundibulum, or pituitary
(head trauma, neurosurgery, brain tumors, surgical ablation/irradiation/resection of pituitary, CNS infection, inflammation)
causes of nephrogenic DI
failure of renal tubules to respond to ADH
(congenital, injury, medications (lithium, amphotericin B, declomycin), hypokalemia, hypercalcemia
causes of dipsogenic DI
hypothalamus defect (thirst mechanism)
(head injury, surgery, infection, inflammation, tumor)
causes of gestational DI
rare, excessive vasopressinase activity (pregnancy)
physical exam for DI
neuro - HA, dizziness, lethargy, confusion
HEENT - dry mucous membranes, decreased skin turgor
cardiac - tachycardia, thready weak pulse
GI - increased PO liquids
GU - increased UO
muscle skeletal - twitching, spasms, weakness
psychological - irritable
VS - hypotensive, tachycardia
key assessment findings in DI
onset - insidious or abrupt
large volume of urine output in absence of ADH (>250 ml/hr) = polyuria
dilute urine = urine specific gravity of <1.005
polydipsia (2-20L of fluid daily)
hypernatremia (>145 mEq/L)
restricting fluids ineffective
diagnostics for DI
fluid deprivation test
plasma levels of ADH - low (CDI) versus normal (NDI)
plasma and urine osmolality
serum osmolality
desmopressin trial (synthetic vasopressin)
tx for central DI
correct/treat underlying etiology
replace ADH (DDAVP - desmopressin acetate, 1-deamino-8-D-arginine vasopressin) oral/intranasal
fluid replacement with hypotonic solutions
chlorpropamide and thiazide diuretic prn for mild form ?
tx for nephrogenic DI
correct/treat underlying etiology
mild salt restriction
prostaglandin inhibitors ?
chlorpropamide and thiazide diuretic ?
Nursing Diagnosis for DI
deficient fluid volume
Decreased cardiac output
electrolyte imbalance
nausea
knowledge deficit
nursing interventions for DI
I&O, foley insertion
frequent weights
monitor VS (tachycardia, hypotension)
PE - neuro checks, mucous membranes
IVF & medication administration (side effects)
ample access to free water ?
diet restriction (low salt, low protein for NDI)
psychological support
education
*tx risks - water intoxication, dehydration, electrolyte imbalance, seizures death
syndrome of inappropriate antidiuretic hormone (SIADH)
hyper-ADH
excessive ADH (vasopressin) secretion
excessive water retention - causes hyponatremia (dilutional) and hypervolemia
causes of SIADH
lung disorders (lung CA, PNA, pneumothorax) ?
CNS disorders (head injury, brain tumors or infections) = direct overstimulation of pituitary gland (increased ADH)
meds - phenothiazines, TCAs, thiazide diuretics, nicotine
infection
hypothyroidism ?
clinical manifestation of SIADH
neuro - HA, AMS, lethargy, delirium, seizures, coma, paralysis
cardiac - HTN, peripheral edema
pulmonary - SOB, crackles
GI - anorexia, nausea and vomiting (early), abdominal pain
GU - decreased UO
MS - cramping, weakness
psychiatric - irritability
SIADH diagnostics
serum hypoosmolality - decreased 2 degree dilution (280 mOsm/kg)
serum hyponatremia - decreased 2 degree dilution (136 - 145 mmol/l)
urine hyperosmolarity - increased 2 degree oliguria (100 mOsm/kg)
urine hypernatremia - increased 2 degree oliguria (20 mEq/l)
plasma levels of ADH - normal or elevated
renal function - normal
SIADH management
acute symptomatic vs chronic asymptomatic
identify and eliminate underlying cause
fluid restriction (1-1.5/d)
salt tablets PO - increase sodium level
loop diuretics - promote water excretion
Urea powder PO - promotes osmotic water loss
vasopressin-2 antagonist - vaptan therapy blocks ADH activity in kidneys
frequent sodium labs
0.9% saline IVF in some types ?
tx of emergent symptomatic hyponatremia
hypertonic saline (3% saline) if severely symptomatic
commonly rate limited to prevent osmotic demyelination syndrome (ODS)
ODS occurs due to rapid sodium correction causing myelin sheath damage (brain stem)
small bolus used in severely symptomatic states
sodium deficit formula for milder cases
nursing interventions for SIADH
monitor VS and serum sodium
monitor I&O closely
fluid restrictions
frequent neuro checks for pts at risks
telemetry
supplemental salt, oxygen prn
urine and blood chemistries
support measures
educational - pathology, procedures, meds, tx
tx risks - electrolyte imbalance, ODS, seizures, coma, death
parathyroid glands
four glands on the posterior thyroid gland
parathyroid glands secrete parathyroid hormone (parathormone) aka PTH
increased PTH - increased blood calcium, decreased blood phosphorus
thyroid secretes calcitonin (and T3, T4)
PTH, calcitonin, and vit. D regulate calcium and phosphorus
hyperparathyroidism
overproduction of parathyroid hormone
increased calcium levels and characterized by bones softening and kidney stones
hypercalcemia > 10.5 mg/dl (normal range 8.5 - 10.2 mg/dl)
hyperparathyroidism incidence
one of most common hormone disorders
occurs 2 to 4 times more often in women
types of hyperparathyroidism
primary - enlargement of one or more of the glands which leads to an overproduction of PTH (80 - 90% of cases)
secondary - overactivity of parathyroids due to low calcium e.g. vit. D deficiency, CKD
tertiary - due to chronic secondary hyperparathyroidism e.g. kidney, transplant, ESRD on dialysis
role of calcium
bone and tooth health
facilitates bodily/cellular functions
stabilizes cells membranes
activities muscle concentrations
initiates neurotransmission
maintain depolarized states
endocrine cell use
activates/stabilizes enzymes
motility, metabolic processes, proliferation, etc
clinical manifestations for hyperparathyroidism
neuro - fatigue, muscle weakness
cardiac - arrhythmias (short QT interval)
GI - nausea, vomiting, constipation, anorexia
GU - nephrolithiasis, kidney damage
MS - skeletal/joint pain, absent reflexes
psych - irritability, neurosis, psychoses
diagnostics for hyperparathyroidism
lab analysis
elevated calcium and PTH levels
radioimmunoassay for PTH
double antibody parathyroid hormone test
radiologic
X-ray and bone scans
US, CT, MRI, thallium scan, fine-needle biopsy
medical tx for asymptomatic hyperparathyroidism
primary hyperparathyroidism - surgery
parathyroidectomy for asymptomatic pts with primary hyperparathyroidism meeting 1 or more of these criteria:
younger than 50yrs of age
those unable/unlikely to follow up
serum Ca+ more than 1mg/dL above normal
GFR < 60 mL/min
urinary calcium > 400 mg/day
bone density with T score < -2.5 (osteoporosis)
presence of nephrolithiasis or nephrocalcinosis
medical tx for symptomatic hyperparathyroidism
promote urinary excretion
rehydrate - require fluid intake of >2000ml. promotes calcium excretion. avoid thiazide and dehydration
loop diuretic - inhibits calcium reabsorption in LOH
increase GI excretion
glucocorticoids - affect vit D and decreased calcium reabsorption)
prevent bone resorption (calcium released from bone)
oral phosphates - decreases calcium, short term only - CaPO4 deposits
bisphosphonates (osteoporosis), calcitonin - inhibits osteoclasts (bone catabolism)
diet - limit calcium
mobility - weight bearing-aids with bone resorption
hypercalcemic crisis
when - extreme elevation of serum calcium levels > 13 - 14mg/dL (normal 8.6 - 10.2)
what - life threatening neurologic, cardiovascular, and kidney symptoms
tx for hypercalcemic crisis
rapid rehydration - large volume IV isotonic saline fluids (INS to keep UOP at 100 ml - 150ml/hr)
emergent cocktail - calcitonin and corticosteroids
dialysis - used in emergent situation not responding to tx
nursing interventions for hyperparathyroidism
ongoing assessment - neuromuscular, cardiac
hydration therapy - I&O
mobility - weight bearing (bone building)
diet - hydration, limit calcium, laxatives, protein (if ulcer)
med administration - routine vs emergent, surgery
blood work - calcium, phosphorous, PTH, vit D
monitor/tele - arrhythmias
tx risks - electrolyte imbalance, arrhythmias, tetany
parathyroidectomy nursing management
maintain ABCs, use high semi-fowlers position
promote hydration and ambulation
monitor for tetany post-op
education: need for follow up - hypocalcemia
Hypoparathyroidism
deficiency of PTH
low PTH = hypocalcemia (loss through bone, kidney, GI)
hyperphosphatemia
types - acquired, autoimmune, congenital, familial, postoperative parathyroidectomy hyperparathyroidism is leading cause (acquired)
clinical manifestations for hypoparathyroidism
tetany due to impaired neuromuscular signal, irritability, muscle hypertonia
hypocalcemia lowers the threshold for neuronal activation
tremors, spasmodic or uncoordinated contractions
numbness, tingling, cramps, stiffness
anxiety, irritability, depression, delirium
ECG changes and hypotension (cardiovascular/cardiopulmonary collapse)
assessment findings:
trousseau sign
positive chvostek
diagnostics for hypoparathyroidism
lab studies:
low serum calcium (normal - 8.6 - 10.2 mg/dl)
low serum vit. D (normal - 20 - 50 mg/dl)
elevated phosphate levels (normal: 2.4 - 4.1 mg/dl)
radiologic:
bone shows increased density
calcification of subcutaneous tissue (or parts of brain)
medical management for hypoparathyroidism
identify and treat etiology - tx depends on symptoms and cause
goal - normalization of serum calcium level (goal 9 or 10 mg/dl)
medication cocktail - calcium, magnesium, and vitamin D2 or D3, thiazide diuretic ?
low stimulus environment (due to neuromuscular irritability)
calcium supplementation - calcium salts and calcium gluconate
aluminum hydroxide gel or aluminum carbonate (gelusil, amphojel) after meals binds phosphate and promotes GI excretion
following parathyroidectomy: if hypocalcemia and tetany present, emergent tx with IV calcium gluconate, and sedative agents and resp. support prn
diet for hypoparathyroidism
high calcium (green leafy vegetable, broccoli, kale fortified OJ, breakfast cereals)
low phosphorus diet (limit milk/products, egg yolks, soft drinks)
low oxalates (limit spinach, meats, nuts)
nursing interventions
ongoing assessment - neuro (seizures), tetany, cardiac, pulmonary
postoperative care - s/p para/thyoidectomy, radical neck dissection - detect early signs of low calcium, related complications (tetany, seizures, resp distress)
med admin - calcium gluconate IV for emergencies; several meds, arrhythmias, (cardiac hx)
cardiac monitoring - arrhythmias
education - diet modifications, meds, restrictions, signs/symptoms of hypo/hypercalcemia
______ typically contraindicated
calcium gluconate and digoxin
digoxin can exacerbate cardiac hypokalemia symptoms
calcium and digoxin increase systolic contraction and synergistic effect resulting in fatal arrhythmias