Endocrine Flashcards
what is hypopituitarism
under activity of the pituitary gland
most often caused by a benign pituitary tumor
other causes: brain surgery head trauma infections of the brain radiation stroke subarachnoid hemorrhage
hypopituitarism manifestations
hypogonadism
- failure of the gonads
- testes in males
- ovaries in females
amenorrhea
infertility
breast and uterine atrophy
vaginal dryness
loss of libido
sexual dysfunction
loss of armpit and pubic hair
hypothyroidism
hypoadrenism
SIADH
diltuional hyponatremia
decreased GH
hypopituitarism diagnostic studies
history and physical exam
neuro-opthalmaological exam
X-ray of pituitary fossa and radio immunoassays of anterior pituiary hormones
CT scan or MRI lab test: serum ACTH cortisol estradiol FSH LH TSH, T4 testosterone
hypopituitarism pharmacological care
hormone replacement therapy
steroid therapy
endocrine problems often amnifest differently in an older adult than a younger person
what is hyperpituitarism
anterior pituitary gland secretes too much GH
acromegaly occurs when growth plates are closed
gigantism occurs when growth plactes are still open
acromegaly: enlargement of hands, feet, face
overproductions of ACTH leads adrenal gland to overproduce cortison –> Cushings disease
hyperpituitarism manifestations
excess prolactin
- headache
- visual disturbances
- growth failure
- pubertal arrest with menstrual abnomralities in girl
excess ACTH
- weight gain with concurrent growth failure
excess GH causes: - mild to moderate obestiy -gigantism - macrocephaly: overly large head - cardiovascular disease - coarse facila features - tumors 0 endocrinopathies
physical changes of acromegaly are irreversible
hyperpituitarism diagnostic studies
hx and physical exam
CT
plasma homrone levels
hyperpituitarism care
microsurgery to remove tumor
- common treatment surgery for patient with pituitary tumors but can cause infertility
pituitary radiation
gamma knife radiation
growth hormone suppressant
- bromocriptine or octreotide
hyperpituitarism management
restrict soidum intake
assess signs for diabetes inspidus
treatment usually produces hypopituitiarism
lifelong hormone replacement therapy with regular check ups
what is diabetes insipidus
occurs when posterior pituitary fland makes TOO LITTLE antidiuretic hormone
- causing failure of tubular reabsorption of water in kidney
you being to pee a lot and often feel thirsty
- it fails to reabsorb so it just comes out
central DI is the most common form
- usually caused by damage to hypothalamus or pituitary gland
nephrogenic DI: defect in tubular reabsorption of water back into bloodstream
diabetes inspisidus manifestations
polydipsia polyuria nocturia dehydration conspitation
diabetes inspidus diagnostic studies
water deprivation tests
- measures body’s inability to concentrate urine
osmotic stimulation
CT scan or MRI
diabetes inspidius pharmacological care
pharmacological interventions: desmopressin and vasopressin chlorpropamide carbamazepine diuretics surgical removal of a tumor
nephrogenic DI: if cause is due to lithium then discontinue or damage may become permanent
diabetes insipidius management
monitor findings of dehydration
measure urine and specific gravity
administer meds
monitor fluids and give IV fluids
intake and output
weigh daily
monitor and care for clients with increased intracranial pressure
health promotion: - teach how record intake and output - about prescribed medications and side effects - avoid fluids with diuretic effects (caffeinated beverages) - check urine specific gravity
what is SIADH
too much ADH with water intoxification and a decrease in sodium concentration
you have too much water in your body
SIADH manifestations
changes in level of consciousness and mental status
tachycardia
hyponatremia
weight gain
urinary specific gravity will be greater than 1.030
hypertension
SIADH pharmacological care
diuretics:
furosemide
bumetanide
careful administration of hyperteonic 3% NaCl Iv solution
- too rapid of an infusion rate can cause permanent neurologic defects
osmotic diuretics - mannitol
vasopressor receptor antagonists
- conivaptan
- tolvaptan
SIADH management
monitor intake and output
sxs for fluid overload and hyponatremia
weigh daily
electrolytes and enruologic strokes
restrict fluid intake as ordered
sodium replacement therapy
seizure precautions
SIADH can be chronic and clients will need to learn to manage the condition at home
- should weigh themselves daily and adhere to prescribed fluid restriction typically 800-1000mL/ day
what is hypothyroidism
thyroid gland does not make enough thyroid hormones
myxedema crisis or come = loss of brain function
- happens as a result of severe, lnogstanding hypothyroidism
hypothyroidism causes
hashimotos thyroditis
atrophic thyroiditis
lithium
amiodarone
interferon alpha
genetics
radiation treatments to the neck or brain
radioactive iodine
surgical removal of all or part of thyroid gland
hypothyroidism manifestations
early symptoms; constipation increased sensitivity to cold fatigue heavy menstrual period joint and muscle pain pale dry skin depression brittle hair and nails weight gain
if left untreated: decrease in taste and smell hoarseness puffy face puffy hands and feet slow speech thickening of skin thinning of eyebrows
hypothyroidism pharmacological care
most accurate and sensitive test to measure thyroid function is TSH level
- often first test done to evaluate thyroid function and monitor effectivenss of homrone replacement therapy
pharamacologic interventions:
levothyroixine
liothyronine
myxedema crisis/coma management will include:
- mechanical ventilation
- treatment of associated infection
- correct hypothermia
- IV thyroid hormone replacement therapy
- conserve energy
- avoid stress
hypothyroidism diagnostic studies
hx and physical exma
labs: INCREASED: - TSH - cholesterol and triglycerides - liver enzymes - prolactin
DECREAED:
- T3 and T4
- serum sodium
- serum glucose
CBC anemia
hypothyroidism management
meds
signs for myxedema
restful environment
protect client from cold
levothyroxine life threatening side effects: cardiac dysrhythmias
- check with HCP to switch to a different brand
what is hyperthyroidism
overactive thyroid makes too much thyroid
thyroitoxic crisis (thyroid storm) rare but potentially fatal
causes: Graes disease too much iodine thyroditis non-cancerous growth of thyroid gland over dosage of thyroid hormone
hyperthyroidism manifestation
difficuly concentrating
fatigue
hyperphagia - excessive or extreme hunger
weight loss
diarrhea
goiter
heat intolerance
exopthalamos
tachycardia
palpitation
restlessness
thing, brittle hair
pliable “plummers” nails
irregular menstrual priods
insomnia
hyperthyroidism diagnostic studies
hx and physical exam
goiter
hyperactive reflexes
labs: increased T3 and T4 increased radioactive iodine uptake presence of thyroid nodules decreased TSH levesl
hyperthyroidism pharmacological care
pharamcologic: radioactivie iodin methimazole antithyroid (propylthiouracil) beta adrenergic blocking agents (propanolol)
surgical intervention: thyroidectomy
exopthalamos: classic finding of graves disease
- cornea can become dry, irritated and devleop ulcerations
hyperthyroidism management
vital
Hr
quiet restful, cool environment
diet therapy, extra fluids
diet high in calories, protein and carbs
stress avoidance
energy conservation
what is hypoparathyroidism
parathyroid hormone produces too little parathyroid hormone
results in hypocalcemia
most common cause: injury to parathyroid glands during thyroid surgery
other causes;
low serum amgnesium levels
metabolic alkalosis
hypoparathyroidism manifestations
neuromuscular irritability
muscle weakness or cramping
personality changes
numbness of fingers and caropedal spams
tetany - muscular spasms
seizures
laryngospasm
dry, scaly skin and hair loss
abdominal cramping
hypoparathyroidism diagnostic studies
hx and physical exma
positive chvosteks facial signs - cheek
positive trousseaus signs - BP cuff
ECG shows abdnormal heart rhythms
labs: decreased: - calcium - magnesium - PTH levels - urine
increased: phosphate
hypoparathyroidism pharmacological care
calcium replacement therapy
Vit D preparations
calcium rich, low phosphorus diet
hypoparathyroidism management
monitor signs of tetany
place an oral airway, suction equipment and tracheostomy tray at clients bedisde
seizure precautions
monitor vitals
have calcium gluconate available if signs of low calcium
reduce phosphrous intake, no:
- fish
- eggs
- cheese
- cereals
what is hyperparathyroidism
parathyroid secretes too much parathyroid hormone
results in hypercalcemia
primary hyperparathyroidism
enlargement of one or more of the parathyroid glands
no known causes
secondary hyperparathyroidism
body produces extra parathyroid hormones because calcium levels are too low
tertiary hyperparathyroidism
parathyroid continues to produce too much even though calcium levels are back to normal
occurs with kidney disease
hyperparathyroidism manifestations
constipation
nausea and vomiting
anorexia
bone pain
deminieralization
deformities
kdieny stones
blurred vision
muscle weakness and fatigue
depression
hyparathyroidism diagnostic studies
hx and physical exam
increase calcium
decrease phosphorus
x-rays and DEXA revel bone demineralization
CT scan
MRI
ultrasound of the neck
hyparathyroidism pharmacological care
drink more fluids
avoid thiazide type diuretics
surgical interventions to remove parathyroid glands
hyperparathyroidism management
postoperatively, observe signs of hypocalcemia
monitor laryngeal damage
monitor renal involvement
increase their fluid intake to dilue calcium levels in blood and urine
consume a diet rich in calcium and vitamin D
what is addisons disease
decreased production of cortisol and aldosterone
symptoms of addison disease do not become apparent until around 90% of the adrenal cortex is destroyed
addison diseae manifestation
fatigue weakness dehydrartion low BP decreased resistance to stress
hyperpigmentation and alopecia
weight loss pathological fractures depression lethargy emotional lability
addison crisis clinical manifestation
nausea and vomiting abdominal pain fever extreme weakness severe hypoglycemia, hyperkalemia and dehydration
BP falls which can lead to shock and coma
death if not treated
addison diseasee diagnostic studies
hx and physical exam
labs:
ACTH stimulation test - low cortisol level
hypoglycemia
electrolytes - low sodium and high potassium
24 hour urine output
addison disease pharmacgologial care
hydrocortison
fludrocortison acetate
diet high in protein, carbs and sodium
low in potassium
addisonian crisis interventions
emergency management
IV hydrocortisone
carefully monitor IV infusion of 0.9% NaCl or D5W/NaCl
Iv glucose or glucagon
insulin with dextrose in normal saline
potassium-binding and excreting resin
vitals
addison disease management
weigh daily
monitor electrolytes
preserve clients energy by assisting with ADLs
collaborate with dietician
measure intake and output
monitor blood sugar levels
health promotion;
lifelong hormone replacement therapy
avoid or manage stress
add more sodium to diet
avoid extra potassium
have quick acting sugar
increasing fluid intake to 2,000-3,000 ml/day
- clients with addison disease will require lifelong hormone therapy with glucocorticoids and mineral corticoids
- taking these with an extended periods of time can lead to serous complication and side effects
what is cushings syndrome
occurs when adrenal galnd secrete too much cortisol
overproduction can be due to:
- cushings disease
- tumors of the pituitary gland
- tumors in other organs and glands in the body that produce cortisol or ACTH
cushings syndrome manifestation
upper body obesity with thin arms or legs
buffalo hump
moon face
acne
striae (purple marks) on abdomen, thighs, breasts
easy bruising
backache
bone pain or tenderness
excess hair growth on face, neck, chest, abdomen, thighs for women
for men, impotent or have decreased libido
personality changes
fatigue
cushings syndrome diagnostic studies
hx and physical exam
labs: 3 standard tests - 24 hour urinary free cortisol - late night salivary cortisol - overnight dexmethasone suppression test
labs will include an increase in cortisol, sodium, and glucose
a decrease in potassium
if underlying cause for cushings syndrome is pituitary adenoma surgical removal of pituitary gland will most likely be required
cushings syndrome pharmacological care
if cause is by corticosteroid use, slowly decrease medication under medical supervision
if cause is by pituitary tumor or tumor that release ACTH, the tumor will be removed (transphenoidal surgery)
if cause if due to an adrenal tumor or other tumors, the tumor will be removed
- if tumor cannot be removed then medicatioin will be needed to block the release of cortisol
pharmacological interventions:
- agents that inhibit steroidogenesis:
- metyrapone
- mitotane
- ketocoriazole
diet including sufficient calcium and vitamin D
cushings syndrome management
monitor signs of hypokalemia and vit
health promotion:
need for lifelong treatment
medication management
need to increase activities, slowly and gradually
body changes from disease may reverse but can take months to years to see changes
monitor signs of depression or difficulty coping
what is pheochromocytoma
benign tumor of the adrenal medulla
causes the adrenal medulla to secrete too much epinephrine and norepinephrine
pheochromocytoma manifestations
abdominal pain chet pain irritabiltiy nervousness severe stress response unusual skin pallor palpitations with tachycardia severe headache diaphoresis weight loss tremors hypertension difficulty coping
pheochromocytoma diagnostic studies
adrenal biopsy
abdominal CT scan
MRI
MIBG scintiscan
- tet that uses injected radioactive material and special scanner to locate or confirm pheochromocytoma
labs:
-24 hour urine collection
- increase catecholamines
serum glucose levels
a client with hypertension, especially if it severe and reffractory to medication should be evaluated
pheochromocytoma pharmacological care
pharamcological intervention:
pre-operatively:
- antihypertensives
- antidysrhythmic
beta adrenergic blocking: propanolol and nadolol
tyrosin inhibitors
alpha adrenergic blocking agents: post-operatively
- phenoxybenzamine
pheochromocytoma management
vitals
meds
keep phentolamine available for treatment of a hypertensive crisis
DO NOT palpate the abdomen
if bilateral adrenalectomy is performed, lifelong steroid therapy will be required
what is diabetes mellitus
pancreas produced too little insulin or cells to stop responding to insuline
results in hyperglycemia
type 1: thought to be genetic autoimmune response
type 2: lifestyle factors
diabetes mellitus manifestations
hyperglycemia
fatigue
weight loss with type 1 only
blurred vision
possible vaginal infections
slow wound healing
polydipsia
polyuria
polyphagia
diabetes mellitus diagnostic exams
hx and physical
labs;
fasting blood sugar
oral glucose tolerance test
glycosylated hemoglobin test
diabetes mellitus pharmacological care
eat foods high in nutrition and low in fat and calories
exercise to lower glucose levels
meds for type 1 diabetes mellitus
insulin
hypertensive meds:
- ACE inhibitors
- ARBs
cholesterol-lowering drugs
- statins
Pramlinitide
meds for type 2 diabetes mellitus
oral hypoglycemic meds
- sulfonylureas
- meglitinides
- biguanides
- thiazolidinediones
metofmrin is the first line therapy for most clients
diabetes mellitus management
teach about med interactions with insulin and oral hypoglycemic meds
teach client to maintain:
balanced diet
eat carbohydrate shake with protein before strenuous exercise
self monitor blood glucose
carry rapid absorbing carbs
self monitor blood glucose
perform appropriate foot care
wear a med alert bracelet
receive regular eye exams
meds that can increase blood glucose levels
- glucocorticoids
- thiazide diuretics
- thyroid agents
- oral contraceptive
- estrogen
meds that can decrease blood glucose levels
aspirin alcohol oral anticoagulants beta blockers tricyclic antidepressants tetracyclines MAOIs
proper foot care for diabetes mellitus
wash feet daily with soap and water
do not soak feet
pat to dry, not rub
attend to corn, calluses but never cut on your own
lotion, but not in between toes
cotton socks and can change if seaty
no heating pads, electric blankets on feet
do not wear circular garters
hypoglycemia manifestations
diaphoresis
cold, clammy skin
anxiety
tremors
headache
slurred speech
client will be weak
nausea and experience mental confusion
hypoglycemia management
if client is conscious and able to swallow; give at least 15 g of carbs - 4 oz of orange juice - regular soda - 2 tbsp of raisins - 4-5 saltine cracklers - 4 tsp of sugar - 1 tbsp of honey or corn syrup
check blood sugar 15 min after intervention
if still less than 70, then repeat the intervention
retinopathy
cause blindness
nephropathy
progressive decrease in kidney function
eventually leading to end stage renal disease
neuropathy
deterioration of nervous system
what is diabetic ketoacidosis
acute complication of DM
severe insulin deficiency and has sudden onset
typically caused by undiagnose diabetes or the inadequacy of prescribed therapy
DKA manifestations
blood sugar greater than 300
pH less than 7.35
fruity sweet odor in breath
Kussmauls rrespirations
flushed appearance
dry skin
metabolic acidosis
thirst
polyuria
anorexia
vomiting
can lead to shock and coma if not treted properly
DKA care
correct fluid depletion - IV fluids
correct electrolyte depletion
- potassium
correct metbolic acidosis
- by lowering the blood sugar with short acting insulin
- given continuous infusion
when blood sugar levels fall below 250, IV should be changed to dextrose containing solution
- 0.9% NaCl
- 5% dextrose
what is hyperosmolar hyperglycemic state (HHS)
complication of diabetes mellitus type 2
untreated high blood sugar levels in high serum osmolality without ketoacidosis
has a gradual onset
HHS manifestations
severe hyperglycemia
usually greater than 600
pH less than 7.4
negative ketones
prfound dehydration
altered level of consciousness
usually precipitated by physcial stress, such as an infection
in non-diabetics, HHS can occur due to tube feedings without supplemental water or because of a too rapid rate of infusion for parenteral nutrition
HHS pharmacological care
aggressive IV rehydration with normal saline or LR
lowering the blood sugar with short-acting insulin (regular)
when blood sugar levels falls below 250 –> IV solution should be changed to dextrose containing solution
- 0.9% NaCl
- 55 dextrose
