Chapter 12: endocrine disorders Flashcards
purpose of hormones
regulate activity of certain cells/organs essential for ADLs
(digestion, metabolism, growth, reproduction, mood control)
major hormones
- thyroid
- parathyroid
- pancreatic insulin and glucagon
- epinephrine and norepinephrine
- several steroids
- gonadal hormones
what do hormone regulate
- digestive secretions and motor activity
- energy production/regulation
- internal homeostasis
- reproduction/lactation
- growth and development
- adaptation (acclimatization and immunity)
what are the 3 kinds of hormones
protein, amine, steroid
mechanisms of action for protein hormones
exerts effects on receptors in the membrane and bind to receptors on the outside of the membrane
which type of hormone has the most rapid effect
protein hormones
mechanism of action for amine hormones
also protein hormones so they show similar fast response
mechanism of action of steroid hormones
bind to the intercellular receptors and have slow action
negative feedback
hormone produces a physiologic effect that. When it is strong enough, further secretion of the hormone is inhibited, which then inhibits the physiologic effect
what could cause increased hormone secretion
stimuli from emotions, perceptions, or behaviors
primary hypothyroidism
decreased T3 and T4 levels
elevated TSH
secondary hypothyroidism
decreased T3, T4, and TSH
what type of things can cause secondary hypothyroidism
hashimotos disease, iatrogenic causes, drugs with iodine (lithium)
when are thyroid hormones NOT used for replacement
transient hypothyroidism during recovery phase of acute thyroiditis
levothyroxine sodium/thyroxine/L-thyroxine (T4)
(Synthroid, Levoxyl, Unithroid)
clinical uses
increase basal metabolism
enhace gluconeogensis
stimulates protein synthesis
liothyronine
(Cytomel, Triostat)
mechanism of action
enhances oxygen consumption by most tissues and increases basal metabolic rate
how is myxedema treated
with liothyronine and synthroid
metabolism of all thyroid preparations
liver
all thyroid preparations are excreted
through feces via bile
undergo enterohepatic recirculation
long term thyroid hormone usage can result in
decreased bone density of the hip and spine
protocol for reaching therapeutic dose of thyroid hormones
monitor TSH q2-3 months and adjust dose 10-25mcg at 6-8 week intervals until normal TSH levels are reached
What decreases T4 absorption
bile acid sequestrants, iron salts, antacids
what may decrease response to T4
estrogen
What medications are made less effective by T4
beta blockers, digoxin, warfarin
T4 contraindications
recent MI
thyrotoxicosis if uncomplicated by hypothyroidism
what is the T4 drug of choice and why
Thyroxine because od consistent potency, good absorption, and prolonged duration of action
Liothytonine
(Cytomel, Triostat)
mechanism of action
enhances oxygen consumption by most tissues and increases basal metabolic rate
liothyronine
(Cytomel, triostat)
clinical uses
treatment of myxedema (with synthroid)
short term suppression of TSH for patients having surgery for thyroid cancer
how hypothyroid medications interact with anticoagulants
thyroid increases catabolism of vitamin K-dependent clotting factor
how hypothyroid medications interact with hypoglycemics
may have to increase dose of hypoglycemic
how do hypothyroid medications interact with bile acid sequestrants
they impair absorption of T4 and T3
how do hypothyroid medications interact with tricyclics
increases tricyclic antidepressant effects because it makes receptors more sensitive
how do hypothyroid medications interact with digoxin
causes digoxin toxicity
decreased dosages of digoxin are needed
liothyronine contraindications
diagnosed but untreated adrenal cortical insufficiency
untreated thyrotoxicosis
hypersensitivity
Is Synthroid or liothyronine more cardiotoxic?
liothyronine
liothyronine conscientious considerations
it has a shorter half-life than other thyroid preparations
dosage adjustment with hepatic impairment
Liotrix
(Thyrolar, Euthroid)
mechanism of action
increases metabolic rate of body tissues by promoting gluconeogenesis and increasing the utilization of glycogen stores
Liotrix (Thyrolar) clinical uses
any type of hypothyroidism except during recovery from subacute thyroiditis
treatment/prevention of euthyroid goiters
supression testing
What is Liotrix a combination of
liothyronine (T3) and levothyroxine (T4)
Signs of hyperthyroidism
weight loss, palpitations, increased apetite, tremors, nervoussness, tachycardia, headache, HTN, menstrual irregularities)
when should thyroid medications be held
HR >100bpm
patient education for thyroid hormones
same time every day (morning)
TFTs at least yearly
how long until you see the full effect of thyroid hormones
a month
what is the most common cause of hyperthyroidism
Grave’s disease
liotrix contraindications
thyrotoxicosis
MI without hypothyroidism
hypersensitivity
older patient with cardiac problems
Grave’s disease
thyroid hyperfunction leads to TSH suppression because the feedback loop from elevated levels of thyroid hormone are not being controlled by the immune system
what should be monitored for a patient taking medication for hyperthyroid
TSH and CBC for first 3 months for agranulocytosis
weight 2-3x/week
conscientious considerations for hyperthyroid medications
may cause goiter or cretinism in fetus
may need to decrease doses of beta-blockers, digoxin, theophylline
hyperthyroid medications
patient education
evenly space doses throughout the day
dietary sources of iodine
call if: fever, sore throat, bleeding, rash, jaundice, N/V
drugs used to treat hypothyroidism
T4
T3
combinations of the 2
drugs used to treat hyperthyroid
PTU
methimazole
propylthiouracil (PTU)
mechanism of action
inhibits oxidation of iodine in thyroid gland and blocks synthesis of T3 and T4
(time released)
PTU clinical uses
pallative treatment of hyperthyroidism
adjunct in prep for thyroidectomy or radioactive iodine therapy
control hyperthyroidism while awaiting spontaneous remission
treatment of thyroxicosis
PTU and warfarin
anticoagulant effect may be increased
PTU contraindications
pregnancy and breastfeeding
Which is preferred for treating thyroid storm
PTU or methimazole and why
PTU because it better inhibits synthesis and peripheral conversion of thyroid hormone
Patient education for PTU
take the same time every day in regard to meals
(either always with meals or always between meals)
methimazole mechanism of action
inhibits synthesis of thyroid hormone
methimazole clinical uses
same as PTU
when can you see the peak effect of methimazole (tapazole)
4-10 weeks
how long can a patient be on a maintenance dose of methimazole
up to 2 years
methimazole and warfarin
may decrease anticoagulant effect
what medications will be decreased by methimazole
codein, hydrocodone, oxycodone, tramadol
cause pf primary hyperparathyroidism
adenomas, chief cell hyperplasia, or hypertophy
causes of secondary hyperparathyroidism
chronic kidney failure on dialysis
why does chronic kidney failure cause hyperparathyroidism
failing kidneys do not convert vitamin D to active form and do not excrete as much phosphorus
hyperparathyroid drugs can be broken into what 2 main groups
antiresorptive drugs
drugs that interfere with PTH secretion
what 2 categories are antiresorptive drugs broken into
estrogen-like compounds, SERMS
biophosphates and calcitonin
what is the only marketed SERM
evista
cinacalcet (sensispar)
mechanism of action
intereferes with PTH secretion by increasing the sensitivity of calcium-sensing receptors on the parathyroid gland
clinical uses of cinacalcet
hyperparathyroidism in dialysis patients
hypercalcemia in patients with parathyroid carcinoma
cinacalcet interactions
amitriptyline and nortriptylene will increse the presence of cinacalcet
what should patient on cinacalcet be monitored for
hypocalcemia
signs of hypocalcemia
paresthesia, myalgias, tetany, cramping, and convulsions
Sensispar in patients with primary hyperparathyroidism
Not approved by FDA
patient education for sensispar
take with food
hypoparathyroidism
decreased levels of PTH that lead to hypocalcemia
(removal of parathyroid gland)
symptoms of hypoparathyroidism
muscle spasms
convulsions
gradual paralysis with dyspnea
idiopathic hypoparathyroidism
serum calcium is decreased
serum phosphate is increased
drug treatment of hypoparathyroidism consist of
either phosphorus or calcium, or both
calcitrol mechanisms of action
- stimulates calcium and phosphate absorption from small intestine
- promotes secretion of calcium from bone to blood
- promotes renal tubule phosphate reabsorptionacts on parathyroid gland to suppress hormone synthesis and secretion
- an analogue of fat-soluble vitamin D
clinical uses of calcijex (calcitrol)
hypocalcemia
adjunct in renal dialysis
reducing elevated parathyroid hormone levels
clinical use of rocaltrol (calcitrol)
postmenopausal osteoporosis
calcitrol interactions
CCBs
how often should seum calcium be monitored when starting treatment with calcitrol
twice weekly early in treatment
what are early signs of calcitrol overdose
weakness, headache, nausea, metallic taste, vomiting, constipation, muscle/bone pain
what are late signs of calcitrol overdose
poluria, polydipsia, anorexia, somnolence, weight loss, photophobia, rhinorrhea, prititus, hallucinations, hyperthermia, HTN, arrythmias
hormones secreted by the ANTERIOR pituitary gland
- growth hormones
- follicle stimulating hormone
- lutenizing hormone
- TSH
- lactogenic factor (Prolactin)
- ACTH
- melanocyte-stimulating hormone
hormones secreted by teh POSTERIOR pituitary gland
vasopressin and oxytocin
diabetes insipidus
insufficient secretion of vasopressin causes the body to loose the ability to concentrate urine
oversecretion of vasopressin causes
syndrome of inapropriate antidiuretic hormone
examples of drugs that affect the posterior pituitary
vasopressin
oxytocin
desmopressin
lypressin
what should be monitored in patients taking medications that affect the posterior pituitary
urine osmolality and volume
ECG
Vasopressin (Pitressin) is also called
antidiuretic hormone
vasopressin mechanism of action
increases water resorption by renal tubules and stimulates smooth muscle receptors in GI tract and arterioles. This causes peristalsis and vasoconstriction
clinical uses of vasopressin
treat diabetes insipidus
prevent abdominal distention post-op
GI hemorrhage
vasodilatory shock
in diabetes insipidus, vasopressin may be administered how
intranasaly
what should be monitored while on vasopressin and why
ECH, fluid/electrolytes because extravasation and necrosis may occur
Oxytocin (Pitocin, Syntocinon)
mechanism of action
stimulates contraction of uterine smooth muscle and enhances lactation
clinical uses of oxytocin
Dosage specific to:
induce labor, abortion, control postpartum bleeding
oxytocin interactions
dinoprostone and misoprostol increase effect
oxytocin contraindications
anticipation of nonvaginal delivery
Desmopressin (DDAVP, stimate)
mechanism of action
increases reabsorption of water by increasing permeability of collecting ducts in the kidney
clinical uses of desmopressin
primary nocturnal enuresis
diabetes insipidus
hemophilia and von Willebrand’s disease
what medications increase the effect of desmopressin
chlorpropamide and ethanol
what medications decrease effect of desmopressin
demeclocycline and lithium
desmopressin contraindications
mild to moderate renal impairment
patient education for desmopressin
drink only enough water to satisfy thirst
How is Lypressin (Diapid) manufactured
lysine derivative of vasopressin
harvested from pituitary glands of swine and then stabilized
Lypressin mechanism of action
promotes the reabsorption of water by increasing the cellular permeability of the kidney’s collecting ducts. This decreases urine output by increasing the osmolality of urine
clinical uses of lypressin
antidiuretic and vasopressor to control symptoms of diabetes insipidus
what medications increase lypressin effect
carbamazepin, chlorpropamide, clofibrate
which medications decrease effect of lypressin
demeclocycline, lithium, and norepinephrine
what should be monitored every 3-6 months during therapy with drugs that affect the anterior pituitary
bone age and growth
Somatrem (Protrpin), and recombinant somatropin (Genotropin, humatrope, norditropin, nutropin, serostim)
drug makeup
biosynthesized chain of 192 poypeptide amino acids that is produced by recombinant DNA processes using E. coli as a carrier
somatrem and recombinent somatropin mechanism of action
minimics human growth hormones
medicated by insulin-like growth factore
Somatrem, and recombinent somatrem
clinical uses
- long term treatment of growth failure caused by pituitary growth hormone deficienfiency (pituitary dwarfism)
- hypopituitarism from disease, radiation, surgery, ot traum
- negative response to standard growth hormone stimulation test
Examples of recombinanat somatropin
- genotropin
- humatrope
- norditropin
- nutropin
- serostim
what medications interact with somtrem and recombinant somatropin
anabolic steroids
thyroid hormones
contraindications for somatrem and recumbinant somatropin
closure of epiphyses
active neoplasms
what happens with prolonged use of somatrem and recombinanat somatropin in a person who does not have acromegaly
acromegaly develops
organ enlargement
DM
arteriosclerosis
HTN
carpal tunnel syndrome
what conditions must be determined prior to placing a patient on somatrem or recombinant somatropin
sensitivity to any growth hormone products
concomittent use of corticosteroids of ACTH
any untreated hypothyroidism
what must be monitored while a patient is on somatrem or
recumbinant somatropin
growth curves
periodic thyroid function tests, glucose, and IGF-1 levels
for Prader-Willi syndrome
Turners syndrome
symptoms of prader willi syndrome
sleep apnea, respiratory infections, snoring
symptoms of Turner syndrome
ear and cardiovascular disorders
what happens after 2 years of treatment with growth hormones
growth rate decines
what is the result of growth hormone therapy in adults
increase in lean body mass, total body water, and physical performance
decrease in body fat and waist circumference
when is octreotide (Sandostatin) used
to reduce growth hormones in patients with acromegaly that have not responded to other treatment
octreotide (Sandostatin)
mechanism of action
reducing blood levels of growth hormone and IGF-1
by mimicing the action of somatostatic
(8 sided protein salt)
clinical uses for octreotide (Sandostatin)
acromegaly
supress severe diarrhea and flushing associated with metastatic cancer
which medications may need dosage adjustment if patient is placed on actreotide (Sandostatin)
insulin and oral hypoglycemics, beta blockers, CCBs, any drug affecting fluid/electrolyte balance
any drugs with low therapeutic index should be used with caution because it is cleared by CYP450 enzymes
contraindications for octreotide (Sandostatin)
hypersensitivities
Acromegaly patients are already at risk for a number of factors that usage of otreotide (Sandostatin) potentiates. What are they
diabetes, hypothyroidism, cardiovascular disease
patient on octreotide (Sandostatin) for up to a year must be monitored for what
gallbladder stones or sludge
patient education for octreotide )Sandostatin)
has many side effects
where are adrenal glands located
top of each kidney
what is secreted by the inner portion of the adrenal gland
epinephrine and norepinephrine and dopamine
what is secreted by the outer portion of the adrenal gland
aldosterone and cortisol
what is produced by outermost layer of adrenal cortex
mineralocorticoids
what is produced by the middle layer of the adrenal cortex
glucocorticoids, cortisol
what is roduced by the innermost layer of the adrenal cortex
androgens, primarily dehydroepiandrosterone
what are the most frequently used drugs for anti-inflammatory and immunosuppressive properties
glucocorticoids
glucocorticoid mechanism of action
suppress inflammatory and immune systems through inhibiting prostaglandins, leukotrienes, and histamine
glucocorticoid clinical uses
hormone replacement in Addison’s disease
cancer therapy
decrease inflammation in SLE (lupus)
RA
IBD
asthma/COPD
respiratory distress syndrome in infants
acute renal insufficiency
shock
simple inflammatory rashes
glucocorticoids predominantly affect what
metabolism of carbohydrates
to a lesser extentfats and proteins
chronic treatment with glucocorticoids
may lead to adrenal suppression
use lowest possible dose for shortest possible time
monitor hematological values, serum electrolytes, serum and glucose levels
glucocorticoids in relation to strss and infection
dosing may need adjusted with stress
signs of infection may be masked
when should glucocorticoids be administered
in the morning to coincide with body’s natural secretion of cortisol
give with meals if PO
shake suspension if given SC or IM
glucocorticoid patient education
avoid people with contagious diseases and vaccines
do not have surgery
wear medical alert bracelet
diet should be high in protein, calcium, potassium and low in sodium and carbs
avoid alcohol
abrupt withdrawals
glucocorticoids and oral anticoagulants
may increase prothrombin time
glucocorticoids and potassium-depleting diuretics
risks for hypokalemia
glucocorticoids and cardiac glycosides
increased risk for cardiac toxicity and arrhythmia
glucocorticoids and calcium
interferes with calcium absorption
glucocorticoids and St. John’s wort
decreases absorption of glucocorticoids
glucocorticoid contraindications
fungal disease
live virus vaccine
HTN
HF
renal impairment
infections resistant to ABT treatment
serious effects of long term glucocorticoid use
hypocalcemia, osteoporosis, edema, muscle wasting, fluid/electrolyte disturbance, spontaneous fractures, amenorrhea, cataracts, glaucoma, peptic ulcer disease, CHF
serious effects of abrupt glucocorticoid withdrawal from long term therapy
anorexia, nausea, fever, headache, joint pain, rebound inflammation, fatigue, weakness, lethargy, dizziness, orthostatic hypotension
why must discontinuation of glucocorticoids be gradual
symptoms of abrupt withdrawal can last up to a year
conscientious consideration for glucocorticoids
page 216
fludrocortisone (Florinef)
clinical uses
replace aldosterone in Addison’s disease
congenital adrenal insufficiency
fludrocortisone (Florinef)
drug make-up
synthetic corticosteroid
florinef in low doses
acts on distal tubules to increase potassum and hydrogen ion secretion, thereby replacing sodium
florinef in high doses
inhibits exogenous adrenal cortical secretion, thymic activity, and secretion of corticotropin in the pituitary gland
what medication interact with Fludrocortisone (Florinef) by causing excessive potassium depletion
amphotericin
loop diuretics
thiazide diuretics
florinef and digitalis
can induce dig toxicity and hypokalemia
which medications will decrease effect of florinef
rifampin
barbituates
hydantoins
serious side effects can result if florinef is taken with
oral contraceptives
other corticosteroids
how long should florinef therapy last and why
no longer than a few weeks cause it can be addictive
signs of florinef overdose requiring emergency attention
muscle weakness, HYN, unusual weight gain, hypokalemia, water retention
symptoms of abrupt florinef withdrawal
anorexia, nausea, fever, headache, joint pain, rebound inflammation, fatigue, weakness, lethargy, dizzines, and orthostatic hypotension
florinef with pregnancy
contraindicated, can absorb just by touching
what should be avoided while a patient is taking florinef
skin tests
vaccinations
alcohol
diet while on florinef
high protein
low salt
potassium rich
drugs used to treat adrenal insufficiency
aminoglutamide (Cytadren)
fludrocortisone (Florinef)
anastrozole (Arimidex)
aminoglutamide (Cytadren)
mechanism of action
adrenal androgen inhibitor
blocks corticosteroids from being made which stops them from signaling the body to produce more hormones
aminoglutamide (Cytadren)
clinical uses
- suppression of adrenal function in certain patients with cushings syndrome
- adrenal carcinoma and ectopic ACTH-producing tumors
- treatment of breast cancer in postmenopausal women
- treatment of metastatic prostate cancer
aminoglutethimide (Cytadren)
interactions
all corticosteroids
cytadren contraindications
hypersensitivities
pregnancy/lactation
what labs should be monitored while on cytadren
thyroid function, baseline hematological, serum glutamicoxaloacetic transaminase, alkaline phosphatase, bilirubin
other conscientious considerations for cytadren
page 218
anastrozole (Arimedex)
mechanism of action
orally active, potent, third line aromatase inhibitor in the management of hormone-sensitive breast cancer
can decrease tumor mass or delay progression of tumor growth
anastrozole (Arimedex)
clinical uses
breast cancer in postmenopausal women
adjuvant therapy for early estrogen receptor positive breast cancer
first line therapy for metastatic breast cancer
advanced therapy if treatment with tamoxifen fails and disease progression continues
anastrozole (Arimedex)
interactions
decreased effects with estrogen replacement therapy
page 219
anastrozole (Arimedex) contraindications
Pregnancy
implications for pregnant, pediatric, geriatric patients
page 219-220
