Medications Affecting the Endocrine System by Linda Self

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Transcript Medications Affecting the Endocrine System by Linda Self

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Endocrine glands
Hormones—chemical messengers
Water-soluble, protein derived hormones
have short duration of action
Lipid-soluble steroid and thyroid hormones
have longer mechanism of action
Endocrine and nervous systems
interconnected
Circadian cycles-ACTH, cortisol and GH
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Anterior pituitary hormones-GH,
corticotropin, TSH, FSH, LH, prolactin
Posterior pituitary hormones-ADH
(vasopressin) and oxytocin
Adrenal cortex hormones—cortisol and
aldosterone
Thyroid hormones—T3 (triiodothyronine) and
T4 (thyroxine)
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Parathyroid hormone—PTH
Ovarian hormones—estrogens and
progesterone
Testicular hormone—testosterone
Placental hormones-chorionic gonadotropin,
estrogen, progesterone, human placental
lactogen
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Cholecystokinin
Erythropoietin
WBCs which produce cytokines
Prostaglandins and leukotrienes
Sometimes neoplasms
Three mechanisms
Inactivated by liver and kidney enzymes
Sometimes conjugated by the liver and
excreted in bile or urine
Inactivated at receptor sites by enzymes
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Hypofunction-Type 1 diabetes, Addison’s
Hyperfunction—Cushing’s, Grave’s,
Gigantism
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Hypothalamus releases inhibitory and
releasing hormones
Corticotropin releasing hormone—released
during sleep. Increased by vasopressin and
decreased by somatostatin
Growth-hormone releasing hormone—
affected by dopamine, norepinephrine,
epinephrine, GABA, acetylcholine and
serotonin. Is blocked by somatostatin
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Somatostatin decreases the release of growth
hormone, CCK, vasoactive intestinal peptide,
TRH, others
TRH causes release of TSH
GRH (gonadotropin releasing hormone)
causes release of FSH and LH
Prolactin-releasing factor active during
lactation
Prolactin inhibitory factor active at times
other than lactation
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Two act directly on target organs—growth
hormone and prolactin
Five act indirectly by stimulating target
organs to produce hormones:
Corticotropin –ACTH
TSH
FSH
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Luteinizing hormone—gonadotropin,
maturation and rupture of ovarian follicle;
produces corpus luteum; in men, affects
Leydig’s cells and testosterone
Melanocyte stimulating hormone
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Antidiuretic hormone—vasopressin, affects
renal tubules to regulate water balance
Oxytocin—uterine contractions and
movement of milk from breast glands to
nipples
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Equivalent to GnRH
Zoladex (goserelin)
Vantas (histrelin)
Lupron (leuprolide)
Synarel (nafarelin)
Initially stimulate LH and FSH with chronic
administration, inhibits stimulation
Results in equivalent to castration in males and
menopause in women
Cannot be given orally
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Octreotide- Sandostatin; pharmacologically
similar to somatostatin
Use for acromegaly—reduces GH and insulin
like growth factor
Useful in vasoactive intestinal peptide tumors
AIDS
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Cortrosyn (cosyntropin)—synthetic ACTH is
used to test for adrenal insufficiency; IV or IM
Humatrope (growth hormone)-for growth
failure, Turner’s, renal failure growth
retardation. Monitor ephiphyses.
Chorex (HCG)-luteinizing hormone. In men to
evaluate ability of Leydig’s (testosterone); Tx
hypogonadism in pituitary problems and in
cryptorchidism
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Ovidrel (HCG alpha) used w/ menotropins to
induce ovulation
Pergonal (menotropins)-contains FSH and LH;
obtained from urine of menopausal women
Somavert (pegvisomant)—GH receptor
antagonist.
Follistim (follitropin beta)—drug preparation
of FSH used sequentially with HCG
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DDAVP (desmopressin) and Pitressin
(vasopressin)—ADH; used in neurogenic DI,
hemostasis in Von Willebrand’s
Pitocin (oxytocin)-induction of labor, control
postpartum bleeding
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Does not increase muscle mass or strength
greater than seen with exercise alone
Not indicated for anti-aging formula
Adverse effects include—acromegaly,
diabetes, hypertension, increased risk of
cardiovascular disease, tumor growth and
cancer
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Glucocorticoids or steroids
Adrenal cortical secretion
Corticotropin releasing
hormone>>corticotropin>>>>cortisol
With stress, increase in norepi, epi and
cortisol; negative feedback system overruled
Prototype is hydrocortisone
Mineralocortocoid activity is intermediae in
hydrocortisone, prednisolone and low in
newer agents
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Increased glucose production
Decreased cellular use of glucose 2ndary to
decreased effect of insulin
Increased breakdown of protein into amino
acids
Decreased rate of protein formation
Increased breakdown of adipose tissue
Decreaed inflammatory response by
decreasing production of inflammatory
chemicals, decreases numbers of antibodies,
#s of lymphocytes
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Modifies vascular smooth muscle tone
increasing pressor effects of catecholamines
Stimulates renal glucocorticoid and
mineralocorticoid receptors
Can cause muscle atrophy
Decrease bone formation, growth and
increase bone breakdown
Opens airways
Stabilize mast cells
Decrease viscosity of gastric mucous
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Class of steroids affecting fluid and
electrolyte balance
Conserve sodium and eliminate potassium
Controlled by kidney function/Reninangiotensin system
Inadequate secretion causes hyperkalemia,
hyponatremia and ECF deficit
Excessive secretion causes hypokalemia,
hypernatremia and ECF excess
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Male = androgens
Female = estrogens and progesterone
Are secreted by both sexes
Secondary sexual characteristics in men
Affect libido and hair growth in women;
excessive amounts can cause masculizing
effects in women
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Addison’s Disease
Secondary adrenocortical insufficiency
Cushing’s disease
Hyperaldosteronism
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Inhibits arachidonic acid metabolism thus
affecting prostaglandins and leukotrienes
Stabilizes biologic membranes also affecting
prostaglandins and leukotrienes
Inhibits production of interleukin 1, TNF and
other cytokines
Impairs phagocytosis—cells can’t move to
injured site
Impairs functioning of lymphocytes
Inhibit growth of tissues thus delay wound
healing
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Allergic or hypersensitivity disorders
Collagen disorders-lupus, scleroderma and
periarteritis
Dermatologic
Endocrine disorders
Inflammatory bowel disorders
Neoplastic disease—suppress lymphocytes
Neurologic disorders-cerebral edema,
myasthenia gravis
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Asthma and COPD
Arthritis—if three or fewer joint, can give joint
injections; no more than three per year
Chemotherapy induced emesis—strong antiemetic effect, mechanism unknown. Usually
give dose with serotonin antagonist and
Reglan.
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Systemic fungal infections
Hypersensitivity
Those at risk for infections
Diabetes mellitus (be cautious)
Peptic ulcer disease
Heart failure
Renal insufficiency (can accumulate and cause
s/s of hypercorticism)
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Beconase-beclamethasone nasally
Nasonex (mometasone)
Celestone-(betamethasone) orally
Decadron (dexamethasone) po or IM
Hydrocortisone—IV, IM, rectally
Solu-Medrol (methylprednisolone)—po, IM, IV
Kenalog(triamcinolone)—IM or topical
Florinef
(fludrocortisone)*****mineralocorticoid
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Daily administration of 15-20mg of
hydrocortisone or its equivalent for 2 weeks
suppresses the HPA axis
MUST taper down
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Thyroid produces three hormones: thyroxine,
triidothyronine and calcitonin
T3 more potent but with a shorter duration of
action
Production of thyroid hormones is dependent
on iodine and tyrosine (needed to form
thyroglobulin)
Control rate of cellular metabolism, linear
growth, brain function, dentition, bone
development and neural development
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Inhibition of pituitary release of TSH
Increassesd fat metabolism
Increased carbohydrate metabolism
Increased heart rate, force of contraction and
cardiac output
Increase rate of cellular metabolism and
oxygen consumption
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Common causes include: Hashimoto’s
thyroiditis, secondary to treatment for
hyperthyroidism
Treatment with amiodarone, lithium or iodine
preparations
Congenital—cretinism
Myxedema –can progress to coma
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Bruising
Decreased cardiac output
Decreased heart rate
Cardiomegaly
ASHD
Apathy, lethargy
Forgetfulness
Drowsiness
Cold intolerance
Constipation
Fatigue
Puffiness
Increased susceptibility to infections
Increased sensitivity to narcotics, barbiturates, anesthetics
Excessive production of thyroid hormone
 Associated with Graves Disease, nodular
goiter, thyroiditis, overtreatment with thyroid
drugs, pituitary adenoma or thyroid cancer
 Subclinical=reduced TSH but normal T3/T4
Can result in osteoporosis
 Thyroid storm aka thyrotoxicosis
 Have been reported cases of iodine-induced
hyperthyroidism
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Tachycardia
Increased cardiac output
Increased BP
Dysrhythmias
Heart failure
Nervousness, restlessness, insomnia
Heat intolerance
Weight loss
Diarrhea
Weakness
Tremors
Amenorrhea
Increased susceptibility to infection
exophthalmos
 Prototype and drug of choice is Synthroid, Levothroid
(levothyroxine)
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Maximum absorption if taken on empty
stomach
Is T4
TSH (0.5 to 4.2 microunits/L) desired level
Goal is euthyroid with TSH level
Most drugs given will have prolonged effect
Lifelong therapy is indicated
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Thioamide derivatives-- Propylthiouracil and
methimazole. Used before radioactive iodine
therapy
Results may not be apparent for 3 months or
longer
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Thioamide preparation to achieve euthyroid state
Then Iodine preparations—Lugol’s and SSKI
Iodine preparations may be used to reduce size
and vascularity of thyroid before surgery
Can cause: goiter, hyperthyroidism, benefits are
temporary
Radioactive iodine cannot be used effectively for
prolonged time in those who have received
iodine preparations (insufficient uptake
thereafter)
OK TO GIVE THIOAMIDE THEN IODINE
PREPARATION BUT NOT IODINE THEN THIOAMIDE
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Thyroid disorders change metabolism of
other drugs
Children w/congenital hypothyroidism, tx
should be started within 6 weeks of birth
Drug of choice is levothyroxine
Monitor ht. and wt.
If hyperthyroid, can use PTU or methimazole,
discourage radioactive iodine in children
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s/s of thyroid disorders may mimic other
disorders in older adults
Thorough PE and diagnostic workup
Levothyroxine is appropriate
Start with small doses, may increase in small
increments monthly
Monitor vitals closely
For hyperthyroidism, use PTU or
methimazole. May use radioactive iodine.
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Thyrotoxicosis manage in intensive care