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Pharmacology > Chapter 12: endocrine disorders > Flashcards

Chapter 12: endocrine disorders Flashcards

1
Q

purpose of hormones

A

regulate activity of certain cells/organs essential for ADLs

(digestion, metabolism, growth, reproduction, mood control)

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2
Q

major hormones

A
  • thyroid
  • parathyroid
  • pancreatic insulin and glucagon
  • epinephrine and norepinephrine
  • several steroids
  • gonadal hormones
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3
Q

what do hormone regulate

A
  • digestive secretions and motor activity
  • energy production/regulation
  • internal homeostasis
  • reproduction/lactation
  • growth and development
  • adaptation (acclimatization and immunity)
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4
Q

what are the 3 kinds of hormones

A

protein, amine, steroid

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5
Q

mechanisms of action for protein hormones

A

exerts effects on receptors in the membrane and bind to receptors on the outside of the membrane

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6
Q

which type of hormone has the most rapid effect

A

protein hormones

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7
Q

mechanism of action for amine hormones

A

also protein hormones so they show similar fast response

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8
Q

mechanism of action of steroid hormones

A

bind to the intercellular receptors and have slow action

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9
Q

negative feedback

A

hormone produces a physiologic effect that. When it is strong enough, further secretion of the hormone is inhibited, which then inhibits the physiologic effect

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10
Q

what could cause increased hormone secretion

A

stimuli from emotions, perceptions, or behaviors

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11
Q

primary hypothyroidism

A

decreased T3 and T4 levels

elevated TSH

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12
Q

secondary hypothyroidism

A

decreased T3, T4, and TSH

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13
Q

what type of things can cause secondary hypothyroidism

A

hashimotos disease, iatrogenic causes, drugs with iodine (lithium)

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14
Q

when are thyroid hormones NOT used for replacement

A

transient hypothyroidism during recovery phase of acute thyroiditis

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15
Q

levothyroxine sodium/thyroxine/L-thyroxine (T4)

(Synthroid, Levoxyl, Unithroid)

clinical uses

A

increase basal metabolism

enhace gluconeogensis

stimulates protein synthesis

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16
Q

liothyronine

(Cytomel, Triostat)

mechanism of action

A

enhances oxygen consumption by most tissues and increases basal metabolic rate

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17
Q

how is myxedema treated

A

with liothyronine and synthroid

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18
Q

metabolism of all thyroid preparations

A

liver

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19
Q

all thyroid preparations are excreted

A

through feces via bile

undergo enterohepatic recirculation

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20
Q

long term thyroid hormone usage can result in

A

decreased bone density of the hip and spine

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21
Q

protocol for reaching therapeutic dose of thyroid hormones

A

monitor TSH q2-3 months and adjust dose 10-25mcg at 6-8 week intervals until normal TSH levels are reached

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22
Q

What decreases T4 absorption

A

bile acid sequestrants, iron salts, antacids

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23
Q

what may decrease response to T4

A

estrogen

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24
Q

What medications are made less effective by T4

A

beta blockers, digoxin, warfarin

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25
Q

T4 contraindications

A

recent MI

thyrotoxicosis if uncomplicated by hypothyroidism

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26
Q

what is the T4 drug of choice and why

A

Thyroxine because od consistent potency, good absorption, and prolonged duration of action

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27
Q

Liothytonine

(Cytomel, Triostat)

mechanism of action

A

enhances oxygen consumption by most tissues and increases basal metabolic rate

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28
Q

liothyronine

(Cytomel, triostat)

clinical uses

A

treatment of myxedema (with synthroid)

short term suppression of TSH for patients having surgery for thyroid cancer

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29
Q

how hypothyroid medications interact with anticoagulants

A

thyroid increases catabolism of vitamin K-dependent clotting factor

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30
Q

how hypothyroid medications interact with hypoglycemics

A

may have to increase dose of hypoglycemic

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31
Q

how do hypothyroid medications interact with bile acid sequestrants

A

they impair absorption of T4 and T3

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32
Q

how do hypothyroid medications interact with tricyclics

A

increases tricyclic antidepressant effects because it makes receptors more sensitive

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33
Q

how do hypothyroid medications interact with digoxin

A

causes digoxin toxicity

decreased dosages of digoxin are needed

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34
Q

liothyronine contraindications

A

diagnosed but untreated adrenal cortical insufficiency

untreated thyrotoxicosis

hypersensitivity

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35
Q

Is Synthroid or liothyronine more cardiotoxic?

A

liothyronine

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36
Q

liothyronine conscientious considerations

A

it has a shorter half-life than other thyroid preparations

dosage adjustment with hepatic impairment

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37
Q

Liotrix

(Thyrolar, Euthroid)

mechanism of action

A

increases metabolic rate of body tissues by promoting gluconeogenesis and increasing the utilization of glycogen stores

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38
Q

Liotrix (Thyrolar) clinical uses

A

any type of hypothyroidism except during recovery from subacute thyroiditis

treatment/prevention of euthyroid goiters

supression testing

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39
Q

What is Liotrix a combination of

A

liothyronine (T3) and levothyroxine (T4)

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40
Q

Signs of hyperthyroidism

A

weight loss, palpitations, increased apetite, tremors, nervoussness, tachycardia, headache, HTN, menstrual irregularities)

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41
Q

when should thyroid medications be held

A

HR >100bpm

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42
Q

patient education for thyroid hormones

A

same time every day (morning)

TFTs at least yearly

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43
Q

how long until you see the full effect of thyroid hormones

A

a month

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44
Q

what is the most common cause of hyperthyroidism

A

Grave’s disease

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45
Q

liotrix contraindications

A

thyrotoxicosis

MI without hypothyroidism

hypersensitivity

older patient with cardiac problems

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46
Q

Grave’s disease

A

thyroid hyperfunction leads to TSH suppression because the feedback loop from elevated levels of thyroid hormone are not being controlled by the immune system

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47
Q

what should be monitored for a patient taking medication for hyperthyroid

A

TSH and CBC for first 3 months for agranulocytosis

weight 2-3x/week

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48
Q

conscientious considerations for hyperthyroid medications

A

may cause goiter or cretinism in fetus

may need to decrease doses of beta-blockers, digoxin, theophylline

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49
Q

hyperthyroid medications

patient education

A

evenly space doses throughout the day

dietary sources of iodine

call if: fever, sore throat, bleeding, rash, jaundice, N/V

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50
Q

drugs used to treat hypothyroidism

A

T4

T3

combinations of the 2

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51
Q

drugs used to treat hyperthyroid

A

PTU

methimazole

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52
Q

propylthiouracil (PTU)

mechanism of action

A

inhibits oxidation of iodine in thyroid gland and blocks synthesis of T3 and T4

(time released)

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53
Q

PTU clinical uses

A

pallative treatment of hyperthyroidism

adjunct in prep for thyroidectomy or radioactive iodine therapy

control hyperthyroidism while awaiting spontaneous remission

treatment of thyroxicosis

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54
Q

PTU and warfarin

A

anticoagulant effect may be increased

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55
Q

PTU contraindications

A

pregnancy and breastfeeding

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56
Q

Which is preferred for treating thyroid storm

PTU or methimazole and why

A

PTU because it better inhibits synthesis and peripheral conversion of thyroid hormone

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57
Q

Patient education for PTU

A

take the same time every day in regard to meals

(either always with meals or always between meals)

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58
Q

methimazole mechanism of action

A

inhibits synthesis of thyroid hormone

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59
Q

methimazole clinical uses

A

same as PTU

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60
Q

when can you see the peak effect of methimazole (tapazole)

A

4-10 weeks

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61
Q

how long can a patient be on a maintenance dose of methimazole

A

up to 2 years

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62
Q

methimazole and warfarin

A

may decrease anticoagulant effect

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63
Q

what medications will be decreased by methimazole

A

codein, hydrocodone, oxycodone, tramadol

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64
Q

cause pf primary hyperparathyroidism

A

adenomas, chief cell hyperplasia, or hypertophy

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65
Q

causes of secondary hyperparathyroidism

A

chronic kidney failure on dialysis

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66
Q

why does chronic kidney failure cause hyperparathyroidism

A

failing kidneys do not convert vitamin D to active form and do not excrete as much phosphorus

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67
Q

hyperparathyroid drugs can be broken into what 2 main groups

A

antiresorptive drugs

drugs that interfere with PTH secretion

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68
Q

what 2 categories are antiresorptive drugs broken into

A

estrogen-like compounds, SERMS

biophosphates and calcitonin

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69
Q

what is the only marketed SERM

A

evista

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70
Q

cinacalcet (sensispar)

mechanism of action

A

intereferes with PTH secretion by increasing the sensitivity of calcium-sensing receptors on the parathyroid gland

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71
Q

clinical uses of cinacalcet

A

hyperparathyroidism in dialysis patients

hypercalcemia in patients with parathyroid carcinoma

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72
Q

cinacalcet interactions

A

amitriptyline and nortriptylene will increse the presence of cinacalcet

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73
Q

what should patient on cinacalcet be monitored for

A

hypocalcemia

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74
Q

signs of hypocalcemia

A

paresthesia, myalgias, tetany, cramping, and convulsions

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75
Q

Sensispar in patients with primary hyperparathyroidism

A

Not approved by FDA

76
Q

patient education for sensispar

A

take with food

77
Q

hypoparathyroidism

A

decreased levels of PTH that lead to hypocalcemia

(removal of parathyroid gland)

78
Q

symptoms of hypoparathyroidism

A

muscle spasms

convulsions

gradual paralysis with dyspnea

79
Q

idiopathic hypoparathyroidism

A

serum calcium is decreased

serum phosphate is increased

80
Q

drug treatment of hypoparathyroidism consist of

A

either phosphorus or calcium, or both

81
Q

calcitrol mechanisms of action

A
  • 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
82
Q

clinical uses of calcijex (calcitrol)

A

hypocalcemia

adjunct in renal dialysis

reducing elevated parathyroid hormone levels

83
Q

clinical use of rocaltrol (calcitrol)

A

postmenopausal osteoporosis

84
Q

calcitrol interactions

A

CCBs

85
Q

how often should seum calcium be monitored when starting treatment with calcitrol

A

twice weekly early in treatment

86
Q

what are early signs of calcitrol overdose

A

weakness, headache, nausea, metallic taste, vomiting, constipation, muscle/bone pain

87
Q

what are late signs of calcitrol overdose

A

poluria, polydipsia, anorexia, somnolence, weight loss, photophobia, rhinorrhea, prititus, hallucinations, hyperthermia, HTN, arrythmias

88
Q

hormones secreted by the ANTERIOR pituitary gland

A
  • growth hormones
  • follicle stimulating hormone
  • lutenizing hormone
  • TSH
  • lactogenic factor (Prolactin)
  • ACTH
  • melanocyte-stimulating hormone
89
Q

hormones secreted by teh POSTERIOR pituitary gland

A

vasopressin and oxytocin

90
Q

diabetes insipidus

A

insufficient secretion of vasopressin causes the body to loose the ability to concentrate urine

91
Q

oversecretion of vasopressin causes

A

syndrome of inapropriate antidiuretic hormone

92
Q

examples of drugs that affect the posterior pituitary

A

vasopressin

oxytocin

desmopressin

lypressin

93
Q

what should be monitored in patients taking medications that affect the posterior pituitary

A

urine osmolality and volume

ECG

94
Q

Vasopressin (Pitressin) is also called

A

antidiuretic hormone

95
Q

vasopressin mechanism of action

A

increases water resorption by renal tubules and stimulates smooth muscle receptors in GI tract and arterioles. This causes peristalsis and vasoconstriction

96
Q

clinical uses of vasopressin

A

treat diabetes insipidus

prevent abdominal distention post-op

GI hemorrhage

vasodilatory shock

97
Q

in diabetes insipidus, vasopressin may be administered how

A

intranasaly

98
Q

what should be monitored while on vasopressin and why

A

ECH, fluid/electrolytes because extravasation and necrosis may occur

99
Q

Oxytocin (Pitocin, Syntocinon)

mechanism of action

A

stimulates contraction of uterine smooth muscle and enhances lactation

100
Q

clinical uses of oxytocin

A

Dosage specific to:

induce labor, abortion, control postpartum bleeding

101
Q

oxytocin interactions

A

dinoprostone and misoprostol increase effect

102
Q

oxytocin contraindications

A

anticipation of nonvaginal delivery

103
Q

Desmopressin (DDAVP, stimate)

mechanism of action

A

increases reabsorption of water by increasing permeability of collecting ducts in the kidney

104
Q

clinical uses of desmopressin

A

primary nocturnal enuresis

diabetes insipidus

hemophilia and von Willebrand’s disease

105
Q

what medications increase the effect of desmopressin

A

chlorpropamide and ethanol

106
Q

what medications decrease effect of desmopressin

A

demeclocycline and lithium

107
Q

desmopressin contraindications

A

mild to moderate renal impairment

108
Q

patient education for desmopressin

A

drink only enough water to satisfy thirst

109
Q

How is Lypressin (Diapid) manufactured

A

lysine derivative of vasopressin

harvested from pituitary glands of swine and then stabilized

110
Q

Lypressin mechanism of action

A

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

111
Q

clinical uses of lypressin

A

antidiuretic and vasopressor to control symptoms of diabetes insipidus

112
Q

what medications increase lypressin effect

A

carbamazepin, chlorpropamide, clofibrate

113
Q

which medications decrease effect of lypressin

A

demeclocycline, lithium, and norepinephrine

114
Q

what should be monitored every 3-6 months during therapy with drugs that affect the anterior pituitary

A

bone age and growth

115
Q

Somatrem (Protrpin), and recombinant somatropin (Genotropin, humatrope, norditropin, nutropin, serostim)

drug makeup

A

biosynthesized chain of 192 poypeptide amino acids that is produced by recombinant DNA processes using E. coli as a carrier

116
Q

somatrem and recombinent somatropin mechanism of action

A

minimics human growth hormones

medicated by insulin-like growth factore

117
Q

Somatrem, and recombinent somatrem

clinical uses

A
  • 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
118
Q

Examples of recombinanat somatropin

A
  • genotropin
  • humatrope
  • norditropin
  • nutropin
  • serostim
119
Q

what medications interact with somtrem and recombinant somatropin

A

anabolic steroids

thyroid hormones

120
Q

contraindications for somatrem and recumbinant somatropin

A

closure of epiphyses

active neoplasms

121
Q

what happens with prolonged use of somatrem and recombinanat somatropin in a person who does not have acromegaly

A

acromegaly develops

organ enlargement

DM

arteriosclerosis

HTN

carpal tunnel syndrome

122
Q

what conditions must be determined prior to placing a patient on somatrem or recombinant somatropin

A

sensitivity to any growth hormone products

concomittent use of corticosteroids of ACTH

any untreated hypothyroidism

123
Q

what must be monitored while a patient is on somatrem or

recumbinant somatropin

A

growth curves

periodic thyroid function tests, glucose, and IGF-1 levels

for Prader-Willi syndrome

Turners syndrome

124
Q

symptoms of prader willi syndrome

A

sleep apnea, respiratory infections, snoring

125
Q

symptoms of Turner syndrome

A

ear and cardiovascular disorders

126
Q

what happens after 2 years of treatment with growth hormones

A

growth rate decines

127
Q

what is the result of growth hormone therapy in adults

A

increase in lean body mass, total body water, and physical performance

decrease in body fat and waist circumference

128
Q

when is octreotide (Sandostatin) used

A

to reduce growth hormones in patients with acromegaly that have not responded to other treatment

129
Q

octreotide (Sandostatin)

mechanism of action

A

reducing blood levels of growth hormone and IGF-1

by mimicing the action of somatostatic

(8 sided protein salt)

130
Q

clinical uses for octreotide (Sandostatin)

A

acromegaly

supress severe diarrhea and flushing associated with metastatic cancer

131
Q

which medications may need dosage adjustment if patient is placed on actreotide (Sandostatin)

A

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

132
Q

contraindications for octreotide (Sandostatin)

A

hypersensitivities

133
Q

Acromegaly patients are already at risk for a number of factors that usage of otreotide (Sandostatin) potentiates. What are they

A

diabetes, hypothyroidism, cardiovascular disease

134
Q

patient on octreotide (Sandostatin) for up to a year must be monitored for what

A

gallbladder stones or sludge

135
Q

patient education for octreotide )Sandostatin)

A

has many side effects

136
Q

where are adrenal glands located

A

top of each kidney

137
Q

what is secreted by the inner portion of the adrenal gland

A

epinephrine and norepinephrine and dopamine

138
Q

what is secreted by the outer portion of the adrenal gland

A

aldosterone and cortisol

139
Q

what is produced by outermost layer of adrenal cortex

A

mineralocorticoids

140
Q

what is produced by the middle layer of the adrenal cortex

A

glucocorticoids, cortisol

141
Q

what is roduced by the innermost layer of the adrenal cortex

A

androgens, primarily dehydroepiandrosterone

142
Q

what are the most frequently used drugs for anti-inflammatory and immunosuppressive properties

A

glucocorticoids

143
Q

glucocorticoid mechanism of action

A

suppress inflammatory and immune systems through inhibiting prostaglandins, leukotrienes, and histamine

144
Q

glucocorticoid clinical uses

A

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

145
Q

glucocorticoids predominantly affect what

A

metabolism of carbohydrates

to a lesser extentfats and proteins

146
Q

chronic treatment with glucocorticoids

A

may lead to adrenal suppression

use lowest possible dose for shortest possible time

monitor hematological values, serum electrolytes, serum and glucose levels

147
Q

glucocorticoids in relation to strss and infection

A

dosing may need adjusted with stress

signs of infection may be masked

148
Q

when should glucocorticoids be administered

A

in the morning to coincide with body’s natural secretion of cortisol

give with meals if PO

shake suspension if given SC or IM

149
Q

glucocorticoid patient education

A

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

150
Q

glucocorticoids and oral anticoagulants

A

may increase prothrombin time

151
Q

glucocorticoids and potassium-depleting diuretics

A

risks for hypokalemia

152
Q

glucocorticoids and cardiac glycosides

A

increased risk for cardiac toxicity and arrhythmia

153
Q

glucocorticoids and calcium

A

interferes with calcium absorption

154
Q

glucocorticoids and St. John’s wort

A

decreases absorption of glucocorticoids

155
Q

glucocorticoid contraindications

A

fungal disease

live virus vaccine

HTN

HF

renal impairment

infections resistant to ABT treatment

156
Q

serious effects of long term glucocorticoid use

A

hypocalcemia, osteoporosis, edema, muscle wasting, fluid/electrolyte disturbance, spontaneous fractures, amenorrhea, cataracts, glaucoma, peptic ulcer disease, CHF

157
Q

serious effects of abrupt glucocorticoid withdrawal from long term therapy

A

anorexia, nausea, fever, headache, joint pain, rebound inflammation, fatigue, weakness, lethargy, dizziness, orthostatic hypotension

158
Q

why must discontinuation of glucocorticoids be gradual

A

symptoms of abrupt withdrawal can last up to a year

159
Q

conscientious consideration for glucocorticoids

A

page 216

160
Q

fludrocortisone (Florinef)

clinical uses

A

replace aldosterone in Addison’s disease

congenital adrenal insufficiency

161
Q

fludrocortisone (Florinef)

drug make-up

A

synthetic corticosteroid

162
Q

florinef in low doses

A

acts on distal tubules to increase potassum and hydrogen ion secretion, thereby replacing sodium

163
Q

florinef in high doses

A

inhibits exogenous adrenal cortical secretion, thymic activity, and secretion of corticotropin in the pituitary gland

164
Q

what medication interact with Fludrocortisone (Florinef) by causing excessive potassium depletion

A

amphotericin

loop diuretics

thiazide diuretics

165
Q

florinef and digitalis

A

can induce dig toxicity and hypokalemia

166
Q

which medications will decrease effect of florinef

A

rifampin

barbituates

hydantoins

167
Q

serious side effects can result if florinef is taken with

A

oral contraceptives

other corticosteroids

168
Q

how long should florinef therapy last and why

A

no longer than a few weeks cause it can be addictive

169
Q

signs of florinef overdose requiring emergency attention

A

muscle weakness, HYN, unusual weight gain, hypokalemia, water retention

170
Q

symptoms of abrupt florinef withdrawal

A

anorexia, nausea, fever, headache, joint pain, rebound inflammation, fatigue, weakness, lethargy, dizzines, and orthostatic hypotension

171
Q

florinef with pregnancy

A

contraindicated, can absorb just by touching

172
Q

what should be avoided while a patient is taking florinef

A

skin tests

vaccinations

alcohol

173
Q

diet while on florinef

A

high protein

low salt

potassium rich

174
Q

drugs used to treat adrenal insufficiency

A

aminoglutamide (Cytadren)

fludrocortisone (Florinef)

anastrozole (Arimidex)

175
Q

aminoglutamide (Cytadren)

mechanism of action

A

adrenal androgen inhibitor

blocks corticosteroids from being made which stops them from signaling the body to produce more hormones

176
Q

aminoglutamide (Cytadren)

clinical uses

A
  • 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
177
Q

aminoglutethimide (Cytadren)

interactions

A

all corticosteroids

178
Q

cytadren contraindications

A

hypersensitivities

pregnancy/lactation

179
Q

what labs should be monitored while on cytadren

A

thyroid function, baseline hematological, serum glutamicoxaloacetic transaminase, alkaline phosphatase, bilirubin

180
Q

other conscientious considerations for cytadren

A

page 218

181
Q

anastrozole (Arimedex)

mechanism of action

A

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

182
Q

anastrozole (Arimedex)

clinical uses

A

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

183
Q

anastrozole (Arimedex)

interactions

A

decreased effects with estrogen replacement therapy

page 219

184
Q

anastrozole (Arimedex) contraindications

A

Pregnancy

185
Q

implications for pregnant, pediatric, geriatric patients

A

page 219-220

Pharmacology (28 decks)

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