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GT BSN/CNL PHARM > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

1
Q

risks of tight glucose control

A

hypoglycemia
hypoglycemic coma

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2
Q

mechanism of action of insulin

A

binds insulin receptor, stimulates GLUT4 channel membrane proliferation (via exocytosis). GLUT4 channels allow glucose to enter the cell

end result: higher intracellular glucose, lower extracellular (plasma) glucose

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3
Q

do the various insulin formulation differ in their pharmacokinetic or pharmacodynamic principles?

A

pharmacokinetic

all are identical pharmacodynamically to endogenous insulin

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4
Q

actions of insulin

A

glycogenesis & cellular uptake of glucose
protein synthesis from amino acids
triglyceride production from fatty acids

(all anabolic actions)

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5
Q

Can you give insulin PO? IV?

A

Only SubQ or IV

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6
Q

Which type of insulin is closest to endogenous insulin (pharmacokinetically)?

A

regular insulin

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7
Q

list the rapid acting insulins

A

aspart
lispro
glulisine

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8
Q

How long after administration is the peak action of rapid acting insulin

A

30-60minutes

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9
Q

NPH is a ______-acting insulin.

A

intermediate

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10
Q

_______ is an insulin with no peak time of activity

A

glargine

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11
Q

which insulins can be mixed together in the same syringe?

A

NPH & short acting insulins

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12
Q

what medication class is metformin

A

biguanide (oral antidiabetic medication)

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13
Q

which two classes of oral antidiabetic medications carry a hypoglycemia risk when administered alone?

A

sulfonylureas
meglitinides

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14
Q

adverse effects of metformin

A

most common: GI upset

decreased B12 & folate absorption
lactic acidosis with toxicity

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15
Q

why do some oral antidiabetics carry a hypoglycemia risk and some don’t?

A

those that do promote insulin release

those that do not work via other mechanisms (decreased insulin resistance, decreased glucose absorption or glucose excretion)

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16
Q

when should metformin be held?

A

hypoperfusion states

such as sepsis, cardiac failure, renal failure, etc.

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17
Q

what is the difference between the meglitinides and the sulfonylureas?

A

meglitinides are shorter acting & only taken with meals

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18
Q

why do thiazolidinediones not work for type 1 diabetics?

A

insulin must be present since the drug works by increasing insulin sensitivity

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19
Q

mechanism of action of alpha glucosidase inhibitors?

A

inhibition of alpha glucosidase enzyme
results in delayed carbohydrate absorption

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20
Q

mechanism of action of sodium glucose cotransporter 2 inhibitors (SGLT2 inhibitors)?

A

inhibition of SGLT2 in renal tubules = increased renal excretion of glucose

SGLT2 is responsible for 90% of glucose reabsorption back into the plasma

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21
Q

actions of glucagon

A

glycogenolysis (increased free glucose)
decreases glyconeogenesis
stimulates glucose production from the liver

opposite of insulin

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22
Q

treatment for growth hormone deficiency?

A

exogenous growth hormone (somatotropin - identical to endogenous)

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23
Q

routes of administration for somatropin?

A

IM or SubQ

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24
Q

adverse effect of somatropin

A

hyperglycemia

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25
Q

treatment for prolactin excess?

A

dopamine agonists
i.e. cabergoline or bromocriptine

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26
Q

function of ADH

A

increase water reabsorption in the collecting ducts (preserves H2O & concentrates the urine)

at very high doses = vasoconstriction & GI smooth muscle contraction

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27
Q

Two ADH replacements?

A

vasopressin
desmopressin (DDAVP)

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28
Q

actions of vasopressin

A

vasoconstriction
smooth muscle contraction

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29
Q

actions of desmopressin (DDAVP)

A

anti-diuresis (H2O reabsorption in collecting ducts)
no vasoconstriction

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30
Q

route of administration of DDAVP

A

PO
intranasal

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31
Q

primary endogenous glucocorticoid?

A

cortisol

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32
Q

primary endogenous mineralocorticoid?

A

aldosterone

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33
Q

s/s cortisol deficiency

A

hypotension
hypoglycemia
cachexia
depression/lethary

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34
Q

s/s cortisol excess

A

HPA axis suppression
hypertension
hyperglycemia
fat redistribution (buffalo hump, etc.)
osteoporosis
menstrual irregularities
infection risk
CNS excitation

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35
Q

s/s aldosterone deficiency

A

hyponatremia
hyperkalemia
acidosis
cellular dehydration

late & untreated can lead to renal failure, CV collapse, death

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36
Q

s/s aldosterone excess

A

myocardial & vascular remodeling & fibrosis
SNS activation
baroreceptor reflex disruption

untreated this leads to decreased contractility, dysrhythmias, hypertension to heart failure & MI

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37
Q

how does ketoconazole treat glucocorticoid excess?

A

blocks glucocorticoid synthesis

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38
Q

What is the drug used for mineralocorticoid excess? What is the drug class?

A

spironolactone
potassium sparing diuretic

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39
Q

What time of day should adrenal hormone replacement therapy be administered?

A

morning
(mimics endogenous secretion)

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40
Q

Is the dose of gluco/mineralocorticoid HIGHER for replacement therapy or for anti-inflammation?

A

Anti-inflammation

for replacement therapy, we just give the dose that results in the patient having normal hormone levels (not suppressing inflammation). Only higher doses (i.e. putting the patient in “excess”) result in decreased inflammation & infection risk

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41
Q

How much higher dose is a stress dose

A

up to 10x

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42
Q

Which glucocorticoid is identical to cortisol?

A

hydrocortisone

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43
Q

what does fludrocortisone do?

A

exogenous mineralocorticoid
(fluid retention, potassium excretion)

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44
Q

Does dexamethasone have more glucocorticoid or mineralocorticoid activity?

A

glucocorticoid. very little mineralocorticoid

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45
Q

What two hormones does the thyroid gland release?

A

T3 & T4

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46
Q

Which is more physiologically active, T3 or T4?

A

T3

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47
Q

A high TSH indicates a _____(low/high) T3 and/or T4 level?

A

low

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48
Q

Which thyroid hormone has a longer half life?

A

T4
(7 days vs. 1 day T3)

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49
Q

Which thyroid hormone is more potent?

A

T3

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50
Q

actions of thyroid hormone

A

increased basal metabolic rate (increased O2 consumption & heat production)

increased HR & contractility (increased CO & myocardial O2 demand)

promotion of growth & development

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51
Q

How many half lives does it take for a drug to reach a plateau level in the body?

A

4

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52
Q

How long does it take levothyroxine to reach steady state

A

approximately one month

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53
Q

Routes of administration of levothyroxine?

A

primarily PO
IV in emergency

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54
Q

levothyroxine is taken 30mins before meals because:

A

absorption is reduced by food

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55
Q

treatment for thyrotoxic crisis (thyroid storm)?

A

medications to suppress thyroid hormone synthesis & release (thionamides)

supportive care:
- beta blockers to attenuate tachycardia
- sedation
- cooling
- fluids

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56
Q

mechanism of action of thionamides?

A

inhibit peroxidase, which results in decreased thyroid hormone synthesis

57
Q

onset of action of thionamides

A

Only decrease synthesis of NEW thyroid hormone. So already synthesized hormone isn’t affected

Thus, full effect can take 3-12 weeks

58
Q

methimazole is preferred over PTU because:

A
  1. longer 1/2 life
  2. more potent
  3. the serious adverse effects are less common
59
Q

adverse effects of methimazole & PTU (thionamides)

A

pruritic rash with initial therapy
arthralgias

rare: agranulocytosis, hepatotoxicity, vasculitis

overdose = hypothyroid symptoms

60
Q

which thionamide is preferred in 1st trimester pregnancy and why?

A

PTU

less placental crossing

61
Q

adverse effect of radioactive iodine (iodine 131)

A

bone marrow depression (results in low RBC, WBC, platelet counts)

62
Q

care precautions for the nurse when caring for a patient taking radioactive iodine

A

less than 30mins per day of patient contact
follow facility protocols for disposal of body wastes

63
Q

high doses of lugol solution can result in

A

hyperthyroid symptoms

64
Q

use for lugol solution

A

rapid and temporary decrease in thyroid hormone

65
Q

how is estrogen metabolized & excreted?

A

hepatic metabolism (CYP450), renal excretion

66
Q

how is progesterone metabolized & excreted?

A

hepatic metabolism (CYP450) & renal excretion

67
Q

non-reproductive effects of estrogen

A
  • maintain bone density & mass
  • vasodilation, decrease LDL, increase HDL
  • increase coagulation & fibrin breakdown
  • CNS protection
  • glucose homeostasis
68
Q

adverse effects of exogenous estrogen administration

A

endometrial CA (d/t hyperplasia)
breast CA
CV thromboembolic events
gall bladder disease

69
Q

non-reproductive effects of progesterone

A

constipation
maternal immune suppression
growth/proliferation of breast ducts

70
Q

adverse effects of exogenous progesterone administration

A

breast tenderness
headache
abdominal discomfort

71
Q

naturally, which hormone is increasing during the proliferative phase of the menstrual cycle

A

estrogen

thus, it should make sense that exogenous estrogen can result in strong endometrial proliferation & thus endometrial CA

72
Q

effects of menopause - i.e. why do women seek treatment?

A

vasomotor symptoms
sleep disturbances
urogenital atrophy
altered lipid metabolism
changes in cognition & sexual response

73
Q

why is hormone therapy for menopause controversial?

A

risk of increased thromboembolic events (CV events like blood clots, MI, CVA, etc.)

74
Q

Why is progesterone added to HT and oral birth control?

A

to prevent endometrial CA

(estrogen only = unopposed proliferation of the endometrium!)
**no uterus, no need to add progesterone!

75
Q

absolute contraindications to HT or hormonal birth control

A

pregnancy
breast or endometrial CA
acute liver disease
uncontrolled hypertension
thrombosis (DVT, MI, CVA)
undiagnosed vaginal bleeding

76
Q

Is a 40 year old heavy smoker a good candidate for hormonal birth control?

A

no (increased risk for thromboembolic events)
but it is not absolutely contraindicated

77
Q

what does SERM stand for and what does it mean?

A

selective estrogen receptor modulator

agonize some estrogen receptors, antagonize others - attempts to provide benefits w/out risks

78
Q

what is the main difference between tamoxifen & raloxifene?

A

raloxifene doesn’t result in endometrial proliferation (i.e. no endometrial CA risk)

79
Q

risks of SERM therapy?

A

endometrial CA risk (only tamoxifen)
increased hot flashes
increased thromboembolism risk

80
Q

benefits of SERM therapy?

A

breast CA prevention
osteoporosis prevention
improved lipid profile

81
Q

why do some women get HT for osteoporosis prevention and others don’t?

A

those that are very high risk for osteo require lifelong therapy.

it is not standard for all women because of the high risk for thromboembolic events as one ages

82
Q

Which hormones are in oral contraceptives?

A

estrogen AND progesterone

or

just progesterone

83
Q

mechanism of action of combination oral contraceptives?

A

suppression of ovulation: high estrogen provides negative feedback to suppress FSH (follicle cannot mature, no ovulation occurs)

also alters cervical mucus & endometrium

84
Q

mechanism of action of minipills?

A

cervical secretion changes

85
Q

what are minipills?

A

progestin-only OCs

86
Q

how many days in a cycle for minipill administration?

A

n/a - this medication is taken continuously throughout the cycle (no placebo)

87
Q

list several other formulations of contraceptives

A

transdermal patch
vaginal ring
subdermal implants
IM/subQ injections
IUDs

88
Q

which two drugs are used for medical abortion?

A

mifepristone (antiprogestin)
misoprostol (prostaglandin)

89
Q

mechanism of action of mifepristone w/ misoprostol

A

mifepristone blocks progesterone receptors, which results in detachment of conceptus as well as cervical softening/dilation

misoprostol is a prostaglandin that directly stimulates uterine contractions

90
Q

what percent of infertility is due to the female?

A

50%

91
Q

mechanism of action of clomiphene

A

blocks estrogen receptors in hypothalamus & pituitary

normally estrogen binds these receptors & provides negative feedback, leading to decreased LH & FSH

when receptors are blocked, LH & FSH continue to be secreted = ovulation

92
Q

what is ovarian hyperstimulation syndrome (OHSS)

A

exogenous hormone administration for infertility leads to exaggerated response –> ovaries swell, leak fluid, & are painful.

Can be dangerous - fluid can collect in abdomen/chest, electrolyte disturbances can occur, blood clots, renal failure, etc.

93
Q

how do menotropins work?

A

they are a 50/50 mixture of LH/FSH. So just work like endogenous LH/FSH –> result in follicular maturation & ovulation

94
Q

adverse effect of menotropins

A

OHSS

95
Q

when should exogenous hCG be administered during fertility treatmnets?

A

after clomiphene or menotropin

(those drugs are for follicular growth, hCG is for ovulation - commonly called “trigger shot”)

96
Q

list four classes of tocolytics

A

beta 2 agonists
calcium channel blockers
COX inhibitors
oxytocin receptor blockers

97
Q

what are tocolytics?

A

drugs that suppress uterine contractions

98
Q

what is terbutaline & how does it work?

A

B2 agonist

agonizes B2 on uterine smooth muscle, resulting in decreased contractions

99
Q

adverse effects of terbutaline?

A

pulmonary edema
hypotension
hyperglycemia
tachycardia

100
Q

what is indomethacin & how does it suppress uterine contractions?

A

COX inhibitor

inhibits prostaglandin synthesis, which results in decreased contractions via cAMP-mediated pathway

101
Q

adverse effects of indomethacin

A

nausea
gastric irritation
increased postpartum bleeding

102
Q

why is magnesium sulfate given for premature labor?

A

fetal neuroprotective effects

103
Q

adverse effects of magnesium sulfate administration?

A

hypotension
flushing
headache & dizziness

SEVERE: hypothermia, paralytic ileus, pulmonary edema

104
Q

fetal effects of magnesium sulfate administration? (i.e. when baby is born, what do you expect?)

A

hypotonia
sleepiness

associated w/ increased infant mortality

105
Q

what drug is indicated to PREVENT preterm labor before it starts?

A

hydroxyprogesterase caproate

106
Q

contraindications of induction of labor

A

umbilical cord prolapse
transverse fetal position
active genital herpes
h/x c-section or myomectomy
placenta previa

107
Q

what are prostaglandins used for in an induction of labor?

A

ripen cervix primarily, but can also contribute to uterine contractions

108
Q

how to administer dinoprostone?

A

transvaginally

109
Q

nursing consideration when administering prostaglandin for induction of labor?

A

monitor fetal heart rate & contractions

fetal distress can occur, tachysystole (rapid contractions) can occur

110
Q

what is oxytocin?

A

endogenous hormone

exogenous version is identical to endogenous

111
Q

effects of oxytocin?

A

uterine stimulation
milk ejection
water retention

112
Q

besides induction of labor, when else is oxytocin given?

A

augmentation of spontaneous labor
postpartum bleeding
abortion

113
Q

most common cause for postpartum hemorrhage?

A

uterine atony (80%)

114
Q

drug of choice for postpartum hemorrhage due to uterine atony?

A

oxytocin

115
Q

besides oxytocin, what else can be given for postpartum hemorrhage?

A

misoprostol (Cytotec)
caboprost tromethamine (Hemabate)
methylergonovine (Methergine)

116
Q

mechanism of action of caboprost tromethamine (Hemabate)

A

prostaglandin that results in uterine contractions and INTENSE vasoconstriction

117
Q

contraindications of caboprost tromethamine (Hemabate)

A

pelvic inflammatory disease
cardiac disease
pulmonary disease
renal disease
liver disease

caution in asthma, hypertension, diabetes

118
Q

adverse effects of caboprost tromethamine (Hemabate)

A

abdominal pain, nausea/vomiting due to smooth m stimulation

hypertension

bronchoconstriction

119
Q

adverse effects of methylergonovine (Methergine)

A

HTN (severe!)
nausea, vomiting
headache

dangerous –> only give in emergencies!

120
Q

how does tranexamic acid work?

A

inhibits plasmin
thus the fibrin mesh doesn’t dissolve (hemostasis is preserved)

121
Q

serious adverse effect of tranexamic acid (TXA)?

A

thrombosis (can lead to PE, MI, CVA)

122
Q

adverse effect of 17-alpha-alkylated compounds?

A

hepatotoxicity

123
Q

medical uses for exogenous testosterone?

A
  • male hypogonadism
  • testosterone replacement therapy (TRT)
  • delayed puberty
  • menopause symptoms (for women)
  • cachexia
  • anemias
  • transgender men
124
Q

why is PO testosterone not preferred?

A

because both formulations are 17-alpha-alkylated compounds and risk hepatotoxicity

125
Q

caution with transdermal testosterone therapy?

A

drug transfer with skin-to-skin contact (especially think with women or children)

126
Q

adverse effects of testosterone therapy?

A

hepatotoxicity
virilization (male characteristics)
premature epiphyseal closure
atherosclerosis
edema
abuse
in high doses = sterility
psychologic effects

127
Q

what drug class does sildenafil belong to?

A

PDE5 inhibitor

128
Q

how do phosphodiesterase 5 inhibitors work?

A

inhibit PDE5 = increase cGMP. Thus with stimulation, erection can occur

129
Q

adverse effects of PDE5 inhibitors

A

hypotension
priapism
increase OSA
HA
flushing

130
Q

contraindications of PDE5 inhibitors

A

MI, unstable angina
hypotension
heart failure

NITROGLYCERIN! (require 24hrs between doses)

131
Q

what can occur with concurrent administration of sublingual nitroglycerin and sildenafil?

A

severe hypotension

132
Q

how do the injectable ED (erectile dysfunction) drugs work?

A

vasodilation that allows rapid inflow of arterial blood

133
Q

list two main pharmacologic interventions for premature ejaculation

A

selective serotonin reuptake inhibitors (SSRIs)
local anesthetics

134
Q

what medication class is finasteride?

A

5-alpha-reductase-inhibitor

135
Q

how do 5-alpha-reductase inhibitors work?

A

inhibit 5-alpha-reductase, which is the enzyme that converts testosterone to DHT (the active form in the prostate)

thus, regression of prostate epithelial tissue & decreased mechanical obstruction occurs

136
Q

adverse effects of 5-alpha-reductase inhibitors

A

decreased libido
gynecomastia

137
Q

how do alpha1 adrenergic antagonists work in treating BPH?

A

relax smooth muscle & decrease dynamic obstruction

some are selective for the receptors on the prostate = less adverse effects

138
Q

adverse effects of nonselective a1 adrenergic antagonists?

A

hypotension
dizziness
nasal congestion

**hypotension can be severe with other drugs that can decrease BP

GT BSN/CNL PHARM (26 decks)

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