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Clinical Medicine > MSK Pharm 1 > Flashcards

MSK Pharm 1 Flashcards

1
Q

Arachidonic acid results in

A

Cox-1 and Cox-2

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2
Q

Cox-1 leads to

A

prostaglandin (PG) and Tranexamic acid (TXA)

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3
Q

Cox-2 leads to

A

prostaglandin (PG)

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4
Q

Cox-1 PG is responsible for

A

mucosal protection

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5
Q

Cox-1 TXA is responsible for

A

platelet aggregation, vasoconstriction

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6
Q

Cox-2 PG is responsible for

A

pain, inflammation, fever, uterine contraction, vasodilation, inhibition of platelet aggregation

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7
Q

Three types of endogenous adrenal hormones

A

mineralocorticoids, androgens, glucocorticoids

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8
Q

Ex of mineralocortiocids

A

aldosterone

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9
Q

Ex of androgens

A

DHEA

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10
Q

Ex of glucocorticoid

A

cortisol, corticosterone

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11
Q

6 effects of glucocorticoids

A

1) increase blood sugar via catabolism of protein and conversion into sugars and fats (gluconeogenesis) 2) enhance sympathetic response 3) stimulate CNS (irritabiilty, insomnia) 4) decrease WBCs 5) stabilize intracellular lysosomes (decrease cell energy) 6) inhibit synthesis of histamin, kinins, prostaglandins

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12
Q

Prednisolone/prednisone mimics actions of

A

cortisol

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13
Q

Prednisolone/prednisone inhibits

A

phospholipase

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14
Q

Uses for prednisolone/prednisone (4)

A

1) immunosuppressant 2) decrease cellular injury 3) anti-inflammatory 4) inhibit collagen synthesis (decrease scar tissue formation)

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15
Q

What drug is most like cortisol?

A

hydrocortisone

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16
Q

AE of corticosteroids

A

Cushing’s syndrome, muscle atrophy, osteoporosis, decreased immune response, GI bleeding and ulcers, hyperglycemia, sodium retention (increased BP), hypokalemia, insomnia, irritability/instability, increased appetite, hirsuitism, amenorrhea, adrenal suppression

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17
Q

Symptoms of adrenal suppression

A

weakness, lethargy, anorexia, nausea, myalgia

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18
Q

What is adrenal suppression?

A

atrophy of adrenal cortex

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19
Q

Why does adrenal suppression occur?

A

glucocorticoids suppress pituitary release of ACTH, zona fasiculata (cells that produce cortisol in the adrenal gland) does not receive stimulation, adrenal atrophy occurs

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20
Q

How long does it take for adrenal suppression to occur?

A

several weeks of treatment; long acting and high dose preparations have highest risk

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21
Q

What can we do to prevent adrenal suppression?

A

Do not abruptly discontinue; gradually taper doses over weeks to months

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22
Q

What’s the preferred treatment for adrenal insufficiency

A

hydrocortisone

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23
Q

What conditions require caution with corticosteroids?

A

infection (predisposes to infection, don’t give with live vaccines), diabetes, peptic ulcer disease, osteoporosis, Myasthenia gravis, cataracts/glaucoma, pregnancy, CNS disorders

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24
Q

Using corticosteroids in pregnancy can cause?

A

cleft palate, hypoadrenalism

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25
Q

Mechanism of action of NSAIDs

A

block the production of prostaglandins via cyclooxygenase inhibition (COX)

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26
Q

What’s the original, prototypical NSAID?

A

Aspirin

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27
Q

Function of NSAIDS (2)

A

antipyretic and anti-inflammatory

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28
Q

Dosing of ASA for antiplatelet

A

<300 mg/day

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29
Q

Dosing of ASA for analgesia, antipyretic?

A

300-2400 mg/day

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30
Q

Dosing of ASA for anti-inflammatory?

A

2400-4000 mg/day

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31
Q

ASA impacts bleeding time, but not?

A

PT or PTT

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32
Q

Does ASA reversibly or irreversibly inhibit cox-1?

A

irreversibly

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33
Q

What are the most common side effects of ASA use?

A

GI upset and ulcer

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34
Q

What are SE of ASA use?

A

GI upset and ulcer, bleeding, salicylism, increased risk of gout attack

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35
Q

Symptoms of salicylism?

A

vomitting, tinnitus, hearing loss, vertigo

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36
Q

What’s the weirdness with gout and ASA?

A

increased risk of gout attack (doses over 3 gm/day increase uric acid excretion however)

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37
Q

Overdose levels of ASA

A

20-35 tablets of 325 mg

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38
Q

Symptoms of ASA overdose

A

respiratory alkalosis and metabolic acidosis, hyperthermia, seizures/coma/death

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39
Q

How is an ASA overdose treated?

A

activated charcoal (if ingestion is recent), hemodialysis if very severe or worsening

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40
Q

What do we worry about with ASA and asthma?

A

Samter’s Triad

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41
Q

Why don’t we use ASA with children and teens?

A

Reye’s syndrome

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42
Q

What’s Reye’s Syndrome?

A

swelling in brain and liver

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43
Q

Ecotrin is an example of ?

A

ASA

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44
Q

motrin is an ex of?

A

ibuprofen

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45
Q

anaprox is an ex of?

A

naproxen

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46
Q

bufferin is an ex of?

A

ASA

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47
Q

advil is an ex of?

A

ibuprofen

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48
Q

Naprelan is an ex of?

A

naproxen

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49
Q

indocin is an example of?

A

indomethacin

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50
Q

Toradol is an ex of?

A

ketorolac

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51
Q

celebrex is an ex of?

A

celecoxib

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52
Q

mobic is an ex of?

A

meloxicam

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53
Q

Do NSAIDs (other than ASA) reversibly or irreversibly bind to cox-1?

A

reversibly

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54
Q

What med is used to close patent ductus arteriosus?

A

indomethacin

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55
Q

What’s a short-term NSAID used for opiod level pain?

A

ketorolac

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56
Q

What’s the issue with ketorolac?

A

high rate of GI events and renal toxicity; poor anti-inflammatory effects

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57
Q

How are NSAIDs excreted?

A

renal predominately; some undergo enterohepatic recycling

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58
Q

Metabolism of NSAIDs

A

phase 1, phase 2 or both

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59
Q

How is absorption of NSAIDs?

A

well absorbed, no interference from food

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60
Q

Repeated dosing of NSAIDS is detectable in?

A

synovial fluid

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61
Q

SE of NSAIDS

A

GI (N/V, GI bleed/ulcer), fluid retention, anemia/dyscrasias, allergy, tinnitus, MI/CHF, HTN

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62
Q

Ibuprofen dosing for inflammation

A

600 mg qid

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63
Q

ASA dosing for inflammation

A

1200-1500 mg tid

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64
Q

Naproxen dosing for inflammation?

A

375 mg bid

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65
Q

What class is acetaminophen?

A

para-aminophenols

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66
Q

Acetaminophen AKA

A

n-acetyl-para-aminophenol (APAP)

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67
Q

MOA of acetaminophen

A

blocks central (not peripheral) prostaglandin production; mechanism not fully understood

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68
Q

Uses for acetaminophen

A

antipyretic, analgesic NOT anti-inflammatory

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69
Q

Advantages of acetaminophen

A

No GI irritation, almost no allergy, no bleeding issues

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70
Q

SE of acetaminophen use

A

methomoglobinemia, leukopenia, liver toxicity

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71
Q

What’s the dangerous metabolite of acetaminophen?

A

N-acetyl-p-benzoquinone imine

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72
Q

Regular strength acetaminophen

A

325 mg

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73
Q

extra strength acetaminophen

A

500 mg

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74
Q

arthritis formulation acetaminophen

A

650 mg

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75
Q

Excedrin of 2 tablets = pain relief of x tablets of APAP or ASA

A

4 tablets

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76
Q

Excedrin consists of

A

APAP 250 mg, ASA 250 mg, caffeine 65 mg

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77
Q

Max daily dose for children for acetaminophen

A

75 mg/kg/day

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78
Q

Max daily dose for adults for acetaminophen

A

4000 mg

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79
Q

minimum hepatotoxic single dose of acetaminophen for children

A

150 mg/kg

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80
Q

minimum hepatotoxic single dose of acetaminophen for adults

A

7.5-10 grams

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81
Q

What is the crude resin from opium poppies containing several alkaloids, one of which is morphine?

A

opium

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82
Q

what is the natural compound structurally related to those found in opium?

A

opiate

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83
Q

An synthetic agent with the same functional and pharmacological properties of opiates ?

A

opioid

84
Q

How do opiates work?

A

activates mew receptors in thalamus and limbic system

85
Q

Common SE of opiates?

A

sedation, lethargy, muscle relaxation, amnesia, respiratory depression and euphoria

86
Q

What are results of using opiates?

A

suppression of cough reflex and stimulation of CTZ (emesis); miosis; histamine release (bronchoconstriction and hypotension); decreased GI motility and urinary retention

87
Q

Routes of administration of opiates?

A

oral, transdermal, parenteral, sublingual/buccal, subQ, insufflation, epidural, itrathecal, rectal

88
Q

Bio-availability of opiates

A

is a problem and oral doses are often much higher than other routes

89
Q

What will highly lipophilic opioids do?

A

accumulate in fatty tissues

90
Q

How do opioids distribute out of the blood?

A

quickly to high perfused tissues

91
Q

Metabolism of opiods

A

glucuronidation

92
Q

which opioids utilize the cytochrome system?

A

meperidine, fentanyl, alfentanil, sufentanil

93
Q

Excretion of opioids?

A

primarily renal

94
Q

Clinical effects in CNS of opioids

A

analgesia, euphoria/dysphoria, sedation without amnesia/disrupted sleep architecture, respiratory depression, cough suppression, miosis, truncal rigidity, N/V

95
Q

No tolerance develops with the opiod SE of?

A

miosis and constipation

96
Q

Clinical effects of opioids in the periphery

A

minor bradycardia, constipation, urinary retention, itching, sweating, flushing

97
Q

Therapeutic uses of opioids

A

analgesia, acute cardiogenic pulmonary edema, cough suppression, non-infectious diarrhea, shivering, anesthesia

98
Q

What type of analgesia use is appropriate for opioids?

A
  • severe, chronic pain

- sharp, intermittent pain

99
Q

What’s the assumed mechanism for opioid use in treatment of acute cardiogenic pulmonary edema/

A

decreased anxiety

100
Q

Describe tolerance of opioids

A

decrease in apparent effectiveness of a drug; reversible; surmountable; shift in dose curve to the right

101
Q

What’s dependence?

A

neuronal adaptation to repeated drug exposure leading to a withdrawal syndrome upon cessation

102
Q

What will precipitate withdrawal of opioids?

A

IV naloxone

103
Q

Symptoms of opiate withdrawal?

A

rhinorrhea, lacrimation, yawning, chills, goosebumps, hyperventilation, hyperthermia, mydriasis, aching, vomiting, diarrhea, anxiety, hostility

104
Q

Which opiates are more likely to foster addiction?

A

short acting opiates

105
Q

What diseases should be cautioned if using opioids?

A

respiratory disase, gallbladder disase, depression, history of drug abuse, epilepsy, diabetes, pregnancy, use of other narcotics or CNS depressants

106
Q

Mechanism of action of local anesthetics

A

work on afferent nerve fibers; LA given in unionized form, enters neuron, ionizes and cannot leave cell, binds to NA channel, stops Na from entering neuron and prevents generation and conduction of action potential

107
Q

Membrane penetration and LA? Unionized.

A

penetrate membranes

108
Q

Membrane penetration and LA? Ionized.

A

do not penetrate membranes well

109
Q

Membrane penetration and LA? weak bases

A

if enters a slightly acidic area, it becomes unable to cross barriers

110
Q

Which type of administration of LA has the lowest systemic absorption?

A

SC Injections

111
Q

What does an Epi additive do to LA?

A

vasoconstrictor (keeps drug in area for a longer period of time); prolongs block

112
Q

What are issues to an Epi additive do to LA?

A

skin necrosis; some people are sensitive and will become tachycardic

113
Q

What does a base additive do to LA?

A

maintain unionized form for a quicker onset of action but decreases duration of action

114
Q

Opioid additive to LA?

A

neuraxial synergy

115
Q

Alpha-2-adrenergic agonists additive to LA?

A

inhibit peripheral nerve conduction

116
Q

How are ester LAs hydrolized?

A

hydrolized by pseudocholinesterases to PABA

117
Q

What’s the cause of ester LA allergy?

A

PABA; some people lack pseudocholinesterase activiity

118
Q

How are amide LAs metabolized?

A

in liver by cytochroms

119
Q

SE with LA?

A

HA, dizziness, confusion, CNS depression (except cocaine), vasodilation (except cocaine)

120
Q

Describe lidocaine

A

rapid, moderate acting, also an antiarrythmic

121
Q

When is lidocaine beneficial?

A

when intubating and extubating

122
Q

Describe bupivicaine

A

slow onset, long lasting, cardiotoxic

123
Q

What is a huge issue with LA?

A

methemoglobinemia

124
Q

Prilocaine is a problem in?

A

neonates and patients with poor heart or lung function (MetHb)

125
Q

Benzocaine oral prepration use over time may cause?

A

MetHb

126
Q

How is methemoglobinemia treated?

A

IV methylene blue

127
Q

What is methemoglobinemia?

A

higher than normal levels of ferric hemoglobin; can’t bind oxygen normally; can’t transport oxygen/starving tissues

128
Q

Describe toxicity issues with LA?

A

a progression may occur as more nerves are affected; lightheadedness, tinnitus, periorbital numbness, seizures, coma, respiratory arrest, cardiovascuar collapse; rare neural toxicity; transient neurological symptoms

129
Q

Describe transient neurological symptoms (TNS)

A

pain in lower extremities (gluteus and moving down), resolves within a week

130
Q

What’s a likely culprit of TNS?

A

lidocaine

131
Q

Which LAs are often culprits of arrhythmias?

A

bupivacaine and ropivacaine

132
Q

What do you use to combat seizures from LA?

A

benzos

133
Q

What do you use to combat arrhythmias from LA?

A

amiodarone

134
Q

What’s used to manage cardiovascular collapse?

A

IV lipid

135
Q

What is the most common cause of pyogenic osteomyelitis?

A

s. aureus

136
Q

What is the most common cause of non-pyogenic osteomyelitis?

A

mycobacterium tuberculosis

137
Q

What’s the most common cause of osteomyelitis in those with sickle cell?

A

s. aureus, salmonella

138
Q

What are the four routes of infection of osteomyelitis?

A

hematogenous ,contiguous spread, direct inocluation

139
Q

approach to osteomyelitis treatment?

A

empiric therapy, must identify organism and primary site, acute v.s chronic, treatment for 4-6 weeks

140
Q

What route of administration is preferred for osteomyelitis treatment?

A

parenteral

141
Q

When do you collected bone sample?

A

before you treat

142
Q

Oral treatment of osteomyelitis may be appropriate after identification of organism if,

A

confirmed infection, initial response to parenteral therapy, suitable oral medication available, pt will be compliant

143
Q

If vertebral, hematogenous osteomyelitis treat with:

A

vancomycin + [ceftriaxone OR cefipime OR levofloxacin]

144
Q

If extremity, hematogenous osteomyelitis treat with:

A

vanco + [ceftazidime OR cefipime]

145
Q

If confirmed MRSA, hematogenous osteomyelitis treat with:

A

vanco +/- rifampin

146
Q

If confirmed MSSA hematogenous osteomyelitis treat with:

A

nafcillin OR oxacillin OR cefazolin

147
Q

If confirmed salmonella hematogenous osteomyelitis treat with:

A

ciprofloxacin or levofloxacin

148
Q

If osteomyelitis with contiguous spread without vascular insufficiency and thinking MRSA treat with:

A

vanco + ceftazidime OR cefepime

149
Q

If osteomyelitis with contiguous-spread without vascular insufficiency and thinking p. aeruginosa treat with:

A

ciprofloxacin OR levofloxacin OR cefepime

150
Q

Who do you suspect has pseudomonas osteomylitis?

A

IV drug abuse, puncture wounds of the foot, long bone internal fixation

151
Q

How do you treat osteomyelitis that’s contiguous with vascular insufficiency?

A

debridement, bone sample, treated based on C&S for 6 weeks

152
Q

Who should be treated for osteoporosis?

A

postmenopusal women and men 50 years and older who have: a hip or vertebral fracture, t-score <2.5 at hip or lumbar spine, osteopenia and FRAX-calculated 10 year hip fracture risk of 3% or major fracture risk of 20%

153
Q

If you initiate treatment for osteoporosis, what should be corrected first?

A

hypocalcemia

154
Q

x mg of calcium per day for women 51 and older and men 71 and older?

A

1200 mg

155
Q

Men 50-70 should consume x mg of calcium?

A

1000 mg

156
Q

x IU of vitamin D per day for patients 50 and older

A

800-1000 IU

157
Q

% daily value of calcium based on?

A

1000 mg calcium per day

158
Q

No more than x mg per dose of calcium due to saturation of transporters

A

500 mg

159
Q

What are the two calcium supplements available?

A

calcium carbonate, calcium citrate

160
Q

Which is less expensive: calcium carbonate or calcium citrate?

A

calcium carbonate

161
Q

Calcium carbonate require?

A

acidic environment for absorption, must be taken immediately after a meal

162
Q

SE of calcium carbonate

A

gas and bloating

163
Q

What’s unique about calcium citrate?

A

contains less calcium per dose, can be taken with or without food, no GI problems

164
Q

What are lifestyle changes that are important in osteoporosis?

A

weight-bearing exercise

165
Q

What improves spine BMD?

A

non-weight bearing when combined with weight bearing

166
Q

Bisphosponates MOA

A

decrease bone turnover; inhibit remodeling of bone (osteoblasts have time to work); inhibit resorption; slows but does not stop bone formation

167
Q

Bisphosphonate instructions

A

take first thing in the day, empty stomach, 8 oz of water, no other food/drink for 30 minutes, remain upright for 30-60 minutes

168
Q

Serious SE of bisphosphonate?

A

erode the esophagus

169
Q

Examples of bisphosphonates

A

alendronate and ibandronate and risedronate and zoledronic acid

170
Q

Alendronate dosing

A

10 mg daily OR 70 mg weekly

171
Q

Who is alendronate approved for?

A

postmenopausal women, men, steroid-induced osteoporosis

172
Q

What is binosto?

A

An alendronate; dissolved in 4 oz room temp water, wait 5 min after fizzing stops then stir 10 seconds then drink

173
Q

What’s a con of binosto?

A

1500 mg of sodium

174
Q

Dosage of ibandronate

A

150 mg monthly or 3 mg IV every 3 months

175
Q

Who is ibandronate approved for?

A

postmenopausal women only

176
Q

Dosing for risedronate

A

5 mg daily OR 35 mg weekly OR 75 mg two consecutive days each month OR 150 mg monthly

177
Q

Who is risedronate approved for?

A

postmenopausal women, men, steroid-induced osteoporosis

178
Q

Zoledronic acid dosage

A

5 mg IV oncea year

179
Q

Who is zoledronic acid approved for?

A

postmenopausal women, men, steroid-induced osteoporosis; secondary prevention s/p hip fracture given within 90 days of fracture

180
Q

SE of osteoporosis meds?

A

GI (pain, nausea, dyspepsia, esophageal ulceration and possible perforation), muscle pain, hypocalcemia, osteonecrosis of the jaw

181
Q

When is osteonecrosis likely in treating osteoporosis?

A

cancer patients after receiving invasive dental work

182
Q

Criteria for drug-induced osteonecrosis of the jaw?

A

-the patient has taken or is taking antiresporptive or antiangiogenic agents -for 8 weeks, there has been exposed bone or bone that is able to be probed through a fistula in the maxillofacial area -there is no history of radiation or metastatic disease to the jaw area

183
Q

Controversy with osteoporosis med?

A

esophageal cancer risk, increased atypical (sutrochanteric, diapheeal) fractures–maybe associated with steroid or PPI use

184
Q

What’s the benefit of IV osteoporosis meds?

A

bypasses GI effects; but reserve for pts who can’t tolerate oral, are n on-compliant or unable to follow directions

185
Q

Raloxifene dose

A

60 mg qd

186
Q

Raloxifene indication

A

postmenopausal women

187
Q

Raloxifene class

A

selective estrogen receptor modulation (SERM); agonist at bone receptor, antagonist in breast and uterine tissue

188
Q

Results of raloxifene?

A

increases BMD in hip and spine and decreased vertebral fractures (not shown to decrease nonvertebral or hip fx)

189
Q

SE of raloxifene

A

hot flashes, leg cramps, increased DVT/PE

190
Q

What’s a good choice if you think a patient has risk of estrogen dependent cancer and osteoporosis?

A

raloxifene

191
Q

Route of calcitonin

A

injectable and nasal spray

192
Q

What’s the indication of calcitonin?

A

prevention of fx in postmenopausal women

193
Q

Calcitonin and fracture risk

A

has not demonstrated reduced fx risk

194
Q

Recommendations for calcitonin

A

for use only as an alternative to other therapies in women who have been postmenopausal for at least 5 years; use only when other therapies are not tolerated or patient insists on using this product

195
Q

SE of calcitonin

A

rhinitis, epistaxis, nose bleeds, allergic reactions, cancer risk

196
Q

What is teriparatide?

A

amino acids 1-34 of human PTH

197
Q

How does teriparatide work?

A

anabolic–increases bone formation; stimulates osteoclast maturation, regulates calcium and phosphate reabsorption in kidneys, increases calcium absorption in gut

198
Q

What happens when teriparatide is given intermittently?

A

osteoblasts are stimulated over osteoclasts

199
Q

SE of teriparatide?

A

nausa, insomnia, hypercalcemia, increased risk of osteosarcoma

200
Q

contraindications of teriparatide

A

bone cancer, paget’s disease, hyperparathyroidism, hypercalcemia

201
Q

Who is teriparatide approved for?

A

severe osteoporosis (osteoporosis with fracture)

202
Q

teriparatide dose?

A

Sq 20 mcg per day

203
Q

Denosumab what is it?

A

monoclonal antibody against RNKL

204
Q

What does denosumab do?

A

decreases osteoclast formation and function; blocks RANKL from binding to RANK

205
Q

Dose of denosumab

A

60 mg Sq every 6 months

206
Q

SE of denosumab

A

increased risk of skin infections, increased risk of hypocalcemia, osteonecrosis of jaw, arthraliga, back pain

Clinical Medicine (13 decks)

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