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Advanced Pharmacology > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Drugs for mild pain

A

APAP, Aspirin, NSAIDs, Cox-2 inhibitors

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2
Q

Drugs for moderate pain

A

NSAIDs, Opioid + APAP, Tramadol

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3
Q

Drugs for severe pain

A

Opiods

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4
Q

APAP MoA

A
  • Inhibit the synthesis of prostaglandins in the CNS

- work peripherally to block pain impulse generation

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5
Q

Dosing for APAP

A

325-650 mg q4h or 100 mg Q6h or

1000 mg Q6h

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6
Q

Max dosing for liver patient on APAP

A

2 gram/day

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7
Q

Max dosing for APAP

A

4 grams/day

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8
Q

APAP routes

A

PO, PR. IV is very expensive

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9
Q

APAP adverse effects

A

hepatotoxicity

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10
Q

Function of cox-1

A

cytoprotective: protects GI, lungs, and kidneys; plays part in platelet aggregation and vasoconstriction

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11
Q

Function of cox-2

A

Inflammatory: Inflammation, pain • Antiplatelet •Vasodilation

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12
Q

Aspirin MoA

A

irreversibly binds to cox-1 and cox-2

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13
Q

Aspirin properties

A

analgesia
anti-inflammatory
antipyretic
antiplatelet (irreversible)

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14
Q

Aspirin antiplatelet MoA

A

prevents synthesis of thromboxane A (a vasoconstrictor and iducer of platelet aggregation)

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15
Q

Aspirin onset

A

15-20 minutes

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16
Q

Aspirin peak

A

1-3 hours

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17
Q

Aspirin duration

A

3-6 hours

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18
Q

Aspirin half-life

A

3 hours

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19
Q

Aspirin elimination

A

urine and liver

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20
Q

Aspirin adverse effects

A

GI bleeding, salycylism, reye’s syndrome, asthma patients: bronchospasm, uticaria, angiodema

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21
Q

Salicylism

A

dizziness, deafness, tinnitus

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22
Q

Important NSAIDs

A

Ibuprofen, Indomethacin, Ketoralac, Naproxen

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23
Q

NSAIDs properties

A

analgesic, antinflammatory, antipyretic, antiplatelet (reversible)

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24
Q

NSAID adverse effects

A 
cardio: fluid retention, htn, edema
GI: irritation, ulcers, bleeding, perforation
Respiratory: bronchospasm
Skin: rash
Renal: insufficiency or liver failure
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25
Q

NSAID black box warning

A

serious CV event, GI bleed perforation

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26
Q

Which med is used for periop pain in CABG

A

NSAIDs

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27
Q

Ketorolac route

A

IV and IM

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28
Q

Ketorolac usage

A

short term mgmt of mod to sever pain (max 5 days)

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29
Q

Ketorolac adverse effects

A

severe post-op bleeding; renal failure

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30
Q

Advantages of cox-2 inhibitor

A
  • decreased pain and inflammation with minimal GI side effects
  • no effect on platelet aggregation/improved bleeding profile
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31
Q

Disadvantages of cox-2 inhibitor

A
  • renal dysfunction
  • avoid in pts who have sulfa allergy
  • CV events (increased vasoconstriction)
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32
Q

Morphine routes

A

PO, PR, IV, IM, SubQ, epidural, intrathecal

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33
Q

Morphine doses*

A

PO: 15-30 q4h PRN

IV_ 2-4 mg q4h PRN

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34
Q

Morphine elimination*

A

renally

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35
Q

Unique morphine properties

A

2 active metabolites; histamine release (hypotension and pruritis)

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36
Q

Hydromorphone trade name

A

dilaudid

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37
Q

Hydromorphone routes

A

PO, PR, IV, IM, SubQ, epidural

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38
Q

Hydromorphone dosing*

A

PO: 2-4 mg q4-6 h
IV: 0.2-1 mg q2-3h

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39
Q

Hydromorphone metabolism

A

half life: 2-3 hours
not renally cleared
no active metabolites

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40
Q

Methadone route

A

PO, IV, IM, SubQ

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41
Q

Methadone metabolism

A
  • biphasic elimination: analgesic 1/2 life: 8-12 h; terminal 1/2 life: 24-36h
  • renally cleared
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42
Q

Methadone adverse effects

A

QT prolongation*; serotenergic effects; lower seizure threshold

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43
Q

Meperidine route

A

PO, IV, IM, SubQ

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44
Q

Meperidine dosing

A

IV: 50-150 mg q4-6h

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45
Q

Meperedine metabolism (and active metabolite)

A

renally; normeperidine

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46
Q

Meperedine adverse effects

A

anxiety, tremors, serotolinergic effects

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47
Q

Drug used for post op shivering

A

Meperidine

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48
Q

Codeine dosing

A

15-60 mg q4h

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49
Q

Codeine usage

A

mild to moderate acute pain; antitussive

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50
Q

Codeine metabolism

A

major CYP 2D6 substrate–if pt lacks enzyme they won’t experience benefits

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51
Q

Codeine route

A

PO only

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52
Q

Hydrocodone route

A

PO only

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53
Q

Hydrocodone dose

A

5-10 mg q4-6h

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54
Q

Hydrocodone usage

A

acute mod to severe pain in pts w/ limited opiod use

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55
Q

Hydrocodone combos (immediate release)

A

Vicodin (Hy+APAP)

Vicoprofen (Hy+ibuprofen)

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56
Q

Hydrocodone combos (extended release)

A

Zohydro (ER 12hrs)

Hysingla (ER 24 hrs)

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57
Q

Fentanyl routes

A

transdermal ,IV, lozenge, buccal, intranasal, sublingual, epidural

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58
Q

Fentanyl dose

A

IV: 25-50 mcg q2-3 h

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59
Q

Fentanyl metabolism

A
  • metabolized by CYP3A4
  • preferred agent in liver failure
  • high potency and lipid solubility=rapid onset
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60
Q

Fentanyl adverse effects

A

bradycardia and chest wall rigidity

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61
Q

Partial agonist med

A

buprenorphine

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62
Q

Antagonist action

A
  • Compete with endogenous and exogenous opiods at mu receptors
  • prevent or reverse opioid-induced side effects
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63
Q

Naloxone usage

A
  • to reverse toxic effects of agonists and agonist-antagonist
  • may be used orally to prevent opioid-induced constipation
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64
Q

Naloxone disadvantages

A
  • repeated dosing may be necessary based upon half-life of agonist
  • Poor systemic bioavailability due to extensive first pass
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65
Q

Naltrexone route

A

IM depot and PO

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66
Q

Naltrexone usage

A 
opioid dependence (if they slip up and take opioid it won't have intended effect)
NOT for acute reversal of toxic effects
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67
Q

Naltrexone adverse effects

A

Hepatotoxic

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68
Q

Methylnaltrexone route

69
Q

Methylnaltrexone usage

A

to treat opioid induced constipation with chronic opioid use

NOT for acute reversal of toxic effects

70
Q

Methylnaltrexone metabolism

A

renally eliminated

doesn’t cross blood brain barrier (acts on peripheral mu receptors like GI tract)

71
Q

Methylnaltrexone adverse effect

A

potential GI perforation

72
Q

Morphine conversion

A

P 10: O 30

73
Q

Hydromorphone conversion

A

P 1.5: O 7.5

74
Q

Mepiridine conversion

A

P 100: O 300

75
Q

Codeine conversion

A

P 100: O 200

76
Q

Buprenorphine conversion

A

P 0.3: O 0.4 (sl)

77
Q

Tramadol route

78
Q

Tramadol MoA

A
  • weak opiate mu receptor binding

- inhibition of norepinephrine and serotonin reuptake

79
Q

Tramadol dosing

A

25-100 mg q4-6h

80
Q

Tramadol metabolism

A
  • extensive CYP 2D6

- renally and hepatically cleared

81
Q

Tramadol adverse effects

A
  • lower seizure threshold
  • sedation
  • less respiratory depression and GI motility; less euphoria
82
Q

Class-wide opioid adverse effects

A

respiratory depression, sedation, constipation, fatigue, confusion, hallucinations/nightmares, GI, N/V, brady

83
Q

Tolerance to resp depression

A

w/in 5-7 days

84
Q

Tolerance to sedation

A

within days to weeks

85
Q

Opioid effects that pt never gains tolerance to

A

miosis, constipation, seizures

86
Q

High tolerance development to

A 
Analgesia 
Euphoria/dysphoria 
Mental clouding 
Sedation 
Respiratory depression 
Antidiuresis Nausea/vomiting 
Cough suppression
87
Q

Moderate tolerance development to

A

bradycardia

88
Q

Meds to treat opioid addiction

A

methadone, buprenorphine, naloxone, naltrexone

89
Q

Chronic pain regimen (opioid)

A

long acting with short acting for breakthrough pain

90
Q

Calculation for breakthrough pain

A

10-15% of daily dose of reg sched opioid

91
Q

Opiods with active metabolites

A

meperidine, morphine

92
Q

Meds for neuropathic pain

A

SNRIs, TCA, Calcium channel a2-δ ligands; lidocaine patch (2nd line); opioids (3rd line)

93
Q

SNRIs

A

duloxetine, venlafaxine

94
Q

TCAs

A

nortirptyline, despiramine

95
Q

First line meds for migraine

A

ASA, APAP, NSAIDs, triptans

96
Q

APAP combos for migraine

A

Exedrin - w/ caffeine
Floricet - caffeine/butalbital
NSAIDs

97
Q

Triptan MoA

A

Selective agonists of 5-HT1B and 5-HT1D receptors
• Normalizes dilated intracranial arteries through enhanced
vasoconstriction
• Peripheral neuronal inhibition
• Inhibition of transmission through second-order neurons of the trigeminocervical complex

98
Q

Triptan effective up to ___ hours after onset

99
Q

Triptan contraindications

A

• Heart disease
• Peripheral vascular disease • Cerebrovascular disease
-Severe hepatic impairment
• Uncontrolled hypertension

100
Q

Triptan considerations

A

Use within 24 hours of ergotamine derivatives
Use within 2 weeks of therapy with monoamine
oxidase inhibitors (MAOI)

101
Q

DMARD characteristics

A

Should initiate within first 3 months of symptom onset
Given to reduce mortality and prevent progression of RA
Onset: delayed weeks to months before benefit seen • No direct analgesic or anti-inflammatory effect
Narrow range of effectiveness
Unique adverse event profile: use often limited by
toxicities
Consists of nonbiologic and biologic agents

102
Q

First line DMARD

A

Methotrexate

103
Q

Methotrexate onset

A

2-3 weeks (max 4 -6)

104
Q

Methotrexate route

A

oral or subq

105
Q

Methotrexate MoA

A

• Folic acid antagonist, immunosuppressant

Inhibits T-lymphocytes proliferation and cytokine production

106
Q

Hydroxychloroquine route

107
Q

Hydroxychloroquine adverse options

A

Relatively safe and well tolerated
• Lack myelosuppressive, renal, hepatic toxicities
• GI toxicity (nausea, vomiting, diarrhea); ocular toxicity (corneal deposits, irreversible retinopathy: baseline and q6 month eye exams)
• Rash, alopecia, skin pigmentation changes

108
Q

Hydroxychloroquine route

109
Q

Hydroxychloroquine MoA

A

Unknown but has some anti-inflammatory properties

-Onset may be delayed up to 6 weeks

110
Q

Adalimubab (Humira)

dosage

A

subQ injections every other week

111
Q

Adalimubab (Humira)

metabolism

A

Onset: 1 – 4 weeks

Half-life: about 10 – 20 days

112
Q

Adalimubab (Humira) Role in therapy

A

monotherapy OR in combination with methotrexate

113
Q

Adalimubab (Humira) adverse effects

A

local site injections

114
Q

Tofacitinib (Xeljanz®) MoA

A

Janus Kinase (JAK) Inhibitor

Major 3A4 substrate

115
Q

Tofacitinib (Xeljanz®) indications

A
  • Moderate to severe RA

* Adequate / Intolerant response to methotrexate

116
Q

Tofacitinib (Xeljanz®) adverse effects

A

URIs, HA, diarrhea, increased LFTs, bone marrow suppression (lymphopenia, neutropenia, anemia), GI perforation, interstitial lung disease

117
Q

TB Screening for Biologic Agents

A

Initially: TST (TB skin test) or IGRA (interferon-gamma- release assay)
• Negative: start biologic
• Positive: chest x-ray, sputum for AFB
Latent TB: treat at least one month then start biologic
Active TB: complete treatment for TB then start
biologic
If risk factors, screen annually

118
Q

Goals for gylcemic control

A
  • A1c < 6.5 – 7.0%
  • Fasting glucose 80 – 130 mg/dL
  • Peak postprandial glucose (1–2 hours after a meal) <180 mg/dL
119
Q

Rapid acting insulin

A 
Insulin lispro (Humalog) 
Insulin aspart (NovoLog)  Insulin glulisine (Aventis)
120
Q

Rapid acting insulin onset

A

15-30 minutes

121
Q

Short acting insulin

A

Regular Humulin R

122
Q

Short acting insulin onset

A

30 minutes

123
Q

Intermediate acting insulin

A

NPH Humulin N

NPH Novolin N

124
Q

Long acting insulin

A 
Insulin glargine (Lantus) – 100 units/mL
Insulin glargine (Basaglar) – 100 units/mL
Insulin glargine (Toujeo) -- 300 units/mL
Insulin detemir (Levemir)  Insulin degludec (Tresiba)
125
Q

Glargine onset

126
Q

Glargine duration

A

22-24 hours

127
Q

Detemir onset

128
Q

Detemir peak

129
Q

Detemir duration

A

14-24 hours

130
Q

Initial type 2 insulin dosing

A

0.2 units/kg/day

131
Q

1 unit of insulin will lower blood glucose by ____ mg/dL

132
Q

Sulfonylureas MoA

A

increase secretion of insulin from beta cells, increase insulin sensitivity

133
Q

Sulfonylureas metabolism

A
  • hepatically metabolized

- renal w/ glyburide

134
Q

Sulfonylureas adverse effects

A
  • hypoglycemia (most common)
  • derm rash, sensitivities
  • GI disturbances
  • weight gain
135
Q

Sulfonylureas

A

Glyburide, glipizide, glimepiride

136
Q

Biguanides MoA

A
  • lowers hepatic glucose output

- increases peripheral glucose uptake and utilization

137
Q

Biguanides contraindications

A

renal impairment def
possibly hepatic impairment and CHF
eGFR<30

138
Q

When to hold biguanides for 48 hours?

A

eGFR 30-60 + contrast dye

139
Q

When to re-evaluate biguanides dosing?

A

eGFR goes < 45

140
Q

When to avoid starting biguanides?

A

eGFR 30-45

141
Q

Incretins

A

GLP1 and DPP4 inhibitors

142
Q

GLP1

A

glucagon like peptide

143
Q

Biguanides adverse effects

A

N/V/D, metallic taste, rarely lactic acidosis

144
Q

Biguanides advantages

A
  • no hypoglycemia
  • weight loss
  • lowers triglycerides
145
Q

GLP1 function

A
  • stimulate insulin release
  • delay gastric emptying
  • suppress postprandial glucagon release
146
Q

GLP-1 agonists

A

Exenatide
Liraglutide
Albiglutide
Dulaglutide

think glip tide

147
Q

GLP-1 adverse effects

A

N/V - slow gastric emptying
HA
pacreatitis (rare)

148
Q

GLP -1 administration

A
  • pre-filled pens for subQ injections

- admin once or twice daily to once weekly

149
Q

DPP-4 inhibitors

150
Q

DPP-4 MoA

A

Inhibits DPP-4 enzyme that is responsible for the breakdown on incretin hormones GLP-1

151
Q

DPP-4 advantages

A

demonstrates CV safety (but doesn’t reduce risk)

152
Q

SGLT inhibitors

153
Q

SGLT MoA

A

increase glucose in urine, and increase loss of glucose through the kidney (lowers blood sugar)/reduces reabsorption of glucose

154
Q

SGLT advantages

A

weight loss

  • low risk of hypoglycemia
  • blood pressure lowering
  • renal protection
  • lowers CHF exacerbation
155
Q

SGLT concerns

A
  • limb amputation (rare)
  • electrolyte distrubacnes
  • UTI
  • yeast infections
  • malignancy
156
Q

Thioureas

A

propylthiouracil

methimazole

157
Q

Thiourea MoA

A

shuts down production of thyroid hormones

158
Q

Thioureas adverse effects

A

rash
fluid retention
leukopenia

159
Q

Drug of choice for thyroid replacement

A

Levothyroxine

160
Q

Levothyroxine MoA

A

produces physiologic levels of both T4 and T3

161
Q

Levothyroxine onset

162
Q

Levothyroxine adverse effects

A

heart failure
MI
Angina
Hyperthyroidism

163
Q

Triptan names

A

Sumatriptan and Zolmitriptan

164
Q

Hydromorphone trade name

165
Q

DM meds that can cause hypoglycemia

A

Insulin and sulfanylureas

166
Q

Serotoninergic effects

A

Methadone
meperidine
tramadol
triptans

167
Q

Cox-2 selective pros and cons

A
  • increase CV events

- decrease GI effects

168
Q

Cox-1 selective pros and cons

A
  • cardioprotective at low doses

- increase risk for GI effects

Advanced Pharmacology (8 decks)

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