MSK Flashcards
1
Q
What two medications are used to close a patent ductus arteriosus?
A
Indomethacin and Acetaminophen
2
Q
What causes gout?
A
An excess of uric acid in the blood
3
Q
What are the 3 types of medications used to treat gout?
A
NSAIDs, colchicine, and steroids
4
Q
What is the best non-pharmacologic way to manage gout?
A
To stay hydrated
5
Q
What is the goal to treat acute gout?
A
To reduce inflammation and pain
6
Q
Why can colchicine be toxic to bone marrow?
A
Because it affects rapidly dividing cells
7
Q
What conditions is colchicine used for?
A
Acute gout, Behçet’s disease, and familial Mediterranean fever
8
Q
What is the mechanism of action (MOA) for colchicine in gout?
A
It concentrates in PMN cells and inhibits microtubule polymerization, preventing neutrophil migration and activity related to gout symptoms
9
Q
What is the most common side effect of colchicine?
A
Diarrhea, which often precedes the patient getting better
10
Q
Is aspirin effective in treating gout?
A
No, it is not effective and can inhibit the excretion of uric acid, potentially causing gout flares
11
Q
What is the target of chronic gout treatment?
A
Urate lowering therapy
12
Q
What are the 3 ways to achieve urate lowering therapy?
A
Decrease synthesis of uric acid, increase excretion of uric acid, and increase metabolism of uric acid
13
Q
What drugs decrease the synthesis of uric acid?
A
Allopurinol (purine) and Febuxostat (non-purine), which are xanthine oxidase inhibitors
14
Q
What enzyme is inhibited to reduce uric acid?
A
Xanthine oxidase
15
Q
What is the first line therapy for reducing uric acid?
A
Xanthine oxidase inhibitors, specifically allopurinol
16
Q
When is Febuxostat used in gout treatment?
A
As a second option for gout prophylaxis, usually if the patient has failed allopurinol
17
Q
What may happen when starting xanthine oxidase inhibitors?
A
They may cause gout attacks when first started, so a medication for acute gout like colchicine may be paired with it initially
18
Q
What are uricosuric agents?
A
A class of medications that increase the production of uric acid.
19
Q
What is uric acid elevation in chemotherapy a sign of?
A
It is one of the first signs of tumor lysis syndrome, usually from hyperkalemia and arrhythmia.
20
Q
What prophylactic treatments should be started at the beginning of therapy to avoid gout flares?
A
Colchicine or NSAIDs.
21
Q
What is febuxostat?
A
A potent and selective inhibitor of xanthine oxidase that is more effective in lowering serum urate levels than allopurinol.
22
Q
What risks are associated with febuxostat?
A
Greater risks for all-cause and cardiovascular mortality.
23
Q
What drug classes increase excretion of uric acid?
A
Probenecid, sulfinpyrazone, and benzbromarone.
24
Q
What is the mechanism of action of probenecid?
A
Inhibits renal tubular urate resorption and penicillin secretion, increasing uric acid excretion by the kidney.
25
What are tophaceous deposits?
They are reabsorbed, providing relief of arthritis and remineralization of bone.
26
What level should the uric acid level be below?
6.
27
What should be done if the patient is not getting low enough with probenecid?
It can be added to a xanthine oxidase inhibitor.
28
Why is moving to a metabolizing agent not first line?
Because it is expensive and an injection, and it is only done when all other options have been exhausted.
29
What does Rasburicase convert uric acid to?
Rasburicase converts uric acid to allantoin, which is a water-soluble metabolite.
30
What are the patient education points for taking bisphosphonates?
Remain upright for 30 mins after taking, take on an empty stomach. Bisphosphonates should not be used by patients with Barrett esophagus.
31
What is osteonecrosis of the jaw?
Osteonecrosis of the jaw is a necrotic, nonhealing lesion of the jaw that occurs, particularly after tooth extraction.
32
What is the usual treatment course with bisphosphonates?
The usual treatment course with bisphosphonates is 3–5 years due to the increasing risk of atypical femoral fractures after that time.
33
What should be done for patients with continued osteoporosis and high fracture risk?
For patients with continued osteoporosis and a high fracture risk, bisphosphonates may be continued for another 2 years.
34
What is the absorption rate of bisphosphonates?
Less than 10% of an oral dose of these drugs is absorbed. Food reduces absorption even further, necessitating their administration on an empty stomach.
35
What is the step-based approach for choosing medications for MSK symptoms?
Prescribe the lowest dose required to control, add ASA 81mg, add PPI, and monitor BP.
36
What is the Beers Criteria for Ketorolac?
Beers Criteria: Potentially inappropriate in older adults. Ketorolac should not be used for longer than 5 days due to nephrotoxicity.
37
What drug is a selective COX-2 inhibitor?
Celecoxib is a selective COX-2 inhibitor that is about 10-20 times more selective for COX-2 than for COX-1.
38
What should be labeled as an allergy if a patient has a rash from Celecoxib?
The patient should be labeled allergic to sulfa drugs.
39
What are the common adverse effects of Naproxen?
The incidence of upper GI bleeding in over-the-counter use is low but still double that of over-the-counter ibuprofen.
40
What is the CNS BB warning for NSAIDs?
The CNS BB warning for NSAIDs is tinnitus.
41
What are the common adverse effects of NSAIDs?
Common adverse effects of NSAIDs include GI injury and renal injury.
42
What are the analgesic and antipyretic agents equivalent to aspirin?
They possess no significant anti-inflammatory effects but are important in treatment.
43
What factors assess risk and address harms of opioid use?
Check PDMP for high dosages and prescriptions from other providers, avoid concurrent benzodiazepine and opioid prescribing, and use immediate-release opioids when starting.
44
What are the goals of treatment in acute pain management?
Goals should be meaningful to the patient, such as treating pain to comfort while ensuring the patient is alert enough to cough and deep breathe.
45
How is chronic pain defined?
Chronic pain is pain that persists longer than 3-6 months.
46
What is nociceptive pain?
Nociceptive pain is the normal response to any type of stimulus that results in tissue damage.
47
What are the two types of nociceptive pain?
Visceral pain and somatic pain.
48
What is visceral pain?
Visceral pain arises from the body’s organs and may be cramping, throbbing, or vague.
49
What is somatic pain?
Somatic pain results from issues within the body’s bone, joints, muscles, skin, or connective tissue and may be localized and stabbing, aching, or throbbing.
50
What is neuropathic pain?
Neuropathic pain results from damage to or abnormal processing of the peripheral or CNS and may be sharp, stabbing, burning, tingling, or numb.
51
What is referred pain?
Referred pain originates in one location but spreads to another location, such as with a myocardial infarction.
52
What is the first step in managing chronic pain?
Assess the patient and chronic pain, including the cause and severity.
53
How would you describe the pain of a 16-year-old boy who twisted his ankle?
Acute pain in relation to tissue injury that will not cause long-term pain.
54
What is the first-line treatment for acute pain from a sprained ankle?
A non-opioid plus adjuvants (SSRIs, ACE bandage).
55
What should be done for a patient with chronic pain syndrome who has failed non-opioid therapy?
A mild-moderate opioid in addition to NSAIDs, usually in combination with medications and/or adjuvant treatment.
56
What does an 85-year-old patient with a broken hip need for long-term pain control?
Surgery or an invasive or minimally invasive procedure.
57
What is the mechanism of action of opioids?
Opioid agonists produce analgesia by binding to specific G protein-coupled receptors (GPCRs) located in the brain and spinal cord involved in pain transmission and modulation.
58
What is the direct application of opioid agonists?
Direct application to the spinal cord provides a regional analgesic effect while reducing unwanted respiratory depression, nausea, and vomiting.
59
What are endorphins?
Endorphins relieve pain, reduce stress, and improve mood and sense of well-being.
60
What are dynorphins?
Dynorphins are neurotransmitters that bind to the kappa receptor, modulating mood and emotional behaviors.
61
What are enkephalins?
Enkephalins are endogenous ligands that bind to opioid receptors to help regulate pain.
62
What are the physical results of the actions of mu receptors?
Analgesia, euphoriant effects, respiratory depression, and physical dependence properties of morphine.
63
What is morphine?
Morphine is the prototypical opioid agonist.
64
What are opioids also called?
Opioids are a generic term for natural or synthetic substances that bind to specific opioid receptors in the CNS, producing an agonist action. They are also called narcotics.
65
What receptors do opioid drugs act on?
Opioid drugs act primarily on the μ (mu)-opioid receptor, as well as c (delta) and j (kappa) nociception/opioid-receptor-like subtype 1 (ORL-1) receptors.
66
What is tolerance?
Tolerance is the gradual loss of effectiveness with frequently repeated therapeutic doses of morphine or its surrogates.
67
What is physical dependence?
Physical dependence is characterized by withdrawal or abstinence syndrome when a drug is stopped or an antagonist is administered.
68
What is the MOA of tramadol?
Tramadol is a centrally acting synthetic analgesic, structurally related to opioids. Its mechanism of action involves both nonopioid and opioid receptors.
69
What are the naturally occurring alkaloids?
Morphine, codeine, thebaine, and papaverine.
70
What are the 3 opioid receptors?
Mu (primary opioid receptors), delta, and kappa.
71
What are the 3 endogenous opioids?
Endorphins, enkephalins (primarily delta), dysmorphins (primarily kappa).
72
Tissue injury is what type of pain?
Nociceptive either somatic or visceral.
73
Why are opioids more potent in an IV form?
Because given PO, they go through first pass metabolism.
74
What is the phenomenon when chronic pain medication stops working?
Tolerance.
75
What is miosis?
Pinpoint pupils.
76
Which opioid is most potent?
Oxycodone, prescribed at higher doses as immediate release or controlled-release forms for moderate to severe pain.
77
How does a bolus with a button for the patient control overdose?
It is timed, and if they are too sleepy, they can’t press the button.
78
Oxycontin or oxycodone to treat acute pain?
Oxycodone.
79
What drug is well absorbed after oral administration but may undergo rapid first-pass metabolism?
Naltrexone.
80
How are neuromuscular blockers used?
Used during surgical procedures and in the intensive care unit (ICU) to produce muscle paralysis.
81
What is Baclofen?
A GABA-B agonist.
82
What is the MOA of Baclofen?
Acts both pre- and postsynaptically by crossing the blood-brain barrier and acting at the spinal cord for spasticity of cerebral and spinal cord origin.
83
Define antispastics.
Spasmolytics used to decrease spasticity that is usually associated with upper motor neuron problems.
84
Define antispasmodics.
Antispasmodic agents reduce musculoskeletal pain and spasms associated with strain or injury.
85
What does the AAOS recommend in relation to use for NSAIDs?
Recommends oral NSAIDs (or topical NSAIDs or tramadol) in patients with symptomatic OA of the knee.
86
What enzyme do NSAIDs inhibit?
COX.
87
What is the indication for NSAIDs with cancer?
Several NSAIDs (including aspirin) reduce the incidence of colon cancer when taken chronically.
88
What are the common adverse effects of NSAIDs?
The most common adverse effects of NSAIDs (including aspirin) are GI injury and renal injury.
89
How is Ketorolac an NSAID?
KETOROLAC is an NSAID that can be administered intramuscularly or intravenously (toxic, but used a lot in the hospital, but not for extended periods of time).
90
What are the two primary COX enzymes?
COX-1 is present in the stomach; COX-2 is not present in the stomach.
91
What do DMARDs do?
DMARDs slow down and reverse joint damage.
92
What is a classic finding in patients with RA?
Ulnar deviation.
93
What question do we ask when suspecting RA?
Morning stiffness.
94
What are the different classes of DMARDs?
1. Synthetic nontargeted/conventional 2. Synthetic, targeted DMARDs (e.g., JAK inhibitors) 3. Biologic DMARDs developed from biological compounds.
95
What are the first-line treatments for RA?
Analgesics and anti-inflammation (NSAIDs, corticosteroids).
96
What is a fast-acting treatment for RA symptoms?
NSAIDs and corticosteroids provide symptomatic relief but do not prevent erosions or alter disease progression.
97
What is JAK?
A targeted synthetic DMARD.
98
What is the most common Biologic DMARD?
Adalimumab (Humira).
99
What is the initial synthetic DMARD of choice for RA?
Methotrexate, which usually works in 2-6 weeks.
100
What is a key safety concern for Leflunomide?
It is teratogenic and has a half-life of 2 weeks.
101
What is Hydroxychloroquine sulfate used for?
It is the antimalarial agent most often used against rheumatoid arthritis.
102
What is required due to the risk of pigmentary retinitis with Hydroxychloroquine?
Ophthalmologic examinations every 12 months are required.
103
What should patients be screened for before receiving Janus kinase inhibitors?
Latent tuberculosis if they have ever been positive.
104
How can Janus kinase inhibitors be used?
As monotherapy or in combination with methotrexate.
105
What is an occasional treatment option for RA?
Gold salts.
106
What warning do gold salts have?
A black-box warning for bone marrow toxicity.
107
What is an sDMARD?
Synthetic DMARD.
108
What is a reasonable alternative to a non-steroidal medication for RA?
A steroid like methotrexate + steroid (be conscious of tapering steroids).
109
What are the black box warnings for Leflunomide?
Embryo-Fetal Toxicity and Hepatotoxicity.
110
What is a cDMARD?
Conventional DMARD, which means the same thing as a synthetic non-targeted DMARD.
111
What is Hydroxychloroquine also used for besides RA?
Malaria prophylaxis and SLE, but requires an annual ophthalmic exam.
112
What does Tofacitinib inhibit?
Janus-associated kinases (JAK) 1, 2, and 3.
113
What are the black box warnings for Tofacitinib?
Risk of serious infection, pulmonary and extrapulmonary TB, invasive fungal infections, mortality, malignancies, and thrombosis.
114
Can Biologic DMARDs be used as combination therapy?
No, never use two biologics together, but you can pair a biological with a medication from another class.
115
What are TNF inhibitors?
Etanercept, infliximab, adalimumab. They are frequently added to the treatment of patients who have not responded adequately to methotrexate and are increasingly used as initial therapy in combination with methotrexate for patients with poor prognostic factors.
116
What are the 3 biologic DMARDs?
Abatacept, Rituximab, Tocilizumab.
117
What is Abatacept?
A recombinant protein that blocks T-cell co-stimulation and produces clinically meaningful responses in approximately 50% of individuals whose disease did not respond to the combination of methotrexate and a TNF inhibitor.
118
What is Rituximab?
A humanized mouse monoclonal antibody that depletes B cells and can be used in combination with methotrexate for patients whose disease has been refractory to treatment with a TNF inhibitor.
119
What is Tocilizumab?
A monoclonal antibody that blocks the receptor for IL-6, an inflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. It is used most often in combination with methotrexate for patients whose disease has been refractory to treatment with a TNF inhibitor.
120
Initial treatment for newly diagnosed 33-year-old presenting with moderate to severe RA?
First-line: Methotrexate (MTX). Often combined with: short-term low-dose prednisone to control symptoms while waiting for MTX to take effect.
121
What class of DMARDs should never be used in combos?
Biologic DMARDs.
122
Definition of DMARDs
DMARDs are a class of medications used to treat autoimmune conditions like rheumatoid arthritis (RA) by slowing disease progression, reducing inflammation, and preventing joint damage.
123
What are bDMARDs? Which ones are taken by mouth?
bDMARDs (Biologic DMARDs): Target specific components of the immune system (e.g., TNF-α, IL-6, B cells). Examples: TNF inhibitors: etanercept, infliximab, adalimumab; IL-6 inhibitor: tocilizumab; T-cell modulator: abatacept; B-cell depleter: rituximab. Oral bDMARDs? → None are taken orally.
124
Is prednisone + methotrexate + infliximab OK?
Yes, with careful monitoring. This is a standard regimen for moderate to severe RA.
125
Is prednisone + hydroxychloroquine + tofacitimib OK?
Yes, with caution. Hydroxychloroquine is mild, and tofacitinib (a JAK inhibitor) is potent.
126
Which DMARD does not have a BB warning?
Hydroxychloroquine (Plaquenil): No BB warning. Often used in mild RA or in combination with other DMARDs. Monitor for retinopathy.
127
What are some combination DMARDS?
As a general rule, DMARDs have greater efficacy when administered in combination than when used individually.
128
What is the most commonly used combination DMARD?
The most commonly used combination is methotrexate with one of the TNF inhibitors, which is more effective than methotrexate alone.
129
What is the most common to use triple therapy of Methotrexate, sulfasalazine, and hydroxychloroquine?
This is to allot for cost, insurance, coverage, etc.
130
What would prompt us to add a biologic right off the bat?
Poor prognostic factors, because we might not have time to wait for escalation of therapy.
131
What is the first treatment option for low disease activity?
Hydroxychloroquine (Plaquenil)
## Footnote
Initial treatment consideration.
132
What is the second treatment option for low disease activity?
Sulfasalazine (Azulfidine)
## Footnote
Initial treatment consideration.
133
What is the third treatment option for low disease activity?
Methotrexate
## Footnote
Initial treatment consideration.
134
What is the fourth treatment option for low disease activity?
Leflunomide (Arava)
## Footnote
Initial treatment consideration.
135
What medication puts rapid metabolizers at higher risk of death?
Codeine, commonly used in cough syrups and pain medications.
136
Why should a patient suspected of opioid overdose be observed?
They may need serial dosing of naloxone due to the short half-life of opioids.
137
What is the cause of nausea, vomiting, muscle pain, and hyperthermia in a known drug user?
Opioid withdrawal syndrome.
138
What is the alternative opioid agonist commonly used for opioid dependence?
Methadone.
139
What medication is a GABA-3 agonist used for significant spasticity?
Diazepam.
140
What opioid-like medication may not be fully reversed by naloxone?
Tramadol.
141
What reversal agent can trigger seizures in a patient who took Xanax?
Flumazenil.
142
Why must patients receiving reversal agents be monitored in the ICU?
The medications have a short half-life.
143
What GABA B agonist is used for patients with significant spasticity?
Baclofen.
144
What muscle relaxer is recommended for acute low back pain?
Flexeril (cyclobenzaprine).
145
What is the mechanism of action of diphosphonates?
They inhibit osteoclast cell turnover.
146
What should be monitored after 3-5 years of bisphosphonate treatment?
DEXA scan.
147
Before starting alendronate, where should a patient be referred?
To a dentist due to the risk of osteonecrosis of the jaw.
148
What is the first choice for urate lowering therapy in a patient with recurrent gout?
Allopurinol.
149
What should be given alongside allopurinol to manage acute gout?
NSAID or colchicine.
150
What is the second best option for chronic gout if xanthine oxidase inhibitors are not tolerated?
Probenecid.
151
What medications can be used for a first episode of acute gout?
NSAIDs, colchicine, and steroids.
152
What do xanthine oxidase inhibitors do?
They decrease uric acid production.
153
What is the next choice for treatment if febuxostat fails and the patient is allergic to probenecid?
Peglodicase.
154
What class of medication is etanercept?
TNF inhibitor.
155
What is the first-line treatment for moderate to severe RA?
Methotrexate.
156
What is the alternative for patients who cannot take bisphosphonates?
Prolia for SC injection every 6 months.
157
What is Suboxone used for?
Opioid dependence treatment.
158
What should be avoided when escalating treatment for RA?
Do not use two biological DMARDs together.
159
What opioid patch is good for chronic and cancer patients?
Fentanyl.
160
What is the first-line treatment for osteoporosis?
Bisphosphonates.
161
What is the mechanism of action for probenecid?
It blocks reabsorption of uric acid.
162
What is chronic pain defined as?
Pain lasting more than 3-6 months.
163
What type of pain is characterized by burning, tingling, and numbness?
Neuropathic pain.
164
What type of pain is abdominal pain and cramping?
Nociceptive, visceral pain.
165
How do NSAIDs work?
They inhibit COX and block production of prostaglandins.
166
What is the black box warning for NSAIDs?
Increased risk of cardiovascular thrombotic events and GI ulceration and bleeding.
167
What NSAID is contraindicated for use longer than 5 days?
Ketorolac/Toradol.
168
What is the best NSAID for a patient with a history of PUD and no history of CVD?
Celecoxib.
169
What is the first-line treatment for a patient with a first episode of acute gout?
NSAIDs or colchicine.
170
What should be used for a premenopausal woman with musculoskeletal pain and a history of gastritis?
NSAID (meloxicam, etc.) + PPI.
171
What is the spectrum of NSAIDs from highly selective to non-selective?
Meloxicam is semi-selective or preferentially selective.
172
What is the irreversible NSAID that inhibits platelets?
Aspirin.
173
What OTC opioid can be used for diarrhea?
Imodium (loperamide).
174
What oral opioid antagonist is FDA-approved for alcohol use disorder?
Naltrexone.
175
What drugs are used for muscle spasticity?
Baclofen, Dantrolene, Diazepam.
176
What are the three strategies for urate lowering therapy?
Decrease uric acid production, increase uric acid excretion, increase uric acid metabolism.
177
How do you classify the pain of a 35-year-old patient with ongoing pain after an MVC 7 months ago?
Chronic pain (>3-6 months)
178
What type of pain is described by a 63-year-old morbidly obese patient with burning, tingling, and numb feelings?
Neuropathic pain
179
How do you classify the abdominal pain of a 38-year-old female with dull, cramping pain that has progressively worsened over 2 days?
Nociceptive visceral pain
## Footnote
Associated with tissue injury or damage; visceral is for internal organs.
180
What is the purpose of a pain assessment scale when evaluating a patient post-surgery?
Selection of initial therapy and modifications
## Footnote
Used to determine what to do next.
181
What is the next choice for a patient with cancer whose pain has progressed after initial treatment with non-opioids and mild-moderate opioids?
Strong opioid therapy and adjuvant
## Footnote
Know which medicines are in which categories.
182
What can a 27-year-old pregnant female take for pain and fever?
Acetaminophen
## Footnote
Safe and effective for pain and fever in pregnant women.
183
What is the BBW for all NSAIDs?
CVD, GI ulceration, & GI bleeding
184
What medication would you use to treat a patient with moderate to severe RA who has evidence of ulnar deviation?
Methotrexate
185
How do NSAIDs work?
They inhibit the COX enzyme and reduce the production of prostaglandins.
186
What medication would be best for a patient with chronic MSK pain who has a history of gastritis and peptic ulcer disease?
COX-2 selective NSAID; Celecoxib
## Footnote
Could do Meloxicam too because NSAIDs are a spectrum.
187
What is the best NSAID for a patient with a history of peptic ulcer disease and no history of CVD?
COX-2; Meloxicam
188
Which NSAID is contraindicated for a 17-year-old male with a sprained ankle needing 7-10 days of NSAIDs?
Ketorolac (Toradol)
## Footnote
Not indicated for > 5 days for high risk of toxicity.
189
What is the drug of choice for treating the acute gout of a 43-year-old male with severe pain in the right great toe?
NSAIDs (Indomethacin) or Colchicine
190
What is the drug of choice for a premenopausal woman with MSK pain who has a history of gastritis?
NSAID + PPI
191
What NSAID should be avoided in a patient with a history of nasal polyps, bronchospastic reaction to ASA, and angioedema?
Ibuprofen, ASA
192
How would you classify Meloxicam in terms of NSAID selectivity?
Semi-selective or preferentially selective
## Footnote
More selective for COX-2 rather than COX-1.
193
What NSAID are you most concerned about for its risk of GI & renal toxicity?
Ketorolac
194
What schedule is cocaine?
Schedule II
195
What credentials do you need to prescribe schedule II medications?
Federal DEA number and SC DHEC controlled substance license
196
What do you do to adjust the dosage when transitioning a patient from IV opioid to PO opioid post-surgery?
Increase their dose because PO medication has to undergo first pass metabolism.
197
Which receptor mediates the side effects of opioid medications?
MU receptor
## Footnote
As opposed to kappa and delta receptors.
198
What is it called when a patient requires higher and higher doses of medication to manage their skeletal bone pain?
Tolerance
199
What class of antidepressants cannot be used with all opioid uses?
MAOI (uncommonly used)
200
What is it called when a newly delivered infant shows withdrawal symptoms?
Physical dependence
## Footnote
When the medication is taken away.
201
What could cause hepatotoxicity in a 3-year-old who swallowed a lot of acetaminophen?
Hepatotoxicity
202
What OTC medication can a chronic alcoholic with mild-moderate cirrhosis take for a headache?
Ibuprofen
203
What medication can a post-operative patient who cannot tolerate PO medications take that is effective for the short term?
Ketorolac (Toradol)
## Footnote
Great alternative to opioids, but must be used for only 3-5 days.
204
What NSAID irreversibly inhibits the target enzyme, separating it from other NSAIDs?
ASA
## Footnote
Irreversibly inhibits platelets & its target enzyme, thromboxane.
205
What OTC medication can you get for profuse diarrhea before a pharm exam?
Imodium (Loperamide)
206
What medication is approved to promote alcohol abstinence?
Naltrexone
207
What medication puts children who are rapid metabolizers at highest risk for death?
Codeine
208
Why would a patient suspected of opioid overdose still need to be admitted to the hospital after receiving Narcan?
Narcan has a short ½ life so they will decompensate again and need more.
209
What is the most likely cause of nausea, vomiting, and muscle aches in a drug addict using IV drugs?
Opioid abstinence syndrome aka withdrawal
## Footnote
Benzo and alcohol withdrawal is life-threatening, opioid withdrawal is not life-threatening.
210
What is the next step in the ladder of pain control for a patient requiring progressive medication?
Methadone
## Footnote
An alternative opioid agonist that has less risk of withdrawal.
211
What GABA-A receptor agonist would you give to a patient with cerebral palsy and significant spasticity?
Diazepam (Benzodiazepine)
212
What opioid-like medication did a patient take if they showed some response to naloxone but not complete reversal of symptoms?
Tramadol
213
What is the reversal medication for a patient who is very sedated and obtunded after taking Xanax?
Flumazenil
214
Why do patients who receive reversal agents for benzodiazepines have to be monitored in the ICU?
The medications have a short ½ life.
215
What GABA-B medication would you transition a patient with cerebral palsy and spasticity to if they were previously on diazepam?
Baclofen
216
What muscle relaxer would you recommend for significant spasm of paraspinal muscles causing low back pain?
Cyclobenzaprine
217
What is the MOA of bisphosphonates prescribed for a 72-year-old woman with osteoporosis?
Inhibits osteoclasts
218
How long can a patient be treated with bisphosphonates after showing benefit on a DEXA scan?
3-5 years
219
Before starting Ibandronate for osteoporosis, which medical provider should you refer the patient to?
Dentist for an exam
220
What is the first choice for urate lowering therapy in a patient who has had 5 episodes of acute gout in the last 11 months?
Allopurinol
221
What other medication should a patient starting on allopurinol be started on and why?
NSAID or colchicine to prevent risk of acute attack.
222
What medication used to treat acute gout flares inhibits leukocyte migration and phagocytosis and can cause bone marrow toxicity?
Colchicine
223
What is the second-line therapy for a patient with chronic gout who cannot tolerate xanthine oxidase inhibitors?
Probenecid
224
What are the three classes of medication for acute treatment of gout?
NSAIDs, colchicine, and steroids
225
What strategy do xanthine oxidase inhibitors use for urate lowering therapy?
Decrease production of uric acid → increase excretion → metabolize to soluble compound
226
What would you treat a patient with >10 uric acid levels who has failed xanthine oxidase inhibitors and has an allergy to probenecid?
Pegloticase
227
What class of medication is Etanercept for a patient with RA who has been on NSAIDs and methotrexate?
Biologic DMARD
228
What is the first-line treatment for mod-severe RA?
Methotrexate
## Footnote
Can add NSAID because it adds short-term symptom relief.
229
What can be added to methotrexate for severe RA or with flare?
Corticosteroids
230
How else can patients who cannot take bisphosphonates take their medication?
Infusible alternative, Denosumab
231
What is Suboxone used for in opioid dependence treatment?
A combination of Buprephenoide (partial agonist) and antagonist naloxone
## Footnote
Use because naloxone is inert when taken PO, discourages disuse of the medication.
232
What must we remember in the escalation of RA treatment with biologic medications?
Do not use two biologics together!
233
What should you not do if failing a biologic and need to change therapy?
Don’t change the class of the biologic to a medication of the same class (ex: TNF)
234
What patch of opioid is used for chronic pain in cancer patients?
Fentanyl
235
What is the first-line treatment for osteoporosis?
Bisphosphonates
236
What is the MOA of Probenecid?
Block reabsorption of uric acid that has been filtered into the urine; decrease excretion of PCN
