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MSK > Pharm > Flashcards

Pharm Flashcards

1
Q

What are the three primary categories of AEs associated with NSAIDs, and why do they occur?

A
  1. ) GI problems: increased risk of bleeding/ulcers, due to impact of mucus layer caused by interruption of prostaglandin function
  2. ) Nephrotoxicity: Due to NSAID effect on afferent arterioles, reducing ability to regulate GFR
  3. ) CV effects: all NSAIDs have risk of thrombosis due to effects on thromboxane
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2
Q

What is the MOA of NSAIDs?

A

Block cyclooxygenase enzymes (COX I and II); analgesic effect is from blocking COX-II. Reduces production of prostaglandins and thromboxane, thus reducing pain and inflammation.

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3
Q

What is the precursor of COX-I and COX-II?

A

Arachidonic acid

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4
Q

What is the only IV administered NSAID used for analgesia?

A

Ketorolac

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5
Q

What is the only COX-II specific NSAID on the market?

A

Celecoxib (only weakly selective).

More selective NSAIDs were removed from market due to increased thrombosis risk

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6
Q

Regarding effect on platelets, what is the major difference between aspirin and other NSAIDs?

A

Aspirin irreversibly inhibits platelet function (via acetylation of the N-acetyl chain of COX).
Other NSAIDs reversibly inhibit platelet function.

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7
Q

Where is acetaminophen metabolized and what are the special considerations?

A
  • Liver, then cleared by kidneys
  • A small percent is metabolized to a toxic metabolite
  • Glutathione is needed to remove the toxic metabolite
  • We can run out of glutathione if too much acetaminophen is ingested, causing a buildup of toxic metabolite and causing liver damage
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8
Q

What is the treatment for acetaminophen overdose and how does it work?

A

N-acetylcysteine: repletes glutathione so the toxic metabolite of acetaminophen can be cleared

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9
Q

When switching a patient from one opioid to another, how should dosages change and why?

A

Start by cutting the dose in half and then titrate up.

While analgesic effects can be matched between opioids, pharmacokinetics and tolerance levels to AEs will differ in unpredictable ways.

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10
Q

What are some AEs of opioids that are NOT subject to tolerance?

A 
Miosis
GI effects (constipation)
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11
Q

Where is morphine metabolized?

A

Liver, however, the analgesic metabolite will accumulate in patients with renal dysfunction.
With either liver or liver dysfunction, dose will need to be adjusted.

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12
Q

Seizures are an AE of which opioid? Why?

A

Meperidine. Meperidine gets metabolized to normeperidine which is excreted renally. In patients with poor renal function, it can build up and cause seizures.

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13
Q

How is methadone different from other drugs used in opiate use disorders?

A

Methadone is a long-acting mu receptor agonist, and also blocks NMDA receptors.

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14
Q

Fentanyl, sufentanil, alfentanil, and remifentanil have what in common?

A

All are very short acting and used in the OR setting. Fentanyl is also available as a patch for use outside of the OR.

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15
Q

What is the partial opioid agonist we studied?

A

Buprenorphine - can displace morphine from the mu receptor. Slowly dissociates from the mu receptor. Used in opioid addiction.

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16
Q

What are the receptors involved in opioid MOA?

A

Mu 1, 2, and kappa receptors
(Open K+ channels and close VGCa2+ channels, causing decrease in neurotransmission: decreased release of ACh, dopamine, NE, and substance P)

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17
Q

With which opioid is there a particular risk of cardiac AEs?

A

Morphine, IV administration, can cause hypotension

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18
Q

Which analgesic drug can cause itching?

A

Morphine: when given IV can increase histamine release

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19
Q

Which opioid has the longest half-life?

A

Methadone

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20
Q

Pure opioid agonists share what important quality regarding dose?

A

No ceiling effect

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21
Q

What are the mixed opioid agents we studied?

A

Pentazocine, butorphanol, and nalbuphine

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22
Q

Which opioid antagonist is most commonly used during opioid overdose?

A

Naloxone

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23
Q

Your patient has severe constipation for which laxatives and other therapies have failed. What drug could be considered?

A

Methylnaltrexone is an opioid antagonist. It does not enter the CNS. It works on opioid receptors in the GI. SubQ administration.

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24
Q

Consider prescribing _____ when starting a patient on an opioid.

A

A laxative

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25
Q

This drug is technically not an opiate, but can be addictive, can cause seizures, serotonin syndrome, and n/v/c.

A

Tramadol

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26
Q

Steroids are used for what effects in RA?

A

Decrease inflammation

Suppress immune system

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27
Q

When should steroids be used in RA?

A

Flares/short term

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28
Q

What is the first line tx for RA?

A

Methotrexate, a DMARD

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29
Q

How does methotrexate work?

A

Inhibits purine metabolism: decreases DNA synthesis by inhibiting tetrahydrofolate production.

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30
Q

What labs must be monitored in a patient on methotrexate?

A

CBC
WBC
LFTs
Pulm function

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31
Q

What are some potential AEs of methotrexate?

A 
Lots of GI effects
Stomatitis
Myelosupression (leukopenia, thrombocytopenia)
Hepatotoxicity
Pulmonary toxicity
Nephrotoxicity
Increased risk of infections

Teratogenic!

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32
Q

Which agent used in the treatment of RA has ocular AEs?

A

Hydroxychloroquine - can cause ocular opacities

33
Q

Which RA drug works by inhibiting the JAK/STAT pathway?

A

Tofacitinib (Xelganz)

34
Q

What is the second-line DMARD for use in RA and it’s MOA?

A

Leflunomide: inhibits pyrimidine synthesis

35
Q

What are two TNF blockers used for the tx of RA, and how are they used?

A
  • Etanercept
  • Infliximab
    (Those were the two that were emphasized, but also adalimumab, certolizumab, and golimumab)

These are most often used in conjunction with methotrexate in pts with moderate-severe RA

36
Q

What is the MOA of anakinra?

A

IL-1 blocker; do not use with TNF blockers

37
Q

Which drug used in the treatment of RA works by blocking interleukin 6?

A

Tocilizumab

38
Q

What is the name and MOA of the last-line RA drug we learned about?

A

Abatacept: this inhibits T-cell co-stimulatory signaling: B-cells (–> immunoglobulins) or macrophages (–> TNFs/ILs)

39
Q

On what cells does Rituximab work?

A

B-cells

40
Q

What are some special considerations when using a biologic in a patient with RA?

A 
Must r/o TB before initiating
Educate about de-myelination
May worsen HF
Long-term risks are not well understood
Cannot receive live vax
Cannot use biologics with an active infection
CBC must be monitored
Increased risk of infection when using with methotrexate
41
Q

What are 3 drugs used in the treatment of acute gout attacks?

A

NSAIDs
Steroids
Colchecine

42
Q

What cell type is the target of colchecine’s MOA?

A

PMNs

43
Q

What are some AEs to be expected with colchecine administration?

A

Nausea
Vomiting
Diarrhea

44
Q

What are 3 classes of drugs used for gout prophylaxis?

A

Xanthine oxidase inhibitors (reduces production of uric acid)

Uricosuric agents (increase excretion of uric acid via action on proximal tubule)

Urate oxidase enzymes (catalyzes oxidation of uric acid for excretion)

45
Q

Which drugs, used in prophylaxis of acute gout flares, are first line? What is their (general) MOA?

A

Xanthine oxidase inhibitors:
Allopurinol
Febuxostat

These reduce uric acid production

46
Q

What is a special consideration when prescribing allopurinol?

A

Must be adjusted for renal function

47
Q

What are some common uricosuric agents; what do they do; and what are some important considerations?

A

Probenecind - NEED GFR of 30+ cc/min!!! Also lots of drug interactions. Lesinurad is a new drug, works just like probenecid

Losartan (lowers BP)

Fenofibrate (lowers TGs, raises HDL)

48
Q

What drug works to prevent gout attacks by converting uric acid to allantoin for excretion?

A

Pegloticase- a urate oxidase enzyme

49
Q

What are 5 drugs that increase uric acid levels?

A 
Thiazide diuretics
Loop diuretics
Niacin
Low dose aspirin
Cyclosporin
50
Q

What is the first line treatment for OA pain?

A

NSAIDs - consider topical

51
Q

What drugs have been shown to slow the progression of OA?

A

None

52
Q

True allergies are associated with what subtype of local anesthetic?

A

Esters

53
Q

What is added to local anesthetics to promote a more rapid onset of action?

A

Bicarb

54
Q

What is added to local anesthetics to promote a longer duration of action?

A

Epinephrine; reduces peak serum concentration due to delay of distribution that results from vasoconstriction

55
Q

What is the general MOA of local anesthetics?

A

Inhibition of voltage-gated Na+ channels, preventing AP propogation

56
Q

During what state do local anesthetic drugs gain access and act on Na+ channels?

A

Open/activated state

57
Q

During what state do local anesthetic drugs bind to Na+ channels?

A

Inactive state

58
Q

What factors affect the rate of dissociation of local anesthetic drugs from Na+ gates?

A

Size
Charge
Lipophilicity

(Small/low lipophilicity = faster dissociation)

59
Q

What is a secondary MOA of local anesthetic drugs?

A

Blockade of K+ channels

This blocks conduction in the dorsal root ganglia/dorsal horns and delays repolarization (thereby increasing the refractory period).

60
Q

Which class of local anesthetics has a longer duration of action?

A

Amides

Esters undergo hydrolysis and have a shorter duration of action

61
Q

A local anesthetic that is very lipophilic will have what qualities compared to a drug that is less lipophilic?

A

Increased potency
Slower onset of action
Prolonged duration of action
Less systemic distribution (fewer systemic AEs)

62
Q

What pharmacokinetic parameters correlate with toxicity risk?

A

Cmax and time to Cmax - peak serum concentration and how quickly that concentration is reached.

63
Q

Why are ester-based local anesthetics associated with hypersensitivity reactions?

A

Metabolism of esters by esterases –> PABA metabolites

64
Q

How can you tell ester- or amide-based local anesthetics apart based on names?

A

Amides all have 2 “i”s in their names (lidocaine, prilocaine)

Esters only have 1

65
Q

Less lipid solubility is associated with what characteristic in local anesthetics?
Higher lipid solubility?

A

Local anesthetics must have some lipid solubility to cross membranes

Less lipid solubility = less potency
Too much lipid solubility = delayed onset of action

66
Q

Given two formulations of the same imaginary local anesthetic: Drug A has a very low potency but quick onset of action; Drug B’s onset of action is twice as long as A’s, but it is more potent. Compare their lipid solubilities.

A

Drug A has low lipid solubility.

Drug B has high lipid solubility.

67
Q

Are myelinated or unmyelinated nerves more sensitive to local anesthetics? Why?

A

Myelinated nerves are more sensitive: activation occurs at nodes more readily.

Unmyelinated nerves require more concentration to overcome AP propogation

68
Q

What type of nerve fibers do local anesthetics affect?

A

Primarily a-delta fibers (touch, temp, and sharp/fast pain)

69
Q

Which 2 local anesthetics are most selective for sensory effects?

A

Bupivacine

Ropivacaine

70
Q

What types of AEs are most common with lidocaine?

A

CNS and some respiratory (cardio AEs are rare).

71
Q

What is the most common feature of severe local anesthetic toxicity?

A

Seizure. Can progress to catastrophic cardiac collapse.

72
Q

Which local anesthetic is most likely to cause CV AEs, and why?

A

Bupivacaine, due to its vasodilatory effects (allowing more rapid systemic distribution)

73
Q

Your patient presents with seizures, respiratory distress, and hypotension after inadvertent IV administration of a local anesthetic (not by you, hopefully). How is this patient treated?

A

Immediate administration of 20% IV lipid emulsion.

Benzos can be given for seizures.

Initiate ACLS as appropriate.

74
Q

Identify 4 characteristics of benzocaine

A
  • Ester
  • Topical use
  • Can cause metahemoglobinemia
  • 100% charge neutral
75
Q

Identify 3 characteristics of chloroproacine

A
  • Ester
  • Fast onset (due to halide substitution)
  • Rapid metabolism
76
Q

Identify 3 characteristics of cocaine (as a local anesthetic)

A
  • Ester
  • Often used during ENT procedures
  • Vasoconstrictor
77
Q

Identify 3 characteristics of tetracaine

A
  • Ester
  • Often used topically in the eyes
  • Long duration (for an ester)
78
Q

Identify 5 characteristics of bupivacaine

A
  • Amide
  • Frequently used as an epidural
  • Cardiotoxicity > CNS toxicity
  • Low maximum dose
  • Long duration of action
79
Q

Identify 4 characteristics of lidocaine

A
  • Amide
  • Rapid onset
  • Low maximum dose
  • Often combined with epinephrine (vasoconstriction from epi reduces systemic distribution, allowing a higher dose to be used)

MSK (4 decks)

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