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Pharmacology > 22) NSAIDs, Gout, RA > Flashcards

22) NSAIDs, Gout, RA Flashcards

1
Q

Inflammation

A
  • Response to cell injury
  • Primarily occurs in vascularized connective tissue
  • Often involves the immune response
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2
Q

Inflammation causes

A
  • Pain

- If cell injury, can result in a chronic condition of pain and tissue damage (like rheumatoid arthritis)

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3
Q

Drugs often used to control pain/inflammation

A
  • NSAIDs

- Acetaminophen

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4
Q

Treatment strategies that target the immune processes

A
  • Glucocorticoids

- Disease-modifying antirheumatic drugs (DMARDs)

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5
Q

Gout

A
  • Metabolic with precipitation of uric acid crystals in joints
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6
Q

Treatment of Gout

A
  • Aacute episode treatment targets inflammation

- Chronic gout treatment targets both inflammatory processes and the production and elimination of uric acid

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7
Q

Why NSAIDs exacerbate asthma?

A
  • Inhibiting prostaglandins potentiates the leukotriene pathway
  • Leukotriene pathway worsens asthma
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8
Q

Functions of the prostaglandins

A
  • Stimulate hypothalamus to increase body temp
  • Stimulate immune cells to cause inflammation
  • Sensitize nerves to pain
  • Produce protective mucous in the stomach
  • Initiate blood clotting
  • Constrict or dilate blood vessels
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9
Q

Prostaglandin function is inhibited by

A
  • NSAIDs
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10
Q

Major difference between the MOA of aspirin and other NSAIDs

A
  • Aspirin acetylates and thereby IRREVERSIBLY inhibits cyclooxygenase
  • Inhibition produced by other NSAIDs is reversible
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11
Q

The irreversible action of aspirin results in

A
  • Longer duration of antiplatelet effect

- Basis for its use as an antiplatelet drug

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12
Q

Arachidonic acid derivatives are important mediators of

A
  • Inflammation

- Cyclooxygenase inhibitors reduce inflammation

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13
Q

NSAIDs also suppress

A
  • Prostaglandin synthesis in the CNS stimulated by pyrogens (produce fever)
  • Reduce fever (antipyretic action)
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14
Q

3 therapeutic dose ranges of aspirin

A
  • The low range (<300 mg/d) = reduce platelet aggregation
  • Intermediate doses (300–2400 mg/d) = antipyretic and analgesic effects
  • High doses (2400–4000 mg/d) = anti-inflammatory effect
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15
Q

Release of phospholipids from damaged cell membrane initiates

A
  • Arachidonic acid cascade COX

- Synthesizes prostaglandins

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16
Q

Analgesics act on

A
  • Both PNS and CNS
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17
Q

Analgesics include

A
  • Acetaminophen (Tylenol), known as Paracetamol in Europe (APAP)
  • NSAIDs: salicylates (aspirin), ibuprofen, naproxen …
  • Others non-OTC (e.g. Opioids as morphine/ oxycodone/ coxib/ and others)
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18
Q

OTC NSAIDs generic/brand names

A
  • Ibuprofen (Advil)
  • Naproxen (Aleve, All day relief, Naprosyn)
  • Aspirin (Bufferin, Ecotrin, Bayer aspirin)
  • Mefenemic acid (Ponstel)
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19
Q

Ibuprofen (Advil) classification

A
  • Propionic acid derivative
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20
Q

All of the OTC NSAIDs site of action

A
  • CNS and PNS
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21
Q

All of the OTC NSAIDs uses

A
  • Analgesic
  • Anti-inflammation
  • Anti-pyretic
  • Antiplatelet (Blood thinning)
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22
Q

Naproxen (Aleve, All day relief, Naprosyn) classification

A
  • Propionic acid derivative
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23
Q

Aspirin (Bufferin, Ecotrin, Bayer aspirin) classification

A
  • Salicylates: Acetyl salicylic acid (ASA)
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24
Q

Mefenamic acid (Ponstel) classificaiton

A
  • Fenamate
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25
Q

Acetaminophen brand names

A
  • Fever-all

- Tylenol

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26
Q

Acetaminophen classification

A
  • Acetyl para-aminophenol (APAP)
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27
Q

Acetaminophen site of action

A
  • CNS
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28
Q

Acetaminophen uses

A
  • Analgesic
  • Antipyretic
  • NOT an anti-inflammatory
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29
Q

Aspirin MOA

A
  • Non-selective and irreversible COX 1 and 2 inhibitor
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30
Q

Ibuprofen, Naproxen, and mefenamic acid MOA

A
  • Non-selective and reversible COX 1 and 2 inhibitor
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31
Q

Aspirin, Ibuprofen, Naproxen, Mefenamic acid (NSAIDs) side effects

A
  • Risk of bleeding (in ASA), bruising
  • NSAIDs allergy (contraindication)
  • GI ulcers, heartburn, nausea
  • Renal monitoring: increase BUN, serum creatinine
  • Exacerbate asthma
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32
Q

Aspirin DOA

A
  • 4-6 h
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33
Q

Ibuprofen and Mefenamic acid DOA

A
  • 6-8 h
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34
Q

Naproxen DOA

A
  • 12 h
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35
Q

NSAIDs metabolism and excretion

A
  • Hepatically (liver) metabolized

- Renally excreted

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36
Q

Metabolism definition

A
  • Process where body breaks down and converts medication into active chemical substances
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37
Q

Symptoms of NSAID toxicity

A
  • Ringing in the ears
  • Nausea and vomiting
  • Abdominal pain
  • Fast breathing rate
  • Fever
  • Low blood glucose and potassium
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38
Q

Complications with NSAID toxicity

A
  • Swelling in the brain
  • Seizures
  • Low blood sugar
  • Cardiac arrest
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39
Q

Selective COX-2 inhibitor

A
  • Celecoxib (Celebrex)
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40
Q

Selective COX-2 inhibitor advantage

A
  • Reducedrisk of GI effects (gastric ulcers and serious GI bleeding)
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41
Q

COX-2 inhibitors risks and side effects

A
  • Same risk of renal damage as COX inhibitors (nephrotoxicity)
  • Increase risk of heart attacks or stroke, hypertension
  • Increase GI bleeding
  • Anemia
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42
Q

Celebrex cannot be given to

A
  • Patients with sulfur allergues (sulfa drug)
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43
Q

Celecoxib (Celebrex) metabolism

A
  • Hepatic
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44
Q

APAP details

A
  • MOA unknown
  • Reduces COX activity
  • Liver metabolized, renal excretion
  • DOA = 4-6 h
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45
Q

APAP side effects

A
  • Nausea, vomiting
  • Constipation
  • Increased aspartate aminotransferase
  • Rash, pruritus
  • Hypokalemia, hyperglycemia
  • Hepatotoxicity
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46
Q

In cases of APAP overdose,

A
  • The sulfate and glucuronide pathways become saturated
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47
Q

Under normal conditions, NAPQI is detoxified by

A
  • Conjugation with glutathione
48
Q

More APAP is shunted to the cytochrome P450 system to produce

A
  • NAPQI

- As a result, hepatocellular supplies of glutathione become depleted

49
Q

APAP causes NAPQI to remain in its toxic form in the liver

A
  • Reacts with cellular membrane molecules
  • Hepatocyte damage and death
  • Acute liver necrosis
50
Q

APAP when following a therapeutic dose in normal patients

A
  • Mostly converted to nontoxic metabolites by conjugation with sulfate and glucuronide (phase II metabolism)
  • Small portion oxidized via cytochrome P450 system
51
Q

Acetaminophen toxicity

A
  • More than 4 g per 24 hours
52
Q

Signs and symptoms of acetaminophen toxicity occure in 3 phases

A
  • Phase 1 (hours after overdose)
  • Phase 2 (24-72h)
  • Phase 3 (3-5 days)
53
Q
  • Phase 1 acetaminophen toxicity (hours after overdose)
A
  • Nausea and vomiting
  • Pale appearance
  • Sweating
54
Q

Phase 2 acetaminophen toxicity (24-72h)

A
  • Jaundice, signs of liver damage (i.e. right upper quadrant pain followed by acute renal failure)
55
Q

Phase 3 acetaminophen toxicity (3-5 days)

A
  • Liver necrosis
  • Low blood sugar
  • Coagulation problems
  • Brain swelling
  • Multiple organ failure and death
56
Q

Liver damage results from one of APAP metabolites

A
  • N-acetyl-p-benzoquinone imine (NAPQI)
57
Q

Acetaminophen overdose antidote/treatment

A
  • N-acetylcysteine (NAC)

- IV form not the OTC oral product (that becomes GSH)

58
Q

ASA vs. APAP structure

A
  • ASA = salicylate

- APAP = para-amino phenol derivative

59
Q

ASA vs. APAP indication

A
  • ASA = analgesic, antipyretic, anti-inflammatory

- APAP = analgesic, antipyretic

60
Q

ASA vs. APAP gastric side effects

A
  • ASA = yes (inhibition of COX-1 in the gastric area)

- APAP = not major

61
Q

ASA vs. APAP at low doses

A
  • ASA = has anti-platelet activity (mediated by COX-1)

- APAP = no anti-platelet activity

62
Q

ASA vs. APAP antidote

A
  • ASA = no specific

- APAP = N-acetylcysteine (NAC)

63
Q

DMARDs

A
  • Disease-modifying antirheumatic drugs
  • Anti-inflammatory actions in several connective tissue diseases
  • Can slow, or even reverse joint damage
64
Q

DMARDs activity/progression

A
  • Slow acting because it may take 6 weeks to 6 months for their benefits to become apparent
65
Q

Corticosteroids

A
  • Can be considered anti-inflammatories with intermediate rate of action (ie, slower than NSAIDs but faster than other DMARDs)
  • Too toxic for routine chronic use
66
Q

Corticosteroid use

A
  • Temporary control of severe exacerbations

- Long-term use in patients with severe disease not controlled by other agents

67
Q

Glucocorticoid side effects

A
  • Decreased growth in children
  • Glaucoma
  • Centripetal distribution of body fat
  • Osteoporosis (negative calcium balance)
  • Increased risk of infection (impaired wound healing)
  • Hirsutism
  • Increased appetite
  • Emotional disturbances (euphoria, depression)
  • Peptic ulcer
  • Hypertension
  • Peripheral edema
  • Hypokalemia
68
Q

Glucocorticoid hyperglycemia/diabetes side effect mechanism

A
  • Gluconeogenesis
69
Q

Glucocorticoid central obesity, moon face, buffalo hump side effect mechanism

A
  • Dramatic redistribution of body fat
70
Q

Glucocorticoid muscle weakness and wasting side effect mechanism

A
  • Breakdown of proteins

- Diversion of amino acids to glucose production

71
Q

Glucocorticoid weight gain side effect mechanism

A
  • Increased appetite (CNS effect)
  • Increased need for insulin over time (because of gluconeogenesis which results from weight gain)
  • Mineralocorticoid activity (Na+/water retention)
72
Q

Glucocorticoid osteoporosis side effect mechanism

A
  • Decreased reabsorption of calcium by the kidney
73
Q

Glucocorticoid avascular necrosis of femur head side effect mechanism

A
  • Increased levels of serum lipids
  • Results in both increased formation of microemboli in bone nutrient arteries, and fat-related blockage of venous flow from bone (lipolysis)
  • IRREVERSIBLE
74
Q

Glucocorticoid skin bruising and poor wound healing side effect mechanism

A
  • Anti-proliferative effect
75
Q

Glucocorticoid hirsutism and acne side effect mechanism

A
  • Due to ACTH-mediated increase of adrenal androgens
76
Q

Glucocorticoid increased infections side effect mechanism

A
  • Immunosuppression
77
Q

Glucocorticoid hypomania, depression, psychosis side effect mechanism

A
  • Normal cortisol levels maintains emotional balance
78
Q

DMARDs names

A
  • Abatacept (T-cell modulator)
  • Anti-IL-1
  • Anti-IL-6
  • Anti-TNF-alpha
  • Belimumab
  • Cyclosporine
  • Hydroxychloroquine, chloroquine
  • Leflunomide
  • Methotrexate
  • Penicillamine
  • Rituximab
  • Sulfasalazine
  • Gol compounds
  • Tofacitinib
79
Q

Abatacept MOA

A
  • Interfere with activity of T-lymphocytes
80
Q

Abatacept toxicity when used for RA

A
  • Infection

- Exacerbation of COPD

81
Q

Anti-IL-1 drug names

A
  • Anakinra
  • Rilonacept
  • Canakinumab
82
Q

Anti-IL-1 drugs MOA

A
  • Recombinant human IL-1 receptor antagonist

- Acts as a cysteine inhibitor

83
Q

Anti-IL-1 drugs toxicity when taken for RA

A
  • Infection

- Neutropenia

84
Q

Anti-IL-6 drug names

A
  • Tocilizumab
85
Q

Tocilizumab MOA

A
  • IL-6 antagonist
86
Q

Tocilizumab (anti-IL-6 drug) toxicity when taken for RA

A
  • Upper respiratory tract infections
  • Hypertension
  • Increase LFT
87
Q

Anti-TNF-alpha drug names

A
  • Infliximab
  • Etanercept
  • Adalimumab
  • Golimumab
  • Certolizumab
88
Q

Anti-TNF-alpha drugs MOA

A
  • Biological agent

- Inhibits action of TNF-alpha

89
Q

Anti-TNF-alpha drugs toxicity when taken for RA

A
  • Infection
  • Lymphoma
  • Hepatotoxicity
  • Hematological effects
  • Cardiovascular toxicity
90
Q

Belimumab MOA

A
  • Anti-B cell activating factor (MAb)

- Inhibits B lymphocyte stimulator (BLyS)

91
Q

Belimumab toxicity when taken for RA

A
  • Nausea, vomiting

- Respiratory tract infection

92
Q

DMARD drugs that interfere with T-lymphocytes

A
  • Cyclosporine
  • Hydrocychloroquine, chloroquine
  • Leflunomide
  • Sulfasalazine
93
Q

Cyclosporine toxicity when taken for RA

A
  • Nephrotoxicity
  • Hypertension
  • Liver toxicity
94
Q

Hydroxychloroquine, chloroquine toxicity when taken for RA

A
  • Diarrhea
  • Dermatitis
  • Hematological abnormalities
95
Q

Leflunomide toxicity when taken for RA

A
  • Rash
  • GI disturbance
  • Myopathy
  • Neuropathy
  • Ocular toxicity
96
Q

Methotrexate MOA

A
  • Cytotoxic drug that reduces the number of immune cells
97
Q

Methotrexate toxicity when taken for RA

A
  • Teratogenic
  • Hepatotoxicity
  • GI
  • Skin reaction
98
Q

Penicillamine toxicity when taken for RA

A
  • Nausea
  • Mucosal ulcers
  • Hematotoxicity
  • Hepatotoxicity
  • Teratogenicity
99
Q

Rituximab MOA

A
  • Interfere with the activity of B-lymphocytes
100
Q

Rituximab toxicity when taken for RA

A
  • Proteinurea
  • Dermatitis
  • GI
  • Hematological
101
Q

Sulfasalazine toxicity when taken for RA

A
  • Cardiac toxicity
102
Q

Gol compounds MOA

A
  • Interfere with the activity of macrophages
103
Q

Tofacitinib MOA

A
  • Janus kinase inhibitor
104
Q

Tofaciitinic toxicity when taken for RA

A
  • Infection
  • Neutropenia
  • Anemia
  • Increased LDL and HDL
105
Q

Colchicine

A
  • A selective inhibitor of microtubule assembly
106
Q

Paclitaxel

A
  • Stabilizes and protects microtubule against disassembly
107
Q

Drugs used in gout

A
  • Microtubule assembly inhibitors
  • Uricosurics
  • Xanthine oxidase inhibitors
  • Uricase
108
Q

Microtubule assembly inhibitors

A
  • Colchicine

- Taken orally

109
Q

Colchicine side effects

A
  • Diarrhea

- Liver and kidney damage with overdose

110
Q

Uricosurics

A
  • Probenecid
  • Lesinurad
  • Both taken orally
111
Q

Uricosurics (probenecid, lesinurad) MOA

A
  • Inhibition of renal reabsorption of uric acid
112
Q

Xanthine oxidase inhibitors

A
  • Allopurinol
  • Febuxostat
  • Both taken orally
113
Q

Xanthine oxidase inhibitors (allopurinol, febuxostat) MOA

A
  • Allopurinol = irreversible inhibior

- Febuxostat = reversible inhibitor

114
Q

Xanthine oxidase inhibitors (allopurinol, febuxostat) side effects

A
  • GI upset

- Bone marrow suppression

115
Q

Uricases

A
  • Pegloticase

- IV administration

116
Q

Pegloticase MOA

A
  • Recombinant mammalian uricase

- Converts uric acid to soluble form allantoin

117
Q

Pegloticase side effects

A
  • Rapid change in uric acid levels can precipitate gout

Pharmacology (27 decks)

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