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Pharmacology > 22) NSAIDs, Gout, RA > Flashcards

22) NSAIDs, Gout, RA Flashcards

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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
Acetaminophen brand names
- Fever-all | - Tylenol
26
Acetaminophen classification
- Acetyl para-aminophenol (APAP)
27
Acetaminophen site of action
- CNS
28
Acetaminophen uses
- Analgesic - Antipyretic - NOT an anti-inflammatory
29
Aspirin MOA
- Non-selective and irreversible COX 1 and 2 inhibitor
30
Ibuprofen, Naproxen, and mefenamic acid MOA
- Non-selective and reversible COX 1 and 2 inhibitor
31
Aspirin, Ibuprofen, Naproxen, Mefenamic acid (NSAIDs) side effects
- Risk of bleeding (in ASA), bruising - NSAIDs allergy (contraindication) - GI ulcers, heartburn, nausea - Renal monitoring: increase BUN, serum creatinine - Exacerbate asthma
32
Aspirin DOA
- 4-6 h
33
Ibuprofen and Mefenamic acid DOA
- 6-8 h
34
Naproxen DOA
- 12 h
35
NSAIDs metabolism and excretion
- Hepatically (liver) metabolized | - Renally excreted
36
Metabolism definition
- Process where body breaks down and converts medication into active chemical substances
37
Symptoms of NSAID toxicity
- Ringing in the ears - Nausea and vomiting - Abdominal pain - Fast breathing rate - Fever - Low blood glucose and potassium
38
Complications with NSAID toxicity
- Swelling in the brain - Seizures - Low blood sugar - Cardiac arrest
39
Selective COX-2 inhibitor
- Celecoxib (Celebrex)
40
Selective COX-2 inhibitor advantage
- Reduced risk of GI effects (gastric ulcers and serious GI bleeding)
41
COX-2 inhibitors risks and side effects
- Same risk of renal damage as COX inhibitors (nephrotoxicity) - Increase risk of heart attacks or stroke, hypertension - Increase GI bleeding - Anemia
42
Celebrex cannot be given to
- Patients with sulfur allergues (sulfa drug)
43
Celecoxib (Celebrex) metabolism
- Hepatic
44
APAP details
- MOA unknown - Reduces COX activity - Liver metabolized, renal excretion - DOA = 4-6 h
45
APAP side effects
- Nausea, vomiting - Constipation - Increased aspartate aminotransferase - Rash, pruritus - Hypokalemia, hyperglycemia - Hepatotoxicity
46
In cases of APAP overdose,
- The sulfate and glucuronide pathways become saturated
47
Under normal conditions, NAPQI is detoxified by
- Conjugation with glutathione
48
More APAP is shunted to the cytochrome P450 system to produce
- NAPQI | - As a result, hepatocellular supplies of glutathione become depleted
49
APAP causes NAPQI to remain in its toxic form in the liver
- Reacts with cellular membrane molecules - Hepatocyte damage and death - Acute liver necrosis
50
APAP when following a therapeutic dose in normal patients
- Mostly converted to nontoxic metabolites by conjugation with sulfate and glucuronide (phase II metabolism) - Small portion oxidized via cytochrome P450 system
51
Acetaminophen toxicity
- More than 4 g per 24 hours
52
Signs and symptoms of acetaminophen toxicity occure in 3 phases
- Phase 1 (hours after overdose) - Phase 2 (24-72h) - Phase 3 (3-5 days)
53
- Phase 1 acetaminophen toxicity (hours after overdose)
- Nausea and vomiting - Pale appearance - Sweating
54
Phase 2 acetaminophen toxicity (24-72h)
- Jaundice, signs of liver damage (i.e. right upper quadrant pain followed by acute renal failure)
55
Phase 3 acetaminophen toxicity (3-5 days)
- Liver necrosis - Low blood sugar - Coagulation problems - Brain swelling - Multiple organ failure and death
56
Liver damage results from one of APAP metabolites
- N-acetyl-p-benzoquinone imine (NAPQI)
57
Acetaminophen overdose antidote/treatment
- N-acetylcysteine (NAC) | - IV form not the OTC oral product (that becomes GSH)
58
ASA vs. APAP structure
- ASA = salicylate | - APAP = para-amino phenol derivative
59
ASA vs. APAP indication
- ASA = analgesic, antipyretic, anti-inflammatory | - APAP = analgesic, antipyretic
60
ASA vs. APAP gastric side effects
- ASA = yes (inhibition of COX-1 in the gastric area) | - APAP = not major
61
ASA vs. APAP at low doses
- ASA = has anti-platelet activity (mediated by COX-1) | - APAP = no anti-platelet activity
62
ASA vs. APAP antidote
- ASA = no specific | - APAP = N-acetylcysteine (NAC)
63
DMARDs
- Disease-modifying antirheumatic drugs - Anti-inflammatory actions in several connective tissue diseases - Can slow, or even reverse joint damage
64
DMARDs activity/progression
- Slow acting because it may take 6 weeks to 6 months for their benefits to become apparent
65
Corticosteroids
- 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
Corticosteroid use
- Temporary control of severe exacerbations | - Long-term use in patients with severe disease not controlled by other agents
67
Glucocorticoid side effects
- 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
Glucocorticoid hyperglycemia/diabetes side effect mechanism
- Gluconeogenesis
69
Glucocorticoid central obesity, moon face, buffalo hump side effect mechanism
- Dramatic redistribution of body fat
70
Glucocorticoid muscle weakness and wasting side effect mechanism
- Breakdown of proteins | - Diversion of amino acids to glucose production
71
Glucocorticoid weight gain side effect mechanism
- Increased appetite (CNS effect) - Increased need for insulin over time (because of gluconeogenesis which results from weight gain) - Mineralocorticoid activity (Na+/water retention)
72
Glucocorticoid osteoporosis side effect mechanism
- Decreased reabsorption of calcium by the kidney
73
Glucocorticoid avascular necrosis of femur head side effect mechanism
- 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
Glucocorticoid skin bruising and poor wound healing side effect mechanism
- Anti-proliferative effect
75
Glucocorticoid hirsutism and acne side effect mechanism
- Due to ACTH-mediated increase of adrenal androgens
76
Glucocorticoid increased infections side effect mechanism
- Immunosuppression
77
Glucocorticoid hypomania, depression, psychosis side effect mechanism
- Normal cortisol levels maintains emotional balance
78
DMARDs names
- 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
Abatacept MOA
- Interfere with activity of T-lymphocytes
80
Abatacept toxicity when used for RA
- Infection | - Exacerbation of COPD
81
Anti-IL-1 drug names
- Anakinra - Rilonacept - Canakinumab
82
Anti-IL-1 drugs MOA
- Recombinant human IL-1 receptor antagonist | - Acts as a cysteine inhibitor
83
Anti-IL-1 drugs toxicity when taken for RA
- Infection | - Neutropenia
84
Anti-IL-6 drug names
- Tocilizumab
85
Tocilizumab MOA
- IL-6 antagonist
86
Tocilizumab (anti-IL-6 drug) toxicity when taken for RA
- Upper respiratory tract infections - Hypertension - Increase LFT
87
Anti-TNF-alpha drug names
- Infliximab - Etanercept - Adalimumab - Golimumab - Certolizumab
88
Anti-TNF-alpha drugs MOA
- Biological agent | - Inhibits action of TNF-alpha
89
Anti-TNF-alpha drugs toxicity when taken for RA
- Infection - Lymphoma - Hepatotoxicity - Hematological effects - Cardiovascular toxicity
90
Belimumab MOA
- Anti-B cell activating factor (MAb) | - Inhibits B lymphocyte stimulator (BLyS)
91
Belimumab toxicity when taken for RA
- Nausea, vomiting | - Respiratory tract infection
92
DMARD drugs that interfere with T-lymphocytes
- Cyclosporine - Hydrocychloroquine, chloroquine - Leflunomide - Sulfasalazine
93
Cyclosporine toxicity when taken for RA
- Nephrotoxicity - Hypertension - Liver toxicity
94
Hydroxychloroquine, chloroquine toxicity when taken for RA
- Diarrhea - Dermatitis - Hematological abnormalities
95
Leflunomide toxicity when taken for RA
- Rash - GI disturbance - Myopathy - Neuropathy - Ocular toxicity
96
Methotrexate MOA
- Cytotoxic drug that reduces the number of immune cells
97
Methotrexate toxicity when taken for RA
- Teratogenic - Hepatotoxicity - GI - Skin reaction
98
Penicillamine toxicity when taken for RA
- Nausea - Mucosal ulcers - Hematotoxicity - Hepatotoxicity - Teratogenicity
99
Rituximab MOA
- Interfere with the activity of B-lymphocytes
100
Rituximab toxicity when taken for RA
- Proteinurea - Dermatitis - GI - Hematological
101
Sulfasalazine toxicity when taken for RA
- Cardiac toxicity
102
Gol compounds MOA
- Interfere with the activity of macrophages
103
Tofacitinib MOA
- Janus kinase inhibitor
104
Tofaciitinic toxicity when taken for RA
- Infection - Neutropenia - Anemia - Increased LDL and HDL
105
Colchicine
- A selective inhibitor of microtubule assembly
106
Paclitaxel
- Stabilizes and protects microtubule against disassembly
107
Drugs used in gout
- Microtubule assembly inhibitors - Uricosurics - Xanthine oxidase inhibitors - Uricase
108
Microtubule assembly inhibitors
- Colchicine | - Taken orally
109
Colchicine side effects
- Diarrhea | - Liver and kidney damage with overdose
110
Uricosurics
- Probenecid - Lesinurad - Both taken orally
111
Uricosurics (probenecid, lesinurad) MOA
- Inhibition of renal reabsorption of uric acid
112
Xanthine oxidase inhibitors
- Allopurinol - Febuxostat - Both taken orally
113
Xanthine oxidase inhibitors (allopurinol, febuxostat) MOA
- Allopurinol = irreversible inhibior | - Febuxostat = reversible inhibitor
114
Xanthine oxidase inhibitors (allopurinol, febuxostat) side effects
- GI upset | - Bone marrow suppression
115
Uricases
- Pegloticase | - IV administration
116
Pegloticase MOA
- Recombinant mammalian uricase | - Converts uric acid to soluble form allantoin
117
Pegloticase side effects
- Rapid change in uric acid levels can precipitate gout

Pharmacology (27 decks)

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