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Bone and Joint 1 Flashcards

1
Q

Most common joint disorder in the US?

A

Osteoarthritis

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2
Q

Non-pharmacological tx for osteoarthritis

A

weight loss, range of motion exercises, strength training, prosthetics

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3
Q

Pharmacological tx for osteoarthritis

A

guided by the degree of joint dysfunction and pain; incudes acetaminophen to NSAIDs

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4
Q

Inflammation occurs causing release of chemical mediators (histamine, cytokines, leukotrienes, and prostaglandins), however, these can only be produced in the presence of?

A

cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and lipoxygenase

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5
Q

COX-1

A

expressed systematically and continuously - role in regulation of platelets, endothelium, and cells of the GI tract and kidney

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6
Q

COX-2

A

inducible enzyme that is synthesized in response to pain and inflammation

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7
Q

Drugs to tx osteoarthritis

A

NSAIDs
Acetylsalicylic acid (Aspirin)
Ibuprofen (Advil, Motrin, Nuprin)
Meloxicam (Mobic)
Acetaminophen (Tylenol)
Misoprostol (Arthrotec, Cytotec)
Cyclooxygenase-2 (COX-2) Inhibitors

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8
Q

Why are NSAIDs more effective than acetaminophen?

A

provide both analgesic and anti-inflammatory actions.

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9
Q

What affects the choice of NSAIDs?

A

determined through trial and error and is affected by factors such as adverse effects, cost, duration of action, and patient preferences

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10
Q

What age-related diseases raise the chance of adverse rxn with the ingestion of NSAIDs?

A

renal and hepatic dysfunction

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11
Q

NSAIDs causing GI upset should be prescribed with what?

A

H2 blockers

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12
Q

What can NSAIDs damage?

A

Renal

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13
Q

Why should NSAIDs be avoided in late pregnancy?

A

Should not be used during late pregnancy because they may cause closure of ductus arteriosus.

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14
Q

Why should NSAIDs be stopped before surgery?

A

Prolong bleeding times

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15
Q

When should NSAIDs be d/c before surgery?

A

1 wk prior

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16
Q

What is the problem with NSAID dosing increase?

A

Taking higher-than-recommended doses does not increase the effectiveness of the NSAID

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17
Q

How should NSAIDs be taken to increase their effect?

A

take NSAIDs 30 minutes before food or 2 hours after meals

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18
Q

What should be watched out for in a pt taking NSAIDs?

A

Watch for signs of hepatic failure (fatigue, lethargy, pruritus, jaundice, upper right-quadrant tenderness, persistent headache, visual disturbances, weight gain, and flu-like symptoms) or GI ulceration (black tarry stool, skin rash, edema, or weight gain)

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19
Q

NSAID + EtOH can increase the chance of what?

A

GI bleed

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20
Q

Common NSAIDs

A

Ibuprofen
Naproxen
Diclofenac - PO and gel
Indomethacin
Sulindac
Meloxicam
Ketorolac
Etodolac
Celecoxib

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21
Q

What kind of NSAID is celecoxib?

A

COX 2 inhibitor

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22
Q

How are NSAIDs used?

A

Antipyretic, analgesic, anti-inflammatory

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23
Q

NSAID MOA

A

COX 1 leads to the production of prostaglandins E and I
(E – works to decrease gastric secretion, I – works to increase the protective mucosa of the epithelial cells)
NSAIDs inhibit COX 1 therefore less inhibition of gastric secretions – increased chance of gastric ulcers
Block prostaglandin cascade - gives NSAIDs all its effects

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24
Q

COX 1 specific NSAIDs

A

ASA
Indomethacin
Piroxicam

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25
COX 2 specific NSAIDs
Celecoxib
26
NSAID SE
Edema Rashes, itching Tinnitus GI bleed, peptic ulcerations Renal failure Prolonged bleeding times, decreased hemoglobin Increased liver enzymes SALICYLISM: Poisoning by NSAIDs and salicylates**
27
Which NSAID has less GI SE?
Celecoxib
28
Salicylism Sxs
headache, dizziness, tinnitus*, hearing loss*, mental disturbances, sweating, thirst, hyperventilation*, nausea, and vomiting
29
Severe salicylate intoxication Sxs
Hyperthermia is usually present Dehydration often occurs
30
Who is at risk of salicylism and why?
Elderly individuals or those with underlying psychiatric disorders may consume an increasing amount over several days to alleviate arthralgias - perpetual spiral
31
Salicylism tx
Sodium bicarb used to alkalinize urine to increase elimination - to alkalinize the urine
32
What prevents further salicylate absorption?
Gastric lavage or induction of emesis will prevent further absorption if performed within 1-2 hours after ingestion +/- activated charcoal
33
Common NSAID interactions?
May increase hypoglycemic effects of insulin and oral hypoglycemics. May see increased risk of bleeding with warfarin, and drugs affecting platelet function. Note: All NSAIDs have drug interactions with anticoagulants, beta adrenergic blockers, phenytoin, lithium, and loop diuretics.
34
When are NSAIDs contraindicated?
NSAIDS are contraindicated during the third trimester
35
Aspirin MOA
- Analgesic action - low to moderate pain - Antipyretic action - lowers elevated body temperature by resetting the hypothalamus "set point" - Anti-inflammatory effects - Inhibition of prostaglandin and thromboxane synthesis is the mechanism of anti-inflammatory action - Antiplatelet effect - reduces the incidence of stroke and myocardial infarction in patients at risk by altering platelet aggregation - Acetylation effect - reducing the formation of thromboxane A2, which promotes platelet aggregation
36
Aspirin does not inhibit the formation of?
Aspirin does not inhibit the formation of leukotrienes via the lipoxygenase pathway.
37
What is the acetylation effect?
ASA covalently acetylates a serine at the active site of platelet cyclooxygenase, thereby reducing the formation of thromboxane A2, which promotes platelet aggregation
38
How long does the acetylation effect last?
acetylation of the enzyme is irreversible, the inhibitory effect of aspirin on platelet aggregation lasts for up to 8 days, until new platelets are formed
39
How is absorption of enteric coated ASA?
enteric-coated preparations may be erratic and slow - AVOID in cases of MI (Prefer chewable ASA)
40
What type of kinetics does ASA undergo?
Biphasic
41
ASA biphasic kinetics means what?
At high and toxic doses, metabolism is limited and occurs according to zero-order kinetics (once blood is saturated, then there is a large concentration increase with small dosing) At lower doses, metabolism proceeds according to first-order kinetics (linear increases slowly)
42
How are salicylates excreted?
Salicylate is excreted in the urine
43
What happens to ASA when pH of urine increases?
- More is excreted - As the pH of the urine increases (alkalization) more is excreted.
44
ASA use
Anti-inflammatory Antipyretic Analgesic Cardiovascular disease
45
ASA SE
Edema Rashes, itching Tinnitus GI bleed, peptic ulcerations Renal failure Prolonged bleeding times, decreased hemoglobin Increased liver enzymes Reye’s syndrome
46
Who is at risk of ASA allergy?
Pts with nasal polyps, and asthma may have an increased risk of salicylate sensitivity
47
When should ASA NOT be given?
FDA recommends aspirin or aspirin-containing products NOT be given to any child <12 yo who has a fever.
48
ASA dosage limit
Adults should not take 325-mg doses of aspirin for any longer than 10 days unless directed otherwise
49
Ibuprofen MOA
Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes
50
Ibuprofen uses
Mild to moderate pain Musculoskeletal aches and pains (joint pain, back pain) because of its anti-inflammatory properties Antipyretic Rheumatoid arthritis Osteoarthritis Dysmenorrhea
51
Ibuprofen SE
Edema Rashes, itching Tinnitus GI bleed, peptic ulcerations Renal failure Prolonged bleeding times, decreased hemoglobin Increased liver enzyme
52
Ibuprofen interaction
May increase hypoglycemic effects of insulin and oral hypoglycemics. May see increased risk of bleeding with warfarin (or chamomile, garlic, ginger, and ginko), and drugs affecting platelet function.
53
What is in chewable tablets of ibuprofen?
Chewable tablets of ibuprofen contain aspartame, which is contraindicated in those sensitive to it.
54
Downfall of ibuprofen?
Short duration of action
55
Meloxicam MOA
Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes
56
Meloxicam use
Rheumatoid arthritis, including juvenile rheumatoid arthritis. Osteoarthritis. Anti-inflammatory. Analgesic. Antipyretic activity.
57
Meloxicam SE
Edema Rashes, itching, stevens-Johnson syndrome* Tinnitus GI bleed, peptic ulcerations Renal failure Prolonged bleeding times, decreased hemoglobin, thrombocytopenia Increased liver enzymes
58
Meloxicam Interactions
May reduce antihypertensive effects of ACE inhibitors. May reduce diuretic effects of furosemide and thiazide diuretics
59
Which NSAID has the LEAST GI toxicity?
Meloxicam
60
Acetaminophen (Tylenol) is the preferred drug for what?
Acetaminophen is the preferred drug for mild to moderate pain if there is no accompanying inflammation.
61
Acetaminophen dosage max
- Acetaminophen, in doses up to 1 gm, four times a day, may be prescribed for mild to moderate pain - Excessive use is more than 4 gm a day; can lead to hepatotoxicity
62
Acetaminophen DOES NOT do what?
Because it has no action on COX-1 and COX-2, acetaminophen has no anti-inflammatory action and does not cause GI adverse events
63
Acetaminophen MOA
Inhibits a previously unknown COX-3 substance in the brain and spinal cord, which explains its ability to reduce fever and pain without causing the unwanted GI side effects
64
Acetaminophen use
Relief of mild to moderate pain. Reduce fever.
65
Acetaminophen SE
Increased liver enzymes, hepatic failure, hepatotoxicity (overdose)
66
Chronic high doses of acetaminophen can cause what?
- Chronic high doses increase the risk of bleeding. - Hepatotoxicity is additive with other drugs, especially alcohol
67
Acetaminophen contraindication
hepatic disease
68
Tylenol toxicity
dose-dependent, potentially fatal hepatic necrosis that runs a course of 7 to 8 days
69
Acetaminophen poisoning tx
Treatment must begin immediately; includes removal of the remaining drug from the stomach, supportive therapy, and initiation of therapy to protect against hepatic damage
70
In Acetaminophen poisoning, what is used as a protection against hepatic damage?
N-acetylcysteine (Mucomyst) is effective if given less than 24 hours after ingestion of acetaminophen; even more effective when administered within 10 hours.
71
Acetaminophen Poisoning/Tylenol Toxicity progression
- Day 1: nausea, vomiting, diaphoresis, vomiting - Day 1–2: liver enzymes, alanine aminotransferase (ALT), bilirubin, and prothrombin rise (GI sxs may temporarily subside) - Day 3–4: peak hepatotoxicity (major hepatic injury occurs) - Day 7–8: death or recovery
72
What is the Rumack-Matthew nomogram?
Graph that helps determine the need to tx tylenol toxicity based on concentration of ingestion and the time since ingestion
73
Misoprostol MOA
Synthetic prostaglandin (E1) analogue with anti-secretory and mucosal protective properties
74
Misoprostol use
Patients with OA at high risk of developing gastric and duodenal ulcers
75
Misoprostol SE
Miscarriage
76
Misoprostol contraindication
Pregnancy: Increases uterine contractility.
77
Misoprostol Interactions
- Potential increased toxicity of methotrexate, digoxin, cyclosporine, lithium - May increase K+ when used with K+-sparing diuretics.
78
Celecoxib MOA
Inhibits prostaglandin synthesis by decreasing the activity of the enzyme COX-2
79
What is the advantage of Celecoxib over other NSAIDs?
Celebrex does not exhibit any antiplatelet activity, which is an advantage over other NSAIDs.
80
Celecoxib use
Rheumatoid arthritis Osteoarthritis Dysmenorrhea
81
Celecoxib SE
Lower extremity edema and HTN, increased risk of MI and stroke GI bleeding Renal toxicity is worse than with other NSAIDs
82
Celecoxib black box warning
May increase risk of serious cardiovascular thrombotic events, MI, and stroke
83
Celecoxib contraindications
CV, renal, or hepatic disease Avoid use in third trimester Use in the setting of CABG surgery
84
What causes joint changes in RA?
- Increase presence of inflammatory cytokines - Proliferation of the synovium - Erosion of cartilage and bone
85
Which drugs HALT the loss of bone in RA?
Disease-Modifying Anti-rheumatic Drugs (DMARDs)
86
Mild cases RA tx
NSAIDs, glucocorticoid joint injections, or low doses of prednisone may be indicated
87
How long do DMARDs take to work?
Wks to months
88
High level of RA tx
Those with a high level of disease or poor prognosis may be given DMARDs as first-line treatment

Pharm 2 (8 decks)

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