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Pharm 2 > Bone and Joint 1 > Flashcards

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
Q

COX 2 specific NSAIDs

A

Celecoxib

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26
Q

NSAID SE

A

Edema
Rashes, itching
Tinnitus
GI bleed, peptic ulcerations
Renal failure
Prolonged bleeding times, decreased hemoglobin
Increased liver enzymes
SALICYLISM: Poisoning by NSAIDs and salicylates**

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27
Q

Which NSAID has less GI SE?

A

Celecoxib

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28
Q

Salicylism Sxs

A

headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation*, nausea, and vomiting

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29
Q

Severe salicylate intoxication Sxs

A

Hyperthermia is usually present
Dehydration often occurs

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30
Q

Who is at risk of salicylism and why?

A

Elderly individuals or those with underlying psychiatric disorders may consume an increasing amount over several days to alleviate arthralgias - perpetual spiral

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31
Q

Salicylism tx

A

Sodium bicarb used to alkalinize urine to increase elimination - to alkalinize the urine

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32
Q

What prevents further salicylate absorption?

A

Gastric lavage or induction of emesis will prevent further absorption if performed within 1-2 hours after ingestion
+/- activated charcoal

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33
Q

Common NSAID interactions?

A

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.

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34
Q

When are NSAIDs contraindicated?

A

NSAIDS are contraindicated during the third trimester

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35
Q

Aspirin MOA

A
  • 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
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36
Q

Aspirin does not inhibit the formation of?

A

Aspirin does not inhibit the formation of leukotrienes via the lipoxygenase pathway.

37
Q

What is the acetylation effect?

A

ASA covalently acetylates a serine at the active site of platelet cyclooxygenase, thereby reducing the formation of thromboxane A2, which promotes platelet aggregation

38
Q

How long does the acetylation effect last?

A

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
Q

How is absorption of enteric coated ASA?

A

enteric-coated preparations may be erratic and slow - AVOID in cases of MI
(Prefer chewable ASA)

40
Q

What type of kinetics does ASA undergo?

A

Biphasic

41
Q

ASA biphasic kinetics means what?

A

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
Q

How are salicylates excreted?

A

Salicylate is excreted in the urine

43
Q

What happens to ASA when pH of urine increases?

A
  • More is excreted
  • As the pH of the urine increases (alkalization) more is excreted.
44
Q

ASA use

A

Anti-inflammatory
Antipyretic
Analgesic
Cardiovascular disease

45
Q

ASA SE

A

Edema
Rashes, itching
Tinnitus
GI bleed, peptic ulcerations
Renal failure
Prolonged bleeding times, decreased hemoglobin
Increased liver enzymes
Reye’s syndrome

46
Q

Who is at risk of ASA allergy?

A

Pts with nasal polyps, and asthma may have an increased risk of salicylate sensitivity

47
Q

When should ASA NOT be given?

A

FDA recommends aspirin or aspirin-containing products NOT be given to any child <12 yo who has a fever.

48
Q

ASA dosage limit

A

Adults should not take 325-mg doses of aspirin for any longer than 10 days unless directed otherwise

49
Q

Ibuprofen MOA

A

Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes

50
Q

Ibuprofen uses

A

Mild to moderate pain
Musculoskeletal aches and pains (joint pain, back pain) because of its anti-inflammatory properties
Antipyretic
Rheumatoid arthritis
Osteoarthritis
Dysmenorrhea

51
Q

Ibuprofen SE

A

Edema
Rashes, itching
Tinnitus
GI bleed, peptic ulcerations
Renal failure
Prolonged bleeding times, decreased hemoglobin
Increased liver enzyme

52
Q

Ibuprofen interaction

A

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
Q

What is in chewable tablets of ibuprofen?

A

Chewable tablets of ibuprofen contain aspartame, which is contraindicated in those sensitive to it.

54
Q

Downfall of ibuprofen?

A

Short duration of action

55
Q

Meloxicam MOA

A

Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes

56
Q

Meloxicam use

A

Rheumatoid arthritis, including juvenile rheumatoid arthritis.
Osteoarthritis.
Anti-inflammatory.
Analgesic.
Antipyretic activity.

57
Q

Meloxicam SE

A

Edema
Rashes, itching, stevens-Johnson syndrome*
Tinnitus
GI bleed, peptic ulcerations
Renal failure
Prolonged bleeding times, decreased hemoglobin, thrombocytopenia
Increased liver enzymes

58
Q

Meloxicam Interactions

A

May reduce antihypertensive effects of ACE inhibitors.
May reduce diuretic effects of furosemide and thiazide diuretics

59
Q

Which NSAID has the LEAST GI toxicity?

A

Meloxicam

60
Q

Acetaminophen (Tylenol) is the preferred drug for what?

A

Acetaminophen is the preferred drug for mild to moderate pain if there is no accompanying inflammation.

61
Q

Acetaminophen dosage max

A
  • 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
Q

Acetaminophen DOES NOT do what?

A

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
Q

Acetaminophen MOA

A

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
Q

Acetaminophen use

A

Relief of mild to moderate pain.
Reduce fever.

65
Q

Acetaminophen SE

A

Increased liver enzymes, hepatic failure, hepatotoxicity (overdose)

66
Q

Chronic high doses of acetaminophen can cause what?

A
  • Chronic high doses increase the risk of bleeding.
  • Hepatotoxicity is additive with other drugs, especially alcohol
67
Q

Acetaminophen contraindication

A

hepatic disease

68
Q

Tylenol toxicity

A

dose-dependent, potentially fatal hepatic necrosis that runs a course of 7 to 8 days

69
Q

Acetaminophen poisoning tx

A

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
Q

In Acetaminophen poisoning, what is used as a protection against hepatic damage?

A

N-acetylcysteine (Mucomyst) is effective if given less than 24 hours after ingestion of acetaminophen; even more effective when administered within 10 hours.

71
Q

Acetaminophen Poisoning/Tylenol Toxicity progression

A
  • 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
Q

What is the Rumack-Matthew nomogram?

A

Graph that helps determine the need to tx tylenol toxicity based on concentration of ingestion and the time since ingestion

73
Q

Misoprostol MOA

A

Synthetic prostaglandin (E1) analogue with anti-secretory and mucosal protective properties

74
Q

Misoprostol use

A

Patients with OA at high risk of developing gastric and duodenal ulcers

75
Q

Misoprostol SE

A

Miscarriage

76
Q

Misoprostol contraindication

A

Pregnancy: Increases uterine contractility.

77
Q

Misoprostol Interactions

A
  • Potential increased toxicity of methotrexate, digoxin, cyclosporine, lithium
  • May increase K+ when used with K+-sparing diuretics.
78
Q

Celecoxib MOA

A

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme COX-2

79
Q

What is the advantage of Celecoxib over other NSAIDs?

A

Celebrex does not exhibit any antiplatelet activity, which is an advantage over other NSAIDs.

80
Q

Celecoxib use

A

Rheumatoid arthritis
Osteoarthritis
Dysmenorrhea

81
Q

Celecoxib SE

A

Lower extremity edema and HTN, increased risk of MI and stroke
GI bleeding
Renal toxicity is worse than with other NSAIDs

82
Q

Celecoxib black box warning

A

May increase risk of serious cardiovascular thrombotic events, MI, and stroke

83
Q

Celecoxib contraindications

A

CV, renal, or hepatic disease
Avoid use in third trimester
Use in the setting of CABG surgery

84
Q

What causes joint changes in RA?

A
  • Increase presence of inflammatory cytokines
  • Proliferation of the synovium
  • Erosion of cartilage and bone
85
Q

Which drugs HALT the loss of bone in RA?

A

Disease-Modifying Anti-rheumatic Drugs (DMARDs)

86
Q

Mild cases RA tx

A

NSAIDs, glucocorticoid joint injections, or low doses of prednisone may be indicated

87
Q

How long do DMARDs take to work?

A

Wks to months

88
Q

High level of RA tx

A

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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