Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

c. pharm exam 3 (w13) > anti-inflammatories 3/ 18 > Flashcards

anti-inflammatories 3/ 18 Flashcards

1
Q

OBJECTIVES:
The participant will be able to understand:
– Mediators of inflammation
– The MOA of NSAIDs
– Their pharmacokinetic and dynamic properties

A

– The adverse reactions
– Clinical uses of the class
– Anesthetic implications
– Specific properties of selected agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 5 mediators of the inflammatory response?

A
  1. Eicosanoids (which has 4 products)
  2. bradykinin
  3. serotonin
  4. histhamine
  5. nitric acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the 4 products of eicosanoid synthesis?

A

–Prostaglandins
– Prostacyclin
– Leukotrienes
– Thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. what are ecosinoids (what chemical) and what are they made from?
  2. what are the main subgroups (again)?
  3. what stimulate the synthesis of eicosanoids?
A

1• Eicosanoids are an important group of endogenous fatty acid derivatives produced from arachidonic acid (from cell membranes)
2• Main subgroups are the prostaglandins, prostacyclin, thromboxane and leukotrienes
3• Active eicosanoids are synthesized in response to various stimuli such as tissue injury and immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The Inflammatory Process:

  1. how is aracadonic acid released?
  2. what is arachaonic acid turned into? by what process?
  3. what is arachidonate metabolized into (2 paths):
    a) what enzyme is active in the liner path, what is thenproduct?
    b) what enzymes is active in the cyclic pathway and what are the products?
A

1• The inflammatory stimuli activates phospholipases in the cell membrane or cytoplasm and arachidonic acid is released
2• Arachidonic Acid is esterized to Arachidonate
3• Arachidonate is then metabolized by either:
a)lipoxygenase (linear path to produce Leukotrienes or lipoxins) or…
b) cyclooxygenase (cyclic path to produce prostacyclin, prostaglandins, or thromboxane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Corticosteroids (glucocorticoids):

  1. how does phospholipase A2 contribute to inflammation?
  2. what do corticosteroids do to phospholipase A2?
A

1• Phospholipase A2 hydrolyzes the ester linkage between a fatty acid and the hydroxyl at carbon 2 of the glycerol backbone of arachadonic acid, releasing the fatty acid (i.e., arachidonate) and a lysophospholipid as products.
2• Corticosteroids are anti-inflammatory because they inhibit Phospholipase A2, reducing arachidonate release. (some COX2 inhibition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
Eicosanoid Synthesis (once again)
1. what are the 2 pathways?
A
  1. cyclic or linear pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

eicosinoid synthesis:

  1. a.what pathway makes 3 products?
  2. what is the group name and what are the 3 enzymes that make them?
A

1• Cyclic Pathway–

2• Cyclic endoperoxides (PGH2, PGI2, TXA2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

eicosinoid synthesis:

  1. what pathway makes 1 product?
  2. what is the group name, and what is the enzyme that makes it?
A

1• Linear Pathway–

2• Hydroperoxides (5-Lipoxygenase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cyclic Pathway

  1. step 1 (_____converts_____ to _______)?
  2. step 2 (_______ are converted to _____,_____ & ______)?
A

1• Cyclooxygenase converts arachidonate to cyclic endoperoxides
2• Cyclic endoperoxides are converted to prostaglandins, prostacyclins, thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Inflammatory Process:

  1. what does COX stand for?
  2. how many forms of ‘cox’ are there?
  3. where are they found and what do they do?
A
  1. cyclooxygenast
    2• Cyclooxygenase exists in at least 2 forms(COX-1 and COX-2) {there is likely more than 2}
    3 cox 1 and 2:
    • COX-1 is found in many tissues and the prostaglandins formed by it are important for a variety of normal physiologic processes
    • COX-2 is mainly in inflammatory cells and the products of it play a major role in tissue injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Prostaglandins:

  1. what enzyme is imperitive in prostaglandin synthesis? what does it do?
  2. what do different cells do to PGH2?
  3. what do cells do once prostaglandins and other compounds are synthesized?
  4. how do most prostaglandins work? what receptors do they work at?
  5. what might the prostaglandins activate at the cell
A

1• Prostaglandin H2 Synthase (PGH2 Synthase) catalyzes the committed step in the “cyclic pathway” that leads to production of prostaglandins, prostacyclins, and thromboxanes
2• Different cell types convert PGH2 to different compounds
3• Prostaglandins and related compounds are transported out of the cells that synthesize them
4• Most affect other cells by interacting with plasma membrane G-protein coupled receptors
5• Depending on the cell type:
a)the activated G protein may stimulate or inhibit formation of cAMP
b)or may activate a phosphatidylinositol signal pathway leading to intracellular Ca++ release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

prostaglandins: thromboxane:
1. where is thromboxane synthesized?
2. what enzyme converts ____ to thromboxane?
3. what is a prostaglandin synthesized by endothelial cells? what does it do?

A

1• Thromboxane is synthesized in platelets
2• TXA2 synthase converts cyclic endoperoxides to thromboxane
3• Prostacyclin is a prostaglandin synthesized in endothelial cells of vessels which acts to vasodilate and inhibit platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Linear Pathway

  1. what enzyme catalyzes the first step in leukotriene synthesis?
  2. what do lipoxygenase enzymes act on? what do most of the products do?
  3. what enzyme found in leukocytes catalyzes the conversion of what___ to what___?
  4. what is 5HPETE converted to___and what do these products do?
  5. what enzyme may have a role in cancer? what might it do?
A

1• The first step for synthesis of leukotrienes is catalyzed by Lipoxygenase.
2. Various lipoxygenase enzymes catalyze oxygenation of various polyunsaturated fatty acids at different sites. Many of the products have signal roles.
3• 5-Lipoxygenase, found in leukocytes, catalyzes conversion of arachidonate to 5 HPETE (5-hydroperoxyeicosatetraenoic acid).
4• 5-HPETE is then converted to various leukotrienes and lipoxins that induce inflammation and asthmatic constriction of the bronchioles.
5• Lipoxygenase is in abundance in cancer cells and thought to have a role in producing vascular genesis needed for tumor growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. linear pathway makes what ?

2. cyclic pathway makes what?

A
  1. leukotrienes

2. prostaglandins, prostacyclins, thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects of eicosanoids:

  1. where do eicosinoids occur?
  2. what are they most envolved in?
  3. what does the ‘SRS-A” stand for in the class that leukotrienes belong to?
  4. what are other jobs (important jobs) of other eicosanoids?
A
  1. Occur in platelets, smooth muscle, CNS and other tissue
  2. Those most involved with pathologic effects are PGF2a, thromboxane A2, (TXA2) and the leukotrienes (LTC4 and LTD4)
  3. Leukotrienes comprise the “slow reacting substance of anaphylaxis” (SRS-A)
  4. Various eicosanoids have effects in protection of gastric mucosa, endogenous vasodilation, smooth muscle relaxation, labor, maintaining patency of the ductus arteriosus during development and platelet clotting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nitric Oxide:

what 2 elements is it formed from?

A

Nitric Oxide
• Formed by nitrogen and oxygen at high temps (formed in lightning
Non biological implications (can be converted in the air to nitric acid which is implicated in acid rain,)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is NO formed in the body?

A

NO synthase from vascular cells, activated by Ca++ to cause NO to accumulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  1. how is NO utilized in the nerves?
  2. how is NO used in inflammation?
  3. how does endothelium use NO?
  4. how is it used to fight bacteria? what does it do in cases of sepsis?
    5.
A

1• Acts as a messenger by its effects on cGMP synthesis
Serves as a neurotransmitter (due to it’s small molecular size it diffuses and therefore not limited to single synapse)
2• Most inflammatory cells express NO synthase when activated by cytokines
3• The endothelium of vessels uses NO to signal smooth muscle relaxation. Result is vasodilation, increased vascular permeability and PG release
4• Macrophages produce NO in combating bacteria
In severe infection causing sepsis over production of NO causes vasodilation
5• Also involved in signaling inhibition of platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NO: how is it used as a medicine/drug?

A

Some drugs used for vascular effects (NTG, amyl nitrate, sildenafil (viagra) are converted to NO or prolong NO to exert their actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are chemical properties of NO?

A

• Because it’s a gas it diffuses easily. It has a very short chemical half life (1-5 seconds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

nsaids:

  1. how often prescribed?
  2. what are they used for?
  3. are all NSAIDS really nsaids?
  4. why are they used?
A
  1. most prescribed drug
    2 • Used for anti-inflammatory and analgesic properties and to supplement anesthesia
    3• Term is used to describe drugs from several different structural classifications (tylenol is actually not an NSAID).
    4• Often used for their ability to avoid opiate side effects however, they also have effects to be aware of
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how NSAIDS WORK:

  1. how many forms of cox? (what does cox stand for)?
  2. what are they ?
A

1• Cyclooxygenase has at least 2 isoforms

2• COX-1 is mainly in non-inflammatory areas whereas COX-2 is activated (cox 2 is the bad one).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how NSAIDS WORK:

-what is the mech of action?

A

• Primary MOA is to inhibit COX activity and thereby decreasing prostaglandin synthesis which decreases inflammatory response and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how NSAIDS WORK:

  1. what drugs inhibit all COX?
  2. why are cox selective drugs good?
A

1• Aspirin and older nonselective drugs inhibit all COX activity so prostaglandins needed for normal function are depleted
2• COX-2 selective NSAIDs should have less effect on prostaglandins involved in normal function than nonselective agents

27
Q

what are effects of NSAIDS?

the 5 things Nsaids do in the body:

A

1• Suppress Prostaglandin synthesis in CNS stimulated by pyrogens (antipyretic)
2• Decrease activation of pain receptors by prostaglandins
3• COX inhibitors reduce inflammation but have no effect on tissue damage or immunologic reaction
4• Inhibition of platelet aggregation
5• Reduce prostaglandin mediated cell protection in GI tract and autoregulation of renal function

28
Q

clinical uses of nsaids:

A 
1• Analgesia
2• Anti-inflammation
– injury,
– Bowel disease
3• Antipyretic
4• Antigout
5• Antirheumatic (slow acting or disease modifying)
29
Q

what are the Propionic acid derivative nsaids?

A

Ibuprofen, Naproxen, ketoprofen

30
Q

what isthe Indole derivative NSAID?

A

• Indole derivative= (Indomethicin)

31
Q

what is the Pyrollopyrol derived nsaid called?

A

•Pyrollopyrol= (Ketorolac)

32
Q

what is the Acetylated nsaid called?

A

• Acetylated =(aspirin)

33
Q

what is the Nonacetylated NSAID?

A

• sodium salicylate

sodium salicylate is major metabolite of aspirin usually given as aspirin

34
Q

what is the”nsaid” that really isnt?

A

• Acetaminophen

35
Q

what is the GI nsaid (aka Sulfasalazine)?

A

• Asacol

36
Q

nsaid…?

A

• Carboxylic acids

37
Q
  • Pharmacokinetics:
    1. what type chemical are all NSAIDS? Except for what drug (which is a ____)?
    2. how do they help with arthritis?
A

1• All NSAIDs are weak organic acids (except for Nabumetone {Relafen- antiarthritic}, which is a ketone prodrug metabolized to the active form)
2• All NSAIDs are found in synovial fluid after repeat dosing

38
Q

Nsaid pharmacokinetics:

  1. metablized where?
  2. elimination
A

1• Highly metabolized in the liver (CP450 families)
2• Percent excreted unchanged in kidney varies–Renal excretion is most important route but some biliary elimination occurs

39
Q

Pharmacokinetics:

  1. what type of metabloism?
  2. protein binding?
  3. volume of distribution?
  4. duration…
A

1• Low first pass extraction
2• Highly protein bound to plasma albumin
3• Small vD
4• Variances between drugs in terms of durations, pKa and effects

41
Q

adverse effects of NSAIDS:

  1. Most frequent type of adverse effect?
  2. what causes it?
  3. what are effects?
A

1-GI
2• Caused by their interference with role of prostaglandins in normal GI physiology
3• Effects range from dyspepsia to gastric erosion, ulceration and perforation

42
Q

Adverse Effects: Renal:

  1. affects in normal kidney?
  2. what is prostaglandins in the kidney?
A

1• Usually no effects in normal healthy kidney

2• Prostaglandins influence renal blood flow, glomerular filtration and tubular transport

43
Q

what does chronic inhibition of prostaglandin do to kidney?

A

-• In higher doses or chronic use inhibition of prostaglandin synthesis can cause renal medullary ischemia

44
Q

what NSAID is safest for kidney patients?

A

-• Aspirin is thought to be safest of NSAIDs for renal patients

45
Q

what pre-existing conditions magnify toxic effects of nsaids?

A

• NSAID renal toxic effects are magnified by preexisting disease, CHF, hypovolemia, concurrent use of other renal toxic drugs, contrast dye and liver disease

46
Q

Adverse Effects: Coagulation

  1. Inhibition of COX activity results in?
  2. Extent and duration of coagulation effects:
  3. is NSAID inhibition reversible?
A
  • inhibition of platelet aggregation
  • varies by drug
  • NSAID inhibition is reversible but lasts longer than drugs T1/2 (except for ASA)
47
Q

Adverse Effects: Coagulation

  1. aspirin 75mg causes what to platelets?
  2. how long does it last?
A
  • Aspirin (75 mg/day) causes irreversible inactivation of platelet COX
  • Effects last life of the platelet (7-10 days)
48
Q

Adverse Effects: Coagulation

  1. What are some surgical implications of antiplatelet functions?
  2. what is the DX test for COX effect on bleeding?
A

1• can cause postop bleeding
-deliberate use for microvascular surgery?
2• Diagnostic test is bleeding time, not platelet count (platelet count doesnt change, they just become inactivated).

49
Q

Adverse Effects: Cardiovascular

• COX2 inhibitors have been associated with…?

A

• an increased risk of stroke and MI

50
Q

Adverse Effects: Cardiovascular

• A study looking at Rofecoxib efficacy in colon polyps incidentally found what?

A

• a doubled increase in rate of cardiovascular disease as compared to placebo

51
Q

Adverse Effects: Cardiovascular
1• COX2 inhibitors have been associated with…?
2• what is the mechanism?

A

1• an increased risk of stroke and MI
2• Mechanism is unclear. Studies suggest COX2 plays a role in protective affect of estrogen in preventing plaque and sclerosis. (Estrogen binds to a receptor which activates COX2 which then increase prostacyclin PGI-2)

52
Q

what should you always check for before giving an NSAID?

A

Always check the patient for factors that increase risk of renal toxicity before giving an NSAID!

53
Q

Adverse Effects: Drug interactions (ADRs):

  1. concurrent use of what drugs causes increased risk of bleeding (especially where)?
  2. use with what drugs can increase what electrolyte levels?
  3. decreases effects of what medications?
  4. if it has effects on this organ, can cause what to other drugs?
  5. what 2 conditions can increase drug reactions?
A

Adverse Effects: Drug interactions (ADRs)
1• Concomitant use with anticoagulants results in increase risk of bleeding (especially GI)
2• Use with K+ sparing diuretics can cause hyperkalemia
3• Can decrease effects of antihypertensives
4• If NSAID renal effects are present, can decrease clearance of other drugs
5• ADRs magnified in elderly and those with organ failure

54
Q

Perioperative Use of NSAIDs:

  1. what can nsaids be used for in pre-op?
  2. what should be checked before using intra-op?
  3. what are post op benefits? what is one issue with “effect” (unlike opiates)?
A 
Perioperative Use of NSAIDs
1• Preemptive analgesia in preop
2• Intraop use
– Check with surgeon
– Check renal and hydration status
3• Postoperative analgesia
– ? Benefit of reduced opiate induced N&V 
– Ceiling "effect" (unlike opiates)
55
Q

NSAIDs
Aspirin (Bayer brand name)
1. what is the chemical name?
2. how is it made (think of the name)?
3. salicylic acid comes from where?
4. where else is salicylic acid used?
5. asa is broken down to what? where?
6. what type of COX is asa/ salicylic acid?
7. how about renal cox effect?
8. does it affect leukotriene pathway?
9. where is it mostly absorbed? also where?
10. what causes decreased absorption?
11. what preparations is it also given as (ex. bufferin)?
12. where is it metabolized (what method) and into what?
13. where is salicylic acid excreted? how much in acidic and how much in alkaline? what if the urine is alkilinized; what should you do with dose?
14. by what method is salicylic acid broken down in the liver? is that the end of it?
15. what is the t-1/2 of asa ; salicylic acid T-1/2?

A

NSAIDs
Aspirin (Bayer brand name)
1• The magic drug- acetylsalicylic acid
2• Derived from acetylation of salicylic acid
3• Salicylic acid is prepared commercially but also found naturally in willow bark where it’s use goes back to Hippocrates and ancient Egypt
4• Salicylic acid is also used in skin creams and topical analgesics
5• Aspirin is hydrolyzed to salicylate in GI
6• Nonselective COX inhibition
7• Weak inhibition of renal COX hence it’s safety profile in these patients
8• No effect on Leukotriene pathway
9• Rapidly absorbed mainly in small intestine but also stomach
10• Absorption is decreased by presence of food as well as increased gastric pH (increased ionization)
11• Given as buffered and effervescent preparations
12• Rapidly hydrolyzed by the liver to salicylic acid (reversible inhibitor)
13• Salicylic acid is excreted in urine, ranging from 5% in acidic urine and 85% in alkaline urine (alkilinization of urine may mean increased dose requirement)
14• Salicylic acid is conjugated in the liver and also has active effects
15• T1/2 aspirin is 15-20 minutes, T1/2 of salicylic acid is 2-3 hours

56
Q

Aspirin Uses

A

Aspirin Uses
• Pain (headache, musculoskeletal, arthritis)
• Antipyretic (inhibition of prostaglandin release in CNS, mainly hypothalamus)
• Antiplatelet for at risk cardiac patients
– Dose range below analgesic dose
• Angina and acute MI
– effects attributable to antiplatelet properties
–– Sometimes combined with heparin therapy

57
Q

Aspirin: Toxicity

  1. gastric effects?
  2. renal effects? but not which one?
  3. liver effects? lesser or greater than other NSAIDs?
  4. bleeding effects?
  5. what does inhibition of prostaglandin cause in asthma patients? why? what do nasal polyps have to do with it? is it just asa?
  6. allergies: how rare? how serious?
  7. what are symptoms?
  8. which one more likely asa or salicylic?
  9. are there cross-sensitivities?
  10. what are ear effects?
  11. ph changes lead to? which in turn causes?
  12. what serious side effects?
  13. condition in children (? caused by virus) called what? leads to what liver and brain issues?
A

Aspirin: Toxicity
• Gastric upset-GI bleed
• Chronic use can lead to acute renal failure and interstitial nephritis (not likely ESRD)
• Possible hepatic damage in OD (< other NSAID)
• Increased bleeding time
• Inhibition of prostaglandin in hypersensitive patients can cause asthma symptoms
– Result of increased Leukotriene synthesis?
– History/presence of nasal polyps=at risk patient – 8-20% of all asthma patients?
– Other NSAIDs also implicated in these patients
• Allergic reactions are rare but serious
• Usual symptoms
• More likely in aspirin than salicylic acid
• Cross sensitivity to other NSAIDs exist
• Tinnitus, vertigo
• Hyperventilation (from Metabolic acidosis) leading to alkalosis,
—Dehydration, hyperthermia, coma, death
• Correlation with Reyes syndrome in children with viral infections
– hepatic fatty degeneration and encephalopathy

58
Q 
Aspirin: Doses
how many theraputic ranges?
1. low range? for what?
2. medium range? for what?
3. high range? for what?
A

Aspirin: Doses
• 3 therapeutic ranges
• Low range, 2400 mg/day – anti-inflammatory

59
Q

Acetaminophen

  1. what is it?
  2. where does it work? on what?
  3. doses?
  4. uses?
  5. used for the same indications as what dose of asa (high, med, low)?
  6. good for what patient population with viruses?
  7. how well absorbed po
  8. metabolized where?
  9. T-1/2 time in normal hepatic?
A

Acetaminophen
1• Analgesic with weak anti-inflammatory properties (minimal COX inhibition in peripheral tissues)
2• Exact MOA is unclear but it more effectively inhibits prostaglandin synthesis in CNS (greater central effect!)
3• Useful as analgesic and antipyretic
4• Dose is 325-650 mg Q 4-6 hours
5• Useful for same indications as intermediate dosed aspirin
6• Good aspirin replacement/substitute for kids with viral infections
7• Well absorbed PO
8• Metabolized in the liver
9• T1/2 2-3 hours in normal hepatic function

60
Q

Acetaminophen: Toxicity

  1. what is affected?
  2. what are s/s?
  3. antidote?
  4. is it renal toxic? how?
  5. does it cause end stage renal disease?
  6. be cautious of what other drugs?
A

Acetaminophen: Toxicity
• Very few side effects in therapeutic ranges
• Severe hepatotoxin in patients with significant liver impairment, OD or patients who regularly take >/= 3 ETOH drinks/day
• Occurs when substrates for phase 2 conjugation are absent, resulting in phase 1 oxidation creating cytotoxic substances
• Symptoms include, jaundice, bleeding disorders,
• Antidote is acetylcysteine (Mucomyst, also used for COPD pts to decrease secretions) to minimize hepatic damage
• Mechanism of renal toxicity differs from other NSAIDs which cause inhibited prostaglandin resulting in medullary ischemia
• Metabolites concentrate in renal papillae and is nephrotoxic
• Thought to account for a significant amount of ESRD
• Certain genetic deficiencies can result in other toxic manifestations such as methemoglobinemia and hemolytic anemia
• Beware of combination drugs such as Darvocet or Vicodin for exceeding therapeutic ranges

61
Q

Toradol (Ketorolac)
1. how good of an analgesic? how good of an antinflammatory?
2. why can/should you only give so much toradol?
3. what is it good for periopertively? what is 30 mg = to?
4. what are concerns?
5. what are concerns with labor and newborn?
6. does it affect MAC?
7. what is po potency?
8 not for what kind of anesthetic use?

A

Ketorolac- Toradol
1• Excellent analgesic, Moderate anti-inflammatory effect
2• Ceiling effects (like all NSAIDs)
3• Advantage as perioperative analgesic lies mainly in reduced opiate side effects; 30mg is said to = 9mg of MSO4
4• Renal concerns exist!
– May cause GI ulceration/bleed, incidence more frequent than aspirin
– Platelet inhibition is a concern, often avoided as premed
5• Contraindicated during L&D due to adverse effect on fetal circulation and inhibition of contractions (prostaglandins)
–Present in breast milk
6• No effect on MAC
7• Less potent PO, 10-20mg = 2 Tylenol #3, (600mg/codeine 60 mg)- but still pretty good!
8•Not for epidural or intrathecal use due to alcohol in preparation

62
Q

toradol:

  1. onset?
  2. peak onset?
  3. duration?
  4. dosing (discontinue after ___days?)
    - -single dose?
    - -multiple doses? daily max?
    - -cut dose by ___ in what patients? or _____?
A

1• Onset: < 1 minute IV, <10 IM
2• Peak onset: 1-3 hours, IV/IM
3• DOA: 3-7 hours, IV/IM
4• Dosing: (Dc after 5 days max)
– Single dose 30 mg (0.5 mg/kg) IV, 60 mg IM
– Multiple, 30mg IV/IM Q 6h max 120mg/day
– Cut dose in half in elderly and decreased renal function ( if even used at all)

63
Q

Propionic Acid Derivatives:

  1. name them?
  2. what are conserns and s/e?
  3. what binding is of concern?
A

Propionic Acid Derivatives
1• Ibuprofen, Naproxen, Ketoprofen (Orudis)
2• Classic NSAID concerns and effects
3• Some are highly bound to proteins and may cause drug interactions (think coumadin)
• Be aware of the potential for side effects as these are very commonly taken OTC drugs!

c. pharm exam 3 (w13) (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions